Psychiatry - H.T. Sonnyk 2003

Epilepsy

Epilepsy is a chronic progressive Brain disorder characterized by seizures (convulsive, sensory, or their equivalents) and The Development of persistent mental alterations (epileptic personality changes or epileptic dementia).

Human imagination has always been struck by the severity and peculiar nature of a major generalized seizure. The very word "epilepsy" meant to the ancient Greeks something that attacks a person, seizing them against their will. Among the many names, this particular term proved to be the most appropriate.

In the ancient world, epilepsy was known as the "sacred disease," since those afflicted with it were attributed with supernatural abilities. The counterpart to "sacred" was the term "demonic disease," as many believed the devil took possession of the person. Such interpretations led to patients often becoming outcasts. The name "Hercules' disease" was also occasionally used due to the notion of extraordinary strength inherent in epileptics.

There was a period when epilepsy was called the lunar disease (morbus lunaticum). This emphasized The connection between the condition's manifestations and the Phases of the moon, as well as phenomena such as somnambulism and sleepwalking. Today, it has been established that these are not synonymous with epilepsy. In Ancient Rome, a fairly common name was morbus comitalis, or the disease of the assembly. If a Roman senator suffered an epileptic seizure, the meeting was immediately suspended, as the seizure was believed to indicate that the proceedings were flawed. Names such as the "black disease" or the "falling sickness" are still encountered today.

The mystery that surrounded epilepsy for centuries has resulted in a considerable number of people even today not being entirely free from superstitious fear associated with this disorder. However, prejudice against epileptics is completely unjustified. It is worth recalling that epilepsy afflicted such prominent figures of various eras as Pythagoras, Democritus, Julius Caesar, Plutarch, Alexander the Great, the Prophet Muhammad, Avicenna, Peter the Great, Napoleon, Walter Scott, Lord Byron, Fyodor Dostoevsky, and others.

Historical Background.

The first detailed description of a major convulsive seizure was provided by Hippocrates. In one of his scientific monographs entitled On the Sacred Disease, he views epilepsy as a brain disorder caused by natural rather than supernatural factors. Hippocrates and some of his contemporaries created the first classifications of epileptic seizures and identified prodromal signs and aura.

Since then, grand mal has remained at the center of neuropsychiatrists' attention, signifying epilepsy regardless of its Etiology. A major contribution to The Study of this pathology was made by Jean Fernel (1497–1558), physician to Catherine de' Medici. He authored a treatise that accurately differentiated the types of the disease. A whole constellation of scientists from this period—Paracelsus, Erastus, Esquirol, Reynolds—studied and described increasingly new forms of epilepsy. Thanks to their work, non-convulsive epileptic seizures were isolated and designated as minor seizures (petit mal).

It was only in the mid-19th century, following the works of Falret and Samt, that the focus shifted to studying psychopathological disorders, particularly personality changes in epilepsy. Significant contributions to this issue were made by Emil Kraepelin (who detailed chronic mental alterations in epilepsy), William Gowers (who demonstrated The Link Between convulsive and non-convulsive manifestations), and John Hughlings Jackson (who contrasted epileptiform and epileptic paroxysms).

The subsequent development of epileptology primarily concerned the study of its etiology and the evolution of classifications. Weighty contributions to clarifying these matters were made by Russian and Soviet scientists such as Sergei Korsakov (1893), Ivan Pavlov (1895), Vladimir Osipov (1931), Vasily Gilyarovsky (1954), Ivan Sluchevsky (1957), Viktor Kovalyov (1979), and others.

PREVALENCE.

According to global statistics, 0.6–0.7% of the world's population suffers from epilepsy, with a higher prevalence among males. In approximately 75% of cases, the onset of the disease occurs before the age of 20.

Epilepsy is diagnosed significantly more often in childhood than in adulthood (3–7% of children). Early and accurate Diagnosis, identification of the triggers causing the disease, and adequate comprehensive Treatment should facilitate a return to normal functioning and, in A number of cases, completely eliminate this affliction.

ETIOLOGY.

The factors contributing to the development of epilepsy can be divided into hereditary (increased seizure susceptibility) and exogenous (associated with organic brain lesions).

