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PubMed2002

Vascular dementia may be the most common form of dementia in the elderly.

Cerebrovascular lesions, mainly lacunes and white matter ischemia, are common in elderly patients with dementia. Vascular dementia (VaD) is the second most common cause of dementia, after Alzheimer's disease (AD). However, lacunar strokes have become an important factor in the clinical expression of AD. Also, population-based studies indicate that vascular risk factors increase the risk of developing AD. It is postulated here that the two main causes of VaD-stroke and ischemic heart disease (IHD)-may be responsible for the majority of cases of dementia in the elderly. STROKE RELATED VaD: Cerebrovascular disease (CVD) is the second leading cause of death worldwide. About 1/3 of stroke survivors [range: 25-41%] 65 years old and above develop VaD within 3 months following the ictus. In the USA alone, 125,000 new cases/year of VaD occur after ischemic stroke (about 1/3 of the 360,000 incident cases of AD). Therefore, more than 1 million elderly people are currently affected by poststroke VaD in the USA. Since current criteria identify "pure" cases of AD and VaD, it is likely that "AD plus CVD" ("mixed" dementia) could be responsible for a large number of cases currently diagnosed as probable AD. CARDIOGENIC VAD: By 2020, IHD leading to congestive heart failure (CHF) will become the leading cause of disability worldwide. Vascular cognitive impairment occurs in 26% of patients discharged from hospitals after treatment for CHF. Cognitive dysfunction correlates with left ventricular dysfunction and systolic blood pressure below 130 mm Hg. CHF is a leading cause of hospital admissions in Western nations (4.5 million cases in the USA alone) and is a growing problem in developing countries. Furthermore, over 800,000 patients/year undergo coronary artery bypass graft (CABG) surgery worldwide, including 300,000 patients in the USA. Measurable cognitive dysfunction occurs post-CABG in 80-90% of patients at hospital discharge. Long-term (5 years) incidence of cognitive defects is 42%. Finally, an international study found short-term postoperative cognitive dysfunction in 26% of patients (>60 years) after abdominal or orthopedic surgery; most of them may be instances of VaD. In conclusion, VaD may be the most underdiagnosed and undertreated form of dementia in the elderly.

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PubMed2000

Withdrawal of synthetic hormones during the perimenopause: a case study.

A single case study was used to explore the experiences of a perimenopausal woman following withdrawal of synthetic hormones. The respondent, aged 51 years, had experienced severe physiologic, affective and cognitive dysfunction following withdrawal of synthetic hormones. She was approached while attending a family planning clinic in regional New South Wales, Australia. Information was obtained through a retrospective chart review and in-depth interview. The findings suggest that affective and cognitive dysfunction may be triggered by the sudden withdrawal of artificial hormones in perimenopausal women. Practitioners should be aware that some women, especially those unable to produce sufficient natural hormones, might experience severe physiologic, affective and cognitive dysfunction when hormone supplements are withdrawn. Detailed history-taking and close monitoring following the withdrawal or introduction of hormones may alert practitioners to the incidence of withdrawal symptoms or side-effects. Moving beyond the scientific interpretations, future research should address these concerns and investigate the potential for addiction when hormones are prescribed.

Anxiety↗

PubMed1997

Quantitative magnetic resonance analysis in vascular dementia.

