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Fact Sheet: Stroke

Definition--Stroke is an injury to the brain caused by an interruption of the brain's blood supply.

Strokes may be caused by:

Thrombosis: A gradual narrowing and eventual blockage of a brain or neck artery, usually from the accumulated buildup of cholesterol and fatty deposits. Approximately 60% of all strokes are caused by thrombosis.

Embolism: A blockage of a brain or neck artery by a clot or "embolus." Clots can be blood clots which form elsewhere in the body (usually the heart) and travel to the brain, or they can be small pieces which break off of fatty deposits lining the arteries. Approximately 20% of all strokes are caused by embolism.

Hemorrhage: A rupture of an artery in the brain or on its surface. Such ruptures can be caused by an aneurysm (a thin, weak area on an artery wall) or by a congenital malformation of the brain's circulatory system. Hemorrhages may occur within the brain itself, or in the space between the brain and its protective outer membrane. Approximately 20% of all strokes are caused by hemorrhage.


Stroke remains our nation's third-leading killer. According to the National Stroke Association, stroke strikes about 500,000 Americans each year--killing 150,000 and forever altering the lives of the 350,000 who survive. There are an estimated 3 million stroke survivors living in the U.S. today.


Some strokes are preceded by warning signs called transient ischemic attacks (TIAs). TIAs cause a temporary interruption of blood flow within or leading to the brain. (A stroke is a permanent cutoff of blood to a region of the brain.)

TIA or stroke warning signs include: Numbness, weakness, or paralysis of the face, arm, or leg--especially on one side of the body. Sudden blurred or decreased vision in one or both eyes. Difficulty speaking or understanding simple statements. Loss of balance, dizziness, or loss of coordination, especially when combined with another warning sign. Severe, unexplained, localized headache with rapid onset. It's important to learn to recognize these serious warning signs.

Although they may not cause pain and may disappear quickly, they are clear warning signs that a stroke may soon follow. If you experience any stroke warning signs, call 911 immediately!


The particular aftereffects experienced by a stroke survivor will depend upon the location and extent of the stroke. For example, strokes which occur in the left hemisphere (half) of the brain can affect communication and memory as well as movement on the right side of the body. Strokes which occur in the right hemisphere of the brain can affect spatial and perceptual abilities as well as movement on the left side of the body. Large strokes (which damage a significant portion of brain tissue) generally result in a greater number of effects and/or an increase in their severity.

Although no two stroke survivors will experience exactly the same injuries or disabilities, physical, cognitive and emotional symptoms common to many stroke survivors include:

Paralysis--Usually on one side of the body (the side opposite the hemisphere in which the stroke occurred), including the face and mouth. Patients may have difficulty swallowing.

Vision problems--Patient may be unable to focus, may have a blind spot, one-sided neglect or may have problems with peripheral vision.

Communication difficulties--Aphasia is a term used to describe a collection of communication difficulties, including problems with speaking, understanding, reading, and writing.

Emotional lability--Uncontrollable, unexplained outward displays of crying, anger or laughter which have no connection to patient's actual emotional state. Episodes generally come and go quickly and dissipate over time.

Depression--A natural reaction, with origins in physiological and psychological causes. Some important factors in predicting the presence and severity of post-stroke depression include previous history of depression, location of the stroke, and size of the stroke.


Improved medical technology has increased physicians' ability to accurately diagnose strokes and assess the damage to the brain. However, it is not always easy to recognize small strokes because symptoms may be dismissed by the patient and family as changes due to the aging process, or may be confused with symptoms of other neurological illnesses. As discussed earlier, any episode of stroke warning signs requires immediate emergency evaluation.


As mentioned previously, stroke warning signs require immediate emergency medical evaluation. One reason for this urgency is that researchers have recently discovered that stroke-related brain damage can extend far beyond the area directly involved in the stroke and can progress and worsen over the first 24 hours.

Researchers are attempting to limit or prevent this secondary damage by testing the brain-protecting effects of drugs administered within the first six hours post-stroke. When stroke occurs, hospitalization is necessary to determine the cause of the stroke as well as to treat and prevent any complications that may result. Once the stroke survivor's condition is stabilized and neurological deficits no longer appear to be progressing, rehabilitation begins.

Rehabilitation may include intensive retraining in a variety of areas: movement; balance; perception of space and body; bowel and bladder control; language; and new methods of psychological and emotional adaptation. Stroke rehabilitation programs consist of the coordinated efforts of many health professionals. Approximately 80% of all stroke survivors have physical, perceptual and language deficits which can be helped through rehabilitation. Many do not receive the services they need because they are not referred to these services or because government or private insurers do not cover these services.A social worker can be useful in making special financial arrangements for long-term care.

Risk Factors

There are several risk factors which can make a person more likely to experience a stroke. These risks are divided into controllable (those you can change) and uncontrollable (those you cannot change).

