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)

An 18-year-old Morgan mare was presented to the Veterinary Medical Teaching Hospital, University of Illinois, with a 10-day history of watery diarrhea, depression, and dysphagia. On admission, the animal was severely dehydrated, depressed, and unable to swallow and had no clinical signs of diarrhea. The respiratory and heart rate and body temperature were within normal limits. Following fluid therapy, the mare developed severe watery diarrhea and continued to be depressed, incoordinated, and dysphagic. The animal died on the fourth day after admission and was sent to the Laboratories of Veterinary Diagnostic Medicine for necropsy. Gross postmortem findings were consistent with an acute cerebral infarction in the right cerebral hemisphere, an acute necrotizing typhlocolitis, multifocal petechial and ecchymotic hemorrhages, enlarged and congested pars intermedia of the pituitary gland, and marked bilateral adrenocortical hyperplasia with multifocal areas of necrosis and hemorrhage. Histologic evaluation of the affected brain demonstrated an area of coagulative necrosis of the gray matter, with hemorrhage, vasculitis, and thrombosis. There were many fungal hyphae 3.5-6.0 microm, pale basophilic, septate, and occasionally branching at 45 degrees present in the arterial walls and throughout the necrotic tissue. Immunohistochemical analysis revealed Aspergillus niger as the etiologic agent responsible for the mycotic vasculitis and infarction in the brain. Bacteria culture and immunohistochemical staining of the colon and cecum failed to demonstrate specific pathogens.
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PMID:Necrotizing mycotic vasculitis with cerebral infarction caused by Aspergillus niger in a horse with acute typholocolitis. 1042 Nov 5

1. We examined 156 patients 33 years after CO poisoning occurred at the Miike Mikawa Mine, Fukuoka, Japan. The subjects were classified according to age as follows: between 55 and 59 years (n = 14), 60 and 69 years (n = 62), 70 and 79 years (n = 60), and 80 and 87 years (n = 18). The mean age was 69.2 years old. Concerning the duration of coma that occurred soon after the accident, 64 remained comatose from 0 to 6 hours, 46 from 6 to 12 hours and 46 from 12 to 48 hours. 2. Subjective symptoms were observed in 96.8% of the patients. Among them, forgetfulness was noted in 89.7%, followed by irritability in 66.7%, headache in 59.6%, insomnia in 55.8%, limb pain in 46.8%, dull head feeling in 42.9% and dizziness in 36.5%. 3. Intellectual disturbances were observed in 68.6% of the patients, including impression disturbance in 58.3%, memory disturbance in 51.9%, calculation disturbance in 63.5%, thinking disturbance in 61.5% and disorientation in 14.1%. 4. Apathy and disorder of volition and interest which were found in 72.4% were included in personality change because all symptoms persisted for many years. Personality change was classified as follows: weakness of emotion and will (hypobulia) in 54.4%, infantilism in 35.2%, hyperactive, talkactive and lack of inhibition in 18.5%, lack of self-possession and unstable temper in 9.6%, depression in 15.3%, neurosis in 7.6% and schizophrenic state in 2.5%. Among these symptoms of personality change, weakness of emotion and will and infantilism were conspicuous among the patients who remained in a coma for more than 6 hours soon after the accident but showed no relationship with age. 5. Neurological symptoms that were found in 48.7% of the patients were classified as sensory disturbance in 25.6%, peripheral nerve symptoms in 16.0%, pyramidal symptoms in 14.1%, ataxia and cranial nerve symptoms in 7.1%, paroxysmal symptoms in 6.4% and focal symptoms in 4.5%, extrapyramidal symptoms in 21.8% (Parkinsonism in 4.5%, tremor in 10.9% and muscle rigidity in 16.0%) and vegetative symptoms in 37.2%. 6. At the time of investigation, 5 CO poisoning patients were classified as serious cases (3.2%), 20 as comparatively serious (12.8%) medium-degree cases, 28 as comparatively mild (17.9%) medium-degree cases, 37 as comparatively serious (23.7%) mild cases, 42 as comparatively mild (26.9%) mild cases, 24 (15.4%) as having symptoms which were not problematic, and 24 (15.4%) as having symptoms that markedly worsened due to complication. 7. A total of 138 (88.4%) cases had complications were classified as follows: 78 cases (50.0%) of hypertension, 62 cases (39.7%) of cerebral infarction, 24 cases (15.4%) of cardiac disturbance, 21 cases (13.5%) of diabetes mellitus, 14 cases (9.0%) of hepatic disturbance and six cases of silicosis (3.8%). 8. Cranial MRI was carried out for 129 cases (82.7%). Of the abnormal findings identified, cerebral atrophy accounted for 72.0% (93 cases), including moderate and severe cases in 47.2% (61 cases), pallidum lesion for 37.9% (49 cases), lacunar infarction (including cerebral infarction) for 52.7% (68 cases), and hippocampal atrophy for 18.6% (24 cases). Many cases of cerebral atrophy and hippocampal atrophy were observed in patients who remained in the initial coma for more than 12 hours and were 80 years of age or old. The cases of pallidum lesion were observed in patients who remained in the initial coma for more than 6 hours, and no relationship with age was found. The other findings, cerebral atrophy and lacunar infarction showed a slight relationship with age. 9. Among the moderate and serious cases of intellectual disturbance, cerebral atrophy constituted to 62.5%, lacunar infarction 68.7% and pallidum lesion 50.0%. Among the moderate and serious cases of personality change, cerebral atrophy constituted 78.5%, lacunar infarction 35.0% and pallidum lesion 50.0%. Moreover, among extrapyramidal symptoms, pallidum lesion constituted 58.6%, cerebral atrophy 55.1% and lacun
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PMID:[Long-term follow-up study on sequelae of carbon monoxide poisoning; serial investigation 33 years after poisoning]. 1050 96

