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PubMed2002

Neuropsychiatric involvement in systemic lupus erythematosus.

The correct diagnosis of central and peripheral nervous system manifestations in patients with systemic lupus erythematosus (SLE) can be challenging because of many SLE-related and non-SLE-related processes that can be present in a patient. The American College of Rheumatology (ACR) has published case definitions for 19 neuropsychiatric SLE (NPSLE) syndromes, with careful attention to important exclusion criteria. These criteria were developed for research purposes but can be helpful to clinicians with a patient who has nervous system dysfunction. This report reviews the data regarding the application of the ACR NPSLE criteria and the influence of ethnicity and disease duration on the development of NPSLE syndromes. Cognitive dysfunction and psychiatric disorders are the two most common manifestations. The work-up and treatment of nervous system syndromes are also discussed.

Angiography↗

PubMed2004

Cognition and immunity; antibody impairs memory.

Patients with lupus (SLE) experience progressive cognitive loss without evidence of CNS vascular disease or inflammation. SLE patients produce anti-DNA antibodies that crossreact with NMDA receptors and are capable of mediating excitotoxic death. We now show that mice induced by antigen to express these antibodies have no neuronal damage until breakdown of the blood-brain barrier occurs. Following administration of lipopolysaccharide (LPS) to immunized mice, antibodies gain access to the brain. They bind preferentially to hippocampal neurons and cause neuronal death with resulting cognitive dysfunction and altered hippocampal metabolism on magnetic resonance spectroscopy. Memantine, an NMDA receptor antagonist, given prior to LPS administration, prevents neuronal damage. Thus, systemic immune responses can cause cognitive impairment in the absence of an inflammatory cascade, implicating the immune system in yet another arena of human pathobiology. Furthermore, NMDA receptor antagonists prevent antibody-mediated damage and may constitute a new approach to therapy in SLE.

Animals↗

PubMed2006

Depression predicts the pattern of cognitive impairment in early Parkinson's disease.

OBJECTIVE: To estimate the pattern of cognitive impairment in early Parkinson's disease (PD) associated with depression. Also, the prediction of potentially relevant demographic/clinical factors in early PD on cognitive functioning was tested. METHOD: The study comprised 80 consecutive early PD patients (16 with major depression (PDMD), 10 PD patients with dysthimic disorder (PDDD), and 54 nondepressed PD patients (PDND)). Thirty_seven healthy subjects matched for age, gender and education were also included in the study. The cognitive evaluation included the comprehensive classical neuropsychological battery and the Cambridge Neuropsychological Test Automated Battery (CANTAB). RESULTS: The two different patterns of cognitive impairment in early PD patients were obtained even when the confounding influences of general cognitive abilities and motor slowness were taken in account. One pattern was common to all PD patients either they were depressed or not, and it is conceived etiologically as dysexecutive. The PDDD group presented only the quantitative increment of the common deficit observed in PD. The second pattern was present in PDMD patients, involved episodic/working memory and language deficits alongside with background executive impairment. Depression was extensively associated with the cognitive dysfunction in early PD, whereas severity of the disease, age at onset and treatment were less favorable as predictors. CONCLUSIONS: This study provides evidence that the pattern of cognitive impairment in early PD may be predicted by depression severity. Therefore, the recognition and treatment of depressive disorder in early PD is important.

Aged↗

PubMed2006

Insight and frontal cortical function in schizophrenia: a review.

Insight into illness has been identified as a clinically important phenomenon, in no small part due to an association with treatment-adherence. An increasing number of studies, but not all, have observed poor insight to be a reflection of cognitive dysfunction in schizophrenia. A review of 34 published English-language studies found a significant number (i.e., 21) reporting a relationship between insight deficits and impaired performance on cognitive tasks primarily mediated by frontal cortex. A significant number of reviewed studies examined insight function in more than one psychiatric population, including bipolar and schizoaffective disorder. The most replicated findings from these studies were the correlations between insight deficits and impaired performance on the Wisconsin Card Sorting Test (WCST). More specifically, WCST perseverative errors correlated positively and the number of categories completed correlated negatively with poor insight, suggesting that impaired insight may be mediated by deficiencies in conceptual organization and flexibility in abstract thinking. Since the WCST requires the ability to demonstrate conceptual flexibility through the generation, maintenance and switching of mental sets along with the capacity to use verbal feedback to correct errors, it would appear that such 'executive' functions are most related to insight. In addition, recently identified structural correlates of poor insight in schizophrenia show some association with anosognosia in neurological patients. This review will discuss the implications of these findings and directions for future research.

