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PubMed2004

Perceptual span deficits in adults with HIV.

Studies have found that infection with the Human Immunodeficiency Virus (HIV) leads to cognitive dysfunction. In fact, attention problems have been reported to be the most frequent cognitive symptom in HIV-infected adults. One question is how early in the course of information processing can attention impairment be detected? To address this issue, performance on a perceptual span task was examined in 54 HIV-infected adults and 19 seronegative controls. In this task a target had to be identified in a briefly presented (50 ms) array of 1, 4, or 12 letter-characters. Response accuracy was differentially worse in the HIV+ group relative to seronegative controls in the most difficult condition, the 12-item array, but not in the easier conditions. There was no evidence of a group difference in response strategy due to disinhibition or in psychomotor speed. These data suggest that HIV infection leads to a reduction in early visual processing capacity (or span of apprehension). The present results illustrate a new type of attentional deficit in HIV and show the impact of HIV on cognition at an earlier point in information processing than has been previously reported.

Adult↗

PubMed2002

Neuropsychological impairment in patients with chronic hepatitis C.

Hepatitis C is the most common cause of chronic liver disease in the United States and it significantly reduces quality of life. The role of cognitive deficits contributing to the morbidity of this disease has not been well characterized. The purpose of this study was to examine cognitive functioning in patients with chronic hepatitis C and to investigate relationships among parameters of disease severity and performance on neuropsychological tests. Sixty-six patients with chronic hepatitis C and 14 patients with other chronic liver diseases were administered a brief battery of neuropsychological tests assessing attention, visuoconstructional ability, learning, memory, and psychomotor speed. Cognitive impairment in patients with chronic hepatitis C ranged from 0% on a visuoconstructional task to 82% on a measure of sustained attention and concentration. Test scores of patients with chronic hepatitis C did not differ from those of patients with other chronic liver diseases. Hence, patients with and without chronic hepatitis C experience cognitive deficits, especially in tasks requiring attention and psychomotor speed. In addition, there was a significant relationship between fibrosis stage and test performance, with greater fibrosis associated with poorer performance. However, both patients with and without cirrhosis exhibited cognitive dysfunction. In conclusion, these findings suggest that progressive hepatic injury may result in cognitive problems even before the development of cirrhosis. Future studies need to determine the effect of this decrease in cognitive function on quality of life.

Adult↗

PubMed2005

Homocysteine and cognitive function.

The prevention and treatment of age-related cognitive impairment and dementia is one of the greatest and most elusive challenges of our time. The prevalence of dementia increases exponentially with age, as does the prevalence of those with micronutrient deficiency. Several studies have shown that elevated homocysteine is correlated with cognitive decline and with cerebral atrophy and that it predicts the subsequent development of dementia in cognitively intact middle-aged and elderly individuals. If elevated homocysteine promotes cognitive dysfunction, then lowering homocysteine by means of B-vitamin supplementation may protect cognitive function by arresting or slowing the disease process.

Cognition↗

PubMed1993

Neuropathology of herpes simplex virus encephalitis in a rat seizure model.

Herpes simplex virus type 1 (HSV-1) is the cause of a serious and often fatal encephalitis. Patients who survive herpes simplex encephalitis (HSE) experience behavioral abnormalities including profound cognitive dysfunctions. We have developed a rat model of acute HSE to investigate the cognitive impairments caused by HSV-1 central nervous system (CNS) infection. Following intranasal inoculation of Lewis rats with a neurovirulent strain of HSV-1, animals shed virus in both ocular and nasal secretions and developed clinical signs of infection, including partial complex motor seizures that eventually generalized. Homogenization assays demonstrated infectious virus in the trigeminal ganglia, olfactory bulbs, and the piriform and entorhinal cortices. Histopathological assessment revealed inflammatory and hemorrhagic lesions in the trigeminal ganglia, olfactory bulbs, amygdala, hippocampus, the piriform and entorhinal cortices, and the spinal trigeminal nuclei. Viral antigens and nucleic acids were also detected within these structures by immunofluorescence microscopy and in situ hybridization, respectively. Viral-induced astrocytic hypertrophy in the CNS was demonstrated by glial fibrillary acidic protein immunoreactivity. Together, these results indicate that HSV-1 has the ability to invade, replicate, and induce site-specific CNS damage in the Lewis rat.

