Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We administered local botulinum toxin injections on the leg adductors of 12 patients with spastic paraparesis (9 patients with HAM, 2 patients with spinal spastic paraparesis, 1 patient with an identified degenerative disease). Two of them were wheelchair-bound and the other patients could walk with or without help. The patients were assessed by the time to walk 10 m and the spasticity score which was derived from the degree of muscle tone and spasm frequency of leg adductors. After the initial injection, 7 of the 12 patients improved spasticity scores and 8 of the 10 patients could walk 10 m within a shorter time. The time to walk 10 m was markedly shortened in moderate cases. However, one patient complained of leg weakness and the time to walk 10 m was prolonged. Five of the 12 patients received injections 3 to 7 times, and were followed up for a mean of 16.2 months. In 4 of the 5 patients, repeated injections could maintain the improvement of spasticity score and time to walk 10 m. However, injection was discontinued in one patient because of leg weakness. The other side effects were pain and swelling at the injected site and dysarthria. However, these side effects were slight and transient and did not require treatment. No other systemic side effects were observed. In conclusion, the beneficial effects of botulinum injections to spastic paraparesis were (1) improvement of objective symptoms in mild cases, (2) improvement of ADL in moderate cases, and (3) improvement of objective symptoms and ease of nursing care in severe cases. Furthermore, we confirmed the long-term efficacy and safety of botulinum toxin.
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PMID:[Treatment of spastic paraparesis with botulinum toxin with reference to beneficial effects, disease severity and long-term treatment]. 761 46

Cerebellar symptoms at onset are unusual in HTLV-I/II-associated tropical spastic paraparesis (TSP). A prospective study of neurological disorders in Panama (1985-1990) revealed 13 patients with TSP and 3 with HTLV-I/II-associated spinocerebellar syndrome (HSCS) presenting at onset loss of balance, wide-based stance and gait, truncal instability, and mild leg ataxia (vermian cerebellar syndrome), with absent upper limb dysmetria but with postural tremor, downbeat nystagmus, and dysarthria. In 4-5 years, spinal cord manifestations of TSP developed, including spastic paraparesis, pyramidal signs, bladder and sphincter disturbances. Two patients were infected with HTLV-I and another one, a Guaymi Amerindian woman, with HTLV-II. Magnetic resonance imaging (MRI) demonstrated cerebellar atrophy involving predominantly the superior vermis. Mild axonal peripheral neuropathy in the lower limbs, dorsal column involvement and inflammatory myopathy were found by neurophysiology studies. There are 14 similar cases reported in Japan and Canada, but to our knowledge these are the first documented cases of HSCS in the tropics. A cerebellar syndrome constitutes another form of presentation of HTLV-I/II infection of the nervous system.
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PMID:Spinocerebellar syndrome in patients infected with human T-lymphotropic virus types I and II (HTLV-I/HTLV-II): report of 3 cases from Panama. 1087 59