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S Berent

Publications and source records attributed to S Berent.

At least 19 recordsLinked to original sources
PubMed2006

Cognition and behavior in children with benign epilepsy with centrotemporal spikes (BECTS).

Characteristics of cognitive deficits in benign childhood epilepsy with centrotemporal spikes (BECTS) remain unclear. The authors screened 200 BECTS children presenting for a clinical trial, finding relative weaknesses in fine motor control, visual learning, and attention in the presence of overall normal intellect, with simple partial seizures associated with more difficulty. Parental concerns for psychosomatic and learning problems were noted. Monitoring select cognitive and behavioral features in BECTS appears appropriate.

Anticonvulsants↗
PubMed2006

Chlorpyrifos exposure and biological monitoring among manufacturing workers.

AIM: To use biological monitoring data to evaluate the soundness of job based exposure classifications. METHODS: The authors studied 52 chlorpyrifos manufacturing workers and 60 referent workers to compare chlorpyrifos exposure estimations from job titles and work areas to urinary excretion of 3,5,6 trichloro-2-pyridinol (TCP), a metabolite of chlorpyrifos. Work history records and industrial hygiene monitoring data were used to establish cumulative interim exposure. Chlorpyrifos exposure during the study year was assessed biologically by urinary excretion of TCP. RESULTS: Exposure as measured by three urinary TCP samples was significantly higher among the chlorpyrifos workers (188 microg/l) than it was for the referent subjects (7 microg/l). Urinary TCP also correlated well with specific exposure categories of negligible (0.73-1.98 mg/m3 days), low (1.99-4.91 mg/m3 days), and moderate (4.92-15.36 mg/m3 days). The weighted Kappa coefficient was 0.80 (95% CI 0.72 to 0.87) for the mean TCP over the study period. CONCLUSIONS: The estimates of chlorpyrifos exposure based on job classifications and industrial hygiene measurements were significantly related to urinary TCP excretion, indicating that the ambient estimates are useful for providing exposure estimates among chlorpyrifos manufacturing workers.

Adult↗
PubMed2004

The effects of occupational exposure to chlorpyrifos on the peripheral nervous system: a prospective cohort study.

AIMS: To determine whether chronic occupational exposure to chlorpyrifos at levels associated with various aspects of manufacturing produced a clinically evident or subclinical peripheral neuropathy. METHODS: Clinical and quantitative nerve conduction study (NCS) examinations were performed on two occasions on chlorpyrifos manufacturing workers who had measurable chlorpyrifos exposure and a referent group. Baseline evaluations were performed on 53 of 66 eligible chlorpyrifos subjects and on 60 of 74 eligible referent subjects; one-year evaluations were completed on 111 of the 113 subjects evaluated at baseline. RESULTS: Chlorpyrifos and referent groups differed significantly in measures of 3,5,6 trichloro-2-pyridinol excretion and plasma butyrylcholinesterase (BuChE) activity, indicating substantially higher exposures among chlorpyrifos subjects. Few subjects had clinically important neurological symptoms or signs. NCS results were comparable to control values, and there were no significant group differences in NCS results at baseline, one year, or change over one year. No chlorpyrifos subject fulfilled conventional criteria for confirmed peripheral neuropathy at baseline or one-year examinations. The odds ratios for developing any diagnosable level of peripheral neuropathy among the chlorpyrifos subjects was not increased at baseline or at one year compared to referents at baseline. Mixed regression models used to evaluate subclinical group-by-time interactions showed numerous significant NCS differences attributable to near-nerve temperature differences among all subjects between the baseline and one-year examinations, but only a few disparate effects related to group. CONCLUSIONS: Chronic chlorpyrifos exposure during the manufacturing process sufficient to produce biological effects on BuChE activity was not associated with clinically evident or subclinical peripheral neuropathy at baseline or with measurable deterioration among chlorpyrifos subjects compared to referents after one year of additional exposure.

Adolescent↗
PubMed2002

Patterns of neuropsychological performance in multiple system atrophy compared to sporadic and hereditary olivopontocerebellar atrophy.

