Transfusion therapy lowers the risk for a new silent stroke in children who have both abnormal cerebral artery blood flow velocity, as detected by transcranial Doppler, and previous silent infarct, even when the initial MRI showed no abnormality. A finding of elevated TCD ultrasonographic velocity warrants MRI of the brain, as those with both abnormalities who are not provided transfusion therapy are at higher risk for developing a new silent infarct or stroke than are those whose initial MRI showed no abnormality.

Preventive measures that can be taken to avoid sustaining a silent stroke are the same as for stroke. Smoking cessation is the most immediate step that can be taken, with the effective management of hypertension the major medically treatable factor.

After taking the patient’s history, a thorough neurologic exam is needed to identify focal neurologic deficits, paying attention to the cranial nerve, motor, sensory, and coordination components of the exam. After the history and physical exam, clinicians may move on to laboratory workup and imaging.

Laboratory workup

Laboratory tests should focus on ruling out metabolic conditions that may mimic TIA (e.g. hypoglycemia causing altered mental status), in addition to further evaluating a patient’s risk factors for ischemic events. All patients should receive a complete blood count with platelet count, blood glucose, basic metabolic panel, prothrombin time/international normalized ratio, and activated partial thromboplastin time as part of their initial workup. These tests help with screening for bleeding or hypercoagulable conditions. An electrocardiogram will also be necessary to rule out abnormal heart rhythms such as atrial fibrillation that can predispose patients to clot formation and embolic events. Other lab tests, such as a full hypercoagulable state workup or serum drug screening should be considered based on the clinical situation and factors such as age of the patient and family history. A fasting lipid panel is also appropriate to thoroughly evaluate the patient’s risk for atherosclerotic disease and ischemic events in the future.

Imaging:

According to guidelines from the American Heart Association and American Stroke Association Stroke Council, patients with TIA should have head imaging “within 24 hours of symptom onset, preferably with magnetic resonance imaging, including diffusion sequences”. MRI is a better imaging modality for TIA than computed tomography (CT), as it is better able to pick up both new and old ischemic lesions than CT. CT, however, is more widely available and can be used particularly to rule out intracranial hemorrhage. Diffusion sequences can help further localize the area of ischemia and can serve as prognostic indicators. Presence of ischemic lesions on diffusion weighted imaging has been correlated with a higher risk of stroke after a TIA.

Vessels in the head and neck may also be evaluated to look for atherosclerotic lesions that may benefit from interventions such as carotid endarterectomy. The vasculature can be evaluated through the following imaging modalities: magnetic resonance angiography (MRA), CT angiography (CTA), and carotid ultrasonography/transcranial doppler ultrasonography. Carotid ultrasonography is often used to screen for carotid artery stenosis, as it is more readily available. However, all of the above imaging methods have variable sensitivities and specificities, making it important to supplement one of the imaging methods with another to help confirm the diagnosis (for example: screen for the disease with ultrasonography, and confirm with CTA). Confirming a diagnosis of carotid artery stenosis is important because the treatment for this condition, carotid endarterectomy, can pose significant risk to the patient, including heart attacks and strokes after the procedure. For this reason, the U.S. Preventive Services Task Force (USPSTF) "recommends against screening for asymptomatic carotid artery stenosis in the general adult population". This recommendation is for asymptomatic patients, so it does not necessarily apply to patients with TIAs as these may in fact be a symptom of underlying carotid artery disease (see "Causes and Pathogenesis" above). Therefore, patients who have had a TIA may opt to have a discussion with their clinician about the risks and benefits of screening for carotid artery stenosis, including the risks of surgical treatment of this condition.

Cardiac imaging can be performed if head and neck imaging do not reveal a vascular cause for the patient’s TIA (such as atherosclerosis of the carotid artery or other major vessels of the head and neck). Echocardiography can be performed to identify patent foramen ovale (PFO), valvular stenosis, and atherosclerosis of the aortic arch that could be sources of clots causing TIAs, with transesophageal echocardiography being more sensitive than transthoracic echocardiography in identifying these lesions. Prolonged cardiac rhythm monitoring can be considered to rule out arrhythmias like paroxysmal atrial fibrillation that may lead to clot formation and TIAs, however this should be considered if other causes of TIA have not been found.

