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Results for “Cognitive Dysfunction”

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PubMed1984

Use of P300 and a dementia rating scale in the evaluation of cognitive dysfunction in MS.

The assessment of mental dysfunction in multiple sclerosis and discrimination from the secondary effects of sensory and motor deficits has comparability to similar work done on dementia in Alzheimer's disease and Parkinson disease. Two approaches to testing might include adaptation of the Alzheimer Disease Assessment Scale and inclusion of the P300 component of the event-related auditory evoked potential.

Alzheimer Disease↗

PubMed1992

Toward the clarification of the construct of depersonalization and its association with affective and cognitive dysfunctions.

Little consensus or systematic research exists regarding the symptoms that constitute depersonalization and its association with affective and perceptual dysfunctions. A scale was constructed to measure depersonalization experiences reported in the literature and four items representing psychotic symptoms. Five factors representing different types of depersonalization emerged: Inauthenticity, Self-Negation, Self-Objectification, Derealization, and Body Detachment. Based on the factors, scales were constructed; these scales have internal consistency ranging from .78 to .84. Each of these factor scales was factorially distinguishable from psychosis and correlated between .48 and .58 with the Jackson and Messick (1972) Feelings of Unreality Scale, suggesting divergent and convergent validity. Inauthenticity, the most frequent and pervasive form of depersonalization experience, was best predicted by a cognitive style featuring intense, critical examination of self and others. In contrast, Self-Objectification was best predicted by thought disorganization and perceptual distortion and was experienced somewhat infrequently by relatively few subjects. All forms of depersonalization were associated with depression, except Inauthenticity.

Adult↗

PubMed1998

Cognitive dysfunction in patients with pituitary tumour who have been treated with transfrontal or transsphenoidal surgery or medication.

OBJECTIVE: This study was carried out to examine the neuropsychological status of patients treated for pituitary tumour by transfrontal surgery, transphenoidal surgery or medical treatment only, with or without radiotherapy. DESIGN AND MEASUREMENTS: Three groups of 23 patients who had been treated for pituitary tumour were compared with 23 healthy controls on a range of neuropsychological measures. The surgical patients were also subdivided into two groups and compared. The neuropsychological measures were standardized psychological tests designed to assess aspects of attention, memory and executive function. PATIENTS: The patients were those who had been treated with transfrontal surgery (n = 23), transsphenoidal surgery (n = 23) and medication only (n = 23). The groups did not differ with respect to age, education or premorbid ability level as assessed by the National Adult Reading Test. All participants were free of known sources of cognitive impairment other than pituitary tumour. RESULTS: Comparison of the four groups revealed that nearly half of the transfrontal, one-third of the transsphenoidal and one-quarter of the non-surgical group had three or more neuropsychological tests scores below the 10th percentile compared to less than 5% of the controls. Impairments in memory and executive function were found in both surgical groups. The non-surgical patients appeared to have problems only on tasks requiring high levels of cognitive processing. Differences were found between the two surgical groups with respect to the severity of the cognitive impairment, the transfrontal patients having more severe impairment than the transsphenoidal. No significant negative effects on cognitive functioning were associated with radiotherapy; however, transfrontal surgery patients who had not been treated with radiotherapy were found to be more impaired than other patients. This was thought to be related to radical surgery. CONCLUSIONS: Many patients with treated pituitary tumour suffer significant cognitive impairment. The severity and nature of impairment differs between treatment groups, although the cause of this could not be addressed by this study. Recommendations are made for future research and clinical practice.

Adult↗

PubMed2004

Aortic atheroma burden and cognitive dysfunction after coronary artery bypass graft surgery.

