PubMed Health⌕ Search

Biomedical subjects

F J Huff

Publications and source records attributed to F J Huff.

At least 37 records · Page 2Linked to original sources
PubMed1989

Automatic and attentional mechanisms of semantic priming in Alzheimer's disease.

Previous studies using a word-naming task have suggested that in demented patients, semantic priming results only from automatic spreading activation and not from attention-dependent processes. If this is true, then on a lexical-decision task where attention-dependent processes are a major source of the semantic-priming effect, demented patients should show little or no priming. To test this prediction, three groups of 16 subjects (young and normal-old individuals and patients with Alzheimer's disease) were given a Word-Naming and a Lexical-Decision task. In both tasks, the amount of semantic priming (the difference in response time to a word preceded by a semantically unassociated vs. a semantically associated word) was determined. Demented patients showed significantly greater semantic priming than either normal group on both tasks. This result argues against the hypothesis that the semantic priming found in demented patients is due solely to automatic processes.

Adult↗
PubMed1988

Neuropsychological function in Alzheimer's disease. Pattern of impairment and rates of progression.

Although patients with Alzheimer's disease (AD) generally have impairments in multiple areas of cognitive function, there are those patients who appear to have neuropsychological deficits more prominent in one domain than in other domains. We examined the neuropsychological status of 86 patients with probable AD and 92 elderly control subjects and identified the patterns of impairments in the patients with AD. Independent deficits of visuoconstructional and lexical/semantic abilities were identified in a subset of patients by a principal components analysis. Individual patients were identified who were predominantly impaired in one, but not the other, neuropsychological domain. There were no striking relationships between the demographic characteristics of the patients and their pattern of deficits at the initial evaluation. There were no significant differences in age at onset or rate of progression of dementia among patients with different patterns of cognitive dysfunction. A review of the results of this and other studies suggests that the language impairment in AD may be associated with two distinct neuropsychological abnormalities: a lexical/semantic impairment that is unrelated to onset or progression of symptoms, and a syntactic impairment that may be associated with earlier onset and more rapid progression of dementia.

Aged↗
PubMed1988

Familial risk of dementia associated with a biologic subtype of Alzheimer's disease.

Increased platelet membrane fluidity is a stable familial trait that identifies a prominent subgroup of patients with Alzheimer's disease. Patients in this subgroup have distinct clinical features, including an early age at symptomatic onset and a rapidly progressive course. The morbid risk of Alzheimer's-type dementia was studied in 421 first-degree relatives of 43 patients who met current consensus criteria for probable Alzheimer's disease and 47 healthy controls. Relatives of patients showed an approximate 50% (90- to 95-year) lifetime risk of dementia, regardless of the platelet membrane phenotype of the respective proband, which was over four times the control value. However, relatives of patients with increased platelet membrane fluidity who developed dementia exhibited symptoms significantly earlier than relatives of patients with normal platelet membrane fluidity. Alternative genetic models that describe the relationship of platelet membrane fluidity and Alzheimer's disease are discussed.

Actuarial Analysis↗
PubMed1988

Cognitive function and platelet membrane fluidity in Alzheimer's disease.

Increased platelet membrane fluidity, as reflected by a decrease in the fluorescence anisotropy of diphenylhexatriene in labeled membranes, identifies a clinically distinct subgroup of approximately 50% of patients at our center who meet NINCDS-ADRDA clinical criteria for Alzheimer's disease. In the current study, we compared the cognitive impairments of patients in this subgroup to those observed in the residual subgroup of patients with Alzheimer's disease who had normal platelet membrane fluidity. No significant differences in the number or distribution of deficits in six cognitive domains were observed between the two subgroups. However, in the subgroup with increased platelet membrane fluidity, there were significantly more patients who exhibited dissociation of deficits on tests related to left and right parietal lobe function than in the residual subgroup. Moreover, the cases with dissociation of deficits consisted almost entirely of patients with deficits on tests reflecting left parietal lobe function and no deficit on tests of right parietal lobe function.