Nutrition, specifically the Mediterranean-style diet, has the potential for decreasing the risk of having a stroke by more than half. It does not appear that lowering levels of homocysteine with folic acid affects the risk of stroke.

When a stroke has been diagnosed, various other studies may be performed to determine the underlying cause. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary since the cause of stroke varies with age, comorbidity and the clinical presentation. The following are commonly used techniques:

- an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral arteries;

- 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 abnormal heart rhythms;

- an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation);

- blood tests to determine if blood cholesterol is high, if there is an abnormal tendency to bleed, and if some rarer processes such as homocystinuria might be involved.

For hemorrhagic strokes, a CT or MRI scan with intravascular contrast may be able to identify abnormalities in the brain arteries (such as aneurysms) or other sources of bleeding, and structural MRI if this shows no cause. If this too does not identify an underlying reason for the bleeding, invasive cerebral angiography could be performed but this requires access to the bloodstream with an intravascular catheter and can cause further strokes as well as complications at the insertion site and this investigation is therefore reserved for specific situations. If there are symptoms suggesting that the hemorrhage might have occurred as a result of venous thrombosis, CT or MRI venography can be used to examine the cerebral veins.

Diagnosis of TIA involves a combination of asking the patient questions about their symptoms and medical history, physical exam, and head imaging. History taking includes defining the symptoms and looking for mimicking symptoms as described above. Bystanders can be very helpful in describing the symptoms and giving details about when they started and how long they lasted. The time course (onset, duration, and resolution), precipitating events, and risk factors are particularly important. Finally, a thorough review of symptoms is necessary to rule in or out other items on the differential diagnosis of TIA. These include, but are not limited to:

Diagnosis of cerebrovascular disease is done by (among other diagnoses):

- clinical history

- physical exam

- neurological examination.

It is important to differentiate the symptoms caused by a stroke from those caused by syncope (fainting) which is also a reduction in cerebral blood flow, almost always generalized, but they are usually caused by systemic hypotension of various origins: cardiac arrhythmias, myocardial infarction, hemorrhagic shock, among others.

Prognostics factors:

Lower Glasgow coma scale score, higher pulse rate, higher respiratory rate and lower arterial oxygen saturation level is prognostic features of in-hospital mortality rate in acute ischemic stroke.

Although the mechanism is not entirely understood, the likelihood of a watershed stroke increases after cardiac surgery. An experiment conducted in a five-year span studied the diagnosis, etiology, and outcome of these postoperative strokes. It was observed that intraoperative decrease in blood pressure may lead to these strokes and patients who have undergone aortic procedures are more likely to have bilateral watershed infarcts. Furthermore, bilateral watershed strokes are associated with poor short-term outcomes and are most reliably observed by diffusion-weighted imaging MRI. Thus future clinical research and practice should focus on the identification of bilateral stroke characteristics. This identification can help discover affected areas and increase correct diagnosis.

Hemodynamic impairment is thought to be the cause of deep watershed infarcts, characterized by a rosary-like pattern. However new studies have shown that microembolism might also contribute to the development of deep watershed infarcts. The dual contribution of hemodynamic impairment and microembolism would result in different treatment for patients with these specific infarcts.

Diagnostic methods include:

- Angiogram

Due to positive remodeling the plaque build-up shown on angiogram may appear further downstream on the x-ray where the luminal diameter would look normal even though there is severe narrowing at the real site. Because angiograms require x-rays to be visualized the number of times an individual can have it done over a year is limited by the guidelines for the amount of radiation they can be exposed to in a one-year period.

- Magnetic resonance imaging (MRI)

Magnetic resonance imaging has the ability to quantify the plaque anatomy and composition. This allows physicians to determine certain characteristics of the plaque such as how likely it is to break away from the wall and become an embolus. MRI does not use ionizing radiation, so the number of times that it is used on a single person is not a concern; however since it uses strong electric fields those who have metal implants in cannot use this technique.

- Computed tomography (CT)

Multidirectional computed tomography (MDCT) is better than regular CT scans, because it can provide a higher spatial resolution and it has a shorter acquisition time. MDCT uses x-rays to obtain the image; however it can identify the composition of the plaque. Thus it can be determined whether the plaque is calcified plaque and lipid-rich plaque, so the inherent risks can be determined. Subjects are exposed to a substantial amount of radiation with this procedure, so their use is limited.