Animals↗

PubMed1998

Cognitive deficits in the acute stage after subarachnoid hemorrhage.

OBJECTIVE: In spite of fundamentally improved medical management of subarachnoid hemorrhage (SAH), many patients remain mentally impaired. However, the causes of these disturbances are unclear. The present study was performed to elucidate the significance of the hemorrhage itself and related events in the neuropsychological performance of patients in the acute stage after SAH. METHODS: A series of 51 patients were examined, by means of a battery of cognitive tests, 1 to 13 days (mean, 5.9 d) after SAH. Thirty-three patients had experienced ruptured aneurysms, and 18 had sustained SAH of unknown origin. Furthermore, 25 patients who had undergone surgical treatment (a mean of 5.0 d earlier) of prolapsed lumbar discs served as a control group. RESULTS: The cognitive deficits of the patients after aneurysmal SAH proved to be comparable to those after spontaneous SAH of unknown origin, with the single exception of a significantly worse (P = 0.003) concentration capacity in the surgically treated group. The severity of SAH in computed tomographic scans correlated (up to r = 0.57, P < 0.001) with poor performance on tests of memory, concentration, divided attention, and perseveration. Frontal intracerebral hemorrhage led to significantly more errors in an aphasia screening test (P < 0.001) and a test of perseveration (P < 0.001). If acute hydrocephalus was present, the patients exhibited worse long-term memory (P < 0.001), showed slower reaction times (P = 0.01), and made more errors in the perseveration test (P = 0.004). Patients with intraventricular blood performed at significantly lower levels in the concentration (P = 0.001), divided attention (P = 0.01), long-term memory (P < 0.001), and perseveration (P = 0.003) tests. CONCLUSION: The results emphasize that the severity of SAH (Fisher score) is the most important factor related to cognitive dysfunction, but frontal hematoma, intraventricular hemorrhage, and acute hydrocephalus were also associated with cognitive deficits, compared with patients with SAH without these findings.

Adult↗

PubMed2006

Anterior-medial thalamic lesions in dementia: frequent, and volume dependently associated with sudden cognitive decline.

BACKGROUND: The anterior-medial thalamus (AMT), which is associated with memory processing, is severely affected by Alzheimer's disease pathology and, when damaged, can be the sole cause of dementia. OBJECTIVE: To assess the frequency of magnetic resonance imaging (MRI) hyperintensities affecting the AMT, and their relationship with sudden cognitive decline. METHODS: 205 consecutive participants from a university cognitive neurology clinic underwent clinical evaluation, neuropsychological testing and quantitative MRI. RESULTS: AMT hyperintensities >5 mm3 occurred in 0 of 34 normal controls but were found in 5 of 30 (17%) participants with cognitive impairment with no dementia (CIND), 9 of 109 (8%) patients with probable Alzheimer's disease, 7 of 17 (41%) with mixed disease and 8 of 15 (53%) with probable vascular dementia (VaD). AMT hyperintensities occurred more often in participants with stepwise decline than in those with slow progression (chi2 = 31.7; p<0.001). Of the 29 people with AMT hyperintensities, those with slow progression had smaller medial temporal width (p<0.001) and smaller anterior-medial thalamic hyperintensities (p<0.001). In a logistic regression model, both variables were significant, and the pattern of decline was correctly classified in 86% of the sample (Cox and Snell R2 = 0.56; p<0.001). Those with AMT hyperintensities >55 mm3 were likely to have stepwise decline in cognitive function regardless of medial temporal lobe width; in contrast, those with smaller AMT hyperintensities showed a stepwise decline only in the absence of medial temporal lobe atrophy. All patients with VaD had left-sided AMT hyperintensities, whereas those with CIND had right-sided AMT hyperintensities. CONCLUSIONS: AMT hyperintensities >55 mm3 probably result in symptomatic decline, whereas smaller lesions may go unrecognised by clinicians and radiologists. Only half of those with AMT hyperintensities had diagnoses of VaD or mixed disease; the other AMT hyperintensities occurred in patients diagnosed with Alzheimer's disease or CIND. These silent hyperintensities may nevertheless contribute to cognitive dysfunction. AMT hyperintensities may represent a major and under-recognised contributor to cognitive impairment.