Although neuropsychological symptoms are associated with multiple system atrophy (MSA), sporadic olivopontocerebellar atrophy (sOPCA), and dominantly inherited olivopontocerebellar atrophy (dOPCA), the differences between these groups have not been explored. We compared 28 MSA patients on psychiatric rating scales and neuropsychological measures to 67 sOPCA patients, 42 dOPCA patients, and 30 normal controls. Patients with dOPCA, sOPCA, and MSA all exhibited significant deficits on motor-related tasks, as well as relatively mild deficits in cognitive functioning. Patients with MSA had greater neuropsychological dysfunction, particularly in memory and other "higher order" cognitive processes, than patients with either sOPCA or dOPCA.

Cognition Disorders↗
PubMed2001

Mild cognitive impairments predict dementia in nondemented elderly patients with memory loss.

BACKGROUND: Some elderly individuals exhibit significant memory deficits but do not have dementia because their general intellect is preserved and they have no impairments in everyday activities. These symptoms are often a precursor to Alzheimer disease (AD), but sometimes dementia does not occur, even after many years of observation. There is currently no reliable way to distinguish between these 2 possible outcomes in an individual patient. We hypothesized that clear impairments in at least 1 cognitive domain in addition to memory would help identify those who will progress to AD. OBJECTIVE: To determine whether nondemented patients with impairments in memory and other domains are more likely than those with memory impairment alone to develop AD. DESIGN AND METHODS: In a retrospective study, we evaluated 48 nondemented, nondepressed patients with clinical and psychometric evidence of memory impairment who were followed up for 2 or more years. Age-adjusted normative criteria were used to identify whether additional impairments were present in language, attention, motor visuospatial function, and verbal fluency at this initial evaluation. The presence or absence of dementia after 2 years and at the most recent neurological evaluation was compared in subjects with normal scores in all 4 of these cognitive areas apart from memory (M-) and those with impairment in 1 or more of these areas (M+). Outcomes were adjusted for age, intelligence at initial evaluation, and years of education. RESULTS: Of the 48 nondemented patients with memory loss, 17 met M- criteria, leaving 31 in the M+ group. Deficits in block design were the most frequent abnormality other than memory loss. At the 2-year follow-up, 1 M- subject (6%) had progressed to AD, whereas 15 (48%) of the M+ group had progressed to AD (P =.003). At the most recent follow-up (mean +/- SD, 4.0 +/- 2.0 years), 4 (24%) of the M- patients progressed to AD compared with 24 (77%) of the M+ patients (P<.001). CONCLUSIONS: Among nondemented elderly patients, memory loss alone rarely progresses to dementia in the subsequent 2 years. However, the risk of dementia is significantly increased among patients with clear cognitive impairments beyond memory loss. Further study is needed to determine whether patients with impairments limited to memory loss have a distinctive clinical course or pathophysiology.

Aged↗
PubMed2001

Evaluation of blink reflex results obtained from workers previously diagnosed with solvent-induced toxic encephalopathy.

We reviewed blink reflexes recorded from 51 railroad workers with long-term occupational exposure to solvents who were diagnosed by others with solvent-induced toxic encephalopathy. No worker fulfilled conventional clinical criteria for dementia or trigeminal mononeuropathy. All workers had normal R1 and R2 blink reflex latencies. R1 latencies correlated significantly with several nerve conduction measures, including F wave latencies, suggesting that some intersubject variability reflected intrinsic conduction properties, not isolated brain-stem function. Although normal, the workers' R1 latencies were significantly prolonged compared with historical control groups, including gender-matched control subjects of similar mean age (11.2 ms vs 9.9 ms; P < 0.0001). Stepwise multiple regression models demonstrated significant associations of R1 latency with age and use of CNS-active prescription medications (P = 0.003), but duration of occupational solvent exposure did not enter into the models. Paradoxically, workers using CNS-active medications had significantly shorter R1 latencies compared with workers not using such medications (10.9 vs 11.7 ms; P = 0.01). Job title, another potential surrogate measure of exposure, was not significantly related to reflex latencies. The geographical site of predominant solvent exposure did influence R1 latency, and workers from one site had longer exposure duration and longer R1 latencies than remaining workers. However, an interaction between age and exposure duration (r = 0.39; P = 0.003) confounded interpretation of this observation. Disability or work status, mental status findings, or classification of encephalopathy did not influence blink reflex latencies. The overall results do not support, but do not entirely exclude, a possible relationship between subclinical blink reflex abnormalities and occupational exposure to solvents. Nevertheless, it is clear from these results that the small group differences in R1 latency between exposed workers and control subjects are of no diagnostic importance and of uncertain physiologic importance, and they may reflect unrecognized confounders and technical factors.

