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Hope Through Research Traumatic Brain Injury National Institute of Neurological Disorders and Stroke National Institutes of Health

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Hope T

hrough Research

TraumaticBrain Injury

National Institute of Neurological Disordersand StrokeNational Institutes of Health

Cover: Gary Weinstein of Takoma Park, Maryland,pictured with his wife Julie Wiatt and his son Zak,suffered a severe head injury when a ball shatteredhis skull while he was coaching a baseball team practicein the spring of 2001. A year after his injury, he returnedto work and is back to coaching.

This pamphlet was written and published by the NationalInstitute of Neurological Disorders and Stroke (NINDS),the United States’ leading supporter of research on disordersof the brain and nerves, including traumatic brain injury.NINDS, one of the U.S. Government’s National Institutesof Health in Bethesda, Maryland, is part of the PublicHealth Service within the U.S. Department of Healthand Human Services.

Table of Contents

Page

Introduction............................................. 1

What is a Traumatic Brain Injury? ................ 3

What Are the Signs and Symptomsof TBI? ................................................... 3

What Are the Causes of and RiskFactors for TBI? ....................................... 4

What Are the Different Types of TBI? ............ 5

What Medical Care Should a TBIPatient Receive? ........................................ 6

How Does a TBI Affect Consciousness? ......... 10

What Immediate Post-Injury ComplicationsCan Occur From a TBI? ............................ 13

General Trauma ................................. 16

What Disabilities Can Result From a TBI?..... 18

Are There Other Long-Term ProblemsAssociated With a TBI? ............................. 23

What Kinds of Rehabilitation Shoulda TBI Patient Receive? ............................. 25

How Can TBI be Prevented? ...................... 27

What Research is the NINDS Conducting? ..... 28

Clinical Trials Research ....................... 34

Where Can I Find More Information?............ 35

Glossary ................................................ 36

Information Resources

Traumatic Brain Injury Research Centers(see pocket inside back cover)

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Introduction

Traumatic brain injury (TBI) is a major publichealth problem, especially among male adolescentsand young adults ages 15 to 24, and among elderlypeople of both sexes 75 years and older. Childrenaged 5 and younger are also at high risk for TBI.

Perhaps the most famous TBI patient in the his-tory of medicine was Phineas Gage. In 1848, Gagewas a 25-year-old railway construction foremanworking on the Rutland and Burlington Railroadin Vermont. In the 19th century, little was under-stood about the brain and even less was knownabout how to treat injury to it. Most serious injuries

to the brain resulted in deathdue to bleeding or infection.Gage was working with explo-sive powder and a packingrod, called a tamping iron,when a spark caused anexplosion that propelledthe 3-foot long, pointedrod through his head. Itpenetrated his skull at thetop of his head, passedthrough his brain, andexited the skull by his temple.Amazingly, he survived theaccident with the help ofphysician John Harlow whotreated Gage for 73 days.Before the accident Gage wasa quiet, mild-mannered man;after his injuries he became

This computer-generated graphicshows how, in 1848, a 3-foot long,pointed rod penetrated the skullof Phineas Gage, a railwayconstruction foreman. The rodentered at the top of his head,passed through his brain, andexited his skull by his temple.Gage survived the accident butsuffered lasting personality andbehavioral problems.

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an obscene, obstinate, self-absorbed man. Hecontinued to suffer personality and behavioralproblems until his death in 1861.

Today, we understand a great deal more aboutthe healthy brain and its response to trauma,although science still has much to learn about howto reverse damage resulting from head injuries.

TBI costs the country more than $48 billion a year,and between 2.5 and 6.5 million Americans alivetoday have had a TBI. Survivors of TBI are oftenleft with significant cognitive, behavioral, andcommunicative disabilities, and some patientsdevelop long-term medical complications, suchas epilepsy.

Other statistics dramatically tell the story ofhead injury in the United States. Each year:

• approximately 270,000 people experiencea moderate or severe TBI,

• approximately 70,000 people die from headinjury,

• approximately 1 million head-injured peopleare treated in hospital emergency rooms,

• approximately 60,000 new cases of epilepsyoccur as a result of head trauma,

• approximately 230,000 people are hospitalizedfor TBI and survive, and

• approximately 80,000 of these survivorslive with significant disabilities as a resultof the injury.

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What is a Traumatic Brain Injury?

TBI, also called acquired brain injury or simplyhead injury, occurs when a sudden trauma causesdamage to the brain. The damage can be focal —confined to one area of the brain — or diffuse —involving more than one area of the brain. TBIcan result from a closed head injury* or a pen-etrating head injury. A closed injury occurs whenthe head suddenly and violently hits an objectbut the object does not break through the skull.A penetrating injury occurs when an objectpierces the skull and enters brain tissue.

What Are the Signs and Symptoms of TBI?

Symptoms of a TBI can be mild, moderate, orsevere, depending on the extent of the damage tothe brain. Some symptoms are evident immediately,while others do not surface until several days orweeks after the injury. A person with a mild TBImay remain conscious or may experience a lossof consciousness for a few seconds or minutes. Theperson may also feel dazed or not like himself forseveral days or weeks after the initial injury. Othersymptoms of mild TBI include headache, confusion,lightheadedness, dizziness, blurred vision or tiredeyes, ringing in the ears, bad taste in the mouth,fatigue or lethargy, a change in sleep patterns,behavioral or mood changes, and trouble withmemory, concentration, attention, or thinking.

* Terms in Italics are defined in the Glossary, page 36.

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A person with a moderate or severe TBI mayshow these same symptoms, but may also havea headache that gets worse or does not go away,repeated vomiting or nausea, convulsions or sei-zures, inability to awaken from sleep, dilation ofone or both pupils of the eyes, slurred speech,weakness or numbness in the extremities, loss ofcoordination, and/or increased confusion, restless-ness, or agitation. Small children with moderate tosevere TBI may show some of these signs as wellas signs specific to young children, such as per-sistent crying, inability to be consoled, and/orrefusal to nurse or eat. Anyone with signs ofmoderate or severe TBI should receive medicalattention as soon as possible.

What Are the Causes of and RiskFactors for TBI?

Half of all TBIs are due to transpor-tation accidents involving automo-biles, motorcycles, bicycles, andpedestrians. These accidents arethe major cause of TBI in peopleunder age 75. For those 75 andolder, falls cause the majority ofTBIs. Approximately 20 percent ofTBIs are due to violence, such asfirearm assaults and child abuse,and about 3 percent are due tosports injuries. Fully half of TBIincidents involve alcohol use.

The cause of the TBI plays a rolein determining the patient’s out-come. For example, approximately

Transportation accidentsinvolving automobiles,motorcycles, bicycles,and pedestrians accountfor half of all TBIs andare the major causeof TBIs in peopleunder age 75.

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91 percent of firearm TBIs (two-thirds of whichmay be suicidal in intent) result in death, whileonly 11 percent of TBIs from falls result in death.

What Are the Different Types of TBI?

Concussion is the most minor and the most commontype of TBI. Technically, a concussion is a shortloss of consciousness in response to a head injury,but in common language the term has come tomean any minor injury to the head or brain.

Other injuries are more severe. As the first lineof defense, the skull is particularly vulnerable toinjury. Skull fractures occur when the bone of theskull cracks or breaks. A depressed skull fractureoccurs when pieces of the broken skull press intothe tissue of the brain. A penetrating skull fractureoccurs when something pierces the skull, such as abullet, leaving a distinct and localized injury tobrain tissue.

