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ischemia mid brain


A. Arterial Supply and Anastomoses 

The brain receives its blood supply from paired vertebral and internal carotid arteries as well as from anastomotic channels derived from extracranial vessels. You should be familiar with the pattern of arterial supply in the brain. 

1. Anastomotic Channels 

a. Circle of Willis (via anterior communicating and posterior communicating arteries) 

b. Channels between external and internal carotid arteries, especially via the ophthalmic artery. 

c. Leptomeningeal anastomoses between peripheral branches of the anterior, middle and posterior cerebral arteries. 

B. Venous Drainage 
The veins of the brain drain into the dural venous sinuses and through them to the internal jugular veins. Since the surface veins of the brain have abundant anastomoses of large caliber, localized venous obstructions may produce few effects. Because the veins of the CNS are valveless, blood may flow in or out of the skull through these connections, providing a potential route for infection. 
C. Factors Affecting CNS Blood Flow 
Normally, autoregulation in the brain keeps cerebral blood flow constant over a wide range of perfusion pressures. The mechanism by which arterioles dilate when perfusion pressure falls and constrict when perfusion pressure rises is poorly understood, but several factors are known to regulate these phenomena. The most potent effect is exerted by carbon dioxide, i.e., increased carbon dioxide causes increased cerebral blood flow. 
D. Factors Operating to Ensure Normal Substrate Requirements 
1. Increased extraction of glucose and oxygen from the perfusing blood 

2. Autoregulation of blood flow in response to changes in perfusion pressure 

3. Anastomoses 
4. Increased percentage of systemic blood flow to the CNS 



A. General Characteristics 

Ischemia, the failure of cerebral blood flow to a region, results in infarction (complete necrosis). Experimental studies suggest that the rapidly lethal effects on neurons are due not only to the sensitivity of those cells to hypoxia but also to the inability of the cerebrovascular bed to recover from a period of severe ischemia, i.e. glial cells swell and compress capillaries. 

The most common cerebrovascular lesions are ischemic in nature - 85% of "strokes" are due to thrombosis or occlusive vascular disease. The vasculature that leads from the heart to the brain is the most common location of occlusive disease. 

The site of infarction and resulting clinical signs depend on many factors in addition to the site of occlusion, including the extent of collateral circulation, the presence of anomalies and the suddenness of occlusion. For example, when occlusion of the internal carotid artery occurs, the infarction is most commonly in the distribution of the middle cerebral artery because the area supplied by the anterior cerebral artery receives blood via the anterior communicating artery. 
Occasionally cerebrovascular lesions result from generalized reduction of cerebral perfusion. For example, if a failing myocardium inadequately perfuses a vascular system already interrupted by moderate amounts of occlusive disease, infarctions of the brain may result. These may be either "watershed" infarcts or localized to distributions of specific arterial branches. In addition, generalized reduction of blood flow is associated with hypoxic encephalopathy, with widespread damage. Hypoxic encephalopathy is discussed further in the Toxic-Metabolic-Nutritional Disorders unit. 
B. Thrombosis (Arterial)--Pale Infarction
1. Pathogenesis 

a. Vascular occlusion due to atheroma - most common cause of stroke. The most common sites are the origins of the internal carotid arteries, vertebral arteries and middle cerebral arteries. 

b. Variations in coagulability of blood; e.g. post-operative changes, polycythemia 

c. Reduction of circulation in an impaired system; e.g. sleep, hypotension, immobilization for fracture. 

d.Vascular occlusion secondary to vasculitis 

2. Incidence



Since the majority of cases of thrombosis are related to atherosclerosis, cerebral thrombosis generally occurs in individuals who have one or more risk factors producing accelerated atherosclerosis. These factors include hypertension, diabetes mellitus, obesity, hyperuricemia, hypothyroidism, abnormal serum lipid levels, and smoking. In young women, the combination of smoking and birth control pills is a significant risk factor. 

