Please confirm that your email address is correct, so you can successfully receive this alert.
SIR: The World Health Organization defines a stroke as rapidly developing clinical signs of a focal (or global) disturbance of the cerebral function, with symptoms lasting 24 hours or longer or leading to death, with no apparent cause other than of vascular origin. A stroke represents a major public health problem, but relatively little work has been directed toward identifying and treating the common neuropsychiatric disorders occurring after stroke.1 Psychosis is a rare complication of stroke, while 2% to 7% people with epilepsy have been reported to suffer from psychosis. The prevalence of psychosis in patients with temporal lobe epilepsy and/or refractory epilepsy varies from 10% to 19%, in most studies.2 Forced normalization is often observed in psychosis of epilepsy. In 1953, Landolt3 described a group of patients with poorly controlled epilepsy who had psychotic episodes associated with the remission of their seizures and the disappearance of epileptiform activity on their EEGs. He called this phenomenon "forced normalization." Upon suppression of seizures, some patients with interictal psychosis may require modification of the antiepileptic medication which is responsible for the excessive inhibition of seizures.4,5 We herein report a case of interictal psychosis which developed after stroke with forced normalization.
A 56-year-old right-handed woman had her first seizure when she was 24 years old. Her natal, perinatal, and previous medical histories were unremarkable. There were no past or family histories of neuropsychiatric disorders. Her seizure type was of complex partial seizures evolving into generalized tonic-clonic seizures. Immediately after the first epileptic seizure, she was referred to the neuropsychiatric department of our hospital for the first time and treatment with antiepileptic drugs was started. Her epileptic seizures were refractory and occurred a few times a week after the long and adequate treatment with antiepileptic drugs (carbamazepine, 1100 mg/day; phenytoin, 325 mg/day; clobazam, 20 mg/day). An EEG demonstrated a 9 Hz basic rhythm activity with many spike and slow wave activities in the left temporal lesion while no definite MRI abnormality was observed. At 55 years of age, she awoke with headache, dizziness, and dysarthria. As these symptoms persisted, she was admitted to the neurological department of our hospital. A magnetic resonance imaging (MRI) scan demonstrated a cortico-subcortical infarction in the left temporal and parietal region. Antiepileptic drugs were not altered after her stroke. About 4 months after her stroke, when no residual symptoms of her stroke remained, she experienced auditory hallucinations that spoke ill of her for the first time. She was very anxious and afraid of the people around her. She was readmitted to the neuropsychiatric department of our hospital and a regimen of haloperidol (4.5 mg/day) was prescribed for the treatment of her psychotic symptoms. About 6 months later, she was discharged from our hospital. Although she still experiences the auditory hallucinations that speak ill of her, they are mild enough as to not disturb her activities of daily living. On the other hand, no epileptic seizures or epileptiform activities on her EEG after her stroke have been observed for 18 months up until the present time.
The occurrence of psychotic episodes independent of the stroke in this case may be a possibility regarding the cause of this patient’s symptoms. It seems unlikely because no psychotic episodes had been observed for 31 years after the onset of epileptic seizures while they appeared only 4 months after her stroke. Psychosis has been reported to develop an average of 14 years after the onset of epileptic seizures.6 Moreover, psychotic episodes after her stroke were associated with the remission of epileptic seizures and the disappearance of any epileptiform activity on the EEGs, which correspond to the clinical criteria recently proposed for the diagnosis of forced normalization.5 The occurrence of psychotic episodes due to a stroke independent of epilepsy may also be a possibility in this case. However, it seems unlikely because psychosis has been reported to be an extremely rare complication of stroke and there have been only a few reports on psychosis due to stroke, all of which suggested an association between a right hemisphere stroke and a schizophreniform disorder.6—11 The reason why forced normalization was observed after stroke in this case is unclear. In the first place, the mechanism of forced normalization is still poorly understood although the kindling phenomenon, the phenomenon of long-term potentiation, and the channel disorder paradigm have all been proposed as viable animal models for forced normalization.4 With the development of new and powerful antipsychotic drugs and other treatments with the propensity to switch off seizures, the development of psychosis associated with forced normalization is therefore expected to become a more and more frequently encountered problem. The present case may help to clarify the mechanism of forced normalization, while providing some helpful suggestions regarding the diagnosis and the treatment of the psychotic symptoms observed in a stroke.
Download citation file:
Web of Science® Times Cited: 2