Insomnia; and Other Disorders of Sleep

by Henry M. Lyman

The dependence of the waking state upon the presence and activity of a sufficient quantity of a peculiarly unstable form of protoplasm in the brain is an hypothesis which presents no great difficulty of comprehension. But how may we explain the lapse from the intelligent vivacity of that waking state into the unconscious inactivity of sleep? I have elsewhere[20] discussed the manner in which artificial sleep is produced by impregnation of the brain with anæsthetic substances that interfere with sensibility, and finally produce stupefaction, by hindering the normal processes of intra-molecular oxidation in the protoplasm of the nervous tissues. The same general line of argument may be extended to cover the action of every narcotic agent with which the living substance of the body may become surcharged. Accepting, then, the hypothesis advocated by Obersteiner and Preyer, it becomes an easy thing to account for the gradual onset of sleep by supposing an accumulation of the “fatigue producing” products of intra-molecular oxidation. But we cannot thus explain the rapid and, as it were, voluntary passage from wide awakefulness into a condition of deep sleep, such as may be commonly observed among sailors and others who have formed the habit of going at once to sleep at regularly recurring hours of the day or night. Certain writers have endeavored to account for this fact by imagining a special mechanism at the base of the brain (choroid plexuses of the fourth ventricle, etc.,) by means of which the current of the blood through the brain may be voluntarily diminished, with a consequent arrest of conscious activity. But, still adhering to the hypothesis of Pflüger, we shall obtain a clearer explanation of the facts by considering the phenomena connected with the succession of impressions upon the organs of sense. It has been ascertained[21] that such impressions must persist for a certain measurable length of time in order to excite conscious perception. A sound must be prolonged for at least fourteen-hundredths of a second, a ray of light must agitate the retina for about eighteen to twenty-hundredths of a second, an ordinary contact with the surface of the skin must continue from thirteen to eighteen-hundredths of a second, in order to awaken any knowledge of sound and light and tactile sensation. For the simplest act of perception from two to four-hundredths of a second are necessary. It is, therefore, perfectly reasonable to suppose that when the “explosive material” of the brain has been sufficiently “dampened” by the accumulation of acid refuse which accompanies prolonged cerebral effort, the impressions of sense may no longer suffice to excite in the cortical protoplasm vibrations of sufficient length, or following each other in sufficiently rapid succession, to sustain consciousness. The cortex of the brain may then be likened to a body of water into which bubbles of partially soluble gas are introduced from below. When the bubbles are large, and when they follow each other rapidly, a continual effervescence is maintained upon the surface of the water. But if the size of the bubbles be reduced, or if the solvent capacity of the liquid be increased, the surface will become almost, if not quite, perfectly tranquil. In some such way, without any great danger of error, may we picture forth the manner in which the generation of ideas in the field of consciousness is related to the molecular movements in the space occupied by the protoplasmic substance of the brain. Returning, now, to the rapid induction of sleep, we find that it is usually the experience of people who lead an active life in the open air, and are compelled to endure frequent interruption of their rest. The sailor who is trained to work four hours on deck, and then to sleep four hours below, has been virtually transformed by this habit into a denizen of a planet where the days and the nights are each but four hours long. His bodily functions become accommodated to this condition; his nervous organs store up in sleep a supply of oxygenated protoplasm sufficient only for an active period of four or five hours; so that, when the watch on deck is ended, he is in a state as well qualified for sleep as a laborer on shore at the close of a day of twelve or fifteen hours. Moreover, the majority of those who can thus easily fall asleep are individuals whose waking life is almost entirely sustained by external impressions. So soon, therefore, as such excitants are shut out by closing the eyes in a place of shelter from the sounds and turmoil of the air, comparatively little remains for the stimulation of ordinary consciousness, and sleep readily supervenes through mere lack of cerebral excitement, especially if the excitable matter of the brain has been previously overwhelmed by the products of active exertion.

