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PubMed1995

A prospective evaluation of cognitive decline in early Huntington's disease: functional and radiographic correlates.

We examined prospectively the relationship between progressive disability in Huntington's disease (HD) and concomitant alterations in neuropsychological functioning and brain imaging indices in a cohort of 60 patients who were enrolled and followed for 30 to 42 months in a controlled clinical trial. Standardized measures of functional capacity and neuropsychological performance were collected, and CT was performed, at regular intervals every 6 to 12 months. Psychomotor skills showed the most significant and consistent decline among the cognitive functions assessed. Memory disturbances were already present at the time of enrollment, but memory did not deteriorate until patients reached advanced stages. Other cognitive operations, such as visual construction and semantic knowledge, manifested small and variable changes over time. CT indices of striatal atrophy correlated only with changes in psychomotor function, while the CT index of frontal atrophy weakly predicted memory and semantic knowledge scores at 42 months. These results confirmed earlier cross-sectional findings and extended our knowledge of the evolution of cognitive dysfunction in HD.

Adult↗

PubMed1997

Is it Alzheimer's disease?

According to one estimate, Alzheimer's disease has been diagnosed in more than 4 million Americans. As our population continues to age, we can expect to see a sharp increase in this number. By the middle of the next century, there are projected to be almost as many Americans over age 80 as there now are over age 65. Primary care physicians are bound to see more and more patients who appear to have Alzheimer's disease, and the burden is on them to rule out other, treatable forms of dementia. Dr. Gambert describes how to distinguish the true cognitive dysfunction of Alzheimer's disease and where to go from there.

Affective Symptoms↗

PubMed2001

Education and cognitive decline in Parkinson's disease: a study of 102 patients.

OBJECTIVE: To understand the correlation between low education level (EL) and the cognitive impairment in Parkinson's disease (PD). PATIENTS AND METHODS: This is a cross-sectional study of cognitive function in 102 non-demented PD patients, from a special clinic (behavioral neurology) in a referral medical center. PD patients were divided into low, middle and high EL groups. We used the Chinese version of the Cognitive Ability Screening Instrument as a neuropsychological test, which covers nine domains of cognitive function. A full score is 100. When determining the abnormality rate of each item of CASI, we used age/education stratified normal control groups as reference to obliterate the influence of education and age on cognitive decline. RESULTS: Recent memory, language and attention are the three items in which there were differences between the groups, in terms of abnormal performance rates. The high EL group is at less risk of recent memory impairment, but at more risk of impairment in language and attention. The other six items and total score showed no differences among the groups. Thirty-eight percent of the patients had a total score below 1.5 SD of the means of the general population. CONCLUSION: This study shows that high EL exerts no protective effect on the cognitive decline in PD patients in general, except in recent memory. The rate of cognitive dysfunction in PD patients is high. This deserves more attention.

Aged↗

PubMed2004

[Neuroprotective effects of magnesium on cerebral ischemia and cerebral contusion].

Neuroprotective effects of magnesium (Mg(2+)) have been shown in experimental studies by using animal models of the cerebral ischemia and cerebral contusion. We review the neuroprotective effects of Mg(2+) in the histological and behavioral studies. In the animal models of cerebral ischemia, Mg(2+) treatment reduces the infarct volume, inhibits the neuronal death, and attenuates the motor impairments. In the animal models of cerebral contusion, Mg(2+) treatment inhibits the neuronal death and edema, and attenuates not only the motor impairments but also cognitive dysfunction.

Animals↗

PubMed2003

Cognitive efficiency declines over time in adults with Type 1 diabetes: effects of micro- and macrovascular complications.

