JURNAL

Stroke
Also called: Brain attack
A stroke is a medical emergency. Strokes happen when blood flow to your brain stops. Within minutes, brain cells begin to die. There are two kinds of stroke. The more common kind, called ischemic stroke, is caused by a blood clot that blocks or plugs a blood vessel in the brain. The other kind, called hemorrhagic stroke, is caused by a blood vessel that breaks and bleeds into the brain. "Mini-strokes" or transient ischemic attacks (TIAs), occur when the blood supply to the brain is briefly interrupted.
Symptoms of stroke are
• Sudden numbness or weakness of the face, arm or leg (especially on one side of the body)
• Sudden confusion, trouble speaking or understanding speech
• Sudden trouble seeing in one or both eyes
• Sudden trouble walking, dizziness, loss of balance or coordination
• Sudden severe headache with no known cause
If you have any of these symptoms, you must get to a hospital quickly to begin treatment. Acute stroke therapies try to stop a stroke while it is happening by quickly dissolving the blood clot or by stopping the bleeding. Post-stroke rehabilitation helps individuals overcome disabilities that result from stroke damage. Drug therapy with blood thinners is the most common treatment for stroke.
A stroke is the rapidly developing loss of brain function(s) due to disturbance in the blood supply to the brain. This can be due to ischemia (lack of blood supply) caused by thrombosis or embolism or due to a hemorrhage. As a result, the affected area of the brain is unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or inability to see one side of the visual field.[1] In the past, stroke was referred to as cerebrovascular accident or CVA, but the term "stroke" is now preferred.[citation needed]
A stroke is a medical emergency and can cause permanent neurological damage, complications, and death. It is the leading cause of adult disability in the United States and Europe. In the UK, it is the second most common cause of death, the first being heart attacks and third being cancer. It is the number two cause of death worldwide and may soon become the leading cause of death worldwide.[2] Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation.[3] High blood pressure is the most important modifiable risk factor of stroke.[1]
The traditional definition of stroke, devised by the World Health Organization in the 1970s,[4] is a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours.[1] With the availability of treatments that, when given early, can reduce stroke severity, many now prefer alternative concepts, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.[5]
A stroke is occasionally treated with thrombolysis ("clot buster"), but usually with supportive care (speech and language therapy, physiotherapy and occupational therapy) in a "stroke unit" and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole), blood pressure control, statins, and in selected patients with carotid endarterectomy and anticoagulation.[1]
Strokes can be classified into two major categories: ischemic and hemorrhagic. Ischemia is due to interruption of the blood supply, while hemorrhage is due to rupture of a blood vessel or an abnormal vascular structure. 80% of strokes are due to ischemia; the remainder are due to hemorrhage. Some hemorrhages develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhages actually start off as ischemic stroke.[1]
[edit] Ischemic stroke
Main articles: Cerebral infarction and Brain ischemia
In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are four reasons why this might happen: thrombosis (obstruction of a blood vessel by a blood clot forming locally), embolism (idem due to an embolus from elsewhere in the body, see below),[1] systemic hypoperfusion (general decrease in blood supply, e.g. in shock)[6] and venous thrombosis.[7] Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.[1][8]
There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.[9][10] The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).[1][11]
[edit] Hemorrhagic stroke
Main articles: Intracranial hemorrhage and intracerebral hemorrhage


CT scan showing an intracerebral hemorrhage with associated intraventricular hemorrhage.
Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g. headache, previous head injury). Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging hematoma (pooling of blood).[citation needed]
Ischemic





Ischemic stroke accounts for about 85 percent of all cases. View a detailed animation of ischemic stroke.
Ischemic strokes occur as a result of an obstruction within a blood vessel supplying blood to the brain. The underlying condition for this type of obstruction is the development of fatty deposits lining the vessel walls. This condition is called atherosclerosis. These fatty deposits can cause two types of obstruction:






