Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have observed discreet subgroups of male patients with psychotic disorders who have unirhinal olfactory identification deficits (microsmia). The purpose of this study was to examine the relationship between left or right nostril microsmia and performance on literalised neuropsychological tests sensitive to lesions in brain areas implicated in the pathogenesis of schizophrenia. Sixty-six male patients diagnosed with schizophrenia or related disorders were assessed with a battery of neuropsychological tests, sensitive to literalised and regional (temporal and frontal lobe) dysfunction. The University of Pennsylvania Smell Identification Test (UPSIT) was administered unirhinally and resultant scores were used to classify patients into olfactory subgroups. Neuropsychological test scores were compared amongst subgroups. A mixed design MANOVA was performed on cognitive domains with olfactory status (right microsmic; RM, n=8, left microsmic; LM, n=20, and normosmic schizophrenic controls; NSzC, n=38) as the between subject factor while hemisphere (left versus right) and domain (executive/fluency versus memory) were within-subject factors. A three-way (olfactory subgroup by hemisphere by region) interaction was observed. Non-verbal memory impairment was observed in the right and left microsmic subgroups. Verbal memory deficits were demonstrated in patients with left nostril microsmia. These results indicate that unirhinal olfactory performance may provide a meaningful manner by which to subtype patients with schizophrenia. Moreover, the data suggest that olfactory deficits in patients with schizophrenia are associated with dysfunction of temporal lobe, rather than frontal lobe abnormalities. The data are consistent with reports linking the right temporal lobe integrity to adequate olfactory processing.
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PMID:Unirhinal olfactory identification deficits in young male patients with schizophrenia and related disorders: association with impaired memory function. 1207 70

Previous research has found frontal lobe involvement in memory impairment in schizophrenia. In the present study, proton magnetic resonance spectroscopy was performed in 13 young patients with schizophrenia and 13 normal control subjects. Spectra were obtained from a voxel of 2 x 2 x 1.5 cm(3) in the bilateral inferior frontal gyrus and thalamus. Subjects were given a verbal learning task and stimulus category repetition (SCR) was calculated from the performance of the task. Significantly reduced N-acetylaspartate (NAA)/choline-containing compounds ratios were found in the left inferior frontal cortex of patients compared with controls. The total number of words recalled by patients was significantly lower than that recalled by controls. In all subjects, SCR scores were positively correlated with NAA/phosphocreatine ratios of the left inferior frontal cortex, which showed a trend towards a decrease in patients. These results support the notion of metabolic abnormalities in the left inferior frontal region related to verbal memory deficits in patients with schizophrenia.
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PMID:Proton magnetic resonance spectroscopy of the inferior frontal gyrus and thalamus and its relationship to verbal learning task performance in patients with schizophrenia: a preliminary report. 1219 38

Memory deficits are frequently observed in schizophrenia but their intrinsic characteristics have not been clarified. We studied remote memory in a group of 20 schizophrenics and 20 healthy age and education matched controls using a newly devised public event questionnaire (PEQ) that employs a free recall, progressive cueing and recognition protocol and requires dating of events. Results indicate that patients with chronic schizophrenia perform significantly more poorly on the PEQ than a group of age and education matched controls both in terms of content and dating of events. The number of events recalled does not improve with progressive cuing or recognition. No distinctive pattern was observed in their temporal gradient. There was no significant difference in content scores for pre- and post-onset events in the schizophrenics. These findings indicate that remote memory deficits in chronic schizophrenics arise from deficient encoding rather than from a retrieval deficit secondary to executive dysfunction.
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PMID:Memory and dating of past events in schizophrenia. 1224 Jul 51

Nicotine has been shown in a variety of studies to improve memory performance. The cognitive effects of nicotine are particularly important with regard to schizophrenia. In the current studies nicotine interactions with three different antipsychotic drugs, haloperidol, clozapine and risperidone, were assessed with regard to memory function. Female Sprague-Dawley rats were trained on the radial-arm maze to asymptotic levels of choice accuracy. They were then administered nicotine alone or in combination with haloperidol, clozapine or risperidone. Acute haloperidol (0.04 mg/kg) did not by itself affect memory performance. Co-administration of haloperidol with nicotine, however, decreased memory performance compared with nicotine administration in isolation. Acute clozapine (1.25 and 2.5 mg/kg) caused a significant memory impairment, an effect reversed by acute nicotine co-treatment. Risperidone (0.05 mg/kg), like haloperidol, did not by itself affect memory performance. Risperidone co-administration with nicotine, however, did significantly attenuate the improvement caused by nicotine administration in isolation. The similar interaction of haloperidol and risperidone with nicotine may be due to their common action of blocking D(2) receptors, a mechanism of action not shared by clozapine. In contrast to the interaction of nicotine with haloperidol or risperidone, nicotine effectively reversed clozapine-induced memory impairment. These studies demonstrate interactions between nicotine and antipsychotic drugs in terms of memory, which may have important impacts on the treatment of schizophrenia.
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PMID:Nicotine interactions with haloperidol, clozapine and risperidone and working memory function in rats. 1237 90

