Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012:2012:989487.
doi: 10.1155/2012/989487. Epub 2012 Dec 26.

Brain temperature: physiology and pathophysiology after brain injury

Affiliations

Brain temperature: physiology and pathophysiology after brain injury

Ségolène Mrozek et al. Anesthesiol Res Pract. 2012.

Abstract

The regulation of brain temperature is largely dependent on the metabolic activity of brain tissue and remains complex. In intensive care clinical practice, the continuous monitoring of core temperature in patients with brain injury is currently highly recommended. After major brain injury, brain temperature is often higher than and can vary independently of systemic temperature. It has been shown that in cases of brain injury, the brain is extremely sensitive and vulnerable to small variations in temperature. The prevention of fever has been proposed as a therapeutic tool to limit neuronal injury. However, temperature control after traumatic brain injury, subarachnoid hemorrhage, or stroke can be challenging. Furthermore, fever may also have beneficial effects, especially in cases involving infections. While therapeutic hypothermia has shown beneficial effects in animal models, its use is still debated in clinical practice. This paper aims to describe the physiology and pathophysiology of changes in brain temperature after brain injury and to study the effects of controlling brain temperature after such injury.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Heat production during energy metabolism. This schema is valid whatever the cell type.
Figure 2
Figure 2
Relationship between oxygen partial pressure (PO2) and oxygen saturation of hemoglobin (SO2). Hypothermia increases the affinity of hemoglobin for oxygen, according to Tremey and Vigué [51].

Similar articles

Cited by

References

    1. Shigemori M, Abe T, Aruga T, et al. Guidelines for the Management of Severe Head Injury, 2nd edition guidelines from the Guidelines Committee on the Management of Severe Head Injury, the Japan Society of Neurotraumatology. Neurologia Medico-Chirurgica. 2012;52(1):1–30. - PubMed
    1. Cairns CJ, Andrews PJ. Management of hyperthermia in traumatic brain injury. Current Opinion in Critical Care. 2002;8(2):106–110. - PubMed
    1. Fernandez A, Schmidt JM, Claassen J, et al. Fever after subarachnoid hemorrhage: risk factors and impact on outcome. Neurology. 2007;68(13):1013–1019. - PubMed
    1. Greer DM, Funk SE, Reaven NL, Ouzounelli M, Uman GC. Impact of fever on outcome in patients with stroke and neurologic injury: a comprehensive meta-analysis. Stroke. 2008;39(11):3029–3035. - PubMed
    1. Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P. Molecular Biology of the Cell. 4th edition. Garland Science; 2002.

LinkOut - more resources