Click to enlarge


Cerebral thrombosis refers to a thrombus (blood clot) that develops at the clogged part of the vessel.
Cerebral embolism refers generally to a blood clot that forms at another location in the circulatory system, usually the heart and large arteries of the upper chest and neck. A portion of the blood clot breaks loose, enters the bloodstream and travels through the brain's blood vessels until it reaches vessels too small to let it pass. A second important cause of embolism is an irregular heartbeat, known as atrial fibrillation. It creates conditions where clots can form in the heart, dislodge and travel to the brain.
Hemorrhagic
Hemorrhagic stroke accounts for about 15 percent of stroke cases. View a detailed illustration of hemorrhagic stroke.
It results from a weakened vessel that ruptures and bleeds into the surrounding brain. The blood accumulates and compresses the surrounding brain tissue. The two types of hemorrhagic strokes are intracerebral hemorrhage or subarachnoid hemorrhage.
Hemorrhagic stroke occurs when a weakened blood vessel ruptures. Two types of weakened blood vessels usually cause hemorrhagic stroke: aneurysms and arteriovenous malformations (AVMs).
An aneurysm is a ballooning of a weakened region of a blood vessel. If left untreated, the aneurysm continues to weaken until it ruptures and bleeds into the brain. Learn more about cerebral aneurysm.
An arteriovenous malformation (AVM) is a cluster of abnormally formed blood vessels. Any one of these vessels can rupture, also causing bleeding into the brain. Learn more about AVM.
Transient ischemic attacks
Also called TIAs, transient ischemic attacks are minor or warning strokes. In a TIA, conditions that can cause an ischemic stroke are present and the typical stroke warning signs develop. However, the obstruction (blood clot) occurs for a short time and tends to resolve itself through normal mechanisms.
Even though the symptoms disappear after a short time, TIAs are strong indicators of a possible major stroke. Steps should be taken immediately to prevent a stroke. View a detailed animation of TIA.


Causes

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Thrombotic stroke
In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus." Thrombotic stroke can be divided into two types depending on the type of vessel the thrombus is formed on:
• Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Diseases that may form thrombi in the large vessels include (in descending incidence): atherosclerosis, vasoconstriction (tightening of the artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia.
• Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery. Diseases that may form thrombi in the small vessels include (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) and microatheroma (small atherosclerotic plaques).
Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. A stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.[18]
Embolic stroke
An embolic stroke refers to the blockage of an artery by an embolus, a travelling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).
Because an embolus arises from elsewhere, local therapy only solves the problem temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.
Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain.
Cardiac causes can be distinguished between high and low-risk:[19]
• High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of the mitral or aortic valve disease, artificial heart valves, known cardiac thrombus of the atrium or vertricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction, chronic myocardial infarction together with ejection fraction <28 percent, symptomatic congestive heart failure with ejection fraction <30 percent, dilated cardiomyopathy, Libman-Sacks endocarditis, Marantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial myxoma and coronary artery bypass graft (CABG) surgery
• Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in the ascending aorta or proximal arch
Systemic hypoperfusion
Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by the major cerebral arteries. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This phenomenon is also referred to as "last meadow" to point to the fact that in irrigation the last meadow receives the least amount of water.
Venous thrombosis
Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.[7]
Intracerebral hemorrhage
It generally occurs in small arteries or arterioles and is commonly due to hypertension, trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g. amphetamines or cocaine), and vascular malformations. The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage.
Ischemic

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Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the ischemic cascade. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after a few hours will suffer irreversible injury possibly leading to death of the tissue, i.e., infarction. Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries. These break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels.
Due to collateral circulation, within the region of brain tissue affected by ischemia there is a spectrum of severity. Thus, part of the tissue may immediately die while other parts may only be injured and could potentially recover. The ischemia area where tissue might recover is referred to as the ischemic penumbra (medicine).
As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis.
Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the apoptosis cascade by means of redox signaling.[18]
These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs.
Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that scavenge Reactive oxygen species, inhibit apoptosis, or inhibit excitotoxic neurotransmitters, for example, have been shown experimentally to reduce tissue injury due to ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of the radical-scavenging spintrap phenylbutylnitrone, is reported be neuroprotective in stroke. This agent appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable results in one large-scale clinical trial, a second trial failed to show favorable results.[18]
In addition to injurious effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.
As is the case with any type of brain injury, the immune system is activated by cerebral infarction and may under some circumstances exacerbate the injury caused by the infarction. Inhibition of the inflammatory response has been shown experimentally to reduce tissue injury due to cerebral infarction, but this has not proved out in clinical studies.
[edit] Hemorrhagic


