- Kentucky One Healthcare, University of Louisville Hospital, 530 S Jackson St, Louisville, KY 40202, USA
Kimberly S. Meyer
Kentucky One Healthcare, University of Louisville Hospital, 530 S Jackson St, Louisville, KY 40202, USA
DOI:10.4103/2152-7806.144632Copyright: © 2014 Meyer KS. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
How to cite this article: Meyer KS. Understanding paroxysmal sympathetic hyperactivity after traumatic brain injury. Surg Neurol Int 13-Nov-2014;5:
How to cite this URL: Meyer KS. Understanding paroxysmal sympathetic hyperactivity after traumatic brain injury. Surg Neurol Int 13-Nov-2014;5:. Available from: http://sni.wpengine.com/surgicalint_articles/understanding-paroxysmal-sympathetic-hyperactivity-traumatic-brain-injury/
Background:Paroxysmal sympathetic hyperactivity (PSH) is a condition occurring in a small percentage of patients with severe traumatic brain injury (TBI). It is characterized by a constellation of symptoms associated with excessive adrenergic output, including tachycardia, hypertension, tachypnea, and diaphoresis. Diagnosis is one of exclusion and, therefore, is often delayed. Treatment is aimed at minimizing triggers and pharmacologic management of symptoms.
Methods:A literature review using medline and cinahl was conducted to identify articles related to PSH. Search terms included paroxysmal sympathetic hyperactivity, autonomic storming, diencephalic seizures, and sympathetic storming. Reference lists of pertinent articles were also reviewed and these additional papers were included.
Results:The literature indicates that the understanding of PSH following TBI is in its infancy. The majority of information is based on small case series. The review revealed treatments that may be useful in treating PSH.
Conclusions:Nurses play a critical role in the identification of at-risk patients, symptom complexes, and in the education of family. Early detection and treatment is likely to decrease overall morbidity and facilitate recovery. Further research is needed to establish screening tools and treatment algorithms for PSH.
Keywords: Paroxysmal sympathetic hyperactivity, sympathetic storming, traumatic brain injury
Traumatic brain injury (TBI) affects 1.4 million Americans annually.[
PSH has been discussed in the literature under a variety ofnames. Early in the recognition of this phenomenon, the term diencephalic seizure was used.[
PSH is a poorly understood phenomenon with varied symptomatology. As a result, identification of the condition is often delayed.[
PSH is thought to occur in stages. The first stage is often asymptomatic due to the heavy sedation and paralytics required for the acute management of intracranial hypertension and other trauma-related injuries. The second stage is characterized by the onset of symptom clusters and the third stage, by a decline in posturing and dystonia.[
Various dissociation theories provide the theoretical framework for PSH. These include those of structural disconnection, where lesions in the mesencephalon cause disruptions in relay from the medulla/hypothalamus, and the more widely accepted excitatory: Inhibitory ratio (EIR) model, where dysfunction of the diencephalic–brainstem inhibitory center that normally controls afferent stimulus processing in the spinal cord occurs.[
There is no accepted treatment algorithm for the management of PSH. Treatment is aimed at mitigating signs and symptoms to decrease associated adverse events such as cardiac hypertrophy, dehydration, muscle wasting, contractures, and delayed recovery which contribute to increased morbidity [
In cases of medication failure, a case series of six demonstrated that hyperbaric oxygen (HBOT) controlled autonomic discharges and posturing in the subacute TBI phase.[
Early identification and treatment of PSH is critical to facilitate recovery from TBI and avoid permanent organ dysfunction. Expensive diagnostic testing is rarely warranted. Instead, the observational and analytical skills employed by most ICU nurses are more useful in recognizing PSH. In addition to communication of findings in order to facilitate diagnosis and treatment, nursing surveillance also affords the opportunity to identify and, therefore, potentially mitigate triggers. A final contribution of nursing involves family and caregiver teaching. In this role, the nurse explains the concept of PSH, along with its causes and treatments, thereby aiding the family member to better cope with the paroxysms that can be very frightening or chaotic to watch.
Early initiation of symptom-specific therapy, although beyond the scope of this paper, is thought to decrease complication rates and ICU length of stay and to facilitate recovery.[
PSH should be considered when patients emerging from coma exhibit multiple, concurrent symptoms of sympathetic overactivity: Hyperthermia, posturing, dystonia, tachycardia, tachypnea, diaphoresis, or hypertension. Nurses play a pivotal role in identifying the condition of PSH, observing and mitigating the triggers which precipitate the event, communicating patient needs to the interdisciplinary team, and finally, educating the family/caregivers. Ongoing research should include efforts to develop scales to document the frequency and severity of these paroxysmal episodes and treatment algorithms to guide the clinician in the management of PSH.
