Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hallux valgus and hallux flexus associated with cerebral palsy foot deformity may be due to equinovalgus and/or metatarsus primus adductus or combinations of these. Occasionally the condition occurs in equinovarus feet. Hallux flexus or "dorsal bunion" is usually due to a weak extensor hallucis longus, overpull of the anterior tibial muscle on the first metatarsal and spasticity or contracture of the flexor hallucis longus or brevis. A weak peroneus longus muscle has not caused this deformity. The condition is usually predictable in the growing child if all factors related to gait, collagen stability and foot alignment are observed. Treatment includes soft-tissue and bone realignment. Release of the adductor hallucis, lateral collateral ligaments of the metatarsophalangeal joint, plication of the medial capsule and of the abductor hallucis and centralization of the extensor hallucis longus will realign the first ray. The flexor hallucis longus is transferred to athe extensor hallucis longus proximal to the metatarsophalangeal joint and the anterior tibial tendon is transferred to the second metatarsal. An osteotomy at the base of the first metatarsal and at the base of the proximal phalanx will realign the skeleton. Twenty-six great toes in 16 patients have been observed for two to 20 years. The correction has been maintained without arthrodesis of the metatarsophalangeal joint except where chondromalacia occurred. Once the pattern of deformity is evident, progression is unrelenting and treatment is indicated in order to prevent chondromalacia of the articular cartilage.
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PMID:Hallux valgus and hallux flexus associated with cerebral palsy: analysis and treatment. 724 69

Motor control and body representation in the central nervous system (CNS) as well as musculoskeletal architecture and physiology are shaped during development by sensorimotor experience and feedback, but the emergence of locomotor disorders during maturation and their persistence over time remain a matter of debate in the absence of brain damage. By using transient immobilization of the hind limbs, we investigated the enduring impact of postnatal sensorimotor restriction (SMR) on gait and posture on treadmill, age-related changes in locomotion, musculoskeletal histopathology and Hoffmann reflex in adult rats without brain damage. SMR degrades most gait parameters and induces overextended knees and ankles, leading to digitigrade locomotion that resembles equinus. Based on variations in gait parameters, SMR appears to alter age-dependent plasticity of treadmill locomotion. SMR also leads to small but significantly decreased tibial bone length, chondromalacia, degenerative changes in the knee joint, gastrocnemius myofiber atrophy and muscle hyperreflexia, suggestive of spasticity. We showed that reduced and atypical patterns of motor outputs, and somatosensory inputs and feedback to the immature CNS, even in the absence of perinatal brain damage, play a pivotal role in the emergence of movement disorders and musculoskeletal pathologies, and in their persistence over time. Understanding how atypical sensorimotor development likely contributes to these degradations may guide effective rehabilitation treatments in children with either acquired (ie, with brain damage) or developmental (ie, without brain injury) motor disabilities.
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PMID:Early movement restriction leads to enduring disorders in muscle and locomotion. 2943 46