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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

15 patients suffering from DSM-III-R major depression were compared with 15 age-, sex- and intelligence-matched controls on a battery of memory tests, aimed at fractionating memory dysfunction in depression. Patients were unimpaired relative to controls on measures of short-term memory, recognition, semantic memory and implicit memory. There was no evidence of a hedonic bias in recall of positive vs. negatively valenced stimuli, nor was there any correlation between depression severity and level of memory impairment. Psychotic patients did not demonstrate greater memory impairment relative to nonpsychotic depressed patients. As a group, however, depressed patients demonstrated deficits in psychomotor speed and in free recall of material (both immediate and delayed). The selective recall deficit suggests that material has been encoded but that patients are particularly impaired with regard to search and retrieval processes.
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PMID:An analysis of memory dysfunction in major depression. 855 82

The consequences for cognitive functioning of normal aging, depression and dementia are well known. However, the borderline between normal and pathological cognitive aging is less well understood. Recently, it has been found that it is important to differentiate between 'successful', 'usual' and pathological cognitive aging. This article reviews existing views on this borderline. Recently, it has been found that health-related factors, or biological life events, may determine the rate of cognitive aging. Various different, but similar, diagnostic descriptions of age-related cognitive dysfunction exist simultaneously: benign senescent forgetfulness, malignant senescent forgetfulness, age-associated memory impairment, age-consistent memory impairment, late-life forgetfulness, mild cognitive changes (subthreshold) and cognitive impairment disorders are some examples of different diagnostic categories. There are also various diagnostic tools to obtain these experimental diagnoses; for example, the Global Deterioration Scale, the Clinical Dementia Rating Scale and the Cambridge Mental Disorders of the Elderly Examination. A diagnosis is considered important for the early detection of dementia. Pharmacological treatments are still in the experimental stage. Improvement of cognitive function has particularly been studied in clinical trials with groups of patients with Alzheimer's disease as well as patient groups with age-associated memory impairment. Future strategies may orient more towards treating symptoms of cognitive dysfunction, probably also on the basis of diagnosis of health-related factors, in age-related cognitive decline and depression.
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PMID:Cognitive impairment in elderly people. Predisposing factors and implications for experimental drug studies. 860 Oct 53

We examined the effects of p.o. administered 3-[1-(phenylmethyl)-4-piperidinyl]-1-(2,3,4,5-tetrahydro-1H-1-b enzazepin-8- yl)-1-propanone fumarate (TAK-147), a novel AChE inhibitor, on impaired learning and memory in animal models. At 1 to 3 mg/kg, TAK-147 ameliorated the passive avoidance deficit induced by diazepam. TAK-147 did not affect delayed-matching-to-position (DMTP) performance of normal rats at doses of 1 to 30 mg/kg assessed by using a three-lever operant chamber, but 9-amino-tetrahydroacridine disrupted the DMTP response at 5 to 20 mg/kg. Scopolamine (0.02-0.1 mg/kg s.c.) impaired DMTP performance, whereas methylscopolamine did not affect the DMTP task. TAK-147 ameliorated the impairment of DMTP performance induced by scopolamine without affecting the general behavior of the rats; however, 9-amino-tetrahydroacridine produced no significant amelioration of the impairment. The intraventricular injection of AF64A disrupted differential-reinforcement-of-low-rate 10-sec performance in rats, as demonstrated by marked decreases in reinforcement rate and response efficiency. TAK-147 slightly increased the reinforcement rate in AF64A-treated rats at a low dose of 1 mg/kg, but the effect was not significant statistically. TAK-147 had no significant effect on the duration of immobility in rats in a forced swimming test at doses of 2 to 10 mg/kg. 9-Amino-tetrahydroacridine prolonged the duration of immobility at 5 to 20 mg/kg. Furthermore, TAK-147 reversed reserpine-induced hypothermia and ptosis in mice at doses of 3 to 10 mg/kg, a result that implies an antidepressant-like action. These results indicate that TAK-147 ameliorates learning and memory impairment in animal models without affecting the general behavior or causing behavioral depression and suggest that TAK-147 may be useful for the treatment of Alzheimer's disease.
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PMID:Effects of 3-[1-(phenylmethyl)-4-piperidinyl]-1-(2,3,4,5-tetrahydro-1 -H-1-benzazepin-8-yl)-1-propanone fumarate (TAK-147), a novel acetylcholinesterase inhibitor, on impaired learning and memory in animal models. 866 90