Skull fractures can cause bruising of brain tissuecalled a contusion. A contusion is a distinct areaof swollen brain tissue mixed with blood releasedfrom broken blood vessels. A contusion can alsooccur in response to shaking of the brain backand forth within the confines of the skull, an injurycalled “contrecoup.” This injury often occurs incar accidents after high-speed stops and in shakenbaby syndrome, a severe form of head injury thatoccurs when a baby is shaken forcibly enough tocause the brain to bounce against the skull. Inaddition, contrecoup can cause diffuse axonal

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injury, also called shearing, which involvesdamage to individual nerve cells (neurons) andloss of connections among neurons. This canlead to a breakdown of overall communicationamong neurons in the brain.

Damage to a major blood vessel in the head cancause a hematoma, or heavy bleeding into oraround the brain. Three types of hematomascan cause brain damage. An epidural hematomainvolves bleeding into the area between the skulland the dura. With a subdural hematoma, bleed-ing is confined to the area between the dura andthe arachnoid membrane. Bleeding within thebrain itself is called intracerebral hematoma.

Another insult to the brain that can cause injuryis anoxia. Anoxia is a condition in which there isan absence of oxygen supply to an organ’s tissues,even if there is adequate blood flow to the tissue.Hypoxia refers to a decrease in oxygen supplyrather than a complete absence of oxygen. With-out oxygen, the cells of the brain die within severalminutes. This type of injury is often seen in near-drowning victims, in heart attack patients, or inpeople who suffer significant blood loss from otherinjuries that decrease blood flow to the brain.

What Medical Care Should a TBIPatient Receive?

Medical care usually begins when paramedics oremergency medical technicians arrive on the sceneof an accident or when a TBI patient arrives at theemergency department of a hospital. Because

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little can be done to reverse the initial braindamage caused by trauma, medical personneltry to stabilize the patient and focus on preventingfurther injury. Primary concerns include insuringproper oxygen supply to the brain and the rest ofthe body, maintaining adequate blood flow, andcontrolling blood pressure. Emergency medicalpersonnel may have to open the patient’s airway orperform other procedures to make sure the patientis breathing. They may also perform CPR to helpthe heart pump blood to the body, and they maytreat other injuries to control or stop bleeding.Because many head-injured patients may also havespinal cord injuries, medical professionals takegreat care in moving and transporting the patient.Ideally, the patient is placed on a back-boardand in a neck restraint. These devices immobilizethe patient and prevent further injury to thehead and spinal cord.

As soon as medical personnelhave stabilized the head-injured patient, they assessthe patient’s condition bymeasuring vital signs andreflexes and by performinga neurological examination.They check the patient’stemperature, blood pressure,pulse, breathing rate, andpupil size in response to light.They assess the patient’s levelof consciousness and neurologi-cal functioning using theGlasgow Coma Scale,a standardized, 15-point test that uses three

Medical professionals takegreat care in moving andtransporting head-injuredpatients. Often back-boardsand neck restraints are usedto immobilize patients andprevent further injury.

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measures — eyeopening, best verbalresponse, and bestmotor response — todetermine the sever-ity of the patient’sbrain injury.

The results of thethree tests are addedup to determine thepatient’s overallcondition. A totalscore of 3 to 8 indi-cates a severe headinjury, 9 to 12 indi-cates a moderatehead injury, and13 to 15 indicatesa mild head injury.

Imaging tests helpin determiningthe diagnosis andprognosis of a TBIpatient. Patientswith mild to moder-ate injuries mayreceive skull andneck X-rays to checkfor bone fracturesor spinal instability.The patient shouldremain immobilized

in a neck and back restraint until medical person-nel are certain that there is no risk of spinal cord

Glasgow Coma Scale

The eye opening part of the GlasgowComa Scale has four scores:

• 4 indicates that the patient can openhis eyes spontaneously.

• 3 is given if the patient can open hiseyes on verbal command.

• 2 indicates that the patient opens hiseyes only in response to painful stimuli.

• 1 is given if the patient does not openhis eyes in response to any stimulus.

The best verbal response part of the testhas five scores:

• 5 is given if the patient is oriented andcan speak coherently.

• 4 indicates that the patient is disorientedbut can speak coherently.

• 3 means the patient uses inappropriatewords or incoherent language.

• 2 is given if the patient makes incom-prehensible sounds.

• 1 indicates that the patient gives noverbal response at all.

The best motor response test has six scores:

• 6 means the patient can move his armsand legs in response to verbal commands.

• A score between 5 and 2 is given if thepatient shows movement in response toa variety of stimuli, including pain.

• 1 indicates that the patient shows nomovement in response to stimuli.

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injury. For moderate to severe cases, the goldstandard imaging test is a computed tomography(CT) scan. The CT scan creates a series of cross-sectional X-ray images of the head and brain andcan show bone fractures as well as the presence ofhemorrhage, hematomas, contusions, brain tissueswelling, and tumors. Magnetic resonance imaging(MRI) may be used after the initial assessment andtreatment of the TBI patient. MRI uses magneticfields to detect subtle changes in brain tissue con-tent and can show more detail than X-rays orCT. Unfortunately, MRI is not ideal for routineemergency imaging of TBI patients because it istime-consuming and is not available in all hospitals.

Approximately half of severely head-injuredpatients will need surgery to remove or repairhematomas or contusions. Patients may alsoneed surgery to treat injuries in other partsof the body. These patients usually go to theintensive care unit after surgery.

Sometimes when the brain is injured swellingoccurs and fluids accumulate within the brainspace. It is normal for bodily injuries to causeswelling and disruptions in fluid balance. Butwhen an injury occurs inside the skull-encasedbrain, there is no place for swollen tissues toexpand and no adjoining tissues to absorb excessfluid. This increased pressure is called intra-cranial pressure (ICP).

Medical personnel measure patients’ ICP usinga probe or catheter. The instrument is insertedthrough the skull to the subarachnoid level and isconnected to a monitor that registers the patient’s

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ICP. If a patient has high ICP,he or she may undergo a ventric-ulostomy, a procedure thatdrains cerebrospinal fluid(CSF) from the brain to bringthe pressure down. Drugs thatcan be used to decrease ICPinclude mannitol or barbitur-ates, although the safetyand effectiveness of thelatter are unknown.

How Does a TBI Affect Consciousness?

A TBI can cause problems with arousal, conscious-ness, awareness, alertness, and responsiveness.Generally, there are five abnormal states of con-sciousness that can result from a TBI: stupor,coma, persistent vegetative state, locked-insyndrome, and brain death.

Stupor is a state in which the patient is unre-sponsive but can be aroused briefly by a strongstimulus, such as sharp pain. Coma is a statein which the patient is totally unconscious, unre-sponsive, unaware, and unarousable. Patientsin a coma do not respond to external stimuli,such as pain or light, and do not have sleep-wakecycles. Coma results from widespread and diffusetrauma to the brain, including the cerebral hemi-spheres of the upper brain and the lower brain orbrainstem. Coma generally is of short duration,lasting a few days to a few weeks. After this time,some patients gradually come out of the coma,some progress to a vegetative state, and others die.

