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Sclerosing Spinal Pachymeningitis1 a Complication of Intrathecal Administration of Depo-Medrol2 for Multiple Sclerosis

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Sclerosing Spinal Pachymeningitis1 a Complication of Intrathecal Administration of Depo-Medrol2 for Multiple Sclerosis J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.11.1124 on 1 November 1976. Downloaded from Journal ofNeurology, Neurosurgery, and Psychiatry, 1976, 39, 1124-1128 Sclerosing spinal pachymeningitis1 A complication of intrathecal administration of Depo-Medrol2 for multiple sclerosis J. L. BERNAT3, C. H. SADOWSKY, F. M. VINCENT, R. E. NORDGREN, AND G. MARGOLIS From the Departments ofMedicine (Neurology) and Pathology, Dartmouth-Hitchcock Medical Center, Hanover, New Hampshire, USA SYNOPSIS Reported complications of intrathecal steroid therapy include aseptic meningitis, infectious meningitis, and arachnoiditis. We report a case of sclerosing spinal pachymeningitis com- plicating the attempted intrathecal administration of Depo-Medrol for multiple sclerosis. The lesion is characterised by concentric laminar proliferation ofneomembranes within the subdural space ofthe by guest. Protected copyright. entire spinal cord and cauda equina, resulting from repeated episodes ofinjury and repair to the spinal dura mater by Depo-Medrol. There is clinical and laboratory evidence that Depo-Medrol produces meningeal irritation and that the vehicle is the necrotising fraction. Intrathecal corticosteroids have been used to treat a What has clearly been learned from multiple trials variety of neurological disorders, notably multiple is that the use of intrathecal steroids is not without sclerosis, arachnoiditis, and herniated intervertebral risk. There have been reports of associated adhesive disc. The efficacy of intrathecal steroids in the treat- arachnoiditis (Dereux et al., 1956; Goldstein et al., ment of arachnoiditis has been demonstrated 1970; Nelson et al., 1973; Dullerud and Morland, (Feldman and Behar, 1961; Sehgal and Gardner, 1976; Nelson, 1976), aseptic meningitis (Goldstein et 1962; Savastano, 1968). Subarachnoid and epidural al., 1970; Nelson et al., 1973; Schock and Wieczorek, injections of steroids have been shown to be of value 1974), tuberculous meningitis (Roberts et al., 1967), in the palliation of radicular symptoms of herniated cryptococcal meningitis and epidural abscess (Shealy, intervertebral disc (Gardner et al., 1963; Winnie et al., 1966), in addition to the transient immediate effects of 1972; Dilke et al., 1973). The efficacv of intrathecal leg paraesthesiae (Nelson et al., 1973), bladder steroids in the treatment of multiple sclerosis, how- paralysis (Van Buskirk et al., 1964; Lance, 1969), ever, remains controversial. Treatment has been and meningeal irritation (Feldman and Behar, 1961). reported to reduce spasticity (Lance, 1969), improve The infectious meningitides presumably reflect poor gait and sphincter control (Baker, 1967), and lead to technique or an immunosuippressive steroid effect, http://jnnp.bmj.com/ a more rapid remission of symptoms (Boines, 1963). while the transient and aseptic complications are con- However, other studies have failed to document sidered to represent a chemical inflammatory res- improvement or have demonstrated only transient ponse to an irritant present in the steroid preparation. benefit (Van Buskirk et al., 1964; Goldstein et al., The following case demonstrates an additional 1970; Nelson et al., 1973). untoward complication occurring when the steroid preparation gains access to the subdural space. ' Presented at the Twenty-Eighth Annual Meeting of the American Academy of Neurology, Toronto, April 1976. CASE REPORT on September 25, 2021 2The trade name is used as the authors attribute the complication described to the vehicle ofthe injection fluid and not to methylpredniso- When first examined in 1972, this 35 year old woman lone acetate. Editor. described a 10 year history of remitting and relapsing s Address for correspondence: Dr James L. Bernat, Division of Neurology, Dartmouth-Hitchcock Medical Center, Hanover, New symptoms including transient limb paraesthesiae, Hampshire 03755. USA. gait unsteadiness, visual blurring, headaches, vertigo, (Accepted 9 July 1976.) tinnitus, urinary retention, and hand tremor. Exam- 1124 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.11.1124 on 1 November 1976. Downloaded from Sclerosing spinal pachymeningitis 1125 ination revealed bilateral temporal disc pallor, right strated sharply bordered foci of demyelination with homonymous hemianopia, bilateral internuclear axonal sparing, loss of oligodendroglia, and astro- ophthalmoplegia, vertical nystagmus, diminished cytic hyperplasia. More active lesions exhibited position and vibration sensation below the knees, phagocytosis of degenerating myelin by foamy truncal ataxia, diffuse hyperreflexia, a right