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Background
Non-ketotic hyperglycaemia (NKH) in poorly controlled patients with diabetes presenting with hemichorea-hemiballismus is rare. 1-5 It is often described to have a typical triad; unilateral involuntary movements, contralateral striatal abnormality on imaging and resolution of symptoms after correction of hyperglycaemia. 3 6 Imaging plays an important role to separate this entity from other causes of movement disorders for rapid and correct initiation of treatment. We describe in this report, emphasising on the CT and MRI brain findings, the characteristic abnormalities in the basal ganglia while reviewing the relevant literatures.
Case presentation
A 62-year-old man with long-standing diabetes mellitus, hypertension and hypercholesterolaemia on medications was presented with a week history of progressive involuntary movement of the right-upper and lower limbs. His conscious level and speech was normal. There was no history of trauma, previous cerebrovascular accidents, thyroid disease or family history of movement disorders. He did not take any neuroleptic medications.
On examination, he was well oriented, normotensive and afebrile. At rest, he demonstrated quasipurposive writhing movements of the right-upper and lower limbs. The power and deep tendon reflexes of upper and lower limbs were normal. The examination of cranial nerves and cerebellar signs were unremarkable.
Investigations
The laboratory studies demonstrated high serum glucose (26 mmol/L) and glycated haemoglobin of 14%. There was no evidence of ketosis or other metabolic abnormalities.
Cross-sectional imaging of the brain was performed to rule out basal ganglia pathology. A CT scan demonstrated unilateral faint hyperdensity of the left striatum ( figure 1 ). MRI confirmed the left striatal abnormality, which was hyperintense in T1-weighted (T1W) images, hypointense in T2-weighted (T2W) images and non-diffusion restricted in diffusion-weighted images ( figure 2 ). The ipsilateral internal capsule was preserved. There was no mass effect or perilesional oedema seen.
Differential diagnosis
The differential diagnosis of T1W hyperintense basal ganglia lesions includes deposition of paramagnetic substances namely iron, copper (Wilson's disease), melanin (malignant melanoma), manganese (chronic liver disease) and intracellular methaemoglobin in subacute haematoma. 1 2 Other causes include chronic hepatic encephalopathy, postcardiac-arrest encephalopathy, hypoglycaemic coma and mild local ischaemia. 4 In most of the metabolic causes however, bilateral involvement is expected. NKH on the other hand is known to be a unique entity presenting unilateral T1W hyperintensity. Differentiation from haemorrhage and tumour,...