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bibliography * The PainScience Bibliography contains plain language summaries of thousands of scientific papers and others sources, like a specialized blog. This page is about a single scientific paper in the bibliography, Mackinnon 2002.

Pathophysiology of nerve compression

updated
Mackinnon SE. Pathophysiology of nerve compression. Hand Clin. 2002 May;18(2):231–41. PubMed #1237102.
Tags: neck, back pain, chronic pain, head, surgery, head/neck, spine, pain problems, treatment

PainSci summary of Mackinnon 2002?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided at the bottom of the page, as often as possible.

From the abstract: “Both ischemic and mechanical factors are involved in the development of compression neuropathy.” In other words, mechanical factors only — just being pinched — probably does not cause nerve pain.

original abstractAbstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Both ischemic and mechanical factors are involved in the development of compression neuropathy. Experimental studies suggest a dose response curve such that the greater the duration and amount of pressure, the more significant is neural dysfunction. With changes of axonal injury, significant neurologic dysfunction would be anticipated; however, the vast majority of patients with CTS present with symptoms in association with electrophysiologic findings of demyelination (prolonged latency). Frequently, the prolongation in latency is minimal and some patients may even present with normal electrodiagnostic studies, still complaining of significant symptomatology. This would support the concept that in the majority of patients with CTS, the symptoms relate to problems with the connective tissue "container" of the nerve rather than pathology of the nerve fiber itself. This would be in keeping with the histopathologic findings of fibrosis, with thickening of the external epineurium and perineurium. These changes would interfere with blood flow as the vessels pass through the epineurium and perineurium and produce dynamic ischemia to the nerve fibers. As well, this fibrosis would decrease the excursion of the nerve fibers, resulting in traction, and prevent the nerve fibers themselves from going through a full range of movement without traction and decreased gliding. The importance of neural gliding and movement of the nerve in the extremity has been recently emphasized in the clinical management of patients with multilevel nerve compression. Clinical maneuvers that put the nerve on stretch will provoke patients' symptoms and have been used to diagnose specific compression neuropathies (neural tension test). Similarly, physical therapy modalities to stretch the nerves and restore neural gliding are frequently successful in relieving patients' symptoms [33]. This physical therapy approach is based on the premise that the connective tissue "container" of the nerve is tight and short and needs to be mobilized. This is in keeping with the histopathologic findings of increased connective tissue at the perineurial and epineurial levels. A greater understanding of the pathophysiology of compression neuropathy will have immediate impact on our management of this problem and likely result in emphasis on conservative management and physical therapy rather than surgical intervention.

related content

These two articles on PainScience.com cite Mackinnon 2002 as a source:


This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights: