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Results for “Cognitive Dysfunction”

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At least 433 records · Page 24Linked to original sources
PubMed2001

Activation of cyclo-oxygenase-2 contributes to motor and cognitive dysfunction following diffuse traumatic brain injury in rats.

1. Post-traumatic inflammation may play a significant role in the development of delayed secondary brain damage following traumatic brain injury. 2. During post-traumatic inflammation, metabolic products of arachidonic acid, known as prostanoids (prostaglandins and thromboxanes) are released and aggravate the injury process. Prostanoid synthesis is regulated by the enzyme cyclo-oxygenase (COX), which is present in at least two isoforms, COX-1 (the constitutive form) and COX-2 (the inducible form). 3. In the present study, we examine the temporal and spatial profiles of COX-2 expression and the effects of the COX-2 inhibitor nimesulide on motor and cognitive outcome following diffuse traumatic brain injury in rats. 4. Adult male Sprague-Dawley rats were injured using the 2 m impact acceleration model of diffuse traumatic brain injury. At preselected time points after injury, animals were killed and the expression of COX-2 was measured in the cortex and hippocampus by western blotting techniques. 5. Increased expression of COX-2 was found in the cortex at 3 days and in the hippocampus as early as 3 h postinjury and this persisted for at least 12 days. 6. Administration of nimesulide (6 mg/kg, i.p.) at 30 min after injury and daily over a 10 day post-traumatic neurological assessment period resulted in a significant improvement compared with vehicle (2% dimethylsulphoxide diluted in isotonic saline)-treated controls in cognitive deficits, as assessed by the Barnes circular maze. There was also a significant improvement in motor dysfunction as assessed by the rotarod test on days 1 and 2 post-trauma compared with vehicle-treated controls. 7. These results implicate the involvement of COX-2 in cognitive and motor dysfunction following diffuse traumatic brain injury.

Animals↗
PubMed1987

Cognitive dysfunction in psychiatric consultation subgroups: use of two screening tests.

Elderly patients are highly vulnerable to illness-related and drug-induced cognitive changes, especially during the acute phase of a medical or surgical illness. Using a structured cognitive screening examination enhances the accurate identification of patients with cognitive impairment. We compared the cognitive portion of the Alzheimer's Disease Assessment Scale (ADAS-COG) to the Mini-Mental State Examination (MMSE) in screening for the presence of organic brain dysfunction. Using cutoff scores, the two tests were in agreement in 94.4% of 36 cases, with total scores on the two tests correlated at r = -.90 (P less than .01). Of these 36 patients for whom psychiatric consultations were requested, 14 (38.8%) were found to be cognitively impaired. We discuss the relationship of test scores to the stated reason for the consultation, as well as variables influencing test results. Finally, we demonstrate the usefulness of cognitive testing in patients who refuse treatment.

Adult↗
PubMed1996

Cognitive dysfunction following surgery for intracerebral glioma: influence of histopathology, lesion location, and treatment.

This study examined the relationship between cognitive function, tumor malignancy, adjunctive therapy, and lesion lateralization following surgery for intracerebral glioma. Neuropsychological test battery results showed no difference between patients with highly malignant gliomas and those with less malignant gliomas, but differences were found for tumor lateralization and type of therapy. Scores on a test of graphomotor speed were lowest for patients who had received radiation or a combination of radiation and chemotherapy, regardless of lesion location. Other test results did not differ according to type of prior treatment but were related instead to tumor lateralization. Left hemisphere lesions were associated with lower scores on verbal tests, while right hemisphere lesions were related to lower scores on a test of facial recognition. These findings suggest that neuropsychological tests may be useful for distinguishing between the diffuse side effects of brain tumor therapy and the focal effects of tumors and surgery on brain functions. In addition, it appears that any differences in cognitive function due to tumor malignancy are eliminated or reduced following surgical intervention.

Adult↗
PubMed1999

Cognitive dysfunction in schizophrenia: unifying basic research and clinical aspects.

Seeking to unite psychological and biological approaches, this paper links cognitive and cellular hypotheses and data about thought and language abnormalities in schizophrenia. The common thread, it is proposed, is a dysregulated suppression of associations (at the behavioral and functional neural systems level), paralleled by abnormalities of inhibition at the cellular and molecular level, and by an abnormal anatomical substrate (reduced MRI gray matter volume) in areas subserving language. At the level of behavioral experiments and connectionist modeling, data suggest an abnormal semantic network connectivity (strength of associations) in schizophrenia, but not an abnormality of network size (number of associates). This connectivity abnormality is likely to be a preferential processing of the dominant (strongest) association, with the neglect of preceding contextual information. At the level of functional neural systems, the N400 event-related potential amplitude is used to index the extent of "search" for a semantic match to a word. In a short stimulus-onset-asynchrony condition, both schizophrenic and schizotypal personality disorder subjects showed, compared with controls, a reduced N400 amplitude to the target words that were related to cues, e.g. cat-dog, a result compatible with behavioral data. Other N400 data strongly and directly suggest that schizophrenics do not efficiently utilize context.

