|Year : 1999 | Volume
| Issue : 4 | Page : 332--3
Postictal mania following primary generalized seizures.
S Chakrabarti, VM Aga, R Singh
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India., India
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
A 29 year old male with primary generalized seizures for 13 years stopped his anticonvulsants leading to an increase in seizure frequency. Five months later he developed a severe manic episode postictally which responded well to a combination of neuroleptics and anticonvulsants. Postictal psychoses usually follow complex partial seizures. Manic episodes are uncommon. This case had some similarities with other cases of postictal psychoses reported previously. It underlines the need for further investigation of several facets of this complex relationship between mood disorders and epilepsy.
|How to cite this article:|
Chakrabarti S, Aga V M, Singh R. Postictal mania following primary generalized seizures. Neurol India 1999;47:332-3
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Chakrabarti S, Aga V M, Singh R. Postictal mania following primary generalized seizures. Neurol India [serial online] 1999 [cited 2021 Sep 27 ];47:332-3
Available from: https://www.neurologyindia.com/text.asp?1999/47/4/332/1575
Postictal psychosis, though a well recognized clinical entity, is relatively rare. Such psychotic states are usually associated with complex partial seizures. Psychotic episodes are preceded by an increase in seizure frequency and have a lucid interval before onset. Psychopathology is mainly polymorphic. Although abnormal mood states are common, well defined episodes of mania or hypomania are infrequent. A case of postictal mania following primary generalized seizures is reported below.
A 29 year old single trainee lawyer with no previous psychiatric problems was admitted to the in-patient unit with acute onset of irritability, grandiosity and violent behaviour. He had generalized tonic-clonic seizures for 13 years which were poorly controlled, despite having received various anticonvulsants. About 5 months before the onset of his current problems, he had stopped taking his drugs and tried indigenous medicines for a while. His seizures had become more frequent and he was noticed to have become a bit short tempered. Soon thereafter, he developed a full blown manic episode quite rapidly. He became extremely irritable, abusive and violent. He talked almost continuously, would argue with everyone and pick up Figurehts unnecessarily. He was very restless and hardly slept. He claimed that he was a famous advocate and commanded the local police force. He became excessively religious, believed he was Lord Shiva and wanted others to treat him likewise. He was not confused, disorientated or hallucinating. There was no family history of psychiatric problems and no particular psychosocial stressors. He had a seizure on the day of admission and for the first few days was uncooperative and aggressive. He refused food, drink and medicines. Treatment was initiated with parental lorazepam and haloperidol; and carbamazepine was added later. He improved significantly within a week, though he remained a bit irritable and occasionally voiced grandiose ideas. Lorazepam was discontinued. He was maintained on oral haloperidol (10mg/day) and carbamazepine (1200mg/day). The EEG was suggestive of primary generalized seizures, with no temporal lobe focus or evidence of status. CT showed a calcified disc lesion in the right caudate with no oedema; the ventricular system was prominent (VHR-0.4 : 1). Similar EEG and CT findings had been reported previously. The serology for neurocysticercosis was negative and other investigations were normal. His blood pressure was mildly raised, so he was started on enalapril maleate (5 mg/day). He remained as an inpatient for 3 weeks and was asymptomatic at discharge. Unfortunately he had a seizure immediately afterwards, although his manic symptoms did not recur. Sodium valproate was later added by the neurologists for more effective seizure control.
This patient had a postictal psychotic episode by virtue of developing psychotic symptoms in clear consciousness, of brief duration within a week of onset of seizures and in the absence of extraneous factors such as anticonvulsant toxicity, previous interictal psychosis, EEG evidence of minor status, and drug intoxication. The psychiatric diagnosis of this particular episode according to ICD-10 was mania with psychotic symptoms. The clinical profile was partly similar to earlier reports of mania or psychosis in the postictal period.,, This included onset of pychosis following increase in fit frequency and a lucid interval between seizures and the begining of psychosis. The sequence of events was set off by discontinuation of anticonvulsants. The role of anticonvulsant withdrawal in precipitating postictal psychosis is uncertain. Probably, the two are only indirectly related, i.e. withdrawal causes an increase in seizures which results in psychosis., A short duration, four weeks in this case, and a good response to a combination of neuroleptics and anticonvulsants are also frequently encountered in these episodes. Confusion, though common, is not invariable. This patient did not have any confusion or clouding of consciousness throughout his psychotic episode. There was no evidence of previous interictal pathology or family history of mental illness. The age at onset of epilepsy was 16 years and there was a gap of 13 years between this and the psychotic episode. Such clinical features are characteristic of the cases reported previously., There was a predominance of religious themes in this patient's symptoms, which also seems to be quite common. However, in most reported cases of postictal psychosis (or mania), the epilepsy is of complex partial type, while our patient had primary generalized seizures. The EEG done twice did not show a temporal lobe focus, however, temporal lobe foci cannot be ruled out entirely since specialized procedures like depth recording and video EEG were not done. Secondary generalization in cases of complex partial epilepsy does not seem to be necessary for emergence of postictal psychosis, although it has been reported in an overwhelming large number of cases; 11 of the 14 in one series and 8 out of 9 cases in another., Some authors suggest that spread of excitation involving several brain areas may contribute to development of psychosis. Thus, generalization may be a common predisposing factor which would explain the occurrence of postictal psychotic episodes even in primary generalized seizures, albeit with a lesser frequency. Mood disorders in epilepsy are said to be associated with right sided foci, though this has not been confirmed. A right sided calcified lesion was detected on CT in our patient, but its nature and relation to seizures or psychosis was not clear. Focal neuropathological lesions have been found to be a risk factor for psychosis, although in this case it is difficult to speculate on the role of structural lesions or possible brain damage in causing the psychotic episode.
Phenomenological pleomorphism is usual in postictal cases, but our patient had a relatively fixed picture which varied little with time. Seizures recurred after discharge but did not lead to an exacerbation in his psychosis. It remains to be seen whether he goes on to develop interictal symptoms, as a proportion of patients do.
This case illustrates that postictal manic episodes, though uncommon, can occur in primary generalized seizures. The clinical features appear to be no different from cases of postictal psychosis of varied phenomenology associated with complex partial seizures. The relationship between mood disorders and epilepsy is a complex one and certainly merits further investigation.
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