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Results for “Cognitive Dysfunction”

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PubMed1994

The P300 ERP component: an index of cognitive dysfunction in depression?

A number of measures of brain function have suggested that depression is associated with cerebral hypoactivity. This study examines the late components of the event-related potential (ERP), in particular the P300 component, in depression. The P300 component is thought to index the updating of neurocognitive models which are concerned with the prediction of future events. Cognitive theories of depression include the proposition that depression may be characterized by abnormalities in the prediction of future events. The P300 component may therefore provide one neurophysiological index of cognitive dysfunction in depression. Twenty-seven subjects (14 medicated, 13 drug-free) fulfilling DSM-III criteria for Major Depression were compared to 27 age- and sex-matched normal controls. The amplitudes and latencies of N100, P200, N200 and P300 ERP components, reaction time and task accuracy were recorded during a standard auditory discrimination task. No significant differences were found in any ERP component measure or in reaction-time between the groups. Depressed subjects performed the experimental task significantly less accurately than normal controls, but this was not reflected in the ERPs.

Antidepressive Agents, Tricyclic↗

PubMedDate not supplied

Age-dependent cerebral atrophy and cognitive dysfunction in SAMP10 mice.

Findings obtained from a series of studies to characterize age-dependent changes in brain morphology and behavior of inbred SAMP10 mice are reviewed. Following apparently normal development, SAMP10 mice developed brain atrophy with advancing age. The neocortex was diffusely atrophic in aged SAMP10 mice, with the frontal cortex being most affected. The entorhinal cortex, amygdala, and nucleus accumbens were also atrophic. Other subcortical structures were mildly atrophic, but the hippocampus was not atrophic. Mild to moderate hypertrophic astrocytosis was seen in the atrophied regions. Alzheimer's type pathology was not seen. The cortical atrophy was due to both loss and shrinkage of neurons. Brain atrophy was not remarkable in normal aging control SAMR10 mice. In accordance with above morphological changes, SAMP10 mice developed cognitive impairments with advancing age that were demonstrated by poor performance in passive avoidance and conditional avoidance tasks. All of these features of SAMP10 mice were inherited. SAMP10, therefore, is a unique model of age-dependent, inherited cerebral atrophy with cognitive dysfunction.

Aging↗

PubMed1996

Actual versus self-reported cognitive dysfunction in HIV-1 infection: memory-metamemory dissociations.

The relationship between subjective awareness and objective neuropsychological status in HIV-1 infection remains unclear. Forty-six HIV-1 seropositive males were administered a battery of neuropsychological measures assessing episodic memory, metacognition, and depression. Results of ANOVA revealed a dissociation between subjects' self-complaint of neuropsychological impairment and objective performance, with subjects who denied cognitive impairment performing worse on memory testing. Three subgroups were identified: A group whose self-reported cognitive impairment exceeded deficits demonstrated on memory testing (37% of subjects); a group who denied impairment but evidenced deficits on memory testing (26% of subjects); and a group whose self-appraisal was consistent with performance (37% of subjects). These data suggest that self-report of cognitive dysfunction among HIV-1 infected subjects is frequently at variance with objective neuropsychological testing and that diminished awareness of decline among medically symptomatic HIV-1 infected subjects can be identified.

Acquired Immunodeficiency Syndrome↗

PubMed2001

[Reduced metabolism in cerebral cortex correlates with MRI changes and cognitive dysfunction in patients with disseminated sclerosis].

INTRODUCTION: Magnetic resonance imaging (MRI) lesion load is widely used in the clinical evaluation of patients with multiple sclerosis (MS), but little is known about the associated changes in cortical activation. For this purpose, we studied the association between the corticocerebral metabolic rate of glucose (CMRglc) and the MRI T2-weighted total lesion area (TLA). In addition, we investigated the correlation between cognitive and neurological disability and CMRglc. METHODS: Twenty-three patients with clinically definite MS underwent measurements of the CMRglc, TLA, motor-evoked potentials (MEP), and cognitive and neurological disability. CMRglc was calculated with positron emission tomography (PET) and 18-F-deoxyglucose (FDG) and compared to that of nine healthy controls. RESULTS: A reduction in CMRglc (p < 0.01) was found in cortical global and regional lobar measurements. Furthermore, regional CMRglc (rCMRglc) was reduced in the dorsolateral prefrontal cortex, orbitofrontal cortex, caudate, putamen, thalamus, and hippocampus. Global cortical CMRglc correlated with TLA (rho = -0.66; p = 0.001), and rCMRglc correlated with the regional lesion load in all cerebral lobes (p < or = 0.05). Global cortical CMRglc and cognitive disability were also correlated (rho = 0.58; p = 0.015), and stepwise regression analysis showed a significant association between rCMRglc of the right thalamus and cognitive performance, as well as the TLA. There was no correlation between CMRglc and neurological disability (expanded disability status scale [EDSS]) or MEP. CONCLUSION: Global and regional cortical CMRglc is significantly reduced in patients with MS compared to healthy controls. The reductions in CMRglc furthermore correlate with the TLA, as well as with cognitive dysfunction, which indicates that MRI white matter lesion burden has a deteriorating effect on corticocerebral neural function.