Databases, Factual↗

PubMed2002

Long-term neurodevelopmental outcomes in school-aged children after neonatal arterial switch operation.

OBJECTIVE: Neurodevelopmental status of children between 8 and 14 years of age after neonatal arterial switch operation for transposition of the great arteries has not previously been systematically evaluated. METHODS: Within a longitudinal study, 60 unselected children operated on as neonates with combined deep hypothermic circulatory arrest and low-flow cardiopulmonary bypass were reevaluated at the age of 7.9 to 14.3 years (mean +/- SD 10.5 +/- 1.6 years). Clinical neurologic status and standardized tests to assess gross motor function, intelligence, acquired abilities, language, and speech were carried out, and the results were related to preoperative, perioperative, and postoperative status, to management, and to neurodevelopmental status at a mean age of 5.4 years. RESULTS: Neurologic and speech impairments were evidently more frequent (27% and 40%, respectively) than in the general population. Intelligence and socioeconomic status were not different (P =.29 and P =.11), whereas motor function, acquired abilities, and language were reduced (P < or =.04 for each). Overall rate of developmental impairment in one or more domains was 55%, compared with 26% at age 5.4 years. Multivariable analysis showed that severe preoperative acidosis and hypoxia predicted reduced motor function (mean deficit 52.7 points, P <.001), whereas longer bypass duration predicted both neurologic (odds ratio per 10 minutes of bypass duration 1.8, P =.04) and speech (odds ratio per 10 minutes of bypass duration 1.9, P =.02) dysfunction, and perioperative and postoperative cardiocirculatory insufficiency predicted neurologic (odds ratio 6.5, P =.04) and motor (mean deficit 6.8 points, P =.03) dysfunction. CONCLUSIONS: The neonatal arterial switch operation with combined circulatory arrest and low-flow bypass is associated increasingly with age, with reduced neurodevelopmental outcome but not with cognitive dysfunction. In our experience, the risk of long-term neurodevelopmental impairment after neonatal corrective cardiac surgery is related to deleterious effects of the global perioperative management and to special adverse effects of prolonged bypass duration. Severe preoperative acidosis and hypoxia and postoperative hemodynamic instability must be considered as important additional risk factors.

Adolescent↗

PubMed2002

Plasma HDL levels highly correlate with cognitive function in exceptional longevity.

BACKGROUND: Families of centenarians have high levels of plasma high-density lipoprotein (HDL) cholesterol, which may have neurological as well as cardiovascular protective effects during aging. Because plasma HDL level declines progressively with aging, we examined whether centenarians with higher plasma HDL levels have better cognitive function. METHODS: Total plasma cholesterol, low-density lipoprotein (LDL) cholesterol, HDL, triglycerides, and apolipoprotein levels were measured in a group of centenarians (N = 139; older than 95 years) and were correlated with their cognitive function (measured by Mini-Mental State Examination [MMSE]). RESULTS: Plasma HDL levels correlated significantly with MMSE (r =.32; p <.0001). Each decrease in plasma HDL tertile (74.9 +/- 2.1, 50.6 +/- 0.5, and 36.8 +/- 1.0 mg/dl) was associated with a significant decrease in MMSE (23.4 +/- 1.5, 17.7 +/- 1.8, and 12.4 +/- 1.8; p <.04 for each plasma HDL tertile). As expected, increased plasma apolipoprotein A-I and decreased plasma triglyceride levels were also correlated with a significantly superior cognitive function. Biological markers of hydration and nutritional status did not differ between the groups with the higher or lower plasma HDL or MMSE. CONCLUSIONS: These data demonstrate that cognitive dysfunction in centenarians is associated with a progressive decline in plasma HDL concentrations. This underscores the protective effects of increased plasma HDL and its role in maintaining superior cognition in longevity.

Aged↗

PubMed2006

Aging: impact upon local cerebral oxygenation and blood flow with acute isovolemic hemodilution.

