What is infarct in brain

Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction. A brain infarct is more commonly known as a stroke, which occurs when the blood supply to part of the brain is suddenly interrupted or when a blood vessel in the brain bursts, spilling blood into the spaces surrounding brain cells. In the same way that a person suffering a loss of blood flow to the heart is said to be having a heart attack (myocardial infarction), a person with a loss of blood flow to the brain or sudden bleeding in the brain can be said to be having a “brain attack” or brain infarct.

Brain cells die when they no longer receive oxygen and nutrients from the blood or when they are damaged by sudden bleeding into or around the brain. Ischemia is the term used to describe the loss of oxygen and nutrients for brain cells when there is inadequate blood flow. Ischemia ultimately leads to infarction, the death of brain cells which are eventually replaced by a fluid-filled cavity (or infarct) in the injured brain.

When blood flow to the brain is interrupted, some brain cells die immediately, while others remain at risk for death. These damaged cells make up the ischemic penumbra and can linger in a compromised state for several hours. With timely treatment these cells can be saved.

Even though a stroke occurs in the unseen reaches of the brain, the symptoms of a stroke are easy to spot. They include sudden numbness or weakness, especially on one side of the body; sudden confusion or trouble speaking or understanding speech; sudden trouble seeing in one or both eyes; sudden trouble walking, dizziness, or loss of balance or coordination; or sudden severe headache with no known cause. All of the symptoms of stroke appear suddenly, and often there is more than one symptom at the same time. Therefore stroke can usually be distinguished from other causes of dizziness or headache. These symptoms may indicate that a stroke has occurred and that medical attention is needed immediately.

There are two forms of brain infarct (stroke): ischemic – blockage of a blood vessel supplying the brain, and hemorrhagic – bleeding into or around the brain.

Ischemic stroke

An ischemic stroke occurs when an artery supplying the brain with blood becomes blocked, suddenly decreasing or stopping blood flow and ultimately causing a brain infarction. This type of stroke accounts for approximately 80 percent of all strokes. Blood clots are the most common cause of artery blockage and brain infarction. The process of clotting is necessary and beneficial throughout the body because it stops bleeding and allows repair of damaged areas of arteries or veins. However, when blood clots develop in the wrong place within an artery they can cause devastating injury by interfering with the normal flow of blood. Problems with clotting become more frequent as people age.

Blood clots can cause ischemia and infarction in two ways. A clot that forms in a part of the body other than the brain can travel through blood vessels and become wedged in a brain artery. This free-roaming clot is called an embolus and often forms in the heart. A stroke caused by an embolus is called an embolic stroke. The second kind of ischemic stroke, called a thrombotic stroke, is caused by thrombosis, the formation of a blood clot in one of the cerebral arteries that stays attached to the artery wall until it grows large enough to block blood flow.

Ischemic strokes can also be caused by stenosis, or a narrowing of the artery due to the buildup of plaque (a mixture of fatty substances, including cholesterol and other lipids) and blood clots along the artery wall. Stenosis can occur in large arteries and small arteries and is therefore called large vessel disease or small vessel disease, respectively. When a stroke occurs due to small vessel disease, a very small infarction results, sometimes called a lacunar infarction, from the French word “lacune” meaning “gap” or “cavity.”

The most common blood vessel disease that causes stenosis is atherosclerosis. In atherosclerosis, deposits of plaque build up along the inner walls of large and medium-sized arteries, causing thickening, hardening, and loss of elasticity of artery walls and decreased blood flow.

Hemorrhagic stroke

In a healthy, functioning brain, neurons do not come into direct contact with blood. The vital oxygen and nutrients the neurons need from the blood come to the neurons across the thin walls of the cerebral capillaries. The glia (nervous system cells that support and protect neurons) form a blood-brain barrier, an elaborate meshwork that surrounds blood vessels and capillaries and regulates which elements of the blood can pass through to the neurons.

When an artery in the brain bursts, blood spews out into the surrounding tissue and upsets not only the blood supply but the delicate chemical balance neurons require to function. This is called a hemorrhagic stroke. Such strokes account for approximately 20 percent of all strokes.

Hemorrhage can occur in several ways. One common cause is a bleeding aneurysm, a weak or thin spot on an artery wall. Over time, these weak spots stretch or balloon out under high arterial pressure. The thin walls of these ballooning aneurysms can rupture and spill blood into the space surrounding brain cells.

Hemorrhage also occurs when arterial walls break open. Plaque-encrusted artery walls eventually lose their elasticity and become brittle and thin, prone to cracking. Hypertension, or high blood pressure, increases the risk that a brittle artery wall will give way and release blood into the surrounding brain tissue.

A person with an arteriovenous malformation (AVM) also has an increased risk of hemorrhagic stroke. Arteriovenous malformations are a tangle of defective blood vessels and capillaries within the brain that have thin walls and can therefore rupture.

Bleeding from ruptured brain arteries can either go into the substance of the brain or into the various spaces surrounding the brain. Intracerebral hemorrhage occurs when a vessel within the brain leaks blood into the brain itself. Subarachnoid hemorrhage is bleeding under the meninges, or outer membranes, of the brain into the thin fluid-filled space that surrounds the brain.

The subarachnoid space separates the arachnoid membrane from the underlying pia mater membrane. It contains a clear fluid (cerebrospinal fluid or CSF) as well as the small blood vessels that supply the outer surface of the brain. In a subarachnoid hemorrhage, one of the small arteries within the subarachnoid space bursts, flooding the area with blood and contaminating the cerebrospinal fluid. Since the CSF flows throughout the cranium, within the spaces of the brain, subarachnoid hemorrhage can lead to extensive damage throughout the brain. In fact, subarachnoid hemorrhage is the most deadly of all strokes.

Transient ischemic attacks

A transient ischemic attack (TIA), sometimes called a mini-stroke, starts just like a stroke but then resolves leaving no noticeable symptoms or deficits. The occurrence of a TIA is a warning that the person is at risk for a more serious and debilitating stroke. Of the approximately 50,000 Americans who have a TIA each year, about one-third will have an acute stroke sometime in the future. The addition of other risk factors compounds a person’s risk for a recurrent stroke. The average duration of a TIA is a few minutes. For almost all TIAs, the symptoms go away within an hour. There is no way to tell whether symptoms will be just a TIA or persist and lead to death or disability. The patient should assume that all stroke symptoms signal an emergency and should not wait to see if they go away.

Recurrent stroke

Recurrent stroke is frequent; about 25 percent of people who recover from their first stroke will have another stroke within 5 years. Recurrent stroke is a major contributor to stroke disability and death, with the risk of severe disability or death from stroke increasing with each stroke recurrence. The risk of a recurrent stroke is greatest right after a stroke, with the risk decreasing with time. About 3 percent of stroke patients will have another stroke within 30 days of their first stroke and one-third of recurrent strokes take place within 2 years of the first stroke.

Risk factors for brain infarct

Many factors can increase your risk of an brain infarct. Some factors can also increase your chances of having a heart attack. Potentially treatable stroke risk factors include:

Lifestyle risk factors

• Being overweight or obese
• Physical inactivity
• Heavy or binge drinking
• Use of illicit drugs such as cocaine and methamphetamines

Medical risk factors

• High blood pressure (hypertension) — the risk of stroke begins to increase at blood pressure readings higher than 120/80 millimeters of mercury (mm Hg). Your doctor will help you decide on a target blood pressure based on your age, whether you have diabetes and other factors.
• Cigarette smoking or exposure to secondhand smoke.
• High cholesterol.
• Diabetes.
• Obstructive sleep apnea — a sleep disorder in which the oxygen level intermittently drops during the night.
• Cardiovascular disease, including heart failure, heart defects, heart infection or abnormal heart rhythm (atrial fibrillation).

Other factors associated with a higher risk of brain infarct include:

• Personal or family history of stroke, heart attack or transient ischemic attack.
• Being age 55 or older.
• Race — African-Americans have a higher risk of stroke than do people of other races.
• Gender — Men have a higher risk of stroke than women. Women are usually older when they have strokes, and they’re more likely to die of strokes than are men. Also, they may have some risk from some birth control pills or hormone therapies that include estrogen, as well as from pregnancy and childbirth.

