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PubMed2004

Working memory and processing speed deficits in systemic lupus erythematosus as measured by the paced auditory serial addition test.

As many as 66% of systemic lupus erythematosus (SLE) patients have been reported to have cognitive deficits. These deficits are often associated with information processing speed and working memory. Similarly, processing speed and working memory impairments are the hallmark of cognitive dysfunction in multiple sclerosis (MS). The Paced Auditory Serial Addition Test (PASAT) places high demands on processing speed and working memory. Fisk and Archibald, however, demonstrated that the total score of the PASAT does not accurately reflect impairments in these cognitive processes. They found that MS patients used a chunking strategy to obtain correct responses and reduce the cognitive demands of the task. In the present study, PASAT performance was examined for 45 SLE patients and 27 controls using alternative scoring procedures. Although the total number of correct responses did not differ between SLE and controls at the 2.4 or 2.0 s presentation rates, SLE patients had fewer dyads (correct consecutive responses) than controls at the faster rate, and more chunking responses than controls at both rates. Disease activity, disease duration, depression, fatigue, and corticosteroids could not account for these differences. The findings suggest that SLE patients, like MS patients, chunk responses more often than controls, and that this scoring procedure may better reflect the working memory and processing speed deficits present in SLE.

Acoustic Stimulation↗

PubMed1999

Adrenal steroid dysregulation in dystrophia myotonica.

OBJECTIVE: To evaluate circulating adrenal steroid hormones, cortisol diurnal rhythm and the negative feedback function of the cortisol axis in patients with dystrophia myotonica (DyM), a disease where metabolic disturbances, peripheral insulin insensitivity and cognitive dysfunction are common features. DESIGN: Morning serum levels of dehydroepiandrosterone sulphate, androstenedione, 17 alpha-hydroxy progesterone and cortisol; morning serum levels of testosterone and insulin; diurnal rhythm of saliva cortisol; and an overnight dexamethasone suppression test, together with a cognitive screening test in men with DyM and in controls. SETTING: Outpatient clinic in co-operation with Umeå University Hospital. SUBJECTS: Fifteen men with DyM and 13 age-matched controls. MAIN OUTCOME MEASURES: Adrenal steroid hormone levels, diurnal rhythm of saliva cortisol, dexamethasone suppression test and Mini Mental State Examination scores. RESULTS: Morning serum levels of dehydroepiandrosterone sulphate, androstenedione and 17 alpha-hydroxy progesterone were significantly decreased in DyM after inclusion of age and body mass index in multiple regression analyses (48, 26 and 32% decreases, respectively). An abnormal diurnal rhythm of saliva cortisol was present in all patients, mean saliva cortisol levels being significantly increased (33%) in DyM patients. Dexamethasone suppressibility did not differ between groups. DyM patients scored significantly lower on the Mini Mental State Examination (P < 0.001). CONCLUSIONS: These results indicate an abnormal adrenal steroid hormone secretion in DyM, which may contribute to peripheral insulin sensitivity as well as cognitive impairment in these patients.

17-alpha-Hydroxyprogesterone↗

PubMed2003

Apathy and executive function in depressed elderly.

Apathy and executive cognitive dysfunction (ECD) are important though conceptually different aspects of late-life depression. The primary objective of this study was to evaluate the relationship of apathy to ECD. The authors also evaluated the relationship of apathy and ECD to global cognitive impairment and word generation. Fifty-two elderly subjects with major depression and MMSE scores of 15 or greater were evaluated with apathy-related items from the Hamilton rating scale for depression (ApHRSD), the Executive Interview (EXIT), the Dementia Rating Scale (DRS), and the Controlled Oral Word Association test (COWA). ApHRSD scores were not significantly correlated with any of these variables. EXIT scores were correlated significantly with DRS and COWA. The results suggest that apathy and ECD may be independent of each other in some samples of elderly with late-life depression. Correlations may have been reduced by low variance for the variables of interest and by psychometric limitations of the ApHRSD.

Aged↗

PubMedDate not supplied

[Neuropsychiatric disorders in multiple sclerosis].