1. Baguley IJ. Nomenclature of “paroxysmal sympathetic storms”. Mayo Clin Proc. 1999. 74: 105-
2. Baguley IJ. Excitatory: Inhibitory Ratio Model (EIR Model): An integrative explanation of acute automonic overactivity syndromes. Med Hypotheses. 2008. 70: 26-35
3. Baguley IJ, Nicholls JL, Felmingham KL, Crooks J, Gurka JA, Wade LD. Dysautonomia after traumatic brain injury: A forgotten syndrome?. J Neurol Neurosurg Psychiatry. 1999. 67: 39-43
4. Baguley IJ, Heriseanu RE, Gurka JA, Nordenbo A, Cameron ID. Gabapentin in the management of dysautonomia following severe traumatic brain injury: A case series. J Neurol Neurosurg Psychiatry. 2007. 78: 539-41
5. Baguley IJ, Heriseanu RE, Nott MT, Chapman J, Sandanam J. Dysautonomia after severe traumatic brain injury: Evidence of persisting overresponsiveness to afferent stimuli. Am J Phys Med Rehabil. 2009. 88: 615-22
6. 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: 409-17
7. Baguley IJ, Nott MT, Slewa-Younan S, Heriseanu RE, Perkes IE. Diagnosing dysautonomia after acute traumatic brain injury: Evidence for overresponsiveness to afferent stimuli. Arch Phys Med Rehabil. 2009. 90: 580-6
8. Baguley IJ, Perkes IE, Fernandez-Ortega JF, Rabenstein AA, Dolce G, Hendricks HT.editors. Paroxysmal sympathetic hyperactivity after acquired brain injury: Consensus on conceptual definition, nomenclature, and diagnostic criteria. J Neurotrauma 2104. Epub; 2014. p.
9. Boeve BF, Wijdicks EF, Benarroch EE, Schmidt KD. Paroxysmal sympathetic storms (“diencephalic seizures”) after severe diffuse axonal head injury. Mayo Clin Proc. 1998. 73: 148-52
10. Bullard DE. Diencephalic seizures: Responsiveness to bromocriptine and morphine. Ann Neurol. 1987. 21: 609-11
11. Last accessed on 2011 Apr 15. Available from: http://www.cdc.gov/TraumaticBrainInjury/index.html .
12. Cuny E, Richer E, Castel JP. Dysautonomia syndrome in the acute recovery phase after traumatic brain injury: Relief with intrathecal Baclofen therapy. Brain Inj. 2001. 15: 917-25
13. Fernandez-Ortega JF, Prieto-Palomino MA, Munoz-Lopez A, Lebron-Gallardo M, Cabrera-Ortiz H, Quesada-Garcia G. Prognostic influence and computed tomography findings in dysautonomic crises after traumatic brain injury. J Trauma. 2006. 61: 1129-33
14. Hendricks HT, Heeren AH, Vos PE. Dysautonomia after severe traumatic brain injury. Eur J Neurol. 2010. 17: 1172-7
15. Hinson HE, Sheth KN. Manifestations of the hyperadrenergic state after acquired brain injury. Curr Opin Crit Care. 2012. 18: 139-45
16. Lemke DM. Sympathetic storming after severe traumatic brain injury. Crit Care Nurse. 2007. 27: 30-7
17. Lv LQ, Hou LJ, Yu MK, Qi XQ, Chen HR, Chen JX. Risk factors related to dysautonomia after severe traumatic brain injury. J Trauma. 2011. 71: 538-42
18. Payen D, Quintin L, Plaisance P, Chiron B, Lahoste F. Head injury: Clonidine decreases plasma catecholamines. Crit Care Med. 1990. 18: 392-5
19. Penfield W. Diencephalic autonomic epilepsy. Arch NeurPsych. 1929. 22: 354-78
20. Rossitch E, Bullard DE. The autonomic dysfunction syndrome: Aetiology and treatment. Br J Neurosurg. 1988. 2: 471-8
21. Russo RN, O’Flaherty S. Bromocriptine for the management of autonomic dysfunction after severe traumatic brain injury. J Paediatr Child Health. 2000. 36: 283-5