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A condition in which exaggerated or abnormal changes in body temperature occur spontaneously or in response to environmental or internal stimuli.


Impaired thermoregulation is a known complication of many of the diagnoses commonly seen among patients in a PM&R practice. It is seen in patients with spinal cord injury, traumatic brain injury, stroke, and other conditions that cause damage to the brainstem. It also can be seen in patients who take certain medications such as anesthetic agents, tranquilizers, antihypertensive drugs, opioids, and sedatives, in addition to alcohol.

Epidemiology including risk factors and primary prevention

The frequency of impaired thermoregulation is not known. This problem is associated with spinal cord injury above level T6 and with severe traumatic brain injury. In spinal cord injury, it occurs more frequently during extremes of ambient temperature. In patients with traumatic brain injury or brainstem stroke, it can occur frequently in the presence of noxious stimuli, although it occurs more frequently spontaneously in the absence of environmental triggers.


In the normal state, powerful mechanisms exist to measure, assess, regulate, and adjust core temperatures. There are sensory, integrator/regulator, and effector components of thermoregulation. The sensory components of the thermoregulatory control system derive from both internal and external sources. There are cutaneous cold and warm receptors located throughout the skin and superficial tissues, which are more concentrated in the fingers, face, and genitalia, and less concentrated proximally. There also are deep body thermal sensors, located in the abdomen and elsewhere. These sensors send impulses with thermal information through projections into the spinal cord, carried predominantly through C-fiber afferents. These fibers, with cell bodies in the dorsal root ganglion, enter the spinal cord and ascend contralaterally in the spinothalamic tracts through the medial lemniscus to the thalamus, which in turn, has fibers that project directly to the somatosensory cortex to enable conscious appreciation of temperature. The ascending fibers also have additional important projections to the hypothalamus to facilitate unconscious autonomic control of temperature. The preoptic hypothalamus receives and interprets the internal and external temperature information, generates the thermal set point, and integrates thermoregulatory responses. Efferents from the hypothalamus control the bodyâ’s response to thermal changes through descending noradrenergic and cholinergic fibers exiting the spinal cord below the C7 level. The strategies which these effectors use to regulate core temperature include changes in vasomotor (causing peripheral vasoconstriction and vasodilatation) and sudomotor (causing sweating) tone, nonshivering and shivering thermogenesis, and piloerection. Conscious awareness of temperature changes, based in the cortex, enables behavioral adaptations to control temperature, including changing location, adjusting environmental temperatures (e.g., via heating or air conditioning), making postural adjustments, or changing clothing. When core body temperature decreases, sympathetic noradrenergic mechanisms normally induce piloerection, shivering, and vasoconstriction to produce body heat and to shunt blood away from the cool surface. Core body temperature is the result of the balance between heat production and heat loss, both of which are adjusted by the central hypothalamic thermoregulatory controller. When core body temperature rises, vasodilatation and sweating normally help the body to lose some of its internal heat. Medical and neurological problems that interfere with the flow of sensory information and/or motor output reduce the ability of the system to assess and mount a response to changes in temperature. Also, direct damage to the hypothalamus controller can result in dysregulation of temperature control.

In spinal cord injury (SCI), the normal connections are lost between the hypothalamus and both its motor and sensory projections. In high SCI, most of the skin is insensate, and so the person may have little or no sensitivity to heat or cold. In addition, the lack of sympathetic outflow on the effector side results in loss of vasoconstriction or vasodilatation, so heat cannot be conserved or lost in response to central temperature changes. In addition, heat production is limited in response to cold stimuli because of the loss of shivering ability resulting from motor deficits. Sweating is ineffective below the level of injury. With high SCI, heat production may increase only slightly over baseline, so central hypothermia in a cold environment is a significant risk for these patients. The amount of impairment of thermoregulation tends to vary according to level and possibly completeness of injury. Practically, the significant risk of hypothermia in cold external environments occurs more commonly in patients with SCI levels above T6 because of the large surface area for which sensation and shivering ability are lost in those patients.

The preoptic area of the anterior hypothalamus, which houses the main thermoregulatory center, can be damaged by trauma, leading to manifestations of thermodysregulation. Other causes of hyperthermia after traumatic brain injury (TBI) include post-traumatic cerebral inflammation and secondary infection. The development of post-traumatic hyperthermia (PTH) can be seen as a secondary effect of TBI that may negatively influence outcome. An increase in body temperature after injury is associated with increased cytokine release, and both hyperthermia itself and the cytokine release can exacerbate neuronal damage, through the mechanisms of increased oxidative stress, glutamate release, increased metabolic expenditure, increasing blood brain barrier permeability, cerebral edema, and raising intracranial pressure.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Thermodysregulation can occur early or late after spinal cord injury. Although it also can occur at any time after traumatic brain injury or brainstem damage, it tends to be more frequent during the early post-injury period. It is distinctly episodic.