Adult↗
PubMed2000

Controversies in neurotoxicology: current status.

Several controversial neurotoxic syndromes have received notoriety in the past several decades. For each, the controversy involves the most fundamental question about the existence of the disorder as a clinically diagnosable entity. Interestingly, the most controversial of these syndromes share several features, including argument about the existence of each syndrome in the courtroom. The authors focus their discussion on three problems (painter's encephalopathy, silicone breast implant neurotoxicity, and the Gulf War syndrome) for which no scientific consensus has been reached that would establish them as diagnosable disorders. These syndromes do not meet traditional disease criteria, and until a clear set of symptoms and objective signs can be defined, a definite course and clear cause demonstrated, and specific tests and treatments identified, these syndromes are likely to remain highly controversial.

Breast Implants↗
PubMed2000

Neurologic evaluation of workers previously diagnosed with solvent-induced toxic encephalopathy.

We examined 52 railroad workers with long-term occupational solvent exposures (average 22 years duration) who had been previously diagnosed by others as having solvent-induced toxic encephalopathy. All described episodes of transient intoxication associated with occupational solvent exposure. Persistent symptoms developed, an average, 16 years after exposure onset and included impaired memory (38), altered mood (21), imbalance (18), and headache (17). Thirteen workers had mild mental status abnormalities, but none fulfilled conventional clinical criteria for encephalopathy or dementia. None had abnormal blink reflex (51) or abnormal electroencephalographic (39) studies. Eight of 47 magnetic resonance imaging studies showed evidence of scattered ischemic lesions among workers with known diabetes mellitus (2), elevated blood pressure (4), or peripheral vascular disease (2). One magnetic resonance imaging scan showed mild cortical atrophy. In stepwise multiple linear and logistic regression models, no statistically significant (P < 0.05) dose-response relationships were found between exposure duration and symptoms or signs that were suggestive of encephalopathy. However, the number of symptoms (P < 0.001) and the number of signs (P = 0.05) were associated with current use of central nervous system-active medications. Further, lower Mini-Mental Status Examination scores were associated with a history of alcohol abuse (P = 0.01) and lower educational level (P = 0.03). The number of chief symptoms involving memory, mood, balance, or headache differed significantly among workers in different geographic sites (F(3.48) = 2.94, P = 0.04), a finding that was not explained by job title or exposure duration. There also was a significant (P = 0.0001) inverse relationship between initial exposure year (r2 = 0.60) or total years of exposure through 1987 (r2 = 0.56) and interval to major neurologic symptom onset, suggesting that factors other than solvent exposure account in part for worker complaints. We found no objective neurologic evidence supportive of toxic encephalopathy or any other uniform syndrome among these individuals, and most complaints were explained by neuropsychological factors or conditions unrelated to occupational solvent exposure.

Adult↗
PubMed1999

Decrease in cortisol reverses human hippocampal atrophy following treatment of Cushing's disease.

