Volume 5 — DISEASES OF THE NERVOUS SYSTEM. (continued 25)

TREATMENT.—The treatment of chronic hydrocephalus is general and local, the first being the most important, although in many cases it is difficult to enforce it, from lack of intelligence and of means on the part of those in charge of the patient. Proper ventilation, good drainage, and cleanliness are essential. The child should be bathed daily, and should be protected against changes in temperature by suitable clothing. If his strength allow, he should be taken into the open air daily in fine weather. A wet-nurse should be provided for infants whose mothers are unable to suckle them. Older patients should take milk, cream, animal broths, farinaceous substances, etc., with wine or brandy. Tonics, especially cod-liver oil, hypophosphite of lime, and some preparation of iron or of the iodide of iron, are important, the choice being determined by the effect apparently produced. The internal and external employment of mercurial preparations, once in vogue, is now almost entirely abandoned by the best authorities. The evacuation of the fluid by puncture, followed by compression of the head by bandaging, has been occasionally resorted to, and in a few instances with success, but the cases in which it is indicated are rare. Thomas Young Thompson⁶ reports a case in which puncture was followed by recovery. The child, fourteen days old, fell, apparently without ill effects, but three weeks afterward a protuberance appeared on the crown of the head which continued to enlarge, and the signs of chronic hydrocephalus were unmistakable. In three months the circumference over the parietal eminences measured 20 inches, and a year afterward 24½ inches. In spite of energetic internal and external treatment the enlargement continued to progress, until the head was punctured, and about three hundred grammes of a clear, transparent fluid, free from albumen, were evacuated. Five weeks later a second puncture was made, and sixty grammes of a milky fluid withdrawn. The child recovered, and two years later was in good health, the head not being disproportioned to the rest of the body. West considers the cases in which the effusion is apparently external—that is, confined to the arachnoid cavity, rather than ventricular, and in which there are no indications of active cerebral disease—to be the most favorable for the operation. The proper situation for the puncture is the coronal suture, about an inch or an inch and a half from the anterior fontanel. A few ounces of fluid only should be withdrawn at a time, and compression should be carefully applied both during the escape of the fluid and afterward.

⁶ Med.-Chir. Transactions, vol. xlvii., 1864.

CONGESTION, INFLAMMATION, AND HEMORRHAGE OF THE MEMBRANES OF THE SPINAL CORD.

BY FRANCIS MINOT, M.D.

Congestion of the Spinal Membranes.

The blood-vessels of the spinal membranes communicate freely with the general circulation, and there is less opportunity for their obstruction than in the case of the meninges of the brain. Hyperæmia of the dura and pia mater is therefore seldom met with, except in connection with disease of the cord; and, indeed, but little is known on the subject, which is only alluded to as possible by authorities of the present day, although the affection was formerly supposed to be a common one, giving rise to various symptoms, such as numbness and formication of the extremities, muscular weakness, and even paraplegia—symptoms which are now known to be caused by structural diseases of the cord only. As Erb¹ remarks, “It is hardly possible that any considerable hyperæmia of the meninges should exist without a similar condition existing in the cord also, as the vascular supply of both is the same.”

¹ “Krankheiten des Rückenmarks,” von Wilhelm Erb, in Ziemssen's Handbuch, Leipzig, 1876; Am. trans., vol. xiii. p. 99.

ETIOLOGY.—Hyperæmia of the spinal membranes is found after death from convulsions, especially in cases of tetanus, hydrophobia, eclampsia, strangulation, poisoning from narcotics, etc., in which the effect is evidently due to asphyxia. An interesting case of extensive hyperæmia of the spinal membranes, as well as of those of the brain, complicating mania, is reported by M. R. G. Fronmüller.² A girl of eighteen years, previously well, being accused of theft, fell into a state of melancholia, passing into mania, with frequent convulsions, screaming, etc. There was no spinal tenderness. The urine contained no albumen. The temperature was never elevated. No opisthotonos. The sphincters became relaxed, and she died at the end of about three weeks. The dura was found to be normal, but the pia mater of the brain, cerebellum, medulla oblongata, and cord was strongly injected. The brain and cord were normal; no ventricular effusion. Here the meningeal hyperæmia was doubtless caused by asphyxia resulting from the convulsions.

² See Schmidt's Jahrbücher, 1883, No. 7.

Congestion of the spinal membranes has been attributed to sudden suppression of the menstrual flow or of hemorrhoidal bleeding, and to portal obstruction, but the evidence of this is very meagre. Exposure to cold and wet, as from sleeping on the damp ground, is an alleged and plausible cause.

The SYMPTOMS attributed to hyperæmia of the spinal membranes are pain in the back extending to the legs, with numbness and tingling of the toes, sensation of weight in the limbs, muscular weakness, appearing suddenly without fever and usually of transient duration. There is no evidence that it gives rise to paralysis. Considering that temporary congestion of the membranes must occasionally happen from convulsions, as in epilepsy, etc., it is remarkable that no symptoms attributable to it have been observed under these circumstances.³

³ See Epilepsy and other Chronic Convulsive Diseases, etc., by W. R. Gowers, M.D., London, 1881, p. 106.

MORBID ANATOMY.—We must be careful not to mistake post-mortem staining of the tissues from imbibition of the coloring matter of the blood—the result of decomposition aided by the position of the body—for true congestion. The latter is recognized by fine vascular arborization covering the surface of the dura or pia, often accompanied with small punctate hemorrhages. More extensive extravasations in the connective tissue, surrounding and between the membranes, are sometimes found. The spinal fluid is usually increased in amount, and often tinged with red. On account of the free vascular connection between the membranes and the cord the latter almost always partakes of the congestion.

DIAGNOSIS.—From what has been said it follows that simple hyperæmia of the spinal membranes can hardly be distinguished from that of the cord. (See the article on DISEASES OF THE SUBSTANCE OF THE BRAIN AND SPINAL CORD.) When the symptoms are unaccompanied by fever, are of very moderate severity, and of short duration, we may perhaps infer that the lesion is confined to the membranes.

