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Postural Hypotension in a Patient with Acute Myelitis

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Postural Hypotension in a Patient with Acute Myelitis 180 Kalita, Misra Postgrad Med J: first published as 10.1136/pgmj.72.845.180 on 1 March 1996. Downloaded from Postural hypotension in a patient with acute myelitis J Kalita, UK Misra Summary by asking the patient to blow to raise the A case of acute transverse myelitis with mercury column by 40 mm for 10 s with ongo- severe postural hypotension is described. ing ECG recording. The ratio of the longest RR interval after the strain and the shortest RR Keywords: hypotension, myelitis interval during the strain was 0.9 (nor- mal > 1.4). Schimer's test was negative and salivation was normal. Pupils were 3 mm, sym- Acute transverse myelitis is an acute loss of metrical and reacted normally to light and sensory, motor and bladder functions without accommodation. The patient's skin was dry evidence of antecedent neurologic disease or and scaly below the waist and there was no spinal cord compression.' Autonomic dysfunc- sweating in the groin and lower limbs after tion in acute myelitis is common and manifests keeping him in a warm environment for with bowel, bladder and sexual dysfunction, 30 min, although there was sweating on face, although postural hypotension is extremely axilla and palm. The patient had faecal incon- rare. tinence and retention of urine although urodynamic studies were not possible. Case report His haemoglobin, blood counts and urinalysis were normal. Erythrocyte sedimen- A 43-year-old man was admitted with a history tation rate was 32 mm for the first hour. Blood of acute onset of lower limb weakness which urea, serum creatinine, blood sugar and liver reached its peak within 48 hours. He also noted function tests were normal. Antinuclear anti- impaired sensations below the midthoracic bodies, rheumatoid factor, anti-dsDNA and region, retention of urine and faecal incon- VDRL were negative. Cerebrospinal fluid tinence. On the tenth day ofhis illness, he had a revealed 60 mg/dl protein, 48 mg/dl sugar, and syncopal attack when he tried to sit up. There 7 lymphocytes/mm3 without any acid-fast was no history of preceding fever, vaccination, bacilli, or fungi. Spinal magnetic resonance http://pmj.bmj.com/ sexually transmitted diseases, tuberculosis or a imaging (MRI) revealed diffuse hyperintense similar illness in the past. lesions on T2 in the whole ofthe thoracic spinal The patient was of average build and nutri- cord and hypointensity on T2 in the conus tion. His neurological examination revealed medullaris. A few areas of hyperintensity were wasting of both legs, with flaccid, areflexic seen in all the sequences in the thoracic cord paraplegia (grade 0 on the 0-5 scale of the which was suggestive of haemorrhage (figure). Medical Research Council). Truncal power The vertebral bodies were normal. Motor was below 60% but the upper limbs were pathways to the lower limbs were inexcitable on September 29, 2021 by guest. Protected copyright. normal. Pinprick and vibration sensations were on both cortical and spinal stimulation. Central reduced below the sixth thoracic spinal level motor conduction time to the upper limbs was and the joint position sensations were absent in normal. Tibial somatosensory-evoked poten- both lower limbs. There was no vertebral tials (SEPs) were unrecordable bilaterally but tenderness or deformity. median SEPs were normal. Nerve conduction Autonomic function tests: the pulse was 82 studies revealed unrecordable peroneal con- beats/min and regular. After recording the duction due to severe neurogenic wasting, but resting blood pressure, whichwas 100/64 mmHg, sural sensory nerve conduction velocity was the patient was made to sit up with his legs normal (43.9 m/s, 19.0 pV). Concentric needle hanging down from the bed; immediately after electromyograms revealed fibrillations and Department of sitting his blood pressure fell to 62/36 mmHg sharp waves in vastus medialis, tibialis anterior, Neurology, Sanjay and he developed syncope. In a supine position gastrocnemius, extensor digitorum brevis and Gandhi Postgraduate the patient was asked to clinch his fist for 5 min lumbar paraspinal muscles. Motor unit poten- Institute ofMedical following which his blood pressure did not tials were unrecordable from the lower limb Sciences, Lucknow - reveal any change. After putting his left arm in muscles. Electromyogram of the abductor pol- 226 014, India ice cold water for one minute the blood pres- J Kalita licis brevis, biceps, and branchioradialis were UK Misra sure in the right arm was 100/68 mmHg. normal. The patient was managed by intermit- Electrocardiogram (ECG) did not reveal sinus tent catheterisation, bulk laxatives, arrhythmia. On deep breathing (six/min) the indomethacin 50 mg bid, elastic leg bandage