In their review of the incidence of organic personality disorder (OPD) in their final sample of 28 TBI patients interviewed within two weeks of the injury and subsequently at six months postinjury using a structured clinical interview based upon the International Classification of Diseases (ICD)-10 criteria, Franulic, Horta, Maturana, Scherpenisse and Carbonell (2000) diagnosed 32% of their sample with OPD. Unfortunately however, they did not indicate a breakdown of the types of OPD observed. However, the authors did note that using the neurobehavioural rating scale developed by Levin, High, Goethe et al. (1987) that the OPD patients differed from the non-OPD patients on measures of cognition and energy, preoccupation with somatic and anxiety-related concerns, and language. The participants with OPD predominantly had frontal injuries. Once again in common with a number of observations in the literature, they noted that the difference in behavioural outcome was independent of the cognitive impairments.
Streeter, van Reekum, Shorr and Bachman (1995) noted that in a comparison of 54 males with borderline personality disorder to 49 psychiatric control patients there was a much higher incidence (42%) of TBI in the borderline group as compared to the controls (4%). As the TBI had occurred before the full expression of the personality disorder, the authors felt that the TBI had been a cause rather than a result of the TBI. Hibbard, Bogdany et al. (2000) noted that using the Structured Clinical Interview for the DSM-IV on 100 participants recruited from a larger pool of 438 TBI patients, 24% of the sample could be diagnosed with a personality disorder prior to the TBI, whereas 66% met the diagnostic criteria for at least one personality disorder after the injury. The most common forms of post-TBI personality disorder were borderline (34%), avoidant (26%), paranoid (26%), obsessive-compulsive (27%), and narcissistic (14%). Those patients who had had personality disorder before the TBI were more likely to show personality disorder afterwards.
Many investigators agree that the most commonly reported personality change following TBI is increased irritability (Prigatano, 1992) accompanied by the associated features of frustration, aggression, egocentricity, impulsiveness, impairment of judgment and insight, and inappropriate expression of affection (Franulic et al., 2000). These changes seem to generate greater distress for patients in the period more than six months following the injury rather than in the acute stage.
Haboubi, Long, Koshy, and Ward (2001) report that irritability is the third most commonly reported complaint in their large cohort of patients assessed 6 months postinjury. At one year, a number of investigators (e.g., 30-35%: Deb, Lyons, & Koutzoukis, 1998, 1999; 33.3%: Kim, Manes, Kosier, Baruah, & Robinson, 1999; 32%: van der Naalt, van Zomeren, Sluiter, & Minderhoud, 1999) note approximately one-third of patients complain of irritability in the year following the injury with the highest level of endorsement being in the mild to moderately injured group and the lowest being in the severe patients. In summarizing this data, Alderman (2003) has noted that "studies are in general agreement that about a third of patients with mild head injuries report irritability. However, this symptom also remains a persistent complaint in the longer term" (p. 212).
Some investigators have expressed the opinion that the individuals who make the best recovery post-TBI are those who show a high level of agitation postinjury (O'Shanick & O'Shanick, 2005). For example, there is a high correlation between the level of the catecholamines and their measured metabolites and quality of outcome post-TBI (Clifton, Ziegler, & Grossman, 1981; Woolf, Hamill, Lee, Cox, & McDonald, 1987).
Injury to the frontal lobe as a result of TBI can exist with relative preservation of performance on standardized tests of frontal functioning. Satish, Streufert and Eslinger (1999) have noted their study of a 48-year-old woman who was involved in a motor vehicle accident (MVA) that culminated in a 2-week period of posttraumatic amnesia (PTA) and damage to the ventral frontal region involving the lateral orbital gyrus including Brodmann's Areas (BA) 12 and 13 and extending into the deep white matter to the tip of the frontal horn. While most of her scores on intelligence, memory, language, spatial and perceptual functioning were in the normal range, she did demonstrate mild attenuation in her performance on the WCST, Trail Making Test Part B and the Paced Auditory Serial Addition Task (PASAT).
Her living circumstance, however, underwent a much more profound change. She was demoted to routine office work whereas before her injury she had been an independent telephone company service operator with high skill in computer processing for the five years preceding her injury. Following the injury, she demonstrated marked difficulty in tracking information changes, completing tasks with efficiency, and organizing herself.
Assessment of this woman using a tool employed in industrial and organizational psychology in the form of the Strategic Management Simulation technique revealed impaired scores on a variety of decision-making measures. These included impairment in initiative, information utilization, breadth of strategy development, and the ability to opportunistically and flexibly deal with rapidly changing situations. She did, however, demonstrate better performance on tasks within context and when she was required to focus on only one aspect of the situation (Satish et al., 1999).