The potential role of magnetic resonance imaging (MRI) in differentiating between specific causes of cognitive decline in patients with vascular dementia (VD) has not yet been fully established. We therefore decided to assess the supratentorial cerebral contents in 24 patients with a diagnosis of probable VD and in 24 normal subjects, matched for age and education level, using MRI volumetric parameters obtained by means of a quantitative method. The volumes of subarachnoid and ventricular spaces, cerebral tissue, and hyperintense areas on T2-weighted images were calculated. In order to reduce interindividual variability caused by differences in intracranial size, each absolute measurement was normalized to the relative size of the intracranial volume. In addition, we calculated the ratio between the areas of the corpus callosum (CC) and supratentorial brain at the same level on the T1-weighted image midsagittal plane. The MRI data were correlated with the deterioration of cognitive functions. Patients with VD showed significantly lower cerebral tissue volume and CC area, and higher ventricular space volume than normal subjects. Furthermore, the total volume of the T2 signal alterations was higher in VD patients than in normal subjects. In VD patients, this volume was found to be proportional to the increase in the volume of the ventricular space. On the other hand, no correlation was found between the volume of the T2 signal alterations and the area of the CC. The degree of global cognitive dysfunction and the score of each neuropsychological test did not show any correlation with the MRI data. Our results suggest that ventricular enlargement in VD patients is correlated with the increase in volume of the T2 signal abnormalities, but that the degree of global cognitive dysfunction is not influenced by the volume of these T2 signal abnormalities. Furthermore, the CC atrophy does not influence the score of any neuropsychological test or the degree of global cognitive dysfunction.

Age Distribution↗

PubMed1992

Time dependency of cognitive recovery with cobalamin replacement: report of a pilot study.

OBJECTIVE: To examine the effects of cobalamin repletion on cognition in elderly subjects with low serum cobalamin and evidence of cognitive dysfunction. DESIGN: Time series data collected in an open trial of parenteral cobalamin therapy. SETTINGS: Outpatient geriatric assessment centers, inpatient geropsychiatry unit, and tertiary care university hospital. PARTICIPANTS: Twenty-two subjects with low serum cobalamin (less than 150 pmol/L) and evidence of cognitive dysfunction were entered consecutively over an 8-month period of time. Eighteen subjects completed the study. INTERVENTIONS: Subjects received 1000 micrograms of cyanocobalamin intramuscularly daily for 1 week, then weekly for 1 month, then monthly thereafter for a minimum of six months. OUTPATIENT MEASURE: The Mattis Dementia Rating Scale (DRS) was administered both before and at least 6 months after full cobalamin replacement therapy. The hypothesis that cognitive improvement was dependent on the duration of cognitive symptoms was formulated a posteriori. RESULTS: After a minimum of 6 months of cobalamin therapy, 11 of 18 patients showed cognitive improvement. There was a striking correlation between duration of cognitive symptoms and response to therapy. Patients symptomatic for less than 12 months gained an average of twenty points on the DRS (paired t test P = 0.0076), whereas patients symptomatic greater than 12 months lost an average of three points (paired t test P = .34). Two patients symptomatic for only 3 months normalized their DRS scores, gaining 31 and 28 points, respectively. CONCLUSION: There may be a time-limited window of opportunity for effective intervention in patients with cognitive dysfunction and low serum cobalamin.

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PubMedDate not supplied

Development of treatments for toxicant-induced cognitive deficits.

A wide variety of toxicants have been found to impair cognitive function. Some such as lead, organophosphate pesticides, and polychlorinated biphenyls are quite widespread in the environment. Others such as alcohol, nicotine, and cocaine are widely used drugs of abuse. Many people are chronically exposed to these toxicants. Lasting cognitive deficits can result, especially after developmental exposure. Considerable research has been directed at developing pharmacological agents to treat the cognitive dysfunction associated with Alzheimer's Disease, Unfortunately, other types of cognitive dysfunction, such as toxicant-induced cognitive deficits, have not received the same degree of attention, despite the fact that they are quite widespread and may be more amenable to development of useful therapeutic treatments. Animal models can be particularly useful because the agents causing these deficits are known. In addition, for a variety of neurotoxic compounds, information concerning the nature of the cognitive effect and mechanism of toxic action can help in development of treatments. Prevention of toxic exposure is ideal. Removal from the source of pollution after exposure can help, but for those who already carry the burden of persistent deficits, development of efficacious therapeutic treatments is a necessity.

Animals↗

PubMed2006

Differential effects of cyclooxygenase inhibitors on intracerebroventricular colchicine-induced dysfunction and oxidative stress in rats.

