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J H Atkinson

Publications and source records attributed to J H Atkinson.

At least 19 recordsLinked to original sources
PubMed1999

Cortical synaptic density is reduced in mild to moderate human immunodeficiency virus neurocognitive disorder. HNRC Group. HIV Neurobehavioral Research Center.

Dendritic and synaptic damage (without frank neuronal loss) may be seen in milder human immunodeficiency virus (HIV)-related cognitive disorders. Synapse volume estimates, performed by stereological methods, could enhance the ability to detect subtle neuronal changes that may accompany cognitive impairment in HIV infection. For the present study, synaptic density and neuronal number were assessed by combined stereology/confocal microscopy and these measures were then correlated with ante-mortem levels of cognitive performance in AIDS patients. Three-dimensional stereological measures showed a significant correlation between reduced synaptic density and poor neuropsychological performance. To evaluate the specificity of any observed associations, additional variables including viral burden, astrogliosis and number of calbindin-immunoreactive neurons were measured. Factor analysis of a set of neuropathological variables revealed two factors; one defined by synaptic density and volume fraction, calbindin pyramidal neuronal densities and viral burden; the second by astrocytosis and calbindin interneuron density. Only the first factor correlated significantly with neuropsychological functioning during life. It is concluded that a combination of factors including synaptic damage, specific neuronal loss and increasing viral load underlies HIV-associated cognitive impairment. As synaptic damage is potentially reversible, early diagnosis and treatment of mild cogntive disorders may improve functioning and prevent the progression of brain disease.

AIDS Dementia Complex↗
PubMed1998

Cerebrospinal fluid tau protein is not elevated in HIV-associated neurologic disease in humans. HIV Neurobehavioral Research Center Group (HNRC).

We measured the concentrations of the neuron-specific protein, tau, in the cerebrospinal fluid (CSF) of 32 neurologically characterized HIV-infected (HIVpos) subjects and nine matched seronegative (HIVneg) controls using a sensitive ELISA assay. Of 32 HIVpos subjects, nine had HIV-associated neurocognitive disorders, and nine had clinically diagnosed peripheral neuropathies. CSF tau levels in subjects with HIV-associated neurocognitive disorders were similar to those in HIVneg subjects (185 +/- 83 vs. 223 +/- 106 pg/ml; P = 57). CSF tau levels in HIVpos subjects with peripheral neuropathies did not differ from those without neuropathies (320 +/- 190 vs. 251 +/- 185; P = 23). In summary, CSF tau levels were not elevated in patients with HIV-associated neurologic disease.

AIDS Dementia Complex↗
PubMed1998

Randomized double-blind placebo-controlled trial of peptide T for HIV-associated cognitive impairment.

