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PubMed2005

The effect of neuroleptic treatments on executive function and symptomatology in schizophrenia: a 1-year follow up study.

Cognitive dysfunctions (as in memory, attention and executive function) have been recognized as fundamental features of schizophrenia. Executive dysfunction is a major obstacle to functional outcome, community functioning and rehabilitation success and it is crucial to assess the effects of so-called neuroleptic (NLP) medications in this domain of cognitive functioning. Risperidone, an atypical NLP, has been reported to improve executive function in schizophrenia (SZ), but there is controversy regarding these findings. The aim of the current study was to assess the differential effects of risperidone (2-6 mg) and conventional (2-40 mg haloperidol) NLPs on executive skills in 31 individuals with SZ over a 12-month period. The performance of both NLP groups was compared to the performance of 17 age- and education-matched healthy controls. In this randomized, double blind study, the Wisconsin Card Sorting Test (WCST) was administered at baseline, 3, 6, and 12 months after initiating medication. The relationship between executive functioning and the course of clinical symptoms, as assessed by the Positive and Negative Syndrome Scale (PANSS) was also investigated. Results showed that, relative to healthy controls, individuals with SZ showed marked impairment in WCST from baseline through 12 months of treatment. Also, participants under haloperidol or risperidone NLP medication performed similarly on the WCST at all assessment periods showing that risperidone and haloperidol do not differ in their effect on executive functioning. Risperidone treatment, however, was more effective in the reduction of negative symptoms. The differential efficacy of risperidone over negative symptoms and WCST performance strongly suggests that the executive impairments are to some extent the result of brain abnormalities independent of those that produce the major psychopathology manifestations seen in SZ.

Adult↗

PubMed2002

Subclinical impairment of brain function in chronic hepatitis C infection.

BACKGROUND/AIMS: Central nervous system abnormalities such as fatigue and depression occur more frequently in chronic hepatitis C virus (HCV) infection than in many other causes of chronic liver disease. The finding that fatigue is unrelated to activity of hepatitis or mode of infection could indicate an independent effect of HCV on brain function. This study tested the hypothesis of a subclinical cognitive dysfunction in HCV-infected patients. METHODS: One-hundred untreated HCV-RNA positive biopsy-proven patients were investigated by P300 event-related potentials, a sensitive electrophysiologic test of cognitive processing. Health-related quality of life and fatigue were assessed using the SF-36 questionnaire and the Fatigue Impact Scale, respectively. RESULTS: Cognitive brain function was subclinically impaired in the cohort of HCV-infected patients as indicated by significantly prolonged P300 latencies (P=0.01 for comparison to matched healthy subjects) and reduced P300 amplitudes (P<0.001, respectively). Seventeen of the 100 HCV-infected patients had P300 latencies outside the age-adjusted normal range. Abnormal P300 characteristics were not related to the degree of histologic or biochemical activity of hepatitis, severity of fatigue or mental health impairment. CONCLUSIONS: This study demonstrates that patients with HCV infection showed a slight but significant neurocognitive impairment, possibly indicating a further extrahepatic manifestation of chronic hepatitis C.

Adult↗

PubMed1998

School failure in early adolescence: the psychopathological risk.

School difficulties and learning disorders in adolescence can become significant risk factors for psychopathology. This study investigates emotional and cognitive patterns in adolescents with school difficulties. Four clinical conditions that can determine adolescence-onset learning disorders are outlined. These are adolescent turmoil, intellectual inhibition, delay in reasoning development, and metacognitive dysfunctioning. Cognitive, emotional and behavioral features of these conditions are discussed in terms of diagnostic and therapeutic implications.

Achievement↗

PubMed1999

Cognitive therapy for a major depressive episode in residual schizophrenia.

