1 Social and communication disorders following traumatic brain injury
Leanne Togher, Skye McDonald and Chris Code
Traumatic brain injury (TBI) is the most common form of brain injury in the modern Western world. While TBI is sustained in people of all ages, the peak incidence is during early adulthood resulting in devastating disabilities for many young adults without any truncation of lifespan. These disabilities span physical, emotional, and cognitive and behavioural domains of function. Impairments in communication and social functioning may be a consequence of disabilities within and across these domains and collectively represent a unique area of investigation for clinicians and researchers alike. The past four decades have seen a major evolution in the way in which such disorders have been described and this chapter will provide an overview and introduction to the various approaches used.
Definitions
The term traumatic brain injury refers to brain injury caused by trauma rather than disease, vascular accidents, alcohol, etc. Traumatic brain injury is a consequence of a head injury of sufficient severity to cause damage to the brain beneath and can be either penetrating or blunt. Penetrating or open head injuries are an uncommon cause of traumatic brain injury, with the exception of war-wounds. Penetrating injuries occur when a missile, such as a bullet, pierces the skull and traverses the brain tissue. High velocity missile wounds cause catastrophic focal and diffuse damage and are usually fatal while low velocity missiles or missile fragments produce focal lesions restricted to the area of direct damage (Grafman & Salazar, 1987). Loss of consciousness is relatively uncommon following such injuries (Salazar et al., 1986) and the functional sequelae often closely resemble that of other kinds of focal neurological lesions often leading to discrete and specific kinds of cognitive impairment (Grafman & Salazar, 1987). Research into aphasia following penetrating head injuries has been important in the development of theoretical approaches to aphasia and aphasia classification. Unfortunately, wars provided the circumstances for the first detailed studies of traumatic brain injury. For instance, Goldstein (1942) developed hospital treatment for brain-injured soldiers in Frankfurt during the First World War where he assessed and treated over 2,000 patients. This work influenced his theoretical approach, although he also had extensive experience with vascular lesions. Russell and Espir (1961) studied the records of 1,166 brain-injured patients examined in Oxford during the Second World War. They estimated that about 60 per cent of left hemisphere damaged patients had aphasia of some degree. Perhaps the most well-known neuropsychologist whose approach to aphasia is influenced by his experience with penetrating head injury is Luria. His famous book, Traumatic Aphasia (Luria, 1970), was first published in Russia in 1947 and details his theoretical approach which developed during his work with Russian soldiers during the Second World War.
More recently, the wars in Iraq and Afghanistan has resulted in a different type of TBI arising from exposure to improvised explosive device (IED) explosions with up to 60 per cent of returned service personnel sustaining brain injuries (Warden et al., 2005). These blast injuries create a sudden increase in air pressure by heating and accelerating air molecules and, immediately thereafter, a sudden decrease in pressure that produces intense wind. These rapid pressure shifts can injure the brain directly, producing concussion or contusion. Air emboli can also form in blood vessels and travel to the brain, causing cerebral infarcts. In addition, blast waves and wind can propel fragments, bodies, or even vehicles with considerable force, causing head injuries by any of these mechanisms (Bell et al., 2009; Summers et al., 2009). Even so, the majority of moderate to severe blast injuries are associated with penetrating fragments (Masel et al., 2012).
Blunt head injuries are by far the most common type of head injury in peacetime (Grafman & Salazar, 1987). Most of these are caused by the rapid acceleration and deceleration of the head such as occurs during motor vehicle accidents, falls or sporting injuries. This kind of injury produces multi-focal pathology in the brain, is associated with altered consciousness in the acute stages and generally causes widespread deficits quite unlike penetrating head injuries. Henceforth the term TBI in this book will refer to traumatic brain injury caused by blunt head injuries. It should also be noted that the term head injury is sometimes used interchangeably, since both this and the more specific term âclosed head injuryâ has had wide usage in the TBI literature.