The pattern of impulsivity following TBI can also be extended to the issue of increase in aggression subsequent to the injury (Kim, 2002). Impulsive aggression (IA), either physical or verbal, is a common sequela of TBI (Eslinger, Grattan, & Geder, 1995). In their study of this phenomenon in 45 severe TBI participants, Greve et al. (2001) have noted that 26 of their sample (i.e., 58%) had persisting problems with aggression. This group had a higher incidence of premorbid aggressive behaviours and tended to be younger and were more irritable, impulsive, and antisocial than the nonaggressive controls. Interestingly, the researchers noted once again that the level of IA was not related to self-regulatory behaviour as assessed by measures of neuropsychological functioning as there were no differences between the IA and non-IA-head-injured controls. The authors contend that their finding supported the notion that "the brain injury did not cause a personality change, but simply further disinhibited an already impulsive and aggressive individual such that they continued to have aggressive outbursts, even in a highly structured and controlled environment" (p. 260).
This notion of the preexistence of antisocial tendencies in the impulsive aggressive individual following TBI supports a number of other findings in the literature regarding aggression. Rosenbaum and Hoggs (1989) note that of 31 consecutive patients referred for evaluation of marital violence, 19 (61.3%) had prior histories of severe TBI. Of this group, a large percentage (48.4%) had coincidental high levels of alcohol abuse. The suggestion that TBI and impulsive aggression may be implicated in forensic presentation was also observed by Allgulander and Nilsson (2000) in their epidemiological study of 1739 homicides between 1978 and 1994 in Sweden. They found that TBI, physical abuse, alcohol dependence, and criminal recidivism increased the risk of being murdered.
Blair (1995, 2001, 2004; Blair & Cipolotti, 2000; Blair, Jones, Clark, & Smith, 1997) has raised an interesting explanation for why this result might occur. His contention is that the notion of "acquired sociopathy" as originally proposed by Dama-sio, Tranel and Damasio (1990) may develop as a consequence of brain injury.
Blair (1995) proposes a violence inhibition mechanism wherein submissive social cues from a victim inhibit the expression or proliferation of the violent behaviour on the part of the perpetrator. Blair contends that moral socialization of the individual reduces aggressive behaviour on the part of the individual as a result of the convergent behavioural modification techniques of aversive conditioning and instrumental learning.
Blair (2004; Blair, Mitchell, & Blair, 2005) contends that the role of the VMPFC in impulsive aggressive behaviours is twofold: (1) the VMPFC is responsible for calculating the expectation of reward attached to the behaviour (an observation consistent with the work of Edmund Rolls (2000) who contends that rather than being an inhibitory mechanism per se, the VMPFC involves the learning of stimulus-reward associations and the alteration of responses on the basis of alteration of behavioural contingencies); and (2) the VMPFC is responsible for the recognition of social cues related to aggression, a process Blair refers to as "social response reversal." Social cues (e.g., disapproval by others, shame, embarrassment, etc.) often serve to modulate the expression of reactive aggression. However, if this system is impaired the impulsive aggression becomes more likely.
One of Blair's (Blair & Cipolotti, 2000; Blair, 2004; Blair, Mitchell, & Blair, 2005) patients, JS, a 56-year-old electrical engineer who was found unconscious with evidence of trauma to the right frontal lobe, shows this pattern of change. On presentation JS had a Glasgow Coma Scale (GCS) of 9, and an enhanced computed tomography (CT) scan showed low-density abnormalities involving the orbital pre-frontal cortex (i.e., the VMPFC) as well as the left temporal lobe almost certainly involving the left amygdala. This case presents a graphic illustration of the types of changes associated with the construct.
JS "failed to conform to social norms" and was notably "irritable and aggressive." His episodes of property damage and violence were frequent and were elicited after little provocation; e.g., an alteration in routine. He was "reckless regarding others personal safety;" on one occasion he continued to push around a wheel-chair bound patient despite her screams of terror. His "lack of remorse"
was striking; he never expressed any regrets about the nurses he hit. He failed to accept responsibility for his actions, justifying his violent episodes in terms of the failure of others (e.g., they were too slow). (Blair & Cipolotti, 2000, p. 1124)
JS also demonstrated failure to plan ahead and an inability to sustain consistent work behaviour. He fulfilled all of the criteria for acquired sociopathy with the exception of premorbid aberrant behaviour (Blair & Cipolotti, 2000).