How to prevent a brain infarct

Knowing your brain infarct risk factors, following your doctor’s recommendations and adopting a healthy lifestyle are the best steps you can take to prevent a stroke. If you’ve had a stroke or a transient ischemic attack (TIA), these measures may help you avoid having another stroke. The follow-up care you receive in the hospital and afterward may play a role as well.

Many stroke prevention strategies are the same as strategies to prevent heart disease. In general, healthy lifestyle recommendations include:

• Controlling high blood pressure (hypertension). One of the most important things you can do to reduce your stroke risk is to keep your blood pressure under control. If you’ve had a stroke, lowering your blood pressure can help prevent a subsequent transient ischemic attack or stroke.

Exercising, managing stress, maintaining a healthy weight, and limiting the amount of sodium and alcohol you eat and drink are all ways to keep high blood pressure in check.. In addition to recommending lifestyle changes, your doctor may prescribe medications to treat high blood pressure.

• Lowering the amount of cholesterol and saturated fat in your diet. Eating less cholesterol and fat, especially saturated fat and trans fats, may reduce the fatty deposits (plaques) in your arteries. If you can’t control your cholesterol through dietary changes alone, your doctor may prescribe a cholesterol-lowering medication.
• Quitting smoking. Smoking raises the risk of stroke for smokers and nonsmokers exposed to secondhand smoke. Quitting tobacco use reduces your risk of stroke.
• Controlling diabetes. You can manage diabetes with diet, exercise, weight control and medication.
• Maintaining a healthy weight. Being overweight contributes to other stroke risk factors, such as high blood pressure, cardiovascular disease and diabetes. Weight loss of as little as 10 pounds may lower your blood pressure and improve your cholesterol levels.
• Eating a diet rich in fruits and vegetables. A diet containing five or more daily servings of fruits or vegetables may reduce your risk of stroke. Following the Mediterranean diet, which emphasizes olive oil, fruit, nuts, vegetables and whole grains, may be helpful.
• Exercising regularly. Aerobic or “cardio” exercise reduces your risk of stroke in many ways. Exercise can lower your blood pressure, increase your level of high-density lipoprotein cholesterol, and improve the overall health of your blood vessels and heart. It also helps you lose weight, control diabetes and reduce stress. Gradually work up to 30 minutes of activity — such as walking, jogging, swimming or bicycling — on most, if not all, days of the week.
• Drinking alcohol in moderation, if at all. Alcohol can be both a risk factor and a protective measure for stroke. Heavy alcohol consumption increases your risk of high blood pressure, ischemic strokes and hemorrhagic strokes. However, drinking small to moderate amounts of alcohol, such as one drink a day, may help prevent ischemic stroke and decrease your blood’s clotting tendency. Alcohol may also interact with other drugs you’re taking. Talk to your doctor about what’s appropriate for you.
• Treating obstructive sleep apnea, if present. Your doctor may recommend an overnight oxygen assessment to screen for obstructive sleep apnea (OSA). If obstructive sleep apnea is detected, it may be treated by giving you oxygen at night or having you wear a small device in your mouth.
• Avoiding illicit drugs. Certain street drugs, such as cocaine and methamphetamines, are established risk factors for a TIA or a stroke. Cocaine reduces blood flow and can cause narrowing of arteries.

Preventive medications

If you’ve had an ischemic stroke or TIA, your doctor may recommend medications to help reduce your risk of having another stroke. These include:

• Anti-platelet drugs. Platelets are cells in your blood that initiate clots. Anti-platelet drugs make these cells less sticky and less likely to clot. The most commonly used anti-platelet medication is aspirin. Your doctor can help you determine the right dose of aspirin for you. Your doctor may also consider prescribing Aggrenox, a combination of low-dose aspirin and the anti-platelet drug dipyridamole, to reduce the risk of blood clotting. If aspirin doesn’t prevent your TIA or stroke, or if you can’t take aspirin, your doctor may instead prescribe an anti-platelet drug such as clopidogrel (Plavix).

• Anticoagulants. These drugs, which include heparin and warfarin (Coumadin), reduce blood clotting. Heparin is fast-acting and may be used over a short period of time in the hospital. Slower acting warfarin may be used over a longer term. Warfarin is a powerful blood-thinning drug, so you’ll need to take it exactly as directed and watch for side effects. Your doctor may prescribe these drugs if you have certain blood-clotting disorders, certain arterial abnormalities, an abnormal heart rhythm or other heart problems. Other newer blood thinners may be used if your TIA or stroke was caused by an abnormal heart rhythm.

Brain infarct signs and symptoms

What are the signs and symptoms of an brain infarct

The signs and symptoms of a stroke vary from person to person, but usually begin suddenly.

As different parts of your brain control different parts of your body, your symptoms will depend on the part of your brain affected and the extent of the damage.

The main stroke symptoms can be remembered with the word F.A.S.T.:

• Face – the face may have dropped on one side, the person may not be able to smile, or their mouth or eye may have drooped.
• Arms – the person with suspected stroke may not be able to lift both arms and keep them there because of weakness or numbness in one arm.
• Speech – their speech may be slurred or garbled, or the person may not be able to talk at all despite appearing to be awake.
• Time – it’s time to dial your local emergency immediately if you notice any of these signs or symptoms.

It’s important for everyone to be aware of these signs and symptoms, particularly if you live with or care for somebody in a high-risk group, such as someone who is elderly or has diabetes or high blood pressure.

Other possible symptoms

Symptoms in the F.A.S.T. test identify most strokes, but occasionally a stroke can cause different symptoms.

Other symptoms and signs may include:

• Sudden numbness, paralysis or weakness of the face, arm or leg (especially on one side of the body)
• Sudden loss or blurring of vision in one or both eyes
• Dizziness
• Sudden trouble walking, dizziness, loss of balance or coordination
• Sudden confusion, trouble speaking or understanding speech
• Difficulty understanding what others are saying
• Problems with balance and co-ordination
• Difficulty swallowing (dysphagia)
• Sudden and very severe headache resulting in a blinding pain unlike anything experienced before
• Loss of consciousness

However, there may be other causes for these symptoms.

Transient ischemic attack (TIA)

The symptoms of a TIA, also known as a mini-stroke, are the same as a stroke, but tend to only last between a few minutes and a few hours before disappearing completely.

Although the symptoms do improve, a TIA should never be ignored as it’s a serious warning sign of a problem with the blood supply to your brain. It means you’re at an increased risk of having a stroke in the near future.

Brain infarct diagnosis

To determine the most appropriate treatment for your stroke, your emergency team needs to evaluate the type of stroke you’re having and the areas of your brain affected by the stroke. They also need to rule out other possible causes of your symptoms, such as a brain tumor or a drug reaction. Your doctor may use several tests to determine your risk of stroke, including:

Physical examination. Your doctor will ask you or a family member what symptoms you’ve been having, when they started and what you were doing when they began. Your doctor then will evaluate whether these symptoms are still present. Your doctor will want to know what medications you take and whether you have experienced any head injuries. You’ll be asked about your personal and family history of heart disease, transient ischemic attack or stroke.

Your doctor will check your blood pressure and use a stethoscope to listen to your heart and to listen for a whooshing sound (bruit) over your neck (carotid) arteries, which may indicate atherosclerosis. Your doctor may also use an ophthalmoscope to check for signs of tiny cholesterol crystals or clots in the blood vessels at the back of your eyes.