Adult↗

PubMed1981

Cognitive dysfunction and imipramine in outpatient depressive.

A group of moderately depressed, nonpsychotic outpatients had impaired performance on a short-term item-recognition memory task (compared with a group of matched normal controls) without evidence of impaired speed or attention on two simpler tasks. Compared with placebo, treatment with imipramine hydrochloride in a multiple crossover design using three-week treatment periods led to improved performance on the memory task without either clinically apparent improvement in depression or significantly improved performance on the other task rather than a specific impairment of short-term memory, but the data do support the presence of cognitive dysfunction in depression, even in ambulatory patients without substantial impairments of attention or motor functioning. The results also indicate that antidepressant drugs can produce improvement in cognitive function, possibly as a forerunner of clinical improvement.

Adult↗

PubMed1996

Incidental white-matter foci on MRI in "healthy" subjects: evidence of subtle cognitive dysfunction.

The clinical significance of incidental white-matter foci seen on MRI is controversial. Mainly using a computer-assisted neuropsychological test battery, we tested the hypothesis that there is a clinical correlate of these foci. We studied 41 individuals aged 45-65 years with no history of neurological or psychiatric disorder, in whom no indication of central nervous system abnormalities was found on standardised neurological examination. A computer-assisted neuropsychological test battery, with the advantage of precise measuring of both time and deviation (e.g. in position memory tests), and rating scales for emotional dysfunction were administered; selected soft neurological signs were assessed. In 16 subjects (39%) MRI showed high-signal foci in the white matter on spin-echo sequences. White-matter foci not adjacent to the lateral ventricles were found to be related to performance on immediate visual memory/visuoperceptual skills, visuomotor tracking/psychomotor speed and, to a lesser degree, learning capacity and abstract and conceptual reasoning skills. Subtle cognitive dysfunction would appear to be a clinical correlate of punctate white-matter foci on MRI of otherwise "healty" individuals.

Aged↗

PubMed1986

An unusual cluster of tardive dyskinesia in schizophrenia: association with cognitive dysfunction and negative symptoms.

Factors associated with the emergence or nonemergence of involuntary movements (tardive dyskinesia) during long-term neuroleptic treatment were investigated in an atypical, isolated population of 31 schizophrenic inpatients with an unusually high prevalence of this syndrome. Patients with involuntary movements could not be distinguished from those without such movements by general characteristics or conventional indices of neuroleptic or anticholinergic treatment. However, they were more likely to show either marked cognitive dysfunction or muteness. These findings support the proposal that, at least in schizophrenia, subtle organic changes may contribute to vulnerability to the emergence of involuntary movements.

Adult↗

PubMed2000

Dysfunctional cognitions in children with social phobia, separation anxiety disorder, and generalized anxiety disorder.

According to cognitive theories of anxiety, anxious adults interpret ambiguous situations in a negative way: They overestimate danger and underestimate their abilities to cope with danger. The present study investigated whether children with social phobia, separation anxiety disorder, and generalized anxiety disorder have such a bias, compared to a clinical and a normal control group. Children were exposed to stories in which ambiguous situations were described, and asked to give their interpretations, using open and closed responses. Results showed that anxious children reported more negative cognitions than control children. However, anxious children did not overestimate danger on the free responses, but they did judge the situations as more dangerous on the closed responses. Anxious children had lower estimations of their own competency to cope with danger than the control groups on both open and closed responses. The results indicate that children with anxiety disorders have dysfunctional cognitions about ambiguous situations.

Adolescent↗

PubMed1977

Schizophrenic cognitive dysfunction: a deficit in rule transfer.

