Changes in Personality
John J. Campbell III
I. Background
A. Definitions
Personality refers to the characteristics of a person that are enduring, pervasive, and distinctive. Personality has been defined as “the dynamic organization within the individual of those psychophysical systems that determine his unique adjustments to his environment.”
Those characteristics are known as traits. Traits occur throughout the population in a bell-shaped data distribution. Traits have probabilistic influences on behavior that are known as tendencies. These tendencies produce patterns of behavior that are consistent over time.
Temperament factors are heritable biases in information processing reflected as automatic, preconceptual responses to social stimuli. Four dimensions of temperament include novelty seeking, harm avoidance, reward dependence, and persistence.
Character refers to behavioral tendencies related to concepts of the self. Initially, temperament influences the development of character. Eventually, insights gained through the developing character can modify the temperament. Three dimensions of character are self-directedness, cooperativeness, and self-transcendence.
B. Classification of changes in personality
Efforts to establish a lexicon for personality change related to neurologic disorders have culminated in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision (DSM-IV-TR) diagnostic criteria for the diagnosis of personality change because of a general medical condition. These criteria include a persistent personality disturbance that represents a change from the individual’s previous characteristic personality pattern with evidence from the history, physical examination, or
laboratory findings that the disturbance is the direct physiologic consequence of a general medical condition. The disturbance must not occur exclusively during the course of delirium and is not better accounted for by another mental disorder. Further, the disturbance must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
There are five specified types of DSM-IV-TR personality change because of a general medical condition. The labile type, is characterized by affective lability, the disinhibited type, if the predominant feature is poor impulse control, the aggressive type, if aggressive behavior predominates, the apathetic type, are characterized by marked apathy and indifference, and the paranoid type, if suspiciousness or paranoid thinking are prominent. In addition, there is an other type, if a feature not noted above is present, a combined type if more than one feature predominates the clinical picture, and an unspecified type. This new diagnostic nomenclature can be used to provide a formal DSM-IV diagnosis of acquired changes in personality.
The neuropsychiatric perspective presented in the subsequent text relies more strongly on established brain-behavior relationships than upon description of the acquired symptoms in the DSM-IV paradigm, which has not yet been widely applied to research populations.
C. Epidemiology
Little is known about the prevalence of changes in personality within neuropsychiatric populations. The few published reports vary in nomenclature and methodology and therefore preclude accurate conclusions. It is clear from these reports, however, that personality change is a common occurrence in most, if not all, neuropsychiatric disorders, particularly in those conditions that involve the prefrontal–subcortical neural networks.
D. Prognosis
Only a small literature exists on the course and prognosis of personality changes associated with neuropsychiatric disorders, primarily in the area of traumatic brain injury (TBI). These limited data suggest that personality changes can be chronic and disabling.
II. Neurobiology and Pathophysiology of Personality Change
A. Normal personality
The neurobiology of human personality is not fully understood. The basis for all human behavior unequivocally involves the final product of the processing and integration of information by widely distributed neural networks within the human brain. Disorders that affect the physical or neurochemical balance within these networks will alter the otherwise stable expression of personality and therefore provide astute clinical observers with signs of incipient neuropsychiatric conditions.
Numerous case reports and case series with clinicopathologic correlation have implicated the neural networks of the prefrontal cortex as a major contributor to human personality and behavior. Alexander and Crutcher have defined these networks as distinct
cortico-striato-pallido-thalamo-cortical loops or circuits. Three of these circuits, involving the dorsolateral convexity of the frontal lobe, the mesial frontal cortex, and the orbitofrontal cortex, have the capacity to mediate “executive” or metacognitive functions that enable us to achieve success in our social environment.
cortico-striato-pallido-thalamo-cortical loops or circuits. Three of these circuits, involving the dorsolateral convexity of the frontal lobe, the mesial frontal cortex, and the orbitofrontal cortex, have the capacity to mediate “executive” or metacognitive functions that enable us to achieve success in our social environment.
B. Dysexecutive syndromes
Prefrontal cortical gray matter, subcortical gray matter (striatum), and white matter are each vulnerable to particular kinds of pathology. Therefore there are numerous conditions that damage these networks and may ultimately manifest as changes in personality. The term frontal lobe syndrome has become synonymous with acquired changes in personality and there is no doubt that focal lesions involving the prefrontal cortex produce predictable changes in executive cognition and behavior. However, sufficient evidence exists demonstrating that lesions distant from the frontal cortical mantle may produce similar clinical findings. Hence the term dysexecutive syndrome is a more appropriate descriptor for patients who manifest personality changes with executive cognitive deficits.