extensor macrophages and early perivascular lymphocytic plantar response, and euphoria. Her cerebrospinal cuffing. fluid (CSF) protein was 0.46 g/l with 25.9 % gamma A 5 x 5 x 5 cm recent haematoma occupied the globulin. The diagnosis of multiple sclerosis was white matter of the left cerebral hemisphere, lateral made. A two weeks course ofintramuscular ACTH 40 and superior to the basal ganglia, without sub- units twice daily failed to produce objective improve- arachnoid or ventricular extension. The brain ment. parenchyma surrounding it was oedematous and Over the next year she received six intrathecal yellowish. There was no apparent relationship injections of Depo-Medrol 80 mg. With each injec- between the borders of the haemorrhage and the tion, she claimed transient benefit but no objective demyelinative plaques. improvement was documented. The entire spinal cord and cauda equina were Repeat examinations in 1973 and 1974 revealed encased by a firm, brownish, dense new tissue obliter- progression of her illness to include a diminished right ating and enlarging the subdural space, and adhering corneal reflex, flattening of the right nasolabial fold, the thickened dura mater to the arachnoid mater diminished gag reflexes, spastic paraparesis, and a (Fig. 1). There was no evidence of secondary vascular neurogenic bladder. A trial of percutaneous epidural compromise of the cord or nerve roots. The new sub- dorsal column stimulation failed to reduce her dural tissue changes ranged from early and active to by guest. Protected copyright. spasticity. In February 1975, she was given intrathecal old and established. The most recent lesion was a Depo-Medrol 80 mg without subsequent subjective linear zone of coagulative necrosis in the posterior or objective improvement. The CSF opening pressure dura mater and epidural tissues in the region of the was 90 mm H20; the protein content was 1.33 g/l; cauda equina, probably the tract of a necrotising there were no cells and the fluid was sterile. injection mass. Fresh haemorrhage, early fibroblastic On 8 October 1975, she suddenly developed head- and endothelial proliferation, and macrophage ache, right-sided weakness, and difficulty in speaking. reaction bordered this lesion in the subdural space. On examination, she was alert and presented new The prominent process was that of organising findings of right hemiparesis, right hemihypaesthesia, granulation tissue and scar formation reflecting the and nonfluent dysphasia. There were no signs of various stages ofrepair ofa necrotising, haemorrhagic meningeal irritation. A course of ACTH was begun, lesion. A layered pattern of reaction was seen indica- then terminated when she became febrile and devel- tive ofrepeated episodes ofinjury and repair, with the oped oedema. Lumbar puncture was performed on older inner laminae overlain by newer laminae the sixth hospital day. Opening pressure and mano- (Fig. 2). These neomembranes were generally closely metrics were unobtainable. The CSF contained apposed and adherent to both inner dural and outer 34 x 106 red blood cells per litre, no leucocytes, arachnoid membranes. The subarachnoid space was protein content of 16 g/l and glucose of 5.0 mmol/l. involved in a similar but less severe manner, with both The fluid was sterile. Depo-Medrol 80 mg was instilled old and recent changes. intrathecally. She suffered a sudden cardiorespiratory arrest on the tenth hospital day. DISCUSSION Notably, she had neither undergone myelography http://jnnp.bmj.com/ nor intrathecal injections of any medication except A sclerosing spinal pachymeningitis resulted from Depo-Medrol. At no time were there clinical or the unintentional repeated subdural injections of laboratory findings indicative of meningitis. Depo-Medrol. That a necrotising agent present in Depo-Medrol was responsible for the pachymening- PATHOLOGY itis is suggested by the presence ofcoagulative necrosis surrounding the most recent needle tract, and the con- Three major central nervous system pathological centric subdural laminar proliferation resulting from processes were present at postmortem: multiple repeated episodes of injury and repair to the inner on September 25, 2021 sclerosis, intracerebral haemorrhage, and sclerosing dura mater. That the Depo-Medrol was injected into spinal pachymeningitis. the subdural space is suggested by the zero opening Typical demyelinative plaques ofall ages and stages pressure and the CSF protein of 16 g/l of the final ofactivity were present throughout theperiventricular lumbar puncture. We presume the formation of a white matter, centrum semiovale, midbrain, pons, 'second sac' (Rogoff et al., 1974) early in her course, medulla, and spinal cord. The older lesions demon- either by an unintentional subdural Depo-Medrol J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.11.1124 on 1 November 1976. Downloaded from 1126 J. L. Bernat,
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