This study examined conceptual rule learning (RL) deficit in male schizophrenic Ss categorized into three groups as defined by Whitaker Index of Schizophrenic Thinking (WIST). Ss were administered a conjunctive, disjunctive, conditional or biconditional rule learning task, WIST, and Shipley-Hartford Memory Scale. It was shown that: (a) the WIST reliably differentiates among three levels of thought disorder as reflected by a deficit in inter-problem transfer of rule learning; (b) certain WIST and Shipley parameters reliably predict RL performance; and (c) phenothiazine dosage levels show no influence on the WIST and no correlation with RL. The findings indicate that cognitive dysfunction in schizophrenics is evidenced by limited inductive reasoning, insufficient channel capacity for filtering out irrelevant information, and inability to gain from antecedent RL experience. Principal locus of schizophrenic thought disorder is examined within a stimulus encoding-information processing paradigm.

Adult↗

PubMed1994

Effect of hyperketonemia and hyperlacticacidemia on symptoms, cognitive dysfunction, and counterregulatory hormone responses during hypoglycemia in normal humans.

The brain usually depends almost exclusively on glucose for its energy requirements. During hypoglycemia associated with prolonged fasting or strenuous exercise, circulating ketone-body and lactate levels increase several-fold; in both situations, certain signs and symptoms of hypoglycemia are diminished. Therefore, to test the hypothesis that hyperketonemia or hyperlacticacidemia of the magnitude seen during certain clinical situations can substitute for glucose as an energy source for the brain and alter physiological responses to hypoglycemia, we assessed autonomic and neuroglycopenic symptoms, counterregulatory hormone responses, and cognitive function during standardized insulin-induced hypoglycemia in normal volunteers with and without infusion of beta-hydroxybutyrate (BOHB) or lactate designed to reproduce circulating levels of these substrates seen during prolonged fasting and strenuous exercise. Compared with paired control experiments, infusion of BOHB and lactate increased the glycemic threshold (required greater hypoglycemia for initiation) and reduced the magnitude of autonomic and neuroglycopenic symptoms, counterregulatory hormone responses, and cognitive dysfunction (all P < 0.05). The hypoglycemic threshold for autonomic symptoms increased from 3.8 +/- 0.1 to 3.1 +/- 0.2 mmol/l during BOHB infusion and from 3.7 +/- 0.1 to 2.8 +/- 0.1 mmol/l during lactate infusion, and the threshold for neuroglycopenic symptoms increased from 2.8 +/- 0.1 to 2.4 +/- 0.1 and 2.3 +/- 0.1 mmol/l, respectively. The magnitude for autonomic symptoms decreased from 12 +/- 2 and 11 +/- 1 to 6 +/- 2 and 4 +/- 1 during BOHB and lactate infusion, respectively. Neuroglycopenic synptoms decreased from 11 +/- 2 to 3 +/- 1 during both series of experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗

PubMed2000

Circumscribed cognitive dysfunction in middle-aged adults with type 2 diabetes.

OBJECTIVE: To examine the extent to which type 2 diabetes is associated with poorer performance on measures of learning, memory, psychomotor speed, and problem-solving in middle-aged adults. RESEARCH DESIGN AND METHODS: This cross-sectional study evaluated 50 adults (age range 34-65 years, mean 50.8) with type 2 diabetes and 50 demographically similar community control subjects without diabetes. Each subject received a thorough physical examination and a detailed neuropsychological assessment. Factor analysis was used to assign specific tests to 1 of 4 cognitive domains (learning, memory for stories, problem-solving, and psychomotor speed). Hierarchical regression analysis was used to identify demographic and biomedical variables associated with cognitive dysfunction. RESULTS: Learning, memory, and problem-solving skills were unaffected by type 2 diabetes. In contrast, psychomotor slowing was predicted by a diagnosis of diabetes (r2 change = 0.075, P < 0.002) with additional variance in psychomotor efficiency explained independently by HbA1 (r2 = 0.064, P < 0.003) and vibratory threshold (r2 = 0.112, P < 0.0001). The magnitude of psychomotor slowing on specific tests ranged from 12% (Digit Vigilance) to 23% (Grooved Pegboard). CONCLUSIONS: Middle-aged adults with type 2 diabetes manifest psychomotor slowing that is associated with poorer metabolic control, whereas learning, memory, and problem-solving skills appear to be largely intact. The development of psychomotor slowing may be a manifestation of a "central neuropathy" induced by chronic hyperglycemia.

