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)

Suicide and suicide attempts occur at a significantly greater rate in schizophrenia than in the general population. Common estimates are that 10% of people with schizophrenia will eventually have a completed suicide, and that attempts are made at two to five times that rate. Demographically associated with suicidality in schizophrenia are being young, being early in the course of the illness, being male, coming from a high socioeconomic family background, having high intelligence, having high expectations, not being married, lacking social supports, having awareness of symptoms, and being recently discharged from the hospital. Also associated are reduced self-esteem, stigma, recent loss or stress, hopelessness, isolation, treatment non-compliance and substance abuse. Clinically, the most common correlates of suicidality in schizophrenia are depressive symptoms and the depressive syndrome, although severe psychotic and panic-like symptoms may contribute as well. This review specifically explores the issue of depression in schizophrenia, in relation to suicide, by organizing the differential diagnosis of this state and highlighting their potentially treatable or correctable causes. This differential diagnosis includes both acute and chronic disappointment reactions, the prodrome of an acute psychotic episode, neuroleptic induced akinesia and akathisia, the possibility of direct neuroleptic-induced depression, negative symptoms of schizophrenia, and the possible co-occurrence of an independent depressive diathesis. The potential beneficial roles of 'atypical' antipsychotic agents, including both clozapine and more novel agents, and adjunctive treatment with other psychopharmacological medications are considered, and the important roles of psychosocial factors and interventions are recognized.
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PMID:Suicide and schizophrenia. 1144 86

Idiopathic Parkinson's disease (IPD) is characterized by motor signs such as akinesia, rigidity, and often tremor at rest. In addition to these symptoms, depression is a common finding affecting 40% of patients with IPD. This study evaluates the effect of the selective serotonin reuptake inhibitor, citalopram, on motor and nonmotor symptoms of depressed and nondepressed patients with IPD. Forty-six nondemented patients with IPD (24 men, 22 women; mean age 64 +/- 5.3 years; mean +/- SD disease duration, 6.4 +/- 3.2 years; mean +/- SD Hoehn-Yahr stage, 2.8 +/- 1.2) were included in the study. Patients were divided in two subgroups: depressed (n = 18) and nondepressed (n = 28). Citalopram was added in an unblinded manner, starting with 10 mg/d, and, after a week, increased up to 20 mg/d in the depressed subgroup (n = 18) and in half of the nondepressed subgroup (n = 14). Parkinsonian and depressive symptoms were evaluated before and after 1 and 4 months of treatment. Statistical evaluation was made by analysis of variance for repeated measures. Citalopram did not worsen motor performance in IPD, but improved bradykinesia and finger taps after 1 month and 4 months of treatment both in patients with and without depression (p < 0.05 versus baseline). A clear improvement in mood was also observed in 15 of 16 patients with depression. Although case reports indicate that citalopram can potentially worsen the motor symptoms in patients with PD, to date this effect has not been confirmed. Many of the symptoms, typically associated with depression, can be observed in nondepressed patients with IPD, because signs thought to represent depression can be produced by Parkinson's disease. In this study, we observed that when combined with levodopa, citalopram induces an improvement of motor performance, in particular of subscores 23 and 31 of Unified Parkinson's Disease Rating Scale both in depressed and in nondepressed patients with IPD.
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PMID:The SSRI, citalopram, improves bradykinesia in patients with Parkinson's disease treated with L-dopa. 1185 92

Mental rotation (MR) performance may be used as an index of mental slowing or bradyphrenia, and may reflect, in particular, speed of motor preparation. MR was employed with a sample of both melancholic (n=8) and non-melancholic (n=9) unipolar depressed patients and healthy controls (n=10) to determine if motor slowing associated with depression might be reflected in slowed motor preparation (as reflected in slope of the MR function) independent of actual motor slowing (overall response time). Both melancholic and non-melancholic patients showed a generalised slowing relative to controls, perhaps reflecting bradykinesia and akinesia. This effect was significantly greater in the melancholic group than in the non-melancholic group. Relative to both the controls and the non-melancholic groups, the melancholic patients showed a progressive slowing with increasing angle of orientation indicating a specific slowing of MR. This deficit suggests a role of slowed motor planning in the psychomotor retardation of patients with melancholic depression.
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PMID:Mental rotation in unipolar major depression. 1193 28