Data from the neurosurgical critical care arena demonstrate a correlation between cerebral oxygenation, survival, and cognitive function. Transfusion may increase and hemodilution decrease cerebral oxygenation. Both acute and chronic anemia have been associated with cognitive dysfunction. Aggressive blood conservation protocols have been instituted across all age groups without conclusive evidence for their impact upon outcome. Aged subjects are at the greatest risk of cognitive sequelae after major surgery associated with significant blood loss. We hypothesize that cerebral physiologic changes associated with "normal" aging may compromise cerebral oxygenation in the presence of severe anemia.Fischer 344 rats, the NIH National Institute of Aging normal aging rat model, underwent a stepwise isovolemic hemodilution protocol. Age groups (Age Grp) studied were as follows: Age Grp-A (3 months), n=14; Age Grp-B (9 to 12 months), n=14; and Age Grp-C (24 months), n=14. Brain oxygen tension (PBrO2), laser Doppler flow, and mean arterial pressure were measured. Final hemoglobin averaged 6.1+/-0.9 g/dL. PBrO2 levels decreased from a baseline of 18.1+/-4.1 to 17.5+/-6.8 mm Hg (P=0.49), and laser Doppler flow increased by 18+/-20% (P<0.0001) after hemodilution. Employing repeated measures multiple regression, Age Grp (P=0.30) was not a significant controlling covariate of PBrO2 in response to isovolemic hemodilution. PBrO2 levels were actually higher in Age Grp-C animals at all time points of the hemodilution protocol, although this was not statistically significant. Aged animals were also fully capable of mounting a robust local cerebral hyperemic response to the anemic challenge that was not separable from the response of younger animals.

Aging↗

PubMed1996

Neuropsychological features of early Alzheimer's disease: preclinical and clinical stages.

In the preclinical stage of Alzheimer's disease (AD), studies of asymptomatic mutation carriers have identified impairments in episodic memory. Other cognitive functions show no or slight impairment suggesting that preclinical AD is a unifunctional cognitive syndrome; the brain is affected selectively and predominantly in the medial temporal structures. In the early clinical stage, deficits occur in episodic memory, verbal abilities, visuospatial functions, attention, and executive functions. AD becomes a multifunctional cognitive syndrome and the brain's association cortices are affected. Nevertheless, sensory-motor performance and procedural memory seem to be intact and only slight impairment may be seen in primary memory. In advanced AD, cognitive dysfunction including deficits is global in primary memory, although sensory-motor performance may be well preserved. The brain's association cortices are severely affected. The sequence of cognitive decline; from unifunctional to global deficits, conforms to the three-stage development of neurofibrillary tangles described by Braak and Braak.

Alzheimer Disease↗

PubMed1992

Using subtests of the Brain Age Quotient to screen for cognitive deficits among substance abusers.

The subtests of the Brain Age Quotient, a brief neuropsychological battery, were used to screen for cognitive impairment in a sample of 112 substance abusers. Each of the subtests was scored, using newly developed T scores corrected for age, education, and gender, for which a mean battery score of T less than 40 indicates general cognitive impairment. The chance-corrected agreement in finding cognitive dysfunction between this battery and the Average Impairment Rating T score from the Halstead-Reitan battery was adequate, kappa = .81. This result suggests that, for discerning global cognitive impairment, this relatively brief neurodiagnostic screening device may be an attractive alternative to the more time-consuming Halstead-Reitan battery.

Adolescent↗

PubMed1994

The cognitive model and treatment of depression.

1. Research indicates that depression is best treated using a combination of drugs and psychological interventions. 2. The Beck psychological model of depression has led to a specific treatment formulation. 3. Beck sees the dysfunctional cognitions which arise in how person sees him- or herself, the world, the future, as contributory to the illness. 4. Research using both qualitative and quantitative analysis has shown cognitive therapy to be an effective form of treatment for depression.

Cognitive Behavioral Therapy↗

PubMed2003

Early and pre-symptomatic neuropsychological dysfunction in the PPND family with the N279K tau mutation.

The N279K mutation on the tau gene of chromosome 17 leads to an inherited condition that involves pallido-ponto-nigral degeneration (PPND). Patients with PPND develop dementia, but the pattern and onset of cognitive dysfunction has not yet been delineated. Four affected patients underwent neurocognitive evaluation within the first 2 years of PPND motor onset; one of whom underwent five serial neurocognitive evaluations, and another who was not diagnosed with PPND until the third annual evaluation. Impaired letter fluency was found in the early stages of PPND and was also shown to precede the onset of motor symptoms by 2 years. Trail Making A (visual scanning and motor speed) and Trail Making B (divided attention) were impaired within the first 2 years of the disease in all but one patient, but this individual showed clinically significant decline on these tasks by the third year of the disease. Learning, memory, and timed visuospatial sequencing skills were variably affected. Results reveal disproportionate frontal-executive dysfunction early in PPND disease course, a pattern similar to what has been reported in other FTDP-17 kindreds and in sporadic PSP. In addition, results suggest that letter fluency may be a sensitive predictor of incipient PPND.