Adult↗

PubMed1994

Evaluation of the neurobehavioral functioning of patients before, during, and after bone marrow transplantation.

PURPOSE: To evaluate the cognitive and emotional functioning of patients undergoing bone marrow transplantation (BMT) in the protected environment (PE). PATIENTS AND METHODS: Patients were given tests of cognition and mood before their hospitalization in the PE, after 2 weeks, at discharge, and at 8 months post-BMT. Locus of control, degree of social support, previous biotherapy, and on-treatment psychiatric consultation were also analyzed. RESULTS: Before BMT, 20% of patients had mild cognitive dysfunction, and nearly 40% had significant anxiety. Although few patients developed problems with cognition or mood during the study, short-term memory deficits nearly doubled at follow-up compared with baseline. Anxiety decreased significantly during hospitalization and remained low at follow-up. In contrast, depression increased throughout hospitalization, but decreased at follow-up. Pre-BMT emotional status and cognitive functioning were highly related to long-term outcome. Type of BMT, locus of control, and degree of social support were related to psychologic distress and cognitive functioning, both during and after BMT. Patient age was not a predictor of neurobehavioral symptoms during or after BMT. CONCLUSION: Pretransplant emotional and cognitive functioning are important determinants of long-term outcome and quality of life (QOL) in BMT patients. In addition, a few patients undergoing BMT develop short-term memory difficulties and mood disturbance that may persist. Pretransplant identification of patients at risk for neurobehavioral difficulties may guide early interventions during hospitalization. Posttransplant assessment may then be used to develop rehabilitation programs and other interventions for individuals with persisting complaints.

Adult↗

PubMedDate not supplied

[Clinical-therapeutic study of dementia in people with Down syndrome and the effectiveness of donepezil in this population].

INTRODUCTION: People with Down syndrome have an early aging process, especially form their 40s. There is a significant average of them who initiate, from that age on, a progressive decline of their cognitive and functional abilities, due to a primary degenerative process Alzheimer's disease type. When assessing response to treatment with, pilot clinical trials on this population have demonstrated real benefits therapeutically. AIMS: To assess the efficacy and safety of a pharmacological treatment with donepezil over cognitive and behavioral disturbances on patients with Down syndrome older than 40 years, areas where family and professional educators of reference have observed cognitive and behavioral changes in comparison with their previous level of disability. PATIENTS AND METHODS: Patients have been selected from different institutions affiliated at the Catalan Foundation for the Down syndrome and by the Catalan Federation Pro Persons with Psychic Disability. Several deterioration, behavioral and functional assessment scales have been used, all of them validated into this population. RESULTS: The results of study demonstrated that donepezil slowed the progression of the cognitive dysfunction, especially during the first three months of treatment. This occurred for both cognitive and social-behavioral outcomes. CONCLUSIONS: Donepezil appears to be effective in the treatment of cognitive and behavioural disturbances associated with the progressive dementia syndrome in Down's. However, the sample sizes used in this, and all published studies are small and this emphasizes the need for a larger, multi-center trial to fully evaluate the nature and extent of the response of Down's syndrome patients to anticolinesterase therapy.

Adult↗

PubMed2006

Community dysfunction in schizophrenia: rate-limiting factors.

The purpose of the present study was to investigate the impact of cognitive functioning, psychopathology, and severity of extrapyramidal side effects on community outcome in a group of Greek outpatients with schizophrenia. Participants were 40 outpatients with schizophrenia (25 men). Social adjustment was assessed with the Quality of Life Scale (QLS). Severity of symptoms of schizophrenia was measured with the Positive and Negative Syndrome Scale (PANNS), and extrapyramidal symptoms with the Extrapyramidal Symptom Rating Scale (ESRS). Finally, a battery of neuropsychological tests was administered in order to assess the following cognitive domains: executive functioning/set shifting, executive functioning/inhibition, fluency, verbal memory, visual memory, working memory, attention, visuospatial ability, and psychomotor speed/visual scanning. Total scores on the QLS were significantly correlated with negative symptoms, parkinsonism, and performance on the fluency tasks. Interpersonal relations subscale was significantly related with negative symptoms and fluency. No significant relationship was found between the Instrumental Role Functioning subscale and the PANSS, ESRS, or any cognitive domain. Scores on the Intrapsychic Foundation subscale were significantly correlated with negative symptoms and fluency. Finally, scores on the Common Objects and Activities subscale were significantly related with severity of negative symptoms, parkinsonism and visual memory. Our findings suggest that severity of negative symptoms, cognitive dysfunction, especially performance on fluency tasks and visual memory, as well as parkinsonism, are important determinants of functional outcome in schizophrenia.

