Stroke - Types, Treatments, Preventions (Dangerous Disease, Causing Death)
Stroke (English: stroke, cerebrovascular accident, CVA) is a condition that occurs when the blood supply to a part of the brain is suddenly interrupted. In brain tissue, the lack of blood flow causes a series of biochemical reactions, which can damage or kill nerve cells in the brain. Death of brain tissue can cause loss of function that is controlled by the network. Stroke is the third leading cause of death in the United States and many industrialized countries in Europe (Jauch, 2005). When can be saved, sometimes patients experience paralysis in limbs, loss of memory or speech. In recent years more and more popular the term brain attack. This term corresponds to the term that is well known, "heart attack".
Stroke occurs because blood vessels branch obstructed by emboli. Emboli can be either cholesterol or air.
Classification
Stroke is divided into two types of ischemic stroke and Hemorrhagic strokes. A prognosis of the results of a study in Korea stated that, 75.2% of ischemic strokes suffered by men with a prevalence of hypertension, smoking and alcohol consumption. Based on the TOAST system, the composition is divided into Laas 20.8%, 17.4% LAC, CEI 18.1%, 16.8% and 26.8% ude ODE.
Hemorrhagic Stroke
In Hemorrhagic stroke, ruptured blood vessels thereby inhibiting the normal flow of blood and blood seeps into the region in the brain and damage it. Bleeding can occur in all parts of the brain such as caudate putamen; thalamus; hippocampus; frontal, parietal, and occipital cortex; hypothalamus; suprachiasmatic area; cerebellum; pons, and midbrain. Nearly 70 percent of cases of hemorrhagic stroke attack patients with hypertension.
Hemorrhagic strokes are divided into subtypes intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), cerebral venous thrombosis, stroke and spinal cord. ICH further divided into parenchymal hemorrhage, hemorrhagic infarction and punctate hemorrhage.
Ischemic Stroke
In ischemic stroke, blockage can occur in arteries along the path leading to the brain. Blood to the brain is supplied by two internal carotid arteries and two vertebral arteries. These arteries are branches of the aortic arch of the heart (aortic arch).
Aetiological classification system
Several classification systems are based on considerations have been applied to the etiology of ischemic stroke. Some of these systems failed to follow the changing times and no longer used, some other systems can still be accepted by most people and used within a limited scope. Here are the most current classification system and the most widely used.
TOAST system
TOAST system (English: Trial of ORG 10172 in Acute Stroke Treatment) first developed the therapy of acute ischemic stroke in early 1990. The system is largely based on clinical features but still consider diagnostic information from CT, MRI, transthoracic echocardiography, extracranial carotid ultrasonography, and if possible, cerebral angiography.
TOAST system is divided into 5 subtypes of stroke, large artery atherosclerosis (Laas), cardiaoembolic infarct (CEI), small artery occlusion / lacunar infarct (LAC), a stroke of another determined cause / origin (ODE), and strokes of an undetermined cause / origin (Ude).
CCS Systems
CCS classification system (English: causative Classification of Stroke System) is similar to the system with the TOAST subtype differences in large artery atherosclerosis can be divided into occlusive and stenotic. For example, ≥ 50% diameter reduction, or reduction in diameter of <50% with plaque ulceration or thrombosis. And undetermined cause subtypes differentiated further into unknown, incomplete evaluation, unclassified stroke (more than one etiology), and cryptogenic embolism.
ASCO System
ASCO is the acronym of atherothrombosis, small vessel disease, cardiac Causes, and other Causes uncommon. ASCO is a classification system based on system phenotype. Each phenotype is still divided into levels 0, 1, 2, 3 or 9. Level 0 means the disease is completely absent, 1 means definitely a potential cause of the index stroke, 2 and 3 for causality uncertain for Unlikely a direct cause of the index stroke (but disease is present), 9 for the grading is not possible due to insufficient work-up.
In this system, patients can be categorized into more than one etiological subtype, for example, patients with carotid atheroma causing stenosis of 50% and atrial fibrillation with atherosclerosis and cardiac embolism, or translated into as A1-S9-C0-O3.
UCSD Stroke Databank System
UCSD system classification ischemic stroke into large-vessel stenotic, large-vessel occlusive, stenotic Small-vessel, small-vessel occlusive, embolic and unknown cause. While the classification of Hemorrhagic strokes are divided into the same subtype of the type of intracerebral and subarachnoid.