A computed tomography scan createsX-ray images of the head and brain.This imaging test can show bonefractures, hemorrhages, hematomas,contusions, brain tissue swelling, andtumors, and can help determine theprognosis of TBI patients.

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Patients in a vegetative state are unconsciousand unaware of their surroundings, but theycontinue to have a sleep-wake cycle and can haveperiods of alertness. Unlike coma, where thepatient’s eyes are closed, patients in a vegetativestate often open their eyes and may move, groan,or show reflex responses. A vegetative state canresult from diffuse injury to the cerebral hemi-spheres of the brain without damage to the lowerbrain and brainstem. Anoxia, or lack of oxygento the brain, which is a common complicationof cardiac arrest, can also bring about avegetative state.

Many patients emerge from a vegetative statewithin a few weeks, but those who do not recoverwithin 30 days are said to be in a persistent vege-tative state (PVS). The chances of recovery dependon the extent of injury to the brain and the patient’sage, with younger patients having a better chanceof recovery than older patients. Generally adultshave a 50 percent chance and children a 60 per-cent chance of recovering consciousness from aPVS within the first 6 months. After a year, thechances that a PVS patient will regain conscious-ness are very low and most patients who do recoverconsciousness experience significant disability.The longer a patient is in a PVS, the more severethe resulting disabilities will be. Rehabilitationcan contribute to recovery, but many patientsnever progress to the point of being able to takecare of themselves.

Locked-in syndrome is a condition in which apatient is aware and awake, but cannot move orcommunicate due to complete paralysis of the body.

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Unlike PVS, in which theupper portions of the brainare damaged and the lowerportions are spared, locked-in

syndrome is caused by damage to specific portionsof the lower brain and brainstem with no damageto the cerebral hemispheres of the upper brain.Most locked-in syndrome patients can communi-cate through movements and blinking of theireyes, which are not affected by the paralysis.Some patients may have the ability to move cer-tain facial muscles as well. The majority oflocked-in syndrome patients do not regainmotor control, but several devices are avail-able to help patients communicate.

With the development over the last half-century ofassistive devices that can artificially maintain bloodflow and breathing, the term brain death has comeinto use. Brain death is the lack of measurablebrain function due to diffuse damage to the cere-bral hemispheres and the brainstem, with lossof any integrated activity among distinct areasof the brain. Brain death is irreversible. Removalof assistive devices will result in immediate cardiacarrest and cessation of breathing.

Advances in imaging and other technologies haveled to devices that help differentiate among thevariety of unconscious states. For example, animaging test that shows activity in the brainstembut little or no activity in the upper brain wouldlead a physician to a diagnosis of vegetative stateand exclude diagnoses of brain death and locked-insyndrome. On the other hand, an imaging test that

“Advances in imaging andother technologies haveled to devices that help

differentiate among the varietyof unconscious states.”

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shows activity in the upper brain with little activityin the brainstem would confirm a diagnosis oflocked-in syndrome, while invalidating a diagnosisof brain death or vegetative state. The use of CTand MRI is standard in TBI treatment, but otherimaging and diagnostic techniques that may be usedto confirm a particular diagnosis include cerebralangiography, electroencephalography (EEG),transcranial Doppler ultrasound, and singlephoton emission computed tomography (SPECT).

What Immediate Post-Injury ComplicationsCan Occur From a TBI?

Sometimes, health complications occur in theperiod immediately following a TBI. Thesecomplications are not types of TBI, butare distinct medical problems that ariseas a result of the injury. Althoughcomplications are rare, therisk increases with the severityof the trauma. Complicationsof TBI include immediateseizures, hydrocephalus orpost-traumatic ventricularenlargement, CSF leaks, infec-tions, vascular injuries, cranialnerve injuries, pain, bed sores,multiple organ system failurein unconscious patients, andpolytrauma (trauma to otherparts of the body in additionto the brain).

A medical technician carefullymonitors a patient undergoing anelectroencephalogram, a diagnostictechnique used to detect abnormali-ties in brain waves.

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About 25 percent of patients with brain contusionsor hematomas and about 50 percent of patientswith penetrating head injuries will develop immedi-ate seizures, seizures that occur within the first24 hours of the injury. These immediate seizuresincrease the risk of early seizures — defined asseizures occurring within 1 week after injury —but do not seem to be linked to the developmentof post-traumatic epilepsy (recurrent seizuresoccurring more than 1 week after the initialtrauma). Generally, medical professionals useanticonvulsant medications to treat seizuresin TBI patients only if the seizures persist.

Hydrocephalus or post-traumatic ventricularenlargement occurs when CSF accumulates inthe brain resulting in dilation of the cerebralventricles (cavities in the brain filled with CSF)and an increase in ICP. This condition can developduring the acute stage of TBI or may not appearuntil later. Generally it occurs within the first yearof the injury and is characterized by worseningneurological outcome, impaired consciousness,behavioral changes, ataxia (lack of coordinationor balance), incontinence, or signs of elevated ICP.The condition may develop as a result of meningitis,subarachnoid hemorrhage, intracranial hematoma,or other injuries. Treatment includes shunting anddraining of CSF as well as any other appropriatetreatment for the root cause of the condition.

Skull fractures can tear the membranes that coverthe brain, leading to CSF leaks. A tear between thedura and the arachnoid membranes, called a CSFfistula, can cause CSF to leak out of the subarach-noid space into the subdural space; this is called

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a subdural hygroma. CSF can also leak from thenose and the ear. These tears that let CSF out ofthe brain cavity can also allow air and bacteriainto the cavity, possibly causing infections suchas meningitis. Pneumocephalus occurs whenair enters the intracranial cavity and becomestrapped in the subarachnoid space.

Infections within the intracranial cavity are adangerous complication of TBI. They may occuroutside of the dura, below the dura, below thearachnoid (meningitis), or within the space ofthe brain itself (abscess). Most of these injuriesdevelop within a few weeks of the initial traumaand result from skull fractures or penetratinginjuries. Standard treatment involves antibioticsand sometimes surgery to remove the infectedtissue. Meningitis may be especially dangerous,with the potential to spread to the rest of thebrain and nervous system.

Any damage to the head or brain usually resultsin some damage to the vascular system, whichprovides blood to the cells of the brain. The body’simmune system can repair damage to small bloodvessels, but damage to larger vessels can result inserious complications. Damage to one of the majorarteries leading to the brain can cause a stroke,either through bleeding from the artery (hemor-rhagic stroke) or through the formation of a clotat the site of injury, called a thrombus or throm-bosis, blocking blood flow to the brain (ischemicstroke). Blood clots also can develop in other partsof the head. Symptoms such as headache, vomiting,seizures, paralysis on one side of the body, andsemiconsciousness developing within several days

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of a head injury may be caused by a blood clot thatforms in the tissue of one of the sinuses, or cavities,adjacent to the brain. Thrombotic-ischemic strokesare treated with anticoagulants, while surgery is thepreferred treatment for hemorrhagic stroke. Othertypes of vascular injuries include vasospasm andthe formation of aneurysms.

Skull fractures, especially at the base of the skull,can cause cranial nerve injuries that result incompressive cranial neuropathies. All but threeof the 12 cranial nerves project out from thebrainstem to the head and face. The seventhcranial nerve, called the facial nerve, is themost commonly injured cranial nerve in TBIand damage to it can result in paralysis offacial muscles.

