SEARCH · PubMed Health

Results for “Cognitive Dysfunction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources

PubMed2005

Case of prolonged alcohol withdrawal syndrome accompanied with hyperthyroidsim.

Hyperthyroidism is associated with increased psychiatric morbidity. It may alter the clinical course of alcohol withdrawal syndrome. We report a 69 year old man who presented prolonged alcohol withdrawal syndrome associated with hyperthyroidism. Initially, he developed typical alcohol withdrawal syndrome including tremor, disorientation, delirium and visual hallucination of small animals. Thyroid function tests revealed a free triiodothyronine (T3) of 6.1 pg/dl (range, 3.0 to 5.8), a free thyroxine (T4) of 2.3 ng/dl (range, 0.85 to 2.15) and a thyroid stimulating hormone (TSH) of 0.003 microU/ml (range, 0.3 to 4.0), and thiamazole was administered. Even after a month, he continuously presented persecutory delusion, auditory hallucination and cognitive dysfunction. Although these symptoms did not respond to the medication including antipsychotics, they totally passed away after the thyroid function reached down to the normal level (free T3 3.0 pg/ml, free T4 1.1 ng/dl, TSH 0.004 microU/ml). In addition, cognitive function was recovered to the normal level as he scored 28/30 on the Mini Mental State Examination. We propose that hyperthyroidism contributed to the occurrence of psychotic symptoms and cognitive dysfunction.

Aged↗

PubMed2002

Emboli, inflammation, and CNS impairment: an overview.

Perioperative stroke occurs in 2-3% of adult cardiac surgery patients, and significant cognitive dysfunction is experienced by 40-60% of patients in the first postoperative week. Perioperative neurocognitive abnormalities are associated with a greatly increased risk of perioperative mortality, lengthy intensive care and hospital stay, and more intensive rehabilitative care. Long-term cognitive dysfunction, ranging from months to years, occurs in 25-40% of adult cardiac surgery patients, resulting in a decreased quality of life. Cerebral emboli are an important cause of perioperative neurocognitive abnormalities. Aortic cannulation, clamping, and manipulation during surgery may dislodge atheromatous materials into the cerebral circulation, leading to perioperative or postoperative stroke. Nevertheless, acute and chronic neurocognitive dysfunction frequently occurs in non-cardiac surgery patients as well, suggesting that some element of surgery and/or anesthesia itself causes or contributes to this phenomenon. One possible cause may be central nervous system (CNS) responses to peripheral tissue injury or inflammation. The CNS is sensitive to systemic pro-inflammatory mediators such as endotoxin and the cytokines interleukin-6 and interleukin- 8, which are activated by surgical trauma. This article discusses the behavior and effects of these inflammatory agents and their intensification in combination with postoperative hyperthermia. The potential beneficial role of pharmacological agents such as heparin, lidocaine, and aprotinin is also examined.

Anti-Inflammatory Agents↗

PubMed2003

[Relationship between three neuropsychological tests and cerebral glucose metabolism in Alzheimer's disease].