Clonidine added to local anaesthetics prolongs the duration of anaesthesia and analgesia of peripheral, neuraxial and retrobulbar blocks. The present randomized blinded controlled study was conducted to evaluate the effect of the addition of clonidine to local anaesthetic mixture on the quality, onset time, duration of peribulbar block, perioperative analgesia and patients' comfort. The study comprised two groups of 12 patients each. Group A (control) patients received 7 ml of a mixture of 2% lignocaine and hyaluronidase with 1 ml normal saline, while group B (clonidine group) patients had clonidine 1 microg/kg added to the above mixture. Onset and duration of lid akinesia, globe anaesthesia and akinesia, time to first analgesic medication and total analgesic requirement were assessed. Patients were monitored for heart rate, blood pressure, sedation and respiratory depression. Addition of clonidine to local anaesthetic mixture resulted in a significant increase in duration of lid akinesia (85.4+/-25.6 vs 173.3+/-35.3 min, P<0.001), globe anaesthesia (63.2+/-6.9 vs 78.8+/-17.5 min, P=0.012) and globe akinesia (161.3+/-24.3 vs 201.2+/-45.7 min, P=0.016). The onset time and quality of block were similar in both the groups. No significant haemodynamic, respiratory or sedative effects were recorded. The perioperative pain scores and the analgesic requirements were significantly (P<0.01) lower in group B patients. We found that addition of clonidine 1 microg/kg to local anaesthetic mixture significantly increases the duration of anaesthesia and analgesia after peribulbar block.
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PMID:Effect of addition of clonidine to local anaesthetic mixture for peribulbar block. 1218 May 81

Changes in cognitive function and disturbances in behavior are commonly seen in parkinsonian patients and they are inherent features of the disease. Estimates on the prevalence of dementia in this disorder are quite variable, ranging from 15 to 25%. Advanced age, depression, severity of akinesia, and the presence of dopaminomimetic psychosis, are considered as risk factors in the development of cognitive deterioration within this patient population. Cognitive dysfunction may manifest as relatively circumscribed deficits or overt dementia. The finding of mild cognitive deficits is common in Parkinson's disease, such as reduced flexibility, psychomotor slowing, reduction in learning capacity and information retrieval, and disturbances in visuospatial tasks. The most prevalent cognitive disturbance is an impairment in visuospatial tasks, not necessarily related to the degree of motor disability. Dementia, when present early on in the course of the disease may suggest alternative diagnoses (Diffuse Lewy body dementia, Alzheimer's disease with extrapyramidal features, Fronto-temporal dementia, etc.), while in those cases in whom the dementing disorder develops at a later stage, it is assumed to be an integral part of the disease, albeit corresponding to variable pathogenetic mechanisms.
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PMID:[Dementia and cognitive impairment in Parkinson disease]. 1240 19

A 22-year-old woman presented with sudden onset of chest pain. Echocardiography showed a ruptured aneurysm of the noncoronary sinus of Valsalva in the right atrium. Slight ST segment depression was observed on initial electrocardiography (ECG). The patient was transferred to a tertiary care centre 10 h after the onset of symptoms. Surgery consisted of patch closure of the noncoronary sinus and tricuspid valve resuspension through the right atrium. Postoperatively, myocardial infarction (MI) was diagnosed based on a significant increase in cardiac enzymes and a new septal and apical akinesia on echocardiography. The etiology of MI in such a setting is multifactorial. Decreased coronary perfusion secondary to the severe aortic valve regurgitation and increased left ventricular end diastolic pressure, coupled with increased myocardial workload and delay before surgery may be implicated in the genesis of MI.
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PMID:Myocardial infarction in a young woman secondary to a rupture of a noncoronary sinus of Valsalva aneurysm without coronary artery disease. 1277 25

Parkinsonism is a clinical syndrome characterized by akinesia, muscular rigidity, and resting tremor. The most frequent cause of parkinsonism is Parkinson's disease (PD). Progressive loss of substantia nigra neurons together with the occurrence of Lewy bodies are considered essential neuropathological features of PD. Recent neuropathological studies suggest that nigral degeneration is only part of a more extended brain degeneration that starts in the medulla oblongata and then spreads to the mesencephalon and cerebral cortex. Correspondingly, the clinical symptoms occurring in PD go far beyond parkinsonism. Depending on the disease stage, autonomic dysfunction, olfactory disturbances, depression, and dementia are frequently encountered in PD. These neuropathological and clinical observations have major implications for future research in PD. In particular, the analysis of the properties that the neuronal cell types involved in PD have in common and that might make them susceptible to degeneration is essential.
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PMID:Parkinson's disease: clinical aspects. 1536 14

