Psychiatry - O. K. Napryeyenko 2001

Clinical Psychiatry
Epilepsy

Epilepsy (from Greek epilepsia — a seizure) is a polyetiological, monopathogenetic, and progressive neuropsychiatric disorder. It is characterized by recurrent convulsive and non-convulsive mental attacks (paroxysms), as well as acute mental disorders that evolve into chronic, persistent conditions. Since biblical times, various mystifications have surrounded this disease—and some still persist today. It has been called the "sacred disease", "demonic illness", "black sickness", "black weakness", "unclean affliction", and "scourge", among other names.

The term "epilepsy" first appears in the works of Avicenna (980–1037). In the majority of cases (70–80%), the disease debuts before the age of 20. Depending on diagnostic criteria, the prevalence of epilepsy is estimated at 0.3–1%, with an average of 0.5%.

To date, there is no unified concept regarding The Essence of epilepsy. Some psychiatrists distinguish between genuine and symptomatic epilepsy, while others view it as a disease of diverse genesis. There is no universally accepted Classification of epilepsy. Although classifications of epileptic seizures exist, their schematic division based on a single principle (either clinical or by the localization of the lesion) is hardly acceptable, since the localization of the lesion and the clinical Structure OF THE seizure may change over the course of the disease. Primary partial and secondary generalized seizures can evolve into primary generalized ones and vice versa.

To unify the nosological Diagnosis of clinically similar yet etiologically distinct pathological manifestations, some researchers suggest using the terms "epileptic reaction" and "epileptic syndrome", replacing the previously used Definitions "epileptiform reaction" and "epileptiform syndrome".

An epileptiform reaction manifests as paroxysms of varying Clinical presentation in response to harmful factors such as elevated body Temperature, various poisonings, traumatic Brain injury, electrical or Insulin Shock, oxygen deficiency (Hypoxia), or an excess of oxygen in the Blood (hyperbaric phenomena). In emotionally labile children, respiratory-affective convulsions can be triggered by fear, pain, or anger. During such episodes, breathing stops upon exhalation during a cry, the face turns cyanotic, and the limbs spasm. Nocturnal terrors, twilight states, dysphoria, and vegetative-visceral crises may present as isolated or recurring paroxysms. Such isolated seizures typically disappear without antiepileptic Treatment and do not recur.

Epileptiform syndromes develop in the presence of active pathological cerebral processes (inflammation, tumors, parasitic infestations, atherosclerosis, aneurysms, etc.). The diagnosis is established based on the underlying disease. An epileptiform syndrome can be an integral component of the clinical picture of organic brain damage of various origins. Paroxysmal convulsive, non-convulsive, and psychopathological disorders are directly linked to the primary illness.

True (genuine) epilepsy is an independent process-based disease with specific Clinical Features, notably persistent mental alterations. Symptomatic (syndromal, residual) epilepsy is also distinguished. Both conditions involve genetic and exogenous-organic determinants. Differentiating between epilepsy and epileptiform syndromes in patients with residual organic brain lesions is considered challenging. This is due both to similarities in their genesis and symptomatology, and to their differences. In general, residual-organic epileptiform syndrome tends to transform into a progressive disease—epilepsy.

Most authors classify as symptomatic epilepsy those conditions that arise on The basis of residual effects of organic brain damage (most commonly of traumatic and infectious origin), accompanied by focal seizures and mental changes characteristic of a psycho-organic syndrome. In other cases, symptomatic epilepsy resulting from birth trauma, meningoencephalitis, and other exogenous-organic brain lesions in children leads, in later stages of its course, to typically epileptic personality changes characteristic of true epilepsy.

Clinical differentiation of epilepsy as a distinct disease is of great importance for diagnosis, treatment, and expert evaluation.

Etiology AND Pathogenesis

The main direction in studying the etiology of epilepsy is identifying the interplay between genetic and exogenous factors involved in The Development of the disease. S. N. Davydenko (1960) emphasized The Role of heredity, noting that the frequency of direct transmission of epilepsy to descendants is 10 times higher than the frequency of sporadic cases in the general population. According to Lennox, the concordance rate for epilepsy in monozygotic twins is 84%, compared to only 17% in dizygotic twins. On the other hand, the incidence of the disease in children born to parents with epilepsy ranges from 3.6% to 8%. The risk of developing epilepsy for close relatives does not exceed 4–4.2%.

The identical hereditary burden in children born to parents with epilepsy is 8%. It is believed that what is inherited in epilepsy is not the disease itself, but a constitutional predisposition to it. However, this predisposition may not only be inherited but can also develop As a result of intrauterine or postnatal exogenous-organic lesions of The Nervous system.

Epilepsy is regarded as a polyetiological yet monopathogenetic disease. Exogenous etiological factors in the development of epilepsy in adults include: traumatic brain injury (24.7%), infections (14.1%), alcohol (4.8%), psychological trauma (2.2%), atherosclerosis (3.7%), and other causes such as maternal illness during Pregnancy, fetal asphyxia, and intoxications (10.2%), among others. Exogenous factors can provoke a seizure if a predisposition to convulsive and other paroxysms exists. According to O. Z. Holubkov, in 5–25% of patients—and according to H. L. Voronkov, in 15–60%—the etiology cannot be established.