BACKGROUND: Decreased hippocampal volume is observed in patients with Cushing's syndrome and other conditions associated with elevated cortisol levels, stress, or both. Reversibility of hippocampal neuronal atrophy resulting from stress occurs in animals. Our study investigated the potential for reversibility of human hippocampal atrophy. METHODS: The study included 22 patients with Cushing's disease. Magnetic resonance brain imaging was performed prior to transsphenoidal microadenomectomy and again after treatment. RESULTS: Following treatment, hippocampal formation volume (HFV) increased by up to 10%. The mean percent change (3.2 +/- 2.5) was significantly greater (p < .04) than that of the comparison structure, caudate head volume (1.5 +/- 3.4). Increase in HFV was significantly associated with magnitude of decrease in urinary free cortisol (r = -.61, p < .01). This relationship strengthened after adjustments for age, duration of disease, and months elapsed since surgery (r = -.70, p < .001). There was no significant correlation between caudate head volume change and magnitude of cortisol decrease. CONCLUSIONS: Changes in human HFV associated with sustained hypercortisolemia are reversible, at least in part, once cortisol levels decrease. While many brain regions are likely affected by hypercortisolemia, the human hippocampus exhibits increased sensitivity to cortisol, affecting both volume loss and recovery.

Adult↗
PubMed1999

Absence of polyneuropathy among workers previously diagnosed with solvent-induced toxic encephalopathy.

An association between polyneuropathy and occupational exposure to trichloroethylene, trichloroethane, perchloroethylene, or similar solvents alone or in combination is controversial. We sought to determine whether workers previously diagnosed with solvent-induced toxic encephalopathy had objective evidence of polyneuropathy. Thirty railroad workers previously diagnosed with toxic encephalopathy were examined in the context of litigation against their employers. All described long-term occupational solvent exposure averaging 20 years in duration (range, 10 to 29 years) and producing acute intoxication on a regular basis. The diagnosis of subclinical or clinical polyneuropathy was established using a combination of symptoms, signs, and nerve conduction study (NCS) measures, consistent with standard clinical practice. Potential confounders were identified. NCS results were compared with historical controls, including unexposed workers matched by gender, age, and body mass index. Dose-response relationships were evaluated using simple linear and stepwise regression models. Three workers fulfilled clinical polyneuropathy criteria. The only worker fulfilling NCS criteria for confirmed clinical polyneuropathy had diabetes mellitus. Mean NCS values for most measures were similar to control values, and existing differences in sensory amplitudes disappeared when compared with the matched control group. NCS measures were not significantly influenced by exposure duration or job title. Separation into groups on the basis of the presence or absence of polyneuropathy symptoms, previous diagnosis of polyneuropathy, disability status, and severity or type of encephalopathy did not demonstrate significant NCS differences. The complaints of these workers claiming neurotoxic injury from occupational solvent exposure are not explained by peripheral nervous system dysfunction.

Adult↗
PubMed1997

Metabolic reduction in the posterior cingulate cortex in very early Alzheimer's disease.

This study investigated cerebral glucose metabolism in very early Alzheimer's disease, before a clinical diagnosis of probable Alzheimer's disease is possible, using [18F]fluorodeoxyglucose positron emission tomography. First, 66 patients with probable Alzheimer's disease with a spectrum of dementia severity (Mini-Mental State Examination score, 0-23) were recruited and studied. Cortical metabolic activity was analyzed topographically using three-dimensional stereotactic surface projections. Regression analysis was performed for each brain pixel to predict metabolic patterns of very early disease. Predictions were tested prospectively in a group of 8 patients who complained only of memory impairment without general cognitive decline (Mini-Mental State Examination score, 25 +/- 1) at the time of scanning but whose condition later progressed to probable Alzheimer's disease. Both results were compared to cerebral metabolic activity in 22 age-similar normal control subjects. Prediction and analysis of actual patients consistently indicated marked metabolic reduction (21-22%) in the posterior cingulate cortex and cinguloparietal transitional area in patients with very early Alzheimer's disease. Mean metabolic reduction in the posterior cingulate cortex was significantly greater than that in the lateral neocortices or parahippocampal cortex. The result suggests a functional importance for the posterior cingulate cortex in impairment of learning and memory, which is a feature of very early Alzheimer's disease.