The present paper describes cognitive approaches to the treatment of a major depressive episode in a patient with residual schizophrenia. The goal of therapy was to increase and stabilize the patient's physical activity through decreasing dysfunctional cognition pertinent to inertia. A therapeutic strategy of 'scheduling activities' was first selected, but to no effect. The vicious circle of alternating excessive activity and total inertia remained unchanged. Based on a revised cognitive case conceptualization, a second strategy, 'scheduling inertia', was then introduced, in which the patient was asked to stay in bed or take a rest for planned periods of time every day. This intervention helped the patient to counteract her perfectionist beliefs. The results suggest that 'scheduling inertia' may be a useful strategy for improving inactivity in a major depressive episode during the residual phase of schizophrenia.

Activities of Daily Living↗

PubMed2001

Dissociation between intentional and incidental sequence learning in Huntington's disease.

The ability to acquire and act upon serial order information is fundamental to almost all forms of adaptive behaviour. There is growing evidence that such knowledge may be acquired through a number of different means, each perhaps with its own neuronal substrate. One major distinction is between serial order information acquired intentionally and leading to explicit conscious knowledge of the sequence structure, and information acquired incidentally through experience. While this latter form of knowledge influences behaviour, it may do so without the participant being aware of the sequential information, i.e. it is acquired implicitly. Evidence from physiological and lesion studies in animals and imaging studies in humans suggests that these two forms of learning may have dissociable neuronal substrates. Specifically, the striato-thalamo-cortical circuit centred on the caudate nucleus is proposed to be involved in intentional sequence learning and that based on the putamen on incidental learning. The present study tested one part of this proposed dissociation by assessing patients with Huntington's disease on tasks of the two forms of learning. On the test of trial-and-error intentional learning there were marked deficits, which were closely related to disease progression and to measures of executive cognitive dysfunction. This finding was in contrast to the finding from the incidental learning task. Performance of the Huntington's disease group was essentially normal and unrelated to measures of disease progression and cognitive status. The results, although supportive of the proposed dual-system hypothesis, offer only partial confirmation. Further direct study is required using similar tasks in patients with putamenal disorder or lesions within the skeletomotor striato-thalamo-cortical circuit.

Adult↗

PubMed2000

Central nervous system complications of cardiac surgery.

The neurological complications of cardiac surgery are associated with significantly increased mortality, morbidity and resource utilization. The use of new surgical techniques, introduction of wider indications for surgery and increased public expectation has led to an increase in the average age of cardiac surgical patients and an increased incidence of repeat procedures. With these changes has come an increased risk of neurological complications. The likelihood of perioperative stroke varies between 1% and 5% in most published series and is dependent on a multitude of risk factors. Of these, patient age, aortic atheroma, symptomatic cerebrovascular disease, diabetes mellitus and the type of surgery appear to be most important. Cognitive deterioration after cardiac surgery is far more common, affecting as many as 80% of patients a few days after surgery and persisting in one-third. Despite an increase in the age of the cardiac surgical population, the reported incidence of cognitive dysfunction after cardiac surgery seems to have fallen in recent years. Whether this is a real phenomenon or the result of changes in the use of psychometric testing and the definition of cognitive decline remains unclear. Recognition that certain equipment, surgical practices and patient factors contribute to neurological morbidity has prompted 'neuroprotective' interventions. Some of these (e.g. arterial line filtration and alpha-stat management) have been shown to improve outcome. Despite these measures, a small number of patients will inevitably sustain cerebral injury during otherwise successful cardiac surgery. Although pharmacological neuroprotection may, in the future, offer some of these patients an improved outcome, it is unlikely that any single agent will prevent neurological injury. In the meantime, the CNS complications of cardiac surgery remain a fertile area of research.

Biomarkers↗

PubMed2005

Prenatal ethanol exposure in rats decreases levels of complexin proteins in the frontal cortex.

