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The sailor who won’t follow orders
CASE: An unlikable patient
Mr. L, age 56, is admitted to the psychiatric unit at our Veterans Affairs Medical Center for active suicidal ideation; he has a history of self-injurious behaviors that include mutilation and overdose. He also has a history of alcohol dependence and multiple inpatient psychiatric admissions. He has never married and conflicts with his siblings—in whose home he has been staying—have led to frequent homelessness.
His affect is silly and shallow. He also shows signs of haughtiness, disinhibition, grandiosity, and confabulation. For example, he says that while in the Navy he had 82 sexual exploits and developed a drug that cured herpes.
We start Mr. L on divalproex, 1,500 mg/d, and quetiapine, titrated to 200 mg/d. After 3 days he is discharged, but this begins a cycle of repeated suicide gestures and readmissions—9 within the next 3 months. Each time he is discharged, Mr. L fails to follow through on treatment recommendations and is indifferent to our staff’s annoyed reactions.
The author’s observations
Some of our staff members regard Mr. L’s suicidal gestures as manipulative and feel angry and demoralized by his poor adherence to outpatient treatment plans. Their negative countertransference might have impacted how they evaluated Mr. L through repeated admissions and discharges. During Mr. L’s ninth admission, we decide to reevaluate his longitudinal history for clues to his noncompliant behavior.
History: Undocumented injury
Mr. L says he began drinking alcohol at age 16. He reports that he has grown marijuana but has not smoked it since 1991. He denies using heroin or other drugs.
Mr. L states that he suffered a head injury in 1975 after falling off a ladder on a Navy ship. He describes losing consciousness for a brief but uncertain duration. He reports that he has developed a seizure disorder since this fall and a history of amnesia secondary to past seizures. His medical records contain no witnessed seizures. Mr. L also says he was hospitalized a few years ago and placed on a ventilator for 7 days for an undetermined reason.
The authors’ observations
Based on Mr. L’s report of a possible traumatic brain injury (TBI), we order a neurologic evaluation. A year earlier, MRI of the brain without contrast demonstrated minimal, nonspecific periventricular and subcortical, punctuate hyperintensities on flair and T2 weighted sequences that are nonspecific. Overall, the impression was “diffuse involutional changes and mild nonspecific periventricular and subcortical white matter hyperintensities,” which might reflect covert vascular brain injury.
Our frustration over Mr. L’s repeated readmissions for suicidal gestures led us to seek outside evaluation and consultation from a senior psychiatrist for assistance with discharge and treatment planning. Unlike our staff, the consulting psychiatrist did not harbor strong negative feelings toward the patient.
Mr. L’s history of deterioration in psychosocial functioning prompted this psychiatrist to perform a thorough mental status examination that focused on cognitive elements and request formal neuropsychological testing.
Evalutation: Cognitive Deficits
During mental status examination, Mr. L has difficulty recalling 3 items and uses a memory strategy to assist himself. He fails to recollect in reverse order the last 5 U.S. presidents. He spells “world” backward, but has difficulty repeating 6 digits forward and 4 backward. He is unable to do serial 7 subtractions from 93 to 65 correctly. He adequately copies interlocking pentagons and draws a clock with the correct time. He achieves a score of 28/30 on the Folstein Mini Mental State Exam, missing the date by 4 days and recalling 2 of 3 words.
These results suggest Mr. L has difficulty with attention and working memory, short-term memory, fund of general information and long-term memory, and ability to perform simple calculations. Most important, they indicate the need for further study, especially a neuropsychological test battery.
Mr. L’s abnormal neuropsychological test results are summarized in the Table. He manifests concretization of thought. His loss of conceptual fluidity is documented formally by measures of perseverative errors and categories completed on the Wisconsin Card Sorting Test (WCST). These findings support a diagnosis of acquired dementia.