Aged↗
PubMed1997

Unmasking the heterogeneity of Alzheimer's disease: case studies of individuals from distinct neuropsychological subgroups.

Case descriptions of patients with probable Alzheimer's disease (AD) who were reliably classified into three neuropsychological subgroups (global [GAD], right-hemisphere [RAD], and left-hemisphere [LAD]) in an earlier cluster analytic study (Fisher et al., 1996) are presented. Concordance between the neuropsychological patterns and clinical histories of randomly selected and hand-selected cases from within each subgroup was high. Longitudinal analysis revealed stable subgroup-specific neuropsychological progression patterns. Results are discussed in terms of future research avenues worth pursuing, in addition to the conceptual shift in research design necessary to uncover both quantitative and qualitative subgroup-specific ability differences.

Aged↗
PubMed1997

Cerebral metabolic differences in Parkinson's and Alzheimer's diseases matched for dementia severity.

UNLABELLED: Despite controversial clinicopathological distinctions between Parkinson's disease with dementia (PDD) and Alzheimer's disease (AD), similar patterns of metabolic reduction in the posterior brain were reported previously using PET with [18F]fluorodeoxyglucose. The current study was designed to examine more specific regional differences in cerebral glucose metabolism between PDD and AD using accurate and objective brain mapping techniques. METHODS: This study included nine normal subjects, nine PDD patients and nine AD patients. PDD and AD groups were matched carefully for age, sex and general dementia severity as measured by Mini-Mental State Examination and Clinical Dementia Rating scales. Each subject underwent [18F]fluorodeoxyglucose-PET and neuropsychological testing. After anatomic standardization of PET image sets and stereotactic data extraction, absolute and normalized cerebral metabolic rates were assessed by region of interest and pixel-by-pixel analyses. RESULTS: PDD and AD showed global glucose metabolic reduction with similar regional accentuation involving the lateral parietal, lateral temporal and lateral frontal association cortices and posterior cingulate cortex in comparison to normal controls. When comparing between PDD and AD, however, PDD showed greater metabolic reduction in the visual cortex and relatively preserved metabolism in the medial temporal cortex. CONCLUSION: Although a common feature of metabolic abnormalities in the posterior brain exists in PDD and AD, the presence of regional metabolic differences suggests different degrees and combinations of disease specific underlying pathological and neurochemical processes.

Aged↗
PubMed1996

Visual-spatial deficits expalin visual symptoms in Alzheimer's disease.

PURPOSE: To determine whether the visual symptoms of patients with Alzheimer's disease are related to visual-spatial dysfunction. METHODS: We administered a test battery modified from existing neuropsychometric materials that taxed visual-spatial skills, form identification, color vision, and visual memory. We tested 14 patients with Alzheimer's disease who had visual symptoms prominent enough to prompt ophthalmologic consultation, 11 patients with Alzheimer's disease who lacked such visual symptoms, and a control group of 53 subjects without Alzheimer's disease. The groups with Alzheimer's disease were matched for Wechsler Adult Intelligence Scale-Revised scores. RESULTS: Patients with Alzheimer's disease who had prominent visual symptoms differed significantly from those without prominent visual symptoms only in their relatively poor visual-spatial test scores. CONCLUSIONS: Visual symptoms in Alzheimer's disease are related primarily to visual-spatial deficits. These findings are consistent with previous evidence that patients with Alzheimer's disease who have prominent visual symptoms have accentuated histologic and metabolic abnormalities in the parieto-occipital regions known to process visual-spatial information. The findings support the view that pathways mediating visual-spatial and form identification are at least partially segregated in the brain, and emphasize that tests used to screen visually symptomatic patients with Alzheimer's disease will be more effective if they prominently assess visual-spatial skills.

Aged↗
PubMed1996

Neuropsychological subgroups of patients with Alzheimer's disease.