If neurotoxicity of MDMA (ecstasy) is now well documented in animals, it is not the same in humans. MDMA intoxication puts the problem of its possible link with the serotonin syndrome and the neuroleptic malignant syndrome. Neuropathological consequences following MDMA intake have been reported, including hemorrhaging and cerebral infarction, cerebral venous sinus thrombosis, and acute inflammatory CNS disease. However, the physiopathology of these complications remains unclear. In the same way, there have been various reports that have attributed MDMA to precipitating the onset of a wide range of psychiatric disorders including sleep disorders, cognitive disorders, panic attacks, depression, flashbacks, psychosis and severe paranoia. Findings suggest that these psychiatric manifestations might be consequences of MDMA induced brain serotonin neurotoxic lesions. All these data are examined from a critical review of the literature.
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PMID:[Neuropsychiatric disorders induced by MDMA ("Ecstasy")]. 1066 3

A mail survey was conducted to elucidate the influential factors on heath-related quality of life (HRQOL) after cerebral vascular disease. Questionnaires for clinicians and their patients were mailed to 2,587 hospitals with more than 100 beds, which have at least one of the following departments: neurosurgery, neurology, psychiatry or rehabilitation. Each mailing contained a request to the clinician and questionnaires for 5 cases. 378 effective questionnaires could be collected, meaning the collection rate was 2.9%. The questions for the physicians concerned diagnosis (cerebral infarction or hemorrhage), duration of illness, activities of daily living(ADL), manifestation of paralysis and psychiatric symptoms and so forth. The questionnaire for the patients was composed of items from the EuroQol clinical version (EuroQol). Geriatric Depression Scale short form (GDS) and inquiries concerning family living with the patients, their housekeeping and so on. A visual analogue scale (VAS) concerning health state of the EuroQol was used as a measure of HRQOL. Coefficients of determination between VAS and other inquiries were calculated by regression analysis or ANOVA, revealing that "anxiety/depression", "GDS" and 16 other items were statistically significant on VAS (p < 0.05). General linear model (GLM) analysis using VAS as a criterion variable and these 18 items as predictor variables showed that "sleep disturbance" and GDS score were most influential on VAS according to the F value of the type 3 sum of squares. "Health state today compared to that during the past one year", "shopping as housekeeping", "ADL" and "pain/discomfort" also have some influence on VAS. In conclusion, sleep disturbance and depression had the most deleterious effect on HRQOL.
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PMID:[Influential factors on health-related quality of life after cerebral vascular disease]. 1103 29

