- Email: [email protected]
Case report: Arachnoiditis following intracranial ‘Thorotrast’
ClinicalRadiology(1992)
45, 141 143
Case Report: Arachnoiditis Following Intracranial 'Thorotrast' p. M . P A N D Y A
a n d A . J. K E O G H
Department of Neurological Surgery, Royal Preston Hospital, Preston A patient is reported with a painless, progressive cauda equina lesion due to arachnoiditis, the result of the contrast medium 'Thorotrast' (thorium dioxide) introduced into the brain over 30 years previously. Contrast medium introduced into the lumbar spine can give rise to aseptic adhesive inflammation (arachnoiditis). It rarely gives rise to clinical problems but, when it does so, is usually associated with back pain and only very rarely with progressive neurological deficit. P a n d y a , P . M . & K e o g h , A . J . ( 1 9 9 2 ) . Clinical Radiology 4 5 , 1 4 1 - 1 4 3 . C a s e R e p o r t : Arachnoiditis
Following
Intracranial
'Thorotrast'
CASE REPORT In October 1954 the patient, aged 21, developed a right temporal abscess, complicating chronic otitis media, and haemolytic streptococci were cultured from the pus. The abscess was aspirated and 8 cm 3 o f the contrast medium 'Thorotrast' were instilled into the cavity. Subsequently the abscess ruptured into the ventricular system, plain films of the skull revealing 'Thorotrast' in the lateral ventricles as well as in the abscess cavity. Despite this complication he recovered well, save for deafness in the right ear. In August 1955 he presented with a history of hacmoptysis, weight loss and occasional chest pain. Chest radiography showed right upper zone shadowing and a diagnosis of pulmonary tuberculosis was made, although tubercule bacilli were never isolated. His symptoms resolved and the chest film appearances returned to normal after anti-tuberculous therapy. In 1983, aged 50, he developed paraesthesiae in the left leg and foot. Myelography revealed appearances suggestive of arachnoiditis, whilst examination of the cerebrospinal fluid (CSF), apart from a protein level of 1.2 g/litre, was otherwise unremarkable. Over the next 2 years his sensory symptoms slowly progressed to affect the whole of both legs. Retention of urine with overflow incontinence developed, so that a diversionary urinary ileostomy was necessary. Over the next few years he also had progressive leg weakness, so that by November 1989 his walking was reduced to a precarious shuffle, and he had to use at least a stick to prevent falling. Examination confirmed a severe lower motor neurone paraparesis in the lower limbs with diffuse wasting, most marked on the left, reduced muscle tone and sensory loss to all modalities to the level of L2 on the left and St on the right; tendon reflexes or plantar responses could no longer be elicited. Plain films of his lumbar spine showed outlining of the dura mater (Fig. l) and further myelography revealed irregular narrowing, with obliteration of nerve root sleeves (Fig. 2), the rest of the spine being normal. Examination of the CSF again showed a raised protein at 1.9 g/ litre, but was otherwise normal. Computed tomography (CT) of the brain showed residual 'Thorotrast' (Fig. 3). At operation thick, somewhat yellow dura mater was found throughout the lumbar region, the arachnoid mater being opaque and the cauda equina a tangled, adherent mass. Histological examination of the arachnoid mater revealed dense fibrous tissue with fine calcification, with no evidence of tuberculosis.
DISCUSSION P l a i n f i l m s o f t h e l u m b a r s p i n e in t h i s p a t i e n t s h o w e d outlining of the dura mater, presumed to be due to thorium dioxide, there being no other explanation for the appearance. Although calcification was seen on histologiCorrespondence to: P. M. Pandya, Neurosurgical Registrar, Department of Neurological Surgery, Royal Preston Hospital, Preston PR2 4HT.
Fig. 1 - Lateral plain radiograph of the lumbar spine showing faintly outlined theca.
142
CLINICAL RADIOLOGY
Fig. 3 CT scan: residual 'Thorotrast' scattered throughout thc ventricular system.
Fig. 2 Lumbar myelogram: smooth and featureless theca with irregular narrowing.