• Blood tests. You may have several blood tests, which tell your care team how fast your blood clots, whether your blood sugar is abnormally high or low, whether critical blood chemicals are out of balance, or whether you may have an infection. Managing your blood’s clotting time and levels of sugar and other key chemicals will be part of your stroke care.
• Computerized tomography (CT) scan. A CT scan uses a series of X-rays to create a detailed image of your brain. A CT scan can show a hemorrhage, tumor, stroke and other conditions. Doctors may inject a dye into your bloodstream to view your blood vessels in your neck and brain in greater detail (computerized tomography angiography).
• Magnetic resonance imaging (MRI). An MRI uses powerful radio waves and magnets to create a detailed view of your brain. An MRI can detect brain tissue damaged by an ischemic stroke and brain hemorrhages. Your doctor may inject a dye into a blood vessel to view the arteries and veins and highlight blood flow (magnetic resonance angiography, or magnetic resonance venography).
• Carotid ultrasound. In this test, sound waves create detailed images of the inside of the carotid arteries in your neck. This test shows buildup of fatty deposits (plaques) and blood flow in your carotid arteries.
• Cerebral angiogram. In this test, your doctor inserts a thin, flexible tube (catheter) through a small incision, usually in your groin, and guides it through your major arteries and into your carotid or vertebral artery. Then your doctor injects a dye into your blood vessels to make them visible under X-ray imaging. This procedure gives a detailed view of arteries in your brain and neck.
• Echocardiogram. An echocardiogram uses sound waves to create detailed images of your heart. An echocardiogram can find a source of clots in your heart that may have traveled from your heart to your brain and caused your stroke. You may have a transesophageal echocardiogram. In this test, your doctor inserts a flexible tube with a small device (transducer) attached into your throat and down into the tube that connects the back of your mouth to your stomach (esophagus). Because your esophagus is directly behind your heart, a transesophageal echocardiogram can create clear, detailed ultrasound images of your heart and any blood clots.

Brain infarct infarct

Emergency treatment for stroke depends on whether you’re having an ischemic stroke blocking an artery — the most common kind — or a hemorrhagic stroke that involves bleeding into the brain.

Ischemic stroke

To treat an ischemic stroke, doctors must quickly restore blood flow to your brain.

Emergency treatment with medications

Therapy with clot-busting drugs must start within 3 hours if they are given into the vein — and the sooner, the better. Quick treatment not only improves your chances of survival but also may reduce complications. You may be given:

• Aspirin. Aspirin is an immediate treatment given in the emergency room to reduce the likelihood of having another stroke. Aspirin prevents blood clots from forming.

• Intravenous injection of tissue plasminogen activator (TPA). Some people can benefit from an injection of a recombinant tissue plasminogen activator (TPA), also called alteplase. An injection of TPA is usually given through a vein in the arm. This potent clot-busting drug needs to be given within 4.5 hours after stroke symptoms begin if it’s given in the vein. TPA restores blood flow by dissolving the blood clot causing your stroke, and it may help people who have had strokes recover more fully. Your doctor will consider certain risks, such as potential bleeding in the brain, to determine if TPA is appropriate for you.

Emergency procedures

Doctors sometimes treat ischemic strokes with procedures that must be performed as soon as possible, depending on features of the blood clot:

• Medications delivered directly to the brain. Doctors may insert a long, thin tube (catheter) through an artery in your groin and thread it to your brain to deliver TPA directly into the area where the stroke is occurring. The time window for this treatment is somewhat longer than for intravenous TPA but is still limited.

• Mechanical clot removal. Doctors may use a catheter to maneuver a tiny device into your brain to physically break up or grab and remove the clot.

However, recent studies suggest that for most people, delivering medication directly to the brain (intra-arterial thrombolysis) or using a device to break up or remove clots (mechanical thrombectomy) may not be beneficial. Researchers are working to determine who might benefit from this procedure.

Other procedures to decrease your risk of having another stroke

To decrease your risk of having another stroke or transient ischemic attack, your doctor may recommend a procedure to open up an artery that’s narrowed by fatty deposits (plaques). Doctors sometimes recommend the following procedures to prevent a stroke.

Options will vary depending on your situation:

• Carotid endarterectomy. In a carotid endarterectomy, a surgeon removes plaques from arteries that run along each side of your neck to your brain (carotid arteries). In this procedure, your surgeon makes an incision along the front of your neck, opens your carotid artery and removes plaques that block the carotid artery. Your surgeon then repairs the artery with stitches or a patch made from a vein or artificial material (graft). The procedure may reduce your risk of ischemic stroke. However, a carotid endarterectomy also involves risks, especially for people with heart disease or other medical conditions.

• Angioplasty and stents. In an angioplasty, a surgeon gains access to your carotid arteries most often through an artery in your groin. Here, he or she can gently and safely navigate to the carotid arteries in your neck. A balloon is then used to expand the narrowed artery. Then a stent can be inserted to support the opened artery.

Hemorrhagic stroke

Emergency treatment of hemorrhagic stroke focuses on controlling your bleeding and reducing pressure in your brain. Surgery also may be performed to help reduce future risk.

Emergency measures

If you take warfarin (Coumadin) or anti-platelet drugs such as clopidogrel (Plavix) to prevent blood clots, you may be given drugs or transfusions of blood products to counteract the blood thinners’ effects. You may also be given drugs to lower pressure in your brain (intracranial pressure), lower your blood pressure, prevent vasospasm or prevent seizures.

Once the bleeding in your brain stops, treatment usually involves supportive medical care while your body absorbs the blood. Healing is similar to what happens while a bad bruise goes away. If the area of bleeding is large, your doctor may perform surgery to remove the blood and relieve pressure on your brain.

Surgical blood vessel repair

Surgery may be used to repair blood vessel abnormalities associated with hemorrhagic strokes. Your doctor may recommend one of these procedures after a stroke or if an aneurysm or arteriovenous malformation (AVM) or other type of vascular malformation caused your hemorrhagic stroke:

• Surgical clipping. A surgeon places a tiny clamp at the base of the aneurysm, to stop blood flow to it. This clamp can keep the aneurysm from bursting, or it can prevent re-bleeding of an aneurysm that has recently hemorrhaged.
• Coiling (endovascular embolization). In this procedure, a surgeon inserts a catheter into an artery in your groin and guides it to your brain using X-ray imaging. Your surgeon then guides tiny detachable coils into the aneurysm (aneurysm coiling). The coils fill the aneurysm, which blocks blood flow into the aneurysm and causes the blood to clot.
• Surgical arteriovenous malformation (AVM) removal. Surgeons may remove a smaller AVM if it’s located in an accessible area of your brain, to eliminate the risk of rupture and lower the risk of hemorrhagic stroke. However, it’s not always possible to remove an AVM if its removal would cause too large a reduction in brain function, or if it’s large or located deep within your brain.
• Intracranial bypass. In some unique circumstances, surgical bypass of intracranial blood vessels may be an option to treat poor blood flow to a region of the brain or complex vascular lesions, such as aneurysm repair.
• Stereotactic radiosurgery. Using multiple beams of highly focused radiation, stereotactic radiosurgery is an advanced minimally invasive treatment used to repair vascular malformations.

Brain infarct recovery

Following emergency treatment, stroke care focuses on helping you regain your strength, recover as much function as possible and return to independent living. The impact of your stroke depends on the area of the brain involved and the amount of tissue damaged.

If your stroke affected the right side of your brain, your movement and sensation on the left side of your body may be affected. If your stroke damaged the brain tissue on the left side of your brain, your movement and sensation on the right side of your body may be affected. Brain damage to the left side of your brain may cause speech and language disorders.

In addition, if you’ve had a stroke, you may have problems with breathing, swallowing, balancing and vision.

People who survive a stroke are often left with long-term problems caused by injury to their brain.

Some people need a long period of rehabilitation before they can recover their former independence, while many never fully recover and need support adjusting to living with the effects of their stroke.

Most stroke survivors receive treatment in a rehabilitation program. Your doctor will recommend the most rigorous therapy program you can handle based on your age, overall health and your degree of disability from your stroke. Your doctor will take into consideration your lifestyle, interests and priorities, and the availability of family members or other caregivers.

Your rehabilitation program may begin before you leave the hospital. It may continue in a rehabilitation unit of the same hospital, another rehabilitation unit or skilled nursing facility, an outpatient unit, or your home.

Every person’s stroke recovery is different. Depending on your condition, your treatment team may include:

• Doctor trained in brain conditions (neurologist)
• Rehabilitation doctor (physiatrist)
• Nurse
• Dietitian
• Physical therapist
• Occupational therapist
• Recreational therapist
• Speech therapist
• Social worker
• Case manager
• Psychologist or psychiatrist
• Chaplain

Psychological impact

Two of the most common psychological problems that can affect people after a stroke are:

• Depression – many people experience intense bouts of crying, and feel hopeless and withdrawn from social activities
• Anxiety – where people experience general feelings of fear and anxiety, sometimes punctuated by intense, uncontrolled feelings of anxiety (anxiety attacks)

Feelings of anger, frustration and bewilderment are also common.

