Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The post cardiotomy state is typically delirious and although organic factors are important it is multi-determined. Cerebral ischaemia has been implicated in the development of psychological disorder after resuscitation but longer term neurotic disorders also occur. Affective disturbances, particularly depression, are associated with the coronary care experience. The following conditions are directly related to an increased incidence of psychological disorder: age, loss of sleep, sensory deprivation, stressful experiences, pre-operative morbidity (both physical and mental), the severity of both surgical trauma and the post-operative medical state. For both the staff who administer intensive therapy and the patient who receives it there are unique psychological hazards, the management of which depends largely on mutual understanding and support.
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PMID:The psychiatric aspects of cardiac intensive therapy: a review. 110 11

3 cases of transient global amnesia (TGA) are reported. Transient ischaemia is probably the cause of the condition in the majority of cases although other mechanisms, particularly epilepsy, may be responsible in some. TGA may not be reported by the patient and may be misdiagnosed as a psychiatric disturbance. An acute confusional or delirious state can also produce an episode of amnesia with inability to remember events which occurred during the period of cerebral dysfunction. In TGA, however, there is an acute and temporary failure to record events without the evidence of more generalised dysfunction which occurs in delirium. During the 3 episodes reported here the patients were able to carry on with their everyday activities and to complete structured tasks, such as the preparation of a meal. TGA appears, at least in some individuals, to carry the prognosis of transient cerebral ischaemia.
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PMID:Transient global amnesia. 730 49

Heatstroke is a life-threatening illness characterized by an elevated core body temperature (>40 degrees C) and dysfunction of central nervous system, which results in delirium, convulsions, or coma. Despite adequate hypothermia or other care-therapy, heatstroke is often fatal. On the basis of our knowledge of the pathophysiology on heatstroke, we hypothesized that heatstroke is a form of hyperthermia associated with the acute physiological alterations, the cytotoxicity of heat, systemic inflammatory response, oxidative damage and attenuated heat-shock response leading to a syndrome of multi-organ dysfunction. In view of above-mentioned situation, the physiological factors underlying heatstroke and the corresponding possible therapeutic strategies to avert the complications of this disorder would be summarized in this review so as to provide some therapeutic guidelines for heatstroke. Heatstroke is a very complicated process. Acute physiological alterations, such as low arterial hypotension, intracranial hypertension, cerebral hypoperfusion, cerebral ischemia, and increased intracellular metabolism rate, occurred while exposed to a high ambient temperature. Hyperpyrexia caused cytotoxicity, resulting the degradation and aggregation of extensive intracellular proteins, influencing the change of membrane stability and fluidity, damaging the transmembrane transport of protein and the function of surface receptor, and inducing different cytoskeletal changes. Heatstroke resembles sepsis in many aspects, and endotoxemia and cytokines may be implicated in its pathogenesis. The concentration of interleukin-6 was positively correlated with the severity of heatstroke. The excessive accumulation of cytotoxic free radicals and oxidative damage may occur in the brain tissues during the genesis and development of heatstroke. The circulatory shock and cerebral ischemia resultant from heatstroke correlated closely with the free radicals (especially free radicals of peroxide and superoxide), the peroxidation of lipids, and low activity of antioxidase in the brain. Heat-shock proteins (Hsps) played a critical role during the process obtaining thermotolerance, therefore, protected from stress-induce cellular damage. Host factors or physiologically limiting factors, for instance, aging, existing illness, dehydration, deep insomnia, lack of acclimation to heat, inadequate physical fitness, and certain genetic polymorphisms were associated with a low level of Hsps expression and might favor the progression from heat stress to heatstroke. Some measures, such as molecular chaperonines, anti-inflammatory agents, antioxidant agents, and modulators of Hsps would be good for the patients with heatstroke.
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PMID:Pathophysiological factors underlying heatstroke. 1663 16

Delirum is a common complication in hospitalized patients and it is characterized by acute disturbances of consciousness, attention, cognition, and perception. Despite the frequency with which it is observed, ischemic stroke is generally considered as an unusual cause of delirium. A subtype of brain embolism is characterized by multiple small emboli in different vascular territories, a condition known as "brain microembolism." Given the high contrast of acute ischemic lesions in diffusion weighted imaging (DWI) this technique is particularly helpful to detect these small infarctions. We present here a patient with pulmonary metastases who was treated with bronchial artery embolization and who subsequently developed delirium due to brain microembolism. The embolic material crossed through pulmonary arteriovenous fistulas, producing multiple areas of cerebral ischemia. The ischemic lesions could be visualized only on DWI, and they affected the periventricular region, caudate nucleus, thalamus, and cerebellum.
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PMID:Delirium due to brain microembolism: diagnostic value of diffusion-weighted MRI. 1744 40

