Recurrent leukoencephalopathy in a cocaine abuser

Bianco, Federico; Iacovelli, Elisa; Tinelli, Emanuele; Lepre, Chiara; Pauri, Flavia

doi:10.1016/j.neuro.2011.03.005

Cited by 27 publications

(43 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the very few reports of cocaine-associated leukoencephalopathy, the presence of levamisole has been suspected but never demonstrated [1][2][3][4]. One originality of the present observation is that a significant exposure to levamisole was proven by hair testing.…”

Section: Discussionmentioning

confidence: 54%

See 1 more Smart Citation

Susac-Like Syndrome in a Chronic Cocaine Abuser: Could Levamisole Play a Role?

et al. 2014

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 54%

“…Despite the wide abuse of cocaine, toxic leukoencephalopathy remains still a relatively rare complication [1,2]. The possible synergistic role of adulterants is frequently debated, and among them, levamisole is an agent that has been associated with leukoencephalopathy [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Susac-Like Syndrome in a Chronic Cocaine Abuser: Could Levamisole Play a Role?

et al. 2014

View full text Add to dashboard Cite

“…In addition, the medication has been directly associated with leukoencephalopathy [8][9][10][11] . The pathology is believed to be similar to other spongiform encephalopathies, where fluid entrapment is found in small vacuoles within the myelin lamellae 1 . The apparent progression of the brain images despite the steady clinical improvement is due to the expansion of such vacuoles 1 .…”

mentioning

confidence: 81%

“…The pathology is believed to be similar to other spongiform encephalopathies, where fluid entrapment is found in small vacuoles within the myelin lamellae 1 . The apparent progression of the brain images despite the steady clinical improvement is due to the expansion of such vacuoles 1 . There is no general consensus on the treatment of toxic leukoencephalopathy.…”

mentioning

confidence: 81%

Cocaine-Induced Recurrent Leukoencephalopathy

González‐Duarte

Williams²

2013

Neuroradiol J

View full text Add to dashboard Cite

SUMMARY -Cocaine-induced leukoencephalopathy is a rare neurological complication. It is most likely related to the substances used to adulterate the cocaine. Levamisole is one of the most common Case ReportA 40-year old woman with chronic daily use of cocaine was admitted to the ER for acute onset of confusion, altered language and mild fever. At entry, her blood pressure was 110/70 mmHg, temperature was 38.5ºC and she exhibited motor aphasia. The rest of the examination was normal. Laboratory tests were within normal limits and HIV was negative. A lumbar puncture showed leucocytes of 200 cells/ mm 3 (75% PMN, 25% MN), glucose of 85 mg/dl, proteins of 35 mg/dl, negative gram and fungal stains, and negative PCR for HSV-1 and 2 and Mycobacterium tuberculosis. Serum HIV and skin tuberculin tests were negative. T2 and FLAIR sequences of the brain MRI displayed areas of hyperintense signal in the white matter of the left parietal lobe ( Figure 1A,B). The DWI/ADC sequences and resonance angiography were normal. Presumptive treatment for an incipient brain abscess was initiated with ceftriaxone, metronidazole and dexamethasone. A transesophageal echocardiogram was normal. ENT and dental evaluations did not reveal any focus of infection. The blood and CSF cultures taken at entry were negative. The patient recovered completely after two days. A follow-up lumbar puncture after ten days showed leucocytes of 10 cells/mm 3 , glucose of 72 mg/dl and proteins of 17 mg/dl, but the MRI indicated only mild improvement of the lesion. Because she was asymptomatic, she was discharged after 14 days of IV antibiotics.Ten days later she began experiencing sudden visual changes and weakness of the left arm. MRI showed resolution of the previous lesion but displayed a new one in the right frontal lobe ( Figure 1C,D). She was readmitted and IV imipenem, linezolid and dexamethasone were begun. The patient recovered completely after a few days. Serum antibodies against Borrelia and Hystoplasma, anti-phospholipid and antinuclear antibodies were negative. A lung biopsy of a small nodule was negative for granulomas, stains and cultures. After one week she was discharged with the same IV treatment administered by a nurse at her home.Seven days later she had a new episode consisting of motor aphasia. The patient was unable to talk, read or write. The MRI showed a third lesion in the left frontal lobe with resolution of the previous lesions ( Figure 1E,F). The patient and her family refused a brain biopsy. A spinal MRI did not show spinal lesions consistent with autoimmune demyelinating disease. PET-CT ( Figure 1G,H) failed to show lesions suggestive of lymphoma. Complete clinical recovery was achieved within two weeks. After the last episode she admitted she had consumed cocaine at home. After a year of follow-up she has not presented new episodes.

show abstract

“…It has also been reported that cocaine-dependent subjects have lower gray matter volume than healthy subjects [10]. Finally, cognitive disturbance might be the result of acute toxic leukoencephalopathy due to cocaine abuse [11,12], most likely caused by adulterants [13]. Toxic leukoencephalopathy is characterized by progressive damage to myelin and other white matter in the brain and is often accompanied by severe neurological symptoms.…”

mentioning

confidence: 99%

Chronic Stimulant Use: An Upcoming Cause of Neurocognitive Disorder in Later Life?

Jacobs¹

2016

Clin Med Rev Case Rep

View full text Add to dashboard Cite

Recurrent leukoencephalopathy in a cocaine abuser

Cited by 27 publications

References 15 publications

Susac-Like Syndrome in a Chronic Cocaine Abuser: Could Levamisole Play a Role?

Susac-Like Syndrome in a Chronic Cocaine Abuser: Could Levamisole Play a Role?

Cocaine-Induced Recurrent Leukoencephalopathy

Chronic Stimulant Use: An Upcoming Cause of Neurocognitive Disorder in Later Life?

Contact Info

Product

Resources

About