Blair and Cipolotti (2000) subjected JS to a number of tasks designed to specifically identify the nature of the deficits in social cognition associated with the behavioural change. These included tasks aimed at assessing reversal learning (i.e., tasks including the Iowa Gambling Test (IGT); tasks that assess the ability to recognize emotional expression and emotional responding including tasks of processing of facial expression, autonomic responses to environmentally salient visual stimuli and face processing tasks; social cognition tasks including tasks of verbal comprehension, emotional attribution, theory of mind, moral/conventional distinction tasks, and social situations tasks.
Blair and Cipolotti (2000) observed that the consistent pattern of deficit noted in JS' case was his impairment in recognizing and responding to angry and disgusted expressions and his poor performance in tasks that assessed the ability to deal with social situations; most notably, an inability to appropriately attribute the emotions of fear, anger, and embarrassment to protagonists in a story and the ability to identify violations of social behaviour.
Blair and Cipolotti (2000) further proposed that as a consequence of his injury, JS had sustained damage to a brain system responsible for apprehending the angry expressions and concerns of another that would ordinarily result in cessation of the aberrant behaviour and an inability to be able to modify his behaviour in response to these signals.
This observation fits in quite well with observations made by Grattan and Eslinger (1989) who noted that brain-injured subjects displayed significantly lower scores on Hogan's Empathy measure than did the comparison group. The impaired empathy performance relates to impairment in neuropsychological tasks of cognitive flexibility, however, not to tasks of abstraction abilities. This seemed to be particularly the case for injuries associated with the right hemisphere.
Blair et al. (1997) also support the notion of brain injury culminating in impairment of empathy. Their study investigated the psychophysiological responsiveness of psychopathic individual to the distress cues and to threatening or neutral stimuli. Relative to the control sample, the psychopathic individuals showed reduced elec-trodermal response to distress cues. Blair (2001) considers that acquired sociopathy is most likely the consequence of impairment in the brain systems that respond to threat. He contends that these behaviours are a consequence of inability to socialize due to an impairment in the capacity to form associations between emotional unconditioned stimuli (particularly distress cues) and conditioned stimuli (specifically representations of transgressions). If the person is raised in a social environment (for example, poverty) where there are advantages for engaging in antisocial behaviour, they will engage in this behaviour but will not experience aversion to the distress of their victims. (p. 730)
A number of studies have attempted to identify which brain regions are activated during social reasoning tasks. Social reasoning causes activations of the left superior frontal gyrus, the orbitofrontal gyrus, and the precuneus in tasks that required the subjects to engage in empathic and forgiveness-related responding. Activation associated with empathy was also noted in the left anterior middle temporal and left inferior frontal gyri, whereas forgiveness caused activation of the posterior cingulate (Farrow et al., 2001).
The association between executive deficits and antisocial behaviour (including criminality, antisocial personality disorder, and psychopathy) has received further endorsement from the meta-analysis undertaken by Morgan and Lilienfield (2000), which supported a correlational link between these phenomena. They noted a moderate to large effect size (0.62) between the two, and the relationship was not moderated by age, gender, level of intelligence, or ethnicity. They noted their largest effect size was observed with the Porteus mazes test and the smallest with the Stroop test.
It is not always the case that the personality changes associated with TBI are a bad thing. Lishman (1987) has noted that "occasionally patients indeed could be said to have shown improvement in personality, in that they were now less prone to worry and were more outgoing and sociable" (p. 161).
In their report of three cases showing marked changes following brain injuries, Labbate, Warden and Murray (1997) describe a case in which a 20-year-old soldier who reported shyness, blushing, and anxious feelings as a child and a teenager, and who used alcohol to help his social anxiety, needed to drink fluids to the point of pain to successfully complete the mandatory urine drug testing in the army. He was subsequently hit in the forehead with a brick causing a brief loss of consciousness (LOC) and six hours of PTA. Subsequent to the blow, he met DSM-IV criteria for personality change due to traumatic brain injury, disinhibited type. After his injury he felt more comfortable in group settings, rarely blushed, and became unconcerned about public urination. The changes related to his social anxiety continued at follow-up, seven months postinjury.
The second type of pattern of organic personality change to emerge following TBI is the apathetic/pseudodepressed/abulic/negative symptom/disorder of drive syndrome and is characterized by apathy or lack of motivation not attributable to intellectual impairment (i.e., not dementia), emotional distress (i.e., not depression) or a diminished level of consciousness (i.e., not delirium) (Marin, 1991).