You’ll receive a psychological assessment from a member of your healthcare team soon after your stroke to check if you’re experiencing any emotional problems.

Advice should be given to help deal with the psychological impact of stroke. This includes the impact on relationships with other family members and any sexual relationship.

There should also be a regular review of any problems of depression and anxiety, and psychological and emotional symptoms generally.

These problems may settle down over time, but if they are severe or last a long time, doctors can refer people for expert healthcare from a psychiatrist or clinical psychologist.

For some people, medicines and psychological therapies, such as counselling or cognitive behavioral therapy (CBT), can help. Cognitive behavioral therapy (CBT) is a therapy that aims to change the way you think about things to produce a more positive state of mind.

Cognitive impact

Cognitive is a term used by scientists to refer to the many processes and functions our brain uses to process information.

One or more cognitive functions can be disrupted by a stroke, including:

• Communication – both verbal and written
• Spatial awareness – having a natural awareness of where your body is in relation to your immediate environment
• Memory
• Concentration
• Executive function – the ability to plan, solve problems and reason about situations
• Praxis – the ability to carry out skilled physical activities, such as getting dressed or making a cup of tea

As part of your treatment, each one of your cognitive functions will be assessed and a treatment and rehabilitation plan will be created.

You can be taught a wide range of techniques that can help you relearn disrupted cognitive functions, such as recovering your communication skills through speech and language therapy.

There are many ways to compensate for any loss of cognitive function, such as using memory aids, diaries and routines to help plan daily tasks.

Most cognitive functions will return after time and rehabilitation, but you may find they don’t return to the way they were before.

The damage a stroke causes to your brain also increases the risk of developing vascular dementia. This may happen immediately after a stroke or may develop some time after the stroke occurred.

Movement problems

Strokes can cause weakness or paralysis on one side of the body, and can result in problems with co-ordination and balance.

Many people also experience extreme tiredness (fatigue) in the first few weeks after a stroke, and may also have difficulty sleeping, making them even more tired.

As part of your rehabilitation, you should be seen by a physiotherapist, who will assess the extent of any physical disability before drawing up a treatment plan.

Physiotherapy will often involve several sessions a week, focusing on areas such as exercises to improve your muscle strength and overcome any walking difficulties.

The physiotherapist will work with you by setting goals. At first, these may be simple goals, such as picking up an object. As your condition improves, more demanding long-term goals, such as standing or walking, will be set.

A careworker or carer, such as a member of your family, will be encouraged to become involved in your physiotherapy. The physiotherapist can teach you both simple exercises you can carry out at home.

If you have problems with movement and certain activities, such as getting washed and dressed, you may also receive help from an occupational therapist. They can find ways to manage any difficulties.

Occupational therapy may involve adapting your home or using equipment to make everyday activities easier, and finding alternative ways of carrying out tasks you have problems with.

Communication problems

After having a stroke, many people experience problems with speaking and understanding, as well as reading and writing.

If the parts of the brain responsible for language are damaged, this is called aphasia, or dysphasia. If there is weakness in the muscles involved in speech as a result of brain damage, this is known as dysarthria.

You should see a speech and language therapist as soon as possible for an assessment and to start therapy to help you with your communication.

This may involve:

• exercises to improve your control over your speech muscles
• using communication aids – such as letter charts and electronic aids
• using alternative methods of communication – such as gestures or writing

Swallowing problems

The damage caused by a stroke can interrupt your normal swallowing reflex, making it possible for small particles of food to enter your windpipe.

Problems with swallowing are known as dysphagia. Dysphagia can lead to damage to your lungs, which can trigger a lung infection (pneumonia).

You may need to be fed using a feeding tube during the initial phases of your recovery to prevent any complications from dysphagia.

The tube is usually put into your nose and passed into your stomach (nasogastric tube), or it may be directly connected to your stomach in a minor surgical procedure carried out using local anesthetic (percutaneous endoscopic gastrostomy, or PEG).

In the long term, you’ll usually see a speech and language therapist several times a week for treatment to manage your swallowing problems.

Treatment may involve tips to make swallowing easier, such as taking smaller bites of food and advice on posture, and exercises to improve control of the muscles involved in swallowing.

Visual problems

Stroke can sometimes damage the parts of the brain that receive, process and interpret information sent by the eyes.

This can result in losing half the field of vision – for example, only being able to see the left- or right hand side of what’s in front of you.

Strokes can also affect the control of the movement of the eye muscles. This can cause double vision.

If you have any problems with your vision after a stroke, you’ll be referred to an eye specialist called an orthoptist, who can assess your vision and suggest possible treatments.

For example, if you’ve lost part of your field of vision, you may be offered eye movement therapy. This involves exercises to help you look to the side with the reduced vision.

You may also be given advice about particular ways to perform tasks that can be difficult if your vision is reduced on one side, such as getting dressed.

Bladder and bowel control

Some strokes damage the part of the brain that controls bladder and bowel movements. This can result in urinary incontinence and difficulty with bowel control.

Some people may regain bladder and bowel control quite quickly, but if you still have problems after leaving hospital, help is available from the hospital, your GP, and specialist continence advisers.

Don’t be embarrassed – seek advice if you have a problem, as there are lots of treatments that can help.

These include:

• bladder retraining exercises
• medications
• pelvic floor exercises
• using incontinence products

Sex after brain infarct

Having sex won’t put you at higher risk of having a stroke. There’s no guarantee you won’t have another stroke, but there’s no reason why it should happen while you’re having sex.

Even if you’ve been left with a severe disability, you can experiment with different positions and find new ways of being intimate with your partner.

Be aware that some medications can reduce your sex drive (libido), so make sure your doctor knows if you have a problem – there may be other medicines that can help.

Some men may experience erectile dysfunction after having a stroke. Speak to your GP or rehabilitation team if this is the case, as there are a number of treatments available that can help.

Driving after brain infarct

If you’ve had a stroke or TIA, you can’t drive for one month. Whether you can return to driving depends on what long-term disabilities you may have and the type of vehicle you drive.

It’s often not physical problems that can make driving dangerous, but problems with concentration, vision, reaction time and awareness that can develop after a stroke.

Your doctor can advise you on whether you can start driving again a month after your stroke, or whether you need further assessment at a mobility center.

Preventing further brain infarcts

If you’ve had a stroke, your chances of having another one are significantly increased.

You’ll usually require long-term treatment with medications aimed at improving the underlying risk factors for your stroke.

For example:

• medication – to help lower your blood pressure
• anticoagulants or antiplatelets – to reduce your risk of blood clots
• statins – to lower your cholesterol levels

You’ll also be encouraged to make lifestyle changes to improve your general health and lower your stroke risk, such as:

• eating a healthy diet
• exercising regularly
• stopping smoking if you smoke
• cutting down on the amount of alcohol you drink

Caring for someone who’s had brain infarct

There are many ways you can provide support to a friend or relative who’s had a stroke to speed up their rehabilitation process.

These include:

• helping them practise physiotherapy exercises in between their sessions with the physiotherapist
• providing emotional support and reassurance their condition will improve with time
• helping motivate them to reach their long-term goals
• adapting to any needs they may have, such as speaking slowly if they have communication problems

Caring for somebody after a stroke can be a frustrating and lonely experience. The advice outlined below may help.

Be prepared for changed behavior

Someone who’s had a stroke can often seem as though they’ve had a change in personality and appear to act irrationally at times. This is the result of the psychological and cognitive impact of a stroke.

They may become angry or resentful towards you. Upsetting as it may be, try not to take it personally.

It’s important to remember they’ll often start to return to their old self as their rehabilitation and recovery progresses.

Try to remain patient and positive

Rehabilitation can be a slow and frustrating process, and there will be periods of time when it appears little progress has been made.

