Mild Traumatic Brain Injury: An Update for Advanced Practice Nurses

Esther Bay, PhD APRN BC CCRN; Samuel A. McLean, MD MPH

Disclosures

J Neurosci Nurs. 2007;39(1):43-51. 

In This Article

Pathogenesis of Mild Brain Injury

MBI can be a result of domestic violence, motor vehicle crash, sport-related concussion, fall, or bicycling-related injury (CDC, 1999). The neural mechanisms mediating the development of MBI symptoms remain poorly understood. A complex cascade of ionic, metabolic, and physiological events, including release of excitatory transmitters, mitochondrial dysfunction, diminished glucose metabolism, and axonal injury are related to clinical signs and symptoms (Giza & Hovda, 2001). Regardless of the cause, a dynamic and complex process of events occurs involving injuries to the axon or injuries to neurons and glial cells, or both.

Axonal injury, often termed diffuse axonal injury (DAI), is a common consequence of brain injury and is associated with poor outcomes (Bramlett & Dalton, 2004). There are three grades of DAI ( Table 1 ). Grade I is associated with widespread axonal damage of the white matter of the cerebral hemisphere and is found in persons who do not experience coma or those with milder injuries. Grade II

DAI consists of tissue tear hemorrhages and axonal abnormalities in the cerebral hemispheres and corpus callosum. Grade III DAI, the most severe, consists of grade II findings in addition to abnormalities in regions of the brainstem (Gennarelli, Thibault, & Graham, 1998). For patients with milder injuries, the presence of DAI can be unclear (Shaw, 2002).

Neuronal and glial cell injury can be associated with secondary injury or disrupted blood flow. A series of events occurs leading to accumulation of excitatory amino acids that could result in calcium influx and cell death (Giza & Hovda, 2001; Marshall, 2000). Neurochemical processes involved in this complex cascade are under study as are processes of apoptosis or programmed cell death, changes in glucose metabolism, and calcium-mediated neuronal injury. Following MBI, cerebral function may be impaired for weeks with significant changes in cerebral metabolism (Bramlett & Dalton, 2004; Marshall). This underscores the need for in-depth clinical assessments in order to uncover neurocognitive correlates of MBI.

In addition, alterations in neurosensory processing may occur via mechanisms other than direct mechanical neuronal injury and its secondary consequences. For example, stress systems are activated in individuals experiencing a traumatic event to mobilize the optimal response to the event. Numerous animal and human studies have demonstrated that many aspects of cognitive and sensory processing are modulated by stress response system function (Diatchenko, Ackley, Slade, Filling, & Mainer, 2006; Pitman & Delahanty, 2005). The degree to which the dysregulation of these physiologic systems may contribute to disordered neurosensory processing is an active area of investigation.

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