A system of practical medicine. By American authors. Vol. 5

by Unknown

ANÆMIA AND HYPERÆMIA OF THE BRAIN AND SPINAL CORD.

BY E. C. SPITZKA, M.D.

---

Cerebral Hyperæmia.

Up to within a few years it was a favorite mode of explaining the results of the administration of certain narcotic and stimulant drugs, and certain of the active symptoms of mental derangement, to attribute them to an increased blood-supply of the nerve-centres. This view seemed to harmonize so thoroughly with the physiological dictum that functional activity depends on the supply of oxygenated blood that the first attempts at questioning it were treated as heresies. To-day, however, few authorities can be found to adhere unreservedly to this once-popular and easy explanation. The drift of physiological and medical opinion is in the direction of regarding some subtle molecular and dynamic state of the nerve-elements as the essential factor in intoxications as well as in maniacal and other forms of insane excitement: if they be complicated by active or passive congestions, this is probably a secondary occurrence of modifying but not of intrinsic determining power. While this change in our views is the natural result of progress in experimental pharmacology and pathology, it does not justify the extreme assertion that there is no disorder of the brain functions deserving the name of congestion and hyperæmia. This assertion seems to have been provoked by the careless manner in which these terms have been employed to designate conditions which are in reality the most different in nature that can be well conceived. No one familiar with the extent to which the term “congestion of the base of the brain” has been abused in this country will marvel that the reaction provoked by it has overstepped the boundaries of cautious criticism. That there are physiological hyperæmias of the brain is now universally admitted; the most recent experimental observations, indeed, conform most closely to the claims of the older investigators. It naturally follows that pathological hyperæmias are both possible and probable, and even if the observations in the dead-house do not strongly sustain the existence of pathological hyperæmias and congestions independently of gross disease, clinical analysis and the gratifying results of appropriate treatment justify us in retaining these designations in our nomenclature with the limitation here implied.

One great difficulty in determining the precise nature of the disorders which the physician is called upon to treat on the theory of hyperæmia lies in the number of factors which may contribute to or modify its development. If, for example, the action of the heart be increased through hypertrophy, the result to the cerebral circulation will obviously be different in a plethoric and in an anæmic person; it will be also very much different in the event of the stimulation of the centres which contract the calibre of the cerebral blood-vessels from what it would be if there were a state of vascular relaxation. Should the cardiac hypertrophy be associated with renal disease, other disturbing elements may be introduced, such as arterio-fibrosis, or the presence in the blood of certain toxic substances having direct effects of their own on the nerve-elements. The picture may be still more complicated by variations in the intracranial pressure. It is impossible to prove, either by direct or indirect evidence, that there is such a pathological state as a simple cerebral hyperæmia; indeed, there is one fact which militates strongly against, if it be not fatal to, such an assumption. Were a physiological hyperæmia to become intensified to a pathological degree, we should have corresponding clinical phenomena. In other words, the culmination of the morbid process should be preceded by an exaggerated physiological excitation similar to that observed with intoxications. But this is rarely the case, and we accordingly find that the more cautious writers, like Nothnagel,¹ do not commit themselves to the view that the results of mental overstrain² are to be classed as simple cerebral hyperæmia. Similar restrictions are to be made regarding the established congestive states, such as those following sunstroke. It has been usually supposed that insolation directly produces cerebral hyperæmia, even to the degree of engorgement, and that the after symptoms in persons who recover are due to the non-return of the meningeal and cerebral blood-vessels to their normal calibre, and to other more remote results of vascular stasis. The latter half of this proposition is in part correct; the former is contradicted by numerous pathological observations. Thus, Arndt,³ who had the opportunity of studying over one hundred cases occurring in the course of a forced march of a division of infantry from Berlin to Pankow, many of which terminated fatally, found almost uniformly a pale brain, with peculiar color-changes, denoting rather structural than circulatory trouble.⁴ The whole list of causes of what is commonly designated cerebral hyperæmia, congestion, and engorgement may be gone through with and similar modifying statements be found to apply to them. The nearest approach to an ideal cerebral congestion is that found with acute alcoholic intoxication. This is at first accompanied by cerebral hyperæmia, which, with the comatose climax, becomes an engorgement; accordingly, many of the results of acute alcoholic intoxication are attributed to the circulatory condition alone. The congestive troubles due to alcoholism which come to the special ken of the physician, however, are those found with the chronic form, and here a more complex pathological condition is found to underlie it; the organization of the brain is altered, the vascular channels more or less diseased, and the vaso-motor mechanism continuously deranged. This disorder, as well as the apoplectiform states attributed to vascular stasis, and the active and passive hyperæmias associated with tumors, meningitic and other gross diseases of the brain, as well as with the status epilepticus, are usually included in the discussion of cerebral congestion, and serve to swell up the chapters devoted to it. They will be found discussed in more appropriate situations in this volume. In this place it is proposed to consider only those congestive states which present themselves to the physician, independently of conditions which, if associated, preponderate in clinical and therapeutic importance.⁵

¹ Ziemssen's Cyclopædia, “Nervous System,” i. p. 39, 2d German ed.

² It has repeatedly happened during the past decade that young persons competing for admission to higher institutions of learning in New York City through the channel of a competitive examination died with symptoms of cerebral irritation; the death certificates in several such cases assigned meningitis or cerebral congestion as the cause of death, and attributed the disorder to mental overstrain. It is not so much the intellectual effort that has proved hurtful to the pupils as the emotional excitement attending on all competitive work, the dread of failure, the fear of humiliation, and anxiety developed by the evident futility of the cramming process. Some years ago I recorded the results of some inquiries on this head in the following words: “The mental-hygiene sensationalists, who periodically enlighten the public through the columns of the press whenever an opportune moment for a crusade against our schools and colleges seems to have arrived, are evidently unaware of the existence of such a disease as delirium grave, and ignorant of the fact that the disorder which they attribute to excessive study is in truth due to a generally vitiated mental and physical state, perhaps inherited from a feeble ancestry. Our school system is responsible for a good deal of mischief, but not for meningitis” (Insanity, its Classification, Diagnosis, and Treatment). Since then I had an opportunity of obtaining an excellent description of such a case which had been attributed to the combined effects of malaria and educational overstrain, presenting opisthotonos, fulminating onset, and an eruption!

³ Virchow's Archiv, lxiv.

⁴ The observations of Gärntner (Medicinische Jahrbucher, 1884, 1) harmonize with this. He found that radiant heat contracts the blood-vessels of the frog's mesentery.

⁵ The same applies to conditions which are discussed under this head in textbooks, although they have either only a medico-legal bearing or are inconstant factors, such as the injection of the brain in death from strangulation. I need but instance the vascular condition of brains of criminals executed by hanging. In the case of one where the strangulation had been slow I found an engorgement of all the vessels and arachnoidal as well as endymal hemorrhages; in a second, where the criminal had been carried half fainting to the drop, and death ensued quickly and without signs of distress, the brain was decidedly anæmic.

It has been also considered best to omit treating of the collateral hyperæmia of the brain sometimes found with erysipelas of the face and scalp. This I regard as essentially of the same nature as the metastatic meningitis of erysipelas, if it be not in reality a first stage of the latter.

ETIOLOGY.—An individual predisposition to cerebral congestion was one of the unquestioned facts of the older medical writers. It undoubtedly exists, and to-day we attribute it to inherited vascular conditions either affecting the calibre and coats of the blood-vessels or the vigor of the vaso-motor apparatus. I have remarked the transmission of that weakness of the latter which underlies the congestive phenomena of later life much more frequently in the female than in the male sex.

It has been claimed that external refrigeration produces hyperæmia of the brain, as of other internal organs, and that this accounts for the greater frequency of the disorder in cold weather. Niemeyer indeed speaks of persons who, suffering from this condition, appear and act in such a way as to convince the laity that they are intoxicated; and Andral, Falret, and Hammond note the occurrence of a much larger number of cases in the winter than in the summer months. I apprehend that the condition described by Niemeyer must be extremely uncommon, both from individual experience and the rarity of its mention as an independently observed fact. With regard to the alleged greater frequency of the disorder in winter, it must be remembered that all the three observers cited include in their computation a number of cases in which congestion was a collateral feature; they did not limit themselves to the disorder as spoken of here. Certainly, the physician will see few if any persons who consult him because of the hyperæmia-producing effects of a cold day.

The suppression of habitual discharges, of the hemorrhoidal flux, and the cessation of menstruation are associated in many instances with the more formidable grades of cerebral hyperæmia. Many phenomena of so-called climacteric insanity depend on congestive states. The sudden closure of an old ulcer or the removal of hemorrhoids in advanced life has in some well-established instances provoked alarming seizures not unlike those noted with paretic dementia. The chain of proof establishing the direct influence of physiological and pathological discharges on the vascular controlling apparatus of the brain is most complete. Not alone cumulative clinical observation, but the occasional happy result of therapeutical procedure based on this supposed interdependence, support it. Thus, the congestive cerebral state is recovered from when the menstrual or hemorrhoidal flow is re-established, or an issue is formed in the nape of the neck, or an old ulcer is allowed to reopen.⁶

⁶ The treatment of paretic dementia, particularly of the congestive type, is also based on this relation. The irritating antimonial ointment and issues in the nape of the neck, etc. have been lauded by older observers, and in two of my own cases had the best results—in one, indeed, with established restitutio ad integrum of now nearly two years' duration. I am inclined to suppose that its abandonment is due to an improper selection of cases; in the ordinary premature senility and syphilitic types such treatment is altogether ineffective. It is applicable to but a minority of cases at best, and to them only at an early period. It is probably to a similar form of congestion that Bouchut refers when (“Les Nèvroses congestives de l'Encéphale,” Gazette des Hôpitaux, 1869) he speaks of a cerebral hyperæmia developing under the mask of a meningitis—an expression that may be allowed if understood in the same sense as the comparison between hydrocephaloid and hydrocephalus.

The origin of most cases that are brought to the physician's attention is more or less complicated. A business-man, lawyer, or student suffering from worry incident to his profession, living so irregularly as to provoke gastric disturbances, becomes afflicted with insomnia, and in addition is also constipated. Straining at stool, he finds a dull, heavy sensation affecting the upper part of his head; attempting to resume his work, this is aggravated, and after a series of temporary remissions the condition to be later described becomes continuous. In such a case the insomnia, usually due to neural irritability, if not aggravated by an existing dyspepsia, leads to such a one, and a circulus vitiosus familiar to all physicians is established. Each of the factors concerned involves strain of the cerebral vaso-motor apparatus, but none more so than the insomnia. It is not so much the intensity of the strain as its long duration and the exhaustion of the centre which in sleep is supposed to be at comparative rest. This rest is not obtained, and, in conformity to the laws of neural exhaustion, that centre becomes morbidly irritable. Now, gastric irritation is competent to produce a reflex influence on even the healthy cerebral organ; to do so it must be a severe one; but with the class of persons alluded to the slightest indiscretion in food or drink is sufficient to set up reflex vertigo or headache. The current theory regarding these symptoms is that they are due to stimulation of the vaso-constrictors and ensuing cerebral anæmia; but the subjects before us will usually be found to flush up instead of becoming pale, as in simple vertigo a stomacho læso, or if there be initial paleness, there is a secondary flush, as if the tired arterial muscle had become exhausted by the effort at obeying the reflex stimulus. In addition, a profuse perspiration sometimes breaks out on the upper part of the body.

The influence of traumatic causes and insolation in producing a tendency to repeated and severe cerebral congestion is recognized, particularly among alienists. It is supposed that an abnormal irritability of the vaso-motor apparatus is provoked by these causes. Abundant evidences are sometimes found in the brains of such persons of an altered state of nutrition of the brain and its membranes, and which point in the direction of congestion.

In the conditions thus far alluded to it can be fairly assumed that the determination of blood to the cerebral blood-vessels is more or less active. Passive congestion due to impeded return circulation is of secondary interest, as the primary disease, be it a pertussis or a laryngeal, cardiac, pulmonary, or surgical condition, will constitute the main object of recognition and management. Certain quasi-physiological acts, as coughing, hurried breathing, holding the breath while straining at stool, and placing the head in a dependent position while acting in the direction of passive hyperæmia, are to be considered in connection with the active forms of congestion which they may momentarily aggravate.

MORBID ANATOMY.—Owing to the non-fatality of the commoner forms of cerebral hyperæmia, no pathological observations of them are at our disposal, nor can we assume from analogy that the appearances would be well marked if they could be made. What little knowledge we have is derived from a study of more serious conditions of which cerebral hyperæmia is an initial, collateral, or episodial feature.

In pronounced cerebral hyperæmia the entire brain is, as it were, tumefied, so that the dura appears tensely stretched over its surface and the gyri are flattened; both the meningeal vessels proper and those of the pia are injected. According as the hyperæmia is active or passive the color of this injection varies, being of a brighter red in the former, of a purple or bluish color in the latter case. The purest instances of active cerebral hyperæmia which I have seen were found in patients dying in the apoplectiform phases of paretic dementia (progressive paralysis of the insane). Here the cortex on section exhibited a beautiful rosy tint, which was distributed in darker and lighter strata in correspondence with the distributional areas of the short and the long cortical arteries; there were numerous puncta vasculosa both in the cortex and in the white substance, and in some instances the arachnoid or the ventricular fluid was tinged with blood, albeit no vascular rupture could be discovered. The red blood-corpuscles undoubtedly escape by diapedesis from the surface as well as the endymal vessels; the same thing occurs in the intracerebral blood-vessels, whose adventitial spaces are often crowded with accumulations of red blood-discs, while groups or single ones are found scattered in the surrounding parenchyma, and even in the periganglionic spaces. Occasionally accumulations of pigment found near the vascular channels remain to attest the former existence of other hyperæmias, and indeed slight accumulations of this kind are found in the brains of most persons who have reached adult life. These are to be regarded as remnants of the physiological hyperæmias to which all active individuals are subject. It is only when the accumulations become considerable and numerous, as in the chronic insane, or are associated with those changes in the blood-vessels which are discussed in the articles on thrombotic and hemorrhagic cerebral disease, that they can be regarded as indications of a pathological condition.

Acute simple meningitis is ushered in by cerebral hyperæmia of the active form. This is not alone demonstrated by the early symptoms of this disease, but also by the fact, which I have observed in two cases, that where this form of meningitis originates on one side, as from extension of the middle-ear trouble, the opposite cerebral hemisphere exhibited intense congestion of the ideal type.

In that serious form of mental disease known variously as grave or acute delirium and typhomania (Luther Bell) a form of cerebral hyperæmia is observed which in its intensity approximates inflammatory congestion. The surface of the brain appears marbled and mottled; blood seems to exude from the gyri after the pia is removed; the cortical lamination is invisible, owing to the hyperæmic discoloration of the gray substance; and the parenchymatous elements themselves appear to be in a state of cloudy swelling. In one case I have observed transudation of a hyaline proteinaceous substance and an exudation of fibrin around the larger arterioles. In some cases of typhus fever a less intense but similar congestive hyperæmia is found. The hyperæmias of paretic dementia, of acute delirium, and of typhus fever agree in this one feature: that all districts of the brain, from the cortex and white substance of the cerebral hemispheres to the medulla oblongata, are involved nearly to the same degree. In the hyperæmia of simple meningitis of the convexity it is chiefly confined to the pia mater and the most superficial cortical strata.

Congestion of the brain from stagnation of the venous return circulation should not be confounded with active hyperæmia. With this condition, which may be due to thrombosis of the sinuses, morbid growths near the jugular foramen or in the neck around the internal jugular veins, or, finally, to certain cardiac and pulmonary disorders, there is rather a lesser than a greater amount of blood sent to the brain; and it is not infrequently found that while the surface of the brain appears congested, owing to the prominence of the cerebral veins, the deeper parts are quite anæmic; and if the injection be general, it will be found that the blood, whether in arteries or veins, has the venous character. An excellent example of this form of congestion is afforded by persons dying in the status epilepticus. In their brains the venous channels stand out, filled to their extreme capacity with blood almost black in color; and in prepared sections, particularly such as are taken from the pons and medulla oblongata, a beautiful natural injection of the vessels is found. But that rosy color which is so characteristic of active hyperæmia is absent, the tissues appearing purplish, bluish, or chocolate-colored.

SYMPTOMATOLOGY.—There are few symptoms attributable to the nervous system which have not been enumerated among the characteristics or the occasional manifestations of cerebral hyperæmia. Thus, Hammond not only follows Andral in enumerating apoplectic, convulsive, comatose, and maniacal symptoms as acute manifestations of active cerebral congestion, but assures us that aphasia may occur under the same circumstances. In the course of his work on the subject, “an absolute want of power to get correct ideas of even simple matters,” confusion of ideas, weakening of the judgment, vacillation of purpose, diminished logical power, illusions and hallucinations of every sense, delusions, morbid apprehension of impending evil, imperative, suicidal, and other impulses, suspicion, hypochondriasis, furious delirium, and the use of profane and obscene language, are enumerated among the characteristic or prominent symptoms of various forms and cases of cerebral hyperæmia.⁷ Not one but several of the recognized forms of insanity have yielded a fair quota of their symptoms to this long array. Among somatic signs he in like manner names neuralgic pains, numbness, spasms, paralysis, false impotence, hyperæmia of the tympanum, choked disc, abolition or perversion of the sense of smell, taste, and sight, fibrillary or fascicular twitches, various states of the urinary excretions, diplopia, and monoplegias. It is here equally evident that the initial symptoms of a considerable number of organic and clearly defined affections have been included. It is on account of the confusion engendered by this wide interpretation of the meaning of the term congestion of the brain that I have determined to limit the term as previously indicated, and to consider only the active form here.

⁷ A Treatise on the Diseases of the Nervous System, 7th ed., pp. 1-53. The natural inference following a perusal of this chapter, as well as the monographs to which their author refers, is that he has gathered together all states in which cerebral hyperæmia was an associated factor, as well as those in which he appears to assume its existence on theoretical grounds, and designated them as cerebral congestion. In some instances he uses the terms hypochondria and cerebral hyperæmia interchangeably (p. 50, loc. cit.).

A feeling of head-pressure, associated with a more or less severe dull pain, aggravated by mental exertion, by stooping down, by straining at stool, or when out of breath, and accompanied by a subjective sense of mental dulness, is the most constant feature of the ordinary cases. There is usually a vertiginous sensation, and an irritability of the eye and ear not unlike that described in the article on Cerebral Anæmia. Sleep is at first disturbed by vivid and sometimes frightful dreams; later, it becomes interrupted, and ultimately complete insomnia may develop. The action of the heart is accelerated and exaggerated in some cases; in that event increased pulsation of the carotids, flushing of the face, injection of the conjunctiva, and a subjective sense of heat in the head and face are experienced. Hammond, in accord with Hasse and Krishaber, believes that febrile symptoms may develop under these circumstances; most authorities, however, deny this for the uncomplicated form. I have never found an objective rise of the general temperature.

Such a condition as that described is usually slowly produced, several weeks, or even months, being occupied in its development. At first the unpleasant symptoms occur only at certain hours of the day, with temporary exacerbations and remissions. It may be arrested with comparative ease at any time; if neglected, the mental faculties become affected, not in the grave sense in which Hammond and the older authors describe it, so as to carry the patient into actual dementia or delusional insanity, but rather in the way of diminished working-power. It is more difficult to fix attention, to recollect words, names, and figures, or to keep up a protracted mental effort, than in health, but the formal judgment does not suffer. I have known patients to be in this condition for many months, and several for more than one year, without any grave deterioration. It is true that in the prodromal periods of some forms of insanity, such as acute mania, there is a condition very similar to that of these patients; and this has led to regarding mania as a possible phase of cerebral hyperæmia. But the very fact that, typically, mania is preceded by such a stage—which is always of brief duration—that maniacal excitement is a constant and unavoidable consequence upon it, while, as far as known, the condition here described may last for years without leading to a true psychosis, should prevent one regarding the two conditions as identical, however similar they may be for the time being.

In sufferers from cerebral hyperæmia who pass into the chronic state of this disorder the disturbance of sleep and of the digestive organs becomes very prominent, and continually reinforces the acting causes of the disorder. In a large number of cases the head-sensations become more or less localized; that is, while the general feeling of pressure or dull ache may continue, a special area, which can be covered by the palm of one hand, either in the middle part or to one side—usually the left—of that part of the vertex, is the seat of a more severe pain, complained of as a hot pressure. The patients frequently claim that the temperature is higher at this spot, and, contrary to what might be anticipated on a priori grounds, the statement will be confirmed, not alone by the coarse method of using the hand, but by the surface thermometer. The locality where this occasional rise of temperature and the more common sense of pressure are experienced corresponds to that part of the longitudinal sinus where the largest cerebral veins enter. It is a noteworthy fact that nearly all the important admunctories of this sinus empty into it within the short space of two inches at this point.

Not all sufferers from cerebral hyperæmia give a history of a gradual development of their symptoms. A few date their trouble from some single intellectual, physical, or emotional strain. In one case, complicated by marked evidences of cerebro-spinal exhaustion, the patient, a lady, had during an illness of her husband, being deserted by her servants, and the water-supply having been cut off, carried all the water required for the invalid and domestic as well as sanitary purposes up three flights of stairs for two unusually hot days in July. In two others, strikingly similar in many details of their cases, both being cornet-players, both attributing their illness to an extra call upon their instrument, it was brought on in the older patient within a few hours after playing on a hot day at the State Camp at Peekskill, and in the second at Narragansett Pier as he left the sultry concert-room and became exposed to a draught. In both these cases, as in a large number since examined, some stomach trouble could be positively determined to have antedated these symptoms. I mention this because it is only in such cases that I have found the nausea or vomiting which some writers regard as an occasional occurrence of, and due to, the lighter form of cerebral hyperæmia.

There are no ophthalmoscopic evidences of cerebral hyperæmia of this form. I have never found the optic disc presenting variations in tint beyond those found within normal limits, except in a case of saturnine encephalopathy with predominant signs of cerebral congestion. I believe that the statement of Hammond⁸ as to the existence of choked disc in cerebral hyperæmia is generally regarded as due to the interpretation of organic diseases as congestive states. It is not confirmed by authorities.

⁸ Loc. cit., p. 41, lines 29-36.

