Neurophysiological classification of carpal tunnel syndrome: assessment of 600 symptomatic hands.
ABSTRACT Following the AAEM electrodiagnostic guidelines, we developed a neurophysiological classification of carpal tunnel syndrome (CTS). Six hundred hands with clinical CTS (mean age 51.4 yr., female/male ratio 5.5/1, right/left ratio 1.8/1) were prospectively evaluated and divided into six classes of severity only on the basis of median nerve electrodiagnostic findings: extreme CTS (EXT-absence of thenar motor responses), severe CTS (SEV-absence of sensory response and abnormal distal motor latency-DML), moderate CTS (MOD-abnormal digit-wrist conduction and abnormal DML), mild CTS (MILD-abnormal digit wrist conduction and normal DML), minimal CTS (MIN-exclusive abnormal segmental and/or comparative study), and negative CTS (NEG-normal findings at all tests). Using this neurophysiological classification, the CTS groups appeared normally distributed (EXT 3% of cases, SEV 14%, MOD 36%, MILD 24%, MIN 21%, NEG 3%), and the age of patients and clinical findings appeared to be related to neurophysiological abnormalities. Significant differences in median neurophysiological parameters not included in the classification (such as palm-wrist sensory conduction velocity) were observed in the different CTS groups. The analysis of the groups showed that: 1) the majority of advanced cases (SEV and EXT) occurred in older patients (60-80 years), 2) most of the milder cases (MIN and MILD) occurred in young female patients. The aim of this study was to standardise the neurophysiological evaluation of CTS.
SourceAvailable from: Annina Schmid[Show abstract] [Hide abstract]
ABSTRACT: Surprisingly little is known about the impact of entrapment neuropathy on target innervation and the relationship of nerve fibre pathology to sensory symptoms and signs. Carpal tunnel syndrome is the most common entrapment neuropathy; the aim of this study was to investigate its effect on the morphology of small unmyelinated as well as myelinated sensory axons and relate such changes to somatosensory function and clinical symptoms. Thirty patients with a clinical and electrophysiological diagnosis of carpal tunnel syndrome [17 females, mean age (standard deviation) 56.4 (15.3)] and 26 age and gender matched healthy volunteers [18 females, mean age (standard deviation) 51.0 (17.3)] participated in the study. Small and large fibre function was examined with quantitative sensory testing in the median nerve territory of the hand. Vibration and mechanical detection thresholds were significantly elevated in patients with carpal tunnel syndrome (P50.007) confirming large fibre dysfunction and patients also presented with increased thermal detection thresholds (P50.0001) indicative of C and Ad-fibre dysfunction. Mechanical and thermal pain thresholds were comparable between groups (P40.13). A skin biopsy was taken from a median nerve innervated area of the proximal phalanx of the index finger. Immunohistochemical staining for protein gene product 9.5 and myelin basic protein was used to evaluate morphological features of unmyelinated and myelinated axons. Evaluation of intraepidermal nerve fibre density showed a striking loss in patients (P50.0001) confirming a significant compromise of small fibres. The extent of Meissner corpuscles and dermal nerve bundles were comparable between groups (P40.07). However, patients displayed a significant increase in the percentage of elongated nodes (P50.0001), with altered architecture of voltagegated sodium channel distribution. Whereas neither neurophysiology nor quantitative sensory testing correlated with patients’ symptoms or function deficits, the presence of elongated nodes was inversely correlated with a number of functional and symptom related scores (P50.023). Our findings suggest that carpal tunnel syndrome does not exclusively affect large fibres but is associated with loss of function in modalities mediated by both unmyelinated and myelinated sensory axons. We also document for the first time that entrapment neuropathies lead to a clear reduction in intraepidermal nerve fibre density, which was independent of electrodiagnostic test severity. The presence of elongated nodes in the target tissue further suggests that entrapment neuropathies affect nodal structure/myelin well beyond the focal compression site. Interestingly, nodal lengthening may be an adaptive phenomenon as it inversely correlates with symptom severity.Brain 10/2014; DOI:10.1093/brain/awu288 · 10.23 Impact Factor
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ABSTRACT: The distribution of sensory symptoms in carpal tunnel syndrome is strongly dependent on the degree of electrophysiological dysfunction of the median nerve. The association between carpal tunnel syndrome and ulnar nerve entrapment is still unclear. In this study, we measured ulnar nerve function in 82 patients with carpal tunnel syndrome. The patients were divided into group I with minimal carpal tunnel syndrome (n = 35) and group II with mild to moderate carpal tunnel syndrome (n = 47) according to electrophysiological data. Sixty-one age- and sex-matched subjects without carpal tunnel syndrome were used as a control group. There were no significant differences in ulnar sensory nerve peak latencies or conduction velocities from the 4(th) and 5(th) fingers between patients with carpal tunnel syndrome and the control group. The ulnar sensory nerve action potential amplitudes from the 4(th) and 5(th) fingers were lower in patients with carpal tunnel syndrome than in the control group. The ratios of the ulnar sensory nerve action potential amplitudes from the 4(th) and 5(th) fingers were almost the same in patients with carpal tunnel syndrome as in the control group. These findings indicate that in patients with minimal to moderate carpal tunnel syndrome, there is some electrophysiological evidence of traction on the adjacent ulnar nerve fibers. The findings do not indicate axonal degeneration of the ulnar nerve.Neural Regeneration Research 05/2013; 8(15):1418-22. DOI:10.3969/j.issn.1673-5374.2013.15.009 · 0.23 Impact Factor
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ABSTRACT: Carpal tunnel syndrome (CTS) is the most common median nerve neuropathy, accounting for 90% of all neuropathies. Carpal tunnel syndrome presents in 3.8% of the general population, with a higher prevalence among women. There are several risk factors associated with CTS, including both medical and non medical factors. The pathophysiologic mechanisms involved in the median nerve compression and traction are thought to be complex, and as yet are not fully understood. The present review aimed to provide an overview of the pathophysiology of median nerve neuropathy in the carpal tunnel, and subsequent development of CTS.