Table of Contents

Epilepsy and Psychiatry


Epilepsy is the most common serious neurological condition. New cases arise at a rate of 50-70 cases per year of causes not including febrile seizures. The greatest number arise in young children and the elderly.

At any time there is around 5-10 people with epilepsy among 1000 persons of the population. The lifetime prevalence (percentage of people who had epilepsy at any time during their life) is  2-5% of the population. The condition is slightly more common in males than females and slightly more common in lower social classes.

Frequency of seizure activity in population

A third of patients has less than one seizure per year. Another third has 1-12 seizures per year and the remaining has more than 1 seizure per month. Two third of people with active epilepsy also have other neuropsychiatric problems such as learning difficulty, behavioural disturbance, discrete cognitive impairment and focal neurological deficit.

Classification of Seizures

A) Primary Generalised Epilepsy

Widespread involvement of both hemispheres simultaneously lead to this type of seizure. The exact mechanism is usually unknown.

Clinical Manifestations:

In Generalise Grand Mal seizures:

  • Sudden loss of consciousness
  • Tonic phase (EEG- 8-12/sec high amplitude spikes)
  • Clonic phase (EEG - as above but interrupted by slow waves)
  • Phase of sleep or disorientation (EEG shows low amplitude delta waves)

B) In Petit Mal

There are absence attacks of altered consciousness EEG - 3 cycles/seconds spike and wave complexes.

C) Atonic seizure

- causing loss of muscle tone

D) Partial Epilepsies:

A focal epileptogenic activity in the brain gives rise to symptoms reflecting function of area involved. If the activity \'progresses\' to involve motor areas patients may get a secondary generalised seizure.

1. Simple Partial Seizures:

There is no loss of consciousness with motor or sensory disturbance. The lesion is in the primary cortex.

2. Complex Partial Seizures:

There is altered consciousness and disturbance of higher mental function. The lesion is usually in the association cortex or limbic system.

Occurrence of seizures types in population

40% primary generalised tonic-clonic seizures

20% secondary generalised tonic-clonic seizures

20% complex partial seizures

12% mixed tonic-clonic and partial seizures

3% simple partial seizures

5% absence and other types

Epileptic Auras

Psychological or neurological symptoms may appear immediately before onset of a seizure as the early seizure activity arising from the epileptic focus before any progression. Changes arising from frontal lobe appear in the form of motor symptoms such as discrete movements or speech arrest. Temporal lobe symptoms involve psychomotor changes similar to temporal lobe epileptic phenomena or autonomic symptoms such as epigastric discomfort, salivation, flushing or vertigo. Parietal lobe foci give sensory symptoms and disorders of body image. The occipital lobe auras take the form of visual disturbances such as areas of changes in the visual fields (scotomata) or simple visual hallucinations.

Changes in the limbic areas lead to psycho-sensory phenomena such as illusions, hallucinations, depersonalisation, or deja vu experience.

Cognitive aural symptoms include disturbance of speech, thought and memory while affective symptoms may show as fear, anxiety, depression, or rarely pleasure.

Psychomotor Epilepsy

This is manifested as complex behaviours representing ongoing epileptic discharge which does not necessarily arise from a temporal lobe focus. It takes the form of:

  • Automatisms : which last for minutes and may be part of ictal or post-ictal phases. It involves impaired consciousness, simple or complex movements and amnesia.
  • Fugue : this may last for hours or days. It may be post-ictal and involves impaired consciousness, abnormal complex behaviour and also amnesia.
  • Twilight States: which takes hours in duration and may occur in ictal or post-ictal phases in the form of impaired consciousness, cognitive and affective changes, delusions and hallucinations followed by partia1 recall of events.
  • Petit Mal Status Epilepticus: This may be for minutes to hours in duration and occur in ictal phase. During which there is speech perseveration, incoordination, psychomotor slowing and is terminated by environmental stimuli. It is followed by amnesia.

Aetiology of Epilepsy

The Clinical-Pathological Basis of Epilepsy:

The cause of epilepsy may be obscure (cryptogenic) due to minor congenital anomalies in the brain which are difficult to establish by traditional investigations such as a CT scan, although the abnormal brain activity may appear in an EEG (electro-encephalography which is a printed tracing of the brain waves detected by electrodes attached to the scalp of the head). This is usually the case in primary epilepsy.

There is a genetic basis for such abnormality leading to a neuronal developmental defects.

15%of cases of epilepsy are due to cerebrovascular disease in the brain. 6% of cases are alcohol related, and 3% are post-traumatic (following head injury), 3% post-infective ( for example after meningitis). Other causes of secondary epilepsy are neuro-developmental disorders, neurodegenerative disease, tumours, and metabolic disorders.

Cellular and Molecular and Basis of Epilepsy:

Epilepsy is the result of excessively synchronous discharge of an aggregate of neurones. Some of the hypothetical causes include:

A. Disorder of neuronal migration:

This may occur due to a genetic cause or intrauterine infection such as cytomegalovirus (CMV). For example in temporal lobe epilepsy, it is suggested that heterotopia (misplacement and displacement of cells from their programmed locations in the brain) leads to clusters of abnormal neurones in the sub-cortical white matter. In primary generalised epilepsy, there is a postulated microdysgenesis (microscopic malformation of cortical development characterized by heterotopic neurones and abnormal cortical architecture).