BACKGROUND: Neurocognitive dysfunction (NCD) after coronary artery bypass graft (CABG) surgery is a common problem. Atherosclerotic disease of the aorta is a known risk factor for stroke after cardiac surgery, but its relationship to NCD is unclear. This study investigates the relationship between aortic atherosclerotic disease and NCD after CABG. PATIENTS AND METHODS: Patients undergoing primary elective CABG were enrolled in an ongoing investigation of NCD after CABG. Intraoperative transesophageal echocardiography (TEE) of the thoracic aorta was performed and analyzed off-line to quantify atheroma burden. Neurocognitive evaluation was performed, both preoperatively and at 6 weeks after surgery. Multivariable linear regression (controlling for age, years of education, and base line cognitive index) was used to determine the relationship between NCD and atheroma burden in the ascending, arch, and descending aorta. RESULTS: One hundred sixty-two patients who had a complete neurocognitive evaluation and adequate TEE images were studied. No significant relationship was found between NCD and atheroma burden in the ascending (p = 0.22), arch (p = 0.89) or descending aorta (p = 0.64). CONCLUSIONS: Although the etiology of NCD is likely multifactorial, our results suggest that aortic atherosclerosis may not be the primary factor in the pathogenesis of post-CABG cognitive changes.

Aged↗

PubMed2002

Histaminergic modulation of stress-induced analgesia and cognitive dysfunction.

Physiological stress is known to produce analgesia and memory disruption. A large body of evidence favors the nonopiate mediation of stress-induced analgesia. It is suggested that brain histamine mediates nonopiate analgesia and participates in learning and memory in rodents. Histamine is released during stress, although the nature of histaminergic involvement in stress response is not clearly defined. Therefore, we studied the effect of L-histidine and histamine-receptor antagonists on antinociception and impaired retention induced by immobilization stress. In the present study, immobilization stress produced a naloxone-resistant analgesia that was potentiated by L-histidine and antagonized by pretreatment with the histamine receptor antagonists chlorpheniramine and cimetidine. L-histidine attenuated the memory disruption induced by immobilization stress, which was significantly reversed by chlorpheniramine but not by cimetidine. Thus the involvement of the central histaminergic system, through histamine H1- and H2-receptors, may be speculated in analgesia and cognitive deficit induced by immobilization stress.

Analgesia↗

PubMed1994

Central nervous system lupus: concomitant occurrence of myelopathy and cognitive dysfunction.

Reported are two cases of patients with central nervous system systemic lupus erythematosus (SLE) with clinical features of a myelopathy confirmed by magnetic resonance imaging (MRI). In one case, further evaluation including Single Photon Emission Computerized Tomography (SPECT) and neuropsychological testing, indicated higher cortical deficits which improved after treatment with monthly pulse intravenous cyclophosphamide. Subsequent cessation of cyclophosphamide was associated with further progression of the neurological disease in this patient.

Adult↗

PubMed2003

Anticholinergic and antiglutamatergic agents protect against soman-induced brain damage and cognitive dysfunction.

Soman, a powerful inhibitor of acetylcholinesterase, causes an array of toxic effects in the central nervous system including convulsions, learning and memory impairments, and, ultimately, death. We report on the protection afforded by postexposure antidotal treatments, combined with pyridostigmine (0.1 mg/kg) pretreatment, against these consequences associated with soman poisoning. Scopolamine (0.1 mg/kg) or caramiphen (10 mg/kg) were administered 5 min after soman (1.2 LD50), whereas TAB (i.e., TMB4, atropine, and benactyzine, 7.5, 3, and 1 mg/kg, respectively) was injected in rats concomitant with the development of toxic signs. Atropine (4 mg/kg) was given to the two former groups at the onset of toxic symptoms. Caramiphen and TAB completely abolished electrographic seizure activity while scopolamine treatment exhibited only partial protection. Additionally, no significant alteration in the density of peripheral benzodiazepine receptors was noted following caramiphen or TAB administration, while scopolamine application resulted in a complex outcome: a portion of the animals demonstrated no change in the number of these sites whereas the others exhibited markedly higher densities. Cognitive functions (i.e., learning and memory processes) evaluated using the Morris water maze improved considerably by the three treatments when compared to soman-injected animals; the following rank order was observed: caramiphen > TAB > scopolamine. Additionally, statistically significant correlations (r = 0.72, r = 0.73) were demonstrated between two learning parameters and [3H]Ro5-4864 binding to brain membrane. These results show that drugs with a pharmacological profile consisting of anticholinergic and antiglutamatergic properties such as caramiphen and TAB, have a substantial potential as postexposure therapies against intoxication by organophosphates.

Animals↗

PubMed2003

Quantitative EEG abnormalities and cognitive dysfunctions in frontotemporal dementia and Alzheimer's disease.