Alzheimer's disease is a progressive neurological and psychiatric disorder. Oxidative stress and neuroinflammation have been implicated in pathophysiology of Alzheimer's disease. Inflammatory cells, such as astrocytes and microglia, are activated in areas of the brain affected by amyloid plaques and inflammatory mediators including cytokines, chemokines, prostaglandins, oxygen free radicals and reactive nitrogen species may have a crucial role in Alzheimer's disease pathogenesis. Central administration of colchicine, a microtubule-disrupting agent, causes loss of cholinergic neurons and cognitive dysfunction that is associated with excessive free radical generation. The present study was aimed to evaluate the effects of cyclooxygenase inhibitors against colchicine-induced cognitive dysfunction and oxidative stress in rats. Following intracerebroventricular (i.c.v.) administration of colchicine (15 microg/5 microl), rats exhibited poor retention of memory in Morris water maze and elevated plus maze task paradigms and oxidative stress in rats. Chronic treatment with naproxen (per se; 20 and 40 mg/kg, p.o.) or valdecoxib (per se; 5 and 10 mg/kg, p.o.) daily respectively for a period of 25 days beginning 4 days prior to colchicine injection significantly improved colchicine-induced cognitive impairment. Intracerebroventricular colchicine injection resulted in free radical generation characterized by alterations in oxidative stress markers with a significant increase in malondialdehyde and nitrite levels and depletion of reduced glutathione levels in the brains of rats. It also caused a decrease in acetylcholinesterase activity. Besides, improving cognitive dysfunction, chronic administration of cyclooxygenase inhibitors (naproxen and valdecoxib) significantly reduced elevated malondialdehyde, nitrite levels and restored reduced glutathione levels and acetylcholinesterase activity. The results of the present study indicated that naproxen (per se; 20 and 40 mg/kg, p.o.) or valdecoxib (per se; 5 and 10 mg/kg, p.o.) treatment has a neuroprotective role against colchicine-induced cognitive impairment and associated oxidative stress. The present findings further support the potential use of cyclooxygenase inhibitors in treatment of neurodegenerative diseases such as Alzheimer's disease.

Acetylcholinesterase↗

PubMed1993

Disturbed frontal regulation of attention in Parkinson's disease.

Parkinson's disease is characterized not only by tremor, akinesia and rigidity, but also by frontal cognitive dysfunction, that can be understood as a disturbance in the 'Supervisory Attentional System' (SAS). This concept refers to a system, located in the frontal cortex, that regulates attentional processes under novel, non-routine conditions. The hypothesis that cognitive dysfunction in Parkinson's disease results from a disturbance in the SAS was investigated by recording 'processing negativity' in 33 parkinsonian patients and 17 controls. Processing negativity is an event-related potential that reflects neuronal activity during selective attention. The contribution of the frontal cortex to selective attention can be studied directly using processing negativity. Parkinsonian patients were also scored for clinical symptoms and subjected to a neuropsychological test battery. Processing negativity was clearly disturbed in the parkinsonian patients. Moreover, parkinsonian patients with the lowest scores on 'frontal' neuropsychological tests such as Stroop, Trail Making and Word Fluency, also had the lowest processing negativity. Our results support the hypothesis that cognitive dysfunction in Parkinson's disease might be understood as a disturbance in the frontal regulation of attentional processes. Degeneration of the dopaminergic mesocortical innervation of the frontal cortex in Parkinson's disease is a possible neurochemical substrate of these frontal attentional disturbances.

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PubMed1996

Cognition enhancers in age-related cognitive decline.