Adult↗

PubMed1986

Behavioral impairments related to cognitive dysfunction in the autoimmune New Zealand black mouse.

The possibility that autoimmunological disorders involving neuronal constituents as autoantigens can result in measurable behavioral impairments prompted the behavioral analysis of the New Zealand black (NZB) mouse strain, known to have high levels of brain-reactive antibodies. Sensorimotor competence and performance in tasks requiring learning and memory were assessed in 7-10-month-old NZB and contrasted with those of CFW mice. The NZB mice showed pronounced deficits in performance of passive and active shock avoidance responses. These deficits could not be accounted for by the slight sensorimotor disadvantage of NZB mice relative to CFW mice. No difference between the two mouse strains was seen in passive avoidance behavior at 1.5 months of age. It is concluded that NZB mice display a behavioral deficit related to cognitive dysfunction and that autoimmune mechanisms may be involved in the etiology of this deficit. Such behavioral disturbances produced by an autoimmune mechanism may have relevance for the neurological declines observed in aging, since the incidence of autoimmune disorders increases markedly in old age.

Animals↗

PubMed1999

SPECT with 99mTc-HMPAO in subjects with HIV infection: cognitive dysfunction correlates with high uptake.

We prospectively studied a cohort of 25 HIV-1 infected individuals with no clinical signs of encephalopathy with 99mTc-HMPAO-SPECT. The findings were correlated with magnetic resonance imaging (MRI), neuropsychological testing and clinical staging aiming at the early diagnosis of HIV encephalopathy by single photon emission computed tomography (SPECT). A total of 25 matched seronegative controls were subject to neuropsychological testing only. A total of 24 patients and controls were monitored for 6-46 months (mean and median 26 months). No patients developed AIDS dementia complex during the study; 3 patients developed minimal symptoms (MSK classification stage 0.5). There was a significant decline in 99mTc-HMPAO uptake over time and neuropsychological abnormalities progressed. Unexpectedly, there was a correlation of high cortical and subcortical 99mTc-HMPAO uptake and low performance in cognitive dysfunction tests, indicating a possible inflammatory reaction in the brain with increased blood flow due to HIV infection. We conclude that, in non-demented HIV-infected individuals, both the 99mTc-HMPAO uptake and functional level slowly decrease over time, but the regional cerebral blood flow decrease could be masked by a direct HIV-induced inflammatory reaction in the brain, which gives a 99mTc-HMPAO hyperfixation.

AIDS Dementia Complex↗

PubMedDate not supplied

Classic conditioning and dysfunctional cognitions in patients with panic disorder and agoraphobia treated with an implantable cardioverter/defibrillator.

OBJECTIVE: A model for the development of anxiety disorders (panic disorder with or without agoraphobia) is needed. Patients with an implantable cardioverter/defibrillator (ICD) are exposed to repeated electric shocks. If the theory of anxiety development by aversive classic conditioning processes is valid, these repeated shocks should lead to an increased risk of anxiety disorders. To study this hypothesis, we retrospectively studied 72 patients after implantation of an automatic ICD. METHODS: Patients were assessed with the semistructured Diagnostic Interview of Psychiatric Disease 1 to 6 years after implantation of an automatic ICD. Panic disorder and/or agoraphobia was diagnosed in patients who fulfilled all DSM-III-R criteria for those conditions. RESULTS: Anxiety disorder developed in 15.9% of patients after ICD implantation. This was significantly related to the frequency of repeated defibrillation (shocks) to stop malignant ventricular arrhythmias. Dysfunctional cognitions are an additional vulnerability factor. CONCLUSIONS: The data support both the conditioning hypothesis and the cognitive model of anxiety development. These findings suggest that ICD patients are an appropriate risk population for a prospective study of the development of anxiety disorders.

Aged↗

PubMed2001

Treatment of cognitive dysfunction associated with Alzheimer's disease with cholinergic precursors. Ineffective treatments or inappropriate approaches?

