Epilepsy

EPILEPSY. Contents: History...531. Etiology...532. Distribution...536. Pathological anatomy...537. Experimental pathology...539. Pathogenesis...540. Course and symptoms...544. Diagnosis...547. Prognosis...549. Treatment...549. Prophylaxis and social significance...552. Mental disorders...553. Surgical treatment of epilepsy...560. Epilepsy, epilepsia (from Greek epilambano - I seize), morbus sacer, morbus divinus, falling sickness, a disease known to humanity since ancient times and manifesting as a sudden, convulsive seizure occurring as if in the midst of perfect health. Epilepsy belongs to diseases whose clinical picture is generally well known, but whose pathogenesis and essence remain, to this day, far from clear, if not entirely unclear. The literature on epilepsy is enormous, and at the present time, more than a hundred scientific works on various questions of epilepsy are published annually. History: The manifestations of epilepsy were well known in antiquity. In Indian medicine of the Vedic period (at least 8 centuries B.C.), there is a reference to epilepsy among the diseases noted in a girl's family, with whom a Brahmin was forbidden to marry. Hippocrates, in 'On the Sacred Disease,' no longer sees anything sacred or supernatural in it; religious measures regarding it are useless; epilepsy is a disease of the nervous system and, in particular, of the 'brain,' the 'organ of reason and intellect.' Hippocrates, considering epilepsy a somatic disease, speaks out against the sympathetic and superstitious methods of treatment practiced in his time. He also provided observations corresponding to clinical reality regarding the influence of heredity in epilepsy, a description of the aura, and the seizure itself. Aretaeus (1st century B.C.) provides a description of mental disorders in epilepsy, both in the form of short-term psychoses and equivalents, and in the form of epileptic dementia. Caelius Aurelianus (4th–5th centuries A.D.) recommended for epilepsy baths and sun treatment; he condemned the castration used in his time, which 'vires amputat, non epilepsiam solvit' [amputates strength, does not resolve epilepsy], as well as turtle blood, or the heart of a hare or camel. Later, until the beginning of the 19th century, Paracelsus, Morgagni, Boerhaave, Stahl, Pinel, and others wrote about epilepsy. In French literature, there exists a study by Josat (1856) on the history of the doctrine of epilepsy. One must also mention the monographs of Tissot (1770), Wenzel (1811), Portal (1827), the work of Bravais (1827) on cortical partial epilepsy, as well as the completely original work (1850s) of the Dutchman Schroeder van der Kolk, who provided anatomical data in favor of a new understanding of the pathogenesis of epilepsy as a disease standing in connection with the peculiarities of the width of the capillaries of the medulla oblongata. In the modern era, the development of neuropathology is reflected in the evolution of the doctrine of epilepsy; the subcortical, or rather, medullary theory of understanding the pathogenesis of the seizure (Kussmaul, Nothnagel) is being replaced by the cortical one in connection with the general study of the motor zone of the cerebral cortex (Jackson, Hitzig, Fritsch, Muratov, Foerster, and others), and then, in recent years, the thought of at least some researchers is returning to bringing the role of subcortical formations to the fore; the doctrines of internal secretion, the autonomic nervous system, intracranial pressure, the state of the blood, acid-base balance, metabolism, constitution, the role of infection in the brain, heredity, etc.—all these moments find their reflection in the understanding and construction of new representations, concepts, and theories in the doctrine of epilepsy. Of great importance in the general doctrine of epilepsy is the question of general genuine, or essential, epilepsy and local epilepsy. It remains an unresolved problem whether, in an unfolding epileptiform seizure, we always have only a syndrome (symptom complex), or whether, alongside such existing general symptomatic epilepsy, one should also recognize the existence of genuine epilepsy as a special independent pathological entity or disease. Etiology. In some cases, the etiological moment of epilepsy is clear, as, for example, in the case of syphilitic or traumatic epilepsy; in others, it can be substantiated, suspected, or assumed with greater or lesser probability; in others, the causes of the onset of the disease are dark and incomprehensible; in these cases, they speak of the endogenous origin of the disease. In many cases, one can speak of the summation of etiological moments, of an existing predisposition, and of provocative moments that cause the disease as well as individual seizures. Here we encounter the fact of the existence of symptomatic epilepsy, i.e., cases where the seizure (in these cases it is better to call it not epileptic, but epileptiform) is only a manifestation of some definite disease (progressive paralysis, cerebral hemorrhage, cerebral arteriosclerosis, inflammation of the brain or its membranes, tumor, trauma, cerebral syphilis, multiple sclerosis, brain parasite, uremia, eclampsia, etc.), and the difficult question of the existence of a special, idiopathic, essential, spontaneous, genuine epilepsy. Epileptic seizures of the latter most often do not have a definite etiological moment or are linked in the past to trauma or infection, but subsequently arise as if spontaneously according to a once-established mechanism, developing independently and at the same time as if according to a template. These cases force one to believe that, as long as we still do not know much about the pathogenesis and etiology of epilepsy, we cannot consider the question of the existence of independent genuine epilepsy as a special kind of disease to be resolved. Further on, when isolating individual exogenous and endogenous etiological moments, the question is illuminated mainly from the point of view of genuine epilepsy. Speaking of epilepsy of infectious origin, one has in mind an encephalitis underlying it, resulting from some acute or chronic infection. Epidemic or sporadic encephalitis, meningitis, typhus, scarlet fever, tuberculosis, syphilis are the most frequently encountered etiological infectious moments. Darkshevich views epilepsy as a whole as an infection of the brain (this cannot be agreed with); attempts were made to find and isolate a specific pathogen of epilepsy, but without success. As exogenous intoxications causing epilepsy, alcoholism is of particularly great importance, and to a lesser extent, ergotism, absinthe, arsenic, and other poisons; insofar as there are isolated indications in the literature on the link between epilepsy and very many poisons, one can think that in these casuistic observations, the main role is played not by exogenous intoxication, but by the endogenous individual predisposition of the subject. Trauma plays a large role in the emergence of both gross, local, symptomatic, and genuine, general epilepsy. Injuries and wounds of the skull, contusions of the brain, and its concussion during urban, transport, industrial, agricultural, and especially military traumatism are to a very large extent (up to 20–30% of cases) the cause of subsequent epilepsy. To a certain extent, one can agree with Bykhovsky that every person wounded in the skull is a candidate for epilepsy. A large role in the origin of the disease is played by traumatism during the act of childbirth (birth with a narrow pelvis, obstetric operations). In the clinical picture of Little's disease, epileptic seizures are often noted. A special position is occupied by the question of reflex epilepsy, i.e., the emergence of seizures due to a scar existing after trauma on the periphery, irritating some nerve or peripheral nerve endings; besides a scar, such an irritating moment can be some foreign body. It remains unclear to what extent the predisposition of the subject plays a role in all cases of traumatic and reflex epilepsy; its role is likely not small. Very curious is the dependence of seizures on cosmic, atmospheric, and climatic influences. According to Gallus, the maximum number of seizures occurs in March (especially), April, August, and the minimum in January, June, October, November, December. It is possible that the cosmic influence turns out to be complex and for different places, different in climatic respects, and the data obtained are different, appearing contradictory. Overheating in the sun can cause a seizure. Staying in a higher-altitude locality (for us, for example, Kislovodsk, 800 m) can also cause a seizure compared to conditions of being in a lower-altitude one (for example, Pyatigorsk, 500 m above sea level). Amman found a parallelism between seizures and atmospheric electricity and terrestrial magnetism. Lukashev managed to notice the dependence of seizures on the average monthly temperature: the greatest increase in seizures occurred at the coldest and warmest average monthly temperatures. Brezina and Schmidt found that rapid fluctuations in barometric pressure with large amplitude can cause seizures. Ratner raised the question of seasonal epilepsy, believing that in a number of cases there are spring and autumn increases in seizures; he links this to a change in autonomic tone in the spring towards the parasympathetic system, and in the autumn towards the sympathetic. It is known that in some patients, seizures occur exclusively at night, in others only during the day.

All this speaks of likely existing cosmic influences on epilepsy and encourages the systematic collection of data on individual patients and individual localities. Hereditary influences turn out to be transitional between exogenous and endogenous etiological factors. It is often possible to note that several epileptics are found in a family, especially along collateral lines. Occasionally, direct epileptic heredity appears very vividly (see Myoclonus). According to Davidenkov, epilepsy, being a hereditary disease, is apparently transmitted recessively; alcoholism, migraines, chorea, paralysis, extreme nervousness, neuroses, and hysteria characterize the epileptic family. In direct transmission, epilepsy is more often transmitted from father to son or from mother to daughter than crosswise. However, for hereditary transmission of epilepsy, it is necessary to have bilateral burdening. In the majority of cases, in the families of epileptics, alcoholism (from 4% to 26%) is found; conception of the patient in a state of intoxication, psychopathy, diseases of the cardiovascular system, migraines, metabolic disorders, but often even with more detailed and persistent questioning, it is not possible to identify the expected characteristic data in the patient's pedigree. This circumstance should apparently be evaluated as evidence that epilepsy should by no means always be considered a constitutionally congenital and endogenous disease. The age factor plays a significant role in the onset of epilepsy. At the birth of a child, he sometimes has eclampsia; this is not epilepsy, but if in the anamnesis of an epileptic we find a mention of eclampsia that he had, then, of course, the question arises about the possible connection between the two phenomena, about a possible predisposition that existed from early childhood. The same applies to the fact of the appearance in children at an early age of epileptiform convulsions (the so-called "infantile" [convulsions]). If a small child reacts to intoxication, elevated temperature (or some other factor) with a convulsive seizure, then on the basis of this alone, a doctor will not yet speak of epilepsy, since such a phenomenon may never repeat itself throughout life; however, in the event of the subsequent development of epilepsy in him, the fact of "infantile" [convulsions] is naturally given the significance of an early, clear sign of predisposition to the disease. Epilepsy in children most often arises in connection with birth trauma, in connection with illness from meningitis, encephalitis, or some other infection, in connection with a strong emotion of fear (fright), as a result of overheating of the head, etc., but often seizures begin in a child without any discernible causes or triggers, idiopathically. In older children, the disease arises in connection with the period of puberty, especially in girls during development; at the same time, a close connection between seizures and menstruation is noted (appearance of seizures before, during, or after menstruation; replacement of menstruation with seizures, etc.). In an adult woman, seizures sometimes begin during pregnancy, before childbirth, and after them, showing a kinship between epilepsy and the eclampsia of pregnant women, women in labor, and the puerperal period. According to some data, women generally fall ill more often than men, according to others—the opposite. Genuine epilepsy usually develops at the age of up to 12-20 years, and it can be called, based on the onset of the disease, a disease of young age. If epilepsy debuts with a seizure at the age of 30 or later, there is a great deal of data to suspect that we are dealing with either some other, usually organic, disease of the brain, or epilepsy on the basis of syphilis. The development of epilepsy at a later age (epilepsia tarda), the age of sexual decline, if there is no progressive paralysis or other organic disease of the brain, usually forces one to think about arteriosclerosis of the brain. The development of epilepsy is also possible in old age. To what extent epilepsy, beginning at different ages and in persons of different sexes, while having to a large extent the same clinical manifestations, is a homogeneous disease, remains open. Epilepsy that began in infancy, epilepsy of old age, epilepsy of the puberty period and late epilepsy, epilepsy in a man and epilepsy arising during pregnancy or manifesting in connection with menstruation—all these are apparently diseases that are different in their pathogenesis, manifesting with the same syndrome. Further, the following question arises: is there always, in all these heterogeneous forms, the same pathogenesis of the seizure itself, or can the seizure in different cases be conditioned by different factors and relationships, just as the localization of the seizure can have different topica. The constitution of epileptics appears as follows: a) the predominant type is dysplastic, athletic, or mixed dysplastic-athletic; b) asymmetries in the development of individual organs are very often noted; c) most often encountered (Chizh) is a special "heavy," "leaden" gaze and luster of the eyes, or in children, eyes with wide pupils and a gaze directed into the distance ("Vasnetsov" eyes); d) weakness of the organization of the vascular system (narrowness of the aorta, early arteriosclerosis, tendency to vascular spasm, etc.); e) unstable metabolism; f) accelerated blood clotting; g) psychological peculiarities (epileptic character): increased sharp irritability for inappropriate reasons, unmotivated mood swings, slowness, rigidity, viscosity of thoughts, exaggerated circumstantiality, petty neatness, selfishness, obsequiousness, hypocrisy, tendency to complain, touchiness, manifestation of anger, tendency to twilight states of consciousness, etc. Insofar as there are grounds to distinguish the features of an epileptic constitution, this thereby emphasizes the great role of predisposition to epilepsy, the readiness in a suitable organism for a seizure to begin suddenly, and the presence in the organism of epileptics of certain endogenous factors and internal etiological factors for the development of the disease. Endogenous etiological factors in epilepsy have the closest relation to the question of understanding the pathogenesis of the seizure. In the constitution of epileptics, from a pathophysiological point of view, the question of unstable metabolism is put forward. There are grounds to believe that only fat metabolism in epileptics appears to be stable. The instability of metabolism concerns the most diverse aspects (nitrogen, carbohydrate, salt, water, basal, intermediate, etc.). The difficulty of the question lies in the fact that for now we still have very little concrete data and a great deal that is contradictory. Apparently, the difficulties of the question depend to a greater extent on rapidly passing disturbances in metabolism, the visible diversity of disorders that can lead to some fundamental disturbance leading to a seizure or resolving it, i.e., from that same fact of great metabolic instability. Insofar as spasmophilia is understood as a state of the organism in which all kinds of convulsive phenomena occur more easily, then, of course, the question of calcium metabolism and the role of the parathyroid glands for epilepsy is of very great interest, however, fully definite conclusions do not yet exist here. -The endocrine glands are closely connected with metabolism. The connection of epilepsy with the period of menstruation and pregnancy in one way or another emphasizes the significance of the sex glands in its etiology. The onset of epilepsy in the majority of cases before the end of adulthood also points to the probable role in this of a disturbance in the process of growth and development of the organism, which proceed with the participation of both glands that gradually lose their significance (pineal, thymus), and those whose influence is felt throughout life (adrenal, thyroid, pituitary), not to mention those mentioned above. -Metabolism and endocrine glands are most closely connected with the autonomic nervous system. It is natural that the instability of the latter, its influence, for example, on such systems important for the clinic of epilepsy as the cardiovascular [system], cannot but have great significance in the sense of the manifestation of such peculiar clinical symptoms that are characteristic of epilepsy (disturbances in the field of blood circulation, frequent nocturnal seizures of the disease, the influence of cosmic changes, the great significance of emotional-affective factors). -The state of the blood of patients with epilepsy appears to be a very important factor in an etiological respect, both in relation to its composition and especially its bio-physico-chemical properties (coagulation, viscosity). -Speaking of such internal etiological factors for the onset of epilepsy as metabolism, endocrine glands, the autonomic nervous system, and blood, one must also point to one more factor, which is, of course, closely connected with those just listed, being itself a product of disturbances in the field of metabolism, but at the same time occupies, from the angle of different points of view, an independent position; this is the processes of autointoxication (see); insofar as an epileptic in the interictal state appears more or less healthy, insofar as an epileptic seizure is to a large extent a clinical expression of some internal self-poisoning of the organism by unknown pathogenic products, to that extent an epileptic can be considered as a subject periodically poisoned by some substances, which are subsequently either neutralized or excreted. Prevalence of epilepsy. Epilepsy is undoubtedly a frequently encountered disease, prevalent apparently in all countries and among all peoples.