In the majority of cases, epilepsy begins in childhood. Unfortunately, even before birth, the fetus is exposed to numerous adverse influences—so-called embryofactors—that can trigger epilepsy. These include:

✵ Fetal Hypoxia resulting from maternal cardiovascular diseases, rhesus incompatibility, uterine Hemorrhage, anemia, lack of fresh air, poor Nutrition, etc.;

✵ fetal traumatic brain injury (during labor stimulation, prolonged labor, etc., which can result in microstrokes and asphyxia). The application of Obstetric Forceps or a vacuum extractor can play an extremely negative role;

✵ maternal infections;

✵ maternal intoxications (which cause damage to the fetal Central Nervous system, such as The Use of embryotoxic drugs or smoking);

✵ maternal trauma (abdominal trauma is especially dangerous);

In the postnatal period, A wide variety of factors can provoke epilepsy. First and foremost are neuroinfections (meningitis, meningoencephalitis, including tuberculous, and encephalitis).

Cases of brain damage in children arising in connection with vaccination are known. Childhood diseases accompanied by hyperthermia-induced seizures (febrile seizures) are extremely dangerous, as cerebral hypoxia frequently develops during these episodes.

Infectious diseases play one of the primary roles in the development of epilepsy not only in children but also in adults. Etiological factors relevant to both adults and children include Influenza, otitis media, chronic tonsillitis, and rheumatism. In the case of rheumatism, epilepsy develops several years after the acute phase of the illness or against the background of a sluggish, chronic process. It should be emphasized that adult-onset epilepsy is considerably less common.

In adults, apart from meningitis and encephalitis, arachnoiditis of various origins plays an important role in the development of epilepsy. In general, inflammatory brain lesions provide a very favorable environment for the development of epilepsy. Traumatic brain injury is of great significance in the onset of epilepsy, typically resulting from domestic accidents in adults.

One of the widespread phenomena causing irreversible changes, such as cavities and softening of the brain tissue, is prolonged alcohol consumption. In addition to general personality disorders, individuals suffering from alcoholism face an increased risk of epileptic seizures. Isolated epileptiform seizures can develop even against the background of a single heavy episode of alcohol intake.

Pathogenesis.

Epilepsy is a polyetiological yet monopathogenetic disease. In the pathogenetic development of this pathology, cerebral and somatogenic (general somatic) mechanisms are distinguished.

Under normal conditions, Excitation and Inhibition processes circulate freely between the Cerebral Cortex AND other brain structures. This ensures proper communication within the central nervous system.

This dynamic continues until The Emergence of the so-called epileptogenic focus—a source of organic (e.g., a scar) or functional (e.g., stress) origin that irritates (excites) surrounding Neurons. To isolate it, adjacent neurons create a protective zone of negative induction around it. If this zone proves ineffective, the surrounding neurons enter a state of hyperexcitation, resulting in epi-discharges, which are hypersynchronized bioelectric potentials (hyperpolarization of synaptic membranes) that form high-voltage synchronous oscillations on the EEG.

An epileptic focus is a group of neurons involved in a focal epi-discharge. Sometimes, secondary "mirror" epileptic foci may appear, which do not fade when The activity of the primary focus drops. This accounts for the clinical polymorphism. As a rule, secondary foci merge into a common complex, but they can also function autonomously.

Through the lens of cerebral mechanisms, a major convulsive seizure unfolds as follows. The cortex, gripped by excitation, becomes exhausted and transitions into a state of protective inhibition. At this point, freed from cortical control within the subcortical-Brainstem structures, the myotonic centers of the extrapiramidal system are excited first (tonic phase), followed by the motor-coordination centers where excitation pulses reciprocally, i.e., bilaterally (clonic phase). Meanwhile, the concomitant excitation of subcortical vegetative-visceral centers triggers a spasm of the smooth Muscles in Internal Organs. The onset of protective inhibition in the aforementioned centers indicates the Termination of the seizure and the onset of coma or other post-ictal states.

An absence seizure occurs in the event of instantaneous, complete cortical inhibition without the involvement of subcortical structures.

Minor convulsive seizures are manifestations of narrowly localized excitation in the motor cortex against the backdrop of its general inhibition. In this case, only isolated muscles contract.

Non-convulsive seizures are the result of excitation that is insufficient to generate a convulsive discharge; consequently, both the cortex and subcortex are fixed in a phase state of incomplete inhibition.

