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Paroxysmal Sympathetic Hyperactivity (PSH) is a syndrome of disproportionate and pathological sympathetic overreaction that can be triggered by nociceptive or environmental stimuli,1 which occurs after severe acquired brain injury. It is characterized by “simultaneous, paroxysmal transient increases in sympathetic (elevated heart rate, blood pressure, respiratory rate, temperature, sweating) and motor (posturing) activity” by an International Consensus Group of experts in 2014.2

PSH has been referred to by at least 31 separate terms in literature,2 including diencephalic or autonomic seizures, brainstem attack, autonomic storming, paroxysmal hyperthermic autonomic dysregulation, and dysautonomia.3 These older terminologies should be considered to be historical to minimize confusion.


Paroxysmal Sympathetic Hyperactivity (PSH) can occur after any brain lesion from trauma, infection, hemorrhage, infarction, brain tumor, global anoxia-ischemia, autoimmune encephalitis, or degeneration. The clinical presentation does not appear to differ depending on the underlying etiology.4

A review of 349 case reports of PSH published before 2010 found that about 80% occurred after traumatic brain injury (TBI), about 10% occurred after hypoxic brain injury, and about 5% occurred after stroke; the remainder of cases had variable etiologies, including hydrocephalus, tumor, and infection.5

Epidemiology including risk factors and primary prevention

The estimated incidence of PSH in adults with TBI ranges from 8-33%.5 The main risk factor for developing PSH after brain injury is increased injury severity; individuals with mild brain injuries typically do not develop PSH6 but may develop autonomic nervous system anomalies that are harder to define.7-10

Individuals who develop PSH tend to be younger in age and male.5,11 In a study of 407 pediatric individuals with acquired brain injury, those who developed PSH also tended to be younger in age and male predominant.1 In another study, patients with diffuse axonal injury (DAI) and brainstem lesions are at high risk.12 Among patients with severe TBI, decreased fractional anisotropy in the splenium of the corpus callosum and posterior limb of the internal capsule is associated with occurrence of PSH.13


The precise pathophysiology of PSH is still poorly understood however sympathetic overdrive can be explained by multiple mechanisms.

Structural damage due to acquired brain injury disrupts higher-order autonomic regulatory centers.14 Sympathetic activation originates in the hypothalamus and medulla; injury to these centers can cause sympathetic hyperactivity. In addition, injury to fibers connecting the hypothalamus to cortical areas and inhibitory pathways coming from the forebrain may also result in sympathetic hyperactivity.15 This results in unregulated sympathetic activity, thus driving autonomic instability.3,16

Another hypothesis, known as the excitatory:inhibitory (EIR) model, proposes that a lesion in the inhibitory centers in the brainstems and diencephalon reduces tonic descending inhibition to afferent sensory information from spinal cord circuits. This amplifies normally non-nociceptive afferent input from the periphery and leads to over-excitation of the sympathetic response.3,17

There is also evidence to support an association between PSH and catecholamine release, which could help account for the exaggerated sympathetic response to non-noxious stimuli.18 In one study, catecholamine levels rose 200-300% above baseline during paroxysms in individuals with PSH, with no similar change found in the control group; this was consistent with prior case study data.19 An Increase in glutamate transmission or decrease in GABA transmission can also result in sympathetic hyperactivity.20

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

Natural History and Trajectory

Acute (days-weeks)
PSH usually develops in the acute phase following brain injury.21 Symptoms, which are paroxysmal and episodic, first appear as early as the first week after TBI.18 In one prospective cohort study, PSH tended to occur about 6 days post-injury.17 Initially, the onset of PSH may be challenging to distinguish from other conditions, including acute withdrawal of sedation and sepsis.5

Most episodes, manifested by hypertension, tachycardia, hyperthermia, tachypnea, diaphoresis, and posturing, are provoked by noxious or non-noxious stimuli such as pain, urinary retention, or repositioning.18 In one study, episodes were associated with a triggering event in 72% of individuals.19

Individual episodes vary in intensity and duration but rarely persist for more than several hours. In one prospective cohort study, episodes tended to last about 30 minutes (ranging 15-50 minutes) and occurred an average of 5 times per day.17 Other studies have found a wide range in duration of episodes, from 3 minutes to 1-2 hours.6

Chronic/stable (weeks-months)
The duration of PSH is variable, from less than 2 weeks to several months.17 The occurrence of PSH tends to diminish over time. In one study, 24% of individuals had increased autonomic responses at one week post-injury while only 8% were diagnosed with dysautonomia at two weeks post-injury.22

Spasticity and dystonia may be persistent even after resolution of PSH. It is unclear if residual hypertonia is a true sequela of PSH or rather a consequence of damage to supraspinal motor tracts, which occurs during initial brain injury.18

Autonomic dysfunction may rarely be associated with life-threatening cardiac arrhythmias or myocardial infarction.

