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Abstract

A 42-year-old woman and active cocaine user complained of subacutely worsening blurred vision and imbalance. Examination of the brain MRI showed rapidly expanding white matter lesions. Brain biopsy was consistent with inflammatory demyelination. Given an unusual presentation and a history of cocaine use, a broad differential diagnosis was considered including neurologic toxidromes.

Case Presentation

A 42-year-old African American woman with a history of polysubstance abuse presented with a 2-week history of worsening headache, dizziness, imbalance, and worsening blurred vision. Her headache was sharp and focal without meningismus or positional changes. Her blurred vision was bilateral. History of substance use included cocaine, marijuana, and ecstasy pills, but no heroin or IV drug use. She had no other significant medical, surgical, family, or medication history. A review of systems was positive for night sweats, but negative for fever, rash, weakness, sensory changes, or weight loss. She had no recent travel history.
Physical examination, including a skin examination, was unremarkable. Neurologic examination was notable for normal mentation and language; poor visual acuity with only light and hand motion perception; otherwise, intact cranial nerves including pupillary responses; no sensory or motor deficit; normal reflexes; and intact limb coordination but ataxic gait.
Blood cell counts, chemistries, erythrocyte sedimentation rate, and C-reactive protein were normal. Urine drug screen was positive for cocaine and benzodiazepine. Brain MRI showed large, confluent, asymmetric, and sharply demarcated T2/FLAIR hyperintensities involving the bilateral white matter extending from periventricular to subcortical regions of the parietofrontal lobes and the right temporal lobe (Figure 1A). Subcortical U fibers were spared, and perilesional edema was minimal. Associated gadolinium enhancement was nodular in some areas, prominent at the peripheral edges, or ring enhancing in other areas. There was no hemorrhage or infarction.
Figure 1 Brain MRI
(A) Brain MRI at presentation. A.a–A.d shows axial (a and b) fluid attenuation inversion recovery (FLAIR) sequence images in axial view (a and b) and right hemisphere sagittal view (c) and left hemisphere sagittal (d) view. A.e–A.h shows corresponding postgadolinium injection T1 sequences images (T1 Gd). (B) At hospital day 14, brain MRI shows progression of FLAIR hyperintense signal change including a new FLAIR hyperintense lesion (arrow) separated in space from prior lesions. (C) At the 5-month follow-up, FLAIR sequences (C.a–C.d) show improvement in hyperintense signal change with complete resolution of gadolinium enhancement (C.e–C.h).
Testing was negative for syphilis, Lyme, tuberculosis, and JC virus antibody. Serologies were also negative for antinuclear antibody, double-stranded DNA antibody, Smith antibody, Ro antibody, La antibody, antineutrophil cytoplasmic antibody, aquaporin-4 antibody, and myelin oligodendrocyte glycoprotein antibody, and very long-chain fatty acid levels were normal. Serum autoimmune encephalopathy panel was negative. CSF testing showed lymphocytic pleocytosis (39 WBC/mm3, 95% lymph), normal red cell counts, elevated CSF protein at 61 mg/dL, and 52 mg/dL of glucose. CSF Gram stain and culture were negative, as were viral studies (HIV, enterovirus, CMV, EBV, and VZV by PCR and West Nile IgG/IgM). CSF MBP was >160 ng/mL (normal level: <4 ng/mL) and 4 CSF-specific oligoclonal bands were detected.
