Entrapment neuropathies: pathophysiology and pathogenesis
Section snippets
Human pathophysiology
Entrapment neuropathies usually occur near joints where the nerve passes through a fibrous tunnel as it courses from one body segment to the next. Examples are carpal tunnel syndrome, an injury to the median nerve at the wrist, and cubital tunnel syndrome, an injury to the ulnar nerve at the elbow. The diagnosis is easily made when the sensory and/or motor deficit corresponds to the tissues innervated by the nerve and a nerve conduction study documents conduction slowing [19]. The diagnosis is
Acute effects of compression
The effects of extraneural compression on microcirculation have been studied under a microscope while a balloon surrounding the nerve was inflated to different pressures [3], [26]. Pressures of 20–30 mmHg interfere with venous blood flow while pressures of 35–50 mmHg reduce capillary flow. A pressure of 70 mmHg causes complete ischemia.
A brief (4 h) period of low-pressure (30 mmHg), extraneural compression of the nerve, causes increased vascular permeability leading to edema formation within
Short-term compression studies
The biological effects of a brief, controlled nerve compression were studied in the rat sciatic nerve using small, inflatable cuffs [5], [20]. In 91 rats, pressures of either 0, 30 or 80 mmHg were applied for 2 h to the nerve, then the cuff was removed and the incision closed. At regular intervals up to 28 days the nerves were removed and examined for evidence of injury. Within 4 h, endoneurial edema formed within all compressed nerves and persisted for the entire time of the study.
Chronic compression models
To model chronic nerve compression, short silicon tubes have been secured loosely around the rat sciatic or sural nerve [14], [35]. Pain and nerve histologic changes occured after 1–3 months. The biological response of the nerve was similar to that found in the cuff experiments, with early perineural edema followed by a short-term macrophage recruitment, fibrosis, demyelination, and, finally, nerve fiber degeneration.
One of the limitations of the tube models is that it is not possible to
Repetitive loading model
Recently, an entrapment neuropathy model associated with repeated loading of the digits was developed using a rabbit model [24]. The goal was to develop a model in which the finger repetition rate and applied force could be precisely controlled. The model involved stimulating the flexor digitorum profundus muscle at a controlled frequency, duty cycle, and duration. The third digit was attached to a load cell and the stimulation voltage was adjusted to achieve the desired finger twitch force.
Summary
The critical compression pressures that alter blood flow in the nerve are known; effects on the venous flow are observed at pressures as low as 20 mmHg. A delayed nerve injury is observed after pressures as low as 30 mmHg are applied to the nerve for 2 h. These pressures initially cause capillary leakage, the accumulation of intra- and extra-neurial edema and a persistently increased intraneurial pressure. These initial changes are followed, over the next 30 days, by a brief inflammatory
Acknowledgements
National Institute for Occupational Safety and Health RO3 OHAR03664, RO1 OH07359; National Institutes of Health RO1 AR46174.
David Rempel is Professor of Medicine at the University of California at San Francisco, Professor of Bioengineering at UC Berkeley and director of the ergonomics graduate training program at UC Berkeley. Dr. Rempel’s research has focused on understanding mechanisms of injury to nerve and tendon due to cyclical loading and the design and evaluation of engineering interventions to prevent hand and arm disorders (e.g., tendonitis and carpal tunnel syndrome).
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David Rempel is Professor of Medicine at the University of California at San Francisco, Professor of Bioengineering at UC Berkeley and director of the ergonomics graduate training program at UC Berkeley. Dr. Rempel’s research has focused on understanding mechanisms of injury to nerve and tendon due to cyclical loading and the design and evaluation of engineering interventions to prevent hand and arm disorders (e.g., tendonitis and carpal tunnel syndrome).
Edward Diao gained a BA from Harvard College in 1977, and an MD from Columbia University in 1981. He is currently Associate Professor at the Department of Orthopaedic Surgery, University of California, San Francisco. His special interests include: hand and microvascular surgery, Flexor tendon repairs and animal model for carpal tunnel syndrome.
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