Pain is a common symptom of TBI and can bea significant complication for conscious patientsin the period immediately following a TBI. Head-ache is the most common form of pain experiencedby TBI patients, but other forms of pain can alsobe problematic. Serious complications for patientswho are unconscious, in a coma, or in a vegetativestate include bed or pressure sores of the skin,recurrent bladder infections, pneumonia orother life-threatening infections, and progres-sive multiple organ failure.

General Trauma

Most TBI patients have injuries to other parts ofthe body in addition to the head and brain. Physi-cians call this polytrauma. These injuries requireimmediate and specialized care and can compli-cate treatment of and recovery from the TBI. Other

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medical complications thatmay accompany a TBIinclude pulmonary (lung)dysfunction; cardiovas-cular (heart) dysfunctionfrom blunt chest trauma;gastrointestinal dysfunc-tion; fluid and hormonalimbalances; and otherisolated complications,such as fractures, nerve injuries, deep vein throm-bosis, excessive blood clotting, and infections.

Trauma victims often develop hypermetabolismor an increased metabolic rate, which leads to anincrease in the amount of heat the body produces.The body redirects into heat the energy neededto keep organ systems functioning, causing musclewasting and the starvation of other tissues. Com-plications related to pulmonary dysfunction caninclude neurogenic pulmonary edema (excess fluidin lung tissue), aspiration pneumonia (pneumoniacaused by foreign matter in the lungs), and fatand blood clots in the blood vessels of the lungs.

Fluid and hormonal imbalances can complicatethe treatment of hypermetabolism and high ICP.Hormonal problems can result from dysfunctionof the pituitary, the thyroid, and other glandsthroughout the body. Two common hormonalcomplications of TBI are syndrome of inappro-priate secretion of antidiuretic hormone (SIADH)and hypothyroidism.

Blunt trauma to the chest can also cause cardio-vascular problems, including damage to bloodvessels and internal bleeding, and problems with

In addition to head and brain injuries,most TBI patients have injuries in otherparts of the body — a condition calledpolytrauma. The formation of bloodclots deep inside a vein (shown above),referred to as deep vein thrombosis, isone of the many medical complicationsthat may occur with TBI.

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heart rate and blood flow. Blunt trauma to theabdomen can cause damage to or dysfunctionof the stomach, large or small intestines, andpancreas. A serious and common complicationof TBI is erosive gastritis, or inflammation anddegeneration of stomach tissue. This syndromecan cause bacterial growth in the stomach,increasing the risk of aspiration pneumonia.Standard care of TBI patients includes adminis-tration of prophylactic gastric acid inhibitors toprevent the buildup of stomach acids and bacteria.

What Disabilities Can Result From a TBI?

Disabilities resulting from a TBI depend upon theseverity of the injury, the location of the injury,and the age and general health of the patient.Some common disabilities include problems withcognition (thinking, memory, and reasoning),sensory processing (sight, hearing, touch, taste,and smell), communication (expression and under-standing), and behavior or mental health (depres-sion, anxiety, personality changes, aggression,acting out, and social inappropriateness).

Within days to weeks of the head injury approxi-mately 40 percent of TBI patients develop a hostof troubling symptoms collectively called post-concussion syndrome (PCS). A patient need nothave suffered a concussion or loss of consciousnessto develop the syndrome and many patients withmild TBI suffer from PCS. Symptoms includeheadache, dizziness, vertigo (a sensation of spinningaround or of objects spinning around the patient),memory problems, trouble concentrating, sleeping

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problems, restlessness, irritability, apathy, depres-sion, and anxiety. These symptoms may last for afew weeks after the head injury. The syndrome ismore prevalent in patients who had psychiatricsymptoms, such as depression or anxiety, beforethe injury. Treatment for PCS may include medi-cines for pain and psychiatric conditions, andpsychotherapy and occupational therapy todevelop coping skills.

Cognition is a term used to describe the processesof thinking, reasoning, problem solving, informa-tion processing, and memory. Most patients withsevere TBI, if they recover consciousness, sufferfrom cognitive disabilities, including the loss ofmany higher level mental skills. The most commoncognitive impairment among severely head-injuredpatients is memory loss, characterized by someloss of specific memories and the partial inabilityto form or store new ones. Some of these patientsmay experience post-traumatic amnesia (PTA),either anterograde or retrograde. AnterogradePTA is impaired memory of events that happenedafter the TBI, while retrograde PTA is impairedmemory of events that happened before the TBI.

Many patients with mild to moderate head injurieswho experience cognitive deficits become easilyconfused or distracted and have problems withconcentration and attention. They also haveproblems with higher level, so-called executivefunctions, such as planning, organizing, abstractreasoning, problem solving, and making judgments,which may make it difficult to resume pre-injurywork-related activities. Recovery from cognitivedeficits is greatest within the first 6 months after

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the injury andmore gradualafter that.

Patients with moderate to severe TBI have moreproblems with cognitive deficits than patientswith mild TBI, but a history of several mild TBIsmay have an additive effect, causing cognitivedeficits equal to a moderate or severe injury.

Many TBI patients have sensory problems, espe-cially problems with vision. Patients may not beable to register what they are seeing or may beslow to recognize objects. Also, TBI patientsoften have difficulty with hand-eye coordination.Because of this, TBI patients may be prone tobumping into or dropping objects, or may seemgenerally unsteady. TBI patients may have diffi-culty driving a car, working complex machinery,or playing sports. Other sensory deficits mayinclude problems with hearing, smell, taste, ortouch. Some TBI patients develop tinnitus, aringing or roaring in the ears. A person withdamage to the part of the brain that processestaste or smell may develop a persistent bittertaste in the mouth or perceive a persistentnoxious smell. Damage to the part of the brainthat controls the sense of touch may cause aTBI patient to develop persistent skin tingling,itching, or pain. Although rare, these condi-tions are hard to treat.

Language and communication problems arecommon disabilities in TBI patients. Some mayexperience aphasia, defined as difficulty withunderstanding and producing spoken and writtenlanguage; others may have difficulty with the more

“The most common cognitive impairmentamong severely head-injured patients ismemory loss, characterized by some loss

of specific memories and the partialinability to form or store new ones.”

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subtle aspects of communication, such as bodylanguage and emotional, non-verbal signals.

In non-fluent aphasia, also called Broca’s aphasiaor motor aphasia, TBI patients often have troublerecalling words and speaking in complete sentences.They may speak in broken phrases and pausefrequently. Most patients are aware of these defi-cits and may become extremely frustrated. Patientswith fluent aphasia, also called Wernicke’s aphasiaor sensory aphasia, display little meaning in theirspeech, even though they speak in complete sen-tences and use correct grammar. Instead, theyspeak in flowing gibberish, drawing out theirsentences with non-essential and invented words.Many patients with fluent aphasia are unawarethat they make little sense and become angry withothers for not understanding them. Patients withglobal aphasia have extensive damage to the por-tions of the brain responsible for language andoften suffer severe communication disabilities.

TBI patients may have problems with spokenlanguage if the part of the brain that controlsspeech muscles is damaged.In this disorder, calleddysarthria, the patient canthink of the appropriatelanguage, but cannot easilyspeak the words because theyare unable to use the musclesneeded to form the words andproduce the sounds. Speechis often slow, slurred, andgarbled. Some may haveproblems with intonation orinflection, called prosodic

Communication disabilities such aslanguage and speech problems arecommon among TBI patients. Above,a speech therapist uses a mirror inher work, performing exercises tohelp a patient relearn speaking skills.

