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Motor Latency (motor + latency)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Electrophysiological features in the distinction between hereditary demyelinating and chronic acquired demyelinating neuropathies

JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004
F Poglio
We carried out an electrophysiological retrospective study in 55 patients with chronic demyelinating acquired and hereditary neuropathies. Alterations of motor nerve conduction velocities (MNCV), distal motor latencies (DML), conduction blocks (CB) and compound muscle action potential (CMAP) were compared, considering the whole number of nerves for each disease. MNCV, DML, CB and CMAP were considered suggestive of demyelination when meeting the American Academy of Neurology (AAN) criteria. Abnormally slow MNCV was found respectively in the 46% of all the CMTX female nerves studied, in the 56.5% of CMTX males, 84% of CMT1A, 74% CIDP and 70% of MAG-PNP. Prolonged DML was observed in the 25% of the CMTX female nerves studied, in the 49.5% of CMTX males, 81% of CMT1A, 63% of CIDP and 71% of MAG-PNP. Moreover, CB were quite often evidenced in CIDP and MAG-PNP nerves (respectively in 48% and 29%) and rarely in hereditary neuropathies. Finally, we observed CMAP reduction in the 45% of all the CMTX female nerves studied, in the 50% of CMTX males, 63% of CMT1A, 49% of CIDP and 60% of MAG-PNP. A well-characterized pattern generally allows an electrophysiological distinction between CMT1A, CMTX males, MAG-PNP on one side and CIDP and CMTX females on the other side. A clear electrodiagnostic distinction result is often hard between CMTX males and MAG-PNP and between CIDP and CMTX females. [source]

Electrophysiological studies in a mouse model of Schwartz,Jampel syndrome demonstrate muscle fiber hyperactivity of peripheral nerve origin

MUSCLE AND NERVE, Issue 1 2009
Andoni Echaniz-Laguna MD
Abstract Schwartz,Jampel syndrome (SJS) is an autosomal-recessive condition characterized by muscle stiffness and chondrodysplasia. It is due to loss-of-function hypomorphic mutations in the HSPG2 gene that encodes for perlecan, a proteoglycan secreted into the basement membrane. The origin of muscle stiffness in SJS is debated. To resolve this issue, we performed an electrophysiological investigation of an SJS mouse model with a missense mutation in the HSPG2 gene. Compound muscle action potential amplitudes, distal motor latencies, repetitive nerve stimulation tests, and sensory nerve conduction velocities of SJS mice were normal. On electromyography (EMG), neuromyotonic discharges, that is, bursts of motor unit action potentials firing at high rates (120,300 HZ), were constantly observed in SJS mice in all muscles, except in the diaphragm. Neuromyotonic discharges were not influenced by general anesthesia and disappeared with curare administration. They persisted after complete motor nerve section, terminating only with Wallerian degeneration. These results demonstrate that perlecan deficiency in SJS provokes a neuromyotonic syndrome. The findings further suggest a distal axonal localization of the generator of neuromyotonic discharges. SJS should now be considered as an inherited disorder with peripheral nerve hyperexcitability. Muscle Nerve, 2009 [source]

Neurophysiological testing in anorectal disorders

MUSCLE AND NERVE, Issue 3 2006
Jean-Pascal Lefaucheur MD, PhDArticle first published online: 15 JUL 200
Abstract The neurophysiological techniques currently available to evaluate anorectal disorders include concentric needle electromyography (EMG) of the external anal sphincter, anal nerve terminal motor latency (TML) measurement in response to transrectal electrical stimulation or sacral magnetic stimulation, motor evoked potentials (MEPs) of the anal sphincter to transcranial magnetic cortical stimulation, cortical recording of somatosensory evoked potentials (SEPs) to anal nerve stimulation, quantification of electrical or thermal sensory thresholds (QSTs) within the anal canal, sacral anal reflex (SAR) latency measurement in response to pudendal nerve or perianal stimulation, and perianal recording of sympathetic skin responses (SSRs). In most cases, a comprehensive approach using several tests is helpful for diagnosis: needle EMG signs of sphincter denervation or prolonged TML give evidence for anal motor nerve lesion; SEP/QST or SSR abnormalities can suggest sensory or autonomic neuropathy; and in the absence of peripheral nerve disorder, MEPs, SEPs, SSRs, and SARs can assist in demonstrating and localizing spinal or supraspinal disease. Such techniques are complementary to other methods of investigation, such as pelvic floor imaging and anorectal manometry, to establish the diagnosis and guide therapeutic management of neurogenic anorectal disorders. Muscle Nerve, 2005 [source]