Brain↗
PubMed2006

Significant cognitive dysfunction in non-delirious patients identified during and persisting following critical illness.

OBJECTIVE: Recent studies have shown significant cognitive problems some months after critical illness. However there has been no research examining cognitive function within the intensive care unit (ICU) in non-delirious patients. DESIGN AND SETTING: A prospective study in an ICU. PATIENTS AND PARTICIPANTS: Using the Cambridge Neuropsychological Test Automated Battery (CANTAB), 30 long-stay, tracheal-intubated ICU patients were tested. Prior to testing on ICU the Confusion Assessment Measure (CAM-ICU) was administered and only those patients clearly not delirious and off sedation for several days were tested. The CANTAB tests were repeated a week after ICU discharge on the general ward and then again at 2 months. Sixteen patients completed the follow-up. RESULTS: While on ICU all 30 patients showed significant problems with strategic thinking and problem solving; 20 patients had some problems with memory. The degree of difficulty with problem solving on ICU was correlated with length of ICU stay (p=0.011), age (p=0.036) and length of hospital stay post ICU (p=0.044). Problems with memory in ICU and on the general ward were correlated with admission APACHE II score (p=0.004 and p=0.005 respectively). At the 2-month follow-up 5 of 16 patients (31%) scored below the 25 percentile for memory and 8 of 16 (50%) below the 25 percentile for problem solving (Slater TA, Jones C, Griffiths RD, Wilson S, Benjamin K (2004) Cognitive impairment during and after intensive care: a pilot study. Intensive Care Med 30 [Suppl 1]:S199). CONCLUSIONS: Difficulties with problem solving and poor memory remained a significant issue for 2 months after ICU discharge.

Adolescent↗
PubMed2005

Antihypertensive agents for aging patients who are at risk for cognitive dysfunction.

Observational and experimental data continue to accumulate about the impact of blood pressure (BP) and antihypertensive agents on cognitive function. Current evidence suggests that there is a U-shaped association between BP earlier in life and poor cognitive function and clinical dementia, including Alzheimer's disease. This association has been identified more consistently in longitudinal surveys due to the fact that BP declines when cognitive symptoms start. Lowering BP provides protection against this complication of high BP. This effect is present in the cognitively intact and in those with dementia. Antihypertensives that cross the blood brain barrier and affect the renin-angiotensin-aldosterone system (such as perindopril or losartan) or brain calcium metabolism (nitrendipine) provide additional protection beyond BP control against cognitive decline. These drugs may be preferred in such clinical situations.

Age Factors↗
PubMed2003

The utility of computerized neuropsychological assessment of cognitive dysfunction in patients with relapsing-remitting multiple sclerosis.

Traditional paper-and-pencil neuropsychological batteries used to document cognitive deficits in multiple sclerosis (MS) patients lack timing precision. This makes it difficult to accurately measure psychomotor slowing, a central cognitive symptom of MS. Additionally, traditional batteries lack multiple alternate forms necessary to control for practice effects when assessing cognition over time. Finally such batteries are lengthy and expensive. Computerized neuropsychological batteries address many of these shortcomings. They measure response time more precisely, require less administration time, include alternate forms, and are ideal for rapid screening/triage. Although there are normative data on the reliability and validity of computerized measures, there have been no controlled validation studies with MS patients. The current study was designed to validate a computerized neuropsychological battery (ANAM) for use with relapsing-remitting (RR) MS patients. Prior to initiation of interferon-beta-1a (Avonex) treatment, subjects participated in a neuropsychological evaluation consisting of traditional and computerized measures. Moderate-to-high correlations were found between computerized and traditional measures. Computerized tests accurately predicted performance on key traditional tests. The battery was also concordant with traditional measures in identifying RR MS patients with and without neurocognitive impairment. Findings are discussed with respect to increased accuracy and accessibility of neuropsychological evaluations for MS patients.

Adolescent↗
PubMed1998

Higher cerebrospinal fluid MHPG in subjects with dementia of the Alzheimer type. Relationship with cognitive dysfunction.

The authors sought to determine the relationships between cerebrospinal fluid (CSF) levels of three neurotransmitter monoamine metabolites and cognitive function. CSF was collected from subjects with dementia of the Alzheimer's type ([DAT] n = 28) and control subjects (n = 10) for determination of CSF 5-hydroxyindole acetic acid (5-HIAA), 3-methoxy-4-hydroxy-phenylglycol (MHPG), and homovanillic acid (HVA) levels. All subjects underwent systematic assessment to determine cognitive function. Subjects with DAT had higher concentrations of CSF MHPG. In the overall sample, cognitive function was inversely correlated with CSF levels of MHPG but not with 5-HIAA or HVA. Within the DAT sample, these correlations did not achieve significance.

Aged↗
PubMed1996

Cognitive dysfunction in chronic schizophrenia followed prospectively over 10 years and its longitudinal relationship to the emergence of tardive dyskinesia.