Using the Squire Subjective Memory Questionnaire (SSMQ), depressed patients rated their memory functioning prior to a course of brief pulse, electroconvulsive therapy (ECT) within the 1 week following the course and 2 months later. Normal controls made similar ratings at comparable intervals. Prior to ECT, patients reported poorer memory functioning than controls. There was marked improvements in the patients' self-reports shortly following ECT, and at 2-month follow-up SSMQ scores were generally comparable in patients and controls. At all time points, the severity of depressive symptoms was strongly associated with patients' reports of memory dysfunction. SSMQ subscales ("depression" and "ECT" items) were not differentially sensitive to effects of ECT or depression. Relations between ECT treatment parameters and changes in patients' self-evaluations only emerged after controlling for clinical state change. Shortly following ECT, there were no relations between SSMQ scores and objective measures of cognitive functioning. However, 2 months following ECT, there was a suggestion that greater retrograde amnesia for autobiographical memories was associated with self-rating of greater memory impairment.
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PMID:Subjective memory complaints prior to and following electroconvulsive therapy. 870 66

It is well established that head injury often causes brain damage leading to long term physical, cognitive and behavioural changes in the injured patients. Whereas the physical effects ranging from sensori-motor disturbances to posttraumatic epilepsy are often reported as well as cognitive sequelae, deteriorations of emotional and behavioural aspects are often neglected. Recent advances in imaging technology and clinical neuropsychology research have greatly contributed to increase our understanding of the effect of traumatic brain injury on diverse behavioural functions. After a brief review of the current status of problems facing the brain injured patients, this paper discusses the neuropsychological aspects of 3 long term brain injured patients. All 3 patients showed important behavioural and emotional distress several years after the accident. Whereas case report of patient A and C discuss the emotional and personality disturbance characterised by anxiety, depression and irritability, case report of patient C which is a case of classic frontal syndrome showed important memory impairment with emotional disturbance characterised by apathy, lack of motivation and complete indifference to his surrounding environment. Whatever the mechanisms involved, psychoaffective disturbances in the brain injured patients appear as important problems in the long term. These emotional difficulties must be considered in the treatment and rehabilitation procedures of these victims in order to help them to improve their social adjustment and quality of life aspects. Neuropsychological test data can be used to develop treatment strategies tailored for an individual's specific cognitive strengths and deficits.
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PMID:Traumatic brain injury, cognitive and emotional dysfunction. Impact of clinical neuropsychology research. 871 91

The subcortical dementias are a heterogeneous group of disorders in which the predominant pathological lesions occur in subcortical structures such as basal ganglia, brainstem nuclei, and the cerebellum. When the cerebral cortex is involved, the lesions are most often in the frontal lobes. These pathologic lesions are associated with cognitive changes that include bradyphrenia, personality change (apathy, depression, irritability), memory impairment, and impaired manipulation of acquired knowledge (calculation, abstraction). Aphasia, apraxia, and agnosia are commonly seen in the cortical dementias, but are absent in the subcortical dementias. Progress in research on the anatomy and connectivity of cortical-subcortical structures has led to refinement in our understanding of the cortical dementias. Despite the connectivity between the cortical and subcortical structures, patterns of cognitive impairment in subcortical dementias remain distinct.
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PMID:Subcortical dementia: a neurobehavioral approach. 881

In clinical practice, Alzheimer's disease (AD), multi-infarct Dementia (MID) and depression are often difficult to differentiate and may coexist. This study reports the findings of CT and MRI focused on hippocampal atrophy (HA). Quantitative volumetric MRI measurements of the hippocampus showed a reduced volume in AD patients compared to normal controls with no overlap. CT studies reported a significant widening of the hippocampal fissure in AD patients. Because volumetric measurements are not available for routine examinations, so far we are required to use the finding of hippocampal lucency in CT and dilatation of the directly visible hippocampal fissure in coronal MRI scans as criteria for HA. These findings were visually classified on a 4-point scale by 2 neuroradiologists, who had no knowledge of the clinical diagnosis. The examinations of 80 patients (42 with AD, 22 with major depression, 3 with MID, 6 classified as age-associated memory impairment (AAMI) and 8 'normals' with only subjective memory impairment) showed that the HA strongly supports the diagnosis of AD, by correctly identifying 95% of the AD patients and 47.8% of the patients without AD. These results suggest that CT and MRI examinations of the hippocampus are capable of demonstrating HA in clinical practice, which is strongly correlated with the diagnosis of AD.
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PMID:Atrophy of hippocampus in patients with Alzheimer's disease and other diseases with memory impairment. 883 80