AIMS/HYPOTHESIS: Mild cognitive dysfunction is not uncommon in adults with Type 1 diabetes, but its pathogenesis remains unclear. Previous cross-sectional studies had suggested that microangiopathy might affect brain integrity and lead to "central neuropathy." To assess the relationship between changes in cognitive performance and the incidence of new micro- and macrovascular complications, 103 young and middle-aged adults (mean age: 40 yrs) with childhood-onset Type 1 diabetes were followed over a 7-year period, and were compared to 57 demographically-similar adults without diabetes. METHODS: All subjects completed a comprehensive battery of neurocognitive tests on two occasions. Diabetic subjects also received repeated medical assessments to diagnose the onset of clinically significant complications. RESULTS: Relative to control subjects, diabetic adults showed significant declines on measures of psychomotor efficiency; no between-group differences were evident on learning, memory, or problem-solving tasks. The development of proliferative retinopathy and autonomic neuropathy during the follow-up period predicted decline in psychomotor speed (p<0.01), as did incident macrovascular complications (p<0.05), systolic blood pressure at follow-up (p<0.01), and duration of diabetes (p<0.01). CONCLUSION/INTERPRETATION: This study shows that cognitive efficiency may decline over time in diabetic adults, and that this neurocognitive change may be linked, at least in part, to the occurrence of complications like proliferative retinopathy and elevated blood pressure. Therapeutic interventions that reduce the risk of vascular complications may have a similarly beneficial effect on the brain and reduce the risk of neurocognitive dysfunction in diabetic patients.

Adult↗

PubMed2005

Comparative and interactive human psychopharmacologic effects of ketamine and amphetamine: implications for glutamatergic and dopaminergic model psychoses and cognitive function.

BACKGROUND: In healthy individuals, ketamine hydrochloride and amphetamine sulfate produce cognitive, behavioral, and subjective effects resembling endogenous psychoses. Studying the comparative and interactive effects of these agents may provide insights into the roles of the glutamate and monoamine systems in psychosis and cognition. OBJECTIVES: To directly compare the effects of ketamine and amphetamine and to explore their interactive effects within individuals. DESIGN: Placebo-controlled, randomized, double-blind psychopharmacologic trial. SETTING AND PARTICIPANTS: Forty-one healthy individuals recruited from the community who completed up to 4 test days. MAIN OUTCOME MEASURES: On each test day, participants received amphetamine (a 1-minute infusion of amphetamine sulfate, 0.25 mg/kg, or saline) and ketamine (a 1-minute intravenous infusion of ketamine, 0.23 mg/kg, followed by a 1-hour infusion of 0.5 mg/kg or an identical saline bolus and infusion). The order of amphetamine and ketamine infusions was randomized. RESULTS: At the doses studied, ketamine and amphetamine produced positive symptoms and euphoria. However, perceptual changes were produced only by ketamine, and hostility, grandiosity, and somatic concern were stimulated only by amphetamine. Amphetamine and ketamine produced conceptual disorganization, but only ketamine produced concrete ideation and unusual mannerisms. Ketamine produced negative symptoms and disrupted delayed recall. Ketamine and amphetamine showed 3 types of interactive effects: (1) amphetamine attenuated the impairment of working memory produced by ketamine; (2) amphetamine and ketamine had additive effects on thought disorder, arousal, and euphoria; and (3) amphetamine and ketamine had less-than-additive effects on psychosis. CONCLUSIONS: These findings implicate N-methyl-D-aspartate glutamate receptors and dopamine systems in psychosis. However, glutamate and dopamine may differentially contribute to psychosis, thought disorder, and euphoria. Regarding medication development for cognitive dysfunction, the pattern of the interactive effects of ketamine and amphetamine is consistent with the hypothesis that facilitation of prefrontal cortical dopamine levels would attenuate some cognitive impairments associated with deficits in N-methyl-D-aspartate receptor function.

Amphetamine↗

PubMed2003

Acute effects and recovery time following concussion in collegiate football players: the NCAA Concussion Study.

