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Stroke
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
A transient ischemic attack (TIA) involves symptoms of stroke that usually last for less than 1 hour. It is defined as focal brain ischemia, with sudden neurologic deficits. There is no visualization of any acute cerebral infarction when evaluation is done with diffusion-weighted MRI. The condition is similar to an ischemic stroke except that most TIAs last for less than 5 minutes. If deficits resolve in 1 hour, infarction is extremely unlikely. Deficits resolving between 1 and 24 hours usually have infarction. At this point, they are no longer considered to be TIAs. Within the first 24 hours, TIAs greatly increase risks of having an actual stroke. Hypertensive patients with diabetes mellitus have an increased frequency of transient ischemic attacks.
Stroke and Transient Ischemic Attacks of the Brain and Eye
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
The clinical diagnosis of stroke is often based on the history, but the anatomical localization of the site and extent of the focal brain ischemia or hemorrhage, and the relevant vascular supply, is often determined by the neurologic examination (Table 12.16). For example, eliciting a visual field defect, particularly a superior or inferior quadrantanopia, points to a lesion in the contralateral temporal or parietal lobe, respectively, and a homonymous hemianopia to a lesion in the optic tract or occipital lobe. Eliciting a cranial nerve palsy in conjunction with associated motor (corticospinal tract) and sensory (e.g. spinothalamic tract) signs usually points to a lesion in the nucleus or fascicle of the cranial nerve and adjacent long tracts within the brainstem.
Pea
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Brain ischemia can result from a variety of disease states including trauma, hypoxia, toxicity, cytokines, etc. Mast cells are the human body’s defense against pathogens as well as inflammation. In brain ischemia, mast cells relocate to the site of damage and degranulate, causing the release of inflammatory mediators. Parrella et al.21 found that PEA, in addition to the flavonoid luteolin, exerts a mast cell modulatory effect in the context of brain ischemia cellular models. The addition of PEA-luteolin prevented the degranulation of mast cells in response to oxygen and glucose deprivation and provided a direct synergistic neuroprotective effect. This research provides a basis for the potential use of PEA in the treatment and management of brain ischemia.
Neurotrophins in carotid atherosclerosis and stenting
Published in Annals of Medicine, 2023
Teodora Yaneva-Sirakova, Latchezar Traykov, Kiril Karamfiloff, Ivo Petrov, Julieta Hristova, Dobrin Vassilev
Carotid ultrasound was done with Vivid E95 General Electric linear transducer 7–13 MHz with reference to the national and European recommendations. We used the NASCET method for assessment [16–19]. With reference to the cited recommendations, [20] we used the following definitions:Unstable plaque – with heterogenous structure with high risk for embolization.Stable plaque – homogenous structure, smooth surface, and good fibrous cap.Symptomatic patient – with transitory visual or neurological symptoms, non-specific symptoms which may be associated with brain ischemia.Non-significant plaque – less than 50% and without characteristics of unstable or high-risk, with peak systolic velocity less than 125 cm/sec and ratio Internal carotid artery/common carotid artery less than 2.5.
Moyamoya syndrome in a male pseudohermaphrodite patient with congenital adrenal hyperplasia – a rare association. Case report and review of literature
Published in British Journal of Neurosurgery, 2023
Remesh Chirayil Vasudevan, Reshma Vachali Madayi, Rohit Ravindranath Nambiar
Moyamoya syndrome is a cerebrovascular condition that causes progressive stenosis of intracranial internal carotid arteries and their proximal branches with compensatory development of collateral vessels. Moyamoya vasculopathy along with well recognized associated conditions is called moyamoya syndrome, whereas Moyamoya vasculopathy with no known associated risk factors is called moyamoya disease. Children and middle-aged adults are affected. It may present either as brain ischemia or as hemorrhage from collateral vessels. Stenosis of vessels results from both hyperplasia of smooth muscles and luminal thrombosis. Pathogenesis may be related to genetic factors, with loci on chromosome 3, 6, 8 and 17 thought to be responsible.1,2 Familial cases may be polygenic or inherited as an autosomal dominant condition with incomplete penetrance. Many growth factors, enzymes and peptides are seen in increased level in these patients. Important among them include fibroblast growth factor, transforming growth factor, vascular endothelial growth factor and matrix metalloproteinases.
Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Mingjuan Cao, Yuqing Fang, Wei Jia, Yao Wang, Jingyi Sun, Dingbo Tao
Cerebral ischemia is also called as brain ischemia or cerebrovascular ischemia, which refers to a situation that the blood supply to the brain is insufficient to satisfy the requirement of metabolism [1,2]. Ischemia can give rise to miscellaneous alterations in brain metabolism and energy crisis [3]. Moreover, cerebral ischemia is usually discovered in the pathological processes of diversified neurological diseases, comprising cerebrovascular disease and brain tumours [4]. The aetiology of cerebral ischemia is complex, which might be linked to cerebral arteriosclerosis [5]. The impairments triggered by cerebral ischemia encompass vision, speaking and physical activity [6,7]. Currently, there is no valid management for cerebral ischemia, which can only be controlled by relevant drugs [8]. It is generally known that cerebral ischemia can evoke hypoxic injury in brain nerve cells [9]. Hence, to probe the molecular mechanism and mediation of hypoxic-triggered nerve cell injury is extremely important for remedying nerve injury after cerebral ischemia.