A review of recently published studies on the effect of cognition enhancers in non-demented human study participants is presented. The heterogeneity of the therapeutic target, age-associated cognitive decline, can be improved by separately treating groups in whom age-extrinsic factors may underlie cognitive pathology. Standardisation of cognitive assessments is necessary, since many different tests are applied to answer the same question. Modelling cognitive dysfunction, either by pharmacological or nonpharmacological means, in humans is highly recommended since it allows hypotheses to be tested in a clearly operationalised way. Predictive validity of the currently applied models for the clinical situation remains a problem, however. The scopolamine (hyoscine) model has, to a reasonable extent, predictive validity for the cholinergic agents. The results of 67 single-dose studies and 30 multiple-dose studies are summarised. All single-dose studies and 14 multiple-dose studies were carried out in young or elderly human volunteers. In 45 of 81 volunteer studies, models of cognitive dysfunction were employed. The scopolamine model was the most used (n = 21); the other studies induced cognitive dysfunction by means of benzodiazepines (8), hypoxia (7), alcohol (5) and sleep-deprivation (4). The remaining 16 multiple-dose studies were clinical trials of a duration varying between 2 weeks and 1 year (average duration was 14 weeks). In these trials, the effects of cognition enhancers were assessed in elderly people in whom impairment of memory, psychomotor performance or cognitive function was determined. These included age-associated memory impairment (AAMI) and age-associated cognitive decline (AACD). There were many studies in which the cognition enhancing properties of substances in humans were reliably demonstrated. The cognition enhancing properties of substances that are widely used, such as caffeine, nicotine and vitamins, may already be active against AACD. New developments such as serotonin (5-hydroxytryptamine3; 5-HT3) antagonists and N-methyl-D-aspartate (NMDA) antagonists have provided marginal and disappointing results in AAMI. There is no cognition enhancer that has reliably and repeatedly been demonstrated to be efficacious for the treatment of AACD. However, this situation may change as the selectivity, specificity and adverse effect profiles of substances that are being developed for the treatment of AD may be expected to be improved in the future.

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PubMed2003

Postoperative hypoxia is a contributory factor to cognitive impairment after cardiac surgery.

OBJECTIVE: Cognitive dysfunction and postoperative hypoxia are common sequelae of coronary artery bypass grafting, but there has been no study to determine whether there is any relationship between them. METHODS: Arterial blood gas measurements were performed before surgical intervention and on the second and fifth postoperative day, and neuropsychological assessments were performed before surgical intervention and 5 days and 3 months postoperatively by using a battery of 10 psychometric tests in 175 patients undergoing coronary artery bypass grafting. An estimate of overall performance on the battery at each assessment point was provided by a simple aggregate cognitive index score calculated from the mean z scores of 4 normally distributed test variables. Multiple regression analysis was performed by using the cognitive index score at day 5 as the dependent variable, with age, sex, duration of the operation, presence or absence of cardiopulmonary bypass, preoperative cognitive index score, and arterial oxygenation and percentage of saturation at day 5 as independent variables. RESULTS: The mean cognitive index score decreased significantly in 115 (66%) patients who agreed to neuropsychological test battery assessment on the fifth postoperative day but improved significantly beyond baseline at 3 months. Mean arterial oxygen tension and percentage of saturation decreased significantly 2 days after the operation and, although improving over the following 3 days, remained decreased at day 5. Decreased cognitive index scores at day 5 strongly predicted cognitive impairment at 3 months (r = 0.36). The only significant independent predictors of the day 5 cognitive index score in the multiple regression analysis were preoperative cognitive index score and arterial oxygenation tension at day 5 (r = 0.24, P <.03). CONCLUSIONS: We report a significant correlation between postoperative cognitive dysfunction and hypoxia 5 days after coronary artery bypass grafting. This finding might have therapeutic implications because early postoperative cognitive dysfunction influences long-term impairment.

Cognition Disorders↗

PubMed2005

IADL functions, cognitive deficits, and severity of depression: a preliminary study.