Encouraging and praising any progress, no matter how small it may appear, can help motivate someone who’s had a stroke to achieve their long-term goals.

Make time for yourself

If you’re caring for someone who’s had a stroke, it’s important not to neglect your own physical and psychological wellbeing. Socializing with friends or pursuing leisure interests will help you cope better with the situation.

Ask for help

There are a wide range of support services and resources available for people recovering from strokes, and their families and carers. This ranges from equipment that can help with mobility, to psychological support for carers and families.

The hospital staff involved with the rehabilitation process can provide advice and relevant contact information.

Lacunar infarct

Lacunar infarctions are defined as small subcortical lesions with a size of less than 15 mm in diameter caused by occlusion of a penetrating artery from a large cerebral artery, most commonly from the Circle of Willis ¹. These penetrating arteries arise at sharp angles from major vessels and are thus, anatomically prone to constriction and occlusion. Other common sources of these penetrating arteries include the middle cerebral artery and the basilar artery.

Lacunar syndromes are clinical manifestations of lacunar infarctions.

The term “lacune” was first described in the late 19th and early 20th century based on pathologic analysis and adapted after imaging technology confirmed the initial hypothesis in the 21st century. A lacune usually describes a small, chronic cavity that represents the healed phase of lacunar infarction ². However, there have been cases reported in which a lacune results from a larger infarct or intracerebral hemorrhage. Dr. Miller Fisher first described arterial pathology under lacunes in the mid-1900s. These vessels contained focal enlargements and small hemorrhagic extravasations through the endothelium of the arteries. Fibrinoid tissue replaces subintimal foam cells that then obliterates the vascular lumens. This process was described as fibrinoid degeneration and lipohyalinosis ³.

The anatomic distribution of lacunar infarctions is most commonly the basal ganglia (globus pallidus, putamen, thalamus, and caudate), the pons, and the subcortical white matter structures (internal capsule and corona radiate). These anatomical sites correspond to lesions at the lenticulostriate arteries, the anterior choroidal artery, thalamoperforant arteries, paramedian branches of the basilar artery, and the recurrent artery of Heubner from the anterior cerebral artery ⁴.

Lesions at these specific sites account for many of the symptoms of lacunar infarctions. There are over 20 lacunar syndromes that have been described, but the most common ones are pure motor hemiparesis, pure sensory stroke, ataxic hemiparesis, sensorimotor stroke, and dysarthria-clumsy hand syndrome.

One community-based study in Rochester, MN estimated that around 16% of first ischemic strokes in the United States are lacunar strokes ⁵.

In a similar community-based study of African-Americans in Cincinnati, lacunar infarctions accounted for 22% of first-time ischemic stroke events ⁶.

Data comparing the frequency of lacunar strokes among different sexes, races, and worldwide populations are not readily accessible. One study in Japan does state that the frequency of lacunar infarcts has decreased since the 1960s due to more aggressive control of risk factors, primarily hypertension ⁷.

Lacunar infarct causes

Multiple mechanisms have been proposed as the cause of lacunar infarction. The usual cause of small lacunar infarctions (between 3 mm and 7 mm) is lipohyalinosis of the small perforating arteries feeding deep subcortical structures. Another mechanism is micro-atheroma formation at the origin of penetrating arteries from major cerebral arteries like the middle cerebral artery, Circle of Willis, or the distal basilar artery. These first two mechanisms are proven pathologically and likely due to chronic hypertension and resulting in small vessel disease ⁸.

If the size of lacune is larger than 5 to 7 mm, it is often not caused by occlusion of 1 or 2 lenticulostriate arterial branches but from an atherothrombotic lesion involving the mainstem middle cerebral artery. These infarcts are named striatocapsular infarcts by Bladin and Berkovic ⁹.

Other proposed mechanisms that have been failed to be proven pathologically include tiny emboli causing obstruction and cerebral arteriolar and capillary endothelial dysfunction leading to small vessel disease as a result of extravasation of blood products.

Out of all the causes of lacunar infarctions, hypertension is the most common modifiable risk factor for stroke. For every 10mm Hg decrease in blood pressure, there is a 1/3rd lowering of stroke risk in primary prevention. So it is extremely important to control the blood pressure effectively to prevent future strokes. Cigarette smoking doubles stroke risk.

The pathophysiology of lacunar infarction is inherently linked to 2 vascular pathologies of the penetrating arteries from major intracranial and extracranial arteries: (1) thickening of the media resulting in decreased arterial diameter and (2) obstruction of the origins by microatheroma formation. Chronic hypertension, diabetes, and other genetic factors cause medial thickening by fibrinoid necrosis, smooth muscle hypertrophy, and other connective tissue elements. As a result, occlusive disease in these penetrating arteries causes a small infarct in the territory that the small vessel supplies. Since collateral circulation in these distant pontine and subcortical areas is so limited, and multiple penetrating vessels are likely affected in these patients, areas of infarct coalesce to form lake-like areas of infarcted/edematous brain tissue. Healing of this tissue ultimately forms “lacunes” ³.

Lacunar infarct symptoms

Most commonly, lacunar infarct symptoms affect the elderly with long-standing hypertension. Otherwise, younger patients with lacunar infarct may have a diagnosis of rare genetic conditions, such as CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy). The presenting complaint would usually not include cortical signs such as:

• Agnosia (loss of the ability to identify objects or people),
• Aphasia (impairment of language, affecting the production or comprehension of speech and the ability to read or write),
• Neglect,
• Apraxia (inability to perform a movement or task when asked despite having the desire and physical capability to carry it out),
• Hemianopsia (blindness (anopsia) in half the visual field).

These lacunar infarcts usually cause symptoms over minutes to hours but may progress with a stuttering course. The clinical features and physical exam findings of lacunar infarct are characteristic of the type of lacunar syndrome:

• Pure motor hemiparesis: Patient presents with weakness on one side of the body (face, arm, and leg) without cortical signs and sensory symptoms.
• Pure sensory stroke: Patient presents with unilateral numbness of the face, arm, and leg without cortical signs or motor deficits. All sensory modalities will be impaired.
• Ataxic hemiparesis: These patients present with unilateral limb ataxia and weakness that is out of proportion to the strength/motor deficit. Patient’s may also exhibit other ipsilateral cerebellar signs such has dysarthria, dysmetria, and nystagmus without exhibiting cortical signs.
• Sensorimotor stroke: Patients present with weakness and numbness of the face, arm, and leg without cortical signs. Cortical function testing must be done meticulously to distinguish between a frontoparietal lobe (MCA = middle cerebral artery) stroke and a subcortical stroke (posterior thalamus and internal capsule).
• Dysarthria-clumsy hand syndrome: This is the least common of all lacunar syndromes. Patients present with facial weakness, dysarthria, dysphagia and dysmetria/clumsiness of one upper extremity.

Lacunar infarct diagnosis

Initial evaluation of a suspected lacunar infarct involves brain imaging with a brain CT and MRI. Since small perforating arteries are hard to visualize with CT angiography (CTA) and magnetic resonance angiography (MRA) scan, the diagnosis is made by matching a patient’s clinical features with a small, noncortical infarct seen on CT/MRI. The initial CT/MRI is also useful in ruling out life-threatening conditions such as intracerebral hemorrhage or herniation.

MRIs have been shown to have a higher sensitivity and specificity than CT ¹⁰. Diffusion-weighted imaging (DWI) is particularly important because it has higher sensitivity for acute infarcts when compared with T2 weighted MRI/FLAIR sequences.

In most cases, mapping a patient’s history of hypertension or diabetes and his/her clinical features with findings of acute ischemia on brain imaging is all that is needed for diagnosis of lacunar infarcts. However, if the patient is young and has no cerebral risk factors, further investigation may be required to determine if there is an embolic source. Vascular imaging and transcranial Doppler is warranted at the same time of initial CT/MRI to rule out large vessel ischemia ¹¹.

