A case of useless hand as a first demyelinating event
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LETTER TO THE EDITOR
A case of useless hand as a first demyelinating event Tarik Benhsain1 · Zaynab Abdulhakeem1 · Bouchra El Moutawakil2 · Mohammed Abdoh Rafai2 · Hicham El Otmani2 Received: 6 October 2018 / Accepted: 26 February 2019 © Belgian Neurological Society 2019
Keywords Pseudoathetosis · Athetosis · Multiple sclerosis · Useless hand
Introduction Athetosis is a clinical syndrome in which slow, writhing, vermicular, sinuous, cramp-like movements seem performed with great deliberation and force. Lesions associated with athetotic syndromes are generally located in the basal ganglia but can also be found in the thalamus, subthalamic nucleus, corticospinal tract, brainstem, and can exceptionally be seen in parietal, frontal, or temporal cortex lesions [1]. Pseudoathetosis is clinically indistinguishable from athetosis and is caused by impaired proprioception. Spinal pseudoathetosis has been reported in association with various causes, including demyelination, inflammation, and syringomyelia [2]. We report the case of a patient who presents a first demyelinating event revealed by an isolated pseudoathetosis following a cervical spinal cord lesion.
Case report A 56-year-old man was admitted for a 1-month history of difficulty manipulating objects and inability controlling his left hand. Neurological examination revealed involuntary, constant, slow, and writhing movements of left hand fingers as the patient stretched out his arms leading to a useless hand. When asked to close his eyes, the pseudoathetoid Electronic supplementary material The online version of this article (https://doi.org/10.1007/s13760-019-01109-3) contains supplementary material, which is available to authorized users.
movements increased (Online Resources 1 and 2). Sensory examination showed a severely impaired vibratory sensation in the left hand while pain, temperature, and touch sensations were normal. Deep tendon reflexes were increased on the left side but neither Babinski nor Hoffmann signs were present. Otherwise motor function and cranial nerves testing were normal. Brain magnetic resonance imaging (MRI) revealed T2 hyperintense lesions in subcortical, juxtacortical, and periventricular white matter (Fig. 1). Spinal cord MRI showed a posterior T2 hyperintense lesion at C3 level which covers less than half of the cord area on axial cut. This lesion was not swollen and has not shown any contrast enhancement (Fig. 2), but was always clinically symptomatic probably due to the fact that the MRI was performed 1 month after symptom onset. Cerebrospinal fluid examination revealed normal cell counts, no protein nor glucose abnormalities but a positive oligoclonal bands and increased IgG index. Routine blood and urine analyses were normal. Immunologic and serological studies excluded infectious and systemic causes. He was treated with methylprednisolone resulting in a complete cessation of the abnormal movements 5 days later. Brain and spinal cord MRI check-ups at 01 and 02 years revealed no additional or enhancing lesions but did not
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