BACKGROUND: Cognitive impairment is a common consequence of human immunodeficiency virus (HIV) infection, and dementia is one of the diseases that defines the acquired immunodeficiency syndrome. Peptide T (d-ala-peptide-T-amide) has been reported to block the binding of gp120 to brain tissue and to protect neurons from the toxic effects of gp120 in vitro. In pilot studies, administration of peptide T to HIV-positive patients with cognitive impairment was associated with improvement in cognition and constitutional symptoms. OBJECTIVE: To determine whether the intranasal administration of peptide T would improve cognitive function of HIV-positive patients with cognitive impairment. PATIENTS AND METHODS: This was a 3-site, double-blind, placebo-controlled trial of peptide T given intranasally at a dosage of 2 mg 3 times a day for 6 months. Participants were HIV-seropositive persons with evidence of cognitive deficits on a screening test battery. Concomitant antiretroviral therapy was allowed. Randomization to the 2 study arms was balanced according to several stratification variables, such as CD4+ cell count, severity of cognitive impairment, and antiretroviral therapy at study entry. A comprehensive neuropsychological (NP) battery, which yielded 23 scores, was administered at baseline and the study end point. The primary outcome measure was a global NP score derived from the 23 standardized scores. The efficacy end point was the change in NP score at 6 months compared with baseline. Secondary efficacy measures were 7 cognitive domain scores and deficit scores of global and domain performance. The patients who completed the baseline and final NP evaluations (after at least 4 months in the randomized treatment arm) were included in the efficacy analyses. Additional analyses were conducted on subgroups of patients according to the CD4+ count and baseline NP deficit. The incidence of NP improvement in the 2 treatment arms was also compared. RESULTS: There was no statistically significant difference between the peptide T and placebo groups on the global NP change score, the individual domains, or the deficit scores. Because of an imbalance in the baseline CD4+ cell count between treatment arms, analyses were also adjusted for this variable. These CD4+-adjusted analyses suggested (P = .07; analysis of covariance [ANCOVA]) a greater improvement in the peptide T group. Subgroup analyses indicated a treatment effect for patients whose CD4 cell count was above 0.200 x 10(9)/L (200 cells/microL) at baseline. Moreover, peptide T treatment was associated with overall cognitive improvement in patients with baseline global deficit scores of at least 0.5, while overall deterioration was more common among the placebo group (P = .02; Mantel-Haenszel chi(2) test). CONCLUSIONS: Peptide T was not significantly different from placebo on the study primary end points. However, additional analyses indicated that peptide T may be associated with improved performance in the subgroup of patients with more evident cognitive impairment (ie, NP global deficit score > or = 0.5) or with relatively preserved immunological status (ie, CD4+ cell count > 0.200 x 10(9)/L).

AIDS Dementia Complex↗
PubMed1998

Progressive cerebral volume loss in human immunodeficiency virus infection: a longitudinal volumetric magnetic resonance imaging study. HIV Neurobehavioral Research Center Group.

OBJECTIVE: To compare rates and anatomical patterns of brain atrophy during 3 stages of human immunodeficiency virus (HIV) disease. DESIGN: Comparisons of multiple serial brain magnetic resonance images in men without HIV infection and HIV-infected men in Centers for Disease Control and Prevention (CDC, Atlanta, Ga) stages A, B, and C. SETTING: Longitudinal cohort study of the San Diego HIV Neurobehavioral Research Center, San Diego, Calif. PARTICIPANTS: Eighty-six HIV-1-positive (HIV-positive) and 23 HIV-negative men who were similar in age and risk group. The number of HIV-positive men in each CDC stage was as follows: A, 33; B, 19; C, 34. All HIV-positive men were free of clinically detectable opportunistic neurologic illness. MAIN OUTCOME MEASURES: Regional volumes of serial magnetic resonance images converted to standardized slope estimates of change in regional volumes of interest. RESULTS: Medically asymptomatic men (CDC stage A) and medically symptomatic men (CDC stage C) had more rapid loss of cortical tissues than did HIV-negative men as manifested by higher slopes (Tukey honestly significant difference test, P=.02 and P=.001, respectively) for cortical fluid volume. Accelerated ventricular volume enlargement occurred only in men with CDC stage C disease. Reduction in the volume of white matter was accelerated in participants with CDC stage C disease compared with participants with CDC stage A disease. Of the gray matter regions, only the caudate nucleus sustained accelerated volume loss during CDC stage C disease. Participants whose systemic disease progressed to a higher CDC stage had significantly accelerated ventricular volume increases and caudate atrophy. Rates of cortical and subcortical fluid volume increases and reductions in the volumes of white matter and the caudate nucleus were significantly related to the rate of decline in the CD4+ lymphocyte count. CONCLUSIONS: In the absence of cerebral opportunistic disease, HIV infection causes progressive atrophy within the gray and white matter in the brain. These changes were most severe in the most advanced stage of disease but were evident even in medically asymptomatic HIV-positive persons. Within the gray matter, the caudate nucleus exhibited progressive volume loss linked to disease stage and the rate of decline of the CD4+ cell count. Structural brain changes can begin in the early stages of HIV infection and accelerate during advanced illness.

