Sub-clinical entrapment neuropathy in man

Neary, D.; Ochoa, José L.; Gilliatt, R. W.

doi:10.1016/0022-510x(75)90248-8

Cited by 197 publications

(73 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is this degeneration that leads to denervation of muscle and subsequent atrophy. 41,42,95 After nerve compression is relieved, nerve repair occurs. With lesions involving only the myelin sheath, repair can occur rapidly over days to weeks.…”

Section: Electrodiagnosticmentioning

confidence: 99%

Clinical and Electrodiagnostic Testing of Carpal Tunnel Syndrome: A Narrative Review

MacDermid¹,

Doherty²

2004

J Orthop Sports Phys Ther

View full text Add to dashboard Cite

Carpal Tunnel Syndrome (CTS) is a pressure-induced neuropathy that causes sensorimotor disturbances of the median nerve, which impair functional ability. A clear history that elicits relevant personal and work exposures and the nature of symptoms can lead to a high probability of a correct diagnosis. Hand diagrams and diagnostic questionnaires are available to provide structure to this process. A variety of provocative tests have been described and have variable accuracy. The Phalen's wrist flexion and the carpal compression tests have the highest overall accuracy, while Tinel's nerve percussion test is more specific to axonal damage that may occur as a result of moderate to severe CTS. Sensory evaluation of light touch, vibration, or current perception thresholds can detect early sensory changes, whereas 2-point discrimination changes and thenar atrophy indicate loss of nerve fibers occurring with more severe disease. Electrodiagnosis can encompass a variety of tests and is commonly used to assess the presence/severity of neuropathic changes and to preclude alternative diagnoses that overlap with CTS in presentation. The pathophysiologic changes occurring with different stages of nerve compression must be considered when interpreting diagnostic test results and predicting response to physical therapy management.

show abstract

Section: Electrodiagnosticmentioning

confidence: 99%

Clinical and Electrodiagnostic Testing of Carpal Tunnel Syndrome: A Narrative Review

MacDermid¹,

Doherty²

2004

J Orthop Sports Phys Ther

View full text Add to dashboard Cite

show abstract

“…Fibers teased from these nerves revealed thinning and retraction of the myelin and intercalated segments indicative of previous demyelination. 26 Limited human studies on compressed sensory nerves that were removed to treat refractory pain have revealed a similar thinning of the myelin and thickening of the endoneurium, microvessels within the endoneurium, and perineurium in the region of compression. 21 Further characterization of the pathological mechanisms following CNC injury, however, has proved to be difficult when using human tissue.…”

mentioning

confidence: 99%

Understanding the mechanisms of entrapment neuropathies

Gupta

2009

FOC

View full text Add to dashboard Cite

Compression neuropathies are highly prevalent, debilitating conditions with variable functional recovery following surgical decompression. Due to the limited amount of human nerve tissue available for analysis, a number of animal models have been created to help investigators understand the molecular and cellular pathogenesis of chronic nerve compression (CNC) injury. Evidence suggests that CNC injury induces concurrent Schwann cell proliferation and apoptosis in the early stages of the disorder. These proliferating Schwann cells downregulate myelin proteins, leading to local demyelination and remyelination in the region of injury. In addition, the downregulation of myelin proteins, in particular myelin-associated glycoprotein, allows for axonal sprouting. Interestingly, these changes occur in the absence of both morphological and electrophysiological evidence of axonal damage. This is in direct contrast to acute injuries, such as transection or crush, which are characterized by axonal injury followed by Wallerian degeneration. Because the accepted trigger for Schwann cell dedifferentiation is axonal injury, an alternate mechanism for Schwann response must exist in CNC injury. In vitro studies of pure Schwann cells have shown that these cells can respond directly to mechanical stimuli by downregulating myelin proteins and proliferating. These studies suggest that although the reciprocal relationship between neurons and glial cells is maintained, chronic nerve compression injury is a Schwann cell-mediated disease.