Chromosomes, Human, Pair 17↗

PubMed2001

Cognitive function and cholinergic neurochemistry in weanling rats exposed to chlorpyrifos.

Previous studies have shown that moderate to high levels of chlorpyrifos (CPF) alter cognitive function in adult and immature rats. In the present study, we tested the hypothesis that lower-level exposure to CPF before or immediately after weaning causes deficits in cognitive function. A total of 78 Long-Evans rats were injected subcutaneously with 0, 0.3 or 7.0 mg/kg CPF every 4 days before or after weaning and were tested with the Morris swim task from postnatal day 24 through 28. Exposure to CPF before weaning did not cause signs of overt cholinergic intoxication or impaired growth nor did the exposures cause significant inhibition of regional brain cholinesterase (ChE) activity or reduction in muscarinic receptors 24 h after the last injection. However, spatial learning was impaired after 5 days of training in the group of weanling rats administered 7.0 mg/kg CPF. Rats administered 0.3 or 7.0 mg/kg CPF after weaning were also impaired in the task, without significant changes in brain ChE activity. These data indicate that low-level exposure to CPF caused deficits in cognitive function in weanling rats, and these effects did not appear to be mediated by the inhibition of brain ChE. It is suggested that the alteration of cognitive function in juvenile rats is an important functional correlate of the cellular and molecular effects of CPF in the immature brain. The mechanisms for CPF-induced cognitive dysfunction are unknown.

Animals↗

PubMed2003

The other side of estrogen replacement therapy: outcome study results of mood improvement in estrogen users and nonusers.

The effect of estrogen on the brain and body of women is a controversial topic that has received a tremendous amount of attention in the past few years. Recent reviews have focused on hormone replacement therapy (HRT), medical risks, and effects on brain metabolism, cognition, risk of Alzheimer's disease, and mood. This article summarizes HRT and mood improvement in postmenopausal women. For nondepressed women, experimental designs provide no clear evidence for mood improvement associated with HRT, whereas observational studies are more likely to report mood improvement. There appears to be moderate evidence that HRT facilitates the improvement of clinical depression and the efficacy of antidepressants. Heterogeneity among studies makes it difficult to generalize and recommend HRT for mood improvement in postmenopausal women, but there is a clear need to examine the necessary duration of HRT for neuroprotection to decrease a woman's risk for depression, cognitive dysfunction, and development of Alzheimer's disease.

Affect↗

PubMed2003

Pitfalls in the assessment of disability in individuals with low-grade gliomas.

In this study, the presence of motor and cognitive disability is described in a cohort of patients with low-grade glioma recruited from a geographical area with a well-defined population located in the middle of Sweden. The study group consisted of 35 patients, of which 24 were evaluated by both a neurologist and a neuropsychologist, and 11 only by a neurologist. The test battery according to EFIT (Edinburgh Functional Impairment Test) was used by the neurologist to measure impairments of limb function, memory and speech. Patients were asked to self-evaluate their deficits in motor function and cognition by responding to a specific questionnaire. In addition, a neuropsychological test battery was used by an experienced neuropsychologist who had no previous contact with the patients. In general, motor impairment was mild and predominantly found in the upper limb. Neuropsychological assessment revealed moderate or severe cognitive impairment in more than half of the patients. This impairment was not detected by neurological examination, and only to some extent reported by the patients them selves. The results show statistical differences in cognitive function, memory and language as recorded by the three assessors. In conclusion, this study demonstrates the usefulness of neuropsychological assessment as a complement to neurological examination to detect cognitive dysfunction in patients with low-grade gliomas.

Adult↗

PubMed1982

The recovery of the severely disable stroke patient.

