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Acute neutrophilic meningitis treated successfully with corticosteroids.

Abstract: This report describes a cocaine user who presented with polymorphonuclear pleocytosis in cerebrospinal fluid mimicking bacterial meningitis. Thorough investigation of the cerebrospinal fluid did not reveal evidence of bacteria or fungi. Clinical deterioration was observed in spite of empiric treatment with antibiotics. The patient had a favorable outcome after corticosteroid treatment.


Multiple acute and long-term neurologic complications have been reported with cocaine abuse, including headaches, seizures, cerebral hemorrhage, cerebral infarction, cerebral atrophy, and cerebral vasculitis. (1) We report a case of acute neutrophilic meningitis probably caused by cocaine-induced cerebral vasculitis treated successfully with corticosteroids.

Case Report

A 33-year-old man presented with severe headache and fever (39[degrees]C) of 10 days' duration. He was an occasional intranasal cocaine user. Neurologic examination was normal. Serum concentration of C-reactive protein was increased (18 mg/L), with a high erythrocyte sedimentation rate (83 mm/h). Leukocytosis (18,700 cells/ [mm.sup.3]) and thrombocytosis (600,000 cells/[mm.sup.3]) were present in the peripheral blood. A lumbar puncture revealed 300 cells/rmn3 with 90% neutrophils, protein 76 mg/dl, immunoglobulin (Ig) G 17.1 mg/dl, glucose 54 mg/dl (102 mg/dl in the serum), and an increased cerebrospinal fluid (CSF) IgG index without oligoclonal bands. CSF stains for bacteria and fungi were negative. Results of CSF and blood cultures and cryptococcal antigen were negative. Polymerase chain reaction for mycobacteria and viruses in CSF and human immunodeficiency virus in the serum was negative. Serologic tests for syphilis, listeria, rickettsias, and mycoplasma were negative. Antineutrophil cytoplasmic, anticardiolipin IgG and IgM, antineuronal, antinuclear, and anti-DNA antibodies in the serum were all negative. Cocaine metabolites were not detected in his urine. Magnetic resonance imaging of the brain showed thickness of the meninges. He was treated empirically with antibiotics for bacterial meningitis, with no improvement. On hospital Day 11, his condition deteriorated, with development of signs of meningism, disorientation, confusion, and bilateral hearing impairment. The persistent fever, the clinical deterioration, and the persistent inflammatory changes in CSF without identification of any infectious pathogen together with the failure of antibiotics led us to suspect a cocaine-induced cerebral vasculopathy. A magnetic resonance angiogram of the brain was reported as normal. No permission for a brain biopsy was obtained. Prednisolone was initiated at a dose of 1 mg/kg for 1 month and the patient rapidly improved, with no residual neurologic deficit. The dose was tapered over a period of 3 months.


Cerebral vasculitis related to cocaine has been reported in eight cases in the literature, proven by either angiugraphy or biopsy. (2) Angiographic evidence of vasculitis was absent in three of the described cases as in our case, because the disease can be limited to the small vessels. (3) Leptomeningeal and cortical biopsies are the diagnostic procedures of choice in the absence of angiographically proven cerebral vasculitis. Only one of the cases reported had CSF neutrophilic pleocytosis mimicking bacterial meningitis as in the present report. (2) The mechanism by which cocaine induces polymorphonuclear pleocytosis in CSF has not been established. It has been proposed that it may be a consequence of a vasculitic hypersensitivity reaction of small meningeal vessels to cocaine. Therapy with corticosteroids has been empiric, aiming at suppressing the ongoing inflammatory process. The role of corticosteroids in this condition is still controversial, but some authors recommend its use in cases where abstinence some cocaine does not stabilize the clinical course. (4)


Cocaine-induced cerebral vasculitis should be included in the differential diagnosis of neutrophilic meningitis in cocaine users when no pathogen can be detected and the antibiotics fail to control the inflammatory process. Whether early treatment with corticosteroids prevents residual neurologic deficits or death needs further evaluation.

Key Points

* Cerebral vasculitis is a rare complication of cocaine abuse.

* Eight cases of cerebral vasculitis have been reported in the literature.

* One reported case presented with polymorphonuclear pleocytosis in cerebrospinal fluid mimicking bacterial meningitis.

* Acute neutrophilic meningitis may rarely be associated with cocaine use when no other causative agent can be detected and the antibiotic treatment has failed.


(1.) Warner EA. Cocaine abuse. Ann Intern Med 1993; 119:226-235.

(2.) Gradon JD, Wityk R. Diagnosis of probable cocaine-induced cerebral vasculitis by magnetic resonance angiography. South Med J 1995; 88: 1264-1266.

(3.) Case records of the Massachusetts General Hospital: Weekly clinicopathological exercises--Case 27-1993: A 32-year-old man with the sudden onset of a right-sided headache and left hemiplegia and hemianesthesia. N Engl J Med 1993; 329:117-124.

(4.) Giang DW. Central nervous system vasculitis secondary to infections, toxins, and neoplasms. Semin Neurol 1994; 14:313-319.

From the Academic Department of Medicine, Hippokration General Hospital, Athens, Greece.

Reprint requests to Alexandra Alexopoulou, MD, 20 N. Politi Street, 16346 Hilioupolis, Athens, Greece. Email:

Accepted April 8, 2002.
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Article Details
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Title Annotation:Case Report
Author:Dourakis, Spyros P.
Publication:Southern Medical Journal
Geographic Code:4EUGR
Date:Sep 1, 2003
Previous Article:Severe acute respiratory syndrome: an overview.
Next Article:Large dopamine-secreting pheochromocytoma: case report.

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