Nicotinic receptor systems are involved in a wide variety of behavioral functions including cognitive function. Nicotinic medications may provide beneficial treatment for cognitive dysfunction such as Alzheimer's disease, schizophrenia, and attention deficit hyperactivity disorder (ADHD). Nicotine has been shown to improve attentional performance in all of these disorders. Better efficacy with fewer side effects might be achieved with novel nicotinic ligands selective for particular nicotinic subtypes. To develop these novel selective nicotinic ligands it is important to use animal models to determine the critical neurobehavioral bases for nicotinic involvement in cognitive function. Nicotine-induced cognitive improvement in rats is most consistently seen in working memory tasks. We have found that both acute and chronic nicotine administration significantly improves working memory performance of rats in the radial-arm maze. The pharmacologic and anatomic mechanisms for this effect have been examined in our laboratory in a series of local drug infusion studies. Both alpha 4 beta 2 and alpha 7 nicotinic receptors in the ventral hippocampus and basolateral amygdala are involved in working memory function. Working memory impairments were caused by local infusion of either alpha 4 beta 2 or alpha 7 antagonists. Ventral hippocampal alpha 4 beta 2 blockade-induced working memory deficits are reversed by chronic systemic nicotine treatment, while ventral hippocampal alpha 7 blockade-induced working memory deficits were not found to be reversed by the same nicotine regimen. Interestingly, alpha 4 beta 2 and alpha 7 induced deficits were not found to be additive in either the ventral hippocampus or the basolateral amygdala. In fact, in the amygdala, alpha 7 antagonist cotreatment actually reversed the working memory impairment caused by alpha 4 beta 2 antagonist administration. These studies of the neural nicotinic mechanisms underlying cognitive function are key for opening avenues for development of safe and effective nicotinic treatments for cognitive dysfunction.
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PMID:Nicotinic receptor subtypes and cognitive function. 1243 26

Evidence is presented that verbal memory impairment distinguishes a subgroup of patients with schizophrenia who also differ in symptom profile and illness adjustment. On the basis of the California Verbal Learning Test (CVLT), a sample of patients was partitioned into memory-impaired (n=16) and memory-unimpaired groups (n=16). Groups were matched for age, sex, IQ, and anti-psychotic medication. These groups were then compared using the Brief Psychiatric Rating Scale (BPRS) and the Sickness Impact Profile (SIP). Results indicate that memory-impaired schizophrenia patients experience significantly more positive symptoms and a poorer quality of life than their memory-unimpaired counterparts. This finding supports the idea that neurocognitive measures are a valuable way of organizing the heterogeneous disease states of schizophrenia.
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PMID:Schizophrenia and memory impairment: evidence for a neurocognitive subtype. 1246 49

Some psychotropic medications frequently prescribed in schizophrenia, especially agents that contain anticholinergic properties, have adverse effects on learning and memory. Given the impact of memory on both functional and symptomatic outcome in schizophrenia, it is important to determine if patients suffer from medication-related memory impairment. This study provides a statistical methodology for identifying medication-related changes in memory functioning. Reliable change estimates were determined for Rey Auditory Verbal Learning Test performance in 38 inpatients with schizophrenia. When an 80% confidence criterion was applied, improvement or decline of 12 words in the total score (sum score: Trials 1-5) cannot be attributed to measurement error. These findings should help clinicians better understand cognitive side effects and facilitate decision making regarding changes to individual patient's psychopharmacotherapy.
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PMID:Reliable change indexes for memory performance in schizophrenia as a means to determine drug-induced cognitive decline. 1278 86

Phencyclidine (PCP) is an N-methyl-D-aspartate (NMDA) glutamate receptor channel noncompetitive antagonist that produces some of the symptoms of schizophrenia, including delusions, hallucinations, and negative symptoms as well as cognitive impairment. Thus, administration of PCP to rodents and nonhuman primates has been suggested to provide a potential animal model for schizophrenia. There have been some reports that 7-14 days of PCP administration can bring about enduring impairments in working memory in rodents but not all studies have been consistent in this regard. The present study determined whether repeated PCP administration impaired spatial performance in rats or mice trained to make minimal errors in an eight-arm radial maze task with a delay. Male Sprague-Dawley rats and C57BL/6J mice received 14 daily injection of vehicle or PCP (10 mg/kg, s.c.) followed by a withdrawal period of 1 week. The number of arm reentry errors and the distance traveled to complete the task were not significantly different between PCP-treated and vehicle-treated rats on 2, 8, and 14 days of PCP administration or 8 days following withdrawal of PCP. Mice treated with PCP for up to 2 weeks also had no significant differences in the number of arm reentry errors, travel distances, the numbers of visits to different arms during the first eight choices, or latencies to take all eight pellets compared to the vehicle-treated group. Thus, the present study failed to demonstrate that repeated administration of PCP to rats or mice produces enduring memory impairment. Factors potentially contributing to the discrepancies between various studies are discussed.
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PMID:Effect of repeated administration of phencyclidine on spatial performance in an eight-arm radial maze with delay in rats and mice. 1287 24

Long-term memory impairment is often found in schizophrenia. The question remains whether this is caused by other cognitive deficits. One hundred eighteen first-episode patients were compared with 45 control participants on several memory tasks. The role of processing speed and central executive functions on memory performance was examined with regression analysis for all participants and for patients separately. Deficits were found in general verbal learning performance and retrieval in episodic memory and semantic memory. Processing speed reduced disease-related variance in all memory variables. Coordination, organization of information, and speed of processing were the best predictors for long-term memory deficits in patients. The amount of explained variance, however, is small, especially in general verbal learning performance.
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PMID:Long-term memory deficits in schizophrenia: primary or secondary dysfunction? 1459 67

Item recognition memory judgment can be based on two processes: item familiarity and/or the conscious recollection of the initial event. On the other hand, associative recognition relies preferably on conscious recollection. Since evidence points to a specific deficit of conscious recollection in schizophrenia, these patients could show greater impairment during associative recognition tasks relative to item recognition tasks. A meta-analysis of 23 studies of recognition memory in schizophrenia was conducted to test this hypothesis. The impairment is indeed 20% greater (p=0.04) for associative recognition relative to item recognition. This study supports the hypothesis of a specific conscious recollection deficit underlying episodic memory impairment in schizophrenia.
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PMID:Is associative recognition more impaired than item recognition memory in Schizophrenia? A meta-analysis. 1460 30


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