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PubMed2005

Cognitive deterioration and electrical status epilepticus during slow sleep.

The results of long-term follow-up of 10 children with global or specific cognitive deterioration and, on the electroencephalogram, electrical status epilepticus during sleep (ESES) are described. They were referred because of cognitive deterioration and underwent repeated neurological and neuropsychological examinations and all-night electroencephalography. A previous cognitive level was known or could be estimated in all. Seven children had a continuous spikes and waves during sleep (CSWS) syndrome, with global cognitive deterioration in four and more specific cognitive decline in three, and another three children had Landau-Kleffner syndrome (LKS). Of the last three, two children never had seizures, while the other had localization-related epilepsy. No children experienced aggravation of clinical seizures. However, therapy was disappointing. Cognitive dysfunction did not respond to valproate and/or benzodiazepines in 9 of the 10 children. A frontal epileptic focus was found in 5 of 7 children with CSWS, and a left temporal focus in 2 of 3 children with LKS. The ESES persisted in CSWS for 5-9 years and in LKS for 1-5 years, and disappeared at puberty. Good cognitive recovery after disappearance of ESES occurred in only one child, and partial recovery in four. An unfavorable prognosis of cognitive deterioration seems to be related to long-duration ESES and/or early onset epileptic activity. The authors are of the opinion that cognitive deterioration in children, with or without manifest epileptic seizures, should mandate electroencephalographic investigation during sleep.

Adolescent↗

PubMed1999

Effects of a small dose of triazolam on P300.

Ten healthy men (mean age, 33.9 years) participated in two experimental sessions cross-overed randomly in a double-blind manner: one with the placebo and another with 0.125 mg of triazolam (TRZ). Resting electroencephalography and event-related potential under oddball paradigm were recorded before the drug administration, and 1, 2, 4, 6 and 8 h after that. P300 waveforms were analyzed by peak amplitudes and 30-ms bin data. Triazolam may cause cognitive dysfunction without general sedation or apparent sleepiness, and this effect appeared 2 h, 4 h and 6 h, most prominently 6 h, after TRZ administration.

Adult↗

PubMed2005

Subjective well-being and quality of life following traumatic brain injury in adults: a long-term population-based follow-up.

PRIMARY OBJECTIVE: To assess subjective well-being and quality-of-life in nationally representative samples of patients at long intervals following traumatic brain injuries. METHODS AND PROCEDURES: Patients with either cranial fractures or cerebral lesions were identified in a national computer-based register of hospital admissions and random samples were selected among those who had suffered the injury at 5, 10 or 15 years prior to the follow-up. Postal questionnaires were sent to them covering quality of life, e.g. return to employment, family relations and current subjective well-being in terms of symptomatology, e.g. somatic complaints, cognitive dysfunction. A response rate of 76% was obtained, comprising 114 patients with cranial fracture and 126 with cerebral lesions. MAIN OUTCOMES AND RESULTS: The group with cerebral lesions had markedly poorer quality of life and subjective well-being than the group with cranial fractures and this did not vary across time. In both groups, the most common symptoms concerned cognition. Among the cerebral lesion group, quality of life outcome was fairly well predicted by severity of injury, but subjective well-being was less well predicted. CONCLUSIONS: The negative consequences of traumatic cerebral lesions are marked and do not vary at long periods following injury.

Activities of Daily Living↗

PubMed2000

Childhood cognitive functioning in schizophrenia patients and their unaffected siblings: a prospective cohort study.

While it is known that children of schizophrenia parents perform more poorly on tests of cognitive functioning than children of normal parents, less certain is the degree to which such deficits predict schizophrenia outcome, whether cognitive functioning deteriorates during childhood in preschizophrenia individuals, and whether nongenetic etiologic factors (such as obstetric complications) contribute to these deficits. In the present study, 72 patients with schizophrenia or schizoaffective disorder, 63 of their siblings not diagnosed with schizophrenia, and 7,941 controls with no diagnosis were ascertained from a birth cohort whose members had been evaluated with standardized tests of cognitive functioning at 4 and 7 years of age. Adult psychiatric morbidity was ascertained via a longitudinal treatment data base indexing regional public health service utilization, and diagnoses were made by review of all pertinent medical records according to DSM-IV criteria. Both the patients with schizophrenia and their unaffected siblings performed significantly worse than the nonpsychiatric controls (but did not differ from each other) on verbal and nonverbal cognitive tests at 4 and 7 years of age. Preschizophrenia cases and their siblings were increasingly overrepresented across decreasing quartiles of the performance distributions. There was not significant intra-individual decline, and there were no significant relationships between obstetric complications and test performance among the preschizophrenia subjects. These results suggest that during the period from age 4 to age 7 years, premorbid cognitive dysfunction in schizophrenia represents a relatively stable indicator of vulnerability deriving from primarily genetic (and/or shared environmental) etiologic influences.