3. Clinical Features 

Infarction of the brain in an area supplied by a cerebral artery tends to produce a clearly recognizable clinical syndrome. Occlusion is preceded by transient ischemic attacks in about 50% of cases. The onset of symptoms is sudden, and gradual improvement may occur beginning after a few days. Specific symptoms depend on the site of infarction. A brief summary of the syndromes produced by infarction in the territory of major arteries is provided below: 

Middle cerebral artery: paralysis of the contralateral face, arm and leg; sensory impairment over the contralateral face, arm and leg; homonymous hemianopsia or homonymous quadrantonopsia; paralysis of conjugate gaze to the opposite side; aphasia if the lesion is on the dominant side (usually the left side of brain); unilateral neglect and agnosia for half of external space if the lesion is on the non-dominant side (usually right side). 
Anterior cerebral artery: paralysis of contralateral foot and leg; sensory loss over toes, foot and leg; impairment of gait and stance. 
Posterior cerebral artery: homonymous hemianopsia; hallucinations; sensory loss and spontaneous pain (if central territory including thalamus is involved - called thalamic syndrome); third nerve palsy and contralateral hemiplegia (if central territory including midbrain is involved - called Weber's syndrome). 
Posterior inferior cerebellar artery: pain, numbness, impaired sensation in face ipsilateral to lesion; impaired pain and temperature sensation in bocy contralateral to lesion; ataxia of limbs; falling to side of lesion; nystagmus, vertigo, Horner's syndrome, dysphagia, hoarseness.



4. Gross Pathology 

a. In the first 48 hours a lesion is difficult to discern at autopsy. After fixation, the infarcted area appears soft and swollen. 

b. Edema reaches a maximum in 4-5 days. Edema acts as a space-occupying lesion and may cause adjacent damage. 

c. Cell loss, myelin breakdown, phagocytosis and glial scar production result in shrinkage and distortion of structure; cysts may form in large infarcts and compensatory ventricular enlargement may occur. 

This image shows a recent infarct in the temporal lobe on the right, with edema indicated by blurring of margin between gray and white matter, gyri pushed out, cracking between temporal lobe white matter and the adjacent gray matter. 

This coronal section shows an old lacunar infarct in putamen and internal capsule on right side of image. 

This coronal section shows an old infarct in distribution of middle cerebral artery; cyst formation and compensatory verticular enlargement are prominent. 

Sections of caudal pons, rostral pons and midbrain from the brain shown at left illustrate Wallerian degeneration of corticospinal tract on right side of each image secondary to the infarct in the distribution of the middle cerebral artery.


5. Microscopic Pathology 

a. After about 12 hours: neuronal nuclear pyknosis and cytoplasmic eosinophilia (red neurons) 

b. After 2 days: polymorphonuclear leukocyte infiltrate; capillary prominence; endothelial swelling; vacuolation of white matter 

c. After 3-5 days: macrophages appear 

d. After 7-21 days: astrocytes proliferate and may become gemistocytic; glial fibers increase; cysts are traversed by blood vessels and surrounded by firm glial tissue 

A microscopic field (high-power) from an old infarct shows lipid-laden macrophages (brownish cytoplasm) and glial fibrils (pink) in a cystic region. 


C. Embolism 

1. Pathogenesis



Emboli are circulating bodies which lodge in vessels, generally involving the smaller vessels. The commonest cause of cerebral embolism is a thrombotic embolus in the middle cerebral artery. After an embolus occludes a vessel, the tissue undergoes infarction and the distal portion of the vessel becomes necrotic. If the occlusive material breaks up or moves into the necrotic area of the vessel, blood disgorges through the weakened wall and floods into the area that has been infarcted. The result is a hemorrhagic infarction. Hemorrhagic infarction often occurs with emboli, but pale infarctions may also result. 

2. Incidence 

Thromboemboli occur most often in patients with valvular heart disease, cardiac disease with atrial fibrillations, or myocardial infarction. Fat emboli may occur following lung injury or surgery. Nitrogen bubbles may form with rapid decompression in deep sea divers. 

3. Clinical Course



Clinical symptoms consist of sudden onset of focal impairment, within seconds to minutes. Most patients survive and marked clinical improvement often occurs. 