Specific secondary or associated conditions and complications

Resting energy expenditure during episodes of PSH is as high as three times the norm. Therefore, adequate nutrition is essential to prevent severe weight loss.23 Body weight losses of 25% have been reported during the acute period in individuals with PSH.5

Individuals with PSH are at increased risk of developing heterotopic ossification.5 Prolonged sympathetic hyperactivity associated with PSH may lead to cardiac damage (including tachyarrhythmia and stress-induced cardiomyopathy), pulmonary edema, intracranial hypertension, rhabdomyolysis, nutritional deficiencies, and skin breakdown.3,20 Furthermore, patients with PSH were found to have a longer hospital stay and higher hospital costs; they were also found to have a higher rate of complications and made less neurological recovery in acute care after brain injury.24,25

Essentials of Assessment


Paroxysmal sympathetic hyperactivity (PSH) presents with non-specific findings and is, therefore a diagnosis of exclusion. Repeated episodes of rapid-onset tachycardia, hypertension, tachypnea, fever, diaphoresis, and rigidity with dystonic posturing are most common. Urinary retention and ileus may also be seen.15 All features are not typically present in all episodes. However, several features must be observed simultaneously for PSH to be considered. Parasympathetic features are absent.15,26

When assessing for PSH, clinicians should first consider other conditions that could present similarly, such as systemic inflammatory response syndrome, infection, noxious stimuli  (fractures, heterotopic ossification, pressure wounds, constipation), seizures, intracranial hypertension, hydrocephalus, medication or substance withdrawal, serotonin syndrome and neuroleptic malignant syndrome.3 Neuroleptic malignant syndrome may present very similarly and should be especially considered in the setting of recent antipsychotic use.

History should look for possible triggers, which can be painful or non-painful, such as passive movement, turning, and endotracheal tube suctioning.2 Episodes can also occur spontaneously. Persistently elevated blood pressure, respiratory rate, heart rate, and temperature are less likely to be consistent with PSH, and other diagnoses should be excluded first.  

Physical examination

Patients with PSH may have paroxysmal increases in heart rate, respiratory rate, blood pressure, and temperature with the return to baseline vital signs in between episodes. During episodes, they may have worsened level of consciousness, dilated pupils, and diaphoresis. Episodes are also associated with dystonia, muscle rigidity, and posturing.2,4,17 This may include decorticate or decerebrate rigidity, bruxism, and opisthotonos.

Patients should have a thorough physical exam to assess for other causes of vital sign changes, such as infection. They should also be assessed for potential consequences of PSH, such as skin breakdown and heterotopic ossification.

Clinical functional assessment

These patients often have severe brain injuries, may present in disorders of consciousness, and may be dependent for care. It is important to perform passive range of motion testing of all joints to evaluate for spasticity.6

Laboratory studies

PSH cannot be diagnosed based on laboratory studies. However, certain studies may be useful in evaluating other conditions that present similar to PSH. A complete blood cell count along with blood, urine, or sputum cultures as indicated, can assess for infection. A comprehensive metabolic panel can evaluate electrolyte abnormalities or gastroenterological pathology that may be causing pain. Patients should also be evaluated for nutritional deficiencies that may occur due to increased energy expenditure during episodes of PSH.


Imaging is not diagnostic for PSH. However, diffuse brain damage and injury to the deep brain structures, including the periventricular white matter, corpus callosum, diencephalon, or the brainstem, are associated with PSH.12,17

Imaging may be useful to evaluate other intracranial pathologies, including herniation, intracranial hemorrhage, infection, or hydrocephalus.

Other imaging studies, such as chest CT angiography, may help to rule out pulmonary embolism.

Supplemental assessment tools

In 2014, a consensus on diagnostic criteria was developed by an international, multidisciplinary group to aid in diagnosing PSH. The Paroxysmal Sympathetic Hyperactivity – Assessment Measure (Figure 1) helps to determine PSH diagnostic likelihood. The first section, the Diagnostic Likelihood Tool, assesses the presence of PSH features and the second portion, the Clinical Feature Scale, measures the severity of PSH features. The PSH-AM is designed for serial use with maximum values from the prior 24-hour period documented. It can be used to monitor clinical trends and aid in treatment.2

Figure 1

PSH CMAD Table 1Download

Evaluation to rule out other causes of paroxysmal symptoms (e.g., seizures, thyroid storm, medication withdrawal) is indicated based on clinical considerations.