cal examination of the dura and arachnoid mater, this was fine and sparse and clearly insufficient to outline the theca. A diagnosis of arachnoiditis was established from the myelographic appearances and confirmed at surgery. Arachnoiditis has no established associated clinical synd r o m e (Kendall, 1987) and, although back pain may occur, neurological deficit is rare (Shaw, 1978). It is related to a variety o f probable causes, including mechanical lumbar disease (French, 1946), infection, especially tuberculosis (Wadia and Dastur, 1969) and intraspinal contrast media (Jorgensen et al., 1975; Keogh, 1974); although m o d e r n contrast media do not appear to cause arachnoiditis, magnetic resonance imaging ( M R I ) is probably now the investigation o f choice as it is safe and p r o b a b l y sufficiently accurate (Ross et al., 1987). There was no question o f mechanical lumbar disease in this patient, and although his history was complicated by
p u l m o n a r y tuberculosis some 27 years before the onset of his current illness, there was no evidence that tuberculosis was the cause of the arachnoiditis. There was a long interval between the two episodes, his current illness had a very protracted course and there was no evidence to suggest tuberculosis either on repeated examination of the CSF, or on subsequent histological examination of the affected arachnoid mater. Although once p o p u l a r as a contrast medium, ' T h o r o trast', a radioactive c o m p o u n d predominantly a betaemitter, has long been discontinued. Ascending spinal cord damage following injection directly into the spine has been described and attributed to prolonged exposure to radiation (Dale and G r a f t o n Love, 1967). This does not seem to be the case here, as there was no evidence o f a myelopathy. This patient demonstrates arachnoiditis in the lumbar spine giving rise to a painless, slow, relentless and quite devastating c a u d a equina syndrome which would appear most likely to be due to intracranial ' T h o r o t r a s t ' introduced over 30 years previously.
REFERENCES
Dale, AJD & Grafton Love, J (1967). Thorium dioxide myelopathy. Journal of the American Medical Association, 199, 606 609. French, JD (1946). Clinical manifestations of lumbar spinal arachnoiditis. Report of 13 cases. Surgery, 20, 718 729. Jorgensen, J, Hansen, PH, Steenskov, V & Ovesen, N (1975). A clinical and radiological study of chronic lower spinal arachnoiditis. Neuroradiology, 9, 139-144.
ARACHNOIDITIS FOLLOWING INTRACRANIAL 'THOROTRAST' Kendall, B (1987).-More Dilemmas in the Management of the Neurological Patient, pp. 96 I05. Churchill Livingstone, Edinburgh. Keogh, AJ (1974). Meningeal reactions seen with myodil myelography. Clinical Radiology, 25, 36l 365. Ross, JS, Masaryk, T J, M0dic, MT, Deamater, R, Bohlman, H, Wilbur, G et al. (1987). MR imaging of lumbar arachnoiditis. American Journal of Neuroradiology, 8, 885 892.
143
Shaw, MDM, Russell, JA & Grossart, KW (1978). The changing pattern of spinal arachnoiditis. Journal of Neurology, Neurosurgery and Psychiatry, 41, 97 107. Wadia, NH & Dastur, DK (1969). Spinal meningitides with radiculomyetopathy. Journal of the Neurological Sciences, 8, 239 297.
45, 141 143
Case Report: Arachnoiditis Following Intracranial 'Thorotrast' p. M . P A N D Y A
a n d A . J. K E O G H
Department of Neurological Surgery, Royal Preston Hospital, Preston A patient is reported with a painless, progressive cauda equina lesion due to arachnoiditis, the result of the contrast medium 'Thorotrast' (thorium dioxide) introduced into the brain over 30 years previously. Contrast medium introduced into the lumbar spine can give rise to aseptic adhesive inflammation (arachnoiditis). It rarely gives rise to clinical problems but, when it does so, is usually associated with back pain and only very rarely with progressive neurological deficit. P a n d y a , P . M . & K e o g h , A . J . ( 1 9 9 2 ) . Clinical Radiology 4 5 , 1 4 1 - 1 4 3 . C a s e R e p o r t : Arachnoiditis
Following
Intracranial
'Thorotrast'
CASE REPORT In October 1954 the patient, aged 21, developed a right temporal abscess, complicating chronic otitis media, and haemolytic streptococci were cultured from the pus. The abscess was aspirated and 8 cm 3 o f the contrast medium 'Thorotrast' were instilled into the cavity. Subsequently the abscess ruptured into the ventricular system, plain films of the skull revealing 'Thorotrast' in the lateral ventricles as well as in the abscess cavity. Despite this complication he recovered well, save for deafness in the right ear. In August 1955 he presented with a history of hacmoptysis, weight loss and occasional chest pain. Chest radiography showed right upper zone shadowing and a diagnosis of pulmonary tuberculosis was made, although tubercule bacilli were never isolated. His symptoms resolved and the chest film appearances returned to normal after anti-tuberculous therapy. In 1983, aged 50, he developed paraesthesiae in the left leg and foot. Myelography revealed appearances suggestive of arachnoiditis, whilst examination of the cerebrospinal fluid (CSF), apart from a protein level of 1.2 g/litre, was otherwise unremarkable. Over the next 2 years his sensory symptoms slowly progressed to affect the whole of both legs. Retention of urine with overflow incontinence developed, so that a diversionary urinary ileostomy was necessary. Over the next few years he also had progressive leg weakness, so that by November 1989 his walking was reduced to a precarious shuffle, and he had to use at least a stick to prevent falling. Examination confirmed a severe lower motor neurone paraparesis in the lower limbs with diffuse wasting, most marked on the left, reduced muscle tone and sensory loss to all modalities to the level of L2 on the left and St on the right; tendon reflexes or plantar responses could no longer be elicited. Plain films of his lumbar spine showed outlining of the dura mater (Fig. l) and further myelography revealed irregular narrowing, with obliteration of nerve root sleeves (Fig. 2), the rest of the spine being normal. Examination of the CSF again showed a raised protein at 1.9 g/ litre, but was otherwise normal. Computed tomography (CT) of the brain showed residual 'Thorotrast' (Fig. 3). At operation thick, somewhat yellow dura mater was found throughout the lumbar region, the arachnoid mater being opaque and the cauda equina a tangled, adherent mass. Histological examination of the arachnoid mater revealed dense fibrous tissue with fine calcification, with no evidence of tuberculosis.
