Carpal tunnel syndrome

Pathogenesis and pathophysiology

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By Mamatha Pasnoor MD and Mazen M Dimachkie MD

The pathogenesis and pathophysiology of carpal tunnel syndrome is predominantly attributable to

nerve dysfunction secondary to chronic mechanical compression. Histological abnormalities consist of
paranodal myelin retraction with bulbous paranodal swellings, segmental demyelination, and variable
degrees of axonal degeneration as well as remyelination and axonal regeneration. There is also a focal
increase in endoneurial and perineurial connective tissue and thickening of the blood vessels. The
contribution of superimposed ischemia in causing some of these connective tissue changes and axonal
degeneration is not well defined.
The most detailed histological data are from studies in guinea pigs who spontaneously develop
entrapment neuropathy in the feet when housed in wire cages (Ochoa and Marotte 1973) The findings
correlate in general with the limited number of available autopsy studies in humans.
Nerves entrapped in the carpal tunnel are more likely than normal nerves to become symptomatic
with ischemia (Fullerton 1963). Muscle weakness and clinical sensory loss correlate with the severity
of abnormalities on nerve conduction studies, whereas pain and paresthesias do not correlate with
electrodiagnostic data. It is postulated that the paresthesias reflect spontaneous activity in the
damaged nerve induced by ischemia.
Pressure measurements in the carpal tunnel with a wick catheter support the concept of increased
pressure as a cause of carpal tunnel syndrome. Increased pressures of 30 mm Hg, which is just below
the threshold for sensory symptoms, have been demonstrated in patients with carpal tunnel syndrome
at rest. Wrist flexion and extension produce further increases and eventual neurologic dysfunction