Japanese encephalitis (JE) causes at least 10 000 deaths each year. Death is presumed to result from infection, dysfunction and destruction of neurons. There is no antiviral treatment. Seizures and raised intracranial pressure (ICP) are potentially treatable complications, but their importance in the pathophysiology of JE is unknown. Between 1994 and 1997 we prospectively studied patients with suspected CNS infections referred to an infectious disease referral hospital in Ho Chi Minh City, Vietnam. We diagnosed Japanese encephalitis virus (JEV), using antibody detection, culture of serum and CSF, and immunohistochemistry of autopsy material. We observed patients for seizures and clinical signs of brainstem herniation, measured CSF opening pressures (OP) and, on a subset of patients, performed EEGs. Of 555 patients with suspected CNS infections, 144 (26%) were infected with JEV (134 children and 10 adults). Seventeen (12%) patients died and 33 (23%) had severe sequelae. Of the 40 patients with witnessed seizures, 24 (62%) died or had severe sequelae, compared with 26 (14%) of 104 with no witnessed seizures [odds ratio (OR) 4.50, 95% confidence interval (CI) 1.94-10.52, P < 0.0001]. Patients in status epilepticus (n = 25), including 15 with subtle motor seizures, were more likely to die than those with other seizures (P = 0.003). Patients with seizures were more likely to have an elevated CSF OP (P = 0.033) and to develop brainstem signs compatible with herniation syndromes (P < 0.0001). Of 11 patients with CSF OP > or =25 cm, five (46%) died, compared with seven (9%) of 80 patients with lower pressures [OR 8.69, 95% CI 1.73-45.39, P = 0.005). Of the 50 patients with a poor outcome, 35 (70%) had signs compatible with herniation syndromes (including 19 with signs of rostro-caudal progression), compared with nine (10%) of those with better outcomes (P < 0.0001). Of 11 patients with CSF OP > or =25 cm, five (46%) died, compared with seven (9%) of 80 patients with lower pressures (OR 8.69, 95% CI 1.73-45.39, P = 0.005). The combination of coma, multiple seizures, brainstem signs and illness for 7 or more days was an accurate predictor of outcome, correctly identifying 42 (84%) of 50 patients with a poor outcome and 82 (87%) of 94 with a better outcome. These findings suggest that in JE, seizures and raised ICP may be important causes of death. The outcome may be improved by measures aimed at controlling these secondary complications.

Prolonged, multiple seizures complicate a high proportion of cases of childhood cerebral malaria, and several studies have shown an association between these and neurological sequelae. We prospectively studied 65 patients (38 female) admitted to Kilifi Hospital in 1994. Electroencephalographic recordings (EEGs) were made at 12-hourly intervals, with continuous recordings made on a cerebral function analysing monitor (CFAM). Survivors were seen one month after discharge. Cerebral computerized tomography was performed on children with neurological sequelae. Sixty-two percent of patients had seizures following admission, of whom half had an episode of status epilepticus. Fifty-two percent of seizures were partial motor, 34% generalized tonic-clonic, and 14% partial with secondary generalization. In 22%, coma appeared to be due to a prolonged postictal state. Ten children had subtle motor seizures. Posterior parieto-temporal discharges were the most common EEG finding. Seven children died, eight developed neurological sequelae, and 50 (77%) recovered fully. Status epilepticus was associated with the development of neurological sequelae. Prolonged, multiple seizures may play an important part in the pathogenesis of coma in childhood cerebral malaria, and are likely to contribute to both the morbidity and mortality of this disease.

This is a prospective study of 107 repairs of obstetric brachial plexus palsy carried out between January 1990 and December 1999. The results in 100 children are presented. In partial lesions operation was advised when paralysis of abduction of the shoulder and of flexion of the elbow persisted after the age of three months and neurophysiological investigations predicted a poor prognosis. Operation was carried out earlier at about two months in complete lesions showing no sign of clinical recovery and with unfavourable neurophysiological investigations. Twelve children presented at the age of 12 months or more; in three more repair was undertaken after earlier unsuccessful neurolysis. The median age at operation was four months, the mean seven months and a total of 237 spinal nerves were repaired. The mean duration of follow-up after operation was 85 months (30 to 152). Good results were obtained in 33% of repairs of C5, in 55% of C6, in 24% of C7 and in 57% of operations on C8 and T1. No statistical difference was seen between a repair of C5 by graft or nerve transfer. Posterior dislocation of the shoulder was observed in 30 cases. All were successfully relocated after the age of one year. In these children the results of repairs of C5 were reduced by a mean of 0.8 on the Gilbert score and 1.6 on the Mallett score. Pre-operative electrodiagnosis is a reliable indicator of the depth of the lesion and of the outcome after repair. Intra-operative somatosensory evoked potentials were helpful in the detection of occult intradural (pre-ganglionic) injury.