OBJECTIVE: Despite the documented association of cognitive dysfunction with impairment in instrumental activities of daily living (IADLs) in geriatric depression, the relationship among deficits in distinct IADLs with severity of depression and specific cognitive impairments remains to be clarified. The authors examined the relationship of depression severity and the cognitive domains of attention, initiation/perseveration, construction, conceptualization, and memory to nine distinct IADLs. METHODS: The subjects were 105 nondemented elderly patients but with impairment in at least one IADL and a history or presence of major depression. Impairment in IADLs and severity of depression were assessed with the Philadelphia Multilevel Assessment Instrument (MAI) and the 24-item Hamilton Depression Rating Scale (Ham-D), respectively. Cognitive dysfunction was assessed with the Mini-Mental State Exam (MMSE) and the Mattis Dementia Rating Scale (DRS). RESULTS: Six IADLs were influenced by impairment in at least one of the cognitive domains. Abnormal scores in initiation/perseveration, an aspect of executive dysfunction, was the cognitive impairment affecting most IADLs; it interfered with the ability to shop for groceries, prepare meals, take medicine, and manage money. Impairment in initiation/perseveration had a most prominent effect in the presence of depressive symptoms and affected shopping for groceries and preparing meals. Lack of interest and motivation, part of the depressive syndrome, compounded by behavioral abnormalities resulting from executive dysfunction, may account for this interaction. CONCLUSIONS: These relationships may provide the background for developing interventions targeting functional deficits associated with specific cognitive dysfunctions and depression.

Activities of Daily Living↗

PubMed2002

Bicaudate ratio as a magnetic resonance imaging marker of brain atrophy in multiple sclerosis.

CONTEXT: Brain atrophy has emerged as a useful surrogate marker of disease involvement in multiple sclerosis (MS). The relationship between whole-brain or regional atrophy and cognitive dysfunction is poorly understood. OBJECTIVES: To determine whether the bicaudate ratio (BCR)-the minimum intercaudate distance divided by brain width along the same line-is increased in MS and to compare the ability of the BCR, whole-brain atrophy, and other magnetic resonance imaging markers to predict cognitive dysfunction. DESIGN: Case-control study. SETTING: University-affiliated clinic. PARTICIPANTS: Sixty patients with MS and 50 age- and sex-matched control subjects. MAIN OUTCOME MEASURES: Bicaudate ratio, whole-brain atrophy, T2 lesion load, T1 ("black hole") lesion load, and caudate volume were measured quantitatively using fluid-attenuated inversion recovery, T1-weighted, and gradient-echo magnetic resonance imaging scans. Symbol Digit Modalities Test was used to assess cognitive function. RESULTS: The BCR (mean [SD]) was higher in patients with MS (0.11 [0.03]) than in controls (0.09 [0.02]) (P<.001), suggesting subcortical atrophy in MS. The BCR was related to total T2 (r = 0.56, P<.001) and T1 (r = 0.40, P<.002) lesion volumes, but not caudate volume in patients with MS. Regression modeling selected BCR (P<.05), but not whole-brain atrophy, T1 or T2 lesion volume, or caudate volume as predictive of Symbol Digit Modalities Test score in patients with MS. CONCLUSIONS: The BCR is increased in MS and is more closely associated with cognitive dysfunction than are other magnetic resonance imaging surrogate markers including whole-brain atrophy. Increased BCR is best explained by frontal horn ventricular enlargement due to atrophy of deep frontal subcortical white matter. This highlights the close relationship between subcortical atrophy and cognitive impairment in patients with MS.

Adult↗

PubMed2002

Capacity to provide informed consent for participation in schizophrenia and HIV research.

OBJECTIVE: The degree to which people with psychiatric symptoms and cognitive dysfunction can provide informed consent to participate in research is a controversial issue. This study was designed to examine the capacity of subjects with schizophrenia and subjects with HIV to provide informed consent for research participation and to determine the relationships among cognitive dysfunction, psychiatric symptoms, and decisional capacity. METHOD: Twenty-five men and women with a DSM-IV diagnosis of schizophrenia and 25 men and women with HIV were recruited. The groups were compared in terms of neuropsychological functioning, psychiatric symptoms, and ability to provide informed consent to a hypothetical drug trial. RESULTS: Eighty percent of the subjects with schizophrenia and 96% of the HIV-positive subjects demonstrated adequate capacity to consent to the hypothetical drug trial, but subjects in the schizophrenia group had significantly lower scores on two of the four aspects of decisional capacity. For the subjects with schizophrenia, neuropsychological functioning and psychiatric symptoms (e.g., apathy and avolition), but not psychotic symptoms (e.g., hallucinations and delusions), were significantly associated with decisional capacity. CONCLUSIONS: The majority of subjects who are recruited and willing to participate in schizophrenia or HIV research will have adequate capacity to provide consent. Cognitive dysfunction and the symptoms shown to be associated with impaired decisional capacity are not unique to schizophrenia and may occur with many other forms of illness. These findings underscore the importance of considering how decisional capacity will be assessed in all types of research, regardless of the specific condition being studied.

