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Dystonia is a neurological condition which causes sustained muscular contractions of an involuntary and patterned nature that induce abnormal postures and twisting movements of the affected body region. A complete understanding of the pathogenesis of dystonia remains to be established, however recent studies suggest abnormalities in somatosensory processing play a key role in the initiation of dystonia. We present the case of a young male who developed sustained, patterned, involuntary movements of his upper limbs following cervical myelopathy induced by a whiplash injury. The movements were not altered after eye closure, therefore were dystonic rather than pseudoathetoid in nature. The dystonia was associated with markedly impaired upper limb proprioception secondary to the myelopathy. Both the dystonia and proprioception improved following a C3-C6 cervical laminectomy and lateral mass fusion surgical procedure. Our case is very rare and only one similar case has previously been reported. We propose that this gentleman developed dystonia due to impaired proprioception caused by his cervical myelopathy. This interesting and important case provides further evidence for the proposal that impaired sensory function is involved in the pathophysiology of dystonia. An improved understanding of the mechanisms causing dystonia will hopefully lead to improved treatment for this disabling condition.

Levodopa-carbidopa intestinal infusion (Duodopa) has proven efficacy in the management of motor complications of Parkinson9s disease (PD). Recent case reports describe subacute axonal neuropathy in patients receiving Duodopa. We report three cases of subacute peripheral neuropathy complicating Duodopa therapy, including two in whom demyelinating features were identified. Three patients with PD (age range 48–68 years) treated with Duodopa (1740–2240 mg/day) presented with a 6–12-week history of paraesthesiae and numbness in upper and lower limbs, with preserved power. Neurophysiological examination revealed absent or attenuated sensory responses in all cases; in two cases there was significant motor conduction slowing and F-wave prolongation. Homocysteine levels were elevated in all patients, and vitamin B12 level in one patient was borderline. There was no evidence of any alternative underlying cause for neuropathy, and CSF examination was normal in both patients with demyelinating features. All patients improved or stabilised clinically following treatment including vitamin B12 supplementation; two stopped Duodopa, while one continued Duodopa along with prednisolone. Duodopa-induced neuropathy may have a demyelinating component, in contrast to previous reports in the literature. Given the putative association between levodopa use, raised homocysteine levels and peripheral neuropathy, clinicians should be alert to this potential complication of Duodopa therapy.

A 20-year-old man with a 6-year history of infrequent nocturnal focal motor seizures with secondary generalization attended an epilepsy clinic. During the seizures, the patient was stiff and rigid, exhibiting left-side convulsive movements. After each episode he had a short-lived left hemiparesis with associated intense vasomotor disturbance. There was no tongue biting or incontinence, but in the morning the patient would complain of being stiff and sore. These seizures had occurred once every 2 to 4 months. He had never had any daytime episodes, although there was a history of occasional daytime jerking of the limbs. Otherwise the patient had been fit and well. Clinical examination was normal, and it was believed that these seizures originated from the right hemisphere. Brain EEG and CT were unremarkable at the time. Three months later, the patient’s condition had deteriorated dramatically. His affect seemed inappropriate, and he had marked ataxia, as well as …