Lacunar infarct treatment

The acute treatment of lacunar infarctions is like that of acute ischemic strokes. Within 4.5 hours of symptom onset, patients should receive intravenous (IV) alteplase therapy. The contraindications to IV thrombolysis is the same as those for other types of acute ischemic strokes, some of which include ischemic stroke/head trauma in the past 3 months, previous intracranial hemorrhage, gastrointestinal (GI) malignancy or hemorrhage in the past 21 days, intracranial/spinal surgery in the past 3 months, and intra-axial intracranial neoplasm. For those patients not eligible for IV alteplase therapy, aspirin therapy is recommended. Otherwise, the acute treatment involves stabilization and early involvement of rehabilitation with speech and physical therapy.

The most important aspect of treatment for these patients is preventative. Aggressive blood pressure control, early high-dose statin therapy, and antiplatelet therapy are crucial. Anti-platelet therapy with aspirin, clopidogrel, or fixed-dose aspirin with dipyramidal are all acceptable medications. With the results of the CHANCE trial and the POINT trial, dual antiplatelet therapy for 3 weeks followed by single antiplatelet will provide the best scheme of therapy. More prolonged dual antiplatelet therapy (clopidogrel + aspirin) has not been shown to decrease the risk of recurrent strokes and resulted in a significantly increased risk of bleeding and death ¹². The present-day scheme of “aggressive medical therapy” with antiplatelet treatment, aggressive blood pressure control with a target of 120/80 mm Hg, high dose statin, good blood sugar control, stopping smoking, sodium reduction, and good weight control and lifestyle modification should be able to prevent at least 80% of strokes ¹³. The LDL “bad” cholesterol should be lowered to less than 100 with a high-intensity statin. Usually a high-intensity statin decrease LDL “bad” cholesterol approximately 50% on an average. Strategies to reduce HbA1C less than 7 are also very important.

After initial stabilization and neurology evaluation, many consultations are not required in the acute phase setting. Physical therapy, speech therapy, occupational therapy, and rehabilitation services led by a Physical Medicine and Rehabilitation physician must be made immediately. Lacunar infarct patients must be initially evaluated in the hospital as well as followed closely in the outpatient setting to ensure that the patient recovers as quickly as possible.

Furthermore, close contact between the patient’s neurologist, primary care physician, Physical Medicine and Rehabilitation physician, and physical therapy/speech therapy/occupational therapy providers after hospital discharge further aids in the prevention of recurrent lacunar/ischemic strokes.

Side effect of  lacunar infarction treatment

The main adverse event to be hypervigilant for in patients with acute lacunar infarctions is a hemorrhagic transformation or adverse bleeding events after IV alteplase therapy. Close monitoring with frequent neurologic exams and a high degree of suspicion can prevent these devastating events.

Preventative treatment is generally well tolerated. However, patients should be notified that there is an increased risk of bleeding on long-term antiplatelet therapy. Side effects of antihypertensive therapy, such as orthostatic hypotension and an increased risk of falls should also be explained to the patient. No data exists that lacunar infarct patients are at increased risk of statin myopathy over the general population. These medications should be prescribed at the lowest therapeutic dose.

Lacunar infarction prognosis

The short-term prognosis of lacunar infarctions is better than other infarcts due to other stroke mechanisms. Multiple population-based epidemiological studies on lacunar infarcts have shown significantly better survival among patients who suffered from lacunar infarctions compared to those who suffered from non-lacunar infarcts ⁵. These studies showed a case fatality of 0% to 3% within the first month and 3% to 9% within the first year, compared with 14% and 28%, respectively.

Though the short-term prognosis for patients with lacunar infarctions is better, there is not as stark a difference in the long-term prognosis when compared with non-lacunar events. Multiple studies have shown that the stroke recurrence rate and the risk of death between lacunar infarcts and non-lacunar infarcts are similar after 5 years. The main reason for the better 5-year survival rate in lacunar syndrome patients is attributed to the lower mortality within the first year of the ischemic event ⁵.

As expected, patients that suffered from a lacunar infarction with worse initial neurologic deficits had a worse functional outcome. However, data does not exist comparing patient functional outcome and long-term prognosis between different mechanisms of lacunar infarction production.

Multi infarct dementia

Multi-infarct dementia is defined as cognitive impairment resulting from multiple lesions and infarcts in both white and gray matter that follow occlusions in cerebral arteries and arterioles ¹⁴. Multi-infarct dementia is considered the most common form of vascular dementia, a primary cause of dementia second to Alzheimer’s disease ¹⁵. Multi-infarct dementia was used as a nearly interchangeable term with vascular dementia before the recognition of dementia subtypes resulting from single infarcts or genetic arteriopathy ¹⁶. Vascular pathology has been found to be the root cause of dementia in about 8–10% of all clinical cases of cognitive impairment, and 25–80% of Alzheimer’s disease patients display vascular lesions that may contribute to their dementia ¹⁷. Multi-infarct dementia and other vascular dementia subtype symptomology variably includes prominent impairment in executive functions involving attention, working memory and perceptual speed, mild episodic memory deficits, affective disturbances, and gait abnormalities, which progressively interfere with daily life activity of the patient and increase the emotional and economic burden for caregivers ¹⁸:S296–S304)). Vascular dementia was also estimated to have the highest annual cost per patient among the most common dementias, likely due to a higher rate of recurrent hospital admissions ¹⁹. However, no approved treatment currently exists to modify cognitive decline once it has become apparent ²⁰. As such, prevention of strokes and management of risk factors are the only universally and medically accepted means of controlling the onset of multi-infarct dementia ²⁰.

Multi-infarct dementia causes

Vascular dementia results from conditions that damage your brain’s blood vessels, reducing their ability to supply your brain with the amounts of nutrition and oxygen it needs to perform thought processes effectively.

Common conditions that may lead to vascular dementia include:

• Stroke (infarction) blocking a brain artery. Strokes that block a brain artery usually cause a range of symptoms that may include vascular dementia. But some strokes don’t cause any noticeable symptoms. These silent strokes still increase dementia risk. With both silent and apparent strokes, the risk of vascular dementia increases with the number of strokes that occur over time. One type of vascular dementia involving many strokes is called multi-infarct dementia.
• Narrowed or chronically damaged brain blood vessels. Conditions that narrow or inflict long-term damage on your brain blood vessels also can lead to vascular dementia. These conditions include the wear and tear associated with aging, high blood pressure, abnormal aging of blood vessels (atherosclerosis), diabetes, and brain hemorrhage.

Risk factors for multi-infarct dementia

In general, the risk factors for vascular dementia are the same as those for heart disease and stroke. Risk factors for vascular dementia include:

• Increasing age. Your risk of vascular dementia rises as you grow older. The disorder is rare before age 65, and the risk rises substantially by your 90s.
• History of heart attack, strokes or ministrokes. If you’ve had a heart attack, you may be at increased risk of having blood vessel problems in your brain. The brain damage that occurs with a stroke or a ministroke (transient ischemic attack) may increase your risk of developing dementia.
• Abnormal aging of blood vessels (atherosclerosis). This condition occurs when deposits of cholesterol and other substances (plaques) build up in your arteries and narrow your blood vessels. Atherosclerosis can increase your risk of vascular dementia by reducing the flow of blood that nourishes your brain.
• High cholesterol. Elevated levels of low-density lipoprotein (LDL), the “bad” cholesterol, are associated with an increased risk of vascular dementia.
• High blood pressure. When your blood pressure’s too high, it puts extra stress on blood vessels everywhere in your body, including your brain. This increases the risk of vascular problems in the brain.
• Diabetes. High glucose levels damage blood vessels throughout your body. Damage in brain blood vessels can increase your risk of stroke and vascular dementia.
• Smoking. Smoking directly damages your blood vessels, increasing your risk of atherosclerosis and other circulatory diseases, including vascular dementia.
• Obesity. Being overweight is a well-known risk factor for vascular diseases in general, and therefore, presumably increases your risk of vascular dementia.
• Atrial fibrillation. In this abnormal heart rhythm, the upper chambers of your heart begin to beat rapidly and irregularly, out of coordination with your heart’s lower chambers. Atrial fibrillation increases your risk of stroke because it causes blood clots to form in the heart that can break off and go to the brain blood vessels.