Table
Abnormal findings on Mr. L’s neuropsychological testing
| Cognitive domain | Test | Score | Interpretation |
|---|---|---|---|
| Mental status and effort | |||
| Mental status | MMSE total score | 28/30 | 2 of 3 items recalled after delay |
| Orientation | MMSE orientation questions | 9/10 | Date off by 4 days |
| Premorbid IQ estimate | WRAT-4 Reading Standard | 66th percentile | Within normal limits. Inconsistent with educational attainment, but could be impacted by temporal lobe findings |
| Verbal memory | |||
| Immediate memory | RBANS Immediate Memory Index (List and Story Learning) | 1st percentile | Severe impairment |
| Delayed memory | RBANS Delayed Memory Index | 1st percentile | Severe impairment |
| Recognition memory | List Learning | Severe impairment | |
| Visuospatial memory | |||
| Delayed memory | RBANS Figure Recall | 3rd percentile | Severe impairment |
| Executive functioning | |||
| Cognitive flexibility | Trails B | 10th percentile | Severe impairment based on educational attainment |
| WCST | Low scores: Nonperseverative errors, perseverative errors, and categories completed | ||
| * Tests of mental status effort, visuomotor processing speed, confrontation naming, visuospatial function, attention, and executive functioning fluency/initiation were within normal limits | |||
| MMSE: Mini Mental State Exam; WRAT: Wide Range Achievement Test; RBANS: Repeatable Battery for the Assessment of Neuropsychological Status; WCST: Wisconsin Card Sorting Test | |||
The authors’ observations
Mr. L’s history, cognitive testing, head imaging, and behavioral observations suggest that several pathogenic factors contribute to his impaired functioning. First, he describes a TBI of unknown severity occurring in 1975. Although brain scans did not show evidence of midline shift or encephalomalacia, a direct blow to the head after falling from a height combined with possible post-injury seizures suggests a TBI of at least moderate severity.
Second, Mr. L describes an incident in which he required inpatient respiratory assistance. Although the precipitating medical event was unclear, anoxia or hypoxia is likely. A recent CT revealed low attenuation in the left temporal region that could represent an infarct.
Mr. L’s severe memory impairment and moderate to severe impairment in cognitive flexibility are commonly reported after a TBI of moderate severity. If an ischemic incident were the primary contributor, a lateralized pattern of cognitive dysfunction—which Mr. L does not exhibit—would be expected.
Although Mr. L likely has vascular dementia, his MRI findings do not indicate sufficient disease to account for his memory scores. Vascular dementia is associated with slow, stepwise cognitive deterioration, which is not consistent with severely impaired memory in a 56-year-old patient.
Finally, alcoholism is associated with cognitive difficulty in memory, visuospatial functioning, and abstract reasoning. Mr. L demonstrated significant difficulty in memory and abstract reasoning, but his visuospatial functioning was largely intact. In the absence of Wernicke’s encephalopathy, chronic alcoholics generally do not show memory decrements in line with Mr. L’s. His MRI results indicated only minimal ventricular and sulcal enlargement. Because atrophy is present in approximately 60% of chronic alcoholics, this finding provides evidence of a contribution, but the other contributory factors are associated with more definitive medical outcomes. Thus, alcoholism must be viewed as a secondary contributor to Mr. L’s impaired functioning.
Taking into account all known contributors, TBI emerges as the primary diagnosis.
Consider neurologic injury
Recognizing and characterizing personality changes related to neurologic injury and disease is often problematic and unreliable, even when psychometrically validated instruments and structured diagnostic interviews are used (Box 1).1-5 Mr. L’s presentation differed from the more commonly reported “impulsive aggression” associated with closed head injury. Sequelae from TBI were contributing to his clinical presentation but was obscured by his shallow and silly affect, inability to accurately assess social cues, and lack of empathy.
Mr. L reported suffering a head injury from falling off a ladder. Personality changes that result from traumatic brain injury (TBI) of the sudden deceleration type—even when mild—are frequently referable to the frontal lobe, especially focal orbital and/or ventromedial damage of the prefrontal cortex.1-5 This is because of the physical proximity of the sphenoid wing to the orbitofrontal region and effects of shearing.
As a result of this damage, patients lack insight into their accompanying cognitive and behavioral abnormalities, such as the egocentricity and impaired empathy shown by Mr. L. These changes might not be detected in clinical interviews and over brief periods.2 Appreciating an acquired personality disturbance may require evaluating the patient’s behavior over months or years.2
In retrospect, Mr. L’s seeking repeated inpatient psychiatric hospitalizations is consistent with poor planning and problem-solving skills. He has a limited repertoire of adaptive behaviors and has learned that suicidal gestures lead to admission and caretaking. These are important to him because he is frequently homeless. His lack of insight is seen in his unrealistic plans for employment in jobs requiring specialized technical skills.
Mr. L’s case emphasizes the importance of considering brain injury as an etiologic factor in personality changes. It also highlights the complex—and seemingly nonoverlapping—functions and dysfunctions of the frontal lobe, including:
- source memory
- working memory
- sustained attention
- conceptual fluidity
- imaginative thinking
- impulse regulation
- planning and problem-solving skills.