I have never found the tympanic membrane hyperæmic independently of ear disease, even when tinnitus was marked. It is claimed to exist by Hammond, and he adduces as analogous the observation of Roosa that quinine produces an injection around the handle of the malleus.⁹

⁹ It certainly is not necessary to look to the injection of the tympanum as an explanation for the tinnitus of cerebral hyperæmia, based on such an analogy. The tinnitus of cinchonism is more central in location, being producible in persons who have pathological or no tympanic membranes, just as the tinnitus of cerebral hyperæmia occurs indifferently under like circumstances.

The congestive states which follow traumatism and insolation are properly considered in connection with the traumatic neuroses and certain forms of insanity. But there are some milder cases in which the symptoms remain within such compass as is comprised in this section. The patient, after a fall or a blow on the head, suffers from insomnia, has a sensation of fulness and ache in the head, complains of a pulsating feeling in the occipital region and an inability to concentrate his thoughts on subjects which previously were parts of his routine. Under appropriate treatment recovery ensues, but there remains behind an intolerance of alcoholic beverages, and at times the patient experiences momentary fits of abstraction, which may be regarded as mild analogies of the more serious episodes of the full-blown traumatic neurosis. Thus, he may be walking along the street and suddenly lose his train of thought for an instant, to regain it on observing that he has inadvertently made a misstep. Or in the midst of an address a previously fluent orator in attempting to find a certain by-law in the rules of a society is unable to recollect which he was in search of, and is compelled to take his seat with a rambling apology. But for the fact that similar sequelæ are noted in cerebral hyperæmia from other causes, it would be questionable whether it be proper to attribute them to the congestive element engendered by the traumatic influence. They are usually noted when the hyperæmic phenomena proper have become latent or disappear, and, with other symptoms customarily treated of as mere results of circulatory trouble, may be regarded as signs of neural exhaustion or inadequacy rather than of insufficient ensanguination.

A more serious form of cerebral hyperæmia occurs in females in conjunction with the climacteric period, and in both sexes in consequences of the suppression of any habitual discharge in advanced, and exceptionally in middle and juvenile, life. The advent of the symptoms is rapid, a few hours or days sufficing for the development of the attack. The face is flushed, the carotids throb violently, the general cutaneous surface is congested, and the patient is incoherently talkative. The one side, usually the right, is heavy and tremulous, the fingers are devoid of their usual skill, and the speech is more or less thick. The sleep is disturbed or replaced by a stuporous condition, whose similitude to an apoplectiform seizure is sometimes heightened by stertorous breathing. After one or several days the patient emerges from this condition by degrees or suddenly with complete restitutio ad integrum. But the attack may recur, and ultimately it is noted in the event of repeated attacks that the return to the normal state is slower and less complete: the disorder then undergoes a transition into the congestive type of paretic dementia described in another portion of this volume.

DIFFERENTIAL DIAGNOSIS.—In some of its clinical aspects cerebral hyperæmia closely resembles cerebral anæmia. This is not surprising when we bear in mind that both constitute nutritive disturbances of the same organ, and that, notwithstanding the apparent difference in the surface injection of an anæmic and a hyperæmic brain, the state of affairs in the ultimate capillary districts may be much more alike than might be anticipated on theoretical grounds. In congestion we have wider vessels, and perhaps, though not necessarily, a better quality of blood; but at the same time the intracranial pressure may be such that the venous emunctories can labor but slowly: the result will be that although there is more blood in the brain, the lessened rate of flow places the nerve-elements under nearly the same nutritive disadvantage that they are placed under with the narrower and vitiated but more rapid blood-column of ordinary anæmia.¹⁰ It is particularly the symptoms dependent on those nerve-centres and tracts which are, so to speak, dynamically sensitive, which resemble each other so much that an intrinsic difference—both being placed side by side—is not always determinable. This is true of the aural and optic symptoms. Tinnitus, photophobia, scotomata, and blurring or darkening of the visual field occur in both, and in about the same varieties. In my experience the acuteness of hearing is more apt to be interfered with by the subjective sounds with hyperæmic than with anæmic tinnitus. The scotomata of hyperæmia are more distinct and coarser than those of anæmia; darkening of the visual field is more apt to occur with sudden rising in anæmia, while in hyperæmia it is provoked by coughing, straining at stool, or other cause operating directly or indirectly on the return circulation. It may be stated, as a general rule, that if any of these symptoms are aggravated on lying down or stooping, they are due to hyperæmia; while if the same procedures are resorted to in anæmia, amelioration ensues. But in many chronic cases these symptoms seem to continue as indications of a permanently altered activity of the nerve-elements themselves; that is, as a sort of pathological habit. In that case the position test may not be decisive. In one respect there is a decided difference between the anæmic and hyperæmic forms; there is never amaurosis in the latter, while it is approached, and occasionally fully developed, in the former. Much more importance attaches to the differentiation of tinnitus due to nutritive brain disorders and that due to aural disease. As a rule, the tinnitus from cerebral hyperæmia is symmetrical; if unilateral, it is of short duration. The procedure of Valsalva¹¹ aggravates the tinnitus of hyperæmia, and relieves that which is due to the commoner forms of ear disease; the former is aggravated and the latter relieved by noise.

¹⁰ It is also admitted that the blood stagnating in the larger veins and accumulating in the arteries, the limits of compressibility of the other cerebral contents being passed, the capillaries will suffer, so that with injected and turgescent arterioles and venules there may be capillary anæmia.

¹¹ I would caution against Politzer's method in cases of ear disease coexisting with cerebral congestion. In a patient now under my treatment each session at the aurist's was followed by a distinct exacerbation of the cerebral symptoms.

In the table on p. 773 I have attempted to formulate the principal differential relations of the protracted forms of cerebral anæmia and hyperæmia.

There are a number of so-called functional nervous states which, aside from the fact that they are unwarrantably confounded with cerebral congestion, do not require mention in a differential relation. Such are the masturbatory neurosis, certain hysterical states, and the asthenia resulting from nervous shock and overwork. These states have found a provisional resting-place under the comprehensive and non-committing title of neurasthenia or nervous exhaustion—a term which includes conditions fully recognized by Robert Whytt and Isenflamm in the last century.

Symptomatic State.	In Cerebral Anæmia.	In Cerebral Hyperæmia.
Pupils.	Usually dilated and mobile.	Usually small or medium.
Respiration.	Often interrupted by sighing or by a deep breath, even when at rest.	Normal.
Headache.	Either sharp and agonizing, and then in a limited area, or a general dull ache, intensified in the temples and over or behind the eyes.	If localized, accompanied by a subjective and objective (always?) feeling of heat; if general, is compared to a bursting or steady pressure.
Activity.	There is lassitude.	There is indisposition to exertion, yet patient is restless.
Temperament.	Lethargic, with exceptions.	Choleric, with exceptions.
Intellect.	Inability to exert.	Rather confusion than inability of.
Sleep.	Insomnia, interrupted by trance-like conditions, in which the patient is comparatively comfortable. Dreams often pleasant.	Insomnia, with great restlessness, variegated by unpleasant and confused dreams.
Influence of upright position of body.	Aggravates all the symptoms.	Either without influence or beneficial.
Influence of recumbent position of body and dependent position of head.	Amelioration.	Aggravation.
Influence of acts involving deep inspiration, such as blowing, straining at stool, sneezing, etc.	If any, a sharp headache may ensue, but the other symptoms are not aggravated.	Aggravated.

TREATMENT.—Ergot of rye with its preparations may be regarded as the cardinal drug in cerebral hyperæmia. There are few drugs in the domain of neurological therapeutics which are so directly antithetical to the pathological state as this one. There is scarcely a case of cerebral hyperæmia that is brought to the physician's attention but may be regarded as being in part due to an over-distension of the cerebral vascular tubes. This is directly overcome by ergot, and the quantity which such patients will sometimes bear without showing signs of ergotism is something remarkable, in notable contrast with the subjects of cerebral anæmia, who are usually very sensitive to it. About three grains of Bonjean's ergotin may be regarded as a safe trial-dose for an adult, and unless a distinct effect is produced within two or three days this dose may be raised to six grains twice or three times within twenty-four hours. It is not advisable to combine strychnia with the ergotin, as is often done; the effect of that alkaloid is to increase the psychical and sensorial irritability of the patient. Chloral hydrate or bromide, or both in combination, is as useful an adjuvant here as it would be hurtful in cerebral anæmia.

It is not usually necessary to employ special hypnotics in cerebral congestion. The same drug whose beneficial effect is so potently marked during the daytime that tinnitus, cerebral pressure, and subjective drowsiness will disappear before it, if not as rapidly, more enduringly, than the symptoms of cerebral anæmia disappear before nitrate of amyl, will also overcome the insomnia in the majority of cases. Where it fails, warm pediluvia or sitz-baths will prove more efficient than the majority of hypnotics. Their use, at all events, involves no hurtful effect on a—possible already—disordered stomach, and their certainty of action is much more even. Their temperature should be about 40-42° Centigrade, and the immersion continue from fifteen to twenty-five minutes.¹²

¹² A number of experiments, the most recent of which were by Musso and Bergesio (Rivista sperimentale di Freniatria e di Medicina legale, 1885, xi. p. 124), have shown that in such baths the cerebral pulsations become less excursive and that the volume of the brain decreases. The same applies to general warm baths.

In those cases where the subject sensations accompanying hyperæmia, active or passive, are intensified in the posterior segment of the head or the nuchal region, leeches at the mastoid process, or cupping, wet or dry according to the severity of the symptoms, will often give immediate relief. Burning with the actual cautery, or, what is equivalent and a much neater application, the heated glass rod, has an equally happy effect in that class of cases where throbbing and pain are intensified low down. It should be done as near the spot indicated by the patient's complaints as possible.¹³

¹³ In a case of gliomatous hypertrophy of the pons oblongata transition marked by the development of numerous tortuous and enlarged blood-vessels the episodes of the disease were found to be of the congestive type, and yielded to no other treatment than that with the cautery.

The diet of patients who are suffering from or subject to cerebral hyperæmia should not be stimulating nor difficult of digestion. It is much more important to avoid distension or overstrain of the stomach than to reduce the nutritive value of the food in the majority of cases, for true plethora is much less common than is supposed. The bowels should be so regulated that the patient have at least one, and that an easy, movement a day. The saline cathartics, particularly the Carlsbad salt, are to be used to effect this if necessary. The clothing around the neck should be free and not compress the parts.

In those severe forms of cerebral congestion attending the climacteric period, or occurring in consequence of the suppression of discharges, and similar causes, the symptoms are often so alarming as to render energetic measures, such as bleeding, immediately necessary. This may be affected by applying leeches to the nose, the temples, or by bleeding at the arm. If due to the suppression of hemorrhoidal discharges or menstruation, the leeches should be applied to the anus and hot sitz-baths taken. In the milder forms a pill composed of aloes, podophyllin, and ox-gall, recommended by Schroeder van der Kolk, will be found effective.

Cerebral Anæmia.

The oft-confirmed observation of Treviranus, that the brain is paler in the sleeping than in the waking state, supplemented as it has been by more elaborate observations, which show that the difference between the intracranial blood-amounts, as estimated in these opposite states, is equivalent to one-twenty-fourth part of the total blood-amount of the body, has been made the basis of much dazzling theory and premature speculation. Hyperæmia of the central nervous apparatus or of certain of its provinces becomes regarded as synonymous with over-activity, and anæmia, general or provincial, as the expression of the opposite functional state. Elaborate directions may be found, even in recent treatises on the subject, how to diagnose, not alone hyperæmia and anæmia of the brain and spinal cord, but also of special lobes of the former and particular columns of the latter. These directions are in most instances based on assumptions which are not supported by direct or tangible evidence, and the consequence is that they have failed to stand the tests of experience, where this gauge is applicable, and necessarily failed to advance in any way either our theoretical or practical knowledge of those states of the brain mechanism which are due to alterations in its nutrition.

Much of the unsatisfactory state of our knowledge on this head is due to the grouping together of the physiological anæmia of sleep and the pathological anæmia with which the physician has to deal. The anæmia of the brain in a sleeping person is probably a secondary factor; it ensues after the person falls asleep, the first step in the latter process being probably an altered dynamic state of the brain which lessens the requirements of that organ for blood. This can be readily demonstrated in the case of infants whose anterior fontanelle has not yet closed. In deep sleep the fontanelle is deeply sunken in, but this sinking in does not occur simultaneously with the child's falling asleep, but shortly thereafter. On the other hand, the fontanelle does not rise simultaneously with the child's awakening, unless it cry, which adds a disturbing factor. There are a number of other facts which show that while a comparison between the sleeping state and cerebral anæmia may be made for the purposes of theoretical discussion, yet there are many important points in which they are at variance. To illustrate this I need but refer to the fact that in deep sleep the pupils are in a state of immobility and pinhole contraction,¹⁴ while in chronic cerebral anæmia of young persons a dilated and mobile pupil is the commoner condition. In acutely-produced cerebral anæmia an initial contraction has been noted, but it is not then persistent.

¹⁴ Inability to counterfeit this feature is one of the most reliable tests of simulation, and served to convince me that in the well-known case of a colored cadet, who was tried by a court-martial on charges involving simulation, the latter was proven. There are persons who can voluntarily contract the pupils, but as they are compelled to innervate all the muscles supplied by the third pair, in so doing they are compelled to converge the optic axes—an act which does not take place in sleep.

One of the main reasons of our imperfect knowledge of the nutritive disorders of the brain is the unsatisfactory state of their post-mortem evidence. Little has been learned in this field, except in those extreme cases where the suddenness and intensity of the circulatory catastrophe were sufficient to prove fatal. Even where all observations made during life justify us in supposing that the amount of blood sent to the brain is small, that the velocity of its current is reduced, and its quantity poor, the autopsy may reveal conditions apparently conflicting with the supposition based on ante-mortem observations. This is amply illustrated by the experience of alienists who have studied the relation between nutritive states of the brain and certain forms of insanity. It is generally held that in so far as the antithetical forms of mental disorder known as anæmia and melancholia can be connected with nutritive disorders, the former is indicative of hyperæmia and the latter of anæmia. A number of facts can be adduced in support of this view, particularly as regards the latter condition. It is found, however, in some examinations made of the brains of patients dying melancholic that the brain is apparently hyperæmic; the length of time elapsing before an autopsy is made, the form of somatic disease with which the patient dies, the position of the body after death,—all these may play a part in the production of cerebral injections which do not correctly indicate the condition of the brain as it existed prior to the moribund period, and when the symptoms of supposed anæmia or hyperæmia could be satisfactorily differentiated.

ETIOLOGY.—The best studied form of cerebral anæmia is that ensuing after extensive hemorrhages or from compression and ligature of either of the common carotid arteries.¹⁵ In the latter case symptoms are produced which are in harmony with the doctrine of localization, and permit us to form a conception of the mode in which a diminution of the cerebral blood-supply influences the functions of the brain. The chief symptoms are noted on the side of the body opposite to that on which the common carotid artery is tied. Thus if the left artery be tied, there is at first felt a tingling or pricking feeling on the right half of the body; this is followed by a warm, sometimes a cold, and ultimately by a numb, feeling. This sensory disturbance may become of what might be called the capsular type—that is, a complete hemianæsthesia; but at first it is distinctly like that which is found with cortical and subcortical disease, being limited to the muscular sense and the intelligent contact-perceptions of objects, the æsthesiometer showing but little or no impairment of the cutaneous space-sense. With the loss of muscular sense the movements become heavy, and later true paresis may appear with perhaps total anæsthesia. Aphasia is sometimes noted in such cases, and, in obedience to the predominant location of the speech-faculty in the left side of the brain, is rarely if ever found¹⁶ when the right common carotid artery is the one ligated.

¹⁵ As the conditions of the cerebral circulation resulting from surgical and other rare causes are not apt to be brought to the physician's attention separately from conditions of more immediate importance, their symptoms are discussed in the etiological portion of this section in order to avoid complicating the semeiological picture of cerebral anæmia of every-day experience. For similar reasons the anomalies of the cerebral circulation of an embolic and thrombotic nature, and those associated with eclampsia and epilepsy, are not mentioned in this connection, as their full discussion properly belongs to other portions of this work.

¹⁶ I am unaware of the record of any case where aphasia occurred with ligature of the right common carotid artery. There is a singular observation by Hagen-Torn of permanent paralysis of the right hypoglossal nerve after such an operation, but the report to which I have access does not state whether this may not have been due to some peripheral involvement of that nerve.

In this series of symptomatic sequelæ it is seen that the functional manifestations of the highest centres are the first to be involved, and this establishes that of all parts of the cerebrum the cortex and subcortical tracts are the more vulnerable to the influence of a deficient blood-supply.¹⁷ As we shall see, it is precisely to the insufficient nutrition of these parts that the more important symptoms of the cerebral anæmia of ordinary practice are attributable.

¹⁷ To this there is an apparent exception: when blindness occurs in consequence of ligature of one carotid artery, it is monocular and limited to the side of the ligation. The visual disturbance of cortical and subcortical disease is bilateral, being of the character known as hemianopsic. The blindness due to tying of the carotid is, however, not due to cerebral, but to retinal, anæmia, and its monocular character does not therefore invalidate the observation in the text. Litten and Hirschberg (Berliner klinische Wochenshrift, 1885, No. 20) found complete bilateral amaurosis in a chlorotic girl of fifteen, and on ophthalmoscopic examination the peripheral origin of the blindness was conclusively proven by the existence of an exquisite choked disc. Both the morbid ophthalmoscopic appearance and the amaurosis disappeared under tonic regimen. It is well to recollect that choked disc may occur in chlorosis, and thus be perhaps erroneously attributed to a coexisting hysteria, as was done in some cases at least by Rosenthal in his textbook.

With bilateral ligature¹⁸ of the primary carotids—and this applies in the main to cerebral anæmia from profuse hemorrhages or sudden changes in the blood-pressure, such as occur in enteric affections, ruptures of aneurisms, in obstetric practice, and after brusque tapping for ascites—the same phenomena noted with unilateral compression are observed on both sides of the body, and usually in slighter intensity. In addition, there is a profound and characteristic disturbance of respiration; a cold sweat breaks out; the senses of sight and hearing become greatly impaired or perverted; the mind becomes clouded, consciousness blurred; complete syncope may ensue, and pass to a fatal termination. In other cases vertigo preponderates or vomiting, and finally convulsions appear. It would seem that the respiratory centre exceeds even the cortex in susceptibility to the evil influence of anæmia. It differs from them in two features: firstly, it appears to require bilateral involvement of the brain for its production; secondly, although the respiratory disturbance precedes that of the higher cerebral functions, it does not become as intense, for at a time when the intellectual functions are abolished, as in anæmic coma and syncope, the respiratory function, however disturbed, is in most cases sufficiently well carried on to bear the organism safely through the crisis. The disturbance is marked by the following characters: The respiration is at first deep and sighing, perhaps frequent; it later becomes slow, and is associated with a subjective sense of oppression; the patient feels as if he could not fill his lungs properly; there is an unsatisfied sensation, as if a deeper breath should be taken, and when, in obedience to this subjective need, a full deep breath is taken, the patient feels as if he had stopped short of completing the act, and remains as unsatisfied as before.¹⁹ Yawning and moaning are often accompaniments of this symptom.²⁰ As we shall see, these signs are often among the chief sources of complaint in the less grave forms of anæmia of every-day experience. In the serious condition before us the Cheyne-Stokes phenomena may follow.

¹⁸ I exclude the observations of Flemming, Hammond, and Corning on carotid compression by external pressure, owing to the difficulty of determining whether or no, and what, other important structures are compressed at the same time.

¹⁹ The occurrence of this functional respiratory trouble is a feature of toxic as well as of anæmic irritation of the respiratory centre; it is accordingly found in cases of profound alcoholic poisoning.

²⁰ It is somewhat difficult to understand why in cases of anæmia induced in both carotid districts the symptoms of anæmia should be marked in the functions of that part of the brain-axis which through the basilar trunk derives its blood from the vertebral arteries. Here the blood-current must necessarily be increased. That the disturbance of breathing, the yawning, and the sighing belong to the group of irritative symptoms due to anæmia is in harmony with the general physiological law which is illustrated in the initial contraction of the pupil, which is found in experimental cerebral anæmia. Observations on anæmia of the brain-axis are too few, and, so far as noted, have been so rapidly fatal that it is not possible to derive from them any facts bearing on the physiological reactions of the respiratory centre to high-graded anæmia. One of the curiosities of medicine appertaining to this subject is the observation recorded in Virchow's Archiv, lxix. p. 93, of the case of a man who had fractured the base of the skull in its posterior fossa, and, the basilar artery becoming caught and pinched in the crack, death occurred rapidly with all the signs of cerebral anæmia, verified by the post-mortem appearances.

Anæmia of the brain may develop at any period of life, not excluding the intra-uterine period. Kundrat and Binswanger regard the deformity of the brain known as porencephaly as the result of an anæmic (non-embolic) necrosis of brain-substance, developed either in the fœtal or the infantile period. The occasional symmetry of the deformity is in favor of this view. That there are other conditions of cerebral malnutrition,²¹ masking themselves in defective development and imperfect isolation of the conducting tracts, and that the consequent differing rate of maturation of these tracts has some relation to the absence or presence of a predisposition to chorea and other disturbances of nervous equilibrium so common at this period of life, I regard as at least probable. But it is at the period of puberty that we encounter the most important discrepancies between the requirements of brain-nutrition and the furnished blood-supply. The disposition to uncomplicated cerebral anæmia is greatest at this period of life and in the female sex. Beneke²² has shown that as the human being grows the arteries, which in children are very large in proportion to the length of the body, get to be relatively smaller and smaller toward the period of puberty—that after this period they widen to again attain a large circumference at old age. There is thus added to the other and more obscure factors which may determine general anæmia at puberty a diminished calibre of the arteries in both sexes. To some extent the disadvantageous influence of (relatively) narrow vascular channels may be overcome by increased cardiac action, and the almost sudden increase in size of the heart about this period is probably the result of the demand made upon its compensatory power. But, as we learn from the same observer that the female heart remains relatively as well as absolutely smaller than that of the male, we can understand why the female should be less able to overcome the pubescent disposition to cerebral (and general) anæmia than the male. Menstruation, which in a certain proportion of girls scarcely maintains the semblance of a physiological process, acting rather as a drain than a functional discharge, is added to the anæmia-producing factors. It is among those who marry in the ensuing condition, who bring forth child after child in rapid succession, perhaps, in addition, flooding considerably at each confinement, that we find the classical symptoms of chronic cerebral anæmia developed.