Adult↗

PubMed2002

Transplanted neural stem cells survive, differentiate, and improve neurological motor function after experimental traumatic brain injury.

OBJECTIVE: Using the neural stem cell (NSC) clone C17.2, we evaluated the ability of transplanted murine NSCs to attenuate cognitive and neurological motor deficits after traumatic brain injury. METHODS: Nonimmunosuppressed C57BL/6 mice (n = 65) were anesthetized and subjected to lateral controlled cortical impact brain injury (n = 52) or surgery without injury (sham operation group, n = 13). At 3 days postinjury, all brain-injured animals were reanesthetized and randomized to receive stereotactic injection of NSCs or control cells (human embryonic kidney cells) into the cortex-hippocampus interface in either the ipsilateral or the contralateral hemisphere. One group of animals (n = 7) was killed at either 1 or 3 weeks postinjury to assess NSC survival in the acute posttraumatic period. Motor function was evaluated at weekly intervals for 12 weeks in the remaining animals, and cognitive (i.e., learning) deficits were assessed at 3 and 12 weeks after transplantation. RESULTS: Brain-injured animals that received either ipsilateral or contralateral NSC transplants showed significantly improved motor function in selected tests as compared with human embryonic kidney cell-transplanted animals during the 12-week observation period. Cognitive dysfunction was unaffected by transplantation at either 3 or 12 weeks postinjury. Histological analyses showed that NSCs survive for as long as 13 weeks after transplantation and were detected in the hippocampus and/or cortical areas adjacent to the injury cavity. At 13 weeks, the NSCs transplanted ipsilateral to the impact site expressed neuronal (NeuN) or astrocytic (glial fibrillary acidic protein) markers but not markers of oligodendrocytes (2'3'cyclic nucleotide 3'-phosphodiesterase), whereas the contralaterally transplanted NSCs expressed neuronal but not glial markers (double-labeled immunofluorescence and confocal microscopy). CONCLUSION: These data suggest that transplanted NSCs can survive in the traumatically injured brain, differentiate into neurons and/or glia, and attenuate motor dysfunction after traumatic brain injury.

Animals↗

PubMed1995

Cognitive function in early adult and adult onset myotonic dystrophy.

INTRODUCTION: Most studies revealing intellectual deficits in myotonic dystrophy (MyD) involved heterogeneous groups of patients with respect to intelligence and onset of disease. The present study was undertaken to investigate whether patients with early adult and adult MyD show subtle cognitive deficits despite a normal intelligence. MATERIALS AND METHODS: We compared 26 MyD patients of normal intelligence with mild symptoms and early adult and adult onset to 25 matched control subjects (CS) on a range of neuropsychological tests and a number of motor tasks of increasing complexity, which required increasing cognitive control. RESULTS: The groups did not differ as far as the neuropsychological tests were concerned, with the exception of the Stroop Color Word Test. With respect to motor performance, the MyD patients were poorer scorers on simple and automatic motor tasks than CS, but the difference disappeared as the complexity of the tasks increased and required correspondingly more cognitive control. CONCLUSION: We found hardly any evidence of cognitive dysfunction in our group of MyD patients with early adult and adult onset.

Adult↗

PubMed1994

Cognitive therapy with schizophrenic patients: conceptual basis, present state, future directions.

Schizophrenia may nowadays be most readily understood as a systemic disorder in which changes in the brain structure underlie individual cognitive abnormalities which for their part interact with environmental factors at the onset of the illness and during its course. From this, one may deduce the rationale for cognitive therapy for schizophrenic patients. Existing approaches may be systemised as direct, indirect and combined procedures. The latter are based on the assumption of the pervasive effects of elementary and complex cognitive dysfunctions at the levels of open behaviour. However, in a mirror-design study with 21 schizophrenic patients according to DSM-III-R in which the effects of various intervention sequences were examined, it was not possible to find confirmation for this. This and other open questions have led to doubts expressed in current literature concerning the utility of cognitive therapy, especially with respect to the locus, nature and malleability of cognitive disorders, as well as the possibility of generalizing cognitive improvements. The latter are discussed in detail and possible future directions in cognitive therapy for schizophrenic patients are shown.

Adult↗

PubMed1993

A prospective controlled investigation of the cognitive effects of amateur boxing.