BACKGROUND: Rodents that are prenatally exposed to ethanol have been shown to exhibit a wide range of cognitive deficits, including impairments in memory, attention and executive function. To determine a potential molecular substrate for cognitive dysfunction in adulthood, we measured regional levels of the presynaptic proteins complexin I and II in a rat model of prenatal ethanol exposure, as levels of these proteins are altered in cognitive-related synaptic plasticity. METHODS: Pregnant female rats received either a liquid ethanol diet (36% ethanol-derived calories) or a liquid control diet (maltose-dextrin isocalorically substituted for ethanol, matched in amount [g/kg body wt/day of gestation] to an ethanol-consuming partner), or were given ad libitum-fed access to standard laboratory chow and water. Levels of complexin I, II and the ubiquitous presynaptic marker synaptophysin were measured in the frontal cortex and hippocampus of adult male offspring, using ELISA. RESULTS: Prenatal exposure to ethanol did not alter levels of presynaptic proteins in the hippocampus or levels of synaptophysin in the prefrontal cortex. However, rats prenatally exposed to ethanol displayed significantly lower levels of both complexin I and II in the prefrontal cortex compared to control animals. CONCLUSIONS: These data indicate that prenatal exposure to ethanol is associated with a selective loss of complexin proteins in the frontal cortex. These proteins are known to be important for activity-dependent neurotransmission, and have previously been shown to mediate synaptic plasticity and cognition. These combined findings suggest that further study of complexin proteins as a substrate for cognitive impairment related to prenatal exposure to ethanol is warranted.

Adaptor Proteins, Vesicular Transport↗

PubMed2005

Delirium in elderly people: an update.

PURPOSE OF REVIEW: To review recent studies on epidemiology, diagnosis, pathophysiology, treatment and prevention of delirium in elderly people. RECENT FINDINGS: There is no evidence that the clinical picture of delirium in elderly people differs from that in younger patients, although it may run a more chronic course. Diagnosing delirium in demented patients, however, may be difficult due to overlap in symptoms of delirium and dementia. Systematic use of screening and diagnostic instruments may help to diminish the common underdiagnosis of delirium. Delirium is best understood as the result of multiple interacting predisposing and precipitating factors. In the elderly, predisposing factors that make patients more susceptible for delirium include cognitive dysfunction and older age, while important precipitating factors that directly cause delirium are any somatic events and the use of anticholinergic drugs. Delirium has a significant negative prognostic impact on functional and cognitive outcome, as well as on morbidity and mortality. Haloperidol remains the standard treatment for delirium, while there is some evidence for the efficacy of risperidone. Other atypical antipsychotics, as well as cholinesterase inhibitors, have not yet been sufficiently studied. Results of studies on the effectiveness of systematic screening of populations at risk and standardized interventions to prevent delirium have been inconclusive. SUMMARY: In recent years, the emphasis in the approach to delirium has shifted from ad hoc treatment to systematic screening and prevention. Interest has been raised in treatment options other than haloperidol, such as atypical antipsychotics and procholinergic drugs.

Journal Article↗

PubMed1998

Phenytoin: effective but insidious therapy for epilepsy in people with intellectual disability.

Phenytoin (5,5-diphenylhydantoin), which has been in use for 60 years, is still an important antiepileptic drug. Its primary mechanism of action is modulation of the sustained repetitive firing of neurones by direct inhibition and blockage of voltage-gated sodium channels in the neuronal cell membrane, and by delay of cellular reactivation. The plasma protein binding of phenytoin is normally between 90% and 95%. The drug is rapidly distributed from the blood to the tissues and is almost completely metabolized in the liver. The plasma phenytoin concentration normally reaches the steady-state level within 1-2 weeks. The half-life of phenytoin is less than 20 h in low doses, but is prolonged in high doses, newborn infants and elderly people. The half-life is shortened when phenytoin is given concomitantly with an enzyme-inducing drug, such as phenobarbital or carbamazepine. Phenytoin is effective for treating generalized tonic-clonic seizures, partial seizures with or without generalization, and convulsive status epilepticus. Over the years, many new, and even serious, adverse effects of phenytoin have been recognized. Phenytoin encephalopathy, manifesting as cognitive impairment and a cerebellar syndrome, is an important adverse neurological effect, the development of which depends on the saturation kinetics of phenytoin, individual differences in phenytoin metabolism, an inhibitory effect of certain drugs on phenytoin metabolism, or the ability of certain drugs to displace phenytoin from plasma proteins, leading to an increase in the plasma level of unbound phenytoin. Because of its potentially adverse effects, phenytoin is not recommended as the first choice for treating epileptic seizures, except as a co-drug for managing convulsive status epilepticus. In patients with epilepsy who also have intellectual disability, and are susceptible to balance disturbances and cognitive dysfunction, it is wise to replace phenytoin with another drug, such as carbamazepine or oxcarbazepine. The long-term use of phenytoin is not recommended for patients with loss of locomotion, marked cognitive impairment, or symptoms and signs of cerebellar disease. The prevention of phenytoin intoxication, with the subsequent development of phenytoin-induced encephalopathy, depends on careful observation of the patients and frequent monitoring of plasma levels of phenytoin and other concomitantly administered antiepileptic drugs.