²¹ I have found in three children under fourteen months of age, who died with symptoms not unlike those of slowly-developed tubercular meningitis, including convulsions, strabismus, temperature disturbance (slight), and terminal coma, without nuchal contracture or pupillary anomalies, a remarkably anæmic brain. The sulci gaped; there were few or no puncta vasculosa; the cortex extremely pale, and the white substance almost bluish-white. On attempting to harden the brain of the youngest of these children, using every precaution and a sufficient number of sets of hardening fluids, including the chromic salts and alcohol, I found that small cavities formed in the cortex, varying from the scarcely visible to two-thirds of a millimeter in diameter. Their existence were demonstrable the day after the death and almost immediate autopsy performed in this case. There had been no antecedent disease in any one of these cases; the children had been lethargic, inactive, and the oldest had made no attempt to walk or talk. There was no morphological or quantitative defect in cerebral or cranial development, and microscopic examination showed that the cavities were not perivascular. In all these cases the patients belonged to the tenement-house population.

²² An excellent abstract of Beneke's original monograph, by N. A. P. Bowditch, will be found in volume i. Transactions of the Massachusetts Medico-Legal Society.

In the male sex the period of adolescence has not the same profound influence in producing cerebral anæmia that it has in females. To some extent, however, habitual self-abuse and early sexual excess of the former produce results similar to those occurring in consequence of perverted physiological processes in the latter. Many of the symptoms presented by the inveterate masturbator are probably due to cerebral anæmia; there are, however, in his case and in that of the early libertine certain vaso-motor complications frequently present which render the clinical picture a mixed one.²³ In addition, abuse of the sexual apparatus has a direct—probably dynamic and impalpable—exhausting effect on the central nervous apparatus.

²³ Kiernan of Chicago has described peculiar trophic disturbances—dermato-neuroses, color-changes of the hair, etc.—in a case of masturbatory mental trouble associated with marked anæmia. The patient whenever he flushed up heard a noise as of a pistol snapped near the mastoid region. In the case of a young man of eighteen who—the pampered son of wealthy parents—became his own master at fifteen, and had at that age indulged in sexual orgies which were continued to an almost incredible extent, it was found that he gradually lost his memory, and on one occasion had a violent epileptiform attack. During his convalescence from the stuporous state which followed it was noted that the patient was quite bright in the morning, but that after he had been up a while he relapsed into a state of apathy, with amnesia, which, decreasing in intensity from week to week, was eventually only noted toward evening, and finally disappeared, the case terminating in complete recovery.

In the vast majority of cases anæmia of the brain is but a part of general anæmia, and all conditions which tend to impoverish the character of the blood and to reduce the rapidity of movement and fulness of the cerebral blood-column are apt to be associated with signs of cerebral malnutrition. As early an observer as Addison noticed the wandering of the mind in pernicious anæmia, in which disorder anæmia and wasting of the brain have been found post-mortem. In two cases of extreme chlorosis I heard the sound known as the cephalic soufflé with great distinctness;²⁴ this sound, when the other morbid conditions that may lead to it can be excluded, indicates a high degree of anæmia. Both patients were somnolent and subject to fainting-spells. In leucocythæmia a rambling delirium is not infrequently noted toward the close of the patient's life, and the habitual sadness and depression of many leukæmic patients is due, as are also certain phases of melancholia, to cerebral malnutrition. In some stages of most, and in all stages of some, forms of renal disease the conditions of cerebral anæmia are present; and it is reasonable to attribute to it some share in the production of the head symptoms of Bright's disease; but here, as in cases of cardiac disease, symptoms due to other influences—uræmia in the former, and insufficient oxygenation of the blood in the latter instance—obscure or conceal those due to the anæmia strictly speaking.

²⁴ When an anæmic murmur at the base of the heart coexists with the cephalic soufflé, the latter may be regarded as an evidence of anæmia; but where the former is absent—that is, when the cephalic soufflé is an isolated, independent symptom—there is reason to suspect the existence of a tumor or some other cause of compression of the carotid artery at or after its entry into the cranium. In one of the cases referred to in the text, pressing on one or the other carotid produced numbness and tingling in the opposite arm, leg, and cheek. Similar observations were made by Tripier (Revue de Médecine, March, 1881), who strenuously maintains the existence of the cephalic soufflé in the adult, against Henry Roger, and in consonance with the observations of Fisher and Whitney. In the last-mentioned case of mine the sound could be heard a distance from the head.

All exhausting diseases, many febrile affections, notably typhoid, starvation from any cause, and exhausting discharges, may produce cerebral anæmia. Under the latter head belong the diarrhœal affections of childhood, which not infrequently lead to an aggravated form of anæmia of the brain known as hydrocephaloid. In addition to the provoking causes of cerebral anæmia there are certain accessory ones: prominent among these is the upright position and sudden rising. The reason of this influence is self-evident, as is also the fact that it is most apt to manifest itself in cases of cardiac enfeeblement. Many a convalescent from an exhausting fever or other disease has on rising from bed fainted; some have fallen dead from cerebral anæmia already existing, but fatally intensified by this sudden change of position. A number of cases are on record by Abercrombie, Forbes Winslow, J. G. Kiernan, and others where persons manifested the symptoms of cerebral anæmia only when in the upright position and even in lying on one side or the other; these are, however, far rarer than is claimed by some later writers.

The purest form of acute cerebral anæmia, aside from that produced by surgical interference with the cerebral circulation or extensive hemorrhages, is that induced by mental influences, such as fright, a disagreeable odor, or a disgusting or harrowing spectacle. Some persons, not suffering from general anæmia or any diseased condition thus far mentioned, on experiencing the emotional influences named will be observed to turn pale, to breathe heavily, and either sink into a chair or fall on the floor partly or entirely unconscious. They are then suffering from a spasm of the cerebral arteries resulting in acute and high-graded cerebral anæmia or syncope. This condition is marked by some of the symptoms previously mentioned as occurring with bilateral ligature of the carotids: thus, the feeling of oppression on the chest, vertigo, heaviness of the limbs, nausea, and vomiting are characteristic; a cold sweat breaks out on the forehead; the visual field becomes darkened; and hearing is rendered difficult by the tinnitus.²⁵ The pulse is small and of low tension, but regular.

²⁵ Most authors claim that the sense of hearing is blunted, as that of vision is. This is so in some, but certainly not in a large number of other cases. I have now under observation a girl whose physical conformation—her neck is very long and her shoulders tapering—and extreme susceptibility combine to favor the occurrence of syncope. She faints in my office whenever an examination is made, even though it be entirely verbal; and after recovering frequently lies down to answer by deputy, as experience has shown her that she is less likely to faint in this position. I have repeatedly satisfied myself from her subsequent statements that she heard what was said, while she appeared to be quite unconscious and “saw everything black or through a cloud.” It is not improbable that the impressions which most writers on the subject convey were derived from the experience of novices in fainting; these, in the alarm and anxiety of their condition, and confused by the tinnitus, might well fail to hear what the bystanders said, particularly as on many such occasions the fainting person is apt to be surrounded by a confused Babel of tongues. While the auditory nerve is as sensitive to the irritative influence of anæmia as any, and there is a case of a boy on record (Abercrombie) who could only hear well when lying down, and was deaf when he stood up, yet the conclusions of other authorities who have studied the subject would lead one to think that there are individual differences in this respect. How often does not the dying person, after feeling for the hands of a relative whom he cannot see, converse with him responsively! And how much need is there not of the humane physician to remember that the sense of hearing is the last intellectual sense to die, lest he speak unguardedly at the bedside!

As a rule, the subjects of simple syncope recover, the horizontal position, which is assumed perforce in most cases, carrying with it the chief remedial influence—namely, the facilitating of the access of a fuller blood-supply to the brain. While, as stated, the tendency to syncope may exist in healthy non-anæmic individuals, it is far more common with those who suffer either from chronic cerebral anæmia or from many of its predisposing conditions. The arterial spasm which causes syncope is an exaggeration of what occurs within physiological limits²⁶ in all persons when subjected to emotional or violent external impressions of any kind.

²⁶ It has been experimentally determined by Istomanow (St. Petersburg Dissertation, 1885) in persons whose brain-surface had become partially accessible to observation through traumatic causes that pain, warmth, pleasant smells, and sweet tastes cause a contraction of the cerebral vessels and a sinking in of the brain-surface, while tickling, unpleasant odors, bitter and sour tastes, produce the reverse condition; that is, bulging of the brain-surface and increased injection of the vessels. Istomanow's results are verified by other observations, particularly by the fact that with the latter class of impressions there is an increase in the general blood-pressure, with sinking of the surface-temperature, and, as measured by Mosso's method, decrease in the volume of the extremities. While there is a general correspondence between these observations and clinical experience, there are a few unexplained discrepancies.

MORBID ANATOMY.—In those severe cases of cerebral anæmia which terminate fatally the entire brain appears bloodless. Since the color of this organ under ordinary circumstances is in great part due to the vascular injection, it appears very different when this admixture is lessened or removed. Then the gray substance, instead of presenting a reddish-gray tint, is of a pale buff color in infants, and a pale gray in adults who have died of acute or intense cerebral anæmia. The white substance exhibits few or no puncta vasculosa, and there is no indication of the faint rosy tinge which even the white substance has in the normal brain. All these appearances can be imitated in the brain of an animal that is bled to death; they are also met with in those who have died of inanition, particularly in cases of melancholia attonita, the subjects of which had long refused food. Most writers state that the ventricular and subarachnoid fluids are increased in amount,²⁷ and that the sulci appear wider in anæmic than in normal brains. That these fluids must be increased to compensate for the diminished blood-amount is evident. But it is not unlikely that exaggerated estimates of the increase have been made; and for this reason: Since the meninges and choroid plexuses are comparatively bloodless, the cerebro-spinal fluids are more likely to present themselves free from that admixture of blood which renders the obtaining and measuring of their quantity so difficult under ordinary circumstances. The gaping of the sulci has not been verified by me either in animals that had been bled to death or in cases of cerebral anæmia in rapidly-fatal atonic and phthisical melancholia. In protracted cases of this nature I frequently found gaping of the sulci: here, from the nature of the cases, the patients dying either from self-starvation, imperfect assimilation, or wasting diseases, the occurrence of a certain amount of atrophy of the brain-substance proper could not be excluded.²⁸

²⁷ Hammond, on the other hand (Diseases of the Nervous System, p. 77), has the ventricles generally empty.

²⁸ Up to within a very short time ago it would have appeared heretical to claim that any considerable amount of brain-wasting could ensue from starvation alone, as the oft-cited experiments of Chossat seemed to show that mammals, birds, reptiles, and amphibians lose in body-weight while being starved, but that the brain-weight is not disturbed to any appreciable extent. Six years ago I examined the brain of a tortoise (Cestudo Virginica) which had starved fully a year through ignorance of the keeper of an aquarium. The atrophy of the brain was so marked that it had undergone demonstrable changes of contour. Since then Rosenbach (Archiv für Psychiatrie, xvi. p. 276) has demonstrated that brain-wasting and other changes do occur in starved rabbits.

With protracted fevers accompanied by inanition—and this applies particularly to the later period of typhoid fever—a condition of cerebral anæmia is found which is of the greatest interest to the clinician. The brain as a whole is bloodless; there may or may not be apparently hyperæmic districts, but the injection is altogether on the surface; the consistency of the brain is considerably diminished, and this organ is often distinctly œdematous. In exceptional cases the œdema is so great that softening results, the white substance becoming fluidified at the cortical limit near the base of the sulci and at the ventricular walls. This is due perhaps as much to post-mortem maceration as to pre-mortem œdema, but that the latter condition exists is shown by the condition of the brain as a whole. The loss of memory, the difficulty of correlating the past and present, the rambling, incoherent conversation, and anenergic stupor observed in the decline of typhoid and other exhausting fevers, especially in older subjects, may be properly attributed to the injurious effects of post-febrile anæmia and anæmic œdema of the brain. Aside from fevers, œdema is apt to be associated with anæmia where venous stagnation is a complicating feature; consequently, it is not uncommon with certain uncompensated valvular lesions, emphysema, and other chronic pulmonic troubles.

Positive observations of tissue-changes from simple cerebral anæmia have not been recorded. Even in extreme cases the essential nervous structures, the ganglionic bodies, the nerve-fibres, their sheaths, and the neuroglia, appear healthy. The adventitial and pericellular spaces are sometimes enlarged, and variations in the number and distribution of the free nuclei of the neuroglia and the border bodies of the periadventitial districts have been observed by me, but not with such constancy as to justify more than this mere mention. In his researches on starvation Rosenbach found the brain œdematous and the ventricles dilated; there were also microscopical changes which indicated a profound disturbance of nutrition; the large cells of the anterior spinal horn and cerebellum had lost their transparency, being in a condition resembling cloudy swelling. The neuroglia appeared to be in a similar condition as that of nerve-cells. Singular as it may appear on first sight, the capillaries were found crowded with blood-corpuscles, and there were many evidences of diapedesis of such. This may indicate a passive accumulation due to deficient cardiac and vascular contractility. The changes, as a whole, were not unlike those found in myelitis,²⁹ except in so far as no actual inflammatory signs were present.

²⁹ Several distinguished neurologists, notably Westphal, who were present when Rosenbach presented his conclusions, were unable to recognize so profound a deviation from the normal structural conditions as he claimed (Archiv für Psychiatrie, xvi. p. 279).

SYMPTOMS.—The clinical phenomena of acute cerebral anæmia have been in the main related in connection with the etiology of this disorder. We shall now proceed to detail those which occur with cases more likely to engage the attention of the practitioner either on account of their gravity or protracted duration.

Uncomplicated Chronic Cerebral Anæmia of Adolescents and Adults.—This condition is one of the common manifestations of general anæmia. Most anæmic persons are languid, drowsy, suffer from insomnia, tinnitus aurium, and other signs of imperfect cerebral irrigation. In some these troubles become alarmingly prominent and may approach the confines of mental derangement. This is particularly apt to occur with women who have borne and nursed a large number of children. In addition to the typical signs of cerebral anæmia, they exhibit depression, may suffer from hallucinations, and even become afflicted with lachrymose or suicidal melancholia (insanity of lactation of the somato-etiological school). Depression of the mental functions is the most constant symptom of cerebral anæmia, and the one which most frequently directs the physician's attention to its existence; its subjects appear mentally blunted, the apperceptive powers are diminished, and it is difficult for the patient to interest himself in anything, or when interested to keep up a mental effort—that is, his attention—any length of time. In more severe grades of the trouble the patients become somnolent in the daytime. Contrary to what those who regard sleep as essentially due to cerebral anæmia might expect, sleep is disturbed, and the patient is wakeful or suffers from vivid and frightful dreams, or even deliria. Others pass a quiet night, but are rather in a trance-like condition than a healthy sleep. Lethargic as the cerebral anæmic person is on the whole, and unable as he feels himself to exert his will-power (aboulia), yet he is often irritable, perverse, and petulant in consequence of that morbid excitability which is a universal attribute of the overworked or imperfectly nourished nerve-element. The younger the patient the more likely is the condition apt to impress one as a stupor, while with older patients irritability is more prominent. In the former the obtuseness is often rapidly overcome when the patient assumes the horizontal position.

It was supposed by Abercrombie that an acute exacerbation of cerebral anæmia of this form in weakly and aged individuals might terminate in death. This condition corresponded to the so-called serous apoplexy of the old writers. With increasing accuracy in our autopsies this condition is more and more rarely recorded, although the possibility of its occurrence as a pathological rarity cannot be denied. As a rule, the chronic form of cerebral anæmia when it terminates fatally, which is exceptional, is marked by a deepening coma and gradual extinction of the vital processes, the Cheyne-Stokes phenomenon preceding this.

Patients suffering from chronic cerebral anæmia are afflicted with morbid irritability of the optic and auditory nerves. Loud sounds and bright lights are very annoying to them. Roaring, buzzing, and beating sounds in the ear are common, and scintillations, muscæ volitantes, and temporary darkening of the visual field—particularly noticed when the head is suddenly raised—are complained of in all cases. It is often found that the tinnitus disappears and the hearing power improves on assuming the horizontal position.

Headache of greater or less severity is found in the majority of cases: it is more severe in the rapidly-developed forms, and I have found it to be complained of in agonizing intensity by women who had risen from childbed and who had flooded considerably. As a rule, the headache, whether severe or mild, is symmetrical and verticalar, in some cases associated with an ache subjectively appearing as if it extended to the back of the orbit. It is remarkable for its constancy, and its exacerbations are often complicated with vertigo and nausea, so that it is not infrequently interpreted as a reflex evidence of gastric disorder. A stitch-like feeling, located in both temples, is often associated with it.

Occasionally sufferers from chronic cerebral anæmia experience seizures, or rather exacerbations, of their disorder which approach in character, while not equalling in degree, an attack of syncope. Whether in bed or in a chair, they then feel as if their limbs were of lead; they deem that they cannot stir hand or foot; the other symptoms related are aggravated; they yawn and breathe deeply, but hear all that is said by those near them, and do not lose consciousness. They express themselves as feeling as if everything around them were about to pass away. One of my patients would frequently find that if this condition overtook her while lying on one side, that side would remain numb for some time and be the seat of a tingling sensation which disappeared on the parts being rubbed. The same was noticed when she awoke in the morning in a similar position. To what extent these features were due to the general anæmia is doubtful. As previously stated, true syncope occurs in chronic cerebral anæmia, but much less frequently in those subjects of this disorder who have reached middle life than in adolescents.

The radial pulse in cerebral anæmia does not necessarily show the anæmic character; not infrequently the general blood-pressure is increased at the onset of the acute form, and if long continued this may be followed by a decrease of the same. The pulse-character may therefore vary greatly in frequency, resistance, and fulness. In protracted cases it is soft, easily compressible, and rapid.

It is not uncommon to find indications of a slight unilateral preponderance of the signs of cerebral anæmia. In one case which terminated in recovery, and was otherwise pure, vertigo was not produced on turning from the left to the right, but it was produced to a distressing degree on turning in the opposite direction; in a second, equally typical, there was for a long time a subjective sensation of falling over toward the right side.

There appears to be much less constancy in the relationship of the deficient blood-supply to the severity of the symptoms than is usually supposed. Much depends upon the time of life at which the disorder develops: a brain that has acquired stability through education and exercise is less vulnerable to the influence of general anæmia than one that has not. The nerve-centres appear, to some extent at least, to regulate their own blood-supply; and whether it be through a change in the blood-current rapidity or some other factor neutralizing the evil effects of the intrinsically inferior quality of the blood, we must attribute to the self-regulating nutrition power of the brain the not uncommon phenomena of an active mind in an anæmic body. And where the general anæmia reaches so high a degree as to involve the brain, under such circumstances we find that irritability to sensory impressions and fretfulness are more prominent than the lethargy and indifference which characterize the juvenile chlorotic form. Although this distinction is less marked between these two classes in regard to acutely-produced anæmia, yet it is observable even there. If in a youth or girl while undergoing phlebotomy cerebral anæmia were to reach such a degree as to cause subjective sounds, they would either approach or fall into a faint; but Leuret, the distinguished cerebral anatomist, while being subjected to the same procedure, hearing a hissing sound, did not lose consciousness, but complained that some one must have upset a bottle of acid on a marble table in the same room, as he supposed he was hearing the sound of effervescence thus produced.

Much, too, appears to depend on dynamic and other thus far undiscovered intrinsic conditions of the brain-tissue itself, irrespective of the mere amount and rapidity of the blood-current. If the subject be exposed to wasting diseases, to blood-poisons, or to vicissitudes of temperature and to physical exhaustion in addition to the causes producing cerebral malnutrition, deliria of a cortical nature are more apt to characterize the case than in simple anæmia. These are known as the deliria of inanition, and present themselves under two forms. The first has been frequently observed in sailors, travellers, and others who have undergone starvation in exposed situations, and is tinctured by the psychical influences incident to such a condition. Just as the Greeley survivors at Cape Sabine, when reduced to their miserable rations of seal-skin boot-leather and shrimps, entertained each other with the enumeration of imaginary culinary luxuries, so others who have suffered in the same way declaim about gorgeous banquets in the midst of a howling wilderness, or, as occurred to a miner who lost his way in Idaho a few winters ago, experienced hallucinatory visions of houses, kitchen utensils, and persons with baskets of provisions. In others the terror of the situation leads to the development of rambling and incoherent delusions of persecution.

The second form, regarded as a variety of starvation delirium, is found in the post-febrile periods of typhoid and other exhausting fevers. In aged persons it may even develop shortly after the onset of the disease. It is usually unsystematized, of a depressive cast, and may be associated with a condition resembling melancholia agitata. In a small proportion of cases insanity of the ordinary types, but more commonly of the special kinds comprised in the group of post-febrile insanity, develops from the anæmic fever delirium as its starting-point.

The spurious hydrocephalus (hydrocephaloid, hydrencephaloid) of Marshall Hall and Abercrombie, referred to in the section on Etiology, is an important condition for the diagnostician to recognize. A child suffering from this disorder presents many symptoms which are customarily regarded as characteristic of tubercular meningitis or of chronic hydrocephalus; thus the pupils are narrow—sometimes unequal;³⁰ there is strabismus, and there may be even nuchal opisthotonos, while the somnolent state in which the little patient usually lies may deepen into a true coma, in which the pupils are dilated, do not react to light, nor do the eyelids close when the cornea is touched. Ominous as this state appears, it may be completely recovered from under stimulating and restorative treatment. On inquiry it is found that the symptoms above mentioned were preceded by cholera infantum or some other exhausting complaint, such as a dysentery or diarrhœa, and that the somnolent condition in which infants are often found toward the close of such complaints passed gradually into the more serious condition described.³¹ The infants thus affected do not, however, sleep as healthy children do, but moan and cry, while apparently unconscious of their surroundings. The surface of the body is cool and pale; the pulse and respiration are normal, except in the comatose period, but the former is easily compressible. The chief points distinguishing hydrocephaloid from true hydrocephalus and other diseases associated with similar symptoms are the following: 1st, There is no rise of temperature; 2d, the pupils are equal; 3d, the fontanelle is sunken in; 4th, the pulse and respiration, with the exception stated, are natural; 5th, there is an antecedent history of an exhausting abdominal disorder; 6th, also a facial appearance characteristic of the latter.