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dysfunction. An important aspect of speech,inflection conveys emotional meaning andis necessary for certain aspects of language,such as irony.

These language deficits can lead to miscommuni-cation, confusion, and frustration for the patientas well as those interacting with him or her.

Most TBI patients have emotional or behavioralproblems that fit under the broad category ofpsychiatric health. Family members of TBIpatients often find that personality changesand behavioral problems are the most difficultdisabilities to handle. Psychiatric problemsthat may surface include depression, apathy,anxiety, irritability, anger, paranoia, confusion,frustration, agitation, insomnia or other sleepproblems, and mood swings. Problem behaviorsmay include aggression and violence, impulsivity,disinhibition, acting out, noncompliance, socialinappropriateness, emotional outbursts, childishbehavior, impaired self-control, impaired self-awareness, inability to take responsibility oraccept criticism, egocentrism, inappropriatesexual activity, and alcohol or drug abuse/addic-tion. Some patients’ personality problems maybe so severe that they are diagnosed with border-line personality disorder, a psychiatric conditioncharacterized by many of the problems mentionedabove. Sometimes TBI patients suffer from devel-opmental stagnation, meaning that they fail tomature emotionally, socially, or psychologicallyafter the trauma. This is a serious problem forchildren and young adults who suffer from aTBI. Attitudes and behaviors that are appropriate

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for a child or teenager become inappropriatein adulthood. Many TBI patients who showpsychiatric or behavioral problems can behelped with medication and psychotherapy.

Are There Other Long-Term ProblemsAssociated With a TBI?

In addition to the immediate post-injury compli-cations discussed on page 13, other long-termproblems can develop after a TBI. These includeParkinson’s disease and other motor problems,Alzheimer’s disease, dementia pugilistica, andpost-traumatic dementia.

Alzheimer’s disease (AD) — AD is a progressive,neurodegenerative disease characterized bydementia, memory loss, and deteriorating cogni-tive abilities. Recent research suggests an asso-ciation between head injury in early adulthoodand the development of AD later in life; the moresevere the head injury, the greater the risk ofdeveloping AD. Some evidence indicates that ahead injury may interact with other factors totrigger the disease and may hasten the onset ofthe disease in individuals already at risk. Forexample, people who have a particular form ofthe protein apolipoprotein E (apoE4) and suffera head injury fall into this increased risk category.(ApoE4 is a naturally occurring protein that helpstransport cholesterol through the bloodstream.)

Parkinson’s disease and other motor problems —Movement disorders as a result of TBI are rarebut can occur. Parkinson’s disease may develop

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years after TBI as a result ofdamage to the basal ganglia.Symptoms of Parkinson’sdisease include tremor ortrembling, rigidity or stiffness,slow movement (bradykinesia),inability to move (akinesia),shuffling walk, and stoopedposture. Despite many scien-tific advances in recent years,Parkinson’s disease remains

a chronic and progressive disorder, meaning thatit is incurable and will progress in severity untilthe end of life. Other movement disorders thatmay develop after TBI include tremor, ataxia(uncoordinated muscle movements), and myo-clonus (shock-like contractions of muscles).

Dementia pugilistica — Also called chronictraumatic encephalopathy, dementia pugilisticaprimarily affects career boxers. The most com-mon symptoms of the condition are dementia andparkinsonism caused by repetitive blows to thehead over a long period of time. Symptoms beginanywhere between 6 and 40 years after the startof a boxing career, with an average onset ofabout 16 years.

Post-traumatic dementia — The symptomsof post-traumatic dementia are very similarto those of dementia pugilistica, except thatpost-traumatic dementia is also characterizedby long-term memory problems and is causedby a single, severe TBI that results in a coma.

Dementia pugilistica is a conditioncaused by repetitive blows to thehead over a long period of time.Symptoms of the disorder, whichprimarily affects career boxers,include dementia and parkinsonism.

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What Kinds of Rehabilitation Shoulda TBI Patient Receive?

Rehabilitation is an important part of therecovery process for a TBI patient. Duringthe acute stage, moderately to severely injuredpatients may receive treatment and care in anintensive care unit of a hospital. Once stable,the patient may be transferred to a subacuteunit of the medical center or to an independentrehabilitation hospital. At this point, patientsfollow many diverse paths toward recoverybecause there are a wide variety of optionsfor rehabilitation.

In 1998, the NIH held a Consensus DevelopmentConference on Rehabilitation of Persons withTraumatic Brain Injury. The Consensus Develop-ment Panel recommended that TBI patients receivean individualized rehabilitation program basedupon the patient’s strengths and capacities andthat rehabilitation services should be modifiedover time to adapt to the patient’s changing needs.*The panel also recommended that moderately toseverely injured patients receive rehabilitationtreatment that draws on the skills of many special-ists. This involves individually tailored treatmentprograms in the areas of physical therapy, occupa-tional therapy, speech/language therapy, physiatry(physical medicine), psychology/psychiatry, andsocial support. Medical personnel who provide thiscare include rehabilitation specialists, such as

* National Institutes of Health Consensus Development ConferenceStatement, October 26–28, 1998. Rehabilitation of Persons withTraumatic Brain Injury. Bethesda, MD, September 1999.

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rehabilitation nurses, psychol-ogists, speech/language patholo-gists, physical and occupationaltherapists, physiatrists (physicalmedicine specialists), socialworkers, and a team coordi-nator or administrator.

The overall goal of rehabilitation after a TBIis to improve the patient’s ability to function athome and in society. Therapists help the patientadapt to disabilities or change the patient’s livingspace, called environmental modification, tomake everyday activities easier.

Some patients may need medication for psychia-tric and physical problems resulting from theTBI. Great care must be taken in prescribingmedications because TBI patients are moresusceptible to side effects and may react adverselyto some pharmacological agents. It is importantfor the family to provide social support for thepatient by being involved in the rehabilitationprogram. Family members may also benefitfrom psychotherapy.

It is important for TBI patients and their familiesto select the most appropriate setting for rehabili-tation. There are several options, includinghome-based rehabilitation, hospital outpatientrehabilitation, inpatient rehabilitation centers,comprehensive day programs at rehabilitationcenters, supportive living programs, independentliving centers, club-house programs, school-based programs for children, and others. TheTBI patient, the family, and the rehabilitationteam members should work together to find thebest place for the patient to recover.

Rehabilitation therapy is an important partof the recovery process of TBI patients.Above, a physical therapist works with apatient to help improve her ability to walk.

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How Can TBI be Prevented?

Unlike most neurological disorders, headinjuries can be prevented. The Centers forDisease Control and Prevention (CDC) haveissued the following safety tips* for reducingthe risk of suffering a TBI.

• Wear a seatbelt every time you drive orride in a car.

• Buckle your child into a child safety seat,booster seat, or seatbelt (depending on thechild’s age) every time the child rides in a car.

• Wear a helmet and make sure your childrenwear helmets when

— riding a bike or motorcycle;

— playing a contact sport such asfootball or ice hockey;

— using in-line skates orriding a skateboard;

— batting and runningbases in baseballor softball;

— riding a horse;

— skiing or snowboarding.

• Keep firearms and bulletsstored in a locked cabinetwhen not in use.