OBJECTIVE: Neuropsychological investigations over the past 20 years have shown the high prevalence of cognitive dysfunction in multiple sclerosis, although there are still large gaps. In this article we review current concepts regarding the different types of neuropsychiatric disorders, their physiopathology, diagnosis and treatment. DEVELOPMENT: We present a classification of the most important types of cognitive and psychiatric alterations in multiple sclerosis, and their physiopathology. We review the methods used in diagnosis, follow up and assessment of these patients. Finally, we analyze the current treatment available for each of these disorders. CONCLUSIONS: Although considerable advances have been made in understanding the neuropsychological disorders occurring in multiple sclerosis, there are still many questions to be answered. There is a need for a unified, agreed, validated battery of neuropsychological tests for the study of specific cognitive deficits in multiple sclerosis so that results may be compared. There is also a lack of biological markers which would help in diagnosis and prognosis. Finally the design and carrying out of clinical trials in the search for specific, effective drugs for the treatment of neuroconductual disorders of multiple sclerosis is necessary.

Adjuvants, Immunologic↗

PubMed2006

Long-term neurological complications after hypoxic-ischemic encephalopathy.

Hypoxic-ischemic encephalopathy accompanying cardiac arrest is a common cause of long-term neurological dysfunction. With the improvement in prehospital emergency systems, larger numbers of people are resuscitated from cardiac arrests, although with the increased prospect of neurological sequelae. Neurological impairment after cardiac arrest is dependent on the degree of brain damage suffered during the arrest. Although the duration and severity of brain ischemia is often difficult to determine, clinicians are often faced with difficult issues related to predicting outcome related to awakening and long-term neurological deficits after the arrest. Neurological impairments range from mild cognitive deficits to severe motor and cognitive deficits that preclude independence in many activities of daily living. Several neurological syndromes have been described in patients who awaken from hypoxic-ischemic coma with lasting motor and cognitive deficits. This review will address many of the common syndromes after hypoxic-ischemic encephalopathy, including persistent vegetative states, seizures, myoclonus, movement disorders, cognitive dysfunction, and other neurological abnormalities.

Brain↗

PubMed1991

Passive avoidance behaviour deficit in the mdx mouse.

Thirty per cent of boys with Duchenne muscular dystrophy (DMD) suffer from various degrees of mental retardation. Since dystrophin, the protein absent in muscles of boys with DMD, is produced also in the brain, it was postulated that the deficiency of brain dystrophin might account for the mental retardation found in DMD boys. The mdx mouse, a mouse model of DMD, fails to produce dystrophin in muscle and brain. This prompted us to study the cognitive function of these animals. Learning and memory processes were studied in 10 mdx females and 9 genetically matched controls using the passive avoidance test. Statistically significant differences in the retention of the passive avoidance response was detected between mdx and control mice, indicating an impairment in passive avoidance learning in mdx mice. Our data reinforce the view that brain dystrophin deficiency is correlated with cognitive dysfunction and indicate that mdx mice might be a model for the mental retardation found in DMD boys.

Animals↗

PubMed2004

Neuropsychological impairment in borderline personality disorder.

In spite of accumulating evidence from neurological, neuroimaging, neuropsychological, and, more recently, developmental studies, borderline personality disorder (BPD) is not considered routinely a neurocognitive disorder. A review of the neuropsychological literature shows that the preponderance of BPD studies failed to examine a broad range of cognitive domains and, in particular, have not adequately evaluated attention. Nevertheless, most neuropsychological studies suggest that these patients' cognitive skills are compromised. The authors administered a neuropsychological battery designed to evaluate nine cognitive domains in twelve female inpatients diagnosed with BPD. Relative to a healthy normative group, inpatients with BPD were impaired in seven cognitive domains, with attention-vigilance and verbal learning and memory most pronounced. Neuropsychological performance was significantly related to degree of psychopathology. The authors recommend that clinicians routinely screen BPD patients for cognitive dysfunction and highlight the roles that this important knowledge can have in treatment.

Adolescent↗

PubMed2003

(-)-9-Dehydrogalanthaminium bromide, a new cholinesterase inhibitor, enhances place and object recognition memory in young and old rats.

In a previous study, we showed that (-)-9-dehydrogalanthaminium bromide, a synthetic galanthamine derivative, was more potent than galanthamine in inhibiting acetylcholinesterase. We studied here the action of this new compound on recognition memory in young and old rats, using a two-trial recognition task designed to test both place and object recognition. (-)-9-dehydrogalanthaminium bromide was injected (0.3, 1, and 3 mg/kg, i.p.) in young and old rats before the acquisition phase, immediately after it, or before the retrieval phase of the task, in order to determine the stage of information processing affected by the compound. (-)-9-dehydrogalanthaminium bromide improved both place and object recognition in young rats, via an enhancement of acquisition (3 mg/kg: place recognition; 1 and 3 mg/kg: object recognition) and consolidation (1 and 3 mg/kg) information processing. In old rats, (-)-9-dehydrogalanthaminium bromide improved performance by acting on the acquisition processes of place (0.3, 1, and 3 mg/kg) and object (1 and 3 mg/kg) recognition. These results provide information on the profile of activity of (-)-9-dehydrogalanthaminium bromide on memory processes, and suggest that this new compound could have utility in the treatment of cognitive dysfunction occurring in Alzheimer's disease or in the normal course of aging.

