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)

Normal pressure hydrocephalus (NPH) may suggest its presence by behavioral symptoms. Initally, the symptoms often manifest themselves as depression with marked psychomotor retardation. Older patients without a prior psychiatric history who have soft, nonlocalizing neurological signs and fluctuating cognitive and memory deficits in association with prominent affective and/or psychotic symptomatology of recent onset, such as the case reported here, should raise the clinician's index of suspicion. In such cases, the Halstead-Reitan neuropsychological battery may be helpful in differentiating an underlying dementia from a primary psychological dysfunction. When the presence of a dementing process is suspected, etiological diagnosis should be vigorously pursued with a CAT scan and, as indicated on clinical grounds, confirmatory and further delimiting studies such as pneumoencephalography, ventriculography, RISA scanning, electroencephalography, constant-infusion manometric testing, and/or angiography. Treatment of NPH includes one of several forms of shunting procedures and appropriate neuroleptic therapy for behavioral symptoms. Althoug there is a substantial risk (40 to 50 percent)ioral symptoms. Although there is a substantial risk (40 to 50 per cent) of shunt-related complications, as many as 60 per cent of operated patients will show objective imprvement, making the diagnosis of and referral for appropriate surgical treatment of NPH an important challenge for the psychiatrist.
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PMID:Psychiatric and behavioral manifestations of normal pressure hydrocephalus. A case report and brief review. 83 Aug 2

The prevalence of depression was examined in 54 patients recruited by speech pathologists and separated into four groups according to aphasia type (Broca's vs Wernicke's) and the duration of illness (less than six months vs more than six months). Evaluation of depression was made through questionnaires, completed by the spouse or speech pathologist, and patient interviews. The four groups were similar in demographical variables, in severity of aphasia and in lesion size (from CAT scan analyses). The prevalence of depression for the total sample was low (15%). Univariate analyses (ANOVA) did not show significant differences between the groups on the depression scales. The severity of depression was not correlated with lesion size or location. It was concluded that Wernicke's aphasics do not experience depression less often nor less severely than Broca's aphasics and that the incidence of depression in aphasia is not high. These results are in contrast with those obtained in earlier studies. Reasons for the discrepancies between this and other studies are discussed.
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PMID:The relationship of depression to symptomatology and lesion site in aphasic patients. 174 34

The case is described of a 43 year old woman with spasmophilic syndrome. For 12 years she had suffered from fainting fits, marked morning asthenia, anxiety, depression, widespread arthromyalgia, blood pressure fluctuations, precordial pains, paresthesia and painful nocturnal cramp. This clinical picture appeared in a subject with a double left kidney and stones in the supernumerary ureter, enlargement of the pancreatic head and tail revealed by a CAT scan and an earlier cholecystectomy. Given the multiplicity of symptoms diagnosis was necessarily by a process of elimination. The data providing grounds for optimism were a positive Chvostek's sign, stable calcium phosphorus profiles, a reduction in ionised calcium and favourable eletromyographic readings.
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PMID:[A case of spasmophilic syndrome]. 360 Nov 38

The method of clinico-pathological correlation for drawing inferences about the localization of particular cerebral functions has a long history of use, and well established theoretical limitations. Release phenomena, loss of excitatory drive, as well as non-specific tissue responses to injury may all have a bearing on observed behavioral change. Nevertheless, the consistent observation that severity of depression in stroke patients is greater for left hemispheric strokes, and greater for left frontal versus left occipital strokes is of considerable interest. Site of lesion appears to have greater explanatory power for this emotional symptom than the obvious psychological explanations in terms of loss of self-esteem and loss of function. Depression is greater for strokes in general than would be expected for equivalent loss of motor function with orthopedic etiology. Loss of cognitive function likewise is a poorer guide to severity of depression than site of lesion. On the other hand, accuracy of lesion assessment using present static anatomical methods (CAT scan), and reliability and validity of the psychopathological examination present methodological difficulties which are discussed. As newer brain imaging techniques that are sensitive to function are developed, this line of enquiry holds considerable promise for furthering our understanding of the anatomy and physiology of emotion.
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PMID:Cerebral localization of emotion based on clinical-neuropathological correlations: methodological issues. 387 61

