Stiff-man syndrome

Muscle relaxant As an adjunct for the relief of skeletal muscle spasm because of reflex spasm caused by local pathology, spasticity caused by uppermotor neuron disorders, athetosis, stiff-man syndrome, used parenterally in the treatment of tetanus (diazepam). 

An adjunct for the relief of skeletal muscle spasm caused by reflex spasm to local pathology (such as inflammation of the muscles or joints, or secondary to trauma) spasticity caused by upper motor neuron disorders athetosis stiff-man syndrome. Injectable diazepam may also be used as an adjunct in tetanus. 

Butler, M.H., Solimena, M., Dirkz, R.J., Hayday, A. and DeCamilli, P. (1993) Identification of a dominant epitope of glutamic acid decarboxylase (GAD65) recognized by autoanti-bodies in stiff man syndrome. J. Exp. Med., 178, 2097-2106. 

Daw, K., Ujihara, N., Atkinson, M.A. and Powers, A.C. (1996) Glutamic acid decarboxylase autoantibodies in stiff man syndrome and insulin-dependent diabetes mellitus exhibit similarities and differences in epitope recognition. J. Immunol., 156, 818-825. 

De Camilli P, Thomas A, Cofiell R, Folli F, Lichte B, Piccolo G, et al. The synaptic vesicle-associated protein amphiphysin is the 128-kD autoantigen of Stiff-Man syndrome with breast cancer. J Exp Med 1993 178(6) 2219-2223. 

Stiff man syndrome has been described 10 days after the start of oral isotretinoin treatment (1 mg/kg/day) and resolved completely within 2 weeks of withdrawal (103). There were no motor or sensory nerve conduction abnormalities. There were no conditions known to be associated with stiff man syndrome, either at the time or during 5 years of follow up. 

Uncommon forms of immune-mediated diabetes "Stiff-man" syndrome Anti-insulin receptor antibodies Others... 

Benzodiazepines are of value in alleviating the symptoms of cerebral palsy, spasticity resulting from degenerative disorders such as multiple sclerosis, tetanus, stiff-man syndrome, and backache and muscle strain. The effective doses are generally large and may be increased as the disease progresses (e.g., multiple sclerosis). 

The stiff-man syndrome, a disease with excess motor unit activity, is also associated with autoimmune diseases and thyroid disorders (Layzer, 1988). Indeed, despite the heterogeneity of conditions manifesting excessive motor activity, terminal axon sprouting has been demonstrated in muscle biopsies (Oda et al, 1989). Despite elevated thyroid antibody titers in the two patients, there are no reports on the presence of TSHr, Tg, or TPO in the peripheral nerves, neuromuscular junction, or striated muscles. Hence, the role these antibodies play in the generation of neuromuscular manifestations still needs to be elucidated. 

A 50-year-old man who was treated with ziprasidone 40 mg bd for 3 weeks had a substantial rise in creatine kinase activity without any evidence of muscle trauma, stiffness, or swelling or any signs of neuroleptic malignant syndrome (29). There was no renal insufficiency or compartment syndrome. 

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