eMedicine Specialties > Physical Medicine and Rehabilitation > Traumatic Brain Injury

Post Head Injury Autonomic Complications: Follow-up

Author: Stephen Kishner, MD, Residency Program Director, Professor of Clinical Medicine, Department of Medicine, Section of Physical Medicine and Rehabilitation, Louisiana State University School of Medicine
Coauthor(s): Joseph Augustin, MD, Resident, Section of Physical Medicine and Rehabilitation, Louisiana State University School of Medicine; Scott Strum, MD, Director of Traumatic Brain Injury Service, Assistant Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University Medical Center
Contributor Information and Disclosures

Updated: Jul 24, 2008

Follow-up

Further Inpatient Care

  • The length of stay in rehabilitation is usually reported as being longer for those patients who experience ADS. Other than this observation, no specific alterations from a typical multidisciplinary, acute inpatient rehabilitation program are expected in this population.
  • If actual myocardial damage is identified as a result of the syndrome, observe appropriate cardiac rehabilitation principles during the head injury rehabilitation program.

Further Outpatient Care

  • The outpatient setting is rarely the context for ADS to present.
  • The usual outpatient therapy programs and the typical concerns regarding family functioning and community re-integration issues pertain to outpatient care.
  • Rarely, continued medication use is required long term. Thus, monitoring for common side effects and minimizing medications that impair cognition are required.

Transfer

  • Transfer to the neurosurgery service or an ICU setting is rarely necessary for patients with ADS, although it is conceivable in the event of dangerously high blood pressure and tachycardia.

Complications

  • Increased sensitivity of neurons to elevated temperature occurs during the acute phase of TBI. In animals, functional differences are discernible between those with temperatures in excess of 38 º C and those whose temperature is maintained below 38 º C. In one study, 73% of patients with dysautonomia had temperatures above 38 º C for 2 weeks after injury, contrasted with only 18% of patients without dysautonomia.6
  • Posturing increases energy expenditure by 150-250%.6 These features increase the risk that persons with dysautonomia will sustain secondary injury to the brain.

Prognosis

  • Although patients who have dysautonomia can make functional gains, their outcomes — as measured by Glasgow Outcome Scale (GOS) and Functional Independence Measure (FIM) scores — have been found to be poorer than those of patients without dysautonomia.14  Individuals with dysautonomia also have more difficulty with memory and experience longer periods of posttraumatic amnesia (PTA) than do patients without dysautonomia. Research has found that for patients with dysautonomia, the duration of ICU stay is the same as that recorded for controls but that the length of rehabilitation stay is greater. On average, the duration of the dysautonomia (as measured by cessation of sweating) has been found to be about 75 days.

Patient Education

  • Explaining ADS to the patient is rarely an issue, because patients are usually cognitively compromised at the time of manifestation of the syndrome. However, reducing the fear of family members is important. The family should understand that this syndrome is seen in persons with brain injury, that it is almost always controllable with medications, and that it does not usually remain a long-term problem.

Miscellaneous

Medicolegal Pitfalls

  • Failure to recognize and appropriately treat autonomic dysfunction syndrome (ADS)
  • Failure to diagnose and treat a significant infection
  • Failure to recognize and treat one of the other, more life-threatening differentials mentioned above (see Differentials).

Special Concerns

  • There are other forms of hypothalamic instability noted in patients with TBI. The manifestations (described below) include neuroleptic malignant syndrome, lethal catatonia, and malignant hyperthermia.
    • Neuroleptic malignant syndrome - This is an idiosyncratic reaction to neuroleptics and other psychotropic medications. Neuroleptic malignant syndrome is normally seen after use of potent drugs, such as haloperidol, thiothixene, or piperazine, and it is thought to be due to alterations of central neuroregulatory mechanisms. Metoclopramide, another dopamine-altering medication, has also been associated with the syndrome. Blockade, depletion of dopamine, or withdrawal of dopaminergic medications is believed to be causal. The clinical picture is hyperpyrexia, hypertonicity, altered levels of consciousness, and autonomic dysfunction. Abnormal electrolytes, elevated white blood cell (WBC) counts, elevated liver function tests, and elevated creatine kinase levels are common laboratory findings. Bromocriptine and dantrolene are the recommended treatment.
    • Lethal catatonia - A disorder that is similar to neuroleptic malignant syndrome, lethal catatonia was more frequently described before the advent of neuroleptic medications. The relationship between lethal catatonia and neuroleptic malignant syndrome is the subject of speculation. Clinically, lethal catatonia is a syndrome that develops slowly (over 2 wk) and is characterized by intense motor excitement day and night, violence, insomnia, anorexia, intermittent posturing, rigidity, and psychiatric disturbances. Tachycardia, diaphoresis, dehydration, labile or high blood pressure, and high fever also may occur. Exhaustion eventually supervenes, with continued fever and either rigidity or flaccidity, followed by demise due to cardiovascular collapse. Electroconvulsive therapy has been found to be helpful.
    • Malignant hyperthermia - This syndrome is not viewed as hypothalamic in nature. Rather, it is due to hypermetabolism in muscle triggered by medication exposure (typically, anesthetic agents). Typical signs of malignant hyperthermia are hyperpyrexia, tachycardia, muscle rigidity, and elevated potassium, calcium, magnesium, and creatine kinase levels. Treatment consists of discontinuing the causal drug, the use of dantrolene, and supportive care. Stress-induced malignant hyperthermia, without exposure to the usual offending medications, has been reported.
 


