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Dive into the research topics where Gregory G. Brown is active.

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Featured researches published by Gregory G. Brown.


Journal of Clinical and Experimental Neuropsychology | 1979

The problem of premorbid intelligence in neuropsychological assessment

Robert S. Wilson; Gerald Rosenbaum; Gregory G. Brown

Abstract The aim of this study was to compare the utility of two methods of estimating premorbid IQ in the assessment of intellectual deterioration secondary to brain dysfunction. One estimate is based on demographic information, and the other is based on measures of present ability thought to be insensitive to brain dysfunction. Demographic and Wechsler Adult Intelligence Scale data were gathered for two groups: (1) 140 neurologic patients and (2) 140 nonneurologic subjects. This diagnostic dichotomy was regressed separately on two deterioration indices which differed only in the method used to estimate premorbid IQ. The index which relied on the demographic estimate was 11% more accurate than the present ability estimate in case classification. The results suggest that demographic information, when applied systematically, can provide a reasonably accurate and useful estimate of premorbid IQ.


Journal of Clinical and Experimental Neuropsychology | 1985

Analysis of covariance as a remedy for demographic mismatch of research subject groups: Some sobering simulations

Kenneth M. Adams; Gregory G. Brown; Igor Grant

Analysis of Covariance (ANCOVA) is often used in neuropsychological studies to effect ex-post-facto adjustment of performance variables amongst groups of subjects mismatched on some relevant demographic variable. This paper reviews some of the statistical assumptions underlying this usage. In an attempt to illustrate the complexities of this statistical technique, three sham studies using actual patient data are presented. These staged simulations have varying relationships between group test performance differences and levels of covariate discrepancy. The results were robust and consistent in their nature, and were held to support the wisdom of previous cautions by statisticians concerning the employment of ANCOVA to justify comparisons between incomparable groups. ANCOVA should not be used in neuropsychological research to equate groups unequal on variables such as age and education or to exert statistical control whose objective is to eliminate consideration of the covariate as an explanation for results. Finally, the report advocates by example the use of simulation to further our understanding of neuropsychological variables.


Journal of Clinical and Experimental Neuropsychology | 1997

Depression and memory in the elderly: A meta-analysis

Sandra S. Kindermann; Gregory G. Brown

A meta-analysis (N = 40) of the effects of depression on memory in the elderly (sample mean age > or = 55 years) examined variables potentially accounting for divergent findings in the literature. The distribution of effects was bimodal and the effect sizes were heterogeneous. Compared to controls, groups containing unipolar subjects only were significantly less impaired than were mixed unipolar-bipolar; five of six studies mixing depression subtype were associated with the more negative mode. Samples containing younger depressed subjects (< 45 years) were significantly more impaired and were associated with the more negative mode. Significant group differences were found between studies matching their comparison groups reasonably well on years of education and those that did not. Thoroughness of dementia screening yielded no group differences. Although correlated observations precluded significance tests, larger effects were found for (1) figural (vs. verbal) memory; (2) delayed (vs. immediate) memory; and (3) recognition (vs. free recall and incidental or cued recall; incidental and cued recall effects were nearly identical). Similar effects were found for composite memory scores versus constituent and for various presentation paradigms (e.g., single presentation, selective reminding). Effect sizes for these categories were in the moderate range. Difficulties synthesizing this literature are discussed as are suggested remedies and directions for future research.


Journal of the Neurological Sciences | 1996

Vascular pathology in three cases of progressive cognitive deterioration

Leonardo Pantoni; Julio H. Garcia; Gregory G. Brown

The clinical condition known as vascular dementia remains poorly defined. Few studies have attempted a correlative link between the clinical syndrome and the structural abnormalities of the brain. Classically the clinical progression of the vascular dementing process is thought to be a multi-step process punctated by repeated episodes of ischemia, that are clinically expressed as strokes. In most instances it has been assumed that the substrate of vascular dementias consists of atherothrombotic infarcts. The objective of this report is to illustrate 3 cases of progressive (rather than stepwise) cognitive deterioration without clinical evidence of stroke, evolving over a period of several years, in which there were prominent vascular lesions. A complete autopsy and detailed neuropathologic examination demonstrated cerebral vascular lesions involving small arterial vessels (< 200 microns in diameter). The lesions consisted of moderate-to-severe arteriolosclerosis in two cases, and mild-to-moderate arteriolosclerosis in a case of Alzheimers disease with severe cerebral amyloid angiopathy. Parenchymal lesions consisted of small cortical and subcortical infarcts, most of them smaller than 0.1 cm in average diameter, and subcortical leukoencephalopathy severe in two cases and mild-to-moderate in the third case. Severe atherosclerosis not accompanied by large infarcts was also present in one case. Arterial changes affecting small, distal branches causing sometimes small parenchymal lesions in association with diffuse cerebral white matter disease, appear to be the anatomical substrate that accompanies progressive cognitive impairment in some patients who are frequently diagnosed with Alzheimers disease because in their clinical records there is neither history of strokes nor stepwise progression of symptoms.