Correspondence to UK ratio of the RR interval during expiration and and physiotherapy, including postural train- Misra inspiration was 0.8 (normal > 1.2). The RR ing. Accepted 28 June 1995 ratio during valsalva manoeuver was calculated He was discharged after 15 days of hospital Postural hypotension and acute myelitis 181 Causes ofpostural hypotension Primary Postgrad Med J: first published as 10.1136/pgmj.72.845.180 on 1 March 1996. Downloaded from * pure autonomic failure * multisystem atrophy (Shy-Drager syndrome, parkinsonism, olivopontocerebellar atrophy, striatonigral degeneration) * acute or subacute dysautonomia Secondary * central: hypothalamic and midbrain tumours, multiple sclerosis, Wernicke's encephalopathy, syringobulbia, age-related changes, spinal injury, syringomyelia, spinal tumours, myelitis * peripheral: afferent (Guillain Barre syndrome, tabes dorsalis, Holmnes-Adie syndrome); efferent (diabetes, amyloidosis, porphyria, familial dysautonomia, carcinomatus neuropathy); miscellaneous (autoimmune and collagen disorders, Eaton Lambert syndrome, AIDS, renal failure, Chaga's disease, polyganglionoradiculopathy, familial hyperbradykininism, dopamine B hydroxylase deficiency) * neurally mediated syncope: vasovagal and micturition syncope, carotid sinus hypersensitivity, glossopharyngeal neuralgia Box 1 evidenced by lack of rise of blood pressure on cold immersion and handgrip. Spinal MRI -~~~~~~~~~~~~~revealed signal changesIsextending from conus Figure Spinal MRI, T, sequence showing medullaries to the first thoracic level with areas of haemorrhage. Bowel and bladder involve- hyperintense lesion in the dorsal region ment are common in segmental involvement of spinal cord but postural hypotension occurs stay. Three months later he was able to sit only in extensive lesions reaching above the without any symptoms of postural hypoten- fifth thoracic segment.3 Only extensive lesions sion; there was no improvement in motor or of the spinal cord produce postural hypoten- sensory symptoms and he still needed intermit- sion because a decrease of 50%/ of pregang- tent self-catheterisation. lionic sympathetic neurons is necessary.2 Spinal cord diseases very rarely produce pos- http://pmj.bmj.com/ Discussion tural hypotension, which has been reported with cervical cord injuries,3 multisystem Our patient with acute myelitis had an unusual atrophy,4 advanced syringomyelia5 and multiple manifestation of severe postural hypotension sclerosis.2 The higher the spinal cord injury the leading to disabling syncopal attacks which more severe is the fall of blood pressure.6 interfered with his rehabilitation. Autonomic Postural hypotension following spinal cord control of blood pressure is complex, being an injury is most pronounced in the acute stage, but on September 29, 2021 by guest. Protected copyright. interplay between parasympathetic and sym- later the patient develops a tolerance to upright pathetic drive. Vagal stimulation produces posture, attributed to an increased sympathetic vasodilatation and bradycardia leading to vasomotor reflex of the isolated spinal cord and hypotension which is normally counteracted by an altered renal vascular renin receptor sympathetic drive, producing tachycardia and mechanism.7 Our patient developed a similar vasoconstriction.2 The causes of postural tolerance three months after the illness. Decom- hypotension are given in box 1. pression sickness can also result in acute In our patient the extensive spinal cord myelopathy which is attributed to occlusion of damage was evidenced by anterior horn cells epidural veins by nitrogen bubbles leading to loss (muscle wasting and electromyogram venus infarction of spinal cord.8 The MRI changes), posterior column (absent joint posi- picture may reveal haemorrhagic changes tion sense and tibial SEPs) and spinothalamic similar to our patient. In syringomyelia, the involvement (loss of pinprick sensation below involvement of intermediolateral horn cells and sixth thoracic spinal level). The corticospinal descending autonomic pathways have been dysfunction could not be documented because reported to be responsible for postural hypoten- of severe anterior horn cell loss. These findings sion.5 The progressive course, lack ofcompensa- suggest both grey and white matter involve- tion to orthostatic hypotension and characteris- ment. It is likely that intermediolateral horn tic MRI features would be distinctive. cells and descending autonomic pathways were Acute transverse myelitis generally results in also damaged which accounts for severe segmental involvement of the thoracic spinal dysautonomia in this patient. The involvement cord. Recent MRI studies have revealed a higher of sympathetic outflow in our patient was level of signal alteration, of more than six to 10 182 Kalita, Misra segments above the sensory level. We also
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