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Transcranial Doppler sonography in dementia of Alzheimer type.

The intention of this study was to examine the relation of clinical variables and cognitive dysfunction to cerebrovascular blood flow in a sample of patients with Alzheimer's disease without any sign or symptom of cardiovascular or cerebrovascular disease. The patients met DSM-III-R criteria for dementia of Alzheimer type. Blood flow velocities in the anterior, middle (MCA) and posterior cerebral arteries were recorded using transcranial Doppler sonography. Several psychometric tests including the Mini-Mental State Examination (MMSE) were performed. The patients' age correlated significantly with the systolic flow velocity in the left MCA (r = -0.57) explaining 24% of the total variance; there was a reduction of the mean flow velocity of 0.7 +/- 0.2 mm/s for every additional year. The MMSE correlated significantly with the systolic flow velocity in the left MCA (r = 0.62) explaining 29% of the total variance. The correlations of flow velocities with age indicate that even in very old patients there is a progressive reduction of cerebral blood flow velocities. The independent negative correlations of flow velocities with cognitive dysfunction indicate that there are progressive cerebrovascular flow reductions in the course of Alzheimer's disease. Both facts should be taken into account when Alzheimer patients are compared with other samples.

Aged↗
PubMed2004

Increased serum matrix metalloproteinase 9 levels in systemic lupus erythematosus patients with neuropsychiatric manifestations and brain magnetic resonance imaging abnormalities.

OBJECTIVE: To evaluate whether serum matrix metalloproteinase 9 (MMP-9) levels are associated with neuropsychiatric manifestations, particularly cognitive dysfunction, as evaluated by neuropsychological testing and brain magnetic resonance imaging (MRI) abnormalities in patients with systemic lupus erythematosus (SLE). METHODS: MMP-9 determinations were made in 44 patients with SLE and 43 healthy controls who underwent a clinical neurologic and neuropsychological investigation in order to identify neuropsychiatric manifestations. Cerebral MRI scans with volumetric estimation of intracranial cerebrospinal fluid spaces, T1-weighted lesions, and T2-weighted lesions were performed for all subjects. SLE activity was assessed by the European Consensus Lupus Activity Measure (ECLAM) index, and accumulated neuropsychiatric abnormality was assessed by the Systemic Lupus International Collaborating Clinics (SLICC)/American College of Rheumatology damage index. RESULTS: No significant difference was found in serum MMP-9 levels between the overall group of SLE patients and controls. However, SLE patients who had at least 1 neuropsychiatric manifestation (NPSLE patients) had significantly higher serum MMP-9 concentrations than did SLE patients without neuropsychiatric syndromes (P = 0.009). Among patients with NPSLE, those with cognitive deficits had significantly higher concentrations of serum MMP-9 than did those with normal cognitive function (P = 0.027). Furthermore, serum MMP-9 levels had a significant positive correlation with the volumes of T1-weighted and T2-weighted lesions in the brain MRI (P = 0.031 and P = 0.015, respectively). The concentration of serum MMP-9 correlated significantly with the SLICC index but not with the ECLAM index. CONCLUSION: Elevated levels of serum MMP-9 in patients with SLE may reflect neuropsychiatric involvement, particularly cognitive dysfunction. The serum MMP-9 concentration may be associated with small- vessel cerebral vasculopathy and increased risk of cerebral ischemic events in patients with SLE.

Adult↗
PubMed1997

Proton magnetic resonance spectroscopy in dementia of Alzheimer type.

Reduced N-acetyl aspartate (NAA) and increased myo-inositol (MI) levels have been reported in patients with dementia of Alzheimer type (DAT) in comparison with controls. We wished to assess the validity of these findings and to evaluate possible correlations of metabolite proportions with cognitive dysfunction in DAT. Twelve patients with DAT and 10 healthy age-matched controls were included. The severity of dementia was assessed using different scales including the Mini-Mental State Examination. MRS was performed with a conventional 1.5 Tesla scanner in a single voxel in the centrum semi-ovale (TE = 30 ms or TE = 136 ms; TR = 1500 ms). The evaluation of MRS results was limited by low interrater, intermeasurement (different echo times) and test-retest reliabilities, by a high interindividual variance and by the failure to measure absolute metabolite concentrations. These problems in mind, it was remarkable that previously reported reductions of NAA levels in patients with DAT could be reproduced in the present sample. The proportion of NAA was diminished in demented subjects in comparison with controls (37% vs 44.90%, short TE). A non-significant trend towards minor reductions of creatine, choline and MI proportions in these subjects might indicate that proportions of other metabolites necessarily increase when NAA is reduced. Cognitive dysfunction of demented subjects was significantly correlated with reductions of NAA, but not with increases of MI. Due to the present technical and methodological problems and to the non-specificity of findings, proton MRS cannot be applied to support the diagnosis of DAT in a clinical setting.

