Dysautonomia after traumatic brain injury: a forgotten syndrome?

Baguley, Ian; Nicholls, Jodie L; Felmingham, Kim L.; Crooks, Jenelle; Gurka, Joseph; Wade, Lauren

doi:10.1136/jnnp.67.1.39

Cited by 189 publications

(183 citation statements)

References 22 publications

(19 reference statements)

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“…Early recognition of this syndrome and its appropriate management may result in less expensive diagnostic tests, avoidance of pharmacological overdoses, prevention of secondary injury, enhanced nursing care and alleviation of anxiety among healthcare personnel observing periodic episodes in affected patients. (1,2) The essential features of this characteristic syndrome include paroxysms of marked agitation, diaphoresis, hyperthermia, hypertension, tachycardia and tachypnoea accompanied by hypertonia and extensor posturing. (2,3) PAID syndrome mainly manifests in the intensive care setting but may persist for months during the patient's rehabilitation phase.…”

Section: Introductionmentioning

confidence: 99%

Paroxysmal autonomic instability with dystonia (PAID) syndrome following cardiac arrest

Kapoor¹,

Singla²,

Singh³

et al. 2014

smedj

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Section: Introductionmentioning

confidence: 99%

Paroxysmal autonomic instability with dystonia (PAID) syndrome following cardiac arrest

Kapoor¹,

Singla²,

Singh³

et al. 2014

smedj

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“…The reasons by which PSH occurs and its morbid effects have been discussed during years, not only in adult TBI patients but also in pediatric populations and other pathologies [9][10][11][12][13][14][15][16]. Recently Meyer [3] propose that PSH courses in three stages being the first of them asymptomatic because of the strong sedation of the patient and the management of cranial hypertension, the second stage would correspond to the onset of symptom clusters and the third stage would be characterized by dystonia and a decline in posturing.…”

Section: Discussionmentioning

confidence: 99%

“…In summary, this hypothesis of Meyer [3] would indicate that in PSH there will be an increase in the excitatory stimuli without the needed compensatory increase in inhibitory functions. This would lead to a facilitation to develop a highly exaggerated sympathetic efflux triggered by non-nociceptive peripheral stimuli [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20].…”

Section: Discussionmentioning

confidence: 99%

Fever Due to Infection or Muscle Heat?

Devesa

Puell

Castellanos

et al. 2017

MOJAP

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Paroxysmal sympathetic hyperactivity is a frequent condition in patients that suffered a TBI, but also other kinds of brain damage, characterized by a myriad of signs and symptom such as high temperature, tachycardia, tachypnea, hypertension, profuse sweating and spastic extension of legs and arms. The presence of high temperature may lead to suspect about any infective process whose analysis can put at risk the life of the patient, while in fact these symptom appear as a consequence of an increased release of catecholamines occurring because of the disruption of central pathways. Muscle spasticity produces a great heat that contributes to the central origin of hyperthermia. Here we describe two cases that presented PSH after different brain injuries. Both were in coma. One of them after a severe TBI and the other one because of a very important brain infection. PSH in the first case was due to a renal colic and PSH was resolved with propofol. The second case developed PSH suddenly before a session of physiotherapy. The rapid detection of the problem led us to use propranolol and in 40 minutes the patient was in normal conditions. We conclude that the knowledge of PSH and its rapid treatment should be mandatory in hospitals and centers devoted to rehabilitate neurological patients.

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“…Dysautonomia or Paroxysmal sympathethetic storming occurs in around 10-30% of TBI [1][2][3]. It exerts a profound negative influence on the final outcome in affected individuals.…”

Section: Editorialmentioning

confidence: 99%

“…It's in phase 2 where the above said symptoms presents and occurs on stopping sedation. Phase 3 represents the burnt out Dysautonomia which begins with stoppage of diaphoresis and leaves patient in variable dystonia/spasticity [1].…”

mentioning

confidence: 99%

Confronting ‘Paroxysmal Sympathetic Storming’ in Traumatic Brain Injury

Oommen¹

2017

JNSK

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Submit Manuscript | http://medcraveonline.com Tachycardia, Tachypnoea, hypertension, fever, Diaphoresis, rigidity and posturing are the common clinical findings in Dysautonomia. Presence of 5 out of any of the above can be considered diagnostic of Dysautonomia [6][7][8]. Infection or agitation can also mimick Dysautonomia. Correct identification of the syndrome and optimal management is highly detrimental in the management of head injuries [9].Phase 1 which lasts during the initial 1 week where patient is on ventilator and sedated with or without paralysis. It's in phase 2 where the above said symptoms presents and occurs on stopping sedation. Phase 3 represents the burnt out Dysautonomia which begins with stoppage of diaphoresis and leaves patient in variable dystonia/spasticity [1].Goal of managing dysautonomia is to prevent secondary injury caused by the Paroxysmal sympathetic storming. Dysautonomia aggravates secondary brain injury by basically 3 mechanisms, first Hyperthermia, which needs very aggressive control. Second the rigidity and posturing that markedly increases the energy expenditure to upto 200% and resulting in a relative malnutrition. Third there is an elevation of circulating catecholamines which is an independent predictor of poor outcome [10][11][12][13][14][15].Pharmacological interventions to treat Dysautonomia are plenty. Benzodiazepine and Narcotic combination reduces the number and frequency of paroxysms probably by reduction of brain activity. Other medications that have shown success include Clonidine (alpha 2 adrenergic agonist) which decrease central sympathetic outflow. The hypertensive and tachycardia component can be controlled through Labetolol. Bromocriptine (Dopamine D2 agonist) is effective in controlling fever and diaphoresis. Intrathecal Baclofen has been found to be of some help in managing autonomic dysutonomia [16][17][18][19][20][21][22][23][24][25]. EditorialDysautonomia or Paroxysmal sympathethetic storming occurs in around 10-30% of TBI [1][2][3]. It exerts a profound negative influence on the final outcome in affected individuals. Dysautonomia commonly occurs following severe head injury if associated with at DAI, Brain stem Injury, preadmission hypoxia or in the younger age group [4,5]. The pathophysiological basis for dysautonomia is yet to be determined but recent evidences support two recent hypothesis -first, the direct injury to the Hypothalamus causing dysautonomia and second functional disconnection of the hypothalamus and diecephalon from rest of the Central nervous system secondary to the axonal injury to the afferent and efferent pathway [6,7].

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Dysautonomia after traumatic brain injury: a forgotten syndrome?

Cited by 189 publications

References 22 publications

Paroxysmal autonomic instability with dystonia (PAID) syndrome following cardiac arrest

Paroxysmal autonomic instability with dystonia (PAID) syndrome following cardiac arrest

Fever Due to Infection or Muscle Heat?

Confronting ‘Paroxysmal Sympathetic Storming’ in Traumatic Brain Injury

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