Journal of the Neurological Sciences | 1992

Vascular dementia: neuropathologic alterations and metabolic brain changes

Julio H. Garcia; Gregory G. Brown

After reviewing the concepts of dementia, in general, and vascular dementia, in particular, this review discusses potential future approaches that may contribute to an improved definition of the clinical syndrome and the neuropathological features of vascular dementia. Specific brain alterations in high-energy phosphate compounds, as measured by nuclear magnetic resonance, may contribute to the separation between dementias with neurodegenerative diseases and those with ischemic (vascular or hemodynamic) disorders.


Journal of Clinical and Experimental Neuropsychology | 1996

Impaired set-shifting in Parkinson's disease: New evidence from a lexical decision task

Cathleen McDonald; Gregory G. Brown; Jay M. Gorell

On a lexical decision (LD) task, participants quickly decide whether a target letter string is a word. When a target word (e.g., CARROT) is preceded by a category cue (e.g., VEGETABLE), participants respond more quickly than when the target is preceded by a semantically neutral cue (e.g., BLANK). Previously, Spicer, Brown, and Gorell (1994) reported that patients with PD, when tested with a variation of Neelys (1977) LD task, showed hyperpriming. That is, patients with PD exhibited a larger difference in reaction time between the neutral cue and category prime conditions than did controls. The present study found little evidence that PD hyperpriming was explained by difficulties accessing semantic information. Rather, hyperpriming appeared to be related to a general tendency among a subgroup of patients with PD to perseverate.


Journal of Clinical and Experimental Neuropsychology | 1994

Lexical decision in Parkinson disease: lack of evidence for generalized bradyphrenia.

Kevin B. Spicer; Gregory G. Brown; Jay M. Gorell

Twenty-two nondemented patients with idiopathic Parkinson disease (PD) and 22 controls completed a lexical decision task for which the expected relationship between primes and targets was manipulated. Both reaction times and movement times were measured. PD subjects were as effective as controls in utilizing the priming cues to reduce their reaction times compared with a neutral condition. This facilitation occurred even at the shortest stimulus onset asynchrony employed (300 ms), and was observed in a condition requiring a shift of attention, suggesting that PD patients experience no general cognitive slowing and no difficulty efficiently shifting attention to a specified semantic category. The degree of facilitation was significantly greater in the PD group in several comparisons, indicating hyperpriming. Finally, expectancy primes facilitated movement times in the PD group only. Although the results do not support the existence of generalized bradyphrenia in nondemented Parkinson disease, the hyperpriming effect and correlational analyses involving vocabulary scores and choice reaction time do raise the possibility of a subtle semantic processing deficit or an impairment of strategic decision-making in PD.


Psychopharmacology | 1992

Selective dissociations of sedation and amnesia following ingestion of diazepam

Jill B. Rich; Gregory G. Brown

Forty-eight healthy volunteers received 0.2 mg/kg oral diazepam or a placebo in a double-blind manner. The effect of the drug on memory was assessed by the free recall of unrelated word lists, and arousal was assessed by subjective ratings of drowsiness, multiple trials of a digit cancellation task, and the rate at which subjects rehearsed aloud items from the word lists. As expected, diazepam, depressed both memory functioning and all three measures of arousal. However, within the diazepam group, rehearsal rate was the only arousal measure that correlated with performance on the recall task. When looking at change scores, or the degree to which performance deteriorated from baseline to the diazepam condition, digit cancellation reduction was the only arousal measure that correlated with recall deterioration. Analyses also revealed that the three arousal measures did not correlate with each other. Results support the view that the arousal/attentional system is composed of partially independent subsystems with varying relationships to memory functioning.


Journal of Clinical and Experimental Neuropsychology | 1989

Memory functioning following a left medial thalamic hematoma.

Gregory G. Brown; Stuart Kieran; Suresh C. Patel

A patient with a discrete, left medial thalamic hematoma developed a severe anterograde amnesia. The memory deficit was most consistent for verbal materials, but was also observed on several tests of figural memory. The patient appeared to have a normal short-term memory (STM) capacity, performed normally on a STM distractor task and was not abnormally sensitive to proactive inhibition. This case is evidence that unilateral damage to the medial thalamus alone can produce a severe memory deficit.


Clinical Neuropsychologist | 1989

Neuropsychological signs of lateralized arteriovenous malformations: Comparison with ischemic stroke

Gregory G. Brown; Kevin B. Spicer; Wendy M. Robertson; Anne Dull Baird; Ghaus M. Malik

Abstract The accuracy of neuropsychological measures in classifying the laterality of arteriovenous malformations (AVMs) was compared with ischemic strokes. Seven commonly used neuropsychological tests were employed. Information obtained from these measures was studied using three techniques: discriminant function analysis (DFA), clinical judgment, and actuarial signs. Only clinical judgments were significantly related to laterality of AVMs for the complete sample. For all three methods, neuropsychological findings were significantly related to the laterality of ischemic stroke. When neuropsychological evidence of lateralized dysfunction was clearly evident, actuarial signs and clinical ratings were as accurate in classifying the laterality of AVMs as they were in classifying the laterality of ischemic stroke.

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Igor Grant

University of California

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