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Biomedical subjects

Curtis M Steyers

Publications and source records attributed to Curtis M Steyers.

3 recordsLinked to original sources

The prevalence of hereditary neuropathy with liability to pressure palsies in patients with multiple surgically treated entrapment neuropathies.

PURPOSE: Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal-dominant peripheral neuropathy that results from deletion of a 1.5-Megabase pair (Mb) segment of the short arm (p) of chromosome 17. Hereditary neuropathy with liability to pressure palsies increases susceptibility of peripheral nerves to pressure and trauma and can be associated with symptoms at multiple anatomic entrapment sites. Many patients present with multiple upper-extremity entrapment neuropathies and the etiology is uncertain. We hypothesized that some of these patients have an underlying hereditary neuropathy. The purpose of this study was to determine the prevalence of HNPP in patients with multiple surgically treated upper-extremity entrapment neuropathies. METHODS: The inclusion criterion for the study was history of more than 1 carpal tunnel release and/or ulnar nerve transposition. The exclusion criteria were history of diabetes or history of Charcot-Marie-Tooth neuropathy. Fifty-nine patients were in the study group. Two patients known to have the 17p11.2 deletion were used as controls. Genomic DNA was extracted from peripheral blood. Each sample was genotyped using polymerase chain reaction (PCR) amplification with short tandem repeat polymorphism markers within the 1.5-Mb region of 17p deleted in HNPP. Markers were scored as homozygous or heterozygous after resolution by polyacrylamide gel electrophoresis and silver staining. RESULTS: The 2 control patients were homozygous for 11 markers. None of the 59 study patients were homozygous for all markers tested in the deleted region. No study patient had the 17p deletion diagnostic for HNPP. Based on the sample size of 59 patients the 95% confidence interval for the prevalence of the 17p11.2 deletion in this population is 0% to 5%. CONCLUSIONS: We found no evidence for an association between HNPP and patients who have multiple surgical releases for upper-extremity entrapment neuropathies.

Case-Control Studies↗

The effects of graded compression of the median nerve in the carpal canal on grip force.

The relationship between tactile hypoesthesia and precision grip force was examined using compression of the median nerve in healthy adults. Hypoesthesia was graded by varying the pressure that an external clamp exerted over the carpal canal. Electrical stimulation of the median nerve in the forearm evoked a compound sensory nerve action potential (SNAP) that we recorded from the digital nerves of the index finger. Clamp pressure was varied to achieve SNAPs that were 75%, 50%, and 25% of precompression amplitude (100%). Grip force and tactile sensibility (Semmes-Weinstein filaments, cotton wisps, sharp/dull) did not change in parallel with reductions of the SNAP. Subjects reported paresthesias at the thumb and index finger at 75% SNAP. Tactile pressure thresholds increased to the clinical range of 'diminished light touch', but subjects detected cotton wisps stroked along the finger. At 75% SNAP grip force did not change compared to 100% SNAP. Simple prehension can proceed efficiently despite these modest reductions in tactile signals. At 50% SNAP the digits remained sensate, but were reported to feel "thick, like cardboard". No subject could detect cotton wisps and tactile thresholds increased by one filament. Sharp/dull distinctions remained. Grip force increased by 55% compared to grip force at SNAPs of 100% and 75%. There were no changes in skin slipperiness, so the increased grip force represented elevated 'safety margin' (grip force exceeding that needed to prevent slip). At 25% SNAP subjects described the skin innervated by the median nerve as feeling "numb", but grip force increased little compared to 50% SNAP. Grip force continued to reflect changes in grip surface friction, and mechanical transients from setting the object on the table triggered coordinated reductions in grip force. We suspect that the loss of information from SA I and FA I, but not FA II, tactile afferents provoked the increased grip force.

Action Potentials↗

Recurrent carpal tunnel syndrome.

Persistent or recurrent symptoms following carpal tunnel release surgery are an infrequent but challenging clinical problem. A thorough evaluation of these patients is mandatory and must confirm the accuracy of the original diagnosis and rule out the presence of concurrent conditions or disorders that may cause persistent symptoms that mimic carpal tunnel syndrome. If an alternative explanation of the patients' symptoms cannot be identified, and if conservative care is ineffective, then surgical treatment should be considered. Adequate exposure of the median nerve and carpal tunnel are mandatory. The general approach should include gentle mobilization of the nerve from adherent scar tissue and interposition of a biologic barrier between the nerve and surrounding tissues. No published data conclusively demonstrate that internal neurolysis provides superior results. Postoperative care should include early mobilization to encourage tendon and nerve gliding.

Carpal Tunnel Syndrome↗