The most common neurological symptoms following TBI include: headache, pain, nausea, dizziness or vertigo, unsteadiness or poor coordination, tinnitus, hearing loss, blurred vision, diplopia, convergence insufficiency, increased light and noise sensitivity, and altered sense of taste and smell. TBI has been noted to cause injury to each of the cranial nerves (Russell, 1960) with the concomitant disruption of the various sensory and motor functions of the head. Waddell and Gronwall (1984), for example, have noted significant increases in the sensitivity to light and sound stimuli following mild TBI.
The most common neuropsychological deficits include memory difficulties, decreased attention and concentration, decreased speed of information processing, compromise in working memory functioning, communication difficulties, difficulties with executive functions (including initiation and planning, concrete thinking, lack of initiative, inflexibility, the dissociation between thought and action, impulsivity, irritability and temper outbursts, interpersonal communication problems, socially inappropriate behaviours, self-centredness, changes in affect, lack of insight and of self-awareness and alterations in judgment and perception), fatigue and increased sensitivity to lack of sleep, stress, and increased use of drugs and alcohol (Groher, 1977; Levin et al., 1982; Morse & Montgomery, 1992; Pollens, McBrantie, & Burton, 1988; Ponsford et al., 1995).
The published research indicates that cognitive functioning recovers most rapidly during the first few weeks following a mild traumatic brain injury (MTBI) and effectively returns to baseline by one to three months postinjury in non-sports-related injuries (e.g., Iverson, 2005; Schretlen & Shapiro, 2003). The restitution of functioning in sports-related injuries tends to be more rapid, with decrements in neuropsychological test performance resolving in 5 to 10 days (Iverson, 2005). Cognition also improves over the first two years after moderate to severe TBI, but these individuals continue to show compromise greater than two years after the injury.
Depending on the focal point and severity of the injury, more specific deficits in visual, perceptual or language processing may also be added to this list. The language deficits following TBI include naming difficulties and diminution in fluency of speech.
Behavioural and characterological changes are often described in terms of loss of initiative, apathy, increased dependency, irritability, impulsivity, disinhibition, insensitivity to the need of others, childishness, poor judgment in social and financial matters, and either hypersexuality or hyposexuality, with an overall lack of insight into one's personality changes (e.g., Brooks, 1984; Wood, 1990).
Neuropsychiatrie illness is a common concomitant of TBI (Jorge, 2005). Fann and colleagues (2004) compared the frequency of psychiatric diagnoses in 939 TBI patients and 2817 controls. The presence of any psychiatric diagnosis in the first year following the TBI was 49% in the moderate to severe group, 34% following an MTBI, and 18% in the controls. In patients without a prior diagnosis of psychiatric disorder, the adjusted relative risk for psychiatric illness in the first 6 months following a moderate to severe TBI was 4.0 (95% CI, 2.4-6.8). Following an MTBI it was 2.8 (95% CI, 2.1-3.7) in comparison to the noninjured controls. For those patients with a psychiatric diagnosis prior to the injury, the adjusted relative risk in the first six months postinjury was 2.1 (95% CI 1.3-3.3) for moderate to severe TBI and 1.6 (95% CI, 1.2-2.0) for MTBI. Prior psychiatric illness proved to be a significant predictor of psychiatric morbidity post TBI, and these problems tended to persist for these patients. This was particularly the case for patients with a previous history of mood or anxiety disorders or for those with a history of alcohol abuse (Dikmen, Bombadier, Machamer, Fann, & Temkin, 2004; Jorge, 2005; Wilde et al., 2004).
Behavioural disturbances such as impulsivity, poor self-control, inability to organise oneself to complete daily activities, and lack of flexibility (Proctor, Wilson, Sanchez, & Wesley, 2000), can have a devastating impact upon the individual in terms of reintegrating into their preinjury lives and functioning adequately and independently in society. In addition, these individuals may have diminished awareness and understanding of their impairments, which can affect their ability to engage in rehabilitation and learn compensatory strategies to enhance their ability to live independently.
The most common emotional and behavioural difficulties following TBI include emotional lability, irritability and aggression, change in personality, fatigue, decreased energy, anxiety, depression, apathy, disordered sleep, loss of libido, and poor appetite (Anderson, 1995). Fatigue, emotional distress and pain are each very common following TBI irrespective of severity.
As a result of the cognitive impairments such as slowed speed of information processing and attentional difficulties, many tasks that were once automatic for the individual, such as concentrating, monitoring ongoing performance, and warding off distractions, can now be completed only with deliberate effort (Lezak, 1995). This extra effort leads to the individual becoming more easily fatigued, further increasing the amount of energy that the individual has to expend to undertake the task in hand. This increasing effort and the resulting fatigue often leads to the individual becoming irritable, frustrated, and angry.
