Chronic Neuropsychiatric Sequelae II: Behavioral Disturbances

Theodore Tsaousides and Jason Krellman

Acute behavioral manifestations of moderate-to-severe traumatic brain injury (TBI) are common, occurring in varying severity in up to 96% of patients [1]. These acute symptoms include agitation, disinhibition, emotional lability, apathy, and/or aggression, and are typically managed pharmacologically (e.g., with anticholinergics or dopaminergic antagonists) and with environmental modification (e.g., minimization of agitating stimuli). Individuals with lesions in the prefrontal (e.g., orbitofrontal) cortex or temporal lobe, either mesial (e.g., amygdala) or neocortical (e.g., temporal pole), are particularly vulnerable to behavioral sequelae. Behavioral disruption is thought to be due to loss of tonic balance between those neural regions that underlie the expression of affect, impulses, and drives and those regions that inhibit or otherwise modulate that expression based on the environmental context.

Behavioral sequelae of TBI can persist beyond the immediate postinjury period and become chronic in those with lesions in the aforementioned regions. Individuals with premorbid histories of impulsive or aggressive behavior (e.g., as seen in the setting of substance abuse, violence, and/or criminality) are also at higher risk [1]. Therefore, the presence of behavioral symptoms is likely multidetermined, reflecting both the characteristics of the brain injury and the individual. Regardless of etiology, chronic behavioral symptoms often result in significantly poorer outcomes, including response to rehabilitation, employment, psychosocial functioning, and community reintegration.

The long-term behavioral consequences of TBI can be classified into three broad categories: those arising from executive dysfunction, emotional dysregulation, and anosognosia. Though overlapping to some degree, certain behavioral presentations are more common within each category.

EXECUTIVE DYSFUNCTION

“Executive functions” are a set of complex and hierarchically nested cognitive functions that are critical for any type of goal-directed behavior [2]. Executive deficits are associated with frontal lobe pathology, but the sheer number of functions classified under the executive umbrella as well as the high degree of interconnectivity between the frontal lobe and other neural regions means that more posterior neuropathology can also manifest in executive deficits. Patients with lesions of the frontal lobes or within greater frontal systems show impairments in anticipation, planning, execution, and/or self-regulation. Deficits in executive functioning are among the most disabling consequences of TBI and affect critical long-term outcomes such as return to work, community integration, and social autonomy.

The anatomical and functional complexity of the frontal lobes means that damage to this region can result in a broad range of behavioral symptoms that interfere with emotional, social, and vocational functioning. Three different syndromes have been identified in the literature based on the anatomical features of the injury [3].

A. Abulic syndrome
Associated with damage to the medial frontal cortex, abulic syndrome results in an amotivational state characterized by motoric, cognitive, emotional, affective, and motivational apathy. Patients with abulia appear lethargic and unmotivated. They lack initiation, exhibit diminished interest in people and events, respond to stimuli at a reduced pace, have reduced ideational fluency, and are emotionally flat. Very often, patients suffering from abulia are misdiagnosed with depression. Indeed, they appear depressed, but they do not meet criteria for a depression spectrum diagnosis etiologically or symptomatically. This condition has been identified in the literature as pseudo-depression [2–4].

B. Dysexecutive syndrome
Damage to the dorsolateral prefrontal cortex is associated with a dysexecutive syndrome characterized by impairment in different aspects of goal-directed behavior. Goal-directed behavior comprises volition, planning, implementation, monitoring, and adjusting behavior [4]. Patients with dysexecutive problems present with significant difficulties in planning and organization, monitoring, and set-shifting. Behaviorally, they appear distractible, disorganized, and inefficient. They have difficulty suppressing habitual responses, are unable to develop and employ effective strategies, and tend to perseverate [2–4].

C. Disinhibition syndrome
Damage to the orbitofrontal cortex can result in a range of emotional and behavioral disturbances. These include interpersonal disinhibition, poor social judgment, and impulsive decision making. They often exhibit environmental dependence and utilization behavior. They have difficulty appreciating the impact of their behavior on others, they lack empathy and perspective taking, and they disregard social conventions. They can appear childish and selfish. They often engage in aggressive and/or abusive behaviors. Their inability to inhibit behavior and anticipate or appreciate the consequences often results in violating rules, breaking the law, and committing minor crimes. This syndrome has been referred to as pseudo-psychopathy in the literature [2–4].

Treatment

A meta-analysis of studies examining the efficacy of interventions for post-TBI executive dysfunction concluded that the use of metacognitive strategies results in improvements in goal management [5], planning and organization [6], and problem solving [7,8], with favorable results extending to personally relevant functional activities [9]. Metacognitive strategies involve using and internalizing step-by-step procedures to enhance awareness and self-regulation [10]. Interventions for executive functioning are administered individually, in groups or a combination of individual and group treatment [9,10].

Interventions for executive dysfunction have also been embedded in comprehensive-holistic day treatment programs (CDHP) with favorable results in terms of improved problem solving [11,12].

EMOTIONAL DYSREGULATION

Emotional regulation is described as a set of heterogeneous processes involved in monitoring, evaluating, and modifying emotional responses [13]. Individuals with brain injuries often present with difficulty modulating emotions and modulating behavioral responses according to the social or broader environmental context, which increases the negative impact of the already impaired cognition on psychosocial functioning [14]. Emotional dysregulation may also contribute to the higher than general population rates of depression, anxiety, and other types of psychopathology [15].

Emotional regulation deficits have been linked to disruptions in neuropsychological processes involving the frontal and temporal lobes, including the anterior cingulate and amygdala. Three behavioral types of emotional dysregulation have been observed as a function of lesion location [16].

A. Impaired appraisal of emotional valence
Individuals with TBI may lose the ability to appraise their emotional valence (attractiveness or aversiveness) of a stimulus. These individuals have difficulty distinguishing between reward and punishment and sustaining their motivation accordingly. They are unable to avoid situations that elicit undesirable emotions and to select situations that elicit desirable emotions. As a result, they show poor judgment and they appear to gravitate toward situations that eventually have a negative impact both on their mood, as well as on the outcomes of their goal-directed behavior, leaving them frustrated and confused [16].

B. Impaired modulation of emotional response
Individuals with TBI have difficulty manipulating the magnitude of the emotional responses. Their ability both to inhibit as well as amplify emotions is impaired. They appear to be experiencing a type of emotional perseveration. Due to the prolonged latency of and delayed recovery from intense emotions, emotionally laden events have a more profound effect on their moods, and they generate more exaggerated behaviors. Difficulty modulating emotion dynamics leads to rage, explosive temper, aggression, hostility, irritability, and anxiety. Conversely, it may manifest as placidity, passivity, apathy, depression, and blunted affect, due to the diminished ability to alter low-intensity emotional states [16].

C. Impaired production of facial expression of emotions
Individuals with TBI can present with pseudobulbar affect (PBA), pathological crying or laughing following the presentation of a stimulus, which is not commensurate to the internal subjective experience of the individual. PBA is a motor disorder attributable to pathological disinhibition of motor pathways involved in emotional expression and must be distinguished from a mood disorder for proper management [17]. As a result of PBA, individuals with TBI may often laugh or cry inappropriately in social situations, with little ability to consciously control their reactions. In addition, individuals with these types of emotional regulation deficits have difficulty producing facial expressions conforming to social norms in the absence of an emotional experience (e.g., remaining somber at a funeral or smiling when greeting a familiar person).

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