Publication | Open Access
Havana Syndrome Among Canadian Diplomats: Brain Imaging Reveals Acquired Neurotoxicity
27
Citations
32
References
2019
Year
Unknown Venue
Canadian DiplomatsTraumatic Brain InjuryNeuropsychologyUs DiplomatsBrain FunctionNeurological DisorderClinical NeurologyNeuropsychiatryBrain CirculationBrain LesionBrain InjuryNeurologyBrain PathologyNeurorehabilitationNeuropathologyHealth SciencesHavana SyndromeNeuroepidemiologyNeurological MonitoringNeuroimagingCerebral Blood FlowNeurological AssessmentNeuroanatomyNeuroscienceBiological PsychiatryBrain ElectrophysiologyConcussionMedicine
Abstract BACKGROUND In late 2016, US diplomats stationed in Havana began presenting with a variety of neurological manifestations that proved difficult to diagnose. Though previous studies suggested a likely association with brain injury, the mechanism of injury, brain regions involved, and etiology remained unknown. METHODS We conducted a multimodal study examining 26 Canadian diplomats and their family members, the majority of whom presented with symptoms similar to their American counterparts while residing in Havana. Assessments included a medical history, self-reported symptom questionnaires, cognitive assessments, blood tests, and brain imaging assessments (magnetic resonance imaging (MRI) and magnetoencephalography (MEG)). Individuals showing signs of brain injury underwent further neurological, visual, and audio-vestibular assessments. Eight participants were tested both before and after living in Havana. RESULTS Our assessment documents multiple functional and structural impairments, including significant spatial memory impairment, abnormal brain-stem evoked potentials, degradation of fibre tracts in the fornix and posterior corpus callosum, blood-brain barrier injury to the right basal forebrain and anterior insula, and abnormal paroxysmal slowing events of cortical activity. Subsequent mass-spectrometry and blood analyses documented reduced serum cholinesterase activity and the presence of organophosphates (Temephos) and pyrethroid metabolites (3-phenoxybenzoic acid or 3-BPA). CONCLUSIONS Our findings confirm brain injury, specify the regions involved, and raise the hypothesis of overexposure to cholinesterase inhibitors as a plausible etiology. If correct, our hypothesis bears public health ramifications (see Discussion) and suggests a course of action for reducing exposure in the future. FUNDING Global Affairs Canada.
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