Nocturnal disturbances are common in Parkinson's disease (PD) patients, with almost 70% of these patients reporting nocturnal disturbances. The etiology of sleep disturbances in patients with PD is still controversial. They might be dependent on dopaminergic drugs, on disease progression, or on a combination of these two factors. Nocturnal disturbances can be categorized in four groups: 1) PD-related motor symptoms, including nocturnal akinesia, early-morning dystonia, painful cramps, tremor, and difficulty turning in bed; 2) treatment-related nocturnal disturbances; 3) psychiatric symptoms, including hallucinations, vivid dreams, depression, dementia, insomnia, psychosis, and panic attacks; 4) other sleep disorders, including insomnia, REM behavioral disorder (RBD), restless legs syndrome (RLS), periodic leg movements (PLMS), and excessive daytime sleepiness (EDS). Specific treatment options are supplied for every group. A global evaluation of nocturnal disturbances would provide clinicians with a valuable tool to establish an optimal regimen that could positively influence all nocturnal disturbance categories and thus improve PD management on. However, it is important to consider that management of some nocturnal disturbances in a group may worsen nocturnal symptoms of another group or may increase EDS. PD-related symptoms can be treated with long-acting DA agonists to obtain continuous DA receptor stimulation during the night. Both treatment-related nocturnal disturbances and psychiatric symptoms may be related to drug treatment, and therefore, in both cases, drug reduction or discontinuance should be considered. Some sleep disorders, such as RLS and PLMS, may be controlled by DA agents, and others, such as insomnia and EDS, may be improved by reducing dopaminergic stimulation.
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PMID:Treatment of nocturnal disturbances and excessive daytime sleepiness in Parkinson's disease. 1550 42

Depression, negative symptoms, and extrapyramidal signs (EPS) frequently occur together in schizophrenia. Their overlap is due partly to the lack of specificity of assessment instruments. However, to disentangle the three syndromes is clinically important as treatment of schizophrenia requires a differentiated approach. This study investigated the overlap between depression, emotional blunting as a core part of the negative syndrome, and akinesia as manifestation of EPS, using the Calgary Depression Rating Scale (CDSS), the Rating Scale for Emotional Blunting (SEB), and the akinesia score of the Simpson-Angus Scale (SAS) as the most specific assessment instruments presently available. We investigated 57 medicated schizophrenic patients before discharge from hospitalization. Mutual relationships were assessed with linear and partial correlations. Substantial linear associations emerged between SEB and SAS scores. The correlation between CDSS and SAS scores was significantly lower, but also different from zero. When SEB scores were statistically controlled, the association between CDSS and SAS scores dropped to nonsignificance; the correlation between SEB and SAS scores remained nearly unchanged when controlling for depression. The correlation between CDSS and SEB scores decreased to nonsignificance when controlling for SAS scores. Neither gender, age, illness duration, nor type of medication had an influence on the findings. High levels of akinesia were related to emotional blunting but not independently to depressive symptoms in medicated schizophrenic patients. Although the results cannot be assumed to be specific for schizophrenia, they corroborate the partial independence of depression and affective blunting in schizophrenia and the relationship of negative symptoms to EPS.
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PMID:Depression, emotional blunting, and akinesia in schizophrenia. Overlap and differentiation. 1560 62

The frequency, phenomenology, and risk factors of hallucinations and delusions were investigated in 64 consecutive inpatients with Parkinson's disease. Fifty patients were admitted to our hospital with symptoms related to Parkinson's disease: psychiatric problems 27 (psychosis 22; anxiety 2; depression 2; mania 1): motor symptoms, 20 (wearing-off 5; akinesia 4; freezing 4; postural instability 4; dyskinesia 2; tremor 2; dystonia 1), and sensory symptoms, 3. Fourteen patients were admitted with other medical problems (pneumonia 4; cerebral infarction 3; bone fracture 3; lumbago 2; seizure 1; cat bite 1). Totally 49 patients had psychiatric problems. Psychosis was present in 43 patients, dementia in 10, depression in 8, mania in 1, anxiety in 10, agitation in 6, stereotypy in 2, and hypersexuality in 2. Of the 43 patients with psychoses, 40 presented with visual hallucinations, 18 with auditory hallucinations, and 23 with delusions. To determine what the clinical correlates with the severity of psychosis were, we divided the patients into 3 groups: the severe group, 22 patients admitted because of psychotic symptoms; the mild group, 21 patients admitted because of problems other than psychosis but presenting psychotic symptoms; and the control group, 21 patients who had no psychotic symptoms. Incidences of auditory hallucinations and delusions were higher in the severe group as compared to the mild group. Patients in the severe group had higher Hoehn-Yahr stages, lower Mini-Mental State Examination scores, decreased H/M ratios of cardiac 123I-MIBG uptake, and lower frequencies of background activity on electroencephalograms. There were no differences in age at admission, age at onset of Parkinson's disease, duration of illness, amounts of levodopa and dopamine agonists received, Hamilton's depression rating scores, and brain MR findings, including atrophy and ischemic changes. Emergence of psychotic symptoms in parkinsonian patients appears to be clearly associated with impaired cognitive function. Therefore, it may be associated with the disease process itself. Terms such as dopaminomimetic or levodopa-induced psychosis may not be appropriate when describing psychosis in Parkinson's disease.
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PMID:[Psychoses in patients with Parkinson's disease; their frequency, phenomenology, and clinical correlates]. 1571 92


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