Fifty-three stroke patients with severe functional loss at two weeks, following the stroke were followed up for one year. No improvement occurred in 47% during this time and this was associated with abnormalities of muscle tone, incontinence of urine or faeces, perceptual disorders and previous disabilities affecting locomotion. Remedial therapy continued for long periods especially in the group who did not improve. It is suggested that rehabilitation resources could have been used more appropriately. Further research is required to determine whether intensive therapy is of value in the severely disabled stroke patient especially those with perceptual and cognitive dysfunction.

Activities of Daily Living↗

PubMed1995

[Cognitive symptoms in persons with snoring and sleep apnea. An epidemiologic study of 1.504 women and men aged 30-60 years. The Dan-MONICA II study].

The objective of the study was to evaluate the relation between every-night (habitual) snoring, sleep apnoea and cognitive complaints (concentration and memory complaints) in an adult population-based sample. In the DAN-MONICA (MONItoring trends in CArdiovascular iseases) 1504 males and females aged 30, 40, 50 and 60 years were classified according to their snoring habits. Nocturnal respiration was measured in 748 participants. The following measures were regarded as potential confounders: age, gender, unintended sleepiness, insomnia, depression, hypnotic use, alcohol consumption by questionnaire, body mass index (BMI) and blood pressure. Concentration and memory problems were both related to depression, insomnia and unintended sleepiness. Snoring and sleep apnoea (defined as a respiratory distress index-RDI > or = 5) were associated with concentration problems and unintended sleepiness. The odds ratios (95% confidence intervals) between snoring, concentration and memory problems, calculated by logistic regression analysis after adjustments for the above confounders, were 1.90 (1.23-2.91, p < 0.01) and 1.38 (0.97-1.99, NS). For those with sleep apnoea, the odds ratios were 3.53 (1.42-8.73. p < 0.001) and 1.51 (0.81-2.14, NS) for concentration and memory problems, respectively. The main conclusion drawn from this study is that cognitive complaints show a high correlation to mood, insomnia and hypersomnia. Habitual snoring and sleep apnoea show a correlation to concentration problems, but not to memory problems. This suggests that part of the association between snoring, sleep apnoea and cognitive dysfunction is related to the presence of sleep disturbances and daytime sleepiness.

Adult↗

PubMed2000

Neurocognitive correlates of stereotactic thalamotomy and thalamic stimulation in Parkinsonian patients.

In the present paper we have reviewed five different studies that relate to neuropsychological consequences of stereotactic thalamotomy and thalamic stimulation in patients with Parkinson's disease. The neuropsychological results are in a strict sense confined to thalamotomy and thalamic stimulation, although the more general message of the importance of investigating cognitive functions before and after surgery applies to other stereotactic techniques for surgical treatment of movement disorders as well. It is argued in the paper that stereotactic thalamotomy provides a unique model for basic research on the neuropsychology of the thalamus, while in return, neuropsychological tests for cognitive dysfunction after surgery may be the most important clinical follow-up. Three general conclusions seem warranted from the data. (1) Parkinsonian patients are impaired on a range of cognitive functions, including language processing, memory, and executive functions. (2) Stereotactic thalamotomy does not further impair the patient; instead, we observed improvement on some tests, particularly verbal memory. (3) In general, there does not seem to be a laterality effect, depending on which side the thalamotomy lesion is applied. An exception to this are dichotically presented simple speech sounds and autonomic responses. In both instances, left-sided brain stimulation produced enhanced performance, while lesioning the left thalamus impaired dichotic listening performance. Finally, we present a new hypothesis for a mechanism behind the thalamotomy effect, based in part on changes in arousal thresholds.

Aged↗

PubMed2005

Cognitive aging as an extension of brain development: a model linking learning, brain plasticity, and neurodegeneration.

Differences in cognitive aging rates among mammals suggest that the pace of brain aging is genetically determined. In this work, we investigate the possibility that brain aging is an extension of brain development. It is possible that a subset of developmental mechanisms are extreme cases of antagonistic pleiotropy in that they are necessary for reaching adulthood and yet later cause age-related diseases. We derive a model linking development and brain aging in which childhood events essential for brain development later result in neurodegeneration. The hypothesis presented herein involves brain plasticity in which the same mechanisms that shape the adult phenotype continue at later ages contributing to cognitive dysfunction and eventually dementia. The same genetic program that decreases brain plasticity at early ages to focus our mind to the surrounding environment may continue in adulthood resulting in cognitive aging. Experimental implications for understanding neurodegeneration in this context are also discussed.

Aging↗