TBI can also result in a variety of neuropsychiatric disturbances ranging from subtle deficits to severe intellectual and emotional disturbances. In rare cases, it can result in chronic vegetative states. The neuropsychiatric disturbances associated with TBI include cognitive impairments, mood disorders, anxiety disorders, psychosis, and behavioural problems (Rao & Lyketsos, 2000).
The study of the nature of psychiatric illness occurring in the wake of TBI continues to expand our understanding of the brain, emotion, behaviour, cognition, physical illness, disability, and quality of life, and how these factors interact with each other. Because the brain is the common pathway by which are all humans experience well-being and suffering, the study of TBI thus provides the unique opportunity to enhance our understanding of all facets of the human experience (Fann, 1997).
Researchers have observed increased rates of depression, mania, generalised anxiety disorder, psychosis, behavioural dyscontrol, and cognitive deficits following TBI when compared to the rates in the general population. Others have also observed increased rates of obsessive-compulsive symptoms, posttraumatic stress disorder, depersonalisation, and personality disorder. Many of these syndromes are common both with the severely brain injured, as well as in the mildly injured subjects. While these disorders occur in the acute phase of TBI, delayed onset of symptoms also occurs. How these neuroanatomical, psychological, cognitive, medical, and social factors interact to determine the resulting psychopathology still needs to be clarified (Fann, 1997).
The residual emotional and behavioural difficulties that occur for individuals who have sustained a TBI have been well documented in the contemporary literature. Lishman (1997), for example, estimates that "the psychiatric consequences and their social repercussions may be judged to be significant in upwards of a quarter of patients who survive" (p. 161). These issues encompass a complex and interdependent set of variables that can lead on to a number of pathological states including substance abuse, depression, anxiety, chronic suicidal or homicidal ideation and action, poor impulse control, significant increase of frustration, and poor insight into behavioural and emotional processes as well as the numerous psychosocial complications associated with the injury (Delmonico, Hanley-Petersen, & Englander, 1998).
The majority of patients with mild TBI recover fairly quickly and are usually completely restored to their preinjury level of functioning in a relatively brief period of time following the initial injury (Mooney & Speed, 2001). However, a significant minority have prolonged, complicated or incomplete recoveries and display outcomes disproportionately worse than would have been predicted on the basis of the objective factors associated with the biomechanics of the injury. It is those individuals, who as a consequence of the injury, or the interaction of the injury with their preinjury state, have these disproportionately worse outcomes that constitute the principal focus of this discussion.
While it would be appropriate in a discussion such as this to include discussion of neurorehabilitation and the current pharmacological treatment approaches to the various conditions described herein, these are not discussed in detail in this volume for two reasons. The first is the sheer scope of an enterprise, which is beyond the cursory summary in this broader discussion of the complications themselves. As a result, the discussion of treatment is left largely untouched as it would require its own similar monograph to appropriately deal with the subtleties of this process. The reader is directed to a number of fine resources on this topic that have been produced over the last few years including the work of Ponsford (2004), Barbara Wilson (2004), and the comprehensive special issue of the journal Neuropsychological Rehabilitation edited by Huw Williams and Jonathan Evans (2003) as well as to some of our own foundation work on these topics (Curran, Ponsford & Crowe, 2000; Keppel & Crowe, 2000; Perlesz, Kinsella, & Crowe, 2000).
Jorge (2005) succinctly addressed the second issue with particular regard to pharmacological interventions with TBI in a recent review
Although progress in basic research allows us to envision a promising future for therapeutic intervention following TBI, there is a lack of adequately controlled clinical studies to provide a solid scientific basis for neuropsychiatry treatment. Currently, treatment decisions are frequently made on the sole basis of clinical experience or with the limited support of open studies and anecdotal cases. (p. 295)
In their comprehensive review on this topic, Warden and colleagues (2006) noted
Despite reviewing a significant number of studies on drug treatment of neurobe-havioral sequelae after TBI, the quality of evidence did not support any treatment standards and few guidelines due to a number of recurrent methodological problems. Guidelines were established for the use of methylphenidate in the treatment of deficits in attention and speed of information processing, as well as for the use of beta-blockers for the treatment of aggression following TBI. (p. 1469)
Warden et al. presented recommendations for interventions with depression, anxiety and other conditions only as options.
Clearly we have much to learn and a long way to go in just characterizing the nature of the changes contingent upon the injury itself, much less in how to sensibly devise treatment strategies for these. Unfortunately, therefore, these discussions must be left to a possible further volume in the future.
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