show abstract

“…Secondly, it might be argued that acute trauma had precipitated symptoms in a chronically damaged nerve. Neary et al (1975) have recently demonstrated the presence of subclinical entrapment neuropathy of the ulnar nerve in the cubital tunnel in asymptomatic individuals at necropsy. Also, Payan (1970) pointed out that patients with entrapment of the ulnar nerve at the elbow might give a history of the sudden onset of an ulnar palsy.…”

Section: Discussionmentioning

confidence: 99%

Pressure palsy of the ulnar nerve with prolonged conduction block

Harrison

1976

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

SYNOPSIS A patient is described in whom conduction block occurred in the ulnar nerve after a pressure palsy and persisted for 16 weeks. The unusually long delay in recovery is discussed.There have been surprisingly few electrophysiological studies of pressure palsies in man. Trojaborg (1970) reported the findings in a group of patients with different types of radial nerve injury. In 29 cases the lesion was due to pressure during sleep. Trojaborg confirmed that the nerve remained normally excitable below the lesion and inexcitable above, a situation found experimentally by Denny-Brown and Brenner (1944) to be due to local demyelination at the site of nerve pressure. Trojaborg found that clinical recovery occurred in six to seven weeks with restoration of conduction in the radial nerve.Recent experimental work in the baboon Ochoa et al., 1972) has shown that tourniquet palsies may be accompanied by a more prolonged conduction block, and Rudge (1974) has described a patient in whom conduction block lasted for 16 weeks after a tourniquet lesion of the median and ulnar nerves. That a similar delay in recovery due to prolonged conduction block can occur after a pressure palsy has been demonstrated by a recently studied patient. CASE REPORT J.M., a 29 year old business man, awoke with weakness of his right (dominant) hand. He was first seen one week later. Examination on that occasion revealed weakness (MRC grade 4) of all ulnar supplied muscles including flexor carpi ulnaris and flexor digitorum profundus. There was sensory disturbance in the ulnar territory with a two point (Accepted 15 August 1975.) threshold of 1.5-2 cm over the medial 1I fingers.There was no evidence of a generalized peripheral neuropathy. The patient was reviewed frequently until full functional recovery had occurred (20 weeks). He was then able to rock climb with no residual weakness in the fingers. Wasting was never obvious at any stage.ELECTROPHYSIOLOGICAL STUDIES At each visit, the ulnar nerve was stimulated at the wrist, elbow, and in the upper arm. The muscle action potential (map) evoked in abductor digiti minimi was recorded by surface electrodes. A sensory nerve action potential was recorded from the ulnar nerve at the wrist during stimulation of the digital nerves in the little finger (Gilliatt and Sears, 1958). A mixed nerve action potential was recorded from the ulnar nerve at the elbow during stimulation at the wrist (Gilliatt and Thomas, 1960). RESULTSThe initial examination revealed a complete conduction block in the upper arm. The ulnar nerve was inexcitable higher than a point 2.5 cm above the cubital tunnel. Below this, the evoked MAP in the abductor digiti minimi measured 7.8 mV from the point of the elbow and 10 mV from the wrist. The motor conduction velocity (elbow to wrist) was 54 m/s (normal 49.0-65.6 m/s, Thomas et al., 1959), the sensory action potential was 17 ,uV (normal range 8-28 pV, Gilliatt and Sears, 1958), and the wrist to elbow volley 30 ,uV (normal range 33-117 ,uV, Gilliatt and Thomas, 1960

show abstract

Sub-clinical entrapment neuropathy in man

Cited by 197 publications

References 20 publications

Clinical and Electrodiagnostic Testing of Carpal Tunnel Syndrome: A Narrative Review

Clinical and Electrodiagnostic Testing of Carpal Tunnel Syndrome: A Narrative Review

Understanding the mechanisms of entrapment neuropathies

Pressure palsy of the ulnar nerve with prolonged conduction block

Contact Info

Product

Resources

About