The TREATMENT is the same as that for congestion of the spinal cord.

Acute Inflammation of the Spinal Dura Mater.

SYNONYM.—Acute spinal pachymeningitis.

Acute inflammation of the spinal dura mater is chiefly confined to the outer surface of the membrane (peripachymeningitis), and is almost always consecutive to either injury or disease of the vertebræ (fracture, dislocation, caries), to wounds penetrating the spinal cavity, or to suppurative disease in neighboring organs or tissues, which makes its way into the peridural space through the intervertebral openings. The symptoms are complex—in part caused by the original disease, and in part by the pressure of the products of inflammation exercised upon the nerve-roots, and even upon the cord itself. Pain in the back, corresponding to the seat of the disease, is rarely absent, and all movements of the trunk are extremely painful. When the exudation is sufficient to compress the nerve-roots, the pain will extend to the trunk and the limbs, and other signs of irritation, such as a feeling of constriction by a tight girdle, and tingling, numbness, and cutaneous hyperæsthesia in the limbs, will be observed, varying in situation according to the seat of the lesion. In some cases the compression of the cord may be sufficient to cause paraplegia. General symptoms will vary according to the complications of the case. Severe injury or extensive disease of the vertebræ will be accompanied with high fever; but if the external inflammation be moderate and the meningeal complication be limited in extent, the fever may be subacute.

MORBID ANATOMY.—The connective tissue between the dura and the bone is the seat of inflammatory exudation, usually purulent, of greater or less extent, and more abundant in the posterior than the anterior part of the spinal cavity, owing to the position of the patient. A more or less abundant exudation, either of pus or of dry caseous matter, is found upon the outer surface of the dura or infiltrating the connective tissue between it and the bony walls. The dura is thickened, and sometimes the exudation is seen upon its inner walls, but the pia is seldom involved in the inflammation. The cord may be compressed or flattened when the amount of exudation is large, and may in consequence show signs of inflammation in its vicinity. The spinal nerves likewise are sometimes compressed, atrophied, softened, and inflamed. The disease rarely occupies the cervical region, on account of the close union of the dura with the bones of that part; hence there is an absence of pain in the neck and of retraction of the head.

DIAGNOSIS.—The diagnosis is founded on the presence of general symptoms of spinal disease—pain in the back, but not extending to the neck, increased by movements of the trunk; cutaneous hyperæsthesia, tingling, or numbness in various parts of the surface of the body; paresis or paralysis of the lower extremities in severe cases; along with a history of vertebral disease or injury or of suppurative disease in the neighborhood of the spine. The history of the case will generally be sufficient to exclude myelitis, tetanus, or muscular pain (rheumatism, lumbago). From acute leptomeningitis the diagnosis must also be made by the history, but it should be borne in mind that the pia may be involved at the same time with the dura.

PROGNOSIS.—In complicated cases the prognosis is grave if the spinal symptoms are well marked and severe, especially when there is evidence of much pressure on the cord (paraplegia). If the signs of spinal irritation were moderate, the danger would depend upon the nature and extent of the external lesion.

TREATMENT.—This would be addressed mainly to the primitive disease. For the spinal symptoms the treatment would not differ materially from that of inflammation of the spinal pia mater.

Chronic Spinal Pachymeningitis.

This affection generally coexists with chronic inflammation of the pia. Like the acute inflammation of the dura, it is seen in connection with disease or injury of the vertebræ, and it may also arise from tumors of the membrane (chiefly syphilitic) and from myelitis. It is frequent among the chronic insane, and in them is sometimes associated with hemorrhagic effusions analogous to the hæmatoma of the cerebral dura mater. Chronic inflammation of the spinal dura is of unfrequent occurrence, and but little is known of its history and pathology. In a case reported by Wilks⁴ the membrane was thickened to nearly its whole extent, and in the cervical region presented numerous bony plates. The pia was also thickened at this part and adhered closely to the dura. The symptoms, which seemed chiefly due to disease of the cord from compression, were retraction of the lower limbs and violent jerking from excessive reflex action.

⁴ Transactions of the Pathological Society of London, vol. vii., 1856.

A special form of the disease, occupying chiefly the cervical region, was first described by Charcot.⁵ The membrane is thickened by a deposit of successive layers of fibrin, compressing the cord, which is flattened from before backward and inflamed. The nerve-roots are also more or less compressed. The course of the disease may be divided into two stages: First, that of irritation of the spinal nerves, with pain in the back part of the neck, extending to the head and along the upper limbs. The pain is permanent, but liable to exacerbations, and is accompanied with stiffness of the neck and a feeling of numbness and tingling, with muscular weakness of the arms. Sometimes the skin of the arms is the seat of trophic changes, as shown by the presence of bullæ or pemphigus. The second period is that of extension of the disease to the cord. The pain ceases, and is followed by paralysis or muscular atrophy, especially in the domain of the ulnar and median nerves, resulting in extension of the hand on the forearm, with flexion of the fingers toward the palm, giving rise to a claw-like appearance (main en griffe). In some cases an upward extension of the disease implicates the root of the radial nerve, and the hand then assumes a prone position from paralysis of the extensor muscles. The lower portion of the cord may also become involved, with similar results in the lower extremities. Although the disease is generally progressive, it is not always so, and Charcot cites one case in which great improvement took place in the course of some years, though not apparently in consequence of any special treatment.

⁵ Leçons sur les Mal. du Syst. nerv., par J. M. Charcot, Paris, 1875, vol. ii. p. 246. See, also, Maladies du Syst. nerv., par A. Vulpian, Paris, 1879, p. 127; and Clinique méd. de l'Hôpital de la Charité, by the same.

Acute Spinal Meningitis.

SYNONYM.—Leptomeningitis spinalis acuta.

By the term spinal meningitis is usually meant inflammation of both the arachnoid and the pia, the two being, as already stated, in reality one membrane. In connection with meningitis of the brain it constitutes a distinct disease which is usually epidemic, and probably zymotic in its origin. (See EPIDEMIC CEREBRO-SPINAL MENINGITIS.) Sporadic spinal meningitis is a rare disease. It may be acute or chronic.