In Germany, about 1‰ of epileptics, in Italy slightly more, in France up to 1.8‰. Among patients in psychiatric hospitals, epileptics constitute on average about 10%. Only a very small number of epileptics end up in hospitals, as many epileptics suffer from such manifestations of epilepsy (very rare seizures, petit mal seizures, mild manifestations of psycho-epilepsy) which do not actually place them in the position of being constantly ill; there are not a few individuals suffering from rare seizures and at the same time possessing good, even outstanding working capacity and excellent mental qualities, and sometimes even genius (Caesar, Mahomet, Napoleon, Chopin, Byron, Helmholtz, Dostoevsky, Flaubert, Van Gogh, and others). The number of epilepsy patients for Western Europe must be determined as no less than 1-2‰ of the population. It is interesting that the number of those rejected for epilepsy upon induction into military service in the Bulgarian army is 0.24‰, in the Italian 1.15‰, in France 1.5‰, in Switzerland 2.6‰, in Germany from 2.06‰ to 3.4‰, in Sweden 3.5‰, in the Russian (Gorshkov) 0.427‰. According to data from the medical department in 1895, there were fewer than 0.2‰ epileptics in Russia; this figure is, of course, too small. In 1893, in the Moscow Governorate, according to the Yakovenko census, there were 5.1 epileptics per 10,000. The information in Sukhov's monograph on the prevalence of epilepsy in Russia (1906) is outdated for the present time. In 1911, in the Moscow Governorate, there were 5.7 epileptics per 10,000 of the population; in 1913, in the Petersburg Governorate, 5.6 per 10,000, and in the Ufa [Governorate] 11.8 per 10,000 of the population. According to data reported by Prozorov (published in 1931), in the USSR, the number of epileptics is subject to sharp fluctuations by individual regions and localities, though for one and the same specific locality, the figures repeat from year to year. In the Moscow Governorate, among psychiatric patients in a psychiatric hospital, there were 7.5% epileptics, in the Ural Region 11.1%, in the Tula [Region] 13.5%, in the Bashkir Republic 17.4%. On average, in psychiatric hospitals, epileptics constitute about 10% of all psychiatric patients. The ratio of male to female epileptics in psychiatric hospitals is 61:39 (it is interesting that the same ratio exists according to Rühl's data in 1839). Pathological anatomy. Posthumous changes in epilepsy appear to be far from systematized and not unambiguous. If a patient dies during a seizure, the changes in the brain usually bear the character of edema, hyperemia, small thrombi, and multiple small hemorrhages; in a later stage, changes are found in the nerve cells and a large number of lymphocytes (infiltrates) and glial nuclei. To what extent these changes are primary or secondary, as a result of the seizure, is difficult to judge. As early as 1827, Portal wrote: "There is no part of the brain that would not show changes in epilepsy," and on the other hand, often during the autopsy of an epileptic, nothing is found macroscopically in the brain. Since the etiology and pathogenesis of epilepsy are complex, and since epilepsy is a disease of the entire organism, it is natural that the attention of the pathologist should be directed not only to changes in the brain but also to the rest of the nervous system, nerve ganglia, glands, etc. So far, there is still very little detailed data with microscopic examination of all organs. If one attempts to systematize the most frequent findings at autopsy in epileptics, the following can be established. 1. Various developmental anomalies of the skull, brain, muscles, glands; so-called physical signs of degeneration, deformation of the base of the skull, the sella turcica, etc., are often encountered. 2. Hydrocephalus, asymmetry of the cerebral ventricles, and phenomena of brain edema; these data can be established primarily by encephalography. 3. Signs of insufficient development of the vascular system and changes in it: narrowness of the aorta, indications of early arteriosclerosis, dilation of perivascular spaces in the brain, closure of the lumen of vessels (their spasms), swelling and proliferation of the vascular endothelium, the presence of small thrombi, hemorrhages. 4. As the most characteristic changes in the nervous substance, phenomena on the part of the neuroglia in the form of diffuse progressive gliosis. Here one must include the sclerosis of Ammon's horn described as early as 1825 in epileptics (in 50-60% of cases according to Alzheimer), marginal subpial neuroglial sclerosis (Chaslin), in which the glia proliferates between the pia mater and the tangential fibers. It is curious to note that in those epileptics who do not have dementia, there are also no signs of marginal gliosis in the brain. And regarding the proliferation of glia, the question remains unresolved as to what extent the described gliosis is primary or secondary. 5. As for changes in the nerve elements themselves, they cannot be called either specific or more or less uniform. Their localization is scattered. A number of researchers (Jakob, Ranke, Alzheimer, Turner) draw attention to developmental defects in the cerebral cortex, disturbances in the architectonics of the brain of epileptics, an abnormal, as if random, arrangement of nerve cells, the presence in a relatively large number of pluriaxonal Cajal-Retzius cells (according to Turner in 70% of cases of idiopathic epilepsy). Recently, more and more material has been accumulating, speaking of changes in the brainstem region. In the 1850s, a professor from Utrecht, Schroeder van der Kolk, described very wide (2-6 times wider than normal) capillaries in the medulla oblongata in epileptics. Anton draws attention to the relationship between the space occupied by the cerebellum and the space occupied by the entire brain. Spielmeyer points to the particular constancy of changes in epilepsy in the cerebellum and in Ammon's horn (in 80% of cases). Lévy-Valensi and Voisin emphasize the development of gliotic sclerosis, especially in the olives. Over the last few years, quite a lot of data from various researchers has been accumulating in favor of the subcortical or extrapyramidal origin of epilepsy. 6. There are also a number of findings at autopsy regarding the glands of internal secretion. Quite often in epilepsy, an non-atrophied thymus gland is found, the so-called thymus persistens. Changes are noted in the thyroid gland (development of sclerosis in it, changes in the follicles, an increase in the amount of iodine to 0.01 instead of the normal 0.004; Parant), in the ovaries (a decrease in the number of Graafian follicles and corpora lutea, their weak vascularization), in the pituitary gland, adrenal glands, and liver. Of course, these findings are still sporadic, but one should not forget that attention to changes in the glands has only been drawn recently, and even fewer examinations under the microscope have been made. The presented data of a pathological-anatomical nature in epilepsy are far from exhaustive and are far from being considered completely pathognomonic. Epilepsy to a large extent proceeds with such a clinical picture that it often appears to be a disease that, as it were, has no pathological anatomy. Taking into account the complexity of the pathogenesis of epilepsy, the heterogeneity of its symptomatology, and the fact that epilepsy is a disease of the entire organism, one can think that in the future, the pathologist's attention should be especially attracted by signs of deviation in the development of the skull, brain, vascular system, and the entire organism, changes in the circulation, glands of internal secretion, pathological-anatomical findings not only in the cerebral cortex but also in the brainstem and subcortical formations; finally, on the other hand, since genuine general epilepsy should to a large extent be considered as a disease having at its core a disturbed and even unstable metabolism, one can expect a shift in our knowledge if the pathologist approaches epilepsy from the point of view of the pathological anatomy of metabolic disorders. This has not yet been done to the present time. On the other hand, one must approach epilepsy not only from the point of view of pathological-anatomical data obtained at autopsy, but also data obtained in a living epileptic by means of encephalography and by a more detailed study of findings during surgical intervention. Adhesions, foci of limited edema, local serous meningitis, changes in blood supply, pulsation of the brain—all this can be seen and distinguished in the living, and what is especially important, only in living tissues; on a corpse, they lose their clarity. By means of encephalography, one can establish edema of the brain tissue, the difference in the size of the cerebral ventricles, their dilation, changes in their shape, the nature of the subarachnoid spaces, phenomena of porencephaly, etc., not to mention more gross changes in local epilepsy of a symptomatic nature. This is a real biopsy of the brain. Here, systematic examination by obtaining 6 images in different planes (Khoroshko's method) is especially valuable. A whole series of surgeons (Horsley, Doyen, Walter, Leriche, Foerster, and others) have observed that the seizure is preceded by sharp anemia of the brain and the cessation of its pulsations. True, there are also indications of the opposite phenomenon—hyperemia of the brain, its swelling. In the fundus of the eye, it was possible to see, 10-20 seconds before the start of the seizure, a spasm of the retinal arteries, and after the seizure, significant dilation of the veins. Experimental pathology. As early as the mid-19th century.