Controllable Stroke Risk Factors

The good news is that 50% of all strokes can be prevented through medical attention and simple lifestyle changes. Hypertension (high blood pressure): High blood pressure means your blood pressure is consistently higher than 140/90. High blood pressure damages artery walls and can increase blood clotting action, which can lead to the formation of stroke-causing clots. High blood pressure can increase your stroke risk two to six times.

Atrial fibrillation: Atrial fibrillation (AF) is the name of a particular type of irregular heartbeat affecting more than 1 million Americans. In AF, the left atrium (left upper chamber) of the heart beats rapidly and unpredictably. Normally, all four chambers of your heart beat in the same rhythm somewhere between 60 and 100 times every minute. In someone who has AF, the left atrium may beat as many as 400 times a minute. If left untreated, AF can increase your stroke risk from 4 to 6 times. Long-term untreated AF can also weaken the heart, leading to potential heart failure.

Smoking: In addition to harming the lungs, smoking also injures blood vessel walls, speeds up hardening of the arteries, increases how hard your heart has to work, and raises blood pressure. Smoking can double your stroke risk. The good news is that if you stop smoking today, within 2 to 5 years your stroke risk will be the same as that of someone who has never smoked. High cholesterol and excess weight: In adults, a cholesterol level of 200 or lower is best. Excess cholesterol can settle on artery walls and lead to the eventual blockage of these vessels by thrombosis. Being overweight strains the entire circulatory system and predisposes you to other stroke risk factors, such as high blood pressure.

Uncontrollable Stroke Risk Factors

Although you cannot change these risk factors, you can greatly minimize their impact on your overall stroke risk by concentrating efforts on your controllable stroke risk factors.

Age: Stroke risk doubles with each decade past age 55. Gender: Males have a slightly higher stroke risk than females.

Race: African Americans have double the stroke risk of most other racial groups.

Family history: A family history of stroke can mean you are at higher risk.

Diabetes: Circulation problems associated with the disease may increase stroke risk even if blood sugar and insulin levels are closely managed. In addition to these risk factors, stroke has also been associated with heavy alcohol use (especially binge drinking), elevated red blood cell counts, and with the use of high estrogen birth control pills by female smokers over age 30. No direct relationship has yet been demonstrated between stress and stroke risk.

Recurrent Stroke

A personal history of stroke can increase your risk of recurrent stroke by ten times. In addition to addressing controllable stroke risk factors, some stroke survivors may benefit from prescription medication to reduce their stroke risk.

Recommended Readings

Brain Attack: Mapping Out Early Recovery From Stroke, Mary M. Castiglione and Cynthia Johnson, 1995, Pritchett and Hull Associates, 3440 Oakcliff Rd., NE, Ste. 110, Atlanta, GA 30340-3079, (800) 241-4925.

Family Guide to Stroke, Louis R. Caplan, et al., 1994, American Heart Association. Available from the AHA Stroke Connection, (800) 553-6321.

Recovering From a Stroke (Patient and Family Guide) and Post-Stroke Rehabilitation: Assessment, Referral, and Patient Management (Clinical Practice Guideline), U.S. Dept. of Health & Human Services, 1995, AHCPR Publications Clearinghouse, P.O. Box 8547, Silver Spring, MD 20907, (800) 358-9295.

Stroke: An Owner's Manual, Arthur Josephs, 1992, Amadeus Press, P.O. Box 13011, Long Beach, CA 90803.

Stroke Survivors, William Bergquist, Rod McLean & Barbara Koblinski, 1994, Jossey-Bass Publishers, 350 Sansome St., San Francisco, CA 94104.

The Road Ahead: A Stroke Recovery Guide, 1992, and Be Stroke Smart series available from the National Stroke Association. Credits Thelma Edwards, R.N., Director of Program Development, National Stroke Association, May 1996


Two million head injuries occur each year in the United States. Brain injury causes between 70,000 and 100,000 deaths each year. 500,000 people will require hospitalization each year as a result of brain injury.

Every year 70,000 - 90,000 people will suffer life long physical, intellectual and psychological disabilities as a result of their injury.

Each year more than 30,000 New Yorkers suffer a head injury serious enough to be admitted to a hospital. It is estimated that 8,000 of these people will be left with serious or lifelong disabilities as a result of their injury. Brain injuries are the most frequent reasons for visits to physicians and emergency rooms.

A brain injury occurs every 16 seconds; a death from head injury occurs every 12 minutes. One out of 80 children born this year are expected to die of a vehicular related brain injury before their 25th birthday. The typical person with a brain injury is a young male between the ages of 16 and 24 who is injured in a vehicular accident. A severely injured person with a brain injury typically requires between 5-10 years of intensive rehabilitation with long-term follow up.