Documenting Mr. L’s cognitive deficits and acquired dementia diagnosis changed our staff’s perception of his behavior, enabling us to overcome negative countertransference (Box 2). We no longer regarded him as deliberately manipulative and refer him for appropriate treatment.
Countertransference can interfere with optimal workup and treatment of patients with character changes related to traumatic brain injury and neurodegenerative processes. When we interpreted Mr. L’s suicidal gestures and hospitalizations as manipulative and deliberate, we failed to appreciate the limited number of things he could do to obtain a safe and protective environment. We also failed to recognize that his poor planning and problem-solving skills—as well as lack of insight into his illness—prevented him from adhering to outpatient treatment.
Originally, we attributed Mr. L’s egocentricity, lack of empathy, and lack of adherence to axis II pathology.
Our staff’s hostile feelings toward Mr. L led us to insufficiently consider his history—which is consistent with cognitive decline—during biopsychosocial evaluation and treatment planning. Mr. L’s status as a frequently homeless, unemployed person reflects a sharp decline for a highly educated person who served as a Navy officer and performed radiation inspections on nuclear-powered vessels.
Outome: Residential placement
We realize Mr. L needs cognitive rehabilitation—including assistance with planning and problem solving—and arrange for his placement in a residential facility for this specialized rehabilitation. Mr. L receives supportive psychotherapy and cognitive remediation from a psychologist. He also is involved in incentive work therapy with a vocational rehabilitation specialist.
Related resource
- Silver, JM, McAllister TW, Yudofsky SC, eds. Textbook of traumatic brain injury. Washington, DC: American Psychiatric Publishing; 2005.
- Divalproex • Depakote
- Quetiapine • Seroquel
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Tranel D. Functional neuroanatomy: neuropsychological correlates of cortical and subcortical damage. In: Yudofsky SC, Hales RE, eds. The American Psychiatric Publishing textbook of neuropsychiatry and clinical neurosciences. 4th ed. Washington, DC: American Psychiatric Publishing; 2002:71-113.
2. Barrash J, Tranel D, Anderson SW. Acquired personality disturbances associated with bilateral damage to the ventromedial prefrontal region. Dev Neuropsychol 2000;18(3):355-81.
3. Silver JM, Hales RE, Yudofsky SC. Neuropsychiatric aspects of traumatic brain injury. In: Yudofsky SC, Hales RE, eds. The American Psychiatric Publishing textbook of neuropsychiatry and clinical neurosciences. 4th ed. Washington, DC: American Psychiatric Publishing; 2002:625-72.
4. Damasio AR, Tranel D, Damasio HC. Somatic markers and the guidance of behavior: theory and preliminary testing. In: Levin HS, Eisenberg HM, Benton AL, eds. Frontal lobe function and dysfunction. Oxford, UK: Oxford University Press; 1991:217-29.
5. Prigatano GP. The relationship of frontal lobe damage to diminished awareness: studies in rehabilitation. In: Levin HS, Eisenberg HM, Benton AL, eds. Frontal lobe function and dysfunction. Oxford, UK: Oxford University Press; 1991:381-97.
CASE: An unlikable patient
Mr. L, age 56, is admitted to the psychiatric unit at our Veterans Affairs Medical Center for active suicidal ideation; he has a history of self-injurious behaviors that include mutilation and overdose. He also has a history of alcohol dependence and multiple inpatient psychiatric admissions. He has never married and conflicts with his siblings—in whose home he has been staying—have led to frequent homelessness.
His affect is silly and shallow. He also shows signs of haughtiness, disinhibition, grandiosity, and confabulation. For example, he says that while in the Navy he had 82 sexual exploits and developed a drug that cured herpes.
We start Mr. L on divalproex, 1,500 mg/d, and quetiapine, titrated to 200 mg/d. After 3 days he is discharged, but this begins a cycle of repeated suicide gestures and readmissions—9 within the next 3 months. Each time he is discharged, Mr. L fails to follow through on treatment recommendations and is indifferent to our staff’s annoyed reactions.
The author’s observations
Some of our staff members regard Mr. L’s suicidal gestures as manipulative and feel angry and demoralized by his poor adherence to outpatient treatment plans. Their negative countertransference might have impacted how they evaluated Mr. L through repeated admissions and discharges. During Mr. L’s ninth admission, we decide to reevaluate his longitudinal history for clues to his noncompliant behavior.
History: Undocumented injury
Mr. L says he began drinking alcohol at age 16. He reports that he has grown marijuana but has not smoked it since 1991. He denies using heroin or other drugs.