ETIOLOGY.—Among the causes of acute spinal meningitis are injuries to the vertebral column, such as fracture and dislocation from falls, blows, etc.; wounds by stabbing or shooting; violent bodily effort, as in lifting heavy weights, etc. Other causes are local exposure to wet and cold, as from sleeping on the wet ground or standing long in water while at work. Like cerebral meningitis, it may complicate constitutional diseases, as rheumatism, pyæmia, etc., but less frequently than the former. Syphilitic inflammation of the spinal membranes is, however, not unfrequently met with, but chiefly of the chronic form. (See the article on SYPHILIS OF THE BRAIN AND SPINAL CORD.) In tubercular meningitis of the brain the pia mater of the cord is often implicated in the disease. Acute spinal meningitis is most frequently met with in young persons, and is more common in men than in women.

SYMPTOMS.—The onset of the disease is generally sudden, and it is rarely preceded by the usual inflammatory symptoms of chilly sensations, restlessness, headache, etc. A sharp rigor is the first indication of disease in most cases. This is followed by fever, with high temperature and a quick, full, hard pulse. Pain in the back follows, either confined to a limited region or extending throughout the whole extent of the spine, soon becoming acute, and aggravated by any movement of the trunk or even of the limbs. There is usually but little tenderness on pressure upon the spinous processes, and often none at all. The pain extends around the body and throughout the limbs. In the course of a few hours muscular contraction in the region of the back, and also of the limbs, is observed. When the disease is situated in the cervical region, the head is drawn backward, and cannot be moved without severe pain. If it occupies a considerable extent of the spine, the dorsal muscles become rigidly contracted and the body is arched forward (opisthotonos), as in tetanus, so that the patient may even rest upon his occiput and sacrum. Owing to the implication of the muscles of respiration, more or less dyspnœa is common, and may even cause death by asphyxia. There is no paralysis of the limbs, unless there be complication of myelitis, but the patient abstains as far as possible from any movement from dread of pain. Reflex irritability is exaggerated. Retention of urine and constipation are common, probably for the same reason. Hyperæsthesia of the surface of the body in limited areas is sometimes noticed, owing to the irritation of the posterior spinal roots. Provided the extent of the inflammation be comparatively limited, recovery is possible, though rare, at this stage of the disease.

When the course of the disease is unfavorable, symptoms of paralysis appear, from compression of the cord by the products of inflammation. The hyperæsthesia of the skin gives place to insensibility; the muscles lose their reflex function and their reaction to electricity; the bladder and rectum become paralyzed. The invasion of the medulla by the disease, which is announced by paralysis of the muscles of the œsophagus and of the tongue, is a fatal complication. The pulse and the respiration become rapid and irregular from compression of the vagus, the temperature rises to 106° or 108° F., and death ensues through asphyxia or failure of the heart.

The course of acute spinal meningitis is rapid. It sometimes terminates fatally within two or three days, and the average duration of fatal cases is about a week, but exceptionally the disease may last for several weeks or even months. Even then complete recovery may take place, though permanent effects are usually left behind, such as paresis or paralysis of the lower extremities, muscular contractions, muscular atrophy, etc., from injury to the nerve-roots or the cord.

The mind is generally clear in the early stage; afterward there may be delirium, especially along with cerebral complication.

MORBID ANATOMY.—It is rarely that the pia mater is the only tissue involved in the inflammation. Frequently the inner surface of the dura is the seat of a fine injection, with delicate false membranes, and the cord itself—at least its exterior portions—probably always participates more or less in the congestion. The pia is reddened and thickened, the surface showing small bloody extravasations, and the space between its two layers is the seat of a fibro-purulent deposit. The spinal fluid is turbid and flocculent. The seat and extent of the morbid appearances vary in different cases; they are always more abundant in the posterior than the anterior part of the cord, and may be confined to a limited space or extend throughout its whole length. It is remarkable that the region of the medulla oblongata is generally free or only slightly affected; but since bulbar symptoms are often prominent in grave cases, Leyden⁶ accounts for it by supposing that the exudation is washed away by the constant movement of the cerebro-spinal fluid. If the cord be involved in the inflammation, it is softened and injected, the nerve-sheaths are destroyed, and the axis-cylinders swollen in places. The nerve-roots show hyperæmia, infiltration of the interstitial tissue with round cells, and destruction of the nerve-sheaths.

⁶ Klinik der Rückenmarks-krankheiten, von E. Leyden, Berlin, 1874, vol. i. p. 407.

DIAGNOSIS.—Spinal meningitis is easily recognized in most cases by its sudden onset and the severity of its symptoms. The distinguishing symptoms are sudden and acute pain in the back, extending around the body and into the limbs, which is increased by every movement of the trunk, rigidity of the back, hyperæsthesia of the skin, retraction of the head, with difficulty of breathing and of swallowing. The diseases from which it must be distinguished are muscular rheumatism (so called), tetanus, and myelitis. In rheumatism of the dorsal muscles the pain is confined to the back, does not extend to the limbs, and is only excited by movement. The fever is moderate or absent; there are no symptoms of spinal complication, such as cutaneous hyperæsthesia, retraction of the head, paresis of the limbs, etc.; and the result is uniformly favorable. Tetanus is almost always due to some well-marked traumatic cause; the muscles of the jaw are usually first implicated (trismus); and the attacks of general muscular spasm are easily excited by peripheral irritation. Myelitis can be distinguished by the absence of pain in the limbs and by paraplegia, but it must be borne in mind that myelitis and spinal meningitis may coexist.

PROGNOSIS.—Acute spinal meningitis is always a grave disease, hence a guarded opinion should be given even in apparently favorable cases. General mildness of the symptoms, with no indication of extension to the medulla oblongata, would afford ground for encouragement. The unfavorable symptoms are those showing compression or inflammation of the cord, such as paresis, paralysis, twitching of the limbs, muscular contractions, cutaneous anæsthesia, etc. The extension of the disease to the medulla, as shown by difficulty of swallowing, speaking, or breathing, is almost necessarily fatal.