Brain injury kills more Americans under the age of 34 than all other causes combined and has claimed more lives since the turn of the century than all United States wars combined.

Some brain injuries are not preventable, such as in stroke, evasive brain surgeries, aneurysms, and such. It is not realistic for an individual to wear a helmet 24 hours, but what an individual we can do is be diligent in preventing brain injury in as many ways that are possible such as wearing helmets when in active leisure actives, seat belts when in a motor vehicles, being careful to not to bump our heads into cabinets or such, receiving the Lyme disease vaccine and if symptoms arise seeking out a physician immediately for intervention therapy, and when falling down putting out your hands or being conscious of how you are about to fall to as to cushion your skull.

Brain Injury Anatomy


The most widely accepted concept of brain injury divides the process into primary and secondary events. Primary brain injury is considered to be more or less complete at the time of impact, while secondary injury evolves over a period of hours to days after trauma.

Primary Injury

Skull fracture: Breaking of the bony skull; in a depressed skull fracture, these bone fragments exert pressure on the brain. Contusions, or bruises, will often occur under the location of a particular impact. They are also common in the tips of the frontal temporal lobes, where the force of the injury can drive the brain against the bony ridges on the inside of the skull. Hematomas, or blood clots, result when small blood vessels are broken by the injury. They can occur between the skull and the brain (epidural or subdural hematoma), or inside the substance of the brain itself (intracerebral hematoma). In either case, if they are sufficiently large they will compress or shift the brain, damaging sensitive structures in the brain stem. They can also raise the pressure inside the skull and eventually shut off blood supply to the brain. Prompt surgical removal of such large blood clots is often lifesaving. However, certain smaller hematomas can be safely allowed to resolve themselves without surgery. Lacerations: Tearing of frontal and temporal lobes or blood vessels caused by brain rotating across ridges inside skull. Diffuse Axonal Injury: After a closed brain injury, the shifting and rotation of the brain inside the skull will result in shearing injury to the brain's long connecting nerve fibers or axons. This can be microscopic and potentially reversible in mild brain injury, but following more severe brain injury it can be devastating and result in permanent disability or even prolonged coma. At present, there is no special treatment for diffuse axonal injury. However, recent studies have shown that some of the damage to axons progresses over the first 12 to 24 hours after the injury. For this reason, there is hope that it may be possible to prevent this progression in the future with specific treatments. Because of these recent findings, diffuse axonal injury is now thought of as a combination of primary and secondary damage.

Secondary Injuries

Delayed secondary injury at the cellular level has come to be recognized as a major contributor to the ultimate tissue loss that occurs after brain injury. A cascade of physiologic, vascular, and biochemical events is set in motion in injured tissue. This process involves a multitude of systems, including possible changes in neuropeptides, electrolytes such as calcium and magnesium, excitatory amino acids, arachidonic acid metabolites such as the prostaglandins and the leukotrienes, and the formation of oxygen-free radicals. This secondary tissue damage is at the root of most of the severe, long-term deficits a person with brain injury may experience. Procedures that minimize this damage can be the difference between recovery to a normal or near-normal condition or permanent disability.

Diffuse blood vessel damage has been increasingly implicated as a major component of brain injury. The vascular response appears to be biphasic. Depending on the severity of the trauma, early changes include an initial rise in blood pressure, an early loss of the automatic regulation of cerebral blood vessels, and a transient breakdown of the blood-brain barrier. Vascular changes peak at approximately 6 hours postinjury but can persist for as long as 6 days. The clinical significance of these blood vessel changes is still unclear, but may relate to delayed brain swelling that is often seen, especially in younger people. Oxygen-free radical scavenger drugs prevent or reverse these changes experimentally, suggesting that such drugs may come to play an important role in the management of brain injury in the near future.

The process by which brain contusions produce brain necrosis is equally complex and is also prolonged over a period of hours. Toxic processes include the release of free oxygen radicals, damage to cell membranes, opening of ion channels to influx of calcium, release of cytokines and metabolism of free fatty acids into highly reactive substances that may cause vascular spasm and ischaemia. Such processes may also be interruptable by therapeutic agents such as lipid antioxidants, calcium channel blockers, and glutamate antagonists. The search for secure evidence that new classes of drug based on these mechanisms reduce the morbidity and mortality of brain injury will be one of the most important efforts of the nineties.

Free radicals are formed at some point in almost every mechanism of secondary injury. Their primary targets are the fatty acids of the cell-membrane. A process known as lipid peroxidation damages neuronal, glial and vascular cell membranes in a geometrically progressing fashion. If unchecked, lipid peroxidation spreads over the surface of the cell membrane and eventually leads to cell death. Thus free radicals damage endothelial cells, disrupt the blood-brain barrier, and directly injure brain cells, causing edema and structural changes in neurons and glia. Disruption of the blood-brain barrier is responsible for brain edema and exposure of brain cells to damaging blood-borne products.