Data from a two-wave longitudinal study of an elderly community sample were used to assess whether cognitive complaints either predict subsequent cognitive decline or reflect past cognitive decline. Cognitive complaints and cognitive functioning were assessed on two occasions three and a half years apart. Cognitive complaints at Wave 1 were found not to predict future cognitive change on the Mini-Mental State Examination, an episodic memory test or a test of mental speed. Similarly, cognitive complaints at Wave 2 were unrelated to past cognitive changes on these tests after statistically controlling for the effects of anxiety and depression. Furthermore, cognitive complaints did not predict either mortality (after controlling for anxiety and depression) or future dementia. These results are evidence against the inclusion of cognitive complaints in diagnostic criteria for proposed disorders such as age-associated memory impairment, mild cognitive disorder and ageing-associated cognitive decline.
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PMID:Do cognitive complaints either predict future cognitive decline or reflect past cognitive decline? A longitudinal study of an elderly community sample. 912 13

Inositol is a simple polyol precursor in a second messenger system important in the brain. Cerebrospinal fluid inositol has been reported as decreased in depression. A double-blind controlled trial of 12 g daily of inositol in 28 depressed patients for four weeks was performed. Significant overall benefit for inositol compared to placebo was found at week 4 on the Hamilton Depression Scale. No changes were noted in hematology, kidney or liver function. Since many antidepressants are effective in panic disorder, twenty-one patients with panic disorder with or without agoraphobia completed a double-blind, placebo-controlled, four week, random-assignment crossover treatment trial of inositol 12 g per day. Frequency and severity of panic attacks and severity of agoraphobia declined significantly with inositol compared to placebo. Side-effects were minimal. Since serotonin re-uptake inhibitors benefit obsessive compulsive disorder (OCD) and inositol is reported to reverse desensitization of serotonin receptors, thirteen patients with OCD completed a double-blind controlled crossover trial of 18 g inositol or placebo for six weeks each. Inositol significantly reduced scores of OCD symptoms compared with placebo. A controlled double-blind crossover trial of 12 g daily of inositol for a month in twelve anergic schizophrenic patients, did not show any beneficial effects. A double-blind controlled crossover trial of 6 g of inositol daily vs. glucose for one month each was carried out in eleven Alzheimer patients, with on clearly significant therapeutic effects. Antidepressant drugs have been reported to improve attention deficit disorder (ADDH) with hyperactivity symptomatology. We studied oral inositol in children with ADDH in a double-blind, crossover, placebo-controlled manner. Eleven children, mean age 8.9 +/- 3.6 years were enrolled in an eight week trial of inositol or placebo at a dose of 200 mg/kg body weight. Results show a trend for aggravation of the syndrome with myo-inositol as compared to placebo. Recent studies suggest that serotonin re-uptake inhibitors are helpful in at least some symptoms of autism. However a controlled double-blind crossover trial of inositol 200 mg/kg per day showed no benefit in nine children with autism. Cholinergic agonists have been reported to ameliorate electroconvulsive therapy (ECT)-induced memory impairment. Inositol metabolism is involved in the second messenger system for several muscarinic cholinergic receptors. Inositol 6 g daily was given in a crossover-double-blind manner for five days before the fifth or sixth ECT to a series of twelve patients, without effect. These results suggest that inositol has therapeutic effects in the spectrum of illness responsive to serotonin selective re-uptake inhibitors, including depression, panic and OCD, and is not beneficial in schizophrenia, Alzheimer's ADDH, autism or ECT-induced cognitive impairment.
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PMID:Controlled trials of inositol in psychiatry. 916 2

The side-effects and complications of posteroventral pallidotomy are analysed in 138 consecutive patients who underwent 152 pallidotomies. Transient side-effects, lasting less than three months, appeared in 18% of the patients, that is, 16.5% of the surgical procedures. Long term complications, lasting more than 6 months, were noted in 10% of the patients, that is, 9.2% of the surgical procedures. Sixteen complications occurred alone or in various combinations in 14 patients and included fatigue and sleepiness (2), worsening of memory (4), depression (1), aphonia (1), dysarthria (3), scotoma (1), slight facial and leg paresis (2) and delayed stroke (2). Complications such as dysarthria and paresis could be attributed to MR- or CT-verified pallidal lesions lying too medially and encroaching on the internal capsule. Two of the patients with deterioration in memory had some memory impairment before surgery, and the aphonic patient had dysphonia preoperatively. The study suggests that stereotactic MRI and careful impedance monitoring and macro-stimulation of the posteroventral pallidum area should be sufficient for minimizing the risk of complications; the stereotactic lesion should be centered within the posterior ventral pallidum without involvement of internal capsule. It is concluded that pallidotomy is a safe procedure if performed on cognitively alert patients, and it seems that both the incidence and especially the severity of complications are lower for posteroventral pallidotomy than for thalamotomy.
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PMID:The side-effects and complications of posteroventral pallidotomy. 923 12


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