Head CT showing deep intracerebral hemorrhage due to bleeding within the cerebellum, approximately 30 hours old.
Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.[18]
Prognosis

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Disability affects 75% of stroke survivors enough to decrease their employability.[89] Stroke can affect patients physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion.[90] Dysfunctions correspond to areas in the brain that have been damaged.
Some of the physical disabilities that can result from stroke include paralysis, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.
Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.
30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal.[91] Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.
Emotional lability, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the patient's actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or emotion.[89] Some patients show the opposite of what they feel, for example crying when they are happy.[92] Emotional lability occurs in about 20% of stroke patients.
Cognitive deficits resulting from stroke include perceptual disorders, speech problems, dementia, and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.
Up to 10% of all stroke patients develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.[93][94]
[edit] Epidemiology
Stroke could soon be the most common cause of death worldwide.[95] Stroke is currently the second leading cause of death in the Western world, ranking after heart disease and before cancer,[1] and causes 10% of deaths worldwide.[96] Geographic disparities in stroke incidence have been observed, including the existence of a "stroke belt" in the southeastern United States, but causes of these disparities have not been explained.
The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age.[97] Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.[91][18] A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in fetuses.
Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time.[98] The results of this study found that the only significant genetic factor was the person's blood type. Having had a stroke in the past greatly increases one's risk of future strokes.
Men are 1.25 times more likely to suffer strokes than women,[18] yet 60% of deaths from stroke occur in women.[92] Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).[18] Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).
Ischemic Strokes
The term "ischemia" refers to a lack of blood-borne oxygen. Ischemic strokes are more common than hemorrhagic strokes and may be caused by stenosis or thrombosis of the arteries, as well as by the presence of thrombo-emboli in the arteries. Check out the Department of Neurology at Debrecen University Medical School, Hungary.
Stenosis is a general term that means narrowing. In this case, it refers to the narrowing of an artery due to the build-up of plaque. As the artery is not completely blocked, some blood passes through it. However, if 50% of normal blood pressure is not maintained, brain damage will occur.
Thrombosis refers to the total blockage of an artery due to plaque build-up or emboli.
There are a number of drugs taken for heart and circulatory disease that have been shown to slow the build up of plaques that block the internal carotid arteries. The internal carotids take blood to the middle cerebral and anterior cerebral arteries. Blockages in the internal carotids can result in stroke that affects language, speech, and cognition. A study by researcher Dr. Goran Berglund (2001) and his team at Malmo University in Sweden that came out on in the American Heart association Journal, Circulation, reported the first evidence that a beta blocker can slow progression of plaque in the internal carotids. The drug used was metoprolol. It slowed the buildup rate by 40% in otherwise healthy people who had plaque buildup with no overt symptoms. The study involved 793 people aged 49 to 70. Another study by researchers in Canada, also reported in Circulation, showed that ramipril, an ACE inhibitor, slowed the formation of plaques in the internal carotids.
Currently only tissue plasminogen activating agents (t-PA) is approved by the FDA for therapy for acute ischemic stroke. This potent medicine carries with it a risk of cerebral hemorrhage. According to Bhatnager, 2008, it must be administered intravenously within three hours of CVA onset or inter-arterially within six. Drugs that inhibit platelets such as aspirin and Plavix are often used after a person has transient ischemic attacks. Many people who are at risk for stroke are advised by their doctors to take an 80mg aspirin every day.
Thrombo-emboli are pieces of plaque which break loose from thrombi and travel through the arterial system until they reach a narrow area and lodge, cutting off the blood supply to brain tissue beyond that point. This can occur when a normally sedentary person engages in strenuous physical activity.

TIAs or Transient Ischemic Attacks
Two different types of temporary ischemic events are warning signs that a true stroke is likely to occur in the near future. They are transient ischemic attack (TIA) and reversible ischemic neurological defect (RIND).
These are transient disturbances of the blood supply to a localized part of the brain, which produce a temporary, focal lesion. Unlike strokes they resolve in spontaneous and complete recovery.