Anticonvulsants↗

PubMed1999

Sensorimotor gating and thought disturbance measured in close temporal proximity in schizophrenic patients.

BACKGROUND: Sensorimotor gating abnormalities have been previously correlated with thought disturbance in schizophrenic patients. These correlative studies have led to the hypothesis that sensorimotor gating abnormalities may underlie thought disturbance. Several authors have cautioned, however, that this and similar hypotheses are supported by data recorded at different times or during resting states" and therefore incorrectly assume that the observed association represents a concurrent relationship. To address this issue, sensorimotor gating and thought disturbance were measured in close temporal proximity, thus strengthening the evidence for the association of these 2 abnormalities in schizophrenic patients. METHODS: Twenty-one schizophrenic men were assessed on measures of sensorimotor gating and thought disturbance. Sensorimotor gating was examined operationally via the use of prepulse inhibition. Thought disturbance was assessed via the Rorschach test measures of perceptual inaccuracy, disordered cognition, and the expression of normally repressed contents. Symptom rating scales (the Scale for the Assessment of Positive Symptoms and the alogia subscale of the Scale for the Assessment of Negative Symptoms) were also used. RESULTS: Deficient prepulse inhibition correlated significantly with 2 of the 3 Rorschach-derived thought disturbance measures. Prepulse inhibition was not correlated significantly with symptom rating scales. The Rorschach measure of impaired perceptual accuracy independently accounted for 60% of the variance in prepulse inhibition measures and contributed 35% of the unique variance beyond the effect attributable to the Scale for the Assessment of Positive Symptoms. CONCLUSIONS: Assessment of information processing and thought disturbance measures in close temporal proximity resulted in strong evidence that gating deficits correlate highly with measures of perceptual and reasoning disturbances. This relationship may form an important basis for the cognitive dysfunction observed among schizophrenic patients.

Acoustic Stimulation↗

PubMed1986

Choice reaction time performance in hospitalized schizophrenic patients and depressed patients.

The choice reaction time performances of matched groups of hospitalized patients diagnosed schizophrenic or depressed were compared with normal controls to test a hypothesis concerning thought disorder specific to schizophrenia. Both patient groups were abnormal compared to controls providing evidence inconsistent with the diagnostic specificity issue. The results are discussed in terms of cognitive dysfunction in depression, the effects of institutionalization and the problems of diagnostic heterogeneity.

Adult↗

PubMed2005

Transgenic mice expressing mutant (N279K) human tau show mutation dependent cognitive deficits without neurofibrillary tangle formation.