Adult↗
PubMed1998

The contribution of job satisfaction to the transition from acute to chronic low back pain.

OBJECTIVE: To determine the extent to which job satisfaction predicts pain, psychological distress, and disability 6 months after an initial episode of low back pain (LBP). DESIGN: A longitudinal design was used to follow an inception cohort experiencing first-episode low back pain with assessment at 2 and 6 months after pain onset. SETTING: Urban medical center outpatient orthopedic clinic. PATIENTS: The consecutive sample was comprised of 82 men with initial-onset acute LBP (T6 or below, daily pain for 6 to 10 weeks). INTERVENTION: Usual orthopedic care. MAIN OUTCOME MEASURES: The primary study outcomes were pain (Descriptor Differential Scale, Visual Analog Scales); disability (Sickness Impact Profile, Quality of Well-Being); and psychological distress (Beck Depression Inventory, Hamilton Rating Scale for Depression, Automatic Thoughts Questionnaire); predictor variables were orthopedic impairment (Waddell Physical Impairment Index) and job satisfaction (Job Descriptive Index, Work APGAR). RESULTS: Measures of job satisfaction, pain, disability, and psychological distress at baseline and 6 months after pain onset were separately reduced into factors using principle components factor analysis. In hierarchical multiple regression analyses, baseline job satisfaction significantly predicted variance in outcome scores at 6 months after pain onset, beyond the variance explained by control factors (demographics; baseline pain, mood, and disability; orthopedic impairment). Zero-order correlations between job satisfaction and orthopedic impairment were small and nonsignificant, suggesting that these two variables act independently in predicting outcome. Although type of work performed (desk work or work requiring light, moderate, or heavy lifting) and social position were correlated with job satisfaction at baseline, neither contributed to the prediction of outcome at 6 months. CONCLUSIONS: Satisfaction with one's job may protect against development of chronic pain and disability after acute onset back pain and, alternatively, dissatisfaction may heighten risk of chronicity. Vocational factors should be considered in the rehabilitation of acute back injury.

Acute Disease↗
PubMed1998

Transition to chronic pain in men with low back pain: predictive relationships among pain intensity, disability, and depressive symptoms.

Pain intensity, disability, and depressive symptoms are hallmarks of chronic pain conditions, but little is known about the relationships among these symptoms in the transition from acute to chronic pain. In this study, an inception cohort of men with low back pain (N = 78) was assessed at 2, 6, and 12 months after pain onset. At 6 months, pain intensity, disability, and depressive symptoms were predicted only by their respective levels at 2 months after pain onset. At 12 months, pain intensity and depressive symptoms were predicted by heightened disability at 6 months after pain onset; 12-month depressive symptoms also were predicted by 2-month disability. Pain intensity was not predictive of changes in disability or depressive symptoms. These findings suggest that functional disability plays a more prominent role than pain intensity in the transition from acute to chronic pain. A "failure to adapt" conceptual model is presented to account for these results.

Adolescent↗
PubMed1998

Treatment of major depression in HIV-seropositive men. HIV Neurobehavioral Research Center Group.

