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Progressive Paraparesis, Lymphocytic Meningitis, and Stroke in a 37-Year-Old Man

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Progressive Paraparesis, Lymphocytic Meningitis, and Stroke in a 37-Year-Old Man Journal ofNeurology, Neurosurgery, and Psychiatry 1994;57:111-115 ill J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.57.1.111 on 1 January 1994. Downloaded from CLINICOPATHOLOGICAL CASE CONFERENCE Progressive paraparesis, lymphocytic meningitis, and stroke in a 37-year-old man J Bamford, J Ironside, H McNaughton, C P Warlow Case presentation Further investigations which were found to The patient is a right-handed male, born in be normal included: barium meal, upper gas- 195 1, and is married. He is an electronics trointestinal endoscopy, brain CT, MRI of solderer. the brain and cervical cord, sural nerve In January 1989 this man began to feel biopsy, bone marrow aspiration and trephine, tired and lethargic and noticed weight loss serum amylase, antinuclear factor, rheuma- despite a reasonable appetite. He also toid factor, lupus anticoagulant, anticardi- described night sweats, possibly in association olipin antibodies, and complement levels, with a temperature. By March he was begin- B12 and folate, blood porphyrins, Treponema ning to notice weakness in the right leg, and pallidum haemagglutination assay (TPHA), then the left leg. He developed tingling and HIV antibodies, CD4/CD8 ratio, antibodies numbness in the left foot, which spread up to against toxoplasmosis, mycoplasma, borrelia, the knee, and with aching in the left leg. He Epstein-Barr virus, herpes zoster, herpes began to notice pain in the right testicle and simplex, cytomegalovirus, measles, and right leg; the latter gradually became numb. mumps virus titres, and an ultrasound scan of By May he was hardly able to walk and he the abdomen including liver, spleen, and developed urinary retention. His health was kidneys. Nerve conduction was normal in the otherwise good. He did not smoke and drank arms but in the legs, the left sural sensory about three pints (1 7 litres) of beer a day. He action potential was absent and the right was previously had had multiple exostoses (famil- small. There was no conduction in the per- ial) removed from both hands. There was no oneal nerves. Int. the legs, the muscles other family history of illness. appeared to be slightly denervated on EMG. On examination in June 1989 he was thin A muscle biopsy was non-specifically abnor- and was noted at times to have mild pyrexia. mal, however, with no definite evidence of He had lost about 25 kg in weight over the denervation. There was selective type II fibre previous six months. General examination atrophy. http://jnnp.bmj.com/ was otherwise, and remained, normal. On By the end ofJune 1989 the numbness and neurological examination, higher functions, weakness had extended to his abdomen and cranial nerves and both arms were normal. he was still occasionally pyrexial (up to 38°C) He was areflexic in the legs and plantar with night sweats. He was started on cortico- reflexes were bilaterally extensor. Tone was steroids and improved somewhat neuro- normal. Both legs were globally weak, the logically but developed pressure sores. right one more than the left. Pain sensation Azathioprine was added and the steroids were was reduced in both feet on September 26, 2021 by guest. Protected copyright. Department of and along the inner gradually reduced in October. Ten days after Neurology, St James's aspect of the right leg. Joint-position sense the steroids were stopped, he awoke to find University Hospital, was lost in both feet. At this stage a urinary that he was weak in the left arm and face, and Leeds, UK catheter was inserted and he was confined to had slurred J Bamford speech. On examination that day a wheelchair. there was dysarthria and an upper motor neu- Western General Hospital, Edinburgh, The following initial investigations were ron weakness of the left side of his face. He UK found to be normal: full blood count, calcium, was weak in the left arm and the left arm Department of phosphate, protein electrophoresis, alkaline reflexes were brisker than the right. In the Pathology phosphatase, thyroid function, glucose, liver legs he had no movement at all, absent J Ironside function (except y-glutamyltransferase = 69 reflexes, and plantar reflexes were flexor. Department of units/l, normal <42), chest radiograph, ECG, There was a sensory level at T4 and there was Clinical Neurosciences blood cultures, and a full myelogram. The no joint-position sensation in the feet. A CT H McNaughton CSF was xanthochromic, however, and pro- scan on the next day showed a low-density C P Warlow tein levels ranged from 3-1 to 7-0 g/l. The area lateral to the right lateral ventricle. The Correspondence to: immunoglobin G level and index were nor- CSF protein was still raised at 2-3 and Dr H McNaughton, g/l Department of Clinical mal. There were 189 lymphocytes/ml. The there were 38 lymphocytes/1l. All CSF cul- Neurosciences, Western level of glucose in the CSF was 2-6 mmol/l tures were again negative and the blood tests General Hospital, Crewe Road, Edinburgh, compared with 6-2 mmol/l in the blood. were unremarkable. The haemoglobulin was EH4 2XU, UK Cultures for bacteria, fungi, and tuberculosis 11 2 g/l and the erythrocyte sedimentation Received 31 August 1993 were negative on several occasions; India ink rate was 24 mm in the first hour. The and in revised form pre- 12 October 1993. stains were also negative. There were no vious tests were repeated and were again nor- Accepted 18 October 1993 malignant cells. mal. Brain biopsy was declined by the patient. 