HCSR System
HCSR System (English: Harvard Cooperative Stroke Registry) to make a classification into subtypes of stroke are accompanied by thrombosis in the arteries or with lacunar infarction, cerebral embolism, intracerebral hematoma, subarachnoid hemorrhage from an aneurysm or arteriovenous malformation.
NINCDS Stroke Data Bank System
In the Stroke Data Bank of the National Institute of Neurological and Communicative Disorders and Stroke diagnostic subtypes classification be based on patient clinical history, examination, laboratory tests including tomography, noninvasive vascular imaging, and when possible and relevant, angiography. The diagnosis of subtypes of infarcts of undetermined cause (IUC) can be reclassified into subtypes of idiopathic pulmonary embolism, stenosis or thrombosis in the arteries, lacunar infarcts, and superficial infarction nonlakunar syndrome.
Other systems
Some other experts consider the classification based on phenotype such as the existence of the internal carotid artery plaque, intima-media thickness, leukoaraiosis, cerebral microbleeds (CMB), or multiple lacunae.
Hemosiderin deposits intracerebral CMB is contained in the pervaskular. Expression of the CMB is very high in lacunar infarction and infarction aterotrombotik, and low expression in the infarct kardioembolik. CMB and leukoaraiosis very closely related. The results show that the CMB prognosis is found in 47-80% of cases of primary intracerebral haemorrhage and 0-78% in cases of ischemic cerebrovascular disease.
Pathophysiology
Until now, the pathophysiology of stroke is a study which is largely based on a series of studies, of the various processes are interrelated, including the failure of energy, loss of homeostasis ion cells, acidosis, elevated levels of Ca2 + cytosolic, eksitotoksisitas, toxicity by free radicals, production of acid Arachidonic, cytotoxicity with sitokina, activation of the complement system, disruption of the blood brain barrier, glial cell activation and infiltration of leukocytes.
Central area of the exposed brain ischemia will experience a dramatic decrease in blood flow, the level of injury and trigger reactions such as eksitotoksisitas trajectory that led to necrosis of the central area of infarction is surrounded by a penumbra / peri-infarction zone. According to the morphology, cellular necrosis is swelling due to disruption of the cell nucleus, organelles, plasma membrane, and the disintegration of the core structure and the cytoskeleton.
In the area of penumbra, will try to neural apoptosis is inhibited by both mechanisms eksitotoksik and inflammation, because brain cells are still normal derivative would induce the immune system to increase tolerance of brain tissue against ischemic conditions, in order to remain able to perform normal metabolic activities. Proteins such as pancortin typical CNS-2 would interact with the actin modulator proteins, Wiskott-Aldrich syndrome protein verprolin homologous-1 (WAVE-1) and Bcl-xL would form mitochondrial protein complexes for the inhibition process.
Recent research shows that many neurons in the penumbra area may undergo apoptosis after several hours / days as part of the process of tissue recovery post-stroke with two trajectories, ie trajectories extrinsic and intrinsic path.
Ischemia not only affects parenkima brain tissue, but also affects the extracranial system. Therefore, the stroke will induce a dramatic immunosuppression via excessive activation of the sympathetic nervous system, thus allowing the occurrence of bacterial infections such as pneumonia.
Eksitotoksisitas glutamic acid
Glutamic acid is an amino acid neurotransmitters in the brain main eksitatorial, will accumulate in the extracellular space and activates pencerapnya. Activation of perceiving glutamate will affect the concentration of intracellular ions, especially ions Na + and Ca2 +. Increased influx of Na + ions can make the cells become injured at the beginning of ischemia, but research shows that most of the cell damage caused by the toxicity of glutamic acid during ischemia is caused more by an increase in excessive intracellular influx of calcium ions which then cause toxic effects.
Oxidative Stress
Throughout the process of stroke, an increase of free radicals such as superoxide anions, hydroxyl radicals and NO. The main source of oxygen derived free radical compounds commonly called reactive oxygen species in the process of ischemia is the mitochondria. While the production of superoxide during post-ischemic compounds is arachidonic acid metabolism via the cyclo-oxygenase path and lipo-oxygenase. Free radicals can also be produced by activated microglia cells and leukocytes through NADPH oxidase system immediately after reperfusion in ischemic tissue. Oxidation will cause further damage in the network and is an important molecule to trigger apoptosis after ischemic stroke.