³⁰ This is not admitted by most writers, but does occur exceptionally.

³¹ It should not be forgotten, however, that very similar symptoms occur after cholera infantum, with a much graver pathological condition—namely, marantic thrombosis of the sinuses.

One of the gravest and rarest forms of cerebral anæmia is one which occurs as a result of extreme general anæmia in very young infants. In a remarkable case which I have had an opportunity of studying, the abolition of certain cerebral functions reached such a degree that the opinion of a number of physicians was in favor of tubercular meningitis.³² There was at the time of my examination complete extremity hemiplegia, and there had been conjugated deviation, restlessness in sleep, and dulness in the waking hours: all these symptoms except the hemiplegia disappeared whenever a more assimilable and nutritious food was used than the one previously employed. On one occasion there were evidences of disturbed vaso-motor innervation; on several, convulsive movements. This history, associated with ordinary evidences of general anæmia, covered a period of eighteen months, without the slightest abnormality of temperature being noted or discoverable during that period. The mucous surfaces of this child were almost colorless, certainly without any indication of the normal tinge; the mother had nursed it, and her milk had been found to possess scarcely any nutritive value. The case terminated fatally at the age of twenty months.

³² It was stated by an experienced practitioner that death occurred with unmistakable symptoms of tubercular meningitis. Certainly, the absence of temperature disturbance at the time of the hemiplegic and other exacerbations, as well as other important features for a period exceeding a year, shows that whatever favorable soil the earlier condition may have furnished for the secondary development of such or other gross structural disease, tubercular meningitis did not exist at the time; while the absence of pupillary and optic-nerve symptoms, as well as the rapid changes from day to day or week to week under dietetic treatment, militate against the assumption of any other organic affection incident to childhood.

Partial Cerebral Anæmia.—Most writers on cerebral anæmia discuss a number of varieties of partial cerebral anæmia as distinguished from the acute and chronic general forms. Some of the conditions thus described properly appertain to the angio-spastic form of hemicrania, others to epilepsy, and the majority to circulatory disturbances dependent on arterial disease. Aside from the partial cerebral anæmia resulting from surgical causes, I am acquainted with but one evidence of limited cerebral anæmia which can be regarded as independent of the neuroses or of organic disease, and that is the scintillating scotoma. This symptom, in the only case in which I observed it, occurred in a medical student, accompanied by pallor and nausea in consequence of the disgust produced in him by the combined odors of a dissecting-room and of a neighboring varnish-factory. The totally blind area of the visual field was strictly hemianopsic in distribution and bounded by a colored zone scintillating, to use the sufferer's words, like an aurora borealis. The attack, probably protracted by his great alarm at being blind in one-half of the visual field, lasted three hours. As the cause in this case was a psychical impression and accompanied by the ordinary signs of that fainting which is not an uncommon occurrence in the dissecting-room; as, furthermore, the individual in question never had a headache except in connection with febrile affections, and then in the lightest form, and is neither neurotic himself nor has a neurotic ancestry or relatives,—I regard it as the result of a simple arterial spasm intensified in the visual field of one hemisphere, analogous to the more general spasm of ordinary syncope.³³

³³ It may be remembered that Wollaston had scintillating scotomata, and that after his death a small focus of softening was found in the one visual field. Ordinarily, this disturbance is associated with hemicrania.

DIAGNOSIS.—There is so little difficulty in recognizing the nature of those cases of acute cerebral anæmia which depend on recognizable anæmia-producing causes that it is unnecessary to point out their special diagnostic features. With regard to chronic cerebral anæmia, and its differentiation from other circulatory brain disorders, I refer to the last article. In this place it will be necessary only to point to some of the symptoms which, individually considered, are found in other disorders, and may therefore be misinterpreted. The chief of these is vertigo, which, as already stated, being associated with nausea, and even vomiting, is not infrequently confounded with stomachic vertigo, while the opposite error is also, though less frequently, fallen into. The chief differential points are—that stomachic vertigo is relieved by vomiting, and anæmic vertigo is not; that the former is rather episodical, the latter more continuous; that in the free intervals of the former, while there may be some dulness, there is not the lethargy found with anæmia; that the headache with the former is either over the eyes or occipital, and most intense after the passage of a vertiginous seizure, while anæmic headache is verticalar or general, and not subject to marked momentary changes. It is unnecessary to indicate here the positive evidences of gastric disorder which are always discoverable in persons suffering from stomachic vertigo; but it is also to be borne in mind that such disorder is frequently associated with the conditions underlying general and cerebral anæmia, particularly in the prodromal period of some pulmonary troubles.

There are a number of organic affections of the brain which are in their early periods associated with symptoms which are in a superficial way like those of cerebral anæmia. As a rule, focal or other pathognomonic signs are present which render the exclusion of a purely nutritive disorder easy; but with some tumors, as is generally admitted, these signs may be absent. It is not difficult to understand why a tumor not destructive to important brain-centres, nor growing sufficiently rapid to produce brain-pressure, yet rapidly enough to compress the blood-channels, may produce symptoms like those of simple cerebral anæmia. It is claimed that with such a tumor the symptoms are aggravated on the patient's lying down, while in simple anæmia they are ameliorated.³⁴ The latter proposition holds good as a general rule; as to the former, I have some doubts. Not even the ophthalmoscope, although of unquestionable value in ascertaining the nature of so many organic conditions of the brain and its appendages, can be absolutely relied on in this field. Until quite recently, optic neuritis, if associated with cerebral symptoms, was regarded as satisfactory proof that the latter depended on organic disease; but within the year it has been shown by Juler³⁵ that it may occur in simple cerebral anæmia, and both the latter and the associated condition of the optic nerve be recovered from.

³⁴ The increased flow of blood to the brain in anæmia is not always momentarily remedial: if, for example, the patient stoop down, he flushes more easily than a normal person, and suffers more than the latter. The same is observed with regard to stimulants.

³⁵ British Medical Journal, Jan. 30, 1886. In the case reported suppression of the catamenia is spoken of, as well as the fact that treatment was directed to the menstrual disturbance. It is not evident from the brief report at my disposal whether the suspension of the menstrual flow was symptomatic of general anæmia or of a local disturbance. Optic neuritis has been recorded as having been present in a large number of cases with no other assignable cause than a uterine disorder. As previously stated, Hirschberg and Litten found choked disc under like circumstances.

The claim of Hammond and Vance that ordinary anæmia of the brain may be recognized through the ophthalmoscope is almost unanimously disputed by experienced ophthalmoscopists, nor is it unreservedly endorsed by any authority of weight among neurologists. That there may be color-differences to indicate anæmia is, however, not impossible; and the fact that a concentric limitation of the visual field sometimes occurs should not be forgotten. It is distinguished from that found with organic diseases by its variability through the day and in different positions of the body.

TREATMENT.—Chronic as well as acute cerebral anæmia, dependent on general anæmia, usually requires no other medicinal treatment than that rendered necessary by the general anæmic state of which it is a part. This has been discussed at length in the third volume of this work: it remains to speak of certain special precautions and procedures rendered necessary by the nervous symptoms predominating in such cases. As the insufficiently nourished brain is not capable of exertion, mental as well as physical rest is naturally indicated. And this not only for the reason that it is necessary to avoid functional exhaustion, but also because the anæmic brain when overstrained furnishes a favorable soil for the development of morbid fears, imperative impulses, and imperative conceptions. This fact does not seem to have been noticed by most writers. The mind of the anæmic person is as peculiarly sensitive to psychical influences as the anæmic visual and auditory centres are to light and sound; and in a considerable proportion of cases of this kind the origin of the morbid idea has been traced to the period of convalescence from exhausting diseases. The prominent position which masturbation occupies among the causes of cerebral anæmia perhaps explains its frequent etiological relationship to imperative conceptions and impulsive insanity.

Although the radical and rational treatment of cerebral anæmia is covered by the treatment of the general anæmia, there are certain special symptoms which call for palliative measures. Most of these, such as the vertigo, the optic and aural phenomena, improve, as stated, on assuming the horizontal position. The headache if very intense will yield to one of three drugs: nitrite of amyl, cannabis indica, or morphine. I am not able to furnish other than approximative indications for the use of remedies differing so widely in their physiological action. Where the cerebral anæmia and facial pallor are disproportionately great in relation to the general anæmia, and we have reason to suppose the existence of irritative spasm of the cerebral blood-vessels—a condition with which the cephalalgia is often of great severity—nitrite of amyl acts as wonderfully as it does in the analogous condition of syncope.³⁶ Where palpitations are complained of, and exist to such a degree as to produce or aggravate existing insomnia, small doses of morphine will act very well, due precautions being taken to reduce the disturbance of the visceral functions to a minimum, and to prevent the formation of a drug habit by keeping the patient in ignorance of the nature of the remedy. When trance-like conditions and melancholic depression are in the foreground, cannabis indica with or without morphia will have the best temporary effect: it is often directly remedial to the cephalalgia. Chloral and the bromides are positively contraindicated, and untold harm is done by their routine administration in nervous headache and insomnia, irrespective of their origin. Nor are hypnotics, aside from those previously mentioned, to be recommended; the disadvantages of their administration are not counterbalanced by the advantages.³⁷ Frequently, in constitutional syphilis, insomnia resembling and probably identical with the insomnia of cerebral anæmia will call for special treatment. In such cases the iodides, if then being administered, should be suspended, and if the luetic manifestations urgently require active measures, they should be restricted to the use of mercury in small and frequent dosage, while the vegetable alteratives may be administered if the state of the stomach permit.

³⁶ There are disturbances in the early phases of cerebral syphilis, whose exact pathological character is not yet ascertained, which so closely resemble the condition here described that without a knowledge of the syphilitic history, and misled by the frequently coexisting general anæmia, it is regarded as simple cerebral anæmia. Under such circumstances, as also with the cerebral anæmia of old age, amyl nitrite should not be employed.

³⁷ Urethran and paraldehyde have failed in my hands with anæmic persons.

Among the measures applicable to the treatment of general anæmia there are three which require special consideration when the cerebral symptoms are in the foreground: these are alcoholic stimulants, the cold pack, and massage. It is a remarkable and characteristic feature of cerebral anæmia that alcoholic stimulants, although indicated, are not well borne³⁸—at least not in such quantities as healthy persons can and do take without any appreciable effect. I therefore order them—usually in the shape of Hungarian extract wines,³⁹ South Side madeira, or California angelica—to be given at first in such small quantities as cannot affect the cerebral circulation unpleasantly, and then gradually have the quantity increased as tolerated. In fact, both with regard to the solid nourishment and the stimulating or nourishing fluids and restorative drugs the division-of-labor principle is well worth following. The cerebral anæmic is not in a position to take much exercise, his somatic functions are more or less stagnant, and bulky meals are therefore not well borne. Small quantities of food, pleasingly varied in character and frequently administered, will accomplish the purpose of the physician much better.

³⁸ Hammond, who classes many disorders under the head of cerebral anæmia which the majority of neurologists regard as of a different character, has offered a very happy explanation. He says, “Now, it must be recollected that the brains of anæmic persons are in very much the same condition as the eyes of those who have for a long time been shut out from their natural stimulus, light. When the full blaze of day is allowed to fall upon them retinal pain is produced, the pupils are contracted, and the lids close involuntarily. The light must be admitted in a diffused form, and gradually, till the eye becomes accustomed to the excitation. So it is with the use of alcohol in some cases of cerebral anæmia. The quantity must be small at first and administered in a highly diluted form, though it may be frequently repeated.”

³⁹ Such as Meneszer Aszu; there is no genuine tokay wine imported to this country, as far as I am able to learn.

The cold pack, strongly recommended by some in general anæmia, is not, in my opinion, beneficial in cases where the nervous phenomena are in the foreground, particularly in elderly persons. Gentle massage, on the other hand, has the happiest effects in this very class of cases.

Of late years my attention has been repeatedly directed to cerebral anæmia of peculiar localization due to malarial poisoning. It has been noted by others that temporary aphasia and other evidences of spasm of the cortical arteries may occur as equivalents or sequelæ of a malarial attack. I have seen an analogous case in which hemianopsia and hemianæsthesia occurred under like circumstances, and were recovered from. Whether more permanent lesions, in the way of pigmentary embolism or progressing vascular disease, causing thrombotic or other forms of softening, may develop after such focal symptoms is a matter of conjecture, but I have observed two fatal cases in which the premonitory symptoms resembled those of one which recovered, and in which these were preceded by signs of a more general cerebral anæmia, and in one case had been mistaken for the uncomplicated form of that disorder. Where a type is observable in the exacerbation of the vertigo, headache, tinnitus, and lethargy of cerebral anæmia, particularly if numbness, tingling, or other signs of cortical malnutrition are noted in focal distribution, a careful search for evidences of malarial poisoning should be made; and if such be discovered the most energetic antimalarial treatment instituted. It is in such cases that arsenic is of special benefit.

The treatment of syncope properly belongs to this article. Where the signs of returning animation do not immediately follow the assumption of the recumbent position, the nitrite of amyl, ammonia, or small quantities of ether should be exhibited for inhalation. The action of the former is peculiarly rapid and gratifying, though the patient on recovery may suffer from fulness and pain in the head as after-effects of its administration. The customary giving of stimulants by the mouth is to be deprecated. Even when the patient is sufficiently conscious to be able to swallow, he is usually nauseated, and, as he is extremely susceptible to strong odors or tastes in his then condition, this nausea is aggravated by them. By far the greater number of fainting persons recover spontaneously or have their recovery accelerated by such simple measures as cold affusion, which, by causing a reflex inspiration, excites the circulatory forces to a more normal action. Rarely will the electric brush be necessary, but in all cases where surgical operations of such a nature as to render the development of a grave form of cerebral anæmia a possibility are to be performed, a powerful battery and clysters of hot vinegar, as well as the apparatus for transfusion, should be provided, so as to be within reach at a moment's notice.

Inflammation of the Brain.

Before the introduction of accurate methods of examining the diseased brain the term inflammatory softening was used in a much wider sense than it is to-day. Most of the disorders ascribed to inflammatory irritation by writers of the period of Andral and Rush are to-day recognized as regressive, and in great part passive, results of necrotic destruction through embolic or thrombic closure of afferent blood-channels. Two forms of inflammation are universally recognized. One manifests itself in slow vascular and connective-tissue changes and in an indurating inflammation. There are two varieties of it: the first of these, which is associated with furibund vaso-motor explosions and regressive metamorphosis of the functional brain-elements, is known from its typical association with grave motor and mental enfeeblement as paretic dementia or dementia paralytica. The second, which is focal in the distribution of the affected brain-areas, is known as sclerosis. The former is treated of in a separate article; the latter is considered in connection with the spinal affections which either resemble it in histological character or complicate its course. The second form of cerebral inflammation is marked by the formation of the ordinary fluid products of acute inflammation in other organs of the body; this is the suppurative form, usually spoken of as abscess of the brain.

In addition to these two generally recognized inflammatory affections there are a number of rare diseases which are regarded by excellent authority as also of that character. The vaguely-used term acute encephalitis has been recently reapplied with distinct limitations to an acute affection of children by Strümpell. This disease is usually of acute onset, infants under the sixth year of age being suddenly, and in the midst of apparently previous good health sometimes, attacked by fever, vomiting, and convulsions.⁴⁰ Occasionally coma follows, which may last for several days, perhaps interrupted from time to time by recurring convulsions or delirium. The convalescence from this condition is rapid, and in some cases is complete; in others paralysis remains behind in the hemiplegic form. The paralysis is usually greater in the arm than in the leg; in extreme cases it involves the corresponding side of the face, and, as the paralyzed parts are arrested or perverted in growth, considerable deformity, even extending to asymmetry of the skull, may ensue. The deformity is aggravated by contractures. Usually there is some atrophy of the muscles, but in one case I found actual hypertrophy⁴¹ of some groups, probably in association with the hemiathetoid movements.

⁴⁰ As in my case of infantile encephalitis followed by athetoid symptoms (Journal of Nervous and Mental Diseases).

⁴¹ This was followed by atrophy. There are never any qualitative electrical changes.

The sequelæ of acute infantile encephalitis present us with the most interesting forms of post-paralytic disturbances of muscular equilibrium. Hemichorea and hemiathetosis, as well as peculiar associated movements and hemicontracture, are found in their highest development with this class of cases. Occasionally epileptiform symptoms are noted,⁴² and in others true epilepsy is developed. It is under such circumstances that imbecility is apt to be a companion symptom or result; and this imbecility is prominently noted in the moral sphere.

⁴² Which in one case of my own disappeared spontaneously.

The grave set of symptoms briefly detailed here are attributed by Strümpell⁴³ to an acute encephalitis, analogous, in his opinion, to the acute poliomyelitis of children. Its frequent occurrence after measles and scarlatina, as well as the fact that Ross⁴⁴ in a carefully-studied case arrived at the opinion that the disease was an embolo-necrotic result of endocarditis, would lead to the conclusion that it is a focal affection, probably due to the transportation of infectious elements to the brain through the blood-vessels. Its occurrence in children in the midst of apparent health⁴⁵ is consistent with the fact that rheumatism and an attendant slight endocarditis frequently pass unrecognized in infancy. It is supposed that a diffuse form of inflammatory non-suppurative softening exists by some of the Germans, but the proof advanced in favor of this view is not conclusive.

⁴³ As a surmise, for up to his writing no reliable autopsies had been made.

⁴⁴ Brain, October, 1883.

⁴⁵ McNutt (American Journal of Medical Sciences, January, 1885) cites Strümpell as attributing the theory of an inflammatory affection, which is analogous to poliomyelitis in its suddenness and nature, to Benedict, and refers to p. 349 of Strümpell's textbook under the erroneous date of 1864. This work was published in 1883-84, and the theory is advanced by Strümpell as his own. It is only a synonym, hemiplegia spastica infantile, that is attributed to Benedict.

A number of rare forms of interstitial encephalitis have been described. In one, elaborately studied by Danillo, an inflammatory hypertrophy of the cortex, involving the parenchyma as well as the connective and vascular structures, was found in a limited area of the motor province of the right hemisphere. There had been crossed epileptiform convulsions during life.⁴⁶

⁴⁶ Bulletin de la Société de Biologie, 1883, p. 238.

There is some question among pathologists as to the recognition of Virchow's encephalitis of the new-born. Certainly a part of Virchow's material was derived from the imperfect study of a condition of infantile brain-development which, as Jastrowitz showed, is physiological, and on which Flechsig based his important researches of tract-development. More recent studies, however, demonstrate that there is a form of miliary encephalitis in new-born children due to septic causes, such as, for example, suppuration of the umbilical cord. The demonstration by Zenker of the occurrence of metastatic parasitic emboli in cases of aphthous stomatitis, and by Letzerich of a diphtheritic micrococcus invasion in the brain of his own child, show that the subject of early infantile encephalitis merits renewed consideration.⁴⁷

⁴⁷ The attempt of Jacusiel to revive Virchow's encephalitis of the new-born (Berliner klinische Wochenschrift, 1883, No. 7) under the title of interstitial encephalitis does not seem to have met with encouragement, for, besides Jastrowitz, Henoch and Hirschberg opposed this view in the discussion.

Strictly speaking, the reactive changes which occur in the brain-substance bordering on tumors, hemorrhagic and softened foci, belong to the domain of encephalitis; but as they are considered in conjunction with the graver lesions to which they are secondary both in occurrence and importance, it is not necessary to more than refer to them here.

Abscess of the Brain.

As indicated in the last article, there formerly existed much confusion in the minds of pathologists regarding the terms softening and abscess of the brain. As long as softening was regarded as an inflammation, so long was abscess of the brain regarded as a suppurative form of softening. Aside from the fact that there is some resemblance in mechanical consistency between a spot of ordinary softening and one of inflammatory softening, there is no essential similarity of the two conditions. True softening is to-day regarded as the result of a death of brain-tissue produced by interference with the blood-supply; it is therefore a passive process. Inflammatory softening, of which abscess is a form, is due to an irritant, usually of an infectious nature. It is to the results of such irritation that the term suppurative encephalitis should be limited.

MORBID ANATOMY.—In all well-established inflammatory brain troubles the active part is taken by the blood-vessels and connective tissue; the ganglionic elements undergo secondary, usually regressive or necrotic, changes. The brain, considered as a parenchymatous organ, is not disposed to react readily in the way of suppurative inflammation unless some septic elements are added to the inflammatory irritant. Foreign bodies, such as knitting-needles, bullets, and slate-pencils, have been found encapsulated in this organ or projecting into it from the surrounding bony shell without encapsulation and without any evidences of inflammatory change. As a rule, a foreign body which enters the brain under aseptic conditions will, if the subject survive sufficiently long, be found to have made its way to the deepest part of the brain, in obedience to the law of gravity, and through an area of so-called inflammatory red softening which appears to precede it and facilitate the movement downward. This form of softening derives its color from the colored elements of the blood, which either escape from the vessels in consequence of the direct action of the traumatic agent; secondly, in consequence of vascular rupture from the reduced resistance of the perivascular tissue in consequence of inflammatory œdema and infiltration; or, thirdly, in obedience to the general laws governing simple inflammation.

A cerebral abscess may present itself to the pathological anatomist in one of three phases—the formative, the crude, and the encapsulated. In the first it is not dissimilar to a focus of yellow softening, being, like the latter, a diffuse softened area varying from almost microscopical dimensions to the size of a walnut, and of a distinctly yellow tinge. Microscopic examination, however, shows a profound difference. In pure yellow softening there are no pus-cells; in the suppurative encephalitic foci they are very numerous, and congregated around the vessels and in the parenchyma in groups. The crude abscess is the form usually found in cases rapidly running to a fatal termination. Here there is an irregular cavity in the brain, usually the white central substance of the cerebrum or cerebellum, formed by its eroded and pulpy tissue; it is filled with yellow, greenish, and more rarely brownish pus. In the most furibund cases broken-down brain-detritus may be found in the shape of whitish or reddish flocculi, but in slowly-formed abscesses the contents are free from such admixture, and thus the third phase is produced, known as the encapsulated abscess. The cavity of the abscess becomes more regular, usually spheroid or ovoid; the pus is less fluid, more tenacious, and slightly transparent; and the walls are formed by a pseudo-membrane⁴⁸ which is contributed by the sclerosing brain-substance, which merges gradually into the outlying normal tissue. I have seen one acute cerebral abscess from ear disease which might be appropriately designated as hemorrhagic; the contents were almost chocolate-colored; on closer inspection it was found that they were true pus, mingled with a large number of red blood-discs and some small flocculi of softened brain-substance. This hemorrhagic admixture was not due to the erosion of any large vessel, for the abscess had ruptured into the lateral ventricle at that part where it was most purely purulent. In a case of tubercular meningitis, Mollenhauer in my laboratory found an abscess in the white axis of the precentral gyrus, with a distinct purulent infiltration following the line of one of the long cortical vessels. The abscess was not encapsulated, the surrounding white substance exhibited an injected halo, and the consistency of the contents was that of mucoid material.

