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1.
J Neurovirol ; 26(4): 530-543, 2020 08.
Article in English | MEDLINE | ID: mdl-32524422

ABSTRACT

We previously reported that neuropathic pain was associated with smaller posterior cingulate cortical (PCC) volumes, suggesting that a smaller/dysfunctional PCC may contribute to development of pain via impaired mind wandering. A gap in our previous report was lack of evidence for a mechanism for the genesis of PCC atrophy in HIV peripheral neuropathy. Here we investigate if volumetric differences in the subcortex for those with neuropathic paresthesia may contribute to smaller PCC volumes, potentially through deafferentation of ascending white matter tracts resulting from peripheral nerve damage in HIV neuropathy. Since neuropathic pain and paresthesia are highly correlated, statistical decomposition was used to separate pain and paresthesia symptoms to determine which regions of brain atrophy are associated with both pain and paresthesia and which are associated separately with pain or paresthesia. HIV+ individuals (N = 233) with and without paresthesia in a multisite study underwent structural brain magnetic resonance imaging. Voxel-based morphometry and a segmentation/registration tool were used to investigate regional brain volume changes associated with paresthesia. Analysis of decomposed variables found that smaller midbrain and thalamus volumes were associated with paresthesia rather than pain. However, atrophy in the PCC was related to both pain and paresthesia. Peak thalamic atrophy (p = 0.004; MNI x = - 14, y = - 24, z = - 2) for more severe paresthesia was in a region with reciprocal connections with the PCC. This provides initial evidence that smaller PCC volumes in HIV peripheral neuropathy are related to ascending white matter deafferentation caused by small fiber damage observed in HIV peripheral neuropathy.


Subject(s)
Atrophy/diagnostic imaging , Gyrus Cinguli/diagnostic imaging , HIV Infections/diagnostic imaging , Neuralgia/diagnostic imaging , Paresthesia/diagnostic imaging , Peripheral Nervous System Diseases/diagnostic imaging , Thalamus/diagnostic imaging , Adult , Aged , Atrophy/pathology , Atrophy/virology , Brain Mapping , Cross-Sectional Studies , Female , Gyrus Cinguli/pathology , Gyrus Cinguli/virology , HIV/pathogenicity , HIV Infections/pathology , HIV Infections/virology , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Neuralgia/pathology , Neuralgia/virology , Paresthesia/pathology , Paresthesia/virology , Peripheral Nervous System Diseases/pathology , Peripheral Nervous System Diseases/virology , Thalamus/pathology , Thalamus/virology , White Matter/diagnostic imaging , White Matter/pathology , White Matter/virology
2.
Pain Med ; 18(3): 428-440, 2017 03 01.
Article in English | MEDLINE | ID: mdl-27497320

ABSTRACT

Objective: . Despite modern antiretroviral therapy, HIV-associated neuropathy is one of the most prevalent, disabling and treatment-resistant complications of HIV disease. The presence and intensity of distal neuropathic pain is not fully explained by the degree of peripheral nerve damage. A better understanding of brain structure in HIV distal neuropathic pain may help explain why some patients with HIV neuropathy report pain while the majority does not. Previously, we reported that more intense distal neuropathic pain was associated with smaller total cerebral cortical gray matter volumes. The objective of this study was to determine which parts of the cortex are smaller. Methods: . HIV positive individuals with and without distal neuropathic pain enrolled in the multisite (N = 233) CNS HIV Antiretroviral Treatment Effects (CHARTER) study underwent structural brain magnetic resonance imaging. Voxel-based morphometry was used to investigate regional brain volumes in these structural brain images. Results: . Left ventral posterior cingulate cortex was smaller for HIV positive individuals with versus without distal neuropathic pain (peak P = 0.017; peak t = 5.15; MNI coordinates x = -6, y = -54, z = 20). Regional brain volumes within cortical gray matter structures typically associated with pain processing were also smaller for HIV positive individuals having higher intensity ratings of distal neuropathic pain. Conclusions: . The posterior cingulate is thought to be involved in inhibiting the perception of painful stimuli. Mechanistically a smaller posterior cingulate cortex structure may be related to reduced anti-nociception contributing to increased distal neuropathic pain.


Subject(s)
Gyrus Cinguli/pathology , HIV Infections/complications , Neuralgia/pathology , Neuralgia/virology , Adult , Aged , Female , Gray Matter , Humans , Image Interpretation, Computer-Assisted , Magnetic Resonance Imaging , Male , Middle Aged , Young Adult
3.
J Affect Disord ; 175: 475-80, 2015 Apr 01.
Article in English | MEDLINE | ID: mdl-25679203

ABSTRACT

Apathy and depression are inter-related yet separable and prevalent neuropsychiatric disturbances in persons infected with HIV. In the present study of 225 HIV+ persons, we investigated the role of an incident depressive episode in changes in apathy. Participants completed the apathy subscale of the Frontal Systems Behavior Scale during a detailed neuropsychiatric and neuromedical evaluation at visit 1 and again at approximately a 14 month follow-up. The Composite International Diagnostic Interview was used to obtain diagnoses of a new major depressive disorder. At their follow-up visit, participants were classified into four groups depending on their visit 1 elevation in apathy and new major depressive episode (MDE) status. Apathetic participants at baseline with a new MDE (n=23) were at risk for continued, clinically elevated apathy at follow-up, although severity of symptoms did not increase. Of the 144 participants without clinically elevated apathy at visit 1, those who developed a new MDE (n=16) had greater apathy symptomatology at follow-up than those without MDE. These findings suggest that HIV+ individuals, who do not as yet present with elevated apathy, may be at greater risk of elevated psychiatric distress should they experience a new/recurrent depressive episode. Thus, in the context of previous findings, it appears that although apathy and depression are separable constructs, they interact such that a new depressive episode is a risk factor for incident apathy.


