No abstract

Dystonia in association with peripheral trauma is a well-described clinical syndrome. The syndrome goes by many names--"traumatic" dystonia, "fixed" dystonia, peripherally induced dystonia, or complex region pain syndrome (CRPS) dystonia. We reviewed the role of peripheral trauma in the development of dystonia, focusing on 4 subtypes--cervical dystonia, focal limb dystonia, CRPS dystonia, and psychogenic dystonia. We show that peripheral trauma inducing, provoking, or precipitating structural changes within the CNS leading to dystonia is not an accepted concept, and current evidence supporting a pathophysiologic mechanism is virtually nonexistent. A better approach to this clinical syndrome is to define it as fixed abnormal posturing that is most commonly psychogenic. While symptomatic treatment of pain and spasms with medication can be beneficial, early psychological evaluation and patient-specific treatment is important. Modalities such as physical and occupational therapy should be utilized early. Finally, it should be emphasized that like many psychogenic movement disorders, it remains a highly disabling and distressing disorder.

Bruxism associated with antidepressant use is an underrecognized phenomenon among neurologists, and may be treated with the addition of buspirone, dose modification, or medication discontinuation.

No abstract

A 50-year-old male presented with complaints of fatigue, confusion, and memory problems. Neurological evaluation revealed altered cognition, unsteady gait, ataxia, dysmetria, and weakness. MRI of the brain was initially unremarkable. Over several days, the patient experienced improvement of symptoms and a follow-up MRI revealed a small lesion in the splenium of the corpus callosum seen on diffusion weighted and T2 sequences. The patient was discovered to have elevated anti-voltage gated potassium channel serum autoantibodies. Follow-up MRI revealed resolution of the splenial lesion. The patient was treated with intravenous immune globulin, and improved back to his pre-treatment baseline. We believe this to be the first case of a reversible splenial lesion syndrome as a manifestation of the anti-voltage gated potassium channel autoantibody syndrome, and propose a pathophysiologic mechanism.