The Study of The Nature of epilepsy and some of its mechanisms has contributed to uncovering A number of mechanisms underlying brain activity. For instance, the functional principle of the somatotopic Organization OF THE sensorimotor cortex was established (Penfield, 1937), and The Significance of the limbic system was proven (Jackson, 1931). Abundant material has been provided for understanding the functional Asymmetry of the brain.

In studying the pathogenesis of epilepsy, primary attention has been paid to various general somatic Functions. Significant deviations from the norm have been noted in nitrogen-protein, carbohydrate, Water-electrolyte, and Mineral METABOLISM. Disturbances in trace element metabolism (copper, zinc, silver) and acid-base balance (shift towards alkalosis) have been identified. However, it later became apparent that such deviations are not sufficiently specific to epilepsy. Changes in the levels of certain Neurotransmitters and the composition of BIOLOGICALLY ACTIVE SUBSTANCES (blood, CEREBROSPINAL FLUID, tissue fluid) in epilepsy patients have indicated disturbances in the cholinergic and serotoninergic systems, which play a prominent role in the genesis of functional Changes in the Central Nervous System during The formation of various paroxysms. These studies have significantly deepened our understanding of the pathogenesis of convulsive seizures. The overall pathogenesis of epilepsy remains not fully elucidated.

Thus, the foundation of epilepsy rests on two factors: predisposition and adverse exogenous influences leading to organic brain damage. A predisposition to epilepsy may be constitutional or acquired. As a result of this readiness, an epileptic focus is formed. In various areas of the brain—most frequently in the Cerebral Cortex—due to known causes (trauma, inflammation, intoxication, etc.) and unknown causes (such as inhibitory influences from the Diencephalon), certain groups of Neurons begin to generate pathological impulses (with high frequency and low amplitude). This promotes Changes in membrane permeability. Such a neuron becomes overly sensitive and, in turn, desynchronizes The activity of cellular structures in adjacent zones, creating a state of epileptic brain readiness. Several pacemaker neurons of the pathological rhythm (8–10) can form an epileptic focus (EF). EF represents a collection of neural ensembles organized in a specific manner. The spike-wave characteristic of discharges indicates a disruption in the information function and memory of the focal neural ensembles. Imposing this operational mode on other PARTS OF THE brain leads to the appearance of secondary and tertiary mirror epileptic foci. However, an EF of pathological rhythm pacemakers is not yet epilepsy.

The direct realization of epileptic readiness into a paroxysm is hindered by the specific activity of a number of structures in the cerebrum and Cerebellum. Therefore, despite the presence of an EF and epileptic brain activity, epileptic paroxysms may not occur for some time or even throughout a lifetime. However, this dynamic equilibrium between desynchronizing and synchronizing mechanisms can be disrupted by various causes (hypoxia, hypoglycemia, hyponatremia, hyperthermia, intoxication, etc.). The "breakthrough" of epileptic activity from the focus, accompanied by the development of clinical manifestations of the disease, indicates the insufficiency of antiepileptic mechanisms and the formation of an epileptic system. Increased convulsive activity is associated with poor myelination of nerve pathways, increased hydrophilicity of the brain, and lability of calcium metabolism. This can explain, for instance, why seizures occur more frequently in children during infectious diseases, intoxications, psychological trauma, etc.

Sensitivity to paroxysmal influences increases with a decrease in the levels of all biogenic amines in the brain.

The immediate period of seizure risk correlates with an increase in the tone of the cholinergic system and a weakness of the serotoninergic system (O. Z. Holubkov, 1967). However, biochemical and immune changes in epilepsy are non-specific.

Pathomorphological changes in epilepsy can be twofold: a) residual, indicating various developmental disorders or past brain injuries; b) pathomorphological, resulting from the epileptic process itself. The terms "incisural" and "marginal" sclerosis appeared long ago and indicate neuronal depletion and proliferation in the hippocampus. In the convulsive form of epilepsy, acute vascular-hypoxic changes occur in the brain, accompanied by chronic vascular-hypoxic encephalopathy. Significant changes are observed in the hippocampus, cerebral cortex, and subcortical reticular Formation of the Brainstem. These are considered factors driving the progressive Nature of the epileptic process.

Brain atrophy in epilepsy is cited among the primary factors of epileptogenesis. Pathomorphological studies of the neocortex, hippocampus, and amygdaloid complex in epilepsy patients have established a clear reduction with high [integrity of neurons and synapses, which leads to the functional and anatomical deafferentation of neurons, increases the excitability of surviving Nerve Cells, revitalizes mechanisms of autorhythmic neuronal functioning, and leads to their "epileptization". A multilevel "epileptic system" emerges in the central nervous system, involving various brain structures. Synaptic remodeling against the Background of neuronal reduction and the reintegration of surviving nerve cells with new synapses determines changes in excitatory and inhibitory processes characterized by the strength, explosiveness, and periodicity typical of these processes.