Subject(s)
Apathy , Depressive Disorder, Major/psychology , HIV Infections/psychology , Depressive Disorder, Major/complications , Female , HIV Infections/complications , Humans , Longitudinal Studies , Male , Middle Aged , Neuropsychological Tests , Risk Factors
4.
J Neurovirol ; 20(3): 209-18, 2014 Jun.
Article in English | MEDLINE | ID: mdl-24549970

ABSTRACT

Despite modern antiretroviral therapy, HIV-associated sensory neuropathy affects over 50 % of HIV patients. The clinical expression of HIV neuropathy is highly variable: many individuals report few symptoms, but about half report distal neuropathic pain (DNP), making it one of the most prevalent, disabling, and treatment-resistant complications of HIV disease. The presence and intensity of pain is not fully explained by the degree of peripheral nerve damage, making it unclear why some patients do, and others do not, report pain. To better understand central nervous system contributions to HIV DNP, we performed a cross-sectional analysis of structural magnetic resonance imaging volumes in 241 HIV-infected participants from an observational multi-site cohort study at five US sites (CNS HIV Anti-Retroviral Treatment Effects Research Study, CHARTER). The association between DNP and the structural imaging outcomes was investigated using both linear and nonlinear (Gaussian Kernel support vector) multivariable regression, controlling for key demographic and clinical variables. Severity of DNP symptoms was correlated with smaller total cerebral cortical gray matter volume (r = -0.24; p = 0.004). Understanding the mechanisms for this association between smaller total cortical volumes and DNP may provide insight into HIV DNP chronicity and treatment-resistance.


Subject(s)
AIDS Dementia Complex/epidemiology , AIDS Dementia Complex/pathology , Magnetic Resonance Imaging , Neuralgia , AIDS Dementia Complex/drug therapy , Adult , Anti-Retroviral Agents/therapeutic use , Brain Injuries/epidemiology , Brain Injuries/pathology , Brain Injuries/virology , Cerebral Cortex/pathology , Cerebral Cortex/virology , Cognition Disorders/epidemiology , Cognition Disorders/pathology , Cognition Disorders/virology , Confounding Factors, Epidemiologic , Cross-Sectional Studies , Female , Gray Matter/pathology , Gray Matter/virology , Humans , Male , Mental Disorders/epidemiology , Mental Disorders/pathology , Mental Disorders/virology , Middle Aged , Neuralgia/epidemiology , Neuralgia/pathology , Neuralgia/virology , Prevalence , Risk Factors , Substance-Related Disorders/epidemiology , Substance-Related Disorders/pathology , Substance-Related Disorders/virology
5.
J Neurovirol ; 17(1): 3-16, 2011 Feb.
Article in English | MEDLINE | ID: mdl-21174240

ABSTRACT

Combination antiretroviral therapy (CART) has greatly reduced medical morbidity and mortality with HIV infection, but high rates of HIV-associated neurocognitive disorders (HAND) continue to be reported. Because large HIV-infected (HIV+) and uninfected (HIV-) groups have not been studied with similar methods in the pre-CART and CART eras, it is unclear whether CART has changed the prevalence, nature, and clinical correlates of HAND. We used comparable methods of subject screening and assessments to classify neurocognitive impairment (NCI) in large groups of HIV + and HIV - participants from the pre-CART era (1988-1995; N = 857) and CART era (2000-2007; N = 937). Impairment rate increased with successive disease stages (CDC stages A, B, and C) in both eras: 25%, 42%, and 52% in pre-CART era and 36%, 40%, and 45% in CART era. In the medically asymptomatic stage (CDC-A), NCI was significantly more common in the CART era. Low nadir CD4 predicted NCI in both eras, whereas degree of current immunosuppression, estimated duration of infection, and viral suppression in CSF (on treatment) were related to impairment only pre-CART. Pattern of NCI also differed: pre-CART had more impairment in motor skills, cognitive speed, and verbal fluency, whereas CART era involved more memory (learning) and executive function impairment. High rates of mild NCI persist at all stages of HIV infection, despite improved viral suppression and immune reconstitution with CART. The consistent association of NCI with nadir CD4 across eras suggests that earlier treatment to prevent severe immunosuppression may also help prevent HAND. Clinical trials targeting HAND prevention should specifically examine timing of ART initiation.


Subject(s)
AIDS Dementia Complex/drug therapy , AIDS Dementia Complex/epidemiology , Antiretroviral Therapy, Highly Active , HIV Infections/drug therapy , HIV Infections/epidemiology , HIV/pathogenicity , AIDS Dementia Complex/complications , Adult , Female , HIV Infections/complications , Humans , Longitudinal Studies , Male , Middle Aged , Prevalence , Treatment Outcome , Young Adult
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