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Neurology India, Vol. 54, No. 3, July-September, 2006, pp. 248-249 Invited Commentaries Cranial neuropathy in patients with leprosy Gourie-Devi M Institute of Human Behavior and Allied Sciences and Department of Neurophysiology and Senior Consultant in Neurology, Sir Gangaram Hospital, New Delhi Code Number: ni06081 Leprosy is a common cause of peripheral neuropathy in tropical countries including India[1] and neuropathy is observed across the spectrum of leprosy from polar tuberculoid (TT), borderline (BT, BB, BL) to polar lepromatous (LL) types. Diagnosis is not difficult when cutaneous lesions are present, but in the ′pure or primary neuritic′ form where skin lesions are absent, a high index of suspicion is required to look for thickening of nerves and proceed with confirmatory investigations of nerve conduction and biopsy. The delineation of this pure polyneuritic form as a distinct clinical entity and inclusion in the classification of leprosy is a contribution of Indian leprologists.[2] In some of these patients, skin lesions may appear while on treatment.[3] As a result of implementation of the intensive National Leprosy Eradication Program in India, with early case detection and treatment, neurologists may be confronted with partially treated cases with resolution of skin lesions but persisting neuropathy (history of treatment is often not revealed by the patient due to the underlying stigma) or pure neuritic leprosy. Mononeuritis, mononeuritis multiplex or symmetrical polyneuropathy forms are seen in leprosy. Cranial nerve paralysis generally occurs along with any of the above three types of peripheral neuropathy and rarely may also be an isolated feature. The reported frequency varies from 10 to 22%.[4] Facial, trigeminal and olfactory nerves are the commonest nerves to be affected. In this issue, Kumar and colleagues,[5] in the setting of neurology department in a tertiary health care center, observed that 9 of 51 (18%) patients admitted during a period of 8 years (1995 to 2003) with leprous neuropathy had involvement of cranial nerves. They had looked for involvement of only 3rd to 12th cranial nerves. Facial (5 patients) and trigeminal (4 patients) nerves were the commonest to be involved, and oculomotor, auditory, glossopharyngeal, vagus, spinal accessory and hypoglossal nerves were affected in one patient each. There were 4 patients with multiple cranial nerve paralysis. Lepromatous leprosy was the common type (5 patients), and there was a single patient with pure neuritic leprosy. Thickening of peripheral nerves and cutaneous branches, particularly the greater auricular nerve (GAN), is a diagnostic marker of leprosy. Dharmendra[6] cautioned that in some normal individuals, GAN is thickened and therefore in leprosy endemic areas, if there is isolated thickened GAN, it would be necessary to confirm its involvement by nerve conduction study of this nerve.[1],[7] The elegant description by Monrad-Krohn in 1923 of the unique patchy bilateral facial paralysis in leprosy due to affection of small branches and the characteristic paralysis of medial segment of frontalis earlier to the lateral part giving appearance of ′V′ remains unsurpassed even today.[8] Neurologists practicing in countries that were earlier considered to be endemic need to be extra vigilant to recognize leprous peripheral neuropathy and cranial nerve involvement, with its protean manifestations since specific treatment is available. References
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