Adolescent↗

PubMed2000

Genetic and state variables of neurocognitive dysfunction in schizophrenia: a twin study.

To characterize the familiality of cognitive dysfunction in schizophrenia, we studied performance on three tasks (visuospatial attention; visuolinguistic conflict, arrow-word; and Wisconsin Card Sorting Test [WCST]) by monozygotic (MZ) and dizygotic (DZ) twin pairs discordant for schizophrenia. The subject sample consisted of six MZ twin pairs, nine DZ twin pairs, and one MZ and one DZ nonschizophrenia cotwin of a patient with schizophrenia. There were two sources of cognitive dysfunction: a nonheritable, state component and a heritable, trait component. Deficits surfaced during the WCST in nonschizophrenia MZ cotwins; this impairment resolved following training in nonschizophrenia MZ cotwins, but not in the probands with schizophrenia, who performed abnormally in all tasks. The results suggest that nonheritable protective factors modulate the specific, plastic, and sometimes subtle neurocognitive deficits related to the schizophrenia genotype.

Adult↗

PubMed2005

Cerebral ischemic injury and cognitive impairment after off-pump and on-pump coronary artery bypass grafting surgery.

BACKGROUND: Off-pump coronary artery bypass grafting surgery reduces the intraoperative cerebral embolic load and may therefore cause less brain injury. The main aim of this study was to compare off-pump and on-pump surgery with regard to the frequency of new postoperative cerebral ischemic lesions and the prevalence of postoperative cognitive impairment. We also assessed whether preoperative cerebral ischemic injury predicts the risk for cognitive dysfunction after surgery. METHODS: One hundred twenty patients with ischemic coronary artery disease were prospectively randomized to undergo off-pump or on-pump surgery. A detailed neuropsychological assessment and a cerebral magnetic resonance imaging examination were performed on the day before and at 3 months postoperatively. The neuropsychological assessment was repeated at 12 months. RESULTS: There was no significant (p = 0.17) difference between off-pump (8.2%) and on-pump (17.3%) surgery with regard to new postoperative cerebral lesions. The prevalence of cognitive impairment after surgery was also similar in the two groups (3 months: off-pump 20.4%, on-pump 23.1%, p = 0.74; 12 months: off-pump 24.1%, on-pump 23.1%, p = 0.90). The degree of preoperative cerebral ischemic injury was significantly associated with cognitive dysfunction after on-pump (p = 0.02) but not after off-pump (p = 0.22) surgery. None of the patients with normal preoperative radiologic findings were found to have cognitive impairment at 3 months postoperatively (p = 0.04). CONCLUSIONS: Long-term cognitive function and magnetic resonance imaging evidence of brain injury were similar after off-pump and on-pump coronary artery bypass grafting surgery. Preoperative cerebral magnetic resonance imaging can be used to predict the risk for cognitive dysfunction after coronary artery bypass grafting surgery.

Adult↗

PubMed1996

Cognitive visual dysfunction in a child with cerebral damage.

Visual impairment as a sequel to cortical damage can be associated with complex disorders in cognitive visual function. Such dysfunction can be difficult to diagnose with certainty, particularly in children, owing to the child's problems of awareness and communication. The authors describe the case of a 13-year-old girl whose cerebral damage is apparently accompanied by complex cognitive visual disorders. Though she has a good binocular visual acuity, she cannot see rapidly moving objects. She has difficulties with orientation, recognising faces and cognitive depth perception. Despite an absence of detailed psychometric testing, a clinical diagnostic approach such as that used in this case, based on a CT scan and careful history-taking and observation, may be helpful in planning educational strategies.

