Cerebral hyperperfusion and reperfusion injuries are not infrequently encountered following in reperfusion of ischemic or hypoperfused brain. Mechanism of injury could be related to tissue plasminogen activator toxicity, oxidative stress, and hyperperfusion due to impaired cerebral autoregulation in already maximally dilated cerebral vasculature and compromised cerebral hemodynamic reserve. Reperfusion injury can present as headaches and seizures in mild forms and as subarachnoid hemorrhage, intracranial hemorrhage, cerebral edema, and encephalopathy in its most severe manifestation. Prevention and identifying those at risk of hyperperfusion syndromes are the best strategy. Active treatment includes basic neurocritical care with reduction of blood pressure to a reperfused brain and timely neuroprotection and cerebral edema control measures are the mainstay of its management approach.
"Liver or renal dysfunction accompanying sepsis may result in encephalopathy [11, 12]; however, sepsis may result in encephalopathy even in the absence of systemic organ failure. Sepsis is typically regarded as being caused by infectious factors, such as bacteria, viruses, or fungi; however, encephalopathy may also occur with metabolic disorders , exposure to toxins  or radiation , injury [14, 15], disturbances in blood flow , and other factors. Among the many complications of sepsis, septic encephalopathy (SE) is considered the most frequent [4, 18], and it is estimated that 9–71 % of patients with diagnosed sepsis exhibit symptoms of encephalopathy [4, 19, 20]. "
[Show abstract][Hide abstract] ABSTRACT: Every year, more cases of sepsis appear in intensive care units. The most frequent complication of sepsis is septic encephalopathy (SE), which is also the essential determinant of mortality. Despite many years of research, it still is not known at which stage of sepsis the first signs of SE appear; however, it is considered the most frequent form of encephalopathy. Patients have dysfunction of cognitive abilities and consciousness, and sometimes even epileptic seizures. Despite intensive treatment, the effects of SE remain for many years and constitute an important social problem. Numerous studies indicate that changes in the brain involve free radicals, nitric oxide, increased synthesis of inflammatory factors, disturbances in cerebral circulation, microthromboses, and ischemia, which cause considerable neuronal destruction in different areas of the brain. To determine at what point during sepsis the first signs of SE appear, different experimental models are needed to detect the aforementioned changes and to select the proper therapy for this syndrome.
Current Neurology and Neuroscience Reports 10/2013; 13(10):383. DOI:10.1007/s11910-013-0383-y · 3.06 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Following carotid revascularization with either carotid endarterectomy or stenting, the impaired cerebral autoregulation can lead to cerebral hyperperfusion syndrome. This impaired autoregulation and increased flow may also put patients with unruptured aneurysms at risk for subarachnoid hemorrhage in the perioperative period. A patient is reported who underwent carotid endarterectomy for symptomatic carotid stenosis. A small anterior communicating artery aneurysm was identified preoperatively, which ruptured 2 days after carotid endarterectomy. Screening for cerebral aneurysms prior to carotid revascularization will allow operators to minimize this risk, either through prior treatment of the aneurysm or tight blood pressure control in the perioperative period.
Journal of Neurointerventional Surgery 09/2011; 4(5):e27. DOI:10.1136/neurintsurg-2011-010091 · 2.77 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: 1. Ischaemic brain injury is a leading cause of death and disability in many countries. However, the pathological mechanisms underlying ischaemic brain injury, including oxidative stress, calcium overload, excitotoxicity and neuronal apoptosis, are perplexing and this makes it difficult to find effective novel drugs for the treatment of the condition. 2. Recently, gaseous molecules such as nitric oxide (NO), carbon monoxide (CO), hydrogen sulphide (H(2)S) and hydrogen (H(2)) have attracted considerable interest because of their physiological and pathophysiological roles in various body systems. Emerging evidence indicates that gaseous molecules are involved in the pathological processes of ischaemic brain damage. 3. In the present review, we summarize evidence regarding the involvement of gaseous molecules in ischaemic brain injury and discuss the therapeutic potential of targeting gaseous molecules. 4. Collectively, the available data suggest that the application of these biological gas molecules and their pharmacological regulators may be a potential therapeutic approach for the treatment of ischaemic brain injury.
Clinical and Experimental Pharmacology and Physiology 12/2011; 39(6):566-76. DOI:10.1111/j.1440-1681.2011.05654.x · 2.37 Impact Factor
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