More on Post Head Injury Autonomic Complications

Overview: Post Head Injury Autonomic Complications
Differential Diagnoses & Workup: Post Head Injury Autonomic Complications
Treatment & Medication: Post Head Injury Autonomic Complications
Follow-up: Post Head Injury Autonomic Complications
References
[ CLOSE WINDOW ]

References

  1. Baguley IJ, Heriseanu RE, Cameron ID, et al. A critical review of the pathophysiology of dysautonomia following traumatic brain injury. Neurocrit Care. 2008;8(2):293-300. [Medline].

  2. Baguley IJ. The excitatory:inhibitory ratio model (EIR model): An integrative explanation of acute autonomic overactivity syndromes. Med Hypotheses. 2008;70(1):26-35. [Medline].

  3. Srinivasan S, Lim CC, Thirugnanam U. Paroxysmal autonomic instability with dystonia. Clin Auton Res. Dec 2007;17(6):378-81. [Medline].

  4. Blackman JA, Patrick PD, Buck ML, et al. Paroxysmal autonomic instability with dystonia after brain injury. Arch Neurol. Mar 2004;61(3):321-8. [Medline]. [Full Text].

  5. Rabinstein AA. Paroxysmal sympathetic hyperactivity in the neurological intensive care unit. Neurol Res. Oct 2007;29(7):680-2. [Medline].

  6. Baguley IJ, Nicholls JL, Felmingham KL. Dysautonomia after traumatic brain injury: a forgotten syndrome?. J Neurol Neurosurg Psychiatry. Jul 1999;67(1):39-43. [Medline]. [Full Text].

  7. De Tanti A, Gasperini G, Rossini M. Paroxysmal episodic hypothalamic instability with hypothermia after traumatic brain injury. Brain Inj. Dec 20 2005;19(14):1277-83. [Medline].

  8. Baguley IJ, Cameron ID, Green AM, et al. Pharmacological management of dysautonomia following traumatic brain injury. Brain Inj. May 2004;18(5):409-17. [Medline].

  9. Becker R, Benes L, Sure U, et al. Intrathecal baclofen alleviates autonomic dysfunction in severe brain injury. J Clin Neurosci. Jul 2000;7(4):316-9. [Medline].

  10. Baguley IJ, Heriseanu RE, Gurka JA, et al. Gabapentin in the management of dysautonomia following severe traumatic brain injury: a case series. J Neurol Neurosurg Psychiatry. May 2007;78(5):539-41. [Medline].

  11. Chiolero RL, Breitenstein E, Thorin D. Effects of propranolol on resting metabolic rate after severe head injury. Crit Care Med. Apr 1989;17(4):328-34. [Medline].

  12. Rossitch E, Bullard DE. The autonomic dysfunction syndrome: aetiology and treatment. Br J Neurosurg. 1988;2(4):471-8. [Medline].

  13. Russo RN, O'Flaherty S. Bromocriptine for the management of autonomic dysfunction after severe traumatic brain injury. J Paediatr Child Health. Jun 2000;36(3):283-5. [Medline].

  14. Baguley IJ, Slewa-Younan S, Heriseanu RE, et al. The incidence of dysautonomia and its relationship with autonomic arousal following traumatic brain injury. Brain Inj. Oct 2007;21(11):1175-81. [Medline].

