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Results for “Cognitive Dysfunction”

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PubMed2003

CSF galanin and cognition after shunt surgery in normal pressure hydrocephalus.

BACKGROUND: "Normal" pressure hydrocephalus (NPH) is associated with injury to neurotransmitter and neuropeptide systems that recovers after surgery. This could be linked to changes in galanin, a neuropeptide with inhibitory effects on basal forebrain cognitive function. OBJECTIVE: To examine changes in CSF galanin concentrations in patients with normal pressure hydrocephalus undergoing shunt surgery, and to investigate the relation between these changes and cognitive functioning. METHODS: Eight patients underwent surgery for idiopathic normal pressure hydrocephalus. Lumbar CSF galanin determinations, cognitive status, and clinical status were quantified before operation and six months after. Cognition was assessed by an extensive battery of tests measuring attention, memory, speed of mental processing, visuospatial function, and frontal lobe function. RESULTS: CSF galanin concentration decreased after surgery. This reduction correlated with improved clinical and cognitive functioning, specifically with attention and visuomotor speed, visuoconstructive and frontal functioning, and clinical status according to the NPH scale, including the sphincter and cognitive components. CONCLUSIONS: The cognitive and clinical improvement after shunt implantation correlated with CSF galanin levels, suggesting that the distribution or function of this agent involves cerebral structures that have some potential for recovery. In this study, galanin was related to several cognitive functions that may be associated with the fronto-subcortical deficits underlying cognitive dysfunction in normal pressure hydrocephalus.

Aged↗

PubMed1993

Residual cognitive deficits 50 years after lead poisoning during childhood.

The long term neurobehavioural consequences of childhood lead poisoning are not known. In this study adult subjects with a documented history of lead poisoning before age 4 and matched controls were examined with an abbreviated battery of neuropsychological tests including measures of attention, reasoning, memory, motor speed, and current mood. The subjects exposed to lead were inferior to controls on almost all of the cognitive tasks. This pattern of widespread deficits resembles that found in children evaluated at the time of acute exposure to lead rather than the more circumscribed pattern typically seen in adults exposed to lead. Despite having completed as many years of schooling as controls, the subjects exposed to lead were lower in lifetime occupational status. Within the exposed group, performance on the neuropsychological battery and occupational status were related, consistent with the presumed impact of limitations in neuropsychological functioning on everyday life. The results suggest that many subjects exposed to lead suffered acute encephalopathy in childhood which resolved into a chronic subclinical encephalopathy with associated cognitive dysfunction still evident in adulthood. These findings lend support to efforts to limit exposure to lead in childhood.

Cognition Disorders↗

PubMed2006

Differential CSF biomarker levels in APOE-epsilon4-positive and -negative patients with memory impairment.

OBJECTIVES: To investigate the relationships between episodic memory, APOE genotype, CSF markers (total tau, T-tau; phospho-tau, P-tau; beta-amyloid, Abeta42) and longitudinal cognitive decline. METHODS: 124 memory clinic patients were retrospectively divided into 6 groups based on (i) episodic memory function (Rey Auditory Verbal Learning Test, RAVLT): severe, moderate or no impairment (SIM, MIM or NIM), and (ii) APOE genotype (epsilon4+ or epsilon4-). CSF marker levels and cognitive decline were compared across groups. RESULTS: Episodic memory function, according to RAVLT scores, was significantly correlated with CSF marker levels only among epsilon4+ subjects and not among epsilon4- subjects. When comparing the 6 subgroups, SIM epsilon4+ and MIM epsilon4+ groups showed significantly lower Abeta42 levels than the other groups. T-tau and P-tau levels were significantly increased in SIM epsilon4+ when compared to all the other groups, including the SIM epsilon4- group. However, both SIM epsilon4+ and SIM epsilon4- declined cognitively during the follow-up. CONCLUSION: It remains to be determined whether APOE genotype affects the expression of biomarkers in CSF, or whether the different biomarker patterns reflect different types of disease processes in patients with progressive cognitive dysfunction.

Amyloid beta-Protein Precursor↗

PubMed2003

Microtubule-associated tau protein positive neuronal and glial inclusions in ALS.