Age Factors↗

PubMed2004

Neurobehavioral correlates of sleep-disordered breathing in children.

The effects of sleep-disordered breathing (SDB) on neurobehavioral function were examined in two matched groups of children from the general population. Thirty-five children with polysomnographically confirmed SDB were matched for ethnicity, age, gender, maternal educational attainment, and maternal smoking, to healthy children with no evidence of SDB. Children with SDB had significantly lower mean scores on the Differential Ability Scales for General Conceptual Ability (similar to IQ) and for the Non-verbal Cluster. On the neuropsychology assessment battery (NEPSY), children with SDB scored significantly lower than the control group on the attention/executive function domain and two subtests within that domain, one measuring visual attention and the other executive function. In addition, children with SDB scored significantly lower than the controls on one subtest from the NEPSY language domain: Phonological Processing. This subtest measures phonological awareness, a skill that is critical for learning to read. No differences in behavior, as measured by the Child Behavior Checklist (CBCL) or the Conners' Parent Rating Scale, were found between the two groups. Using a novel algorithm to assess sleep pressure, we found that children with SDB were significantly sleepier than controls. Furthermore, total arousal index was negatively correlated with neurocognitive abilities, suggesting a role for sleep fragmentation in pediatric SDB-induced cognitive dysfunction.

Aptitude↗

PubMed1999

QEEG changes during cardiopulmonary bypass: relationship to postoperative neuropsychological function.

The relationship of changes in intraoperative QEEG and postoperative cognitive function was studied in 32 patients undergoing cardiac surgical procedures requiring cardiopulmonary bypass (CPB). All patients were anesthetized with a high dose narcotic technique in which CPB was carried out using moderate hypothermia. EEG recorded continuously throughout each procedure was analyzed using the neurometric technique. Neuropsychological (NP) evaluations were administered to all patients before, 1 week and 2-3 months postoperatively. A decrement in postoperative performance of 2 standard deviations in two or more tests from preoperative testing was defined as a new cognitive deficit. Of the patients studied, 40.6% demonstrated a new postoperative cognitive deficit at 1 week. At 2-3 months postoperatively, 28.1% continued to show a cognitive deficit. Discriminant analysis of the QEEG as a function of NP performance was calculated at select times during the surgical procedure. QEEG prediction of NP performance was just above chance at the 1 week comparison but excellent for the 2-3 month comparisons. This study suggests that with appropriate monitoring protocols, intraoperative QEEG may predict cognitive dysfunction experienced by patients 2-3 months postoperatively.

Anesthesia, General↗

PubMed2003

The effect of zero-balanced ultrafiltration during cardiopulmonary bypass on S100b release and cognitive function.

Zero-balanced ultrafiltration (ZBUF) might reduce the systemic inflammatory response (SIRS) during cardiopulmonary bypass (CPB) by removing inflammatory mediators. The objective of this study was to determine the effect of ZBUF on postoperative serum S100b levels, a marker of neuronal injury. In addition, the possible effects of ZBUF on postoperative neurocognitive function were assessed. Sixty patients undergoing elective coronary bypass grafting were randomly assigned either to a control group or to a protocol group in which ZBUF was performed. Serum S100b levels were measured five minutes after intubation, at the end of bypass and eight and 20 hours after arrival at the intensive care unit (ICU). Cognitive function was assessed with neuropsychological tests on the day before the operation and the sixth day after surgery. The S100b level at 20 hours after arrival at the ICU was 0.27 g/L (SD 0.16) in the control and 0.25 g/L (SD 0.12) in the group with ZBUF. There were no statistical differences at any time between the two groups. S100b was not detectable in the ultrafiltrate, indicating that these results were not obscured by washout of S100b. Thirteen patients (52%) in the control group and 14 patients (56%) in the ZBUF group showed a cognitive deficit. In conclusion, ZBUF during CPB does not decrease the release of S100b. This result is not affected by washout. ZBUF did not reduce the incidence of early neurocognitive deficits. The role of SIRS in the development of cognitive dysfunction following CPB remains to be resolved.