(1851) Brown-Séquard showed that in an animal one can induce convulsions by irritating the most diverse parts of the nervous system, not only the central but also the peripheral, in particular by irritating the sciatic nerve. This provided experimental proof of the possibility of reflex epilepsy. Subsequently, all such experiments using the method of mechanical, electrical, and chemical (strychnine, cocaine, absinthe) irritation (Fritsch, Hitzig, Ferrier, Magnan, Goreli, Munk, and others) particularly confirmed, substantiated, and developed the cortical pathogenesis of the epileptiform seizure. All this was brilliantly confirmed not only in animals but also in humans during brain surgery (Goreli, Krause, Foerster, and others; in our country, especially V. I. Razumovsky and many other surgeons). However, the experiments of Luciani, Vulpian, and Goltz showed the possibility of the development of convulsions even in animals deprived of the cerebral cortex. It was established quite a long time ago (Cooper, Kussmaul, Tenner) that anemia, compression of the carotid and vertebral arteries, causes a seizure, and Landau, Herman, and others showed this also in relation to the cervical veins. Elsberg and Stookey particularly emphasized the significance of the moment of suddenness for the development of convulsions. An interesting step forward in the matter of experimental research was made by the introduction of a combined effect: preliminary operative-mechanical damage to the cortex and subsequent chemical irritation. This method was proposed by Rossolimo (1892) under the name of surgical-toxic, but received general recognition significantly later (some 30-35 years later); in this way, the full significance of both a small local injury (focus) in the brain and a toxic agent (cocaine, strychnine, picrotoxin, absinthe, etc.) in a weak dose, which each individually is not capable of causing a seizure, was demonstrated. Experimentally, the significance of the glands of internal secretion in the development of a seizure was also shown: thus, after thyroidectomy, a seizure occurs more easily; it is possible to induce convulsive attacks with subsequent death by injecting insulin (the significance of progressive hypoglycemia). By intravenously injecting rabbits with an aqueous extract of brain matter (endotoxins of nervous tissue), Khoroshko showed the possibility of the development of an epileptiform seizure in an animal with a demonstrative change in the biophysical-chemical properties of the blood (change in coagulability, appearance of thrombi). A. D. Speransky and his school (Galkin, Fedorov, Pigalov, and others) introduced a new interesting methodology and new, most interesting thoughts into the matter of experimentation; the Speransky laboratory developed a method of experimental freezing of individual and, moreover, different parts of the brain, isolated and emphasized the full significance of the subcortical moment in the development of a seizure in contrast to the cerebral cortex, the significance of combined moments (brain, fluid, periphery, toxins, etc.), the significance not of irritation, but of inhibition of the functions of the cerebral cortex for the development of a seizure by releasing the activity of subcortical apparatuses. Speransky emphasizes the significance at any given moment of the state of the corresponding nervous elements, draws closer the nature of the nervous mechanisms of the epileptiform seizure and sleep (inhibition of the cortex!), and particularly highlights the significance of the environment; "excitation that has arisen in any one point of the cortex can easily cause a process of inhibition in all its other parts"; "in the nervous mechanism of an epileptic attack, the main role is played by the coincidence of irritation of the subcortex with phenomena of diffuse inhibition of the cortex"; "the creation of the necessary combination, ensuring—even with a constant stimulus—the onset of an epileptic attack, is always more or less accidental"; "the place from which an epileptic attack arises can be any point of the nervous system"; "from whatever source the process may arise, it will be realized with the help of a reflex mechanism; therefore, all forms of Epilepsy are reflex." Experimental observation of the phenomena of Epilepsy in humans was limited only to the facts of electrical irritation of the cerebral cortex during operations; there is a whole series of observations of the toxic origin of seizures (absinthe, alcohol, cocaine, sodium chloride, adrenaline, anise, dill; after rapid intravenous injection of a concentrated solution of sodium iodide during the new method of arteriography of the brain); seizures in humans are induced by compression of the carotids (anemia), irritation of the sympathetic and sensory sphere (pressure on the eyes during examination of the oculocardiac reflex, irrigation of the auditory canal with cold water). (All this shows, among other things, how careful one should be with various medical manipulations, since inducing an epileptic seizure without need is undoubtedly contraindicated and even harmful.) Of particularly great interest is the induction of a seizure by hyperventilation, i.e., by rhythmic (10-15 per minute) measured deep inhalation and subsequent deepest possible exhalation of air by the patient for 20 minutes. As a result of this test, phenomena of tetany, increased reflexes, and twitching may develop, and in epileptics—a seizure (Foerster). At the basis of these phenomena lies the developing state of alkalosis of the blood. The experiment showed the significance in the pathogenesis of Epilepsy of a local focus, a toxic moment, the state of blood circulation, and the biochemical and biophysical properties of the blood. Pathogenesis. Since the question of epilepsy as a hereditary disease and of an epileptic constitution has been put forward, when illuminating the pathogenesis of this disease, one must always take into account the presence to one degree or another of a predisposition to Epilepsy as a peculiar idiopathic disease and to the possibility of the development of a seizure, whether it be epileptic or epileptiform. From the point of view of pathogenesis, it is necessary to always distinguish whether we have before us essential, idiopathic, genuine Epilepsy as a specific disease or symptomatic Epilepsy, epilepsy as a syndrome in progressive paralysis, syphilis of the brain, multiple sclerosis, kidney disease, brain parasites, tumor, etc. On the other hand, it is extremely important not to conflate into one the phenomena of general Epilepsy, manifesting immediately with generalized seizures, and the picture of local epilepsy of the Jacksonian, Kozhevnikov type, or the prolonged cortical convulsions of Muratov; in the latter, the entire undoubted significance of a local focus in the brain stands out, expressed clinically by the presence of a specific aura; however, an aura in a stereotypical form can often be observed also in so-called general seizures of Epilepsy; in these cases, the existence of some local focus is also undoubtedly present, but its significance in the pathogenesis of the seizure must be considered much less important. Be that as it may, if one abstracts from the clinical picture of gross-focal symptomatic Epilepsy, as it occurs¹ in tumors, syphilis, abscesses, and large traumatic scars, then still the fact of the presence of a local focus, albeit smaller and more delicate in its pathological-anatomical picture, as we most often observe after an infection (encephalitis) or trauma in the brain, provides grounds for understanding the pathogenesis of a seizure primarily as the accumulation from time to time of irritation of nervous elements. The pathogenesis of an epileptic seizure and of Epilepsy as a disease, due to the insufficiency of our knowledge, does not yet seem possible to present in an impeccable, satisfactory form. We are dealing here only with hypothetical statements and assumptions of a temporary nature based on one or another factual data. Since the cerebral cortex certainly has very great significance in the pathogenesis of Epilepsy, both local and general, especially if the latter is viewed from the angle of the view and significance of local changes in it, one should become acquainted with the conclusions on this matter by Foerster, who put much labor into the study of this question. Foerster distinguishes 8 typical localizations in the cerebral cortex for the development of epileptic seizures: 1) the anterior central gyrus; 2) the frontal field (superior frontal section); onset of the seizure with a turning of the head and eyes to the opposite side, then the trunk, etc.; 3) the frontal oculomotor field (posterior section of the 2nd frontal gyrus); onset of the seizure with clonic twitching of the eyes; 4) the posterior central gyrus; onset with a sensory aura; 5) the parietal field; likewise a sensory aura; appearance of pain at the onset of the seizure; 6) the occipital, oculomotor field; visual aura; 7) the temporal field; auditory, olfactory, gustatory aura; 8) the operculum and the lower section of the central gyri—the field of rhythmic movements; appearance during the seizure of movements of chewing, swallowing, licking, smacking, grunting, groaning, screaming, vomiting. Foerster believes that a seizure can be induced from any part of the brain. Whether a seizure develops as a result of irritation of the cerebral cortex or, as Speransky thinks, the activation of subcortical centers always takes place, it is undoubtedly the case in any event that epileptic seizures also arise as a result of the activation of subcortical mechanisms; to what extent the optic thalami, the lenticular nucleus, the corpus caudatum, and other parts of the diencephalon, the brainstem, and the medulla oblongata play a role here remains as yet unknown. It is also unknown to what extent one should recognize the possibility of the development of an epileptic seizure as a result of some disturbances originating from the medulla oblongata and the brainstem.

If one considers the great connection of this part of the nervous system with the autonomic nervous system and the vascular system, and takes into account the significant participation of disturbances in the state of blood circulation and the properties of the blood in the development of a seizure, then it becomes understandable and acceptable to assume the possibility of the appearance of a seizure through the influence of some kind of effects coming from the brainstem, in particular from the medulla oblongata. From this area, it is easy to assume an effect in the form of a developing shock, leading to general inhibition of the functions of the cerebral cortex and causing loss of consciousness. The quantitative difference in this kind of effect and the phenomena of inhibition finds its clinical reflection in both cases in the rapidly occurring loss of consciousness, while in others—in the gradual development of an unconscious state, twilight consciousness, etc. The sharpness and volume of consciousness are undoubtedly closely connected with the phenomena of attention, on the one hand, and with the energy of circulatory processes—on the other. Thus, it is impossible to imagine, from the point of view of a spatial understanding of the topography of nervous mechanisms, that the development of an epileptic seizure depends on or is localized in any one place (focus) of the brain; it is much closer to the truth to understand the genesis of the seizure as a function of the disturbed activity of the entire brain as a whole, in which one can distinguish, as separate details, the participation of one or another nervous mechanism. A local focus (aura) is a condition for the facilitated occurrence of a seizure, a kind of springboard from which the further presentation begins. But what happens in the focus or near the focus? How to imagine the emergence of some process from which all further development proceeds? Since in epilepsy, after a seizure, there is often a complete restoration to the pre-seizure state of health, this process must be very unstable, easily reversible, far from always leaving behind any traces, and often passing completely without a trace in the pathological-anatomical sense. Not only processes in the tissue of the brain or the central nervous system in general can cause an epileptiform seizure, but also irritations coming from the periphery. From the nasal cavity or the external auditory canal, a seizure can be caused in the order of reflex epilepsy if a foreign body is present there. A scar on a peripheral nerve, a bone spur that has appeared as a result of some injury, irritation of the semicircular canals, inflammatory swelling during teething, intestinal worms—all these are also etiological moments that can cause a seizure in the order of a reflex effect. However, in most cases, a seizure occurs during various disturbances of a humoral nature, in metabolism, in blood circulation, without the presence of such a noticeable irritating cause as in the case of reflex epilepsy. An epileptic may have disturbances in nitrogen metabolism (retention of uric acid, ammonia, ammonium carbamate; Krainsky), in lipid metabolism (decrease in blood cholesterol), carbohydrate (hypoglycemia), mineral (calcium metabolism), water (edema), a decrease in ionized calcium; these disturbances are usually observed in the pre-seizure state, characterized in most cases by blood alkalosis (Bigwood) due to a decrease in the alkaline reserve. The epileptic presents a picture of unstable regulation in metabolism; the concentration of hydrogen ions in the blood of an epileptic gives large fluctuations—from 5.2 to 7.6 (alkalosis). The pre-seizure state (usually alkalosis) apparently appears to be almost the complete opposite of the post-seizure state (acidosis). Alkalosis is probably only a favorable condition for the onset of a seizure. Such factors as menstruation or hyperventilation intensify alkalosis and therefore are very favorable for the development of a seizure. Conversely, infectious diseases in the fever period, pregnancy, certain medications (luminal, potassium bitartrate) weaken alkalosis and therefore create unfavorable conditions for the manifestation of a seizure. Nevertheless, it seems that this instability in metabolism, in acid-base balance, etc., is only the basic background of genuine epilepsy, and some additional, perhaps toxic, factor is required. A weakening of the permeability of capillaries or the blood-brain barrier by preliminary drainage of cerebrospinal fluid during absinthe poisoning (Speransky) increases the readiness for the onset of an epileptic seizure. There are a number of indications of the possibility of understanding an epileptic seizure as an anaphylactic shock (Buscaino)—increased sensitivity to certain nutrients (meat, milk, cheese, butter, sweets, chocolate, beans, eggs, grain bread); in this case, phenomena of the type of Vidal's hemoclasic shock (crisis) or vascular-trophic (vascular-blood) shock (Boucher and Gustin) develop in the body; this is expressed, among other things, by an increase and fluctuation in blood clotting, changes in the amount of fibrin-ferment, fluctuations in the number of blood platelets, leukocytic thrombi, fluctuations between leukopenia and leukocytosis, disturbances in blood pressure, changes in the refractometric index of blood serum, etc. These phenomena are observed both in anaphylactic shock and in an epileptic seizure. The epileptic is undoubtedly a subject with great instability of the vascular-blood apparatus. Some of these phenomena precede the seizure, others usually occur in the phase following the seizure. However, it is also necessary to note the difference between epilepsy (alkalosis, loss of consciousness) and anaphylaxis (acidosis, absence of loss of consciousness). Understanding an epileptic seizure as an anaphylactic shock is probably acceptable only for individual cases of epilepsy. Finally, the fact that the blood serum of epileptics contains some toxic substance which, when injected into animals, causes, among other things, convulsive phenomena, suggests that in epilepsy, some toxic principle probably circulates in the patient's body, perhaps at times, which is presumably a product of disturbed interstitial metabolism of the auto-endointoxication type. Since experiments with aqueous extracts of brain tissue have shown (Khoroshko) the possibility of the development of an epileptiform seizure upon their intravenous administration to an animal, and since similar data have been obtained regarding placental tissue and kidney tissue, it is possible to compare them and express the assumption of an identical pathogenesis of seizure development in eclampsia (placenta), uremia (kidney), and epilepsy (brain), at least for a part of the phenomena. If one abstracts from those cases of epilepsy in which there is some local focus of disease in the brain, expressed by an aura, or in which there is some peripheral reflex-irritating moment, then the understanding of the pathogenesis of general-type epilepsy can be imagined as follows: the patient has an extremely unstable metabolism, an unstable acid-base balance, an unstable vascular-blood apparatus and unstable regulation of it; under the influence of the most diverse, in strength, exogenous and endogenous moments, up to fatigue and mental agitation, the normal chain of vital processes can break in one of these systems—some toxic spasmophilic product appears, or the degree of resistance of the capillary endothelium and nervous mechanisms relaxes, or the susceptibility of the latter to products of interstitial metabolism circulating in the norm, which are completely harmless for the time being, increases; something like an internal shock arises somewhere, causing, via a vegetative reflex, the shutdown of the cerebral cortex and the disinhibition of subcortical mechanisms in the form of a seizure. As a particular case of the pathogenesis of epilepsy, it can be assumed that under the influence of some provocative moment, the interstitial metabolism in the brain tissue is disturbed, its endotoxins enter the bloodstream, where, under their influence, a change in the biophysical properties of the blood occurs in the form of disturbances in its viscosity and clotting; stasis, spasms, thrombi, and other shifts in the vascular-blood system are formed; hence—the development of a seizure either by the type of internal shock and reflex or by the type of transient ischemic irritation. If all disturbances are not persistent and are fully reversible, the general well-being of the organism is restored. If, however, the disturbances that occurred during the seizure or a series of them have gone far, then subsequently a picture of gliosis begins to develop, and the phenomena of epileptic degeneration and dementia gradually increase. The pathogenesis of epilepsy and the seizure should be imagined as diverse—sometimes less, sometimes more complex. It is unknown whether all the above-listed moments of disturbance in metabolism and blood properties stand in any relationship to each other, and whether these correlations are always non-obligatory and can be to a large extent accidental. Understanding the pathogenesis of some cases of epilepsy as auto-endointoxication by products of brain metabolism and subsequent disturbances in the blood and blood bed also explains a number of clinical phenomena and known therapeutic effects. Course and symptoms. Epilepsy begins at different ages.