BACKGROUND: The authors compared tau protein deposition in the frontal cortex of patients with cognitive impairment of amyotrophic lateral sclerosis (ALSci) (n = 6), cognitively intact patients with ALS (n = 6), and age-matched controls (n = 6) in order to determine the pathologic substrate of ALSci. METHODS: Archival paraffin-embedded tissue was examined using Gallyas staining and immunostaining for tau-1 (phosphorylation-dependent tau epitope), tau-2 (phosphorylation independent), Alzheimer-specific tau phosphoepitopes (AT 8; ser(396) phosphorylation), beta-amyloid, glial fibrillary acid protein, SMI 31 (recognizing phosphorylated NFH), alpha-synuclein, or ubiquitin. RESULTS: Tau immunoreactive astrocytic and dense neuronal inclusions were found in both ALS and ALSci, although to a greater extent in ALSci. Superficial linear spongiosis and Gallyas-positive intraneuronal aggregates, immunoreactive with tau-1 and AT 8 but rarely to ser(396) tau, were unique to ALSci. Dense extracellular aggregates were observed by both Gallyas staining and tau-1 immunostaining. Tufted degenerating astrocytes containing tau-1 and AT 8 immunoreactive aggregates and, rarely, dense Gallyas positive neuritic plaques immunoreactive with tau-1 and AT 8, but not with ser(396) tau or beta-amyloid, were observed in ALSci. Tau positive glial coiled bodies were observed in the deep cortical layers and adjacent subcortical white matter in ALSci. Although 3R and 4R tau mRNA isoforms were expressed to similar levels in the frontal cortex of all cases, the total amount of tau mRNA was increased in both ALS and ALSci. Both gray and white matter soluble tau protein expression was similar among control, ALS, and ALSci cases. CONCLUSIONS: Cognitive dysfunction in ALS may reflect abnormal tau protein metabolism.

Aged↗

PubMed2005

The nature and frequency of cognitive deficits in children with neurofibromatosis type 1.

OBJECTIVE: To assess the frequency and severity of specific cognitive deficits in children with neurofibromatosis type 1 (NF1) in a large unbiased cohort. METHODS: Extensive cognitive assessments were performed in 81 children with NF1 ages 8 to 16 years and their performance was compared with that of 49 unaffected sibling controls. RESULTS: Eighty-one percent of the children with NF1 had moderate to severe impairment in one or more areas of cognitive functioning. Although 51% of children with NF1 performed poorly on tasks of reading, spelling, and mathematics, specific learning disabilities (as defined by IQ-achievement discrepancies) were present in only 20% of the children. Sustained attention difficulties were present in 63% of children with NF1, with 38% of children with NF1 fulfilling the diagnostic criteria for attention deficit-hyperactivity disorder. The NF1 neuropsychological profile is characterized by deficits in perceptual skills (visuospatial and visuoperceptual), executive functioning (planning and abstract concept formation), and attention (sustained and switching). Interestingly, both verbal and visual memory was unaffected in NF1 children, and their memory skills were in general stronger than their level of general intellectual function. Although both expressive and receptive language skills were significantly impaired in NF1 children, they appeared to be relatively better preserved than visuospatial abilities once IQ is taken into account. CONCLUSION: There is an extremely high frequency of cognitive problems in children with neurofibromatosis type 1, making cognitive dysfunction the most common complication to affect quality of life in these children.

Adolescent↗

PubMed1998

Cognitive and motor functioning in Parkinson disease: subjects with and without questionable dementia.

