Author(s): Justin Weppner, DO, Varun Mishra, BS
Originally published: September 20, 2013 Last updated: May 22, 2025
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Disease/Disorder

Definition

Impaired thermoregulation is a condition in which exaggerated or abnormal changes in body temperature occur spontaneously or in response to environmental or internal stimuli. Poikilothermia refers to the inability to internally regulate core body temperature.1 Clinically, poikilothermia can manifest with hypothermia (core temperature less than 35°C/95°F) or hyperthermia (core temperature > 37.8°C/100°F). 

Etiology

Impaired thermoregulation arises from various factors that disrupt the body’s ability to maintain core temperature. Neurological conditions, such as spinal cord injury (SCI), particularly those with level of injury above T6, traumatic brain injury (TBI), stroke, and brainstem lesions are significant contributors. Certain medications such as opioids, anesthetic agents, anticholinergic medications, and anti-hypertensive drugs may also contribute to impaired thermoregulation.2,3 

Epidemiology including risk factors and primary prevention

The exact prevalence of impaired thermoregulation remains unclear. Risk factors include loss of afferent input and autonomic control in spinal cord injury, especially in those with a level above T6, often during extremes of ambient temperature. Brain injury patients may also be predisposed due to direct hypothalamic injury or hypothalamic irritation. Thermal dysregulation can arise in the presence of noxious stimuli, though it frequently occurs spontaneously.4,5 

Patho-anatomy/physiology

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 body’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, non-shivering 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 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 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.6 

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

Thermodysregulation is episodic in nature and can arise immediately after or as a later consequence of spinal cord injury. Although it may occur at any time after traumatic brain injury or brainstem damage, it is particularly frequent in the early post-injury period.7,8 

Specific secondary or associated conditions and complications

Thermal dysregulation in spinal cord injury often manifests as poikilothermia, wherein body temperature is influenced by environmental conditions. Patients with high-level spinal cord injuries are susceptible to a greater degree of thermodysregulation.1 This can lead to hypothermia in colder environments or hyperthermia in warm environments or during exercise. Furthermore, idiopathic occurrence of fever, often referred to as “quad fever,” has been observed in spinal cord injury, with significant associated morbidity and mortality.9 

Traumatic brain injuries may be followed by paroxysmal sympathetic hyperactivity (PSH), also known as central dysautonomia and central storming. Clinical manifestations include episodic hyperthermia, hypertension, tachycardia, tachypnea, pupillary dilation, agitation, diaphoresis, hypertonia, and decerebrate posturing. Crucially, this syndrome may mimic other severe conditions in the intensive care setting, including seizure, sepsis, and impending herniation.10 

Symptoms of PSH arise due to imbalance between excitatory and inhibitory central nervous system (CNS) pathways, manifesting with autonomic dysregulation. Damage to the brainstem and select cortical regions (orbitofrontal, anterior temporal, and insula) that influence hypothalamic activity has been implicated in the pathogenesis of PSH. 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.11,12

PSH occurs in up to one-third of patients in coma or vegetative state. PSH is most commonly seen in patients with severe TBI but can also occur in patients with hypoxic brain injury, hydrocephalus, tumor, and CNS infection.13 It is possible to have electrocardiographic changes, arrhythmias, increased intracranial pressure, hypohidrosis, and cool limbs.

Essentials of Assessment

History

History should include the time of onset, duration, triggering events, associated symptoms, and treatments of previous episodes.

Physical examination

For patients with acute spinal cord injury, evaluation of autonomic dysfunction (including impaired thermoregulation) should be done as per the International Standards to Document Remaining Autonomic Function after Spinal Cord Injury. The 2021 guidelines recommend oral temperature measurement with no liquids for 10 minutes prior to taking an oral temperature. Alternatively, temperature can be monitored via rectal measurement or ingestible telemetry capsule. Multiple body temperatures should be taken throughout the day to account for variability associated with circadian rhythm. Exam room temperature should remain between 20-25°C (70-78°F).14,15

A thorough examination for potential triggers, such as sources of infection, should be sought as causes of fever before making a diagnosis of hyperthermia due to temperature dysregulation. Examination should include skin inspection, evaluation of the head & neck region, respiratory system, gastrointestinal tract, and genitourinary systems. 

Functional assessment

The febrile episode and associated symptoms may impair functional ability temporarily. Aging is also associated with an attenuated physiological ability to dissipate heat and the risk of heat-related illness in these individuals is elevated, thus assessing impact of thermal dysregulation on daily activities and overall functional status is essential.

Laboratory studies

Unfortunately, there are no known biomarkers for impaired thermoregulation at this time. However, an autonomic test battery including parasympathetic and sympathetic cardiovascular function measures (deep breathing test, Valsalva maneuver, tilt, or pressor test), can be utilized. More specialized tests include carotid sinus massage, assessment of baroreceptor reflex function, pharmacological tests or cardiac, and regional hemodynamic measurements can also be considered.