CONTEXT: Lack of empirical data on recovery time following sport-related concussion hampers clinical decision making about return to play after injury. OBJECTIVE: To prospectively measure immediate effects and natural recovery course relating to symptoms, cognitive functioning, and postural stability following sport-related concussion. DESIGN, SETTING, AND PARTICIPANTS: Prospective cohort study of 1631 football players from 15 US colleges. All players underwent preseason baseline testing on concussion assessment measures in 1999, 2000, and 2001. Ninety-four players with concussion (based on American Academy of Neurology criteria) and 56 noninjured controls underwent assessment of symptoms, cognitive functioning, and postural stability immediately, 3 hours, and 1, 2, 3, 5, 7, and 90 days after injury. MAIN OUTCOME MEASURES: Scores on the Graded Symptom Checklist (GSC), Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and a neuropsychological test battery. RESULTS: No player with concussion was excluded from participation; 79 players with concussion (84%) completed the protocol through day 90. Players with concussion exhibited more severe symptoms (mean GSC score 20.93 [95% confidence interval [CI], 15.65-26.21] points higher than that of controls), cognitive impairment (mean SAC score 2.94 [95% CI, 1.50-4.38] points lower than that of controls), and balance problems (mean BESS score 5.81 [95% CI, -0.67 to 12.30] points higher than that of controls) immediately after concussion. On average, symptoms gradually resolved by day 7 (GSC mean difference, 0.33; 95% CI, -1.41 to 2.06), cognitive functioning improved to baseline levels within 5 to 7 days (day 7 SAC mean difference, -0.03; 95% CI, -1.33 to 1.26), and balance deficits dissipated within 3 to 5 days after injury (day 5 BESS mean difference, -0.31; 95% CI, -3.02 to 2.40). Mild impairments in cognitive processing and verbal memory evident on neuropsychological testing 2 days after concussion resolved by day 7. There were no significant differences in symptoms or functional impairments in the concussion and control groups 90 days after concussion. CONCLUSIONS: Collegiate football players may require several days for recovery of symptoms, cognitive dysfunction, and postural instability after concussion. Further research is required to determine factors that predict variability in recovery time after concussion. Standardized measurement of postconcussive symptoms, cognitive functioning, and postural stability may enhance clinical management of athletes recovering from concussion.

Acute Disease↗

PubMed1989

Occupational therapy program development for medical-psychiatry units: a cognitive model.

Occupational therapy programs form an essential component of the overall treatment program on medical psychiatry units for patients with depression, physical debilitation, and cognitive dysfunction. This article outlines theoretical and practical aspects of developing an occupational therapy program for medical-psychiatric inpatients. Emphasis is placed on accurate assessment of cognitive and physical functioning to facilitate stratification of patients into appropriate therapeutic activities that are commensurate with their level of functioning. The theoretical basis and orientation of occupational therapy is also discussed vis-à-vis its relevance to the treatment of patients with concurrent medical and psychiatric illness.

Adolescent↗

PubMed2001

Time-related cognitive deficiency in four different types of depression.

Mild cognitive impairment often occurs in depressive illness. But it is unknown whether the occurrence or severity of cognitive deficits has diagnostic specificity. It is of interest to investigate whether there are time-related differences in cognitive functions characteristic of different kinds of depressive diagnoses, and therefore whether such differences might help to distinguish between types of depressive disorder. Eighty inpatients with a DSM-IV depressive episode (unipolar, bipolar, dysthymic and schizoaffective disorder, depressive type) were assessed with a series of neuropsychological tests at the beginning and at the end of their hospital stays. A group of 62 matched healthy controls were assessed with the same series of tests at comparable intervals. The diagnostic sub-groups could not be distinguished by cognitive parameters in the time-course. At the time of admission the inpatient group had a worse performance than the control group. After a significant decrease of their mean depression score, the patients still continued to show an outcome worse than the controls. We conclude that the variation of cognitive dysfunction with time in depression seems to be a phenomenon which does not depend on the kind of depressive sub-diagnosis. The results indicate that cognitive deficits might persist longer than the period of illness, but this seems to be true for all depressive sub-diagnoses.

Adult↗

PubMed2003

Cognitive function in schizophrenia. Deficits, functional consequences, and future treatment.