Other imagings, including MRI of orbits and spine, CT of the chest, abdomen and pelvis, along with CT angiogram of the head, were unremarkable. MR spectroscopy of the brain was nonspecific, showing slightly increased choline and lactate peaks with slightly decreased N-acetyl acetate peak. Flow cytometry and cytology showed no malignant cells.
Her hospital course (Figure 2) was complicated by new-onset seizure on hospital day 7. She received 1 g of IV methylprednisolone daily for 5 days between hospital days 11 and 15, after which she had subjective, but not objective, improvement. A repeat brain MRI on hospital day 13 showed progression with a new enhancing T2/FLAIR hyperintense lesion in the left frontal periventricular region. The right parietofrontal lobe lesion had enlarged, and the left parietofrontal lesion had extended into the left temporal lobe (Figure 1B). Based on these findings, an additional 5-day course of 1 g of IV methylprednisolone was given starting on hospital day 17, followed by plasma exchange.
Figure 2 Timeline of Hospital Course and Treatment
Due to the patient's ongoing disease activity and initial poor therapeutic response, a stereotactic needle biopsy of the right parietal lobe lesion was performed on hospital day 15 to exclude neoplasia and obtain a definitive diagnosis. Histologic and immunohistochemical studies showed abundant macrophages and astrogliosis in the brain parenchyma with focal perivascular inflammation (Figure 3). Luxol fast blue/periodic acid-Schiff stain showed changes consistent with diffuse rather than perivenular demyelination. There was no evidence of a neoplastic process. Staining for the BK virus was negative. The results of the biopsy were thus consistent with an inflammatory demyelinating process.
Figure 3 Brain Pathology
Hematoxylin & eosin (H&E) stain at 20X (A) and at 40X (B) showing sheets of macrophages, reactive astrocytes, and focal perivascular lymphocytic cuffing. Luxol fast blue/periodic acid-Schiff (LFB/PAS) stain at 20X (C) and at 40X (D)showing loss of myelin (blue). (E) Glial fibrillary acidic protein immunohistochemistry shows reactive gliosis. (F) CD68 immunohistochemistry shows sheets of macrophages noted on H&E sections.
Patient was discharged home after a 1-month hospital stay, with a plan for clinical follow-up without starting maintenance immunotherapy. At discharge, examination was notable for impaired vision limited to light and motion perception only and mild gait instability. At the 5-month follow-up, she was independent with activities of daily living and walked unaided. Neurologic examination was notable for impaired visual acuity (finger counting only) with subtle left visual field cut and difficulty with tandem gait. Repeat brain MRI showed marked improvement (Figure 1C).