Risk factors for epilepsy

H. L. Voronkov (1990) described so-called epileptic radicals. The combination of two or more such features—especially in the presence of a history of cerebral-organic diseases—is a direct indication for targeted examination and, if necessary, preventive antiepileptic measures. Epileptic radicals include:

1) early childhood convulsive-spastic states occurring suddenly or against the background of hyperthermia in children under one year of age (less frequently at 2–3 years), and tonic Muscle spasms;

2) primary enuresis persisting into adolescence;

3) "restless early childhood" — the infant is very restless, sleeps poorly, and cries; does not calm down even when rocked or after feeding;

4) frequent nocturnal myoclonic jerks, affective terror;

5) systematic somnambulism followed by amnesia;

6) stereotyped terrifying dreams with night terrors;

7) spontaneous transient hemiplegia or hemiplegia occurring after early childhood seizures;

8) frequent recurrence of paroxysmal migraine-like headaches;

9) motor inhibition, malice, rudeness, timidity;

10) transient mild delay in mental and physical development during childhood.

Classification

In the International Classification of Diseases (ICD-10), epilepsy is coded under Chapter 6 "Diseases of the nervous system".

Clinical Features

It is clear from the definition of epilepsy that recurrent seizures form its core. A seizure occurs against the background of complete well-being or during a sharp exacerbation of a chronic process, manifesting as transient motor, sensory, or psychic signs.

Epileptic seizures are characterized by:

a) sudden onset and termination; b) short duration; c) stereotypy; d) recurrence.

The clinical manifestations of seizures vary. Esquirol (1815) distinguished two types: major convulsive seizures (grand mal) and minor non-convulsive seizures (petit mal). Gowers (1881) differentiated between major, minor, and hysterical seizures. A very important milestone was the division of epileptic seizures into generalized and partial (Jackson, 1931). In 1981, seizures were classified as follows: 1) generalized; 2) partial; 3) unclassified.

Generalized seizures. Major convulsive seizures may be primary or secondary generalized. Primary generalized major convulsive seizures are characterized by: sudden loss of consciousness; falling (most often forward); a tonic seizure phase (up to 30 s) with general tension of all Muscles. Tongue biting, shock, and a clonic seizure phase (1—2 min) may occur. The seizure concludes with a postictal stupor stage. The onset of the seizure may be preceded by distant (1—2 days) or proximal (from 1 h to 30 min) prodromal symptoms such as weakness, general malaise, fatigue, headache, depressed mood, and irritability. In 50% of cases, seizures begin with an aura (Greek *aura* — a breeze), manifested by fleeting sensory (sound, light, smell, numbness, warmth, cold, etc.), motor (convulsive twitching), somatovegetative (nausea, sweating, flushing), and psychic (anxiety, fear) phenomena. The tonic phase is accompanied by respiratory arrest, pallor, and subsequent cyanosis. Pupils do not react to light; involuntary urination and defecation may occur. After the seizure, there is complete amnesia, headache, and a dysthymic mood.

Often, convulsive seizures are atypical and present abortively, with only a tonic or clonic seizure phase, or sometimes with muscle relaxation without convulsions. Major convulsive seizures occurring one after another without the patient regaining consciousness are referred to as status epilepticus.

Generalized seizures include minor seizures:

a) simple absence (2—15 s) with loss of consciousness and a fixed gaze, but without postural disturbance;

b) complex absence — In addition to brief loss of consciousness, changes in the tone of certain facial or Neck Muscles are observed. Atotonic, myoclonic, and vegetative absences are distinguished herein;

c) pyknoleptic seizures — brief loss of consciousness accompanied by facial pallor and hypersalivation. Movements are directed backward. Minor convulsive seizures occurring in rapid succession are called status petit mal.

The electroencephalographic (EEG) sign of minor seizures is bilaterally synchronous spike-wave complexes at a frequency of 3 Hz.

In atypical absences, referred to as pseudo-absences, against the background of loss of consciousness with a fixed gaze, the paroxysm lasts longer than in true absence seizures. Onset and recovery are gradual. The déjà vu phenomenon may occur. Autonomic disorders are observed. The EEG records: fast low-amplitude oscillations (10–20 per second); asynchronous and asymmetric, or bilateral, high-amplitude spike-waves (2 per second). These distinctions are of practical importance for grounding therapy and prognosis.

Myoclonic, or impulsive, seizures are observed less frequently than minor seizures, predominantly during the prepubertal period. They present as sudden jerks of the arm muscles, shoulder girdle, and neck against a background of impaired consciousness. Seizures most often occur in series or as "salvos" (5–20 in a row).

Akinetic seizures are predominantly observed in early childhood. They are manifested by forward Movements of the HEAD AND TORSO. Typical movements include "nodding", "pecking", and "salaam" seizures, which some authors classify as myoclonic.