Free iron, as found in contusions and hematomas, is particularly toxic, probably by catalyzing the formation of hydroxyl radical (one of the most destructive of all the free radicals). Hall and Traystman report that these products may result in progressive secondary injury to otherwise viable brain tissue through several mechanisms, for example, by producing further ischemia or altering vascular reactivity, by producing brain swelling (edema or hyperemia), by injuring neurons and glia directly, or activating macrophages that result in such injury, or in the case of penetrating brain injury, by establishing conditions favorable to secondary infection. In other words, much of the ultimate brain loss may be caused not by the injury itself, but by an uncontrolled vicious cycle of biochemical events set in motion by the trauma. The control of this complex cascade of cellular events remains one of the most important challenges in the acute management of brain injury. As with diffuse axonal injury, it offers a potential therapeutic window of opportunity during which brain swelling and nerve cell death may be prevented during the first few hours after an injury has been sustained.

Secondary Intracranial

Insults In the minutes and hours after a brain injury, a variety of other damage may occur.

Hematoma (epidural, subdural and/or intracerebral)
Brain swelling/edema
Increased intracranial pressure
Cerebral vasospasm
Intracranial infection

In one recent survey of 100 individuals with severe, moderate and minor brain injury associated with other injuries by Andrews, 92% were found to have one or more type of intracranial insult occurring for periods of 5 minutes or longer while being managed in a well staffed and well equipped intensive care unit.

Secondary Systemic Insults

Secondary systemic insults (outside the brain) that may lead to further damage to the brain are extremely common after brain injuries of all grades of severity, particularly if they are associated with multiple injuries. Thus people with brain injury may have combinations of low blood oxygen, blood pressure, heart, and lung changes, fever, blood coagulation disorders, and other adverse changes at recurrent intervals in the days following brain injury. These occur at a time when the normal regulatory mechanism by which the cerebrovascular vessels can relax to maintain an adequate supply of oxygen and blood during such adverse events is impaired as a result of the original trauma.

Some of the more common forms of secondary systemic insults are listed below:

Hypoxemia (Low blood oxygen)
Arterial hypotension (high or low blood pressure)
Hypercarbia (carbon dioxide accumulation)
Severe hypocarbia Pyrexia (fever)
Hyponatremia (low sodium)
Abnormal blood coagulation
Lung changes
Cardiac (heart) changes
nutritional (metabolic) changes

What is coma?

Coma Management and Care

When we hear the word coma, many of us envision a person in a deep, sleep-like state, completely unaware of the outside world. In fact, the word coma simply refers to unconsciousness. This unconsciousness may be very deep, where no amount of stimulation will cause the person to respond. In other cases, however, a person who is in coma may move, make noise, or respond to pain. The process of recovery from coma is a continuum along which a person gradually regains consciousness.

Prolonged coma does not necessarily mean a poor prognosis. All individuals with traumatic brain injury who are initially in a coma will emerge from the coma. Some people will progress and ultimately have a good recovery. Some will emerge but have significant disabilities, and others will be in what is known as the minimally conscious state or the vegetative state for years. In the vegetative state, people may appear to be awake and may even open their eyes and look about the room, but are otherwise unresponsive. A variety of treatments and techniques may be used to care for these people and prevent complications. This section gives an overview of the coma management process.


While a person is in coma, a variety of evaluations may be conducted. Ongoing evaluations of a person in a coma are important to assess the person's status, identify and prevent complications and to adapt medical treatment. The Glascow Coma Scale is usually administered upon admission to determine depth of coma and periodically thereafter to help determine duration of coma more accurately.

Electroencephalograms (EEGs) and Evoked Potentials (EPs) or Event Related Potentials (ERPs) are frequently used to monitor neurophysiologic status. Measurements of cerebral blood flow may also be helpful in evaluating coma. Brain imaging technologies, particularly computerized tomography scans (CT-Scans) and magnetic resonance imaging (MRI) can offer important information about an individual's status over time.

In addition, many evaluations will be conducted by individual members of the treatment team. These include range of motion, respiratory, nutrition, to name a few.

For more detailed information on coma many other related subjects, presented in a personal and comprehensible manner by someone who's "Been There", please visit http://www.waiting.com, also known as "The Waiting Room".

Medical Management

Medical management may involve sensory stimulation programs, positioning programs, medications, surgery, nutrition, hygiene and various other interventions. Professional staff can include physicians, neurologists, surgeons, nurses and many others. Seizures, hypertension, hydrocephalus, aspiration pneumonia, urinary tract infections, hormonal abnormalities and skin ulcers are some of the potential problems that a person in a coma may experience. The medical staff will be prepared to treat these and any other unexpected difficulties.