At the general somatic level, these phenomena are accompanied by multi-level disturbances in protein-Nitrogen METABOLISM (accumulation of ammonium bases, alkalosis, predominance of albumins over globulins), endocrine balance (decrease in glucocorticosteroids and increase in desoxycorticosteroids, impaired metabolism of ACTH, Insulin, and vasopressins), Mineral Metabolism (disorders in copper and zinc metabolism), and cerebral metabolism (decreased norepinephrine, serotonin, GABA, ATP, alongside increased acetylcholine and potassium in the intercellular substance).

Over time, the anomalous influence of epileptic systems contributes not only to the recurrence of seizures but also to The formation of persistent brain function disorders, the development of epileptic personality traits, and memory decline.

Classification of Epilepsy.

For a long time, epilepsy was divided into genuine (or idiopathic) and symptomatic forms.

Genuine epilepsy was associated with negative hereditary factors. It was believed that genuine epilepsy involved no structural Changes in the brain. Later, the term "genuine epilepsy" came to be used for cases of epilepsy where the underlying cause remains undetermined even after a thorough Clinical examination of the patient.

Today, alongside epilepsy as a progredient disease, researchers also distinguish epi-syndromes, which are non-progredient convulsive Reactions of the Organism to pathogenic influences.

To gain a more precise understanding of the varieties of epileptic paroxysms, we present the classification by V. V. Kovalyov (1979).

A. Generalized (centrencephalic, widespread) seizures:

Primary generalized (without aura);

Secondary generalized (with aura);

I. Major convulsive seizures:

a) generalized (fully developed);

б) abortive;

II. Minor (non-convulsive) seizures:

a) absences (simple and complex);

b) pyknoleptic;

c) myoclonic (impulsive);

d) akinetic (propulsive).

III. Status epilepticus:

a) status epilepticus of generalized tonic-clonic seizures;

b) status of minor seizures.

B. Focal (partial) seizures:

I. Motor paroxysms:

a) Jacksonian;

b) adversive;

c) psychomotor;

II. Sensory (hallucinatory, illusory, and elementary variants possible): somatosensory, visual, auditory, olfactory, gustatory.

III. Psychic paroxysms:

a) twilight states;

b) paroxysmal dysphoria;

c) paroxysmal fears;

d) derealization and depersonalization paroxysms;

e) psychopath-like paroxysms.

IV. Speech paroxysms:

a) loss of articulation;

b) aphasic paroxysms.

V. Autonomic-visceral (focal paroxysms).

Clinical presentation.

Epileptic seizures can be convulsive or non-convulsive. In focal or partial seizures, consciousness is generally preserved. In other cases, the state of consciousness may remain impaired for a certain period of time or recover immediately after the seizure.

Generalized tonic-clonic seizure (Grand mal):

Aura (from the Latin for breeze) is the initial phase of an epileptic seizure resulting from the excitation of local brain structures before consciousness is lost. Patients retain memories of this phase. An aura is observed in 60% of patients presenting with convulsive symptoms.

Some researchers consider the aura to be an independent partial seizure followed by secondary generalized epileptic paroxysms. The term was introduced into medical practice by the prominent physician Galen (130-210 AD).

Today, the following forms of aura are distinguished, depending on the localization of the pathological focus:

a) sensory - a brief sensation preceding the loss of consciousness, such as a gentle breeze, an indefinite smell, a crawling sensation (formication), ringing, noise, a melody, etc.;

b) motor - Rotation of the eyes, HEAD, or torso around its axis, and local Muscle twitching, followed by a loss of consciousness and a fall. Sometimes the convulsions spread following the arrangement of cortical centers, generalizing and leading to a loss of consciousness;

c) psychic aura may manifest as fear, dysphoria, or distorted perception of the environment. A feeling of familiarity, or déjà vu, frequently occurs;

d) autonomic-visceral aura - the patient experiences a highly unpleasant, sometimes vague sensation in the epigastric region that rises up to the throat, often accompanied by nausea, less frequently vomiting, and hyperhidrosis.

The aura is often, but not always, followed by a major convulsive seizure, which is the most prominent manifestation of epilepsy.

The patient suddenly loses consciousness and falls forward like a felled tree (due to a generalized relaxation of muscles lasting several seconds), and tonic convulsions ensue. The patient's body may assume various positions: the head is turned, the eyes gaze upward or to the side, the arms are extended or brought toward the torso and clenched into fists, and the legs are usually extended or sometimes flexed.