4. Pathological Changes



Emboli most often produce tiny hemorrhagic infarcts in the cerebral cortex although one larger region may be involved. The area involved is generally smaller than for thrombotic occlusion. 
A recent hemorrhagic infarct is present on the left side of the image and an old pale infarct on the right side. This section shows a large hemorrhagic infarct produced by embolism. 

5. Types of Emboli -- the most common is thromboemboli 

a.Thromboemboli--most frequently from the heart; may also arise from atheromatous plaques on carotid and vertebral-basilar arteries 

b. Fat Emboli--fat globules associated with trauma to long bones 

c. Air Emboli--associated with trauma to heart, lungs, orvessels, e.g in surgical procedures 

d. Metastatic Deposits--from systemic tumors 

e. Septic Emboli--most often seen in bacterial endocarditis; may cause brain abscess or other secondary conditions. 

f. Nitrogen Bubbles--form with rapid decompression (Caisson disease) 

D. Venous or Dural Sinus Thrombosis--Hemorrhagic Infarction
This is the least common pattern of cerebral infarction. Hemorrhagic infarction occurs when blood stasis in large veins or venous sinuses leads to infarction, then, increased pressure disrupts capillaries causing blood to enter the infarcted areas. Abrupt occlusion of several cerebral veins or dural sinuses is necessary to produce a large hemorrhagic infarct. Slowly progressive venous or dural sinus occlusion rarely results in tissue necrosis. Predisposing factors include dehydration in children, spread of infection from adjacent foci (nasal sinus or middle ear) and disorders that cause hypercoagulability of blood. 
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National Institutes of Health, Bethesda, Maryland 20892 

Written May 1997

STROKE ("Brain Attack")


  • What is a Stroke? 
  • What are the risk factors and symptoms of a Stroke?
  • Where can I find more information? (last updated April 7, 1998)

DESCRIPTION: A stroke or "brain attack" occurs when brain cells die because of inadequate blood flow. When blood flow fails, brain cells are robbed of vital supplies of oxygen and nutrients. About 80 percent of strokes are caused by the blockage of an artery in the neck or brain, and the rest by bleeding into or around the brain. Some strokes have little recognizable effect. Others can quickly cause death. Stroke kills about 150,000 Americans each year and is the leading cause of adult disability. As the names "stroke"and "brain attack" imply, it happens suddenly. Many strokes could be prevented by heeding strokes warning signs and treating its underlying risk factors, including high blood pressure, cigarette smoking, diabetes, and heart disease. 

Return to Index

Risk Factors for a Stroke

Stroke prevention is still the best medicine. The most important treatable conditions linked to stroke are: 

  • High blood pressure. Treat it. Eat a balanced diet, maintain a healthy weight, and exercise to reduce blood pressure. Drugs are also available. 
  • Cigarette smoking. Quit. Medical help is available to help quit. 
  • Heart disease. Manage it. Your doctor can treat your heart disease and may prescribe medication to help prevent the formation of clots. If you are over 50, NINDS scientists believe you and your doctor should make a decision about aspirin therapy. 
  • Diabetes. Control it. Treatment can delay complications that increase the risk of stroke. 
  • Transient ischemic attacks (TIAs). Seek help. TIAs are small strokes that last only for a few minutes or hours. They should never be ignored and can be treated with drugs or surgery. 
Symptoms of a Stroke

If you see or have one or more of these symptoms, don't wait, call 911 right away! 

  • Sudden numbness or weakness of  face, arm, or leg, 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
  • Sudden severe headache with no known cause. .
Treatment can be more effective if given directly. Every minute counts!

Return to Index

Standard medical textbooks and health guides found at a local library contain additional information on preventing and treating stroke as well as coping with disability from a stroke. The following articles available from a medical library provide in-depth information on the latest clinical findings in NINDS-sponsored stroke research:

The National Institute of Neurological Disorders and Stroke t-PA Study Group. "Tissue Plasminogen Activator for Acute Ischemic Stroke." The New England Journal of Medicine, 333:24; 1581-1587 (December 14, 1995).

Stroke Prevention In Atrial Fibrillation Study Group Investigators. "Preliminary Report of the Stroke Prevention in Atrial Fibrillation Study." The New England Journal of Medicine, 322:12; 863-868 (March 22, 1990).

