Psychosocial Characteristics of Acquired Brain Injury
LESLIE GUIDOTTI BRETING
An acquired brain injury (ABI) not only causes impairment in the areas of motor, cognitive, and other bodily functions, but also can lead to significant psychological distress and impact the patient and support system, including family. Psychosocial problems associated with ABI may actually be one of the major challenges facing rehabilitation and reintegration into one’s community.
ABI may result in disability with biological, psychological, and social ramifications. How rehabilitation practitioners conceptualize “disability” has important implications in terms of assessment, treatment planning, service delivery, and outcomes. Furthermore, an understanding and adoption of a model of disability helps the rehabilitation practitioner orient psychosocial topics such as coping, adjustment, social support, and intervention into a broader context. Models of disability (i.e., how disability is understood) have evolved from moral models to the medical model to functional models to social models (Chan, Gelman, Ditchman, Kim, & Chiu, 2009) (see Table 15.1). Moral models tended to view a person’s health condition and disability as being indicative of personal failings, or conversely that disability conferred a purified moral superiority (Schillace, 2013). The medical model has traditionally focused almost exclusively on pathology. The primary service providers were physicians who considered the locus of disability as situated entirely within the individual’s body (Smart, 2001).
Functional models focused on how the physiological and psychological consequences of a disorder, disease, or injury may incur functional limitations (Livneh & Robert, 1993; Nagi, 1965). A corollary of this definition is that disability is contextually determined. For example, a surgeon may be deemed disabled based on the functional demands of her occupation after evidencing low average attention and processing speed on neuropsychological testing following an ABI. However, another person with the same injury and test results may not be disabled if the cognitive demands of her occupation are less severe.
Social models of disability define disability as the interaction of biological, functional, social, and environmental factors (Brandt & Pope, 1997; Engel, 1977; Tate & Pledger, 2003; Wright, 1960). Purely social models argue disability is a socially constructed phenomenon that results in the imposition of barriers to equal participation and access on individuals with physiological impairments and functional limitations. For example, a person with severe hemiparesis may have physiologic injury to the primary motor cortex that resulted in functional limitations related to ambulation; however, this individual would not be considered disabled in the area of transportation if his vehicle was modified to accommodate his paralysis thereby allowing him to drive. As such, social model theorists place greater responsibility on society for ameliorating disability (Chan et al., 2009).
The medical and functional models are regarded as disablement models because they are focused primarily on impairment and limitations; social models are characterized by enablement (Masala & Petretto, 2008). These models identify enabling factors such as assistive technology, environmental modification, access to health care, medications, and social support that improve the individual’s engagement in activities and participation in social roles (Brandt & Pope, 1997).
Currently, the most widely adopted conceptualization of disability is the World Health Organization (WHO) International Classification of Functioning, Disability, and Health (ICF) model, which is a companion to the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10; World Health Organization [WHO], 1992). The ICF model integrates aspects of the medical, social, and functional models. It encompasses three broad components: (a) body structure and function, (b) activities and participations, and (c) personal and environmental factors (WHO, 2001). In this model, disability is the multifactorial product of a dynamic interplay between a health condition and contextual factors both environmental and personal. Moreover, it enables a biopsychosocial and person-centered perspective on health care (Alford et al., 2015).
From a psychosocial perspective, personal factors, environmental factors, and participation may be particularly relevant. Personal factors are defined as features of the individual that influence his or her performance of activities and participation (Peterson, 2005; WHO, 2001). These include characteristics such as coping style, social background, demographics, personality, and learning history. Environmental factors include the characteristics of the physical layout of the community, as well as the social environment and attitudinal milieu (Peterson, 2005; WHO, 2001). These factors may serve to facilitate inclusion in the community or buttress barriers to participation. Environmental factors include assistive technologies, the physical environment, social support and relationships, attitudes, service delivery systems, and policies. Participation refers to engagement in and fulfillment of life roles in the community (e.g., vocational, relational, recreational roles) (Peterson, 2005; WHO, 2001). The interplay between the individual’s health condition, ability to engage in activities, environmental factors, and personal factors impacts participation, which in turn affects quality of life (Chan et al., 2009). Consequently, improved and maintained participation in life roles is the primary goal of rehabilitation.
A qualitative study of persons with ABI demonstrated that issues related to participation and inclusion is a vital concern; moreover, perceived psychosocial and instrumental support from family, friends, and health professionals is important in determining the individual’s health status and functioning (Sveen, Ostensjo, Laxe, & Soberg, 2013). However, negative attitudes and beliefs about brain injuries held by the individual’s social network may have a detrimental effect. For example, stigmatizing attitudes of friends, colleagues, and acquaintances may be viewed as a barrier to participation, especially when the validity of impairments are questioned because they are “invisible” (Levack, Kayes, & Fadyl, 2010).
In conclusion, disability is a complex and multifactorial phenomenon (Chan et al., 2009). Depending on one’s perspective, disability in traumatic brain injury (TBI) can be described exclusively in terms of tissue damage in the brain, or as being derived in the interaction between limitations caused by tissue damage and the contextual demands of performing tasks, or as the restrictions imposed on the person by the surrounding social and physical environment. The ICF attempts to integrate each of these perspectives in its conception of disability (WHO, 2001). As a result, psychosocial aspects of disability become critical in a comprehensive understanding of disability in ABI. Understanding a person’s access to social support, family system, coping style, social and vocational roles, personality factors, and cultural background, as well as an appreciation of broader societal attitudes and beliefs, may be just as crucial for the amelioration of disability in ABI as understanding the physiological sequela of brain injury and resultant functional limitations.
