Ali, Tropical Spastic paraparesis and polymysitis.qxp

INTRODUCTION The description of a neurological entity termed “Jamaican peripheral neuritis” by Strachan (1) in 1888 marked the beginning of more than a century of systematic clinical and scientific investigation into an endemic neurological syndrome that is now recognize as tropical spastic paraparesis. It required the work of Scott (2) in 1918 and finally Cruickshank (3) in 1956 to better clinically characterize this entity. Cruickshank identified that “a neuropathic syndrome with features which do not conform to any recognized pattern has been known to occur in the West Indies for some years”. The clinical distinction between a predominantly spastic and an ataxic form was first delineated by Montgomery et al (4) in 1964 with the observation that the proportion of ataxic patients was steadily declining over time. The clinical features of tropical ataxic neuropathy (TAN) were described in detail (3–4). Symptoms were primarily of failing vision, deafness and weak legs. Clinical findings were of optic neuropathy, nerve deafness and prominent posterior column signs with lesser pyramidal signs and mild bilateral peroneal wasting. Cases examined at post mortem demonstrated symmetrical demyelination of posterior columns especially fasciculus gracilis and optic nerves, particularly the papillomacular fibres. Significantly, there were no inflammatory changes with occasional mild patchy demyelination of peripheral nerves. In comparison, the clinical features of the spastic group were quite different with pyramidal findings (100%), bladder symptoms (71%), constipation (65%) and posterior column findings(56%) dominating the clinical picture. Optic atrophy, nerve deafness and wasting were seen in less than 15% of patients (4–5). Pathologically, patchy thickening and opacity of the meninges of the base of brain and especially the spinal cord was observed. Microscopically, a mainly perivascular lymphocytic cellular infiltrate with parenchymal small vessel proliferation and reactive gliosis in damaged neuronal tissue was noted. Demyelination was most prominent in lateral and posterior columns and could extend into the posterior and anterior nerve roots.