Aged↗

PubMed1991

Aseptic meningitis following cardiac transplantation: clinical characteristics and relationship to immunosuppressive regimen.

Neurologic disorders are uncommon but alarming complications of cardiac transplantation. Of 29 patients from the Utah Cardiac Transplant Program (UCTP) who had lumbar puncture because of change in neurologic function, or to assess fever of uncertain etiology, CSF pleocytosis was present in 14 patients, 4 of whom had an active infectious process involving the nervous system. In 10 other patients, CSF pleocytosis with negative cultures appeared following treatment with OKT3 monoclonal antibody. The most prominent clinical signs of this aseptic meningitis syndrome are fever and transient cognitive dysfunction.

Adolescent↗

PubMed2006

[An effect of long-term cerebrolysin therapy in combination with neuroleptics on behavioral and cognitive disturbances in endogenous childhood autism].

An open prospective clinical study included 25 patients with childhood autism aged from 3 to 8 years (mean age 5 years 11 months). Patients received 2 therapeutic courses (15 intramuscular Cerebrolysin injections of 1.0 ml every other day per course) with 2 months interval and basic antipsychotic therapy using typical neuroleptics in age-adjusted dosages. The duration of the study was 180 days. Significant or very significant improvement was achieved after the 1st Cerebrolysin course in 38% patients, after the 2nd course in more than 50% and to the end of the follow-up (180th day) in 71% of patients. There were no cases of deterioration during the trial. The autism severity as measured by the CARS scale consistently decreased from the day 0 to the day 180--from 37.7 to 32.6 scores, respectively (p < 0.001) in all assessments as compared with the baseline. To the end of the study, the patients demonstrated a significant decrease in mental retardation by 0.2 years. A statistically significant improvement was achieved in cognitive activity, attention during task performing as well as in self-service (by 0.3 years), receptive and expressive speech, cognitive performance and perception (by 0.2 years), fine motor function (by 0.1 years). The combined therapy comprising neuroleptics and Cerebrolysin double course can be recommended for correction of behavioral disorders and cognitive dysfunction in patients with mild moderate and moderate/severe autism.

Amino Acids↗

PubMed2006

Proof-of-concept trial of an alpha7 nicotinic agonist in schizophrenia.

CONTEXT: The alpha7 nicotinic acetylcholine receptor gene, CHRNA7, is associated with genetic transmission of schizophrenia and related cognitive and neurophysiological sensory gating deficits. Cognitive dysfunction is responsible for significant psychosocial disability in schizophrenia. Nicotine, a low-potency agonist at the alpha7 receptor, has some positive effects on neurophysiological and neurocognitive deficits associated with schizophrenia, which suggests that more effective receptor activation might meaningfully enhance cognition in schizophrenia. OBJECTIVES: To determine if 3-[(2,4-dimethoxy)benzylidene]anabaseine (DMXB-A), a natural alkaloid derivative and a partial alpha7 nicotinic cholinergic agonist, significantly improves neurocognition, and to assess, by effects on P50 auditory evoked potential inhibition, whether its neurobiological actions are consistent with activation of alpha7 nicotinic receptors. DESIGN: Randomized, double-blind crossover trial of 2 drug doses and 1 placebo. SETTING: General clinical research center. PATIENTS: Twelve persons with schizophrenia who did not smoke and were concurrently treated with antipsychotic drugs. One person was withdrawn because of a transient decrease in white blood cell count. INTERVENTION: Administration of DMXB-A. MAIN OUTCOME MEASURES: Total scale score of the Repeatable Battery for the Assessment of Neuropsychological Status and P50 inhibitory gating. RESULTS: Significant neurocognitive improvement was found on the Repeatable Battery for the Assessment of Neuropsychological Status total scale score, particularly for the lower DMXB-A dose compared with placebo. Effects were greater than those of nicotine in a similar study. Significant improvement in P50 inhibition also occurred. Patients generally tolerated the drug well. CONCLUSIONS: An alpha7 nicotinic agonist appears to have positive effects on neurocognition in persons with schizophrenia. Longer trials are needed to determine the clinical utility of this novel treatment strategy.

Adult↗

PubMed1995

Lack of preservation of higher brain function during hypoglycaemia in patients with intensively-treated IDDM.