TREATMENT.—During the first stage of the disease an effort should be made to reduce the hyperæmia of the membranes by the local abstraction of blood. This is best effected by cupping along each side of the spine and by the application of leeches to the anus; the bleeding should be promoted by poultices. Free purging is likely to be of service, and is best obtained by means of ten grains each of calomel and jalap (for an adult), followed by saline laxatives. Counter-irritation to the back may be induced by the application of blisters or by painting the skin with a strong tincture of iodine (one or two drachms of iodine to an ounce of sulphuric ether). After the effusion of lymph and pus, as shown by symptoms of compression of the nerve-roots and cord, absorbents should be tried, of which the iodide of potassium, in doses of five to ten grains, four times daily, is most likely to be of benefit. Pain must be relieved by opium or morphia and chloral hydrate. The latter, either alone or combined with hyoscyamus and bromide of potassium, will be useful to allay spasmodic twitching, opisthotonos, or muscular contraction. The patient should be enjoined to lie on each side alternately, or on the face if possible, in order to equalize the hyperæmia of the membranes and cord. Liquid nourishment must be freely administered, such as milk, broths, gruel, etc., together with wine and other stimulants in case of exhaustion and threatening of collapse. During convalescence the patient should be carefully protected against cold and fatigue, and the strength must be supported by quinine and iron with suitable diet.

Chronic Spinal Meningitis.

SYNONYMS.—Chronic inflammation of the pia mater of the spinal cord, Chronic spinal leptomeningitis.

Chronic spinal meningitis may follow the acute form, or it may arise from chronic disease of the vertebræ or of the cord, especially myelitis and sclerosis. It is most apt to accompany sclerosis of the posterior columns, and it is often difficult to say in any particular case whether the meningeal affection preceded or followed that of the cord. Probably some cases of chronic myelitis, especially of the disseminated form, owe their origin to chronic meningitis.⁷ It has been thought to follow blows on the back, and also to arise from general concussion without traumatism, and has been considered as a frequent result of accidents from railroad collisions, etc. This view has been disputed by Herbert W. Page,⁸ who says: “Of the exceeding rarity of spinal meningitis as an immediate result of localized injury to the vertebral column we are well assured.... And we know of no one case, either in our own experience or in the experience of others, in which meningeal inflammation has been indisputably caused by injury to some part of the body remote from the vertebral column.” Chronic alcoholism and syphilis, especially the latter, predispose to the disease. In many cases no adequate cause can be assigned.

⁷ Leyden, op. cit., vol. i. p. 442.

⁸ Injuries of the Spine and Spinal Cord, without Apparent Mechanical Lesion and Nervous Shock, in their Medico-legal Aspects, London, 1883, p. 128.

SYMPTOMS.—Gowers⁹ remarks that a large number of symptoms formerly assigned to chronic spinal meningitis have nothing to do with that pathological state, but are now known to be owing to alterations within the cord which are frequently associated with it. The symptoms which are really due to the meningeal inflammation—namely, those arising from interference with the nerve-roots in their passage through the thickened membranes—do not differ essentially from those of chronic pachymeningitis of the spine; the principal are pain in the back, especially on movement, extending to the trunk and limbs, hyperæsthesia of the skin in various regions within the domain of the irritated sensory roots, with diminution or loss of the knee-jerk, and areas of anæsthesia due to their more complete compression. The compression of the motor roots gives rise to symptoms which are similar to those of disease of the anterior cornua, consisting chiefly of muscular wasting, with impairment of motion in corresponding regions, without fever.

⁹ The Diagnosis and Diseases of the Spinal Cord, by W. R. Gowers, M.D., 2d ed., Philada., 1881, p. 73.

The anatomical appearances, which are most pronounced in the posterior aspect of the cord, and diminish from below upward, are often of considerable extent. The membrane is thickened, opaque, and often adherent to the cord. On the inner surface are seen numerous small bodies composed of proliferating connective tissue.¹⁰ These, according to Vulpian, are chiefly found in the lower dorsal and lumbar region and on the cauda equina. The dura is very frequently involved in the inflammation; it is thickened, and its inner surface is adherent to the pia, often showing numerous miliary bodies similar to those found in the pia.

¹⁰ Leyden, op. cit., vol. i. p. 144; A. Vulpian, Mal. du Syst. nerv., Paris, 1879, p. 126.

DIAGNOSIS.—Chronic spinal meningitis so rarely exists apart from disease of the dura or of the cord that its separate diagnosis must be mainly a matter of conjecture. Leyden justly says we must usually be content to diagnosticate chronic meningitis without attempting any further distinction, except in cases which originate in disease of the vertebræ or of their neighborhood, and afterward penetrate into the spinal canal, and which would probably give rise to pachymeningitis. The diseases with which chronic meningitis of the spine is most likely to be confounded are posterior sclerosis (locomotor ataxia) and chronic degeneration of the anterior cornua (progressive muscular atrophy).¹¹ From the former it is distinguished by the absence of ataxia; from the latter, by the irregular distribution of the symptoms; and from both, by the existence of limited areas of anæsthesia and of extensive spinal pain. It must be remembered that inflammation of the cord complicating that of the meninges, or pressure upon the cord by the thickened membranes may give rise to mixed symptoms. The latter is especially observed in syphilitic cases.

¹¹ Gowers, op. cit., p. 74.

PROGNOSIS.—Simple chronic spinal meningitis is rarely if ever fatal. How far it is capable of amelioration or of cure is not, in the present state of our knowledge, known. When complicated with disease of the cord the prognosis will depend upon that of the latter. Syphilitic chronic meningitis is to a certain extent amenable to appropriate medication.

TREATMENT.—The treatment should have for its object (1st) to relieve pain; (2d) to arrest the progress of the inflammation, and especially to prevent it from extending to the cord; (3d) to promote the absorption of the exudation. For the first object the internal or hypodermic employment of morphia should be combined with external applications, such as fomentations, liniments, ice, etc. Counter-irritation by means of dry cupping, blisters, iodine, etc., with leeches, shampooing, and douches of hot water, may be of some use in retarding the progress of the inflammation, and should be aided by the administration of mercurials and the preparations of iodine. The biniodide of mercury would be useful for this purpose in the dose of one-sixteenth to one-eighth of a grain three times daily, its effect being carefully watched in order to prevent salivation. The same means will also aid in favoring the absorption of lymph. In syphilitic cases an appropriate specific treatment is indicated.