BACKGROUND: The purpose of this randomized double-blind, placebo-controlled study was to compare the efficacy and safety of fluoxetine plus group psychotherapy versus group psychotherapy alone in HIV-seropositive men (based on 1986 CDC classes II, III, and IV.C.2) who had been diagnosed with major depressive disorder (DSM-III-R). METHOD: During a 7-week trial, patients were treated with fluoxetine 20-60 mg or placebo 1-3 capsules per day and were seen in weekly supportive group psychotherapy. In addition, subjects were rated on the 17-item Hamilton Rating Scale for Depression (HAM-D-17), Clinical Global Impressions scales for Improvement (CGI-I) and Severity of Illness (CGI-S), and the short version of the Beck Depression Inventory (BDI-13). Of the 47 patients enrolled in the study, 25 were administered fluoxetine and 22 were given placebo. RESULTS: Subjects who received fluoxetine began to show significantly more improvement than patients who received placebo on both self- and observer-rated scales by the end of the first week of treatment. By endpoint, patients treated with fluoxetine experienced greater mean changes from baseline compared with placebo-treated patients on the HAM-D-17 (12.1 vs. 6.6; F = 6.53, df = 1,45; p < .05) and BDI-13 (5.9 vs. 1.2; F = 5.73, df = 1,45; p < .05), and a greater percentage of fluoxetine-treated patients experienced a > or = 50% in HAM-D-17 scores (64% vs. 23%; chi2= 8.60, df = 1, p < .01). Differences were particularly apparent in subjects whose initial depressive episodes were rated as severe (i.e., HAM-D-17 score > or = 24). Severely depressed patients treated with fluoxetine had an endpoint CGI-I of 1.4 compared with an endpoint CGI-I of 2.7 for patients treated with placebo (F = 6.02, df = 1,11; p < .05). Further, side effects were generally mild and transient. The most frequently noted effects reported by subjects treated with fluoxetine were nausea, dry mouth, headache, and diarrhea, in decreasing order of frequency. CONCLUSION: This study supports the efficacy and safety of fluoxetine over and above group psychotherapy for the treatment of HIV-associated major depression.

Adult↗
PubMed1997

Neurocognitive impairment is an independent risk factor for death in HIV infection. San Diego HIV Neurobehavioral Research Center Group.

OBJECTIVE: To determine if mortality is increased in individuals with human immunodeficiency virus type 1 (HIV-1)-associated neurocognitive disorders less severe than frank dementia. DESIGN: A prospective cohort study; median duration of follow-up was 2.4 years. Kaplan-Meier analysis and Cox proportional hazards models were used to compare survival times according to neurocognitive classification. SETTING: University-based research unit. PARTICIPANTS: A volunteer sample of 414 individuals seropositive for HIV-1. Subjects were classified at their baseline evaluation as neuropsychologically (NP) normal or abnormal (impaired in > or = 2 NP test domains). A subgroup of NP abnormal subjects met operational criteria for HIV-associated minor cognitive motor disorder; the remaining subjects were designated NP impaired. Subjects with frank dementia were excluded. MAIN OUTCOME MEASURE: Mortality. RESULTS: At the baseline evaluation, 256 (62%) of 414 subjects were designated normal; 109 (26%). NP impaired; and 49 (12%), minor cognitive motor disorder. One hundred six participants (26%) died during follow-up. Compared with the NP normal group, the unadjusted relative risk (RR) of death for all NP abnormal subjects (minor cognitive motor disorder and NP impaired) was significantly increased (RR, 1.7; 95% confidence interval [CI], 1.2-2.6; P < .005). After adjusting for concurrently measured predictors of survival (CD4 lymphocyte counts, Centers for Disease Control and Prevention HIV disease classification, hemoglobin concentration, and serum beta 2-microglobulin) in proportional hazards models, mortality for all NP abnormal subjects remained elevated (RR, 1.8; 95% CI, 1.2-2.8; P < .01). The elevation in mortality risk for subjects with minor cognitive motor disorder was statistically significant (RR, 2.2; 95% CI, 1.2-3.8; P < .01); for NP impaired subjects it was marginally significant (RR, 1.6; 95% CI, 1.0-2.8; P = .06). CONCLUSIONS: The HIV-infected individuals with NP impairment had a higher risk of dying than those without impairment. This was particularly true for those meeting syndromic diagnostic criteria.

Adult↗
PubMed1997

Cerebrospinal fluid human immunodeficiency virus type 1 RNA levels are elevated in neurocognitively impaired individuals with acquired immunodeficiency syndrome. HIV Neurobehavioral Research Center Group.

