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)

Repeated monthly intracisternal inoculations of N-butyl benzenesulfonamide induced a chronic, slowly progressive myelopathy in young adult New Zealand white rabbits that was manifested by hyperreflexia, spasticity, hypertonia, gait impairment and altered tonic immobility responses. The neuropathological features consisted of scattered neuroaxonal spheroids, fusiform distention of the intramedullary portions of the spinal cord ventral roots and, as defined by microtubule-associated protein-2 (MAP 2) immunoreactivity, an initial distention and subsequent loss of dendritic processes in neurons of the nucleus motoris lateralis with the perikaryon of these cells remaining intact. A similar chronic progressive myelopathy was induced by repeated low dose intracisternal inoculations of aluminum chloride in New Zealand white rabbits. However, the neuropathological changes were more extensive and consisted of dendritic, axonal and perikaryal inclusions of phosphorylated and nonphosphorylated neurofilament localized to spinal motor neurons in the nucleus motoris medialis, substantia grisea intermedia and select brainstem nuclei with only minimal involvement of the nucleus motoris lateralis. The co-administration of these two neurotoxins over the course of 8 months induced striking behavioral changes as well as a fulminant myelopathy. This was accompanied by a loss of neuronal perikarya in the nucleus motoris accompanied by a loss of neuronal perikarya in the nucleus motoris lateralis and topographically extensive neocortical neurofilamentous degeneration. These features suggest that potentiation occurs when the two toxins are co-administered, a view supported by an estimation of the co-neurotoxicity coefficient (CNC greater than 1). Our results have implications for understanding human neurodegenerative disorders in which potentiation of insults may occur, producing a clinical and neuropathological disease state not expected from either agent alone.
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PMID:Potentiation in the neurotoxic induction of experimental chronic neurodegenerative disorders: N-butyl benzenesulfonamide and aluminum chloride. 174 33

[Purpose] To develop a device for measuring the torque of an ankle joint during walking in order to quantify the characteristics of spasticity of the ankle and to verify the functionality of the device by testing it on the gait of an able-bodied individual and an equinovarus patient. [Subjects and Methods] An adjustable posterior strut (APS) ankle-foot orthosis (AFO) was used in which two torque sensors were mounted on the aluminum strut for measuring the anterior-posterior (AP) and medial-lateral (ML) directions. Two switches were also mounted at the heel and toe in order to detect the gait phase. An able-bodied individual and a left hemiplegic patient with equinovarus participated. They wore the device and walked on a treadmill to investigate the device's functionality. [Results] Linear relationships between the torques and the corresponding output of the torque sensors were observed. Upon the analyses of gait of an able-body subject and a hemiplegic patient, we observed toque matrices in both AP and ML directions during the gait of the both subjects. [Conclusion] We developed a device capable of measuring the torque in the AP and ML directions of ankle joints during gait.
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PMID:Development of an ankle torque measurement device for measuring ankle torque during walking. 2615 44