As prodromal phenomena, the following are noted: convulsive seizures in childhood ('infantile'), prolonged urinary incontinence, jumping up, nightmares and screaming in children at night (pavor nocturnus), sleepwalking, somnambulism, lunacy, increased inexplicable irritability, etc. But often an epilepsy seizure occurs quite suddenly. A seizure may begin with a premonition, a feeling by the patient of its onset, sometimes a peculiar experience or perception as if of a breeze blowing (hence the name 'aura'); it is characteristic of the aura phenomenon that it usually always precedes a seizure in a stereotypical form; at the same time, the form of the aura can be most diverse: a general sensation from some part of the body (e.g., the epigastric region, heart, neck, skin, limb), as if experiencing some movement along the body, an olfactory, gustatory, visual, auditory sensation, in some cases with the vividness of a hallucination (sensory, sensitive aura) or a stereotypically repeating movement (twitching of a finger, limb, turning of the eyes, neck, head, screaming, moaning, facial convulsion, grimace, rapid movement, etc.; motor aura), or a vegetative-visceral aura (experiencing fear, terror, various organic, localized, or general phenomena). The seizure itself usually begins with tonic convulsions, which then pass into clonic ones. The convulsions seize the patient either immediately, causing them to fall, sometimes breaking and bruising themselves, or gradually, so that the patient has time to lie down, and sometimes even by strong compression, e.g., of the limb in which the aura began, or by an effort of will, somehow abort (cut off) the further development of the seizure. Sometimes the seizure develops in the order of the arrangement of the cortical centers of the motor zone: twitching on one side of the face passes to the arm, then to the leg of the same side, then to the musculature of the other leg, then to the arm and face of the opposite side. This is Bravais-Jackson cortical epilepsy. During a seizure, labored breathing, salivation (foam at the mouth), biting of the tongue (convulsion in the tongue and masticatory muscles, admixture of blood in the saliva), cyanosis, weakening of the pulse, loss of consciousness, absence of pupillary reaction to light, involuntary urination, sometimes defecation, vomiting, and sweating are observed. Seizures can sometimes follow one after another (status epilepticus) and number in the tens and even hundreds; the temperature as a result of the convulsions sometimes rises to 40° and higher. The frequency of seizures is very diverse in individual patients: in some, 1-2-3 during their entire life, in others 1-2 times a year, in others monthly (especially in women in connection with menstruation), several times a month, either one by one or in series, and finally, seizures occur daily and several times during each day. In individual cases, it is possible to establish a certain rhythm in the appearance of seizures, i.e., their alternation at regular intervals. The strength and degree of the seizure can also be diverse: seizures can be underdeveloped, of greater or lesser duration, accompanied by greater or lesser stupor, malaise, and even loss of consciousness. Amnesia (a complete lack of memory by the patient of what happened to them) occurring after the seizure is characteristic. Upon the return of consciousness, one can often establish in the patient phenomena of amnesic aphasia, a limitation for some time in the use of words (Bernstein's oligophasia). After a seizure, a headache, sleep, hibernation, or drowsiness usually occurs. The seizure lasts 2-3 minutes, but sometimes longer- 5-8 minutes. As a rule, patients do not die from a convulsive seizure, but in a state of status epilepticus, death can often occur. In addition to general convulsive, so-called major (grand mal) seizures, so-called minor (petit mal) seizures are often observed. The most characteristic and mandatory feature for them is the loss of consciousness. The patient may lose consciousness for only a few seconds, change in the face, turn pale, the facial expression changes (but this may not happen), and then they continue to live as before, e.g., continue an interrupted conversation, eat food, etc.; at the same time, some patients know that something happened to them, others notice nothing, as if ignoring their own temporary lapse, absence (absence). In some cases, a minor seizure can be expressed by some action, movement, a series of manipulations, aimless and unnecessary, a smile, crying, the utterance of some phrase or word, etc. A minor seizure ends with a sigh, the restoration of the patient's previous state, sometimes swallowing, chewing movements, smacking of the lips. Sometimes a patient in a state of a minor seizure seems to spin around (epilepsia rotatoria - rotating) or strives to run away (epilepsia procursoria - striving to run forward). Attacks of dizziness in the form of minor seizures (vertigo epileptica) are observed. Some associate attacks of headache in the form of migraine with epilepsy. Minor seizures can alternate with major ones, can be without major ones, and reach high frequency. In children, frequent attacks of loss of consciousness give the picture of so-called pyknolepsy. It is possible that attacks of uncontrollable sleep (narcolepsy) in some cases are also equivalents of a convulsive seizure. Besides psychic equivalents, convulsive seizures of epilepsy can be replaced by other and, moreover, very diverse phenomena, namely various neuralgias, states of malaise and excessive fatigue, sensations of intense heat or cold, blinding, blindness, visual and auditory hallucinations, perversions of taste and smell, spasms of the glottis, attacks of shortness of breath, forced erections, gastralgias, sudden imperative urges to defecate and urinate, attacks of angina pectoris and bradycardia (Adams-Stokes disease). In addition to the main forms of manifestations of epilepsy in the form of seizures of one kind or another, there are also separate forms of epilepsy where seizures of general convulsions are combined with interictal phenomena of hyperkinesis, constant or periodically occurring. Thus, we have the Kozhevnikov form (epilepsia partialis continua), the epilepsia choreica form (Bekhterev), where there are choreic twitchings in the interictal state, the form of Unverricht's myoclonic epilepsy, a special form of nystagmo-myoclonus of Lenoble and Aubineau, where twitchings are localized in the eye muscles. Epilepsy seizures are sometimes expressed by phenomena not of irritation, but of deficit—paralysis. Thus, the following are observed: epileptic apoplectic stroke, described back by Trousseau, transient aphasia, phenomena of paresis or paralysis of a limb. Perhaps some cases described under the name of cataplexy should also be attributed here. After a general convulsive seizure, phenomena of paresis and paralysis in the form of temporary exhaustion are also sometimes observed, and pathological reflexes (Babinski reflex) are noted, indicating the involvement of the pyramidal tract. After a seizure, albuminuria is usually observed, sometimes for several days. Blood pressure drops sharply at the beginning of the seizure, and then subsequently turns out to be elevated. The pressure of the cerebrospinal fluid during a seizure is elevated. The fluid itself usually does not present any special deviations. In the intervals between seizures of the disease, the organism of the epileptic very often does not present any significant noticeable disorders. However, in other patients, signs of an epileptic constitution are well manifested; one can speak of noticeable and detectable disturbances in metabolism, on the part of the autonomic nervous system, the glandular apparatus, the blood, and the psychic state. (For psychic disorders in epilepsy, see below). The working capacity of epileptics turns out to be very different. Every epileptic is ill in their own way, and a template cannot be established. Fluctuations are also observed in the frequency and manifestations of seizures. A past infectious disease (especially scarlet fever, typhus) can always worsen the course of the disease. The same must be said regarding trauma. Sometimes it is noted that in the case of tuberculosis, erysipelas, pneumonia, diphtheria, the course of epilepsy takes on a more favorable character. Usually, epileptics do not live to old age, and death occurs in connection with seizures, especially if the latter become more frequent. Diagnosis. Recognition of epilepsy in most cases, when manifested by frequent typical seizures, does not present difficulties. If, however, the seizure is observed for the first time or one has to judge it by questioning, it is very important to always clarify all characteristic moments (complete loss of consciousness, complete amnesia, cyanosis, enuresis, tongue biting). First of all, it is necessary to differentiate a hysterical and epileptiform seizure, which is sometimes not so easy to do by questioning even for a very experienced specialist. A twilight state of consciousness also occurs in hysteria, an accidental bruising of the body can also occur during a hysterical seizure, the psychogenic moment in hysteria can be hidden, and in the case of an epileptic seizure, on the contrary, it can be very prominent. Some also use the term hystero-epilepsy (see).

