Stroke although rare in children, is an important cause of morbidity in the paediatric age group. Over a period of 8 years, 43 children (17 boys and 26 girls) in the age groups of 1–16 years (mean 8.02 yrs) presented with stroke which constituted 10% of all strokes in the young and 0.7% of all paediatric admissions. The chief clinical features were hemiplegia (86%), convulsions (27%), fever (23%). dysphasia (23%), headache (11%) and altered level of consciousness (11%). Routine laboratory tests were non‐contributory. Cranial computerized tomography (CCT) on 21 patients was abnormal in 95% and was useful in revealing the extent of infarction. Infarction was confined to middle cerebral artery territory, often involving basal ganglionic structures and was associated with focal or diffuse atrophy. Angiograms were abnormal in 78% of the patients (18/23) and were complimentary to the CCT. Etiological factors identified were: Moya‐moya disease 6, arteritis 5, fibromuscular dysplasia 2, scorpion sting 2, and venous sinus thrombosis and small vessel occlusion one each. Though 23% of the patients had fever at onset, no obvious evidence of systemic or CNS infection was noticed. Stroke in children continues to pose a diagnostic challenge.

Heterotopic ossi®cation (HO) is an important complication of spinal cord and brain injuries but is rarely reported among patients with non-traumatic myelopathies. In a prospective study on medical problems seven (6.04%) among the 114 subjects with non-traumatic myelopathies had heterotopic ossi®cation. All of them had involvement of hip joints. The co-morbid conditions were: urinary tract infection, seven; spasticity, three; pressure sores, ®ve; and deep venous thrombosis, one. The initial diagnosis was often other than heterotopic ossi®cation. Erythrocyte sedimentation rate and serum alkaline phosphatase levels were elevated in all subjects. Following rest and non-steroidal anti-in¯ammatory drugs, the range of motion improved in two patients. Heterotopic ossi®cation can occur in patients with non-traumatic myelopathies and has risk factors and clinical features similar to patients with traumatic spinal cord injury. A high index of suspicion about this complication is necessary for early diagnosis and prompt intervention.

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Objectives:The objective of this study was to assess the clinical characteristics, patterns, and factors associated with headache in patients with cerebral venous sinus thrombosis (CVT).Methods:In this prospective cohort study, we recruited conscious CVT patients who were able to give reliable history after consent. Institutional ethics approval was obtained. The diagnosis of CVT was based on the clinical and imaging parameters. Data regarding headache characteristic, severity (visual analog scale [VAS]), imaging findings and outcome was recorded.Results:Forty-seven patients (19 males and 28 females) with mean age 29.7 ± 8.7 years were recruited. The mean duration of headache was 12.6 ± 26.8 days, and VAS was 79.38 ± 13.41. Headache onset was acute in 51.1%, subacute in 42.6%, thunderclap in 4.3%, and chronic in 2.1%; location was holocranial in 36.2%, frontal in 27.7% patients; description was throbbing in 44.7% and aching in 25.5% patients. Superior sagittal sinus and transverse sinus were involved in 63.8% cases each. The prothrombotic factors were anemia in 55.3%, puerperal in 38.3%, hyperhomocysteinemia in 29.8%, and polycythemia in 19.1%.Conclusion:Holocranial and bifrontal headache of increasing severity may be a marker of CVT. This may be useful in clinical judgment in identifying conscious patients with CVT.

Dural venous sinus thrombosis is a rare and potentially devastating disease. Several predisposing factors exist, including oral contraceptive therapy and colitis. First-line therapy consists of systemic anticoagulation. If first-line therapies fail, more aggressive endovascular therapies may be performed. We report our initial experience with the Solitaire FR device for treatment of refractory symptomatic dural venous sinus thrombosis.

Background:Neurological affection in Sjogren's syndrome (SS) can occur in the central and peripheral nervous system. Literature describing the neurological involvement in SS among Indian patients is lacking.Materials and Methods:Six patients of SS fulfilling the histological or serological criteria of the American European Consensus Group for SS were studied prospectively. The patients underwent clinical examination and laboratory investigations. Their clinical and investigation features are described.Results:The age of the patients ranged from 26 to 48 years, with a male to female ratio of 2:4. In our series, peripheral sensori-motor neuropathy and sensory ataxic neuropathy was seen in 3/6, mononeuritis multiplex in 2/6, cranial neuropathy in 2/6, autonomic neuropathy in 1/6, myelopathy in 4/6, optic neuropathy in 2/6, with presence of classical sicca features in 5/6 patients. Positive lip biopsy was seen in three, altitudinal field defect in one and positive Schirmer's test in five patients. Nerve conduction study abnormalities were seen in three and evidence of vasculitis was seen in nerve biopsy of one patient and chronic nonuniform axonopathy was seen in another. Antibody to Ro (SSA) or La (SSB) was positive in five patients.Conclusions:SS involves different parts of the nervous system with varied presentations. Clinical suspicion and adequate laboratory testing helps to diagnose and manage this disorder that is relatively rare in Indian patients.

Wistar rat pups were administered either a high dose of lead acetate (400 micrograms lead/g body weight/day) or a low dose (100 micrograms lead/g body weight/day) by gastric intubation, from 2 days through 60 days of age. The rats on both these doses exhibited statistically significant decreases in body and brain weights throughout the lead treatment period. A group of rats on high dose was also rehabilitated by discontinuing the lead from 60 days of age. In these rats, at 160 days of age, the body weight but not the brain weight recovered to normal levels. During the lead intake, the rats on high dose revealed significant elevations in the levels of noradrenaline (NA) in the hippocampus (HI), cerebellum (CE), hypothalamus (HY), brainstem (BS), and accumbens-striatum (SA). The elevated levels in all the above regions except in the HY persisted even after rehabilitation. The dopamine (DA) levels changed significantly in opposite directions in HY (elevation) and BS (reduction) during the lead treatment, and the HY recovered after rehabilitation. Under lead, the serotonin (5HT) levels were elevated significantly in the HI, BS and MC (motor cortex), while after rehabilitation the abnormality persisted only in the MC. Low dose lead treatment was also effective on the same areas of brain. In the low dose group, estimation of the levels of GABA and glutamate were also done, and a significant decrease of GABA in CE and glutamate in MC was observed. The differences observed in the neurotoxic effects (none or significant) of lead in the different regions for each of the transmitters (NA, DA, 5HT) supports the interesting conclusion that the vulnerability of the axon terminals of any given type is dependent on some regional factors, although the projections of the different regions originate from an apparently similar category of neurons in the brain stem.

Stiff-person syndrome (SPS) is an autoimmune neuronitis with progressive myoclonus and stiffness. It is a rare but treatable disorder with few case reports in children. SPS is due to autoantibodies against the enzyme glutamic acid decarboxylase which is present in neuronal and nonneuronal tissues. This is the case report of an 8-year-old boy with clinical and investigational features suggestive of SPS with associated myoglobin-induced renal failure, who completely recovered with treatment.