NO is generally produced from L-arginina with one isoform of NO synthase, and a cluster of differentiation of neurons throughout the brain as nNOS. Activation of nNOS requires calcium / calmodulin. On the other hand, the expression of iNOS (English: inducible NOS) found in inflammatory cells such as microglia cells and monocytes. Both nNOS and iNOS isoforms have a role that damage the brain in the period of ischemia. However, all three isoforms of eNOS (English: endothelial NOS) has the effect of vasodilation and not destructive.
Activation of NMDA during ischemia perceiving will stimulate the production of NO by nNOS. NO formed will enter into the cytoplasm and reacts with superoxide and produce a kind of highly reactive oxygen species that is peroksinitrita (ONOO-).
Post-ischemia, both types of reactive oxygen species and reactive nitrogen species then serve to activate some metabolic trajectories such as inflammation, apoptosis, and decreased oxygen supply which affects the increase in lactic acid through anaerobic glycolysis or acidosis. Also, it would seem iNOS gene expression in vascular cells or cells undergoing inflammation and COX-2 gene expression in nerve cells in the area between infarct and penumbra. Both of these inflammatory genes will increase ischemic damage.
Lipid peroxidation
In addition to producing a variety of compounds of ROS, the trajectory of acidosis also participated in the process of intracellular protein synthesis. Lipid peroxidation in cell membranes that induces apoptosis of neurons, would result in compounds called aldehydes hidroksinonenal 4-(4-HNE), which will react with membrane transporters such as Na + / K + ATPase, glutamate transporters and glucose transporter.
Damage in the membrane transporter, which causes excessive influx of Ca2 + ions and free radicals, further activates the transcription factor NF-κB such as neuroprotective, HIF-1 and IRF-1. Activation of these transcription factors to induce the production of sitokina inflammation such as IL-1, IL-6, TNF-α, kemokina such as IL-8, MCP-1, cell adhesion molecules such as selectin, ICAM-1, VCAM-1 and pro-inflammatory genes such as IIP-10.
Blood-brain barrier dysfunction
The blood brain barrier which is the endothelium in the brain tissue will respond to the injury resulting from stroke by increasing permeability and decreasing functions, along with the degradation of basal lamina on the walls of veins. Therefore, in acute conditions, stroke will increase the interaction between brain endothelial cells with extravascular cells such as astrocytes, microglia, neurons, with intravascular cells such as platelets, leukocytes, and further contribute to the inflammatory process, in addition to changes in circulating levels of ICAM- 1, trombomodulin, tissue factor and tissue factor pathway inhibitor. endothelial dysfunction which causes a deficiency of the blood brain barrier, impaired cerebral autoregulation and prothrombotic changes are believed to be the cause of cerebral small vessel disease (SVD). Patients (SVD) may have lacunar infarcts, or with accompanying leukoaraiosis.
Of the 594 patients with stroke, leukoaraiosis was found in 55.4% of cerebral large vessel disease (LVD) or atherosclerosis, 30.3% in SVD and 14.3% in cardioembolic disease. In pronosis LVD, leukoaraiosis had a tendency toward intracranial stenosis group with 40.3% for intracranial group, 26.9% for extracranial group and 45.5% for the group a combination of both. No correlation was found between leukoaraiosis with diabetes mellitus, hyperlipidemia, smoking, hypertension and heart disease.
Infiltration of leukocytes
In brain tissue, there are several populations of cells with the capacity to secrete sitokina after stimulation of ischemia, namely endothelial cells, astrocytes, microglia cells and neurons.
The role of post-ischemic inflammatory response by microglia cells, especially in the penumbra area with secretion of pro-inflammatory sitokina, toxic metabolites and enzymes. In addition, microglia and astrocytes cells also secrete neuroprotective factors such as erythropoietin, TGFβ1, and metalotionein-2.
There is ample evidence to demonstrate the role of leukocytes in the pathogenesis of injury due to stroke as a result of reperfusion injury in tissue and microvascular dysfunction. Evidence can be classified into 3 main parts namely,
* Post-ischemia leukocytes accumulate until there is tissue injury
* Simtoma ischemia responded with an increase in neutrophils. In experiments with mice, the low population of neutrophils in the circulation of the blood showed a smaller infarct volume.
* Prevention of cell adhesion between leukocytes with endothelial cells at blood-brain barrier, with a monoclonal antibody shown to provide protection against injury from stroke.