⁴⁸ There is considerable dispute as to the real nature of the tissue encapsulating cerebral abscesses. It is known, through the careful observations of R. Meyer, Goll, Lebert, Schott, and Huguenin, that the capsule may form in from seven to ten weeks in the majority of cases, about eight weeks being the presumable time, and that at first the so-called capsule of Lallemand does not deserve the name, being a mucoid lining of the wall. At about the fiftieth day, according to Huguenin, this lining becomes a delicate membrane composed of young cells and a layer of spindle-shaped connective elements.

In cases where the symptoms accompanying the abscess during life had been very severe it is not rare to find intense vascular injection of the parts near the abscess, and it is not unlikely that the reddish or chocolate color of the contents of some acutely developed abscesses is due to blood admixture derived from the rupture of vessels in this congested vicinity. Sometimes the entire segment of the brain in which the abscess is situated, or the whole brain, is congested or œdematous. In a few cases meningitis with lymphoid and purulent exudation has been found to accompany abscesses that had not ruptured. It is impossible to say whether in this case there was any relation between the focal and the meningeal inflammation, as both may have been due to a common primary cause.⁴⁹ In such cases, usually secondary to ear disease, thrombosis of the lateral sinus may be found on the same side. Where rupture of an abscess occurs, if the patient have survived this accident long enough—for it is usually fatal in a few minutes or hours—meningitis will be found in its most malignant form. A rupture into the lateral and other ventricles has been noted in a few cases.⁵⁰

⁴⁹ Otitis media purulenta in the two cases of this kind I examined.

⁵⁰ In one, observed together with E. G. Messemer, intense injection of the endymal lining, with capillary extravasations, demonstrated the irritant properties of the discharged contents.

Some rare forms of abscess have been related in the various journals and archives which have less interest as objects of clinical study than as curiosities of medical literature. Thus, Chiari⁵¹ found the cavity of a cerebral abscess filled with air, a communication with the nose having become established by its rupture and discharge.

⁵¹ Zeitschrift für Heilkunde, 1884, v. p. 383. In this remarkable rase the abscess, situated in the frontal lobe, had perforated in two directions—one outward into the ethmoidal cells, the other inward into the ventricles, so that the ventricles had also become filled with air. This event precipitated a fatal apoplectiform seizure.

The contents of a cerebral abscess usually develop a peculiarly fetid odor. It has been claimed that this odor is particularly marked in cases where the abscess was due to some necrotic process in the neighborhood of the brain-cavity. The only special odor developed by cerebral abscesses, as a rule, is identical with that of putrid brain-substance, and it must therefore depend upon the presence of brain-detritus in the contents of the abscess or upon the rapid post-mortem decomposition of the neighboring brain-substance.

In two cases of miliary abscess which, as far as an imperfect examination showed, depended on an invasion of micro-organisms, an odor was noticed by me which was of so specific a character that on cutting open the second brain it instantly suggested that of the first case, examined six years previous, although up to that moment I had not yet determined the nature of the lesion.⁵²

⁵² Owing to the lack of proper methods of demonstrating micro-organisms, the first case whose clinical history was known was imperfectly studied; of the second case, accidentally found in a brain obtained for anatomical purposes, the examination is not yet completed.

That form of abscess which, from its situation in or immediately beneath the surface, has latterly aroused so much interest from its important relations to localizations is usually metastatic, and directly connected with disease of the overlying structures, notably the cranial walls. In this case the membranes are nearly always involved. The dura shows a necrotic perforation resembling that found with internal perforation of a mastoid or tympanic abscess. The pia is thickened and covered with a tough fibro-purulent exudation; occasionally the dura and leptomeninges are fused into a continuous mass of the consistency of leather through the agglutinating exudation. The abscess is usually found open, and it is not yet determined whether it begins as a surface erosion, and, bursting through the cortex, spreads rapidly on reaching the white substance, or not. The white substance is much more vulnerable to the assault of suppurative inflammation than the gray, and not infrequently the superficial part of the cortex may appear in its normal contiguity with the pia, but undermined by the cavity of the abscess, which has destroyed the subcortical tissue. Possibly the infecting agent, as in some cases of ear disease, makes its way to the brain-tissue through the vascular connections, which, however sparse at the convexity of the brain, still exist.

CLINICAL HISTORY.—The symptoms of a cerebral abscess depend on its location, size, and rapidity of formation. There are certain parts of the brain, particularly near the apex of the temporal lobe and in the centre of the cerebellar hemisphere, where a moderately large abscess may produce no special symptoms leading us to suspect its presence. There are other localities where the suppurative focus⁵³ indicates its presence, and nearly its precise location and extent, by the irritative focal symptoms which mark its development and by the elimination of important functions which follows its maturation. It is also in accordance with the general law governing the influence of new formations on the cerebral functions that an acutely produced abscess will mark its presence by more pronounced symptoms than one of slow, insidious development. Indeed, there are found abscesses in the brain, even of fair dimensions, that are called latent because their existence could not have been suspected from any indication during life, while many others of equal size are latent at some time in their history.

⁵³ Practically, our knowledge of localization of functions in the human brain begins with the observation by Hitzig of a traumatic abscess in a wounded French prisoner at Nancy named Joseph Masseau. The year of the publication of this interesting case constitutes an epoch in advancing biological knowledge, which will be remembered when even the mighty historical events in which Hitzig's patient played the part of an insignificant unit shall have become obsolete. This, the first case in the human subject where a reliable observation was made was an unusually pure one; the abscess involved the facial-hypoglossal cortical field (Archiv für Psychiatrie, iii. p. 231).

An acute cerebral abscess is ushered in by severe, deep, and dull headache, which is rarely piercing, but often of a pulsating character. The pain is sometimes localized, but the subjective localization does not correspond to the actual site of the morbid focus.⁵⁴ It is often accompanied by vertigo or by a tendency to dig the head into the pillow or to grind it against the wall. With this there is more or less delirium, usually of the same character as that which accompanies acute simple meningitis. As the delirium increases the slight rise in temperature which often occurs in the beginning undergoes an increase; finally coma develops, and the patient dies either in this state or in violent convulsions. The case may run its course in this way in a few days, but usually one to three weeks intervene between the initial symptoms and death.

⁵⁴ Although Ross seems to be of a contrary opinion, it is the exception for the pain to correspond in location to the abscess.

Between the rapid and violent course of acute cerebral abscess detailed, and the insidious course of those which as latent abscesses may exist for many years without producing any noticeable symptoms whatever, there is every connecting link as to suddenness and slowness of onset, severity and mildness of symptoms, and rapidity and slowness of development and progress. It is the encapsulated abscesses which are properly spoken of as chronic, and which may even constitute an exception to the almost uniform fatality of the suppurative affections of the brain. Thus, the symptoms marking their development may correspond to those of an acute abscess, but coma does not supervene, temporary recovery ensues, and the patient leaves the hospital or returns to his vocation. But all this time he appears cachectic, and there will be found, on accurate observation, pathological variations of the temperature and pulse. The appetite is poor; the bowels are usually constipated; there are frequent chilly sensations and horripilations, and a general malaise. This condition slowly passes away in the few cases which recover; in others relapses occur, usually of progressing severity, and terminate life. The period during which the symptoms of the abscess are latent may be regarded as corresponding to the latent period which sometimes intervenes between an injury and the development of the symptoms of acute abscess, and which, according to Lebert, may comprise several weeks or months. In other words, the morbid process may be regarded all this time as progressing under the mask of a remission. It is this latent period which it is of the highest importance for the diagnostician to recognize. There is usually headache, which is continuous and does not change in character, though it may be aggravated in paroxysms. Usually the temperature rises with these paroxysms, and if they continue increasing in severity they may culminate in epileptic convulsions.

Many of the symptoms of cerebral abscess—prominently those attending the rapidly-developed forms and the exacerbations of the chronic form—are due to cerebral compression. It is the pulse and pupils, above all, that are influenced by this factor.

In an affection having so many different modes of origin as cerebral abscess, and occupying such a wide range of possible relations to the cerebral mechanism, it is natural that there should exist many different clinical types. So far as the question of the diagnosis of localized cerebral abscesses is concerned, I would refer to the article dealing with cerebral localization, in order to avoid repetition. With regard to the etiological types, they will be discussed with the respective causal factors.

ETIOLOGY.—Abscess of the brain is so frequently found to be due to metastatic or other infectious causes that it is to be regarded as highly improbable that it is ever of idiopathic occurrence. The most frequent associated conditions are—suppurative inflammation in neighboring structures, such as the tympanic cavity, the mastoid cells, the nasal cavity, or inflammation or injury of any part of the cranium and scalp. The connection of these structures with the brain through lymphatic and vascular channels is so intimate that the transmission of a pyogenic inflammatory process from the former to the latter is not difficult to understand. But disease of far distant organs, such as gangrene of the lung, and general affections, such as typhoid fever, occasionally figure among the causes of cerebral abscess, particularly of the miliary variety.

Among the commonest causes of cerebral abscesses are those which the surgeon encounters. The injury may be apparently slight and limited to the soft parts, or the bone may be merely grazed. Gunshot wounds are particularly apt to be followed by a cerebral abscess; and it has been noted that those which granulate feebly, whose base is formed by a grayish, dirty, and fetid material, are most apt to lead to this ominous complication. The symptoms do not usually develop immediately, and after the surgeon is led to indulge in the hope that danger is past, proper reaction sets in, healthy granulations develop—nay, the wound may close and be undergoing cicatrization—then the patient complains of feeling faint or drowsy, and with or without this premonition he has convulsive movements of one side, sometimes involving both extremities and the corresponding side of the face. Consciousness is usually preserved, but the spells recur, and the patient is noted to be absent-minded during and after the convulsive seizure. On some later day he is noticed to become pale, as in the initial stage of a true epileptic seizure; total abolition of consciousness follows, and the clonic spasms, affecting the same limbs and muscles involved in the first seizures, now recur with redoubled violence. After such an attack more or less paresis is observed in the muscles previously convulsed. A number of such seizures may occur, or a fatal issue terminate any one of them. Not infrequently the field of the involved muscles increases with each fit. Thus the thumb or a few fingers may be the first to show clonic spasm; in the next fits, the entire arm; in succeeding ones, the leg and face may follow suit. In such a case the periphery first to be convulsed is the first to become paralyzed, thus showing that where the disease began as an irritative lesion the cortex is now destroyed, and that around the destructive focus as a centre the zone of irritation is spreading excentrically, first to irritate and then to destroy seriatim the functions of the various cortical fields in their order. According to the teachings laid down in the article on Localization, the order of invasion and extension, as well as the nature, of the focal symptoms will vary. Finally, the attacks become more severe and of longer duration; the patient does not recover in the intervals, but complains of nausea, pain, confusion, and head-pressure. He is noted to be dull, his temperature is slightly raised (100° F.), and the speech may be affected. Several attacks may occur in a day, each leaving the patient more and more crippled as to motility and mind. He is delirious and drowsy at intervals; his temperature may rise after an attack from one to four degrees, usually remaining near 103°–104° F. in the evening; and, coma developing, death occurs, the convulsion or paralytic phenomena continuing at intervals during the moribund period, and the temperature and pulse sometimes running up rapidly toward the last. On examining the parts, it is found that the bone is necrotic at the point of injury, usually only in its outer table, but sometimes in its entire thickness. In exceptional cases the normal continuity of the entire table is not interrupted to all appearances, and a small eroded spot on the inner table is found bathed in pus, or a detached necrotic fragment may be found in the latter. Corresponding to the purulent focus on the inner table the dura mater is detached, discolored, and perforated in one or more places with irregular rents or holes which have a greenish or blackish border. An abscess is found in that part of the brain which corresponds to this opening. There is no question that it was caused by direct infection from the necrotic spot.

Cases have been noted,⁵⁵ apparently of idiopathic origin, in which a sudden paralysis of a few fingers was the first symptom produced by the development of a cerebral abscess. In a few days such a paralysis extends to the other fingers and to the forearm. Occasionally no convulsive phenomena are noted, or choreic movements indicate, in their place, that the cortical field is irritated. Such cases usually run a rapidly fatal course.

⁵⁵ Arthur E. W. Fox, Brain, July, 1885.

The most frequent cause of cerebral abscess in civil practice is suppurative inflammation of the middle ear. It may be safely asserted that the person suffering from this affection is at no time free from the danger of a cerebral abscess, a purulent meningitis, or a phlebitic thrombosis of the sinuses. Cases are on record where the aural trouble had become chronic, and even quiescent, for a period of thirty years, and at that late date led to abscess with a fatal termination. Of 6 cases of this character in my experience, 4 of which were verified by anatomical examination, not one but had occurred at least four years after the commencement of the ear trouble, and 1 happened in a man aged fifty-four who had contracted the latter affection in childhood. In 2 there was in addition diffuse purulent meningitis, limited on the convexity to the side where the abscess was situated.⁵⁶ In 4 the abscess was in the temporal lobe, 1 of them having in addition an abscess in the cerebellar hemisphere of the same side; in a fifth the abscess was in the deep white substance of the cerebral hemisphere, opening into the lateral ventricle, and in the sixth it was in one cerebellar hemisphere alone.

⁵⁶ One of these was seen during life by J. R. Pooley; the other was a paretic dement at the New York City Pauper Asylum.

The course of this class of abscesses is usually obscure: focal symptoms are not commonly present, and the constitutional and local symptoms usually appear as a gradual outgrowth from the aural troubles. Thus there is at first usually little fever, vertigo, and chilliness, but considerable tinnitus, and sometimes pain in the ear. Occasionally local signs of a septic metastasis of the otitis, such as œdema over the mastoid or painful tumefaction of the cervical glands, are visible. The pain previously referred to the region of the ear now becomes general; commonly—even where the abscess is in the temporal lobe—it becomes progressively aggravated in the frontal and sometimes in the nuchal region, and under an increase of the febrile phenomena death may exceptionally occur without further complication. Even large abscesses in one half of the cerebellum occur without producing Ménière's symptom—a fact which leads to the suspicion that the purulent deposit must have been of slow and gradual development. In one case distinct symptoms indicating an affection of the subcortical auditory tract were observed. As a rule, this class of abscesses are accompanied toward the close by active general symptoms—convulsions, coma, narrowing and impaired light-reaction of the pupils. Delirium, when a prominent symptom from the beginning, indicates the probable association of meningitis with the abscess.⁵⁷ Occasionally severe pain, rigor, high temperature, and paralysis may be absent even with rapidly-developed abscess from otitis.⁵⁸

⁵⁷ The same is probably true of oculo-motor paralysis, which Ross (loc. cit., vol. ii. p. 735) refers to uncomplicated abscess.

⁵⁸ This was the case with an abscess containing five ounces of pus recorded by C. S. Kilham at the Sheffield Medical Society (British Medical Journal, February 13, 1886). As illustrating what was stated about the non-correspondence of the pain and the location of the abscess, it may be stated that notwithstanding this large abscess was in the temporal lobe, what pain was present was in the forehead.

Ulcerative endocarditis, infectious osteomyelitis, pulmonary gangrene, general pyæmia, and, as is claimed by a few authors, typhoid fever, are often accompanied by multiple abscesses in the brain-substance. Usually the foci are small, as may be readily inferred from the fact that they are of embolic origin, the emboli being usually so small as to lodge in very small vessels, and that the fatality of the primary disease is so great as to cut short life before the abscess can reach larger dimensions. For the same reasons the symptoms they produce are rarely distinctive. In chronic lung affections accompanied by putrescence in bronchiectatic or other cavities cerebral abscesses are not uncommon occurrences. Under these circumstances, although we must assume an embolic origin, the abscess is rarely multiple, and the symptoms are as marked as in the ordinary varieties. Thus a patient suffering from chronic phthisis, with or without prodromal malaise or somnolence, experiences formications and pain in his right leg; he then notices a slight halt in walking; twitches appear in the affected extremity; it becomes distinctly paretic. The arm then becomes affected in like manner; the pupils become unequal; a severe chill occurs, followed by delirium, convulsions, coma, and death.

DIAGNOSIS.—There is little difficulty in recognizing the existence of a cerebral abscess in which well-marked focal and constitutional symptoms coincide, or where a distinct abscess-producing cause, such as an ear trouble, a head injury, or a putrid bronchiectasis, coexists.⁵⁹ But there are a number of cases, varying from the latent form to forms with obscure general symptoms, whose recognition is impossible or at best a matter of conjecture. Such cases may be readily confounded with certain tumors. The existence of febrile symptoms, although not excluding tumor, as some tumors are accompanied by such, is greatly in favor of abscess. On the other hand, choked disc, which is rare with abscess and found only with the very largest, is in favor of tumor.

⁵⁹ Yet a leading and careful authority was misled into making the diagnosis of abscess in a case of ear disease complicated by a cerebral tumor.

PROGNOSIS AND TREATMENT.—The majority of cerebral abscesses must, from the nature of the case, be regarded as not influenceable by medicinal measures or surgical treatment. The miliary and other abscesses due to general septic causes or to mycotic invasion, being in the nature of the case but features of intrinsically dangerous or fatal primary diseases, do not call for special measures. It is different with those due to local trouble about the head and to surgical causes. Remarkable advances have been made in the operative treatment of cerebral abscesses, chiefly owing to the increasing accuracy of the localization of the affected areas through the disturbance of their function, and to the perfection of surgical methods. A number of cases by Gussenbauer, Wernicke, and others have shown that some abscesses may be accurately located during life by the focal symptoms produced by their presence. Wernicke's observation of a large abscess in the occipital lobe showed two facts. First, it permitted the study of the effect of large abscesses on the cerebral movements, as it was found after trephining that the pulsation movement of the brain was lost and the dura tensely bulging, thus indicating a high degree of cerebral pressure. Secondly, the operation showed that an abscess can be emptied of its contents, under moderate aseptic precautions, without provoking contiguous inflammatory reaction or infecting the meninges. Notwithstanding these favorable local conditions, the patient died. Gussenbauer⁶⁰ was more fortunate. He surmised from the fluctuation of some symptoms and the predominance of others that his patient had an abscess in the frontal lobe. The suspicion was verified: an abscess of the size of an apple was found, opened, and emptied of its contents. The patient recovered without any immediate untoward symptom.⁶¹

⁶⁰ Prager medizinische Wochenschrift, 1885, Nos. 1, 2, and 3.

⁶¹ Epileptic and focal spasms subsequently developed, which shows that a new inflammatory or other destructive process may have set in in the vicinity of the emptied sac.

The uncertainties of localization in some districts of the brain are so great that a number of attempts to repeat the explorations and aspiration of Wernicke and Gussenbauer have failed. In one case recently operated on in New York City the aspirating-needle was run into the brain-substance in several different directions without striking the pus. It is a question under such circumstances whether the chances of an abscess becoming latent, minimal though they be in cases with pronounced signs, are not to be preferred to those which an uncertain operation can give. The superficial encephalitic foci offer far better opportunities for surgical triumphs. Here not only the symptoms are much more constant, and point more unerringly to the site of the morbid spot, but there are often other signs, such as the evidences of impaction of a foreign body, local tenderness on percussion, or bone disease, which aid in determining the proper spot for the application of the trephine. Several operations where traumatic encephalitis existed with or without leptomeningitis of the convexity, followed by complete recovery, were performed by Macewen.⁶²

⁶² The Lancet, 1885, vol. i. p. 881.

The medicinal treatment of abscess of the brain is limited to derivative methods, whose aim is the relief of pressure—an aim whose fulfilment is more frequently illusory than otherwise.

Benefit has been claimed from the energetic use of mercury, chiefly in the form of calomel, by older writers; and recently Handfield Jones has endorsed its administration, attributing to it a remission in a case in which it was employed. It must be remembered, however, that remissions occur spontaneously in this disease, and that the purgative action of calomel may act well for the time being in an affection so apt to be associated with hyperæmia and increased cerebral pressure as is an abscess of the brain.⁶³ In the nature of the case, even this latter momentarily beneficial effect is at the best temporary.

⁶³ Brain, October, 1884, p. 398.

The prophylaxis of cerebral abscess can be carried out only in cases due to cranial and aural affections. The importance of treating all scalp and cranial injuries under aseptic⁶⁴ precautions is recognized by all surgeons. It is generally admitted that the trephining of a bone suspected to be the site of an ostitic or necrotic process involves fewer risks than the allowing it to remain. Similar principles govern the treatment of the inflammatory involvement of the mastoid cells often complicating otitis media. If trephined at all, these should be trephined at the earliest moment. It was a belief among the older aurists that the sudden cessation of an aural discharge was of evil augury, and that cerebral complications were more apt to follow under such circumstances than when the ear discharged freely. Von Tröltsch, Politzer, Gruber, and Toynbee have opposed the exclusive application of the old dogma. In so far as the older ear-surgeons regarded a profuse aural discharge as an encouraging sign, in this respect they were of course wrong. But their observation of the frequent concurrence of cerebral sequelæ with suppression of discharge is, I think, borne out by a large number of cases. It does not apply, however, to the suppression of discharge by the rational employment of aseptic injections.

⁶⁴ This term is used in its widest sense here.

Spinal Hyperæmia.

The spinal cord is found to vary considerably in color in different individuals. To some extent this difference is influenced by the position occupied by the body after death, but not as markedly as in the case of the brain. Thus it will be paler in a body which has been kept in the prone than in one which has been kept in the supine position.⁶⁵ It is usually found more injected in persons who have died of febrile affection than in those who have died of exhausting diseases; notably is this the case with typhus fever and with subjects who die with congestive malarial chill. But the most intense congestion, where the gray substance instead of having the normal rosy hue appears like a blood-soaked sponge, and the white substance instead of the tint to which it owes its name has a pink shade, is found in subjects dying in convulsive disorders complicated by asphyxia, such as epileptic status, tetanus, and certain toxic disorders.

