Venous Insufficiency and Polyneuropathy
August 1, 2000 2 minutes read
Venous Insufficiency and Polyneuropathy
Abstract & Commentary
Source: Reinhardt F, et al. Peripheral neuropathy in chronic venous insufficiency. Muscle Nerve 2000;23:883-887.
Thirty chronic venous insufficiency (cvi) patients (mean age, 55.1 years) were compared to 20 age-matched normal controls to determine whether CVI was associated with peripheral neuropathy. Diagnosis of CVI was (apparently) based on clinical findings of venous dilation, edema, pigmentary skin changes, or ulceration, plus abnormal Doppler or duplex sonography of the peripheral venous system. Exclusionary criteria included other causes for neuropathy such as diabetes, vitamin deficiency or excess, vasculitis, Lyme disease, Sjogren’s syndrome, dysproteinemia, and exposure to neurotoxic agents. All patients underwent neurological examination and compression therapy to relieve edema prior to electrodiagnostic studies. Large-diameter myelinated A-alpha fibers were studied using standard peroneal motor nerve conduction study. A-beta fibers were evaluated by sural sensory nerve conduction study and vibration threshold testing using an electromagnetic vibratester (Vibratester 100, Gottingen, Germany). Warm and cold detection thresholds using the Somedic Thermotest Type I (Stockholm, Sweden) examined thinly myelinated A-delta and unmyelinated C fibers, respectively. Laser Doppler flowmetry determined peripheral vasomotor C fiber function. Autonomic testing using the quantitative sudomotor axon-reflex test (QSART) studied postganglionic unmyelinated C fiber function. Heart rate variability testing excluded systemic autonomic dysfunction. Statistical analysis was performed using the Mann-Whitney U-test with the Bonferroni correction.
Approximately one-third of CVI patients demonstrated signs of neuropathy on examination, with vibration threshold and warm and cold perception significantly reduced compared to controls. Sural nerve recordings, and sudomotor (QSART) and vasomotor (Doppler flowmetry) function were normal in all with only peroneal distal motor latency prolongation on nerve conduction study. A-alpha, A-beta, A-delta, and thermoafferent C fibers are abnormal in CVI, possibly due to ischemia, and may contribute to the development of stasis ulcers.
Commentary
Although this paper does not clearly indicate either how CVI or peripheral neuropathy were diagnosed, nor exactly how many patients had peripheral neuropathy, nevertheless, the association with CVI appears convincing and correlates with the clinical experience of this reviewer. Should a therapeutic clinical trial be initiated using nerve growth factor for stasis ulcers? —michael rubin
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