BACKGROUND: The nature of cognitive performance in subjects with Parkinson disease (PD) without dementia is controversial, perhaps because of failure to exclude subjects with unrecognized very mild dementia. OBJECTIVE: To compare cognitive and motor functioning in well-characterized subjects with PD without overt dementia with healthy elderly control subjects. DESIGN: Subjects' conditions were evaluated clinically and psychometrically at entry into a longitudinal study of cognitive and motor performance in elderly subjects. Measures included a global dementia staging scale, the Washington University Clinical Dementia Rating; psychometric tests, including Logical Memory, Digit Span, Associate Learning, Information, Block Design, Digit Symbol, Trail-making A, Crossing-off, Boston Naming Test, and Word Fluency; and motor measures, including finger tapping, gait velocity, reaction time, and movement time. SETTING: A university-based research facility. SUBJECTS: There were 3 groups of subjects: healthy elderly control subjects (n=43), subjects with PD without dementia (n=58), and subjects with PD with questionable dementia (n=22), each evaluated at time of entry. RESULTS: As expected, both PD groups were impaired on motor measures (gait velocity, finger tapping, and movement time) compared with the healthy elderly control group. Neither PD group showed slowing in reaction time. The subjects with PD with questionable dementia were more impaired on Logical Memory, Block Design, Digit Symbol, and Trailmaking A compared with the subjects with PD without dementia. Although free of clinically evident cognitive dysfunction (Clinical Dementia Rating score, 0), the PD group without dementia was impaired with respect to the healthy elderly control group on all measures from the psychometric assessment except Digit Span, Associate Learning, and Word Fluency. CONCLUSIONS: The PD group without dementia showed global cognitive impairments in comparison with the healthy elderly control group, possibly because the healthy elderly control subjects represented idealized aging. Although the deficits were of small magnitude, this finding suggests that PD may predispose to subclinical cognitive impairment. Longitudinal follow-up is required to determine whether subjects with PD destined to develop overt dementia can be distinguished from those who do not.

Aged↗

PubMedDate not supplied

Course of psychopathology, cognition and neurobiological abnormality in schizophrenia: developmental origins and amelioration by antipsychotics?

It is argued that schizophrenia has origins in events occurring during the first or early second trimester that are reflected in minor physical anomalies and which may at least in part predispose to later obstetric complications. This neurodevelopmental basis underlies certain neuromotor and psychosocial abnormalities of infancy and childhood, which are the early manifestations of what will be reconceptualised later as negative symptoms and (particularly frontal) cognitive dysfunction, but gives rise to positive symptoms only on the maturation of other systems necessary for their expression. This later emergence of psychosis may reflect an active morbid process that is associated with increased accrual of negative symptoms and of general (but not frontal) cognitive impairment that may be ameliorated by effective antipsychotic treatment. The psychological or biological basis of this heuristic process is poorly understood. Contemporary re-appraisal of any impact of antipsychotics on the long-term course of schizophrenia must take into account what is known of the origins of the disease process with which such drugs might interact. Much recent work continues to indicate that very early events, during the embryonic/fetal period, are important in, if not fundamental to, the genesis of schizophrenia; i.e. that there is a neurodevelopmental basis to the disorder. The present article seeks to establish a time-line relating early intrauterine adversity and dysmorphogenesis, through the onset of psychosis, to the chronic phase of the illness over adulthood; from this time-line, a schema is elaborated for a beneficial impact of antipsychotics on the course of psychopathology, cognition and, less clearly, neurobiological abnormality.

Antipsychotic Agents↗

PubMed2005

Neuropsychological function in high-risk breast cancer survivors after stem-cell supported high-dose therapy versus standard-dose chemotherapy: evaluation of long-term treatment effects.

BACKGROUND: Studies on cognitive functioning in breast cancer patients point out that a subset of women exhibit chemotherapy-related neuropsychological impairment. Thereby, high-dose therapy may elevate the risk of cognitive dysfunctions. The primary purpose of the study was to evaluate the impact of high-dose versus standard-dose chemotherapy on the late neuropsychological outcome in randomized assigned high-risk breast cancer survivors. Next to focusing prevalence, function specificity and extent of cognitive impairment, the question as to whether doses-dependent group differences occur was investigated. PATIENTS AND METHODS: Twenty-four high-dose and 23 standard-dose patients 5 years, on average, after treatment underwent a comprehensive neuropsychological assessment. In addition, 29 early-stage breast cancer patients matched for age, education and time since treatment were recruited as a comparison group. RESULTS: Global cognitive impairment was observed in 8% of high-dose versus 13% of standard-dose compared with 3% of early-stage breast cancer patients. Compared with normative data, all patient groups performed worse on one attention subtest measuring the simple reaction time (P < 0.001 in each case). By contrast, no significant between-group differences on the late neuropsychological outcome were found. CONCLUSIONS: Five years after treatment, standard-dose patients were slightly, but not significantly, more impaired in cognitive performance than high-dose patients.

