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.