Aged↗
PubMed1988

A comparison of lexical-semantic impairments in left hemisphere stroke and Alzheimer's disease.

Patients with aphasia due to left hemisphere stroke and patients with Alzheimer's disease, who were matched for severity of naming impairment, were compared on tests of lexical-semantic processing. The results suggest that the lexical-semantic impairments in both groups are due to a combination of impaired access to, and loss of, lexical-semantic information, but that impaired access is more prominent in stroke patients, whereas Alzheimer's disease patients suffer a greater loss of information. The results are discussed in terms of a brain model of the storage and processing of lexical-semantic information, and with respect to implications for treatment strategies.

Aged↗
PubMed1988

Risk of dementia in relatives of patients with Alzheimer's disease.

Using a family history questionnaire, we investigated the occurrence of dementia among relatives of patients with a clinical diagnosis of Alzheimer's disease (AD) and among the relatives of age-matched control subjects. Cumulative lifetime risk of developing AD-type dementia was greater among relatives of AD probands and was consistent with an autosomal dominant genetic mode of transmission. Although the lifetime risk of AD-type dementia was similar among relatives of early-onset and late-onset AD probands, relatives of early-onset probands tended to have an earlier onset of dementia than did relatives of late-onset AD probands. This result raises the possibility that age at onset of dementia in AD may be genetically determined.

Actuarial Analysis↗
PubMed1987

The neurologic examination in patients with probable Alzheimer's disease.

Abnormal findings on a standardized neurologic examination were compared between patients with a clinical diagnosis of probable Alzheimer's disease (AD) and healthy control subjects. Aside from mental status findings, the most useful examination findings for differentiating AD from control subjects were the presence of release signs, olfactory deficit, impaired stereognosis or graphesthesia, gait disorder, tremor, and abnormalities on cerebellar testing. These abnormalities probably reflect the different areas of the central nervous system that are affected pathologically in AD. In the clinical diagnosis of AD, particular attention should be given to these aspects of the neurologic examination.

Aged↗
PubMed1987

Age at onset and rate of progression of Alzheimer's disease.

Age at onset, duration, and severity of dementia were evaluated in 165 patients with a clinical diagnosis of Alzheimer's disease. Rate of progression of dementia was determined in 77 patients by repeated administration of the Blessed Dementia Scale (BDS). The distribution of age at onset among patients was bimodal, with a division at about age 65. Duration of dementia at the time of initial examination was shorter, and rate of progression on follow-up examination was more rapid in senile-onset (age 65 or greater) than in presenile-onset (before age 65) cases. Considerable overlap among values for the two patient groups was observed for both variables, indicating that age at onset is not a strong predictor of rate of progression of dementia in patients with Alzheimer's disease.

Age Factors↗
PubMed1987

Cognitive deficits and clinical diagnosis of Alzheimer's disease.

We used cognitive deficits detected by neuropsychological testing to evaluate clinical diagnosis of Alzheimer's disease. Deficits were defined with respect to performance of control subjects according to procedural guidelines set by a NINCDS-ADRDA Work Group. The most frequent deficits were in recent memory and lexical-semantic language abilities. Clinical diagnosis of Alzheimer's disease was compared with diagnosis based on a criterion of two or more cognitive deficits both on initial neuropsychological testing and on testing repeated a year later in some subjects. Initial clinical diagnosis identified 96% of cases who met the criterion when first tested and 100% of those with multiple deficits at follow-up. Specificity with respect to the criterion was 86% on initial testing and 89% at follow-up. These findings support the validity of clinical diagnosis of Alzheimer's disease using the NINCDS-ADRDA criteria.

Aged↗
PubMed1986

Cholinesterases in cerebrospinal fluid. Correlations with clinical measures in Alzheimer's disease.