This nomenclature is more consistent with current theories that describe large scale distributed neural networks subserving behavior. The nomenclature also provides a more rational template for evaluating patients who acquire changes in personality and the complex behaviors reliant upon executive cognition. Although functional divisions within the prefrontal system have been identified, in clinical practice lesions are seldom confined to any one of these systems. As a result, patients are likely to manifest the clinical features of more than one of the symptom clusters defined in the subsequent text. With this in mind, three distinct dysexecutive syndromes have been identified (see Table 11.1).
1. Disorganized type
The high-level cognitive functions mediated by the dorsolateral prefrontal lobe and its connections include cognitive flexibility, temporal ordering of recent events, planning ahead, regulating actions based on environmental stimuli, and learning from experience. Patients exhibiting dysfunction
in these cognitive domains are concrete and perseverative and show impairment in reasoning and limited mental flexibility. People who were once punctual and successful come to appear stubborn or “scattered” to acquaintances. In addition, they often will “lose set” and engage in purposeless or disorganized activities. The common denominator for these deficits appears to be metacognitive disorganization. It is therefore reasonable to refer to this cognitive and personality symptom cluster as the “dysexecutive syndrome—disorganized type.”
in these cognitive domains are concrete and perseverative and show impairment in reasoning and limited mental flexibility. People who were once punctual and successful come to appear stubborn or “scattered” to acquaintances. In addition, they often will “lose set” and engage in purposeless or disorganized activities. The common denominator for these deficits appears to be metacognitive disorganization. It is therefore reasonable to refer to this cognitive and personality symptom cluster as the “dysexecutive syndrome—disorganized type.”
TABLE 11.1 Primary Clinical Features of the Regional Prefrontal Syndromes | |||||||||||||||
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Examples of this behavior may include slowly progressive loss of ability to manage a checking account, having utilities occasionally cut off because of nonpayment of bills, neglecting home maintenance and personal hygiene, or having a qualitatively or quantitatively limited supply of food at home. In the setting of a disorganized dysexecutive syndrome, old habits and simple patterns predominate. Hot tea and toasted bread become the de facto diet for many elderly people with executive cognitive impairment.
2. Disinhibited type
The orbitofrontal cortex has discrete connections with paralimbic cortex and limbic structures. The orbitofrontal cortex therefore plays a role in the elaboration and integration of limbic drives. Patients with orbitofrontal pathology exhibit poor impulse control, explosive aggressive outbursts, inappropriate verbal lewdness, jocularity, and a lack of interpersonal sensitivity. Because this syndrome is characterized primarily by impulse dyscontrol it would be appropriate to describe it as the “dysexecutive syndrome—disinhibited type.”
Examples of this behavior may include making unwelcome public statements about the appearance of strangers, use of vulgar language, or using inappropriate humor. This syndrome has been described as “pseudopsychopathic,” and it causes great distress to caregivers who observe the loss of the premorbid personality and its evolution into crassness and vulgarity.
3. Apathetic type
Mesial frontal pathology often affects the functional balance between the cingulum and the supplementary motor area. In a sense, this system represents the behavioral outflow of the executive cognitive system and these structures appear to participate in an exploratory system involving a link between motivation and action. Disruption of this neural network frequently leads to a dysmotivational picture ranging from apathy to akinetic mutism (see Chapter 1). These patients often appear outwardly depressed, yet they lack the dysphoria, negative cognitions, and neurovegetative signs of a major depression, such as anorexia or insomnia. This syndrome has also been described as “pseudodepressed.” Because the predominant characteristic of this syndrome is behavioral inertia it is appropriate to describe it as the “dysexecutive syndrome—apathetic type.”
Family members are often frustrated by the inertia of the apathetic patient and mistakenly interpret the patient’s apathy as
deliberate. The patient’s emotional blunting is often erroneously perceived as a lack of caring or concern. The striking lack of spontaneity often contrasts sharply with the premorbid personality.
deliberate. The patient’s emotional blunting is often erroneously perceived as a lack of caring or concern. The striking lack of spontaneity often contrasts sharply with the premorbid personality.