This article has discussed the relationship between cognitive deficits and functional outcome in schizophrenia. This relationship was noted first by Kraepelin and Bleuler at the beginning of the twentieth century. With the introduction of conventional neuroleptics, the focus shifted toward the treatment of positive symptoms. In the past few decades, cognitive dysfunction has been recognized as a fundamental feature of schizophrenia and has been shown repeatedly to have a negative association with functional outcome [6]. Improvement in cognitive functioning became one of the most important clinical targets in the treatment of schizophrenia in the 1990s [82]. Main domains of cognition that are disrupted significantly in schizophrenia include attention, executive function, verbal and visuospatial working memory, and learning and memory. Although conventional antipsychotics are effective in treating positive symptoms, they lack the ability to improve cognitive impairment and produce poor functional outcome. Previous research has shown superior efficacy of atypical antipsychotics on cognitive impairments in schizophrenia compared with conventional antipsychotics. Because the heterogeneity of atypical antipsychotics in their pharmacologic properties, they have differential profiles of cognitive efficacy in patients with schizophrenia. Establishing the cognitive profile of each atypical antipsychotic is an important task. This knowledge can be used to address individual cognitive problems and needs. Because cognitive deficits have been shown to have associations with different aspects of clinical symptoms, limited learning in rehabilitation programs, and functional outcome in schizophrenia, targeting individual cognitive deficits would lead to greater treatment success in terms of clinical and functional outcome. Although atypical antipsychotics have some benefit on cognitive function, further efforts to improve cognitive function are required. Attempts at improving cognition in schizophrenia with specific cognitive enhancers pharmacologically and psychological therapies such as cognitive remediation might lead to better functional outcome in patients with schizophrenia.

Antipsychotic Agents↗

PubMed2003

Impact of comorbid depressive symptoms on nonverbal memory and visuospatial performance in obsessive-compulsive disorder.

INTRODUCTION: Recent research has suggested that some executive dysfunctions in obsessive-compulsive disorder (OCD) represent an epiphenomenon of comorbid depressive symptoms. The present study investigated whether the impact of comorbid depressive symptoms on cognitive dysfunction in OCD extends to nonverbal memory impairment. METHODS: A total of 32 OCD patients and 20 healthy controls took part in the study. Participants were administered a neurocognitive battery with a focus on nonverbal memory and visuospatial functions. RESULTS: While evidence was provided that neurocognitive processes necessitating visuospatial transformation and visuoconstruction are deficient in OCD patients regardless of comorbid depressive symptoms, nonverbal memory dysfunctions were only apparent for patients with elevated scores in the Hamilton Depression (HDRS) Rating Scale (total score > or = 8). Correlations with subscores of the HDRS revealed that core depressive symptoms are related to nonverbal memory deficits in OCD. Mental rotation, middle discrimination, and position discrimination were found to be unaffected in OCD. Y-BOCS scores, length of illness, onset of illness, number of hospital admissions, and checking compulsions were not associated with neurocognitive disturbances. CONCLUSIONS: Nonverbal memory is disturbed in only a subgroup of OCD patients displaying elevated HDRS scores (HDRS > or = 8). It is claimed but awaits further empirical testing that differences in depression profile across OCD studies have contributed to inconsistencies in prior investigations on neurocognitive functioning in OCD. Our results are questioning the hypothesis that nonverbal deficits are a causal factor for the development of checking compulsions.

Journal Article↗

PubMed1994

Neurologic consequences of hypertension and antihypertensive drug therapy.

Untreated essential hypertension leads to cardiovascular and renal disease and stroke, but antihypertensive drug therapy effectively reduces these consequences of hypertension. Several studies indicate that hypertension can negatively impact on cognitive function, especially on learning and memory, but the ability of antihypertensive drugs to ameliorate these cognitive dysfunctions is less clear. None of the recent studies convincingly demonstrates that any of the antihypertensive drugs currently in use has a major deleterious effect on cognition in hypertensive patients, but some of the drugs more reliably benefit cognitive function in the hypertensive patient. As a class, the angiotensin-converting enzyme inhibitors most consistently lead to cognitive improvement in the overall hypertensive population, but beta 1-adrenergic receptor blockers and a subset of calcium channel blockers appear to have very similar effects. Animal studies and clinical studies in demented patients suggest that angiotensin-converting enzyme in the cerebral cortex plays a role in normal learning and memory, a finding that provides a theoretic foundation to the beneficial actions of this class of drugs on cognitive function in hypertensive individuals.

