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Lethal high: acute disseminated encephalomyelitis (ADEM) triggered by toxic effect of synthetic cannabinoid black mamba
  1. Kiran Samra1,
  2. Ian S Boon2,
  3. Gregory Packer3,
  4. Saiju Jacob4
  1. 1 Department of Neurology, National Hospital for Neurology and Neurosurgery, London, UK
  2. 2 Department of Diabetes, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
  3. 3 Clinical Decision Unit, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
  4. 4 Department of Neurology, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
  1. Correspondence to Dr Kiran Samra, kiransamra{at}


A previously well 25-year-old man presented with agitation, double incontinence and left-sided incoordination. His symptoms started after smoking a synthetic cannabinoid (black mamba) 5 days earlier. Over 48 hours, he developed aphasia, generalised hypertonia, hyper-reflexia and dense left hemiparesis. This progressed to profuse diaphoresis, fever, tachycardia, hypertension and a possible seizure necessitating admission to the intensive care unit. CT head and cerebrospinal fluid analysis were unremarkable. MRI brain demonstrated asymmetric multifocal hyperintense lesions in white and grey matter, which raised suspicions of acute disseminated encephalomyelitis (ADEM). An electroencephalogram showed widespread brain wave slowing, indicating diffuse cerebral dysfunction. Cerebral angiogram was normal. Toxicology analysis of the substance confirmed a potent synthetic cannabinoid NM2201, technically legal at the time. The patient made a slow but significant recovery after a course of intravenous methylprednisolone, intravenous immunoglobulins and oral steroids, and was later transferred to a rehabilitation bed.

  • Drug misuse (including addiction)
  • Neuroimaging
  • Neurology
  • Intensive care
  • Toxicology

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  • Contributors KS: Core Medical Trainee 2.

    ISB: Core Medical Trainee 2.

    GP: Specialty Registrar in Acute Medicine/Intensive Care Unit.

    AA: Specialty Registrar in Clinical Neurophysiology.

    VR-K: Consultant Acute Medicine and Clinical Service Lead for Clinical Decision Unit.

    SJ: Consultant Neurologist and Clinical Service Lead for Neurology.

    All authors contributed significantly in collecting data, writing the manuscript, reviewing the literature and approved the final manuscript.

    Joint first authorship: KS and ISB contributed equally to this paper.

  • Competing interests None declared.

  • Patient consent Consent obtained from next of kin.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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