Diencephalic vegetative-visceral seizures are distinguished by polymorphic autonomic disorders (tachycardia, hyperhidrosis, hyperthermia, nausea, polyuria, tremor) accompanied by potential loss or alteration of consciousness.

Focal (partial) seizures are defined as those in which clinical and EEG findings reveal the onset of neuronal activation within a localized region of one cerebral hemisphere. They are classified into simple partial, complex partial, and partial seizures with secondary generalization.

Complex seizures differ from simple ones in that they involve an impaired ability to comprehend ongoing events and to respond appropriately to stimuli at the onset of or during the seizure.

Partial seizures are characterized by a diverse symptomatology—including motor, sensory, autonomic, or psychic manifestations—depending on the localization of the epileptic focus. Jacksonian motor seizures are characterized by focal, cortical-origin convulsions. They begin in one part of the body and subsequently generalize. Oculoclonic, oculogyric, adversive, rotational, and phonatory seizures are also distinguished.

Jacksonian sensory seizures present with elementary or complex sensory manifestations (visual, auditory, gustatory, olfactory, somatosensory). They may remain localized or spread to adjacent somatosensory areas in the cerebral cortex. Partial seizures with autonomic symptoms are characterized by nausea, facial pallor or flushing, diaphoresis, and pupillary dilation. Most frequently, they follow the course of complex seizures, presenting with various visceral manifestations (digestive, respiratory, cardiac, and abdominal).

Partial psychic seizures are associated with neuronal discharges in the temporal or frontal lobes, accompanied by affective and cognitive symptomatology.

Seizures with affective symptomatology are characterized by short duration (seconds to minutes) and emotional experiences ranging from mild to intensely pronounced (fear, anxiety, depression, anger).

Cognitive paroxysms involve a feeling of unreality regarding one's surroundings or oneself. These seizures encompass ideational, dysmnesic, and other disturbances. Feelings of déjà vu or jamais vu are observed in cases of right-sided localization of epileptic foci within the temporal lobe.

A partial seizure (whether complex or simple) may evolve into a generalized convulsive seizure, which has led to the classification of secondary generalized seizures.

NON-CONVULSIVE FORMS OF PAROXYSMS (PSYCHIC EQUIVALENTS)

Within clinical epilepsy, non-convulsive paroxysms with qualitative alterations of consciousness (twilight states, dreamlike states with fantastical daydream-like delusions, ambulatory automatisms) and without disturbances of consciousness (affective paroxysms, cataleptic, psychomotor, etc.) occupy a significant place. The prevalence of psychoses in epilepsy is 7%, and the incidence rate is 10%.

Paroxysms with altered consciousness (according to M. O. Hurevych, 1949) or dreamlike states featuring fantastical experiences of derealization and depersonalization include so-called apperceptive illusions (illusions of jamais vécu and déjà vécu, jamais vu and déjà vu). Disorders of this type vary in duration, and patients experience them as if in a dream.

Dysphoria in epilepsy is characterized by paroxysmal mood disorders tinged with malevolent-angry affect, which serves as a foundation for the development of polymorphic, frequently fragmentary, low-productivity, and mosaic psychopathological symptoms. Depending on the intensity of their expression, these symptoms may reach a psychotic or non-psychotic level. The content of dysphoria may be defined by melancholy, resentment, anxiety, fear, malice, irritability, tension, aggressiveness, distrust, suspicion, despair, depression or elevated mood, paresthesias, illusions, and overvalued or delusional ideas.

Dysphoric reactions and a dysphoric mood background should be distinguished as a non-psychotic level of disorder, whereas dysphoric psychoses and "status" represent the psychotic level.

A dysphoric reaction is defined as a paroxysmal malicious-irritable outburst triggered by any pretext, which patients themselves frequently seek out. Dysphoric reactions resemble affective reactions but, unlike the latter, lack a direct causal relationship with psychogenic factors. The clinical picture develops gradually. To achieve release, patients search for a target object. Dysphoric reactions last from 20 minutes to 1.5 hours, leaving behind a subjective feeling of fatigue. The patient subsequently feels remorse and apologizes for their behavior.

The dysphoric background is generated by subconscious, severe, undifferentiated, yet quite intense emotional fluctuations. This state lasts from 1–2 hours to 1 month, and up to 2–3 months in protracted cases of epilepsy.

Psychotic forms include dysphoric psychoses and dysphoric status characterized by various types of malicious-irritable, depressive, paranoid, and euphoric features. Gross behavioral disturbance and inadequate situation assessment are consequences of intense, paroxysmal affect. The duration of psychoses ranges from 1–2 hours to 5–7 days.

Dysphoric status comprises complex polymorphic states consisting of diverse, mutually succeeding, frequently prolonged dysphoric psychoses and frequent dysphoric reactions, typically unified by a common dysphoric background. They last from 1 to 6 months.

Acute interictal epileptic psychoses present with more complex clinical symptoms and lack paroxysmal features.