Accumulation of T cells occurs after ischemia, and is estimated to cause reperfusion. CD8 T cells can induce brain injury with a molecule of the cytotoxic granules. Th1 cells CD4 + secretion sitokina pro-inflammation including IL-2, IL-12, IFN-γ and TNF-α may exacerbate the effects of stroke, while cells TH2 CD4 + with sitokina anti-inflammatory such as IL-4, IL-5, IL-10 and IL-13 further has a protective role.
Bleeding
In animal experiments on rabbits, at least sitokina TNF-α or antibody play a role on the occurrence of bleeding after ischemic stroke induced by klot. In this case an increase in the prognosis of bleeding from 18.5% to 53.3% and an increase in volume bleeding up to 87%. In addition, the use of tissue plasminogen activator (tPA) with a standard dose of 3.3 mg / kg will increase the likelihood of bleeding from 18.5% to 76.5%, the effect of tPA can be mitigated by the use of anti-TNFα antibodies. Giving EPO after 6 hours of a stroke will worsen the tPA-induced hemorrhage by mediating MMP-9, NF-κB and interleukin-1 receptor-associated kinase-1 (IRAQ-1).
In rats, TNF-α will induce the expression of MMP-9 that lower levels of protein in the blood brain barrier as okludin, and increased permeability in brain capillaries. and modulates MMP-9, gelatinase A for open the blood brain barrier. Bleeding that occurs then the body responds by producing urokinase-type plasminogen activator (UPA). Expression of MMP-9 can also be induced by lipopolysaccharide.
Risk factors
* Smoking
* Alcohol
* Diet
* High levels of cholesterol
* Family history
Hypertension
Hypertension would stimulate the formation of atherosclerotic plaque in the arteries and arterioles in the brain, and induces lipohialinosis trajectory in the basal ganglia vessels, until caused lacunar infarction or brain hemorrhage.
Atrial Fibrillation
Atrial fibrillation is an indication of kardioembolisme, whereas kardioembolisme stock represents 20% of ischemic cause. Kardioembolisme occurs due to the lack of contraction of heart muscle in the left ventricle, called stasis, which occurs by a buildup of the concentration of fibrinogen, D-dimer and von Willebrand factor. This is an indication of prothrombotic status with myocardial infarction, which in turn, would release the thrombus is formed, with consequent increased risk of embolization in the brain. About 2.5% of patients with acute myocardial infarction will have a stroke within 2 to 4 weeks, 8% of men and 11% of women will experience an ischemic stroke within 6 years, because of dysfunction and cardiac left ventricle aneurysm.
Atherosclerosis
Research on the trajectory aterogenesis that trigger atherosclerosis has focused on coronary arteries, but a similar process also occurs in the brain and cause ischemic stroke. Atherosclerosis can affect arteries of the brain such as the carotid arteries, arteries in the midbrain, and basilar arteries, or to the arteriolar vessels of the brain such as lenticulostriate vessels, basilar penetrating and medullary. Some research suggests that the mechanisms of atherosclerosis affecting the arteries can be slightly different from the mechanism of the arteriolar vessels.
Intracranial atherosclerosis is considered as a very rare condition. An autopsy of the brain infarction of 339 stroke patients who died from intracranial atherosclerosis, intracranial plaques found 62.2% and 43.2% intracranial stenosis. An autopsy by the National Cardiovascular Center, Osaka, Japan on 142 stroke patients who died within 30 days starting from an attack of ischemia, suggesting that both types of thrombus that is rich in blood platelets and fibrin-rich developing in culprit plaque in the arteries of the brain is a major factor aterotrombotik stroke. 70% of cases showed the presence of stroke kardioembolik thrombus formation as potential sources of embolism in the heart or veins of patients with patent foramen ovale and tetralogy of Fallot. Generally thrombus platelet-rich veins that settles in the heart, will be detached and form emboli in the arteries of the brain.
Diabetes mellitus
Based on autopsy studies, patients with diabetes mellitus are prone to lacunar infarction and cerebral small vessel disease. Epidemiological studies show that diabetes is a risk factor for ischemic stroke. Pathogenesis of stroke, triggered apparently started from reasi excessive glycation and oxidation, endothelial dysfunction, increased platelet aggregation, fibrinolysis deficiency and insulin resistance. In rats, ischemic strokes that occur in diabetes mellitus will trigger Hemorrhagic strokes are accompanied by an increase in enzyme MMP-9 in the brain that worsen the condition of leukoaraiosis.