Early predictions of outcomes

PSH has been associated with worse clinical outcomes, including more time on mechanical ventilation, more infection, tracheostomy placement, longer ICU stays, and longer total hospitalization.17,24 Duration of PSH may also affect outcome with persistent episodes possibly having worse outcomes.18


Avoid known triggers for episodes and overstimulation.18 It is essential to minimize noise and to promote a regular sleep-wake cycle.

Social role and social support system

PSH can be distressing for family members, friends, and healthcare providers. Clinicians should provide education about PSH, including prognosis. Informed family members and staff can help by reducing overstimulation and identifying triggers.

Professional issues

Patients with more severe brain injuries often require life-sustaining treatment, including mechanical ventilation and surgeries. These treatments may pose ethical dilemmas. Clinicians should be mindful of such situations when caring for patients and consider ethics consultation when appropriate.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Paroxysmal Sympathetic Hyperactivity treatment should include 1) minimizing avoidable stimulation, 2) aborting paroxysms with medication, and 3) preventing further episodes. The first step is avoidance of overstimulation and reduction of noxious stimuli. As for pharmacological treatment, all treatment trials are empirical but are supported by clinical experience.3,18,27–31

A systematic review found a dramatic variety of treatment regimens for PSH; the most commonly prescribed agents were benzodiazepines, beta-blockers, opioids, alpha-2 agonists, and baclofen.32 Shald et al. found monotherapy to be less effective than treatment with multiple agents with different mechanisms of action.33 In the critical care setting, dexmedetomidine may be superior to propofol in controlling several symptoms of PSH.33

Table 2. Medications for Paroxysmal Sympathetic Hyperactivity15,34,35

MedicationMechanismDoseClinical EffectSide Effects
PropranololNoncardioselective beta-blockerStart: 10 mg tid by enteral route Max: 320 mg/dayPreventive; effective for tachycardia, hypertension, and diaphoresis Less effective for feverBradycardia, hypotension, sleep disturbance Contraindicated: asthma, heart-block
LabetalolNoncardioselective beta-blocker; selective α(1)-adrenergic receptor antagonistStart: 50 mg bid by enteral route (IV option available)Preventive; effective for tachycardia and hypertensionBradycardia, hypotension Contraindicated: asthma, heart-block
GabapentinInteracts with α2δ subunit of voltage-gated calcium channels in brain and spinal cordStart: 100-300 mg tid by enteral route Max: up to 3600-4800 mg/dayPreventive; improves most featuresSedation
ClonidineCentral α2-adrenergic receptor agonistStart: 0.1-0.3 mg bid by enteral route Max: 2.4 mg/dayAbortive and preventive; mostly improves tachycardia and hypertensionBradycardia, hypotension, sedation
BromocriptineDopamine D2 receptor agonistStart: 1.25-2.5 mg every 12 hours by enteral route Max: 20-40 mg/dayPreventive; effect tends to be modest and delayedConfusion, agitation, dyskinesia, nausea/emesis, orthostatic hypotension, could reduce seizure threshold
DantroleneInhibits calcium release from sarcoplasmic reticulumStart: 0.5-2 mg/kg/IV every 6-12 hours or 25 mg daily by enteral route Max: 10 mg/kg/IV or 400 mg qid by enteral routeAbortive; improves hypertonicity and dystoniaHepatotoxicity (can be severe), respiratory depression, muscle weakness
BaclofenGABAB agonistStart: 5 mg every 8 hours by enteral route Max: 80 mg/dayPreventive; improves hypertonicity and dystoniaSedation, muscle weakness
MorphineOpioid agonist2-8 mg IV bolusAbortive; improves most featuresRespiratory depression, sedation, hypotension, ileus, emesis, histamine release, developing of tolerance

Some studies have found that antipsychotics/dopamine antagonists such as haloperidol are not useful and may even worsen PSH.36 For severe dystonia or rigidity, treatment with intrathecal baclofen and botulinum toxin injection have also been used with benefit.

