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W Schady

Publications and source records attributed to W Schady.

41 records · Page 3Linked to original sources
PubMed1982

Abnormal spontaneous activity in single sensory nerve fibers in humans.

Spontaneous discharges generated in human motor nerve fibers have long been recognized, and their effects have been comfortably recorded from the muscle target with needle electrodes. Delay in documenting comparable phenomena from sensory fibers is explained by the need to record the abnormal activity directly from nerve fibers using intraneural microelectrodes. The hypothesis that a variety of positive sensory phenomena associated with nerve disease is the result of ectopic impulse generation from within the sensory unit can now be tested with microneurographic techniques. Research inaugurating microneurography in the study of positive sensory phenomena has yielded evidence of ectopic impulse generation from sensory units in subjects actually experiencing paresthesia or pain. The phenomenology of ectopic discharges in sensory fibers has been recorded with intraneural microelectrodes in: (1) transient postischemic paresthesia induced experimentally in otherwise normal nerves; (2) spontaneous paresthesia symptomatic to (probable) structural nerve pathology; and (3) in the sign of Tinel in traumatic neuromas.

Action Potentials↗
PubMedDate not supplied

Effect of angiotensin-converting-enzyme (ACE) inhibitor trandolapril on human diabetic neuropathy: randomised double-blind controlled trial.

BACKGROUND: Diabetes is a common cause of polyneuropathy. The development and progression of nephropathy, retinopathy, and neuropathy are closely related. Angiotensin-converting enzyme (ACE) inhibitors delay progression of both nephropathy and retinopathy. We investigated the effect of ACE inhibition on diabetic neuropathy. METHODS: We recruited 41 normotensive patients with type I or type II diabetes and mild neuropathy into a randomised double-blind placebo-controlled trial. Changes in the neuropathy symptom and deficit scores, vibration-perception threshold, peripheral-nerve electrophysiology, and cardiovascular autonomic function, were assessed at 6 and 12 months. The primary endpoint was the change in peroneal nerve motor conduction velocity. FINDINGS: We found no significant difference at baseline for age, HbA1c, blood pressure, or severity of neuropathy between two groups. There was no change in HbA1c over the treatment period. Peroneal motor nerve conduction velocity (p=0.03) and M-wave amplitude (p=0.03) increased, and the F-wave latency (p=0.03) decreased and sural nerve action potential amplitude increased (p=0.04) significantly after 12 months of treatment with trandolapril compared with placebo. Vibration-perception threshold, autonomic function, and the neuropathy symptom and deficit score showed no improvement in either group. INTERPRETATION: The ACE inhibitor trandolapril may improve peripheral neuropathy in normotensive patients with diabetes. Larger clinical trials are needed to confirm these data before changes to clinical practice can be advocated.

Adult↗
PubMedDate not supplied

Observations on severe ulnar neuropathy in diabetes.

We describe the clinical and neurophysiologic findings in a group of diabetic patients with a severe ulnar neuropathy. All patients attending a large inner-city diabetes center were prospectively screening for hand wasting and weakness due to ulnar nerve disease. Twenty diabetic patients fulfilling the clinical criteria underwent nerve conduction studies and electromyography. All but one patient with a motor ulnar neuropathy had systemic complications, mostly severe: ten were amputees, four had had a renal transplant, and two were blind. The onset of hand weakness was sudden in five. All patients had a classical "ulnar hand" (bilateral in five) but forearm muscles were little affected. Sensory loss was prominent in only one-half. Nerve conduction studies showed markedly reduced ulnar motor responses (mean, 1.2 mV versus 7.4 mV in controls) and ulnar/median motor ratios. Motor conduction was disproportionately slowed across the elbows, with or without conduction block, in only eight of 34 affected ulnar nerves. Five of these patients had a habit of leaning on their elbows and/or a Tinel's sign. Median sensory action potentials (SAPs) were recordable in 12 patients but ulnar SAPs were absent in 30 of 34 affected nerves. Electromyography revealed advanced denervation of ulnar supplied hand muscles. We conclude that motor ulnar neuropathy is not uncommon in patients with diabetes of long standing, especially in those with severe systemic complications. Nerve entrapment at the elbows occurs in some, but in many the lesion is axonal, and damage may occur through ischemia.

Adult↗