OBJECTIVE: To investigate the relationship between quantitative EEG (qEEG) measurements in frontotemporal dementia (FTD), Alzheimer's disease (AD) and healthy controls and to study to what extent qEEG in FTD and AD or neuropsychological test results of FTD and AD patients or a combination of both contribute to classification accuracy. METHOD: The FTD sample consisted of 19 patients, the AD sample of 16 patients, and the control group of 19 subjects. Groups were matched on the group level with respect to demographic variables. For qEEG the global field power was calculated for six frequency bands: delta (1.0-3.5 Hz), theta (4.0-7.5 Hz), alpha (8.0-11.0 Hz), beta1 (12.0-15.5 Hz), beta2 (16.0-19.5 Hz), beta3 (20.0-23.5 Hz), and spectral ratio as the ratio of the sum of fast frequency bands alpha + beta1 + beta2 + beta3 and slow frequency bands delta + theta. RESULTS: In comparison to controls FTD patients were marked by an absence of an increase in slow qEEG activities and a decrease in fast activities, whereas AD patients were marked by an increase in slow activities and a smaller decrease in fast activities. According to the Mann-Whitney U test the cognitive functions of attention, visuospatial thinking and episodic memory were significantly better in FTD than in AD. Using logistic regression analysis the best predictors of FTD and AD were in a model using the delta and theta activities, and high levels of visuospatial ability and episodic memory. Classification accuracy of the model was 93.3%. CONCLUSION: FTD patients reveal a different pattern of qEEG changes than AD patients. This result demonstrates the importance of qEEG for FTD diagnosis. Cognition is selectively better in FTD than in AD. A combination of qEEG and neuropsychology is recommended for differential diagnoses of FTD and AD.

Alzheimer Disease↗

PubMed2004

Cognitive dysfunction in Parkinson's disease: the role of frontostriatal circuitry.

It has been known for many years that the classic motor symptoms of Parkinson's disease are accompanied by deficits of executive function that resemble those seen after frontal lobe damage in humans. What is less clear is how different components of frontostriatal circuitry contribute to these impairments. Recently, improved methods of clinical assessment and classification, combined with novel technical approaches, such as functional neuroimaging, have led to great advances in our understanding of the fundamental mechanisms that drive frontostriatal circuitry. As a direct result, it has been possible to redefine impairments of executive function in Parkinson's disease more precisely in terms of the specific neuropsychological, neuroanatomical, and psychopharmacological mechanisms involved.

Animals↗

PubMed2003

Symptoms and cognitive dysfunction in patients with the late whiplash syndrome.

The aim of the study was to record the severity of symptoms in patients with the late whiplash syndrome and to assess how the symptom load affected the performance on a simple psychometric test. The Rivermead Post-Concussion Symptoms Questionnaire (RPQ) with an additional question on neck pain, modified RPQ (mRPQ), and the Short Test of Mental Status (STMS) were applied on 40 chronic whiplash patients. Symptoms reported by the whiplash group were compared to those of 50 normal controls. The patients scored significantly higher than the controls on all symptoms listed in the mRPQ. The most frequent symptoms reported.

Adult↗

PubMed2002

Electrophysiological correlates of visual categorization: evidence for cognitive dysfunctions in early Parkinson's disease.

Our aim was to examine the electrophysiological correlates of perceptual categorization in Parkinson's disease (PD). We recorded visual event-related potentials (ERPs) in a natural scene categorization task in drug naive idiopathic PD patients and healthy control subjects. In the control group, there was a significant early difference (150-250 ms poststimulus) between ERPs elicited by pictures containing animals and scenes without animals. In spite of relatively preserved basic-level visual functions, this was not observable in the PD group. These results raise the possibility for striatal contributions to visual categorization and may provide a novel protocol for further clinical studies.

Aged↗

PubMed1999

Interleukin-1 receptor antagonist attenuates regional neuronal cell death and cognitive dysfunction after experimental brain injury.