A thorough workup, including complete blood count, urinalysis, urine culture, and chest x-ray should be performed to rule out infection. Testing for other causes of fever in SCI, such as deep vein thrombosis or heterotopic ossification should be considered.

Imaging

Plain films to evaluate sources of fever might include those of the chest, abdomen, and limbs. Brain imaging with computed tomography (CT) or magnetic resonance imaging (MRI) may reveal evidence of severe brain injury or CNS infection.

Environmental

Extremes of heat or cold in the environment may predispose the patient with impaired thermoregulation to hyperthermia or hypothermia, respectively.

Rehabilitation Management and Treatments

Available or current treatment guidelines

The 2021 clinical practice guidelines of the Consortium for Spinal Cord Medicine regarding autonomic dysreflexia and other autonomic dysfunctions offer recommendations for management of thermal dysregulation.

It is necessary first to consider other causes of fever. Once other causes of fever are ruled out, then thermal dysregulation should be considered as a diagnosis. The guidelines recommend monitoring for hypothermia and hyperthermia in patients with SCI at T6 or above.

Treatment typically consists of behavioral and environmental strategies. These include cooling devices, air-conditioning, drinking cool liquids, and/or washing with tepid water to manage hyperthermia. Careful planning on amount and type of clothing is important. SCI patients must also be monitored during exercise due to the risk for hyperthermia. Ambient temperature regulation, insulated clothing, blankets, warm humidified air, and intake of warm fluids are recommended to prevent or manage hypothermia. Avoidance of alcohol in cooler environments is also recommended. Education regarding medications that may impair thermal regulation is essential.14 

For patients with TBI, it is often necessary to use medications. The most commonly used medications are beta blockers. Alpha adrenergic blocker medications have been tried less often. Bromocriptine may reduce hyperthermia and diaphoresis. Dantrolene or baclofen may reduce extensor posturing. For extreme and refractory cases, judicious doses of morphine can be used to stop the episodes.16,17 

At different disease stages

Thermodysregulation is treated similarly at all stages of the condition.

Patient & family education

It is important to teach patients and families about common presenting symptoms, prevention strategies, and methods of immediate treatment.  Measures to prevent hyperthermia include wearing appropriate lightweight and light-colored clothing, maintaining a proper temperature-controlled environment (e.g., use of air-conditioning), maintaining appropriate hydration, water spray or fan when exercising or in a hot environment.  Since alcohol can cause vasodilation and heat loss, those prone to hypothermia should minimize alcohol intake in cold environments.

Emerging/unique interventions

Spinal electrical stimulation has demonstrated benefit as a therapeutic tool for locomotor recovery after spinal cord injury. A systematic review conducted by Flett et al., found that electrical nerve stimulation is also associated with improved autonomic function, including thermal regulation.18 Moussalem et al., investigated phase change material cooling vests to manage thermal dysregulation and thermal comfort in sixteen paraplegic patients. They observed enhanced thermal comfort and decreased skin temperatures but inconsistent reductions in core temperature.19 

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

Episodes are considered resolved when the temperature returns to normal.

It is important to approach the patient with thermal dysregulation with a strong suspicion for infection. When, causes of fever have been ruled out, then impaired thermoregulation should be considered as a diagnosis.

Cutting Edge/Emerging and Unique Concepts and Practice

Techniques to measure functional integrity of sudomotor nerves include the quantitative sudomotor axon reflex sweat test (QSART), analysis of the sympathetic skin response and the thermoregulatory sweat test (TST). In addition to these techniques, more recent developments have been introduced to reduce technical demands and interindividual variability such as Sudoscan, which measures electrochemical skin conductance to assess sudomotor nerves. Recent studies suggest that Sudoscan findings are reliable and with high diagnostic accuracy.20 

