An innovative hand brace for carpal tunnel syndrome: a randomized controlled trial.

We developed a hand brace and studied its efficacy and tolerability in patients with carpal tunnel syndrome (CTS). We randomized 83 subjects into a treated group, which wore the hand brace at night for 4 weeks, and a control group, which received no treatment. The primary efficacy measure was change in the Boston Carpal Tunnel Questionnaire (BCTQ) score. Secondary measures were Subjects' Global Impression of Change Questionnaire (SGICQ), median distal motor latency, sensory conduction velocity and amplitude, and neurophysiological class of severity. The treated group showed a reduction in BCTQ symptomatic score (from 2.75 to 1.54 at 4 weeks; P < 0.001) and functional score (from 1.89 to 1.48; P < 0.001). There were no significant changes in the control subjects. SGICQ documented improvement in all treated subjects (P = 0.006). No significant difference was found in electrophysiological measurements, but overall neurophysiological classification shifted to less severe classes in the treated group (P < 0.05). Thus, the study demonstrates that this hand brace is highly efficient in relieving symptoms and functional loss in CTS.

A relief maneuver in carpal tunnel syndrome.

We describe a maneuver that eases or abolishes paresthesias in carpal tunnel syndrome. With the affected hand palm up, the distal metacarpal heads are gently squeezed together; in some instances stretch of digits III and IV is also required. This maneuver may help in the clinical diagnosis of carpal tunnel syndrome, can be useful as a means of relieving symptoms, and provides the basis for the design of an innovative splint.

Exclusive electrophysiological motor involvement in carpal tunnel syndrome.

OBJECTIVE: To define the frequency of exclusive electrophysiological motor involvement in carpal tunnel syndrome (CTS). METHODS: We reviewed the electrophysiological studies of 2727 consecutive hands with typical symptoms and signs of CTS and at least one abnormal test of the following: median distal motor latency (DML), digit two sensory conduction velocity (D2-SCV), segmental D2-SCV from wrist to palm, median-ulnar sensory latency difference from ring finger stimulation. RESULTS: Thirty-one hands (1.2%) had prolonged median DML ( > 4.4 ms) with normal SCV ( > 48 m/s). In 17 of 31 hands, segmental D2-SCV from wrist to palm or median-ulnar latency difference from ring finger stimulation were also performed with normal results in 8 hands, demonstrating a true exclusive electrophysiological motor involvement. CONCLUSIONS: In CTS, exclusive electrophysiological involvement of median motor fibers is rare. It may be related to preferential compression of the intraneural motor fascicles clumped superficially in the most volar-radial nerve quadrant or, more probably, to the fact that the recurrent thenar branch may exit the carpal tunnel through a separate ligamentous tunnel within the transverse carpal ligament where it may be preferentially or selectively compressed.

Low back pain due to hypertrophic roots as presenting symptom of CIDP.

Attention has recently been drawn to chronic inflammatory demyelinating polyneuropathy (CIDP) with symptomatic nerve root hypertrophy. A 31-year-old woman had fluctuating and worsening low back pain. Absent tendon jerks and a slight weakness of the hand interossei muscles suggested a diffuse neuropathy. The electrophysiological and histological findings were diagnostic for CIDP. Lumbar spine MRI showed marked nerve root enlargement with gadolinium enhancement. This case widens the range of the clinical presentations of CIDP. Further studies are warranted to ascertain whether cauda equina gadolinium enhancement may be a useful tool in the diagnosis of CIDP and a marker of disease activity for monitoring response to therapy.

Conduction block and segmental velocities in carpal tunnel syndrome.

In carpal tunnel syndrome (CTS) standard measurement of median distal motor latency and sensory conduction does not distinguish whether low amplitude responses are due to axonal degeneration or demyelination. In 88 control and 294 CTS hands we recorded amplitude and duration of compound muscle action potential (CMAP) and of antidromic sensory nerve action potential (SNAP) after palm and wrist stimulation to determine wrist to palm amplitude, duration ratios and segmental conduction velocities. In 16% of CTS hands there was an abnormal amplitude reduction without increased duration of CMAP or SNAP from wrist stimulation indicating partial conduction block. In 148 hands distal motor latency to abductor pollicis brevis and/or sensory conduction to digit 2 were abnormal. In the remaining 146 hands wrist to palm motor conduction was less than 35 m/s in 22.6% and wrist to palm sensory conduction was less than 45 m/s in 13%. At least one segmental conduction was abnormal in 27% of hands. Segmental studies allow the discrimination between conduction block and axonal degeneration, increase diagnostic yield in CTS, and might be useful in addressing treatment and predicting outcome.

Acute motor axonal neuropathy with high titer IgG and IgA anti-GD1a antibodies following Campylobacter enteritis.

We describe the first two European cases of acute axonal motor neuropathy with both IgG and IgA anti-GD1a antibodies following Campylobacter enteritis. Both patients acutely developed severe weakness without sensory involvement, had antibodies to Campylobacter jejuni and polyclonal IgG and IgA titers > or = 12,800 to GD1a at onset, which decreased during follow-up. Serial electrophysiologic studies showed: 1, normal or only slightly slowed motor conductions; 2, evidence of a progressive loss of excitability and conduction failure in nerve fibers undergoing axonal degeneration in intermediate nerve segments and evidence of distal axonal involvement in one nerve; 3, normal sensory conductions, sensory potential amplitudes and somatosensory evoked potentials. Although we cannot exclude that axonal degeneration followed demyelination, we think that anti-GD1a antibodies account for the axonal involvement because GD1a is present in the axolemma and exposed at the node of Ranvier and in nerve terminals. The exclusive motor involvement could be explained by the fact that GD1a has a different internal structure in motor and sensory fibers.