Among epileptic psychoses with impaired consciousness, the following are distinguished:

a) epileptic delirium (featuring impaired objective orientation, vivid visual hallucinations, persecutory delusions, fear, anger, and corresponding behavior);

b) epileptic oneiroid (featuring predominantly impaired objective orientation, fantastical visual hallucinations and illusions, along with agitation or stupor);

c) epileptic stupor (featuring motor retardation against the background of a twilight state, accompanied by hallucinations and delusions).

Acute psychoses without impairment of consciousness:

a) epileptic paranoid state (persecutory delusions, illusions, and hallucinations);

б) epileptic depression (anxiety, agitation, self-blame ideas);

в) epileptic mania (euphoric or ecstatic background, ideas of personal grandiosity).

Chronic epileptic Schizophrenia-like psychoses include paranoid, paranoid-hallucinatory, hallucinatory-paranoid, and catatonic types.

Paranoid psychosis manifests as systematized delusions of reference, poisoning, reformism, as well as religious and hypochondriacal ideas. These ideas and activities are permeated by the cognitive inertia, affect stickiness (viscosity), and unctuous speech characteristic of epilepsy. Patients are exceptionally persistent, punctilious, and vindictive.

Paranoid psychosis is characterized by true and pseudohallucinations (visual and auditory), along with Features of the Kandinsky-Clérambault syndrome.

Hallucinatory-paranoid psychosis may present with a paraphrenic structure featuring fantastical hallucinatory and delusional experiences.

Catatonic psychosis is rarely observed; its clinical picture is dominated by substuporous symptoms with negativism and mutism, hebephrenic features, and impulsive agitation accompanied by stereotypies and aggressiveness.

Protracted epileptic psychoses are accompanied by a decrease in seizure frequency or their complete cessation, alongside EEG normalization. Persistent psychological impairments affecting personality and intellect are considered specifically epileptic and are viewed as a crucial diagnostic sign of epilepsy. Personality disturbances are distinguished by polarized emotional-volitional reactions, narrowing of interests, egocentrism, explosiveness, and aggressive acts involving cruelty, humiliation, and unctuous obsequiousness. Patients exhibit a marked neatness, often manifested as a caricatured pedantry regarding order at home and in the workplace. Flattery, heightened sensitivity, and vulnerability are combined with malice and ill-will.

Intellectual alterations begin with the onset of sluggish thinking and circumstantiality. Over time, memory and Abstract thinking deteriorate, accompanied by oligophasia. The following types of epileptic dementia are distinguished:

a) amnestic-oligophasic — memory impairment, oligophasia, cognitive decline, and mental rigidity (developing predominantly in epilepsy with frequent convulsive seizures);

б) affective — explosiveness, egocentrism, dysphoric states, characteristic of patients with episodic epileptic psychosis and psychomotor ("temporal lobe") seizures;

c) paralogical — persistent paranoid delusion (ideas of reference, persecution, grandeur, hypochondriacal, etc.).

THE SPECTRUM OF personality changes in epilepsy is exceptionally broad, ranging from mild characterological shifts to profound manifestations of dementia. Characterological deviations in most patients develop following fully established paroxysms, yet they may also manifest prior to the onset of seizures, driven by an epileptic process that initially lacks overt paroxysmal expression.

In the majority of patients, the course of epilepsy is characterized by a slowly Progressive development of paroxysmal and deficit symptoms. Persistent epileptic alterations in character and intellect emerge 10–20 years after disease onset and are observed in approximately 24% of patients.

The course of epilepsy can be divided into the initial stage and the stage of fully developed manifestations of the epileptic process. During this period, non-convulsive paroxysms, dizziness, headaches, night terrors, somnambulism, somniloquy, psychosensory disorders, and enuresis are noted in nearly 80% of cases. These signs may appear several years prior to the onset of convulsive paroxysms. In 20% of patients, the first sign is a major or abortive convulsive seizure. During the stage of fully developed manifestations, convulsive seizures are combined with non-convulsive paroxysms.

At the same time, a single convulsive paroxysm may be accompanied by a dozen non-convulsive ones.

The types of epilepsy course depend on the CHARACTERISTICS OF THE onset, the form and frequency of paroxysms, pre-existing conditions, individual reactivity and compensatory mechanisms, and the adequacy of the rehabilitation process.

The continuously progressive type is characterized by frequent (up to 15 per month) polymorphic convulsive seizures combined with non-convulsive paroxysms and steady, progressive cognitive impairment. Therapeutic efficacy is low.

The moderately progressive type. The frequency of convulsive paroxysms is up to three per month. Non-convulsive paroxysms are rare. Under The Influence of antiepileptic therapy, the frequency of paroxysms decreases, and personality traits are relatively preserved. Personality deterioration develops very slowly. The rehabilitation effect is very high.

The remittent type proceeds with therapeutic remissions and a high level of social adaptation. Paroxysms are rare (up to one per month).

The stationary type. Adaptation is unimpaired, and mental processes remain practically unchanged. Seizures are rare (1–3 per year) and respond poorly to treatment.

The sluggish type. Convulsions are absent, and the pace of mental processes is moderately slowed. Patients seek medical attention regarding issues of social adaptation.

