The main indication for use of physostigmine is treatment of anticholinergic coma after anaesthesia and intoxication. Generalized epileptic seizures are known complications of physostigmine, whereas focal seizures and non-convulsive status epilepticus (NCSE) have not been described as complications in this setting [1]. Epileptic nystagmus (EN) is a rare clinical sign of seizures defined as repetitive jerking of the eyes secondary to epileptic activity. EN usually occurs as horizontal nystagmus with its fast phase beating away from the epileptogenic hemisphere [2]. Purely vertical beating EN on the contrary is unusual and has been described only a few times in the setting of bilateral epileptic activity [3]. We present a patient in whom cholinergic treatment with physostigmine resulted in right occipital NCSE presenting with upbeat nystagmus and prolonged impairment of consciousness documented on video electroencephalogram (EEG). A 66-year-old woman with history of drug abuse for analgetics and hypnotics but no history of epilepsy was admitted to our intensive care unit presenting with coma [Glasgow Coma Score (GCS) 8, eye 2/verbal 2/motor 4]. Initial computed tomography (CT) scan, CT angiography and perfusion CT revealed no causative abnormalities. An immediate EEG showed severe encephalopathy. On physical examination, signs suggestive of an anticholinergic syndrome (dry skin, dilated pupils and urinary retention) were found, and drug intoxication was suspected. Under continuous EEG recordings, two repeated doses of 1 mg intravenous physostigmine were administered, leading to a right occipital EEG status pattern associated with upbeat nystagmus, as shown in the figure and animation (Fig. 1, online resources 1 and 2). The time relationship between the occipital spikes and the fast phase of the nystagmus was constant at about 100 ms. The patient remained unresponsive. With another 2 mg lorazepam, nystagmus ceased, paralleled by remission of the right occipital EEG status pattern. The patient regained consciousness and was amenable to further treatment (GCS 14, eye 4/verbal4/motor 6). Systemic application of physostigmine may typically lead to generalized epileptic seizures. Our patient showed focal seizure activity. Interestingly, consciousness remained impaired, although physostigmine is expected to raise the level of consciousness immediately in case of anticholinergic coma. We think that NCSE at this moment prevented full recovery in the present case, because GCS improved to nearnormal values after termination of NCSE by lorazepam. The clinical presentation of NCSE generally depends on the cortical area(s) involved. Symptoms may range from very discrete alterations in normal behaviour to alterations in the level of consciousness [4]. Impairment of consciousness may result from widespread unilateral and bilateral seizure discharge. However, there are reports of complete loss of consciousness with lateralized epileptic discharge only (for review, see [5]). It is important to note that epileptic discharge did not occur strictly unilaterally in the present case. However, this does not equate to generalized epileptic seizure. Just in the occipital lobe, epileptic discharge spreads rapidly to contralateral homologous areas via the corpus callosum with predominance on one side [6]. Electronic supplementary material The online version of this article (doi:10.1007/s00415-011-6257-9) contains supplementary material, which is available to authorized users.
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