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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Right ventricular (RV) ischemia occurs in 50% of patients with acute inferior myocardial infarction, and may result in severe hemodynamic compromise associated with poor clinical outcome. Acute right coronary artery (RCA) occlusion proximal to the RV branches results in right ventricular free wall (RVFW) dysfunction. The ischemic, dyskinetic RVFW exerts mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function leads to a decrease in transpulmonary delivery of left ventricular (LV) preload, resulting in diminished cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction and septally-mediated alterations in LV compliance, which are exacerbated by elevated intrapericardial pressure. Under these conditions, RV pressure generation and output are dependent on LV-septal contractile contributions, governed by both primary septal contraction and paradoxical septal motion. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling, thereby resulting in further depression of RV performance and more severe hemodynamic compromise. Bradyarrhythmias limit the output generated by the rate-dependent noncompliant ventricles. Patients with right ventricular infarction and hemodynamic compromise often respond to volume resuscitation and restoration of a physiological rhythm. Vasodilators and diuretics should generally be avoided. In some, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and has a remarkable ability to recover even after prolonged occlusion. Therefore, the term RV infarction appears to be somewhat of a misnomer, for in most patients a substantial proportion of acute RV dysfunction represents ischemic but viable myocardium. Although RV performance improves spontaneously even in the absence of reperfusion, recovery of function may be slow and associated with high in-hospital mortality. Reperfusion enhances the recovery of RV performance and improves the clinical course and survival of patients with ischemic RV dysfunction.
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PMID:Right heart ischemia: pathophysiology, natural history, and clinical management. 944 58

This study examined the stroke knowledge of 60 stroke rehabilitation patients, 46 spouses, 25 family members, and 103 people in the general community. Changes in stroke knowledge with time, and determinants of stroke knowledge, were also examined. Clinical participants were assessed on acute admission, admission to and discharge from rehabilitation, and 6 and 12 months after discharge. Community participants were assessed once. Instruments used were the Stroke Care Information Test, Australian ADL Index, Frenchay Activities Index, Illness Behaviour Questionnaire and Zung Self-rating Depression Scale. The stroke knowledge of all participants, particularly patients, was poor, but improved with time. Better-informed patients were younger, had milder strokes, were less depressed, were less likely to develop abnormal illness behaviour, and made a better functional recovery than patients with poorer knowledge. Structured information programmes are needed for stroke patients and their families. Improved community awareness of stroke may help the prospects for recovery and quality of life for people who have strokes.
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PMID:Knowledge of stroke in rehabilitation and community samples. 954 20

Damage to the brain triggers a host of reactive responses in neurons and glia which are seen at sites of focal injury as well as at sites that are at a distance from the injury. Although many of these responses have been studied extensively, the signals that initiate the different responses have not been fully characterized, and it is still not understood how focal injury affects neurons and glia in distant sites. The present review summarizes recent findings that suggest that physiological events that occur at the time of the injury or during the early postlesion period can play an important and variable role in modulating neuronal and glial responses to injury. We focus on the events that occur in the hippocampal formation following unilateral lesions of the entorhinal cortex - a model system that has been used extensively for studies of cellular responses following focal brain injury. This lesion destroys the cells of origin of a massive excitatory projection to the dentate gyrus and hippocampus proper. Over time, the denervated neurons in the hippocampal formation are almost completely reinnervated as a result of local sprouting of systems that survive the lesion. Thus, this model system has been useful for studying cellular responses to both denervation and reinnervation. We summarize the information that this injury triggers physiological events that can strongly modulate gene expression in neurons and glia, including episodes of spreading depression that occur at the time of the injury, seizures that occur during the early postlesion period, the loss of afferent drive which leads to decreases in postsynaptic activity, and the restoration of activity that occurs in conjunction with reinnervation. We describe recent studies which suggest that some of these physiological events occur to a variable extent in different animals, especially the episodes of spreading depression and the recurrent seizures. Thus, the spatial pattern and temporal dynamics of altered gene expression following this "model" experimental injury may vary from animal to animal. The fact that physiological events strongly modulate the reactive changes in gene expression that occur following injury has important implications for understanding the sequelae of injury, and offers new opportunities for experimental and therapeutic interventions that may improve cellular repair, regeneration, and recovery of function.
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PMID:Injury-induced physiological events that may modulate gene expression in neurons and glia. 954 30

The aim of Programme 38 of the Swiss National Research Foundation is to enhance collaboration between basic science and clinical application, as related to diseases of the nervous system, over a 5-year period. The 15 ongoing projects are described. They are mainly concerned with mechanisms of pathogenesis and recovery of function, and ways of modifying them therapeutically after traumatic lesions or various diseases of the nervous system such as stroke, Parkinson's disease, Alzheimer's dementia, depression, meningitis, HMSN etc.
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PMID:[National Research Program NFP 38: "Diseases of the nervous system"]. 964 54