Clinical forms of epilepsy:

1) convulsive-spastic. Begins at the age of 5–30 years. Major convulsive seizures predominate. Status epilepticus is a rare complication. Epileptic psychoses are uncommon and typically arise following a series of convulsive seizures. Psychological alterations are intense, reaching the level of amnestic-oligophasic dementia;

2) Classical. It begins during Puberty and is characterized by progressive paroxysms with convulsive and psychotic symptoms. At the onset of the disease, it presents with a polymorphic paroxysmal and deficit clinical picture. Against the background of profound epileptic personality changes, the paroxysmal symptoms regress or disappear completely;

3) Psychic. It typically starts between the ages of 17 and 30, presenting predominantly with minor psychopathological paroxysms. The psyche is affected in an affective manner, while intellectual functions remain largely intact. An increased frequency of psychic equivalents can lead to protracted epileptic psychosis;

4) Simple. This form is observed very rarely. Convulsive seizures and psychic equivalents do not occur, whereas alterations in intellect and character develop gradually. Patients seek medical attention specifically due to memory impairment and difficulties with social adaptation. Their Anamnesis indicates only isolated non-convulsive paroxysms;

5) Latent. There are no paroxysms, but the EEG reveals a focus of epileptiform activity. This form is also referred to as bioelectric.

Diagnosis

The diagnosis of epilepsy is straightforward if the clinical presentation reveals the aforementioned seizures, typical paroxysmal psychic disorders, and corresponding personality changes. In the absence of overt signs, diagnosis requires evaluating not only the polymorphic facultative manifestations of the disease, but above all, the specifics of its clinical course and obligatory signs. The latter include: sudden onset and self-termination of disorders, stereotyped recurrence and periodicity, short duration (seconds, minutes), and marked contrast to the patient's usual state of well-being ("strange, inexplicable behavior").

A single seizure should be interpreted as an epileptic reaction rather than epilepsy or epileptiform syndrome.

Epilepsy must be differentiated from hysteria, which is characterized by demonstrative symptoms, Variability, and their occurrence predominantly under the Influence of External triggers in the presence of other people. The encephalographic signs described above are absent in hysteria.

In early childhood, the clinical course of epilepsy can be mimicked by tonic and clonic convulsions in spasmophilia, which is characterized by calcium metabolism disorders, seasonality, laryngospasm, and Erb's, Trousseau's, and Chvostek's signs.

To prescribe treatment, it is essential to establish the underlying cause of the epileptiform syndrome (organic CNS lesion). The appearance of epileptiform symptoms during a somatic (e.g., infectious) process or its exacerbation rules out a diagnosis of genuine epilepsy.

Electroencephalographic data are of great diagnostic significance, particularly paroxysmal EEG changes. Interictal epileptic bioelectric activity is detected in 80–90% of patients with true epilepsy and in only 10–15% of those with symptomatic epilepsy.

Among the pathological types of electrical activity in epilepsy, the most frequently observed are: sporadic or multiple spikes as a typical manifestation of a focal discharge; sharp waves, usually detected within the epileptogenic focus; "sharp wave – slow wave" complexes (frequency of 2 Hz); "wave-spike" rhythm (frequency of 3 Hz); hypersynchronous fast rhythm; and slow waves of theta and delta oscillation types.

EEG changes in epilepsy can vary depending on the nature of Structural and functional impairments in different brain regions. A universally recognized feature is the absence of specific electroencephalographic curves unique to any single form. General manifestations of these changes include hypersynchrony and excessive amplitude (a 10- to 15-fold increase compared to baseline activity). A characteristic feature of the disease's course is the enhancement of pathological waves under the influence of additional stimuli (light, sound, hyperventilation, medication, etc.). For the diagnosis of epilepsy, surface Electroencephalography results alone are insufficient; these findings must be correlated with clinical observation data.

TREATMENT

Historically, the severity of epilepsy was determined primarily by the frequency, duration, and manifestations of paroxysms; consequently, treatment naturally focuses on suppressing seizures. The main principle of therapy for epilepsy patients is continuous, long-term (spanning many years), individualized, and comprehensive treatment. The goal is to achieve complete cessation of seizures for a period of 5 years. Only then can medications be gradually tapered and discontinued. Therapy is carried out chiefly on an outpatient basis. Inpatient treatment aims to determine the causes of epilepsy and, in severe cases, to select adequate drug doses and assess the body's response. Such treatment is best conducted in specialized centers or departments.

Individualized therapy entails: prescribing doses appropriate for each patient that reduce pathological mechanisms and enhance antiepileptic ones; establishing optimal dosages; and creating an effective combination of antiepileptic agents.

The dosage of a drug generally depends on the frequency and nature of the seizures. The higher the monthly seizure frequency, the higher the required dose. A. S. Remezova (1963) proposed a table correlating seizure frequency with the dosage of baseline medications.

