702 - Episodic Hypothalamic Instability with Hypothermia and Bradycardia Following Severe Traumatic Brain Injury

Case Diagnosis: Paroxysmal hypothalamic instability with episodic hypothermia and bradycardia following severe traumatic brain injury (TBI).

Case Description: A 17-year-old female sustained severe TBI following a rollover MVC (GCS 3). MRI showed right MCA/ACA and bilateral occipital infarcts. CT revealed bifrontal hemorrhagic contusions and left subdural hematoma. Course was complicated by central diabetes insipidus, raising suspicion for hypothalamic injury. During inpatient rehabilitation (IPR) she developed recurrent episodic hypothermia and sinus bradycardia. These episode included intermittent changes in mental status, most notably decreased communication but also occurred at neurological baseline. She remained hemodynamically stable despite bradycardia. IPR management included warming measures, frequent temperature checks, infectious workups and neurostimulant titration (methylphenidate, donepezil). Discontinuation of donepezil did not alter episode frequency, suggesting a central cause. She required multiple transfers to acute care due to IPR limitations, including inability for prolonged warming or telemetry during therapy. Acute care evaluation included lumbar puncture, repeat imaging, a negative infectious workup. Endocrine evaluation revealed mild hypothyroidism, however levothyroxine initiation did not change the episode frequency. 

Discussions: Paroxysmal hypothermia is a rare manifestation of hypothalamic dysfunction after severe TBI. While hyperthermia and paroxysmal sympathetic hyperactivity are more commonly seen, episodic hypothermia is infrequently reported. In this case, the absence of infection or significant endocrine pathology supports a central origin for the patient’s autonomic instability. Unlike prior reports of patients with hypothalamic injury who remained minimally conscious, this patient demonstrated command following and functional communication (De Tanti et al.), highlighting variability in presentation and functional outcomes.

Conclusions: Recognition of hypothalamic instability after TBI may prevent unnecessary interventions, guide supportive care, and reduce acute transfers from inpatient rehabilitation. Broader understanding of its varied presentations could optimize therapy participation and recovery trajectories in patients with severe TBI.