That analogous, though not identical, predisposition to unconsciousness may also be rapidly induced by modifications of the cerebral circulation is proved by the sudden reduction of cerebral excitability and consciousness which occurs during the act of fainting. In this counterfeit presentment of sleep the important part played by variations of the blood current through the brain is so conspicuous that certain writers have attempted to show that genuine sleep is the result of a diminution in the flow of blood to the cortex of the brain. An ingenious physician has even attempted to relieve insomnia very much as a surgeon might undertake to cure a popliteal aneurism—by placing tourniquets on the arteries leading to the affected part. But the mere fact that syncope produces unconsciousness does not prove that “cerebral anæmia” should be elevated to the rank of the principal cause of natural sleep. The nervous process is the primary factor. The circulation of the blood is everywhere under the immediate control of the nervous system. Consequently, every change in the condition of the nervous structures is followed by a corresponding change in the state of the circulating apparatus. Wherever an organ is aroused to activity, so delicate are the adjustments by which it is connected with the brain and with the heart that it is at once irrigated by an increased flow of blood. When its functional activity subsides, the same mechanism provides for a corresponding reduction in the supply of blood to its tissues. The brain itself forms no exception to this law. This has been admirably shown by the observations of Professor Mosso, of Turin.[22] The learned professor enjoyed the rare opportunity of observing three individuals who had suffered the loss of a considerable portion of the bony walls of the cranium, exposing the surface of the cerebrum, and affording a view of the pulsation of the vessels of the brain. With the aid of the cardiograph, the sphygmograph, the hydrosphygmograph, and the plethosphygmograph, it became possible to register the circulation of the blood in the brain, and to compare that portion of its course with the coincident circulation in other parts of the body. It was thus shown that every increase of emotional or intellectual activity was attended by an increase in the activity of the cerebral circulation. This increase was procured at the expense of other portions of the body, which exhibited a coincident reduction in the amount of blood received from the heart. The occurrence of sleep caused a diminution in the number of respirations, and a fall of six or eight beats in the pulse. The volume of the brain and its temperature were at the same time slightly reduced, through the diversion of blood from the head to other regions of the body. The consequent dilatation of the vessels in the extremities was readily demonstrated by the use of the plethosphygmograph. The extreme sensitiveness of the nervous centers was further illustrated by the fact that if, during sleep, a ray of light were directed upon the eyelids, or if any organ of sense were moderately excited without waking the patient, his respiration was at once accelerated; the heart began to beat more rapidly, the vessels of the extremities contracted, and the blood flowed more freely into the brain. Similar results accompanied the act of dreaming. The return of full consciousness on waking was followed by an immediate increase in the activity of the intra-cranial circulation.

The extreme susceptibility of the brain to influences proceeding from artificial disturbances in the circulation, was exhibited in the case of one of Professor Mosso’s patients. By compression of the carotid arteries, unconsciousness was induced, and an attack of convulsions was aroused. In no other part of the body can a corresponding disturbance of function be so quickly produced by similar means. A limb may be rendered bloodless for nearly half an hour, by the application of an elastic bandage, and yet its sensory nerves will remain capable of transmitting impressions from the periphery. But in this case, compression of the carotids for only eight seconds was sufficient to abolish consciousness and to excite convulsive movements.

In all such observations it is worthy of note that the nervous impression is the primary event so long as artificial disturbances are not intruded. The changes of blood-pressure and circulation were invariably secondary to the excitement of nerve tissue. Sleep, therefore, must be regarded as the cause, rather than the consequence, of the so-called cerebral anæmia which obtains in the substance of the brain during repose. This condition of “anæmia” is nothing more than the relatively lower state of circulation which may be remarked in every organ of the body during periods of inactivity. Every impression upon the sensory structures of the brain occasions a corresponding liberation of motion in those structures. The movement thus initiated arouses the vaso-dilator nerves of the cerebral vessels and excites the vaso-constrictor nerves of all other portions of the vascular apparatus. Hence the superior vascularity of the brain so long as the organs of sense are fresh and receptive. Hence the diminishing and varying vascularity of the different departments of the brain as sleep becomes more or less profound. These modifications of the brain and of its circulation are well illustrated by the effects of a moderate degree of cold applied to the cutaneous nerves of the body, as not unfrequently happens when the night grows cool towards morning. The disturbance of the sensitive nerves of the skin is transmitted to the brain. The excitement of this organ causes dilatation of its vessels, and increased irritability of the cortical instrument of perception. This becomes the starting point for the projection of impulses upon the field of consciousness, producing dreams, or even a complete awakening from sleep.