It is now well recognized that communication problems following a TBI are distinctly different to those subsequent to a more focal lesion such as occurs in a cerebrovascular accident (or a penetrating head injury) and these require different approaches to assessment and remediation. This has come from the recognition that, due to the multi-focal nature of TBI, there is a complex interplay of cognitive, emotional, linguistic, physical, behavioural and organic psychosocial factors which may contribute to the communication difficulties experienced. These may include anything from word finding problems and impoverished output to excessive talkativeness, poor turn taking and repetitiveness (Snow et al., 1998). In turn, communication problems can have a significant effect on psychosocial outcomes. The ability to communicate successfully is crucial to being able to maintain relationships and to establishing vocational and leisure activities. Overall, loss of communicative competence presents a major obstacle to reintegration into the community because it makes the person more taxing and less rewarding to interact with socially (Bond & Godfrey, 1997). Friends, carers and family begin avoiding them and this generally limits their ability to maintain preinjury relationships (Elsass & Kinsella, 1987; Tate et al., 1989). In addition, they often misjudge social situations, for example they may appear to be overly familiar with potential acquaintances thus interfering with their ability to establish new relationships.
As a result of diminished communication and interpersonal skills, people with TBI become socially isolated, have reduced opportunities for employment and may even require caregivers to help them with everyday tasks such as shopping or pursuing leisure options. But even with caregivers, the poor communication skills of people with TBI are problematic. Caring for people with TBI is stressful, with high levels of caregiver burden and depression (Hanks et al., 2007; Knight et al., 1998; Lefebvre & Levert, 2012; Wedcliffe & Ross, 2001). The main sources of this stress have been identified as problems communicating with the person with TBI (MAA, 1998), behavioural disturbance (Knight et al., 1998) and the level of cognitive processing difficulties and poor insight of the person with TBI (Prigatano et al., 2005; Wallace et al., 1998).
Approaches to assessing communication disorders after traumatic brain injury
The complexity of communication and social problems following TBI has resulted in a range of approaches from varied theoretical backgrounds, including neuropsychology, psychosocial outcomes, pragmatics, sociolinguistics, social skills, discourse analysis and neurophysiology. This chapter will provide a brief overview of these different and often confusing perspectives and will refer the reader to the relevant chapters within the book.
Language assessment from the perspective of aphasia
In the 1970s it was recognized that communication problems following TBI were unique (Groher, 1977; Halpern et al., 1973) differing from those experienced by patients with other types of neurological disorders. Communication was described as being confused (Groher, 1977), confabulatory (Hagan, 1982), tangential (Hagan, 1982; Levin et al., 1979; Thomsen, 1975), full of empty phrases (Heilman et al., 1971) and failing to display logico-sequential relationship between thoughts (Hagan, 1982). While recovery of language function was demonstrated at below the sentence level, it was frequently observed that TBI subjects did not manage at conversational levels (Groher, 1977; Halpern et al., 1973; Levin et al., 1982).
In the absence of appropriate measurement tools, researchers were only able to provide a superficial description of the way in which people with TBI communicated. Use of aphasia test batteries failed to delineate the problems which were observed in day-to-day communication leading to the creation of new definitions such as âsubclinical aphasiaâ (Sarno, 1980) and subsequent debates as to what constitutes aphasic impairment (Holland, 1984). In aphasia the patient has problems which can be described in terms of representational linguistic levels of phonology, morphology, syntax and lexical semantics (Code, 1991). Certainly it was recognized that a TBI might well result in aphasic disturbances. Indeed, early descriptions of language impairment following TBI suggested that aphasia occurred in 2 per cent of 750 cases and 14 per cent of 50 cases respectively (Heilman et al., 1971; Levin et al., 1976). But in addition, while Sarno and colleagues (Sarno, 1980; Sarno & Levita, 1986) indicated that 32 per cent of their TBI subjects evidenced frank aphasia, they also argued that many subjects suffered a form of subclinical aphasia, defined as âevidence of linguistic processing deficits on testing in the absence of manifestations of clinical impairmentâ (Sarno, 1980: 687). The linguistic deficits in the subclinical aphasia group included difficulties with visual naming, word fluency and impaired performance on the Token Test, when compared with a matched dysarthric group. These results have been replicated in later studies with evidence of specific word finding difficulties on naming and word fluency tasks being the most common finding when people with TBI are evaluated on tests of traditional language functioning (Adamovich & Henderson, 1984; Levin et al., 1981; Lohman et al., 1989).