However, this type of term is nosologically completely incorrect, since most often in such cases we are dealing only with some additional hysterical components in epileptics, which does not yet give grounds to speak of a combination of two independent diseases. In other cases, we are dealing only with epileptiform seizures developing against a foreign nosological background. It cannot be denied that true epileptic seizures sometimes respond to suggestion therapy, and, on the other hand, can arise under the influence of a psychogenic moment. If it is established that the seizure is epileptiform, then it is required to distinguish it from a seizure during uremia (albuminuria can be observed for a short time even after a seizure), during progressive paralysis (40-year age, pupillary symptoms, speech, psyche, etc.), during cerebral syphilis (data from cerebrospinal fluid, blood examination), during a tumor (increase in phenomena, headaches, vomiting, stasis in the fundus of the eye, focal symptoms), during cysticercosis or other parasites (eosinophilia), during a brain abscess (phenomena of increased intracranial pressure, leukocytosis, increased temperature), during encephalitis and meningitis (stormy onset, increased temperature, other symptoms, cerebrospinal fluid), during alcoholism, intoxications, and other rarer forms (multiple sclerosis, schizophrenia, hydrocephalus, tuberculosis, subarachnoid hemorrhage, hemorrhage into the brain substance, cerebral embolism, cerebral thrombosis, thrombophlebitis). The question of traumatic Epilepsy is decided by establishing the connection of the disease with the trauma. If seizures begin at the age of over 40, then a diagnosis of late Epilepsy (epilepsia tarda) is made with subsequent clarification of the diagnosis (cerebral arteriosclerosis, senile dementia). The development of an epileptiform seizure in childhood, especially in small children, requires very careful consideration of the issue before a final diagnosis of Epilepsy in the sense of an independent disease is made. In childhood, the doctor is primarily faced with the question: is the seizure a manifestation of some general disease or a local one? In the latter case, all the difficulties of the differential diagnosis of local cortical symptomatic Epilepsy of the Bravais-Jackson type and other similar forms arise. At the same time, it must be remembered that the presence of focal phenomena does not exclude genuine Epilepsy. Careful collection of the anamnesis is extremely important. It is extremely important to establish a connection with infectious diseases of a general nature, as well as meningitis and encephalitis. The question regarding the attitude toward tuberculosis (tuberculous meningitis and solitary tubercle), hydrocephalus, and limited, often cystic meningitis is very responsible, since practically the question of surgical intervention is raised here. The more stereotypically the seizures develop, the more data there is in favor of their focal development; if, however, the seizures manifest with signs of predominant participation of one or the other hemisphere of the brain, then this speaks for a more general cause. All questions of differential diagnosis that arise at the bedside of an adult patient also arise in relation to a sick child. In the latter, one must also remember the existence of favorable moments for the possibility of the development of an epileptiform seizure: increased temperature, intoxication and autointoxication, worm disease, reflex moments. In the clinical picture of a convulsive seizure, the prevalence of the tonic element over the clonic one should be considered a favorable moment regarding the prognosis, since this speaks more for the presence of greater involvement of subcortical mechanisms than for cortical disease. The presence of psychic symptoms and especially their increase (e.g., weakening of memory) also worsens the prognosis, as it testifies to a more general disease. The younger the child, the more moments they may have for the development of an epileptiform seizure as a reaction to a known irritation of a more or less accidental, mild nature with a more favorable prognosis. However, these 'reactions' may turn out to be early signs of a predisposition to Epilepsy in the future. As conditions also requiring differentiation in relation to Epilepsy in children, the following should also be named: spasmophilia, tetany, eclampsia, fainting (cataplexy), pyknolepsy, narcolepsy, hysteria, schizophrenia; difficulties often depend on the fact that regarding some forms, such as pyknolepsy, narcolepsy, it is generally not easy to draw a demarcation line; then the question of disturbances in calcium metabolism in spasmophilia clashes with the unresolved problem of the significance of the same metabolism in Epilepsy; questions of hysteria as a psychoneurosis and psychoepilepsy in application especially to neuropathic and psychopathic children turn out to be very confused in practice. Psychoepilepsy can also occur without convulsive seizures (epilepsia larvata), however, such a diagnosis is very responsible. Besides determining the constitution, observation, and questioning of the patient, a comprehensive examination is of great importance for the diagnosis of Epilepsy: examination of urine, blood (morphology, biochemistry, coagulability, viscosity), cerebrospinal fluid, fundus of the eye, labyrinth function, radiography, encephalography, hyperventilation. Establishing a clinical diagnosis not of symptomatic, but of genuine Epilepsy, the modern neuropathologist must also try to approach the clarification of the pathogenesis of the disease, since only this can move forward in matters of treatment. The question of any local process or disturbance also has practical significance for general genuine Epilepsy. It is extremely important to attempt to establish differences in the interictal, preictal, and postictal states; therefore, all kinds of examinations in patients should be carried out systematically, daily or at short intervals, and repeatedly. Serological and cerebrospinal fluid establishment of the validity of suspicions of syphilis, the nature of traumatic changes in tissues, the picture of deviations in metabolism (sugar, calcium, potassium, cholesterol, blood uric acid), the picture of acid-base balance (alkalosis, acidosis), the biophysical state of the blood, edema of the brain substance, disturbances in water metabolism—all this, if it does not yet provide exhaustive data for solving practical questions, still brings us closer to clarifying complex, confused questions and is apparently the only way to resolve the problem of pathogenesis and therapy in epilepsy. The prognosis in Epilepsy in each individual case depends on the frequency of seizures, their character, the state of the psyche, the specifics of treatment, and the speed of the increase in phenomena. The range of clinical and social significance of the manifestations of Epilepsy is very extensive: from rapidly onsetting dementia and complete, severe disability to the preservation of working capacity throughout the patient's entire life and the absence of obstacles to the manifestation of high giftedness and creative abilities of the patient. Sometimes Epilepsy ceases independently; this is more often observed by the time of puberty and the strengthening of the organism in cases of its onset during the period of formation in girls. The prognosis also depends to a very large extent on the success of therapy in each individual case. The fairly widespread opinion about the incurability of Epilepsy, about the failure of therapy, must be revised. Epilepsy is a disease that must be subjected to treatment and can be stopped. Treatment. If the Epilepsy is symptomatic, cortical, then treatment follows the general rules of therapy for the underlying disease (syphilis, progressive paralysis, kidney inflammation, meningitis, encephalitis, arteriosclerosis, etc.) or the question of surgical treatment is raised (tumor, trauma, skull fracture, etc.). If the diagnosis points to genuine, general Epilepsy, then therapy must be considered from several sides: a) therapeutic effect on the seizure itself or epileptic status; b) treatment in the interictal state; c) predominantly symptomatic treatment; d) treatment according to known indications of an etiopathogenetic nature; e) surgical treatment of general Epilepsy. Since the disease is predominantly expressed by seizures, and seizures occur at different times, it is necessary that the patient themselves or their relatives keep a daily record of seizures. On this record, in women, it is very important to note the time of menstruation; one can also note various other current moments, such as mental and physical fatigue, agitation, psychic traumas, dietary errors, excesses, etc. Such a record allows one to monitor the seizures, by which mainly one has to judge the treatment, to establish correlations with individual moments in the patient's life regimen, making corrections to prescriptions and the structure of their daily life. If seizures are rare, then evaluating the results of treatment is more difficult than in the case when seizures are frequent. In view of the fact that the disease lasts for years and the patient may be under the observation of many doctors during this time, it is very useful to make notes of a therapeutic nature in the patient's records of seizures. During a seizure, usually, nothing needs to be done except for some precautions: lay the patient on their back, place a pillow under their head, loosen the collar, belt, insert a spatula or spoon between the teeth. The seizure ends by itself.

If status epilepticus is present, one can use an enema of chloral hydrate or another narcotic, inject scopolamine, apply leeches, perform a venesection, or a lumbar puncture to release cerebrospinal fluid. The main methods of treatment in the interictal period until recently have been pharmacological agents: bromine, urea derivatives, and borax. Bromine for the treatment of epilepsy was introduced by Locock in 1857. It is given in the form of a single salt or a mixture of salts. In view of the fact that even ammonium bromide can cause convulsions in animals, the use of ammonium salts cannot be considered advisable. Small doses of arsenic are prescribed against the phenomena of bromism. Bekhterev in 1894 proposed using a combination with Adonis for the same purpose. In recent years, bromides have been giving way in the treatment of epilepsy to urea derivatives (introduced into practice in 1913), luminal (a German preparation), gardenal, and rutonal (a French preparation); their advantage lies in the fact that they do not depress the psyche as much as large doses of bromine and do not produce such unpleasant phenomena as bromism. Some (in our country, Korotnev) highly recommend the use of chemically pure borax (sodium borate) up to 4.0-6.0-8.0 g or more per day. Since 1920, instead of borax, at the suggestion of P. Marie, Crouzon, and Bouttier, a boron preparation in the form of a double salt—potassium tartrate-borate (20.0:300.0 of water, initial dose of 1 tablespoon 3 times a day; it is recommended to use a chemically pure preparation)—has begun to come into fashion; it does not possess toxic properties even in large doses and acts well on the psychic sphere. Flechsig (1893) introduced the treatment of epilepsy with opium, which he alternated with bromides. Atropine (belladonna) is also used in combination with bromides. Somnifen and paraldehyde are also used. To enhance the effect of the aforementioned largely symptomatic agents, a lumbar puncture can be performed beforehand. If there are indications of any endocrine disorders (onset of epilepsy during the onset of menstruation, thyroid gland defect, etc.), then appropriate therapy should never be ignored. If the physician suspects disturbed calcium metabolism in epilepsy, the administration of calcium preparations per os and intravenously is indicated, but better results can be expected from general ionogalvanization with calcium, a course of general ultraviolet irradiation (mountain sun), and the use of parathyroid gland preparations. In order to intervene in disturbed cellular metabolism, protein therapy is used in various forms (milk, peptone, etc.). In view of certain indications that there are some defects in the blood of epileptics, autohemotherapy is indicated. If there are indications of a link between the disease and an infection, a course of vaccine therapy (antirabic serum, various vaccines) can be recommended. In view of indications of epilepsy as a disease based on auto-endointoxication due to disturbed metabolism in brain tissue, systematic courses of brain emulsion injections are used. In this case, repeated courses are undoubtedly advisable, since a positive effect often occurs only after several courses. In cases of late-onset epilepsy, a good effect can be observed from a course of general ionogalvanization with iodine. In view of the undoubted instability of the autonomic nervous system in an epileptic and the great importance of circulatory disturbances, methods proposed for influencing the circulation in the head via the sympathetic system (diathermy of the upper cervical region, ionogalvanization with calcium of the same region) can sometimes have a positive effect. There is a proposal to use the Jesionek lamp for epilepsy. If there are indications of cerebral edema, dehydration is used by releasing cerebrospinal fluid and injecting air in its place, i.e., the same manipulation that is performed during encephalography, but for therapeutic purposes. All the listed methods yield some success in a certain number of cases; sometimes this success can be called good and even brilliant. On the other hand, the fact of the existence of very many diverse proposals for therapeutic purposes shows that the problem is still too complex, that the treatment used is often ineffective, but that a positive effect can be exerted from different sides, in different directions, and to a greater extent in connection with the purely individual conditions of the development of the disease in each separate case. It is still far from possible to determine with certainty and precision the characteristics of each patient; therefore, one often has to move forward in the treatment of the epileptic only by groping. But successes are possible and achievable. Great importance is attached to the dietary treatment of epilepsy. The idea of the necessity to limit nitrogenous nutrition (meat, etc., is forbidden) is quite widespread. There should be no sweeping decision here. For such a diet, it is necessary to have more definite indications (an increase in uric acid in the blood, high specific gravity of urine, and finally, the fact of the positive influence of such a diet in a given patient). Toulouse and Richet (1899-1900) proposed depriving patients of table salt during treatment with bromine. Here, too, an individual decision on the issue is needed, especially since such a diet is burdensome, and phenomena of bromism are intensified with it. In view of existing indications of hypoglycemia in some epileptics, Vladychko (1925) considers it advisable to introduce a large amount of sugar in epilepsy, but for this, again, one should proceed from individual data on the decrease in the amount of blood sugar in the patient. Peterman (1925) proposed the so-called ketogenic diet. American authors developed it on a large amount of material. It proceeds from the fact of a decrease in the number of epileptic seizures during fasting and starvation (development of acidosis) and aims to combat alkalosis by creating acidosis in the body. The diet boils down to a sharp restriction of proteins and carbohydrates and abundant consumption of fats. Such nutrition is, of course, very burdensome, however, a number of authors report good results, especially in children, who adapt well to such nutrition. Prevention and social significance. Regarding the prevention of epilepsy, great importance must be attributed to the general regimen of epileptics. As for nutrition first of all, in view of the extreme instability of their metabolism and, apparently, the facilitated onset of autointoxications and the existence of hidden idiosyncrasies, patients generally need moderate nutrition, infrequent meals, and the exclusion of individual food products based on individual characteristics. Wine is, of course, forbidden. Smoking (which causes vasoconstriction) is contraindicated. Good air in the room is very important, especially where the patient sleeps; it is necessary to avoid stuffy, crowded gatherings. Mental and physical work is indicated, but in accordance with strength and without fatigue. Sick children should study, and the cessation of studies is permissible only in case of rapid progression of the disease. General hydrotherapy for the purpose of maintaining the tone of the autonomic nervous system always produces a good effect. The treatment of epileptics requires a definite reform in the sense of attracting great attention to them and creating the necessary conditions for the systematic study, observation, and treatment of this type of patient, who can to a large extent be regarded as healthy and can count on effective treatment. In such a model institution for the treatment of inpatient and outpatient epilepsy patients, it is necessary to have a laboratory with a staff of laboratory technicians, especially biochemists, sufficient for systematic examinations of patients, and proper conditions for dietary nutrition. The diversity of the clinical picture of epilepsy has great social significance. General prevention in relation to genuine epilepsy is to a large extent the same as in relation to psychoses. Progeny for epileptics is contraindicated, although an unconditional threat of epilepsy hangs over children only in the presence of indications of epilepsy in the families of both parents. The fight against alcoholism, syphilis, and traumatism is of particular importance. Patients with symptomatic epilepsy, of course, should not be viewed socially from the same angle as patients with genuine epilepsy. Climatic influences in relation to epilepsy are little studied, but staying at high altitudes (e.g., in Kislovodsk) in the presence of epileptic seizures is contraindicated. When drafted into the army and entering military service, epileptics are exempted from it. Usually, they are admitted for testing to a hospital, where they are observed for a month for the appearance of a seizure and, in the event of its development, the seizure itself is observed. During the testing period, it is possible to use methods of artificial induction of a seizure, such as hyperventilation and carotid compression. Since, under the influence of hyperventilation, it is usually possible to observe the development of a seizure in only approximately 40-50% of epilepsy cases, the method of carotid compression is practically more convenient.