Multi-infarct dementia prevention

The health of your brain’s blood vessels is closely linked to your overall heart health. Taking these steps to keep your heart healthy may also help reduce your risk of vascular dementia:

• Maintain a healthy blood pressure. Keeping your blood pressure in the normal range may help prevent both vascular dementia and Alzheimer’s disease.
• Prevent or control diabetes. Avoiding the onset of type 2 diabetes, with diet and exercise, is another possible way to decrease your risk of dementia. If you already have diabetes, controlling your glucose levels may help protect your brain blood vessels from damage.
• Quit smoking. Smoking tobacco damages blood vessels everywhere in your body.
• Get physical exercise. Regular physical activity should be a key part of everyone’s wellness plan. In addition to all of its other benefits, exercise may help you avoid vascular dementia.
• Keep your cholesterol in check. A healthy, low-fat diet and cholesterol-lowering medications if you need them may reduce your risk of strokes and heart attacks that could lead to vascular dementia, probably by reducing the amount of plaque deposits building up inside your brain’s arteries.

Multi-infarct dementia signs and symptoms

Multi-infarct dementia (vascular dementia) is a general term describing problems with reasoning, planning, judgment, memory and other thought processes caused by brain damage from impaired blood flow to your brain.

Multi-infarct dementia (vascular dementia) symptoms vary, depending on the part of your brain where blood flow is impaired. Symptoms often overlap with those of other types of dementia, especially Alzheimer’s disease dementia.

Multi-infarct dementia (vascular dementia) signs and symptoms include:

• Confusion
• Trouble paying attention and concentrating
• Reduced ability to organize thoughts or actions
• Decline in ability to analyze a situation, develop an effective plan and communicate that plan to others
• Difficulty deciding what to do next
• Problems with memory
• Restlessness and agitation
• Unsteady gait
• Sudden or frequent urge to urinate or inability to control passing urine
• Depression or apathy

Multi-infarct dementia (vascular dementia) symptoms may be most clear-cut when they occur suddenly following a stroke. When changes in your thinking and reasoning seem clearly linked to a stroke, this condition is sometimes called post-stroke dementia.

Sometimes a characteristic pattern of multi-infarct dementia (vascular dementia) symptoms follows a series of strokes or ministrokes. Changes in your thought processes occur in noticeable steps downward from your previous level of function, unlike the gradual, steady decline that typically occurs in Alzheimer’s disease dementia.

But multi-infarct dementia (vascular dementia) can also develop very gradually, just like Alzheimer’s disease dementia. What’s more, vascular disease and Alzheimer’s disease often occur together.

Studies show that many people with dementia and evidence of brain vascular disease also have Alzheimer’s disease.

Multi-infarct dementia diagnosis

Doctors can nearly always determine that you have dementia, but there’s no specific test that confirms you have vascular dementia. Your doctor will make a judgment about whether vascular dementia is the most likely cause of your symptoms based on the information you provide, your medical history for stroke or disorders of the heart and blood vessels, and results of tests that may help clarify your diagnosis.

Today vascular dementia also is diagnosed using the DSM 5 criteria, the International Classification of Diseases, Tenth Edition criteria, the Alzheimer’s Disease Diagnostic and Treatment criteria, the National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche at L’Enseignement en Neurosciences (NINDS-AIREN) criteria ²¹ and the Hachinski ischemic score ²².

Lab tests

If your medical record doesn’t include recent values for key indicators of the health of your heart and blood vessels, your doctor will test your:

• Blood pressure
• Cholesterol
• Blood sugar

Your doctor may also order tests to rule out other potential causes of memory loss and confusion, such as:

• Thyroid disorders
• Vitamin deficiencies

Neurological exam

Your doctor is likely to check your overall neurological health by testing your:

• Reflexes
• Muscle tone and strength, and how strength on one side of your body compares with the other side
• Ability to get up from a chair and walk across the room
• Sense of touch and sight
• Coordination
• Balance

Brain imaging

Images of your brain can pinpoint visible abnormalities caused by strokes, blood vessel diseases, tumors or trauma that may cause changes in thinking and reasoning. A brain-imaging study can help your doctor zero in on more likely causes for your symptoms and rule out other causes.

Brain-imaging procedures your doctor may recommend to help diagnose vascular dementia include:

Computerized tomography (CT) scan. For a CT scan, you’ll lie on a narrow table that slides into a small chamber. X-rays pass through your body from various angles, and a computer uses this information to create detailed cross-sectional images (slices) of your brain.

A CT scan can provide information about your brain’s structure; tell whether any regions show shrinkage; and detect evidence of strokes, ministrokes (transient ischemic attacks), blood vessel changes or tumors. Sometimes you’ll receive an intravenous (IV) injection of a contrast agent that will help highlight certain brain tissues.

Magnetic resonance imaging (MRI). An MRI uses radio waves and a strong magnetic field to produce detailed images of your brain. You lie on a narrow table that slides into a tube-shaped MRI machine, which makes loud banging noises while it produces images.

MRIs are painless, but some people feel claustrophobic inside the machine and are disturbed by the noise. T2-weighted MRI was found to provide the best-contrast image and was ultimately determined to be more sensitive than CT for detecting white matter lesions and infarcts ²³.Today MRI, both T2-weighted and fluid attenuated inversion recovery (FLAIR), are commonly used to study suspected vascular dementia ²⁴.

Carotid ultrasound

This procedure uses high-frequency sound waves to determine whether your carotid arteries — which run up through either side of your neck to supply blood to the brain — show signs of narrowing as a result of plaque deposits or structural problems. Your test may include a Doppler ultrasound, which shows the movement of blood through your arteries in addition to structural features.

Neuropsychological tests

This type of exam assesses your ability to:

• Speak, write and understand language
• Work with numbers
• Learn and remember information
• Develop a plan of attack and solve a problem
• Respond effectively to hypothetical situations

Neuropsychological tests sometimes show characteristic results for people with different types of dementia. People with vascular dementia may have an exceptionally hard time analyzing a problem and developing an effective solution.

They may be less likely to have trouble learning new information and remembering than are people with dementia due to Alzheimer’s disease unless their blood vessel problems affect specific brain regions important for memory. However, there’s often a lot of overlap in exam results for people with vascular dementia and people who also have the brain changes of Alzheimer’s disease.

Multi-infarct dementia treatment

Treatment often focuses on managing the health conditions and risk factors that contribute to vascular dementia.

Controlling conditions that affect the underlying health of your heart and blood vessels can sometimes slow the rate at which vascular dementia gets worse, and may also sometimes prevent further decline. Depending on your individual situation, your doctor may prescribe medications to:

• Lower your blood pressure
• Reduce your cholesterol level
• Prevent your blood from clotting and keep your arteries clear
• Help control your blood sugar if you have diabetes

No treatment has yet moved beyond clinical trials to meet regulatory approval, the research community’s improved understanding of multi-infarct dementia raises the prospect of finding a viable intervention ²⁵. A few of the drugs that initially seemed the most promising included ace tylcholinesterase inhibitors and the antihypertensive calcium channel blocker nimodipine ²⁶.

Several acetylcholinesterase inhibitors are approved for the symptomatic management of moderate Alzheimer’s disease ²⁷. Among these, galantamine and donepezil showed only mild improvements in executive function, no improvement in any other clinical measures, and some deleterious side effects in early multi-infarct dementia clinical trials ²⁶.

Nimodipine was the subject of several therapeutic trials of multi-infarct dementia at the start of the 21st century by Pantoni et al. ²⁸. As nimodipine has a vasodilatory effect on small vessels, it was thought that it would be helpful in maintaining perfusion in areas most sensitive to ischemic events ²⁸. These patients showed improvement versus controls in measures of neuropsychological and executive function but not motor functions [79]. Subsequently, it was discovered that these improvements were limited to the subgroup with subcortical lesions only ²⁸. However, nimodipine has since seen little attention in further clinical trials ²⁵.

Current clinical trials for the treatment of vascular dementia with forthcoming results include rivastigmine (NCT00130338) and cilostazol (NCT00847860). Rivastigmine is another acetylcholinesterase inhibitor with some cognitive benefits in previous clinical trials of vascular dementia when Alzheimer’s disease was also a probable contributor to cognitive dysfunction ²⁹. Cilostazol has been sug gested as a vascular dementia treatment when diabetes is a significant contributing risk factor based on improved Morris water maze performance in rat models of diabetes ³⁰.

