Whiteley et al.¹ reported that higher level of circulating markers of the acute inflammatory response in acute stroke were associated with higher temperatures in normal brain. They found no association between blood markers of inflammation and brain temperature in different regions of brain. The authors measured 3 markers of inflammation: C-reactive protein, interleukin-6, and fibrinogen. Higher temperature in diffusion-weighted imaging–abnormal brain was not associated with higher body temperature at the time of the first scan, but was associated with higher contemporaneous body temperature at the second scan. Was there any correlation between ischemic lesions and markers of inflammation? For example, did ischemic lesions in the infratentorial lesions correlate with one of these measurements? Body temperature is related to brain lesion in the hypothalamus and direct or indirect damage to the hypothalamus could contribute to the findings. In addition to brain cooling, elevating these biomarkers should be explored further.

Author Response

We thank Kano et al. for their comments. All the patients had supratentorial acute ischemic lesions. We did not examine the effect of lesion location on brain or body temperature because the study was not large enough to do this properly. We were interested in whether it was the acute diffusion imaging lesion temperature that was responsible for the rise in body temperature or whether other factors drive body temperature changes after stroke (i.e., general response to inflammation after stroke). Our results suggest the latter given that temperature in normal brain was more closely associated with body temperature early on and with plasma markers of inflammation. We suspect that elevated ischemic lesion temperature is controlled by a different set of factors from those that raise body temperature after stroke.