A quantitative electrophysiological study of acute idiopathic polyneuritis.

Martinez-Figueroa, A; Hansen, Stig; Ballantyne, J. P.

doi:10.1136/jnnp.40.2.156

Cited by 34 publications

(22 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Many of the investigations of segmental demyelination involve acute lesions in previously healthy nerve fibres, and these have shown a capacity for rapid remyelination and the re-establishment of normal conduction velocities (Gilliatt, 1973). Significant axonal dysfunction may be absent in these cases, and indeed, in the more acute demyelinating neuropathy associated with the Guillain-Barr6 syndrome, we have found evidence of an axonal dysfunction (Martinez-Figueroa et al, 1977) but this is less severe than in our patients with diabetic neuropathy. Gilliatt (1973) stated that 'repeated cycles of myelin breakdown and repair produce effects on conduction velocity' [and presumably other parameters] 'very different from those seen in a single demyelinative episode produced in the experimental animal'.…”

Section: Motor Unit Potential Areasmentioning

confidence: 40%

Axonal dysfunction in the neuropathy of diabetes mellitus: a quantitative electrophysiological study.

Hansen¹,

Ballantyne²

1977

Journal of Neurology, Neurosurgery & Psychiatry

Self Cite

View full text Add to dashboard Cite

Section: Motor Unit Potential Areasmentioning

confidence: 40%

Axonal dysfunction in the neuropathy of diabetes mellitus: a quantitative electrophysiological study.

Hansen¹,

Ballantyne²

1977

Journal of Neurology, Neurosurgery & Psychiatry

Self Cite

View full text Add to dashboard Cite

“…However, the limitation of these data makes it impossible to draw firm conclusions about a possible relationship between NC [20],in which smaller and slower conducting myelinated fibers can be evaluated, or motor-unit number estimation (MUNE) [14,15], can contribute to the elucidation of pathophysiological mechanisms of fatigue in GBS. In addition, it can be hypothesized that fatigue is caused by ineffective muscle activation, as a result of a decreased number but larger size of remaining motor units [15]. Recovery after GBS could be accompanied with reinnervation of most muscle fibers, reflected by normal peak muscle strength and normal NC values, but impaired sustained muscle performances.…”

Section: Discussionmentioning

confidence: 99%

Nerve conduction studies in relation to residual fatigue in Guillain-Barré syndrome

Garssen¹,

Doorn²,

Visser³

2006

J Neurol

View full text Add to dashboard Cite

Many Guillain-Barré syndrome (GBS) and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) patients recover well, but suffer from excessive fatigue, which may persist for years and reduce the quality of life considerably. In order to determine whether residual subclinical peripheral nerve dysfunction is a possible underlying mechanism of fatigue, we performed standardized nerve conduction (NC) studies in 16 fatigued patients, mean 6.5 years after diagnosis. Thirteen were relatively well recovered from GBS and 3 had stable CIDP. In contrast to CIDP, most NC values in GBS patients were remarkably restored and within normal values. No correlations were found between the electrophysiological findings and the fatigue scores,muscle strength, or functional scores. This study demonstrates that fatigue in GBS is not explained by residual nerve dysfunction, using conventional NC measurements.

show abstract

“…Despite the rome. 12 considerable reduction in the numbers of functionevidence of a diffuse de-ing motor units in the EDB muscles of these in the form of a reduced patients, reinnervation by the surviving units is Sfecting most, if not all, of relatively poor, indicating a diffuse and widetolic neuropathy. spread disturbance of axonal function.…”

Section: Discussionmentioning

confidence: 99%

Quantitative electrophysiological study of alcoholic neuropathy.

Ballantyne¹,

Hansen²,

Weir³

et al. 1980

Journal of Neurology, Neurosurgery & Psychiatry

Self Cite

View full text Add to dashboard Cite

S U M M A R Y Thirty-one chronic alcoholic patients were investigated using quantitative electrophysiological techniques. Estimates of the numbers of functioning motor units in the extensor digitorum brevis muscles and measurements of the parameters of the potentials of these units are presented along with the values for motor nerve conduction velocities in the inne;vating lateral popliteal nerves. Motor conduction velocities and sensory nerve action potential amplitudes were also measured in the ulnar nerves. The results and their inter-relationships lead us to conclude that the slowing of motor nerve conduction and reduction in sensory nerve action potential amplitudes in alcoholic neuropathy are a consequence of axon loss. We found no evidence of pathological slowing of conduction in surviving axons. Reinnervation by functioning motor axons is poor compared to a number of other neuropathic conditions. In our patients there was no evidence of preferential involvement of sensory axons. The results support a predominant axonal dysfunction in alcoholic neuropathy.The pathological basis of alcoholic neuropathy remains controversial. Some electrophysiological and pathological studies have favoured a primary axonal disturbance'-5 while others support a predominant or concomitant demyelinative pathogenesis.6 7 There is little quantitative information concerning the extent and severity of denervation and compensatory reinnervation in the peripheral motor system in alcoholic neuropathy and such quantitative data as are available, refer to sensory nerve studies and appear to favour the earliest involvement of sensory axons in this neuropathy. 5 We have applied our computer assisted technique for the estimation of the number of functioning motor units in the human extensor digitorum brevis muscle (EDB)8 and the derivation of the parameters of a sample of electrically evoked motor unit potentials (MUPs)9 from the same muscle in a group of patients with alcoholic neuropathy in an effort to quantify the changes in motor parameters in that condition. We have also Address for reprint requests: Dr JP Ballantyne, Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G5 1 4TF, Scotland. Accepted 13 December 1979 measured the fastest motor nerve conduction velocities (FMNCVs) and the shortest distal motor latencies (SDMLs) in the innervating lateral popliteal nerve and FMNCVs, sensory nerve conduction velocities and potential amplitudes in an ulnar nerve in each patient. The relationships between these parameters and their significance for the pathophysiology of alcoholic neuropathy are discussed. Where appropriate comparisons are drawn with the results we have obtained in other neuromyopathies. MethodsThe composition and placement of the surface recording electrodes over the EDB muscle, the properties of the stimulating electrodes over the anterior tibial nerve at the ankle, and the details of the rate and strength of stimulation

show abstract

A quantitative electrophysiological study of acute idiopathic polyneuritis.

Cited by 34 publications

References 21 publications

Axonal dysfunction in the neuropathy of diabetes mellitus: a quantitative electrophysiological study.

Axonal dysfunction in the neuropathy of diabetes mellitus: a quantitative electrophysiological study.

Nerve conduction studies in relation to residual fatigue in Guillain-Barré syndrome

Quantitative electrophysiological study of alcoholic neuropathy.

Contact Info

Product

Resources

About