Additionally, as spasticity and/or dystonia may become a noxious stimulus for patients, a focal treatment of these conditions may lead to resolution of PSH as seen with a case series.37

At different disease stages

New onset/acute

  • Potential curative interventions
    Identify and address precipitating causes. If possible, replace medications that can cause malignant neuroleptic-like syndrome (e.g., metoclopramide). Correct electrolyte imbalance. Remove or reduce noxious stimulation, including spasticity and/or dystonia.
  • Symptom relief
    Medication trial with titration should be initiated. Treatment is empirical and may require switching or addition of a different category, if one medication is not effective. Botulinum toxin injection is considered in case of significant bruxism, opisthotonos, or abnormal posturing. In case of significant bruxism, initiate dental consultation for mouth piece to protect teeth.
  • Rehabilitation strategies intended to stabilize or optimize function or prepare for further interventions at later disease stages. Resting splint and passive range of motion for prevention of joint contractures. Frequent position changes for prevention of decubitus ulcer. Control over or prevention of noxious stimulation in the environment.


  • Secondary prevention and disease management strategies
    Continue passive range of motion and position changes to prevent decubitus ulcer, deep vein thrombosis, joint contractures and heterotopic ossification. When medications fail to ameliorate symptoms, intrathecal baclofen or other focal spasticity treatment can be considered.
  • Symptom relief: as above.
  • Rehabilitation strategies intended to optimize function:
    As long as vital signs are unstable, only minimal rehabilitative intervention is feasible, with monitoring of vital signs. Passive range of motion should be continued.


  • Continue treatment as in subacute phase. As vital signs stabilize, increase mobility; from simple activity (sitting up, standing at tilt table) with monitoring of vital signs. Initiate aggressive treatment for joint contractures or dystonia.

Coordination of care

Close interdisciplinary communication that includes the acute intensive care physician is crucial for optimizing management.

Patient & family education

Family education is important to decrease noxious stimulation and help with maintaining good positioning to prevent joint contractures and decubitus ulcers.

Measurement of patient outcomes

Most evidence suggest that PSH is associated with worse short and long-term outcomes after TBI,1,12,18,24 including longer hospital stay or higher rate of tracheostomy.17 The outcomes measured by Glasgow Outcome Scale (GOS) at 6 and 12 months after brain injury reported poor as well.12,38

Translation into practice

Early treatment with medication that can prevent or abort these features can be effective. Given the significant disturbances of care from PSH, treatment will be beneficial.

Cutting Edge/Emerging and Unique Concepts and Practice

For focal dystonia (bruxism or opisthotonos), botulinum toxin injection is indicated. For bruxism, key target muscles are bilateral masseter and temporalis (if approachable, pterygoid muscles are to be targeted). For severe opisthotonos, key target muscles are paraspinal muscles.

Gaps in the Evidence-Based Knowledge

There is still a paucity of evidence in pharmacological treatment and understanding of pathophysiology. More research in this field is necessary. At this time, it is important to make sure that the awareness of PSH grows to help lead to better definition and treatment.