Eighty six amateur boxers underwent a series of neuropsychological assessments on three occasions--pre bout, immediate post bout and follow up within two years; 31 water polo players and 47 rugby union players acted as controls. The neuropsychological tests were selected as being sensitive to subtle cognitive dysfunction and formed part of a battery of other neurological and ophthalmic assessments. No evidence of neuropsychological dysfunction due to boxing was found, either following a bout or a series of bouts at follow up. None of a range of parameters including number of previous contests, recovery from an earlier bout, number of head blows received during a bout and number of bouts between initial assessment and follow up, were found to be related to changes in cognitive functioning.

Adolescent↗

PubMed2000

Cortical deficits in multiple sclerosis on the basis of subcortical lesions.

Patients suffering from multiple sclerosis have a high frequency of cognitive deficits usually attributable to demyelination and axonal loss in the subcortical white matter. Neurologic abnormalities referable to cortical function are uncommon but have been described. The present study describes three patients with clinically definite MS with deficits in cognitive function referable to cortical location. Two of the patients underwent positron emission tomography and showed profound cortical hypometabolism adjacent to subcortical white matter lesions seen on MRI. This paper points out that neurologic deficits referable to cortical sites may be caused by subcortical white matter lesions and that cognitive dysfunction in patients with MS may progress rapidly in the absence of motoria deficits or other evidence of clinical deterioration. Multiple Sclerosis (2000) 6 50 - 55

Adult↗

PubMed2005

Morris water maze search strategy analysis in PDAPP mice before and after experimental traumatic brain injury.

Traumatic brain injury (TBI) is a common cause of cognitive dysfunction and a major risk factor for Alzheimer's disease (AD). PDAPP mice, a transgenic line overexpressing a mutant human amyloid precursor protein (APP) implicated in familial AD, have markedly impaired behavioral performance in the Morris water maze relative to wild-type (WT) littermates. Performance further deteriorates following experimental TBI in both PDAPP and WT mice. However, the aspects of cognitive function involved are not well understood. Here, we have analyzed search strategies used in the water maze by 3-4 month old PDAPP and WT C57Bl6 littermates both before and after moderate controlled cortical impact TBI. Prior to TBI, PDAPP mice used less spatial strategies and more nonspatial systematic strategies and strategies involving repetitive looping than WT mice. With training, PDAPP mice used more spatial strategies and less repetitive looping. After TBI, PDAPP mice lost use of spatial strategies and relied more on repetitive looping. TBI in WT mice also reduced their use of spatial strategies but instead caused a switch to nonspatial systematic strategies. We also analyzed changes in the efficiency with which mice used each individual strategy, but found that differences in which strategies were used quantitatively accounted for most of the differences in performance between groups. These results demonstrate that suboptimal search strategy use in addition to effects on spatial learning and memory underlies the impaired performance of PDAPP mice and further deterioration following TBI. Human TBI patients may have analogous poor use of problem solving strategies.

Amyloid beta-Protein Precursor↗

PubMed2005

Cognition in schizophrenia: impairments, determinants, and functional importance.

Recent findings support and add to earlier findings of cognitive dysfunction in schizophrenia. Deficits across neurocognitive domains such as attention, working memory, language skills, and executive functioning tend to be moderate, with the most pronounced deficits found in verbal learning and memory. All these neurocognitive domains are related to adaptive and social skills, with executive functions and verbal learning and memory showing more variance across more domains than other neuro-cognitive variables. Negative symptoms and neurocognitive domains, although correlated, are distinct and have differential pathways of change with treatment. General psychopathology symptoms, such as depression and anxiety, may become important treatment targets as strategies are developed for translating cognitive enhancement to real-world functional performance.

Antipsychotic Agents↗

PubMed1993

What may be gained from neuropsychological investigations of tardive dyskinesia?

As an iatrogenic movement disorder, tardive dyskinesia (TD) offers a unique opportunity to study brain-behavior relationships. The authors provide a brief overview of TD and discuss its association to cognitive dysfunction. It is argued that, given the complexity of the variables involved in the study of TD, there is pressing need for greater applications of neuropsychological research paradigms to help elucidate this disorder.

Antipsychotic Agents↗

PubMed2003

Parkin mutation associated parkinsonism and cognitive decline, comparison to early onset Parkinson's disease.

