Riding Out the Storm: Sympathetic Storming after Traumatic Brain Injury

Denise M. Lemke

Disclosures

J Neurosci Nurs. 2004;36(1) 

In This Article

History

Wilson (1923) introduced the term "tonic fit" when describing sudden episodes of intensification of extensor posturing. Throughout the years, terms such as diencephalic autonomic epilepsy (Penfield, 1929), central dysregulation (Bricolo, Turazzi, Alexandre, & Rizzuto, 1977), tonic decerebrate spasms (Cartlidge & Shaw, 1981), tonic cerebellar fits (Davis & Davis, 1982), sympathoadrenal response (Rosner, Newsome, & Becker, 1984), decerebrate rigidity (Klug et al., 1984), diencephalic seizures (Bullard, 1987), autonomic dysfunction syndrome (Rossitich & Bullard, 1988), traumatic apallic syndrome (Hackl et al., 1991), paroxysmal sympathetic storms (Boeve et al., 1998), dysautonomia (Baguley et al., 1999), storming (Thorley, Wertsch, & Klingbeil, 2001) and autonomic dysfunction syndrome (Strum, 2002) have been used to describe these episodes.

Theories on the cause of the episodes range from loss of cortical control over autonomic function (Hortnag et al., 1980), loss of physiological regulatory mechanisms (Klug et al., 1984), disinhibitory control of sympathetic outflow (Bullard, 1987), disruption of the autonomic relay system (Boeve et al., 1998), and dysregulation of the autonomic nervous system (Strum, 2002). Numerous sites of dysfunction have been speculated, from the upper brain stem and diencephalon (Bullard), brain stem (Cartlidge & Shaw, 1981), orbital frontal cortex (Strum, 2002), and, more specifically, the anterior hypothalamus or medulla (Boeve et al.; Hackl et al., 1990). Secondary to lack of diagnostic radiographic tools, early analysis of the anatomic correlate of the episodes was based on interpretation of clinical symptoms.

Recent research has looked further into identifying the possible location of the dysfunction by evaluating electroencephalogram (EEG), computed tomography (CT) and magnetic resonance imaging (MRI). In EEG testing, these individuals have not demonstrated seizure activity during storming episodes (Baguley et al., 1999; Boeve et al., 1988; Do, Sheen, & Bromfield, 2000; Pranzatelli et al., 1991; Rossitich & Bullard, 1988; Strum, 2002; Thorley, Wertsch, & Klingbeil, 2001). A consistent location of the injury has not been demonstrated on CT or MRI, though there have been several case reports of individuals with diffuse axonal injury (DAI) on MRI who exhibited storming (Boeve et al.; Klug et al., 1984; Strum). The DAI may contribute to disassociation of the sympathetic and parasympathetic systems.

Whatever the cause, there is an uncontrolled sympathetic surge that produces a stress response. In a normal state, the parasympathetic system would respond to an increased sympathetic activity by providing compensation, or an inhibitory response, and the body would return to a normal homeostatic state. In storming, there appears to be both an exaggeration of the sympathetic response with a diminished parasympathetic response or alteration in the relay system between the two networks.

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