Literature DB >> 9484376

A prospective quantitative study of sensory deficits after whole sural nerve biopsies in diabetic and nondiabetic patients. Surgical approach and the role of collateral sprouting.

M Theriault1, J Dort, G Sutherland, D W Zochodne.   

Abstract

BACKGROUND: Sural nerve biopsy (Sbx) has been employed for the diagnosis of peripheral neuropathies and for multicenter trials of therapy in diabetic neuropathy. There is only limited prospective information available about what factors influence the resolution of the sensory deficit (Sdef) after biopsy.
METHODS: We prospectively studied the surface area of skin Sdef after whole human Sbx in diabetic and nondiabetic patients for up to 18 months after the procedure. Sdef was determined by mapping, in two dimensions, the area of loss to pinprick and light touch in the sural distribution using a transparent boot-like device with 1-square-cm grid markings. At the same time, patients were interviewed about biopsy-related symptoms.
RESULTS: Overall, the Sdef in all patients declined by an average of 91 +/- 3% at 18 months. The pattern of Sdef decline indicated that collateral sprouting was the mechanism of sensory reinnervation. The extent of Sdef at 6, 12, or 18 months did not differ between diabetics and nondiabetics. In diabetics, there was a correlation between sensory reinnervation with pre-biopsy sural nerve potential amplitude and HbA1C level, but not with age or diabetes duration. Diabetic patients who had nerve resections starting at or below the center of a plane through the lateral malleolus and traveling proximally for 7 cm or less had a Sdef that was less than patients with longer and more proximal nerve resections. The majority of patients had unpleasant but mild mechanically elicited sensory symptoms at 1 year that had improved in most, but not all patients, by 18 months.
CONCLUSIONS: Sbx is associated with prolonged sensory symptoms and sensory loss. Recovery occurs by collateral reinnervation.

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Year:  1998        PMID: 9484376     DOI: 10.1212/wnl.50.2.480

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


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