During this phase, breathing stops after air is expelled from the Lungs. The forced expulsion of air from the lungs (caused by the contraction of Respiratory Muscles) through the spastic glottis often produces a characteristic cry, signaling the onset of the seizure.

During the tonic phase, the patient's face first turns pale, then flushes and rapidly becomes cyanotic and bloated. The eyes, if not closed, bulge and fixate, and the pupils dilate and do not react to light. The Tongue is usually trapped between the Teeth.

The tonic phase typically lasts from a few seconds to half a minute. At the end of the tonic tension, tremors appear as a sign of the waning tonic phase of the convulsions, followed by isolated contractions signaling the transition into the clonic phase.

During the clonic phase, muscle contractions of the head, torso, and limbs become increasingly frequent and severe, sometimes resulting in trauma. Dislocations of the shoulder joint and lower jaw are most common. During this stage, cyanosis gradually disappears, noisy breathing resumes, mucus (resulting from hypersecretion during the tonic phase) is expelled from the Bronchi, and foam appears around the Mouth, often stained red (due to biting the tongue). Incontinence of the bladder, and less frequently of the rectum, often occurs.

The clonic phase can last from 30 seconds to 5 minutes. Following it, a comatose state is observed, sometimes transitioning into a deep Sleep lasting several hours.

After waking, the patient often remains groggy for some time (movements and thinking are slowed, responses to stimuli are delayed, and speech is labored), feels generalized body aches and a headache, and has a depressed, often irritable or angry mood. Consciousness returns to patients gradually after a seizure. Initially, the patient is disoriented, does not understand where they are or what time of day it is, and fails to recognize people around them.

Memory for past events is restored first, followed by recent events, and only after some time are the events immediately preceding the seizure recalled. Memory impairment and disorientation are not equally pronounced in all patients. In some cases, the aftermath of the seizure is mild, and the patient's normal condition is restored almost immediately.

Another variant of generalized epileptic seizures is minor seizures (petit mal), or absences.

Minor convulsive seizure. In contrast to a major seizure, it proceeds without convulsions or with moderate focal convulsions and ends within a few seconds. The patient's posture is often maintained. Operating on inertia, the patient may continue the action they started. The seizure period is amnesized.

Absence seizure. Absences are not always accompanied by a profound alteration of consciousness. There are cases with incomplete impairment of consciousness, where the patient (usually a child) is faintly aware that something has happened to them, or quite confidently notes a brief lapse in consciousness - a simple absence.

In a complex absence, the lapse in consciousness is combined with other symptoms. Here, the numerous and diverse clinical manifestations are primarily associated with tone changes in various muscle groups.

Complex absences are categorized into those characterized by muscle relaxation (atonic absence) and those accompanied by increased muscle tone (hypertonic absence). Some types of seizures are accompanied by elementary automatisms such as lip and tongue movements, hand-rubbing, etc. Autonomic absences are also observed: fever, sweating, and a sensation of heat.

There are also absences accompanied by Urinary Incontinence, as well as those accompanied by coughing or sneezing, among others.

Local, or partial, seizures.

The symptoms of local epileptic seizures depend on the Functions performed by the neuronal structures where the discharge occurs, as well as the areas recruited as the seizure develops. Partial (or local) epileptic seizures often serve as precursors (aura) to secondary generalized seizures.

Local epileptic seizures can also occur independently, without secondary generalization. A Jacksonian seizure most commonly begins at the corner of the mouth or in the thumb or big toe. This is followed by the spread of convulsive contractions along the entire limb, extending to the Muscles of the torso, face, and the opposite limb (the "Jacksonian march"). The apogee of the "Jacksonian march" is typically a generalized convulsive seizure with a loss of consciousness.

Another quite common type of focal seizure is the somatosensory paroxysm. These seizures originate from a lesion in the sensory area (postcentral gyrus) of the cerebral cortex. The most typical manifestations of somatosensory seizures include tingling, numbness in an arm, leg, or face, and various types of unpleasant sensations (paresthesias). Pain is very rare during these episodes. Such sensations may spread in the manner of a "Jacksonian march," potentially culminating in a generalized tonic-clonic seizure.

The Clinical presentation of most sensory seizures (auditory, visual, olfactory, gustatory), dizzy spells, autonomic-visceral symptoms, and episodes accompanied by various psychiatric disorders is frequently associated with lesions in the temporal lobes of the brain.

