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We read with interest the editorial by Kennedy et al,1 detailing the short-term treatment of herpes simplex encephalitis (HSE). We agree with the authors that we cannot overemphasise the seriousness of the neuropsychiatric symptoms that a number of these patients display in the long term.
We report a 55 year old woman who was diagnosed with HSE; diagnosis was confirmed with a positive PCR test for herpes simplex in the CSF and acyclovir was started the following day after presentation. After a few weeks the patient’s recovery was almost complete and she was discharged home. Six months later, there was an abrupt change when the patient developed insomnia and would sit up all night watching children’s videos; she also became hostile and confused. She was admitted to a psychiatric unit where she continued to be confused and agitated with episodes of extreme behaviour such as undressing or trying to attack staff.
MRI showed appearances consistent with severe encephalomalacia of the right temporal lobe with evidence of gliosis in the frontal and temporal lobes consistent with previous HSE. It was surprising that the EEG tracing was normal with no focal or epileptiform features.
The patient remained in the psychiatric unit for seven months during which time she failed to respond to different antipsychotic medications and she was heavily sedated. The nursing staff reported that the patient was generally confused but there were distinctive episodes where the patient would stare and then display abusive and disruptive behaviour for periods of up to an hour once or twice a day. Carbamezepine was started and when the patient reached a dose of 400 mg twice daily these episodes ceased completely and the patient’s behaviour showed dramatic improvement. She continued to have mild cognitive impairment affecting mainly short-term memory.
Psychiatric problems after HSE are not uncommon; Hokkanen et al found that psychiatric problems are the main cause of long term disability in these patients.2 Despite the fact that clinical relapse of HSE is well documented,3 cognitive and psychiatric problems are usually already in place in the acute stage and further deterioration or relapse is uncommon.2 In our case the comparatively long period between recovery and onset of behavioural and psychiatric symptoms seemed to cast doubt about the association with the HSE and uncertainty regarding the appropriate treatment
Vallini et al reported successful treatment of a HSE patient presenting with severe emotional liability and explosive emotional outbursts.4 The patient responded to carbamezepine, which was started after his EEG showed seizure activity detected in temporal structures. Despite the absence of any EEG abnormalities in our case, it showed a similar favourable response to carbamezepine. We feel that any patient with intermittent behavioural or psychiatric symptoms after HSE should have a therapeutic trial of carbamazepine, even in the absence of any clinical or neurophysiological evidence of seizure activity.
Gaber and Eshiett report an interesting case of carbamazepine responsive neuropsychiatric syndrome after herpes simplex encephalitis (HSE). Neuropsychiatric symptoms after HSE are well recognised.1 The frontotemporal and limbic lesions in HSE are particularly likely to cause behavioural and psychiatric symptoms. Retrospective studies have previously implicated HSE in the delayed syndromes of violent psychoses2 and major depression.3 However, psychiatric disorders are also common after non-herpes virus encephalitis. Hunter and others had emphasised the importance of considering encephalitic antecedents, even if clinically unapparent, in the differential diagnosis of psychiatric patients.4 Long term follow up data from the National Childhood Encephalopathy study have shown more recently that 20% of the affected children developed epilepsy and a similar proportion had behavioural problems, hyperactivity or unsociable behaviour.5
Besides being a first line antiepileptic, carbamazepine is also recognised to possess considerable therapeutic value in certain psychoses and is an effective long term treatment for bipolar disorder in some cases.6 Carbamazepine responsiveness in this particular case may not, therefore, imply that the psychiatric symptoms were epileptic in origin. However, EEG signatures of epilepsy are often absent interictally, and the presence of psychoses is known to normalise EEG changes (“forced normalisation”) in epilepsy patients.7 In this particular case, we certainly concur with the authors’ use of carbamazepine and were delighted to learn of the favourable response.
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