Adult↗

PubMedDate not supplied

[Attention impairment in patients suffering from schizophrenia and their relatives of first-degree].

UNLABELLED: Attention dysfunction as assessed by standardised tests has often been reported in schizophrenic patients. Since many cognitive dysfunctions noted in these patients occur also in their close relatives, a supposition arises that they may be indicators not so much of transient states, but rather of a stable feature of cognitive functioning. This feature perhaps is transmitted from generation to generation and might contribute to the onset of the disease. AIM: A comparison of selected attention indicators in schizophrenic patients and their first-degree relatives with these in healthy controls without family history of schizophrenia. METHOD: Participants in the study were 99 patients diagnosed with schizophrenia (according to the ICD-10-DCR criteria) in an early period of remission, their first-degree relatives (N = 56), out of whom 42 were healthy and 14 had a history of psychiatric disorders, and a control group of participants (N = 42) unrelated to the subjects and with no psychiatric history. Several tests of the computer-aided Vienna Test Battery were used, and namely: the RT test measuring reaction time to simple visual or auditory stimuli, and LVT test measuring the accuracy and performance time in a task that consisted in visual tracking of lines, and required concentration of visual perception. RESULTS: As compared to the controls, the patient group was found to manifest attention deficits in the form of longer reaction time to simple stimuli as well as increased performance time and decreased correctness of visual line tracking. The patients had also a somewhat longer reaction time to visual (but not auditory) stimuli, and their line tracking was inferior as compared to that of their healthy relatives. As regards the reaction time to simple stimuli, the latter did not differ significantly from the controls, but in the line tracking test which required more attention, their performance was significantly inferior to that of the control group.

Adult↗

PubMed2006

Neural consequences of sleep disordered breathing: the role of intermittent hypoxia.

Sleep disordered breathing is characterised by periodic breathing, episodes of hypoxia and repeated arousals from sleep; symptoms include excessive daytime sleepiness, impairment of memory, learning and attention. Recent evidence from animal studies suggests that both intermittent hypoxia and sleep fragmentation can independently lead to neuronal defects in the hippocampus and pre frontal cortex; areas known to be closely associated with neural processing of memory and executive function. We have previously shown that sleep disordered breathing is associated with loss of gray matter concentration within the left hippocampus (47). We have now confirmed and extended this finding in 22 right handed, newly diagnosed male patients (mean (sd): age 51.8 (15.4) yrs, apnea/hypopnea index 53.1 (14.0) events/hr, minimum nocturnal oxygen saturation 75 (8.4) %) and 17 controls matched for age and handedness. Voxel-based morphometry, an automated unbiased technique, was used to characterise changes in gray matter concentration. The magnetic resonance images were segmented and grey matter concentration determined voxel by voxel. Analysis of variance was then preformed, adjusted for overall image intensity, with age as a covariant. Additional to the deficit in the left hippocampus, we found more extensive loss of gray matter bilaterally in the parahippocampus. No additional focal lesions were seen in other brain regions. Based on our findings and data from other human and animal studies, we speculate that in patients with sleep disordered breathing intermittent hypoxia is associated with neural deficit, and further that such lesions may lead to cognitive dysfunction.

Adult↗

PubMed1989

The development and initial validation of a sensitive bedside cognitive screening test.