Certain precautions, such as wearinga helmet when riding a bicycle ormotorcycle and wearing a seatbeltwhen driving or riding in a car,greatly reduce the risk of TBI.

*From the CDC, Department of Health and Human Services(http://www.cdc.gov/safeusa/home/tbi.htm).

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• Avoid falls by

— using a step-stool with a grab bar to reachobjects on high shelves;

— installing handrails on stairways;

— installing window guards to keep youngchildren from falling out of open windows;

— using safety gates at the top and bottomof stairs when young children are around.

• Make sure the surface on your child’s play-ground is made of shock-absorbing material(e.g., hardwood mulch, sand).

What Research is the NINDS Conducting?

The National Institute of Neurological Disordersand Stroke (NINDS) conducts and supportsresearch to better understand CNS injury andthe biological mechanisms underlying damageto the brain, to develop strategies and interven-

tions to limit the primaryand secondary brain dam-age that occurs withindays of a head trauma,and to devise therapiesto treat brain injuryand help in long-termrecovery of function.

On a microscopic scale,the brain is made up ofbillions of cells that inter-connect and communicate.

NINDS grantees developed a device thatsimulates the condition of trauma in cellsin culture. The device allows researchers tocontrol the degree of injury to the cells andthen study the biological and physiologicalresponses those cells have to trauma. Thedevice can also serve as a tool to test theeffects of pharmaceutical agents.

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The neuron is the main functional cell of the brainand nervous system, consisting of a cell body (soma),a tail or long nerve fiber (axon), and projections ofthe cell body called dendrites. The axons travel intracts or clusters throughout the brain, providingextensive interconnections between brain areas.

One of the most pervasive types of injury followingeven a minor trauma is damage to the nerve cell’saxon through shearing; this is referred to as dif-fuse axonal injury. This damage causes a seriesof reactions that eventually lead to swelling of theaxon and disconnection from the cell body of theneuron. In addition, the part of the neuron thatcommunicates with other neurons degeneratesand releases toxic levels of chemical messengerscalled neurotransmitters into the synapse orspace between neurons, damaging neighboringneurons through a secondary neuroexcitatorycascade. Therefore, neurons that were unharmedfrom the primary trauma suffer damage from thissecondary insult. Many of these cells cannot survivethe toxicity of the chemical onslaught and initiateprogrammed cell death, or apoptosis. This processusually takes place within the first 24 to 48 hoursafter the initial injury, but can be prolonged.

One area of research that shows promise is thestudy of the role of calcium ion influx into thedamaged neuron as a cause of cell death andgeneral brain tissue swelling. Calcium entersnerve cells through damaged channels in theaxon’s membrane. The excess calcium inside thecell causes the axon to swell and also activateschemicals, called proteases, that break downproteins. One family of proteases, the calpains,

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are especially damaging to nerve cells becausethey break down proteins that maintain thestructure of the axon. Excess calcium within thecell is also destructive to the cell’s mitochondria,structures that produce the cell’s energy. Mito-chondria soak up excess calcium until they swelland stop functioning. If enough mitochondriaare damaged, the nerve cell degenerates. Calciuminflux has other damaging effects: it activatesdestructive enzymes, such as caspases that damagethe DNA in the cell and trigger programmed celldeath, and it damages sodium channels in thecell membrane, allowing sodium ions to floodthe cell as well. Sodium influx exacerbatesswelling of the cell body and axon.

NINDS researchers have shown, in both cell andanimal studies, that giving specialized chemicalscan reduce cell death caused by calcium ion influx.

Other researchers haveshown that the use ofcyclosporin A, whichblocks mitochondrialmembrane permeability,protects axons fromcalcium influx. Anotheravenue of therapeuticintervention is the useof hypothermia (aninduced state of lowbody temperature)to slow the progres-sion of cell death andaxon swelling.

A researcher studies an image generated by animmunofluorescent microscope to understandcell death in the hippocampus, the section ofthe brain that controls memory. The hippocam-pus is frequently affected in TBI patients. Thistechnology allows the researchers to study whathappens to injured cells at the molecular level,and to look for ways to interrupt the chain ofchemical events that causes permanent braindamage after a severe head injury.

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In the healthy brain, the chemical glutamatefunctions as a neurotransmitter, but an excessamount of glutamate in the brain causes neuronsto quickly overload from too much excitation,releasing toxic chemicals. These substancespoison the chemical environment of surroundingcells, initiating degeneration and programmedcell death. Studies have shown that a group ofenzymes called matrix metalloproteinases con-tribute to the toxicity by breaking down proteinsthat maintain the structure and order of theextracellular environment. Other research showsthat glutamate reacts with calcium and sodiumion channels on the cell membrane, leading toan influx of calcium and sodium ions into thecell. Investigators are looking for ways todecrease the toxic effects of glutamate andother excitatory neurotransmitters.

The brain attempts to repair itself after a trauma,and is more successful after mild to moderateinjury than after severe injury. Scientists haveshown that after diffuse axonal injury neuronscan spontaneously adapt and recover by sproutingsome of the remaining healthy fibers of the neuroninto the spaces once occupied by the degeneratedaxon. These fibers can develop in such a way thatthe neuron can resume communication with neigh-boring neurons. This is a very delicate processand can be disrupted by any of a number offactors, such as neuroexcitation, hypoxia (lowoxygen levels), and hypotension (low blood flow).Following trauma, excessive neuroexcitation,that is the electrical activation of nerve cells orfibers, especially disrupts this natural recoveryprocess and can cause sprouting fibers to losedirection and connect with the wrong terminals.

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Scientists suspect that these misconnections maycontribute to some long-term disabilities, suchas pain, spasticity, seizures, and memory problems.NINDS researchers are trying to learn more aboutthe brain’s natural recovery process and whatfactors or triggers control it. They hope thatthrough manipulation of these triggers they canincrease repair while decreasing misconnections.

NINDS investigators are also looking at larger,tissue-specific changes within the brain after aTBI. Researchers have shown that trauma tothe frontal lobes of the brain can damage speci-fic chemical messenger systems, specifically thedopaminergic system, the collection of neuronsin the brain that uses the neurotransmitterdopamine. Dopamine is an important chemicalmessenger — for example, degeneration ofdopamine-producing neurons is the primarycause of Parkinson’s disease. NINDS research-ers are studying how the dopaminergic systemresponds after a TBI and its relationship toneurodegeneration and Parkinson’s disease.

The use of stem cells to repair or replacedamaged brain tissue is a new and excitingavenue of research. A neural stem cell is aspecial kind of cell that can multiply and giverise to other more specialized cell types. Thesecells are found in adult neural tissue and normal-ly develop into several different cell types foundwithin the central nervous system. NINDS research-ers are investigating the ability of stem cells todevelop into neurotransmitter-producing neurons,specifically dopamine-producing cells. Research-ers are also looking at the power of stem cells to

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develop into oligodendrocytes, a type of braincell that produces myelin, the fatty sheath thatsurrounds and insulates axons. One study inmice has shown that bone marrow stem cells candevelop into neurons, demonstrating that neuralstem cells are not the only type of stem cell thatcould be beneficial in the treatment of brain andnervous system disorders. At the moment, stemcell research for TBI is in its infancy, but futureresearch may lead to advances for treatmentand rehabilitation.

