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|Year : 2000 | Volume
| Issue : 4 | Page : 404-5
A case of foot dystonia with peripheral lesion.
Roy J, Mitra K, Gangopadhyay PK, Das S, Roy T, Maity B
|How to cite this article:|
Roy J, Mitra K, Gangopadhyay P K, Das S, Roy T, Maity B. A case of foot dystonia with peripheral lesion. Neurol India 2000;48:404
A Case of Foot Dystonia with Peripheral Lesion : Letter to Editor
Peripheral lesions occassionally associated with focal or segmental dystonias include torticollis, writers cramp, arm dystonia and foot dystonia.,, Arm dystonia after peripheral nerve lesions has been reported. We describe a patient who developed dystonia of right foot, along with sensory disturbances and reflex changes in the distribution of L5-S1 root.
A 42 years old man presented with low back pain and difficulty in walking for the last 18 months. There was no history of trauma to the back. He also noticed abnormal movement of his right foot after walking few steps, which was relieved after taking rest. Clinical examination revealed power grade 4/5 in both dorsiflexors and plantar flexors of right foot. Ankle jerk was absent on right side. Pain and temperature sensation was diminished over L5 and S1 distribution on right side. SLR was positive on right side. Dystonic posture of the right foot on walking for 2-3 minutes was noted with a striatal toe and clawing of other toes and slight inversion of the foot. It was relieved after taking rest. Rest of the neurological examination was normal.
Blood sugar, urea and haemogram were within normal range. Lumbar myelogram showed normal contrast density and flow throughout spinal subarachnoid space from C1 to lower lumbar region. There was evidence of prolapsed disc at L5-S1 level [Figure. 1]
Electrophysiological studies also showed evidence of L5-S1 radiculopathy. Contrast CT brain was normal. Patient was offered spinal surgery but he refused and was discharged on request.
The patient presented with dystonia affecting right foot and dorsi flexors of great toe, on walking. There were no clinical features suggesting intracranial lesion. Normal contrast CT scan brain helped to exclude incranial pathology for dystonia (commonly basal ganglia lesions).
The muscles responsible for dystonia in the present case were flexor digitorium longus and flexor hallucis longus, inverted by L5-S1 nerve roots. There was evidence of sensory and reflex changes, suggesting L5-S1 root dysfunction, which was further confirmed by the electro-physiological test and contrast myelogram (though MRI was a better investigation, it could not be done due to financial reasons). Lumbar canal stenosis has been reported to be associated with dystonia.
Had the patient opted for surgical therapy, our postulation could have been confirmed. There is paucity of Indian literature on peripheral lesion responsible for focal dystonia.
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