Stroke Prevention in Atrial Fibrillation Investigators. "Warfarin Versus Aspirin for Prevention of Thromboembolism Atrial Fibrillation: The Stroke Prevention in Atrial Fibrillation II Study." The Lancet, 343:8899; 687-691 (March 19, 1994).

The North American Symptomatic Carotid Endarterectomy Trial Collaborators. "Beneficial Effect of Carotid Endarterectomy in Symptomatic Patients with High-Grade Carotid Stenosis." The New England Journal of Medicine, 325:7; 445-453 (August 15, 1991).

Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. "Endarterectomy for Asymptomatic Carotid Artery Stenosis." Journal of theAmerican Medical Association, 273:18; 1421-1428 (May 10, 1995).

To Obtain Suggested Resources (click)...


Information is also available from the following organizations (last updated April 7, 1998): 

American Heart Association

7272 Greenville Avenue

Dallas, TX 75231

(214) 373-6300

(800) 242-8721

Agency for Health Care Policy and Research

P.O. Box 8547

Silver Spring, MD 20907

(800) 358-9295

National Stroke Association

96 Inverness Drive East, Suite One

Englewood, CO 80112

(303) 649-9299

(800) 787-6537

National Rehabilitation Information Center

8455 Colesville Road, Suite 935

Silver Spring, MD 20910-3319

(800) 346-2742


Return to Index or NINDS Publications Page 


National Institute of Neurological Disorders and Stroke
National Institutes of Health
Bethesda, MD 20892

Brain Attack

Risk Factors for a Stroke

Stroke prevention is still the best medicine. The most important treatable conditions linked to stroke are: 

Symptoms of a Stroke

If you see or have one or more of these symptoms, don't wait, call 911 right away!  Treatment can be more effective if given directly. Every minute counts!


Return to NINDS Stroke Page.


National Institute of Neurological Disorders and Stroke
National Institutes of Health
Bethesda, MD 20892 


© 1995, American Institute of Preventive Medicine

Strokes, also called cerebrovascular accidents, are the third leading cause of death in the United States. A stroke can be caused by lack of blood (and therefore lack of oxygen) to the brain, usually due to either clogged arteries or a ruptured blood vessel in the brain. In either case, the end result is brain damage (and possible death). Persons who suffer from both high blood pressure and hardening of the arteries are most susceptible to having a stroke. A stroke can happen suddenly, but it often follows years of the slow buildup of fatty deposits inside the blood vessels.

Some people experience a temporary "mini-stroke", or a transient ischemic attack (TIA). The symptoms mimic a stroke, (see below) but clear within 24 hours. TIAs are a warning that a real stroke may follow.

Measures can be taken to prevent a stroke. Here's what to do to reduce the risks of a stroke:

  • Control your blood pressure. Have it checked regularly and, if necessary, take medication prescribed by your physician.
  • Reduce blood levels of cholesterol to below 200 milligrams per deciliter (measured by a blood test).
  • Get regular exercise.
  • Keep your weight down.
  • Don't smoke.
  • Keep blood sugar levels under control if you're diabetic.
  • Use alcohol in moderation, if at all.
  • Avoid taking oral contraceptive pills, if possible. (If you must use them, don't smoke).
  • Learn to manage stress.
  • Ask your doctor about taking aspirin (low-dose, such as a daily baby aspirin). 
  • Ask your doctor to evaluate you for a surgical procedure that scrapes away fatty deposits in one or both of the main arteries in the neck.

Signs and Symptoms
It's important to know the warning signals of a stroke and get immediate medical attention, to minimize the damage. To help you remember what to look out for, the initials of the signs and symptoms spell DANGER.

  • Dizziness.
  • Absent-mindedness, or temporary loss of memory or mental ability.
  • Numbness or weakness in the face, arm, or leg.
  • Garbled speech.
  • Eye problems, including temporary loss of sight in one eye, or double vision.
  • Recent onset of severe headaches.