To determine whether cerebrospinal fluid (CSF) viral burden measurements can assist in the evaluation of human immunodeficiency virus (HIV)-associated neurocognitive disorders, we quantified HIV type 1 (HIV-1) RNA in CSF. Because previous findings suggested that disease stage, lymphocytic pleocytosis, and HIV-1 RNA levels in plasma may influence CSF viral burden, these variables were examined as potential modifying factors. HIV-1 RNA levels were quantified by using a reverse transcriptase-polymerase chain reaction assay. Performance on a comprehensive neuropsychological (NP) battery was noted in 97 prospectively enrolled, HIV-infected subjects. Among subjects with acquired immunodeficiency syndrome (AIDS) (<200 CD4+ lymphocytes), NP impairment was associated with significantly higher CSF RNA levels (3.1 vs 1.8 log10 copies/ml; p = 0.02); most impaired subjects met criteria for HIV-associated dementia or minor cognitive-motor disorder. In subjects without AIDS, CSF RNA and NP impairment were unrelated. Before AIDS, CSF RNA was strongly correlated to plasma RNA and to pleocytosis, but in AIDS, CSF and plasma RNA were independent. In conclusion, we found elevated CSF HIV-1 RNA levels in NP impaired subjects with AIDS. Before AIDS, systemic viral replication, possibly through CD4+ mononuclear cell trafficking, may govern virus levels in CSF, whereas in AIDS, CD4 cell depletion may unmask a correlation between increased productive central nervous system HIV infection and clinical neurocognitive disorders.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Dendritic injury is a pathological substrate for human immunodeficiency virus-related cognitive disorders. HNRC Group. The HIV Neurobehavioral Research Center.

To determine the neuropathological substrate of human immunodeficiency virus (HIV)-associated neurocognitive disorders, we examined persons with acquired immunodeficiency syndrome before their death and related their antemortem neuropsychological performance to postmortem indicators of HIV encephalitis, viral burden, and presynaptic and postsynaptic neuronal injury. Of 20 prospectively examined cases, 9 were neurocognitively normal, 5 showed neuropsychological impairment, 5 had minor cognitive/motor disorder, and 1 was demented. Degree of neurocognitive impairment was strongly related to the amount of dendritic simplification based on microtubule-associated protein 2 immunohistochemical staining, somewhat less so to a semiquantitative viral burden score based on numbers of HIV gp41-immunoreactive cells, and much less so to the presence of multinucleated giant cells or microglial nodules. It appears that even milder neurocognitive impairment reflects microneuroanatomical injury to synaptic structures.

AIDS-Related Opportunistic Infections↗
PubMed1997

The clinical significance of behavioral treatment for chronic low back pain: an evaluation of effectiveness.

The clinical effectiveness of behavioral treatment for chronic low back pain (CLBP) was evaluated using an empirical strategy to quantify individual patient change. Patients with CLBP (n = 17) presenting to an outpatient pain clinic were evaluated at baseline and six months posttreatment on variables of pain, disability and distress. Similar patients receiving usual medical care (n = 17) were evaluated on the same outcome measures and time line for purposes of descriptive comparison. Validated and widely-used measures of pain (McGill Pain Questionnaire), disability (Sickness Impact Profile), and depression (Beck Depression Inventory) served as outcome measures. Forty-seven percent of patients receiving behavioral treatment evidenced clinically significant improvement in at least one of the dimensions of pain, disability and depression associated with CLBP. However, clinically significant improvement across all three measures was rare. These findings are discussed in terms of the viability of behavioral treatment for CLBP, the need to enhance the degree of clinically significant outcome associated with behavioral treatments, and the value of empirical evaluation of clinically significant improvement following treatment interventions.

Adult↗
PubMed1997

The Quality of Well-Being scale in asymptomatic HIV-infected patients. HNRC Group. HIV Neural Behavioral Research Center.

