Skin Complications Other than Pressure Ulcers Following Spinal Cord Injury

RESEARCH UPDATE Newsletter
April, 1993

Skin Complications Other than Pressure Ulcers Following Spinal Cord Injury

by Samuel L Stover M.D.

The skin is the largest organ system of the body affected in individuals with spinal cord injury. Skin complications represent one of the leading causes of anxiety, morbidity and interference with educational, vocational, and social goals. Because pressure ulcers are such a frequent and serious skin complication after spinal cord injury, very little attention has been given to other skin complications which may also affect the lives of persons with SCI and possibly even predispose them to pressure ulcers. There is relatively little information in the literature about skin problems following spinal cord injury that is not related to pressure ulcers.[1,2]
The histology and histopathology of denervated skin have not been studied very extensively. In most of the major dermatology text books, there is no reference to the histopathology of denervated skin. One textbook [3] reports that denervation leads to no definite changes in the form or structure of sweat glands, hairs, blood vessels, and other cutaneous cells. The literature also shows there has been controversy about the affects of denervation on wound healing. [4,5,6,7,8]

A recurring clinical observation in persons with spinal cord injury is the finding of brawny induration (hardening) of the skin, characterized by non-pitting thickening of the skin[9]. An earlier study showed skin biopsies with dermal fibrosis (chronic hardening and shrinking of the connective tissue) similar to that associated with progressive systemic sclerosis (hardening). Indirect immunofluorescence with anti-collagen antibodies against human interstitial collagen Types I and III showed a reduction in Type III collagen (small elastic fibers) in the epidermis, and almost exclusive Type I collagen (large thick bundles) in the entire dermis, including the adipose tissue. [9]

Early pilot studies [references 9 and 10] also suggested that the autonomic nervous system may play some role in the development of this dermal fibrosis since the majority of persons studied with this condition had lesions above the T6 level. Autonomic dysreflexia is known to occur in persons with spinal injuries above T6 and may actually lead to an imbalance of autonomic mediators including either an excess or decrease in certain of the autonomic mediators.

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