Paroxysmal Autonomic Instability After Brain Injury

I congratulate Blackman et al¹ for their valuable effort to bring some order into the chaotic and sketchy literature on autonomic dysregulation after brain injury. They propose the termparoxysmal autonomic instability with dystonia (PAID) to characterize the syndrome. Although I agree with the necessity to introduce a unifying nomenclature, this denomination and the criteria listed by the authors may be too restrictive. In the neurological-neurosurgical intensive care unit, I have often observed patients with brain injuries who have spells of autonomic dysregulation but minimal or no dystonia and in whom no other explanation for these signs can be found. These patients typically respond to the agents cited by the authors (nonselective β-blockers, morphine sulfate, bromocriptine mesylate, or clonidine hydrochloride) and sometimes worsen when they receive haloperidol for sedation. If left untreated, many eventually develop dystonic posturing.

As noted by the authors, early recognition of this condition and prompt intervention may minimize unnecessary testing and medication use. Furthermore, dysautonomic episodes have been associated with poor functional outcome after severe traumatic brain injury.² Although this association may simply reflect the severity of the initial brain injury, the effects of secondary brain insults during dysautonomic episodes—from hyperthermia, an extreme increase in energy expenditure, or a rise in intracranial pressure—on neurological outcome deserve further investigation. Thus, rejecting the diagnosis based solely on the absence of dystonic posturing may have negative consequences. Until the manifestations of this syndrome become better delineated, it may be reasonable to use less restrictive criteria in research protocols.

Correspondence: Dr Rabinstein, Critical Care Neurology, Department of Neurology, University of Miami School of Medicine, 1150 NW 14th St, Suite 304, Miami, FL 33101 (arabinstein@med.miami.edu).