Computed tomography (CT) and MRI scanning will show damaged area in the brain, showing that the symptoms were not caused by a tumor, subdural hematoma or other brain disorder. The blockage will also appear on the angiogram.

Typically, tissue plasminogen activator may be administered within three to four-and-a-half hours of stroke onset if the patient is without contraindications (i.e. a bleeding diathesis such as recent major surgery or cancer with brain metastases). High dose aspirin can be given within 48 hours. For long term prevention of recurrence, medical regimens are typically aimed towards correcting the underlying risk factors for lacunar infarcts such as hypertension, diabetes mellitus and cigarette smoking. Anticoagulants such as heparin and warfarin have shown no benefit over aspirin with regards to five year survival.

Patients who suffer lacunar strokes have a greater chance of surviving beyond thirty days (96%) than those with other types of stroke (85%), and better survival beyond a year (87% versus 65-70%). Between 70% and 80% are functionally independent at 1 year, compared with fewer than 50% otherwise.

Occupational Therapy and Physical Therapy interventions are used in the rehabilitation of lacunar stroke. A physiotherapy program will improve joint range of motion of the paretic limb using passive range of motion exercises. When increases in activity are tolerated, and stability improvements are made, patients will progress from rolling to side-lying, to standing (with progressions to prone, quadruped, bridging, long-sitting and kneeling for example) and learn to transfer safely (from their bed to a chair or from a wheel chair to a car for example). Assistance and ambulation aids are used as required as the patient begins walking and lessened as function increases. Furthermore, splints and braces can be used to support limbs and joints to prevent complications such as contractures and spasticity. The rehabilitation healthcare team should also educate the patient and their family on common stroke symptoms and how to manage an onset of stroke. Continuing follow-up with a physician is essential so that the physician may monitor medication dosage and risk factors.

In last decade, similar to myocardial infarction treatment, thrombolytic drugs were introduced in the therapy of cerebral infarction. The use of intravenous rtPA therapy can be advocated in patients who arrive to stroke unit and can be fully evaluated within 3 h of the onset.

If cerebral infarction is caused by a thrombus occluding blood flow to an artery supplying the brain, definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die. In increasing numbers of primary stroke centers, pharmacologic thrombolysis with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery.

Another intervention for acute cerebral ischaemia is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective, though no differences have been found between newer and older versions of the devices. The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.

Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute cerebral ischaemia. In a systematic review of six uncontrolled, single-center trials, involving a total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90-98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable. This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.

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 performed rapidly after cerebral infarction. Carotid endarterectomy is also indicated to decrease the risk of cerebral infarction for symptomatic carotid stenosis (>70 to 80% reduction in diameter).

In tissue losses that are not immediately fatal, the best course of action is to make every effort to restore impairments through physical therapy, cognitive therapy, occupational therapy, speech therapy and exercise.

It is estimated that lacunar infarcts account for 25% of all ischemic strokes, with an annual incidence of approximately 15 per 100,000 people. They may be more frequent in men and in people of African, Mexican, and Hong Kong Chinese descent.

Some evidence suggests that magnesium sulfate administered to mothers prior to early preterm birth reduces the risk of cerebral palsy in surviving neonates. Due to the risk of adverse effects treatments may have, it is unlikely that treatments to prevent neonatal strokes or other hypoxic events would be given routinely to pregnant women without evidence that their fetus was at extreme risk or has already suffered an injury or stroke. This approach might be more acceptable if the pharmacologic agents were endogenously occurring substances (those that occur naturally in an organism), such as creatine or melatonin, with no adverse side-effects.

Because of the period of high neuronal plasticity in the months after birth, it may be possible to improve the neuronal environment immediately after birth in neonates considered to be at risk of neonatal stroke. This may be done by enhancing the growth of axons and dendrites, synaptogenesis and myelination of axons with systemic injections of neurotrophins or growth factors which can cross the blood–brain barrier.

A stress test, is just that, a test to put stress on the heart through exercise. A doctor will put a patient through a series of exercises to measure the tolerance for stress on the heart. This test uses an ECG to detect the electrical impulses of the heart during physical exertion.

During this test a patient is put on a treadmill or a stationary bike. The incline or resistance of the bike are steadily increased until the patient reaches the target heart rate for the patient's age and weight.

An exercise stress test is not always accurate in determining if one has a blockage in the arteries. Women and those who are young may show abnormalities on their test even though no signs of coronary ischemia or CAD are present.

