Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty German cancer patients (56.9+/-12.7 years old) without brain metastasis underwent neurological PET. The acquired brain data were compared to the data of ten age and sex-matched controls (53.6+/-15. 7). Scores of Zung's Self-rating Depression Scale (SDS) obtained from 15 out of the 20 patients suggested they might be mildly depressed. Scores of Taylor's Manifest Anxiety Scale (MAS), used for additional psychological evaluation, were close to normal distribution. Hypometabolic areas in the German cancer patients were compared with those demonstrated in our previous study in Japanese cancer patients. Common findings in both studies were observed in the limbic structures, such as the anterior and posterior cingulate gyri, the basolateral frontal cortices, as well as in the basal ganglia (especially the caudate nucleus) and frontal cortex. These results are in accordance with many previous PET studies on major depression. The results show that the positron emission tomography and (18)F-fluoro-deoxyglucose ((18)FDG-PET) brain mapping results could be partially reproduced, and suggest that PET brain mapping of cancer patients has a potential clinical application to the field of psycho-oncology and cancer patient care.
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PMID:Reproducibility of PET brain mapping of cancer patients. 1076 53

Test-retest reliability of resting regional cerebral metabolic rate of glucose (rCMR) was examined in selected subcortical structures: the amygdala, hippocampus, thalamus, and anterior caudate nucleus. Findings from previous studies examining reliability of rCMR suggest that rCMR in small subcortical structures may be more variable than in larger cortical regions. We chose to study these subcortical regions because of their particular interest to our laboratory in its investigations of the neurocircuitry of emotion and depression. Twelve normal subjects (seven female, mean age = 32.42 years, range 21-48 years) underwent two FDG-PET scans separated by approximately 6 months (mean = 25 weeks, range 17-35 weeks). A region-of-interest approach with PET-MRI coregistration was used for analysis of rCMR reliability. Good test-retest reliability was found in the left amygdala, right and left hippocampus, right and left thalamus, and right and left anterior caudate nucleus. However, rCMR in the right amygdala did not show good test-retest reliability. The implications of these data and their import for studies that include a repeat-test design are considered.
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PMID:Six-month test-retest reliability of MRI-defined PET measures of regional cerebral glucose metabolic rate in selected subcortical structures. 1084 13

Neuropsychiatric systemic lupus erythematosus (SLE) is frequently associated with deficits in brain glucose metabolism, even if morphological imaging by magnetic resonance imaging (MRI) shows no abnormalities. In these patients it is unclear whether or not the changes of brain metabolism measured by F-18-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) may progress to lesions of cerebral structure. We describe a 20-year-old woman with SLE who presented with depression, headache and impairment of memory. Initially, a cranial MRI was negative, but FDG-PET revealed significant hypometabolism in the frontal and parieto-temporo-occipital regions on both sides as well as hypermetabolism in the nuclei caudati. Within two months the patient developed an acute confusional state, seizures, visual disturbances and cranial MRI became positive showing hyperintensities at the basal ganglia and the temporo-occipital regions. Focal cerebral symptoms responded to treatment with high dose corticosteroids and brain lesions in MRI disappeared. However, a second FDG-PET showed persistent hypometabolism at frontal regions in accordance with the persistence of subclinical depression. To our knowledge, this is the first SLE case report showing that functional brain lesions visualized by FDG-PET may be a risk factor for subsequent structural brain damage seen in MRI. Thus, FDG-PET may help to verify cerebral involvement of SLE earlier than MRI.
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PMID:Alterations of cerebral glucose metabolism indicate progress to severe morphological brain lesions in neuropsychiatric systemic lupus erythematosus. 1087 34