Mr. L states that he suffered a head injury in 1975 after falling off a ladder on a Navy ship. He describes losing consciousness for a brief but uncertain duration. He reports that he has developed a seizure disorder since this fall and a history of amnesia secondary to past seizures. His medical records contain no witnessed seizures. Mr. L also says he was hospitalized a few years ago and placed on a ventilator for 7 days for an undetermined reason.
The authors’ observations
Based on Mr. L’s report of a possible traumatic brain injury (TBI), we order a neurologic evaluation. A year earlier, MRI of the brain without contrast demonstrated minimal, nonspecific periventricular and subcortical, punctuate hyperintensities on flair and T2 weighted sequences that are nonspecific. Overall, the impression was “diffuse involutional changes and mild nonspecific periventricular and subcortical white matter hyperintensities,” which might reflect covert vascular brain injury.
Our frustration over Mr. L’s repeated readmissions for suicidal gestures led us to seek outside evaluation and consultation from a senior psychiatrist for assistance with discharge and treatment planning. Unlike our staff, the consulting psychiatrist did not harbor strong negative feelings toward the patient.
Mr. L’s history of deterioration in psychosocial functioning prompted this psychiatrist to perform a thorough mental status examination that focused on cognitive elements and request formal neuropsychological testing.
Evalutation: Cognitive Deficits
During mental status examination, Mr. L has difficulty recalling 3 items and uses a memory strategy to assist himself. He fails to recollect in reverse order the last 5 U.S. presidents. He spells “world” backward, but has difficulty repeating 6 digits forward and 4 backward. He is unable to do serial 7 subtractions from 93 to 65 correctly. He adequately copies interlocking pentagons and draws a clock with the correct time. He achieves a score of 28/30 on the Folstein Mini Mental State Exam, missing the date by 4 days and recalling 2 of 3 words.
These results suggest Mr. L has difficulty with attention and working memory, short-term memory, fund of general information and long-term memory, and ability to perform simple calculations. Most important, they indicate the need for further study, especially a neuropsychological test battery.
Mr. L’s abnormal neuropsychological test results are summarized in the Table. He manifests concretization of thought. His loss of conceptual fluidity is documented formally by measures of perseverative errors and categories completed on the Wisconsin Card Sorting Test (WCST). These findings support a diagnosis of acquired dementia.
Table
Abnormal findings on Mr. L’s neuropsychological testing
| Cognitive domain | Test | Score | Interpretation |
|---|---|---|---|
| Mental status and effort | |||
| Mental status | MMSE total score | 28/30 | 2 of 3 items recalled after delay |
| Orientation | MMSE orientation questions | 9/10 | Date off by 4 days |
| Premorbid IQ estimate | WRAT-4 Reading Standard | 66th percentile | Within normal limits. Inconsistent with educational attainment, but could be impacted by temporal lobe findings |
| Verbal memory | |||
| Immediate memory | RBANS Immediate Memory Index (List and Story Learning) | 1st percentile | Severe impairment |
| Delayed memory | RBANS Delayed Memory Index | 1st percentile | Severe impairment |
| Recognition memory | List Learning | Severe impairment | |
| Visuospatial memory | |||
| Delayed memory | RBANS Figure Recall | 3rd percentile | Severe impairment |
| Executive functioning | |||
| Cognitive flexibility | Trails B | 10th percentile | Severe impairment based on educational attainment |
| WCST | Low scores: Nonperseverative errors, perseverative errors, and categories completed | ||
| * Tests of mental status effort, visuomotor processing speed, confrontation naming, visuospatial function, attention, and executive functioning fluency/initiation were within normal limits | |||
| MMSE: Mini Mental State Exam; WRAT: Wide Range Achievement Test; RBANS: Repeatable Battery for the Assessment of Neuropsychological Status; WCST: Wisconsin Card Sorting Test | |||
The authors’ observations
Mr. L’s history, cognitive testing, head imaging, and behavioral observations suggest that several pathogenic factors contribute to his impaired functioning. First, he describes a TBI of unknown severity occurring in 1975. Although brain scans did not show evidence of midline shift or encephalomalacia, a direct blow to the head after falling from a height combined with possible post-injury seizures suggests a TBI of at least moderate severity.
Second, Mr. L describes an incident in which he required inpatient respiratory assistance. Although the precipitating medical event was unclear, anoxia or hypoxia is likely. A recent CT revealed low attenuation in the left temporal region that could represent an infarct.