Aged↗
PubMed2002

The partial reinforcement extinction effect in humans: effects of schizophrenia, schizotypy and low doses of amphetamine.

The partial reinforcement extinction effect (PREE) was studied in human subjects. It has been suggested that the PREE depends on neural mechanisms critical to the cognitive dysfunction which underlines acute schizophrenia. We therefore predicted that the PREE should be reduced, through decreased resistance to extinction in the partial reinforcement (PR) condition, in various types of individual: (a) healthy volunteers given low doses of oral amphetamine; (b) those in the acute (but not chronic) phase of a schizophrenic illness and; (c) healthy volunteers with high scores on personality measures of schizotypy. Despite obtaining robust demonstrations of PREE in all experiments, none of these predictions were confirmed. A single, low dose, of amphetamine had no effect on either continuous reinforcement (CR) or partial reinforcement (PR). Acute and chronic schizophrenic patients showed a reduced PREE compared to controls. However this was due to increased resistance to extinction in the CR groups. Finally, high schizotypy scores were associated with greater PREE, attributable to both decreased extinction in the CR condition and increased extinction in the PR condition. The results of these experiments on human PREE provide no support that PREE is a valid paradigm with which to explore the cognitive dysfunction underlying schizophrenia.

Acute Disease↗
PubMed2001

Pulse oximetry for perioperative monitoring.

BACKGROUND: Monitoring with pulse oximetry might improve patient outcome by enabling an early diagnosis and consequently, correction of perioperative events that might cause postoperative complications or even death. Only a few randomised clinical trials of pulse oximetry have been performed during anaesthesia and in the recovery room which describe perioperative hypoxaemic events, postoperative cardiopulmonary complications and cognitive dysfunction. OBJECTIVES: To study the effect of perioperative monitoring with pulse oximetry to clearly identify the adverse outcomes that might be prevented or improved by the use of pulse oximetry. SEARCH STRATEGY: Trials were identified by computerised searches of the Cochrane Library, MEDLINE, EMBASE, and by checking the reference lists of trials and review articles. SELECTION CRITERIA: All controlled trials that randomised patients to either pulse oximetry or no pulse oximetry during the perioperative period, including the operating and recovery room. DATA COLLECTION AND ANALYSIS: We collected data in relation to events detectable by pulse oximetry, any serious complications that occurred during anaesthesia or in the postoperative period, intra- or postoperative mortality, and duration of recovery or intensive care stay. Formal statistical synthesis of individual trials was not performed in view of the variety of outcomes studied. MAIN RESULTS: Searching identified six reports; four studies with data from a total of 21,773 patients were considered eligible for analysis. Only two studies specifically addressed the outcomes in question; both found no effect on the rate of postoperative complications using perioperative pulse oximetry. Two studies used hypoxaemia detectable by pulse oximetry to assess the value of perioperative monitoring, although outcomes were not given. It was found that hypoxaemia was reduced in the pulse oximetry group both in the operating theatre and in the recovery room. During observation in the recovery room, the incidence of hypoxaemia in the pulse oximetry group was 1.5-3 times less. The postoperative cognitive function using the Wechsler memory scale and continuous reaction time was independent of perioperative monitoring with pulse oximetry. The other study showed that postoperative complications occurred in 10% of the patients in the oximetry group and in 9.4% in the control group. The two groups did not differ in cardiovascular, respiratory, neurologic, or infectious complications. The duration of hospital stay was a median of 5 days in both groups, and an equal number of in-hospital deaths was registered in the two groups. REVIEWER'S CONCLUSIONS: The studies confirmed that pulse oximetry can detect hypoxaemia and related events. However, we have found no evidence that pulse oximetry affects the outcome of anaesthesia. The conflicting subjective and objective results of the studies, despite an intense, methodical collection of data from a relatively large population, indicates that the value of perioperative monitoring with pulse oximetry is questionable in relation to improved reliable outcomes, effectiveness and efficiency.