The cause of sleep must, therefore, be sought in the molecular structure of the brain, rather than in fluctuations of the blood-current. In the present state of our knowledge it must be negatively represented as the consequence of a deficiency in the amount of movable oxygen in the nervous tissue. This deficiency may be the result of immaturity, as in the fœtus, or in the new-born infant; or it may result from the accumulation of an excess of the waste-products of intra-molecular oxidation during functional activity—products which hinder the further passage of oxygen into stable combination with the oxidizable elements of protoplasm. Sleep thus produced differs from the artificial sleep induced by narcotic drugs, in the fact that its cause is self-generated by the instrument of thought, while narcotic stupor is caused by the intrusion of substances derived from without—substances which, like the natural refuse of the living cells, more or less completely hinder the processes of oxygenation and oxidation within the tissues of the body. Hence the states of healthy sleeping and waking must necessarily be self-limited and regularly successive; while the state of narcotism is purely accidental, and its duration exactly corresponds with the variable length of the period during which the body may remain impregnated with the hypnotic agent.

Certain morbid forms of sleep further illustrate its dependence upon the persistence of depression in the functional activity of the brain. For some persons this seems to constitute their normal condition. They are either excessively fat, red-faced, and soaked with beer, or they are pale, anæmic, and pulpy, with flabby muscles and a feeble circulation. They fall asleep whenever left to themselves, and never seem to be fully aroused to active life. The fat boy who figures so amusingly in The Pickwick Papers, furnishes a life-like picture of this variety of somnolence.

The introductory stage of the eruptive fevers is often characterized by somnolence. It also frequently appears as the forerunner of coma in the various diseases which terminate in unconsciousness and death. A singular example of this has been observed among the negro inhabitants of the Atlantic coast of tropical Africa. The disorder is known to English writers as sleeping dropsy; by the French it is called maladie du sommeil. It is characterized by daily paroxysms of somnolence which tend to become more and more continuous and profound until they are finally merged in fatal coma. For our knowledge of the disease we are chiefly indebted to the description by Clark,[23] an English surgeon who practised in Sierra Leone, and to the monograph by Guerin,[24] a French naval surgeon, who had enjoyed exceptional opportunities for observation among the laborers who had been carried from Africa to the island of Martinique. Similar cases have been occasionally reported in other regions of the world, but it is among the Africans that it has been principally remarked. The onset of the malady is gradual, commencing with a slight frontal headache. After a few days a disposition to sleep after meals is noted. This becomes increasingly urgent, and the intervals of sleep are prolonged until at length the patient becomes continually soperose. The waking periods are marked by a sluggish state of the intellectual faculties. The pulse is not accelerated, and it remains full and soft. The veins of the sclerotic are turgid, and the eyeball seems unusually prominent. The temperature does not increase, but rather tends to diminish its figure. The skin is dry and moderately cool. The tongue continues moist, and is covered with a white fur. The bowels and the bladder are regularly emptied, and the appetite persists with considerable vigor. Finally, the patient becomes completely comatose, and dies quietly. Sometimes, however, the evolution of the disease is less tranquil. Epileptiform convulsions, followed by progressively deepening periods of coma, interrupt its course, and a continuous muscular agitation marks the closing scene. At the same time the pulse grows weaker and more frequent until its movements cease in death. Recovery is almost unknown, though the duration of the disease often varies from three months to a year or longer. Examination of the body after death yields very negative results; the sinuses and larger vessels of the brain are engorged with blood, but no evidence of inflammation is anywhere apparent. The other organs present no pathological alterations whatever. These observations seem to indicate that the disease originates in some form of general blood-poisoning, rather than in any local inflammation or degeneration. Dr. Clark has called attention to an enlargement of the cervical glands as a feature of the malady. According to Dr. G. H. Bachelder,[25] the native physicians cure the disease by extirpation of the affected glands. He has also observed an initial lesion in the nasal mucous membrane. If this be confirmed, the malady will take its place among the forms of somnolence produced by infection of the blood.