Unilateral cerebral contusion is associated with an early (30 min) increase in norepinephrine (NE) turnover followed by a later (6-24 h) depression of turnover which is bilateral and widespread throughout the brain. Blockade of NE function during the first few hours after traumatic brain injury (TBI) impedes subsequent recovery of function without enlarging the size of the lesion. The current studies were carried out to characterize further the timing of the switch from increased to decreased NE turnover and to investigate the pathogenesis of the delayed recovery of function associated with blocking NE function. Adult male rats had unilateral somatosensory cortex contusions made with a 5 mm diameter impact piston. They were killed after 2 h and their brains analyzed for NE turnover by HPLC with electrochemical detection. In general, NE turnover (the ratio of 3-methoxy-4-hyroxyphenylglycol to NE levels) had returned to sham-lesion control levels in most brain regions by 2 h after either left or right sided contusions. The only exceptions were a persistent 87% increase at the lesion site after right-sided contusions and 22% and 32% increases in the contralateral cerebellum after right- and left-sided contusions, respectively. Blockade of alpha1-adrenoceptors by treatment with prazosin (3 mg/ kg, i.p.) 30 min prior to TBI produced edema in the striatum and hippocampus at 24 h which was not seen saline-treated rats nor in rats where NE reuptake was blocked with desmethylimipramine (DMI; 10 mg/kg, i.p.). DMI increased edema at the lesion site at 24 h, however. These data suggest that the early increase in NE release following unilateral cerebral contusion is protective and that this may act to stabilize the blood-brain barrier in areas adjacent to the injury site. Drugs that interfere with this enhanced noradrenergic function might enhance the damage caused by TBI.
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PMID:Norepinephrine and traumatic brain injury: a possible role in post-traumatic edema. 968 66

We used field potential recording techniques to examine whether felbamate (FBM), lamotrigine (LTG), and lidocaine (LID) protect against the irreversible functional damage induced by transient ischemia. Five minutes of ischemia caused a depression of the field potential in rat cortical slices, which did not recover even after more than 1 h of washout. The N-methyl-D-aspartate (NMDA) antagonist ketamine (50 microM) protected against depression of the field caused by ischemia. On the other hand, the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2.3-dione (CNQX) (10 microM) had protective effects only if co-applied with ketamine. We found that either FBM (30-300 microM), which did not modify the amplitude of the field EPSP, or LTG (10-300 microM), which reversibly depressed the excitatory synaptic transmission, had a marked protective effect when superfused before and during the ischemic insult. After FBM (100 microM) and LTG (100 microM), the field EPSP recovered by 84 +/- 1% and 73 +/- 2.7% of control, respectively. Furthermore, LID (30-300 microM) was less effective than FBM and LTG in inducing a functional recovery from the damage caused by ischemia (58 +/- 1.8%). The rank order of potency, based on the maximal protection caused by the three drugs, was FBM > LTG > LID. Our results suggest that a noticeable neuroprotection can be obtained during glucose and O2 deprivation by preventive therapeutic regimens which use the two recently marketed anticonvulsant drugs, FBM and LTG.
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PMID:An electrophysiological analysis of the protective effects of felbamate, lamotrigine, and lidocaine on the functional recovery from in vitro ischemia in rat neocortical slices. 982 29

Noradrenaline, an important transmitter in the CNS, is involved in cerebral plasticity and functional recovery after injury. Experimental brain injury, including KCl application onto the brain surface, induces a slow-moving cortical depolarization/depression wave called cortical spreading depression (CSD). Interestingly, CSD does not produce neuronal damage but can protect cortical neurons against subsequent neurotoxic insults, although the mechanisms involved are unknown. This study examined the status of alpha- and beta-adrenoceptors (ARs) in cerebral cortex following CSD. Anesthetized rats had unilateral CSD induced by a 10-min topical application of KCl to the frontoparietal cortex and were killed at various times thereafter. Levels of alpha1-, alpha2-, beta1-, and beta2-AR mRNA and binding were examined using in situ hybridization histochemistry and radioligand autoradiography. Levels of alpha1b-AR mRNA in the affected neocortex were significantly increased by 20-40% at 1, 2, and 7 days (P </= 0.01) compared with contralateral levels, but were not significantly above control values at 2 and 4 weeks after CSD induction. Cortical alpha1B-AR binding sites were also increased by 45-65% 1 and 2 weeks (P </= 0.01) after CSD in a similar, but delayed, profile to alpha1b-AR mRNA. CSD rapidly increased beta1-AR mRNA by 45% at 1 h (P </= 0.01) and produced a delayed decrease of 25% in alpha2a-AR mRNA at 2 days and 1 week (P </= 0.05), but had no effect on corresponding levels of binding sites. In contrast, CSD had no effect on the remaining AR-subtype mRNAs or binding levels in neocortex under identical conditions. These results reveal a long-term up-regulation of alpha1B-ARs induced by an acute cortical stimulation/depression. Subtype-selective responses of ARs to CSD reflect an important differential regulation of expression of each receptor in vivo and suggest that alpha1B-ARs are particularly likely to be involved in cortical adaptive responses to physical injury at both local and distant locations.
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PMID:Differential spatiotemporal alterations in adrenoceptor mRNAs and binding sites in cerebral cortex following spreading depression: selective and prolonged up-regulation of alpha1B-adrenoceptors. 987 96

