Diagnosis and management of acute ischemic stroke: speed is critical

Musuka, Tapuwa; Wilton, Stephen B.; Traboulsi, Mouhieddin; Hill, Michael D.

doi:10.1503/cmaj.140355

Cited by 271 publications

(197 citation statements)

References 64 publications

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“…A number of pharmaceutical agents aiming to target distinct microglial markers in ischaemia have shown promising results in experimental studies and clinical trials. Considering the high disease burden of ischaemic stroke, drug repurposing of pre-existing pharmaceutical agents may be an avenue for exploration in addition to the development of new therapeutic agents, which specifically target the phenotypic expression of microglia [1]. It is worth noting that many of these agents have been administered orally and could affect both infiltrating peripheral macrophages and endogenous microglia.…”

Section: Pharmacological Modulation Of Microglia Activation In Ischaementioning

confidence: 99%

“…Ischaemic stroke constitutes about 85% of all stroke events [1]. The underlying pathophysiology of ischaemic stroke is complex and has not yet been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

“…With such a complex and multifaceted pathophysiology, targeting the mechanisms by which stroke is known to cause cerebral damage remains a significant barrier to achieving pre-stroke functionality. At present, many patients who survive an ischaemic attack experience a decline in their quality of life, developing conditions, such as hemiplegic paralysis and aphasia[1]. Microglial biology plays a pivotal role in the pathophysiology of neuroinflammation induced by ischaemic stroke, thus presenting an attractive treatment target for pharmacological intervention.…”

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confidence: 99%

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Post-Ischaemic Immunological Response in the Brain: Targeting Microglia in Ischaemic Stroke Therapy

et al. 2020

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Microglia, the major endogenous immune cells of the central nervous system, mediate critical degenerative and regenerative responses in ischaemic stroke. Microglia become “activated”, proliferating, and undergoing changes in morphology, gene and protein expression over days and weeks post-ischaemia, with deleterious and beneficial effects. Pro-inflammatory microglia (commonly referred to as M1) exacerbate secondary neuronal injury through the release of reactive oxygen species, cytokines and proteases. In contrast, microglia may facilitate neuronal recovery via tissue and vascular remodelling, through the secretion of anti-inflammatory cytokines and growth factors (a profile often termed M2). This M1/M2 nomenclature does not fully account for the microglial heterogeneity in the ischaemic brain, with some simultaneous expression of both M1 and M2 markers at the single-cell level. Understanding and regulating microglial activation status, reducing detrimental and promoting repair behaviours, present the potential for therapeutic intervention, and open a longer window of opportunity than offered by acute neuroprotective strategies. Pharmacological modulation of microglial activation status to promote anti-inflammatory gene expression can increase neurogenesis and improve functional recovery post-stroke, based on promising preclinical data. Cell-based therapies, using preconditioned microglia, are of interest as a method of therapeutic modulation of the post-ischaemic inflammatory response. Currently, there are no clinically-approved pharmacological options targeting post-ischaemic inflammation. A major developmental challenge for clinical translation will be the selective suppression of the deleterious effects of microglial activity after stroke whilst retaining (or enhancing) the neurovascular repair and remodelling responses of microglia.

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Section: Pharmacological Modulation Of Microglia Activation In Ischaementioning

confidence: 99%

“…Ischaemic stroke constitutes about 85% of all stroke events [1]. The underlying pathophysiology of ischaemic stroke is complex and has not yet been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Post-Ischaemic Immunological Response in the Brain: Targeting Microglia in Ischaemic Stroke Therapy

et al. 2020

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“…1 Of all strokes, upto 85% are ischemic and 15% are hemorrhagic. 2 Ischemic stroke syndromes have a multitude of possible causes, characterized by a rule of quarters: 25% cardio embolic, 25% arteroembolic (large-artery disease), 25% lacunar (small-vessel disease) and 25% due to other causes, with global variation in proportions by population. 3 Atherosclerotic risk factors for ischemic stroke are traditional and non-traditional.…”