Medication might be used to treat seizure disorders, infections, muscle spasticity, hypertension, and swelling, to name only a few of the possible reasons. In some cases, medication might be prescribed that has the potential to increase the coma duration, but decrease the swelling in the brain, therefore decreasing the overall extent of damage to the brain tissue.

It has been suggested that people in coma should not receive a lot of medications that have sedative side effects. However, they are often used. When this is the case, physicians will often use the medication for a short period of time, and attempt to decrease the dosage. When any medications are prescribed, it can be important that those who know the person best, such as family members, be vigilant to observe any deterioration in functioning.

There are a number of medications that can increase central arousal, to include psycho-stimulants and antidepressants. These have been used to treat some individuals in coma, but have not always been found to be effective. Sensory stimulation is one way that many coma programs attempt to increase arousal.

Nursing Care

Nursing involves the monitoring of all body systems. A nurse attempts to maintain the persons medical status, anticipate potential complications and work to restore a persons functioning.

Nursing practice for the person in a coma usually requires monitoring vital signs and assessing all peripheral pulses on a regular basis. In addition, circumferential leg measurements will probably be performed to monitor for deep-vein thrombosis. A rehabilitation nurse will frequently take notice of and document skin color and temperature changes, food and liquid intake, and bowel and bladder functioning. Cardiovascular, musculoskeletal and respiratory functioning will also be closely monitored by the nursing staff.

Respiratory Care

Because respiratory problems are extremely common in people with brain injuries, airway control and mechanical ventilation are often a major focus in early treatment. Early aggressive control of the airway, adequate ventilation, and oxygenation have been demonstrated to improve outcome.

The two main objectives of mechanical ventilation are (1) to provide the person with adequate ventilation and oxygenation and (2) to avoid or correct respiratory muscle overload or fatigue. There are several techniques of mechanical ventilation that can be utilized.

Artificial airways are another way to provide adequate respiratory care. Pharyngeal "airways" are not really airways. They are plastic "spacers" that can be inserted through the mouth to hold the back of the tongue away from the back of the throat. Tracheostomies are indicated when prolonged ventilation is anticipated, when airway control is required to prevent aspiration or to relieve upper airway obstruction.

Respiratory therapy has various functions for the person in a coma. Oxygen therapy might be administered if the person requires it. Chest physiotherapy is used to help mobilize secretions from the lower respiratory tract. This involves a combination of percussion, vibration, postural drainage, and coached coughing. Suctioning is used to clear secretions from the pharynx, and should only be performed when needed for people who have endotracheal tubes or tracheostomy tubes in place.


People with severe alterations in consciousness (commonly referred to as the vegetative state) present an array of positional problems requiring special attention to achieve an effective upright position. Abnormal reflexes and reactions cause a pathologic increase in muscle tone and abnormal posturing of the trunk and extremities.

The first goal of positioning the person to a sitting position is to inhibit the elicitation of the abnormal reflexes. The second goal is to help prevent the development of joint contractures. Prolonged positioning in abnormal rigid postures can increase the likelihood of muscle and soft tissue contracture. Preventing the adverse effects of prolonged bed rest by alleviating pressure on the skin is the third goal. The fourth goal is to help alleviate the problems of decreased blood flow to the extremities, decreased systolic blood pressure and decreased red blood cell formation. The final goal is to increase the persons level of awareness through stimulation to the kinesthetic and visual systems.

As positioning programs occur, it can be important that continuous evaluations be completed in order to assess how the intervention is affecting the total body position and the persons behavior. A varying number of devices may be necessary at different times throughout a positioning program.

Finally, a positioning program should include education for the family and other caretakers about the rationale behind the program and the reasons for the use of each devise.

Therapeutic Intervention

Various therapeutic interventions are available to a person in the vegetative state. Sensory stimulation programs are based on the rationale that stimulation will increase the input into the reticular activating system in the brain, and thereby increase the person's arousal level. However, the principles of sensory stimulation have not, for the most part, been established by science.

The main principles of sensory stimulation are to control the environment so there are few distractions, apply one stimulation at a time, conduct brief sessions, stimulation should be attempted in all five senses, and should vary in nature and intensity. Many reports state that stimulus that have emotional significance to the person may be more likely to emit a response. Some programs will use tape-recorded messages from family and friends.

People in the vegetative state often will have difficulties with muscle tone, contractures and heterotopic ossification. Prolonged stretch (including splinting), whirlpool or hubbard tank treatment, electric stimulation, altered body positioning and vibration may all facilitate reductions in muscle tone as well as range of motion exercises. Some people with increased muscle tone may benefit from medications.

Contractures are the loss of passive range of motion due to alterations in the muscle and connective tissue. Range of motion exercises and prolonged stretch may be utilized to help prevent this from happening.

Early symptoms of heterotopic ossification include warmth, swelling and pain response. This usually occurs around the large joints of spastic extremities, and is the appearance of bone in the soft tissue. This problem should be remediated early so as to prevent disfigurement that could require surgery to correct.

