A stroke occurs when blood flow to a part of the brain is interrupted by a blockage (ischemic stroke) or a burst blood vessel (hemorrhagic stroke). This interruption deprives brain cells of necessary oxygen and nutrients, leading to cell death. A frequent consequence of this brain injury is the disruption of the body’s ability to maintain a stable internal temperature, a process called thermoregulation. Unstable body temperature, whether too high or too low, can significantly worsen the outcome and recovery for stroke patients.
How the Brain Regulates Body Temperature
The body maintains a stable core temperature, typically around 37°C (98.6°F), through a finely tuned system controlled by the brain. The hypothalamus, a region deep within the brain, functions as the body’s primary thermostat. This area constantly receives signals about the current temperature from receptors located in the skin and internal organs.
The hypothalamus compares the detected temperature to its internal set point and initiates immediate responses to correct any deviations. If the body is too hot, it triggers heat-loss mechanisms, such as sweating and the widening of blood vessels (vasodilation). If the body is too cold, it initiates heat-conservation and heat-production mechanisms, including shivering and the narrowing of blood vessels (vasoconstriction).
This control ensures the body’s cells can function optimally, as they are highly sensitive to temperature changes. The hypothalamus sends signals through neural pathways to the autonomic nervous system, which controls these involuntary actions. Maintaining this stable thermal environment is essential for survival and proper organ function.
Why Stroke Disrupts Temperature Control
When a stroke occurs, the resulting damage to brain tissue can compromise the thermoregulatory network, leading to temperature instability. The specific location and size of the injury determine the type and severity of this disruption. Strokes that directly affect the hypothalamus or the neural pathways connecting it to the brainstem are the most likely to cause severe problems.
One significant consequence is the development of “central fever,” a form of hyperthermia not caused by infection. This central fever results from neurological damage, which effectively raises the hypothalamic temperature set point or prevents the brain from executing cooling mechanisms. Unlike a typical fever caused by a virus or bacteria, central fever often does not respond well to standard fever-reducing medications like acetaminophen.
Both ischemic and hemorrhagic strokes can cause this failure in temperature control. Large strokes, particularly those involving structures near the brain’s core, are strongly associated with higher and earlier fever onset. In rare cases, severe strokes can disrupt the body’s ability to generate heat, causing a drop in core temperature known as hypothermia.
The Effects of Fever and Hypothermia on Stroke Recovery
Temperature instability, particularly fever, complicates stroke recovery and is associated with worse neurological outcomes. Even a small increase in body temperature can be detrimental to the injured brain. Hyperthermia increases the brain’s metabolic demand for oxygen and glucose at a time when blood supply is already compromised.
This heightened demand accelerates the death of neurons in the penumbra, the at-risk tissue surrounding the core stroke injury. Increased temperature also promotes the breakdown of the blood-brain barrier, leading to cerebral edema, or brain swelling. Fever can also increase the excitability of neurons, raising the risk of seizure activity.
Unintended hypothermia, which is less common than fever, also carries significant risks. An accidental drop in temperature can slow the body’s metabolism and impair the immune system, increasing the risk of infections such as pneumonia. Hypothermia can also interfere with blood clotting, which is a concern in hemorrhagic stroke patients or those receiving anti-clotting medications. Sustained temperature dysregulation is an independent predictor of greater disability and higher mortality rates following a stroke.
Managing Temperature Instability Post-Stroke
Given the negative impact of temperature fluctuations, continuous temperature monitoring is a standard practice in acute stroke care. Clinicians use specialized thermometers to track core body temperature, aiming to maintain a controlled normothermia (36.0°C to 37.5°C). This proactive approach is essential because early fever onset is linked to the poorest outcomes.
To treat fever, standard interventions include administering antipyretics like acetaminophen, although these are often only marginally effective for central fever. More aggressive, non-pharmacological methods are frequently necessary to achieve normothermia, such as using surface cooling blankets or water-circulating pads placed on the patient’s trunk and limbs. In highly controlled hospital settings, advanced intravascular cooling devices may also be used.
For patients who develop accidental hypothermia, treatment focuses on simple, passive warming techniques, such as using blankets and forced-air warmers to gradually increase the core temperature. An entirely separate strategy is therapeutic hypothermia, which involves intentionally cooling the patient to a target temperature (e.g., 33°C to 35°C) as a neuroprotective measure.
While therapeutic hypothermia is promising in animal models and used in cardiac arrest survivors, its application in stroke is highly specialized. It remains an evolving area of research without a definitive proven benefit for routine use.