Section: Introductionmentioning

confidence: 99%

Study of serum homocysteine level in cases of non-diabetic ischemic stroke

Murmu¹,

Mahesh²,

Dash³

et al. 2018

Int J Res Med Sci

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Background: Aim of the study was to measure serum homocysteine levels in non-diabetic ischemic stroke and to co-relate its significance with other risk factors of ischemic stroke. It was a case control study.Methods: The study was done in the Department of Medicine, VSS.I.M.S.A.R, Burla, Odisha. 42 patients of non-diabetic ischemic and 42 age and sex matched controls were included in the study. Adults above the age of 18 years who were non-diabetic presenting with first-ever ischemic stroke, confirmed by CT scan of brain were included. Diabetic patients, haemorrhagic stroke, suspected embolic stroke, patients on vitamin supplementations, chronic usage of phenytoin were excluded. Routine investigations, fasting serum lipid profile and serum homocysteine levels were done.Results: Mean serum homocysteine level in ischemic stroke patients were found to be much higher (25.83 micro mol/L) in comparison to control group (9.77 micro mol/L) which is statistically significant. Mean serum homocysteine levels were found to be higher in patients with age group of more than 60 years, male sex, sedentary lifestyle, vegetarian diet, hypertensive patients and patient with normal fasting lipid profile. Statistical analysis for significance of difference was done using Chi-Square test with Yate’s correction.Conclusions: A statistically significant correlation was found between all the studied risk factors among non-diabetic patients and serum homocysteine levels. Estimation of serum homocysteine is advisable in all cases of non-diabetic ischemic strokes to know the prognosis.

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“…It is estimated that about 15 million new stroke cases occur annually, five million of which lead to mortality and another five million suffer from permanent disability, thus imposing a burden on families and the community (4). Ischemic stroke accounts for 80-85% of all strokes, and is caused by a sudden obstruction of a major feeding vessel, which reduces local blood flow and oxygen and nutrients delivery to the affected brain tissue (4)(5)(6). The hippocampal CA1 region plays an essential role in learning and memory functions.…”

Section: Introductionmentioning

confidence: 99%

Positive Effects of Post-ischemic Forced Treadmill Training on Sensorimotor and Learning Outcomes Following Transient Global Cerebral Ischemia

et al. 2019

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Background and objectives: Stroke is one of the leading causes of death and long-term acquired disability. It is of great importance to seek ways for improving motor, sensory, and cognitive function after stroke and brain injury. In this regard, therapeutic exercise is the most commonly used method of rehabilitation that can significantly reduce the severity of functional damage. The aim of the present study was to investigate effects of eight weeks of forced treadmill training on cognitive and motor functions in ischemic rats.Methods: Fourteen adult male Wistar rats were divided into an exercise group and a control group (no exercise). Occlusion of both common carotid arteries was made to induce cerebral ischemia. Twenty-four hours after the induction of ischemia, the subjects in the exercise group were subjected to treadmill running, five days a week for eight weeks. The skilled ladder rung walking task was used to evaluate motor function before and after the stroke.Results: The number of errors was decreasing in both groups, but significant differences were observed in the motor function between the two groups in the third, fifth, and eighth week.Conclusion: Our results suggest that post-ischemic exercise might modulate ischemia-induced hippocampal injury and ameliorate the subsequent memory and motor impairment.

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Diagnosis and management of acute ischemic stroke: speed is critical

Cited by 271 publications

References 64 publications

Post-Ischaemic Immunological Response in the Brain: Targeting Microglia in Ischaemic Stroke Therapy

Post-Ischaemic Immunological Response in the Brain: Targeting Microglia in Ischaemic Stroke Therapy

Study of serum homocysteine level in cases of non-diabetic ischemic stroke

Positive Effects of Post-ischemic Forced Treadmill Training on Sensorimotor and Learning Outcomes Following Transient Global Cerebral Ischemia

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