Brief bedside cognitive examinations such as the Mini-Mental State Examination are designed to detect delirium and dementia but not more subtle or delineated cognitive deficits. Formal neuropsychological evaluation provides greater sensitivity and detects a wider range of cognitive deficits but is too lengthy for efficient use at the bedside or in epidemiological studies. The authors developed the High Sensitivity Cognitive Screen (HSCS), a 20-minute interview-based test, to identify patients who show disorder on formal neuropsychological evaluation. An initial study demonstrated satisfactory test-retest and interrater reliability. The HSCS was then administered to 60 psychiatric and neurological patients with suspected cognitive deficits but without gross impairment, who also completed formal neuropsychological testing. Results of both tests were independently classified as either normal, borderline, or abnormal. The HSCS correctly classified 93% of patients across the normal-abnormal dichotomy and showed promise for characterizing the extent and severity of cognitive dysfunction.

Adolescent↗

PubMed1983

Social drinking and cognitive function: a review.

Six different studies of social drinkers drawn from California, Oklahoma, Massachusetts and Michigan, using different methodologies, indicate a negative association between social drinking (specifically quantity of alcohol consumed per drinking occasion) and sober cognitive performance. This relationship prevails not only in men but also in women. The decrements in performance are greater in older than in younger individuals, and they are more evident in heavy than in light social drinkers. These findings do not necessarily indicate, albeit they do suggest, a causal link between social drinking and impairments in cognitive functioning. Additional questions raised in this review must be answered before a cause and effect relationship is established between social drinking and cognitive dysfunction.

Adult↗

PubMed2006

Olfactory functions in asymptomatic carriers of the Huntington disease mutation.

Huntington's disease (HD) is a neurodegenerative disorder initially affecting the basal ganglia and especially the head of the caudate nucleus. Neuropsychological research has indicated that olfactory dysfunction may appear early in HD, prior to the onset of significant motor or cognitive dysfunction. The aim of this study was to examine whether asymptomatic carriers of the Huntington disease mutation also exhibit olfactory dysfunction. To address this issue we presented an extensive olfactory test battery comprising tasks assessing olfactory sensitivity, intensity discrimination, quality discrimination, episodic odor memory, and odor identification, to a group of gene carriers and nonmutation carriers of the disease. The results showed that gene carriers were selectively impaired in discriminating odor quality, although performance did not differ from noncarriers across the other tasks. The role played by striatum and then in particular the caudate nucleus for olfactory processing in general, and for odor quality discrimination in particular, is discussed.

Adult↗

PubMed2006

Long-term cognitive and neuropsychological symptoms after global cerebral ischemia in Mongolian gerbils.

The objective of this study was to establish a rodent model of vascular dementia that showed long-term cognitive and neuropsychological deficits, and to correlate those behavioral deficits with the patterns of ischemic lesions, thus providing a platform for future testing of potential therapeutic agents. In Mongolian gerbils, either 5-minute single bilateral common carotid artery occlusion (SBCCAO) or repetitive bilateral common carotid artery occlusion (two 7-minute occlusions, RBCCAO) was induced, and the behavioral deficits were evaluated using 2 tests: a modified open-field test with an escape zone to evaluate changes in anxiety and locomotor activity, and a T-maze test to assess cognitive dysfunction. SBCCAO did not induce anxiety changes but caused transient locomotor hyperactivity and mild cognitive deficits. Only pyramidal neuronal death was found in the bilateral CA1 sector of the hippocampus following SBCCAO. In contrast, RBCCAO induced persistent locomotor hyperactivity, reduced anxiety, and caused severe cognitive deficits at 4 weeks post-ischemia. RBCCAO caused significant atrophy associated with diffuse selective neuronal death in the bilateral cerebral cortex and caudate nucleus, as well as the CA1 region. The repetitive ischemia model appears to be a potentially useful platform for the long-term analysis of cognitive and neuropsychological symptoms associated with vascular dementia.

Animals↗

PubMed2005

Cognitive impairment and diffuse white matter atrophy in alcoholics.

