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MONTREAL — Comorbid antisocial personality disorder blunts the brain dysfunction associated with HIV/AIDS but also blunts the brain benefits associated with antiretroviral therapy, reported Lance Bauer, Ph.D., professor of psychiatry at the University of Connecticut, Farmington.
“There is good evidence that both ASPD [antisocial personality disorder] and HIV affect the same regions of the brain,” he said at the annual conference of the EEG and Clinical Neuroscience Society.
The prevalence of ASPD is disproportionately high in the HIV/AIDS population, with one study estimating it as high as 74%, making it important to screen for this psychiatric disorder, he said in an interview. The diagnosis of ASPD “may provide a context for the treatment plan. Such patients may require more frequent follow-ups to deal with compliance issues or may require a more structured approach for their treatment—for example, greater involvement of the spouse or family member, or simplifying the treatment regimen.”
In his published study, which he presented at the meeting, Dr. Bauer compared the effect of ASPD on brain function in 26 treated and 71 untreated HIV patients, compared with 68 seronegative controls using the P300 event-related potential (ERP) test (Neuropsychobiology 2006;53:17–25).
Using ERP, previous studies have shown increased P300 latency and decreased P300 amplitude associated with untreated HIV. These changes in P300 suggest a subtle underlying dysfunction in the brain that sometimes is accompanied by slowing of motor skills and information processing, as well as impaired attention or memory skills, according to Dr. Bauer. These abnormalities have been shown to be reversible with antiretroviral therapy.
Similarly, in ASPD patients, previous P300 ERP studies have revealed decrements in frontal brain structure and function.
Dr. Bauer's study confirmed previous findings in that ASPD was associated with frontal brain dysfunction, both in HIV-negative and HIV-positive patients on antiretroviral therapy.
But among untreated HIV patients, ASPD appeared to have no deleterious effect on brain function. “ASPD may initially compromise the function of this region to such a degree that the additional effects of untreated HIV/AIDS are blunted,” he suggested.
In addition, among HIV-positive patients, ASPD blunted the ability of antiretroviral therapy to reverse brain dysfunction. This is probably related to the effect of ASPD in diminishing the capacity of the nervous system “to respond to the presence of medications that would normally improve frontal brain function,” Dr. Bauer said.
MONTREAL — Comorbid antisocial personality disorder blunts the brain dysfunction associated with HIV/AIDS but also blunts the brain benefits associated with antiretroviral therapy, reported Lance Bauer, Ph.D., professor of psychiatry at the University of Connecticut, Farmington.
“There is good evidence that both ASPD [antisocial personality disorder] and HIV affect the same regions of the brain,” he said at the annual conference of the EEG and Clinical Neuroscience Society.
The prevalence of ASPD is disproportionately high in the HIV/AIDS population, with one study estimating it as high as 74%, making it important to screen for this psychiatric disorder, he said in an interview. The diagnosis of ASPD “may provide a context for the treatment plan. Such patients may require more frequent follow-ups to deal with compliance issues or may require a more structured approach for their treatment—for example, greater involvement of the spouse or family member, or simplifying the treatment regimen.”
In his published study, which he presented at the meeting, Dr. Bauer compared the effect of ASPD on brain function in 26 treated and 71 untreated HIV patients, compared with 68 seronegative controls using the P300 event-related potential (ERP) test (Neuropsychobiology 2006;53:17–25).
Using ERP, previous studies have shown increased P300 latency and decreased P300 amplitude associated with untreated HIV. These changes in P300 suggest a subtle underlying dysfunction in the brain that sometimes is accompanied by slowing of motor skills and information processing, as well as impaired attention or memory skills, according to Dr. Bauer. These abnormalities have been shown to be reversible with antiretroviral therapy.
Similarly, in ASPD patients, previous P300 ERP studies have revealed decrements in frontal brain structure and function.
Dr. Bauer's study confirmed previous findings in that ASPD was associated with frontal brain dysfunction, both in HIV-negative and HIV-positive patients on antiretroviral therapy.
But among untreated HIV patients, ASPD appeared to have no deleterious effect on brain function. “ASPD may initially compromise the function of this region to such a degree that the additional effects of untreated HIV/AIDS are blunted,” he suggested.
In addition, among HIV-positive patients, ASPD blunted the ability of antiretroviral therapy to reverse brain dysfunction. This is probably related to the effect of ASPD in diminishing the capacity of the nervous system “to respond to the presence of medications that would normally improve frontal brain function,” Dr. Bauer said.
MONTREAL — Comorbid antisocial personality disorder blunts the brain dysfunction associated with HIV/AIDS but also blunts the brain benefits associated with antiretroviral therapy, reported Lance Bauer, Ph.D., professor of psychiatry at the University of Connecticut, Farmington.
“There is good evidence that both ASPD [antisocial personality disorder] and HIV affect the same regions of the brain,” he said at the annual conference of the EEG and Clinical Neuroscience Society.
The prevalence of ASPD is disproportionately high in the HIV/AIDS population, with one study estimating it as high as 74%, making it important to screen for this psychiatric disorder, he said in an interview. The diagnosis of ASPD “may provide a context for the treatment plan. Such patients may require more frequent follow-ups to deal with compliance issues or may require a more structured approach for their treatment—for example, greater involvement of the spouse or family member, or simplifying the treatment regimen.”
In his published study, which he presented at the meeting, Dr. Bauer compared the effect of ASPD on brain function in 26 treated and 71 untreated HIV patients, compared with 68 seronegative controls using the P300 event-related potential (ERP) test (Neuropsychobiology 2006;53:17–25).
Using ERP, previous studies have shown increased P300 latency and decreased P300 amplitude associated with untreated HIV. These changes in P300 suggest a subtle underlying dysfunction in the brain that sometimes is accompanied by slowing of motor skills and information processing, as well as impaired attention or memory skills, according to Dr. Bauer. These abnormalities have been shown to be reversible with antiretroviral therapy.
Similarly, in ASPD patients, previous P300 ERP studies have revealed decrements in frontal brain structure and function.
Dr. Bauer's study confirmed previous findings in that ASPD was associated with frontal brain dysfunction, both in HIV-negative and HIV-positive patients on antiretroviral therapy.
But among untreated HIV patients, ASPD appeared to have no deleterious effect on brain function. “ASPD may initially compromise the function of this region to such a degree that the additional effects of untreated HIV/AIDS are blunted,” he suggested.
In addition, among HIV-positive patients, ASPD blunted the ability of antiretroviral therapy to reverse brain dysfunction. This is probably related to the effect of ASPD in diminishing the capacity of the nervous system “to respond to the presence of medications that would normally improve frontal brain function,” Dr. Bauer said.