NEUROLOGICAL MANIFESTATIONS IN LEPROSY: CLINICAL ASPECTS, DIAGNOSIS, AND THERAPEUTIC IMPLICATIONS

Abstract

Leprosy is a chronic infectious disease caused by Mycobacterium leprae, characterized by its tropism for skin and peripheral nerves. Neurological involvement is the main cause of morbidity and permanent disabilities associated with the disease, resulting in physical deformities and a significant psychosocial impact. Neural damage results from both the direct invasion of Schwann cells by the bacillus and the host's immune response, which can intensify the intraneural inflammatory process. Clinically, leprosy neuropathy manifests asymmetrically, frequently as multiple mononeuropathy, with preferential involvement of superficial nerves such as the ulnar, median, common fibular, and posterior tibial nerves. Early signs include loss of thermal and pain sensation, followed by tactile and motor impairment. Progression can result in muscle weakness, atrophy, and deformities such as claw hand and foot drop. Autonomic involvement is also relevant, presenting with anhidrosis, xerosis cutis, vasomotor changes, and a predisposition to neuropathic ulcers. Leprosy reactions represent acute inflammatory events that worsen neural damage. Type 1 (reversal) reaction is associated with exacerbation of cellular immunity, while type 2 reaction, or erythema nodosum leprosum, involves a systemic immune complex mechanism. Acute neuritis constitutes a medical emergency, characterized by intense pain and rapid functional loss, requiring immediate intervention to avoid irreversible sequelae. The diagnosis is essentially clinical, based on the identification of skin lesions with sensory alteration, peripheral neural thickening, and focal motor or sensory deficits, complemented by tests such as bacilloscopy and electromyography in selected cases. Treatment is based on multidrug therapy standardized by the World Health Organization, associated with the management of inflammatory reactions with corticosteroids and, in specific cases, thalidomide. Although effective in eliminating the bacillus, the therapy does not reverse established neural damage, reinforcing the importance of early diagnosis and systematic follow-up for the prevention of disabilities.