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)

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

Recent-onset noncompaction of the myocardium is a rare but serious entity with uncertain prognosis. Cerebral infarction is among the forms of presentation, and pregnancy and hypercoagulability increase risk. We report the case of a pregnant woman brought to the emergency department with ischemic cerebral infarction. Investigation demonstrated the cause to be cardiac embolism, and noncompaction of the myocardium was diagnosed. She was stabilized and a few days later underwent elective cesarean section under general anesthesia. Surgery and postoperative recovery were uneventful, and she was transferred for rehabilitation. Myocardial injury and progression to cerebrovascular accident must be prevented in such cases; the patient must be stabilized and antiplatelet and/or anticoagulant therapy initiated before surgery. Hemodynamic stability must be maintained throughout the perioperative period and neonatal depression avoided after delivery. Various approaches are available to be adapted to the patient's situation.
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PMID:[Perioperative treatment of a pregnant woman with recent cerebral infarction secondary to noncompaction cardiomyopathy]. 1730 82

In the light of accumulating evidence for the occurrence of spontaneous cortical spreading depression and peri-infarct depolarizations in the human brain injured by trauma or aneurysmal subarachnoid haemorrhage, we used DC electrode recording and laser speckle imaging to study the relationship between depolarization events and perfusion in the ischaemic, gyrencephalic brain. In 14 adult male cats anaesthetized with chloralose, one cerebral hemisphere was exposed and the middle cerebral artery occluded. Surface cortical perfusion in core and penumbral territories was imaged semiquantitatively at intervals of 13 s for 4 h. Cortical surface DC potential was recorded. Time interval between changes in DC potential and in perfusion was examined, and this comparison was repeated using microelectrodes for DC potential in five similar experiments in a second laboratory. Mean pre-occlusion perfusion was 11707 +/- 4581 units (equivalent to CBF (cerebral blood flow) approximately 40.5 +/- SD 14.4 ml/100 g/min), and fell on occlusion to 5318 +/- 2916 (CBF approximately 17.1 +/- 8.3), 5291 +/- 3407 (CBF approximately 17.0 +/- 10.1), and 6711 +/- 3271 (CBF approximately 22.2 +/- 9.6), quickly recovering to 8704 +/- 4581 (CBF approximately 29.5 +/- 14.4), 9741 +/- 4499 (CBF approximately 33.3 +/- 14.1) and 10 314 +/- 3762 (CBF approximately 35.4 +/- 11.4) on the core, intermediate and outer penumbral gyri, respectively. Mean perfusion later fell secondarily on core and intermediate gyri but, overall, was preserved on the outer (upper level of perfusion) gyrus during the period of observation. Pattern and severity of transient changes in perfusion associated with depolarization events varied with gyral location; falls in perfusion were sometimes profound and irreversible, and followed rather than preceded depolarization. In this model of occlusive stroke, reductions in perfusion linked to peri-infarct depolarization events contribute to secondary deterioration in penumbral areas. The findings suggest that such events play a central rather than a subsidiary role in cerebral infarction in the gyrencephalic brain.
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PMID:Peri-infarct depolarizations lead to loss of perfusion in ischaemic gyrencephalic cerebral cortex. 1743 18

Vertigo is one of the most common reasons for a patient to consult the general practitioner, and in the elderly in particular the underlying cause may be varied. Dizziness is not infrequently a side effect of medication, or may be associated with depression. Other possible causes include orthostatic dysregulation, hyperventilation, heart disease, equilibrium disorders, visual problems, paroxysmal positioning vertigo,TIA, cerebral infarction or the presence of a tumor.
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PMID:[Vertigo in the elderly]. 1761 64

