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Typically Seen in MS. (SE,,00180,5 Mm Sagittal 710 Letters to the editor J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.53.8.710-a on 1 August 1990. Downloaded from MRI of thoracic cord in tropical spastic (SEmoo40) 5 mm contiguous parasagittal slices AG KERMODE paraparesis and five P RUDGE using a surface coil. All MS patients AJ THOMPSON TSP patients had additional T2-weighted EPGH DU BOULAY Tropical spastic paraparesis (TSP) is a dis- sequences (SE,o00,8, 5 mm contiguous WI MCDONALD ease occurring in Afro-Caribbeans following parasagittal slices) to detect abnormal signal. The Multiple Sclerosis NMR Research Group, Institute ofNeurology, HTLV- 1 retro-virus infection. There is some Images were reported without knowledge of Queen Square, evidence that the geographical and ethnic the individual diagnosis by one ofthe authors London distribution ofHTLV-1 illness is even wider' (EPGH du B). Correspondence to: Dr Allan G Kermode, NMR and HTLV-1 associated myelopathy (HAM) Atrophy ofthe thoracic cord was seen in six Research Group, Insitute of Neurology, Queen in Japan is probably the same disorder. of nine patients with TSP and five of nine Square, London WC1N 3BG, United Kingdom Abnormalities are found on MRI ofthe brain patients with MS. Three offive patients with The Multiple Sclerosis Work Group is supported in both TSP23 and HAM.4 High signal areas TSP who had T2-weighted images of by the Multiple Sclerosis Society of Great Britain are found in the brain similar to those in thoracic cord had diffuse high signal and all and Northern Ireland, and by the Medical Research multiple sclerosis (MS), though they tend to three had atrophy (fig). Five ofnine with MS Council. 1 Cartier-Rovirosa L, Mora C, Araya F, et al. be less extensive. The thoracic cord (on which had high signal return on T2 weighted HTLV1 positive spastic paraparesis in a tem- the brunt ofthe pathological process falls) has images, one of whom did not have atrophy. perate zone. Lancet 1989;i:556-7. been examined in only three patients, one of The pattern of high signal was diffuse in two 2 Cruickshank JK, Rudge P, Dagleish AG, et al. whom had atrophy.2 Since the clinical picture in three Tropical spastic paraparesis and Human T- and focal or patchy (fig). cell Lymphotropic Virus type 1 in the United ofTSP may resemble that ofprogressive MS, These results confirm the previous MRI Kingdom. Brain 1989;112:1057-90. we have made a systematic comparison of the finding of atrophy in the thoracic cord in a 3 Newton M, Cruickshank JK, Miller D, et al. MRI characteristics of the thoracic cord in proportion of patients with TSP. However, a Antibodies to HTLV-1 in West Indian bom UK resident patients with spastic paraparesis. the two conditions. similar degree ofatrophy is seen as frequently Lancet 1987;i:415-6. Nine patients with TSP who were born in in patients with MS who had a progressive 4 Kira J, Minato S, Itoyama Y, Goto I, Kato M, the Caribbean were compared with an age spastic paraparesis, a finding compatible with Hasuo K. Leukoencephalopathy in HTLV-1- sex of white is associated myelopathy: MRI and EEG data. J and matched group European pathological studies where cord atrophy Neurol Sci 1988;87:221-32. patients with clinically definite MS,' all of present in 72% of patients with MS at 5 Poser CM, Paty DW, Scheinberg L, et al. New whom had a progressive spastic paraparesis. necropsy.7 There was some difference in the diagnostic criteria for multiple sclerosis: Disability was scored using the Kurtzke Dis- pattern of high signal seen in the two groups, guidelines for research protocols. Ann Neurol 1983;13:227-31. ability Status Scale.6 The patients with TSP with more diffuse and uniform high signal in 6 Kurtzke JF. Further notes on disability evalua- were anti-HTLVl positive and had HTLV-1 TSP and focal or patchy high signal in MS. tion in multiple sclerosis with scale modifica- genome integrated into leucocyte DNA. However, these differences in the MRI find- tion. Neurology (Mn) 1965;15:654-61. were The mean was 53 a reliable distinction 7 Ikuta F, Zimmerman HM. Distribution of Eight female. age ings are slight and plaques in seventy autopsy cases of multiple years (range 43-65 years), the mean symptom between the two conditions cannot be made sclerosis in the United States. Neurology duration was 12 years (range 1-5-23 years), on these grounds. 