BACKGROUND: Patients with Parkinson's disease (PD) have cognitive changes resulting, presumably, from a progressive disruption of the functional integrity of frontostriatal circuitry. OBJECTIVE: To assess the cognitive state of two brothers with early onset autosomal recessive (EO-AR) parkinsonism and a large deletion in the parkin gene, and to compare it to that of patients with sporadic young onset PD (YOPD). METHOD: Two brothers with parkinsonism and deletion of axons 4-6 of the parkin gene (ages 51, 55 years; duration of symptoms, 22, 29 years respectively) and 4 randomly selected patients with YOPD (mean age 47.8+/-4.9 years; mean duration of symptoms, 11.5+/-1.9 years) were administered a neuropsychological battery at "on" state. We assessed global cognitive state using the Mini-Mental State Examination (MMSE), orientation, attention, memory, language, ideational praxis, constructive praxis and executive functions (shifting aptitude, verbal fluency, sequencing). RESULTS: The older of the two brothers with EO-AR parkinsonism had dementia according to DSM IV criteria, and MMSE score of 24, whereas the other had normal global cognitive status with mild cognitive changes (MMSE=29). The older brother had impaired memory tasks. Storage and retrieval capacities were defective on both immediate and delayed recalls, naming, constructional praxis, selective attention, shifting aptitude and phonemic and semantic fluency were also affected. The younger brother had difficulties in retrieval on delayed recall, selective attention, phonetic fluency, shifting aptitude and sequencing. This neuropsychological profile clearly differs from that of the YOPD patients, none of whom displayed cognitive dysfunction. CONCLUSIONS: Our patients with parkin mutation performed poorly on neuropsychological tests compared to those with YOPD. This difference could reflect the longer disease duration or the nature of the degenerative process.

Adult↗

PubMed2001

Neurophysiological evaluation of late effects of adjuvant high-dose chemotherapy on cognitive function.

OBJECTIVES: To evaluate late neurotoxicity of adjuvant high-dose (HD) chemotherapy versus standard-dose (SD) chemotherapy by event-related potentials (ERP) and quantitative electroencephalography (qEEG). PATIENTS AND METHODS: From a randomized study in high-risk breast cancer patients on the efficacy of high-dose versus standard-dose adjuvant chemotherapy, late effects on cognitive functioning were analyzed by neuropsychological tests. Cognitive impairment was found in 32% of the HD group, 17% of the SD group and in 9% of a control group of stage I breast cancer patients not treated with chemotherapy. In 17 consecutive patients in the HD group and 16 consecutive patients in the SD group neurophysiological tests were performed, consisting of P300 and qEEG. Results of patients treated with chemotherapy were compared with results of 14 control patients not treated with chemotherapy. All patients were tested two years after treatment. RESULTS: Asymmetry of the alpha rhythm of > or =0.5 Hz was found in 7 HD patients, 2 SD patients and in none of the control patients (p = 0.01). No differences were found between the groups with regard to frequency of alpha rhythm, alpha blocking and latency of P300. No correlation was found between neurophysiological parameters and neuropsychological performance, except for an overall relation between the P300 latencies and the total number of deviant test scores. CONCLUSION: Although the neurophysiological differences are subtle and the relation with the cognitive functioning in individual patients as measured by the neuropsychological examination is equivocal, the results suggest that there is neurophysiological support for cognitive dysfunction as a late complication of high-dose systemic chemotherapy in breast cancer.

Alpha Rhythm↗

PubMed2002

Neuropsychological function in systemic lupus erythematosus: a five-year longitudinal study.

OBJECTIVE: To evaluate potential changes in cognitive functions over a 5-yr period in patients with systemic lupus erythematosus (SLE). METHODS: Twenty-eight patients with SLE were examined at baseline and after a mean follow-up of 60.7+/-5.0 months using standardized neuropsychological tests. Group changes in performance over time were measured and the effects of baseline values for subsequent changes in individual variables after 5 yr were evaluated. RESULTS: When all SLE patients were considered as a group, seven out of nine (78%) neuropsychological variables remained unchanged and two (22%) improved significantly during the observation period, possibly due to methodological bias. Analysis of the importance of the level of initial cognitive performance for subsequent changes during the observation period, demonstrated that cognitive changes were not significantly influenced by baseline levels, except for a trend in three of nine variables. Neither demographic nor disease-associated quantitative factors were associated with cognitive changes over time. CONCLUSION: Cognitive dysfunction seems to be a relatively stable feature of central nervous system involvement in SLE. A decrease in performance over time was not demonstrated consistently in the majority of domains.

Adult↗

PubMed1991

Cognitive function in adult adrenoleukodystrophy: comparison with leukoaraiosis and multiple sclerosis.