C. Gastaut-Geshwind syndrome
Electrical pathology in the brain, in the form of partial complex seizures originating in the anterior temporal lobe, may also influence personality expression. An “Epileptic Interictal Personality,” also known as the Gastaut-Geschwind syndrome, has been described in which a person has a moral or religious preoccupation, diminished libido, propensity to write, verbosity, blandness, and difficulty disengaging from conversations. Attempts to further define this syndrome with the Minnesota Multiphasic Personality Inventory have revealed mixed results, with abnormalities frequently noted on the depression, paranoia, schizophrenia, and psychasthenia scales. However, this instrument does not provide a sensitive index of behavioral parameters for this clinical presentation.
Geschwind et al. hypothesized that these changes reflect an enhanced connection between temporolimbic and cortical heteromodal association areas. This “hyperconnection” could result in a heightened (right hemisphere focus) or diminished (left hemisphere focus) response to the social environment. These hypotheses remain controversial. Still, clinicians who treat patients with temporal lobe epilepsy have little doubt about the existence of interictal disorders of personality. This syndrome is not universal, however, and many patients with temporal lobe epilepsy do not demonstrate these traits.
References
1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed. Text Revision. Washington, DC: American Psychiatric Association; 2000.
2. McRae RR, Costa PT. Personality in adulthood: A five factor theory perspective. New York, NY: The Guilford Press; 2003.
3. Cloninger CR, Svrakic DM, Przybeck TR. A psychobiological model of temperament and character. Arch Gen Psychiatry. 1993;50:975–990.
4. Duffy JD, Campbell JJ. The regional prefrontal syndromes: A clinical and theoretical overview. J Neuropsychiatry Clin Neurosci. 1994;6:379–387.
5. Waxman SG, Geschwind N. The interictal behavior syndrome of temporal lobe epilepsy. Arch Gen Psychiatry. 1975;32:1580–1586.
III. Management
A. Principles of management
In general, the management of personality change in patients with neurologic illness should begin with a clinical interview of the patient and collecting collateral history from an acquaintance or family member. The clinician should then conduct a formal assessment of mental status and cognition, a sensorimotor examination, relevant laboratory and neuroimaging studies, and a biopsychosocial formulation and treatment plan.
1. Perform a diagnostic evaluation
The diagnosis of personality change in patients with neurologic illness is especially challenging. Personality change
secondary to a neurologic illness is a diagnosis of exclusion and should be offered only when delirium, and other mood, anxiety, and substance use disorders have been ruled out.
The clinical interview should establish as clearly as possible the change in the patient’s premorbid personality. While self-report scales have been developed to assess personality, temperament, and character, they are of limited use in this clinical situation. Patients with neurologic illness affecting personality often demonstrate lack of insight and cannot reliably complete these instruments. Further, the personality change precludes objective assessment of premorbid personality, which, in essence, no longer exists. Independent reports of spouses and other collateral informants are required to complete the picture.
Validated instruments can provide a useful framework for collecting data. The Five-Factor Model captures five domains of personality—agreeableness, conscientiousness, openness to experience, extraversion, and neuroticism. Alternatively, the temperament and character inventory, developed by Cloninger et al. measures seven domains of personality. Four temperament dimensions are defined—novelty seeking, harm avoidance, reward dependence, and persistence. The model defines three dimensions of character—self-directedness, cooperativeness, and self-transcendence.
A general physical and neurologic examination should be performed with special attention to the cognitive (including executive cognition) and motor examinations.
Laboratory tests are indicated only to confirm the presence of a general medical disorder, suspected neurologic disorder, or substance use disorder as suggested by the history or examination, or to characterize the status of a known disorder.
Evaluate the safety of the patient or caregiver. Problems with impulsive, risk-taking behavior and aggression are common dimensions of personality change that can imperil safety.
Evaluate the emotional status of the caregiver, who are usually under considerable stress and may require individualized interventions.
2. Implement a biopsychosocial treatment plan
Determine and continually evaluate the treatment setting (inpatient vs. outpatient) based on the patient’s clinical status, safety, available support systems, ability to care adequately for self, and willingness and ability to cooperate with treatment plan.
While few evidence-based treatments exist for personality change secondary to neurologic illness, I recommend a biopsychosocial model that is, the combined use of appropriate biological (somatic) treatments (including acute phase and continuation or maintenance phase treatment),
psychological treatments, and social interventions. Develop contingency plans with caregivers for dealing with acute situations such as aggression or violence.
Evaluate and address functional impairments in interpersonal relationships, work and living conditions, and other health-related needs.
Provide education and support to patient, family, and caregivers.
Enhance treatment adherence by simplifying the treatment regimen, minimizing the cost of the treatment, minimizing side effects, and identifying relevant community support services.Related posts:
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