An 80-year-old man with vascular dementia and coronary artery disease was found comatose in a hot bath. He was hyperthermic (106 F), hypotensive, and tachycardic on arrival to the emergency department. Computed tomography (CT) head and CT angiography head and neck hours showed no acute pathology. Brain magnetic resonance imaging (MRI) 4 days after presentation displayed striking multifocal, bilaterally symmetric abnormalities in the gray matter structures of cerebral and cerebellar cortices, basal ganglia, and thalamus (Figure 1 and Figure 2).
Figure 1.
Images showing bilaterally symmetric increased diffusion-weighted imaging (DWI) and fluid attenuation inversion recovery (FLAIR) signal in the cerebellar cortex (A and B) and pre- and post-central gyri (C and D) as well as increased DWI signal in the right hippocampus (E, arrow).
Figure 2.
Diffusion-weighted imaging, apparent diffusion coefficient, and FLAIR images showing restricted diffusion in addition to increased DWI and FLAIR signal in the bilateral occipital cortex (AC) and globus pallidus internus (DF, arrows).
Cytokine-mediated inflammation, caspase-mediated apoptosis, and excitotoxicity are leading hypothesized causes of hyperthermia induced neuronal injury.1,2 The typical radiologic pattern of injury, demonstrated here, conspicuously resembles brain injury caused by carbon monoxide, cyanide, and hypoxia-ischemia. In these diseases, mitochondrial dysfunction is closely tied to neuronal injury.3-5 Therefore, it is possible that mitochondrial dysfunction may also be an important contributor to neuronal injury in hyperthermia. Heat stress increases inner mitochondrial membrane permeability, leads to uncoupling of oxidative phosphorylation and cellular respiration, and causes direct interference with oxidative phosphorylation during in vitro studies, supporting this hypothesis. 2 Nonetheless, the exact pathophysiology of hyperthermic brain injury remains poorly understood.
This case illustrates classic clinical and imaging features of severe hyperthermic brain injury and, by the pattern of injury on MRI, possibly provides insight about pathophysiology, implicating mitochondrial failure as a contributory process. It also demonstrates the potential for reasonable functional recovery despite coma and striking abnormalities on MRI. During the third week of hospitalization, the patient’s encephalopathy began to rapidly improve. He was discharged on hospital day 26 to a rehabilitation facility, where rapid improvement continued. He returned home with minimal new deficits (wider gait and mild cognitive worsening compared to baseline) 2 weeks later.
Footnotes
Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.
ORCID iD
Dylan G. Jones https://orcid.org/0000-0001-6014-6763
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