Mr. L’s severe memory impairment and moderate to severe impairment in cognitive flexibility are commonly reported after a TBI of moderate severity. If an ischemic incident were the primary contributor, a lateralized pattern of cognitive dysfunction—which Mr. L does not exhibit—would be expected.
Although Mr. L likely has vascular dementia, his MRI findings do not indicate sufficient disease to account for his memory scores. Vascular dementia is associated with slow, stepwise cognitive deterioration, which is not consistent with severely impaired memory in a 56-year-old patient.
Finally, alcoholism is associated with cognitive difficulty in memory, visuospatial functioning, and abstract reasoning. Mr. L demonstrated significant difficulty in memory and abstract reasoning, but his visuospatial functioning was largely intact. In the absence of Wernicke’s encephalopathy, chronic alcoholics generally do not show memory decrements in line with Mr. L’s. His MRI results indicated only minimal ventricular and sulcal enlargement. Because atrophy is present in approximately 60% of chronic alcoholics, this finding provides evidence of a contribution, but the other contributory factors are associated with more definitive medical outcomes. Thus, alcoholism must be viewed as a secondary contributor to Mr. L’s impaired functioning.
Taking into account all known contributors, TBI emerges as the primary diagnosis.
Consider neurologic injury
Recognizing and characterizing personality changes related to neurologic injury and disease is often problematic and unreliable, even when psychometrically validated instruments and structured diagnostic interviews are used (Box 1).1-5 Mr. L’s presentation differed from the more commonly reported “impulsive aggression” associated with closed head injury. Sequelae from TBI were contributing to his clinical presentation but was obscured by his shallow and silly affect, inability to accurately assess social cues, and lack of empathy.
Mr. L reported suffering a head injury from falling off a ladder. Personality changes that result from traumatic brain injury (TBI) of the sudden deceleration type—even when mild—are frequently referable to the frontal lobe, especially focal orbital and/or ventromedial damage of the prefrontal cortex.1-5 This is because of the physical proximity of the sphenoid wing to the orbitofrontal region and effects of shearing.
As a result of this damage, patients lack insight into their accompanying cognitive and behavioral abnormalities, such as the egocentricity and impaired empathy shown by Mr. L. These changes might not be detected in clinical interviews and over brief periods.2 Appreciating an acquired personality disturbance may require evaluating the patient’s behavior over months or years.2
In retrospect, Mr. L’s seeking repeated inpatient psychiatric hospitalizations is consistent with poor planning and problem-solving skills. He has a limited repertoire of adaptive behaviors and has learned that suicidal gestures lead to admission and caretaking. These are important to him because he is frequently homeless. His lack of insight is seen in his unrealistic plans for employment in jobs requiring specialized technical skills.
Mr. L’s case emphasizes the importance of considering brain injury as an etiologic factor in personality changes. It also highlights the complex—and seemingly nonoverlapping—functions and dysfunctions of the frontal lobe, including:
- source memory
- working memory
- sustained attention
- conceptual fluidity
- imaginative thinking
- impulse regulation
- planning and problem-solving skills.
Documenting Mr. L’s cognitive deficits and acquired dementia diagnosis changed our staff’s perception of his behavior, enabling us to overcome negative countertransference (Box 2). We no longer regarded him as deliberately manipulative and refer him for appropriate treatment.
Countertransference can interfere with optimal workup and treatment of patients with character changes related to traumatic brain injury and neurodegenerative processes. When we interpreted Mr. L’s suicidal gestures and hospitalizations as manipulative and deliberate, we failed to appreciate the limited number of things he could do to obtain a safe and protective environment. We also failed to recognize that his poor planning and problem-solving skills—as well as lack of insight into his illness—prevented him from adhering to outpatient treatment.
Originally, we attributed Mr. L’s egocentricity, lack of empathy, and lack of adherence to axis II pathology.
Our staff’s hostile feelings toward Mr. L led us to insufficiently consider his history—which is consistent with cognitive decline—during biopsychosocial evaluation and treatment planning. Mr. L’s status as a frequently homeless, unemployed person reflects a sharp decline for a highly educated person who served as a Navy officer and performed radiation inspections on nuclear-powered vessels.
Outome: Residential placement
We realize Mr. L needs cognitive rehabilitation—including assistance with planning and problem solving—and arrange for his placement in a residential facility for this specialized rehabilitation. Mr. L receives supportive psychotherapy and cognitive remediation from a psychologist. He also is involved in incentive work therapy with a vocational rehabilitation specialist.
Related resource
- Silver, JM, McAllister TW, Yudofsky SC, eds. Textbook of traumatic brain injury. Washington, DC: American Psychiatric Publishing; 2005.