112 Bamford, Ironside, McNaughton, Warlow J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.57.1.111 on 1 January 1994. Downloaded from Figure 1 Non-contrast on axial brain CTscan early since the history is of a global weak- showing haemorrhagic ness in the legs. This, rather than the focal infarct in the region ofthe weakness usually associated with cauda left basal ganglia. equina lesions, suggests cord involvement, albeit that the signs (areflexia and flexor plan- tars), point to a lower motor neuron problem. Additionally, one notes that proprioception is much more affected than spinothalamic modalities. In vasculitic conditions affecting peripheral nerves, the larger myelinated fibres may be picked out preferentially. The normal myelograms reasonably exclude a mass lesion and I note the absence of thickened or infil- trated nerve roots which might have been a source of a tissue diagnosis, although the radiology can be normal even with extensive lymphomatous infiltration of nerve roots. Finally, the testicular pain might be radicular in origin rather than due to primary testicular pathology. So we come to the CSF: there is a very high protein content and the immediate assumption would be that the xanthochromia relates to this, although, in view of subse- quent events, the possibility of a haemor- rhagic pathology needs to be remembered. There is a lymphocyte response and a reduc- tion in the CSF glucose compared with the blood of more than 50%. The differential diagnosis of these abnormalities is extensive, Over the next several months he developed but in the clinical context, tuberculous infected pressure sores, occasional chest meningitis (TBM) must be high on the list. infections, and urinary infections. He had Hospitalised patients with TBM have CSF intermittent pyrexia. In May and June 1990 white cell (predominantly lymphocyte) counts the corticosteroids were being reduced when, of up to 1000/ml with high protein and low on 17 June, he suddenly became aphasic with glucose levels. The direct smear is positive for weakness of the right arm, possibly with a acid-fast bacilli in 10-85% of cases, depend- right homonymous hemianopia. A plain CT ing on technique, with positive cultures in scan (fig 1) showed a haemorrhagic infarct in 45-90%.l The chest radiograph was normal the left basal ganglia. His swallowing was so in this case but up to 50% of patients with badly impaired that a nasogastric tube was TBM have no evidence of tuberculosis else- inserted. An EEG showed widespread slow- where.' So far, polymerase chain reaction ing bilaterally. The corticosteroids were again techniques for rapid diagnosis of TBM have http://jnnp.bmj.com/ increased and there may have been some been disappointing. The clinician here was improvement. He was still completely para- faced with the problem of an active CSF lysed in his legs, catheterised, and confined to compatible with TBM, in a man whose neu- a wheelchair. He was eventually placed in rological condition was deteriorating rapidly. long-term care, and gradually declined. He Furthermore, the use of steroids was being died in January 1992. As far as we know there contemplated. There are those clinicians, and were no further, overt neurological events, I think I may be one of them, who would on September 26, 2021 by guest. Protected copyright. except that, weeks before his death, he had start treatment with antituberculosis drugs in an episode of aphasia and weakness in his this situation while awaiting the results of cul- right arm. A postmortem examination was tures. On the other hand, the normal, con- performed. trast-enhanced CT scan, in particular the absence of basal meningeal enhancement or hydrocephalus, would argue against TBM. Discussion Fungal meningitis was obviously looked for DR JOHN BAMFORD: with India ink stains on multiple CSF speci- This man's initial symptoms are non-specific, mens, although I would have preferred to but give hints of an inflammatory, infective, have had the result of the cryptococcal anti- or neoplastic aetiology. The neurological gen test.2 deterioration was rapid with the initial symp- Sarcoidosis clearly merits consideration. toms of right leg weakness in March, and yet Matthews' review3 remains the most useful by the same summer he was paraplegic and here.
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