  1. Pozzi M, Conti V, Locatelli F, et al. Paroxysmal Sympathetic Hyperactivity in Pediatric Rehabilitation: Clinical Factors and Acute Pharmacological Management. Journal of Head Trauma Rehabilitation. 2015;30(5):357-363. doi:10.1097/HTR.0000000000000084
  2. Baguley IJ, Perkes IE, Fernandez-Ortega JF, Rabinstein AA, Dolce G, Hendricks HT. Paroxysmal sympathetic hyperactivity after acquired brain injury: consensus on conceptual definition, nomenclature, and diagnostic criteria. J Neurotrauma. 2014;31(17):1515-1520. doi:10.1089/neu.2013.3301
  3. Lump D, Moyer M. Paroxysmal sympathetic hyperactivity after severe brain injury. Curr Neurol Neurosci Rep. 2014;14(11):1-7. doi:10.1007/s11910-014-0494-0
  4. Perkes IE, Menon DK, Nott MT, Baguley IJ. Paroxysmal sympathetic hyperactivity after acquired brain injury: A review of diagnostic criteria. Brain Inj. 2011;25(10):925-932. doi:10.3109/02699052.2011.589797
  5. Perkes I, Baguley IJ, Nott MT, Menon DK. A review of paroxysmal sympathetic hyperactivity after acquired brain injury. Ann Neurol. 2010;68(2):126-135. doi:10.1002/ana.22066
  6. Choi HA, Jeon SB, Samuel S, Allison T, Lee K. Paroxysmal sympathetic hyperactivity after acute brain injury. Curr Neurol Neurosci Rep. 2013;13(8). doi:10.1007/s11910-013-0370-3
  7. Johnson BD, O’Leary MC, McBryde M, Sackett JR, Schlader ZJ, Leddy JJ. Face cooling exposes cardiac parasympathetic and sympathetic dysfunction in recently concussed college athletes. Physiol Rep. 2018;6(9):e13694. doi:10.14814/phy2.13694
  8. La Fountaine MF, Toda M, Testa AJ, Hill-Lombardi V. Autonomic Nervous System Responses to Concussion: Arterial Pulse Contour Analysis. Front Neurol. 2016;7. doi:10.3389/fneur.2016.00013
  9. Pertab JL, Merkley TL, Cramond AJ, Cramond K, Paxton H, Wu T. Concussion and the autonomic nervous system: An introduction to the field and the results of a systematic review. NeuroRehabilitation. 2018;42(4):397-427. doi:10.3233/NRE-172298
  10. Miranda NA, Boris JR, Kouvel KM, Stiles L. Activity and Exercise Intolerance After Concussion: Identification and Management of Postural Orthostatic Tachycardia Syndrome. Journal of Neurologic Physical Therapy. 2018;42(3):163-171. doi:10.1097/NPT.0000000000000231
  11. Zafonte RD. Traumatic brain injury: an enduring challenge. Lancet Neurol. 2017;16(10):766-768. doi:10.1016/S1474-4422(17)30300-9
  12. Lv LQ, Hou LJ, Yu MK, et al. Prognostic Influence and Magnetic Resonance Imaging Findings in Paroxysmal Sympathetic Hyperactivity after Severe Traumatic Brain Injury. J Neurotrauma. 2010;27(11):1945-1950. doi:10.1089/neu.2010.1391
  13. Hinson HE, Puybasset L, Weiss N, et al. Neuroanatomical basis of paroxysmal sympathetic hyperactivity: A diffusion tensor imaging analysis. Brain Inj. 2015;29(4):455-461. doi:10.3109/02699052.2014.995229
  14. Letzkus L, Keim-Malpass J, Kennedy C. Paroxysmal sympathetic hyperactivity: Autonomic instability and muscle over-activity following severe brain injury. Brain Inj. 2016;30(10):1181-1185. doi:10.1080/02699052.2016.1184757
  15. Rabinstein AA. Autonomic Hyperactivity. CONTINUUM Lifelong Learning in Neurology. 2020;26(1):138-153. doi:10.1212/CON.0000000000000811
  16. Letzkus L, Keim-Malpass J, Kennedy C. Paroxysmal sympathetic hyperactivity: Autonomic instability and muscle over-activity following severe brain injury. Brain Inj. 2016;30(10):1181-1185. doi:10.1080/02699052.2016.1184757
  17. Fernandez-Ortega JF, Prieto-Palomino MA, Garcia-Caballero M, Galeas-Lopez JL, Quesada-Garcia G, Baguley IJ. Paroxysmal sympathetic hyperactivity after traumatic brain injury: Clinical and prognostic implications. J Neurotrauma. 2012;29(7):1364-1370. doi:10.1089/neu.2011.2033
  18. Meyfroidt G, Baguley IJ, Menon DK. Paroxysmal sympathetic hyperactivity: the storm after acute brain injury. Lancet Neurol. 2017;16(9):721-729. doi:10.1016/S1474-4422(17)30259-4
  19. Fernandez-Ortega JF, Baguley IJ, Gates TA, Garcia-Caballero M, Quesada-Garcia JG, Prieto-Palomino MA. Catecholamines and paroxysmal sympathetic hyperactivity after traumatic brain injury. J Neurotrauma. 2017;34(1):109-114. doi:10.1089/neu.2015.4364
  20. Rabinstein AA. Autonomic Hyperactivity. CONTINUUM Lifelong Learning in Neurology. 2020;26(1):138-153. doi:10.1212/CON.0000000000000811