Protopine, an isoquinoline alkaloidis, is known to produce many effects such as vasodilation, down-regulation of glutamate levels in brain and decrease of intracellular calcium. However, so far there is no report on the effect of protopine in cerebral ischaemia. In this study, the effect of protopine on the focal cerebral ischaemia was investigated in rats. Male Sprague-Dawley rats were divided into five groups: sham-operated group, vehicle-treated group and three doses of protopine-treated groups (0.98, 1.96 and 3.92 mg/kg). Protopine was intraperitoneally administered to rats once daily for 3 days prior to the ischaemia and 0.9% normal saline to rats in the vehicle-treated group in the same pattern. Rats in the sham-operated group were given 0.9% normal saline without the ischaemia. The focal cerebral ischaemia was induced by the middle cerebral artery occlusion for 24 hr via the intraluminal filament technique. The results showed that pre-treatment with protopine reduced the cerebral infarction ratio and serum lactate dehydrogenase activity, and improved the ischaemia-induced neurological deficit score and histological changes of brain in a dose-dependent manner. The further studies demonstrated that protopine increased superoxide dismutase activity in serum, and decreased total calcium and terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL)-positive cells in the ischaemic brain tissue in the middle cerebral artery occlusion rats. The results indicate that protopine is able to produce an effective protection on the injury caused by the focal cerebral ischaemia in rats possibly through the multiple effects of calcium antagonism, antioxidation and depression of cell apoptosis.
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PMID:Protective effect of protopine on the focal cerebral ischaemic injury in rats. 1765 7

The concept of vascular depression includes cases of late- onset depression, with cerebral infarction observed in imaging modalities and cardiovascular risk factors, with cognitive disabilities and poor response to antidepressant drugs. A case of a 71 year-old woman with no psychiatric background and with vascular risk factors who was re-admitted to a psychiatric hospitalization unit for melancholic depression with psychotic symptoms is presented. The magnetic resonance imaging showed a subcortical lacunar lesion and mild leukoaraiosis lesions and the neuropsychological examinations showed mild cognitive impairments. In the previous admissions the symptoms were refractory to several psychopharmacology strategies, responding only to electroconvulsive therapy (ECT). In this admission she received ECT, with remission of the symptoms, and was included in an ECT maintenance program. The vascular depression concept would explain the special features and outcome of this case.
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PMID:Vascular depression with melancholic symptoms: response to electroconvulsive therapy. 1800 78

Several mechanisms are currently thought to contribute to migraine pathogenesis, including interictal neuronal hyperexcitability, cortical spreading depression underlying the symptom of aura, and trigeminal nerve activation at a peripheral and central level. However, these mechanistic concepts incompletely explain migraine susceptibility in individual patients and do not fully account for the well documented association between migraine and ischemic cerebrovascular disease, including increased risk of both clinical stroke and subclinical brain lesions in migraine patients. The circle of Willis is a major source of collateral blood flow supply in the human brain, and developmental morphologic variants of the circle of Willis are extremely frequent. Altered cerebral blood flow (CBF) has been demonstrated in regions supplied by variant circle of Willis vessels. Our central hypothesis is that circle of Willis anomalies correlate with alterations in cerebral hemodynamics and contribute to migraine susceptibility and ischemic complications of migraine. Dysregulation of CBF may allow relative ischemia to develop in the setting of increased metabolic demand related to neuronal hyperexcitability, may trigger cortical spreading depression, and may predispose individuals with migraine to ischemic lesions and stroke. Identification of structural alterations in the cerebral vasculature in migraine patients would have several important pathophysiological and clinical implications. First, it would provide a developmental mechanism for migraine susceptibility that may lead to further insights into genetic predisposition to migraine. Second, it would expand understanding of potential mechanisms underlying migraine aura and linking migraine with both clinical and subclinical cerebral infarction. Third, it could help to identify the subpopulation of patients at risk of progressive cerebral ischemia so as to target preventative therapies appropriately. Fourth, it would suggest a role for further diagnostic evaluation to determine migraine mechanism in individual patients, analogous to the current paradigm in ischemic stroke in which determination of stroke mechanism is critical to therapeutic decision-making.
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PMID:Migraine and circle of Willis anomalies. 1822 67

Paroxetine is often coadministered with low-dose aspirin to treat cerebral infarction patients with depression. In order to assess the ulcerogenic risk induced by the coadministration of these drugs, we examined their effects on gastric secretion using the pylorus ligation method and determined the prostaglandin E(2) (PGE(2)) content in the gastric mucosa using enzyme immunoassay (EIA). Paroxetine stimulated the gastric fluid secretion and acid output, dose-dependently, however, it had no effect on the PGE(2) content in the gastric mucosa. Furthermore, exogenous serotonin inhibited both the gastric fluid secretion and the acid output. The coadministration of low-dose aspirin and paroxetine significantly enhanced the gastric fluid secretion and acid output, thus resulting in gastric bleeding, but it hardly affected the PGE(2) content in the gastric mucosa. The stimulation of gastric secretion by the coadministration of low-dose aspirin and paroxetine is therefore considered to play an important role in the development of gastric injuries.
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PMID:The coadministration of paroxetine and low-dose aspirin synergistically enhances gastric ulcerogenic risk in rats. 1859 77