1976;26 (6, pt 2):26-8. and the mean Kurtzke disability score was seven (range five to eight). The mean age of the MS patients was 42 years (range 35 to 53 years), the mean symptom duration was 11 Lewy bodies and subacute sclerosing ised epileptic seizures, multifocal myoclonus, years (range seven to 17 years), and the mean panencephafltis emotional lability, dysarthria, mild chorea Kurtzke disability score was five (range 4 to and ataxia. Serum measles virus titre was 6). The spine was imaged by a Picker 0-5T The occurrence of Lewy bodies in the elevated. An EEG showed periodic com- superconducting machine with TI weighted nervous system is relatively specific to Park- plexes and cerebrospinal fluid (CSF) showed inson's disease.' Their association with other a paretic Lange curve. His condition stabil- disorders may provide a clue to the aetiology ised, but at the age of 21 years he deteriorated of Parkinson's disease, especially when the again. Six years later he was bed-bound, and cause of these disorders is known. We de- died of bronchopneumonia. scribe Lewy bodies in two patients with The brain showed severe atrophy asso- subacute sclerosing panencephalitis (SSPE). ciated with widespread neuronal and myelin are of survival and the loss, gliosis, and occasional neurofibrillary They examples long http://jnnp.bmj.com/ first has been reported for this reason.2 tangles. Very few nerve cells remained in the A 14 year old boy presented with intellec- substantia nigra with a couple ofLewy bodies tual deterioration and absence attacks. When present in each unilateral section. Lewy seen at the National Hospital he had general- bodies were also present in the locus on September 25, 2021 by guest. Protected copyright. '00- ho W.2 .. E:.!* As, Figure The MRI on the left shows diffuse high signal with atrophy of the thoracic cord in TSP. The right shows the patchy high signal typically seen in MS. (SE,,00180, 5 mm sagittal Figure Locus coeruleus neuron containing a neurofibrillary tangle surrounded by a number of slices). smaller Lewy bodies. Haematoxylin and eosin x 1500. Letters to the editor 711 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.53.8.710-a on 1 August 1990. Downloaded from coeruleus, but not in the dorsal vagal nucleus, 3 Wisniewski K, Jervis GA, Moretz RC, Wisni- from even low doses of anticholinergic ewski HM. Neurofibrillary tangles in diseases agents. nucleus basalis, cerebral cortex, spinal cord, other than senile and presenile dementia. Ann superior cervical sympathetic ganglia, and Neurol 1979;5:288-94. Two points are illustrated by this unusual coeliac ganglia. 4 GibbWRG, Lees AJ. The relevanceofthe Lewy case. First, anticholinergic agents, which do The second case was a nine year old boy body to the pathogenesis ofidiopathic Parkin- not have demonstrable efficacy in NMS3 are son's disease. J Neurol Neurosurg Psychiatry in NMS. presenting with intellectual deterioration and 1988;51:745-52. probably contraindicated Second, an epileptic seizure. A month later, when 5 Cianchetti C, Marrosu MG, Manconi PE, Loi patients with NMS should be carefully admitted to H6pital Ste-Justine, Montreal, M, Cao A. Subacute sclerosing panence- monitored for signs of anticholinergic tox- he was unable to obey simple commands, his phalitis in only one of identical twins. Eur icity. Neurol 1983;22:428-32. affect was inappropriate and there was mild DAVID A BENNETT Rush Alzheimer's Disease Center, orofacial chorea. The left plantar was exten- and Department ofNeurology, sor and his gait ataxic. He developed general- Rush Presbyterian-St Luke's Medical Center, ised myoclonus with occasional opisthotonus, 710 SPaulina Street, 8 North JRB, Chicago, Illinois, and within weeks showed decorticate postur- United States ing. Serum measles virus titre was 1024. CSF 1 Guze BH, Baxter LR Jr. Neuroleptic malignant protein was 0-54 g/l, with no cells, and the Combined neuroleptic malignant syn- syndrome. N EnglJ Med 1985;313:163-6. measles complement fixation titre was 128. 2 Henderson VW, Sooten GF. Neuroleptic malig- drome and the central anticholinergic nant syndrome: a pathogenetic role for An EEG was dominated by low voltage syndrome dopamine receptor blockade? Neurology slowing and periodic high voltage slow-wave 1981;31:132-7. complexes. 3 Kurlan R, Hamill R, Shoulson I. Neuroleptic The neuroleptic malignant syndrome (NMS) malignant syndrome. Clin Neuropharm 1984; His condition stabilised, but he remained is an idiosyncratic reaction to neuroleptic 7:109-20. bed-bound and died at the age of 19 years. drugs characterised by encephalopathy, The brain showed generalised atrophy, with rigidity, dysautonomia and hyperthermia.' profound neuronal loss and gliosis in the Dopamine receptor blockade appears central cerebral cortex and hippocampus with a few to the pathophysiology of the rigidity,2 and microglial nodules and tangles. Some remain- possibly the encephalopathy.3 Because ing neurons showed intranuclear inclusions. cholinergic receptor blockade can also cause Intraoperative aneurysms rupture dur- All central grey nuclei showed severe encephalopathy, the differential diagnosis of ing the predissection stage neuronal loss with glial and microglial re- NMS includes the central anticholinergic actions and several tangles. There was severe syndrome (CAS).' Nevertheless, anticholin- Much has been written about intracranial neuronal loss in the substantia nigra and locus ergics, which are used to treat Parkinsonism aneurysms which rupture as they are being coeruleus with tangles and Lewy bodies (fig).
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