Disclosures: Malcolm K. Moses-Hampton, MD: No financial relationships or conflicts of interest

Case Description: The patient was a 20 year-old-male with PMH of type 1 diabetes and schizophrenia who was admitted after being found unresponsive. Admission blood glucose was 36. After admission, the patient had further medical deterioration developing respiratory failure requiring intubation and significant neurologic deficits (aphasia, cognitive deficits, left-sided spastic hemiplegia).

Setting: Tertiary Care Center

Patient: 20 y.o. male Assessment/

Results: Initial CT head and infectious workup was negative on admission. EEG showed diffuse polymorphic slow and low voltage waveforms. MRI brain at the time was significant for widespread T2 flair and restricted diffusion most notably in the in left centrum semi-ovale, corona radiata, internal capsule, and the basal ganglia: all attributed to prolonged hypoglycemia. Due to the significant functional deficits, the patient was transferred to acute inpatient rehabilitation but transitioned to subacute rehabilitation due to poor progress.

Discussion: Cerebral hypoglycemia results in a release of excitotoxic proteins leading to selective neuronal necrosis. This state shifts cerebral blood-flow away from neocortex, hippocampus, and basal ganglia to mid- and hindbrain structures. In HBI, excitotoxic and ischemic injury are characterized as T2 flair and diffusion restriction on MRI. Frontoparietal and diencephalic structures are most likely to be affected as was the case with this patient. HBI appears to be a diagnosis of exclusion with a preceding hypoglycemic event. Hypoglycemia can result in neurological symptoms, including generalized seizures, bizarre behavior, coma, and focal deficits. Neurologic injury is associated with an overall mortality of 11%. Symptoms can persist beyond normalization of glucose levels, however MRI findings and patient’s symptoms usually normalize. This patient’s course was complicated by continued episodes of glucose abnormalities, possibly leading to prolongation of the patient’s neurologic sequelae.

Conclusion: Most patients fully recover from HBI with good functional outcomes however as in this case, large areas of effect, poor electroencephalographic findings, and broad functional deficits belie a poor prognosis.

Level of Evidence: Level V

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PM&R Meeting Abstracts - https://pmrjabstracts.org/abstract/hypoglycemia-induced-brain-injury-hbi-in-an-adult-with-type-1-diabetes-a-case-report/