Carpal tunnel syndrome as a manifestation of systemic disease.

The syndrome of compression of the median nerve in the carpal tunnel produces well-defined symptoms and signs. Often there is electromyographic evidence of impaired neural conduction at the level of the wrist. The clinical features of the syndrome have been described clearly by Garland, Bradshaw, and Clark (1957) and by Phalen and Kendrick (1957). To appreciate the many aetiological factors which have been incriminated in the causation of the syndrome, an accurate knowledge of the anatomy of the volar aspect of the wrist is required. Robbins (1963) has prepared transverse and longitudinal sections of the cadaveric hand and wrist to display the unyielding boundaries of the carpal tunnel. The relationship of the median nerve to the flexor tendons as they traverse the tunnel are depicted clearly. There is considerable crowding of the structures that lie within the tunnel. Any decrease in its size or increase in the volume of its contents is reflected in alteration of function in the most susceptible structure, the median nerve. Many traumatic disorders have been incriminated in the aetiology of this syndrome of median nerve compression. These include recent and healed Colles' fractures (Lynch and Lipscomb, 1963), dislocation of the lunate bone, and degenerative arthritis of the radio-carpal or intercarpal joints (Robbins, 1963). Of the non-traumatic causes, tumours (e.g. ganglion, lipoma) are not uncommon; primary amyloidosis (Grokoest and Demartini, 1954) and myeloma (Rubio, 1960) are rare causes. Tophaceous gout and rheumatoid and non-specific tenosynovitis have been found associated with the syndrome (Grossman, Kaplan, Ownby, and Grossman, 1961), often in their early stages. Myxoedema and acromegaly, presumably because of alterations in soft tissue metabolism, have produced carpal tunnel syndrome (Johnston, 1960; Skanse, 1961). The fluid retention of pregnancy may also account for the increased incidence of the syndrome in that condition (Heathfield and Tibbles, 1961). At operation, the median nerve, in addition to flattening within the carpal tunnel, may manifest proximal thickening or its sheath may appear hypertrophied. These pathological features are more likely to be the effect than the cause of nerve compression. Although numerous pathological and functional disorders have been described in association with the carpal tunnel syndrome, not in every case can a predisposing factor be elicited. It is recognized that the syndrome can be part of a generalized systemic disorder when such a condition has already manifested itself in other ways. The object of the present investigation is to assess the long-term results of operation for decompression of the median nerve at the wrist, to discover if the syndrome is a prodromal or early phase of a generalized disorder, and to ascertain if there is an association between the syndrome and any degenerative or inflammatory skeletal or soft tissue disease.