Differential Diagnosis

Inflammatory, infectious, neoplastic, and toxic etiologies were considered in the differential diagnosis. The diagnosis of multiple sclerosis (MS) requires objective evidence of CNS lesions disseminated in space and time in the setting of a typical clinically isolated syndrome.1 We considered focal supratentorial syndrome, referable to bilateral optic radiations, as the clinically isolated syndrome in this case. Repeat MRI demonstrated a new T2/FLAIR hyperintense lesion, which provided objective evidence of dissemination in space and time (Figure 1, A and B). However, the atypical clinical and imaging features of this case compelled a comprehensive evaluation for alternative diagnoses.2 Imaging “red flags” included the large confluent lesions and gadolinium enhancement of all lesions on MRI at presentation. MRI lesions were essentially periventricular with no strictly juxtacortical, infratentorial, or spinal cord lesions. The rapid progression on MRI was also considered unusual for MS. Although nonspecific to some extent, the presence of CSF-specific oligoclonal bands and the pathologic confirmation of inflammatory demyelination were in support of an MS diagnosis. Of importance, these results were indicative of an immune-mediated inflammatory process and informed treatment options. Following an extensive evaluation without indication of an alternative, the diagnosis of MS was made based on an inflammatory demyelinating condition with no better explanation. Below we discuss the potential alternative inflammatory demyelinating processes that were carefully considered.
The typical clinical presentation of acute disseminated encephalomyelitis (ADEM)3 involves encephalopathy, which was missing in this case. Characteristic ADEM imaging findings of poorly defined T2 hyperintense lesion borders and involvement of the gray matter were also lacking. The negative serologies and lack of optic nerve and/or spinal cord involvement make myelin oligodendrocyte glycoprotein antibody disease (MOGAD) and neuromyelitis optica spectrum disorder (NMOSD) less likely. Although, we note there can be seronegative cases of NMOSD, which can present early on with isolated cerebral involvement.
Levamisole-induced leukoencephalopathy (LIL) was considered based on a history of drug use and a urinalysis positive for cocaine. The syndrome of LIL may manifest with altered mentation, focal neurologic signs, often ataxia, and seizures. Imaging is often notable for multifocal large gadolinium-enhancing white matter lesions that are frequently indistinguishable from that of MS or ADEM.4 CSF findings in LIL may be normal or show pleocytosis and/or oligoclonal bands.4,5 Lesional biopsy have been reported to show perivascular cuffing with lymphocytic infiltrates, abundant macrophages, and pathologic features generally congruous with active demyelination. Favorable response to treatment with corticosteroids is typical, with occasional need for plasma exchange. Levamisole or its metabolite was not specifically measured in this patient due to LIL being a late consideration in the differential diagnosis. The lack of specific testing for levamisole was a missed opportunity and a limitation in this case. It should be noted that cocaine by itself can induce acute/subacute leukoencephalopathy, which on biopsy demonstrates a vacuolar degeneration, which was not seen on the study of this patient.
Other systemic inflammatory disorders with CNS involvement, including systemic lupus erythematosus, Sjogren disease, Behcet disease, and neurosarcoidosis were considered but felt less likely in the absence of systemic manifestations, negative serologies, and/or lack of characteristic imaging features. Autoimmune encephalitides were also considered; however, imaging findings were atypical, and serum autoimmune encephalitis panel was negative. CSF autoimmune encephalitis panel was sent but could not be completed because of insufficient quantity. CNS vasculitis was considered less likely due to CT angiogram and brain biopsy results. The pathology was reassuring in terms of neoplastic etiologies such as gliomatosis cerebri and primary CNS lymphoma. CNS infections were considered given the CSF lymphocytic pleocytosis (e.g., viral, spirochete, fungal, and mycobacterial etiologies), but testing was negative, and the patient stabilized without antimicrobial administration. Progressive multifocal leukoencephalopathy was less likely based on negative JC virus serology and negative BK virus staining on the brain biopsy specimen. Adrenoleukodystrophy was considered based on imaging features but is less likely based on normal very long-chain fatty acid levels and the female sex of this patient.

Final Diagnosis

A diagnosis of MS was made, after extensive evaluation and serious consideration given to LIL.

