Biomedical subjects

E M Raynor

Publications and source records attributed to E M Raynor.

22 records · Page 2Linked to original sources

PubMed1995

Differentiation between axonal and demyelinating neuropathies: identical segments recorded from proximal and distal muscles.

The presence of significant slowing of motor nerve conduction velocity is considered one of the electrodiagnostic hallmarks of demyelinating neuropathies; however, slowing of conduction velocity may also accompany severe axonal loss. When compound muscle action potential (CMAP) amplitudes are markedly reduced, it is frequently difficult to determine if conduction velocity slowing is due to axonal loss with dropout of the fastest conducting fibers or demyelination. To evaluate the relationship between conduction velocity and axonal dropout, we compared conduction velocities through the same segment of nerve recording from distal and proximal peroneal muscles in patients with chronic neuropathies, in patients with motor neuron disease, and in control subjects. In controls and patients with motor neuron disease, conduction velocities were normal with no significant difference between proximal and distal sites. In patients with axonal neuropathies, conduction velocities were preferentially slowed when recording from distal muscles and relatively normal when recording from proximal sites. Patients with demyelinating neuropathies showed marked slowing of conduction at both sites. We conclude that comparing conduction velocity obtained from proximal versus distal muscle recordings provides a simple, reliable aid for differentiating between chronic axonal and demyelinating polyneuropathies, especially in cases with conduction velocity slowing and low CMAP amplitudes.

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PubMed1994

Sensory and mixed nerve conduction studies in the evaluation of ulnar neuropathy at the elbow.

The relative sensitivities of sensory, mixed nerve, and motor conduction studies in assessing ulnar neuropathy at the elbow have not yet been established. Using surface electrodes, we performed conduction studies across the elbow segment in 43 patients with symptoms referable to the ulnar nerve and 40 control subjects. Segmental slowing of motor conduction localized the lesion to the elbow in 14 of 21 patients (67%) with clear evidence of ulnar neuropathy on physical examination but only in 2 of 22 (9%) with subtle or no physical examination abnormalities. The diagnostic yield was increased by the finding of segmental slowing of sensory or mixed nerve conduction across the elbow to 86% and 68%, respectively, for each of the groups. We conclude that surface-recorded sensory and mixed nerve conduction studies appear to be more sensitive than motor studies in the electrodiagnosis of ulnar neuropathy at the elbow and are especially valuable in patients with subtle clinical involvement.

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PubMed1994

Recurrent inhibition is decreased in patients with amyotrophic lateral sclerosis.

Recurrent inhibitory pathways are powerful modulators of motor neuron excitability. Renshaw cell activation can both inhibit homologous motor neurons and disinhibit antagonists. In spastic spinal-cord-injured patients, recurrent inhibition is consistently increased, and clinical reductions in spasticity are associated with reduced recurrent inhibition. In this study, we evaluated 12 spastic patients with amyotrophic lateral sclerosis (ALS) to see whether a similar mechanism was operating. In contrast to spinal-cord-injured patients, spastic patients with ALS showed strikingly reduced recurrent inhibition, as assessed by a conditioned H-reflex technique, which produces a response (H') whose amplitude is inversely correlated with activity in recurrent inhibitory pathways. The mean ratio of the maximum H' response to the maximum H-reflex response (H'/H ratio) was 0.55, significantly greater than the ratio seen in normal subjects. Amplitude of the H' correlated with amplitude of the Achilles tendon reflex. Thus, in patients with classical ALS, recurrent inhibition appears to be abnormally reduced compared with control subjects, suggesting a different physiology for spasticity in this setting than in spinal cord transection.

Adult↗

PubMed1993

Nonvasculitic, steroid-responsive mononeuritis multiplex.

We report two patients with mononeuritis multiplex, both of whom had focal inflammation of the perineurium and endoneurium on sural nerve biopsy without necrosis of blood vessel walls, histologic evidence of lymphoid malignancy, or mycobacterial infection. The predominant early sensory symptoms were asymmetric pain and paresthesias; subsequently, muscle weakness developed. Electrophysiologic studies showed an asymmetric sensorimotor axon loss radiculoneuropathy with denervation of limb and paraspinal muscles. Spinal fluid protein was elevated in one patient. There was no cause or underlying systemic disease. Marked improvement occurred with steroid therapy.

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