Lumbar puncture in paediatric stroke.

In April, 2010, a 2-year-old, previously healthy boy was referred to our hospital with acute left-sided hemiparesis. His parents reported no preceding illness, except chickenpox 10 months earlier. On neurological exam ination he had left upper motor neuron facial palsy and left-sided weakness of the arm and leg with hyper-refl exia and a positive Babinski sign. At admission, diff usion-weighted brain MRI images showed signs of recent cerebral ischaemia in the right middle cerebral artery territory (fi gure A). Our diff erential diagnosis included cerebral arteriopathy, trauma, infection, cardiac abnor malities, genetic, metabolic, and pro-thrombotic diseases. A week later, gadolinium-enhanced MR-arteriography showed a concentric stenosis of the right M1 and M2 segment compatible with an arteriopathy (fi gure B). Cerebrospinal fl uid (CSF) analysis showed: leucocyte count 8×106/L (normal <5); total protein 0·11 g/L (normal 0·16–0·31); and glucose 31 mmol/L (normal 2·1–4·2). CSF PCR for varicella zoster virus was positive. A full paediatric stroke analysis including cardio logical and thrombophilia screening was normal. He was treated with aspirin 38 mg/day, methyl prednisolone intra venously for 3 days (30 mg/kg daily), and aciclovir intravenously for 7 days (60 mg/kg daily). He recovered but had a left hemiparesis. 6 months later, brain MRI showed an unchanged stenosis of the right middle cerebral artery and no new ischaemic lesions of varicella zoster In April, 2011, at fi nal follow-up, he was stable, with a left hemiparesis but no cognitive problems. Cerebral arteriopathy is a common cause of arterial ischaemic stroke in previously healthy children. Both large and small arteries can be aff ected. If no progression is apparent on follow-up angiography after at least 6 months, transient cerebral arteriopathy can be diagnosed. In most cases arterial stenosis persists, and a unilateral stenosis or occlusion is typically located at the distal internal carotid artery, the proximal anterior cerebral artery, or the proximal medial cerebral artery. Association of varicella zoster with transient cerebral arteriopathy is well established. When transient cerebral arteriopathy occurs within 12 months of a clinical varicella infection it is considered a postvaricella arteriopathy. The proposed mechanism is direct meningeal infi ltration and secondary infl ammation of the cerebral arteries. Post-varicella arteriopathy can be diagnosed by detection of IgG to the virus in CSF, a low serum/CSF ratio of specifi c IgG, or positive PCR for the virus in CSF. Intrathecal varicella zoster IgG antibodies are more often detected than viral DNA with PCR because they remain present much longer, and a possible explanation for the diff erence in sensitivity might be the timing of the CSF analysis. Treatment with a short course of corticosteroids and anti-platelet therapy is recom mended because of a 20–30% recurrence risk and the supposed infl ammatory nature of the disease. Although no large randomised trials have been done, antiviral treatment is currently recommended for patients with post-varicella arteriopathy with signs of active viral replication or reactivation. The number of reported cases of postvaricella arteri opathy confi rmed by CSF testing in paediatric arterial ischaemic stroke is small, which suggests reluctance to do lumbar puncture in such cases. Failure to test CSF analysis for varicella zoster in paediatric stroke might result in undertreatment of these children. Our case emphasises the need for CSF analysis for varicella zoster virus in children, even in the absence of clinical signs or history of infection.