Symptoms of TIAs mimic those of stroke. These attacks may cause temporary aphasia, numbness, and impair speaking, reading, and writing abilities. Dizziness and visual problems, such as blindness in part of the visual field, can also occur. Sometimes, TIAs are very mild and involve only numbness in a limb, or loss of sight in one eye. Severe TIAs cannot be differentiated from a stroke until recovery occurs.
A TIA typically last between 2 and 15 minutes, although such an event could conceivably last as long as 24 hrs. It is also possible to have a series of many brief TIAs during one day. For example, a patient might have 10 or more transient ischemic attacks within a 24 hr. period.
As mentioned above, drugs such as aspirin or Plavix are often prescribed after a TIA.
RIND or Reversible Ischemic Neurological Defect
A RIND is a lengthy TIA. The term RIND is usually applied to attacks that continue for more than 12 hours without interruption, although some may last for several days. As with a TIA, a RIND will resolve in complete recovery, however some neurologists do not consider them temporary. (There is some evidence that RINDs do cause some subtle neurological damage, but these minor changes are nothing like the types of disabilities seen after "real" strokes.)

Ischemic strokes, as well as TIAs and RINDs, are more likely to occur early in the morning. During sleep, blood pressure is at its lowest level. When a person gets out of bed, the sudden increase in blood pressure due to this change in activity level can cause an embolism to break free.
Hemorrhagic Strokes
Hemorrhagic stroke occurs when a cerebral artery ruptures, causing bleeding within the cranium. Such ruptures may be caused by aneurysms or weak spots in arterial walls. (Aneurysms can balloon out rather than bursting. The excess pressure resulting from this swelling can also damage brain tissue.) Bleeding due to stroke can cause the formation of hematomas, or pools of congealed blood, in the epidural space, or the subdural space.
Intraparenchymal bleeding refers to the flow of blood into brain tissue rather than into an existing space like the subarachnoid space or a potential space like the subdural space. The term "parenchyma" means "specific cells of a gland or organ" (Stedman's Concise Medical Dictionary. 1997) Parenchymal hemorrhages occur most frequently in the putamen (part of the lenticular nucleus), thalamus, pons, or cerebellum (Coch & Metter, 1994). The striata artery which supplies the internal capsule with blood is quite thin and easily hemorrhages. This is why it is called the artery of stroke.
Before the advent of sophisticated scanning techniques that allow the identification of small as well as large hematomas, it was believed that prognosis after a hemorrhagic stroke was extremely poor. Now it is recognized that patients often make a better recovery after a hemorrhagic stroke than after an ischemic stroke. Slow parenchymal bleeding may irritate brain tissue rather than damaging it. As the brain absorbs some of the blood flow from the hemorrhage, these areas heal and begin to function again. It is possible for a patient to make a complete recovery from a hemorrhagic stroke.

Because it frequently occurs at a very slow rate and over a lengthy period, neurological problems due to parenchymal bleeding may have an extended spontaneous recovery. For this reason, it may justifiable to continue therapy for a longer period of time with patients who have had parenchymal bleeding than with those who have had other types of hemorrhages.
Strokes can also be divided into the categories of completed or progressive.
Completed strokes are the type most commonly seen. In this case, the infarction of brain tissue has ceased to occur.

Progressive strokes are those that are still evolving, meaning that the patient's condition is continuing to deteriorate. Progressive strokes can last for a week or more. This condition is usually the result of a severe hemorrhage.
If called in to evaluate patients with this diagnosis, the SLP should test the patients but explain in the report that major changes could occur shortly. Even if their aphasia is initially mild it could worsen. Particular caution should be used when evaluating the swallowing status of such patients. They may be able to swallow safely initially, but develop dysphagia later as their condition worsens. Also, progressive strokes tend to happen to people who have very poor cerebral vascular health and are therefore at risk for having another stroke very soon. Cerebral vascular accidents are only some of the medical conditions that result in aphasias and right hemisphere syndrome. Also included are tumors and metabolic encephalopathy. In addition patients may have dementia. I just read a study on coffee and prevention of dementia.