Impact of Body Temperature on Acute Ischemic Stroke Outcomes

Body temperature is a critical modifier of pathophysiological processes following acute ischemic stroke. Even small deviations from normothermia can influence neuronal survival, inflammation, metabolic rate and excitotoxic cascades in the ischaemic penumbra. Hyperthermia in the early phase often exacerbates tissue injury by amplifying inflammatory mediators, increasing blood–brain barrier permeability and promoting free-radical generation. Conversely, mild hypothermia can confer neuroprotective benefits by slowing metabolic demands, stabilising cell membranes and attenuating glutamate-induced excitotoxicity. The temporal profile of temperature change is equally important: peak elevations beyond the first 24–48 hours tend to correlate with larger infarct volumes and poorer functional outcomes, while temperature on admission is a less reliable prognostic marker. Clinical strategies to regulate temperature, including antipyretic protocols and controlled cooling, have therefore emerged as promising adjuncts to reperfusion therapies, with the potential to improve neurological recovery and reduce mortality.

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Impact of Body Temperature on Acute Ischemic Stroke Outcomes publication trend

The graph below shows the total number of articles in impact of body temperature on acute ischemic stroke outcomes across all publications each year (not limited to Nature Index journals).

Technical terms

Acute ischaemic stroke: Sudden loss of brain function caused by an arterial blockage that deprives neural tissue of oxygen and nutrients.

Hyperthermia: Elevation of core body temperature above the normal physiological range, often defined as ≥37.5 °C in stroke settings.

Hypothermia: Reduction of core body temperature below normal, typically managed therapeutically to protect the brain.

Reperfusion: Restoration of blood flow to ischaemic brain tissue through medical or mechanical means, such as thrombolysis or thrombectomy.

Infarct size: Volume of brain tissue irrevocably damaged by ischaemia, usually measured by imaging techniques.

Symptomatic intracranial haemorrhage: Clinically significant bleeding within the skull that presents with new neurological deficits after reperfusion therapy.

References

1. Influence of Temperature Chronobiology on Stroke Outcome. International Journal of Molecular Sciences (2023).
2. Temporal profile of body temperature in acute ischemic stroke: relation to infarct size and outcome. BMC Neurology (2016).
3. Glutamate Excitoxicity Is the Key Molecular Mechanism Which Is Influenced by Body Temperature during the Acute Phase of Brain Stroke. PLOS ONE (2012).
4. Neuroprotection or Increased Brain Damage Mediated by Temperature in Stroke Is Time Dependent. PLOS ONE (2012).
5. Association of Early Increase in Body Temperature with Symptomatic Intracranial Hemorrhage and Unfavorable Outcome Following Endovascular Therapy in Patients with Large Vessel Occlusion Stroke. Journal of Integrative Neuroscience (2022).
6. Association between hyperpyrexia and poststroke outcomes in patients with recanalization after mechanical thrombectomy: a retrospective cohort study. BMC Neurology (2021).
7. Effects of a 4-Step Standard Operating Procedure for the Treatment of Fever in Patients With Acute Stroke. Frontiers in Neurology (2021).