Between the profound unconsciousness of natural sleep and coma may be placed the distinction that the one is always the consequence of healthy physiological processes, while the other is always the result either of injury, of disease, or of some form of intoxication. Comatose unconsciousness may be the result of cerebral compression caused by injury of the head, or by the presence of an inflammatory exudation. Intra-cranial tumors, embolisms, thrombi, diseases of the cerebral arteries, and degenerations of the brain,—in short, every morbid change of which the liquids and the solids within the cranium are capable—may become the cause of coma. Toxæmic conditions of the circulating fluids of the body may benumb the brain with comatose sleep. Few diseases, therefore, exist without the possibility of coma as one of their consequences—a coma which, however, must not be confounded with the genuine sleep which sometimes occupies the larger part of convalescence from acute illness. During such convalescence there is a reversion to the infantile type of nutrition with all its need of prolonged and frequent periods of repose. Like normal sleep, the comatose condition admits considerable variation of intensity. The patient may sometimes be partially roused, as from the coma of alcoholic intoxication, and he may finally recover complete consciousness; but very often the reverse is the fact. The coma deepens into paralysis of the respiratory centres, and death concludes existence without the slightest manifestation of sensibility or intelligence.

Lethargy is a pathological variety of sleep, in which the repose of the body is even more complete than in coma. The victim of coma often presents a countenance suffused with blood; the pulse beats vigorously, and respiration may become stertorous. But in lethargy the abolition of bodily movement is almost absolute. In the milder forms of this disorder the patient may be partially roused, so as to attempt an answer when addressed, appearing like a person in very deep sleep; but in the majority of cases he remains insensible, unconscious, and utterly irresponsive to ordinary forms of irritation. Respiration and circulation are reduced to a minimum, and may, even for a time, become imperceptible. Uncomplicated with hysteria, the disorder is rapidly fatal, but, according to Rosenthal,[26] hysterical lethargy is never mortal.

Many examples of this disease have been afforded by the records of apparent death. I am well acquainted with a lady who, in early childhood, had been laid out for burial at the supposed termination of some infantile illness. Her mother alone insisted that the child was still alive. After some time spent in weeping and expostulation, she applied a blister to the thorax of the babe. This soon excited evidences of painful irritation, followed by a complete recovery. Still more instructive is the case, narrated by Rosenthal,[27] of a young woman, twenty-four years of age, who, in consequence of violent emotional excitement, became unconscious, and presented no signs of life, though tested by placing a mirror before the mouth, and by dropping melted sealing-wax upon the skin. On raising her eyelids, the pupils gave no reaction to light; the limbs remained perfectly flaccid, and the radial arteries were pulseless. Careful auscultation, however, detected a very feeble and intermittent sound in the cardiac region. The walls of the chest exhibited no movement, but the lateral surfaces of the abdomen presented a slow and almost imperceptible oscillation. Gentle faradization of the muscles and nerves of the face, arm, and hand, excited definite muscular contractions. By this method Rosenthal became satisfied that, although the patient had remained for thirty-two hours in this condition, she was only apparently dead. In fact, after continuing forty-four hours in a state of suspended animation, she awoke spontaneously, made a rapid recovery, and seemed to enjoy as comfortable health as an excitable, nervous temperament would permit.