Nearly 64% of people with mild traumatic brain injury (MTBI) experience prolonged symptoms and functional impairments lasting months or years postinjury. Explanations for delayed recovery have varied and lacked a guiding framework, hindering intervention science. Using theory substruction and adapting McLean and associates' biopsychosocial model for chronic pain after trauma, we suggest that perceived psychological stress and associated neurobiological responses may predict risk for functional impairment. This model can be tested using a biopsychosocial approach to determine the interplay of psychological stress and neurobiological responses implicated in functional impairments after MTBI. Testing of this model will advance understanding of pathways to postconcussion syndrome.
Keywords: mild traumatic brain injury; stress; vulnerability; functional status
Stress-related disorders abound in the United States and developing countries. In fact, stress in its more chronic form has become a major focus in research concerned with chronic disorders, including Alzheimer's disease, cancer, heart disease, and depression (McEwen, 2002). Along with the increase of stress-related disorders is the rising worldwide incidence of mild traumatic brain injury (MTBI), also known as the signature wound of Operation Enduring Freedom (Hoge et al., 2008; Schneiderman, Braver, & Kang, 2008). While many people recovering from MTBI will experience full recovery by 12 weeks, sadly as many as 64% will experience prolonged symptoms (Meares et al., 2007), decline from preinjury function (Maio et al., 2006), psychiatric disorders, (Deb, Lyons, & Koutzoukis, 1998), and inability to return to their pre-injury employment (Ruffolo, Friedland, Dawson, Colantonio, & Lindsay, 1999). When such chronic difficulties persist after the expected 12-week recovery period, a diagnosis of postconcussion syndrome (PCS) can be made (American Psychiatric Association, 2000).
Understanding of and treatment for PCS is limited. Currently, scientists theorize that both biological and psychological factors contribute to this complex disorder (Rees, 2003; Wood, 2004). Research has suggested that physiological mechanisms associated with the injury event damage axonal and metabolic processes in the brain and may establish an environment of vulnerability for further damage (Biasca & Maxwell, 2007). Additionally, scientists have identified that pre- and postinjury stress are risk factors for poor outcome after MTBI (Bay & Bergman, 2006; Fenton, McClelland, Montgomery, MacFlynn, & Rutherford, 1993; Mooney, Speed, & Sheppard, 2005; Ponsford et al., 2000). These risk factors include preinjury psychiatric comorbidities, presence of stressful life events, and heightened perceived psychological stress after the injury event. We propose that the combination of the MTBI event (associated with the acceleration-deceleration injury and related damage of axonal structures and metabolic processes) and dysregulated early stress responses (psychological and neurobiological) may set the stage for the development of this disorder. The purpose of this article is to explicate our biobehavioral theory-early stress responses: a vulnerability framework for functional impairment following MTBI.
The community of rehabilitation science is multidisciplinary. This allows for varied approaches to clinical problems but perhaps has limited broad conceptualizations of problems that ultimately lead to standardized treatment approaches. An important first step in designing and testing interventions for complex clinical problem requires theoretically guided frameworks from which hypotheses can be tested and interventions designed. There has been a lack of a broad guiding theory that predicts those likely to have poor recovery, resulting in studies on variables of interest but not building toward a more comprehensive understanding.
We propose a broad conceptualization focused on the phenomenon of early stress responses after MTBI and its ability to predict those at risk for functional impairment. …