Adolescent↗

PubMed2002

Effects of epoetin alfa on cognitive function, mood, asthenia, and quality of life in women with breast cancer undergoing adjuvant chemotherapy.

Several recently published studies describe moderate to severe cognitive dysfunction in breast cancer survivors who were treated with adjuvant chemotherapy 1-5 years before undergoing extensive neuropsychological testing. While these studies are hypothesis-generating and preliminary given their small size and retrospective nature, they consistently suggest that between approximately 15% and 25% of chemotherapy-treated breast cancer patients will have evidence of cognitive dysfunction some years after chemotherapy, compared to about 10% of breast cancer survivors who did not receive chemotherapy. Recent preclinical data strongly suggest that erythropoetin is a potent, endogenous neuroprotective agent that prevents neuronal apoptosis from a variety of insults including hypoxia, trauma, subarachnoidal hemorrhage, and encephalitis. Erythropoietin also appears to enhance learning in a mouse spatial learning maze model. We have conducted a pilot study of epoetin alfa versus placebo in early-stage breast cancer patients who received standard adjuvant anthracycline-based chemotherapy to determine the feasibility of administering standardized neurocognitive assessment tests in the oncology practice setting in order to understand whether the Executive Interview 25 test can detect the subtle cognitive impairment in verbal fluency, attention, and short-term memory observed with chemotherapy, and to assess whether epoetin alfa-treated patients have less evidence of cognitive dysfunction during and 6 months after chemotherapy compared with control-treated patients. We report here the preliminary results of this pilot clinical trial.

Animals↗

PubMed1984

The Brief Psychiatric Rating Scale (BPRS) in geropsychiatric research: I. Factor structure on an inpatient unit.

Factor analysis of symptom ratings recorded on the Brief Psychiatric Rating Scale (BPRS) for a sample of 87 geropsychiatry inpatients resulted in five relatively independent factors. The factor structure differed in two important respects from that previously observed in numerous analyses of BPRS ratings of patients from the general adult psychiatric population. The symptom of depressive mood combined with emotional withdrawal and motor retardation to define a withdrawn depression factor, whereas depressive mood has routinely evidenced greater affinity for anxiety and tension in younger adults. In addition, the unitary thinking disturbance factor that has been observed routinely in data from the younger adult psychiatric population split into separate factors of cognitive dysfunction and psychotic distortion. Construct validity of the cognitive dysfunction factor was examined with reference to an objective mental status questionnaire.

Aged↗

PubMed1994

Type II diabetes and cognitive function. A population-based study of Native Americans.

OBJECTIVE: To explore the relationship between type II diabetes and cognitive function in older Native Americans and to assess the effects of other selected risk factors for cognitive dysfunction on this relationship. RESEARCH DESIGN AND METHODS: Cognitive function was assessed in 80 diabetic and 81 nondiabetic Native Americans who were 45-76 years of age in a cross-sectional population-based sub-study of the Strong Heart Study. Thirteen cognitive function tests were administered during a personal interview. Information about six other risk factors for cognitive dysfunction, including depressive symptoms, physical function, alcoholism, current alcohol use, hypertension, and myocardial infarction, was ascertained from interviews and from abstraction of medical records. RESULTS: Diabetes was associated with impairment on only two tests of cognitive function: verbal fluency (P = 0.004) and similarities (P = 0.010). Depressive symptoms were related to verbal fluency (P = 0.004), but did not explain the diabetes-related difference in performance. The effects of hypertension, depressive symptoms, and current alcohol use explained the diabetes-related performance difference on similarities. Cognitive function was not related to metabolic control (HbA1c level). CONCLUSIONS: We found little evidence that type II diabetes in this population of Native Americans is associated with decrement in cognitive function. Some of the cognitive impairment previously attributed to diabetes may be related, at least in part, to the influence of other risk factors. This should be considered in the design of future studies in other populations.

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