The second and third cases described by Labbate et al. (1997) again prove interesting. The second case involved an initial presentation of a man with antisocial personality disorder, including an extensive forensic history involving incarceration for a hit-and-run offence, theft during his youth, heavy drinking, and a dishonorable discharge from the navy, featured complete remission of his sociopathic tendencies following a motorcycle accident in which he sustained a severely contused frontal lobe and the removal of a volume of his right frontal and temporal areas.
The third case in this series featured a woman who had had a long history of anger dyscontrol, including argumentativeness and rapid resort to physical violence. She was struck by a truck while jogging and suffered six days of PTA, and the magnetic resonance imaging (MRI) revealed bilateral frontal contusion. Subsequent to her recovery, she reported marked personality change, and after the injury she no longer felt angry, did not engage in arguments, and was able to calmly register her complaint about ward nurse behaviour.
Clearly in these last two cases the previously high levels of aggressive and antisocial behaviour were overcome as a result of the effects of the TBI on premorbid personality consistent with the notion of an increase in apathetic responding, in line with the extensive literature on the prefrontal leucotomy and lobotomy procedures (Stuss & Benson, 1986; Valenstein, 1986).
Kant, Duffy, and Pivovarnik (1998) using standardized evaluation tools (Clinical Neuropsychiatric Examination, the self- and family-member-rated version of the Apathy Evaluation Scale [AES]) (Marin, 1991; Marin, Biedrzycki, & Firinciogullari, 1991) and the Beck Depression Inventory, noted that of 83 consecutive TBI patients seen at a neuropsychiatric clinic, 10.84% had apathy without depression, an equivalent percentage had depression without apathy, and another 60% of the patients exhibited both. Younger patients were more prone to apathy and depression than the older patients, and the patients with the more severe injuries were more likely to reflect apathy alone. Interestingly family members observed the apathy syndrome more than the patients themselves, possibly indicating a decrease in the level of self-awareness following the injury.
While these data do indicate that there is overlap between apathy and depressive mentation, these are separable constructs, and the implications of each are quite different in the treatment and management of patients following the TBI (Levy et al., 1998). Recent literature places the conditions associated with diminished motivation on a spectrum spanning from apathy at the least severe end through abulia to akinetic mutism at the most severe end of the disruption of behavioural responding (American Congress of Rehabilitation Medicine [ACRM], 1995; Fisher, 1983; Marin, 1997; Marin & Chakravorty, 2005; Mega & Cohenour, 1997).
Akinetic mutism is characterized by impaired initiation of behaviour and cognition with preservation of visual tracking (ACRM, 1995). Essentially the patient is mute and motionless despite being awake. The symptoms of abulia are similar but somewhat less severe than those of akinetic mutism with poverty of behaviour and speech, lack of initiative, blunting of emotional responding motor slowing, and delay of speech production (Fisher, 1983; Mega & Cohenour, 1997). Apathy is a diminution of motivation in the presence of normal consciousness and other forms of cognition, but with diminution in the quantity rather than the quality of behavioural responding (Marin & Chakravorty, 2005).
In a subsequent replication and extension of the Kant et al. (1998) study discussed above, Andersson, Gundersen and Finset (1999) investigated the levels of apathy and psychophysiological reactivity in a sample of thirty severe TBI participants. Using a cutoff score of 34 on the AES, they noted that 66.7% of the sample featured self-reported levels of apathy above the cutoff. This compares quite favorably with the level noted in the Kant et al. (1998) study that noted an overall level of 71.1%. A subsequent study by Andersson and Bergedalen (2002) noted a level of 62.3%, although an earlier study (Andersson, Krogstad, & Finset, 1999) noted a somewhat lower level of 46.6%. Nonetheless, it is clear that in the range of 47-71% of severe TBI participants feature supra-cutoff levels of apathy in the period following TBI.
A large percentage of these participants will also feature reduced self-awareness as this phenomenon appears to be closely related to levels of motivation and emotional responsivity (Andersson, Krogstad et al., 1999) in this patient group. From a neuro-psychological perspective the apathetic pattern of personality change in TBI is commonly associated with compromise in memory functioning, including impairments of acquisition and recall of information, as well as with compromise in executive functions and diminution of psychomotor speed (Andersson & Bergedalen, 2002). It has been reported that stimulant medications such as amantadine, amphetamine, bromocriptine, buproprion, methylphenidate, and selegeline may be useful in treating this syndrome (Kraus & Maki, 1997a, 1997b; Marin, Fogel, Hawkins, Duffy, & Krupp, 1995; Warden et al., 2006).
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