Post-stroke Fever in Patients without Infectious Diseases: The Involvement of Hypothalamus Confirmed by Autopsy
Background: Post-stroke fever is known to occur even without infection presumably due to central mechanisms. In our rat study, a small hypothalamic infarction caused fever substantially (Stroke 30:2743, 1999). In human subjects, the hypothalamus is supplied by the posterior choroidal artery. Internal carotid artery (ICA) territory ischemia usually spares the hypothalamus except for large infarction which provides secondary damage to the hypothalamus by mass effects. The present study was performed to clarify whether the development of central type fever is related with the size of infarction and the involvement of hypothalamus. Methods: Subjected were 60 patients with acute embolic stroke in ICA territory who were admitted within 24 hours after stroke. Patients with infection were excluded from the study. The patients were divided into 3 groups according to the size of infarction on CT in the chronic phase (small, medium-sized or large). In all the patients, axillary temperature was recorded 4–6 times/day for 1 week. Daily average temperature was compared between the groups. In 6 fatal patients, autopsy studies were performed to find hypothalamic involvement. Results: In the group of small infarction, the average temperature never exceeded 37.0 degrees throughout the 1-week period. In the group of large infarction, the temperature was not elevated at the admission but showed rapid increase thereafter. The average temperature exceeded 37.0 degrees from the 2nd day through the 6th day. In the group of medium-sized infarction, the temperature showed a temporary elevation followed by rapid recovery. Of 6 autopsy patients, 3 had post-stroke fever and the others had no fever. In all the 3 febrile patients, the ipsilateral hypothalamus was involved by ischemia, while in the other 3 patients, the hypothalamus remained intact. Conclusions: Our results suggest that large ICA territory infarction may cause fever due to secondary damage to the hypothalamus. Fever may be a causative factor of poor clinical outcome. It can be said from the different viewpoint that fever may be the consequence of large lesion which likely brings about poor outcome.