Bowel and bladder treatment is an intervention that occurs for people in comas. A person's immobility and liquid diet frequently require a stool softener to be administered. Bladder incontinence may be the result of two interacting factors, the first being an inhibited detrusor reflex (the ability to push down) and depressed cognition.

Unknown source at this time

Childhood BI--Facts and Figures

Some Myths, Facts and Figures About Childhood Brain Injuries

One million children are taken into emergency rooms each year with brain injuries. Traumatic injuries occur when a child's head is struck or hits an object.

Common causes of these injuries are car crashes, bicycle collisions, falls, sports, or beatings. Penetrating brain injuries are caused by an object, such as a bullet entering the brain.

Children may also have acquired brain injuries as th result of illness, infections, loss of oxygen, tumors, strokes, or metabolic disorders. The brain controls the body's many functions and actions. Consequently traumatic and acquired brain injuries can interrupt, delay, or alter a child's development. Estimates suggest that brain injuries to children between birth and age 19 annually result in: 7,000 deaths. 150,000 hospitalizations.

Over $1 billion in hospital costs. 30,000 children becoming permanently disabled. Brain injury is the most frequent diagnosis reported in the National Pediatric Trauma Registry. It is also the diagnosis most likely to result in multiple limitations in function and long term disabilities.

The causes of brain injury vary by children's ages. Physical abuse occurs most among infants. Toddlers are prone to injury from falls. Young children are injured as passengers in car accidents. Pedestrian and bicycle collisions with motor vehicles increase among school age children. Adolescents become injured as drivers as well as occupants of motor vehicles. Injuries due to violence increase among adolescents.

Despite these facts: Most children go directly home from hospitals and trauma centers. Fewer rehabilitation programs are available for children than adults. Children's physical recovery is often more rapid than their cognitive recovery.

Long-term effects of injuries upon children's behavior and abilities to learn may not become evident until later in school and at home.

Myths and Facts

MYTH/FACT Since the student looks good physically, everything must be OK! A student with a brain injury may show no physical signs of a disability. However, the ability to learn may have changed. A student who has a severe brain injury will have a serious and permanent disability.

The severity of the brain injury does not always predict long-term outcome. Recovery from a brain injury is very different from a broken bone. Youth with minor brain injuries can have serious disabilities and those with serious injuries can have good recoveries.

Each injury is different!

The younger the student is when injured, the better the recovery. Younger children have shorter periods of uninterrupted development and skills to draw upon after an injury. Changes caused by an injury to a young child may not appear for many years until the brain is challenged to do more complex tasks and processes. After six months, a student with a brain injury won't get any better. There is no timetable for recovery.

Changes may be most rapid during the first six months after injury, but progress may continue at a slower rate for many months and years. A brain injury erases memory. Many students have post-traumatic amnesia and can't remember events right before or after the injury.

Students with brain injuries tend to retain information learned prior to the injury. It is learning new information that is a common problem. Parents must face reality to adjust. Parents, family members, and students need time to understand changes and adjust their hopes and goals for the future. No one can predict the future. By living with the changes caused by the injury, the family and student can use their experience to prepare for the future when they are ready.

This fact sheet is provided as a public service by:

The May Center for Education and Neurorehabilitation, May Institute
Research and Training Center in Rehabilitation and Childhood Trauma
Department of Physical Medicine and Rehabilitation
Tufts University School of Medicine and New England Medical Center

For additional copies or to learn more, please call:
May Center at (617) 963-3600 or
35 Pacella Park Drive, Randolph, MA, 02368
Or write:
Research and Training Center
Dept. of Physical Medicine and Rehabilitation
Tufts-New England Medical Center
750 Washington Street 75K-R
Boston, MA 02111

Partial funding is provided by the
National Institute od Disability and Rehabilitation Research
U.S. Department of Education (grant No. H133B0044).

Substance Abuse related to Brain Injury

Wernicke-Korsakoff Syndrome (Alcohol-Related Dementia)


Wernicke-Korsakoff Syndrome (WKS) is a neurological disorder. Wernicke's Encephalopathy and Korsakoff's Psychosis are the acute and chronic phases, respectively, of the same disease.

WKS is caused by a deficiency in the B vitamin thiamine. Thiamine plays a role in metabolizing glucose to produce energy for the brain. An absence of thiamine therefore results in an inadequate supply of energy to the brain, particularly the hypothalamus (which regulates body temperature, growth and appetite and has a role in emotional response. It also controls pituitary functions including metabolism and hormones) and mammillary bodies (where neural pathways connect various parts of the brain involved in memory functions).

The disease is typically associated with chronic alcoholism, but may be associated with malnutrition or other conditions which cause nutritional deficiencies.