Animals↗

PubMedDate not supplied

A follow-up study of the family with the Swedish APP 670/671 Alzheimer's disease mutation.

OBJECTIVE: To study the progression of Alzheimer's disease (AD) at a very early stage and to evaluate clinical markers of presymptomatic AD. SETTING: Longitudinal study at a university hospital. SUBJECTS: A Swedish family harboring a double mutation at codons 670/671 of the APP gene on chromosome 21 was followed longitudinally for 3 years. Both mutation carriers and noncarriers participated. OUTCOME MEASUREMENTS: Results from clinical investigations, electroencephalography, neuropsychological and neuroradiological examinations including magnetic resonance imaging, single-photon emission computed tomography and positron emission tomography were assessed and compared on two or more occasions. MAIN OUTCOME: During follow-up, 1 initially asymptomatic mutation carrier who was near the expected age of onset for this family, developed cognitive symptoms, and at the end of the follow-up fulfilled the diagnostic criteria for AD. One mutation carrier with cognitive symptoms at the first examination showed clinical deterioration and was diagnosed with AD. One demented mutation carrier died and was shown to have typical AD neuropathology at autopsy. The two remaining asymptomatic mutation carriers, as well as all the noncarriers were asymptomatic. These mutation carriers who were near the expected age of onset of AD but without clinical signs of the disease, did not show changes in either electrophysiological parameters or volumes of the temporal lobes. However, in these 2 individuals the blood flow in the temporal lobe showed intermediate values between the symptomatic mutation carriers and healthy noncarriers. Two neuropsychological tests showed a deterioration that paralleled clinical symptoms in 1 of the mutation carriers who was close to the expected age of onset and who at the end of the follow-up had clinical signs of AD. In the same subject, brain glucose metabolism was pathologically reduced in the temporal lobes before other clinical symptoms were obvious. CONCLUSION: In this familial form of AD a reduced temporal lobe glucose metabolism was indicative of AD before the expected clinical onset. Reduced glucose metabolism even preceded the development of subjective or objective cognitive dysfunction and might therefore serve as a clinical marker for AD before the onset of clinical symptoms. Reduced cerebral blood flow in the temporal lobes and cognitive deterioration paralleled the clinical decline in the early stage of the disease. Copyrightz1999S.KargerAG,Basel

Adult↗

PubMed2003

The atypical antipsychotic ziprasidone, but not haloperidol, improves phencyclidine-induced cognitive deficits in a reversal learning task in the rat.

The glutamate/N-methyl-D-aspartate receptor antagonist phencyclidine (PCP) has been shown to induce both positive and negative symptoms of schizophrenia, as well as cognitive deficits, thus providing a relatively valid model of psychosis. Isolation rearing from weaning in the rat has been proposed as a non-pharmacological model of psychosis. The aim of the present study was to explore the validity of a combination of these techniques to model cognitive dysfunction associated with schizophrenia. The present study evaluates the effects of the novel antipsychotic ziprasidone and the typical antipsychotic haloperidol in their ability to reverse the cognitive deficit induced by PCP in isolation reared rats and social controls. Rats housed in social isolation (n = 25) or in groups of five (n = 25) from weaning were food deprived and trained to respond for food in an operant reversal learning paradigm. PCP at 1.0 and 1.5 mg/kg (intraperitoneally, i.p.) significantly and selectively impaired reversal task performance in both groups of rats. This impairment was not significantly improved following the coadministration of haloperidol (0.05 mg/kg, i.p.). Higher haloperidol doses (0.1 and 0.25 mg/kg, i.p.) were found to impair task performance, with the social animals being more sensitive than isolation-reared animals. In contrast, ziprasidone (2.5 mg/kg, i.p.) reversed the impairment caused by PCP. This was significant in social animals, while in isolates there was a non-significant enhancement in performance of the reversal task with ziprasidone compared to PCP alone. Thus, PCP produced a selective reversal learning deficit in rats, which was ameliorated following treatment with ziprasidone but not haloperidol. Rearing conditions did not influence performance of the test or the deficit produced by PCP.