A coronary angiography is performed only after a stress test or ECG shows a sign of coronary ischemia or CAD. This test is very important in finding where the blockages are in the arteries.

This test helps determine if an angioplasty or bypass surgery is needed.

During this test the doctor makes a small incision in the patient's groin (femoral) or wrist (radial) and inserts a catheter. The catheter has a very small video camera on the end of it so that the doctor can find the arteries.

Once he has found the arteries, he injects a dye in them so that he/she can detect any blockages in the arteries. The dye is able to be seen on a special x-ray machine.

The test takes one to two hours.

Asymptomatic individuals with intracranial stenosis are typically told to take over the counter platelet inhibitors like aspirin whereas those with symptomatic presentation are prescribed anti-coagulation medications. For asymptomatic persons the idea is to stop the buildup of plaque from continuing. They are not experiencing symptoms; however if more build up occurs it is likely they will. For symptomatic individuals it is necessary to try and reduce the amount of stenosis. The anti-coagulation medications reduce the likelihood of further buildup while also trying to break down the current build up on the surface without an embolism forming. For those with severe stenosis that are at risk for impending stroke endovascular treatment is used. Depending on the individual and the location of the stenosis there are multiple treatments that can be undertaken. These include angioplasty, stent insertion, or bypass the blocked area.

Well-designed clinical trials for stroke treatment in neonates are lacking Recent clinical trials show that therapeutic intervention by brain cooling beginning up to 6 hours after perinatal asphyxia reduces cerebral injury and may improve outcome in term infants, indicating cell death is both delayed and preventable

Pancaspase inhibition and Casp3-selective inhibition have been found to be neuroprotective in neonatal rodents with models of neonatal brain injury, which may lead to pharmacological intervention In a study done by Chauvier, "et al.", it is suggested that a Caspase inhibitor, TRP601, is a candidate for neuroprotective strategy in prenatal brain injury conditions. They found a lack of detectable side effects in newborn rodents and dogs. This may be a useful treatment in combination with hypothermia.

MRI has proven valuable for defining brain injury in the neonate, but animal models are still needed to identify causative mechanisms and to develop neuroprotective therapies. In order to model human fetal or neonatal brain injury, one needs a species in which a similar proportion of brain development occurs in utero, the volume of white to grey matter is similar to the human brain, an insult can be delivered at an equivalent stage of development, the physiological outcome of the insult can be monitored, and neurobehavioral parameters can be tested. Some animals that meet these criteria are sheep, non-human primates, rabbits, spiny mice, and guinea pigs.

Transplantation of neural stem cells and umbilical cord stem cells is currently being trialed in neonatal brain injury, but it is not yet known if this therapy is likely to be successful.

The prognosis for pediatric stroke survivors varies. The following are some common outcomes:

- Cerebral Palsy (often Hemiplegic Cerebral Palsy/Hemiplegia)

- Epilepsy

- Vision Loss

- Hearing Loss

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:

1. Thrombosis (obstruction of a blood vessel by a blood clot forming locally)

2. Embolism (obstruction due to an embolus from elsewhere in the body, see below),

3. Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)

4. Venous thrombosis.

Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.

The U.S. Preventive Services Task Force (USPSTF) recommends against screening for carotid artery stenosis in those without symptoms.

Carotid stenosis is usually diagnosed by color flow duplex ultrasound scan of the carotid arteries in the neck. This involves no radiation, no needles and no contrast agents that may cause allergic reactions. This test has moderate sensitivity and specificity, and yields many false-positive results.

Typically duplex ultrasound scan is the only investigation required for decision making in carotid stenosis as it is widely available and rapidly performed. However, further imaging can be required if the stenosis is not near the bifurcation of the carotid artery.

One of several different imaging modalities, such as angiogram, computed tomography angiogram (CTA) or magnetic resonance imaging angiogram (MRA) may be useful. Each imaging modality has its advantages and disadvantages - Magnetic resonance angiography and CT angiography with contrast is contraindicated in patients with renal insufficiency, catheter angioigraphy has a 0.5% to 1.0% risk of stroke, MI, arterial injury or retoperitoneal bleeding. The investigation chosen will depend on the clinical question and the imaging expertise, experience and equipment available.

70% of patients with carotid arterial dissection are between the ages of 35 and 50, with a mean age of 47 years.