Seizures with autonomic-visceral manifestations also occur. One of the most characteristic signs is an unpleasant sensation in The Stomach (epigastric region). Some patients experience nausea, vomiting, or increased peristalsis, while others report a feeling of emptiness or heartburn.

A dream-like state represents one form of psychosensory seizure. It is precisely during such paroxysms that symptoms of déjà vu ("already seen"), déjà entendu ("already heard"), or déjà vécu ("already experienced") occur. Much less frequently, patients report jamais vu ("never seen") or jamais entendu ("never heard") phenomena. Additionally, patients may experience distortions in the perception of space, shape, size of objects, and their relative positions, as well as disturbances in body image, macropsia, micropsia, metamorphopsia, and others.

During ambulatory automatisms, a patient's actions may appear purposeful: they might cook a meal, wash dishes or sweep the floor, and so on. Sometimes these states last for a prolonged period. The profound impairment of consciousness during these automatic actions is reflected in the patient's facial expression. Their gaze is blank or staring into space. They do not respond to calls or addresses, yet they navigate around obstacles while walking; they may even cross a street, dodging traffic (though not always successfully).

Status Epilepticus.

Status epilepticus is a dangerous complication of epilepsy. The frequency of major convulsive seizures varies among individuals. In some patients, seizures occur 2–3 times a year, while in others, they happen once a week or several times a month. This pattern is referred to as clusters of epileptic seizures.

However, if seizures occur repeatedly over the course of a single day, following one another almost continuously without the patient regaining clear consciousness, status epilepticus develops. The number of seizures can reach 300 or more per day, and this critical state can persist for many hours or even several days.

This condition is life-threatening; without appropriate interventions to terminate the episode, it can result in death. Such outcomes stem from complications including hyperthermia and cardiovascular disturbances, such as rapid, thready pulse and a sharp drop in Blood pressure. Pulmonary edema may also develop.

Psychic Equivalents of Epileptic Seizures.

Twilight states of consciousness occur suddenly. Patients are disoriented in time, place, surroundings, and events. Somnambulism is a variant of this condition, where patients walk around the room, rearrange objects, go outside, and engage in other activities while remaining in a sleep-like state. Amnesia typically follows upon waking.

Epileptic delirium is a profound clouding of consciousness accompanied by vivid hallucinatory experiences and delusional ideas. It is characterized by an affect of ecstasy, terror, or rage, accompanied by corresponding defensive, aggressive, or other behavioral patterns.

Epileptic stupor is characterized by reduced mobility and catalepsy. Patients are disoriented and perplexed; they either fail to answer questions or give incorrect responses, and are unable to name common objects. Waxy flexibility (cerea flexibilitas) and perseveration are typically present. At the same time, patients appear tense, terrified, and inwardly irritable.

Dysphoria refers to episodes of unmotivated mood disturbances. Dysphoric states are most frequently characterized by a sullen, dysphoric mood. Suddenly and unexpectedly to those around them, patients become gloomy, irritable, enraged, and aggressive. Such episodes can last from a few hours to several days.

Personality Changes in Epilepsy.

With a prolonged course of the disease, patients develop specific personality traits that were not previously characteristic of them, leading to the Formation of the so-called epileptic personality. The most prominent features include heightened irritability, hot-temperedness, and malice. Patients tend to be fault-finding, egocentric, and hypochondriacal, yet they may simultaneously exhibit excessive politeness and unctuousness (emotional "polarity"). A predilection for diminutives (e.g., "sis," "pill," etc.), meticulous neatness, and excessive pedantry are also observed. The inertia of nervous processes manifests in patients as mental rigidity, reduced comprehension, and a loss of intuitive insight.

Epileptic dementia (known as "concentric" dementia). It is characterized by a gradual narrowing of the patient's interests around their own personal needs, particularly the physiological functions of their body.

Thinking becomes sluggish, viscous, overly detailed, and concrete, with thoughts fixated on trivial matters. The patient is unable to distinguish the essential from the secondary. Memory suffers, and words are occasionally omitted, rendering speech restricted and monotonous. Patients are exclusively preoccupied with themselves and their health status; scientific, social, and professional interests are lost. This narrowing of the psyche develops gradually and concentrically.

TREATMENT.

