• Mitral annular calcification
• Patent foramen ovale
• 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 (Watershed stroke)

=Venous thrombosis

Hemorrhagic stroke

=Intracerebral hemorrhage

Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging hematoma (pooling of blood). It generally occurs in small arteries or arterioles and is commonly due to hypertension, trauma, bleeding disorders, amyloid angiopathy, illicit drug use (amphetamines and 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.

=Subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) is bleeding into the cerebrospinal fluid (CSF) of the subarachnoid space surrounding the brain. The two most common causes of SAH are rupture of aneurysms from the base of the brain and bleeding from vascular malformations near the pial surface. Bleeding into the CSF from a ruptured aneurysm occurs very quickly, causing rapidly increased intracranial pressure. The bleeding usually only lasts a few seconds but rebleeding is common. Death or deep coma ensues if the bleeding continues. Hemorrhage from other sources is less abrupt and may continue for a longer period of time. SAH has a 40% mortality over 30 day period.

Signs and symptoms

If the area of the brain affected contains one of the three prominent Central nervous system pathways -- the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:

• muscle weakness or numbness (hemiplegia)
• reduction of pain or temperature sensation
• reduction in sensory or vibratory sensation

In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. A stroke affecting the brainstem therefore can produce symptoms relating to deficits in these cranial nerves:

• altered smell, taste, hearing, or vision (total or partial)
• drooping of eyelid (ptosis) and weakness of ocular muscles
• decreased reflexes: gag, swallow, pupil reactivity to light
• decreased sensation and muscle weakness of the face
• balance problems and nystagmus
• altered breathing and heart rate
• weakness in sternocleidomastoid muscle (SCM) with inability to turn head to one side
• weakness in tongue (inability to protrude and/or move from side to side)

If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

• aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area)
• apraxia (altered voluntary movements)
• disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)
• altered vision (involvement of occipital lobe)
• memory deficits (involvement of temporal lobe)
• hemineglect (involvement of parietal lobe)

If the cerebellum is involved, the patient may have the following:

• trouble walking
• altered movement coordination
• dizziness

Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain.

If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

Subarachnoid hemorrhage

The symptoms of SAH occur abruptly due to the sudden onset of increased intracranial pressure. Often, patients complain of a sudden, extremely severe and widespread headache. The pain may or may not radiate down into neck and legs. Vomiting soon occurs after the onset of headache. Usually the neurologic exam is nonfocal --- meaning no deficits can be identified that attributes to certain areas of the brain --- unless the bleeding also occurs into the brain. The combination of headache and vomiting is uncommon in ischemic stroke.

Transient ischemic attack (TIA)

Diagnosis

If a stroke is confirmed on imaging, various other studies may be performed to determine whether there is a peripheral source of emboli:

• an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis)
• an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream)
• a Holter monitor study to identify intermittent arrhythmias
• an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation)

Treatment

Early assessment

If a patient is suspected of having a stroke, emergency services should be contacted immediately. The patient should be transported to the nearest hospital that can provide a rapid evaluation and treatment with the latest available therapies targeted to the type of stroke. The faster these therapies are started for hemorrhagic and ischemic stroke, the chances for recovery from each type improves greatly. Quick decisions about medication and the need for surgery have been shown to improve outcome.

Only detailed physical examination and medical imaging provide information on the presence, type, and extent of stroke.

Studies show that patients treated in hospitals with a dedicated Stroke Team or Stroke Unit and a specialized care program for stroke patients have improved odds of recovery.

Ischemic stroke

In increasing numbers of primary stroke centers, thrombolysis ("clot busting") is used to dissolve the clot and unblock the artery. However, there is a time constraint: the more time that goes by, the more brain that has irreversibly died. There is also a small risk of making the patient worse by causing bleeding. When used within the first 3 hours, thrombolysis improves the outcome in 1 of every 3.1 patients and worsens the outcome in 1 in every 32 patients. The routine use of thrombolysis is not approved beyond 3 hours. As an easily administered therapy that can be given at any hospital with a CAT scanner, thrombolysis is available at most hospitals in the US, but not where no institutional commitment to stroke care has occurred.

Another intervention for acute ischemic stroke is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it up into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. In August 2004, the FDA cleared one such device, called the Merci Retriever.

Whether thrombolysis is performed or not, the following investigations are required:

• Stroke symptoms are documented, often using scoring systems such as the National Institutes of Health Stroke Scale, the Cincinnati Stroke Scale, and the Los Angeles Prehospital Stroke Screen. The latter is used by emergency medical technicians (EMTs) to determine whether a patient needs transport to a stroke center.
• A CT scan is performed to rule out hemorrhagic stroke
• Blood tests, such as a full blood count, coagulation studies (PT/INR and APTT), and tests of electrolytes, renal function, liver function tests and glucose levels are carried out.