Care and Treatment
Tests can be done to locate the obstruction of blood flow to the brain. The doctor may then prescribe appropriate medicines and/or surgery. When an actual stroke occurs, it is crucial to get immediate treatment. Treatment often includes:




Intracerebral hemorrhage, embolism, thrombosis, or vascular insufficiency causing destruction of brain tissue.


Fragility of the vessels of the arterial tree, hypertension, excessive serum cholesterol and triglycerides, kidney damage, electrolyte imbalance and malnutrition are all involved separately or in unison resulting in cerebrovascular accidents. Combine these factors with stress producing exhaustion of adrenals and severe emotional strain and catastrophe results.


A deficiency in vitamin C is very detrimental to strength and integrity of blood vessels and large amounts of vitamin C are needed to prevent a cerebral hemorrhage. Blood cholesterol and triglycerides must be reduced and all nutrients needed to meet the demands of stress and aid the exhausted adrenals as well as to rebuild kidney tissue must be provided. Sodium intake must be reduced and a balance achieved with choline and potassium.

Suggested Nutrition:

Procosanol #760 3 per day. Supplies needed oxygen reserves, and repairs damaged nerves.

C-1000 Plus #453 3 each hour in early stage. Massive amounts of vitamin C are often needed to offset the inroads of arterial destruction

Glyco Plex #970 3 per day. High-potency vitamin B-complex with choline which protects liver and kidney against damage and hemorrhage.

Cerebrovascular Disease

What is stroke?
What causes stroke?
What is an arteriovenous malformation (AVM)?
How do I know I have an AVM?
How Are AVMs Diagnosed?
How are AVMs Treated?
Where Can I Find More Information About Stroke and AVMs?

What is stroke?

In order to operate at its peak performance, the human brain requires a constant supply of energy provided by the oxygen and nutrients delivered by the flowing blood. If blood flow is obstructed or impaired at any point between the vessels connecting the heart and the brain, portions of the brain relying on the obstructed vessel for oxygen and nutrients from the blood now become deprived of oxygen. Because the brain is critically dependent on the flow of blood circulating through the brain, the cells of the brain tissue become injured. Depending on the amount of time blood is kept from the cells, the injury to the brain cells can result in permanent damage to the brain tissue, ultimately resulting in a corresponding loss of human processes and functions. The severe restriction or complete stoppage of blood flow to the brain as the result of any disease process or injury to the blood vessels of the brain is commonly referred to as stroke. 

Stroke is the third leading cause of death and a leading cause of serious, long-term disability in the United States. According to the most recent statistics from the American Heart Association:

Approximately 600,000 people each year will suffer either a new or recurrent stroke;

On average, someone in the United States suffers a stroke every 53 seconds; every 3.3 minutes someone dies of one;

About 4 million stroke survivors are alive today; and, 

Stroke places a substantial burden on the national health care, costing an estimated 30 billion dollars in health care costs and lost productivity.

What causes stroke?

It was stated in the previous section that stroke occurs as a result of a decrease in blood flow to the brain. To better understand exactly how blood flow could be decreased, let us use the analogy of a garden hose which is a long, thin flexible tube to represent a blood vessel. There exist two distinct approaches by which flow through the hose can be impeded: (1) an obstruction or clog within the hose or (2) compression or pinching the hose from the outside. Similarly, two types of stroke that have been identified and recognized clinically correspond to their characteristic mechanisms of flow obstruction: ischemic stroke and hemorrhagic stroke.

Ischemic strokes, which account for 80 percent of strokes, are caused by an obstruction due to a blood clot within the major blood vessels in the cerebral circulation. Hemorrhagic strokes, which account for the remaining 20 percent of all strokes, occur as a result of rupture or breakage of weakened blood vessels within the brain, typically due to an aneurysm or an arteriovenous malformation (AVM). An aneurysm develops as an outpouch or ballooning of a vessel. If left untreated, the aneurysm continues to expand until it eventually ruptures. An AVM is a cluster of abnormal blood vessels which develop at birth. These abnormal blood vessels are enlarged and structurally weak, making them more susceptible to rupture caused by the force of the flowing blood. For each of these types of weakened vessels, rupture causes hemorrhage, bleeding into the surrounding brain tissue, causing the brain to become compressed or pushed aside to accommodate the increase of blood. As the brain is compressed, so are the nearby vessels, resulting in decreased flow through the vessel.