McLeod syndrome is a distinct form of neuroacanthocytosis. Its defining feature is the depression of erythrocyte Kell antigens. The underlying X chromosomal mutations cause a dysfunction of an erythrocyte membrane protein Kx. A choreatic movement disorder with caudate atrophy in CT and MRI has been reported in McLeod syndrome later in the course of the disease. Positron emission tomography with 18F-deoxyglucose (FDG) was performed in two unrelated affected men. In the older patient, progressive chorea was seen from the 5th decade. In the second patient there were no signs of a movement disorder at the age of 28. Positron emission tomography disclosed a reduction of the striatal FDG uptake in both patients, with accentuation in patient 1. Frontal lobe metabolism was not affected. Basal ganglia dysfunction with early impairment of striatal glucose metabolism thus seems obligatory for McLeod syndrome, as found in other forms of chorea with or without acanthocytosis.
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PMID:Reduction of striatal glucose metabolism in McLeod choreoacanthocytosis. 1125 78

This study sought to clarify the effects of bupropion SR on anterior paralimbic function in depressed patients by studying changes in the activation of these structures from waking to REM sleep both before and after treatment. Twelve depressed patients underwent concurrent EEG sleep studies and [18F]fluoro-2-deoxy-D-glucose ([18F]-FDG) positron emission tomography (PET) scans during waking and during their second REM period of sleep before and after treatment with bupropion SR. Nine subjects completed pre- and post-treatment waking PET studies. Five subjects completed pre- and post-treatment waking and REM sleep PET studies. Bupropion SR treatment did not suppress electrophysiologic measures of REM sleep, nor did it alter an indirect measure of global metabolism during either waking or REM sleep. Bupropion SR treatment reversed the previously observed deficit in anterior cingulate, medial prefrontal cortex and right anterior insula activation from waking to REM sleep. In secondary analyses, this effect was related to a reduction in waking relative metabolism in these structures following treatment in the absence of a significant effect on REM sleep relative metabolism. The implications of these findings for the relative importance of anterior paralimbic function in REM sleep in depression and for the differential effects of anti-depressant treatment on brain function during waking vs. REM sleep are discussed.
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PMID:Effects of bupropion SR on anterior paralimbic function during waking and REM sleep in depression: preliminary findings using. 1130 49

The purpose of this study is to examine the relationship between psychological factors, regional brain activity and natural killer cell activity (NKA). Eight patients with malignant diseases were studied by FDG-PET under a resting condition. NKA and degree of anxiety and depression were measured using Taylor's manifest anxiety scale (MAS) and Zung's self-rating depression scale (SDS). Linear correlation of NKA and psychological measures to the regional brain metabolism in cancer patients was examined using statistical parametric mapping (SPM). Positive linear correlation between NKA and regional metabolic rate ratios was identified in the visual association cortex, anterior cingulate gyrus (CG) and sensorimotor area, and negative correlation was identified in the inferolateral prefrontal cortex (ILPFC), prefrontal cortex (PFC), orbitofrontal cortex (OFC) and anterior temporal cortex. Positive linear correlation to the MAS score was identified in the visual association cortex, anterior CG, primary sensorimotor area and the posterior parietal cortex, and negative correlation was detected in the ILPFC, PFC, OFC and anterior temporal cortex. The NKA and MAS scores positively correlated with each other (p<0.001). The result might serve as supporting data for a hypothesis that psycho-immune interaction is also mediated by the cerebral cortex and limbic system.
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PMID:Relationship between trait anxiety, brain activity and natural killer cell activity in cancer patients: a preliminary PET study. 1174 66