Neuropsychological data from 134 patients diagnosed with probable Alzheimer's disease (AD) were studied retrospectively to investigate whether subgroups of patients with qualitatively distinct profiles could be identified. Three empirical classification approaches were undertaken in this regard: Q-type factor analysis, hierarchical agglomerative cluster analysis, and iterative partitioning. Three subgroups were consistently identified across the clustering methods. Subgroup 1, the largest of the groups, was marked by moderate to severe anomia and constructional dyspraxia. Individuals in subgroup 2 displayed relatively spared visual-perceptual/constructional functioning but severe anomia. Members of subgroup 3 exhibited intact naming and nonverbal reasoning and moderate difficulty in copying overlapping figures. The three subgroups did not differ with respect to age, age at disease onset, duration of illness, educational level, or Hamilton depression rating. Detailed description of the data analyses are provided as a tutorial outlining subtyping methodology. Results are discussed in terms of the subgroup and the stage model approaches to the conceptualization of AD.

Aged↗
PubMed1996

Diminished glucose transport and phosphorylation in Alzheimer's disease determined by dynamic FDG-PET.

UNLABELLED: Using dynamic [18F]fluorodeoxyglucose (FDG) and PET, kinetic rate constants that describe influx (K1) and efflux (k2) of FDG as well as phosphorylation (k3) and dephosphorylation (k4) were determined in patients with probable Alzheimer's disease and similarly aged normal controls. METHODS: The regional cerebral metabolic rate for glucose (CMRglu) was calculated from individually fitted rate constants in frontal, temporal, parietal and occipital cerebral cortex, caudate nucleus, putamen, thalamus and cerebellar cortex. Dynamic PET scans were obtained in normal controls (n = 10, mean age = 67) and Alzheimer's disease patients (n = 8, mean age = 67) for 60 min following injection of 10 mCi of FDG. RESULTS: The Alzheimer's disease group was characterized by decreases of the CMRglu ranging from 13.3% in the frontal to 40.9% in the parietal cortex, which achieved significance in all regions except the thalamus. K1 was significantly reduced in the parietal (p < 0.01) and temporal cortices (p < 0.05). Significant declines in k3 were found in the parietal (p < 0.005), temporal and occipital cortex, and in the putamen and cerebellum (p < 0.05). The rate constants k2 and k4 were unchanged in the Alzheimer's disease group. CONCLUSION: These data suggest that hypometabolism in Alzheimer's disease is related to reduced glucose phosphorylation activity as well as diminished glucose transport, particularly in the most metabolically affected areas of the brain, the parietal and temporal cortex.

Aged↗
PubMed1995

Longitudinal neuropsychological and genetic linkage analysis of persons at risk for Huntington's disease.

OBJECTIVE: To determine (1) whether the neuropsychological profiles of healthy individuals at risk (AR) for Huntington's disease who were positive (AR/+) or negative (AR/-) for the Huntington's disease genetic marker differed from those of symptomatic patients with Huntington's disease and normal control individuals and (2) whether the neuropsychological performance of the two AR groups differed from each other on three assessments during a 4-year span. DESIGN: Case-control, double-blind study, with AR status determined by genetic linkage analysis (G8 probe), in addition to examination of trinucleotide repeats for most AR subjects. SETTING: The Neuropsychology Program in the Department of Psychiatry and the Department of Neurology at the University of Michigan Medical Center, Ann Arbor, a tertiary care center. PARTICIPANTS: Eight subjects matched as closely as possible for age, gender, and education in each of the following groups: AR/+, AR/-, normal control, and Huntington's disease. MEASURES: A battery of neuropsychological tasks, including measures of intelligence, memory, problem solving, and motor ability. RESULTS: Although both AR groups demonstrated variability on select intellectual subtests relative to normal subjects, they did not differ from each other on the three assessments during a 4-year span. Patients with Huntington's disease performed more poorly than the other groups across a range of neuropsychological measures. CONCLUSIONS: These results do not support previous evaluations concluding that AR/+ individuals demonstrate cognitive impairments as compared with AR/- individuals. Findings in earlier studies without genetic linkage analysis of lower performance of AR individuals, including children, as compared with normal controls may relate to extraneous environmental and familial issues that interfere with intellectual development.

Double-Blind Method↗