Previous studies showed that bladder hyperactivity after cerebral infarction in Sprague-Dawley (SD) rats was mediated in part by D2 dopaminergic and NMDA glutamatergic mechanisms. In the present experiments, the interaction between dopaminergic and glutamatergic excitatory mechanisms in the control of bladder and external urethral sphincter (EUS) reflexes was investigated in urethane-anesthetized sham-operated (SO) and cerebral-infarcted (CI) SD rats. Occlusion of the left middle cerebral artery or a sham operation was performed under halothane anesthesia. Two hours after either of the two procedures, rats were anesthetized with urethane. Dizocilpine, an N-methyl-d-aspartate (NMDA) glutamatergic antagonist, was administered intravenously in doses of 0.3 or 3 mg/kg to CI rats and 3 mg/kg to SO rats. These doses completely inhibited bladder and EUS activity. The effects of apomorphine (a dopamine agonist with greater efficacy at D2 than D1 receptors) or quinpirole (a selective D2 dopamine receptor agonist) were examined on the dizocilpine-induced depression of bladder contractions and EUS EMG activity. Apomorphine did not antagonize the dizocilpine depression of EUS activity, but it did reestablish the micturition reflex after dizocilpine blockade and did increase the amplitude of bladder contractions and voided volume in a dose-dependent manner (0.0001-10 mg/kg, iv), in both CI rats and SO rats pretreated with dizocilpine. There were no differences between SO rats and CI rats in the apomorphine responses in rats pretreated with doses of 0.3 or 3 mg/kg dizocilpine. A larger dose of dizocilpine (10 mg/kg) did not affect the bladder contractions after apomorphine administration. Quinpirole (0.001-1 mg/kg, iv) also partially reversed the dizocilpine depression of bladder activity in SO and CI rats. These results indicate that NMDA glutamatergic and D2 dopaminergic mechanisms exert independent excitatory influences on bladder activity in both SO and CI rats. D2 dopamine receptor agonists can reverse the effect of NMDA receptor blockade on bladder activity but were ineffective in reversing the block of sphincter activity.
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PMID:Interaction between D2 dopaminergic and glutamatergic excitatory influences on lower urinary tract function in normal and cerebral-infarcted rats. 1131 67

Several studies confirm cognitive impairment and dementia to be increased after stroke in the elderly. Although not necessarily involving memory deficits, the frequency of cognitive impairments may occur in up to 30% of stroke survivors at 3 months. This impairment may be confounded by preexisting cognitive decline or dementia. By contrast, cognitive changes and dementia are widely recognized in familial forms of stroke, such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Several factors, including type of stroke, recurrent episodes, the site and laterality of the lesion(s), volume of cerebral infarction, medial temporal lobe atrophy, and coexistent neurodegenerative pathology predict the degree of impairment. Aphasia, diabetes mellitus, atrial fibrillation, and depression are listed among other biologic factors that further exacerbate cognition and affect long-term survival. There is no clear consensus whether genetic factors, such as the apolipoprotein E e4 allele or angiotensin converting enzyme gene polymorphisms, modify cognitive changes or stroke outcome. Although several neurotransmitter systems may be affected in post-stroke dementia, the amelioration of cholinergic function is a worthy target.
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PMID:Stroke and cognition. 1138

It has been reported that 20-65% of cerebral infarction patients suffers from depression. On the other hand, elderly-onset depression has more cerebro-vascular changes such as deep white matter lesion and periventricular hyperintensity on MRI than young-onset depression. These findings together leads new disease category 'vascular depression' (VD), meaning depression primarily caused by cerebral infarction. VD patients show less family history and symptomatic changes within a day than those with non-vascular depression. Though anti-depressants are effective on VD, they have higher incidence of side effect on VD than on non-vascular depression. Benzodiazepines and cerebral circulation and metabolism enhancers are also used in VD therapy. The prognosis of VD is worse than that of non-VD or cerebral infarction without depression.
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PMID:[Vascular depression]. 1151 62

