Autonomic dysfunction syndromes after acute brain injury

Abstract

The central autonomic nervous system (CAN) is a multifaceted, richly connected neural network incorporating the hypothalamus, its descending tracts through the brainstem, the insular cortex and down into the spinal cord. All levels of the CAN are susceptible to injury following traumatic brain injury (TBI), whether from focal or diffuse injury. Focal injuries would be expected to produce localized damage to CAN control centers, whereas the effects of diffuse injuries are presumed to be more diverse and/or widely distributed. As the combination of focal and diffuse injury following TBI can vary widely from one individual to the next, the impact of focal injuries is best understood with reference to the focal ischemic stroke literature. Subarachnoid hemorrhage (SAH), a common complication following TBI, also has predictable effects on autonomic control that can be understood with reference to spontaneous SAH literature. Finally, paroxysmal sympathetic hyperactivity (PSH), a syndrome incorporating episodes of heightened sympathetic drive and motor overactivity following minor stimulation, is discussed as an example of what happens when central inhibitory control of spinal cord autonomics is impaired.

Keywords: central autonomic network; hyperadrenergic crisis; paroxysmal sympathetic hyperactivity; stroke; subarachnoid hemorrhage; traumatic brain injury.

Fig. 34.1.

Relationship between paraventricular nuclei and neurons directly associated with central autonomic control.

Fig. 34.2.

Major nuclei and pathways of the central autonomic network.

Fig. 34.3.

Normalized heart rate (HR) change for 100 beats before and after endotracheal tube (ETT) suctioning in an intensive care unit. Poststimulus HR increased by 2% in the sTBI group, by 8% in the DYS — group, and by 16% in the DYS+group. DYS+, dysautonomic; DYS−, nondysautonomic; sTBI, standard TBI. (Reproduced from Baguley et al., 2009b.)

Fig. 34.4.

Heart rate over time in a patient with paroxysmal sympathetic hyperactivity following traumatic brain injury. Note the periods of tachycardia contrasted against a background of normal heart rate. (From Baguley (2008), with permission from Jaypee Brothers Medical Publishers Pty. Ltd., India.)