We review applications of the Quality of Well-Being (QWB) scale for use in studies of human immunodeficiency virus (HIV)-infected patients. The QWB scale is a preference-weighted decision theory-based measure that summarizes outcomes in terms of quality-adjusted life years (QALYs). In order to validate the QWB scale for HIV-infected patients, the measure was administered in the University of California, San Diego (UCSD) HIV Neural Behavioral Research Center (HNRC). Data are presented for a cohort of 400 HIV-positive-infected men and 114 HIV-uninfected male controls. The evidence suggests that the QWB scale is a significant prospective predictor of mortality. The QWB scale was concurrently associated with the number of CD4+ lymphocytes and ratings of neurological impairment based upon clinical evaluations. Further, the QWB scale was related to neuropsychological assessments derived from formal tests of cognitive functioning. Neuropsychological impairments may be associated with income loss for affected patients. The QWB scale scores were lower among patients with clinical depression. We conclude that the QWB scale is an appropriate general health outcome measure for use in observational studies and clinical trials for patients with HIV disease.

Case-Control Studies↗
PubMed1997

Memory for verbal information in individuals with HIV-associated dementia complex. HNRC Group.

Patterns of memory performance were examined for 9 participants with HIV-associated dementia (HAD), 15 HIV-seropositive participants without dementia, and 15 HIV-seronegative controls. Episodic and semantic memory were assessed using the California Verbal Learning Test, the Boston Naming Test, and Verbal Fluency tests. The HAD group showed deficits in episodic memory, with relative sparing of semantic memory. In addition, results suggest a retrieval deficit in HAD rather than a deficit in retention of information. This pattern is consistent with the presence of a subcortical dementing process and supports findings from previous neuropathological, neuroimaging, and neuropsychological studies suggesting that subcortical brain dysfunction is frequently associated with HIV disease (e.g., Navia, Jordan, & Price, 1986).

AIDS Dementia Complex↗
PubMed1997

Neuropsychological performance of HIV-1 infected men with major depression. HNRC Group. HIV Neurobehavioral Research Center.

This study sought to determine if human immunodeficiency virus-type 1 (HIV-1) infected depressed men were more likely to be neuropsychologically impaired than their nondepressed counterparts. Subjects were 47 HIV-1 infected men who met DSM-III-R criteria for current major depressive disorder (MDD) and 47 HIV-1 infected nondepressed male controls (M age = 34.2 years) equated on HIV-1 disease severity, demographics, and drug use. The psychiatric interview included the Structured Clinical Inventory for the DSM-III-R, and Hamilton Rating Scale for Depression. The neuropsychological battery included tests covering 8 functional domains based on an expanded Halstead-Reitan Battery. The medical assessment included a history and physical examination, immunologic staging, and evaluation of prescription and recreational drug use. Prevalence of global neuropsychological impairment in the two groups (depressed vs. control) did not differ [53% vs. 38% respectively; chi 2(1, N = 94) = 2.11, p > .05]. While syndromically depressed patients performed less well than nondepressed individuals on memory tests [delayed retention portions of the Story Memory Test: F(1,91) = 5.34, p < .05; and Figure Memory Test: F(1,90) = 4.16, p < .05], the majority of depressed participants (64%) did not have clinically impaired memory. No relationship between neuropsychological impairment and severity of depression was observed. The results suggest that, while HIV-1 infected men with major depression may perform more poorly than nondepressed men on some aspects of memory tasks, they are not more likely to evidence clinically significant neurocognitive impairment.

Adult↗
PubMed1996

Social and psychological characteristics of HIV-infected women and gay men. HIV Neurobehavioral Research Center (HNRC) Group.

In this paper, we examine social and psychological characteristics of 60 HIV+ women and gay men, matched on age and stage of HIV infection. A discriminant function analysis was performed using measures of life adversity, psychological distress, and psychosocial resources. The best combination of predictors for distinguishing between HIV+ women and gay men was comprised of satisfaction with emotional support, network size, use of avoidant coping, Hamilton depression, and loneliness scores [chi 2(7) = 14.8, p < .05]. Women reported more satisfaction with emotional support, although gay men had larger social networks. Gay men used more avoidant coping and had higher lonelines scores as compared to women, although women reported more depressive symptoms. Utilizing this set of psychosocial variables, we correctly classified 73% of the HIV+ women and 67% of the HIV+ men. These findings suggest the importance of considering subgroup differences in the design of counseling programs for HIV+ individuals.