Using [18F]fluorodeoxyglucose and positron emission tomography (PET), the authors examined the regional brain glucose metabolism of six patients with chronic schizophrenia, six patients with chronic depression, and 12 normal control subjects. Three schizophrenic and four depressive patients had CAT scans that showed enlarged ventricles (ventricle-brain ratios higher than 9.0) and widened sylvian fissures. The PET scans of the schizophrenic and depressed patients did not differ significantly from those of the age-matched controls, and a previously reported metabolic "hypofrontality" was not confirmed. The patients with enlarged ventricles and widened sylvian fissures tended to have lower global metabolism.
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PMID:Comparison of PET measurement of local brain glucose metabolism and CAT measurement of brain atrophy in chronic schizophrenia and depression. 394 50

Data are presented on 24 patients with epilepsy and psychosis whose clinical presentation was rated using the Present State Examination (PSE). Seventeen had complex partial seizures and a diagnosis of temporal lobe epilepsy, seven had generalised epilepsy. An association between a CATEGO category of nuclear schizophrenia (NS) and a lesion of the left side was noted. No clear link between depressive symptoms and a right-sided focus was discovered. Affective disorders were noted in both groups of epileptic patients, although paranoid psychoses were commoner in the temporal lobe group. There was also a tendency for the latter to have more delusions of persecution, ideas of reference, and special features of depression. The group rated as NS appear less likely to show evidence of intellectual deterioration than the other psychotic patients; in addition, the interval between the onset of their epilepsy and the onset of their psychosis is shorter. Radiological assessment by CAT reveals few differences between groups, but the psychotic samples do show higher than expected values on a number of variables, in particular the bilateral septum-caudate distance and the size of the third and fourth ventricle.
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PMID:Epileptic psychosis: an evaluation of PSE profiles. 397 33

Thirty left-handed patients hospitalized for stroke were examined for mood disorders. Patients with left hemisphere lesions and nondominant hand impairments had significantly higher depression scores and more depressive diagnoses than patients with right hemisphere lesions and dominant hand impairments. Major depression was strongly associated with left anterior brain injury, and depression severity was significantly correlated with proximity of the lesion on CAT scan to the left frontal pole. These findings are almost identical to previously reported results from right-handed patients and suggest that cerebral lateralization of poststroke mood disorders may be independent of cerebral motor dominance and language dominance.
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PMID:Mood disorders in left-handed stroke patients. 407 5

An initial event in gram-negative bacteremia is activation of the complement cascade with production of C5a. C5a, in turn, acts as a chemotactic stimulus for leukocytic aggregation and, in conjunction with bacterial products, stimulates the release of oxygen free radicals from leukocytes. We have hypothesized that these oxygen free radicals (.O2-, superoxide anion; .OH, hydroxyl radical; H2O2, hydrogen peroxide) contribute to the characteristic myocardial dysfunction of endotoxin shock, Isolated canine cardiac sarcoplasmic reticulum (SR) was used as a subcellular determinant of mechanical function. SR was incubated for 20 min at 37 degrees C in the presence of phorbol myristate acetate activated leukocytes (A-L) and calcium uptake and Ca2+-adenosine triphosphatase (ATPase) activities were measured. Activated leukocytes significantly depressed SR Ca2+ uptake rates (C = 1.12 +/- 0.05 mumol CA2+/mg-min; A-L = 0.73 +/- 0.05). The addition of catalase (CAT; 10 micrograms/ml) or superoxide dismutase (SOD: 10 micrograms/ml) plus CAT reversed the inhibition of SR Ca2+ uptake. SOD further depressed SR Ca2+ uptake (+SOD = 0.55 +/0 0.04 mumol Ca2+/mg-min). Mannitol had no effect. SR ATPase activity was inhibited with A-L (C = 1.41 +/- 0.04 mumol Pi/mg-min; A-L = 0.84 +/- 0.09). Neither mannitol, nor SOD nor CAT alone had any effect on the depression of SR ATPase activity. SOD plus CAT reversed the ATPase depression induced by A-L. It is concluded that phorbol myristate acetate activated leukocytes via free radical-mediated mechanisms can directly affect function and activity of the excitation-contraction coupling system of cardiac muscle. Free radical scavengers identified hydrogen peroxide as a major mediator of depressed Ca2+ uptake rates. In conjunction with the superoxide anion, hydrogen peroxide contributes to the depressed ATPase activity.
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PMID:Interaction of oxygen free radicals and cardiac sarcoplasmic reticulum: proposed role in the pathogenesis of endotoxin shock. 685 Oct 3