Discussion

MS is a chronic relapsing CNS inflammatory demyelinating disorder. An MS diagnosis depends on both clinical and paraclinical data, which are acknowledged to be of limited specificity. Atypical demyelinating syndromes that overlap with MS on clinical or pathologic grounds are well recognized and test the limits of the diagnostic criteria for MS.6 Tumefactive demyelination is a term used to describe inflammatory demyelinating syndromes that present with tumor-like lesions. Many cases of tumefactive demyelination subsequently have a clinical and imaging course typical of MS, indicating that large expansile lesion formation is rare but not inconsistent with the diagnosis of MS.7 Common tumefactive demyelination features on imaging include mass effect, perilesional edema, and T2 hypointense rim, which were not found in this case. Another acute form of MS, the Marburg variant, is a severe rapidly progressive demyelinating syndrome.6 Historically, the Marburg variant was associated with death within a year of clinical presentation, but more recent reports indicate a nonfatal course is possible with aggressive immunotherapy.8 Imaging shows enlarging white matter lesions, and pathology is often more severe than the typical MS, with necrosis superimposed on diffuse inflammatory demyelination. While Marburg variant was an early consideration, it was felt less likely in our case due to a stable clinical course without intense maintenance immunotherapy and improvement on follow-up imaging. Acute hemorrhagic encephalomyelitis and Balo concentric sclerosis were unlikely because the clinical, imaging, and pathology features lacked evidence of hemorrhage, focal perivenous demyelination, or concentric demyelination.
LIL is a rare consequence of exposure to levamisole and should be considered in the context of CNS injury following cocaine use.4,9,10 Levamisole, previously used as an anthelmintic or adjuvant chemotherapy, was withdrawn from the US drug market due to its risk of neutropenia and cutaneous vasculitis.4 It remains, however, a frequent cocaine adulterant detected in up to 70% of the supply in the United States, making illicit drug use an important route of exposure to levamisole.11 Most cases of LIL occurred with therapeutic dosing of levamisole, either as monotherapy or with 5-fluorouracil. However, there have been several reports of LIL associated with cocaine use.5,12 Clinically, LIL is a subacute onset focal neurologic syndrome with or without encephalopathy.4 The clinical course is typically monophasic, with good response to corticosteroids and/or other acute immunomodulatory treatments. On imaging, one finds large multifocal white matter T2 hyperintense lesions with gadolinium enhancement, resembling ADEM or MS. CSF findings can include pleocytosis and CSF oligoclonal bands. Reported LIL biopsies demonstrate active inflammatory demyelination, perivascular inflammatory infiltrates, abundant macrophages, astrogliosis, and loss of myelin. Of importance, the laboratory, imaging, and pathologic features of LIL can be indistinguishable from ADEM and MS. Exposure to levamisole is also associated with a syndrome of cutaneous vasculitis with neutropenia, elevated C-reactive protein, and positive antineutrophilic cytoplasmic antibody, which may be more commonly encountered than LIL.13 Review of the literature indicates there is little overlap between the incidence of LIL and that of the levamisole-induced cutaneous vasculitis. In LIL, levels of C-reactive protein and antineutrophilic cytoplasmic antibody have been normal when reported, and most cases do not mention neutropenia or skin findings. Therefore, the lack of systemic manifestations of levamisole exposure are unlikely to be helpful in excluding an LIL diagnosis. Maintaining a high index of suspicion in the appropriate clinical context for LIL is the best approach and permits timely testing for levamisole or its metabolite, which are detected in the urine for up to 2–3 days following exposure.13
In conclusion, the diagnosis of atypical demyelinating syndromes remains a challenge. Exclusion of infectious, other inflammatory, and neoplastic etiologies is important. Brain biopsy is helpful to exclude alternative diagnoses but often does not provide an exclusive diagnosis. A high index of suspicion for neurologic toxidromes should be maintained in the appropriate clinical context.

Glossary

ADEM
acute disseminated encephalomyelitis
LIL
levamisole-induced leukoencephalopathy
MOGAD
myelin oligodendrocyte glycoprotein antibody disease
MS
multiple sclerosis
NMOSD
neuromyelitis optica spectrum disorder

Appendix Authors

NameLocationContribution
Tolulope O. Amiola, MDDepartment of Neurology, VCU School of MedicineDrafting/revision of the article for content, including medical writing for content; major role in the acquisition of data; and analysis or interpretation of data
Unsong Oh, MDDepartment of Neurology, VCU School of MedicineDrafting/revision of the article for content, including medical writing for content; major role in the acquisition of data; and analysis or interpretation of data
Hope Richard, MD, PhDDepartment of Neuropathology, VCU School of MedicineMajor role in the acquisition of data; analysis or interpretation of data
Scott D. Newsome, DODepartment of Neurology, Johns Hopkins HospitalDrafting/revision of the article for content, including medical writing for content; analysis or interpretation of data
Jennifer Graves, MD, PhDDepartment of Neurosciences, University of California at San DiegoDrafting/revision of the article for content, including medical writing for content; analysis or interpretation of data
Scott S. Zamvil, MD, PhDDepartment of Neurology, Program in Immunology, University of California at San FranciscoDrafting/revision of the article for content, including medical writing for content; analysis or interpretation of data
Myla D. Goldman, MD, MScDepartment of Neurology, VCU School of MedicineDrafting/revision of the article for content, including medical writing for content; major role in the acquisition of data; and analysis or interpretation of data