Spinal Meningeal Hemorrhage.

SYNONYMS.—Spinal meningeal apoplexy, Hæmatorrhachis.

Spinal meningeal hemorrhage may take place between the dura mater and the walls of the vertebral canal, or between the dura and the pia mater—i.e. into the arachnoid space.

ETIOLOGY.—Penetrating wounds, injuries to the vertebræ, fractures and dislocations, and violent blows are apt to give rise to more or less hemorrhage into the spinal canal. Violent convulsions, as in tetanus, epilepsy, uræmic eclampsia, hydrophobia, may be followed by meningeal hemorrhage, owing to the disturbance of the circulation from asphyxia; and excessive muscular effort, as in lifting heavy weights, etc., has been said to cause it. In cerebral meningeal hemorrhage and in effusion into the substance of the brain the blood sometimes escapes into the spinal canal. An aneurism of the aorta has been known to communicate with the canal; such a case was reported by Laennec.¹² In certain diseases with hemorrhagic tendency, as purpura and scurvy, spinal extravasation is occasionally observed.¹³

¹² Traité d'Auscultation médiate, 4th ed., Paris, 1837, vol. iii. p. 443.

¹³ A case of scorbutic spinal hemorrhage is reported in the British Med. Journal, Nov. 19, 1881.

SYMPTOMS.—These vary according to the conditions under which the hemorrhage is produced and to the amount of bleeding. In traumatic cases the signs of hemorrhage are often completely overshadowed by those of the injury of the vertebræ, the membranes, or the cord, and are undistinguishable. When a large amount of blood is suddenly introduced into the spinal canal, it usually gives rise, by pressure on the cord, to paraplegia, which, however, is sometimes of only short duration. Thus in Laennec's case the bursting of an aneurism into the spinal cavity was signalized by a sudden paraplegia, but in half an hour the power of movement returned, though sensation did not. The patient died in a few hours from hemorrhage into the left pleural cavity. The amount of blood in the spinal cavity is not stated, and, in fact, it would appear that the spine was not opened. When the amount of blood is smaller the symptoms indicate irritation of the spinal nerves and of the cord. Pain in the back is always present, extending into the limbs, and is sometimes severe. Its seat corresponds to that of the effusion. There may be a feeling of tingling and numbness in the lower extremities, with anæsthesia or hyperæsthesia of the skin and more or less paresis. A feeling of constriction around the waist or the chest is sometimes complained of. In slight effusions the symptoms may be limited to numbness and formication of the extremities, with slight paresis. There is rarely fever in the early stages, unless the amount of blood is sufficient to give rise to inflammatory conditions of the cord or membranes. If the extravasation be moderate it is generally absorbed, with relief to the symptoms, although slight numbness and paresis of the extremities may continue for a long time.

PATHOLOGICAL ANATOMY.—In hemorrhage outside the dura the loose cellular tissue between the membrane and the bony canal contains more or less coagulated blood according to the circumstances of the case, especially in the posterior region of the canal and covering the nerve-roots. The dura is reddened by imbibition of the coloring matter of the blood. When the amount of the effusion is large, as in traumatic and aneurismal cases, or where cerebral hemorrhage has extended into the spine, the cord may be compressed by it. Hemorrhage into the arachnoid sac, except in cases of violence, etc., is usually of limited amount, sometimes only in the form of drops of blood upon the surface of the dura or pia. When more abundant it may surround the cord more or less completely, but in most cases it is limited in longitudinal extent, being confined to the space of one or two vertebræ. The cord may be more or less compressed, reddened, and softened. In all cases the spinal fluid is discolored and reddened in proportion to the amount of the hemorrhage.

DIAGNOSIS.—When the complications are such that symptoms attributable to hemorrhage are not observed, the diagnosis of spinal hemorrhage is impossible. This may happen in the case of wounds and injuries of the vertebræ and of the passage into the spinal canal of blood from an apoplectic effusion of the brain. In the convulsions of tetanus, epilepsy, etc. the amount of the hemorrhage is rarely sufficient to give rise to distinctive symptoms. In idiopathic and uncomplicated cases the chief diagnostic marks are suddenness of the attack; pain in the back, usually at the lowest part; disturbances of sensation in the extremities (anæsthesia, formication, etc.); paresis or paralysis of the legs; the absence of cerebral or spinal inflammatory symptoms; and, in many cases, the favorable course of the disease. Sometimes an ostensible cause, such as scurvy, purpura, suppressed menstruation, or hemorrhoidal flux, will aid in the diagnosis. The disease for which spinal hemorrhage is most likely to be mistaken is acute myelitis, but this is not sudden in its onset, is accompanied with fever, and gives rise to paralysis both of motion and sensation, and to loss of control over the sphincters, to bed-sores, etc. Hemorrhage of the cord would be accompanied by paraplegia and loss of sensation in the lower extremities and slight tendency to spasmodic manifestations; it is fatal in the majority of cases, or else is followed by permanent paralysis. Hysteria might be confounded with spinal hemorrhage, but the history of the case and the transient duration of the symptoms would clear up all obscurity.

PROGNOSIS.—In traumatic cases the hemorrhage is usually only one element in the gravity of the situation, which depends chiefly upon the character and extent of the original injury. In idiopathic and uncomplicated cases the prognosis, which must always be doubtful, will vary according to the severity of the symptoms as corresponding to the amount of the effusion. The danger is greatest during the first few days; if there should then be diminution of the more important symptoms, an encouraging opinion may be given. The immediate effects may, however, be less grave than the remote, such as bed-sores, cystitis, etc. Except in the very mildest cases the patient is likely to be confined to bed for several weeks. In more severe ones the convalescence may be very protracted, and permanent lameness, etc. may result.