OBJECTIVE: To study the relationship between the scores of 3 neuropsychological scales: MMSE, extended scale of dementia (ESD) and Blessed dementia scale (BDS) and cerebral glucose metabolism in Alzheimer's disease (AD) indicated by positron emission tomography (PET). METHODS: Brain scanning was performed with SIEMENS ECAT 47 PET scanner among 21 AD patients, aged 60 - 83 (10 mild, 6 moderate, and 5 severe), and 15 healthy persons, aged 57 - 73. The ratio of mean radioactivity of cerebral lobe to that of cerebellum as semi-quantitative parameters was used to evaluate the cerebral glucose metabolism. Cognitive function was assessed by three neuropsycholigical scales: MMSE, ESD and BDS. RESULTS: The average MMSE score was 13.3 +/- 6.3 (range 2 - 25), the average ESD score was 120.5 +/- 54.8 (range 28 - 200), and the average BDS score was 4.7 +/- 3.1 (range 0.5 - 10) in the AD patients. The decreases of glucose metabolism in parietal, frontal and temporal lobes were significantly positively correlated with MMSE and ESD scores, and negatively correlated with BDS scores in AD patients (P < 0.05). The correlations between MMSE and ESD (r = 0.886), MMSE and BDS (r = -0.763), and ESD and BDS (r = -0.773) were significant in AD patients (all P < 0.01). Taking the ratio of radioactivity of cerebral lobe to that of cerebellum as an independent variable X, the MMSE, ESD and BDS scorsas dependent variable Y, three regression equations were established as follows: Y = 40.11 * X- 25.32, Y = 309.19 * X- 180.9, Y = 19.97 - 16.53 * X. The independent variable entering the three regression equations was always the ratio of radioactivity of left parietal lobe to that of cerebellum. The ratio of radioactivity of left parietal lobe to that of cerebellum was a significant predictor for cognitive dysfunction measured by MMSE, ESD and BDS in AD patients (P < 0.01). CONCLUSION: MMSE, ESD and BDS scores correlate well with impaired cerebral glucose metabolism in AD. The function of left parietal lobe may play an important role in the progress of the disease. MMSE, ESD and BDS are good measures for cognitive dysfunction.

Aged↗

PubMed1993

Neuropsychiatric disease in Sjögren's syndrome: anti-ribosomal P and anti-neuronal antibodies.

PURPOSE: Patients with Sjögren's syndrome (SS) may develop nonfocal (i.e., psychiatric and/or cognitive dysfunction) as well as focal, neuropsychiatric disease (CNS-SS). Anti-ribosomal P and anti-neuronal antibodies have been associated with nonfocal neuropsychiatric disease in systemic lupus erythematosus (SLE), particularly psychosis and depression. This study examines the spectrum of psychiatric and cognitive dysfunction observed in SS patients with focal, as well as nonfocal, central nervous system (CNS) disease and relates these observations to the presence of serum and cerebrospinal fluid (CSF) anti-ribosomal and anti-neuronal antibodies. PATIENTS AND METHODS: One hundred thirty-one patients--patients with primary SS (n = 91), patients with secondary SS (n = 34), and mothers of infants with neonatal lupus erythematosus (NLE) (n = 6)--were studied. Patients were referred to a large tertiary referral center and the population was highly selected for CNS disease. Patients were evaluated clinically for focal and nonfocal CNS disease. Sera from 131 patients and 34 paired sera/CSF samples were examined by enzyme-linked immunosorbent assay and radioimmunoassay for the presence of anti-ribosomal P and anti-neuronal autoantibodies, respectively. Clinical features were categorized and autoantibody profiles obtained and correlated independently for statistical significance. Data were analyzed using the two-tailed Fisher exact test. RESULTS: Psychiatric or cognitive impairment, usually mild or moderate, occurred in over 80% (63 of 77) of this highly selected population of SS patients, and more than 60% of patients (48 of 77) had both. Anti-ribosomal P antibodies occurred in six (4.6%) patients with SS and related disorders. None of the patients with primary SS had anti-ribosomal P antibodies, whereas they were present in a small number of patients with secondary SS (i.e., 4 of 34 [12%]) and in 2 of 6 mothers of infants with NLE. There was no correlation between nonfocal CNS disease, including psychosis or severe depression, and the presence of anti-ribosomal P antibodies. Paired serum CSF samples from 34 SS patients with active CNS disease, including 6 with psychosis and 5 with severe depression, did not contain either anti-ribosomal P or anti-neuronal antibodies. Anti-ribosomal P and anti-neuronal antibodies were present in a control subset of SLE patients defined serologically by the presence of anti-nDNA antibodies. CONCLUSION: Patients with primary SS associated with CNS disease, including psychosis and depression, do not have serum or CSF autoantibodies to ribosomal P peptide or neuronal antigens, detected by binding to neuroblastoma cells. Thus, autoantibodies associated with nonfocal or diffuse CNS disease in classical SLE (particularly psychosis and depression) are not present in CNS-SS. The observations suggest that nonfocal CNS disease in CNS-SS and CNS-SLE may be mediated by different immunopathologic mechanisms. Potentially, these observations may have diagnostic and therapeutic implications in the management of patients with CNS-SS and patients with CNS-SLE.