The authors report a case of man-in-the-barrel (MIB) syndrome occurring after an extensive revision involving thoracoilium instrumentation and fusion for iatrogenic and degenerative scoliosis, progressive kyphosis, and sagittal imbalance. Isolated brachial diplegia is a rare neurological finding often attributed to cerebral ischemia. It has not been previously reported in patients undergoing complex spine surgery. This 70-year-old woman, who had previously undergone T11-S1 fusion for lumbar stenosis and scoliosis, presented with increased difficulty walking and with back pain. She had junctional kyphosis and L5-S1 pseudarthrosis and required revision fusion extending from T-3 to the ilium. In the early postoperative period, she experienced a 30-minute episode of substantial hypotension. She developed delirium and isolated brachial diplegia, consistent with MIB syndrome. Multiple studies were performed to assess the origin of this brachial diplegia. There was no definitive radiological evidence of any causative lesion. After a few days, her cognitive function returned to normal and she regained the ability to move her arms. After several weeks of rehabilitation, she recovered completely. Man-in-the-barrel syndrome is a rare neurological entity. It can result from various mechanisms but most commonly seems to be related to ischemia and is potentially reversible.
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PMID:Man-in-the-barrel syndrome after thoracoilium fusion. 1903 49

In 2010 Critical Care published a large number of articles on critical care aspects of neurologic and neurosurgical conditions. These aspects included investigation of diagnostic criteria for bacterial meningitis, critical illness myopathy and their relationship to systemic inflammation. A number of studies investigated the biology of sepsis-related delirium, its biomarkers, its relationship to inflammation and its impact on outcome. Other teams reported on the use of magnetic resonance imaging, biomarkers and electroencephalogram to predict outcome in patients who were comatose following cardiac arrest. Our understanding of the pathophysiology as well as management of subarachnoid hemorrhage was addressed in several papers. Topics included the effect of hemodynamic treatment of delayed cerebral ischemia, pulmonary edema and the impact of subarachnoid hemorrhage on endocrine function. Finally, outcome from neurocritical care and patients' retrospective willingness to consent to the treatment they received were reported.
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PMID:Year in review 2010: Critical Care--Neurocritical care. 2214 75

Reversible cerebral vasoconstriction syndrome (RCVS) is a collective term used for transient noninflammatory, nonatherosclerotic segmental constriction of cerebral arteries. The angiopathies of RCVS have previously been defined by several nomenclatures. Current opinion favors the unification of these pathophysiologically related angiopathies because of their similar angiographic features and clinical course. RCVS typically presents acutely as headache, delirium, seizure, cerebral ischemia, and/or hemorrhage. The angiographic features make RCVS an important mimic of CNS vasculitides. In contrast to CNS vasculitis, RCVS is typically a transient condition with relatively good clinical outcomes. Although a complete understanding of the etiological and pathological features of RCVS has not yet been achieved, alterations in vascular tone lead to the observed arterial changes. In this review, we aim to provide a summary of RCVS and provide insight into current perspectives of the underlying pathophysiological processes, diagnosis, and treatment.
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PMID:Reversible cerebral vasoconstriction syndrome: a review of recent research. 2325 Jul 64

Brain dysfunction is a frequent complication of sepsis, usually defined as "sepsis-associated encephalopathy" (SAE). Its pathophysiology is complex and related to numerous processes and pathways, while the exact mechanisms producing neurological impairment in septic patients remain incompletely elucidated. Alterations of the cerebral blood flow (CBF) may represent a key component for the development of SAE. Reduction of CBF may be caused by cerebral vasoconstriction, either induced by inflammation or hypocapnia. Endothelial dysfunction associated with sepsis leads to impairment of microcirculation and cerebral metabolic uncoupling that may further reduce brain perfusion so that CBF becomes inadequate to satisfy brain cellular needs. The natural autoregulatory mechanisms that protect the brain from reduced/ inadequate CBF can be impaired in septic patients, especially in those with shock or delirium, and this further contributes to cerebral ischemia if blood pressure drops below critical thresholds. Sedative agents alter cerebro-vascular reactivity and may significantly reduce CBF. Although disorders of brain perfusion and alteration of CBF and cerebral autoregulation are frequently observed in humans with sepsis, their exact role in the pathogenesis of SAE remains unknown. Brain perfusion can further become inadequate due to cerebral microcirculatory dysfunction, as evidenced in the experimental setting. Microvascular alterations can be implicated in the development of electrophysiological abnormalities observed during sepsis and contribute to neurological alterations in septic animals. The aim of this review is to provide an update on the pathophysiology of brain perfusion in sepsis, with a particular focus on human clinical investigation and novel tools for CBF monitoring in septic patients.
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PMID:Brain perfusion in sepsis. 2350 96

Delirium is an acute brain dysfunction syndrome that is common in adult critical care patients. The pathogenesis of delirium is highly related with neuroinflammation, neurotransmitter imbalance, abnormal stress response, and cerebral ischemia. In intensive care unit (ICU), the occurrence of delirium is accompanied with long-term cognitive impairment in patients. Effective assessment tools can detect ICU delirium as early as possible, and subsequent treatment can improve the clinical outcome. However, there are no specific protocols for the treatment of ICU delirium, and active prevention is of particular important. This narrative review aims to address the risk factors, pathogenesis, diagnosis, treatment and prevention of ICU delirium, with a view to increase the understanding of ICU delirium and standardize management.
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PMID:[Research progress of delirium in intensive care unit]. 3257 62