The effect of systemic administration of human recombinant interleukin-1 receptor antagonist (rhIL-1ra) on behavioral outcome and histopathologic damage after lateral fluid-percussion brain injury of moderate severity was evaluated. In study 1, brain-injured Sprague Dawley rats received timed subcutaneous injections beginning 15 minutes after injury of either 100 mg/kg rhIL-1ra (high dose, total dose = 1900 mg/kg), 10 mg/kg rhIL-1ra (low dose, total dose = 190 mg/kg), or vehicle over 7 days. No effect of low-dose rhIL-1ra was observed in study 1. High-dose rhIL-1ra significantly attenuated posttraumatic neuronal loss in the injured hippocampal CA3 region (P < 0.05), dentate hilus (P < 0.05), and cortex (P < 0.05) but impaired recovery of motor function at 7 days after trauma (P < 0.05). In study 2, rats were pretrained to learn a visuospatial task in a Morris water maze, subjected to fluid-percussion brain injury or sham treatment, and randomly assigned to receive multiple subcutaneous injections at timed intervals of 100 mg/kg rhIL-1ra (total dose = 900 mg/kg) or vehicle over 42 hours, followed by continuous infusion of a lower concentration of rhIL-1ra (20 mg/kg/day, total dose = 100 mg/kg), or vehicle for 5 days using subcutaneously implanted osmotic minipumps. Postinjury administration of rhIL-1ra significantly attenuated cognitive deficits compared with vehicle-treated animals at 42 hours (P < 0.05) but did not affect motor function at 48 hours, 1 week, and 2 weeks. These results suggest that inhibitors of cytokine pathways may be therapeutically useful for the treatment of brain trauma.

Animals↗

PubMed1994

Cognitive dysfunction following subcortical infarction.

OBJECTIVE: To determine the association between computed tomographic scan findings of subcortical infarction, periventricular lucency, and ventricular enlargement and a patient's performance on a range of neuropsychological tests. DESIGN: Prospective study of patients in whom computed tomographic scanning identified discrete areas of subcortical lucency that were consistent with multiple subcortical infarcts and in whom there was no evidence for additional cerebral computer tomographic pathology. SETTING: Hospital practice that included both inpatients and ambulatory patients. PATIENTS: One hundred forty-seven consecutive appropriate computed tomographic scans were identified. Sixty-two patients were excluded because of concomitant medical disorders, and eight refused participation. We describe 77 patients. MAIN OUTCOME MEASURES: Performance on a battery of neuropsychological tests. RESULTS: The number of infarcts but not the volume of infarction, periventricular lucency, and cerebral ventricular enlargement but not cortical atrophy were significantly associated with impaired performance on neuropsychological tests. The number of infarcts correlated with impaired performance on tests, and this impaired performance was thought to be dependent on the function of frontal systems, while periventricular lucency and ventricular enlargement correlated with impaired performance on a wider range of tests, including tests that depended on memory and language. CONCLUSIONS: The number of infarcts, periventricular lucency, and ventricular enlargement are the computed tomographic head scan parameters that correlated with severity of impaired performance on neuropsychological tests in patients with subcortical infarction. Cognitive impairment is presumed to be the result of cortical disconnection following disruption of the connections between the subcortical regions and the frontal cortex.

Aged↗

PubMed1992

Brief communication. Vitamin B1, B2, and B6 augmentation of tricyclic antidepressant treatment in geriatric depression with cognitive dysfunction.

This was a 4-week randomized placebo-controlled double-blind study to assess augmentation of open tricyclic antidepressant treatment with 10 mg each of vitamins B1, B2, and B6 in 14 geriatric inpatients with depression. The active vitamin group demonstrated significantly better B2 and B6 status on enzyme activity coefficients and trends toward greater improvement in scores on ratings of depression and congnitive function, as well as in serum nortriptyline levels compared with placebo-treated subjects (Ss). Without specific supplementation, B12 levels increased in Ss receiving B1/B2/B6 and decreased in placebo Ss. These findings offer preliminary support for further investigation of B complex vitamin augmentation in the treatment of geriatric depression.

Aged↗

PubMedDate not supplied

Cellular delivery of human CNTF prevents motor and cognitive dysfunction in a rodent model of Huntington's disease.

