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)

To study the involvement of motor and sensory pathways in neurolathyrism, 19 patients with lathyrism from Unnao, India, where lathyrism is endemic, were studied. The mean age of the patients at the time of the onset of illness was 35.8 (range 18-70) years. The mean duration of illness was 15.6 (range 2-30) years. The clinical picture comprised walking difficulty due to stiffness and mild weakness in all 19 patients, cramps in the legs in five, frequency or urgency of micturition in five, and flexor spasms in three. There was pronounced leg spasticity with a mean Ashworth score of 4.1 (range 2.9-5). Central motor conduction to the tibialis anterior muscle (CMCT-TA) was slow in 14 of the 17 patients (21 sides). Slowing of peripheral motor nerve conduction, although less pronounced, was significant in the upper limb in four and the lower limb in seven sides. The tibial somatosensory evoked potentials were normal and peroneal nerve conduction was marginally impaired. Values for CMCT-TA correlated with the degree of spasticity (p < 0.02) whereas weakness, crossed adductor reflexes, and clonus did not. The wide variability of CMCT-TA in lathyrism may be due to involvement of different types of fibres. Large diameter fibre involvement may cause pronounced slowing. Small diameter fibre involvement could produce appreciable spasticity and mild weakness but a lesser degree of slowing or even normal conduction.
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PMID:Peripheral and central conduction studies in neurolathyrism. 820 26

The aim of our study was to evaluate Motor Evoked Potentials (MEPs) and cortical excitability, using Transcranial Magnetic Stimulation (TMS) as well as short latency Somatosensory Evoked Potentials (SEPs) in Autosomal Dominant Hereditary Spastic Paraparesis (ADHSP) patients. MEPs were recorded from upper and lower limb muscles in 12 patients (7 m and 5f) affected by ADHSP with spastin mutation (SPG4). We measured: (i) motor threshold (MTh); (ii) total motor conduction time (TMCT); (iii) direct and indirect central motor conduction time (d-CMCT and i-CMCT) calculated by subtracting from the cortical latency those obtained on magnetic spinal stimulation (d-PMCT) and via the F-wave method (i-PMCT); (iv) MEP amplitude (MEP/Mmax ratio%) and (v) duration of the cortical silent period (CSP). Latency, amplitude and persistence of the F-wave obtained with electrical nerve stimulation were also considered; H reflex was also tested from lower extremities. SEPs were recorded from spine and scalp sites following median and posterior tibial nerve stimulation; conventional latency and amplitude measurements were performed. In a comparison with the control group, the MTh recording from lower limbs was significantly higher (67.5 +/- 7.7% versus 52.5 +/- 6.9%), MEPs were absent in one case and showed reduced amplitude in the remainders (22.9 +/- 12.6% versus 66.3 +/- 25.9% of M wave); TMCT resulted to be abnormal (36.5 +/- 3.9 ms versus 27.1 +/- 1.4 ms) and d-CMCT as well as i-CMCT were significantly prolonged (23.1 +/- 3.5 ms versus 13.8 +/- 1.3 ms; and 20.1 +/- 3.4 ms versus 10.6 +/- 1.3 ms, respectively). The CSP, which was normal from the hands, was significantly shortened from the legs and correlated with spasticity scoring (Ashworth scale). Cortical SEPs from lower limbs were abnormal in all cases, whereas SEPs by stimulation of median nerves were normal; F-wave parameters from upper limbs showed no abnormalities, whereas an increased persistence was detected from lower limbs; H reflex amplitudes resulted larger compared with controls. Moreover, shortening of the CSP, being correlated with the Ashworth scale, can be considered an electrophysiological marker of spasticity that seems to arise from impairment of the supraspinal or intracortical inhibitory pathways with an additional contribution of increased segmental motor neuron excitability. These data prove the existence of comparable neurophysiological abnormalities in ADHSP with spastin mutation (SPG4) when long ascending and descending pathways are involved.
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PMID:Motor and somatosensory evoked potentials in Autosomal Dominant Hereditary Spastic Paraparesis (ADHSP) linked to chromosome 2p, SPG4. 1772 May 46