Antineoplastic Agents↗

PubMed2005

Predictors of dyadic adjustment in multiple sclerosis.

Because multiple sclerosis (MS) is usually diagnosed between the ages of 20 and 50, a time during which most people begin serious relationships, dyadic adjustment for MS patients is a salient issue. However, little is known about factors that might contribute to dyadic adjustment problems in MS. In the present study, we predicted that MS patients showing evidence of three common sequelae of MS--depression symptoms, fatigue and cognitive dysfunction--would be most likely to display problems with dyadic adjustment. Sixty-four MS patients and 49 significant others were assessed. Patient-reported dyadic adjustment was significantly (P at least <0.05) associated with depression (r = -0.48) and fatigue (r = -0.31), but not cognitive functioning. Significant other-reported dyadic adjustment was significantly associated with patients' depression (r = -0.38), fatigue (r = -0.30) and executive functioning impairments (r = 0.37). Stepwise regression analyses revealed that depression was the only significant predictor of dyadic adjustment, regardless of whether significant other (r2 change = 0.16) or patient-reported (r2 change = 0.22) dyadic adjustment was used as the criterion variable. If depression leads to dyadic problems in MS patients, treatment of depression may result in improved dyadic adjustment. Conversely, if dyadic problems contribute to depression in MS, then treatment of dyadic problems may lead to relief from depression in these patients.

Adaptation, Psychological↗

PubMed2001

A case of claimed persistent neuropsychological sequelae of chronic formaldehyde exposure: clinical, psychometric, and functional findings.

Many anecdotal cases and some clinical studies have demonstrated that formaldehyde exposure can cause multiple health-related problems and cerebral dysfunction. The U.S. Consumer Product Safety Commission has documented multiple hazards related to formaldehyde exposure. Some of this research has suggested that low levels of exposure can be very hazardous to one's health and can potentially result in heightened chemical sensitivities, seizures, and cognitive decline. Some research suggests that exposure results in long-term immunological changes, cell neurofilament protein changes, and demyelination. Symptomatically, exposure has been associated with respiratory problems, excessive fatigue, headaches, mood changes, and impaired attention, concentration, and memory functioning. This article outlines the case of a biology teacher whose chronic formaldehyde exposure resulted in heightened sensitivity to formaldehyde, three tonic-clonic seizures, and dramatic amnesia as well as other cognitive dysfunction.

Journal Article↗

PubMed1990

Cognitive impairments in abstinent alcoholics.

Impaired cognitive functioning in alcoholics is widespread during the first months of detoxification. Between half and two thirds of abstinent alcoholics exhibit cognitive impairments during this period, with residual deficits persisting for years after detoxification in some patients. The most severe deficits have been observed in visuospatial abilities, perceptual-motor integration, abstract reasoning, and new learning. The most significant predictors of cognitive dysfunction in persons recovering from alcoholism are the time elapsed since the last drink and the person's age. Surprisingly, the pattern and duration of a patient's alcohol abuse are relatively weak determinants of neuropsychological impairment during abstinence. Research investigating the hypothesis that cognitive impairments may be related to alcoholic persons resuming drinking has yielded mixed results, but a higher level of neuropsychological functioning is associated with increased rates of completing treatment programs and with greater success in the work environment after discharge from treatment. The possibility of cognitive limitations should be taken into account in planning treatment programs for alcoholism.

Adult↗

PubMed2000

Cerebral dysfunction after cardiac surgery--are we moving forward?

This review focuses on the effects of cardiac surgery and cardiopulmonary bypass on the brain, with special emphasis on the results of recently conducted studies. The incidence of postoperative neurological and neuropsychological deficits and risk factors for cerebral injury are reviewed. The relationships between cerebral embolic load, release of biochemical markers of brain injury and cognitive dysfunction after cardiac surgery are also reviewed. Finally, recently gained information on the management of cardiopulmonary bypass is discussed, along with the results of recent pharmacological neuroprotective trials in patients undergoing cardiac surgery.