Amino Acid Sequence↗

PubMedDate not supplied

Apolipoprotein E polymorphism and cognitive impairment in a bi-ethnic community-dwelling elderly sample.

The epsilon 4 (epsilon 4) and epsilon 2 (epsilon 2) alleles of the apolipoprotein gene (APOE) located on chromosome 19 have been associated with increased and decreased risk for Alzheimer disease (AD) in older adults, respectively. However, there is a dearth of studies examining the relation of APOE polymorphism with cognitive functioning among community-dwelling ethnic minority elderly. This study examined the risk for cognitive impairment associated with the APOE epsilon 4 and epsilon 2 alleles in a community-based cohort of non-Hispanic white (NHW; N = 739) and white Hispanics (WH; N=321). All patients were recruited consecutively from a memory-screening program and evaluated using standardized assessment procedures. Cognitive impairment was classified according to an age and education adjusted Folstein Mini-Mental State Exam (MMSAdj) score of less than 24. The results indicated the APOE epsilon 4 allele was associated with increased risk for cognitive dysfunction in NHW and WH after controlling for the effects of age, education, and gender. This risk was generally observed to be dose-dependent, with greater risk among epsilon 4 homozygotes in relation to epsilon 4 heterozygotes. The epsilon 2 allele of APOE did not confer decreased risk for cognitive impairment among NHW and WH. This study supports the relation of APOE polymorphism to cognitive dysfunction among two ethnic populations residing in the community.

Aged↗

PubMed2002

Amyloid beta-peptide induces cholinergic dysfunction and cognitive deficits: a minireview.

Amyloid beta-peptide (Abeta) plays a critical role in the development of Alzheimer's disease (AD). Much progress has been made in understanding this age-related neurodegenerative disorder, thus an insight into the cellular actions of Abeta and resulting functional consequences may contribute to preventive and therapeutic approaches for AD. In this review, recent evidence of Abeta-induced brain dysfunction, particularly of cholinergic impairment and memory deficits is summarized. Moreover, proposed mechanisms for Abeta-induced neurotoxicity such as oxidative stress, ion-channel formation, and Abeta-receptor interaction are discussed.

Amino Acid Sequence↗

PubMed2005

Benign childhood epilepsy with occipital paroxysms: neuropsychological findings.

Benign childhood epilepsy with occipital paroxysms is classified among childhood benign partial epilepsies. The absence of neurological and neuropsychological deficits has long been considered as a prerequisite for a diagnosis of benign childhood partial epilepsy. Much evidence has been reported in literature in the latest years suggesting a neuropsychological impairment in this type of epilepsy, particularly in the type with Rolandic paroxysms. The present work examines the neuropsychological profiles of a sample of subjects affected by the early-onset benign childhood occipital seizures (EBOS) described by Panayotopulos. The patient group included 22 children (14 males and 8 females; mean age 10.1+/-3.3 years) diagnosed as having EBOS. The patients were examined with a set of tests investigating neuropsychological functions: memory, attention, perceptive, motor, linguistic and academic (reading, writing, arithmetic) abilities. The same instruments have been given to a homogeneous control group as regards sex, age, level of education and socio-economic background. None of the subjects affected by EBOS showed intellectual deficit (mean IQ in Wechsler Full Scale 91.7; S.D. 8.9). Results show a widespread cognitive dysfunction in the context of a focal epileptogenic process in EBOS. In particular, children with EBOS show a significant occurrence of specific learning disabilities (SLD) and other subtle neuropsychological deficits. We found selective dysfunctions relating to perceptive-visual attentional ability (p<0.05), verbal and visual-spatial memory abilities (p<0.01), visual perception and visual-motor integration global abilities (p<0.01), manual dexterity tasks (p<0.05), some language tasks (p<0.05), reading and writing abilities (p<0.01) and arithmetic ability (p<0.01). The presence of cognitive dysfunctions in subjects with EBOS supports the hypothesis that epilepsy itself plays a role in the development of neuropsychological impairment. Supported by other studies that have documented subtle neuropsychological deficits in benign partial epilepsy, we stress the importance of reconsidering its supposed "cognitive benignity", particularly in occipital types.

