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acute_ischemic_stroke

Acute ischemic stroke

Cerebral ischemia due to cerebral vasospasm is a feared complication in patients following aneurysmal subarachnoid hemorrhage (SAH).

Epidemiology

Of the approximately 795 000 strokes in the United States annually, 87% are from ischemia and result in significant morbidity and mortality.

Clinical Features

Early neurological deterioration (END) is a common condition associated with poor outcome after acute ischemic stroke.

Diagnosis

Diffusion weighted magnetic resonance imaging (DWI) is widely appreciated as an indispensable tool in the examination of the central nervous system. It is considered useful not only for the detection of acute ischemic stroke but also for the characterization and differentiation of brain tumors and abscess.

Treatment

Acute ischemic stroke is inadequately treated in the USA and worldwide due to a lengthy history of neuroprotective drug failures in clinical trials.

The rapid development of a neuroprotective or cytoprotective compound would allow future stroke victims to receive a treatment to reduce disabilities and further promote recovery of function.

A opinion article reviews in detail the enormous costs associated with developing a small molecule to treat stroke, as well as providing a timely overview of the cell-death time-course and relationship to the ischemic cascade. Distinct temporal patterns of cell-death of neurovascular unit components provide opportunities to intervene and optimize new cytoprotective strategies. However, adequate research funding is mandatory to allow stroke researchers to develop and test their novel therapeutic approach to treat stroke victims 1).


Research has reported how excitatory amino acids act as the major excitatory neurotransmitters in the cerebral cortex and hippocampus. Furthermore, other therapeutic targets such as free radical scavenger strategies and the anti-inflammatory neuroprotective strategy have been evaluated with conflicting data in animal models and human subjects with acute ischemic stroke. Whereas promising combinations of neuroprotection and neurorecovery, such as citicoline, albumin and cerebrolysin have been tested with findings worthy of further evaluation in larger randomized clinical trials. Understanding the complexities of the ischemic cascade is essential to developing pharmacological targets for acute ischemic stroke in neuroprotective or flow restoration therapeutic strategies 2).

Endovascular treatment

Hypothermia

Therapeutic hypothermia is increasingly recognized as having a tissue-protective function and positively influencing neurological outcome, especially in cases of ischemia caused by cardiac arrest or hypoxic-ischemic encephalopathy in newborns. Yet, many aspects of hypothermia as a treatment for ischemic stroke remain unknown. Large-scale studies examining the effects of hypothermia on stroke are currently underway 3).

Brain ischemia and treatment are one of the important topics in neurological science. Free oxygen radicals and inflammation formed after ischemia are accepted as the most important causes of damage. Currently, there are studies on many chemopreventive agents to prevent cerebral ischemia damage. The aim of Aras et al is to research the preventive effect of the active ingredient in genistein There is currently no promising pharmacotherapy aside from intravenous or intra-arterial thrombolysis. Yet because of the narrow therapeutic time window involved, thrombolytic application is very restricted in clinical settings. Accumulating data suggest that non-pharmaceutical therapies for stroke might provide new opportunities for stroke treatment 4).

Progression of focal stroke symptoms still constitutes a serious clinical problem for which heparin has insufficient effectiveness in clinical practice. New therapies, ideally preventive, are needed 5).

Omega 3 fatty acid enhance cerebral angiogenesis and provide long-term protection after stroke 6).

After cerebral ischemia, revascularization in the ischemic boundary zone provides nutritive blood flow as well as various growth factors to promote the survival and activity of neurons and neural progenitor cells. Enhancement of angiogenesis and the resulting improvement of cerebral microcirculation are key restorative mechanisms and represent an important therapeutic strategy for ischemic stroke.

Improvements in acute ischemic stroke (AIS) outcomes have been achieved with intravenous thrombolytics (IVT) and intra-arterial thrombolytics vs supportive medical therapy. Given its ease of administration, noninvasiveness, and most validated efficacy, IVT is the standard of care in AIS patients without contraindications to systemic fibrinolysis. However, patients with large-vessel occlusions respond poorly to IVT. Recent trials designed to select this population for randomization to IVT vs IVT with adjunctive endovascular therapy have not shown improvement in clinical outcomes with endovascular therapy. This could be due to the lack of utilization of modern thrombectomy devices such as Penumbra aspiration devices, Solitaire stent-trievers, or Trevo stent-trievers, which have shown the best recanalization results. Continued improvement in the techniques with using these devices as well as randomized controlled trials using them is warranted 7).