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Wu V-C, Huang J-W, Lien H-C, et al. Levamisole-induced multifocal inflammatory leukoencephalopathy: clinical characteristics, outcome, and impact of treatment in 31 patients. Medicine (Baltimore). 2006;85(4):203-213.
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Tollens N, Post P, Martins Dos Santos M, Niggemann P, Warken M, Wolf J. Multifocal leukoencephalopathy associated with intensive use of cocaine and the adulterant levamisole in a 29-year old patient. Neurol Res Pract. 2022;4(1):38.
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Nozaki K, Abou-Fayssal N. High dose cyclophosphamide treatment in Marburg variant multiple sclerosis A case report. J Neurol Sci. 2010;296(1-2):121-123.
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Information & Authors

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Published In

Neurology® Neuroimmunology & Neuroinflammation
Volume 11Number 3May 2024
PubMed: 38285968

Publication History

Received: October 16, 2023
Accepted: November 27, 2023
Published online: January 29, 2024
Published in print: May 2024

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Disclosure

The authors report no relevant disclosures. Go to Neurology.org/NN for full disclosures.

Study Funding

National Multiple Sclerosis Society.

Authors

Affiliations & Disclosures

From the Departments of Neurology (T.O.A., U.O., M.D.G.) and Neuropathology (H.R.), VCU School of Medicine, Richmond, VA; Department of Neurology (S.D.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurosciences (J.G.), University of California at San Diego, La Jolla and Department of Neurology (S.S.Z.), Program in Immunology, University of California at San Francisco.
Disclosure
Financial Disclosure:
1.
NONE
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1.
NONE
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1.
NONE
Legal Proceedings:
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From the Departments of Neurology (T.O.A., U.O., M.D.G.) and Neuropathology (H.R.), VCU School of Medicine, Richmond, VA; Department of Neurology (S.D.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurosciences (J.G.), University of California at San Diego, La Jolla and Department of Neurology (S.S.Z.), Program in Immunology, University of California at San Francisco.
Disclosure
Financial Disclosure:
1.
scientific advisory board - Horizon therapeutics
scientific advisory board - Genentech
Research Support:
1.
NONE
Stock, Stock Options & Royalties:
1.
NONE
Legal Proceedings:
1.
NONE
From the Departments of Neurology (T.O.A., U.O., M.D.G.) and Neuropathology (H.R.), VCU School of Medicine, Richmond, VA; Department of Neurology (S.D.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurosciences (J.G.), University of California at San Diego, La Jolla and Department of Neurology (S.S.Z.), Program in Immunology, University of California at San Francisco.
Disclosure
Financial Disclosure:
1.
NONE
Research Support:
1.
NONE
Stock, Stock Options & Royalties:
1.
NONE
Legal Proceedings:
1.
NONE
From the Departments of Neurology (T.O.A., U.O., M.D.G.) and Neuropathology (H.R.), VCU School of Medicine, Richmond, VA; Department of Neurology (S.D.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurosciences (J.G.), University of California at San Diego, La Jolla and Department of Neurology (S.S.Z.), Program in Immunology, University of California at San Francisco.
Disclosure
Financial Disclosure:
1.
Scientific advisory board - Biogen
Scientific advisory board - Genentech
Scientific advisory board - Bristol Myers Squibb
Scientific advisory board - EMD Serono
Scientific advisory board - Greenwich Biosciences
Scientific advisory board - Novartis
Scientific advisory board - Horizon Therapeutics
Scientific advisory board - TG Therapeutics
Research Support:
1.
Commercial - Roche: Lead PI for clinical trial
Commercial - Roche: Clinical trial (paid directly to institution)
Commercial - Genentech: Clinical trial (paid directly to institution)
Commercial - Biogen: Clinical trial (paid directly to institution)