⁶⁵ I have not seen it noticed anywhere, but it is a fact readily demonstrable in any autopsy made in a well-preserved body that when a short segment of cord is observed at the moment of section the section surface appears pale; but if it be again examined after a few moments, it will show a reddish tinge, marked as a faint injection would be; this tinge distinctly deepens under the eye. I have observed this in specimens which were not held in the hand, so that the influence of pressure can be excluded. Nor do I believe that the elasticity of the tissues is such as to account for the phenomenon.

In attempting to apply the fact that varying degrees of vascular injection are found on post-mortem examinations of the spinal cord to the elucidation of certain clinical phenomena, we encounter the same difficulties and sources of error that confronted us in the study of nutritive brain disorders. The majority of writers have therefore contented themselves with making a careful clinical study of the mostly subjective signs of disorders which, once designated as spinal anæmia and hyperæmia, are now classified under the non-committal titles of spinal irritation and exhaustion (neurasthenia), as in this volume. A number of these disorders, like the so-called anæmic paralysis of Bouchut, Leroy d'Etiolles, Beroliet, Baimer, and Brandis, would to-day be considered as hysterical or reflex; and a few of the instances cited by their contemporaries as cases of spinal hyperæmia have been since demonstrated to resemble the initial phases of organic diseases of the cord.

The causes of active spinal hyperæmia are either direct, as when the spinal centres are overtasked by muscular strain either through over-exertion or through toxic convulsions, surprised by violent shocks, such as concussion accidents, or collateral, as when a physiological discharge (menstruation) or a pathological one (hemorrhoidal flux) is suddenly checked. A few cases are reported where carbonic-oxide-gas poisoning provoked spinal hyperæmia. But, like the alleged cases of spinal hyperæmia after continued and exanthematic fevers, they were probably cases of incipient or established myelitis. Hammond claims that surface chilling exerts the same congesting influence on the cord which he claims for the brain; but no definite observations have been made in this direction.

Passive spinal hyperæmia has been attributed to obstructive cardiac and chronic pulmonary affections. In such cases, as with most causes acting on the circulation of blood in the nerve-centres, the coexisting cerebral congestion usually masks the spinal. It is a question how far the intense hyperæmia of the cord found in some cases of tetanus, strychnia-poisoning, and the condition called hydrophobia⁶⁶ is primary and an indication of neural hyperexcitability, and how far it is secondary to the asphyxia attending the last phases of these convulsive states. The weight of opinion is in favor of an acceptation of the latter as the chief or only factor.

⁶⁶ In a case of hydrophobia clinically as well marked as has been recorded, which I had the privilege of examining through the courtesy of Kretschmar, both brain and cord were found remarkably anæmic.

Over-exertion and sexual excesses are frequently followed by a sensation of fulness and tension in the sacral and lumbar regions, which may be relieved by lying prone, while it is aggravated while lying supine.⁶⁷ From the location of this pain it is evident that it is not due to congestion of the cord or its membranes, but to fulness of the vertebral and spinal veins of the lower segment of the vertebral column. A similar sensation, which may be relieved by the same change in position or by a hemorrhoidal flux, is complained of by patients suffering from portal obstruction. The veritable symptoms of hyperæmia manifest themselves in the parts which receive their nervous supply from the affected districts. The reflexes are usually more active; paræsthesias of different kinds, such as formication, tingling, and creeping sensations, are common; and there is more or less motor weakness, the limbs feeling heavy and sometimes being the seat of an acute pain. As a rule, these symptoms are limited to the lower half of the body.

⁶⁷ Although this fact has been questioned, I have no doubt whatever that it is true, from a large number of observations. In many subjects suffering from the results of excessive venery or masturbation, an intolerable, sometimes pulsating, feeling in the lumbo-sacral region is only relieved by raising the lower end of the trunk with the back up. This condition is influenced by a change of residence to a district having a different level above the sea, and consequently a different barometric condition.

There is very little question when these symptoms exist for any length of time, and become aggravated, that more subtle nutritive changes than are covered by the single term hyperæmia become responsible for them. In a pure hyperæmia the position-test of Brown-Séquard, which shows relief when the patient is upright or prone and aggravation when he is supine, particularly if the gravitation of blood to the cord be facilitated by raising the head and extremities, ought to yield constant results. But in some cases, particularly those of long-standing, the very opposite is noted: the patient's symptoms are aggravated by standing or sitting up, and relieved by lying down. Here there is probably exhaustion or malnutrition of the nerve-elements, rendering them abnormally sensitive to exertion. This view is supported by the fact that molecular disturbances, such as those which probably accompany simple concussion, predispose the patient to the development of the symptoms of spinal hyperæmia, and aggravate them if established previous to such accident.

Hammond,⁶⁸ who in his chapter on Spinal Congestion and Anæmia follows rather the older authors, such as Ollivier, than the newer and either more cautious or more sceptical writers on the subject, describes the symptoms of congestion as comprising belt sensations, paraplegia, erections of the penis, muscular twitches, loss of expulsive power, and incontinence of the bladder, paralysis of the abdominal muscles, paralysis of the anal sphincter, loss or abolition of reflex excitability, diminution of electro-muscular contractility, and occasionally hyperæsthesia and shooting pains. It is not doubtful for a moment that if such a case were to occur in hospital experience it would be regarded as one of organic disease, and not incipient, but well-established organic disease of the cord. Those making the diagnosis would have their opinion strengthened if, as Hammond states, the process took place with great rapidity and had a tendency to extend itself and eventually involve the whole cord, or if, as Brown-Séquard is by him cited as stating, bed-sores occurred in addition. Although Hammond describes certain anatomical changes, such as increased development of blood-vessels and distension and injection of them, I am unable to find any cases recorded as spinal congestion during life, and carefully examined with a due regard to sources of error after death, in which such changes were found. It is true that after strychnine- and cocaine-poisoning an intense hyperæmia⁶⁹ of the cord is found. In mammals it is of a far more pronounced character than in reptiles, and usually more marked in proportion to the existing asphyxia. That the characteristic toxic effects of these drugs is not to be sought for in their direct or indirect congesting influence is shown by the fact that exsanguinated frogs can be made to undergo strychnine tetanus when their blood is replaced by a saline solution according to the method of Salkowski. Little support, therefore, could be derived from a pretended analogy between toxic and pathological hyperæmias, even if the phenomena of both were similar; which is not the case.

⁶⁸ Diseases of the Nervous System, 7th ed., p. 392.

⁶⁹ It is true that in animals which are so organized that the congestion cannot be attributed to asphyxia, as I showed (Hammond Prize Essay of the American Neurological Association, 1878) in some experiments on strychnine, arterial congestion and small foci of hemorrhage were found in the upper cervical cord of frogs who had been kept in continuous strychnine tetanus for over seventy days.

The introduction of subaqueous caissons for workmen engaged in the building of bridges, in which those employed labor under abnormal atmospheric pressure, has led to the development of a previously-unknown cerebro-spinal affection known as the caisson disease, and in which, it is generally supposed, either congestion or hemorrhage of the spinal cord occurs in consequence of sudden changes of vascular pressure resulting from sudden diminution of the barometric pressure. Clinically, this affection has been studied in England, France, and above all in America in connection with the building of the East River Bridge and the one over the Mississippi at St. Louis.⁷⁰ Experiments by Hoppe-Seyler, Bert, and I. Rosenthal have shown that a sudden diminution of pressure leads to hemorrhages in various tissues, and, according to the two first-named, a development of gas occurs in the vascular and other fluids of the body. A number of peculiar symptoms which do not specially interest us here occur in conjunction with the so-called caisson disease: these are—pain in the ear, with or without otitis sicca; peculiar pains in the joints, which occur on leaving the caisson, and are probably due to hyperæmia of the joint-surfaces and sudden increase of the intra-articular fluid; and retardation of the pulse-rate. In some cases cerebral hyperæmia is added, the patients tottering about as if drunk. The spinal symptoms consist of a paraplegiform affection. The paralysis is usually sudden; in some cases the patient a few minutes after stepping from the air-chamber falls down perfectly helpless as far as the lower half of the body is concerned. The expulsive power of the bladder is usually weakened, and there is anæsthesia to all forms of sensation in the affected limbs, as well as diminished electro-cutaneous sensibility. The patient often complains of a strange feeling, as if the lower half of his body were a foreign substance. With this the electro-muscular reactions are normal. In the majority of cases these symptoms disappear entirely in from three to ten days, but occasionally they remain longer; imperfect recovery of motion and sensation occurs, or, as happened in a few cases, one of which was carefully examined during life by Lehwess and after death by Leyden, death occurs as in myelitis. In the only case where an autopsy and careful microscopical examination were made under these circumstances⁷¹ peculiar fissures were found in the substance of the spinal cord, surrounded by areas of reactive myelitis and filled with granule-cells. The absence of any pigmentary relics of a hemorrhage induced Leyden to assume that the lacunæ were not of hemorrhagic origin. He inclines to the view that they were due to the escape of gas from the blood-plasma, and consequent multilocular inflation of the tissue. If his observation be confirmed, it constitutes a strong objection to the hyperæmia theory of the caisson disease. There is neither permanent hyperæmia nor congestive or hemorrhagic myelitis developed, as far as the limited material thus far studied permits a conclusion.

⁷⁰ Clark, St. Louis Med. and Surg. Journ., cited from Hammond, loc. cit.

⁷¹ E. Leyden, Archiv für Psychiatrie, ix. p. 316.

Pure spinal hyperæmia rarely presents itself for treatment. The form due to over-exertion is recovered from by rest in a very short time; that due to suppressed discharges, by the re-establishment of the latter or by the application of leeches to the lumbo-sacral and iliac region. Ergotin is recommended by Hammond in very large doses. It is a question whether this drug may not exert a bad effect in protracted cases where its use has to be continued for a long time.⁷² In using it, it is well to bear in mind that imperfect nutrition of nerve-elements is perfectly compatible with an increased blood-amount.

⁷² A young physician, who for a long period took ergotin in twelve-grain doses for the relief of symptoms regarded as congestive, acquired a tolerance of the drug such as I have not seen recorded anywhere, and in addition presents some obscure signs of cerebellar disease and initial optic-nerve atrophy.

Strychnia has been given with benefit in the caisson disease—another evidence, as this drug is theoretically contraindicated in true hyperæmia, that this disease is not, as Hammond and the majority of authors with him regard it, essentially a congestive affection. The treatment of those numerous cases in which signs of venous fulness accompany spinal exhaustion and irritation is detailed in the articles dealing with those affections.

Spinal Anæmia.

Anæmia of the cord-substance proper, like hyperæmia, is practically inseparable from the corresponding condition of the membranes. The influence of a reduced blood-amount on the functional activity of the spinal cord is more susceptible of exact demonstration than the corresponding nutritive disturbance of the brain. As the functions of this segment of the nervous axis are far simpler than those of the higher organ, there is more unanimity among observers as to the interpretation of their disordered states. In Stenon's experiment, and the more elaborate modifications made by those who have followed his method, it is found that interference with the supply of arterial blood to the spinal cord is followed by abolition of the function of the gray matter; if the supply be still further diminished, the functions of the white tracts become eliminated; next the peripheral nerves, and ultimately the muscles themselves, lose their normal excitability. On the re-establishment of the circulation these various parts regain their functional capacity in the inverse order of its suspension—the muscles first, next the nerves, then the white substance, and last the gray substance of the cord. The initial symptoms of some cases of myelitis from refrigeration correspond more nearly to such a result of artificial anæmia of the cord than they do to anything that is customarily regarded as hyperæmia.⁷³

⁷³ I have seen distinct pallor of the spinal meninges on dipping the posterior extremities of a dog, whose cord had been exposed, into water. It is to be remarked, however, that other observers, notably Hammond, have either obtained different results or interpreted the consequences of refrigeration differently.

No one has gone farther than Hammond in erecting a theoretical anatomical framework which elaborately provides for the accommodation of various symptoms of spinal anæmia. He describes anæmia of the posterior columns, and sharply discriminates between it and anæmia of the antero-lateral columns. It is a question whether the conducting tracts of these columns are seriously affected in their functions by anæmia as long as the centres of innervation are well nourished. Undoubtedly, it is the gray substance of the cord which is most vulnerable to the influence of disturbed circulation and nutrition, as Stenon's experiment has shown; and a glance at the distribution of the blood-vessels will show that a partial anæmia or hyperæmia, limited to special cornua in any considerable length of the cord, is an exceedingly improbable occurrence. With regard to isolated anæmia of the white columns, it is to be admitted that the posterior are most vulnerable to malnutrition. But it is doubtful whether this vulnerability is so great as to allow of an exclusively posterior anæmia, or whether a protracted anæmia of this kind could exist for years as a purely symptomatic—or, as some designate it, functional—disorder.

Hammond candidly states that in specifically locating the lesions in these affections he is aware that post-mortem examinations are wanting to support them, and admits that what he calls anæmia of special parts of the cord is the spinal irritation of most authors, and in part the reflex paraplegia of others.

The most clearly-established form of cerebral anæmia is the one which is indicated by the ischæmic paraplegia of Jaccoud and the paraplegia following profuse hemorrhages. The former is produced by all causes which, by obstructing the flow of arterial blood in the abdominal or thoracic aorta, cut off the proper blood-supply to the cord, which the latter receives through the intercostal and upper lumbar arteries. Aneurism, compression by tumors, and embolism of the aorta produce this result. The consequence is paraplegia corresponding in all features of its development to the phenomena observed in Stenon's experiment. These features, already detailed, suffice to show that it is not the anæmia of the peripheral nerves and muscles that is chiefly responsible for the paraplegia, but the insufficient irrigation of the gray and white substance of the cord itself. The same is true of the paraplegia following hemorrhage which has been noted after uterine, renal, and enteric hemorrhages. Both affections are exceedingly rare.

The influence of general anæmia on the functions of the spinal cord is not susceptible of accurate study. The cerebral enlargement of the nervous axis is so much more unfavorably situated than the cord that it suffers first and most when general anæmia is present. The consequence is that the signs of cerebral anæmia mask those of spinal anæmia. It is supposed, however, by many authorities that the effect of anæmia on the cord may be regarded as an auxiliary factor in the production of hysterical and neurasthenic symptoms.

How far the spinal cord is liable to suffer from arterial spasm is as yet a matter of conjecture. It is supposable that just as a powerful psychical impression provokes a sudden spasm of the cerebral arteries, so a peripheral irritation may provoke a spasm of the spinal arteries. In this way the reflex paralyses, motor and vaso-motor, are explained by many writers.

The subject of reflex palsy has been so much confused by improper cataloguing—if it can be so called—that some of the best authorities have become sceptical as to its occurrence. Among the chief sources of error has been the attributing to irritation of the genital organs various convulsive, psychical, and paralytic disorders. Adherence of the prepuce and its excessive length were charged with being responsible for idiocy, imbecility, epilepsy, and every form of paraplegia and panplegia. It was further claimed that instances of complete cure of each of these affections had followed the removal of the exuberant or adherent prepuce. I cannot find a single instance recorded where such a cure was effected in any of our large medical centres, so as to prove convincing to critical colleagues. On the contrary, L. C. Gray⁷⁴ has shown that various surgical procedures have been needlessly resorted to on this erroneous theory in cases of organic diseases of the spinal cord. I have seen two unfortunate children suffering from the worst forms of anterior poliomyelitis, one afflicted with pseudo-hypertrophic paralysis, and several hydrocephalous and microcephalous idiots, whose prepuces had been sacrificed to the theory alluded to—it is needless to add without any result, good or bad.

⁷⁴ Reflex Irritation from Genital Irritation. In this paper written communications from all or nearly all neurologists in the United States—certainly including all those of national fame and large experience—are cited, in which they testify to never having seen a case of this character cured by operations on the penis (Annals of Anatomy and Surgery, Jan. and Feb., 1882.)

The possibility of a reflex paralysis occurring from genital irritation in the male cannot be denied; among the lower animals a ligature around the spermatic cords sometimes produces paraparesis, and paraplegia is a common complication of renal and vesical troubles in others. But analogous observations in man are rare, and becoming rarer with our increasing acumen in diagnosis. In females peculiar reflex disturbances are found associated with uterine and ovarian derangements. In one case of retroflexion, with possible dislocation of the ovary, referred to me by H. J. Boldt, there is a remarkable vaso-motor paralysis of the right arm during each menstrual period: this member becomes greatly enlarged, of a purplish-blue color, and cold. Equally remarkable are the reflex disturbances resulting from the presence of worms in the intestinal canal. Every form of spinal and cerebral paralysis, even aphasia, has been observed in connection with helminthiasis. Such disorders yield as rapidly as they are developed to the exhibition of vermifuges.

Special interest has been aroused by the discovery laid down in the joint treatise of J. W. Mitchell, Morehouse, and Keen of reflex paralysis following injuries, observed in the War of the Rebellion. The cases cited by them appear singular on first sight. The paralysis is often observed in parts of the body which are not only remote from the seat of injury, but have no direct connection, physiologically or otherwise, with it. The hand may be injured and the opposite leg paralyzed.

Since Mitchell, Morehouse, and Keen first announced the existence of this peculiar form of reflex paralysis a careful search has been made by military surgeons engaged in other campaigns for like results. Notably was this done in the Franco-Prussian War. A number of confirmatory instances have been collected, some of which rival in singularity those related by the discoverers of the affection. In one case a unilateral paralysis agitans followed a punctured wound of the opposite shoulder, and in another reflex aphasia followed a gunshot wound of the lumbar region.⁷⁵ A discrimination is to be made between such cases where the paralysis, anæsthesia, or neuralgia is an immediate result of the injury, and those where they follow after weeks or months. In the latter instance we have not true reflex disorders to deal with, an ascending neuritis having been found in the few cases which could be carefully followed up.⁷⁶

⁷⁵ Sanitäts Bericht über die deutschen Heere im Krieg gegen Frankreich, 1870-71, vol. vii.—abstracted in Neurologisches Centralblatt, 1886, p. 207.

⁷⁶ In a case of Mollenhauer's, vesical paralysis and paresis of the right leg occurred six years ago (1880) in a veteran of our civil war who had a gunshot wound of the right hand, with signs, which are still present, of occasional exacerbation of brachial neuritis. Prodromal signs of paresis were noticed at intervals since his return from the campaign. The bladder trouble and paresis are now apparently stationary. Such a case can be accounted for only on the assumption of an organic cord-change secondary to a neuritis.

The theory that the reflex paralysis from utero-ovarian, intestinal, and surgical affections, when acutely produced, is due to central anæmia, is as acceptable as any other would be in the absence of decisive observations.

Spinal anæmia will but rarely present itself as a subject for special and separate treatment. When not associated with an intrinsically grave condition, such as aortic obstruction, dysentery, fatal hemorrhage, or typhoid fever, it is an exceedingly benign affection, rapidly yielding to tonic and restorative measures combined with rest.

Embolism, Thrombosis, Hemorrhage, and Abscess of the Spinal Cord.

Although the spinal cord is a segment of the same central organ as the brain, nourished in a similar way, and subject to the same physiological and pathological laws, lesions of the vascular apparatus, which play so important a part in brain pathology, play a comparatively insignificant one in that of the spinal cord. Embolic, thrombic, and primary hemorrhagic lesions of the cord are so rare that their possible existence has even been denied. A primary thrombosis of the cord has not yet been satisfactorily demonstrated to occur independently of syphilitic lesions; and when it occurs the ensuing tissue-changes, as described by Heubner, Julliard, and Greiff, are usually in the background as compared to the gummatous, sclerotic, or meningitic changes which coexist. The clinical as well as the anatomical picture is accordingly either one of a myelitis or meningitis, as the cases of Charcot-Gombault, Heubner, McDowell, Wilks, Wagner, Zambaco, Homolle, Winge, Moxon, Schultze, Westphal, Julliard, and Greiff show. (See Myelitis and Spinal Meningitis.)

With regard to the occurrence of hemorrhage into the substance of the spinal cord (hæmato-myelia), it is so rare an occurrence that I can recall but a single case in which I entertained the diagnosis of this lesion; and in that very case I am unable to declare that it was not a hemorrhagic myelitis. Aneurismal changes of the spinal arteries are comparatively of rare occurrence, and as other predisposing causes to primary vascular rupture are rare in the cord, the probability of its occurrence is very much diminished. Hebold,⁷⁷ in a young girl who had developed severe cerebro-spinal symptoms during a period of nine months following an erysipelatous disorder, found the upper dorsal cord, on section, dotted with numerous reddish and round points. These points corresponded to aneurismal dilatations of the vessels. As there were other inflammatory and vascular lesions in the same subject, the author referred their causation to a general constitutional vice, the result either of the phlegmonous or of a tuberculous disorder.

⁷⁷ Archiv für Psychiatrie, xvi. 3. Rupture of miliary and other aneurisms in the meninges has been reported by Astley Cooper, Traube, and others. It is remarkable that such cases are more and more rarely recorded from year to year in inverse ratio to the accuracy of our spinal autopsies. I have never found a miliary aneurism below the uppermost cervical level of the cord. On the other hand, I have found extensive spinal hemorrhage in cases where the vessels of the cord proper were fairly healthy.

It is claimed that suppression of the menses, over-exertion, lifting heavy weights, and concussion are causes of spinal hemorrhage. The same causes are also mentioned for acute hemorrhagic myelitis; and it is a question whether the supposed hemorrhage is an initial lesion or secondary to congestive or anæmic softening.⁷⁸

⁷⁸ I have never found vascular ruptures, although carefully searching for them, in the spinal cord of persons dying instantly after falls from a great height, or, as in one case which I was fortunately able to secure the cord of, where the subject had been violently thrown down. Where hemorrhages have been found under these circumstances they were, as far as I am able to learn from the cases recorded, meningeal.

