SUMMARYA 16-year-old girl was admitted with insidious onset, gradually progressive spastic sensori-motor paraparesis, with a sensory level at D10 dermatome without bowel or bladder involvement for the last 2 months following trivial trauma on the lower back. MRI of the spine showed a low-to-intermediate signal intensity, heterogeneous mass with multiple fluid levels. A diagnosis of aneurysmal bone cyst was made. A D8-D9 laminectomy with near total excision of mass was performed. Histopathology of the mass showed cyst cavity filled with haemorrhage surrounded by bony trabeculae confirming the diagnosis. Following excision the patient had excellent recovery. We report this case owing to its rarity and to emphasise the importance of surgery if there is cord compression. BACKGROUND

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SUMMARYLacunar syndrome is a neurodeficit secondary to a deep cerebral lesion, usually because of microatheroma of small arteries. Ataxic hemiparesis (AH) is a lacunar syndrome with unilateral pyramidal weakness and ipsilateral ataxia. Thalamic tuberculoma, as a cause of AH, has not been previously described in the literature. We describe an elderly man who presented with left hemiparesis and ipsilateral ataxia. Clinical examination revealed upper motor neuron left facial paresis and leftsided hemiparesis. The patient had incoordination in left upper and lower limbs. Mantoux test was positive and erythrocyte sedimentation rate was elevated. MRI of brain showed a conglomerated hypointense lesion in the right thalamus with a peripheral hyperintensity on T1-weighted imaging and a hyperintense lesion in T2-weighted imaging with significant perilesional oedema, suggesting a tuberculoma. The patient was treated with antitubercular therapy and was symptomatically better at the 9 months follow-up. BACKGROUND

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Valproate-induced hyperammonemic encephalopathy is a rare event clinically characterized by impaired sensorium, vomiting, headache, seizures and focal neurological deficits. The pathogenesis of this dreadful complication is not well understood, although hyperammonemia has been implicated in causation of encephalopathy. In this submission, we have highlighted a case of valproate-induced encephalopathy who presented mainly with bilateral cerebellar features and generalized slowing on electroencephalogram. High index of suspicion of valproate-induced hyperammonemic encephalopathy is required if diffuse ataxia is present as it is a potentially reversible clinical disorder.