  21. Hughes JD, Rabinstein AA. Early diagnosis of paroxysmal sympathetic hyperactivity in the ICU. Neurocrit Care. 2014;20(3):454-459. doi:10.1007/s12028-013-9877-3
  22. Baguley IJ, Slewa-Younan S, Heriseanu RE, Nott MT, Mudaliar Y N V. The incidence of dysautonomia and its relationship with autonomic arousal following traumatic brain injury. Brain Inj. 2007;21(11):1175-1181. doi:10.1080/02699050701687375
  23. Mehta NM, Bechard LJ, Leavitt K, Duggan C. Severe weight loss and hypermetabolic paroxysmal dysautonomia following hypoxic ischemic brain injury: The role of indirect calorimetry in the intensive care unit. Journal of Parenteral and Enteral Nutrition. 2008;32(3):281-284. doi:10.1177/0148607108316196
  24. Fernández-Ortega JF, Prieto-Palomino MA, Muñoz-López A, Lebron-Gallardo M, Cabrera-Ortiz H, Quesada-García G. Prognostic influence and computed tomography findings in dysautonomic crises after traumatic brain injury. Journal of Trauma – Injury, Infection and Critical Care. 2006;61(5):1129-1133. doi:10.1097/01.ta.0000197634.83217.80
  25. Baguley IJ. Autonomic complications following central nervous system injury. Semin Neurol. 2008;28(5):716-725. doi:10.1055/s-0028-1105971
  26. Lump D, Moyer M. Paroxysmal sympathetic hyperactivity after severe brain injury. Curr Neurol Neurosci Rep. 2014;14(11):1-7. doi:10.1007/s11910-014-0494-0
  27. Rabinstein AA, Benarroch EE. Treatment of Paroxysmal Sympathetic Hyperactivity. Curr Treat Options Neurol. 2008;10(2):151-157.
  28. Rabinstein AA, Sandhu K. Non-infectious fever in the neurological intensive care unit: Incidence, causes and predictors. J Neurol Neurosurg Psychiatry. 2007;78(11):1278-1280. doi:10.1136/jnnp.2006.112730
  29. Ley EJ, Leonard SD, Barmparas G, et al. Beta blockers in critically ill patients with traumatic brain injury: Results from a multicenter, prospective, observational American Association for the Surgery of Trauma study. Journal of Trauma and Acute Care Surgery. 2018;84(2):234-244. doi:10.1097/TA.0000000000001747
  30. Thomas A, Greenwald BD. Paroxysmal sympathetic hyperactivity and clinical considerations for patients with acquired brain injuries: A narrative review. Am J Phys Med Rehabil. 2019;98(1):65-72. doi:10.1097/PHM.0000000000000990
  31. Patel MB, McKenna JW, Alvarez JAM, et al. Decreasing adrenergic or sympathetic hyperactivity after severe traumatic brain injury using propranolol and clonidine (DASH After TBI Study): study protocol for a randomized controlled trial. Trials. 2012;13(1):1. doi:10.1186/1745-6215-13-177
  32. Tu JSY, Reeve J, Deane AM, Plummer MP. Pharmacological Management of Paroxysmal Sympathetic Hyperactivity: A Scoping Review. J Neurotrauma. 2021;38(16):2221-2237. doi:10.1089/neu.2020.7597
  33. Shald EA, Reeder J, Finnick M, et al. Pharmacological Treatment for Paroxysmal Sympathetic Hyperactivity. Crit Care Nurse. 2020;40(3):e9-e16. doi:10.4037/ccn2020348
  34. Ripley D, Driver S, Stork R, Maneyapanda M. Pharmacologic Management of the Patient with Traumatic Brain Injury. In: Eapen B, Cifu DX, eds. Rehabilitation after Traumatic Brain Injury. Elsevier; 2018:154.
  35. Scott RA, Rabinstein AA. Paroxysmal Sympathetic Hyperactivity. Semin Neurol. 2020;40(05):485-491. doi:10.1055/s-0040-1713845
  36. Baguley IJ, Camerons 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
  37. Edmond A, McKay O, Mehta N, Dabaghian L, Yonclas P. Spasticity management and resolution of paroxysmal sympathetic hyperactivity in the acute care setting: a case series. Brain Inj. 2022;36(6):817-821. doi:10.1080/02699052.2022.2077441
  38. Hendricks HT, Heeren AH, Vos PE. Dysautonomia after severe traumatic brain injury. Eur J Neurol. 2010;17(9):1172-1177. doi:10.1111/j.1468-1331.2010.02989.x

Original Version of Topic

Chong Tae Kim, MD. Cerebrally Mediated Autonomic Dysfunction. 11/10/2011.

Previous Revision(s) of the Topic

Chong Tae Kim, MD. Cerebrally Mediated Autonomic Dysfunction. 9/17/2015.

Kayli Gimarc, MD, Lesleay Abraham, MD, Cherry Junn, MD. Paroxysmal Sympathetic Hyperactivity. 8/3/2020.

Author Disclosure

Cherry Junn, MD
Nothing to Disclose

Kayli Gimarc, MD
Nothing to Disclose