The Specifics of the epileptic process require adherence to the following mandatory principles when organizing and implementing treatment: continuity and prolonged administration of medications, gradual titration of doses and drug substitution, a comprehensive and, whenever possible, pathogenetically sound approach to therapy, and individualized care.

Anticonvulsant pharmacotherapy remains the primary method of treating epilepsy today. The therapeutic regimen can be divided into three stages.

Stage One: the primary objective is to determine the most optimal treatment strategy and utilize it to suppress paroxysms. Treatment begins with low doses of anticonvulsant drugs administered 1–3 times a day, evaluating efficacy every 3–5 days and gradually increasing the dosage.

Treatment should be initiated with a single medication rather than a combination to accurately identify the most effective agent. Phenobarbital is traditionally chosen as the first-line treatment due to its broad spectrum of action and efficacy against major generalized tonic-clonic seizures.

Ratio of seizure frequency to drug dosage for adults and children (in parentheses).

The replacement of a drug (in case of its ineffectiveness or complications) is carried out very cautiously through a fractional, "sliding" substitution with a new agent, adhering to the following equivalent doses relative to phenobarbital: diphenylhydantoin — 1 : 1.5; benzonal — 1 : 2; hexamidine — 1 : 3.

The Second Stage involves consolidating the remission achieved through treatment by means of prolonged (at least five years) systematic administration of optimal doses of the medication.

The Third Stage is verifying the stability of remission through a gradual (over 1.5–2 years) reduction of the anticonvulsant dose. This is only possible after the complete cessation of seizures and the disappearance of signs of paroxysmal activity on the EEG for five years. Following the final discontinuation of treatment, medical monitoring should be performed at least 1–2 times a year.

The therapeutic regimen combines agents that target all pathogenetic links; the main ones include: anti-paroxysmal, resorption-promoting, dehydrating, desensitizing agents, and multivitamin complexes.

Anticonvulsant drugs are prescribed in the majority of epilepsy cases. Their Selection is determined primarily by the specific type of seizure in a given patient.

Thus, carbamazepine, karbasan, finlepsin (0.6–0.8 g daily), phenobarbital (0.05–0.3 g daily), and hexamidine (0.125–2.0 g daily) are advisable for major generalized or psychomotor seizures, whereas benzonal (up to 0.8 g daily) is recommended for partial motor seizures. To treat convulsive forms, M.Ya. Sereisky's mixture is widely used, consisting of phenobarbital (0.02–0.05 g), bromural (0.05–0.2 g), papaverine (0.02–0.05 g), caffeine (0.015 g), and calcium gluconate (0.25–0.5 g).

Diphenylhydantoin (daily dose of 0.2–0.3 g) has an even broader spectrum of action than phenobarbital, but being more toxic, it may cause headache, dizziness, dysarthria, nystagmus, diplopia, and other adverse effects.

For absence seizures, the use of valproic acid group drugs (Orfiril, Depakine, sodium valproate) and trimethadione is effective; for minor seizures, treatment with succinimide group drugs is most effective: ethosuximide, pyknolepsin, morpholep, suxilep, etc.

A number of drugs have proven effective in various minor seizures: clonazepam for myoclonic and propulsive seizures in children at a dose of 0.25 mg/kg daily; Convulex at a dose of 20–30 mg/kg daily for myoclonic seizures in children and adolescents; pyknolepsin at a mean daily dose of 0.75–1.5 g for simple absence seizures and pyknoleptic seizures in children.

A physician faces considerable difficulties when treating myoclonic forms of epilepsy. In such cases, benzodiazepine group drugs are used: seduxen 5–10 mg daily, eunoctine, as well as hormonal agents: dexamethasone, prednisolone.

Finlepsin and benzodiazepines are used to treat dysphoria; in cases of their ineffectiveness (dysphoria of psychotic severity) or the appearance of twilight states of consciousness, neuroleptics are indicated: Tizercin 2.5% - 1 ml, haloperidol 0.5% - 1 ml parenterally.

Typically, anticonvulsants are combined with Other types of therapy aimed at normalizing cerebral metabolism: glutamic acid, Vitamins B1, B6, B12, ascorbic acid, Folic acid, etc.

If patients exhibit signs of elevated intracranial pressure, dehydrating therapy is indicated: furosemide, diacarb, veroshpiron, triampur.

In cases where adhesion or scarring processes in the brain are suspected, resorption-promoting agents are prescribed: lidase, aloe, vitreous body, bioquinol, etc.