Transient ischemic attack (TIA)
Transient ischemic attack (TIA), also called acute cerebrovascular syndrome (ACVS), is one of the risk factors of ischemic stroke.
TIA can be described as a brief episode of neurologic dysfunction that usually occurs due to vascular disorders, in the form simtoma in the brain or retinal ischemia lasting less than 24 hours, or less than 1 hour, without leaving a trace in the form of cerebral infarction acute.
From another perspective, because stroke is a neurologic deficiency due to blood flow changes in brain tissue, so the TIA can be regarded as an indication or simtoma arising from changes in cerebral blood flow that can not be detected clinically within 24 hours.
TIA will not necessarily be indicative of the occurrence of stroke in later life, and are rarely associated with primary Hemorrhagic stroke. In a human population that has been getting old, TIA induced by obstruction of blood flow in large blood vessels mainly due to atherothrombotic, but in patients aged under 45 years of TIAs are usually caused by rupture of blood vessels (English: arterial dissection), migraine and drug- sympathomimetic drugs. TIA also can be caused by:
* Large artery atherothrombosis with distal flow reduction
* Arteriosclerosis in small blood vessel ("lacunar Tias")
* Emboli Kardiogenic and inter-arterial embolism
* Vasospasma
* Vasculitis
* Sludging-polycythemia. sickle cell anemia. Trombositemia and the like
* Hypercoaguable-puerperal states. Oral contraceptive use. 'Sticky platelet syndrome "and the like
* Meningitis
* Cortical vein thrombosis, dehydration. Puerperium. Infection. Neoplasms and the like
* Dysplasia fibromuscular
* Moyamoya Syndrome
* Takayasu arteritis
However, several other conditions can cause symptoms very similar to the TIA, such as focal seizure activity, migraine (? "Spreading depression"), compressive mononeuropathies (carpal tunnel syndrome. Ulnar elbow compression and so forth), Adams-Stokes syndrome, brain tumors with Transient neurologic symptoms, subdural hematoma, demyelinating disease, hypoglycemia, hyperglycemia, primary ocular disease, glaucoma, vitreal hemorrhage. floaters and the like, hysteria-conversion functional disorders, Malingering, hyperventilation.
Cardiac papillary fibroelastoma (CPF)
Of the 725 cases of CPF, 55% were male patients with tumor location, generally, is found in the valvular surface, especially in trikuspidalis aortic valve, but valve mitralis. Tumors were also found in non-valvular surface, as in the left ventricle. Tumor size varies from 2 mm to 70 mm.
CPF clinical manifestations include stroke, myocardial infarction, pulmonary embolism, congestive heart failure and sudden cardiac arrest. However, not all patients show such simtoma.
Cryptogenic cerebral infarction (CCI)
CCI is most commonly found in patients with patent foramen ovale either accompanied or not accompanied by septal aneurysm. Since 1989, CCI is the cause of 40% of cases of ischemic stroke. 4.9% of men and 2.4% of women with mutations of alpha-galactosidase which is indicative of Fabry disease, whereas other studies showed association with thrombophilia. path was estimated to include CCI pathogenesis of atherosclerosis in the arteries of the brain, both intracranial like moderate middle cerebral artery stenosis, such as the extracranial vertebral artery stenosis or proximal origin as thick plaques in the aortic arch that had been considered not related to the pathogenesis of stroke.
Patent foramen ovale (PFO)
Platipnea-ortodeoksia syndrome is a rare condition with simtoma of dyspnea and arterial desaturation. PFO is one form-ortodeoksia platipnea syndrome with orthostatic increase in the area of atrial septal deficiency. The diagnosis of PFO is frequently found on the CCI and migraine, are also thought to cause embolism in patients with arterial thromboembolism.
Diagnosis
Is a clinical diagnosis of stroke and its investigation. Investigations that can be done include head CT scan, MRI. To assess awareness of stroke patients can use the Glasgow Coma Scale. To distinguish the type of stroke can be used a variety of scoring systems, such as the Siriraj Stroke Score, Stroke Algorithm Gajah Mada, or algorithm Junaedi.
Clinical Simtoma
Features a very common ischemic stroke, according to the Uniformed Services University of the Health Sciences, was based on the number of results of physical examination of patient diagnosis were summarized in a single period. USUHS following tables summarize the general public to be used to recognize the clinical symptoms of a stroke as early as possible. And for medical professionals, the National Institutes of Health stroke scale has made the table as a guide to making a diagnosis in less than about 5 to 10 minutes.