If it is possible to organize a daily systematic examination of blood coagulation (due to the difficulty of the methodology), then in epilepsy it is generally possible to establish increased coagulation, and before a seizure, approximately a day in advance, a significant acceleration of blood coagulation. While in civil service, agriculture, and industry, individuals suffering from epilepsy may perform work and retain their ability to work, the question of utilizing the labor of epileptics cannot be resolved indiscriminately, and it is necessary to demand a more individual approach to this issue. General contraindications for the labor of epileptics should be considered: high temperatures at the workplace, work in chemical production, work in transport and security, and work near moving machinery. There exists an International League Against Epilepsy (General Secretary Dr. Muskens in Amsterdam); the league has a special journal, 'Epilepsia'. From time to time, at scientific congresses, the question of epilepsy is placed on the agenda. In our country, under the State Institute of Neuro-Psychiatric Prophylaxis, a commission for the fight against epilepsy was organized (Prof. Minor, Secretary Rosenstein) as early as 1917; by 1927, 24 of its branches had emerged in various cities; it is necessary that the fight against epilepsy be conducted more energetically and that the interested public be involved in this issue much more widely, perhaps even to a certain extent with the participation of the patients themselves who are suitable for this.

V. Khoroshko. Psychiatric disorders in epilepsy. Changes in the psyche are among the fundamental and constant phenomena in epilepsy. Despite the diversity of these changes, they nevertheless have features sufficiently characteristic of epilepsy. One should distinguish between acute psychiatric disorders and chronic changes in the psyche. Acute psychiatric disorders are primarily associated with seizures. In both grand mal and petit mal seizures, a profound disturbance of consciousness and subsequent amnesia are observed. The aura often has a psychiatric character and is expressed by affects of fear and hallucinations, usually of a terrifying nature, associated with a clouding of consciousness. Most often, there are visual hallucinations, both elementary (in the form of sparks, fire, lightning) and more complex (dead people, ghosts, etc.). Other forms of hallucinations are also observed (general sensation, olfactory, auditory), as well as special sensory deceptions in the form of disturbances of the body schema (the head separating from the torso, etc.). It is very characteristic of the psychiatric aura to have a monotonous repetition of the same hallucination before each seizure. Furthermore, both before and after a seizure, more prolonged (sometimes lasting several hours) changes in mood and clouding of consciousness with terrifying hallucinations and motor agitation (the patient runs, attacks those around them, etc.) are often observed. Such acute psychiatric disorders are not always associated with convulsive seizures; they can also develop independently, and in that case, they are called psychiatric equivalents of a seizure. This name emphasizes the similarity of such states to a seizure, with the equivalent, as it were, replacing the seizure. The equivalent, like the seizure, begins endogenously, usually without an external cause, suddenly, and ends just as suddenly. The duration of psychiatric equivalents varies—from fleeting cloudings of consciousness (absence) to disorders lasting a number of hours or even days. Only in rare cases is an attack of an epileptic psychiatric disorder more prolonged and develops into a psychosis, which, however, possesses the fundamental features of a psychiatric equivalent (sudden onset and end, specific symptomatology). Regardless of the duration of the course, acute epileptic psychiatric disorders can be distinguished by their manifestations, and in this regard, the following forms can be identified. The fundamental and most frequent form is twilight states of consciousness. During such states, patients retain the ability to move and act, but perceptions of the surroundings occur unclearly, with the frequent presence of various sensory deceptions; the coherence of thinking is disturbed, and patients are disoriented and cannot correctly evaluate their surroundings. As a result, psychic processes proceed without proper connection and sequence, actions are performed without sufficient motivation, and reactions are not adequate to stimuli. The changes in mood usually observed during twilight states—sometimes depressed, sometimes close to ecstasy, and always tense—as well as frequent affects of fear, hallucinations, and delusional ideas, are the basis for the pathologically incorrect behavior of patients, who are often dangerous to those around them and to themselves. They commit assaults, murders, arson, throw themselves out of windows, etc. Twilight states are accompanied by physical symptoms: increased tendon reflexes, dilation of the pupils and their sluggish reaction, slow and unclear speech, dizziness, increased sweating, and salivation. After the end of the twilight state, amnesia is complete or partial, which to a certain extent can serve as a measure of the depth of the experienced clouding of consciousness. Clinically, one can distinguish individual types of twilight states, but their grouping has a conventional significance, as there are transitional and mixed forms. For individual patients, a stereotypical repetition of twilight states similar in manifestation is very characteristic. Among the most frequent forms of twilight states is somnambulism (sleepwalking). Patients get up in their sleep, leave the house, sometimes climb onto the roof, then return or fall asleep somewhere else. During sleepwalking, the perception of the outside world is insufficient and distorted, and movements are of an automatic nature. No memory of the sleepwalking remains with the patient. Apparently, sleepwalking is associated with nightmarish dreams, which are generally very common for epileptics and in themselves can be considered a peculiar equivalent in sleep. In some cases, a dream-like state develops in patients during the day, during which they do not recognize their loved ones, perceive their surroundings unclearly, sometimes strive to go somewhere, and perform senseless actions. The next form of a twilight state is delirious confusion, characterized by vivid hallucinations and delirium. In this state, affects of fear, anger, and sometimes ecstasy are frequent. It seems to the patients that they are about to be burned, buried alive, etc., and in such a state, they are very dangerous and commit acts of violence and murder. In some cases, patients are sharply stuporous, do not answer questions, and almost do not react to their surroundings (epileptic stupor); sometimes, on the contrary, the consciousness of the patients is not so clouded, they answer questions and express delusional ideas of grandeur and persecution; such cases resemble an acute paranoid syndrome and can then be quite prolonged (several weeks). In cases with a milder clouding of consciousness, patients, upon superficial observation, seem to deviate only slightly from the norm, as if absent-minded. They can perform a series of actions that are more or less purposeful, but their entire behavior as a whole is nevertheless unusual and strange. Perceiving their surroundings unclearly and evaluating them incorrectly, they give inadequate reactions. In such a fogged state, patients can undertake long journeys. Upon regaining consciousness, they usually poorly understand what happened to them and retain only a partial and vague memory of the trance. Sometimes patients retain sufficient memories of their experiences during twilight states, especially if these experiences, as is usual for epileptics, were distinguished by particular vividness, but even then, connections in time are disturbed. It is very characteristic that patients often experience disproportionately long series of events during a short disturbance of consciousness. In cases of incomplete amnesia, after patients come to their senses, remnants of hallucinatory-delusional experiences sometimes seem to get stuck in their consciousness. Such patients, upon emerging from a twilight state, claim, for example, that someone came to them, tore off their skin, or burned them with a red-hot iron, or that they had visions, etc. Painful experiences (and sometimes ecstasy) during twilight states, being distinguished by enormous acuteness and intensity, along with fragments of delirium, can, as it were, go beyond the limits of the twilight states and be the basis for the development of more or less prolonged disorders with delusions of persecution or grandeur (epileptic paranoid). Although, as a rule, twilight states arise endogenously, some external conditioning is sometimes possible. This happens in pathological affect, at the height of which the consciousness of the epileptic is sharply disturbed, and in pathological intoxication; being as a rule intolerant to alcohol, epileptics, from small doses, fall into intoxication with a sharp disturbance of consciousness and a tendency to commit violent acts. The next fundamental form of acute psychiatric disorder in epilepsy is expressed in mood changes (dysthymia). These changes are also characterized by a sudden onset and end, and an endogenous origin without any external cause. The duration of such attacks is several hours or days, more rarely weeks. The mood is usually unpleasant: patients are gloomy, irritable, tense, sometimes experience causeless fear, and pester others with requests and complaints. An elevated mood is observed more rarely, but it is devoid of a joyful character and is also distinguished by tension; in this case, there is no flight of ideas or distractibility, but the slowness and viscosity of psychic processes characteristic of epileptics are preserved. Sometimes an elevated mood has the character of ecstasy and is associated with religious fervor. In some cases, mood changes are the basis for the development of complex behavioral disturbances in patients in the form of prolonged wanderings and travels (so-called poriomania) or bouts of heavy drinking (dipsomania). Sometimes, during mood changes, episodic hallucinations and cloudings of consciousness are observed; such cases are transitional to twilight states of consciousness. Acute psychiatric disorders are, of course, not sharply expressed in all cases of epilepsy; usually, they are combined with convulsive seizures, but there are also cases where psychiatric disorders come to the fore, filling the picture of the disease, sometimes with very rare convulsive seizures and even a complete absence of the latter. For such forms, the terms "psychoepilepsy" or "psychosensory epilepsy" are applicable. The latter name is especially appropriate in cases rich in hallucinations and other sensory disturbances, obviously associated with the peculiarities of the localization of the process (in contrast to the usual convulsive form with predominant motor disorders).