Humans↗
PubMed2007

Glutathione elevation by gamma-glutamyl cysteine ethyl ester as a potential therapeutic strategy for preventing oxidative stress in brain mediated by in vivo administration of adriamycin: Implication for chemobrain.

Oxidative stress in heart and brain by the cancer chemotherapeutic drug adriamycin (ADR), used for treating solid tumors, is well established. Long-term treatment with ADR in breast cancer patients has led to symptoms of cardiomyopathy. Less well recognized, but increasingly well documented, is cognitive dysfunction. After chemotherapy, free radical-mediated oxidative stress has been reported in both heart and brain. We recently showed a significant increase in protein oxidation and lipid peroxidation in brain isolated from mice injected intraperitonially (i.p) with ADR. Systemic administration of ADR also induces tumor necrosis factor-alpha (TNF-alpha), which leads to production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in brain. Circulating TNF also causes mitochondrial dysfunction, leading to apoptotic pathways in brain. Inducible nitric oxide synthase also plays a role in ADR-induced TNF-mediated neurotoxicity. In addition, we previously showed a significant decrease in glutathione (GSH) levels in brain isolated from ADR injected mice, along with increased expression of multidrug-resistant protein-1 (MRP-1), glutathione-S-transferase (GST), glutathione peroxidase (GPx), and glutathione reductase (GR). There was a significant decrease in activity of brain GST. The present study was designed to test the hypothesis that, by elevating brain levels of GSH, the brain would be protected against oxidative stress in ADR-injected mice. gamma-Glutamyl cysteine ethyl ester (GCEE), a precursor of glutathione, injected i.p. (150 mg/ kg body weight) 4 hr prior ADR injection (20 mg/kg body weight) led to significantly decreased protein oxidation and lipid peroxidation in subsequently isolated mice brain compared with brain isolated from ADR-injected mice without GCEE. The GSH levels were restored to the level of brain isolated from saline-injected mice. Furthermore, the enzyme activity of GST was increased in brain isolated from ADR-injected mice previously injected with GCEE compared with the brain isolated from ADR-injected mice previously injected with saline. These results are discussed with regard to potential pharmacological prevention of brain cognitive dysfunction in patients receiving ADR chemotherapy.

Animals↗
PubMed2004

Increased expression of neuronal cyclooxygenase-2 in the hippocampus in amyotrophic lateral sclerosis both with and without dementia.

The pathophysiological basis of cognitive dysfunction, including frontotemporal dementia (FTD), in patients with amyotrophic lateral sclerosis (ALS) and ALS with dementia (ALSD) remains unclear. On the other hand, increased expression of cyclooxygenase-2 (COX-2) in the spinal cord is thought to play a pivotal role in motor neuron degeneration in ALS. In this study, to assess the relationship between the neuronal COX-2 expression in the cerebrum, the formation of tau- and alpha-synuclein-negative but ubiquitin-positive neuronal inclusions (UPIs), and dementia in motor neuron disease (MND), we examined neuronal COX-2 immunoreactivity in the frontal cortex and hippocampus of patients with non-demented ALS without UPIs ( n=11), ALSD with UPIs ( n=6), and normal controls ( n=24) using a quantitative immunohistochemical technique. Neuronal COX-2 expression in all CA1-4 in the hippocampus was significantly up-regulated in the ALSD group, and, to lesser degree but significantly, in the ALS group. Neuronal COX-2 expression in the frontal cortex was also significantly up-regulated in the ALSD group but not in the ALS group. These findings suggest that (1) the frontal cortex and hippocampus of MND are involved in the same pathogenic process associated with COX-2 induction that has been observed in spinal anterior horn cells, (2) COX-2 induction in the cerebrum is a pathogenic process that can occur even in the absence of UPI formation in MND, and (3) COX-2 expression in the cerebrum may be associated with cognitive dysfunction in MND.

Aged↗
PubMed2002

Analysis of cerebral blood flow of subcortical vascular dementia with single photon emission computed tomography: adaptation of statistical parametric mapping.