Research on single and rapid transcranial magnetic stimulation (sTMS/rTMS) indicates an antidepressive efficacy of these methods. In our 4 week study of sTMS, 12 patients affected by severe non-psychotic major depression (DSM-III-R) were enrolled and put on standardized combined antidepressant medication with the serotonin re-uptake inhibitor citalopram, and the serotonin modulating drug, trazodone. They underwent sTMS in a specific method as an add-on therapy. Age, gender, illness and episode duration, episode number, Hamilton Rating Depression Scale-24 (HRDS), Mini-Mental State (MMS), drug levels assessed by HPLC, magnesium and thyroid stimulating hormone (TSH) were recorded. For each patient functional brain imaging was performed by (18)FDG and (99m)Tc HMPAO SPECT at the beginning of the study, as were EEG tracings which also were recorded at the end. Lorazepam was allowed as co-medication. Of the patients, 66.7 per cent (N=8) could be identified as sTMS responders. Possible predictors for sTMS response as add-on therapy may be duration, pattern of improvement in global and in specific single items of the HRDS, lorazepam dosage, functional involvement of basal ganglia and cortical temporal lobe and the initially lower mean frequency and lability of the alpha-activity of EEG. These variables possibly predict the clinical outcome of depressed patients treated by sTMS as an add-on therapy. Copyright 2000 John Wiley & Sons, Ltd.
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PMID:Clinical impacts of single transcranial magnetic stimulation (sTMS) as an add-on therapy in severely depressed patients under SSRI treatment. 1240 5

We describe the case of a patient who came to our attention because of a reversible depression of myocardial contractility, probably due to myocarditis. A positron emission tomography study showed, in correspondence to the malfunctioning segments, a decreased F18-2-fluoro-2-deoxyglucose (F18-FDG) uptake in the presence of a normal perfusion as assessed by means of N13-labeled ammonia uptake. This phenomenon, called "reverse mismatch", shows that viability is not always dependent on FDG uptake and that it could be associated with the recovery of myocardial contractility. Some interpretations of the association between a reversible dysfunction and a reduced myocardial glucose metabolism are presented. The central role of nitric oxide and of cyclic guanosine monophosphate is hypothesized to explain both the mechanical and metabolic abnormalities.
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PMID:Evidence of reverse mismatch with positron emission tomography imaging in a patient with reversible myocardial dysfunction. 1247 22

The pathology of Borderline personality disorder (BPD) is poorly understood and its biological basis remains largely unknown. One functional brain imaging study using [(18)F]Deoxyglucose-PET previously reported frontal and prefrontal hypometabolism. We studied brain metabolism at baseline in 12 medication-free female patients with BPD without current substance abuse or depression and 12 healthy female controls by [(18)F]Deoxyglucose-PET and statistical parametric mapping. We found significant frontal and prefrontal hypermetabolism in patients with BPD relative to controls as well as significant hypometabolism in the hippocampus and cuneus. This study demonstrated limbic and prefrontal dysfunction under resting conditions in patients with BPD by FDG-PET. Dysfunction in this network of brain regions, which has been implicated in the regulation of emotion, may underlie symptoms of BPD.
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PMID:Positron emission tomography in female patients with borderline personality disorder. 1284 64

Prefrontal hypoperfusion and decreased glucose uptake in the prefrontal cortex (PFC) are found in violent criminal offenders, murderers and aggressive psychiatric patients. These abnormalities may be independent of diagnosis and associated with impulsive-aggression as a personality trait. Impulsive-aggression is a clinical characteristic of borderline personality disorder (BPD) where it is associated with assaultive and suicidal behaviors. We conducted FDG-PET studies in 13 non-depressed, impulsive female subjects with BPD and 9 healthy controls to look for abnormalities in glucose metabolism in areas of the PFC associated with regulation of impulsive behavior. Statistical Parametric Mapping-99 (SPM99) was used to analyze the PET data with Hamilton depression scores as covariate. Significant reductions in FDG uptake in BPD subjects relative to healthy controls were found bilaterally in medial orbital frontal cortex, including Brodmann's areas 9, 10 and 11. There were no significant areas of increased uptake in BPD subjects compared to control subjects. Covarying for measures of impulsivity or impulsive-aggression rendered insignificant the differences between groups. Decreased glucose uptake in medial orbital frontal cortex may be associated with diminished regulation of impulsive behavior in BPD.
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PMID:Impulsivity and prefrontal hypometabolism in borderline personality disorder. 1292 3


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