Specific secondary or associated conditions and complications

Uncontrolled fever is a component of the clinical syndrome known as paroxysmal autonomic instability with dystonia (PAID). Also known as central dysautonomia and central storming, this phenomenon results from altered autonomic activity following TBI, resulting in severe hypertension, fever, tachycardia, tachypnea, pupillary dilation, and extensor posturing. It results from injury to the brainstem, but can also occur following brainstem hemorrhage, elevated pressure on the brainstem, and injury to select cortical areas that influence hypothalamic activity can also be a cause. These regions include orbitofrontal, anterior temporal, and insular areas. Subcortical areas that may influence hypothalamic function are the amygdala, the periaqueductal gray matter, nucleus of tractus solitaries, and both the uvula and vermis of the cerebellum. Damage to these areas release control of vegetative function and results in dysregulation of autonomic balance. PAID occurs in up to one-third of patients in coma or vegetative state. It is more common in patients with severe TBI, but also is seen in patients with hydrocephalus and CNS infection. Clinical manifestations are temperature typically greater than 38.5oC, hypertension, heart rate greater than 130 beats per minute, rapid respiratory rate, associated with agitation, diaphoresis, rigidity, or decerebrate postures. It is possible to have electrocardiographic changes, arrhythmias, increased intracranial pressure, hypohydrosis, and cool limbs.



History should include time of onset, duration, triggering events, associated symptoms, and past treatments.

Physical examination

For patients with acute SCI, evaluation of autonomic dysfunction (including impaired thermoregulation) should be done as per the International Standards for Assessing Remaining Autonomic Function.

A thorough examination should be performed looking for conditions that may serve as triggers. In particular, sources of infection should be sought as potential causes. This means that a thorough exam should be performed of the head and neck, pulmonary, abdominal, genitourinary, and skin, looking for potential sources of infection.

Functional assessment

The febrile episode and associated symptoms may impair functional ability temporarily.

Laboratory studies

Unfortunately, there are no known biomarkers for impaired thermoregulation at this time. Therefore, impaired thermoregulation is a diagnosis of exclusion. It is critical to consider and rule out other, more treatable, causes of fever first. This means that a thorough fever workup, including complete blood count, urinalysis, urine culture, and chest x-ray should be performed. Testing for other causes of fever in spinal cord injury, such as deep vein thrombosis or heterotopic ossification should be considered.


Plain films to evaluate sources of fever might include those of the chest, abdomen, and limbs. Brain imaging may reveal evidence of severe brain injury.


Extremes of heat or cold in the environment may predispose the patient to fever or hypothermia, respectively.


Available or current treatment guidelines

It is necessary first to consider other causes of fever. When other causes of fever are ruled out, then thermal dysregulation should be considered as a diagnosis.

In patients with spinal cord injury, treatment typically consists of behavioral and environmental strategies, including changing the environment, posture, and the amount and type of clothing.

For patients with traumatic brain injury, removing any potential triggering noxious stimulus is important, but it is almost always necessary to use medications. Perhaps most commonly used are beta blocker medications. Alpha adrenergic blocker medications have been tried less often. Bromocriptine may reduce hyperthermia and diaphoresis. Dantrolene may reduce extensor posturing. For extreme and refractory cases, judicious doses of morphine can be used to stop the episodes.

At different disease stages

Thermodysregulation is treated similarly at all stages of the condition.

Patient & family education

It is extremely helpful to teach patients and families about this condition, methods of prevention, common presenting symptoms, and methods of immediate treatment.

Emerging/unique Interventions

Episodes are considered resolved when the temperature returns to normal.

Trbovech, et al, concluded that cooling vests helped prevent exercise-induced hyperthermia in athletes with SCI. This small study did not find a significant difference with this intervention.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

It is extremely important to approach the patient with thermal dysregulation with a strong concern about other, treatable, causes of fever. When, and only when, those other causes of fever are ruled out, then impaired thermoregulation should be considered as a diagnosis.




Gaps in the evidence-based knowledge

There is no specific evidence-based protocol or algorithm for behavioral or drug treatment for this condition.



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Lemons DE, Riedel G, Downey JA. Thermoregulation and the effects of thermomodalities. In: Gonzalez E, et al (eds.): Downey and Darling’s Physiological Basis of Rehabilitation Medicine. 3rd ed. pp. Boston, MA: Butterworth; 2001:507-520.

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Original Version of the Topic:

Elliot J. Roth, MD. Impaired thermoregulation. Publication Date:2013/09/20.

Author Disclosure

Felicia Skelton, MD
Accnetive Health: Rehabilitation Medicine Consultant, Monetary payment.