Dysautonomia after pediatric brain injury

Autor: Ericka L. Fink, Elizabeth C. Tyler-Kabara, Maryanne J Henderson, Michael Shoykhet, Jong H Jeong, Katherine A. Kirk, Michael J. Bell
Rok vydání: 2012
Předmět:
Zdroj: Developmental Medicine & Child Neurology. 54:759-764
ISSN: 0012-1622
Popis: Dysautonomia is a severe, debilitating sequela of acquired brain injury (ABI). It is characterized by dysfunction of the autonomic nervous system with resultant disturbances in temperature and hemodynamic homeostasis, and dystonic muscle contractions. Myriad names in the literature (including ‘paroxysmal autonomic instability with dystonia’ and ‘paroxysmal sympathetic hyperactivity,’ among others) and the lack of generalized agreement over precise symptomatology required for diagnosis complicate the development of an organized approach to this disorder.1–3 The most common constellation of clinical signs, however, includes a combination of fever, tachypnea, hypertension, tachycardia, diaphoresis, and dystonia.1,2,4,5 Over a dozen names have been given to this constellation of signs and symptoms (‘sympathetic storms’, ‘thalamic storms’, and others) but for this study we have chosen to adhere to the most predominant term, ‘dysautonomia’.6,7 After injury, symptom onset has been observed between 1 and 60 days, but most reports focus on the first several weeks after injury.1 One prospective study observed widespread autonomic arousal (24%) among its participants within 7 days of injury, but only 8% qualified as having dysautonomia by day 14.8 The duration of dysautonomia symptoms is variable, with some groups proposing two or three distinct phases, or even distinct disorders: a short-duration variant (lasting through the acute recovery stage), as well as a prolonged variant (lasting weeks to 6 or more months).4,6,9 The pathophysiology of dysautonomia is not well understood but may arise from disinhibition of diencephalic autonomic centers, which, in turn, leads to over-responsiveness to innocuous and/or nociceptive sensory stimuli.10 The prevalence and overall outcomes of dysautonomia vary by injury type. In previous studies, the prevalence of dysautonomia has ranged from 8 to 33% after traumatic brain injury (TBI) and from 6 to 29% after non-traumatic or anoxic brain injury.2,5,8,11–13 There is very little in the literature on dysautonomia in children, but its prevalence after TBI has been reported to be 12%, whereas a prevalence of 29% has been observed after anoxic brain injury in a small series.5 Dysautonomia has been prospectively associated with worse outcomes after TBI in adults: patients had longer stays in intensive care units, worse Glasgow Outcome Scale scores, increased frequency of infection, need for tracheotomy, longer duration of post-traumatic amnesia, and increased estimated hospital costs.8,13 Importantly, dysautonomia has also recently been associated with increased mortality in adults after TBI and diffuse axonal injury.14 In the pediatric population, clinical reports about dysautonomia have infrequently extended beyond case reports15,16 despite the fact that brain injury is a leading cause of morbidity and mortality in children. Thus, our aim in this study was to define the epidemiology of dysautonomia in children recovering from ABI, including prevalence, signs, and symptoms used to make the diagnosis, brain injury etiologies, and outcomes. We audited medical records from a regional rehabilitation center for children to accomplish these objectives. In addition, we extracted from these records various medical aspects of the care that these children required during their post-injury period. We hypothesized that after ABI, children with dysautonomia have longer rehabilitation courses and worse functional outcomes than children without it.
Databáze: OpenAIRE
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