In malignant disease progression, pharmacotherapy failure, and the presence of a clearly localized epileptic focus, surgical resection of the corresponding brain area may be indicated.

The management of status epilepticus requires the following mandatory measures: preventing tongue retraction and aspiration of vomitus, arresting convulsions, combating cerebral edema, and supporting Cardiac Activity.

Treatment should begin with the intravenous administration of 4–6 ml of a 0.5% solution of sibazon, followed by a cleansing enema and the rectal administration of up to 60 ml of a 2% chloral hydrate solution in starch paste or 30 ml of a 2% sodium barbital solution. Thirty minutes after the enema, the intramuscular administration of 10–15 ml of a 25% magnesium sulfate solution is indicated.

If sibazon is ineffective, 1.0 g of hexenal or thiopental sodium dissolved in 10 ml of isotonic sodium chloride solution is administered intramuscularly, 0.5 into each buttock. Anticonvulsants are combined with dehydration therapy (furosemide, urea, mannitol), cardiac stimulants, detoxification, and hypotensive therapy.

If seizures persist, recourse is made to the inhalation of nitrous oxide mixed with oxygen in a 2:1 ratio. Anesthesia (at the level of surgical stages I–II) should be maintained for another 1–2 hours after the status is controlled. In severe cases, lumbar puncture is performed with the withdrawal of 15–20 ml of CEREBROSPINAL FLUID.

EXPERT ASSESSMENT.

Medical-labor expertise. Approximately 50% of epilepsy patients require disability status. In the presence of frequent seizures and dementia, they are deemed disabled with the assignment of disability group II. With pronounced concentric dementia, when patients require constant outside care, they are granted disability group I.

Military-medical expertise. In cases of infrequent seizures (less than 2–3 times a year), conscripts are deemed unfit for military service in peacetime and fit for non-combat service in wartime, while officers are deemed fit for non-combat service in both peacetime and wartime. With frequent seizures (more than 2–3 times a year), enlisted personnel are deemed unfit for military service and are deregistered. The presence of twilight states, ambulatory automatism, or persistent epileptic mental changes, regardless of the frequency of paroxysms, serves as the basis for a decision of unfitness for military service and deregistration.

Forensic-psychiatric expertise. The mere establishment of an epilepsy diagnosis does not predetermine the expert Conclusion. The same patient may be deemed sane regarding a crime committed during the interictal period, and exculpated regarding a crime committed during a paroxysm.

The most important and complex task in forensic-psychiatric practice is the differentiation of transient epileptic disorders, which frequently contribute to the commission of socially dangerous acts by patients. Criminal acts committed during a twilight state possess a number of distinctive features: suddenness, motivelessness, lack of intent, absence of precautionary measures or attempts to conceal the crime, infliction of multiple wounds on the victim, motiveless desecration of the corpse, etc. The very nature of such a crime suggests a twilight clouding of consciousness. Additional data regarding the onset of a seizure close to the time of the crime, a sharp change in condition, the patient's "inadequate" appearance (a bewildered look, motor retardation, or motiveless agitation), deep sleep following the offense — where the patient sometimes falls asleep next to the victim — and similar occurrences in the Anamnesis make the diagnosis of a twilight state of consciousness quite convincing.

Offenses committed in a state of dysphoria are less common. Their recognition requires objective data regarding a motiveless, sudden mood change and the presence of similar states in the past. Sometimes patients themselves create obstacles to the qualification of their pathological condition by attempting to attribute the onset of a "bad" mood to some external factor. Forensic-psychiatric evaluation depends on the depth of the dysphoria. The inclusion of delusional experiences and disturbances of consciousness at the peak of dysphoria indicate the necessity of exculpation.

CONTROL QUESTIONS.

1. Define epilepsy and its types.

2. Etiology of epilepsy.

3. Pathogenesis of epilepsy.

4. MAIN CLINICAL MANIFESTATIONS of epilepsy.

5. Clinical Features of a generalized tonic-clonic seizure.

6. Clinical features of a absence seizure (petit mal).

7. What is status epilepticus?

8. What are psychic equivalents?

9. What are dysphoric states?

10. Personality changes in epilepsy.

11. Characteristics of epileptic dementia.

12. Core principles of epilepsy treatment.

13. Management and termination of status epilepticus.

14. Medical and social examination of patients with epilepsy.