Severe hypoglycaemia with cognitive dysfunction is 3 times more common in intensively, rather than conventionally, treated insulin-dependent diabetes mellitus (IDDM). To investigate the effect of diabetes control on higher brain function during acute hypoglycaemia, we studied one of the earliest detectable changes in cognitive function, i.e. the four-choice reaction time, and symptomatic and hormonal responses during euglycaemic and hypoglycaemic clamping in human subjects. There were no changes in symptoms or counterregulatory hormones and four-choice reaction time was stable during 220 min of euglycaemic insulin clamping in five men with IDDM, with a coefficient of variation of less than 2.2% (1% for accuracy) for the cognitive function test. During stepped hypoglycaemic clamping however, hormonal responses and subjective awareness of hypoglycaemia occurred in all groups but started at much lower blood glucose concentrations in eight intensively-treated diabetic subjects (Group 1) than in ten conventionally-treated (Group 2) or in eight non-diabetic subjects (Group 3). For example, for adrenaline, plasma glucose thresholds were 2.7 +/- 0.2 vs 3.4 +/- 0.2 and 3.2 +/- 0.1 mmol/l, respectively, p < 0.05, Group 1 vs Groups 2 or 3 and for subjective awareness of hypoglycaemia 2.3 +/- 0.2 vs 3.0 +/- 0.1 and 3.2 +/- 0.1 mmol/l, p < or = 0.003), as in previous studies. In contrast, deterioration in reaction time occurred at 3.2 +/- 0.3, 3.2 +/- 0.2 and 3.0 +/- 0.2 mmol/l, respectively (p = NS), thus occurring at higher glucose levels than subjective awareness in the intensively-treated subjects only. The altered hierarchy of responses to hypoglycaemia in well-controlled intensively-treated diabetes explains the increased risk of severe hypoglycaemia without warning seen in such patients.

Adult↗

PubMed2005

Neurotransmitter deficits in behavioural and psychological symptoms of Alzheimer's disease.

Behavioural and psychological symptoms of dementia (BPSD) occur in 50-90% of Alzheimer's disease (AD) patients. Imbalance of different neurotransmitters (acetylcholine, dopamine, noradrenaline and serotonin), involvement of specific brain regions responsible for emotional activities (parahippocampal gyrus, dorsal raphe and locus coeruleus) and cortical hypometabolism have been proposed as neurobiological substrate of BPSD. Compared to with respect to the neurochemical component, the cholinergic dysfunction seems to play a major role in contributing to BPSD occurrence. This view is also supported by the findings of recent trials with cholinesterase inhibitors, showing that these drugs are effective in controlling and/or improving BPSD, independent on effects on cognitive dysfunction. On the site of psychotropic drugs, atypical or novel antipsychotics represent the reference drugs for treating BPSD, whereas classic antipsychotic drugs for their profile and the potential side effects should be avoided.

Alzheimer Disease↗

PubMed2000

Minireview: mechanisms by which the metabolic syndrome and diabetes impair memory.

Type 2 diabetes is associated with an increased risk of cognitive dysfunction. These effects seem particularly true for memory functions. This article examines how diabetes and the biological changes that occur with diabetes such as hyperglycemia, changes in insulin concentration, hypertension, and changes in lipid levels might lead to these alterations in cognitive functioning, with an emphasis on the mechanisms leading to changes in memory.

Dementia↗

PubMed1997

Psychomotor and cognitive functioning in cancer patients.

Psychomotor and cognitive dysfunction in cancer patients can be classified into two main categories according to etiology: disease-induced factors (metabolic disturbances, brain metastasis, pain, etc.) and treatment-related factors (drugs, antineoplastic therapy, etc.). In particular, the effects of chronic opioid administration in cancer patients have been subjected to investigations, and most studies have been engaged in assessment and treatment of the cerebral dysfunction. Early studies found that cancer patients in chronic oral opioid therapy had prolonged continuous reaction times, and that the opioids seemed to be mainly responsible for the prolongation. Significant dose escalations of opioids (> or = 30%) caused transiently impaired psychomotor and cognitive functions in cancer patients. Cancer patients in chronic oral opioid therapy did not achieve any advantages changing to epidural opioid therapy with regard to faster continuous reaction times and less pain. Large doses of opioids are often required to control severe pain in cancer patients. As increased sedation and impaired psychomotor and cognitive functions often occur, a number of studies have investigated the use of amphetamine derivatives to counteract the sedative side-effects of opioid. These drugs seem promising during high-dose opioid therapy and their use may be particularly rewarding in poor opioid-responsive pain conditions such as incident and neuropathic pain.

Analgesics, Opioid↗