Acetylcholinesterase and butyrylcholinesterase activities in cerebrospinal fluid were measured in 17 patients with Alzheimer's disease and 6 control patients, as potential clinical measures of impaired cholinergic neurotransmission in Alzheimer's disease. The activity of butyrylcholinesterase was decreased in patients with Alzheimer's disease compared to that observed in control patients, but there was overlap between values in the 2 groups. Low butyrylcholinesterase activity was correlated with severity of dementia, memory impairment, and language disorder. Acetylcholinesterase activity was significantly correlated with visual contrast sensitivity, but not with dementia severity, and did not differentiate patients with Alzheimer's disease from control cases. These results suggest that cholinesterases in cerebrospinal fluid are related to brain cholinesterases, and indicate that the activities of acetylcholinesterase and butyrylcholinesterase should be distinguished in studies of cerebrospinal fluid.

Acetylcholinesterase↗
PubMed1986

Semantic impairment and anomia in Alzheimer's disease.

Impairment in naming visually presented objects was investigated in patients with a clinical diagnosis of Alzheimer's disease. Impaired object naming correlated with difficulty listing the names of objects from a specified semantic category and with erroneous selection of words semantically related to the correct names for objects in a name recognition test. These results suggest that patients with Alzheimer's disease have a semantic impairment characterized by inability to distinguish among objects that are members of the same semantic category, and that this impairment is associated with difficulty producing the names for objects. Semantic impairment was present in patients with normal ability to discriminate visually presented shapes, indicating that the semantic deficit in Alzheimer's disease occurs independently of abnormalities of visuospatial function. Patients tended to make errors on the same items in both confrontation naming and name recognition tests, suggesting that the semantic impairment in Alzheimer's disease involves loss of information about specific objects and their names.

Aged↗
PubMed1986

Neurological abnormalities associated with severity of dementia in Alzheimer's disease.

Abnormal findings on neurological examination were evaluated in 165 patients with a clinical diagnosis of Alzheimer's disease who attended a memory disorders clinic. Severity of dementia was measured by the Blessed Dementia Scale, and associations of abnormalities with dementia severity were evaluated using logistic regression. Presence of aphasia, apraxia, and primitive reflexes on neurological examination were strongly associated with severity, and weak associations were observed for abnormalities of muscle tone and gait. Among these associated neurological features, only aphasia and apraxia were present in mildly demented cases with sufficient frequency to suggest utility as diagnostic signs early in the course of the disease.

Alzheimer Disease↗
PubMed1986

Equivalent forms of the Boston Naming Test.

In order to develop a test of naming ability that is sensitive to changes in performance on repeated testing, but is unbiased by practice effects, the 85 items of the Boston Naming Test (BNT) were divided into two 42-item forms. Both forms were given to 15 healthy adult subjects, 24 patients with a clinical diagnosis of Alzheimer's disease, and 17 patients with other brain lesions. The reliability of the BNT was high as measured by coefficient alpha and interitem correlations. Performance on the two forms of the test was similar as indicated by mean scores and by correlations between scores. The BNT score includes uncued (spontaneous) and cued responses. When uncued responses were analyzed separately, the reliability and equivalence of the forms remained strong. Using uncued scores therefore does not alter the psychometric properties of the test, and considerably reduces administration time. The modification of the BNT described here should be useful in studies in which repeated measurements are obtained for the purpose of detecting changes in naming ability.

Alzheimer Disease↗
PubMed1985

Visual agnosia contrasted with visual-verbal disconnection.

Serial neuropsychological findings are contrasted in two cases: one with a syndrome of visual agnosia, the other with a disorder resulting from visual-verbal disconnection. Both patients were impaired in confrontation naming of objects and pictures, but the patient with visual-verbal disconnection was able to perform tasks of color-object matching and pantomime recognition, whereas the patient with visual agnosia could not do so, demonstrating a failure to establish meaningful nonverbal visual-visual association. Additionally, the performance of the patient with visual agnosia reflected an evolution from the apperceptive to associative forms of the disorder, suggesting that the various impairments of visual identification form a continuum of related disorders.

Agnosia↗