Production of oxygen-free radicals has been proposed as one pathophysiologic mechanism for postburn cardiac contractile dysfunction in adults. To examine this hypothesis in young subjects, we studied the cardiac effects of polyethylene glycol-superoxide dismutase (PEG-SOD) and PEG-catalase (PEG-CAT), each given as 20 U/g of body weight with fluid resuscitation (Parkland formula), after a third-degree burn constituting 33% of the total body surface area in young (6- to 7-day old) guinea pigs (group 3, n = 12). Fluid-treated burns without scavenger therapy (group 2, n = 15) and sham burn controls (group 1, n = 15) were included. Animals were killed 24 hours postburn, and hearts were studied in vitro (Langendorff). Compared with sham burn controls, fluid-treated burns (group 2) had significant cardiac dysfunction as indicated by a lower peak systolic left ventricular (LV) pressure (LVP: 67 +/- 2 vs. 57 +/- 4 mm Hg, p = 0.01, mean +/- SEM), maximal rate of LV pressure development (+dP/dt max: 1169 +/- 45 vs. 988 +/- 45 mm Hg/second, p = 0.01), and fall (-dP/dt max: 1109 +/- 45 vs. 919 +/- 49 mm Hg/second, p = 0.01). In addition, LV function curves calculated for group 2 were shifted downward and to the right of those calculated for sham burn controls in the direction of contractile depression, p = 0.01. PEG-SOD/PEG-CAT treatment in burns did not significantly improve LVP (60 +/- 5 mm Hg), but scavenger therapy improved +/-dP/dt max values (1112 +/- 74 and 988 +/- 98 mm Hg/second, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of toxic oxygen metabolites in a young model of thermal injury. 747 25

Through expression of a glucocorticoid receptor (GR) antisense RNA in brain, we have produced transgenic mice with an hyperactive hypothalamic-pituitary-adrenocortical (HPA) system similar to that seen in depressed patients. This model supports the hypothesis that disturbed corticosteroid receptor regulation could be the primary factor responsible for both the CRH/AVP hyperdrive that leads to increased activity of the HPA system, and the premature escape from the cortisol suppressant action of dexamethasone seen in affective disorders. Although normalisation of the hyperactive HPA system occurs during successful antidepressant therapy of depressive illness, these improvements do not correlate with changes in monoaminergic neurotransmitter systems, suggesting that unknown mechanisms of action may be operative. Work from my laboratory was the first to show that different types of antidepressants increased glucocorticoid receptor (GR) mRNA. We found increased GR mRNA levels irrespective of the preferential inhibitory action of antidepressant on the monoamine neurotransmitter re-uptake and showed increased GR gene transcription in antidepressant-treated mouse fibroblast cells that do not possess monoamine re-uptake mechanisms. We measured changes in glucocorticoid response in cells transfected with a glucocorticoid-sensitive reporter plasmid (MMTV-CAT) and observed increased glucocorticoid-stimulated CAT activity when the cells were treated with antidepressant. A different chimaeric gene construct consisting of a fragment of the GR gene promoter region fused to the CAT gene allowed more direct measurement of antidepressant action and increased CAT activity was also seen when cells transfected with this construct were treated with antidepressant. Finally, GR mRNA concentration and glucocorticoid binding activity were increased in brain tissues of animals chronically treated with antidepressant. The time course of antidepressant actions on corticosteroid receptors coincides with their long-term actions on HPA system activity and follows closely that of clinical improvement of depression. This suggests that antidepressant-induced changes in brain corticosteroid receptors may underlie the observed simultaneous decrease in circulating ACTH and corticosterone levels and the decreased adrenal size. Some of these effects may be mediated through CRH since, in antidepressant-treated transgenic mice hypothalamic CRH mRNA levels were decreased. From this work we have formulated the hypothesis that a primary action of antidepressants could be the stimulation of corticosteroid receptor gene expression that renders the HPA system more susceptible to feedback inhibition by cortisol. The resultant decrease in HPA system activity could induce secondary changes in glucocorticoid-sensitive gene expression and lead to redressment of neurotransmitter imbalance. This work opens up a completely new insight into antidepressant drug action and suggests a line of approach to the development of new drugs by focusing on this action.
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PMID:Modulation of glucocorticoid receptor gene expression by antidepressant drugs. 885 29


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