The delivery of ciliary neurotrophic factor (CNTF) to the central nervous system has recently been proposed as a potential means of halting or slowing the neural degeneration associated with Huntington's disease (HD). The following set of experiments examined, in detail, the ability of human CNTF (hCNTF) to prevent the onset of behavioral dysfunction in a rodent model of HD. A DHFR-based expression vector containing the hCNTF gene was transfected into a baby hamster kidney fibroblast cell line (BHK). Using a polymeric device, encapsulated BHK-control cells and those secreting hCNTF were transplanted bilaterally into rat lateral ventricles. Eight days later, the same animals received bilateral injections of quinolinic acid (QA, 225 nmol) into the previously implanted striata. A third group received sham surgery (incision only) and served as a normal control group. Bilateral infusions of QA produced a significant loss of body weight and mortality that was prevented by prior implantation with hCNTF-secreting cells. Moreover, QA produced a marked hyperactivity, an inability to use the forelimbs to retrieve food pellets in a staircase test, increased the latency of the rats to remove adhesive stimuli from their paws, and decreased the number of steps taken in a bracing test that assessed motor rigidity. Finally, the QA-infused animals were impaired in tests of cognitive function-the Morris water maze spatial learning task, and the delayed nonmatching-to-position operant test of working memory. Prior implantation with hCNTF-secreting cells prevented the onset of all the above deficits such that implanted animals were nondistinguishable from sham-lesioned controls. At the conclusion of behavioral testing, 19 days following QA, the animals were sacrificed for neurochemical determination of striatal choline acetyltransferase (ChAT) and glutamic acid decarboxylase (GAD) levels. This analysis revealed that QA decreased striatal ChAT levels by 35% and striatal GAD levels by 45%. In contrast, hCNTF-treated animals did not exhibit any decrease in ChAT levels and only a 10% decrease in GAD levels. These results support the concepts that implants of polymer-encapsulated hCNTF-releasing cells can be used to protect striatal neurons from excitotoxic damage, produce extensive behavioral protection as a result of that neuronal sparing, and that this strategy may ultimately prove relevant for the treatment of HD.

Animals↗

PubMed2004

Cognitive dysfunction in cholesterol embolic disease.

A patient who developed neurological and renal complications following coronary angiogram and coronary artery bypass grafting is reported. Neurological involvement was in the form of fluctuating sensorium and a subcortical pattern of dementia. Renal failure was seen in the form of raised urea and creatinine levels. Renal biopsy revealed the cause of the renal failure to be due to cholesterol embolic disease. While the sensorium often improved following renal replacement therapy (dialysis), the dementia was poorly responsive to therapy. The patient succumbed due to progressive renal failure. Awareness of the protean manifestations and a high index of suspicion are essential for appropriate diagnosis in order to enable the clinician to accurately prognosticate in this often fatal disease.

Basal Ganglia↗

PubMed1998

Hypoglycemia in children with diabetes: incidence, counterregulation and cognitive dysfunction.

Hypoglycemia remains a critical problem in the treatment of IDDM and often limits our ability to consistently achieve excellent glycemic control. Ongoing studies will be important to increase our understanding of the factors responsible for its occurrence and the impact that hypoglycemia may have, particularly for the brain. Significant differences have been documented between adults and children in the incidence of this complication of insulin therapy as well as in the counterregulatory hormone responses to hypoglycemia and its effects on the CNS. While children with diabetes still need insulin treatment, the prevention of hypoglycemia will be a central aim of management. This will depend on effective and expert diabetes education and support for the patient and his or her family along with better efforts to achieve more physiological insulin replacement.

Adolescent↗

PubMed1996

Pathogenesis of irradiation-induced cognitive dysfunction.

Neurocognitive dysfunction is a common sequela of cranial irradiation that is especially severe in young children. The underlying mechanisms of this disorder have not been described. The present review describes the role of the hippocampus and the anatomically related cortex in memory function and its marked susceptibility to ischemic and hypoxic injury. Based on studies of animal models of human amnesia and histopathological findings in the irradiated brain, the neurocognitive sequela of cranial irradiation can be seen to be mediated through vascular injury, resulting in ischemia and hypoxia in the hippocampal region. Recognition of the site and mechanisms of this injury may lead to the development of techniques to minimize the risks.

Age Factors↗