Simtoma paraklinis
Some biochemical compounds in blood serum that can be used as the basis of diagnosis and prognosis of brain necrosis, among others:
S100-β is a peptide secreted astrocytes during brain injury occurs, the process of neurodegeneration and psychiatric disorders. S100-β is a compound of calcium binding, in vitro, at low levels, interactions with the immune system in the brain will improve the survival of developing neurons, however, at higher levels, S100-β stimulates the production of pro-inflammatory sitokina and apoptosis.
Studies on animals show neuroprotective effects of S100-β with teraktivasinya cellular processes in neurons that NMDA-induced eksitotoksisitas hold. Increased serum S100-β always occur in ischemic stroke, and occur also in other conditions such as traumatic brain injury (TBI), Alzheimer's and schizophrenia.
When there is an ischemic stroke, serum concentrations of S100-β reached a maximum on days 2 through 4. The maximum concentration value of S100-β associated with the NIH stroke scale, and pathophysiology of infarct size, so the higher the maximum value of S100-β, the higher the risk of Hemorrhagic transformation. Increased S100-β is also found in primary Hemorrhagic strokes, which shows the initial hematoma volume.
Elevated levels of S100-β does not have to happen quickly, and many cells other than astrocytes and Schwann cells that get the highest S100-β, so the use value of serum S100-β as one of the basic diagnosis of stroke is still quite vulnerable. However, several studies have shown that serum S100-β is more related to the condition of the blood brain barrier integrity.
Glial fibrillary-associated protein (GFAP)
GFAP is a monomeric intermediate filament protein found in astrocytes and brain ependimal cells that function as part of the cytoskeleton. Serum levels of S100-β and GFAP will rise sharply in 1-2 days according to infarct size, and returned to normal about 3 weeks later.
Serum GFAP is a more sensitive indicator than the S100-β in minor stroke or minor stroke, but the time delay increases in serum was made in diagnostic applications are limited.
MBP is the hydrophilic proteins important for the structure of the myelin sheath. MBP levels in CSF are often used as an indication of pathogen activity in multiple sclerosis. Stroke is also accompanied by elevated levels of MBP in CSF is approximately 1 week after the attack, and returned to normal after the third week.
Fatty acid-binding proteins (FABPs)
FABP is a group of intracellular molecules that play a role in supporting and as long-chain fatty acid transport, which will be secreted into the blood circulation shortly after cell damage. In the human body there are 9 types of FABP are scattered in each of the different tissue types. Four types of FABP found in the nervous system, two of which are only found in the adult central nervous system, namely brain-type (B-FABP) in glia and heart-type (H-FABP) in neurons.
The discovery of H-FABP in various types of tissue are signs of acute myocardial infak. B-FABP in the network in the central nervous system and can not be detected in healthy human blood serum. Serum H-FABP and B-FABP will be sharp in 2-3 hours after a stroke. B-FABP is a very sensitive indication of lacunar infarcts and subcortical infarcts, but does not indicate the level of damage that occurs in neurons, and not a specific indication of the occurrence of stroke. Conversely an increase in H-FABP is directly proportional to the size of the infarct and the level of nerve damage.
Neuron-specific enolase (NSE)
NSE is one of three forms of enolase, an enzyme contained in the trajectory of glycolysis. Although quite specific in neurons, NSE can also be found in the neuroendocrine cell culture and related forms of cancer cells. NSE concentration in CSF would increase as the occurrence of ischemic stroke and a number of other brain injuries such as subarachnoid hemorrhage, ICH, etc., until it begins to be detected after 4-8 hours after the attack. The highest concentration after an ischemic stroke have a correlation with the value on the NIH stroke scale.
Tau protein (TP)
The brain has 6 isomers TP which enables the formation of microtubules with tubulin interaction. Elevated levels of TP occurs very slowly and only 27% of the total concentration increased beyond the upper limit of normal threshold within 24 hours after ischemic stroke, but this concentration value indicates the size of the infarct and stroke strata. Elevated levels of TP in the CSF after stroke is also an indication of the size of the infarct. But the stroke did not affect the levels of β-amyloid, and klusterin ApoE in the CSF.
