Differentiating between hysteria presenting in an epileptiform manner and epilepsy can present diagnostic difficulties. Differentiation is important, however, since management of the two disorders differs. Electrochemical stimulation of the medial basal hypothalamus in animal models increases prolactin release.' Therefore if the abnormal electrical activity in epilepsy passes through the midbrain it should raise the serum prolactin concentration. This paper reports an investigation of this hypothesis.Patients, methods, and results

Thirty newly diagnosed patients with Parkinson's disease and 30 patients with primary depressive illness showed slowing of response on a computerized digit symbol substitution test when compared with 30 matched normal control subjects. Significant slowing was related, in the parkinsonian patients, to structural brain disorder and affective impairment and, in the depressed patients, to motor impairment. A second computerized test, cognitively simpler but requiring the same motor response, was also administered to each subject. Both cognitive and motor slowing seemed to contribute to slowing of response in the digit symbol test in both parkinsonian and depressed patients. The tests were repeated after about six months in 12 subjects from each group. The parkinsonian patients, on dopaminergic treatment, showed neither significant change in motor or affective impairment, nor improvement in response time for the digit symbol test, but change in response time was related to change in depression rating. The depressed patients, on conventional treatment, showed significant improvement in both affective and motor impairment and improvement in response time for the digit symbol test, due to improvement in cognitive slowing. It is proposed that bradyphrenia in Parkinson's disease and psychomotor retardation in depressive illness are closely related, and that impairment of dopaminergic systems may be involved in both.

SUMMARY Postictal values of prolactin, LH To-date most information concerning endocrine changes following seizures derives from studies of electrochemically induced attacks in animals, and from electroconvulsive therapy (ECT) in patients. In rats, direct electrical stimulation of the medial basal hypothalamus has been shown to increase plasma prolactin levels.' In humans, Ohman et al2 first reported that ECT led to increases of serum prolactin in patients with endogenous depression, findings later confirmed by O'Dea et a13 and Trimble.' Arato et al noted similar findings following ECT in schizophrenia.Several investigators have now reported serum prolactin changes following epileptic seizures in patients. Trimble' in a study of nine patients with generalised epilepsy found prolactin levels to rise sharply after the ictus. Since similar rises were noted following unilateral ECT with anaesthesia and muscle relaxation, it was concluded that the changes were consequent on the epileptic activity itself. Abbott et a16 measured serum prolactin and cortisol levels in 26 patients after tonic-clonic seizures, and noted significant increases in both. In these studies, as in the recent reports from Hoppner et a17 and There are less data regarding the effects of seizure activity on gonadotrophin release in man. Ryan et a19 measured levels of gonadotrophins, thyroid stimulating hormone, and growth hormone in men and post-menopausal women after ECU, and noted a significant rise in FSH and LH in some of the males. Vigas et al'0 demonstrated a significant increase in serum LH levels after ECI in female psychiatric patients, although FSH was not affected.In this study we report further data on changes of prolactin and gonadotrophins following a variety of seizure types in patients with epilepsy. Materials and methodsSixty-four patients with epilepsy (42 males and 22 females) who were resident at the Chalfont Centre for Epilepsy, Chalfont St Peter, England, were studied. All subjects were receiving polytherapy with combinations of anticonvulsant drugs. Blood samples were drawn immediately, twenty minutes and one hour following a patient's seizure. A description of the seizure pattern was recorded at the time of the attack by a member of the nursing staff experienced at observing patients with epilepsy and was written on a card which accompanied the blood samples taken in relationship to the seizure. In addition, no fewer than four blood samples were obtained over a period of two hours from each patient during seizure-free intervals to assess baseline hormonal levels.

Laboratroy and clinical evidence indicates that tricyclic antidepressants lower seizure threshold and in high doses may induce generalised seizures. In baboons with photosensitive epilepsy (Papio papio) the effects of 2 tricyclic antidepressants (imipramine and chlorimipramine) and of maprotiline and Nomi fensine have been studied (i.v. dose range 1-20 mg/kg. Imipramine, chlorimipramine and maprotiline (10 mg/kg i.v.) lowered seizure threshold to a comparable extent, whereas Nomifensine (10 mg/kg i.v-) did not enhance myoclinic responses to photic stimulation. Generalised seizures were seen 15-30 min after imipramine or chlorimipramine (20 mg/kg), and these two drugs showed no difference in their epileptogenicity. Administration of 5-hydroxytryptophan (25 mg/kg i.v.) 90 min before chlorimipramine or imipramine (10 mg/kg) completely blocked the usual augmentation of photically-induced epileptic responses. It is concluded that enhancement of serotoninergic activity following blockade of 5-HT re-uptake within the brain is unlikely to be responsible for enhanced myoclonic responses and epileptogenic seizures seen after tricyclic antidepressants. Nomifensine is significantly less epileptogenic than imipramine or chlorimipramine.

No abstract