Status epilepticus

Psychotic disorders in patients with epilepsy

Patients with epilepsy are highly prone to developing acute psychotic states characterized by a wide variety of clinical presentations. Psychoses may occur before the onset of a convulsive seizure, follow it, or develop completely independently of paroxysms.

Main types of acute epileptic psychoses:

• Twilight states. Proceed with prominent productive symptoms. Patients may exhibit pronounced aggression, experience hallucinations and delusions, and be in a state of severe agitation. The most crucial feature is that upon emerging from the psychosis, total amnesia sets in, and the patient has no recollection of what happened.
• Paroxysmal psychoses. Unlike twilight states, memory is preserved in this form. The clinical picture often resembles oneiroid syndrome with fantastic, frequently religious experiences. The patient may exhibit illusions, fragmented visual or auditory hallucinations, phenomena of psychic automatism, and unsystematized delusions (most commonly delusions of persecution).

Differential diagnosis Epileptic psychoses must be distinguished from schizophrenia. The following point in favor of epilepsy:

1. Extremely sharp, sudden onset.
2. Short duration of the episode (from half an hour to several days).
3. Stereotyped repetition of seizures in a specific patient.
4. Absence of negative symptoms typical of the schizophrenic process (emotional flattening, apathy, autism).

Chronic psychoses in this condition are rare. When they do occur, they are usually limited to everyday delusions, less frequently ideas of reference or religious delusions. As for the affective sphere, depression is typical for patients, manifesting as dysphoria—a state of gloomy discontent, irritability, grumbling, and malice.

Patterns of the course of epilepsy

The disease typically has a progressive nature. Over time, patients experience an increased frequency of seizures, new types of paroxysms, a gradual decline in intellect, and the accumulation of specific personality changes (epileptic personality defect).

The rate of progression varies widely. There are both highly malignant forms leading to rapid loss of working capacity and severe dementia, as well as quite favorable variants (especially among juvenile and childhood forms) where the individual maintains their profession and social connections.

Criteria for a favorable prognosis:

• Onset of the disease between 5 and 13 years of age.
• Development of generalized tonic-clonic seizures or typical absences without a preceding aura.
• Sufficiency of treatment with a single antiepileptic drug (successful monotherapy).
• Familial nature of the pathology or idiopathic form (when there is no history of clear brain damage).
• Normal interictal electroencephalogram (EEG) findings.
• Absence of mental retardation and neurological deficit.

Disease development factors

Epilepsy develops under the influence of multiple causes. External (exogenous) factors play a significant role: severe infectious diseases, traumatic brain injuries, complicated pregnancy, and pathological labor.

However, a direct connection is far from always apparent. There is a paradox: even massive brain trauma may not lead to epilepsy, and overall there is no strict correlation between the volume of nervous tissue damage and the risk of seizures. Furthermore, the onset of the disease can occur years after the harmful factor exposure, and in every sixth patient (about 15% of cases), the cause cannot be found at all even upon deep examination.

The genetic factor also matters, although the inheritance mechanisms are complex and not fully understood. The transmission type has been accurately established for only a few specific forms (for example, benign neonatal convulsions). At the same time, in monozygotic twins, the probability of both developing the disease (concordance) reaches 48–83%, which significantly exceeds the figures for dizygotic twins.

Convulsive states in severe poisoning

Epileptiform seizures and convulsive syndromes can act as a formidable complication in psychoactive drug intoxication.

• Stimulants (cocaine). Poisoning is accompanied by severe neuropsychiatric disorders: delirium, aggression, hyperreflexia, and the development of pronounced convulsive seizures. This condition requires immediate relief with tranquilizers (diazepam).
• Tricyclic antidepressants. Intoxication often leads to the patient entering a coma preceded by extreme agitation and convulsions.
• Barbiturates and sleeping pills. In severe poisonings, a comatose state develops. It is important to remember the strictest rule of antidotal therapy: the specific drug bemegride is strictly contraindicated to administer to a patient who has already fallen into a coma, as this directly provokes severe epileptic seizures.
• Opioids. Lead to profound respiratory depression. Against the background of oxygen starvation, both clonic and tonic seizures can develop.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Clinical picture and phases of development of a classical convulsive seizure
• Specific EEG changes in various forms of epilepsy
• Methods for stopping acute status epilepticus
• Extrapyramidal disorders in toxic brain lesions
• Detoxification algorithms for tricyclic antidepressant overdose

Other topics in "Chapter 20. Epilepsy"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.