Previously, we reported a relationship between silent cerebral infarction (SCI), as detected by magnetic resonance imaging (MRI), and late onset major depression. In the present study, we clarify the clinical features of the depressive phase of patients with major depression and SCI, and their response to antidepressant pharmacotherapy. Using clinical charts, we retrospectively examined patients with depression, who were first admitted for antidepressant pharmacotherapy. All patients were classified according to the MRI findings and the age on admission (older or younger than 50 years) into either the young SCI(-) group (n = 23), the elderly SCI(-) group (n = 27) or the elderly SCI(+) group (n = 20).The characteristics of the clinical features were evaluated at the time of admission, after 2 weeks of treatment and at the time of discharge using the Hamilton rating scale for depression (HAMD). These data were compared between each patient group. No differences in the clinical features, as evaluated by HAMD, were observed between the three groups at the time of admission. However, the mean length of treatment was significantly longer and the treatment response, as evaluated by the total HAMD score, was significantly worse in the elderly SCI(+) group than in the other two groups, when examined after 2 weeks of treatment and at the time of discharge. The elderly SCI(+) group demonstrated higher scores in feelings of guilt, suicide, retardation and hypochondriasis than the young SCI(-) group and the elderly SCI(-) group after two weeks of treatment, and higher scores in early insomnia, late insomnia, somatic anxiety and hypochondriasis at the time of discharge. Our findings suggest that while the presence of SCI does not affect the clinical features observed at the time of admission, it does affect the treatment response to antidepressant pharmacotherapy.
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PMID:Clinical features and treatment response of patients with major depression and silent cerebral infarction. 1170 17

In this study, we characterized cognitive functioning in patients with major depression and silent cerebral infarction (SCI), as detected by magnetic resonance imaging (MRI), after they had recovered from depression. Thirty-five patients with unipolar depression who experienced the onset of depression after the age of 50 underwent MRI and were classified as SCI(+) (n = 17) or SCI(-) (n = 18). The Wechsler Adult Intelligence Scale-Revised (WAIS-R) and the Uchida-Kraepelin psychodiagnostic test were administered after the patients had recovered from depression. In addition, the intelligence quotient (IQ) and mental speed of the patients in the two groups were compared. The total, verbal and performance IQ scores, as determined by the WAIS-R, were significantly lower in the SCI(+) group than in the SCI(-) group. The mental speed of patients in the SCI(+) group, as assessed by the Uchida-Kraepelin psychodiagnostic test, was almost half that of the SCI(-) group. Our findings provide further evidence that a comprehensive impairment of cognitive functioning, especially a severe reduction in mental speed, remains after recovery from depression in patients with major depression and SCI.
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PMID:Cognitive dysfunction in recovered depressive patients with silent cerebral infarction. 1180 36

Depression is common after stroke. While several reports have been published on the use of antidepressants such as selective serotonin reuptake inhibitors and tricyclics for the treatment of post-stroke depression (PSD), no previous study has examined the use of a selective serotonin and noradrenaline reuptake inhibitor (SNRI) for this condition. The present study investigated the efficacy and safety of milnacipran, a SNRI, for the treatment of PSD. A 6-week open study was conducted in 12 patients (two males and 10 females) aged 53-88 years. All patients were diagnosed with major or minor depressive disorder according to DSM-IV, where onset was subsequent to a cerebral infarction or haemorrhage (stroke). Severity of depression was assessed using the 21-item Hamilton rating scale for depression (HAM-D). The maximum total daily dose of milnacipran was in the range of 30-75 mg b.i.d. Three patients experienced side-effects, but none of the side-effects were serious. Two patients dropped out of the study. At the end of the study, 58.3% (7/12) of the total patient population and 70% (7/10) of the patients completing the study were in remission (a final HAM-D score of less than 7 and no longer meeting criteria for major or minor depression). These results suggest that milnacipran may be an effective treatment for PSD.
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PMID:Therapeutic effects of milnacipran, a serotonin and noradrenaline reuptake inhibitor, on post-stroke depression. 1198 53


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