- Divalproex • Depakote
- Quetiapine • Seroquel
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
CASE: An unlikable patient
Mr. L, age 56, is admitted to the psychiatric unit at our Veterans Affairs Medical Center for active suicidal ideation; he has a history of self-injurious behaviors that include mutilation and overdose. He also has a history of alcohol dependence and multiple inpatient psychiatric admissions. He has never married and conflicts with his siblings—in whose home he has been staying—have led to frequent homelessness.
His affect is silly and shallow. He also shows signs of haughtiness, disinhibition, grandiosity, and confabulation. For example, he says that while in the Navy he had 82 sexual exploits and developed a drug that cured herpes.
We start Mr. L on divalproex, 1,500 mg/d, and quetiapine, titrated to 200 mg/d. After 3 days he is discharged, but this begins a cycle of repeated suicide gestures and readmissions—9 within the next 3 months. Each time he is discharged, Mr. L fails to follow through on treatment recommendations and is indifferent to our staff’s annoyed reactions.
The author’s observations
Some of our staff members regard Mr. L’s suicidal gestures as manipulative and feel angry and demoralized by his poor adherence to outpatient treatment plans. Their negative countertransference might have impacted how they evaluated Mr. L through repeated admissions and discharges. During Mr. L’s ninth admission, we decide to reevaluate his longitudinal history for clues to his noncompliant behavior.
History: Undocumented injury
Mr. L says he began drinking alcohol at age 16. He reports that he has grown marijuana but has not smoked it since 1991. He denies using heroin or other drugs.
Mr. L states that he suffered a head injury in 1975 after falling off a ladder on a Navy ship. He describes losing consciousness for a brief but uncertain duration. He reports that he has developed a seizure disorder since this fall and a history of amnesia secondary to past seizures. His medical records contain no witnessed seizures. Mr. L also says he was hospitalized a few years ago and placed on a ventilator for 7 days for an undetermined reason.
The authors’ observations
Based on Mr. L’s report of a possible traumatic brain injury (TBI), we order a neurologic evaluation. A year earlier, MRI of the brain without contrast demonstrated minimal, nonspecific periventricular and subcortical, punctuate hyperintensities on flair and T2 weighted sequences that are nonspecific. Overall, the impression was “diffuse involutional changes and mild nonspecific periventricular and subcortical white matter hyperintensities,” which might reflect covert vascular brain injury.
Our frustration over Mr. L’s repeated readmissions for suicidal gestures led us to seek outside evaluation and consultation from a senior psychiatrist for assistance with discharge and treatment planning. Unlike our staff, the consulting psychiatrist did not harbor strong negative feelings toward the patient.
Mr. L’s history of deterioration in psychosocial functioning prompted this psychiatrist to perform a thorough mental status examination that focused on cognitive elements and request formal neuropsychological testing.
Evalutation: Cognitive Deficits
During mental status examination, Mr. L has difficulty recalling 3 items and uses a memory strategy to assist himself. He fails to recollect in reverse order the last 5 U.S. presidents. He spells “world” backward, but has difficulty repeating 6 digits forward and 4 backward. He is unable to do serial 7 subtractions from 93 to 65 correctly. He adequately copies interlocking pentagons and draws a clock with the correct time. He achieves a score of 28/30 on the Folstein Mini Mental State Exam, missing the date by 4 days and recalling 2 of 3 words.
These results suggest Mr. L has difficulty with attention and working memory, short-term memory, fund of general information and long-term memory, and ability to perform simple calculations. Most important, they indicate the need for further study, especially a neuropsychological test battery.
Mr. L’s abnormal neuropsychological test results are summarized in the Table. He manifests concretization of thought. His loss of conceptual fluidity is documented formally by measures of perseverative errors and categories completed on the Wisconsin Card Sorting Test (WCST). These findings support a diagnosis of acquired dementia.