Commercial - Lundbeck: Clinical trial (paid directly to institution)
Society - National MS Society : Clinical trial (paid directly to institution)
Governmental - Department of Defense: Clinical trial (paid directly to institution)
Foundation - Patient Centered Outcome Research Institute: Clinical trial (paid directly to institution)
Foundation - Stiff Person Syndrome Research Foundation: Research support
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NONE
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Jennifer Graves, MD, PhD https://orcid.org/0000-0003-1539-1940
From the Departments of Neurology (T.O.A., U.O., M.D.G.) and Neuropathology (H.R.), VCU School of Medicine, Richmond, VA; Department of Neurology (S.D.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurosciences (J.G.), University of California at San Diego, La Jolla and Department of Neurology (S.S.Z.), Program in Immunology, University of California at San Francisco.
Disclosure
Financial Disclosure:
1.
Steering Committee - Novartis
Advisory Board - Horizon
Advistory Board - TG Therapeutics
Research Support:
1.
NONE
Stock, Stock Options & Royalties:
1.
NONE
Legal Proceedings:
1.
NONE
Scott S. Zamvil, MD, PhD https://orcid.org/0000-0003-2720-9915
From the Departments of Neurology (T.O.A., U.O., M.D.G.) and Neuropathology (H.R.), VCU School of Medicine, Richmond, VA; Department of Neurology (S.D.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurosciences (J.G.), University of California at San Diego, La Jolla and Department of Neurology (S.S.Z.), Program in Immunology, University of California at San Francisco.
Disclosure
Financial Disclosure:
1.
Consulting - Genzyme
Consulting - Alexion
Consulting - Roche
Consulting - Novartis
Consulting - Horizon (Amgen)
Research Support:
1.
NIH - NIAID (1 R01AI131624-01A1): Repertoire selection of AQP4-specific T cells that cause CNS autoimmune disease
NIH - NIAID (1 RO1 AI170863-01A1): Characterization of T cells in MOG antibody-associated disease
Stock, Stock Options & Royalties:
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NONE
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Myla D. Goldman, MD, MSc https://orcid.org/0000-0002-5675-945X
From the Departments of Neurology (T.O.A., U.O., M.D.G.) and Neuropathology (H.R.), VCU School of Medicine, Richmond, VA; Department of Neurology (S.D.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurosciences (J.G.), University of California at San Diego, La Jolla and Department of Neurology (S.S.Z.), Program in Immunology, University of California at San Francisco.
Disclosure
Financial Disclosure:
1.
Advisory Board - Alexion
Consultant - Genetech
Advisory Board - Horizon
Data Safety Monitoring Board - Anokion
Data Safety Monitoring Board - Immunic
Advisory Board - Novartis
Advisory Board - EMD Serono
Research Support:
1.
Foundation - National MS Society: Assessment of the Clinical Importance of Insulin Resistance & Steroid Associated Hyperglycemia in Relapsing Multiple Sclerosis
Governmental - Department of Defense: Systolic Blood Pressure Variability and Multiple Sclerosis Disease Progression
Governmental - PCORI: Determining the Effectiveness of early Intensive Versus Escalation approaches for the treatment of Relapsing-Remitting Multiple Sclerosis (DELIVERMS).
Foundation - National MS Society: Validation of 6MW Gait Speed Trajectory as a Clinical Outcome Measure of Demyelination
Stock, Stock Options & Royalties:
1.
NONE
Legal Proceedings:
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Notes

Correspondence Dr. Amiola [email protected]
Go to Neurology.org/NN for full disclosures. Funding information is provided at the end of the article.
The Article Processing Charge was funded by National Multiple Sclerosis Society.
Submitted and externally peer reviewed. The handling editor was Editor Josep O. Dalmau, MD, PhD, FAAN.

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  1. Levamisole-induced leukoencephalopathy, Radiopaedia.org, (2024).https://doi.org/10.53347/rID-183133
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