Journal Article↗

PubMed1998

Cognitive profiles of autopsy-confirmed Lewy body variant vs pure Alzheimer disease.

OBJECTIVE: To compare the cognitive profiles of patients with autopsy-confirmed Alzheimer disease (AD), with or without concomitant Lewy bodies, on 2 dementia screening measures. METHODS: Profiles on subtests of the Mattis Dementia Rating Scale (range, 105-125) and of component items of the Mini-Mental State Examination were compared between 23 patients with uncomplicated AD and 23 patients with concomitant AD and Lewy body pathology (Lewy body variant [LBV]). RESULTS: Although the groups did not differ significantly regarding age, years of education, total Mini-Mental State Examination score, or total Mattis Dementia Rating Scale score, the AD group performed significantly worse than the LBV group on the Mattis Dementia Rating Scale Memory subscale (P < .005). In contrast, the LBV group demonstrated poorer performance than the pure AD group on the Initiation/Perseveration subscale (P < .02). The groups did not differ significantly on the Attention, Construction, or Conceptualization subscales. The same overall pattern of results was obtained when subgroups with mild to moderate and moderate to severe dementia were examined separately, with the additional finding that in the mild-to-moderate range patients with dementia and LBV performed worse than patients with pure AD on the Construction subscale. CONCLUSIONS: The difference in pattern of cognitive deficits among patients with pure AD vs those with AD and LBV is similar to that seen between AD and more subcortical/frontal dementias (eg, Huntington disease) This suggests that the concomitant Lewy body pathology significantly contributes to the presentation of the cognitive dysfunction in individuals with LBV.

Aged↗

PubMedDate not supplied

Corticosteroids and cognition.

The brain is a major target organ for corticosteroids. It has been observed that excessive circulatory levels of endogenous and exogenous corticosteroids are frequently associated with cognitive impairment in a wide variety of clinical disease states. Cognition and low levels of corticosteroids have been less well studied. In this paper we review the literature on glucocorticosteroid effects on cognition and delineate specific functions that appear to be causally affected. We draw a possible connection to specific areas of brain perturbation, including the hippocampus and frontal lobe regions. The possibility that cognitive dysfunction caused by glucocorticoids can be pharmacologically managed is introduced.

Addison Disease↗

PubMed1999

Screening for impaired cognitive function among the elderly in Spain: reducing the number of items in the Short Portable Mental Status Questionnaire.

The objectives of this work are to assess the agreement in classifying the 10th percentile of the population with impaired cognitive function resulting from different combinations of items in the Short Portable Mental Status Questionnaire, to evaluate the effect of literacy status on the new reduced versions, and to propose items less biased by education. Three data sets of representative samples of non-institutionalized elderly (65-year-olds and older) living in urban and rural communities in Spain were analyzed. Cognitive function was assessed using either the original or a modified Spanish version of the Short Portable Mental Status Questionnaire (SPMSQ). Different combinations of items were excluded from the scale and for each resulting reduced scale the lower 10th percentile of the distribution assessed a cut-off score. Cohen's kappa was used to test the agreement between the whole scale and the reduced scales in identifying the lowest 10th percentile of people with cognitive impairment. To test the effect of literacy status, the three samples were combined. New distributions were obtained for reduced versions of the scale including the items with the highest correlation with cognitive impairment controlling for literacy status. All three samples follow a similar distribution of errors. Most kappa values obtained when excluding one or more items from the original scales were between 0.80 and 0.95, while proportion of agreement varied between 94.2% and 100%. Lack of agreement is highest when eliminating all items that represent one dimension. Shorter versions of the SPMSQ are as reliable as the complete 10-item version in identifying those at risk for cognitive dysfunction. Cut-off points differed by literacy status but remained stable regardless of the number of items included.

Aged↗

PubMed1997

Hierarchy of physiological responses to hypoglycemia: relevance to clinical hypoglycemia in type I (insulin dependent) diabetes mellitus.