Cognitive evaluation of 6 cases of adult adrenoleukodystrophy (ALD) included in a brain magnetic resonance (MR) study are reported: 2 males with adrenomyeloneuropathy and 4 women heterozygous for ALD. Cognition was normal in 4 and MR scan in 2 of them. In the 2 others, there were mild modifications of the white matter. One patient suffered of visual retention disturbances with abnormalities of the white matter in MR scan. In the last, cognitive decline was observed; MR scan showed atrophy of cortex and corpus callosum and periventricular high signal areas. Comparison with leukoaraiosis in healthy adults and with multiple sclerosis suggests that there is probably a relationship between cognition and extension of brain MR abnormalities. Time of appearance and frequency of cognitive dysfunction might be explained by the natural history of each of these diseases.

Adrenoleukodystrophy↗

PubMed2002

Systemic lupus erythematosus in three ethnic groups. X. Measuring cognitive impairment with the cognitive symptoms inventory.

OBJECTIVE: To determine the factor structure of the Cognitive Symptoms Inventory (CSI) in patients with systemic lupus erythematosus (SLE) participating in a multiethnic longitudinal study of outcome, the Lupus in Minority populations, Nature versus nurture (LUMINA) study. METHODS: LUMINA patients of Hispanic (n = 48), African American (n = 64), and Caucasian (n = 44) ethnicity who had a study visit (enrollment or followup) between January 1 and September 30, 2000 were included. Patients completed the CSI, a 21-item self-report measure of cognitive function. Sociodemographic, clinical, immunologic, psychosocial, and behavioral variables were ascertained per protocol and as previously described. Data were analyzed with SPSS. The factor structure of the CSI was determined using the principal axis method with oblique rotation as decided by Gorsuch. All factors having an Eigenvalue greater than 1 were considered. A 4-factor solution was derived that accounted for 42.6% of the common variance. The correlations between patient factor scale scores and variables from the demographic, clinical, psychosocial, and behavioral domains were then examined. RESULTS: The four factors and their respective variance are, Attention/Concentration (28.8%), Pattern Recognition/Activity Management (5.7%), Intermediate Memory (4.7%), and Initiation of Executive Functions (3.4%); each factor correlated with the total CSI score. Overall, patients' factor scale scores were positively and significantly correlated with other measures of cognitive dysfunction such as the Systemic Lupus Activity Measure (neuromotor domain) or the Systemic Lupus International Collaborating Clinics Damage Index (neurocognitive impairment), as well as with measures of fatigue, maladaptive coping skills, poor mental functioning, poor social support, and helplessness. They were, however, not correlated with sociodemographic or clinical variables. CONCLUSIONS: In addition to demonstrating that the CSI can be used to measure cognitive impairment in patients with SLE in the research setting, we have determined a 4-factor solution for the CSI that appears to have adequate metric properties. At present, the CSI may best be used as a screen for difficulties in daily activities involving intermediate memory, concentration, attention, and executive function. Nevertheless, further work with the CSI items and factor scales is necessary to establish internal and test-retest reliability of the factor scales; and provide additional evidence of the convergent and predictive validity of these scales in larger samples of patients from each ethnic subgroup.

Adult↗

PubMed2006

Differential effects of classical neuroleptics and a newer generation antipsychotics on the MK-801 induced behavioural primitivization in mouse.

Cognitive dysfunction plays an important role in mental disorders like schizophrenia and may involve inadequate glutamatergic signalling in different regions of the brain, mediated by e.g. glutamatergic N-methyl-D-aspartate (NMDA) receptors. In rodents, NMDA receptor antagonists often increase motor activity; in addition they induce a more primitive and undifferentiated behavioural pattern, which we believe may correspond to some of the cognitive defects seen in schizophrenia. In the present study, the movement pattern of mice treated with the uncompetitive NMDA receptor antagonist MK-801 in conjunction with six antipsychotic agents, some with reported clinical effects on cognition, was characterised and quantified. The classical neuroleptic drugs chlorpromazine and trifluoperazine, the atypical antipsychotic agents ziprasidone and olanzapine, the gamma-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-receptor potentiator CX516 and the serotonin (5-HT)2A-antagonist M100907 were tested. In accordance with previous observations, MK-801 was found to induce a primitive and monotonous behavioural pattern dominated by forward locomotion; spatial movements, the number of switches between the states moving and stationary, and rearing frequency were reduced. All test substances counteracted MK-801-induced hyperactivity, but differed in their ability to improve behavioural quality. Chlorpromazine and trifluoperazine were unable to restore behavioural diversity while ziprasidone, olanzapine, CX516 and M100907 restored it to varying degrees. A striking similarity in movement pattern was seen between the hypoglutamatergic mice treated with the AMPA-receptor agonist CX516, and those receiving the 5HT2A-antagonist M100907.

Animals↗