OBJECTIVE: Diffuse brain white matter atrophy is often seen in chronic alcoholics, but its relation with cognitive impairment remains to be solved. In order to address this issue, in alcoholics with cognitive impairment at different levels, we studied relations of the central sensory conduction time (CSCT) or brain magnetic resonance imaging (MRI) findings with the cognitive function. METHODS: Subjects were 35 alcoholics with mild cognitive impairment (mini-mental state examination score, MMSE, >/=24; mean+/-SD, 27.7+/-1.9), 12 with moderate to severe cognitive impairment (MMSE<24; 20.3+/-2.7), 15 with Alzheimer's disease (AD) (MMSE, 18.9+/-4.3) (disease control) and 20 healthy volunteers (MMSE, 28.5+/-1.6) (normal control). Median nerve SEPs were recorded in the all subjects, and the latencies and amplitudes of their N9, N11, P13/14, N20 and P25 components were measured. The ventriculocranial ratio (VCR) and the width of cortical sulci were measured on MRIs. These physiological parameters and MRI findings were compared between the 4 groups of the subject, and correlations between those all features were also analyzed. RESULTS: CSCT and VCR were significantly greater in alcoholics with moderate to severe cognitive impairment than those in the other 3 groups. Pearson's product-moment correlation analyses of the alcoholics disclosed that both the CSCT and VCR had significant negative correlations with the MMSE score. Moreover, the CSCT and VCR were positively correlated. CONCLUSIONS: Both physiological and morphological estimates of the white matter function (CSCT and VCR) had a significant correlation with the cognitive dysfunction. SIGNIFICANCE: The diffuse white matter atrophy may be one of the factors causing cognitive impairment in chronic alcoholics.

Aged↗

PubMed2006

GABAB receptor antagonism abolishes the learning impairments in rats with chronic atypical absence seizures.

Chronic atypical absence seizures are a component of the Lennox-Gastaut syndrome, a disorder invariably associated with severe cognitive impairment in children. However, the cause of this intellectual delay remains unclear. The AY9944 model of chronic atypical absence seizures in rats reliably reproduces the electrographic, behavioral, pharmacological and cognitive features of clinical atypical absence. Using this model, we tested the hypothesis that the cognitive impairment associated with this disorder involves a gamma-aminobutyric acid B (GABA(B)) receptor-mediated mechanism. Therefore, we examined the effect of a specific, high affinity GABA(B) receptor antagonist, CGP35348, on the atypical absence seizures, the working memory deficits, and the altered long-term potentiation that we have observed in the AY9944 model. CGP35348 blocked atypical absence seizures, restored long-term potentiation to normal level, and reversed the cognitive deficit in the AY9944-treated animals. However, dose-response studies showed that lower doses of CGP35348 that failed to influence atypical absence seizure activity, completely reversed the spatial working memory deficit. These data suggest that GABA(B) receptor-mediated mechanisms are responsible for the cognitive dysfunction in the AY9944 model of chronic atypical absence seizures and further, that their cognitive impairment is independent of the seizure activity. The data raise the possibility that GABA(B) receptor antagonists may have therapeutic potential for the treatment of cognitive impairment in epilepsy syndromes where atypical absence seizures are a component.

Animals↗

PubMed2005

Deficits in cortico-striatal synaptic plasticity and behavioral habituation in rats with portacaval anastomosis.

Hepatic encephalopathy is characterized by disturbances of motor and cognitive functions involving the basal ganglia. So far no standards for assessment of neuropsychiatric abnormalities (disorders of sleep, mood, anxiety and personality) in subclinical hepatic encephalopathy have been defined. Using an animal model of mild (subclinical) hepatic encephalopathy we investigated now striatum-related behaviors and cortico-striatal synaptic plasticity in rats 2 months after introduction of a portacaval shunt and sham-operated matched controls. In a novel open field portacaval shunt rats displayed less locomotor activity; unlike controls they also showed no habituation to the field and no recall of the field environment after 24 h, indicative of cognitive deficit. The elevated-plus maze test indicated no differences in fear/anxiety in the portacaval shunt animals. Tetanic stimulation of cortical afferents in magnesium-free solution evoked an N-methyl-D-aspartate-dependent long-term potentiation in sham-operated animals. In portacaval shunt animals long-term potentiation was significantly impaired. Histamine, a potent modulator of cortico-striatal transmission, induced a larger long-term depression of field potentials in control compared with portacaval shunt rats. In conclusion, a combination of electrophysiological and behavioral approaches has revealed functional changes in cortico-striatal transmission. These data are relevant for understanding the mechanisms of motor and cognitive dysfunctions in hepatic encephalopathy patients and for the development of precise psychometric tests, evaluating cognitive deficits in subclinical hepatic encephalopathy.

Animals↗