Basic cognitive function was assessed at initial and at 5- and 10-year follow-up assessments among 41 primarily middle-aged in-patients manifesting the severest form of schizophrenia; additionally, the presence and severity of tardive dyskinesia was evaluated on each occasion. Overall, there was a modest but significant deterioration in cognitive function over the decade, particularly among older men. Longitudinally, patients with persistent tardive (orofacial) dyskinesia continued to show poorer cognitive function than those consistently without such movement disorder, though within neither group did cognitive function change over the decade. Those patients demonstrating prospectively the emergence of orofacial dyskinesia showed a marked deterioration in their cognitive function over the same time-frame within which their movement disorder emerged, but this decline did not progress further thereafter. There appears to exist some modes, progressive deterioration in cognitive function even late in the chronic phase of severe schizophrenic illness which appears to derive primarily from patients showing de novo emergence of tardive orofacial dyskinesia.

Adult↗
PubMedDate not supplied

Mode of action: disruption of brain cell replication, second messenger, and neurotransmitter systems during development leading to cognitive dysfunction--developmental neurotoxicity of nicotine.

Developmental exposure to nicotine in rats results in neurobehavioral effects such as reduced locomotor and cognitive function. Key events in the animal mode of action (MOA) include binding to the nicotinic cholinergic receptor during prenatal and/or early postnatal development. This leads to premature onset of cell differentiation at the expense of cell replication, which leads to brain cell death or structural alterations in regional brain areas. Other events include an initial increase followed by a decrease in adenyl cyclase activity, as well as effects on the noradrenergic, dopaminergic, and serotonergic neurotransmitter systems. Because the nicotine receptor is also present in the developing human brain and the underlying biology for DNA synthesis and cell signaling is comparable, this MOA is likely to be relevant for humans. Although the effects of nicotine exposure in developing humans is not well documented, nicotine exposure as a result of cigarette smoking during pregnancy is associated with several physiological and behavioral outcomes that are reminiscent of the effects of nicotine alone in animal models. As data become available with the advent of the use of the nicotine patch in pregnant humans, the question as to the relative importance of smoking per se versus nicotine alone may be determined.

Animals↗
PubMed2000

Role of dopamine in learning and memory: implications for the treatment of cognitive dysfunction in patients with Parkinson's disease.

Along with dementia, Parkinson's disease (PD) is associated with subtle but widespread cognitive impairment even in the absence of clinically apparent cognitive decline. Many of the deficits are reminiscent of those observed in patients with lesions of the prefrontal cortex, that is, failure in executive function that involves skills required for anticipation, planning, initiation and monitoring of goal-directed behaviours. This paper reviews the dopaminergic brain circuitry, and preclinical and clinical evidence supporting the regulation of prefrontal cortex activity by dopamine, and the role of dopamine in cognitive impairment in patients with PD. It addresses the need to integrate these facts and the findings of positive, neutral or detrimental frontal cognitive response to dopaminergic drugs in PD which should be viewed mainly in the context of methodological differences for subject selection. The cognitive effect of levodopa does not much depend on a neuropsychological specificity of the drug, the years of evolution of the disease or the severity of the motor signs. Instead, it may be a function of the level of dopamine depletion in different parts of the basal ganglia and prefrontal cortex. Consequently, dopaminergic agents may enhance cognitive functions in some patients and impair them in others. De novo patients tend to improve during the first year of treatment; stable responders to oral levodopa tend to show no changes; and wearing-off responders tend to deteriorate with acute levodopa challenge. Enhancement and impairment of cognitive function with dopaminergic treatment is incomplete and task-specific, suggesting the need to integrate the above dopamine facts with other neurotransmitter systems findings in PD. Meanwhile, such cognitive dissociation can be useful in refining the definition of the cognitive deficit in PD patients without dementia and emphasising the need to develop new and specific strategies for treatment.

Animals↗
PubMedDate not supplied

[Magnetic resonance imaging correlates of cognitive dysfunction in patients with multiple sclerosis].

INTRODUCTION AND DEVELOPMENT: Studies with conventional magnetic resonance imaging (MRI) support the hypothesis that cognitive impairment in multiple sclerosis (MS) patients is related with the lesion burden. Patterns of frontal lobe cognitive decline were also found to be related with the corresponding regional lesion load, although the total lesion load on T2-weighted MRI scans of the brain seems to be more relevant in determining frontal lobe deficits. Other non-conventional MRI techniques with a higher specificity to the heterogeneous substrates of MS pathology, such as the assessment of hypointense lesion load on T1-weighted scans and the histogram analysis of magnetization transfer ratio maps, have recently been applied to MS cognitive studies. CONCLUSIONS: Results from these studies suggest that three factors play a role in the pathogenesis of MS dementia: the burden of MS lesions, the severity of the pathological damage within individual lesions and that of the normal-appearing white matter.

Cognition Disorders↗