Research on the pathophysiology, etiology, and neuroanatomical correlates of psychiatric and psychosocial difficulties due to brain injury is limited; however, the majority of available literature points to a disruption of the frontal subcortical network to explain the behavioral changes. Changes to the frontal region of the brain are often what occur after a brain injury given the bony protuberances in which it sits.
The incidence of psychological conditions following TBI is often related to pretrauma risk factors, including a history of psychological difficulties and gender. However, posttrauma risk factors also play a role in incidence of psychological conditions. It has been shown that significant life stressors and lack of social support can increase the risk. Clinical research has demonstrated that psychiatric complications are prevalent in ABI, with an incidence of around 40% to 50% for moderate to severe TBI and about 34% after a mild TBI; however, the incidence is not well documented for mild TBI or concussion owing to the fact that many patients at that level do not make it into the health care system (Vaishnavi, Rao, & Fann, 2009).
CLINICAL PRESENTATION/DIAGNOSTIC CONSIDERATIONS
Up to 60% to 80% of family members report that personality change has occurred in their loved one with a brain injury (Brooks, Campsie, Symington, Beattie, & McKinlayl, 1986; Weddell & Leggett, 2006). Personality changes following an ABI involve three factors: pretrauma patterns of emotion regulation and motivation, neurological disturbances to brain structures involved in emotion regulation and motivation (i.e., damage to the amygdala or higher cortical centers), or reactionary disturbances such as failure to cope with the new environmental demands given reduced resources (Prigatano, 1987). Understanding personality changes following ABI is important because of the inevitable impact on psychosocial adjustment, such as integration into society through employment and maintaining interpersonal relationships (Prigatano, 1987). Personality changes frequently observed in patients with brain injury include the following:
Lack of empathy
Anger, irritability, and agitation
Loss of drive, initiative, and motivation
Self-directed in motivation
Loss of spontaneity
Socially inappropriate behavior
Lack of insight
Enhanced sensitivity to distress
Impaired social awareness and inability to recognize emotional expressions in face and voice
Many patients experience depression following ABI, with estimated frequencies ranging between 6% and 77% (Jorge & Arciniegas, 2014). Symptoms of depression include sad mood, loss of interest in activities previously enjoyed, feelings of worthlessness and/or guilt, loss of concentration, decreased energy, slowed thinking and movement, appetite loss, and sleep problems. Like personality changes, the pathophysiology of mood disorders following an ABI involves three factors: pretrauma factors such as genetic vulnerability and prior psychiatric history; factors that relate to the injury itself, such as damage to the emotion regulation systems in the brain; and factors associated with recovery, such as social support (Jorge & Arciniegas, 2014). Although it is thought that the risk of developing depression is highest in the first year post injury, research indicates that the risk of depression onset remains high even decades after ABI. Experts on the subject generally accept an estimated first-year post-ABI depression onset frequency between 25% and 50% (Jorge & Arciniegas, 2014). Approximately one-fourth of patients who were not depressed during the first year post injury developed depression during the second year. Approximately two-thirds of patients who were depressed during the first year post injury continued to exhibit significant depressive symptoms, highlighting the perpetual nature of this disorder in ABI patients. Depressive disorders following ABI are strongly associated with the presence of anxiety disorders.
It is estimated that anxiety disorders occur in 24% to 28% of patients with ABI (Warden & Labbate, 2005). Symptoms of anxiety include fear, worry, restlessness, difficulty concentrating, sleep problems, muscle tension, and feelings of panic. Anxiety may be the result of the brain injury directly, such as damage to the neural circuits involved in development of this disorder, or it may manifest due to the postinjury experience, such as worry about physical injury and possible cognitive decline. As a result of physical injury and/or personality and cognitive deficits, self-consciousness may cause anxiety and lead to avoidance of social settings, hindering reintegration into society (Warden & Labbate, 2005).
Posttraumatic Stress Disorder
Reexperiencing the traumatic event through vivid memories or flashbacks, avoidance of situations related to the trauma, and emotional withdrawal following an ABI suggest the presence of a posttraumatic stress disorder (PTSD). This is the most common psychiatric disorder following ABI (Bryant, Marosszeky, Crooks, Baguley, & Gurka, 2001) and is a serious barrier to rehabilitation. It has been suggested that the likelihood of developing PTSD following a brain injury is mediated by the encoding of traumatic memories. Loss of consciousness and poor recall of the event appear to be protective factors against development of PTSD, which explains why PTSD is more commonly seen in patients with mild brain injuries than in those with moderate to severe brain injuries. Even when patients report poor memory of the event, the partial encoding of some details may lead to reexperiencing and hyperarousal (Mallya, Sutherland, Pongracic, Mainland, & Ornstein, 2015). PTSD is associated with anger and increased arousal, which may exacerbate the aggression experienced after ABI and result in reduced impulse control (Chemtob, Novaco, Hamada, Gross, & Smith, 1997). Avoidance behaviors may impede community integration and minimize social activities, contributing to feelings of loneliness, depression, and ultimately reducing the quality of life of these patients.
Aphasia is infrequent in patients with ABI; however, deficits in communication skills are not. Many individuals with ABI are described as talkative but inefficient, unable to remain on topic, tangential, and prone to irrelevant comments. Conversational style is slow with incomplete responses, and comprehension may also be impaired. Self-focused conversations, immature humor, frequent interruptions, disinhibited remarks, and inappropriate levels of self-disclosure have been commonly observed (McDonald, Togher, & Code, 2013).