Stroke Pentagon: Stroke Management Approach in Resource Poor Settings

Stroke is a neurological condition that is characterized by sudden onset focal neurological deficit due to spontaneous cerebral vascular occlusion or rupture. It is a neurological emergency and its prevalence is very high, especially in developing countries where it assumes an epidemic proportion. It is globally the second most common cause of death after ischaemic heart disease. The poor indices in developing countries are multifactorial and related to late case presentation, ignorance, poverty, and unavailability of comprehensive and well-coordinated stroke care. There is a need to identify the available and cheap stroke management steps in the developing countries and strengthen the system to maximize the benefits in reduction of the morbidity and mortality of stroke. It is against this background that we identified Stroke prevention, acute stroke management, Stroke rehabilitation, Stroke research, and Stroke support as five pillars (stroke pentagon) in stroke management in developing countries. There is a need to sensitize the stakeholders in stroke management as highlighted in the stroke pentagon to assume more responsibility. Moreover, there is the need to have a more coordinated and concerted stroke management approach which will involve all the identified five pillars to ensure improved stroke indices in the developing countries.

Relationship Between Exercise and 18-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography Imaging of Brain in the Elderly

CT were analyzed. The subjects were elderly people aged 55–75 who volunteered for brain 18F of the FDG CT and PET scanning. The elderly who maintained exercise were divided into exercise group and non-exercise group into control group. The images obtained by CT examination showed that the brain of the elderly who insisted on exercise showed a significant increase in glucose metabolism, which indicated that exercise had a preventive effect on brain diseases of the elderly, and reduced the risk of cerebral vascular occlusion and brain atrophy.

Peran Eritropoietin pada Stroke Iskemik Akut

Stroke iskemik merupakan salah satu penyebab stroke tersering, disebabkan oleh oklusi pembuluh darah serebral dan penyebab kematian ketiga. Iskemik otak akan menghasilkan penghasilan mediator inflamasi yang dapat berpartisipasi dalam jejas iskemik di otak. Saat awitan stroke iskemik terjadi, area otak yang diperdarahi oleh pembuluh darah akan kekurangan oksigen dan nutrisi sehingga sel otak terutama neuron berada dalam risiko, neuron ini masih dapat berfungsi yang dikenal sebagai penumbra. Hipoksia jaringan dan iskemik serebral mengaktivasi HIF-1α, yang kemudian mengaktivasi transkripsi gen eritropoietin (EPO) dan Vascular Endothelial Growth Factor (VEGF). Eritropoietin (EPO) merupakan peptida yang juga memiliki efek non–hematopoiesis yaitu berperan mendorong neuroproteksi. Eritropoietin (EPO) dikeluarkan dalam hitungan menit dari proses iskemik dan mencapai puncak dalam 24 jam dari awitan stroke iskemik. Efek neuroproteksi dari EPO yaitu sebagai anti apoptosis, anti oksidan, anti inflamasi, anti eksitoksisitas, neurogenesis, angiogenesis dan neurotropik. Dengan kata lain bahwa EPO dapat mengurangi derajat keparahan akibat oklusi pembuluh darah otak. Role of Eritropoietin in Acute Ischemic StrokeAbstractIschemic stroke is one of the most common causes of stroke, caused by cerebral vascular occlusion and the third cause of death. . Ischemic brain will generate income of inflammatory mediators who can participate in ischemic lesions in the brain. When the recitation of an ischemic stroke occurs, areas of the brain that are obscurated by blood vessels will lack oxygen and nutrients so that brain cells, especially neurons, are at risk, these neurons can still function known as penumbra. Tissue hypoxia and cerebral ischemic activate HIF-1α, which then activates the transcription of the Eritropietin (EPO) and Vascular Endothelial Growth Factor (VEGF) genes. Eritropoietin (EPO) is a peptide that also has the effect of non-hematopoiesis which is responsible for encouraging neuroprotection. Eritropietin (EPO) is issued in minutes of an ischemic process and reaches its peak within 24 hours of the onset ischemic stroke. The neuroprotection effect of EPO is as anti-apoptosis, anti-oxidant, anti-inflammatory, anti-excitation, neurogenesis, angiogenesis and neurotropic. In other words, EPO can reduce the severity due to occlusion of brain blood vessels.

Hypoxia Inducible Factor (HIF) 1-Α dan Vascular Endothelial Growth Factor (VEGF) pada Stroke Iskemik Fase Akut

Stroke iskemik merupakan salah satu penyebab stroke tersering, disebabkan oleh oklusi pembuluh darah serebral dan penyebab kematian ketiga. Saat awitan stroke iskemik terjadi, area otak yang diperdarahi oleh pembuluh darah akan kekurangan oksigen dan nutrisi sehingga sel otak terutama neuron berada dalam risiko, neuron ini masih dapat berfungsi yang dikenal sebagai penumbra. Hipoksik, salah satu karakteristik penumbra merupakan stimulus utama regulasi protein HIF-1α. Hipoksik sendiri merupakan stimulus utama prekondisi iskemik. Prekondisi iskemik akan menghasilkan fenotipe tahan hipoksia yakni protein hypoxia inducible factor (HIF)-1α. HIF-1α merupakan satu-satunya zat yang dikeluarkan oleh jaringan yang mengalami hipoksia. HIF-1α bertindak sebagai protein sinyal yang dapat meregulasi gen protein lain. Efektor HIF-1α antara lain eritropoitin dan vascular endothelial growth factor (VEGF). Pertumbuhan, diferensiasi dan ketahanan sel endotel diregulasi oleh VEGF yang distimulasi dari HIF-1α. Selama iskemik serebral, jaringan yang rusak mencoba untuk meningkatkan pengiriman oksigen melalui induksi angiogenesis melalui produksi VEGF. Hal ini ditandai dengan adanya peningkatan jumlah pembuluh-pembuluh darah mikro di area infark. VEGF dan reseptornya diregulasi oleh HIF-1α dalam hari pertama iskemik.Hypoxia Inducible Factor (HIF) 1-Α and Vascular Endothelial Growth Factor (VEGF) in Acute Ischemic StrokeAbstractIschemic stroke is one of the most common causes of stroke, caused by cerebral vascular occlusion and the third cause of death. When the onset of an ischemic stroke occurs, the area of the brain bleeding by blood vessels will lack oxygen and nutrients so that brain cells, especially neurons, are at risk, these neurons can still function known as penumbra. Hypoxic, one of the characteristics of penumbra is the main stimulus for regulation of HIF-1α protein. Hypoxia itself is the main stimulus of ischemic precondition. The ischemic precondition will produce a hypoxic-resistant phenotype namely protein hypoxia inducible factor (HIF) -1α. HIF-1αis the only substance released by tissue that experiences hypoxia. HIF-1α acts as a signaling protein that can regulate other protein genes. Effectors of HIF-1αinclude erythropoitin and vascular endothelial growth factor (VEGF). Growth, differentiation and endurance of endothelial cells are regulated by VEGF stimulated from HIF-1α. During cerebral ischemia, damaged tissue tries to increase oxygen delivery through induction of angiogenesis through VEGF production. This is characterized by an increase in the number of micro blood vessels in the infarct area. VEGF and its receptors are regulated by HIF-1α in the first day of ischemia.