Baclofen, a muscle relaxant prescribed for the alleviation of symptoms of spasticity acts primarily at the spinal level but with high doses, it penetrates the blood-brain barrier and can result in prominent central nervous depression. Baclofen toxicity has been associated with a variety of symptoms ranging from dizziness to deep coma. We report the clinical course, management, and outcome of a case of baclofen overdose who presented in deep coma with loss of brainstem reflexes and a burst suppression (BS) pattern on his electroencephalogram (EEG). In addition, we reviewed the presentation and outcomes of all reported cases of baclofen toxicity with a BS pattern on EEG to evaluate if those cases share a common clinical presentation and for the presence of signs and symptoms that would help the clinician to consider this diagnosis. There appears to be a common clinical picture associated with severe baclofen toxicity consisting of deep coma associated with loss of all brainstem reflexes including pupillary reactivity, frequent association with seizures/myoclonic jerks, and a BS pattern on EEG. The outcome is generally good, and serial EEGs are recommended to document a reversal of the abnormal electrographic features.

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Hypoxic-ischemic brain injury is a well-known consequence of cardiac arrest and providing an accurate prognostication remains a challenge, especially in decisions related to withdrawal of care. Bilateral absence of the cortical response (N20 potential) on median somatosensory evoked potentials, on days 1 to 3 after the return of spontaneous circulation, is widely considered as the most reliable predictor of poor outcome with a high specificity and a low false-positive rate. The authors describe the case of a young comatose woman after hypoxic injury because of cardiac arrest whose initial median somatosensory evoked potentials revealed bilateral absence of the N20 response associated with evidence of selective injury to both perirolandic cortices and basal ganglia on brain MRI. This patient made a substantial recovery associated with bilateral reappearance of the N20 potential and resolution of the neuroimaging abnormalities.This case revealed that an acute selective and reversible hypoxic injury to both perirolandic cortices may lead to a temporary loss of the N20 responses and an inaccurate prediction of poor outcome after cardiac arrest. It emphasizes on the importance of adopting a multimodal approach in the prognostic assessment of survivors of cardiac arrest.

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Background: Coronavirus disease 2019 (COVID-19) has been associated with many neurological complications affecting the central nervous system. Purpose: Our aim was to describe a case of COVID-19 associated with a probable variant of acute necrotizing encephalopathy (ANE). Results: A 60-year-old man who presented with a 3-day history of dyspnea, fever, and cough tested positive for severe acute respiratory syndrome–coronavirus 2 (SARS-CoV-2). Five days following his admission, the patient was intubated secondary to respiratory failure. Following his extubation 16 days later, he was found to have a left-sided weakness. Magnetic resonance imaging (MRI) of the brain showed hemorrhagic rim-enhancing lesions involving the right thalamus, left hippocampus, and left parahippocampal gyrus. These lesions showed decreased relative cerebral blood flow on MR perfusion and restricted on diffusion-weighted imaging. These neuroimaging findings were consistent with ANE. The left-sided weakness gradually improved over the subsequent weeks. Conclusions: We concluded that COVID-19 can be associated with ANE, a condition believed to be the result of an immune-mediated process with activation of the innate immune system. Future studies must address whether biological drugs targeting the pro-inflammatory cytokines could prevent the development of this condition.