WKS has a relatively low prevalence (0.4% to 2.8% of reported autopsies). However, it is likely that the disease is under-reported and under-diagnosed. An estimated 25% of WKS cases were missed where the brains were not examined microscopically. Another study found that only 20% of clinical WKS diagnoses were made correctly in life when compared to autopsy results. Moreover, WKS appears to be only one distinct disease that causes alcohol-related dementia. Based on clinical research studies, between 22% to 29% of individuals with dementia were found to be heavy drinkers or alcoholics and 9% to 23% of elderly alcoholics in alcoholism treatment were found to also have dementia.

An estimated 1.1 to 2.3 million older Americans have problems with alcohol. Medical researchers are still grappling with how to more fully define the association between heavy alcohol use and symptoms of dementia. Symptoms WKS symptoms may be long-lasting or permanent and should be distinguished from the acute affects of alcohol consumption or from a period of alcohol "withdrawal." The disease is characterized by mental confusion, amnesia (a permanent gap in memory) and impaired short-term memory. An estimated 80% of persons with WKS continue to have a chronic memory disorder. Individuals often appear apathetic and inattentive and some may experience agitation. In addition, WKS tends to impair the person's ability to learn new information or tasks. Individuals with WKS are known to "confabulate" (make up or invent information to compensate for poor memory). Other symptoms include ataxia (weakness in limbs or lack of muscle coordination, unsteady gait), slow walking, rapid, tremor-like eye movements or paralysis of eye muscles Fine motor function (e.g., hand or finger movements) may be diminished and sense of smell also may be affected. In the advanced stages, coma can occur. Although treatable if caught early enough, the death rate from WKS is relatively high, about 10% to 20%.


WKS is often missed as a diagnosis. In the acute phase, a physical examination may reveal skin changes and a red "beefy" tongue. In addition, blood count, electrolytes and liver function tests should be conducted. Even in the chronic phase, an MRI may show shrunken mammillary bodies and other changes in the brain. CT scans have showed enlarged ventricles and diencephalic lesions.

It is important that a full medical history include information about the person's daily drinking habits, both present and past. Family, friends and past medical records should be consulted to obtain the most complete information possible on the person's history with alcohol. Proposed criteria for diagnosing alcohol-related dementia (not strictly WKS) suggest that the diagnosis be made at least 60 days after the last exposure to alcohol and that a "significant" alcohol history would include an average of 35 drinks per week for men (28 for women) for at least five years. Typically, the period of significant drinking must be within three years of the onset of dementia.

Recent medical research also suggests that the genetic marker APOE4 is a significant predictor of global intellectual deficits in people with WKS. Individuals with the ApoE genotype may experience a certain interaction with heavy alcohol use which could predispose them to WKS. Concerns about an inherited susceptibility to WKS should be discussed with a genetic counselor.

In cases of suspected non-alcohol related WKS, the physician may investigate anorexia nervosa, hypermesis gravidarum, severe malnutrition and other disorders or surgical procedures which impair intestinal absorption of thiamine.


If caught early enough, WKS is a preventable, treatable disease. Treatment consists of thiamin replacement therapy, sometimes along with other vitamins. Dosages may vary and should be monitored closely by a physician. If alcoholic consumption stops and treatment is properly administered, individuals with early-stage WKS can expect a marked recovery and may be capable of learning simple, repetitive tasks.

However, the person's confusion may take some time to subside and even incomplete recovery of memory can take up to a year. In the later stages, if damage to the brain is irreversible, individuals are likely to have lasting problems with memory and gait (for example, lack of muscle coordination and numbness or weakness in limbs).

Family Issues

Caring for a family member who has WKS or alcohol-related dementia presents multiple challenges for family caregivers. Lasting symptoms of dementia and other neurological problems are difficult conditions under even the best circumstances. Bizarre behaviors may be interpreted by the family as a continuation of "binge" drinking, even if the person has stopped drinking.

Individuals with a history of alcohol abuse have often isolated themselves from their families and loved ones. Strained relationships are common in families of alcoholics. As a caregiver, you may feel resentful of caring for a parent or spouse with a lifelong history of alcohol abuse. In addition, it may be hard to convince the impaired person to give up drinking, since most WKS-affected individuals have been long-term alcoholics. Discuss with a physician or mental health professional effective strategies for preventing a loved one from drinking. Ironically, people with WKS can be quite apathetic and seldom demand alcohol, yet are likely to accept it if offered.

Families should enlist the help and support of mental health professionals or case workers who have experience in working with alcoholism. Family meetings or support groups also may be helpful in bringing together additional family members to assist the WKS person. A case manager or family counselor can help the family sort through issues and help arrange appropriate support services. In severe cases or when the family is unable to provide appropriate care, a residential facility may be sought. Nursing homes which provide special dementia care should be considered for a confused WKS patient.