A randomized controlled trial evaluating an alternative mouse or forearm support on change in median and ulnar nerve motor latency at the wrist

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 4 2009
Craig F. Conlon MD
Abstract Background The purpose of this study was to determine the effects of an alternative mouse and/or a forearm support board on nerve function at the wrist among engineers. Methods This randomized controlled intervention trial followed 206 engineers for 1 year. Distal motor latency (DML) at baseline and follow-up was conducted for the median and ulnar nerves at the right wrist. Results One hundred fifty-four subjects agreed to a nerve conduction study at the beginning and end of the study period. Those who received the alternative mouse had a protective effect (OR,=,0.47, 95% CI 0.22,0.98) on change in the right ulnar DML. There was no significant effect on the median nerve DML. The forearm support board had no significant effect on the median or ulnar nerve DML. Conclusions In engineers who use a computer for more than 20 hr per week, an alternative mouse may have a protective effect for ulnar nerve function at the wrist. No protective effect of a forearm support board was found for the median nerve. Am. J. Ind. Med. 52:304,310, 2009. © 2009 Wiley-Liss, Inc. [source]

Faecal incontinence after lateral internal sphincterotomy is often associated with coexisting occult sphincter defects: A study using endoanal ultrasonography

ANZ JOURNAL OF SURGERY, Issue 10 2001
Joe J. Tjandra
Background: Troublesome faecal incontinence following a lateral internal sphincterotomy (LIS) is often attributed to faulty surgical techniques: division of excessive amount of internal sphincter or inadvertent injury to the external sphincter. The aim of the present paper was to assess the anatomic and physiological factors that may contribute to faecal incontinence following a technically satisfactory lateral internal sphincterotomy by a group of colorectal specialists. Methods: Fourteen patients (nine women, five men; median age: 38 years; range: 23,52 years) who developed troublesome postoperative faecal incontinence were evaluated by clinical assessment, endoanal ultrasonography and anorectal physiological studies (manometry, pudendal nerve terminal motor latency) by two independent observers. The Cleveland Clinic continence score (0,20; 0, perfect continence; 20, complete incontinence) was used to quantify the severity of faecal incontinence. Fourteen continent subjects after a LIS (nine female patients, five male patients; median age: 36 years; range: 20,44 years) were also evaluated as ,continent' controls (continence score , 4). Results: In the incontinent group, the median postoperative Cleveland Clinic continence score was 9 (range: 6,13) compared with a preoperative score of 1 (range: 0,3). On assessment by endoanal ultrasonography the site of the internal sphincterotomy was clearly identified. There were additional coexisting defects, on endoanal ultrasonography, of the external anal sphincter in seven female patients, of the internal sphincter in two female and two male patients; and a defect of both the external and internal sphincters in a male patient who had had a prior fistulotomy. The pudendal nerve terminal motor latency (PNTML) was prolonged in two female patients on the side contralateral to the lateral internal sphincterotomy. In two of five male patients there was no evidence of any occult sphincter injuries. In the continent controls a defect of the distal portion of the external sphincter was noted in one female patient. None of the patients had a prolonged PNTML. The maximum voluntary contraction was significantly lower in the female subjects than in the female continent controls (92 mmHg vs 140 mmHg; P < 0.05), while the resting anal canal pressures and length of the high pressure zone were similar between the study subjects and the continent controls. Conclusion: Troublesome faecal incontinence after a satisfactorily performed lateral internal sphincterotomy is often associated with coexisting occult sphincter defects. [source]