B. Mesial temporal sclerosis:

This is a selective loss of pyramidal neurones in CAl, CA3 and CA4 subfields of hippocampus. It is a common finding at post mortem examination of institutionalised epileptic patients and also in anterior temporal lobectomy. It is caused by uncurbed seizure activity during brain development. More than half of patients with mesial sclerosis have history of prolonged febrile convulsions in infancy. Cell loss causes secondary regenerative changes promoting focal epileptogenesis later in life. The excessive neuronal sprouting alters excitatory/inhibitory neuronal balance.

C. Decreased GABA Inhibitory Neurotransmission:

GABA (Gamma-Amino-Butyric Acid) is the major inhibitory neurotransmitter system in the brain. Its neurones has long tracts and it is also abundant in interneurones. In hippocampus and cerebral cortex, recurrent GABA interneurones prevent excessively sustained discharge from principle neurones. Drugs blocking GABA transmission are epileptogenic. Benzodiazepines bind to a site on GABA receptor and promote action of GABA and thus act as anti-epileptics.

Genetic deficiency of GABA synthesis occurs in hereditary pyridoxine dependent convulsions in infants.

Alumina (Aluminium oxide) is used to induce experimental epilepsy by applying it directly to the cortex of experimental animals such as monkey cortex. Studies have found specific loss of GABA neurones and consequent seizures following application of Alumina Cream.

D. Increased Glutamate Excitatory Neurotransmission:

Glutamate is an excitatory neurotransmitter with several receptor types such as NMDA, kainate receptors. NMDA receptor antagonists are anticonvulsants in animal models. There is evidence of increased kainate and NMDA receptors in hippocampi of temporal lobectomy specimens. There is also some evidence of enhanced sensitivity of NMDA receptors in humans with Temporal Lobe Epilepsy.

E. Membrane Conductance Abnormalities:

Calcium conductance contributes to the rhythmic firing in thalamus area of the brain. Calcium is probably involved in the 3 cycles/second spike and wave activity characteristic of absence seizures. Calcium conductance is reduced by ethosuximide, a drug which is specific for control of absence seizures.

Psychiatric Disorders in Epilepsy

A. Disorders due to brain damage also causing seizures:

Some conditions may contribute to both Epilepsy and the psychiatric disorder.

  • Neurodegenerative disorders e.g. Alzheimer\'s disease
  • Focal brain injury e.g. tumour, head injury
  • Neurodevelopmental syndromes e.g. infantile spasms, Lennox Gastaut,tuberous sclerosis

Pre-ictal phenomena occurring before the seizure (prodroma) may involve mood change, irritability. The ictal events such as auras of complex partial seizures and post-ictal phenomena such as twighlight states has to be differentiated from psychiatric conditions presenting with a similar picture.

C. Inter-ictal disorders:

Patients with epilepsy may show behavioural changes which are not directly related to the seizures themselves. There is evidence of enduring personality change in life-long epilepsy and some patients may develop a psychotic disorder, sometimes referred to a Epileptic psychosis.

D. Pseudo-seizures

Some clinicians have described a Temporal Lobe Personality Syndrome. Its features include emotionality, with mood changes such as elation and euphoria, sadness, anger, aggression, altered sexual interest. Guilt, very high standard of morals, obsessionality, circumstantiality, resistance to change (viscosity) and a sense of personal destiny. Other features also described in this syndrome include overwhelming urge to write (hypergraphia), religiosity and excessive philosophical interest. The person is usually humourless, and sometimes paranoid or suspicious.

Temporal Lobe Epilepsy and Aggression:

During an automatism, epileptic patients may be aggressive and commit acts of violence. Inter-ictal aggression has been reported in a third of lobectomy patients. Aggression is found more in teenage male epileptics and more in those with left-sided focus of abnormality in the brain. There is evidence of improvement of seizures and aggression following surgery to remove an epileptic focus.

Epileptic Psychoses

A. Directly related to seizures: Symptoms may be similar twilight states. B. Inter-ictal:

Different forms of psychosis may appear in epileptic patients. Transient schizo-affective or affective states, chronic schizophrenia like state are described. 10-15% poorly controlled patients with temporal lobe epilepsy receive the diagnosis of schizophrenia or schizophrenia-like psychosis. This is associated usually with a left-sided focus. In a study of 69 patients with unequivocal epilepsy and subsequent diagnosis of epileptic psychosis, their psychosis have developed after a mean of 14 years following the onset of epilepsy. There is no family history of schizophrenia or history of schizotypal personality traits in the family. Brain damage was found in 50% of cases. Most of these patients had temporal lobe epilepsy. Psychosis was not related to severity of epilepsy or use of medication.

The schizophrenia-like symptoms include paranoid delusions (100%), thought disorder (50%), auditory hallucinations (46%), thought insertion and thought block. However, unlike schizophrenia, Patients have more mystical or religious content, more visual hallucinations (16%), warm affect, their personality is well preserved, and they have good social function.


These are psychogenic seizures, sometimes called hysterical seizures or non-epileptic seizures. They represent up to 20% of referrals to neurology. The view that it is unlikely to occur in those who have not experienced true epilepsy is contentious. There is history of frequent hospital admissions and social problems. There is current or past history of psychiatric disorder especially depression. There may be also history of attempted suicide, sexual maladjustment and sometimes history of extreme childhood adversities such as abuse (10-15%). It is commoner in organic brain disease including mental retardation.

Clinical features:

The patient presents with out of phase limb movements, unresponsive behaviour, side to side head movements, pelvic thrusting, and there is no post-ictal neurological signs. There is also no incontinence or evidence of self harm. Blood tests show prolactin levels are not raised. It is sometimes difficult to distinguish pseudoseizures from frontal lobe seizures.