The observations of the loss of cholinergic function in neocortex and hippocampus in Alzheimer's disease (AD) developed the hypothesis that replacement of cholinergic function may be of therapeutic benefit to AD patients. The different approaches proposed or tested included intervention with acetylcholine (ACh) precursors, stimulation of ACh release, use of muscarinic or nicotinic receptor agonists and acetylcholinesterase (AChE) or cholinesterase (ChE) inhibition. Inhibition of endogenous ACh degradation through ChE inhibitors and precursor loading were treatments more largely investigated in clinical trials. Of the numerous compounds in development for the treatment of AD, AChE and ChE inhibitors are the most clinically advanced, although clinical trials conducted to date did not always confirm a significant benefit of these drugs on all symptom domains of AD. The first attempts in the treatment of AD with cholinergic precursors did not confirm a clinical utility of this class of compounds in well controlled clinical trials. However, cholinergic precursors most largely used such as choline and phosphatidylcholine (lecithin) were probably not suitable for enhancing brain levels of ACh. Other phospholipids involved in choline biosynthetic pathways such as CDP-choline, choline alphoscerate and phosphatidylserine clearly enhanced ACh availability or release and provided a modest improvement of cognitive dysfunction in AD, these effects being more pronounced with choline alphoscerate. Although some positive results cannot be generalized due to the small numbers of patients studied, they probably would justify reconsideration of the most promising molecules in larger carefully controlled trials.

Age of Onset↗

PubMed2001

Cognitive dysfunction in patients with amyotrophic lateral sclerosis is associated with spherical or crescent-shaped ubiquitinated intraneuronal inclusions in the parahippocampal gyrus and amygdala, but not in the neostriatum.

Skeins or skein-like inclusions, one of the two types of ubiquitinated intraneuronal inclusions in amyotrophic lateral sclerosis (ALS), in the neostriatum are not specific to the disease, but it has not yet been determined whether the other, spherical or crescent-shaped inclusions (SCI) are pathognomonic. To clarify this and also to investigate whether the distribution of SCI in particular brain regions is associated with clinical parameters, we examined the occurrence of SCI in the brains of 24 patients with ALS and 94 controls. SCI in the neostriatum were specifically detected in 54% of the ALS cases, but not in any of the controls. No apparent phenotypic denominator, such as disease duration or the occurrence of dementia, correlated to the distribution of SCI in the neostriatum in ALS cases. On the other hand, the occurrence of SCI in both the second and third layers of the parahippocampal gyrus and amygdala was significantly correlated to the presence of dementia in ALS cases. SCI were distributed in association with each other among the parahippocampal gyrus, dentate gyrus of the hippocampus and amygdala, but not between the spinal anterior horn and any non-motor-associated brain regions. These findings suggest that these particular brain regions might be significantly involved in the neurodegenerative process associated with ALS. The relationship of SCI to either ALS pathogenesis or cognitive dysfunction depends on the brain regions in which they are distributed, and this indicates that the neurodegenerative processes in ALS proceed differentially in particular motor-associated and nonmotor-associated brain regions.

Aged↗

PubMed1998

Tinnitus Cognitions Questionnaire: Development and Psychometric Properties of a Measure of Dysfunctional Cognitions Associated with Tinnitus.

The development of the Tinnitus Cognitions Questionnaire (TCQ), a scale designed to assess positive and negative cognitions associated with tinnitus, is described. Psychometric analyses of the TCQ are examined, with a total of 189 subjects from three separate samples. The results indicate good test-retest reliability (r = 0.88) and internal consistency (Cronbach's alpha = 0.91). Factor analysis revealed two factors that were interpreted as positive cognitions and negative cognitions. TCQ negative items and positive items were found to be unrelated (r = 0.09). Correlations between the TCQ and other self-report indices of depression, automatic negative thoughts, and tinnitus-specific symptomatology are reported. The TCQ may provide a useful index of the cognitive responses of tinnitus sufferers and may be employed as a measure of change in outcome research on psychological management of tinnitus.

Journal Article↗

PubMedDate not supplied

Clozapine-induced cognitive dysfunction in mice.

The atypical antipsychotic clozapine was examined for its ability to interrupt cognitive functions in mice on passive avoidance paradigm and elevated plus maze. The posttraining intraperitoneal injection of clozapine (0.1-7.5 mg/kg) induced dysfunction in acquisition as well as retrieval, which was reversed by physostigmine (0.05 mg/kg). Clozapine showed dose-related effects on scopolamine-induced cognitive dysfunction, with higher doses having no significant effect and lower doses reversing the dysfunction. These results are explained on the basis of clozapine's effects on central cholinergic receptors.

Animals↗