Three patients with hemiballism-hemichorea caused by non-ketotic hyperglycaemia are presented, two of whom had hyperosmolar non-ketotic hyperglycaemic syndrome. In two of the three patients, the hyperkinesia was the initial presenting symptom of their diabetes mellitus. The hypersensitivity of the postmenopausal dopamine receptor, decreased y-aminobutyric acid in the brain in non-ketotic hyperglycaemia, coexisting lacunar infarct in the basal ganglion, and pre-existing metabolic dysfunction in the basal ganglion may all have played a part in the pathogenesis of this movement disorder. (7 Neurol Neurosurg Psychiatry 1994;57:748-750) patients, comprises a spectrum ranging from a mild degree of hyperosmolality with minimal symptoms to severe hyperosmolality accompanied by coma.'2 To the best of our knowledge, there have been no reports of this type of hyperkinesia being caused by HNKS. MethodsFrom January 1986 to December 1992, a total of 20 patients with hemiballism-hemichorea were registered at the special clinic for movement disorders in the neurological department of our hospital; in three of these the disease was caused by non-ketotic hyperglycaemia. Two of the three had HNKS (table 1), based on the fact that patients with HNKS have hyperglycaemia, an absence of ketonaemia, and a plasma osmolality greater than 320 mmol/kg.13
Objective-To study regional blood flow of the striatum in non-ketotic hyperglycaemic choreic patients. Methods-Brain SPECT was performed with intravenous injection of 20 mCi 9mTc hexamethylpropylene amineoxime in six non-ketotic hyperglycaemic choreic patients and 10 age matched patients with a similar level of hyperglycaemia without chorea as a control. The focal perfusion defects were analysed by visual interpretation and semiquantitative determination with reference to homolateral occipital blood flow. Recently, PET has been used to measure local cerebral metabolism and has been shown to be useful in the detection of basal ganglia dysfuction in Huntington's disease and other hereditary choreas.'2-16 To date, no report has used imaging techniques to systematically examine non-ketotic hyperglycaemic choreic patients . Furthermore, no study has evaluated the sensitivity of SPECT in the detection of focal perfusion defect in non-ketotic hyperglycaemic chorea.Therefore, we studied six patients who had typical manifestations of hemichorea or generalised chorea due to hyperglycaemia and performed SPECT to show whether a similar pathophysiology of hypometobolism or hypoperfusion of the striatum also occurs in nonketotic hyperglycaemic chorea. Materials and methodsSix patients (four men, two women) with an age range from 58 to 71 presented with either hemichorea (five patients) or generalised chorea (one patient). Besides chorea, these six patients were all characterised by pronounced hyperglycaemia, and an increase in haemoglobin Alc concentration and serum osmolality. Ketone bodies were present in traces or absent. The patients were referred for 99mTc hexamethylpropylene amineoxime (HMPAO) brain SPECT. Those who clearly had underlying diseases causing chorea-for example, hyperthyroidism, hereditary disorders, or lesions shown by MRI over the appropriate anatomic locus to contribute to chorea-were excluded. Another 10 age matched diabetic patients with a similar level of hyperglycaemia and an increase in HbAlc without chorea served as controls.Brain SPECT (Elscint Apex CT system) was performed after intravenous injection of 20 mCi 99mTc-HMPAO with valium (5-10) mg for sedation and reduction of movement artifacts; however, the chorea was not completely abolished at examination.
Ten recruited soldiers developed acute left wrist drop and numbness on the back of the thumb after a three hour military shooting training. Neurological examination disclosed decreased muscle power (0-2/5) of left wrist dorsiflexion, hypalgesia and hypaesthesia on the radial side of the left hand, and diminished brachioradialis reflex. Electrophysiological studies showed prolonged distal latency, reduced amplitude and slowness of left radial nerve motor conduction velocity between the axilla and elbow. Electromyography (EMG) revealed fibrillation potentials at rest, polyphasic motor unit and an incomplete interference pattern at volition over the extensor digitorum communis and brachioradialis. Nine patients recovered completely clinically and electrophysiologically between nine and 12 weeks after the onset of the palsy. Sensation recovered faster than the weakness. One patient failed to recover after three months, possibly because of the longer duration of nerve compression. Longer nerve compression time and sustained, decreased muscle power with signs of active denervation in EMG are indicators of poor prognosis.
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