Animals↗

PubMed2000

[Cognitive therapy for schizophrenic patients].

Neurocognitive deficits of schizophrenic patients are assigned to the following three levels of disorders: Information-processing, basic styles of thinking and emotional management. Cognitive interventions are schematically subdivided in direct, indirect and combined ones. Direct interventions are oriented straight at the disorder and contain exactly definable therapeutic steps inside of an experimental procedure. The focus of indirect interventions are the environment of the disorder with the purpose of modification and reorganisation. Combined interventions connect both approaches to get a decrease of the impairments of the symptoms and a long-term stabilization. Today, connections between the pattern of cognitive dysfunctions and the social functioning of schizophrenic patients are investigated. Verbal memory and vigilance seem to be good predictors of the community functioning. Further developments of cognitive therapies have to include multimodal approaches and unspecific therapeutic influences.

Cognitive Behavioral Therapy↗

PubMed2000

[Psychological concepts and treatments for chronic pain and somatoform syndromes].

Chronic pain syndromes and somatic syndromes not fully explained by organic pathology are common complaints presented by patients in general health care. Studies have shown the major role of psychological factors in the etiology of these disorders leading to new conceptualization of illness and cognitive behavioral approaches to treatment. Chronic pain and somatoform symptoms are dependent on individual resources of stress prevention strategies, coping skills, environmental influences on symptoms and dysfunctional cognitions and beliefs about illness. Psychological concepts, treatment approaches and specific interventions are demonstrated.

Adaptation, Psychological↗

PubMed2002

[Mild cognitive decline in the elderly: nosology and clinical status].

Cognitive impairment without dementia is common in elderly persons and causes significant impairment in capacity to perform everyday activities. A number of nosological entities have been proposed for the classification of sub-clinical cognitive dysfunction. The more recent concepts assume an underlying organic condition, in particular the presence of early stage dementia. While prospective studies suggest that persons with mild cognitive disorder have a high risk of developing dementia, long-term follow-up of subjects with mild cognitive impairment suggests that dementia alone does not explain all cases. Cognitive disorder in the elderly must be construed as a common outcome for a number of interacting pathologies whose expression is also mediated by genetic, environmental and social factors.

Aged↗

PubMed2000

AIDS does not alter the total number of neurons in the hippocampal formation but induces cell atrophy: a stereological study.

Although cognitive dysfunction is a common finding in patients with acquired immunodeficiency syndrome (AIDS) its pathogenesis remains controversial. Given the involvement of the hippocampal formation in the processing of cognitive information and the scarcity of quantitative studies in this brain region, we have examined, using stereological methods, the hippocampal formations of AIDS patients. The study was performed in ten AIDS patients and ten age-matched controls. All cases were male. The Principle of Cavalieri was applied to estimate the volume of the layers of the dentate gyrus and of the CA3 and CA1 hippocampal fields. The fractionator and the nucleator were used as estimators of the total number, and mean somatic and nuclear volumes of the neurons in the cell-containing layers of all hippocampal subdivisions. No cell death was detected in AIDS patients but the global volume of their hippocampal formations was significantly decreased due to the reduced volume of its layers, mainly the cell-containing layers. Furthermore, the somatic and nuclear volumes of the neurons in the hippocampal formation were significantly decreased in AIDS patients. No correlation was found between the estimates obtained and the presence or absence of neurological involvement. Our results show that neurons in the hippocampal formation of AIDS patients display marked morphological changes, despite the maintenance of their total number. These alterations are likely to lead to dysfunction of the hippocampal circuitries and, thus, might contribute to explaining the dementia features which occur in this condition.

AIDS Dementia Complex↗