Mutations in the tau gene, which is located on chromosome 17, were found causative for autosomal dominantly inherited frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). To determine if cognitive deficits could be caused by tau mutations, two transgenic mouse lines were generated expressing a four-repeat isoform of human tau or its mutant, containing one of the FTDP-17 mutations (WILD mice and N279K mice). In open field test, N279K mice showed hyperactivity in locomotion and rearing. In prepulse inhibition test, N279K mice but not Wild mice showed significant deficits. Both transgenic mice, especially N279K mice, showed impairment in acquisition of spatial learning in Morris water maze. Although both N279K mice and Wild mice acquired passive avoidance as well as non-transgenic mice, N279K mice but not Wild mice showed severe deficits in acquisition of active avoidance. Histological analysis of the present mutant mice did not show any signs of neurofibrillary tangle formations in the brain, and cognitive dysfunction seemed to precede such neuropathological changes or occur independently from them. The behavioral phenotype of N279K mice mimics features of human FTDP-17 and provides a basic model for elucidating mechanisms underlying cognitive deficits in not only FTDP-17, but also diverse tauopathies.

Alzheimer Disease↗

PubMed2006

Are deficits in executive sub-processes simply reflecting more general cognitive decline in schizophrenia?

BACKGROUND: Schizophrenia is associated with both global and specific cognitive deficits. We sought to investigate whether deficits in executive subcomponents differed in their relationship to global cognitive impairments. METHOD: 95 patients were classified according to pre-morbid and current general cognitive ability as having either (a) intact pre-morbid and current general cognitive ability; (b) intact pre-morbid but deteriorated current ability, and (c) deteriorated both pre-morbid and current cognitive ability. All patients completed measures of verbal and spatial working memory, sustained selective attention, attentional set sifting, and inhibitory control. RESULTS: Deficits on both measures of working memory were associated with general cognitive ability. None of the attentional control deficits observed were associated with general ability. Further, spatial working memory deficits were also associated with more severe negative symptoms. CONCLUSIONS: These results provide further evidence of the discreet nature of attentional deficits in schizophrenia. By contrast, this study suggests that working memory deficits may to some extent index more general cognitive decline. Awareness of such overlap is important for schizophrenia genetics studies where working memory measures has been used to index supposedly discreet aspects of cognitive dysfunction.

Adult↗

PubMed2002

Latent inhibition as a function of schizotypality and gender: implications for schizophrenia.

In three within-subject experiments, we demonstrated that preexposure to an irrelevant stimulus interfered with performance when that stimulus subsequently predicted the correct location of a target stimulus. This latent inhibition-like effect (LI) was manifest in response time measures, but not errors. As with other related paradigms, LI was a function of an interaction between schizotypy-level and gender. Low schizotypal females and high schizotypal males exhibited significant LI, while high schizotypal females and low schizotypal males failed to produce LI effects. The results, similar to findings with schizophrenic patients, suggest a sexual dimorphism of cognitive dysfunction in schizophrenia, particularly in regard to the processing of irrelevant stimuli.

Adolescent↗

PubMed1991

Obstructive sleep apnea syndrome: pathogenesis of neuropsychological deficits.

Neuropsychological deficits have been documented in patients with obstructive sleep apnea syndrome (OSAS). Both nocturnal hypoxemia and impairement of daytime vigilance have been suggested as the pathogenesis of these deficits, yet it remains difficult to find good correlations between cognitive deficits and either of these physiological parameters. In the present study, 10 normal controls were compared to 10 moderately and 10 severely apneic patients, all recorded in a sleep laboratory for two consecutive nights, with a vigilance and neuropsychological assessment made during the intervening day. Relative to the controls, moderate and severe OSAS showed differences in many cognitive functions, although the severely affected showed the greater differences. Moreover, severe apneics were also worse than moderate apneics on tests that were found to be normal in the latter group. This suggests a discontinuity in the appearance of neuropsychological deficits as OSAS progresses. Further analyses revealed that reductions in general intellectual measures, as well as in executive and psychomotor tasks were all attributable to the severity of hypoxemia, while other attention and memory deficits were related to vigiance impairment. Therefore, both vigilance impairment and nocturnal hypoxemia may differentially contribute to the cognitive dysfunctions found in OSAS.

Adult↗

PubMed2004

Usefulness of a cube-copying test in outpatients with dementia.

