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Mitochondrial Transplantation in Myocardial Ischemia and Reperfusion Injury
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
David Blitzer, Borami Shin, Alvise Guariento, Pedro J. del Nido, James D. McCully
Restoration of blood flow is the best measure to arrest ischemic injury, however reperfusion is accompanied by and activates a cascade of inflammatory pathways that can augment the ischemic injury to heart itself and even extends to distant organs [62–64]. Pathologically, reperfusion can cause hemorrhagic infarct with accompanying contraction band necrosis. Paradoxically, reperfusion can also lead to disruption of the microvasculature, creating a “no-reflow” phenomenon in which blood flow to the ischemic region remains diminished after addressing the arterial occlusion [65–67]. The mechanism by which the reperfusion augments ischemic injury has been the subject of extensive investigations. The investigations have demonstrated that mitochondrial response plays a crucial role in that the rate of oxygen consumption, and thus the synthesis of high energy phosphates, immediately declines with the reduction of blood flow and oxygen supply [55]. When assessed by oximetry in animal models, mitochondrial function is affected by ischemia in a number of ways, notably the decline in state three oxygen consumption and respiratory control index marked by decreases in malate, a substrate of complex I, succinate, a substrate of complex III, and cytochrome c [48,68–76].
Headache associated with vascular disease: migraine and stroke
Published in Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby, Headache in Clinical Practice, 2018
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby
Headache treatment usually consists of high doses of oral acetaminophen. Aspirin should be avoided because of its interaction with anticoagulants. The prognosis of CVT is unpredictable,135 with mortality ranging from 33%121 to 4% (6/160 in Bousser et al’s series). There are three main causes of death: the brain lesion itself (particularly with massive hemorrhagic infarct), intercurrent complications (such as sepsis, uncontrolled seizures, or pulmonary embolism), or the underlying condition (carcinoma, leukemia, septicemia, paroxysmal nocturnal hemoglobinuria, or heart failure).25
Antenatal and postpartum comparison of HD-OCT findings of macula, retinal nerve fiber layer, ganglion cell density between severe preeclampsia patients and healthy pregnant woman
Published in Hypertension in Pregnancy, 2020
Abdullah Tok, Abdullah Beyoğlu
In preeclampsia cases, placental ischemia/hypoxia develops because of abnormal remodeling of the spiral arteries in the maternal placental interface. Inflammatory cytokines, reactive oxygen species, and anti-angiogenic factor sFlt-1 are expressed from the ischemic placenta. As a result of these ischemic placental factors and because of impaired cardiovascular adaptation in normal pregnancies, problems emerge in the cerebrovascular system such as increased cerebral perfusion pressure, impaired autoregulation in the central nervous system, increased permeability of the blood-brain barrier, imbalance in the cerebrospinal fluid electrolytes, sympathovagal imbalance, and reduced baroreceptor reflex sensitivity. These disturbances in the central nervous system can cause white matter lesions, cerebral edema, and hemorrhagic infarct (20).
Complications During Inter-Hospital Transfer of Patients with Acute Ischemic Stroke for Endovascular Therapy
Published in Prehospital Emergency Care, 2020
Denis Sablot, Franck Leibinger, Adrian Dumitrana, Nathalie Duchateau, Laurène Van Damme, Geoffroy Farouil, Nicolas Gaillard, Marlène Lachcar, Laurent Benayoun, Caroline Arquizan, Majo Ibanez, Francis Coll, Bénédicte Fadat, Ludovic Nguyen Them, Lucie Desmond, Thibaut Allou, Philippe Smadja, Adelaïde Ferraro-Allou, Isabelle Mourand, Anais Dutray, Celine Pujol, Maxime Tardieu, Snejana Jurici, Jean-Marie Bonnec, Nadège Olivier, Julie Mas, Vincent Costalat, Alain Bonafe
Overall, 7 patients had a symptomatic hemorrhagic infarct (6 after IVT and 1 without IVT) among whom 3 without clinical signs during inter-hospital transfer. In the other 4, the NIHSS increased by more than 4 points and the final NIHSS was higher than 20. Specifically, 1 patient developed agitation needing sedation, and 1 had airway hemorrhage that required intubation during inter-hospital transfer (as noted previously).
Pathogenesis of epileptic seizures and epilepsy after stroke
Published in Neurological Research, 2018
Huajun Yang, Gary Rajah, Anchen Guo, Yongjun Wang, Qun Wang
Post-stroke seizure refers to seizures or epilepsy developing after a stroke without a prior history of epilepsy, which is due to reversible or irreversible damage caused by the ischemic or hemorrhagic infarct rather than other brain structural abnormalities or metabolic disorders. According to the time of onset of seizures after stroke, they can be divided into early epileptic seizures and late epileptic seizures. Generally, early epileptic seizures are defined as seizures within 2 weeks after a stroke while late epileptic seizures are defined as seizures developing after 2 weeks [1]. In some studies, authors also use 24 hours [2,3] or 1 week [4,5] as a dividing criteria. In 2014, the International League Against Epilepsy (ILAE) had revised the operational clinical definition of epilepsy [6]: Epilepsy is a disease of the brain defined by any of the following conditions: (1) At least two unprovoked (or reflex) seizures occurring >24 hours apart; (2) One unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years; (3) Diagnosis of an epilepsy syndrome. According to the new definition, one or more episodes of seizures after a stroke which has exceeded the time range of acute symptomatic seizures can be considered as post-stroke epilepsy [7]. Cerebrovascular diseases underlie about 11% of all cases of epilepsy and are heterogeneous with various causes [8]. At present, there is a great variation in the incidence of post-stroke seizures and epilepsy in various studies. Recent prospective studies have shown that the incidence of post-stroke epilepsy is 3.1–21.8% [6,8,9]. The variance might be associated with sample size, research population, inclusion criteria, type of stroke, definition of post-stroke epilepsy, and follow-up period. Early epileptic seizures mainly occur within 24 hours after stroke, accounting for 57% of all early seizures; Late epileptic seizures mainly occur at 6–12 months after stroke, and more than 90% of the patients will suffer recurrence. The incidence of post-stroke status epilepticus is less than 1% [10]. Post-stroke epilepsy can aggravate stroke, seriously affect the prognosis and quality of life, and might even be life-threatening [11]. A thorough understanding of post-stroke epilepsy is important for the prevention and treatment of the disease. This article will review the advances in the pathogenesis of epileptic seizures and epilepsy after stroke.