What is an arteriovenous malformation (AVM)?

AVMs are congenital vascular lesions which occur as a result of capillary maldevelopment between the arterial and venous systems. As is the case with aneurysms, AVMs may occur at any point within the human vasculature, but are most common and pose a more substantial risk to the patient when located in the brain. Because an arteriovenous malformation (AVM) is a source of hemorrhagic stroke that tends to occur in the younger population, it poses a significant risk of severe disability and death to persons under the age of 50. To understand more precisely what an AVM is, let us consider the circulation of blood to and from the brain under normal circumstances. 

In the normal human circulation, the blood vessels originate from the heart and consist of a branching arrangement of arteries of continually decreasing size until they feed into a capillary bed before exiting the bed through small veins which increase in size prior to returning to the heart. The capillary bed serves an important purpose in that its vascular resistance slows the flow of blood considerably to allow perfusion of oxygen and nutrients to surrounding tissue and removal of cellular waste. In one form of cerebrovascular disease, arteriovenous malformations (AVMs), the vessels comprising the capillary bed of the brain become malformed during embryonic development and prohibit the opportunity for blood to properly perfuse into the surrounding tissue. 

In people with AVMs, the capillary vessels are weak and enlarged and serve as direct shunts for blood flow between the high pressure arterial system and the low pressure venous system corresponding to a large pressure gradient and small vascular resistance. Because these capillary vessels are now larger and since blood will follow the path of least resistance, more blood is shunted or detoured through the AVM than through the normal vessels of the brain. This results in a decreased supply of blood (and the necessary oxygen and nutrients it contains) to the brain tissue adjacent to the AVM. More importantly, because the AVM vessels are larger, blood is being pushed through the AVM at a speed faster than normal. This increased speed, in turn, results in a greater force exerted by the blood on the fragile and dilated vessels. The continual pounding of blood against the walls of the AVM vessels over a period of time can eventually cause the vessel wall to give way and rupture, resulting in bleeding or hemorrhage.


How do I know I have an AVM?

Unfortunately, AVMs typically lay silent in the brain and give the person absolutely no indication that something is wrong. Because AVMs are believed to be congenital in nature, there is a chance that an individual might have an AVM if there is a family history of AVMs. The majority of AVMs are discovered as the result of either hemorrhage or epileptic seizures. If an AVM is discovered incidentally or by chance, aggressive treatment is highly recommended. 

Approximately 0.14% of the United States population has an intracranial AVM.2 Brain AVMs pose a significant risk and represent a major life threat, particularly to persons under the age of 50. AVMs tend to produce symptoms in those between 10 and 40 years of age, occurring in a young and productive age group in which hemorrhage can be severely incapacitating or fatal.3 By the end of the fourth decade of life, approximately 80% of all AVMs have become symptomatic, and 20% remain silent clinically and are more commonly diagnosed incidentally. Hemorrhage is the most serious sequela of AVMs, accounting for 50% of their clinical presentation and approximately 25% present with epileptic seizures.4 The remaining percentage present as a result of mass effect, neurological deficits, or headaches. The incidence of initial AVM hemorrhage is approximately 3% per year with the mortality rate from an initial hemorrhage ranging from 10 to 17% and a severe disability rate of 20% to 29%.3 Once an AVM has bled, the risk of a second hemorrhage, known as a rebleed, increases from 3% to 6%. In addition, headaches, dizziness, mass effect and neurological deficits may occur as a consequence of brain AVMs


How Are AVMs Diagnosed?

Because the majority of AVMs present themselves only after they have ruptured, the individual will seek immediate medical attention complaining of a severe headache, often referred to as "the worst headache of my life". Once admitted into the hospital, the doctor must diagnose or determine that the cause of the symptoms is due to a stroke and not to another unrelated illness such as a brain tumor. To diagnose an AVM in an individual, imaging tests are performed which allow the doctor to view images of the brain and search for information that would indicate the occurrence of a stroke. In general, the most common type of imaging procedure used in the evaluation of patients suspected of stroke provides anatomical information or images of the structure of the brain. Examples of this type of imaging technique are computed tomography, magnetic resonance imaging, and x-ray angiography.

