Paroxysmal Autonomic Instability With Dystonia After Brain Injury

Abstract

A complication of severe brain injury is a syndrome of intermittent agitation, diaphoresis, hyperthermia, hypertension, tachycardia, tachypnea, and extensor posturing. To capture the main features of this syndrome, derived through literature review and our own case series, we propose the term paroxysmal autonomic instability with dystonia. We reviewed reports of autonomic dysregulation after brain injury and extracted essential features. From the clinical features, consistent themes emerge regarding signs and symptoms, differential diagnosis, and pharmacological therapies. We used these findings to make recommendations regarding diagnosis and treatment. Paroxysmal autonomic instability with dystonia appears to be a distinctive syndrome after brain injury that can mimic other life-threatening conditions. Early recognition may lead to fewer diagnostic tests and a rational approach to management. Prospective trials of specific drugs are needed to determine optimal efficacy.

The Utility of EEG, SSEP, and Other Neurophysiologic Tools to Guide Neurocritical Care

“…As a result, the literature supports the routine use of continuous monitoring for seizure detection in patients with TBI, despite the small amount of prevention afforded by 7 days of prophylactic phenytoin [30]. A secondary role of EEG in TBI is discrimination of seizures from paroxysmal autonomic instability with dystonia, both of which may be associated with elevated intracranial pressure [31,32]. Hypoxic ischemic encephalopathy is also associated with a high rate of seizures, affecting 10 to 33% of patients following cardiac arrest [33,34].…”

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

“…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.…”

Fever Due to Infection or Muscle Heat?

“…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.…”

“…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].…”