Cholinesterase inhibitors have been shown to slow the progression of cognitive decline ²². The side effect profile is significant, to include gastrointestinal distress, symptomatic bradycardia, and agitation. Memantine, an NMDA antagonist, is FDA approved for moderate to severe dementia and has been shown to improve patient functional levels and lessen care dependency. Whether to offer these medications takes a careful conversation with patients and caregivers, weighing the benefits and side effects individualized to their health condition and goals of care.

Multi-infarct dementia prognosis

Overall, patients with vascular dementia have a shortened life expectancy. Those who have already had a cerebrovascular accident have the highest mortality, with a 5-year survival of only 39% ²². Patients with vascular dementia also have coexisting atherosclerotic disease, and death from cardiovascular causes is common.

Other complications

Besides death, other complications of vascular dementia include the following:

• Abnormal behavior, such as delusion, paranoia, or hallucinations
• Aspiration pneumonia
• Depression
• Falls
• Gait difficulties
• Pressure sores and ulcers
• Repeated hospitalizations
• Stress on caregivers

1. Venkataraman P, Tadi P, Lui F. Lacunar Syndromes. [Updated 2019 Mar 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534206[↩]
2. Mok V, Kim JS. Prevention and Management of Cerebral Small Vessel Disease. J Stroke. 2015 May;17(2):111-22[↩]
3. Caplan LR. Lacunar infarction and small vessel disease: pathology and pathophysiology. J Stroke. 2015 Jan;17(1):2-6[↩][↩]
4. Feekes JA, Hsu SW, Chaloupka JC, Cassell MD. Tertiary microvascular territories define lacunar infarcts in the basal ganglia. Ann. Neurol. 2005 Jul;58(1):18-30.[↩]
5. Sacco S, Marini C, Totaro R, Russo T, Cerone D, Carolei A. A population-based study of the incidence and prognosis of lacunar stroke. Neurology. 2006 May 09;66(9):1335-8[↩][↩][↩]
6. Woo D, Gebel J, Miller R, Kothari R, Brott T, Khoury J, Salisbury S, Shukla R, Pancioli A, Jauch E, Broderick J. Incidence rates of first-ever ischemic stroke subtypes among blacks: a population-based study. Stroke. 1999 Dec;30(12):2517-22[↩]
7. Kubo M, Kiyohara Y, Ninomiya T, Tanizaki Y, Yonemoto K, Doi Y, Hata J, Oishi Y, Shikata K, Iida M. Decreasing incidence of lacunar vs other types of cerebral infarction in a Japanese population. Neurology. 2006 May 23;66(10):1539-44[↩]
8. Wardlaw JM, Smith C, Dichgans M. Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging. Lancet Neurol. 2013 May;12(5):483-97[↩]
9. Bladin PF, Berkovic SF. Striatocapsular infarction: large infarcts in the lenticulostriate arterial territory. Neurology. 1984 Nov;34(11):1423-30[↩]
10. Hommel M, Besson G, Le Bas JF, Gaio JM, Pollak P, Borgel F, Perret J. Prospective study of lacunar infarction using magnetic resonance imaging. Stroke. 1990 Apr;21(4):546-54[↩]
11. Khan A, Kasner SE, Lynn MJ, Chimowitz MI., Warfarin Aspirin Symptomatic Intracranial Disease (WASID) Trial Investigators. Risk factors and outcome of patients with symptomatic intracranial stenosis presenting with lacunar stroke. Stroke. 2012 May;43(5):1230-3[↩]
12. SPS3 Investigators. Benavente OR, Hart RG, McClure LA, Szychowski JM, Coffey CS, Pearce LA. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N. Engl. J. Med. 2012 Aug 30;367(9):817-25[↩]
13. Rothwell PM, Giles MF, Chandratheva A, Marquardt L, Geraghty O, Redgrave JN, Lovelock CE, Binney LE, Bull LM, Cuthbertson FC, Welch SJ, Bosch S, Alexander FC, Carasco-Alexander F, Silver LE, Gutnikov SA, Mehta Z., Early use of Existing Preventive Strategies for Stroke (EXPRESS) study. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. Lancet. 2007 Oct 20;370(9596):1432-42[↩]
14. The pathobiology of vascular dementia. Iadecola C. Neuron. 2013 Nov 20; 80(4):844-66.[↩]
15. Vascular dementia: different forms of vessel disorders contribute to the development of dementia in the elderly brain. Thal DR, Grinberg LT, Attems J. Exp Gerontol. 2012 Nov; 47(11):816-24.[↩]
16. Gorelick PB, Scuteri A, Black SE, Decarli C, Greenberg SM, Iadecola C, et al. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42:2672–2713[↩]
17. Jellinger KA. Pathology and pathogenesis of vascular cognitive impairment – a critical update. Front Aging Neurosci. 2013;5:17[↩]
18. Román G. Vascular dementia: distinguishing characteristics, treatment and prevention. J Am Geriatr Soc. 2003;51((suppl dementia[↩]
19. Hill J, Fillit H, Shah S, del Valle MC, Futterman R. Patterns of healthcare utilization and costs for vascular dementia in a community-dwelling population. J Alzheimers Dis. 2005;8:43–50[↩]
20. Baskys A, Cheng JX. Pharmacological prevention and treatment of vascular dementia: approaches and perspectives. Exp Gerontol. 2012;47:887–891[↩][↩]
21. Neuropathological diagnosis of vascular cognitive impairment and vascular dementia with implications for Alzheimer’s disease. Kalaria RN. Acta Neuropathol. 2016 May; 131(5):659-85.[↩]
22. Uwagbai O, Kalish VB. Dementia, Vascular. [Updated 2018 Oct 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430817[↩][↩][↩]
23. Do white matter changes on MRI and CT differentiate vascular dementia from Alzheimer’s disease? Erkinjuntti T, Ketonen L, Sulkava R, Sipponen J, Vuorialho M, Iivanainen M. J Neurol Neurosurg Psychiatry. 1987 Jan; 50(1):37-42.[↩]
24. Neuroimaging in vascular cognitive impairment: a state-of-the-art review. Heiss WD, Rosenberg GA, Thiel A, Berlot R, de Reuck J. BMC Med. 2016 Nov 3; 14(1):174.[↩]
25. Pharmacological prevention and treatment of vascular dementia: approaches and perspectives. Baskys A, Cheng JX. Exp Gerontol. 2012 Nov; 47(11):887-91.[↩][↩]
26. Efficacy and adverse effects of cholinesterase inhibitors and memantine in vascular dementia: a meta-analysis of randomised controlled trials. Kavirajan H, Schneider LS. Lancet Neurol. 2007 Sep; 6(9):782-92.[↩][↩]
27. A cohort study of effectiveness of acetylcholinesterase inhibitors in Alzheimer’s disease. Raschetti R, Maggini M, Sorrentino GC, Martini N, Caffari B, Vanacore N. Eur J Clin Pharmacol. 2005 Jul; 61(5-6):361-8.[↩]
28. Efficacy and safety of nimodipine in subcortical vascular dementia: a subgroup analysis of the Scandinavian Multi-Infarct Dementia Trial. Pantoni L, Rossi R, Inzitari D, Bianchi C, Beneke M, Erkinjuntti T, Wallin A. J Neurol Sci. 2000 Apr 15; 175(2):124-34.[↩][↩][↩]
29. Efficacy, safety and tolerability of rivastigmine capsules in patients with probable vascular dementia: the VantagE study. Ballard C, Sauter M, Scheltens P, He Y, Barkhof F, van Straaten EC, van der Flier WM, Hsu C, Wu S, Lane R. Curr Med Res Opin. 2008 Sep; 24(9):2561-74.[↩]
30. Efficacy of Cilostazol a selective phosphodiesterase-3 inhibitor in rat model of Streptozotocin diabetes induced vascular dementia. Kumar A, Kumar A, Jaggi AS, Singh N. Pharmacol Biochem Behav. 2015 Aug; 135():20-30.[↩]