Chronic changes in the psyche in epilepsy are extremely typical for this disease. They are expressed in changes of character and thinking (epileptic character), develop gradually, progressively, and, being a consequence of a destructive disease process, coalesce into a peculiar epileptic dementia. The earliest sign of such psychiatric degradation is changes in character. Patients become irritable, affective; subsequently, an increase in drives, cruelty, and morbid egoism is discovered. Complaining of insults and oppression from those around them, they are prone to hypocritical sanctimoniousness and at the same time are distinguished by cruelty. Awareness of their severe disease and concerns about health, while the circle of interests narrows, contribute to the development of extreme egocentrism. At the same time, a tendency toward mysticism, superstition, and religiosity has always been considered characteristic of epileptics. These features are partly connected with the increasing dementia, and partly with the circumstance that seizures, with their suddenness and inevitability, create in patients the idea of some dependence on an external force, of possession. Vivid hallucinations, especially visual ones, often associated with a state of ecstasy, further contribute to mystical experiences. It is understandable, therefore, that epileptics played a large role in the history of religions and that the disease itself was considered sacred (morbus sacer). However, in our time, even among epileptics, the religious-mystical content of clinical manifestations is observed less and less frequently in connection with the elimination of corresponding beliefs among the masses. Furthermore, intellectual changes, which are the basis of epileptic dementia, are very peculiar. Slowness, viscosity, and rigidity of thinking, and a lack of flexibility are noted. Intellect and memory gradually weaken, the circle of interests narrows, the store of ideas becomes impoverished, and quick-wittedness decreases. A special viscosity of thoughts is characteristic of the epileptic, an inability to switch in a timely manner, to transition from one topic to another, treading in place; the patient gets confused in details, non-essential particulars, and cannot exit a narrow circle of ideas. The limitations of epileptics correspond to an exaggerated circumstantiality, petty neatness, and a capacity for painstaking detailing. Despite all the monotony of the psychiatric content, polar fluctuations are characteristic of epileptics: from slowness to explosiveness (explosivity), from obsequiousness and servility to extreme cruelty. The poles of this epileptic proportion are unevenly emphasized in individual cases. Of course, chronic changes in the psyche in epileptics are expressed to varying degrees. Sometimes it reaches the point of profound epileptic dementia, when patients are completely helpless, are in a state of marasmus, and become dull and apathetic. In more favorable cases, relatively insignificant changes in the psyche are noted; the patients, while distinguished by a difficult character, still behave generally correctly, can work, and their slowness and reduced quick-wittedness are partly compensated for by detailed circumstantiality and neatness. The degree of chronic degradation of the psyche does not always run parallel to the frequency and strength of convulsive seizures; cases with a predominance of acute psychiatric disorders and rare seizures can also lead to profound chronic changes and dementia. The features of the epileptic psyche (irritability, explosiveness, tendency toward pathological affects) and acute psychiatric disorders (especially twilight states) lead to behavioral disturbances and make these patients difficult in communal living and, as already mentioned, often dangerous to those around them. The most nightmarish murders, sadistic mutilations, rapes, arsons, etc., are committed by epileptics. This determines the great forensic-medical significance of epilepsy accompanied by pronounced psychiatric disorders. Psychiatric disorders in epilepsy deteriorate sharply under the influence of alcoholism, which accelerates the degradation of patients. Intoxication itself in epileptics often has a pathological character, accompanied by severe twilight states with subsequent amnesia. On the other hand, mood disturbances in epileptics with phenomena of painful tension are in some cases accompanied by an irresistible craving for alcohol, which is expressed in a drinking bout. Psychiatric changes in epilepsy in childhood are distinguished by certain features. In this regard, it is especially important that childhood epilepsy entails phenomena of psychiatric underdevelopment, which is all the more pronounced the earlier the disease begins. Thus, the mental retardation of epileptic children is combined with progressive degradation, conditioned by the course of the disease process. Characterological features of epileptics develop in children gradually and are sometimes not clearly enough expressed. Of the acute epileptic disorders, somnambulism and night terrors are most characteristic of children. More complex psychosensory and delusional syndromes are rarely observed in children. It should be said in general that in children, epilepsy is distinguished by less polymorphic symptomatology and is often monosymptomatic. The psychiatric changes described above relate to genuine epilepsy and are generally not characteristic of symptomatic epilepsy, the features of which are determined by other regularities associated with the form of the underlying disease. The similarity of convulsive seizures in genuine and symptomatic epilepsy does not extend to the main psychiatric manifestations, which is connected with the difference in their nosological essence. However, there are some forms of diseases close to epilepsy with similar symptomatology, regarding which the question of their belonging to genuine epilepsy is still unclear. This includes the episodic twilight states of Kleist, which are similar to the corresponding epileptic syndromes but are not accompanied by other epileptic manifestations and degradation. Of even greater significance is the affect-epilepsy of Bratz, which is expressed in sharp affectivity, impulsivity, aggressiveness, antisocial behavior, and convulsive seizures developing at the height of an affect. In addition, in these patients, the following are observed: petit mal, fainting, dizziness, mood disorders, states of confusion of the equivalent type, vasomotor disorders, etc. Despite all this, the Bratz form differs from genuine epilepsy by the reactivity of the seizures and the absence of degradation. Thus, affect-epilepsy to a certain extent approaches epileptoid psychopathy, differing, however, from the latter by the presence of convulsive seizures and, in general, a rich epileptic symptomatology that goes beyond the limits of psychopathies. The differential diagnosis of epileptic psychiatric disorders usually does not present particular difficulties. On the contrary, the presence of these disorders, especially in cases of rare and not always observable convulsive seizures, ensures the diagnosis of epilepsy and its differentiation from other diseases in which symptomatic epileptiform seizures may occur. Peculiar progressive changes in the psyche, great polymorphism of symptomatology, and attacks of twilight states of consciousness decide the diagnosis in favor of genuine epilepsy. Furthermore, of course, in symptomatic epilepsy, the presence of manifestations of the underlying organic disease (tumors, syphilis of the brain, etc.) is important. Significant difficulties may be presented by distinguishing genuine epilepsy from symptomatic alcoholic epilepsy, in which there may be not only typical convulsive seizures but also some psychiatric changes similar to epileptic ones (especially pathological affects). It should be kept in mind that alcoholism, while sometimes being the cause of toxic alcoholic epilepsy, in other cases can provoke the development of true genuine epilepsy (in the presence of a corresponding predisposition). Petit mal and the features of epileptic thinking (slowness, viscosity, rigidity) are not characteristic of alcoholic epilepsy. Similar difficulties may arise when differentiating genuine epilepsy from traumatic epilepsy, since trauma in some cases may be the cause of symptomatic epilepsy, and in others, it may provoke genuine epilepsy. Despite all the similarity (seizures, affectivity, vasomotor phenomena, weakening of intellect and memory), there are also differences: rigidity, viscosity, and circumstantiality of the epileptic psyche are not characteristic of trauma patients; they have more sharply expressed neurotic layers and focal symptoms are often observed. The progressiveness of degradation further allows for the differentiation of epilepsy from epileptoid psychopathy, which is also characterized by affectivity, explosiveness, and polar fluctuations similar to epileptic ones, but without degradation. For the recognition of acute epileptic psychiatric disorders, an endogenous sudden onset with subsequent amnesia is especially characteristic. Analogous hysterical disorders arise psychogenically, are accompanied by expressive movements, and their content is connected with the psychic trauma that gave rise to the disease. When recognizing twilight states, it is important to take into account the patient's state outside of seizures and, in general, the entire totality of painful symptoms and the features of the psyche as a whole.

Mood disorders in epileptics differ from similar disturbances in manic-depressive psychosis by a general tension, a predominance of affects of fear and malice, and in general by the presence of the characteristics of the epileptic psyche with its slowness, explosiveness, viscosity, and tendency toward clouding of consciousness. Epileptics are characterized neither by pure depression with the psychomotor retardation of melancholics, nor by the cheerful, active, distractible excitement of manic patients with their basically intact, non-degrading psyche. The differentiation of epileptic paranoid states from schizophrenic ones is based on their connection with twilight states of consciousness, on more gross manifestations of affectivity and explosiveness, on the predominance of vivid visual hallucinations over auditory ones, and on the absence of the schizophrenic features of paralogical thinking. In some cases, it is necessary to differentiate epileptic dementia from schizophrenic dementia. Besides the features of acute manifestations (seizures, psychiatric equivalents), the differentiation proceeds mainly along the lines of distinguishing the simpler, concrete epileptic psyche, with its slowness, viscosity, and limitation, from the schizophrenic one, which is characterized by peculiar disturbances of thinking, autistic attitudes, detachment from reality, and emotional impoverishment. The therapy of epileptic psychiatric disorders basically coincides with the general methods of treating Epilepsy. It should only be noted that there is a need for the timely placement of epileptics with acute psychiatric disorders (more or less prolonged or frequently recurring) into psychiatric hospitals. With pronounced chronic changes in the psyche, epileptic children, even in the presence of rare seizures, cannot be educated in normal schools and need to be placed in special institutions for education and upbringing. Adults with profound epileptic dementia are subject to placement in colony-type institutions. With regard to epileptics with less significant psychiatric changes and rare seizures, their appropriate vocational guidance is very important. Professions requiring accuracy, punctuality, and detailed painstaking work, and not associated with great responsibility, should be considered more suitable for them; certain types of clerical work, as well as craft and agricultural work, are excellently performed by epileptics. Conversely, work requiring quick thinking, responsible decisions, frequent switching, fast tempos, and work associated with situations where there are possibilities for frequent conflicts is not suitable for them. Proper employment of even demented epileptics yields all the more successful results because these patients remain capable of working and productive for a long time in work that is suitable and accessible to them. Prophylactically, it is especially important to eliminate the possibility of alcoholism, which sharply worsens the condition of these patients. Dispensary registration of all epileptics, children and adults, is a necessary prerequisite for organizing timely psychoneurological assistance for such patients.

