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Tuberculoid Leprosy

The skin lesions are asymmetrical and characteristically macular or maculopapular, depigmented or hypopigmented hyperesthetic patches with raised edges (Fig. 34.2). They occur on the back and on the extensor surfaces of the limbs, and are associated with loss of sensation and reduced sweating. They may heal spontaneously. If they progress, the epidermis becomes thin and the hair actually falls out. Leprosy affects the nerves in the depigmented skin lesions and some of the major peripheral nerves become tender, thickened, and palpable. Pain may be the presenting symptom in tuberculoid or borderline tuberculoid leprosy occurring in nerves before skin lesions have appeared.

The peripheral nerves are commonly damaged where they are superficial or lie over an unyielding surface, e.g., the postauricular nerve over the mastoid, the supraclavicular nerve, the ulnar nerve above the elbow and the antibrachial nerves in the forearm, the radial and median nerves at the wrist, and the peroneal nerve where it passes around the neck of the fibula. When the nerves become acutely swollen, trauma is common and causes further disability. Opening the sheath and decompressing the nerve used to be recommended, but there is doubt that it alters the nerve damage..

Anesthesia seldom brings the patient to the doctor. More commonly the cut or burn or other trauma to a limb causes the visit and the patient may not realize that the limb is anesthetic (Fig. 34.5). Numbness of an individual skin lesion is more common in Asia than elsewhere.

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Fig. 34.5 A, B. Trophic ulceration. A Multiple ulcers on the soles of the feet, some healed. The ulcer on the left foot, below the fourth toe, is penetrating to the underlying bones. The patient was able to walk quite well. B A deep trophic ulcer over the first metatarsal head, which exposed the bone. There are other ulcers over the proximal phalanx of the first toe.

The end result of nerve damage is either motor paralysis or sensory loss. For example, damage to the ulnar nerve causes paresis, followed by paralysis and wasting of the small muscles of the hand (the interossei, lumbrical, thenar, and hypothenar muscles). The uncompensated action of the remainder of the muscles causes flexion and the typical "claw hand" deformity (Fig. 34.6). Where there is combined damage to both the ulnar and median nerves the result is the "main en griffe" deformity. Paralysis of the facial nerve prevents the eyes from closing and there is drying of the cornea and conjunctiva.

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Fig. 34.6A-E. The "claw hand" deformity of leprosy. A A normal hand compared with a severely contracted hand of leprosy. B This child's hand is beginning to contract and there is slight rarefaction of the metacarpal heads. There is a tendency toward metacarpal-phalangeal subluxation. C A different patient with slightly more deformity. The rarefaction of the metacarpal heads is more obvious. D In this patient the fingers are now bent to 90°. There are cystic areas in the fifth metacarpal and around the second metacarpal-phalangeal joint. These are probably due to direct infection. There is generalized osteoporosis. E More advanced deformity: there was soft tissue ulceration on the tips of the fingers and beginning resorption of some of the terminal phalanges.

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