Research indicates that alcoholism often runs in families. Having additional family members who are alcoholic increases the burden of care. Some research has shown that a person whose parent has a history of alcoholism may have an inherited susceptibility to alcohol addiction and alcohol-related neurological problems (peripheral neuropathies). Such findings suggest that people in alcoholic families need to take special precautions to avoid excessive use of alcohol in order to reduce their own risk of alcohol-related health problems.

Caring for the Person with WKS

It is important to ensure that the affected person continues to abstain from drinking alcohol and that the person maintains a balanced diet with adequate thiamin intake. However, even if the person stops drinking and replenishes thiamin, symptoms of the disease (e.g., problem behaviors, agitation, lack of coordination, learning deficits) may continue. In an abstinent (i.e., sober) WKS patient, these symptoms must be recognized as part of the disease caused by irreversible damage to the brain and nervous system.

Family caregivers should take precautions to ensure the safety of the person with WKS, as well as others in the household. The confused or disoriented individual should not be left alone. Supervision is required to ensure that the person does not wander away from home, leave the stove on or the water running.

Short-term memory problems mean that the confused person may repeat the same question again and again. Coping with frequent repetition often involves a trial and error approach and a combination of strategies. First, be patient and deliver responses in a calm manner. The confused person will pick up on your mood and may become more frustrated if your voice is loud or angry. In addition, place reminders in the house to help the person feel more secure. Label inside doors and drawers with words or pictures. Write notes (e.g., dinner is at 6:00 pm). Another strategy is to distract the person with another topic or activity (e.g., a short walk, reminiscing over an old photo, etc.)

If the person continues to be agitated, symptoms should be discussed with a physician, neurologist or psychiatrist. Medications may be available to help control outbursts or anxiety.

Just as important, it is essential that the caregiver get some support and time off from constant caregiving demands. Make sure you leave some time to attend to your own needs, including eating well, getting enough sleep and getting regular medical check-ups. A home care worker, friend or family member may be needed to provide periodic respite assistance to help your loved one and to relieve the stress on you, the family caregiver.

Recommended Readings

Alcohol Problems in Later Life, Vicki Schmall, Corrine Gobeli, & Ruth Stiehl, 1989, Oregon State University, 422 Kerr Administration Bldg., Corvallis, OR 97331, (541) 737-2513.

Alcohol-Induced Brain Damage, Research Monograph 22, 1993 (NIH Publication 93-3549), National Institute on Alcohol Abuse and Alcoholism, Willco Bldg., Ste. 409, 6000 Executive Blvd., Rockville, MD 20892-7003, (301) 443-3860


Carlen, P. L. et al. (1994) Alcohol-related dementia in the institutionalized elderly. Alcoholism: Clinical and Experimental Research, 18(4):1330-1334.

Haugland, S. (1989) Alcoholism and other drug dependencies. Primary Care, June 1989. As cited in Alcohol Abuse Among Older People, American Association of Retired Persons (AARP) PF5179, 1994; Washington, DC.

Jacobson R.R. and Lishman W. A. (1990) Cortical and diencephalic lesions in Korsakoff's syndrome: a clinical and CT scan study. Psychological Medicine, 20: 63-75.

Muramatsu, T. et al. (1997) Apolipoprotein E e4 allele distribution in Wernicke-Korsakoff syndrome with or without global deficits. Journal of Neural Transmission, 104: 913-920.

Oslin, D. et al. (1998) Alcohol related dementia: proposed clinical criteria. International Journal of Geriatric Psychiatry, 13: 203-212.

Parkin, A. J. (1991) Wernicke-Korsakoff syndrome of nonalcoholic origin. Brain and Cognition, 15: 69-82.

Schaefer, S. & Haley, J.A. (1996) Wernicke-Korsakoff syndrome. Journal of the American Academy of Nurse Practitioners, 6(9): 435-436.

Welch L.W. et al. (1997) Fine motor speed deficits in alcoholic Korsakoff's syndrome. Alcoholism: Clinical and Experimental Research, 21(1): 134-139.

Zubaran, C. Fernandes J.G. & Rodnight, R. (1997) Wernicke-Korsakoff syndrome. Post Graduate Medical Journal, 73(855): 27-31.

Pessione, F., Gerchstein, & Rueff, B. (1995) Parental history of alcoholism: A risk factor for alcohol-related peripheral neuropathies. Alcohol & Alcoholism, (306): 749-754.

Novitt-Moreno, A. D. (1995) How Your Brain Works. Ziff-Davis Press: Emeryville, CA. Martin, P. R. & Nimmerrichter, A.A. (1993) Pharmacological treatment of alcohol-induced brain damage. In W.A Hunt & S.J. Nixon (eds.) Alcohol-induced brain damage. National Institute on Alcohol Abuse and Alcoholism (Research Monograph No. 22), Rockville, MD


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