Cerebral infarction producing psychiatric disorders such as depression and mania is a recognized phenomenon. However, resolution of affective disorders following stroke has not been previously reported. We describe the case of a 53-year-old woman with a 25-year history of treatment-resistant bipolar II and panic disorders. At the age of 46, she experienced a subarachnoid hemorrhage with secondary vasospasm that resulted in a stroke. Shortly following the hemorrhage, the patient experienced a complete remission of both psychiatric illnesses that has been sustained for 7 years. Initial computed tomography (CT) and angiography studies revealed subarachnoid hemorrhage with intraventricular extension, communicating hydrocephalus, and aneurysms of the left posterior communicating artery and the right anterior cerebral artery. Following clipping of the left internal posterior communicating artery aneurysm, the patient developed vasospasm with further stroke symptoms. A subsequent CT scan showed a fully developed ischemic infarct in the left temporoparietal region that was confirmed by follow-up magnetic resonance imaging (MRI). We present a 7-year follow-up with complete psychiatric interview, chart review, and MRI. The present case demonstrates the importance of continued efforts to localize neural circuits involved in the pathogenesis and maintenance of affective disorders.
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PMID:Resolution of bipolar II and panic disorders following subarachnoid hemorrhage. 1933 49

According to ICD-10 International Statistical Classification of Diseases anxiety state is different combination of somatic and mental symptoms of anxiety of absence of real menace that is onset attack-like or permanently. Anxious disorder is observed in 5-10% of the population, twice more often at woman than at men. The lengthening of the postinsult period is observed more often in the structure of the patient with old cerebral infarction that is complicated with anxious disorder. Diagnostics, treatment and prevention of anxious disorder in the postinsult period require elaboration of new approaches by the doctors. It is announced that anxious disorder in the postinsult period at such patient may reach 60-70%. Researches have been held on the basis of the clinic "Medina" in Batumi. The main group consisted of 30 out-patients (14 women and 16 men) between 41 and 73 years old who experienced cerebral infarction of 3-18 months prescription. Patients with pancreatic diabetes and unstable accompanying somatic diseases were excluded. Computer or magnetic - resonant tomography of the brain was performed to all patients during insult in order to verify the diagnosis; the clinical-and-psychological and neurological check up was also performed using neurological scale NIH NINDS in order to identify severity of insult as well as using the scale "Renkin" to assess the degree of impairment of vital functions. Depression was assessed with the help of HDRS (Hamilton depression ration scale). The level and presence of anxiety were determined by the scale that assesses the level of reactive and personal - anxiety. The following initial data were received as a result of research from the patients of the comparing groups before treatment: an average age of patients was 55,1+/-1,9 years; prescription of cerebral infarction was 6,35+/-1,0 months; severity of cerebral infarction on scale NIH NINDS was 2,7+/-0,25 points; invalidation degree on "Renkin" scale was 1,95+/-0,25 points. Personal anxiety was 85,4+/-7,27 points according to self assessment scale, reactive anxiety equaled 86,3+/-7,1 points. Depression evidence in comparing groups turned out to be initially high and equaled 14,5+/-2,1 points. The study revealed cognitive functions according to MMSE at 4 men. Therefore, a long effecting social stress leads to development of depression. Unemployed people working under constant pressure, living in overpopulated areas are the most subject to stress as well as those whose mutual relation with associates are broken and who more often gets in disputed situations. The first condition in treatment of the anxious disorders is detailed knowledge of the patient and his understanding the essence of illness. The necessary information and the elementary receptions of treatment for overcoming anxiety and panic attacks are given by the doctor. Frequently, the relief comes only that the patient realizes that it not illness that is unknown and dangerous to a life, but curable anxious disorder. Whenever possible the doctor will advise a relevant method of psychotherapy which will help to cope with the problems caused by prolonged panic disorder.
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PMID:[Anxiety state in patients during postinsult period with old cerebral infarction]. 1957 14


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