BACKGROUND AND OBJECTIVES: Subcortical vascular dementia (VaD) is a relatively homogeneous subtype of VaD, but the mechanisms of cognitive dysfunction of subcortical VaD are not fully understood. This study investigates the changes of cerebral blood flow (CBF) in patients with subcortical VaD and the contribution of the white matter hyperintensity (WMHI) and clinical severity to CBF changes. METHODS: 99mTc-ethyl cysteinate dimer single photon emission computed tomography (SPECT) was performed to measure the regional CBF and statistical parametric mapping SPM99 software was applied to automated and objective analysis of the SPECT image data. Twenty-three patients (12 male, 11 female) with mild to moderate dementia who met both the criteria of the DSM-IV and probable and possible NINDS-AIREN for VaD and had subcortical white matter changes and lacunar infarctions in brain MRI were evaluated against 17 normal control subjects (7 male, 10 female). The severity of the WMHI was measured by the semi-quantitative scale method proposed by Mäntyla. The Clinical Dementia Rating scale measured the severity of dementia. RESULTS: SPM analysis of the SPECT image reveals significantly reduced regional CBF in the right thalamus, left caudate nucleus, cingulate, bilateral superior temporal, and left ventral subcallosal gyri in subcortical VaD patients compared to the normal controls (corrected P<0.001). Of four WMHIs, only the deep WMHI was associated with the small CBF reduction in the left superior temporal gyrus (uncorrected P<0.01). The reduction of the CBF according to the severity of dementia was noted in the anterior and posterior association areas (uncorrected P<0.01). CONCLUSIONS: Our study suggests that cognitive dysfunction of subcortical VaD may be related to the reduction of the CBF in the brain areas mentioned, which are probably not associated with the severity of periventricular WMHI and dementia.

Aged↗
PubMed1996

The cardinal features of cognitive and noncognitive dysfunction and the differential efficacy of tacrine in Alzheimer's disease patients.

The Alzheimer's Disease Assessment Scale (ADAS), frequently used in clinical trials to assess overall pathology of Alzheimer's disease (AD), comprises two subscales. The cognitive subscale (ADAS-COG) consists of 11 items, and the noncognitive subscale consists of 9 items. Factor analyses were carried out on ADAS-COG and ADAS-NONCOG item scores from the most recent and largest (n = 663) placebo-controlled, multicenter, 30-week study (970-61) of tacrine in patients with AD conducted by the clinical research group at Parke-Davis Pharmaceutical Research. Through factor analyses the primary dimensions of variation in the ADAS-COG and ADAS-NONCOG were defined. Obliquely rotated three principal factors of ADAS-COG and three principal factors of ADAS-NONCOG have been interpreted as three cardinal features of cognitive function corresponding to memory, language, and praxis, and three cardinal features of noncognitive function corresponding to agitation, depression, and lack of concentration. Reliably defined factors of ADAS-COG enabled comparisons of longitudinal changes in cognitive dysfunction. Factor scores at week 30, adjusted to baseline factor scores, were used to compare the effects of tacrine with those of placebo on cognitive cardinal features. Additionally, the effect of concurrent depression on cardinal features of cognitive dysfunction was evaluated by gender.

Aged↗
PubMed2002

Cognitive reactivity to sad mood: structure and validity of a new measure.

Cognitive reactivity to the experimental induction of sad mood has been found to predict relapse in recovered depressed patients. The present report describes the development and test of a questionnaire that aims to measure cognitive reactivity independently from a mood induction procedure. The Leiden Index of Depression Sensitivity (LEIDS) was filled out by 198 participants. After Principal Components Analysis, 26 items were retained, which comprised four factors with good psychometric properties: Negative Self-Evaluation; Acceptance/Coping; Indifference; and Harm Avoidance. In a sample of 48 college students, LEIDS scores--particularly Negative Self-Evaluation and Harm Avoidance--were rather strong predictors of cognitive reactivity in a mood induction procedure. In contrast, baseline depression and baseline cognitive dysfunction did not predict cognitive reactivity. It is concluded that the LEIDS is a promising measure of cognitive reactivity, and that clinical studies need to be carried out to test its ability to predict relapse of depression.

Adolescent↗
PubMed2002

Effects of LP-BM5 murine leukemia virus infection on errors and response time in a two-choice serial reaction time task in C57BL/6 mice.