The symptoms attributed to spinal hemorrhage are the same, taking the same locality of the cord, as those of a very rapidly-developed transverse myelitis. It is unnecessary to enumerate these here in anticipation of the next section. They are described as being much more sudden. This suddenness is the only diagnostic aid on which we can rely.⁷⁹ The fate of the patient is said by Erb to be decided within a few days. If he survive the immediate consequences of the hemorrhage, he is apt to recover, as to life, altogether, with such permanent atrophies, paralyses, and anæsthesias as are entailed by the destruction of the tracts and gray substance involved in the hemorrhage. The treatment recommended for this condition consists of rest, either in the lateral or prone position, local depletion and derivation to the intestinal canal, as well as the internal use of ergotin. The local application of ice, which is also advised, is probably based on illusory views.⁸⁰ After the immediate danger is past the case is to be treated as one of myelitis—a very safe recommendation in view of the probability that it was a case of myelitis from the beginning.

⁷⁹ And even this sign is unavailable as a distinguishing feature in supposed hemorrhage from concussion, as sudden paraplegias of motion and sensation are found in some cases of railway spine, and, although a number of cases terminating fatally have been examined, there was not always hemorrhage even in the meninges.

⁸⁰ Until authorities shall have agreed as to what effect the exposure of the bodily periphery to certain temperatures has on the circulation of the cord, it would be premature to make any special recommendations as to the temperature at which they should be kept. I am inclined to believe that while, as is universally accepted, a general cooling of the bodily surface tends to increase vascular fulness in the cord, as in all other internal organs, a partial cooling, as of the feet, produces local anæmia at the level of origin of the nerves supplying the cooled part. Certainly, the bilateral neural effects of unilateral cooling are in favor of this view.

The descriptions given of the hemorrhagic foci as observed after death strengthen the view that they were in the majority of cases of myelitic origin. Usually, they are stated to extend up and down the cord in the direction of least resistance—that is, in the gray substance—resembling an ordinary apoplectic clot. But in their neighborhood there was usually considerable softening, and, to judge by the descriptions given, this softening differed in no wise from that which is the characteristic feature of acute myelitis;⁸¹ and often the transition from a peripheral zone of white softening, through an intermediate zone of red softening, to a central compact clot, is so gradual as to leave it unquestionable that the softening pre-existed, and that a vessel had broken down in the midst of the myelitic detritus. Many ancient foci of myelitis betray the hemorrhagic complication of their initial period by the presence of pigmented residue of the absorbed clot.

⁸¹ In the latest treatise on nervous diseases published in our language (Ross, loc. cit., vol. ii. p. 325) the insufficient foundation on which a whole chapter has been built up is illustrated by the admission that the usual evidence of acute central myelitis may be observed far beyond the limits of the hemorrhagic infiltration. If a large area of softening in the brain were found to contain a central or peripheral clot of blood, and histologically resembling a typical embolic or thrombic softening, no one would be in doubt as to which of the two was the primary lesion.

Embolisms and embolic softenings of that part of the spinal cord which is supplied by the small spinal vessels are so rarely observed in the dead-house that our knowledge of their possible occurrence and character is almost entirely the result of experimental observations or based on analogy. The situation of these vessels, the angle at which their supply-tubes are given off from the aorta, all act as protectors of the cord against what is one of the chief dangers to which the brain is exposed. No definite symptoms have been attributed to the few doubtful cases of simple embolic occlusion of the spinal arteries found accidentally in human subjects. Even those emboli which, when once let loose in the circulation, are found distributed in nearly every organ of the body, those derived from ulcerative endocarditis and those due to the invasion of micrococci, are comparatively rare in the cord. Leyden found multiple capillary emboli in the spinal cord from the former cause. Small grayish white foci in a similar distribution were found to be due to an invasion of cocco-bacteria from a decubitus by Rovigli.⁸² In this latter case an increase of pain and muscular spasm in the history of the case of sclerosis which was thus complicated was attributed to the parasitic affection.

⁸² Rivista sperimentale di Freniatria, 1884, x. p. 227.

Just as simple and infectious embolic lesions are frequent in the brain and rare in the cord, so purulent inflammation or abscess is an exceptional occurrence in spinal as compared with cerebral pathology, and probably for the same reasons.

Simple Acute Myelitis.

SYNONYMS.—Spontane (primäre) acute Rückenmarkserweichung, Softening of the spinal cord, Ramollissement blanc de la moelle, Myélite aiguë.

As Leyden, whose treatise⁸³ may be regarded as the foundation of our knowledge on this subject, correctly avers, it is to Abercrombie and Ollivier that we owe the determination of the existence of that acute structural disease of the spinal cord, now termed myelitis, as an affection independent of meningeal changes. The anatomical descriptions given by these older writers may be accepted at the present day as models of accurate observation by the naked eye. Their statement that in acute myelitis the substance of the spinal cord is softened and changed into a puriform, yellowish, diffluent mass; that while the disorganization is sometimes more marked in the posterior, at others in the anterior, and occasionally in the lateral half, it is most pronounced in the axis of the cord, because the central gray substance is the favorite starting-point of the morbid process,—requires no modification to-day. Considerable doubt existed in the minds of the contemporaries of Ollivier and Abercrombie as to whether this change was the result of a true inflammation; and one of the clearest thinkers of the day, Recamier,⁸⁴ regarded myelitic softening as a lesion peculiar to the nervous apparatus, and different from ordinary inflammation. I believe that the most profound investigators of the present day have not been able to rid themselves of a similar doubt. The discovery of Gluge's so-called inflammatory corpuscles, which was regarded as settling the question, only served to confuse the student by the confidence with which it was urged that they were infallible criteria of the inflammatory process. Under the non-committal designation of granule-cells these bodies still flourish in the annals of cerebro-spinal pathology. As we shall see, a number of products of real disease, of artifice, and of cadaverous change have passed and do pass muster under this name. The first substantial progress in our knowledge of the minute processes underlying inflammation of the spinal cord was made by Frommann and Mannkopf, but it applied altogether to the chronic inflammatory or cirrhotic affections of the cord. The difference between acute and chronic myelitis is greater than is the difference between acute and chronic inflammation in any other organ; and it must be admitted that if Recamier is to be regarded as having erred in asserting that acute myelitis is not a true inflammation, he is justified in so far as he asserted many features of the process to be altogether peculiar to the organ affected. Leyden himself attempted to throw light on the subject by provoking myelitis experimentally in dogs. He injected Fowler's solution into the spinal cords of three dogs, and in each instance produced changes which he interpreted as comparable to the myelitis of human pathology. But the inflammation thus provoked was not of the cord-substance alone; it also involved the membranes, and the inflammatory foci were in several instances purulent. Now, pus never⁸⁵ forms in ordinary myelitis. An abscess of the cord never occurs where a septic agency can be excluded. In six dogs whose spinal cords I wounded in the dorsal and lumbar regions by aseptic methods, and who survived from two to seven days, I never found purulent or indeed any active inflammatory process, as that term is ordinarily understood, but exactly such passive and necrotic or reactive changes as occur in the acute myelitis of human pathology.

⁸³ Klinik der Rückenmarkskrankheiten, ii. p. 115.

⁸⁴ Cited by Leyden.

⁸⁵ In the textbooks and encylopædias, without an exception, the statement that pus may be a product of myelitis is made. This is true of traumatic cases and of such depending on septic and zymotic causes alone. I am unable to find a single carefully observed case of the occurrence of pus in simple myelitis in the literature.

Owing to the advance of clinical and anatomical knowledge made within the past fifteen years many forms of spinal disease classed with the inflammations have been recognized as distinct pathological entities, no longer to be confounded with simple acute myelitis, ordinarily so called. Special forms of acute spinal paralysis, notably acute poliomyelitis anterior of children and the corresponding chronic affection among adults, have become separated in this way, and are accordingly treated of in separate parts of this volume.⁸⁶

⁸⁶ For other and practical reasons the traumatic and compression forms of myelitis are also assigned a separate place.

Some dispute exists as to the propriety of making a distinction between acute and chronic myelitis, since an acute myelitis, if the initial attack be recovered from with life, presents a similar condition clinically as chronic myelitis; and this quiescent or slowly-progressing condition may extend over many years. The term acute with reference to inflammation of the spinal cord refers only to the active period of the disease. Just as an embolic softening of the brain is an acute affection, but may be followed by a chronic paralysis or aphasia, so the acute myelitic process may be followed by a chronic paraplegia. It is improper to call the latter a chronic myelitis. It is merely a protracted symptomatic sequel of the acute process. The latter is distinguished from chronic myelitis both clinically (by the rapidity of its onset) and anatomically (by the early dissolution of nerve-elements in the focus of disease). Limited in this sense, acute myelitis, excluding the special clinical forms already adverted to, is rather a rare disease.

MORBID ANATOMY.—The most recognizable change noted in an acute myelitic focus is one of consistency: the spinal substance is softened. In some cases the softening is so slight that the observer may doubt whether he has a pathological or cadaveric softening to deal with, the dorsal cord, which is most apt to be the site of an acute transverse myelitis, being precisely the part which is most apt to show the latter change even in fairly well-preserved bodies. In extreme cases the softening may be so intense that the cord-substance, completely fluidified, runs out of the meningeal sac, leaving the latter a collapsed membranous cylinder to mark the place where the cord once was. Where the cord-substance is sufficiently firm to permit of sections being made through it, the normal outline of the gray and white substance is found obliterated, either presenting the appearance as if the gray and white matter had been stirred up together or of a more uniform color-change. The color may be either white, reddish, yellowish, or chocolate-like. It depends upon the participation of the blood-vessels in the change. If there be much hyperæmia, there will be developed what is known as red softening; if there be much extravasation and commingling of blood with the diffluent cord-tissue, a chocolate color will mark the diseased area; and similarly one and the same focus may present different tints in different parts according to the age and intensity of the process and the more or less advanced retrogressive metamorphosis of the extravasated fluid. As already stated, the purulent form of softening or abscess does not occur in ordinary myelitis.

There is considerable variation in the extent of the affected areas of acute myelitis. In the typical and severe transverse form the whole thickness of the cord may be disorganized, and the disorganization may extend in the length of the cord, so as to involve the level of exit of from two to five pairs of nerves. In less furibund cases the area of absolute softening is confined to the gray substance and its immediate neighborhood, the submeningeal white substance being but slightly affected or escaping. Sometimes several foci of intense softening are scattered through a short length of the cord and connected by less severely involved areas of softening or œdema. Leyden distinguishes three types of distribution—the transverse, the longitudinal, and the disseminated insular or multiple form. He includes under the longitudinal type the so-called central softening of Albert, but undoubtedly many cases of syringo-myelia have passed under this designation. The submeningeal form of softening which, with Ollivier, he states to occur in association with spinal meningitis, must be a very rare affection, as it is difficult to find a well-established case recorded. The longitudinal form shows the same predilection for the gray substance which the acute myelitic process generally does, but I have seen a finely demarcated fascicular myelitis limited to the lateral column in a paretic negro. In this case the pyramid tract and the contiguous area in front of it were so intensely softened that for a length of twelve centimeters a hollow canal ran through the cord in the place previously occupied by the diseased substance. In recent cases of myelitis the diseased area is usually found surrounded by a transition zone in which, the morbid change gradually becoming less intense, the consistency is firmer, and which merges into that of the normal cord. In cases where death occurs after a few weeks a more abrupt demarcation is usually found; this is due to the reactive changes occurring in the neighborhood. The connective tissue becomes firmer, and thus the softening centre becomes surrounded by a sclerosing capsule. Ultimately, the centre undergoes complete disintegration and absorption, and a cavity is left behind filled with a clear fluid; in short, a cyst surrounded by a firm capsule represents the residua of disease. In cases where the softening at the centre of the focus does not proceed so rapidly nor reach so high a degree as to result in liquefaction, the less vulnerable elements, the blood-vessels and supporting tissues, survive the death of the ganglionic and conducting substance; the connective elements hypertrophy, and thus a firm sclerotic patch is formed, indicating the location of the previously softened field.

It seems to be generally admitted, with Hayem, that the blood found exuded in the hemorrhagic form of myelitis does not necessarily indicate an active determination, but is rather, like some forms of so-called red softening of the brain, the result of capillary rupture or necrosis in the midst of the disintegrated tissue, now rendered incapable of supporting the vessels. The existence of a purely white form of myelitic softening shows that a textural change is the primary occurrence, and that the participation of hyperæmia or congestion is not an essential feature of myelitis. The assumption of an initial inflammatory congestion is made rather on theoretical grounds than on the basis of observation. It is simply incredible that, as Ross⁸⁷ claims, white softening should be a third stage, preceded by red and yellow softening as a first and a second stage! How the extravasated blood, which pathologists generally allow to leave long-lasting traces, manages to disappear, and how blood-vessels in the midst of necrotic or œdematous surroundings suddenly acquire such contractile energy as to produce a total emptying of their contents while the perishable nerve-elements remain behind, are problems which should be solved before attempting to assign to a condition which is often found to be a primary phase of myelitis the position of a late and regressive stage. Erb admits that red softening, to which he also assigns the position of a first stage, is very rarely seen, only traumatic and rapidly fatal cases of central myelitis offering opportunities of examining it. None of the various forms of exudation claimed to occur at this period under the names of vitreous, colloid, or hyaline deposit have been confirmed in any recently well-studied case.⁸⁸ The great mass of authorities, however, still agree in regarding the minute changes of the initial stage of myelitis to correspond to those of ordinary inflammation. The vessels are described as injected, the adventitial spaces as crowded with the formed elements of the blood, and the vascular walls and the neuroglia infiltrated with granule-cells and fatty granular matter. By some, inflammatory changes of the neuroglia are described, but I am unable to find a single case in which these were determined in early fatal cases. As far as our observation goes, the hypertrophy of the neuroglia is a later occurrence.

⁸⁷ A Treatise on Diseases of the Nervous System, 1882, vol. ii. p. 280. The author states no authority, nor does he advance his own observations in support of this statement.

⁸⁸ Baumgarten's case of hyaline exudation, Archiv der Heilkunde, vol. xvii. 276, was an infectious myelitis and associated with anthrax.

As to the nervous elements themselves, they are always found affected. The nerve-cells appear inflated, their processes fragile, sometimes suddenly swollen in their course, at others very thin and brittle. Multiplication of the nuclei of the large multipolar cells has been described. It must be an unusual occurrence, as it has been confirmed by but a few of the numerous observers who have examined into this question. The protoplasm of the nervous elements loses its normal striation and fine molecular granulation; it becomes either coarsely granular or hyaline. The axis-cylinders, both in their intracinereal and their intramyelinic course, show changes similar to those of the cell-processes in the gray matter. Particularly frequent are swellings in their course, the diameter of the cylinder being so much increased as to almost equal that of the myelin tube. This increase in diameter is regarded as an inflammatory swelling by some, as secondary to disturbed nutrition by others; it precedes disintegration: the substance becomes granular, fragile, and in the end dissolves. In the mean time the myelin loses its continuity, irregular segments of it fusing into round and oval masses.⁸⁹

⁸⁹ Many of the bodies represented as granule and colloidal cells are in reality round spheres of myelin, whose resemblance to a nucleated cell is sometimes heightened by their occasional inclusion of a fragment of an axis-cylinder which has not yet lost its power of imbibing carmine and other dyes. Where softening has proceeded farthest, there the spherical and other forms of myelin are found crowding the field, and mingled with them are blood-corpuscles, fragments of blood-pigment, granular detritus, and bodies known as fatty granular cells. A number of bodies of very different origin have received this name, some of them, like the fragments of myelin alluded to, not even meriting the name of cells. Others, however, are veritable formed histological elements, either leucocytes or cellular ingredients of the neuroglia, which, having fed on the products of myelin disintegration, have become enlarged and coarsely granular. The longer the duration of the process the more numerous are these bodies, showing that they are not the coarse and essential factor of the inflammation, but an accompaniment, subserving some conservative process, inasmuch as they either remove effete material or contribute to the permanent organization of the cicatricial or atrophic tissue.

The period now reached by the morbid process may be regarded as a sort of interregnum. The necrotic tissues have not yet disappeared on the one hand, the products of inflammation have not yet organized themselves on the other. It is in this period that the ganglionic elements are described as undergoing certain changes in outline and in appearance. Above all, one change has interested observers, which, consisting in the development of what appear to be spherical vacuoles in the interior of the cell, is termed vacuolization. I can compare it to nothing so nearly as to the appearance which is produced by the formation of gas-bubbles in a putrefying albumen or other semifluid substance.

This vacuolization of ganglion-cells is now regarded as a cadaveric change. It is not agreed, as yet, whether its occurrence in myelitis is so frequent as to suggest its ante-mortem occurrence as a veritable feature of the disease. I have been struck by this change in the neighborhood of wounds artificially produced in dogs, even in the fresh specimen. It must be remembered, however, that under these circumstances, the nutrition of the cell being destroyed and exposure to the macerating effect of the cerebro-spinal and pathologically exuded fluids occurring, a cadaveric change may take place intra vitam.

The influence of phosphorus and alkaloid as well as metallic poisons on the cord has been experimentally studied by a number of observers. Unfortunately, Popow, Tschisch, and Danillo—who described as characteristic a resulting change in the staining reaction of the cells, the development of vacuoli in them, and an atrophy of their processes—had not made a sufficient number of examinations of normal cords under like methods of preparation to recognize which of these deviations is without the physiological confines. Kreyssig⁹⁰ demonstrated the existence of all these conditions in the cords of perfectly healthy animals preserved in chromic acid;⁹¹ and Schultze confirms him, and expresses a surprise, which must be shared by all reflecting investigators, that poisons of so widely different a character should have an identical effect on the cord-substance, as is claimed by the writers named.

⁹⁰ Virchow's Archiv, cii.

⁹¹ He attributes the remarkable difference in staining of nerve-cells of the same ganglionic group and in the same section to the sudden transferral of the hardened specimens to strong alcohol, which seems to be the custom in some German laboratories. He claims that uniformity in staining is effected if the specimen be transferred from the chromic preparation to weak alcohol, then to stronger, and thus by gradual increase of the strength to strong spirit. Possibly, instead of approximating the real structural indications by this method, Kreyssig may obliterate them. In specimens which alcohol is not permitted to touch before staining is completed, very deeply and very lightly stained cells will be found almost side by side. The shorter the hardening process, the more perfect the staining method, the more likely are these differences to be found. It is reasonable to assume that the difference in dye-absorbing power indicates slight differences in the cell-protoplasm, marking the nutritive state of the latter and occurring within physiological limits.

If life be prolonged and the conservative processes assert themselves, the disintegrated material disappears, and as the white color of the greater area of the cord was due to the myelin, and the latter has now become destroyed within the diseased area, the latter presents a grayish color. This phase is often termed gray softening. The consistency is, however, much firmer than in the previous stage. Trabeculæ of connective tissue form, enclosing in their meshes a large number of neuroglia-nuclei and sometimes spaces filled with fluid. According as condensation and retraction or rarefication preponderate the process will terminate either in the formation of a sclerotic focus or of a cyst. Occasionally an irregular spongy tissue containing several small cysts results.

Charcot claims that a restitution of anatomical continuity, and therefore of physiological potentiality, may occur in a myelitic cicatrix. But the experiments of Kahler⁹² and Homén⁹³ prove that when a nerve-tract is once destroyed within the spinal cord all hope of restoring that tract in structure, and thus to restore its functions, is at an end. Unlike the fibres of the peripheral nerves, those of the spinal cord and brain do not seem capable of regeneration.⁹⁴ If a restoration of function is to occur at all, it must occur through other channels than those destroyed—in other words, by vicarious action.

⁹² Prager medizinische Wochenschrift, 1884, No. 31.

⁹³ Contribution expérimentale à la Pathologie et à l'Anatomie pathologique de la moelle épinière, Helsingfors, 1885, abstracted in Centralblatt für die medizinisches Wochenschriften, 1886, No. 16.

⁹⁴ According to the first observer, this is probably due to structural differences. The extramedullary fibres have a sheath and annular constrictions which are absent in the intramedullary.

In a large number of cases myelitis is a limited affection; that is, its ravages remain confined to the area originally involved. But occasionally the morbid process involves the next segments above or below, extending with specially great rapidity through the anterior gray horns. Exceptionally, the entire cord may thus become the site of a generalized myelitis. There is one segment of the cord which may be regarded as possessing an acquired vulnerability when a myelitic focus is in its neighborhood, and that is the lower end. It seems that while the results of a transverse myelitis in the middle dorsal cord may remain stationary for ten or more years, those of a transverse myelitis at the upper lumbar level do not; on the contrary, the entire cord below the lesion appears to be doomed to undergo the same degeneration by contiguity. This is the only occurrence which seems to deserve the name of a descending myelitis: an ascending extension is more frequently noted in other parts of the cord, but the frequency of both the so-called ascending and descending types has been unduly magnified by the inclusion of the secondary degenerations, which are constant sequelæ of all complete destructive transverse lesions of the cord, but which are rather passive phenomena, and probably influence the clinical progress of the case but little, except under such conditions as are potent in that chronic form of myelitis which underlies tabes dorsalis.

CLINICAL HISTORY.—The symptoms of acute myelitis usually correspond to those of any more or less completely transverse lesion of the cord, and accordingly vary with the altitude of the upper level of the lesion. In a general way, they may be stated as consisting of—

First, paralysis of movement in the parts supplied from the nerves given off below the level of the lesion. The reason for this can be easily recognized in those cases where the pyramid tract, which conveys voluntary impulses centrifugally, is interrupted by the softening.

Second, paralysis of sensation in the parts supplied by the same nerves. This is equally explained by the pathological interruption of the centripetal impressions normally conveyed brainward.

Third, alterations in the nutrition of the parts supplied by the nerves arising in the affected level.

Fourth, abolition of those reflexes which are translated in the level of the lesion.

Speaking crudely, then, the symptoms of a transverse myelitis fall into two natural groups. The one which includes the first and second categories enumerated are symptoms due to interruption of cerebral functions; the other, which comprises the last two categories, being due to abolition or perversion of spinal functions. There is a third group comprising certain constitutional symptoms.

Aside from those variations due to the distribution, extent, and intensity of the lesion there are others which depend on the rapidity of its invasion. There are three types in this respect—the apoplectiform, the ordinary acute, and the subacute. The term apoplectiform has been used in two different senses, one being clinical, and referring to the rapidity of onset of the symptoms; the other anatomical, and referring to the nature of the lesion. It is, however, doubtful if a distinction in the latter sense is practically valuable. The presence of a blood-clot in a myelitic focus is itself secondary to the softening, and the intensity and rapidity of the process must have shown itself in the development of the latter.⁹⁵ The term ought, therefore, to be used in a clinical sense only.