Difficulty with naming appears to be one of the most reported persisting communication problems following TBI. Thomsenâs (1975) study of 50 patients with severe TBI found persistent oral expression impairment in half of the subjects when they were examined, on average, 33 months post-injury. Groher (1977) assessed a group of 14 severe TBI patients at monthly periods following resolution of coma. Patients demonstrated intact confrontation naming on the Porch Index of Communicative Abilities (Porch, 1967) four months after regaining consciousness; however their communication was described as lacking in conversational content. Levin et al. (1976) found in their sample of 50 severe TBI patients of varying severity that 40 per cent evidenced impaired naming on the Multilingual Aphasia Examination (Benton, 1967). In a follow-up study of 21 subjects who had been acutely aphasic, Levin et al. (1981) found that 12 showed persistent naming impairments.
Naming impairments have also been investigated in children (Jordan et al., 1992; Jordan et al., 1990) and adults with TBI (Kerr, 1995) using an information processing approach to assessment in the tradition of Coltheart (1987) and Shallice (1987). The advantage of a psycholinguistic perspective is the control it allows over the context in which language production occurs. The sophistication of this approach, widely used in aphasia therapy in describing the nature of naming impairments, holds some promise for word level analysis with TBI patients. Sentence level processing also appears to be affected by brain injury, so that, for example, complex syntactic processing has been associated with increased pause time (Ellis & Peach, 2009).
The information processing approach to word finding impairments has been applied in treatment (Hillis, 1998) to successfully remediate both semantic and phonological impairments (Leemann et al., 2011; Vitali et al., 2007; Wambaugh & Wright, 2007; Yeung & Law, 2010). Recent advances in brain imaging have demonstrated that remediation of naming is associated with re-activation of language brain areas (Vitali et al., 2007) lending support to the use of principles of experience dependent neuroplasticity which is revolutionizing rehabilitation processes worldwide (Kleim & Jones, 2008).
Frank aphasic and specific naming deficits in TBI have been conventionally assessed using standard aphasia batteries such as the Western Aphasia Battery (Kertesz, 1982), The Boston Diagnostic Aphasia Examination (Goodglass & Kaplan, 1972) and the Multilingual Aphasia Examination (Benton et al., 1994) supplemented by specific tests of naming such as the Boston Naming Test (Kaplan et al., 1983) and comprehension e.g. the Revised Token Test (McNeil & Prescott, 1978). The development of the psycholinguistic approach to language assessment has culminated in the production of assessment instruments based upon these principles such as the Psycholinguistic Assessment of Language Processing in Aphasia (Kay et al., 1992) and more recently, the Northwestern Assessment of Verbs and Sentences (NAVS: Cho-Reyes & Thompson, 2012; Thompson, 2012). However, while these instruments may be sensitive to basic linguistic deficits following TBI, such instruments inadequately capture the spectrum of communication deficits experienced in TBI. Nor do they take socially mediated aspects of language functioning into account.
Recognizing the influence of other cognitive disorders
Sarnoâs term âsubclinical aphasiaâ precipitated a debate regarding the terminology researchers and clinicians should be using when describing language impairment following TBI. Holland (1984) argued that language disorders following TBI are not aphasia but are second to cognitive and memory impairments. She objected to Sarnoâs term âsubclinical aphasiaâ as inappropriate labelling. Braun and Baribeau (1987) further criticized Sarno for not reporting nonverbal psychological functions which they felt precluded the differentiation between generalized intellectual dysfunction and aphasia. This foreshadowed the interest which was to follow in the relationship between cognitive impairments and communication.
By the middle to late 1980s increasing awareness of the interplay between cognition and language led to the introduction of the term cognitive-language disorder (Hagan, 1984; Kennedy & DeRuyt...