Adaptation, Psychological↗
PubMed1995

Sleep electroencephalogram delta-frequency amplitude, night plasma levels of tumor necrosis factor alpha, and human immunodeficiency virus infection.

We tested the hypothesis that increases in tumor necrosis factor alpha (TNF-alpha) induced by human immunodeficiency virus (HIV) are associated with the increases in slow-wave sleep seen in early HIV infection and the decrease with sleep fragmentation seen in advanced HIV infection. Nocturnal sleep disturbances and associated fatigue contribute to the disability of HIV infection. TNF-alpha causes fatigue in clinical use and promotes slow-wave sleep in animal models. With slow progress toward a vaccine and weak effects from current therapies, efforts are directed toward extending productive life of HIV-infected individuals and shortening the duration of disability in terminal illness. We describe previously unrecognized nocturnal cyclic variations in plasma levels of TNF-alpha in all subjects. In 6 of 10 subjects (1 control subject, 3 HIV-seropositive patients with CD4+ cell number > 400 cells per microliters, and 2 HIV-positive patients with CD4+ cell number < 400 cells per microliters), these fluctuations in TNF-alpha were coupled to the known rhythm of electroencephalogram delta amplitude (square root of power) during sleep. This coupling was not present in 3 HIV-positive subjects with CD4+ cell number < 400 cells per microliters and 1 control subject. In 5 HIV subjects with abnormally low CD4+ cell counts ( < 400 cells per microliters), the number of days since seroconversion correlated significantly with low correlation between TNF-alpha and delta amplitude. We conclude that a previously unrecognized normal, physiological coupling exists between TNF-alpha and delta amplitude during sleep and that the lessened likelihood of this coupling in progressive HIV infection may be important in understanding fatigue-related symptoms and disabilities.

Adult↗
PubMed1995

Is gender dysphoria dysphoric? Elevated depression and anxiety in gender dysphoric and nondysphoric homosexual and bisexual men in an HIV sample. HNRC Group.

Few if any studies before the AIDS epidemic suggested that male homosexuals may on average have higher levels of depression than male heterosexuals. However, several samples of homosexual and bisexual men in HIV studies suggest that depression and anxiety are high in these populations, and that this psychiatric morbidity began before the AIDS epidemic. We tested the hypothesis that high childhood gender nonconformity (CGN) is associated with depression and anxiety, and so might account for differences in these variables among samples of homosexuals. A total of 254 homosexual or bisexual male subjects were assessed for depression, anxiety, and associated symptoms using various self-report and interview measures, as well as for CGN (using the Freund Feminine Gender Identity scale, FGI). For comparison purposes only, we also evaluated the subjects for the DSM-III diagnosis of Ego-Dystonic Homosexuality. Highly gender nonconforming men (high FGI scores) were more likely to have current symptoms of anxiety and depression by self-report, and to have had a lifetime history of depression by clinical interview. This association was more often due to FGI items dealing with childhood than adulthood. When the FGI was broken into subscales by a prior factor analysis, stepwise regression suggested that the subscale measuring core gender identity nonconformity (so-called "gender dysphoria") was more reliably associated with depression and anxiety than were the factors measuring nonconformity in the areas of masculine and feminine gender roles, or genitoerotic (sexual) roles. This subscale was also the only FGI measure correlating with Ego-Dystonic Homosexuality. AIDS (CDC stage and HIV serostatus) and age did not account for these findings. We conclude that the often-reported higher levels of depression, anxiety, and associated symptoms among homosexual and bisexual men in AIDS studies are more common in the subgroup of such men who are gender dysphoric. Theoretical and clinical implications of these data are discussed.

Adult↗