In addition to the basic research described above,NINDS scientists also conduct broader basedclinical research involving patients. One areaof study focuses on the plasticity of the brainafter injury. In the strictest sense, plasticitymeans the ability to be formed or molded. Whenspeaking of the brain, plasticity means the abilityof the brain to adapt to deficits and injury. NINDSresearchers are investigating the extent of brainplasticity after injury and developing therapies toenhance plasticity as a means of restoring function.

The plasticity of the brain and the rewiring ofneural connections make it possible for one partof the brain to take up the functions of a disabledpart. Scientists have long known that the imma-ture brain is generally more plastic than themature brain, and that the brains of childrenare better able to adapt and recover from injurythan the brains of adults. NINDS researchersare investigating the mechanisms underlying thisdifference and theorize that children have anoverabundance of hard-wired neural networks,many of which naturally decrease through a

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process called pruning. Whenan injury destroys an impor-tant neural network in chil-dren, another less usefulneural network that wouldhave eventually died takes

over the responsibilities of the damaged network.Some researchers are looking at the role ofplasticity in memory, while others are usingimaging technologies, such as functional MRI,to map regions of the brain and record evidenceof plasticity.

Another important area of research involves thedevelopment of improved rehabilitation programsfor those who have disabilities from a TBI. TheCongressional Children’s Health Act of 2000authorized the NINDS to conduct and supportresearch related to TBI with the goal of design-ing therapies to restore normal functioning incognition and behavior.

Clinical Trials Research

The NINDS works to develop treatments that canbe given in the first hours after a TBI, hoping thatquick action can prevent or reverse much of thebrain damage resulting from the injury. A recentlycompleted NINDS-supported clinical trial involvedlowering body temperature in TBI patients to33 degrees Celcius within 8 hours of the trauma.Although the investigators found that the treat-ment did not improve outcome overall, they didlearn that patients younger than 45 years whowere admitted to the hospital already in a hypo-thermic state fared better if they were kept “cool”

“In the strictest sense, plasticitymeans the ability to be formedor molded. When speaking ofthe brain, plasticity meansthe ability of the brain to

adapt to deficits and injury.”

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than if they were brought to normal body tempera-ture. Other ongoing clinical trials include the useof hypothermia for severe TBI in children, theuse of magnesium sulfate to protect nerve cellsafter TBI, and the effects of lowering ICP andincreasing cerebral blood flow.

Where Can I Find More Information?

The National Institute of Neurological Disordersand Stroke is the Federal government’s leadingsupporter of biomedical research on brain andnervous system disorders, including TBI. TheNINDS conducts research in its own laboratoriesat the National Institutes of Health in Bethesda,Maryland, and supports research at institutionsnationwide. The address for the Institute, aswell as information on other organizations thatoffer various services to those affected by TBI,is provided on the Information Resources cardenclosed in the back pocket of this brochure.Information on the NINDS and its researchprograms is also available on the World WideWeb at www.ninds.nih.gov.

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Glossaryaneurysm — a blood-filled sac formed by disease-related stretching of an artery or blood vessel.

anoxia — an absence of oxygen supply to anorgan’s tissues leading to cell death.

aphasia — difficulty understanding and/orproducing spoken and written language.(See also non-fluent aphasia.)

apoptosis — cell death that occurs naturally aspart of normal development, maintenance, andrenewal of tissues within an organism.

arachnoid membrane — one of the threemembranes that cover the brain; it is betweenthe pia mater and the dura. Collectively, thesethree membranes form the meninges.

brain death — an irreversible cessation of measur-able brain function.

Broca’s aphasia — see non-fluent aphasia.

cerebrospinal fluid (CSF) — the fluid thatbathes and protects the brain and spinal cord.

closed head injury — an injury that occurswhen the head suddenly and violently hitsan object but the object does not break throughthe skull.

coma — a state of profound unconsciousnesscaused by disease, injury, or poison.

compressive cranial neuropathies — degenera-tion of nerves in the brain caused by pressureon those nerves.

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computed tomography (CT) — a scan thatcreates a series of cross-sectional X-rays ofthe head and brain; also called computerizedaxial tomography or CAT scan.

concussion — injury to the brain caused bya hard blow or violent shaking, causing a suddenand temporary impairment of brain function,such as a short loss of consciousness or disturb-ance of vision and equilibrium.

contrecoup — a contusion caused by the shakingof the brain back and forth within the confinesof the skull.

contusion — distinct area of swollen braintissue mixed with blood released from brokenblood vessels.

CSF fistula — a tear between two of thethree membranes – the dura and arachnoidmembranes – that encase the brain.

deep vein thrombosis — formation of a bloodclot deep within a vein.

dementia pugilistica — brain damage caused bycumulative and repetitive head trauma; commonin career boxers.

depressed skull fracture — a fracture occurringwhen pieces of broken skull press into the tissuesof the brain.

diffuse axonal injury — see shearing.

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dysarthria — inability or difficulty articulatingwords due to emotional stress, brain injury,paralysis, or spasticity of the muscles neededfor speech.

dura — a tough, fibrous membrane lining thebrain; the outermost of the three membranescollectively called the meninges.

early seizures — seizures that occur within1 week after a traumatic brain injury.

epidural hematoma — bleeding into the areabetween the skull and the dura.

erosive gastritis — inflammation and degenera-tion of the tissues of the stomach.

fluent aphasia — a condition in which patientsdisplay little meaning in their speech even thoughthey speak in complete sentences. Also calledWernicke’s or motor aphasia.

Glasgow Coma Scale — a clinical tool usedto assess the degree of consciousness andneurological functioning – and thereforeseverity of brain injury – by testing motorresponsiveness, verbal acuity, and eye opening.

global aphasia — a condition in which patientssuffer severe communication disabilities as aresult of extensive damage to portions of thebrain responsible for language.

hematoma — heavy bleeding into or around thebrain caused by damage to a major blood vesselin the head.

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hemorrhagic stroke — stroke caused bybleeding out of one of the major arteriesleading to the brain.

hypermetabolism — a condition in which thebody produces too much heat energy.

hypothyroidism — decreased production ofthyroid hormone leading to low metabolic rate,weight gain, chronic drowsiness, dry skin andhair, and/or fluid accumulation and retentionin connective tissues.

hypoxia — decreased oxygen levels in an organ,such as the brain; less severe than anoxia.

immediate seizures — seizures that occur within24 hours of a traumatic brain injury.

intracerebral hematoma — bleeding within thebrain caused by damage to a major blood vessel.

intracranial pressure — buildup of pressure inthe brain as a result of injury.

ischemic stroke — stroke caused by the formationof a clot that blocks blood flow through an arteryto the brain.

locked-in syndrome — a condition in which apatient is aware and awake, but cannot moveor communicate due to complete paralysisof the body.

magnetic resonance imaging (MRI) — a non-invasive diagnostic technique that uses magneticfields to detect subtle changes in brain tissue.