Background-Seizures are a prominent feature of childhood cerebral malaria, and are associated with an increased risk of death and neurological sequelae. We present the electroencephalographic (EEG) findings from a detailed clinical and electrophysiological study. Methods-Children with cerebral malaria had EEGs recorded within six hours of admission, and at 12 hourly intervals until recovery of consciousness. Ten deeply comatose children underwent intracranial pressure monitoring. Children were not mechanically ventilated, which made it possible to directly correlate the clinical and EEG findings. Results-Of 65 children aged 9 months and above, 40 had one or more seizures, and 18 had an episode of status epilepticus. Most seizures were partial motor, and spike wave activity consistently arose from the posterior temporo-parietal region, a border zone area lying between territories supplied by the carotid and vertebrobasilar circulations. Fifteen children had seizures that were clinically subtle or electrographic. Clinical seizures were associated with an abrupt rise in intracranial pressure. Fifty children recovered fully, seven died, and eight had persistent neurological sequelae. Initial EEG recordings of very slow frequency, or with background asymmetry, burst suppression, or interictal discharges, were associated with an adverse outcome. Conclusions-Serial EEG recording has uncovered a range of clinical, subtle, and electrographic seizures complicating childhood cerebral malaria, and has emphasised their importance in the pathogenesis of coma. Further work is required to determine the most appropriate regimen for the prophylaxis and treatment of seizures in cerebral malaria, in order to improve outcome. (Arch Dis Child 2001;84:247-253) Keywords: cerebral malaria; coma; seizures; electroencephalogram Cerebral malaria, a diVuse encephalopathy caused by Plasmodium falciparum, remains a major cause of death and disability in subSaharan Africa.1 The pathophysiology of the disease is complex and poorly understood. 6-8 Despite their importance, and in common with many other causes of childhood coma, there have been few descriptions of the clinical and electroencephalographic features of seizures in cerebral malaria. Electroencephalography (EEG) can supply the clinician with information on the origin and distribution of seizure activity, detect subtle or subclinical seizures, and may reveal abnormal electrical activity of prognostic significance.9 It is therefore of potential value in the clinical management of cerebral malaria, and may improve understanding of the underlying pathophysiology. Here we present the EEG findings from a detailed clinical and electrophysiological study of 65 children with cerebral malaria. 5 Methods STUDY SITEThe study was conducted at the Kenya Medical Research Institute (KEMRI) unit, located at Kilifi District Hospital, on the coast of Kenya. The hospital serves a predominantly rural population, and approximately 5000 children are admitted to the 35 bed paediatric ward annually...

Status epilepticus refractory to first-line therapy is associated with a high morbidity and mortality. Correct diagnosis and adequate treatment of this condition require electrographic monitoring and anaesthetic facilities available in specialist intensive care units (ICUs). We carried out an audit of 26 patients admitted to a neurological ICU with a diagnosis of status epilepticus, to identify deficiencies in diagnosis and management prior to transfer to the ICU, and examine the effectiveness of ICU management. Or transfer, only 14 (54%) were in status epilepticus; six were in drug-induced coma or were encephalopathic, and six had pseudostatus epilepticus, of whom four had been intubated. The commonest treatments prior to transfer were benzodiazepines, chlormethiazole and phenytoin; the loading dose of phenytoin was adequate in at least 7/16 cases. All those in status epilepticus on transfer had their seizures successfully controlled, but ten required general anaesthesia with thiopentone, propofol, ketamine or midazolam. Two died--one had a severe encephalitis and the other had had a cardiac arrest prior to treatment. This study highlights deficiencies in the initial diagnosis and management of status epilepticus, the role of specialist neurological intensive care, and the importance of early referral.