Adolescent↗

PubMedDate not supplied

A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease.

Much evidence indicates that abnormal processing and extracellular deposition of amyloid-beta peptide (A beta), a proteolytic derivative of the beta-amyloid precursor protein (betaAPP), is central to the pathogenesis of Alzheimer's disease (reviewed in ref. 1). In the PDAPP transgenic mouse model of Alzheimer's disease, immunization with A beta causes a marked reduction in burden of the brain amyloid. Evidence that A beta immunization also reduces cognitive dysfunction in murine models of Alzheimer's disease would support the hypothesis that abnormal A beta processing is essential to the pathogenesis of Alzheimer's disease, and would encourage the development of other strategies directed at the 'amyloid cascade'. Here we show that A beta immunization reduces both deposition of cerebral fibrillar A beta and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of A beta in the brain. This implies that either a approximately 50% reduction in dense-cored A beta plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic A beta species.

Alzheimer Disease↗

PubMed1995

Cognitive functioning and magnetic resonance imaging in chronic fatigue.

BACKGROUND: This study examines whether cognitive dysfunction in chronic fatigue may be accounted for by depression and anxiety or is due to brain pathology evident on magnetic resonance imaging (MRI). METHOD: Twenty-six subjects with chronic fatigue, with and without coexisting depression, and 18 age-matched normal controls were recruited from primary care following a presumed viral illness six months previously. Comparison was made with 13 psychiatric controls with depressive illness on standardised cognitive tests. MRI determined the presence of cerebral white-matter lesions. RESULTS: No substantial differences in performance were shown between subjects with chronic fatigue, most of whom met the criteria for chronic fatigue syndrome, and controls. Subjective cognitive dysfunction increased with psychopathology. White-matter lesions were found in a minority from all groups. Improvement in fatigue and depression coincided with improved performance on cognitive measures. CONCLUSIONS: Subjective complaints of cognitive impairment are a prominent feature of chronic fatigue, but objective cognitive and MRI abnormalities are not. Such complaints probably reflect psychopathology rather than a post-viral process.

Adolescent↗

PubMed1988

Medically incongruent chronic back pain: physical limitations, suffering, and ineffective coping.

Chronic low back pain (CLBP) patients with pain and symptomatology incongruent with physical pathology have been found to have a poorer outcome to medical treatment and rehabilitation, and to use health care resources excessively. To examine possible psychological and behavioral bases for this pattern, this investigation contrasted 40 CLBP patients who displayed non-organic physical signs, inappropriate symptoms, and/or anatomically incongruent pain drawings with 40 'control' CLBP patients without incongruent pain criteria. Multivariate analyses revealed that the incongruent CLBP group reported greater pain intensity and depression, received higher observer ratings of pain, displayed more ambulatory/postural pain behavior, and reported more dysfunctional cognitions during pain. Incongruent CLBP patients also were found to have greater physical impairment and disability. When group differences on physical impairment/disability were controlled statistically, all the afore-mentioned differences disappeared, with one exception. Incongruent CLBP patients still displayed more maladaptive and dysfunctional cognitions. These findings indicate that incongruent CLBP patients may be conceptualized as ineffective and overwhelmed in their attempts to cope and as more physically disabled as a result of their pain. The role of cognitive factors, reasons for failure of physically based interventions, and implications for patient management are discussed.

Adaptation, Psychological↗

PubMed2002

The relationship of subcortical MRI hyperintensities and brain volume to cognitive function in vascular dementia.