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meningitis — inflammation of the three mem-branes that envelop the brain and spinal cord,collectively known as the meninges; the meningesinclude the dura, pia mater, and arachnoid.

motor aphasia — see non-fluent aphasia.

neural stem cells — cells found only in adultneural tissue that can develop into several dif-ferent cell types in the central nervous system.

neuroexcitation — the electrical activation ofcells in the brain; neuroexcitation is part of thenormal functioning of the brain or can also bethe result of abnormal activity related to an injury.

neuron — a nerve cell that is one of the mainfunctional cells of the brain and nervous system.

neurotransmitters —chemicals that transmitnerve signals from one neuron to another.

non-fluent aphasia — a condition in whichpatients have trouble recalling words andspeaking in complete sentences. Also calledBroca’s or motor aphasia.

oligodendrocytes — a type of support cell inthe brain that produces myelin, the fatty sheaththat surrounds and insulates axons.

penetrating head injury — a brain injury inwhich an object pierces the skull and entersthe brain tissue.

penetrating skull fracture — a brain injuryin which an object pierces the skull and injuresbrain tissue.

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persistent vegetative state — an ongoing stateof severely impaired consciousness, in whichthe patient is incapable of voluntary motion.

plasticity — ability of the brain to adapt todeficits and injury.

pneumocephalus — a condition in which air orgas is trapped within the intracranial cavity.

post-concussion syndrome (PCS) — a complex,poorly understood problem that may cause head-ache after head injury; in most cases, patientscannot remember the event that caused theconcussion and a variable period of timeprior to the injury.

post-traumatic amnesia (PTA) — a state of acuteconfusion due to a traumatic brain injury, markedby difficulty with perception, thinking, remember-ing, and concentration; during this acute stage,patients often cannot form new memories.

post-traumatic dementia — a condition markedby mental deterioration and emotional apathyfollowing trauma.

post-traumatic epilepsy — recurrent seizuresoccurring more than 1 week after a traumaticbrain injury.

prosodic dysfunction — problems with speechintonation or inflection.

pruning — process whereby an injury destroysan important neural network in children, andanother less useful neural network that wouldhave eventually died takes over the responsibilitiesof the damaged network.

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seizures — abnormal activity of nerve cells in thebrain causing strange sensations, emotions, andbehavior, or sometimes convulsions, musclespasms, and loss of consciousness.

sensory aphasia — see fluent aphasia.

shaken baby syndrome — a severe form of headinjury that occurs when an infant or small childis shaken forcibly enough to cause the brain tobounce against the skull; the degree of braindamage depends on the extent and durationof the shaking. Minor symptoms includeirritability, lethargy, tremors, or vomiting;major symptoms include seizures, coma,stupor, or death.

shearing (or diffuse axonal injury) — damageto individual neurons resulting in disruption ofneural networks and the breakdown of overallcommunication among neurons in the brain.

stupor — a state of impaired consciousness inwhich the patient is unresponsive but can bearoused briefly by a strong stimulus.

subdural hematoma — bleeding confined tothe area between the dura and the arachnoidmembranes.

subdural hygroma — a buildup of protein-rich fluid in the area between the dura andthe arachnoid membranes, usually caused bya tear in the arachnoid membrane.

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syndrome of inappropriate secretion ofantidiuretic hormone (SIADH) — a conditionin which excessive secretion of antidiuretic hor-mone leads to a sodium deficiency in the bloodand abnormally concentrated urine; symptomsinclude weakness, lethargy, confusion, coma,seizures, or death if left untreated.

thrombosis or thrombus — the formation of ablood clot at the site of an injury.

vasospasm — exaggerated, persistent contractionof the walls of a blood vessel.

vegetative state — a condition in which patientsare unconscious and unaware of their surround-ings, but continue to have a sleep/wake cycle andcan have periods of alertness.

ventriculostomy — a surgical procedure thatdrains cerebrospinal fluid from the brain bycreating an opening in one of the small cavitiescalled ventricles.

Wernicke’s aphasia — see fluent aphasia.

Information Resources

The National Institute of Neurological Disorders andStroke, a component of the National Institutes of Health,is the leading federal supporter of research on brain andnervous system disorders. The Institute also sponsorsan active public information office. For information onhead injury or other neurological disorders, contact theInstitute’s Brain Resources and Information Network(BRAIN) at:

BRAINP.O. Box 5801Bethesda, MD 20824301-496-5751800-352-9424www.ninds.nih.gov

In addition, a number of private organizations offera variety of services and information that can helpthose affected by TBI. They include:

Acoustic Neuroma Association600 Peachtree ParkwaySuite 108Cumming, GA 30041www.anausa.org770-205-8211

Brain Injury Association105 North Alfred StreetAlexandria, VA 22314www.biausa.org703-236-6000800-444-6443

Brain Trauma Foundation523 East 72nd Street8th FloorNew York, NY 10021www.braintrauma.org212-772-0608

Family Caregiver Alliance690 Market StreetSuite 600San Francisco, CA 94104www.caregiver.org415-434-3388 (in California: 800-445-8106)

National Rehabilitation InformationCenter (NARIC)1010 Wayne AvenueSuite 800Silver Spring, MD 20910-5633www.naric.com301-562-2400800-346-2742

National Stroke Association9707 East Easter LaneEnglewood, CO 80112-3747www.stroke.org303-649-9299800-STROKES (787-6537)

National Institute on Disabilityand Rehabilitation Research (NIDRR)600 Independence Avenue, S.W.Washington, DC 20013-1492www.ed.gov/offices/OSERS/NIDRR202-205-8134

“Traumatic Brain Injury: Hope Through Research,”2002, NINDS

Head Injury Research Centers: August 2002

To find better ways to prevent and treat head injury,the NINDS research program supports a broadspectrum of studies by investigators at leadingbiomedical research institutions across the country.Information on research activities at these centersmay be obtained by contacting the principalinvestigators listed below.

Donald P. Becker, M.D.UCLA School of MedicineSurgery Department10833 Le Conte Avenue, Room 74-140 CHSLos Angeles, California 90024-6901310-825-3998

W. Dalton Dietrich, Ph.D.Scientific DirectorMiami Project to Cure ParalysisDepartment of Neurological SurgeryUniversity of Miami School of MedicinePost Office Box 016960, MC R48Lois Pope LIFE Center1095 N.W. 14th Terrace, 2nd FloorMiami, Florida 33136305-243-2297

Tracy K. McIntosh, Ph.D.Department of NeurosurgeryHospital of the University of Pennsylvania3320 Smith Walk, Hayden Hall, 105Philadelphia, Pennsylvania 19104-6316215-573-3156

Donald W. Marion, M.D.Department of Neurological Surgery9402 Presbyterian-University Hospital230 Lothrop StreetPittsburgh, Pennsylvania 15213412-647-0956

Claudia Robertson, M.D.Department of NeurosurgeryBaylor College of MedicineScurlock Tower6560 Fannin Street, Suite 944Houston, Texas 77030713-798-4696

Ross Bullock, M.D.Division of NeurosurgeryMedical College of VirginiaVirginia Commonwealth UniversityWest Hospital, 8th Floor, South Wing1200 East Broad StreetRichmond, Virginia 23219804-828-9165

“Traumatic Brain Injury: Hope Through Research,”2002, NINDS

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CreditsWritten by Marcia Vital, Office of Communications and PublicLiaison, NINDS

Illustrations and photos:

William Geiger for NINDS — cover and pages 4, 7, 13, 21, 26, 27, 28, 30Dr. Hanna Damasio, Department of Neurology, University of Iowa — page 1Diagnostic Radiology Department, NIH Clinical Center — page 10

Prepared by:

Office of Communications and Public LiaisonNational Institute of Neurological Disorders and StrokeNational Institutes of HealthBethesda, Maryland 20892-2540

NIH Publication No. 02-158September 2002