Mapping cerebellar degeneration in HIV/AIDS

Klunder, Andrea D.; Chiang, Ming‐Chang; Dutton, Rebecca A.; Lee, Sharon E.; Toga, Arthur W.; López, Oscar L.; Aizenstein, Howard J.; Becker, James T.; Thompson, Paul M.

doi:10.1097/wnr.0b013e328311d374

Cited by 40 publications

(34 citation statements)

References 33 publications

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“…Our cross-sectional analyses confirm limited volumetric reductions in HIV-infected participants with cognitive impairment compared to healthy controls, including regions previously noted to be affected in the setting of HIV, such as the cerebellum, nucleus accumbens and brainstem. 36–38 These findings were driven by HIV-infected participants with HAND and we did not identify differences by HIV serostatus alone. Among the HIV infected group, the baseline volume of the nucleus accumbens and its association to executive functioning is notable.…”

Section: Discussionmentioning

confidence: 64%

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Progressive Brain Atrophy Despite Persistent Viral Suppression in HIV Patients Older Than 60 Years

Clifford

Samboju

Cobigo

et al. 2017

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Background Current HIV treatments are successful at suppressing plasma HIV RNA to undetectable levels for most adherent patients. Yet, emerging evidence suggests viral suppression will inadequately control inflammation and mitigate risk for progressive brain injury. We sought to quantify differences in longitudinal brain atrophy rates among older virally suppressed HIV-infected participants compared to that of healthy aging. Methods We examined longitudinal structural brain MRI atrophy rates employing region of interest assessments and voxel-wise tensor-based morphometry in HIV-infected participants over age 60 years (n=38) compared to age-matched HIV-uninfected healthy and cognitively normal controls (n=24). Results The mean age of participants was 63 years, the mean estimated duration of infection was 21 years and the median of duration of documented viral suppression was 3.2 years. Average proximal and nadir CD4 counts were 550 and 166, respectively; 15/38 (39%) met criteria for HIV-associated neurocognitive disorder. In models adjusting for age and sex, HIV serostatus was associated with more rapid average annualized rates of atrophy in the cerebellum (0.42% vs. 0.02%, p=0.016), caudate (0.74% vs. 0.03%, p=0.012), frontal lobe (0.48% vs. 0.01%, p=0.034), total cortical gray matter (0.65% vs. 0.16%, p=0.027), brain stem (0.31% vs. 0.01%, p=0.026), and pallidum (0.73% vs. 0.39%, p=0.046). Among those with HIV, atrophy rates did not differ statistically by cognitive status. Conclusion Despite persistent control of plasma viremia, these older HIV-infected participants demonstrate more rapid progressive brain atrophy when compared to healthy aging. Either HIV or other factors that differ between older HIV-infected participants and healthy controls could be responsible for these differences.

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Section: Discussionmentioning

confidence: 64%

“…The TBM analyses overcomes this limitation, consequently, a unique focal finding in the cerebellum emerged, consistent, in general, with the total cerebellar differences noted in our ROI examination and with extant literature. 36 …”

Section: Discussionmentioning

confidence: 99%

Progressive Brain Atrophy Despite Persistent Viral Suppression in HIV Patients Older Than 60 Years

Clifford

Samboju

Cobigo

et al. 2017

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…In cART-treated patients, imaging studies associate HIV infection with shrinkage of the basal ganglia, 18 thalamus, 19 hippocampus, 20 cerebellum, 21 cortex, 22 and white matter 19 ; i.e., brain regions in which we have identified volumetric reductions related to HIV DNA. Our findings of smaller brainstem and nucleus accumbens in the pooled HIV1 and D-HIV subjects are novel.…”

mentioning

confidence: 99%

Peripheral blood HIV DNA is associated with atrophy of cerebellar and subcortical gray matter

et al. 2013

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Objective: We evaluated regional brain volumes and cerebral metabolite levels as correlates of HIV DNA in peripheral blood mononuclear cells (PBMCs). Methods:In this cross-sectional study, 35 HIV1 subjects aged $40 years (25 with detectable PBMC HIV DNA; 10 with HIV DNA ,10 copies/10 6 cells, the threshold of detection) and 12 seronegative controls underwent structural brain MRI and magnetic resonance spectroscopy at 3 T. HIV1 subjects were on combination antiretroviral therapy $1 year; all but 1 had plasma HIV RNA ,50 copies/mL. We used logistic regression to evaluate relationships of likely predictor variables to the outcome of PBMC HIV DNA detectability in the HIV1 subjects. Effects of serostatus and HIV DNA on regional brain volumes (normalized to intracranial volume) and on metabolite ratios over creatine were evaluated by analyses of covariance, controlling for age.Results: Relative to the HIV1 group with undetectable HIV DNA, subjects with detectable HIV DNA demonstrated decreased volumes of cerebellar (214%, p 5 0.020) and total subcortical (210%, p 5 0.024) gray matter. Compared to healthy controls, only the detectable HIV DNA group showed significant (p , 0.05) enlargement of lateral ventricles and volumetric reductions of caudate, putamen, thalamus, hippocampus, nucleus accumbens, brainstem, total cortical gray matter, and cerebral white matter. Detectable HIV DNA was not associated with significantly altered cerebral metabolite levels. Glu 5 glutamate; HAND 5 HIV-associated neurocognitive disorders; ICV 5 intracranial volume; MI 5 myo-inositol; MRS 5 magnetic resonance spectroscopy; NAA 5 N-acetylaspartate; PBMC 5 peripheral blood mononuclear cell; PLSD 5 protected least significant difference; SN 5 seronegative; U-HIV 5 HIV1 infected subjects with undetectable peripheral blood mononuclear cells HIV DNA; VRS 5 Virchow-Robin spaces. Conclusion:

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“…In addition, there may be behavioral effects such as apathy and irritability. Psychomotor retardation (associated with damage to the frontal-striatal systems) also may occur [14,15]. The clinical severity of this process ranges from asymptomatic neurocognitive impairment (ANI), to a mild neuro-cognitive disorder (MND), to full-blown HIV-associated dementia (HAD) [16].…”

Section: Clinicalmentioning

confidence: 99%

“…MRS measures brain biochemistry, fMRI measures changes in blood flow related to neural activity in the brain, and morphometry models quantitative changes in neuroanatomical structures. These techniques also have been used to detect changes in the brains of asymptomatic HIV-1-positive patients [10,14,22]. …”

Section: Clinicalmentioning

confidence: 99%