⁹⁵ I am able to recall but a single case in which, even clinically speaking, a primary hemorrhage into the cord-substance was plausible. In this instance a sudden arrest of menstruation had occurred nearly simultaneously with a combined strain and exposure in a young girl.

The constitutional symptoms of acute myelitis—which, however, are often absent—are its most distinctive features in one sense. Disorders of motion and sensation and perversions of nutrition are signs common to all destructive affections of the cord, whether of a traumatic, neoplastic, or a chronic inflammatory character. But fever, headache, and delirium,⁹⁶ associated with gastric and visceral disturbances of acute development, are not found to be initial and intrinsic symptoms with them as with acute myelitis. In their absence the mode of onset is characteristic. A high degree of paralysis, motor or sensory, is developed with a rapidity unequalled in any chronic affection of the cord. Sometimes there is a prodromal period in which formication, numbness, and disorders of movement are observed in the same part of the body which are destined to become paralyzed at a later stage of the malady. Within a few hours, days, or at most weeks, complete paraplegia may become developed. The prodromal symptoms may include any form of disturbed sensation. Lancinating pains, tingling, a feeling of the limbs falling asleep, peculiar and indescribable sensations attending the acts of micturition and defecation or of placing the feet violently on the ground, are common. Occasionally they are found in one limb only, although motor and sensory paralysis may ultimately occupy the symmetrical member as completely as the one first involved. In some cases it has been noted that the patient is unable to lie down, or, if lying, to occupy the dorsal recumbent position. This feature has been utilized to support the theory of an initial congestion, which is supposed to be relieved or aggravated according as the cord is kept elevated or depressed.

⁹⁶ These symptoms are to be regarded as actual parts of the myelitic symptoms only when they accompany the prodromal or initial periods. The later complications, uræmia and septicæmia, the latter arising from pyelitis, cystitis, or decubitus, often lead to constitutional disturbance which is not due to the myelitis as such.

In most cases of transverse myelitis, when the anterior cornua are destructively involved, we possess in the electrical tests valuable and unerring means of determining the altitude and extent of the lesion. Whenever we find the atrophy of a paralyzed muscle accompanied by qualitative electrical changes in myelitis, we must conclude that the cell-group from which that muscle receives its nerve-supply is destructively involved.⁹⁷ These changes are particularly well demonstrable when the cervical or lumbar enlargements are affected. They are not as readily ascertainable in the case of a transverse myelitis in the upper dorsal region, on account of the situation of the muscles supplied by the upper dorsal nerves, and the consequent difficulty of application of the necessary tests.

⁹⁷ The proposition, originally, I believe, made by myself, that there are distinct cell-groups in the spinal cord which are constant with certain animal species, and correspond in relative development to ventral, dorsal, and appendicular muscular groups (“Architecture and Mechanism of the Brain,” Journal of Nervous and Mental Diseases, April, 1880), appears to be confirmed in a general way by the researches and cases of Edinger, Kahler-Pick, Dejerine-Major, Genzmer, Von Monakow, Sahli, Prévost-David, F. Schultze, Remak, and Parrot-Joffroy; for the knowledge of the first and last of which I am indebted to the review of the subject by Starr (“Localization of the Functions of the Spinal Cord,” American Journal of Neurology and Psychiatry, August, 1883).

The disturbance of the deep reflexes with very few exceptions affects the same peripheries as are represented in the destroyed and impaired gray nuclei. Thus, if the lower part of the lumbar enlargement be affected, the reflexes of the Achilles tendon and the gluteal muscles will disappear; if the upper lumbar enlargement, the knee-jerk disappears.⁹⁸ Disease of the lower part of the cervical enlargement is in like manner associated with absence of the wrist-tendon reflexes, while the disappearance of the elbow-tendon reflex suggests a higher involvement at the levels of the fifth and sixth cervical nerve-roots.

⁹⁸ The disappearance of the knee-jerk and similar reflexes was originally supposed to be a phenomenon exclusively pertaining to spinal disease and to a destructive lesion anywhere in the track of the centripetal and centrifugal nerves connected with that segment of the cord in which the reflex is supposed to be translated. But aside from a number of physiological observations⁹⁹ which prove that cerebral conditions may influence the intensity of the jerk, there are pathological ones which show that it may be permanently abolished in disease of the pons and cerebellum, and temporarily abolished or diminished immediately after capsular and ventricular hemorrhage. The associated symptoms in the former case, and the history of the onset and total hemiplegia in the latter, serve to distinguish them from destructive spinal lesions should the occasion for discriminating between them ever arise; which is not likely.

⁹⁹ S. Weir Mitchell and M. J. Lewis found that voluntary effort increases the jerk at first, but if continued diminishes its excursiveness (The Medical News, 1886, Feb. 13th and 20th).

In complete transverse acute myelitis of the cervical region high fever is a constant symptom. In unilateral myelitis of this region flushing of the face and unilateral sweating are produced, together with iridoplegia, sometimes preceded by dilatation, owing to initial irritation and succeeding paralysis of the sympathetic branches originating at this level of the cord.

Just as the disturbed reflexes and the belt sensations enable us to distinguish at what levels of the cord the myelitis is situated, so the distribution of the motor and sensory paralysis affords corroborative evidence of such location and additional proof of its extent and intensity.

Transverse myelitis at and above the level of origin of the phrenic nerve is almost immediately fatal, through its interference with the innervations required in respiration. In the upper part of the cervical enlargement it produces complete paraplegia of motion and sensation in the trunk and all four extremities. In the lowest part of the cervical enlargement it produces paralysis of the same parts, but the serratus magnus and scapular muscles escape. The nuclei of origin of the muscles moving the upper extremity are situated so that those which are farthest removed from the axis of the body when the arms are extended are situated lowest in the cord. The sensory paralysis is distributed in harmony with the motor paralysis; that is, when there is paralysis of motion in the hand and forearm the anæsthesia or subjective numbness is also in the hand and forearm. The same correspondence is not found in affections of the lumbar enlargement, for anæsthesia of the gluteal region accompanies paralysis of the crural muscles when the lesion is low down at the level of the lower lumbar and upper sacral nerves. The distribution of the anæsthesia, in other words, is not by segments of the limb, but by surfaces. The gluteal, posterior femoral, gastrocnemial, and outer pedal surfaces are affected together with the muscles moving the foot, while the thigh and inner side of the leg and foot become anæsthetic, with lesion of the upper part of the lumbar enlargement accompanying paralysis of the quadriceps and deep muscles. It is not difficult to understand this discrepancy when we bear in mind the different plan of distribution followed by the brachial plexus as compared with the lumbar and sacral plexuses. It is not, in my experience, found that the anæsthesia affects that surface which covers the part moved by the paralyzed muscle; which is characteristic of associated paralysis and anæsthesia from cortical disease.

One of the most dreaded occurrences in acute myelitis is the malignant bed-sore. The ordinary decubitus which results from the protracted sojourn of the patient in bed, coupled with the prominence of his trochanters and sacrum resulting from general or atrophic emaciation, is also common, but is comparatively benign and easy to prevent or to manage when established. The malignant bed-sore, on the other hand, is a spontaneous occurrence, due to the same obscure but undeniable trophic influences exerted for good by the normal and for evil by the diseased nerve-centres, which play so large a part in the symptomatology of tabes dorsalis. It cannot be avoided; it is not due to pressure alone, or, as some have claimed, to the macerating influence of the dribbling and decomposing urine. The development of this lesion is exceedingly rapid, and it may be regarded as a sort of local gangrene. The skin shows a livid color; vesicles appear, then burst; the part becomes denuded; and within a few days a deep ulcer with a dark border and base appears, discharging a sanious fluid. The subsequent history is that of a rapid extension and destruction of the neighboring tissues, even down to the bone, and if situated over the sacrum opening into the spinal canal through the necrotic arches of the sacral vertebra, thus leading either to general septicæmia or to putrid infection of the spinal meningeal sac. Occasionally, gangrenous spots coexist on other parts of the body, notably the lower extremities, where neither pressure nor maceration can be accused of playing a part, proving that the process is primarily due to the spinal affection.

Acute central myelitis, as described by Dujardin-Beaumetz, Hayem, Hallopeau, and Erb, usually runs its course very rapidly. Indeed, all of these observers speak of it as the most violent and quickly fatal variety of spinal inflammation. I have, however, seen one case with T. A. McBride at the Presbyterian Hospital in which all the characteristic symptoms of acute central myelitis were markedly developed and present in their characteristic groupings, and yet the patient had been suffering from progressing symptoms of myelitis for one year and a half before that time.¹⁰⁰ Usually, complete anæsthesia and paralysis of the lower half of the body occur in this form. But the most characteristic feature is a rapidly progressive atrophy not only of the paralyzed muscles, but also of some which are still partially under the dominion of the will. With this there is extreme vesical and rectal trouble, the sphincters being paralyzed. As a rule, the deep and superficial reflexes are destroyed—they are always diminished—and trophic disturbances of a malignant type, such as acute decubitus, joint-changes, and œdema, are common. The paraplegia is characterized by the flaccid condition of the limbs; the contractures and spastic symptoms found with other forms of myelitis are entirely absent, and qualitative electrical changes, beginning with disappearance of farado-muscular contractility, are found in the atrophying muscles. There are marked constitutional symptoms with this form; the tendency to an ascent of the process and successive involvement of one segment after another of the gray matter is great, and a fatal issue, as far as known, is inevitable.

¹⁰⁰ At the time the patient had undergone such a profound change in appearance that I failed to remember him, and it was only by accident I learned that I had seen him in private consultation with his family attendent, F. A. McGuire, a year previous. On the latter occasion I had made the diagnosis of subacute myelitis chiefly limited to the posterior columns; there were ataxia, both static and locomotor, slight incontinence, belt sensation, and ocular symptoms, with abolition of the deep reflexes in the lower limbs.

DIAGNOSIS.—The principles governing the determination of the affected region of the cord in acute myelitis are exactly the same as those detailed in the later sections on Chronic Myelitis or Sclerosis, the acuteness of the onset, and the relapses which sometimes occur, and the predominance of irritative spasms—which, however, is an inconstant criterion—serving to distinguish between the acute and chronic form of spinal inflammation. In the present state of our knowledge it is impossible to always differentiate between acute central myelitis and syringo-myelus—a condition in which the formation of a periendymal neoplasm, and its subsequent breaking down in the axis of the cord, lead to the formation of a tubular cavity.¹⁰¹ The neoplasm in this instance is classified among the gliomatous new formations. The symptoms depend, exactly as do those of myelitis, on the distribution of the destructive lesion. In some cases the posterior cornua and columns are chiefly involved, and extreme anæsthesia is found; in others the anterior columns are affected, and the symptoms of a poliomyelitis or an imperfect transverse myelitis may be imitated.¹⁰²

¹⁰¹ This cavity, unlike that of hydro-myelus, is not a dilatation of the central canal, but, lying to one side of it, is excavated in the cord-substance.

¹⁰² Repeated fractures have been noted in cases marked by profound analgesia. It is believed that they are not always due to trophic changes, but may be the result of muscular action, exaggerated on account of the patient's inability to gauge his efforts. Still, in the majority of cases the presence of positive trophic disturbances of the skin seems to indicate the probability of some textural change facilitating the fracture.

As a rule, the sensory disturbance in syringo-myelus is out of proportion to the muscular atrophy developed; that is, it involves a far more extensive province. It is usually of a peculiar character: some forms of sensation are involved but slightly, or even escape, and others may be nearly destroyed. Commonly, it is the pain and temperature-sense which suffer most, while the cutaneous space and pressure, as well as the muscular sense, are not materially disturbed. These peculiarities are not commonly found in cases of myelitis, and when present, and particularly when the paralytic or sensory affections involve all four extremities alike, they suggest the existence of syringo-myelus. As yet we are unable to make more than a probable diagnosis between the two diseases.

DURATION AND PROGNOSIS.—The duration of the disease varies. Cases of the apoplectiform variety are mentioned, in which the process reached its height in a few minutes, or where the patient, having retired in good health the night before, awoke finding himself paralyzed in the lower half of his body. Death may terminate such a case in a few days or weeks. In another class of cases, complicated by serious involvement of the bladder, the fatal termination is often precipitated by putrid cystitis, pyelitis, or uræmic poisoning, and even in cases which have passed the dangers of the early period in safety these ominous complications may develop with the usual result many years after the beginning of the illness. In a number of cases the first period, that in which the morbid process becomes developed, is followed by one of comparative quiescence, in which the paralyses of sensation and motion then established remain stationary for months and years. A number of authors, Erb, Leyden, Strümpell, and Ross, speak of such a case as one in which chronic myelitis has followed an acute myelitis. It seems improper to use the terms acute or chronic in this way. As it is generally understood that the term acute applies to myelitis in which disintegration of the nerve-elements predominates over interstitial proliferation, and in which the secondary sclerosis is rather like the cicatrix of an acute inflammation and necrosis, it should not be confounded at any period, no matter how similar the clinical signs may be, with a process which is essentially an interstitial one from the start. If chronic amaurosis results from an acute glaucoma, we do not change the latter designation to chronic glaucoma.

In cases where the symptoms at the acme indicate rather an involvement of the peripheral than the central paths of the cord, and in which an incomplete motor and sensory paralysis develops, the patients often regain a considerable amount of motor power and sensation, so that they may reach a good age, suffering at most from a paresis of some one muscle or muscular group, occasional bladder trouble, and pains. It has been laid down as a rule that where paraplegia and other signs remain stationary for years, there is no hope of even partial recovery. The following remarkable and well-attested case proves that this rule is not without exceptions:

Isidor K——, æt. forty-four years, worker in tobacco. After over-exertion in the fall of the year 1879 he had numbness, tingling, dorsal pain, and paresis rapidly developed, which induced him to consult the physicians at the clinic of the University of the City of New York. After some slight improvement a relapse occurred, and several others followed, usually provoked by over-exertion, till he became completely paraplegic. He was, according to his account, several times exhibited to a medical class by William A. Hammond, and remembers that this authority spoke of a possible ascent of the affection and ensuing involvement of the arms. His bladder was at no time seriously disturbed. For four years and three months he was totally paraplegic; his lower extremities were without life; and for the greater part of the time he could not move his toes. The limbs were cold and pale, but underwent little atrophy. The only exercise obtained during this time was in a roller carriage. His sexual power was abolished throughout the whole four years and over. Nothing can be learned as to his reflexes in this period.¹⁰³ The paralysis of sensation was as complete as that of motion, and the lower limbs never perspired. The arms remained free. There was a dorsal belt sensation.

¹⁰³ Hammond has no notes of the case, having discontinued the clinic, and Ludwig Weiss, the physician in charge, saw him only occasionally in behalf of a benefit society.

On July 23, 1884, shortly before mid-day, while lying on the bed, in which he had lain a helpless cripple for over four years, except when lifted into the roller carriage, he felt a sudden rush of warmth. Surprised at this first sensation he had felt for years in limbs which had been quasi-foreign appendages, he raised up the bed-clothes and saw that they changed color. There was some tingling for about three minutes, and a perspiration broke out in the affected members. With this he found he could move his feet: half alarmed, half exulting, he sent for his physician, L. Weiss, who found that the patient could stand and walk with considerable freedom. I was then consulted, and found the patient presenting a picture of incomplete transverse myelitis. He could walk, turn about, stand with closed eyes with slight swaying, and his knee-phenomenon was of short excursiveness, but exceedingly spasmodic, and this symmetrically so. He was carefully watched, and against the advice of his physician engaged in peddling cigars, and subsequently took a position as attendant at the pauper asylum on Ward's Island. Here he was on his feet fully twelve hours a day, and his motion, which had continued improving until it was to all practical intents and purposes normal, aside from a slight stiffness, again became impaired, and a joint trouble in the metacarpo-phalangeal articulation of the right little toe, which had troubled him a week after his partial recovery, recurred.¹⁰⁴ On January 15th of the present year I again examined him. His knee-phenomenon was greatly exaggerated, cutaneous sensations scarcely impaired, gait paraparetic, but he could walk great distances, and claimed to suffer less from the exertion than from the tenderness accompanying the joint trouble referred to. There had, therefore, occurred, without any assignable cause—for the patient was not under treatment for a year or more before the event—an almost instantaneous restoration of sensation, locomotion, and sexual power; all of which faculties, notwithstanding the infraction of every medical direction given, remained established for two years, with prospects of so continuing a longer period.

¹⁰⁴ This was a trophic joint trouble.

TREATMENT.—Most of the therapeutic propositions relating to the treatment of the acute myelitic process are based on the theory that it is of a congestive character or associated with congestion. Accordingly, the internal administration of such drugs as ergotin, which diminish the calibre of the blood-vessels, and local measures, such as depletion, wet cupping, and counter-irritation, intended to act in the same way by derivation, are unanimously recommended by authorities. The suggestion of Hammond, that the patient occupy a ventral or lateral, and not the dorsal, position, is based on, and entirely consistent with, this same view. It is difficult to say what effect is attributable to these measures. Remarkable spontaneous changes—retrogressions as well as advances of the morbid process—occur equally under expectant as under active treatment. I have never seen any improvement in the active phase of simple myelitis which I felt confident I could attribute to any special remedy employed with a view of acting directly on the morbid process. Indeed, improvement has been claimed by Jewell as a result of the use of strychnia—a drug which under the very dogmas governing the orthodox treatment of the disease might be expected to do positive damage.¹⁰⁵

¹⁰⁵ Jewell gives very large doses of this alkaloid. L. C. Gray, in a discussion held before the American Neurological Association, cited numerous observations directly conflicting with those of Jewell. I cannot, in view of a recent observation in a typical case of acute anterior poliomyelitis, in which by accident the toxic effects of strychnia were obtained, consider this dispute as at all settled. In direct connection with the toxic symptoms the abolished patellar jerk returned in an exaggerated form; motion also returned, and rapid improvement ensued.

In relapses of acute myelitis which had been brought on by chilling of the feet I have obtained good results by derivation to the lower extremities, and on many grounds think that the morbid process in the cord, if it can be affected at all, can be affected by treating the periphery where the symptoms are noted more readily than by applying the cautery or bleeding over the proven site of the disease. Exposure of the dorsal region to cold has not yet been noted as a cause of acute myelitis, whereas such exposure of the lower extremities is a frequent one. This seems to show that the spinal cord is more vulnerable to influences affecting its nervous distribution than to those which are topographically nearer. If this is true as regards morbid influences, it may be urged that it is plausible as regards remedial influences if these are to drive out the disease tendency by the same door it entered.

Rest is imperative during the active progress of the disease. It may be stated as a canon that the earlier the patient takes to his bed, and the more thoroughly he obeys the injunction to attempt no motion of the affected members, the better, cæteris paribus, will the result obtained be. Countless cases are on record where a relapse was directly traceable to a walk undertaken prematurely or carried farther than was wise. As convalescence or partial restitution advances, gradually increasing exercise is to be attempted, not waiting for the danger-signal of a tired feeling to discontinue it; for that feeling, developed, means positive harm already done. It is therefore necessary to allow the returning function to be utilized only within small limits at first, and extending them slowly.

In all cases of severe myelitis where the formation of bed-sores is to be apprehended the water-bed should be employed. Owing to the low temperature which the rubber sac constituting it has, it is necessary to cover it with some well-warmed and non-conducting material and to have the room well warmed. If bed-sores are already formed, they are to be treated according to ordinary surgical principles. Antiseptic means should be in the foreground in the case of the malignant bed-sore. It is to be remembered that the latter is a gangrenous process, and, in so far as the formation of a line of demarcation between the necrotic and the conserved tissue is concerned, the ordinary expectant rules of surgery govern the case: the water-bath appears to yield the best results. Ordinary bed-sores yield readily to mechanical protection and stimulating ointments or the balsam of Peru. Iodoform is recommended, but it produces granulations of an indolent character as compared with those obtained through the use of resinous ointments.

The warm bath is probably the most useful measure in acute myelitis. In cases due to exposure I do not believe it can be applied too soon. Its temperature should, in the beginning at least, not be higher than about 88° F., and the duration about seven minutes. The continued administration will depend on the immediate effect on the patient, and the sittings can be ultimately prolonged to half an hour or even longer. It should be administered once daily, and, when the patient is not disturbed by the manipulation connected with its use, even oftener. Cold baths are recommended by the Germans, but it seems rather in the passive period of the disease than during its active phase.

The management of the bladder trouble is one of the most critical points in the treatment of most cases. The results of retention of urine are more frequently the cause of a fatal issue than any other single complication. Where there is complete retention continuous catheterization is to be employed, as recommended by Strümpell.¹⁰⁶ In other cases the bladder should be emptied thrice in the twenty-four hours. The catheter is to be thoroughly disinfected, and if the slightest sign of cystitis is noted the bladder should be washed out with astringent and disinfectant solutions. The continuous irrigation with a solution of corrosive sublimate, 1:2000, appears to give the best results.

¹⁰⁶ A. Nelaton's catheter is introduced into the bladder, and kept in place by strips of adhesive plaster fixed to the inner aspect of the thighs. A perforated condom fixed to the catheter, and then fastened to the inguinal region, is in my opinion a better measure, especially in patients who have some motor power left. The catheter is connected with a rubber tube, which should run on a decline in order to effect complete drainage.

If there be a syphilitic taint present—and more particularly is this true of cases where no other cause can be assigned—large doses of iodide of potassium¹⁰⁷ should be administered, and mercurial ointment energetically applied, even to the point of salivation.

¹⁰⁷ Here, if anywhere, the so-called heroic doses are applicable.

I am unable to say anything with regard to the local use of electricity in the active period of the disease. Ascending currents are recommended by Erb, weak currents of about five minutes' duration being employed over the part supposed to be affected. In order to secure sufficiently deep deflection of the current large electrodes are applied. The use of galvanism and faradism on the affected periphery, the former being preferred where atrophic, the latter where anæsthetic conditions preponderate, is to be instituted early and continued through the duration of the disease. The rules stated in the section devoted to electro-therapeutics are to be followed. In cases where the bladder or rectum are paralytic, these organs should have galvanism applied to them by means of electrodes shaped like catheters or sounds.

After the acute phase of myelitis is passed, the secondary period is to be managed according to the principles laid down in the section on the Treatment of the Sclerotic Processes.