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Central nervous system
Published in David A Lisle, Imaging for Students, 2012
Common causes of stroke:Cerebral ischaemia and infarction (acute ischaemic stroke): 80 per centParenchymal (primary intracerebral) haemorrhage: 15 per centUsually due to hypertensionCommon sites: basal ganglia, brainstem, cerebellum and deep white matter of the cerebral hemispheresSpontaneous subarachnoid haemorrhage: 5 per cent (see above)Cerebral venous occlusion: <1 per cent.
Herbal Therapies
Published in Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam, Herbal Product Development, 2020
H. Shahrul, M. L. Tan, A. H. Auni, S. R. Nur, S. M. N. Nurul
Neurological diseases are characterized by progressive dysfunction and death of neurons and the main degenerative disorders manifest predominantly as movement disorders, those of cognition or a mixture of both (Vajda, 2002). Movement disorders include akinetic and rigid forms, predominantly extrapyramidal deficits, hyperkinetic dysregulation of movement, ataxic with features of cerebellar ataxia, and motor neuron disorders (Vajda, 2002). Neuronal damage may be contributed by excitotoxicity, cerebral ischaemia and target deprivation. Excitotoxicity refers to an excessive activation of neuronal amino acid receptors, leading to apoptotic DNA fragmentation and cellular fragmentation (Mark et al., 2001; Vajda, 2002). On the other hand, cerebral ischemia is a condition where cessation of blood supply to the brain tissue leads to necrosis and apoptosis (Lee et al., 2001). Neurological disease is reported as the third most common cause of death. It is the leading cause of adult neurological disability (Carter et al., 2007). Among the important pathological mechanisms include inflammatory reaction, blood-brain barrier (BBB) disruption, oxidative stress, and neuronal apoptosis. They are widely considered as the four major therapeutic targets for acute ischemic stroke (Lalkovičováand Danielisová, 2016). Competition between neurons for innervation of their targets may cause target deprivation-induced neuronal death and is mainly apoptotic and occurs by programmed cell death (Deshmukh and Johnson, 1997; Martin et al., 1998). Environmental factors in neurodegenerative disease comprise physical, toxic and infection related factors. Other possible factors include dietary excitotoxic and bacterial or viral infections (Vajda, 2002). Neuroprotection could possibly result in salvage, recovery or regeneration of the nervous system, its cells, structure and function. It is also used to refer to relative mechanisms that prevents the central nervous system (CNS) from neuronal injuries caused by chronic (e.g., Alzheimer’s and Parkinson’s diseases) or acute (e.g., stroke) neurodegenerative diseases (Elufioye et al., 2017). Numerous herbal plants contain neuroprotective and possess memory enhancing effects. Among well-studied herbs include Ginkgo biloba, Panax ginseng, and Salvia officinalis will be highlighted in this chapter.
Mechanisms Associated with Protective Effects of Ginkgo Biloba Leaf Extracton in Rat Cerebral Ischemia Reperfusion Injury
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Wei Song, Jun Zhao, Xu-Sheng Yan, Xin Fang, Dong-Sheng Huo, He Wang, Jian-Xin Jia, Zhan-Jun Yang
Cerebral ischemia is a pathophysiological phenomenon that often occurs in cerebral infarction characterized by disruption of supply of blood, oxygen, and glucose to the brain. Following cerebral ischemia additional brain tissue injury occurs attributed to reperfusion in this brain area termed cerebral ischemia-reperfusion injury (CIRI) resulting in consequent generation and accumulation of toxic metabolites (Sanderson et al. 2013; Tuma and Steffens 2012). Injury attributed to reperfusion may be more fatal than the initial cerebral ischemia. Several investigators demonstrated that CIRI involves complex pathophysiological processes predominantly related to oxidant stress as evidenced by (1) excessive generation of free radicals accompanied by inhibition of antioxidant enzyme activities, and (2) increased release of inflammatory mediators (Jia et al. 2017; Li et al. 2017; Patel and Saver 2013). Although these underlying mechanisms are known to be involved in CIRI, effective therapeutic measures still need to be established.
Involvement of apoptosis in the protective effects of Dracocephalum moldavaica in cerebral ischemia reperfusion rat model
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Peng Wu, Xu-Sheng Yan, Li-Li Zhou, Xin-Lang Liu, Dong-Sheng Huo, Wei Song, Xin Fang, He Wang, Zhan-Jun Yang, Jian-Xin Jia
The disruption of supply of blood, oxygen, and glucose to the brain referred to as cerebral ischemia results in consequent generation and accumulation of toxic metabolites. Additional damage to brain tissue injury occurs following ischemia-reperfusion (IRI) (Sanderson et al. 2013; Tuma and Steffens. 2012). Injury attributed to reperfusion may be more fatal than ischemia itself. Several investigators demonstrated that cerebral ischemia-reperfusion injury (CIRI) involves complex pathophysiological processes predominantly related to excessive generation of free radicals, inflammatory mediators, excitatory amino acids and apoptosis (Li et al. 2017; Patel and Saver. 2013). It is well known that apoptosis plays a key important role in CIRI (Erfani et al. 2018; Jia et al. 2017; Li et al. 2015; Zhang et al. 2016; Zou et al. 2017).
The protective mechanism underlying total flavones of Dracocephalum (TFD) effects on rat cerebral ischemia reperfusion injury
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Peng Wu, Xu-sheng Yan, Yu Zhang, Dong-sheng Huo, Wei Song, Xin Fang, He Wang, Zhan-jun Yang, Jian-xin Jia
Cerebrovascular disease is a public health concern as the consequential increase in morbidity and mortality places a great burden on society. Ischemic stroke occurs in more than half of the individuals exhibiting cerebrovascular disorders (Dong et al. 2013). Various investigators demonstrated that reperfusion of the ischemic area in the brain is the best way to treat ischemic stroke; however, a more fatal attack to central nervous system (CNS) tissue occurs after reperfusion, which is termed cerebral ischemia reperfusion injury (CIRI) (Xie, Zhang, and Jing 2018; Zhang et al. 2016). In CIRI injury several mechanisms occur including excitotoxicity, inflammatory, neuronal apoptosis and brain edema (Dong et al. 2013; Pillai et al. 2009; Tang et al. 2012). Further, it is well known that acute inflammatory responses and apoptosis play a key role in the secondary damage of neuronal cells produced by brain reperfusion injury (Lu, Deng, and Lu 2012; Wang et al. 2018; Xie, Zhang, and Jing 2018; Zhao et al. 2018, 2010).