Brain Neurorehabil.  2012 Sep;5(2):58-61. 10.12786/bn.2012.5.2.58.

Autonomic Dysfunction after Traumatic Brain Injury

• Bok SK

• KMID: 2270741
• DOI: http://doi.org/10.12786/bn.2012.5.2.58

Abstract

Patients following traumatic brain injury (TBI) sometimes display paroxysmal autonomic and muscle overactivity, which is suspicious to self-limiting or permanent disability. There are still no standard definition and diagnostic tools for autonomic dysfunction after TBI. Dysautonomia has been used as the most dominant term by authors of papers, was defined as simultaneous paroxysmal increases in at least five out of the seven features (heart rate, respiratory rate, blood pressure, temperature, posturing, dystonia and sweating) with episodes persisting for at least 2 weeks after injury. Heart rate variability (HRV) may be helpful to diagnosis the dysautonomia. The available evidence for managing of dysautonomia was intravenous morphine, Gabapentin, Bromocriptine and intrathecal baclofen infusion. Therefore, future efforts should be targeted at multicenter, large sample studies to make the diagnostic criteria and to evaluate the incidence, natural history and management of autonomic dysfunction after TBI.

Keyword

autonomic dysfunction; dysautonomia; heart rate; traumatic brain injury (TBI)

MeSH Terms

Amines
Baclofen
Blood Pressure
Brain Injuries
Bromocriptine
Cyclohexanecarboxylic Acids
Dystonia
gamma-Aminobutyric Acid
Heart Rate
Humans
Incidence
Morphine
Muscles
Natural History
Primary Dysautonomias
Respiratory Rate
Amines
Baclofen
Bromocriptine
Cyclohexanecarboxylic Acids
Morphine
gamma-Aminobutyric Acid

Figure

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  Fig. 1 EIR (excitatory: inhibitory ratio) model by Baguley. MC: Motor centers, BEI: Brain excitatory:inhibitory center, SEI: Spinal excitatory:inhibitory center, +: Excitatory pathways, -: Inhibitory pathways.

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