Post-stroke depression and functional outcome were examined in a population-based stroke register active in four different districts (total population, 134 804) in Finland. Five hundred and ninety four first time strokes were registered. Beck's depression inventory (BDI), with ten as the cutoff point for depression, was applied to 321 of 423 survivors after three months and to 311 of 390 survivors after 12 months. Functional outcome was measured with the Barthel Index (BI) and the Rankin Scale (RS). One hundred and fifty one of 321 (47.0%) and 147 of 311 (47.3%) patients were depressed after three and 12 months, respectively. Depression at three months was associated with poor functional outcome at the one-year follow-up (P = 0.001 for the BI and the RS). On the other hand, poor functional outcome at three months was associated with depression after one year (P = 0.004 and 0.002 for the BI and the RS, respectively). Patients who were depressed at three months were more often in institutional care between three and 12 months later than non-depressed patients (P = 0.005). Post-stroke depression is associated with poor functional recovery of patients. If depression were diagnosed and treated early, it might help patients to recover more completely and/or faster, which could save community healthcare resources by avoiding or shortening the time of institutional care or reducing the need for home care.
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PMID:Post-stroke depression and functional recovery in a population-based stroke register. The Finnstroke study. 1021 Sep 11

The past two decades have witnessed an explosive growth of knowledge regarding postischemic myocardial dysfunction or myocardial "stunning." The purpose of this review is to summarize current information regarding the pathophysiology and pathogenesis of this phenomenon. Myocardial stunning should not be regarded as a single entity but rather as a "syndrome" that has been observed in a wide variety of experimental settings, which include the following: 1) stunning after a single, completely reversible episode of regional ischemia in vivo; 2) stunning after multiple, completely reversible episodes of regional ischemia in vivo; 3) stunning after a partly reversible episode of regional ischemia in vivo (subendocardial infarction); 4) stunning after global ischemia in vitro; 5) stunning after global ischemia in vivo; and 6) stunning after exercise-induced ischemia (high-flow ischemia). Whether these settings share a common mechanism is unknown. Although the pathogenesis of myocardial stunning has not been definitively established, the two major hypotheses are that it is caused by the generation of oxygen-derived free radicals (oxyradical hypothesis) and by a transient calcium overload (calcium hypothesis) on reperfusion. The final lesion responsible for the contractile depression appears to be a decreased responsiveness of contractile filaments to calcium. Recent evidence suggests that calcium overload may activate calpains, resulting in selective proteolysis of myofibrils; the time required for resynthesis of damaged proteins would explain in part the delayed recovery of function in stunned myocardium. The oxyradical and calcium hypotheses are not mutually exclusive and are likely to represent different facets of the same pathophysiological cascade. For example, increased free radical formation could cause cellular calcium overload, which would damage the contractile apparatus of the myocytes. Free radical generation could also directly alter contractile filaments in a manner that renders them less responsive to calcium (e.g., oxidation of critical thiol groups). However, it remains unknown whether oxyradicals play a role in all forms of stunning and whether the calcium hypothesis is applicable to stunning in vivo. Nevertheless, it is clear that the lesion responsible for myocardial stunning occurs, at least in part, after reperfusion so that this contractile dysfunction can be viewed, in part, as a form of "reperfusion injury." An important implication of the phenomenon of myocardial stunning is that so-called chronic hibernation may in fact be the result of repetitive episodes of stunning, which have a cumulative effect and cause protracted postischemic dysfunction. A better understanding of myocardial stunning will expand our knowledge of the pathophysiology of myocardial ischemia and provide a rationale for developing new therapeutic strategies designed to prevent postischemic dysfunction in patients.
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PMID:Molecular and cellular mechanisms of myocardial stunning. 1022 90

Over one-third of Medicare stroke patients are admitted to nursing homes for rehabilitation. Patients with stroke who are admitted to nursing homes are extremely heterogeneous, including both those with minimal physical and cognitive impairment and those who are totally physically dependent. Quality measures that are appropriate for evaluating stroke care in nursing homes include outcome measures, particularly those that are patient-centered, such as self-reported functional recovery and return to the community; process measures involving essential services such as screening for depression and pain; and structural measures such as the availability of a psychologist or presence of an interdisciplinary team. In measuring quality, nursing home professionals must allow sufficient time for outcomes to unfold, such as 3 to 6 months, rather than measuring outcome at discharge from a setting. Nursing home professionals must also take into consideration patient heterogeneity in terms of risk factors for outcomes of interest.
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PMID:Stroke rehabilitation in nursing homes: how do we measure quality? 1049 40


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