Hypoglycemia elicits a characteristic sequence of responses in healthy humans. These responses (and their arterialized venous glycemic thresholds) include: 1) Decreased insulin secretion (approximately 4.5 mmol/L). 2) Increased glucose counterregulatory hormone (glucagon, epinephrine, growth hormone and cortisol) secretion (approximately 3.6-3.8 mmol/L). 3) Symptoms of hypoglycemia (approximately 3.0 mmol/L). 4) Cognitive dysfunction (approximately 2.6 mmol/L). Thus, insulin secretion decreases as plasma glucose levels fall within the physiological range, and counterregulatory hormone secretion increases as plasma glucose levels fall just below the physiological range at substantially higher glucose levels than those required to produce symptoms and impair cognitive function. These data are entirely consistent with the body of evidence that insulin, glucagon and epinephrine stand high in the hierarchy of redundant glucoregulatory factors that prevent, as well as correct, hypoglycemia. When the same methods are used, these thresholds are remarkably reproducible from laboratory to laboratory. Nonetheless, the glycemic thresholds are dynamic rather than static. They vary in relation to recent antecedent glycemia. For example, lower plasma glucose concentrations are required to elicit autonomic, including epinephrine, and symptomatic responses in patients with well controlled IDDM, a phenomenon best attributed to recent antecedent iatrogenic hypoglycemia. This is the basis of the clinical syndrome of hypoglycemia unawareness, which is now known to be reversible with scrupulous avoidance of iatrogenic hypoglycemia. The latter also at least partially reverses reduced epinephrine responses to hypoglycemia, a key component (in the setting of absent glucagon responses) of the syndrome of defective glucose counterregulation. While perhaps seemingly adaptive, these threshold shifts appear to be maladaptive since both defective glucose counterregulation and hypoglycemia unawareness are associated with substantially increased rates of severe iatrogenic hypoglycemia in people with IDDM.

Diabetes Mellitus, Type 1↗

PubMed2003

Cognitive functioning in younger and older HIV-1-infected adults.

In young adults, a major neurologic complication of HIV-1 infection is cognitive motor impairment. Epidemiologic findings suggest that increasing age is a significant risk factor for HIV-1-associated dementia as the AIDS-defining illness. Findings from the few studies that have directly measured cognition in younger and older HIV-1-infected adults, however, have been mixed, in part, because of small sample sizes and other methodologic differences between studies. The authors present preliminary findings on cognitive functioning in symptomatic HIV-1-infected younger (aged 20-39 years) and older (aged 50 years or older) adults. Independent of age, HIV-1 infection was accompanied by learning and memory retrieval deficits, which were significantly associated with high plasma viral loads in the young adults. Relative to the younger and older HIV-1-negative (HIV-1-) groups, only the younger HIV-1-positive (HIV-1+) group had significantly longer reaction times (RTs). Within the older HIV-1+ group, however, longer simple and choice RTs were significantly correlated with higher viral loads and lower CD4 cell counts. Although HIV-1 infection affects cognition independent of age, longitudinal studies involving large numbers of older individuals are needed to determine whether there are age differences in the prevalence, nature, and severity of HIV-1-associated cognitive dysfunction.

Acquired Immunodeficiency Syndrome↗

PubMed1994

Influence of clinical variables on neuropsychological performance in multiple sclerosis.

The effects of age, educational level, duration and course of the disease, physical disability and mood status on several cognitive functions (short- and long-term memory, frontal functions, attention, language and visuospatial skills) have been evaluated in 42 multiple sclerosis (MS) patients. The Hamilton Depression Rating Scale (HDRS) scores and a secondary progressive disease course significantly influenced neuropsychological performance. Factorial analysis revealed that indexes of (1) frontal function impairment, (2) long-term verbal memory and language function impairment, and (3) visuospatial short- and long-term memory and visuoperceptive function impairment accounted for 85% of the variance in neuropsychological performance. Only the first factor was significantly related to the presence of depressive symptomatology, as assessed by the HDRS. These results indicate that both the course of the disease and the presence of affective disorders must be taken into account when evaluating the natural history of cognitive impairment in MS and suggest that depressive symptomatology and cognitive dysfunction in MS are related to the involvement of at least partially overlapping anatomofunctional circuits.

Adult↗