Gaps in the Evidence-Based Knowledge

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

References

  1. Krassioukov A, Stillman M, Beck LA. A Primary Care Provider’s Guide to Autonomic Dysfunction Following Spinal Cord Injury. Top Spinal Cord Inj Rehabilitation. 2020;26(2):123-127. doi:10.46292/sci2602-123
  2. Westaway K, Frank O, Husband A, et al. Medicines can affect thermoregulation and accentuate the risk of dehydration and heat-related illness during hot weather. J Clin Pharm Ther. 2015;40(4):363-367. doi:10.1111/jcpt.12294
  3. Sessler DI. Defeating Normal Thermoregulatory Defenses: Induction of Therapeutic Hypothermia. Stroke. 2009;40(11):e614-e621. doi:10.1161/strokeaha.108.520858
  4. Grossmann F, Flueck JL, Perret C, Meeusen R, Roelands B. The Thermoregulatory and Thermal Responses of Individuals With a Spinal Cord Injury During Exercise, Acclimation and by Using Cooling Strategies–A Systematic Review. Front Physiol. 2021;12:636997. doi:10.3389/fphys.2021.636997
  5. Takahashi C, Hinson HE, Baguley IJ. Traumatic Brain Injury, Part II. Handb Clin Neurol. 2015;128:539-551. doi:10.1016/b978-0-444-63521-1.00034-0
  6. Morrison SF, Nakamura K. Central Mechanisms for Thermoregulation. Annu Rev Physiol. 2019;81(1):285-308. doi:10.1146/annurev-physiol-020518-114546
  7. Wettervik TMS, Engquist H, Lenell S, et al. Systemic Hyperthermia in Traumatic Brain Injury-Relation to Intracranial Pressure Dynamics, Cerebral Energy Metabolism, and Clinical Outcome. J Neurosurg Anesthesiol. 2021;33(4):329-336. doi:10.1097/ana.0000000000000695
  8. Baschieri F, Guaraldi P, Provini F, et al. Circadian and state-dependent core body temperature in people with spinal cord injury. Spinal Cord. 2020;59(5):538-546. doi:10.1038/s41393-020-0521-8
  9. Watson CCL, Shaikh D, DiGiacomo JC, et al. Unraveling quad fever: Severe hyperthermia after traumatic cervical spinal cord injury. Chin J Traumatol. 2022;26(01):27-32. doi:10.1016/j.cjtee.2022.01.006
  10. Ott JL, Watanabe TK. Evaluation and Pharmacologic Management of Paroxysmal Sympathetic Hyperactivity in Traumatic Brain Injury. J Head Trauma Rehabilitation. 2024;39(6):E576-E581. doi:10.1097/htr.0000000000000960
  11. Baik SW, Kang DH, Kim GW. Transdermal opioid patch in treatment of paroxysmal autonomic instability with dystonia with multiple cerebral insults: A case report. Medicine. 2020;99(40):e22536. doi:10.1097/md.0000000000022536
  12. Nancy F, Khowaja A, Khowaja P. Paroxysmal sympathetic hyperactivity: A common consequence of traumatic brain injury. Auton Neurosci. 2025;257:103238. doi:10.1016/j.autneu.2024.103238
  13. Bansal S, Chakrabarti D, Krishnakumar M, et al. The correlation between the severity of paroxysmal sympathetic hyperactivity and plasma catecholamine levels in patients with severe traumatic brain injury. Brain Inj. 2024;38(14):1212-1219. doi:10.1080/02699052.2024.2380460
  14. Krassioukov A, Linsenmeyer TA, Beck LA, et al. Evaluation and Management of Autonomic Dysreflexia and Other Autonomic Dysfunctions: Preventing the Highs and Lows: Management of Blood Pressure, Sweating, and Temperature Dysfunction. Top Spinal Cord Inj Rehabilitation. 2021;27(2):225-290. doi:10.46292/sci2702-225
  15. Wecht JM, Krassioukov AV, Alexander M, et al. International Standards to document Autonomic Function following SCI (ISAFSCI). Top Spinal Cord Inj Rehabilitation. 2021;27(2):23-49. doi:10.46292/sci2702-23
  16. Baguley IJ, Cameron ID, Green AM, Slewa-Younan S, Marosszeky JE, Gurka JA. Pharmacological management of Dysautonomia following traumatic brain injury. Brain Inj. 2004;18(5):409-417. doi:10.1080/02699050310001645775
  17. Asmar S, Bible L, Chehab M, et al. Traumatic brain injury induced temperature dysregulation: What is the role of β blockers? J Trauma Acute Care Surg. 2021;90(1):177-184. doi:10.1097/ta.0000000000002975
  18. Flett S, Garcia J, Cowley KC. Spinal electrical stimulation to improve sympathetic autonomic functions needed for movement and exercise after spinal cord injury: a scoping clinical review. J Neurophysiol. 2022;128(3):649-670. doi:10.1152/jn.00205.2022
  19. Moussalem CK, Mneimneh F, Sarieddine R, et al. Effect of Phase Change Material Cooling Vests on Body Thermoregulation and Thermal Comfort of Patients With Paraplegia: A Human Subject Experimental Study. Glob Spine J. 2021;13(7):1754-1764. doi:10.1177/21925682211049167
  20. Vittrant B, Ayoub H, Brunswick P. From Sudoscan to bedside: theory, modalities, and application of electrochemical skin conductance in medical diagnostics. Front Neuroanat. 2024;18:1454095. doi:10.3389/fnana.2024.1454095

Original Version of the Topic

Elliot J. Roth, MD. Impaired thermoregulation. 9/20/2013.

Previous Revision(s) of the Topic

Felicia Skelton, MD. Impaired thermoregulation. 8/17/2016.

Kareen Velez, MD. Impaired Thermoregulation. 11/17/2021.

Author Disclosure

Justin Weppner, DO
Nothing to Disclose

Varun Mishra, BS
Nothing to Disclose