Table
Abnormal findings on Mr. L’s neuropsychological testing
| Cognitive domain | Test | Score | Interpretation |
|---|---|---|---|
| Mental status and effort | |||
| Mental status | MMSE total score | 28/30 | 2 of 3 items recalled after delay |
| Orientation | MMSE orientation questions | 9/10 | Date off by 4 days |
| Premorbid IQ estimate | WRAT-4 Reading Standard | 66th percentile | Within normal limits. Inconsistent with educational attainment, but could be impacted by temporal lobe findings |
| Verbal memory | |||
| Immediate memory | RBANS Immediate Memory Index (List and Story Learning) | 1st percentile | Severe impairment |
| Delayed memory | RBANS Delayed Memory Index | 1st percentile | Severe impairment |
| Recognition memory | List Learning | Severe impairment | |
| Visuospatial memory | |||
| Delayed memory | RBANS Figure Recall | 3rd percentile | Severe impairment |
| Executive functioning | |||
| Cognitive flexibility | Trails B | 10th percentile | Severe impairment based on educational attainment |
| WCST | Low scores: Nonperseverative errors, perseverative errors, and categories completed | ||
| * Tests of mental status effort, visuomotor processing speed, confrontation naming, visuospatial function, attention, and executive functioning fluency/initiation were within normal limits | |||
| MMSE: Mini Mental State Exam; WRAT: Wide Range Achievement Test; RBANS: Repeatable Battery for the Assessment of Neuropsychological Status; WCST: Wisconsin Card Sorting Test | |||
The authors’ observations
Mr. L’s history, cognitive testing, head imaging, and behavioral observations suggest that several pathogenic factors contribute to his impaired functioning. First, he describes a TBI of unknown severity occurring in 1975. Although brain scans did not show evidence of midline shift or encephalomalacia, a direct blow to the head after falling from a height combined with possible post-injury seizures suggests a TBI of at least moderate severity.
Second, Mr. L describes an incident in which he required inpatient respiratory assistance. Although the precipitating medical event was unclear, anoxia or hypoxia is likely. A recent CT revealed low attenuation in the left temporal region that could represent an infarct.
Mr. L’s severe memory impairment and moderate to severe impairment in cognitive flexibility are commonly reported after a TBI of moderate severity. If an ischemic incident were the primary contributor, a lateralized pattern of cognitive dysfunction—which Mr. L does not exhibit—would be expected.
Although Mr. L likely has vascular dementia, his MRI findings do not indicate sufficient disease to account for his memory scores. Vascular dementia is associated with slow, stepwise cognitive deterioration, which is not consistent with severely impaired memory in a 56-year-old patient.
Finally, alcoholism is associated with cognitive difficulty in memory, visuospatial functioning, and abstract reasoning. Mr. L demonstrated significant difficulty in memory and abstract reasoning, but his visuospatial functioning was largely intact. In the absence of Wernicke’s encephalopathy, chronic alcoholics generally do not show memory decrements in line with Mr. L’s. His MRI results indicated only minimal ventricular and sulcal enlargement. Because atrophy is present in approximately 60% of chronic alcoholics, this finding provides evidence of a contribution, but the other contributory factors are associated with more definitive medical outcomes. Thus, alcoholism must be viewed as a secondary contributor to Mr. L’s impaired functioning.
Taking into account all known contributors, TBI emerges as the primary diagnosis.
Consider neurologic injury
Recognizing and characterizing personality changes related to neurologic injury and disease is often problematic and unreliable, even when psychometrically validated instruments and structured diagnostic interviews are used (Box 1).1-5 Mr. L’s presentation differed from the more commonly reported “impulsive aggression” associated with closed head injury. Sequelae from TBI were contributing to his clinical presentation but was obscured by his shallow and silly affect, inability to accurately assess social cues, and lack of empathy.
Mr. L reported suffering a head injury from falling off a ladder. Personality changes that result from traumatic brain injury (TBI) of the sudden deceleration type—even when mild—are frequently referable to the frontal lobe, especially focal orbital and/or ventromedial damage of the prefrontal cortex.1-5 This is because of the physical proximity of the sphenoid wing to the orbitofrontal region and effects of shearing.
As a result of this damage, patients lack insight into their accompanying cognitive and behavioral abnormalities, such as the egocentricity and impaired empathy shown by Mr. L. These changes might not be detected in clinical interviews and over brief periods.2 Appreciating an acquired personality disturbance may require evaluating the patient’s behavior over months or years.2
In retrospect, Mr. L’s seeking repeated inpatient psychiatric hospitalizations is consistent with poor planning and problem-solving skills. He has a limited repertoire of adaptive behaviors and has learned that suicidal gestures lead to admission and caretaking. These are important to him because he is frequently homeless. His lack of insight is seen in his unrealistic plans for employment in jobs requiring specialized technical skills.
Mr. L’s case emphasizes the importance of considering brain injury as an etiologic factor in personality changes. It also highlights the complex—and seemingly nonoverlapping—functions and dysfunctions of the frontal lobe, including:
- source memory
- working memory
- sustained attention
- conceptual fluidity
- imaginative thinking
- impulse regulation
- planning and problem-solving skills.