Correlation between seizure frequency and drug dosage for adults and children (in parentheses)

Such dosages cannot be prescribed for all forms of epilepsy; they are established for patients with major convulsive seizures. Selecting an adequate dose at the onset of treatment is particularly important. However, during the course of therapy, it may become necessary to increase or decrease the dosage to ensure it remains adequate should the patient's condition change.

Convulsive seizure types are observed more frequently than others and, as most authors note, treatment for typical major convulsive seizures is the most effective.

For major convulsive seizures, finlepsin (tegretol), finlepsin retard, carbamazepine, karbasan, phenobarbital, convulex (sodium valproate, depakine chrono), hexamidine, diphenine, and benzonal are prescribed. For minor seizures, trimethadione, suxilep, ethosuximide, and diamox (fonurit, diacarb) are recommended.

For psychic paroxysms, neuroleptics (chlorpromazine, haloperidol, clopixol, fluanxol, risperidone, lyprexa, solian), tranquilizers (radedorm, tranxene, relatium, sibazon, seduxen, tazepam), and antidepressants (finlepsin, inriptiline, cipramil, prozac, chloracoin) are indicated. For the convulsive form, Sereisky's mixtures (phenobarbital, bromisoval, papaverine hydrochloride, caffeine-sodium benzoate, calcium gluconate) or Vorobyov's mixture (phenobarbital, diphenine, nicotinic acid, glutamic acid, spasmolitin, caffeine-sodium benzoate, glucose) are used. Tablet formulations such as "Glufederal" and "Pagluthe-ral" (containing phenobarbital, oromisoval, caffeine-sodium benzoate, and calcium gluconate) are also prescribed.

For autonomic paroxysms, Gromon's mixture, which includes seduxen, suprastin, and caffeine-sodium benzoate, is administered.

The comprehensive treatment regimen combines drugs that act on all pathogenetic links: a) anti-paroxysmal; b) resolvent; c) dehydrating; d) mild stimulants; e) desensitizing; f) multivitamins, Magne B₆, and berocca. Diet therapy and a regulated daily routine are also prescribed.

Additional information on epilepsy treatment

When selecting antieptic drugs, the type of epileptic seizure is the primary consideration.

Finlepsin (Finlepsin retard), carbamazepine, and karbasan are recommended for tonic-clonic paroxysms, while benzonal is indicated for partial motor seizures.

Valproates, ethosuximide, and trimethadione are more effective for absence seizures; sodium valproate is preferred for polymorphic seizures; and Finlepsin, carbamazepine, and karbasan are also superior for psychosensory seizures.

It is important to consider the pharmacokinetic properties of antiepileptic drugs. For instance, if the half-life is long (24 hours or more), as seen with phenobarbital, diphenylhydantoin, trimethadione, and ethosuximide, therapeutic blood concentrations are maintained with administration 1–2 times daily. Drugs with a half-life of up to 12 hours should be taken 3–4 times daily (hexamidine, benzonal, and valproic acid preparations).

Regarding seizure control, certain correlations have been established between the drug dosage and its concentration in Blood Plasma.

Toxic blood concentrations of antiepileptic drugs frequently fall within the therapeutic range. Therefore, the patient's somatic status must be continuously monitored, particularly regarding changes related to vitamin metabolism.

For morning seizures, stimulating psychostimulants are recommended to prevent the spread of excitation from the epileptic focus.

For sleep-related seizures caused by a deficiency in rapid eye movement (REM) sleep, carbamazepine (karbasan) and diphenylhydantoin are prescribed in combination with a-tryptophan (1.5–3.0 g twice daily).

The influence of endocrinological factors on treatment efficacy must also be taken into account. Since the estrogen-to-progesterone ratio varies depending on the menstrual phase, progesterone administration may be required for correction.

During pregnancy, blood concentrations of antiepileptic drugs often decrease, and this factor must likewise be accounted for.

Thyroid dysfunction typically increases epileptic activity, making the normalization of thyroid function crucial. Hypofunction disrupts metabolic processes, necessitating The Use of calcium supplements and thyreocalcitonin.

Epileptic activity increases during the prepubertal and pubertal periods, often requiring higher drug dosages.

Adverse drug reactions may occur during antiepileptic therapy, driven by their chemical and pharmacological properties. Such complications include aplastic and megaloblastic anemia (associated with hexamidine, diphenylhydantoin, trimethadione, and phenobarbital), hyperplastic gingivitis (diphenylhydantoin), lymphadenopathy (trimethadione, diphenylhydantoin), arthropathies (trimethadione, benzonal, hexamidine, phenobarbital), and Liver and Kidney damage (phenobarbital, hexamidine, diphenylhydantoin, carbamazepine). Folic acid prevents the development of megaloblastic anemia.

Vitamins and reduced doses of antiepileptic drugs are used to manage adverse effects. Antihistamines are prescribed for dermatological manifestations (rash, urticaria, photodermatitis).

Emergency management of status epilepticus requires the immediate Implementation of a set of measures, specifically: 1) preventing asphyxiation due to tongue obstruction, saliva aspiration, or vomiting; 2) halting convulsions; 3) managing cerebral edema; and 4) supporting cardiac function.