The relationship between MRI findings (i.e., subcortical hyperintensities; SH, whole brain volume) and the cognitive dysfunction of vascular dementia (VaD) was examined. Participants included 24 persons that met NINDS-AIREN criteria for VaD (MMSE = 19.9 +/- 4.2) and underwent comprehensive neuropsychological assessment and MRI brain imaging. The volume of subcortical hyperintensities (SH) was strongly associated with executive-psychomotor performance, but not with performance across other cognitive domains or global cognitive functional level. Conversely, WBV was strongly associated with global cognitive functioning and performance across most cognitive domains (memory, language, visual integration), but not with executive-psychomotor functioning. The failure of SH to account for either the global dementia evident in these VaD patients or impairments across most cognitive domains suggests that deep subcortical white matter disease may only indirectly contribute to the global cognitive dysfunction of VaD. That WBV emerged as a stronger correlate of dementia raises further questions regarding the cerebral mechanisms that contribute to the development of VaD.

Aged↗

PubMed2000

Normal pressure hydrocephalus in diabetic patients with recurrent episodes of hypoglycemic coma.

The pathophysiology of brain damage induced by severe hypoglycemia is still unknown. We experienced a case with type 1 diabetes and recurrent severe hypoglycemic coma who showed a central brain atrophy and an abnormal cerebrospinal fluid flow, suggesting normal pressure hydrocephalus. Following this case, the CSF flow was studied using 111In-DTPA cisternography in six consecutive diabetic patients admitted for repeated episodes of hypoglycemic coma. All the patients showed the central brain atrophy on computed tomography and four of them (67%) had the ventricular reflux, with delayed clearance of 111In-DTPA. Two patients with abnormal CSF flow showed cognitive dysfunction by WAIS or WAIS-R. In contrast, none of five randomly selected diabetic patients, without hypoglycemic coma showed abnormal CSF flow. Our results suggest the presence of normal pressure hydrocephalus in diabetic patients with recurrent hypoglycemic coma. It may associate with the cognitive dysfunction.

Aged↗

PubMed2003

Neurological dysfunctions versus regional infarction volume after focal ischemia in Mongolian gerbils.

BACKGROUND AND PURPOSE: With advances in the therapy of stroke at the postacute phase, the use of animal models for chronological and region-specific evaluation of neurological function has become increasingly important. Our aim was to test long-term behavioral dysfunction in gerbils after focal ischemia and to correlate the results with the regional distribution of infarction in the coordinating cortical regions. METHODS: Repetitive unilateral hemispheric ischemia (two 10-minute occlusions, 5-hour interval) was induced in Mongolian gerbils. The elevated body swing test (EBST), bilateral asymmetry test (BAT), and T-maze test were performed to assess asymmetrical motor behavior, somatosensory deficit, and spatial cognitive dysfunction during 4 weeks after ischemia. The results were correlated against the regional infarction volume of the primary motor, somatosensory, and primary visual cortices at 4 weeks after ischemia. RESULTS: In all postischemic gerbils, persistent sensorimotor and cognitive dysfunctions were detectable throughout the postischemic period. Histological examination revealed that a cortical zone of infarction surrounded the selective neuronal death in the ipsilateral cerebral hemisphere. The regional infarction volumes of the primary motor, somatosensory, and visual cortices were significantly correlated with the scores of the EBST, BAT, and T-maze test, respectively. These combinations had the highest regression coefficient of all pairs. CONCLUSIONS: Postischemic motor and somatosensory functions were significantly correlated with regional infarction volumes in the corresponding cortical regions. In gerbils, visual abnormality could be independently detected by the T-maze test. Such regional analyses of ischemic lesions would be useful for investigating the functional outcomes of stroke therapy.

Animals↗

PubMed2001

Molecular mechanism of cholinergic dysfunction and cognitive deficits induced by amyloid beta-peptide.

Amyloid beta-peptide (A beta) plays a critical role in the development of Alzheimer's disease (AD). Much progress has been made in understanding this age-related neurodegenerative disorder; thus an insight into the cellular actions of A beta and resulting functional consequences may contribute to preventive and therapeutic approaches for AD. In this review, recent evidence of A beta-induced brain dysfunction, especially cholinergic impairment and memory deficits, is summarized. Moreover, proposed mechanisms for A beta-induced neurotoxicity such as oxidative stress, ion-channel formation, and A beta-receptor interaction are discussed.