TREATMENT.—In the early stage absolute rest in bed, with cold applications to the back and moderate purging, should be employed. Large doses of ergot are recommended, but there is little evidence of benefit from this medicine. In traumatic cases no rules for treatment of the hemorrhage can be laid down. If the extravasation evidently depends upon a constitutional diathesis, as in purpura, scurvy, etc., the remedies appropriate for these diseases should be employed, especially tonics and astringents, such as the tincture of the chloride of iron, in doses of from fifteen to thirty drops three times daily, quinine, and the vegetable acids. Should there be evidence of blood-pressure from suppressed discharge, as in amenorrhœa, arrested hemorrhoidal flow, etc., leeches should be applied to the anus, and blood may be taken from the region of the spine by cupping. In the later stages an attempt may be made to aid the absorption of the effused blood by the administration of the iodide of potassium or the protiodide of mercury, and by the application of blisters or strong tincture of iodine to each side of the spine. Pain must be relieved and sleep obtained, when necessary, by means of opium, chloral hydrate, or other anodynes. Electricity, rubbing, bathing, etc. will be useful for combating the paralytic symptoms which may remain after the disease itself is relieved.

SPINA BIFIDA.

BY JOHN ASHHURST, JR., M.D.

DEFINITION.—By the term spina bifida is meant a congenital malformation of the vertebral column, consisting in the absence of a part—commonly the spinous processes and laminæ—of one or more of the vertebræ, and thus permitting a protrusion of the spinal meninges, which, with their contents, form a tumor of variable size and shape, usually in the lumbo-sacral region.

SYNONYMS, ETC.—Of the various names which have been proposed for this affection, most are objectionable, as not expressing with sufficient definiteness what is meant. Thus, hydrorachis (the term generally employed by French writers), hydrorachitis, spinal hydrocele, etc., convey merely the notion of an accumulation of fluid within the spinal canal, and are as applicable to simple serous effusions in that part, whether occurring as a complication of hydrocephalus or as the result of injury, as to the special affection under consideration. Again, myelochysis—pouring out or protrusion of the spinal marrow—would imply that the cord itself was necessarily involved in the tumor, which is certainly not always the case. The terms schistorachis (cleft spine) and atelorachidia (defective spine—a name suggested by Béclard) would be preferable, and are really more accurate than the name spina bifida, since, as a matter of fact, the spinous processes are, as a rule, not bifid, but totally deficient. The latter term, however, has the advantage of being more familiar, and may be retained simply as a matter of convenience. It is said by Itard to have been first employed by the Arabian physicians.

HISTORY.—Spina bifida does not appear to have been known to the ancients, the earliest recorded observations of the affection being found in the writings of Bauhinus (1560-1624), of Tulpius (1593-1674), of Bonetus (1620-89), and of Ruysch (1638-1731). Good accounts of the affection may be found in the Dictionnaire des Sciences médicales (tome xxii., Paris, 1818), and particularly in Holmes's Surgical Treatment of the Diseases of Infancy and Childhood (2d ed., London, 1869), in Follin and Duplay's Traité de Pathologie externe (tome iii.), and in Treves's article on “Malformations and Injuries of the Spine” in the International Encyclopædia of Surgery (vol. iv., New York, 1884).

ETIOLOGY.—There are two conditions essential to the formation of a spina bifida: (1) an arrest of development, or at least a defective closure, of the vertebral arches; and (2) a dropsical condition either of the central canal of the spinal cord or of the subarachnoid spaces; but which of these is the antecedent condition it is, as justly remarked by Erb, impossible to decide. Spina bifida often occurs as a complication of hydrocephalus, and is itself often complicated with an atrophic and deformed condition of the lower extremities—a circumstance which led Tulpius to suggest that the malformation was caused by a malposition of the fœtus in utero, an explanation which it seems hardly necessary to waste time in considering. Salzmann observed spina bifida in two children born of the same mother, and Camper noticed it in twins.

SYMPTOMATOLOGY.—Spina bifida forms a tumor—or, more rarely, several tumors—in the region of the vertebral column, usually discovered at birth, but occasionally not noticed until a later period. Thus, Lancisi mentions a case in which the tumor first made its appearance in a hydrocephalic child at the age of five years, and J. L. Apin one in which the patient reached the age of twenty before any swelling was manifested. If these records are accepted as authentic, the only satisfactory explanation is that of Itard—viz. that the bony deficiency existed from the time of birth, and that the dropsical protrusion did not occur until afterward: this seems to me more reasonable than the suggestion of the younger Andral, that the vertebræ underwent a process of secondary softening and absorption. The part most frequently affected is the lumbar region, but cases are not wanting of the occurrence of spina bifida in the cervical, dorsal, and sacral regions, and even, in at least one case (Genga's), in the coccyx. The tumor almost invariably occupies the median line, and projects directly backward: in at least four cases, however, recorded by Bryant, Emmet, and Thomas, the tumor protruded anteriorly from deficiency of the vertebral bodies.

The size of a spina bifida varies from that of a walnut to that of a child's head, or even larger: in some rare instances, such as those recorded by Lezelius and Richard, the whole spinal column has been cleft, and the tumor has extended from nucha to sacrum; but cases of this kind seldom come under the surgeon's observation, as children with such extensive deformity usually perish shortly after birth. The shape of the swelling is rounded, or more often oval; it is commonly sessile, but occasionally pedunculated; and it is sometimes lobulated, the lobules being separated by more or less distinct sulci. The skin covering the tumor is in some cases normal, with more or less fat in the subcutaneous connective tissue, but more often thin, tightly stretched, red, shining, and occasionally ulcerated; more rarely it is thickened and leathery, as in a case referred to by Sir Prescott Hewett. Sometimes a navel-like depression is found at some part of the surface, corresponding, as pointed out by Follin and Duplay, and by Erb, to the place of attachment, on the interior of the sac, of the terminal extremity of the spinal cord. The cutaneous investment is sometimes altogether wanting, the spinal dura mater itself forming the external covering of the tumor. It is in these cases especially that ulceration and rupture are apt to occur.