Computed tomography (CT or CAT scans) uses x-rays to obtain images of the internal structures of the body. CT represents the most efficient means in the evaluation of a person presenting with stroke-like symptoms. From a CT scan, the doctor can: (1) confirm whether or not a stroke has occurred; (2) identify the type of stroke (ischemic or hemorrhagic); and (3) in most instances, localize the source of the stroke. Magnetic resonance imaging (MRI) utilizes a magnetic field to generate images of the human body. MRI reveals structural information of the brain at high resolution and is particularly useful in the diagnosis of brain vessel abnormalities such an aneurysms and AVMs. X-ray angiography uses x-rays and a contrast agent injected into the bloodstream to provide high quality images of the blood vessels of the body. X-ray angiography is used to identify the source and location of the obstruction as well as provide anatomical information of aneurysms and AVMs.


How are AVMs Treated?

The objective for treatment of AVMs is to reduce the risk that one of the weakened vessels will rupture and bleed and to re-establish blood flow to the surrounding brain tissue. Three methods that are commonly used to accomplish this task include: neurosurgical resection, endovascular embolotherapy, and radiosurgery.

In neurosurgical resection, the neurosurgeon performs a craniotomy or surgically opens a portion of the skull to gain direct access to the AVM. Once the arteries feeding or supplying blood into the AVM and the veins draining or removing blood from the AVM are identified, the neurosurgeon carefully dissects and removes the mass of abnormal vessels comprising the AVM and rejoins or resects the normal circulation within the brain.

Endovascular embolization is a procedure, performed by interventional neuroradiologists, in which access to the AVM is obtained from within or inside the vessels directly connected to the AVM. In such a procedure, a catheter or long, thin, flexible tube is inserted into an artery, usually in the thigh, and navigated through the various arteries of the circulatory system until it reaches an artery that feeds directly into the AVM. Once the catheter is in position, the neuroradiologist delivers a chemical or mechanical agent which results in the physical occlusion or clogging of the vessels within the AVM. By clogging the vessels of the AVM, blood is prevented from further harming the weakened vessels and redirecting blood through the normal parts of the brain.

In radiosurgery, the procedure involves the use of a radiation beam focussed with high precision onto the region of the brain where the AVM has previously been localized. As radiation penetrates the skull and strikes the tissue of the AVM, it induces a biological response that ultimately results in the death and subsequent closure of the abnormal AVM vessels while the normal healthy vessels can withstand the damage and heal themselves.


Where Can I Find More Information About Stroke and AVMs?

AVM Database

AVM Survivor Page

Brain Aneurysm and Arteriovenous Malformation Center at MGH-Harvard

Arteriovenous Malformation (AVM)

Cerebrovascular Disorders

National Organization for Rare Disorders, Inc. (NORD)

American Heart Association

Aneurysm & AVM Support Page

The Whole Brain Atlas



- Symptomatic or asymptomatic stenosis of carotid arteries.

- Patients that present with hemispheric transient ischemic attacks (TIA), hemispheric cerebrovascular accidents (CVAs) or transient monocular blindness (amaurosis fugax), should undergo duplex analysis of the carotid and vertebral arteries in the Vascular Surgery Clinic.
- Asymptomatic carotid stenosis is generally discovered during carotid duplex obtained for carotid bruit or non-hemispheric symptoms.
- Management is based upon presence or absence of significant occlusive disease of the carotid artery.
- Initial management should be duplex imaging of the carotid and vertebral arteries in the neck.

- All patients should have risk factor reduction and management of comorbid conditions. Specifically, smokers should be encouraged to quit smoking, people with elevated cholesterol and lipids should have this controlled and diabetics should have their disease maximally managed.
- Management of concomitant cardiac and pulmonary disease, which is often associated with cerebrovascular occlusive disease, should be managed appropriately along with control of obesity.
- In individuals who have hemispheric symptoms, but no evidence of carotid stenosis, alternative etiologies should be sought for the cause of the symptoms.