Amyloid beta-Peptides↗

PubMed2002

Topiramate antagonizes MK-801 in an animal model of schizophrenia.

The phencyclidine (PCP) model of schizophrenia suggests that N-methyl-D-aspartate (NMDA) receptor hypofunction and its consequences may play an important role in the pathophysiology of this psychiatric disorder. Moreover, the schizophreniform psychosis caused by PCP resembles schizophrenia in all of the relevant domains of psychopathology, especially negative symptoms and cognitive dysfunction. Because of interest in the PCP model and possible NMDA receptor hypofunction in schizophrenia, animal behaviors elicited by PCP and its analogues have been characterized. These preclinical models may serve to identify candidate compounds that possess therapeutic efficacy in schizophrenia. Ideally, negative symptoms and cognitive dysfunction would also serve as therapeutic targets for these novel medications. In the current study, the ability of topiramate to attenuate the severity of a specific behavior elicited by MK-801 (dizocilpine), a high affinity analogue of PCP was studied in mice. Topiramate was chosen because it addresses two of the predicted pathological consequences of NMDA receptor hypofunction. Specifically, topiramate potentiates GABAergic neurotransmission and antagonizes the excitotoxic actions of glutamate at the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate (KA) classes of glutamate-gated channels. Topiramate was shown to inhibit MK-801-elicited "popping" behavior in a complex dose-dependent manner.

Animals↗

PubMed1997

The first neurophysiological evidence for cognitive brain dysfunctions in children with CATCH.

CATCH syndrome, caused by a microdelection in chromosome 22, is characterized by cleft palate and cardiac anomalies. The majority of these children also have learning difficulties or speech and language deficits. These problems are often due to the dysmorphology of the articulatory system. In the present study, the duration of auditory sensory memory, which is of central importance to speech perception and understanding, was investigated. As a research method we used mismatch negativity (MMN), an attention independent event-related potential, which provides an objective electrical index of auditory sensory memory. The present data suggest that the duration of this memory span is considerably shorter in 6-10-year-old children with CATCH than in healthy controls. Thus, the language-related problems encountered in children suffering from CATCH syndrome are likely to be caused also by CNS dysfunctions.

Abnormalities, Multiple↗

PubMedDate not supplied

Erythropoietic agents in the management of cancer patients. Part 2: studies on their role in neuroprotection and neurotherapy.

Cognitive dysfunction has been reported in subsets of cancer patients and has been related to their underlying disease (small-cell lung cancer [SCLC]) or to a specific therapy (prophylactic cranial irradiation in SCLC, chemotherapy in breast cancer). Patients with uremic encephalopathy who have had their hemoglobin levels normalized by erythropoietic therapy have shown improved cognitive function in some studies. The mechanism responsible for the improvement is unknown and might reflect either a direct neuroprotective effect of erythropoietins on the central nervous system or the benefit of increased tissue oxygenation secondary to the correction of peripheral anemia. Whether erythropoietic agents can affect the cognitive dysfunction reported among some cancer patients is currently being investigated. The current state of knowledge about the use of erythropoietic agents for neuroprotection or the treatment of neurologic syndromes is described.

Antineoplastic Agents↗

PubMed1989

Cognitive loss in multiple sclerosis. Case reports and review of the literature.

Neuropsychological and neuroradiologic evidence of cerebral lesions is described for 12 patients with multiple sclerosis in whom cognitive disability was far greater than any other neurologic disability. Cognitive dysfunction resulted in significant functional impairment at work or home in three fourths (9 of 12) of the patients described here, despite mild physical disability (mean Kurtzke Expanded Disability Status Scale score, 3.2). A unique feature of the neurologic examination in these patients was the presence of prominent frontal release signs (gait apraxia and placing response) in the lower extremities. Two new scales, a Cognitive Function Scale and a Frontal Release Scale, were adapted for the investigation of these patients. The extensive literature relating to cognitive dysfunction in multiple sclerosis is reviewed and discussed with regard to its clinical relevance.

Adult↗