DISCUSSION P l a i n f i l m s o f t h e l u m b a r s p i n e in t h i s p a t i e n t s h o w e d outlining of the dura mater, presumed to be due to thorium dioxide, there being no other explanation for the appearance. Although calcification was seen on histologiCorrespondence to: P. M. Pandya, Neurosurgical Registrar, Department of Neurological Surgery, Royal Preston Hospital, Preston PR2 4HT.
Fig. 1 - Lateral plain radiograph of the lumbar spine showing faintly outlined theca.
142
CLINICAL RADIOLOGY
Fig. 3 CT scan: residual 'Thorotrast' scattered throughout thc ventricular system.
Fig. 2 Lumbar myelogram: smooth and featureless theca with irregular narrowing.
cal examination of the dura and arachnoid mater, this was fine and sparse and clearly insufficient to outline the theca. A diagnosis of arachnoiditis was established from the myelographic appearances and confirmed at surgery. Arachnoiditis has no established associated clinical synd r o m e (Kendall, 1987) and, although back pain may occur, neurological deficit is rare (Shaw, 1978). It is related to a variety o f probable causes, including mechanical lumbar disease (French, 1946), infection, especially tuberculosis (Wadia and Dastur, 1969) and intraspinal contrast media (Jorgensen et al., 1975; Keogh, 1974); although m o d e r n contrast media do not appear to cause arachnoiditis, magnetic resonance imaging ( M R I ) is probably now the investigation o f choice as it is safe and p r o b a b l y sufficiently accurate (Ross et al., 1987). There was no question o f mechanical lumbar disease in this patient, and although his history was complicated by
p u l m o n a r y tuberculosis some 27 years before the onset of his current illness, there was no evidence that tuberculosis was the cause of the arachnoiditis. There was a long interval between the two episodes, his current illness had a very protracted course and there was no evidence to suggest tuberculosis either on repeated examination of the CSF, or on subsequent histological examination of the affected arachnoid mater. Although once p o p u l a r as a contrast medium, ' T h o r o trast', a radioactive c o m p o u n d predominantly a betaemitter, has long been discontinued. Ascending spinal cord damage following injection directly into the spine has been described and attributed to prolonged exposure to radiation (Dale and G r a f t o n Love, 1967). This does not seem to be the case here, as there was no evidence o f a myelopathy. This patient demonstrates arachnoiditis in the lumbar spine giving rise to a painless, slow, relentless and quite devastating c a u d a equina syndrome which would appear most likely to be due to intracranial ' T h o r o t r a s t ' introduced over 30 years previously.
REFERENCES
Dale, AJD & Grafton Love, J (1967). Thorium dioxide myelopathy. Journal of the American Medical Association, 199, 606 609. French, JD (1946). Clinical manifestations of lumbar spinal arachnoiditis. Report of 13 cases. Surgery, 20, 718 729. Jorgensen, J, Hansen, PH, Steenskov, V & Ovesen, N (1975). A clinical and radiological study of chronic lower spinal arachnoiditis. Neuroradiology, 9, 139-144.
ARACHNOIDITIS FOLLOWING INTRACRANIAL 'THOROTRAST' Kendall, B (1987).-More Dilemmas in the Management of the Neurological Patient, pp. 96 I05. Churchill Livingstone, Edinburgh. Keogh, AJ (1974). Meningeal reactions seen with myodil myelography. Clinical Radiology, 25, 36l 365. Ross, JS, Masaryk, T J, M0dic, MT, Deamater, R, Bohlman, H, Wilbur, G et al. (1987). MR imaging of lumbar arachnoiditis. American Journal of Neuroradiology, 8, 885 892.
143
Shaw, MDM, Russell, JA & Grossart, KW (1978). The changing pattern of spinal arachnoiditis. Journal of Neurology, Neurosurgery and Psychiatry, 41, 97 107. Wadia, NH & Dastur, DK (1969). Spinal meningitides with radiculomyetopathy. Journal of the Neurological Sciences, 8, 239 297.