Biomedical subjects

Victoria Di Sclafani

Publications and source records attributed to Victoria Di Sclafani.

7 recordsLinked to original sources

PubMed2006

Sub-diagnostic psychiatric comorbidity in alcoholics.

BACKGROUND: Psychiatric comorbidity in alcohol use disorders is clearly established, however most studies ignore data on psychiatric symptom counts that do not meet criteria for a diagnosis. We examined psychiatric symptom counts and psychological measures in the domains of anxiety, mood and externalizing pathology in 48 long-term abstinent alcoholics (LTAA) compared to 48 age/gender comparable light/non-drinking controls (NC). METHODS: Continuous measures of pathology (i.e., symptoms counts and psychological assessments) in each domain were compared between groups for: (1) all study participants, (2) excluding individuals with a lifetime psychiatric diagnosis in the domain, and (3) excluding individuals with a current psychiatric diagnosis in the domain. RESULTS: Psychiatric symptom counts and psychological pathology were greater in LTAA than NC. The differences between groups on these measures were not reduced by removal of individuals with lifetime or current diagnoses. CONCLUSIONS: The bulk of the difference between LTAA and NC in psychiatric illness was carried by sub-diagnostic psychopathology. In comparison to the limited view provided by using only symptomatology that meets criteria for a diagnosis, the use of continuous measures of psychiatric symptomatology and psychological abnormality yields a much more accurate picture of psychiatric illness co-occurring with alcoholism.

Alcoholism↗

PubMed2006

Statistical parametric mapping of brain morphology: sensitivity is dramatically increased by using brain-extracted images as inputs.

A major attraction of voxel-based morphometry (VBM) is that it allows researchers to explore large datasets with minimal human intervention. However, the validity and sensitivity of the Statistical Parametric Mapping (SPM2) approach to VBM are the subject of considerable debate. We visually inspected the SPM2 gray matter segmentations for 101 research participants and found a gross inclusion of non-brain tissue surrounding the entire brain as gray matter in five subjects and focal areas bordering the brain in which non-brain tissue was classified as gray matter in many other subjects. We also found many areas in which the cortical gray matter was incorrectly excluded from the segmentation of the brain. The major source of these errors was the misregistration of individual brain images with the reference T1-weighted brain template. These errors could be eliminated if SPM2 operated on images from which non-brain tissues (scalp, skull, and meninges) are removed (brain-extracted images). We developed a modified SPM2 processing pipeline that used brain-extracted images as inputs to test this hypothesis. We describe the modifications to the SPM2 pipeline that allow analysis of brain-extracted inputs. Using brain-extracted inputs eliminated the non-brain matter inclusions and the cortical gray matter exclusions noted above, reducing the residual mean square errors (RMSEs, the error term of the SPM2 statistical analyses) by over 30%. We show how this reduction in the RMSEs profoundly affects power analyses. SPM2 analyses of brain-extracted images may require sample sizes only half as great as analyses of non-brain-extracted images.

Adult↗

PubMed2006

Cognitive performance in long-term abstinent alcoholic individuals.

BACKGROUND: There are few investigations of the potential recovery of neurocognitive function in chronic alcoholic samples after very-long-term abstinence. The current study examined cognitive abilities in middle-aged (mean age 46.8 years), long-term abstinent alcoholic individuals (LTAA). Twenty-five LTAA men and 23 LTAA women abstinent for an average of 6.7 years were compared with an equal number of gender and age-comparable normal controls (NC). We examined the association of neurocognitive variables with age, duration of abstinence, alcohol use measures, and the density of a family history of problem drinking. METHODS: Long-term abstinent alcoholic individuals and NC underwent comprehensive neuropsychological assessment. Performance was measured in the following 9 domains: abstraction/cognitive flexibility, attention, auditory working memory, immediate memory, delayed memory, psychomotor function, reaction time, spatial processing, and verbal skills. RESULTS: Long-term abstinent alcoholic individuals performed similarly to NC, except for deficits in the spatial processing domain. The spatial processing results must be interpreted with caution because of multiple comparison issues; however, spatial processing deficits are among the impairments most often reported in abstinent alcoholic individuals. None of the cognitive measures were associated with length of abstinence, any alcohol use variable, or family history measure. CONCLUSIONS: Very-long-term abstinence resolves most neurocognitive deficits associated with alcoholism, except for the suggestion of lingering deficits in spatial processing.

Adult↗

PubMed2004

Controlling for premorbid brain size in imaging studies: T1-derived cranium scaling factor vs. T2-derived intracranial vault volume.

