The possibility that so‐called anti‐epileptic drugs (AEDs) may aggravate epilepsy must always be borne in mind by the clinician. Many reports of such aggravation of seizures have been published. Most such reports are anecdotal and speculative, and suggest that many such reactions are idiosyncratic. However, for some there is a sufficient body of evidence to suggest that some AEDs used in certain epilepsies may consistently cause worsening of seizures. Seizure aggravation may include increase in the frequency or severity of existing seizures, emergence of new types of seizure, or the occurrence of status epilepticus. The pathophysiology of seizure aggravation is poorly understood including nonspecific effects such as those associated with sedation, druginduced encephalopathy, and paradoxical or inverse pharmacodynamic effects. For some epilepsies the choice of AEDs may be inappropriate, and although the mechanism of seizure aggravation is not clear, its occurrence may be fairly predictable. This is best documented for the use of carbamazepine in idiopathic generalized and myoclonic epilepsies. Most other AEDs have been reported occasionally to cause seizure aggravation. The lowest risk of seizure aggravation appears to be with valproate. Risk factors for worsening of seizures are epileptic encephalopathy, polytherapy, high frequency of seizures, and cognitive impairment. Advances in pharmacogenomics may in the future enable such adverse effects to be predicted for individual patients. Meanwhile, a systematic approach to reporting AED‐induced seizure aggravation should be developed.

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SUMMARY Intracerebral haemorrhage is rare in childhood. We have reviewed the last 10 years' experience, in our referral area, of parenchymatous intracerebral haemorrhage in children from 1 month to 16 years of age. There were 27 cases, five of which were intracerebellar and two predominantly intraventricular. The commonest aetiology was vascular malformation (10), followed by haemorrhage into tumour (four), and coagulopathies (five).Clinical features were non-specific, but altered consciousness, headache, vomiting, and focal signs were the most common. Focal signs were, however, rare in the patients with intracerebellar haemorrhage. There was an overall mortality of 54% (14 out of 27). Nine patients were handicapped on follow up, but none severely so. For the diagnosis of intracerebral haemorrhage a high level of clinical suspicion is needed with early use of computed tomography. Maintenance of homeostasis, relief of raised intracranial pressure, and evacuation of haematoma are the aims of management.

Summary.Vincristine is an anti-neoplastic agent for intravenous use. Inadvertent intrathecal administration of vincristine tends to follow a predictable clinical sequence of a progressive ascending radiculomyeloencephalopathy, usually fatal in outcome. We report a case of a 10-year-old girl who suffered an inadvertent intrathecal vincristine administration. We have outlined the management strategy used and her consequent neurological progress. She has survived but with a significant neurological deficit. Her outcome is, however, less severe than in previous literature reports; this may in part be attributable to early aggressive neurological management. This case also serves to highlight the tragic consequences of human error when handling chemotherapeutic agents of this nature.