Spinæ bifidæ are usually soft and fluctuating, and occasionally partially reducible; their tension and elasticity are increased when the child is in the upright position or during the acts of expiration and crying, and are diminished during inspiration or when the child is laid upon its face. When the part is relaxed a bony prominence can be felt on either side, and the aperture in the vertebral column can be more or less distinctly outlined. The swelling is apt to be painful on pressure. If the tumor is of moderate size and covered with healthy skin, there are usually no constitutional symptoms, and, even where ulceration and rupture occur, the opening may heal and a spontaneous cure may possibly ensue. More often, as the tumor increases in bulk—or at any time if pressure be made upon it—various nervous symptoms are observed: drowsiness, muscular twitchings, convulsions, and often paraplegia and paralysis of the sphincters. Rupture is usually followed by the development of spinal meningitis, or may prove directly the cause of death by the loss of cerebro-spinal fluid which it causes; in other instances, however, if the rupture be a small one, healing may occur (as already mentioned) or a fistulous opening may persist; in rare cases the fluid may escape by a process of transudation without rupture, as in an example recorded by Laborie.

As may be inferred from what has already been said, the course of spina bifida is usually rapid and toward a fatal termination. In some instances, however, as in cases observed by Holmes, and more recently by Lithgow, spontaneous recovery has followed the obliteration of the channel which unites the sac with the cavity of the spinal membranes; and in other instances, without a cure having been effected, life has been prolonged for very many years. Thus, Behrend reports a case in which a patient with spina bifida lived to the age of fifty, and Holmes refers to another in which death resulted from an independent disease at the age of forty-three. But a still more remarkable case was recorded by Callender, the patient in this instance having reached the age of seventy-four.

PATHOLOGY AND MORBID ANATOMY.—The most important points for consideration in respect to the anatomy of spina bifida are the relations which the spinal cord and spinal nerves bear to the sac, and the nature of the contained fluid. It is ordinarily said that the spinal cord itself commonly enters the sac of a spina bifida—the report of the London Clinical Society's committee gives the proportion of cases in which it does so at 63 per cent.—and Holmes figures a specimen from the museum of St. George's Hospital, London, in which this condition is obviously present; on the other hand, Mayo-Robson in eight operations only once found the cord implicated; and the late John B. S. Jackson of Boston—whose name will be recognized as one of high authority in regard to all questions of morbid anatomy—once assured me that he had made very many dissections of spinæ bifidæ, and that he had invariably found that the cord stopped short of the sac, and that only the nerves entered the latter: this, as negative evidence, cannot of course contravene such positive evidence as that of the specimen referred to by Holmes, but it would seem to show that the condition was a less common one than is generally supposed, and that in at least a fair proportion of cases the cord itself did not form part of the sac contents. This remark applies especially to those cases in which the fluid is accumulated in the subarachnoid space, and in which, as pointed out by Sir P. Hewett, the cauda equina or spinal nerves are pushed by the vis a tergo into the sac; but when the dropsical effusion occupies the central canal of the cord, this is apt to be flattened and spread out like a thin lining to the sac, just as the brain is spread over the inner wall of the skull in cases of internal hydrocephalus; and, on the other hand, when the accumulated fluid fills the cavity of the arachnoid the cord is apt to be pushed forward, and the sac may be entirely devoid of all nerve-structures. Such, too, according to Giraldès, is the case in spina bifida of the cervico-dorsal region.

The committee of the London Clinical Society classify cases of spina bifida in three divisions: (1) Those in which the membranes only protrude (spinal meningocele); (2) those in which the protrusion involves both the cord and membranes (meningo-myelocele); and (3) those in which the central canal of the cord itself forms the cavity of the sac (syringo-myelocele). The last variety is the rarest, as the second is the most common. In meningo-myeloceles the spinal cord with its central canal is continued within the median, vertical portion of the sac, and at this part there is no covering of true skin; the nerve-roots which traverse the sac arise from this intramural portion of the central nervous system.

Humphry of Cambridge, England, makes a somewhat similar classification of spinæ bifidæ, recognizing as the most common variety the hydrorachis externa anterior, in which the fluid occupies the subarachnoid space in front of the spinal cord, and in which “the cord and the nerves are stretched backwards and outwards upon the sac, and are there confluent, together with the arachnoid, pia mater, and dura mater, or their representatives, in the thin membrane which forms the hindmost part of the wall of the sac;” rarer forms are the hydro-meningocele, or hydrorachis externa posterior, in which the fluid accumulates behind the cord, which does not enter the sac, and the hydro-myelocele or hydrorachis interna, in which the fluid occupies the central spinal canal.

The theory which, according to the Clinical Society's committee, best explains the pathological anatomy of spina bifida is that which assumes a primary defect of development of the mesoblast from which the structures closing in the vertebral furrow are developed.

The fluid of spina bifida appears to be identical in character with the cerebro-spinal fluid. Bostock found that it was very slightly clouded by the application of heat, and that it contained, in 100 parts, 97.8 of water, 1.0 of chloride of sodium, 0.5 of albumen, 0.5 of mucus, 0.2 of gelatin, and some traces of lime. Five specimens more recently analyzed by Hoppe-Seyler gave an average of 98.8 parts water, 0.15 parts proteids, and 1.06 extractives and salts. Turner found a reaction somewhat similar to that of grape-sugar, as had been previously found by Bussy and Deschamps in cerebro-spinal fluid itself, but in two specimens analyzed by Noad for Holmes it was at least very doubtful whether sugar was actually present. “The first specimen was found to be completely neutral; its specific gravity was 1.0077; it contained phosphates, but no reaction could be obtained resembling that of sugar. The second specimen ... did give a reaction with copper like that of sugar, but no trace of fermentation could be obtained.” Three analyses, however, made by Halliburton for the London Clinical Society's committee showed uniformly a decided trace of sugar, with a diminution in the quantity of proteids, which appeared to consist entirely of globulin.

In some cases the sac of a spina bifida contains, besides nerve-structures and cerebro-spinal fluid, both fibrous and fatty tissues.