Intracranial vault (ICV) volume, obtained from T2-weighted magnetic resonance imaging (MRI), is generally used to estimate premorbid brain size in imaging studies. T1-weighted sequences lack the signal characteristics for ICV measurements [they have poor contrast at the outer boundary of sulcal cranium scaling factor (CSF)] but are valuable in imaging studies due to their excellent gray vs. white matter contrast. Smith et al. [NeuroImage 17 (2002) 479] suggested a T1-derived cranium scaling factor as an alternative control variable for premorbid brain size in cross-sectional studies. This index, which is computed using the SIENAX software, is a scaling factor comparing an individual's skull to a template skull derived from the Montreal Neurological Institute (MNI) average of 152 T1 studies (the MNI152). SIENAX computes coarsely defined estimates for the individual and MNI skulls rather than well-defined volumes. To test how well this approach would work as a control variable for premorbid brain size in cross-sectional studies, we compared the T1-derived cranium scaling factor to T2-derived ICV measurements in a sample of 92 individuals: 39 white males, 22 white females, and 31 African-American males, with an age range of 26-78 years. The correlation between T1- and T2-derived variables was 0.94 and did not differ across subject groups. The T1-derived cranium scaling factor accounted for a statistically significant portion (87%) of the variance of the T2-derived ICV measure and thus is a good surrogate for ICV measurement of premorbid brain size as a reference measure in MRI atrophy studies. Furthermore, neither race, sex, nor age accounted for any additional variance in ICV, indicating that neither race-, gender-, nor age-associated cranial bone thickness effects were present in this data set.

Adult↗

PubMed2004

Cerebral reserve capacity: implications for alcohol and drug abuse.

Cerebral reserve capacity (or functional reserve) refers to the brain's ability to maintain function when confronted by degenerative processes. Functional reserve can be estimated by several associated measures, including premorbid brain size, premorbid IQ, and level of education attained. There is accumulating evidence that the magnitude of reserve capacity is important in determining the onset and progression of the clinical manifestations of neurodegenerative brain diseases. Normal aging also whittles away at this cerebral reserve, and there may be a consequent unmasking of morbid effects that was not clinically evident when this compensatory reserve was sufficient. We review the evidence supporting this model for a number of degenerative brain processes, including Alzheimer's disease, presenile dementia, HIV dementia, aging, and chronic (multiyear) substance abuse. The concept of cerebral functional reserve has important implications for alcohol and drug abuse morbidity. First, given the high genetic contribution to substance abuse, there is an increased likelihood that the parents of substance abusers were substance abusers themselves. Substance abuse during pregnancy can inhibit brain growth, resulting in reduced brain size and reduced reserve capacity (and therefore less ability to compensate for loss of function later in life). Second, substance abuse is often coupled with poverty, and both substance abuse and poverty are associated with some of the same conditions that reduce brain growth. Finally, we comment on the most important public health implication of the cerebral reserve capacity model (vis-à-vis addiction).

Alcoholism↗

PubMed2002

Prefrontal cortical volume reduction associated with frontal cortex function deficit in 6-week abstinent crack-cocaine dependent men.

BACKGROUND: This study examined regional cortical volumes in 6-week abstinent men dependent on crack-cocaine only (Cr) or on both crack-cocaine and alcohol (CrA). Our goal was to test the a priori hypothesis of prefrontal cortical volume reduction, along with associated impairments in frontal mediated functions, and to look for differences between the Cr and CrA groups. METHODS: Structural magnetic resonance imaging (MRI) of the brain and neuropsychological assessment were performed on 17 6-week abstinent Cr subjects, 29 six-week abstinent CrA subjects, and 20 normal controls. Cortical volume was quantified in the prefrontal, parietal, temporal and occipital regions. RESULTS: Cr and CrA subjects showed comparable reductions in prefrontal gray matter volume compared to controls; this reduction was negatively associated with performance impairments in the executive function domain. CONCLUSIONS: Dependence on Cr (with or without concomitant alcohol dependence) was associated with reduced prefrontal cortical volume. Cr dependence with concomitant alcohol dependence was not associated with greater prefrontal volume reductions than Cr dependence alone. The existence of these findings at 6-week abstinence indicates that they are not a result of acute cocaine or alcohol exposure. The association of reduced prefrontal cortical volume with cognitive impairments in frontal cortex mediated abilities suggests that this reduced cerebral volume has functional consequences.

Adult↗

PubMed2002

Neuropsychological performance of individuals dependent on crack-cocaine, or crack-cocaine and alcohol, at 6 weeks and 6 months of abstinence.

BACKGROUND: Little data exist on the neuropsychological effects of crack-cocaine dependence or crack-cocaine and alcohol dependence. This study examined cognitive function in abstinent crack dependent and crack and alcohol dependent individuals at 6 weeks and 6 months abstinence. METHODS: a comprehensive neuropsychological battery, including the MicroCog computerized assessment, was administered to 20 abstinent crack dependent subjects, 37 abstinent crack and alcohol dependent subjects, and 29 normal controls. Depression was examined as a covariate, and the association between substance use variables and neuropsychological performance was examined. RESULTS: the two substance dependent groups had similar neuropsychological profiles at 6 weeks abstinent, with both groups exhibiting significant cognitive impairment in a wide range of functions compared to controls. The substance dependent groups were still impaired significantly at 6 months of abstinence. Only mild effects of depression on neuropsychological performance were observed. CONCLUSIONS: crack dependence and crack and alcohol dependence may lead to severe and persistent neuropsychological deficits over a wide range of domains. The strongest predictor of brain damage associated with substance dependence in this sample was dose (particularly quantity and duration of peak dose).

Adult↗