Acute stroke patients are usually given BC-20 302, or microplasmin, oxygen, fitted to enter the infusion of fluids and nutrients, is then given mannitol or corticosteroids to reduce swelling and pressure inside the brain, due to blood cell infiltration white. Recent research shows that paralysis and other symptoms can be prevented or restored if recombinan tissue plasminogen activator (rtPA) or streptokinase which serves to destroy embolism administered within 3 hours, after the onset of stroke. Thrombolysis with rtPA proved useful in the management of acute stroke, although it can increase the risk of cerebral hemorrhage, especially in areas that open the blood brain barrier.
Some compounds are given together with rtPA to reduce those risks, among others, batimastat (BB-94) and marimastat (BB-2516), which inhibits MMP enzymes, compounds such as the spin trap agent alpha-phenyl-Nt-butylnitrone (PBN) and disodium-[tert-butylimino) methyl] benzene-1 ,3-disulfonate N-oxide (NXY-059), and compound anti-ICAM-1.
Method of treatment using the albumin hemodilution is still controversial, but research by The Amsterdam Stroke Study provide a prognosis of mortality reduction from 27% to 16%, increase self-reliance activities from 35% to 48%, while 3 months after an attack of acute stroke .
Recovery
Stroke associated with limited recovery of brain function, although the peri-infarct area becomes more neuroplastik thus allowing improvement sensorimotorik perform remapping function in brain areas that were damaged. At the cellular level, there are two processes of regeneration in the peri-infarct cortex, the axons will experience a change in phenotype of neurotransmitters into the regenerative status, and stick the stems to create a new connection under the influence trombospondin, , laminin, and NGF results Schwann cell secretion, and neuronal progenitor cell migration into the peri-infarct cortex. Almost all the attacks occurred 1 month after stroke, peri-infarct region will experience a decline in the growth inhibitor molecule. At this time, neurons will activate genes that stimulate growth, in an undulating rhythm. Neurogenesis intertwined with angiogenesis also occurs wavy migrating neuroblasts that begin with the expression of GFAP, which is in subventrikular zone into peri-infarct cortex. Migration is mediated by several compounds such as erythropoietin, stromal-derived factor 1 (SDF-1) and angiopoietin-1, to generate neuroblasts with mileage and a longer migration timescales shorter cytokinesis.
Inhibition of GABA ekstrasinaptik perceiving function in peri-infarct area caused by the dysfunction of the GABA transporter GAT-3/GAT-4, in rats, can be restored by administering benzodiazepines.
Prevention
In men without risk factors for stroke with age below 65 years, the risk of stroke in 1 year range at 1%. Upon the occurrence of a mild stroke or TIA, the use of compounds such as anti-coagulant warfarin, a drug used for patients with atrial fibrillation, will reduce the risk of stroke from 12% to 4% in one year. While the use of anti-platelet compounds such as aspirin, generally at a daily dose of 30 mg or more, will only provide protection with a reduced risk to 10.4%. The combination of aspirin with dipyridamole provide further protection to the annual risk reduction into 9 , 3%.
The best way to prevent stroke is to identify people at high risk and control risk factors for stroke as much as possible, such as smoking, hypertension, and stenosis in the carotid arteries, set up a healthy diet and avoid foods that contain cholesterol (LDL), and olaraga regularly. Stenosis is an endothelial vasodilation effect that is generally caused by a decline in the secretion of NO by endothelial cells, ascorbic acid can be mitigated to increase the secretion of NO by endothelial cells through the trajectory of NO synthase or cyclase guanilat, reduce nitrita into NO and inhibit oxidation of LDL on the trajectory of atherosclerosis.
Some health institutions such as the American Heart Association or the American Stroke Association Council, Council on Cardiovascular Radiology and Intervention provides prevention guide that starts with careful handling of the various diseases that can be caused by atherosclerosis, the use of anti-thrombotic compounds to kardioembolisme and anti-platelet compound for the case non-kardioembolisme, followed by controlling risk factors such as arterial dissection, patent foramen ovale, hyperhomocysteinaemia, hypercoagulable states, sickle cell disease; cerebral venous sinus thrombosis; stroke during pregnancy, stroke due to post-menopausal hormone use, use of anti-coagulant compound after the occurrence of cerebral hemorrhage; hypertension, hypertension, smoking, diabetes, atrial fibrillation, dyslipidemia, carotid stenosis, obesity, metabolic syndrome, excessive alcohol consumption, excessive consumption of drugs, contraceptive drug consumption, snoring, migraines, increased lipoprotein and phospholipase.
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