Other immediate strategies to protect the brain during stroke include ensuring that blood sugar is as normal as possible (such as commencement of an insulin sliding scale in known diabetics), and that the stroke patient is receiving adequate oxygen and intravenous fluids. The patient may be positioned so that his or her head is flat on the stretcher, rather than sitting up, since studies have shown that this increases blood flow to the brain. Additional therapies for ischemic stroke include aspirin (50 to 325 mg daily), clopidogrel (75 mg daily), and combined aspirin and dipyridamole extended release (25/200 mg twice daily).

It is common for the blood pressure to be elevated immediately following a stroke. Studies indicated that while high blood pressure causes stroke, it is actually beneficial in the emergency period to allow better blood flow to the brain.

If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence.

If the stroke has been the result of cardiac arrhythmia (such as atrial fibrillation) with cardiogenic emboli, treatment of the arrhythmia and anticoagulation with warfarin or high-dose aspirin may decrease the risk of recurrence.

Hemorrhagic stroke

Care and rehabilitation

Good nursing care is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.

For most stroke patients, physical therapy is the cornerstone of the rehabilitation process. Often, assistive technology such as a wheelchair and standing frame may be beneficial. Another type of therapy involving relearning daily activities is occupational therapy (OT). OT involves exercise and training to help the stroke patient relearn everyday activities sometimes called the Activities of daily living (ADLs) such as eating, drinking and swallowing, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with problems understanding speech or written words, or problems forming speech.

Patients may have particular problems, such as complete or partial inability to swallow, which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still unsafe after a week, then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.

Stroke rehabilitation can last anywhere from a few days to several months. Most return of function is seen in the first few days and weeks, and then improvement falls off. Complete recovery is unusual but not impossible. Most patients will improve to some extent.

Prognosis

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, vision loss, and pain. If the stroke is severe enough, 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 (Post stroke depression), which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal. 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. Some patients show the opposite of what they feel, for example crying when they are happy. 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 perpetually unaware of his or her own disabilities or even the fact that he or she has suffered a stroke. In a condition called agnosia, or neglect, a patient is unable to see anything on the left or right side and is unaware of and unable to conceive of anything on the neglected side.

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 seizureReith J, Jorgensen HS, Nakayama H, Raaschou HO, Olsen TS. Seizures in acute stroke: predictors and prognostic significance. The Copenhagen Stroke Study. Stroke 1997;28:1585-9. PMID 9259753.Burn J, Dennis M, Bamford J, Sandercock P, Wade D, Warlow C. Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project. BMJ 1997;315:1582-7. PMID 9437276..

Risk factors and prevention

One of the most significant stroke risk factors is advanced age. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.--> 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.

Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, also increases stroke risk. Stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.

Men are 1.25 times more likely to suffer CVAs than women, yet 60% of deaths from stroke occur in women. Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002). Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT). Stroke seems to run in some families.

Prevention is an important public health concern. Identification of patients with treatable risk factors for stroke is paramount. Treatment of risk factors in patients who have already had strokes (secondary prevention) is also very important as they are at high risk of subsequent events compared with those who have never had a stroke. Medication or drug therapy is the most common method of stroke prevention. Aspirin (usually at a low dose of 75 mg) is recommended for the primary and secondary prevention of stroke. Treating hypertension, diabetes mellitus, smoking cessation, control of hypercholesterolemia, physical exercise, and avoidance of illicit drugs and excessive alcohol consumption are all recommended ways of reducing the risk of stroke.^*

In patients who have strokes due to abnormalities of the heart, such as atrial fibrillation, anticoagulation with medications such as warfarin is often necessary for stroke prevention.^*

Procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. These procedures have been shown to prevent stroke in certain patients, especially where carotid stenosis leads to ischemic events such as transient ischemic attack.

Pathophysiology

Within the region of brain tissue affected by ischemia there is a spectrum of severity of the ischemia such that 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.

As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenine triphosphate (ATP) fails leading to failure of energy dependent processes necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. Among these is the loss of membrane ion pump function that leads to electrolyte imbalances in brain cells, the release of excitatory neurotransmitters, which have toxic effects in excessive concentrations, the release of oxygen free radicals that react with and damage a number of cellular elements, and the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis..

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 reduce oxygen free radicals, 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. However, no neuroprotective agents have been shown to be effective in humans..

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.

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.

Epidemiology