Treatment begins with the intravenous administration of sibazone (seduxen) — 2–4 ml of a 0.5% solution (up to 80 ml per day). This is followed, after a cleansing enema, by up to 60 ml of a 2% chloral hydrate solution in a starch mucilage or 30 ml of a 2% sodium barbital solution. Thirty minutes after the enema, 10–15 ml of a 25% magnesium sulfate solution is administered intramuscularly. Hexenal and sodium thiopental are prescribed if sibazone (seduxen) proves ineffective. Dissolve 1.0 g of hexenal or sodium thiopental in 10 ml of isotonic sodium chloride solution and administer 0.5 ml intramuscularly into each buttock. If seizures persist, intravenous sodium oxybate (10 ml of a 20% solution), diphenylhydantoin (250 mg dissolved in 50 ml of bidistilled water), methindione (10 ml of a 5% solution), or viadril (0.5 g dissolved in isotonic sodium chloride solution) should be administered.

When these measures fail, inhalation of nitrous oxide mixed with oxygen (a 2:1 ratio) should be initiated, and lumbar puncture should be considered. Anesthesia (at the level of surgical stages I–II) must be maintained for 1–2 hours after the cessation of status epilepticus. Anticonvulsants are combined with dehydration therapy (furosemide, urea, mannitol), alongside cardiac, detoxifying, and antihypertensive agents.

Antidepressants, antipsychotics, and tranquilizers are used to treat epileptic psychoses.

In many countries, Surgical treatment is prescribed when a localized epileptic focus is identified (V. I. Tsimlyuk et al., 1997). Experimental correction of cerebral seizure activity has been performed via embryonic neural tissue transplantation. This method has proven effective in treating a range of other conditions by restoring structural integrity and reversing functional deficits in the brain.

Optimal treatment outcomes, as well as primary, secondary, and tertiary Prevention, can be achieved by establishing a proper regimen of work and rest. Patients should avoid physical and mental overexertion, overheating, hypothermia, excessive sun exposure, infections, TRAUMATIC BRAIN INJURIES, and intoxications. It is important to follow recommendations such as limiting dietary fluids, salt, spicy seasonings, protein-rich foods (especially meat), and caffeine (coffee, cocoa, chocolate), while completely eliminating alcoholic beverages.

Primary prevention measures for epilepsy include: counseling individuals with this and other endogenous psychiatric disorders about the significant risk of passing the pathology on to their offspring before marriage; ensuring an uncomplicated course of Pregnancy and Childbirth; preventing and properly treating organic brain diseases; dispensary monitoring of patients with a history of epileptic or epileptiform reactions or markers; administering sedative and dehydrating therapy; and EEG monitoring.

As a primary prevention measure for epilepsy in the presence of early signs (epileptic markers), and to stabilize the disease course alongside appropriate dietary, general strengthening, and other measures, prolonged (up to 3 months) courses of sedative and anticonvulsant therapy are recommended.

Prognosis

In terms of recovery, the prognosis is often guarded. Complete remission is rarely achieved. Prolonged epilepsy leads to specific character changes and cognitive decline. The disease is also life-threatening due to accidents (head trauma, falls into water or fire, encounters with moving objects, electrical sources, falls from heights, etc.); suicidal behavior during dysphoric episodes; self-harm during twilight states; and fatal complications arising from status epilepticus.

Expert Evaluation

Medical and social evaluation aims to assess the level of social functioning in patients and develop a rehabilitation plan. A disability status is established in cases of prolonged convulsive and non-convulsive paroxysms and pronounced psychological impairment. However, patients should be rationally employed within reasonable limits, taking into account contraindications for certain types of occupational activities. Premature disability significantly reduces the level of clinical and social adaptation.

Military Expert Evaluation. In accordance with Article 22 of the Order of the Minister of Defense of Ukraine No. 2 dated January 4, 1994, "On Approval of the Regulation on Military Medical Examination and Medical Screening in the Armed Forces of Ukraine," individuals with epilepsy are deemed unfit for military service and are deregistered from the military.

Forensic Psychiatric Evaluation. If an offense is committed in a psychotic state, particularly with a twilight state of consciousness, or in cases of severe epileptic dementia, the individual is recognized as legally insane (not guilty by reason of insanity). In the event of a serious crime and the risk of recidivism, the court decides on the compulsory Treatment of the examinee. Patients with pronounced psychological deficits are declared legally incompetent, and a guardianship is established over them.

Review Questions

1. Definitions of epilepsy, Epidemiology, etiology, and pathogenesis.

2. Clinical presentation of generalized tonic-clonic seizures.

3. Minor epileptic paroxysms and their varieties.

4. Episodic psychotic states (psychic equivalents).

5. Status epilepticus, emergency care.

6. Epileptic personality traits. Early diagnosis of epilepsy, risk factors for epilepsy.

7. Intellectual-mnestic and emotional-volitional disorders in epilepsy.

8. Prevention, treatment, and rehabilitation in epilepsy.

9. Prognosis and expert evaluation in epilepsy.