Human immunodeficiency virus type 1 (HIV-1) infection is often accompanied by cognitive, motor, and behavioral dysfunction. Cognitive function diminishes in indices of attention, psychomotor speed, and learning and memory. These are collectively termed acquired immunodeficiency syndrome dementia complex (ADC or neuroAIDS). Inoculation with the LP-BM5 murine leukemia virus (MuLV) causes profound immunosuppression (murine acquired immunodeficiency syndrome, or MAIDS) in C57BL/6 mice. Previous studies show that the LP-BM5 MuLV impairs learning and memory without gross motor impairment. Since learning and memory performance deficits can be related to attention deficits, we assessed the effect of LP-BM5 MuLV infection on sustained attention performance using a two-choice serial reaction time task. This task required the animals to detect a visual stimulus presented randomly on the right or the left unit and respond by a nose-poke in the illuminated hole within a 5 s period for water reward. The LP-BM5 MuLV infected group, like the control group, improved sustained attention performance until 7 weeks of virus infection in all measures including choice accuracy, response omission, and correct response time. However, during the late stage of infection, LP-BM5 MuLV infected mice showed selective sustained attention performance deficits. From 8 weeks after LP-BM5 MuLV infection, the virus infected mice started to lose their improved sustained attention performance in response omission and began to make correct responses more slowly than the control mice when the duration of stimulus light was 5 s. Moreover, at 13 and 14 weeks after LP-BM5 MuLV infection, the virus infected group made correct choices significantly less accurately than the control group when duration of stimulus light was shortest (1 s). These data show that LP-BM5 MuLV infection causes not only the previously reported learning and memory deficits but also produces sustained attention performance deficits in mice.

Animals↗
PubMed1998

Scopolamine model of dementia: electroencephalogram findings and cognitive performance.

BACKGROUND: Memory and cognitive functions are known to decline with advancing age. Studies have suggested that this may be due to a decrease in cholinergic function in the brains of elderly people. This review aims to assess studies documented in the literature dealing with the 'scopolamine model' of dementia. METHODS: Sources included MedLine searches from the last 10 years (search for 'scopolamine model', 'dementia', 'electroencephalogram', 'cognition') and references from original and review articles. The aim was to include human and animal studies occupying the cholinergic hypothesis in cognitive dysfunction. Electroencephalographic (EEG) and cognition findings were considered. RESULTS: Scopolamine influences delta, theta, alpha and beta activity in EEG and partially mimics the EEG changes found in patients with senile dementia or dementia of the Alzheimer type. Effects on different cognitive functions have been extensively documented. CONCLUSION: Scopolamine produces similar memory deficits seen in the elderly, but the drug cannot induce the full range of deficits seen in patients with Alzheimer's disease. Various aspects of memory were unaffected by scopolamine administration. Memory improvements in elderly subjects can be achieved after cholinergic stimulation.

Aged↗
PubMed2002

Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: partial reversal by feeding acetyl-L-carnitine and/or R-alpha -lipoic acid.

Accumulation of oxidative damage to mitochondria, protein, and nucleic acid in the brain may lead to neuronal and cognitive dysfunction. The effects on cognitive function, brain mitochondrial structure, and biomarkers of oxidative damage were studied after feeding old rats two mitochondrial metabolites, acetyl-l-carnitine (ALCAR) [0.5% or 0.2% (wt/vol) in drinking water], and/or R-alpha-lipoic acid (LA) [0.2% or 0.1% (wt/wt) in diet]. Spatial memory was assessed by using the Morris water maze; temporal memory was tested by using the peak procedure (a time-discrimination procedure). Dietary supplementation with ALCAR and/or LA improved memory, the combination being the most effective for two different tests of spatial memory (P < 0.05; P < 0.01) and for temporal memory (P < 0.05). Immunohistochemical analysis showed that oxidative damage to nucleic acids (8-hydroxyguanosine and 8-hydroxy-2'-deoxyguanosine) increased with age in the hippocampus, a region important for memory. Oxidative damage to nucleic acids occurred predominantly in RNA. Dietary administration of ALCAR and/or LA significantly reduced the extent of oxidized RNA, the combination being the most effective. Electron microscopic studies in the hippocampus showed that ALCAR and/or LA reversed age-associated mitochondrial structural decay. These results suggest that feeding ALCAR and LA to old rats improves performance on memory tasks by lowering oxidative damage and improving mitochondrial function.

Acetylcarnitine↗
PubMed2005

Alleviative effects of gamma-aminobutyric acid (GABA) on behavioral abnormalities in aged dogs.

gamma-aminobutyric acid (GABA, 30 mg/kg) was administered to aged dogs with recent history of veterinary clinic visits (mean age: 15.3 years old) once daily for 2 weeks by mixing with food. Their owners subjectively evaluated the effects of GABA on behavioral signs often associated with aging in the dogs. Improvement in some of behavioral signs was notable without any observable adverse effects. Dogs administered with GABA tended to exhibit improvement in emotional states and signs may be caused by neurovegetable dysfunction, though effects on cognitive dysfunction syndrome were not always observed. Thus, GABA administration may be one of the effective means of improving the quality of life of aged dogs.