With the emergence of new technologies in imaging, thrombolysis and endovascular intervention, the treatment modalities of acute ischemic stroke will enter a new era 8).

Within 3 h from symptom onset, the existence of FLAIR-positive lesions on pretreatment MRI is significantly associated with an increased bleeding risk due to systemic thrombolysis. Therefore, considering FLAIR-positive lesions on baseline MRI might guide treatment decisions in ischemic stroke 9).

Outcome

Early neurological deterioration (END) is a common condition associated with poor outcome after acute ischemic stroke.

The majority of victims must endure life-long disabilities that not only affect their livelihood, but also have an enormous societal economic impact.

Blood pressure (BP) variability is independently and linearly associated with the development of neurologic deterioration in acute stage of ischemic stroke 10).

1)
Lapchak PA, Zhang JH. The High Cost of Stroke and Stroke Cytoprotection Research. Transl Stroke Res. 2016 Dec 30. doi: 10.1007/s12975-016-0518-y. [Epub ahead of print] PubMed PMID: 28039575.
2)
Tuttolomondo A, Pecoraro R, Arnao V, Maugeri R, Iacopino DG, Pinto A. Developing drug strategies for the neuroprotective treatment of acute ischemic stroke. Expert Rev Neurother. 2015 Oct 15:1-14. [Epub ahead of print] PubMed PMID: 26469760.
3)
Han Z, Liu X, Luo Y, Ji X. Therapeutic hypothermia for stroke: where to go? Exp Neurol. 2015 Jun 6. pii: S0014-4886(15)30017-0. doi: 10.1016/j.expneurol.2015.06.006. [Epub ahead of print] PubMed PMID: 26057949.
4)
Chen F, Qi Z, Luo Y, Hinchliffe T, Ding G, Xia Y, Ji X. Non-pharmaceutical therapies for stroke: Mechanisms and clinical implications. Prog Neurobiol. 2014 Jan 6. pii: S0301-0082(13)00147-0. doi: 10.1016/j.pneurobio.2013.12.007. [Epub ahead of print] PubMed PMID: 24407111.
5)
Rödén-Jüllig A, Britton M. Effectiveness of heparin treatment for progressing ischaemic stroke: before and after study. J Intern Med. 2000 Oct;248(4):287-91. PubMed PMID: 11086638.
6)
Wang J, Shi Y, Zhang L, Zhang F, Hu X, Zhang W, Leak RK, Gao Y, Chen L, Chen J. Omega-3 polyunsaturated fatty acids enhance cerebral angiogenesis and provide long-term protection after stroke. Neurobiol Dis. 2014 Apr 29. pii: S0969-9961(14)00103-X. doi: 10.1016/j.nbd.2014.04.014. [Epub ahead of print] PubMed PMID: 24794156.
7)
Serrone JC, Jimenez L, Ringer AJ. The role of endovascular therapy in the treatment of acute ischemic stroke. Neurosurgery. 2014 Feb;74 Suppl 1:S133-41. doi: 10.1227/NEU.0000000000000224. PubMed PMID: 24402482.
8)
Lu AY, Ansari SA, Nyström KV, Damisah EC, Amin HP, Matouk CC, Pashankar RD,Bulsara KR. Intra-arterial treatment of acute ischemic stroke: the continued evolution. Curr Treat Options Cardiovasc Med. 2014 Feb;16(2):281. doi:10.1007/s11936-013-0281-2. PubMed PMID: 24398801.
9)
Hobohm C, Fritzsch D, Budig S, Classen J, Hoffmann KT, Michalski D. Predicting intracerebral hemorrhage by baseline magnetic resonance imaging in stroke patients undergoing systemic thrombolysis. Acta Neurol Scand. 2014 Jul 18. doi: 10.1111/ane.12272. [Epub ahead of print] PubMed PMID: 25040041.
10)
Chung JW, Kim N, Kang J, Park SH, Kim WJ, Ko Y, Park JH, Lee JS, Lee J, Yang MH, Jang MS, Oh CW, Kwon OK, Jung C, Kim BJ, Han MK, Gorelick PB, Bae HJ. Blood pressure variability and the development of early neurological deterioration following acute ischemic stroke. J Hypertens. 2015 Jul 31. [Epub ahead of print] PubMed PMID: 26237556.
acute_ischemic_stroke.txt · Last modified: 2017/01/03 22:53 (external edit)