- Any patient with a hemispheric symptom to include TIAs, amaurosis fugax, stroke or evidence of global hypoprofusion of the brain should undergo referral to the Vascular Surgery Clinic for carotid duplex imaging.
- Any patient with a question of carotid bruit should undergo screening carotid duplex imaging via referral to the Vascular Surgery Clinic.
- Patients with asymptomatic high-grade carotid stenoses are considered for CEA based on degree of stenosis and associated comorbid conditions.
- Patients with clearly hemispheric symptoms ipsilateral to a high-grade carotid lesion should be considered for carotid endarterectomy (CEA).

- Patients found to have no significant carotid stenosis should be returned back to the primary care provider.
- Patients undergoing carotid endarterectomy are followed lifelong in the Vascular Surgery Clinic to monitor their carotid arteries.
- Patients should be concomitantly followed by their primary care provider to assist in risk factor reduction and management of comorbid factors.
- Patients with carotid artery stenosis not requiring CEA should be followed by both the Vascular Surgery Clinic and their primary care provider.

DISCLAIMER - Adherence to these guidelines will not ensure successful treatment in every situation. Further, these guidelines should not be considered inclusive of all accepted methods of care or exclusive of other methods of care reasonably directed to obtaining the same results. The ultimate judgment regarding the appropriateness of any specific procedure, therapy or referral must be made by the physician in light of all circumstances presented by an individual patient.

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- A cerebrovascular condition that accompanies either an ischemic or hemorrhagic lesion in one of the hemispheres which results in loss of motor and sensation to the opposite side of the body.
- Cognitive and perceptual changes that usually occur as a result of a right hemispheric lesion include decreased spatial perception, decreased vision on the left side of both eyes, impulsivity, poor judgment of abilities, dizziness, decreased coordination and poor balance.
- Changes in language that usually occur as a result of left hemisphere lesion include receptive and/or expressive aphasia, decreased vision on the right side of both eyes, right hemiparesis, decreased coordination and poor balance.

- History and Physical exam.
- Plain films not required.
- MRI/CT is indicated.
- Active/passive range of motion of affected extremities.
- Proper positioning to prevent joint deformities.
- Evaluation of functional performance in self-care, work, and leisure skills to determine impact on quality of life.
- Clinical activities to enhance balance, posture and mobility.
- Clinical activities to increase independence in feeding and hygiene.

- 1-3 times a week, one hour sessions in treatment activities to increase balance, strength, coordination, dexterity, sensation, or cognition/perception with resolution and/or progress expected within two weeks or six sessions.
- Home retraining programs to increase safety, offer patients and significant others opportunities to learn/practice/habituate compensatory strategies until "quality of life" achieved, and increase motor and/or cognitive skills with reevaluation once every two weeks.
- 1 or 2 time sessions to teach caregivers specific strategies and/or compensatory techniques that will improve functional independence in self-care, work, or leisure tasks.
- 4 - 16 "weekly" sessions.

- A change in motor function resulting in a decreased level of independence in self-care on home management, work, or leisure pursuits.
- A change in cognitive function also affecting independence to carry out normal routine and perform daily tasks in an effective or efficient manner.
- Inability to perform normal work routine or do normal job-related tasks as a result of either a physical or cognitive limitation.
-Inability to emotionally cope with ramifications of residual dysfunction.
-Language problem affecting interactions.

- No resolution or change in functional status with O.T. intervention.
- Completed specialty care evaluation demonstrating new/sudden decrease in physical and/or mental performance that requires evaluation/care at primary care level.
- Chronic condition that can be managed at primary care level with intermittent special care evaluation as needed

DISCLAIMER - Adherence to these guidelines will not ensure successful treatment in every situation. Further, these guidelines should not be considered inclusive of all accepted methods of care or exclusive of other methods of care reasonably directed to obtaining the same results. The ultimate judgment regarding the appropriateness of any specific procedure, therapy or referral must be made by the physician in light of all circumstances presented by an individual patient.

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Last Updated on December 9, 1998 by Dr.DANIL HAMMOUDI