DIAGNOSIS.—Ordinary fatty tumors have been mistaken for spinæ bifidæ, but such an error could only be committed through carelessness: more difficult is the diagnosis from certain forms of congenital cyst, occupying the median line of the back, and still more difficult the diagnosis from the several affections known as false spina bifida. In the former case the distinction might be made by noting the irreducibility, constant shape, and unchanging tenseness of the cyst, and perhaps, as suggested by T. Smith, by tracing the line of spinous processes beneath it; some information, too, might perhaps be gained by chemical examination of the fluid obtained by puncture. Under the name of false spina bifida Holmes includes three distinct conditions: these are—(1) a true spina bifida, in which the connection with the spinal membranes has in some way been obliterated, the sac then communicating with the vertebral canal, but not with the theca; (2) a congenital, cystic, or fatty tumor, taking its origin within the vertebral canal, and projecting through an opening caused by a gap in the laminæ; and (3) a tumor containing fœtal remains, and properly regarded as an example of included fœtation. In any of these cases a positive diagnosis might be impossible, and the probable nature of the tumor could only be inferred by noting the absence of one or more of the characteristic symptoms of true spina bifida.

PROGNOSIS.—The prognosis of spina bifida is without question unfavorable; at the same time the affection is by no means to be considered, as it was formerly, one of an invariably fatal character, for, apart from the fact already mentioned that several cases are on record in which patients with untreated spina bifida have reached adult life, and even old age, the modern method of treatment has proved so much more successful than those formerly employed that in favorable cases surgical interference affords at least a reasonable prospect of recovery. The circumstances which especially furnish grounds for an unfavorable prognosis are the rapid growth of the tumor, the thinning or ulceration of its coverings, and the occurrence of nervous symptoms, and particularly of paralysis or convulsions.

TREATMENT.—This may be either palliative or radical. If the tumor be not increasing materially in size, the surgeon may properly content himself with palliative measures—applying equable support and perhaps slight pressure by the use of a well-padded cap of gutta-percha or leather, an air-pad, or, as advised by Treves, a simple pad of cotton smeared with vaseline, and a bandage; if the tumor be small and covered with healthy integument, painting its surface with collodion may be of service through the contractile property of that substance. Radical measures are only indicated when the child, otherwise healthy, seems to have his life threatened by the rapid growth of the tumor, causing risk of ulceration and rupture, or giving rise to convulsions or paralysis. The principal modes of treatment to be considered under this heading are—(1) simple tapping or paracentesis; (2) injection of iodine; (3) ligation of the neck of the sac; and (4) excision.

(1) Paracentesis, a simple evacuation of the fluid contents of the sac, is the only operation ordinarily justifiable in cases attended by paralysis or other grave nervous manifestations. The puncture should be made in the lower part of the sac and at a distance from the median line (in the course of which the nerve-structures are particularly distributed), and only a small quantity of fluid—a few drachms or at most one or two ounces—should be removed at a time, the instrument being at once withdrawn if convulsions follow, and the wound being instantly closed with lint dipped in compound tincture of benzoin. Either an aspirator-tube or a small trocar may be used, and the operation may be repeated if necessary, pressure being maintained during the intervals. Paracentesis has occasionally though not often proved curative.

(2) Injection of Iodine.—This mode of treatment was introduced about the same time by Velpeau and by Brainard of Chicago. The latter surgeon's method consists in injecting, after only partially emptying the tumor, a solution of iodine with iodide of potassium (iodine, 5 grs.; iodide of potassium, 15 grs.; water, 1 fl. oz.), allowing it to flow out again, washing out the sac with water, and finally reinjecting a portion of the cerebro-spinal fluid originally evacuated; and the former's, in completely evacuating the tumor, and then injecting a mixture of iodine and iodide of potassium, each one part to ten parts of water. Each of these plans has met with a fair measure of success;¹ but the modification introduced by James Morton of Glasgow is a great improvement, and affords what is actually the most successful mode yet devised for dealing with spina bifida. Morton employs a solution of iodine in glycerin (iodine, 10 grs.; iodide of potassium, 30 grs.; glycerin, 1 fl. oz.), which has the advantage of being less diffusible than the aqueous solution, and therefore less liable to enter the spinal canal. The tumor is about half emptied, and a small quantity—from fluid drachm ss to fluid drachm iij of the solution—is then slowly injected, and allowed to remain. The operation is repeated after a few days if necessary. Of 50 cases known to Morton as having been treated in this way up to May, 1885, 41 were regarded as successful; but of 71 cases collected by the London Clinical Society's committee, only 39 had been benefited by the operation.

¹ In a case recently recorded by Woltering, however, iodine injection was followed by death within half an hour.

The introduction of iodine into the sac of a spina bifida is, according to Morton, only justifiable in cases unattended by paralysis; under opposite circumstances I should be disposed to try a plan recently employed with success by Noble Smith in a case of meningocele—viz. injecting the iodo-glycerin solution into the coverings of the sac, and as close to it as possible without perforating it.

(3) and (4). Ligation and excision have each occasionally effected a cure, but more often have but helped to precipitate a fatal issue. A successful case of ligation followed by excision has been recently recorded by Löbker. The elastic ligature, applied around the neck of the sac (if this be pedunculated), has been employed by Laroyenne, Ball, Colognese, Baldossare, Mouchet, and other surgeons, and of 6 cases collected by Mouchet, 3 ended in recovery. Another success has been recently recorded by Turretta. The écraseur has been used, but its employment cannot be recommended. Compression by clamps is advised by Schatz of Rostock. Ligation is best adapted to cases occurring in the cervical and dorsal regions, in which, as pointed out by Giraldès, nerve-elements are less likely to be involved. Excision, supplemented by transplantation of a strip of periosteum from a rabbit, has been successfully resorted to by Mayo-Robson and by R. T. Hayes of Rochester, N. Y.; and simple excision, with suture in separate lines of the sac and integuments, by Mayo-Robson, Atkinson, and Jessop. The Clinical Society's committee in all refers to 23 cases treated by excision, 16 of which are said to have been successful.

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.