OBJECTIVE: To clarify whether a quantitatively scored cube-copying test could rapidly assess dementia patients, predicting thier performance in cognitive tests. METHODS: Subjects were 171 outpatients with amnesia who were including 92 with Alzheimer's disease (AD); 59 vascular dementia (VD); 17 frontotemporal dementia (FTD); and three lewy body disease (DLB) and 32 normal healthy subjects. Subjects asked to copy a perspective drawing of a cube. Points of connection and plane-orientation errors were scored using Maeshima's method. The Mini-Mental State Examination (MMSE), an auditory verbal learning test (AVLT), a word fluency test and Raven's Coloured Progressive Matrices (RCPM) were administered. Age, clinical disease severity, symptom duration, specific diagnosis and neuropsychological scores were evaluated for relationships with constructional ability. RESULTS: The cube-copying test showed errors in most dementia patients and 11 of 32 normal subjects. Only three patients each with AD and VD copied correctly, but 11 patients with 17 FTD drew the cube correctly. Numbers of connections completed and plane-orientation errors correlated significantly with MMSE, AVLT, word fluency and RCPM scores. CONCLUSION: The cube-copying test is useful for routine clinical dementia screening, however the test examines only one aspect of cognitive function. While not an alternative to conventional neuropsychological examinations, quantitatively scored cube copying can provide a rough estimate of cognitive dysfunction in dementia patients.

Aged↗

PubMed1989

Cognitive event-related potentials in multiple sclerosis.

Twenty-three patients with multiple sclerosis (MS) and 1 patient with isolated optic neuritis (mean age 37.5 yrs, average duration of disease 10 yrs) were tested with auditory and visual cognitive event-related potentials (ERPs) using an oddball paradigm. The results were compared with data from 19 age-matched healthy controls. All patients had magnetic resonance imaging (MRI) head scans and 19 had comprehensive neuropsychological testing. The stimulus-related components of the ERPs were normal for nearly all patients, but 10 showed abnormalities of the later cognitive-related components and another 3 had waveforms in which the cognitive components could not be identified. These abnormalities were found mainly for the auditory test. Of these 13 patients, 11 had significantly prolonged reaction times (RT) or reduced target recognition performance. Five of 8 MS patients with normal IQ and memory function tests had abnormal ERPs with the reverse being true for 4 of 10 patients. Patients with abnormal ERPs showed a higher MRI cerebral lesion score and had a longer duration of illness and greater physical disability than patients with normal ERPs. It is concluded that the generation of ERPs is in part dependent on the integrity of cerebral white matter and that ERPs may indicate subtle degrees of cognitive dysfunction not always detected by standard tests of intellect.

Adult↗

PubMed1998

Pharmacological differentiation of classical and novel antipsychotics.

The symptoms of schizophrenia are treated through the blockade of mesolimbic and mesocortical dopamine activity. However, if dopamine activity in the nigrostriatal region is also blocked, extrapyramidal syndromes (EPS) are induced, and EPS are a major cause of noncompliance. It is therefore important for antipsychotic drugs with selective pharmacological profiles to be developed. Animal models for limbic selectivity and dose-response separation between behavioural and pharmacological parameters, which are analogous to EPS and antipsychotic effects, can now be used to differentiate between novel antipsychotics with few or no EPS and classical antipsychotics. Schizophrenic patients also often experience cognitive dysfunction, and it is important that antipsychotic drugs are developed that do not exacerbate this. Again, animal models can be used to give an indication of whether a compound has any effect on cognition. Both behavioural and electrophysiological rat models indicate that novel antipsychotic drugs, such as sertindole, but not classical antipsychotic drugs, such as haloperidol, demonstrate marked limbic selectivity. Nonhuman primate models of EPS show that the novel antipsychotics have a much greater separation between dose-response curves for antipsychotic effect and the development of EPS. The Morris water maze confirmed that sertindole does not adversely affect spatial learning or memory in rats. This paper reports on the differentiation between classical and novel antipsychotics using animal models.

Animals↗