  15. Baguley IJ. Nomenclature of "paroxysmal sympathetic storms". Mayo Clin Proc. Jan 1999;74(1):105. [Medline].

  16. Boeve BF, Wijdicks EF, Benarroch EE. Paroxysmal sympathetic storms ("diencephalic seizures") after severe diffuse axonal head injury. Mayo Clin Proc. Feb 1998;73(2):148-52. [Medline].

  17. Cheshire WP, Freeman R. Disorders of sweating. Semin Neurol. Dec 2003;23(4):399-406. [Medline].

  18. Clifton GL, Robertson CS, Kyper K. Cardiovascular response to severe head injury. J Neurosurg. Sep 1983;59(3):447-54. [Medline].

  19. Clifton GL, Ziegler MG, Grossman RG. Circulating catecholamines and sympathetic activity after head injury. Neurosurgery. Jan 1981;8(1):10-4. [Medline].

  20. Fernández-Ortega JF, Prieto-Palomino MA, Muñoz-López A, et al. [Dysautonomic seizures in patients admitted to an intensive care unit following severe traumatic brain injury]. Rev Neurol. Oct 16-31 2004;39(8):715-8. [Medline].

  21. Hamill RW, Woolf PD, McDonald JV. Catecholamines predict outcome in traumatic brain injury. Ann Neurol. May 1987;21(5):438-43. [Medline].

  22. Horn LJ, Sherer M. Rehabilitation of traumatic brain injury. In: Grabois M, Garrison SJ, Hart KA, et al, eds. Physical Medicine and Rehabilitation: The Complete Approach. Malden, Mass: Blackwell Science; 2000:1290-1.

  23. Meythaler JM, Stinson AM. Fever of central origin in traumatic brain injury controlled with propranolol. Arch Phys Med Rehabil. Jul 1994;75(7):816-8. [Medline].

  24. Ropper AH. Acute autonomic emergencies and autonomic storm. In: Low PA, ed. Clinical Autonomic Disorders. Boston, Mass: Little, Brown; 1993:747-56.

  25. Sandel ME, Abrams PL, Horn LJ. Hypertension after brain injury: case report. Arch Phys Med Rehabil. Jul 1986;67(7):469-72. [Medline].

  26. Scott JS, Ockey RR, Holmes GE. Autonomic dysfunction associated with locked-in syndrome in a child. Am J Phys Med Rehabil. May-Jun 1997;76(3):200-3. [Medline].

  27. Sherman MA, Shutov AA. [Clinical course of autonomic nervous system disorders in veterans with consequences of combat mild brain injury]. Zh Nevrol Psikhiatr Im S S Korsakova. 2003;103(1):17-20. [Medline].

  28. Shiozaki T, Taneda M, Kishikawa M, et al. Transient and repetitive rises in blood pressure synchronized with plasma catecholamine increases after head injury. Report of two cases. J Neurosurg. Mar 1993;78(3):501-4. [Medline].

  29. Thorley RR, Wertsch JJ, Klingbeil GE. Acute hypothalamic instability in traumatic brain injury: a case report. Arch Phys Med Rehabil. Feb 2001;82(2):246-9. [Medline].

  30. Whyte J, Filion DT, Rose TR. Defective thermoregulation after traumatic brain injury. A single subject evaluation. Am J Phys Med Rehabil. Oct 1993;72(5):281-5. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

autonomic dysfunction syndrome, ADS, dysautonomia, paroxysmal sympathetic storm, autonomic storm, neurostorming, diencephalic seizure, acute midbrain syndrome, brainstem attack, hypothalamic-midbrain dysregulation syndrome, hyperpyrexia associated with muscle contraction, paroxysmal autonomic instability with dystonia, PAID, traumatic brain injury, TBI, hydrocephalus, brain tumor, subarachnoid hemorrhage, intracerebral hemorrhage

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Stephen Kishner, MD, Residency Program Director, Professor of Clinical Medicine, Department of Medicine, Section of Physical Medicine and Rehabilitation, Louisiana State University School of Medicine
Stephen Kishner, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Association of Neuromuscular and Electrodiagnostic Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph Augustin, MD, Resident, Section of Physical Medicine and Rehabilitation, Louisiana State University School of Medicine
Disclosure: Nothing to disclose.

Scott Strum, MD, Director of Traumatic Brain Injury Service, Assistant Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University Medical Center
Scott Strum, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Medical Editor

Teresa L Massagli, MD, Residency Director, Professor, Department of Rehabilitation Medicine and Pediatrics, University of Washington School of Medicine
Teresa L Massagli, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Physical Medicine and Rehabilitation, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.