M. Gurevich. Surgical treatment of epilepsy. Surgical treatment for epilepsy must be divided into three sections: operations for genuine epilepsy, operations for symptomatic-focal and traumatic epilepsy, and operations for reflex epilepsy. I. A. Operations for genuine epilepsy are in turn divided into a) operations of a general nature and b) operations within the cranial cavity, i.e., on the meninges and on the brain substance itself. The former include: 1) Lumbar punctures, proposed in their time by Quincke. This measure currently has only historical interest. 2) Encephalography. This surgical intervention essentially belongs to diagnostic operations and is usually performed before surgical intervention—trepanation. It was noted that those cases of epilepsy which, for one reason or another, were not operated on after encephalography, proceeded very favorably in the future. The patients themselves felt subjectively better, seizures became less frequent and acquired a rudimentary character. However, this method as a therapeutic one did not gain recognition among surgeons and neuropathologists in view of unfulfilled hopes. 3) The same attitude developed toward the proposal to perform a puncture of the corpus callosum (Balkenstich) for genuine and traumatic epilepsy. 4) Operations on the sympathetic nervous system in the form of extirpation of the superior cervical sympathetic ganglia (first proposed by Alexander, recently recommended by Leriche, Brüning, and others). This operation was performed in a small number of cases and was met with great skepticism, although its defenders did put forward arguments not devoid of physiological significance. The named authors attempted to change the function of the neurovascular system of the brain, based on the change in the volume of brain vessels during epileptic seizures, to which Kocher first drew attention. In reality, the operation brought little benefit; therefore, at the present time, it does not find application, just as the operation of periarterial sympathectomy, which is close to it in theoretical justification. 5) Only for the sake of completeness of the review can one mention the proposal to perform ligation of the vertebral artery, carotid artery, or their constriction by means of various methods for genuine epilepsy. There are only isolated observations, and the results are not very convincing and the dangers are great. 6) Operations on the adrenal glands. Theoretical considerations and experimental observations gave reason to hope for the possibility of weakening convulsions, the most characteristic and severe symptom, by weakening the activity of the adrenal glands and especially the cortical substance (Fischer). Facts refuted both the theoretical premises and destroyed hopes for the effectiveness of this method. The same fate befell proposals for the treatment of epilepsy by intervention on other glands of internal secretion, e.g., the ovaries. B. Operations for genuine epilepsy with opening of the skull (trepanation) and intervention on the meninges and brain substance. The basis for these operations was two facts: firstly, the presence in genuine epilepsy of certain anatomical changes in the soft meninges in the form of edema of the arachnoid membrane or in the form of chronic leptomeningeal changes. It must be said, however, that these changes are not always encountered, and moreover, their character is extremely diverse, so that the term "leptomeningeal changes" can be accepted conditionally: sometimes grayish-white stripes are found along the vessels and yellowish spots scattered in various areas of the arachnoid membrane. Secondly, Kocher observed during epileptic seizures on the operating table a bulging of the brain from the trepanation opening and explained the epileptic seizure by the onset of increased intracranial pressure, taking the consequence for the cause. Thus, the theoretical justifications for the "valve" operation are the same as for the operation on the sympathetic nervous system, as was already indicated above. The most popular operation from this cycle was the operation of creating a "valve" (see Brain, operations for brain tumors). Since the theoretical justification was more of a conjecture than an interpretation of the essence of the epileptic seizure, this operation, which found very many adherents due to its ease and relative safety, nevertheless did not yield a great therapeutic effect, as can be seen from the attached table. Table 1. Short- Author Number of op- time of ob- improved and worsened Improvement Recov- Died erations servation ery (According to) . . Weispfennig (Weispfennig) Pussep 9 (1-3 years) F. Krause . . . - Mintz and Korot- koe ..... - .- Burdenko . . 2 (5-10 years) The evaluation of the presented data requires very large comments and reservations regarding the understanding of the terms recovery, improvement, and the duration of postoperative observations. P. Krause at one time proposed five years as the minimum observation period. It is already clear from the table provided that different authors choose shorter durations (see, for example, Pussep's data). Finally, the very concept of genuine epilepsy is understood differently by different authors. As a consequence of this, precise conclusions cannot be drawn. But, be that as it may, introducing all corrections, one still cannot recognize the "valve" operation as very effective, although, as can be seen from the table, all authors note a significant percentage of improvements. By improvement is understood a decrease in the number of seizures and a change in their character. The "valve" operation was at one time proposed as a measure to combat status epilepticus. According to literary data, in this case, it yielded doubtful success: while some authors report positive results, others speak of complete uselessness and believe that the intervention contributed to accelerating the lethal outcome (Neuding, Seeligor). Finally, for genuine epilepsy, the Goreli proposal of partial removal of the cortex is applied. In some forms of genuine epilepsy, there are hints of specific centers from the irritation of which the epileptic seizure begins, the so-called epileptogenic zones. Although it must be admitted that in so-called genuine epilepsy there must be some morphological changes in the brain substance, in the practice of the neuropathologist and surgeon, there are few cases where it is possible to identify epileptogenic zones. In view of this, the Goreli method did not receive wide distribution. Thus, in relation to genuine epilepsy, we currently do not have strictly developed methods of surgical treatment. II. Operations for symptomatic epilepsy (focal, Jacksonian epilepsy). From the extensive group of symptomatic epilepsy, in particular, focal epilepsy has always been considered an object of the most effective surgical intervention, promising a definite positive result. In focal epilepsy, in the majority of cases, there are organic processes of one nature or another in the craniocerebral cavity. In these cases, however, seizures are sometimes observed not only of the focal type but also general convulsions. Epileptic seizures of the same character are observed in some forms of intoxications and infections (uremia, lead and arsenic poisoning, alcohol poisoning, malaria, some forms of syphilis, and finally, fresh inflammatory processes). The different nature of the processes causing epileptic seizures determines the indications for operability and inoperability and the methods of operations. Focal forms (Jacksonian epilepsy). In this group, inoperable cases include forms where the basis is intoxication and infection (early stage). Operations are not recommended in early childhood, in old age, during pregnancy, and menstruation. The question of status epilepticus from the point of view of contraindications in these forms must be considered open. An extremely important question for surgical intervention is the time of surgical intervention after the appearance of the first seizures. Is it necessary to proceed immediately to an operation following the diagnosis of symptomatic focal epilepsy? This question, posed in such a way, sounds somewhat abstract. If the cause of symptomatic epilepsy is organic lesions of the cortex and subcortical substance, as well as the meninges (inflammation, neoplasms), trauma with its gross anatomical disturbances, and finally, increased intracranial pressure, then the decision on the time of the operation cannot be formulated in one dogmatic form or another. In some forms, one can wait, trying one therapeutic measure or another; conversely, in others, the observation periods must be shortened, e.g., with the increase of hypertension phenomena, with the threat of loss of vision, as is the case with tumors, cysts, and abscesses. A big mistake is made by neuropathologists and surgeons in epilepsy in children suffering from spastic paralysis or paresis as a result of trauma intra partum. Here, the treatment process is delayed too long, and irreparable general changes in the cortex occur, even though it is possible to completely remove the pathologically altered area, e.g., a cyst or limited scar masses. The question of intervention in traumatic epilepsy is more definite. In trauma, one distinguishes 1) early seizure attacks and 2) late ones. In early attacks, if there is an open injury to the skull, the question is decided without hesitation—in this case, the intervention coincides with the primary treatment of the wound, albeit with consideration of the phenomena of shock and general cerebral insult.

In closed injuries, with intact soft tissues and bones of the skull, the nature of the seizures, their frequency and strength (e.g., a tendency to progress into st. epilepticus), determine both the time and place of intervention. The necessity to reckon with the phenomena of shock is more persistent here than in cases of open injuries: in these cases, one has to resolve the question of topical diagnosis, which determines the site of surgical intervention; in a shock state, establishing the depression or loss of function of one or another center appears difficult, and sometimes impossible until the shock phenomena are eliminated. In late epileptic seizures arising on the basis of trauma, the indications for intervention are more complex. Here, one has to establish the cause of the seizures. Often, the site of the injury does not correspond to the epileptogenic centers of the cortex. Furthermore, there are cases where the trauma did not precede the seizures but was received during the first seizure by the patient, who himself was not aware of this; the patient tells of a second seizure, placing it in a causal connection with a head contusion during the first, unconscious seizure; finally, sometimes the trauma is so insignificant that it is difficult to assume any serious damage to the brain substance or its membranes; here one has to think about a preceding epileptic predisposition. Only upon excluding these factors and in the presence of pyramidal symptoms or residual phenomena in the form of post-paroxysmal pareses or prolonged paralyses can one confidently speak of a causal connection between the trauma and the disease and precisely mark the site of intervention. In late epileptic seizures after closed trauma, determining the time of intervention is a serious question. In late epileptic seizures after open injuries that proceeded with signs of infection, regardless of whether the primary treatment was perfect or unsatisfactory or did not take place at all, one must consider the possibility of an exacerbation of a dormant infection, of course if it is not a case of clear osteomyelitis of the skull bones or an abscess. Usually, it is advised to wait for a six-month period after the complete closure of the wound by a scar. In closed forms, it is also recommended to wait for a certain period both for the application of medicinal treatment and for clarifying the topography of the injury. However, the waiting period should not be dragged out too long here either, for fear of obtaining secondary irreparable changes in the cortex. From the group of traumatic Epilepsy, special attention must be paid to gunshot injuries both in peacetime and in wartime. The guiding principles here remain to a large extent the same as in traumatic Epilepsy of non-gunshot origin, but one cannot pass over in silence cases of focal Epilepsy in blind gunshot wounds, when the foreign body lies far from the sensory-motor area, as well as those cases where there are multiple wounds with varying degrees of visible damage. Here, one can also assume the formation of so-called late abscesses, which can form at various points of the bullet track. Type of intervention in symptomatic Epilepsy. 1. In focal, non-traumatic cases, including here mainly the group of the Jacksonian type, an osteoplastic operation is usually performed. After trepanation, a thorough examination of the membranes, vessels, and cortex of the brain is performed. In the presence of one or another morphological change, the latter are removed according to the general rules of neurosurgery. Depending on the type of lesion, either a radical removal of scars, neoplasms, or cysts is performed, or a partial one if, due to anatomical conditions, a radical one is unfeasible. In any case, a thorough hemostasis must be performed; it is best to use an 'electric knife'. In some cases, temporary drainage has to be done. In the case of abscesses, it is done as a rule with one or another modification in the technique of execution. Sometimes in focal Epilepsy in the epileptic zone, there are no changes to the naked eye. Then, after carefully examining the overlying section of the cortex, one should move it aside with a thin spatula and examine the neighboring sections, which is possible at least for 2-3-4 cm under the edge of the cranial incision. In an extreme case, upon discovering a suspicious spot, one has to expand the trepanation opening in the direction of this spot. In this case, the changed spot should be removed, sparing, if possible, the sensory-motor area. In the absence of changes on the surface of the brain, the question of subcortical foci arises. In this case, cautious punctures are made, and in an extreme case, incisions. If all these investigations prove negative, the question arises of removing the primary convulsive center (epileptogenic zone) according to Horsley or of subcortical transection of communication pathways as proposed by Trendelenburg. Practically, it is very important in this regard to determine the planar dimensions of the zone to be removed and the depth to which one should penetrate. F. Krause, who has great experience in operations of this kind, advises removing 25-30 mm², more rarely up to 60 mm² in plane, while the depth is determined from 2.5-3 to 4.5 mm. The justification for the latter figures, however, needs physiological verification. In subcortical transections according to Trendelenburg, the plane of the incision is also recommended to be located at a depth of 3-4 mm. With the same goal—to exclude the activity of epileptogenic centers—massage of the epileptogenic zone (Bircher) and alcohol injections into these zones (Razumovsky, Kolyubakin, and Nazarov) were proposed. In traumatic Epilepsy and in Epilepsy after gunshot injuries, the type of intervention is determined by the degree and type of destruction. Here, one has to remove depressed parts of the skull, excise scars of the membranes, scar masses of the cortex, and separate adhesions between the cortex, the arachnoid, and the dura mater (meningolysis). During these manipulations, one often has to deal with foci of dormant infection, as well as with scars extending into the depth of the brain substance. In the first case, it is necessary to reckon with the possibility of a recurrence of the infectious process and limit oneself to the minimal dimensions of the intervention, in any case, to refuse meningolysis. In the second case, it is desirable to remove as large a part of the scar formations as possible. During operations for traumatic Epilepsy, one often has to remove the scarred dura mater over a large extent. Then the question of its plasty arises. Many different methods have been proposed; of all of them, one should dwell on plasty with a fascial-fat flap or the method of splitting the dura mater. These methods provide some guarantee against secondary adhesions. This refers only to late operations. In fresh, contaminated wounds, including gunshot ones, it is not possible to recommend the performance of plastic operations, especially in a military field setting, in the first zone of the location of surgical institutions. 2. Symptomatic focal, as well as general Epilepsy, depending on hypertension and hydrocephalus, is treated surgically either according to the causal principle, i.e., by eliminating the cause of increased intracranial pressure, or symptomatically. An example of operations of the first type in symptomatic Epilepsy can be the operation of removing tumors, cysts, parasites, and in hydrocephalus of the occlusive type—the elimination of adhesions disrupting the patency of communication pathways (between the ventricles, the cistern, and the subarachnoid space). An example of operations of the second type is the above-described operations of subtemporal trepanation, the 'valve' according to Kocher, trepanation of the occipital bone, the Anton-Bramann operations, the Anton-Schmieden operations, and all types of drainage of the subarachnoid space, including uretero-dural anastomosis (Heile's method). The outcomes of surgical interventions in various forms of symptomatic Epilepsy (focal) must be considered by separate groups. Of these, the groups of greatest practical interest are: 1) focal forms—Jacksonian Epilepsy with limited local foci; 2) Epilepsy in tumors; 3) traumatic Epilepsy; 4) Epilepsy in hydrocephalus. 1. Focal forms in various anatomically limited processes yield, according to the statistics of various authors, 10% recoveries and 20-30% improvements. 2. Epileptic seizures in small tumors, as well as in voluminous, well-demarcated meningiomas, disappear in the majority of cases completely upon radical removal. 3. Epilepsy after peacetime traumas yields 30-35% (Krause)—14% improvements with surgical intervention. Epilepsy after gunshot injuries of wartime in early forms yields a high percentage of cures, namely 48-50%, in chronic late forms—18.8% (combined statistics of Krause-Schumm). 4. Statistics of cured cases of Epilepsy in hydrocephalus, in view of the small number of observations by various authors who used different methods, do not make it possible to provide any reliable percentages and indicate a method of choice. III. Operative treatment in reflex Epilepsy boils down, after a thorough study of the pathogenesis of these seizures, to the liquidation of the suspected pathological processes. Views regarding this type of Epilepsy in the sense of etiopathogenesis are not established, although facts of the cessation of epileptic seizures after operations on the periphery are noted.

The most reliable data in this direction relate to operations on peripheral nerves, in the form of freeing nerve trunks from scars formed at the site of trauma, nerve sutures, and to operations in the region of the accessory nasal sinuses and the pharynx. As for interventions in the abdominal and thoracic cavities, they were isolated and did not yield an effect: for example, with the goal of curing epilepsy in a patient suffering from chronic constipation, the entire large intestine was removed, but the operation proved useless regarding the epilepsy.

N. Burdenko.