Aging↗
PubMed1991

Chronic low-dose MPTP in nonhuman primates: a possible model for attention deficit disorder.

Schneider and Kovelowski (1990) showed that chronic low-dose N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration to monkeys caused cognitive dysfunction without significant motor impairment on tasks thought to be related to the caudate-frontal axis. The cognitive difficulties were similar to those seen in monkeys with frontal lesions, normal young monkeys, and normal young children. The caudate-frontal dysfunction is consistent with the cognitive difficulties that are thought to exist in children with attention deficit disorder (ADD). The caudate-frontal dysfunction is also consistent with the distribution of decreased cerebral blood flow and, presumably, decreased metabolism that has recently been found in children with ADD. In monkeys given chronic low-dose MPTP, pilot neurochemical studies have suggested abnormalities in dopamine and norepinephrine metabolism, the two neurotransmitters most frequently linked with ADD. We suggest that chronic low-dose MPTP induced cognitive dysfunction in primates may not only be a model for the cognitive disturbances that accompany Parkinson's disease but may also aid in understanding the cognitive dysfunction seen in children with ADD.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2026

Ultra-high-field 7T MRI reveals neural abnormalities of attention networks in relation to cognitive impairment in hypertension.

Hypertension is a significant risk factor for cognitive impairment (CI), yet the corresponding neural network abnormalities remain underexplored. In this study, we examined the associations among global and domain-specific cognitive dysfunction, neuroimaging measures, and blood pressure in a subgroup of hypertensive patients with CI (N&#xa0;=&#xa0;41) from a randomized controlled trial who underwent ultra-high-field 7&#xa0;T MRI. Structural atrophy related to CI was localized to regions overlapping the attention networks. Both whole-brain and within-network dysfunction of the attention networks were associated with worse global cognitive performance. Notably, hyperconnectivity within key attention network hubs, including the right anterior insula and posterior intraparietal sulcus, was associated with declined processing speed in hypertensive patients, mediating the association between pulse pressure and processing speed. These findings provide new insights into the neural pathophysiology of hypertension-related CI and suggest potential network-based targets for intervention.

Magnetic Resonance Imaging↗
PubMed2005

Small ischemic brain lesions after cardiac valve replacement detected by diffusion-weighted magnetic resonance imaging: relation to neurocognitive function.

OBJECTIVE: Following coronary artery bypass graft surgery, some studies using magnetic resonance imaging (MRI) have demonstrated new small ischemic brain lesions in patients without apparent neurological deficits. We aimed to prospectively evaluate brain injury after cardiac valve replacement using MRI and to determine the relationship to neurocognitive function. METHODS: Thirty patients with a mean age of 64.9+/-9.8 years (range, 32-82, 12 female) receiving cardiac valve replacement (aortic valve replacement [AVR], n = 24; mitral valve replacement [MVR], n = 2; AVR and MVR, n = 2; AVR and mitral valve repair, n = 2) were investigated. Study protocol included neurological examination, comprehensive neuropsychological assessment and diffusion-weighted (DW) MRI. The investigations were performed before surgery and 5 days and 4 months after surgery. RESULTS: Postoperative DW MRI detected new focal brain lesions in 14 patients (47%). No patient revealed a focal neurological deficit. Six patients (43%) had multiple (> or = 3) lesions (range, 1-7). Lesion volume ranged from 50-500 mm3 except 1 territorial infarct of 1900 mm3. Of a total of 41 lesions, 27 (66%) were located in the right hemisphere and 32 in a subcortical location. By 5 days postoperatively, significant neurocognitive decline was observed in 5 of 13 tests affecting memory, attention and rate of information processing. By 4 months, dysfunction had recovered in all cognitive areas. The presence of new ischemic lesions was not associated with neurocognitive decline at discharge. There was also no significant correlation between clinical and operative variables and the presence of new DW lesions or neuropsychological outcome. CONCLUSIONS: Following cardiac valve replacement, new small ischemic brain lesions were detected by diffusion-weighted MRI. Neurocognitive decline was present early after operation, but resolved within 4 months. A correlation of new ischemic lesions to postoperative cognitive dysfunction or clinical variables was not found.

Adult↗