Documenting Mr. L’s cognitive deficits and acquired dementia diagnosis changed our staff’s perception of his behavior, enabling us to overcome negative countertransference (Box 2). We no longer regarded him as deliberately manipulative and refer him for appropriate treatment.
Countertransference can interfere with optimal workup and treatment of patients with character changes related to traumatic brain injury and neurodegenerative processes. When we interpreted Mr. L’s suicidal gestures and hospitalizations as manipulative and deliberate, we failed to appreciate the limited number of things he could do to obtain a safe and protective environment. We also failed to recognize that his poor planning and problem-solving skills—as well as lack of insight into his illness—prevented him from adhering to outpatient treatment.
Originally, we attributed Mr. L’s egocentricity, lack of empathy, and lack of adherence to axis II pathology.
Our staff’s hostile feelings toward Mr. L led us to insufficiently consider his history—which is consistent with cognitive decline—during biopsychosocial evaluation and treatment planning. Mr. L’s status as a frequently homeless, unemployed person reflects a sharp decline for a highly educated person who served as a Navy officer and performed radiation inspections on nuclear-powered vessels.
Outome: Residential placement
We realize Mr. L needs cognitive rehabilitation—including assistance with planning and problem solving—and arrange for his placement in a residential facility for this specialized rehabilitation. Mr. L receives supportive psychotherapy and cognitive remediation from a psychologist. He also is involved in incentive work therapy with a vocational rehabilitation specialist.
Related resource
- Silver, JM, McAllister TW, Yudofsky SC, eds. Textbook of traumatic brain injury. Washington, DC: American Psychiatric Publishing; 2005.
- Divalproex • Depakote
- Quetiapine • Seroquel
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Tranel D. Functional neuroanatomy: neuropsychological correlates of cortical and subcortical damage. In: Yudofsky SC, Hales RE, eds. The American Psychiatric Publishing textbook of neuropsychiatry and clinical neurosciences. 4th ed. Washington, DC: American Psychiatric Publishing; 2002:71-113.
2. Barrash J, Tranel D, Anderson SW. Acquired personality disturbances associated with bilateral damage to the ventromedial prefrontal region. Dev Neuropsychol 2000;18(3):355-81.
3. Silver JM, Hales RE, Yudofsky SC. Neuropsychiatric aspects of traumatic brain injury. In: Yudofsky SC, Hales RE, eds. The American Psychiatric Publishing textbook of neuropsychiatry and clinical neurosciences. 4th ed. Washington, DC: American Psychiatric Publishing; 2002:625-72.
4. Damasio AR, Tranel D, Damasio HC. Somatic markers and the guidance of behavior: theory and preliminary testing. In: Levin HS, Eisenberg HM, Benton AL, eds. Frontal lobe function and dysfunction. Oxford, UK: Oxford University Press; 1991:217-29.
5. Prigatano GP. The relationship of frontal lobe damage to diminished awareness: studies in rehabilitation. In: Levin HS, Eisenberg HM, Benton AL, eds. Frontal lobe function and dysfunction. Oxford, UK: Oxford University Press; 1991:381-97.
1. Tranel D. Functional neuroanatomy: neuropsychological correlates of cortical and subcortical damage. In: Yudofsky SC, Hales RE, eds. The American Psychiatric Publishing textbook of neuropsychiatry and clinical neurosciences. 4th ed. Washington, DC: American Psychiatric Publishing; 2002:71-113.
2. Barrash J, Tranel D, Anderson SW. Acquired personality disturbances associated with bilateral damage to the ventromedial prefrontal region. Dev Neuropsychol 2000;18(3):355-81.
3. Silver JM, Hales RE, Yudofsky SC. Neuropsychiatric aspects of traumatic brain injury. In: Yudofsky SC, Hales RE, eds. The American Psychiatric Publishing textbook of neuropsychiatry and clinical neurosciences. 4th ed. Washington, DC: American Psychiatric Publishing; 2002:625-72.
4. Damasio AR, Tranel D, Damasio HC. Somatic markers and the guidance of behavior: theory and preliminary testing. In: Levin HS, Eisenberg HM, Benton AL, eds. Frontal lobe function and dysfunction. Oxford, UK: Oxford University Press; 1991:217-29.
5. Prigatano GP. The relationship of frontal lobe damage to diminished awareness: studies in rehabilitation. In: Levin HS, Eisenberg HM, Benton AL, eds. Frontal lobe function and dysfunction. Oxford, UK: Oxford University Press; 1991:381-97.