Classification and Complications of Traumatic Brain Injury

Classification and Complications of Traumatic BrainInjury

Author: Percival H Pangilinan Jr, MD; Chief Editor: Denise I Campagnolo, MD, MS more...Updated: Oct 26, 2012

EpidemiologyTraumatic brain injury (TBI), also known as acquired brain injury, head injury, or brain injury, causes substantial disabilityand mortality. It occurs when a sudden trauma damages the brain and disrupts normal brain function. TBI may haveprofound physical, psychological, cognitive, emotional, and social effects. The diagnosis of mild TBI appears to bevastly underdiagnosed in the setting of systemic trauma, even in trauma centers.[1]

According to the Center for Disease Control and Prevention's National Center for Injury Prevention and Control, thefollowing annual statistics apply in the United States[2] :

At least 1.4 million people sustain a TBI.Approximately 50,000 people die from a TBI.Approximately 475,000 TBIs occur among infants, children, and adolescents aged 0-14 years.About 80,000-90,000 people experience the onset of a long-term disability due to a TBI.

The following groups are at particular risk for TBI[2] :Males are about twice as likely as females to sustain a TBI.Infants and children aged 0-4 and adolescents aged 15-19 years are the 2 age groups at highest risk for a TBI.Adults aged 75 years or older have the highest rates of TBI-related hospitalization and death.

A TBI is caused by an excessive force, blow, or penetrating injury to the head. The leading causes of TBI are asfollows[2] :

Falls (28%)Motor vehicle crashes (20%)Being struck by or against objects (19%)Assaults (11%)

Mortality rates after brain injury are highest in people with a severe TBI. In the first year after a TBI, people who surviveare more likely to die from seizures, septicemia, pneumonia, digestive conditions, and all external causes of injury thanare other people of similar age, sex, and race.[3]However, the mortality rate after severe TBI has decreased since thelate 20th century.[4]

In one study, researchers estimated that the economic burden of TBI in the United States was approximately $37.8billion in 1985.[5] This estimate included $4.5 billion in direct expenditures for hospital care, extended care, and othermedical care and services; $20.6 billion in work-related losses and disability; and $12.7 billion in lost income frompremature death.

See also the following related Medscape Reference topics:

Medscape ReferenceReference

NewsReferenceEducationMEDLINE

Classification and Complications of Traumatic Brain Injury http://emedicine.medscape.com/article/326643-overview

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Initial Evaluation and Management of CNS InjuryTraumatic Brain Injury in ChildrenTraumatic Brain Injury: Definition, Epidemiology, Pathophysiology

See also the following related Medscape resource:Resource CenterTrauma

PathophysiologyClassification as Primary or Secondary injuryTBI may be divided into primary injury and secondary injury. Primary injury is induced by mechanical force and occursat the moment of injury. Secondary injury is not mechanically induced. It may be delayed from the moment of impact,and it may superimpose injury on a brain already affected by a mechanical injury.[6]

Primary injuryThe 2 main mechanisms that cause primary injury are contact (eg, an object striking the head or the brain striking theinside of the skull) and acceleration-deceleration. Primary injury due to contact may result in injury to the scalp, fractureto the skull, and surface contusions. Primary injury due to acceleration-deceleration results from unrestrictedmovement of the head and leads to shear, tensile, and compressive strains. These forces can cause intracranialhematoma, diffuse vascular injury, and injury to cranial nerves and the pituitary stalk.[6]

Contusions are distinct areas of swollen brain tissue.[7] They are typically found on the poles of the frontal lobes, theinferior aspects of the frontal lobes, the cortex above and below the operculum of the sylvian fissures, and the lateraland inferior aspects of the temporal lobes.Intracranial hematoma is the most common cause of death and clinical deterioration after TBI. Hematomas arecategorized as follows[6] :

Epidural hematomas - These are usually caused by fracture of the temporal bone and rupture of the middlemeningeal artery. With epidural hematomas, clotted blood collects between the bone and the dura. Becausethe source of bleeding is arterial, this type of hematoma can grow quickly and create pressure against the braintissue.Subdural hematomas - Such hematomas are usually caused by rupture of the bridging veins in the subduralspace. They can grow large enough to act as mass lesions, and they are associated with high morbidity andmortality rates.Subarachnoid hematomas - These result from damage to blood vessels in the posterior fossa stalk.

Diffuse axonal injury (DAI) is one of the most common and important pathologic features of TBI. It constitutes mostlymicroscopic damage, and it is often not visible on imaging studies. The main mechanical force that causes DAI isrotational acceleration of the brain, resulting in unrestricted head movement. Rotational acceleration produces shearingand tensile forces, and axons can be pulled apart at the microscopic level. Microscopic evaluation of the brain tissueoften shows numerous swollen and disconnected axons. Rapid stretching of axons is thought to damage the axonalcytoskeleton and, therefore, disrupt normal neuron function.[8]

Secondary injurySecondary injury may occur hours or even days after the inciting traumatic event. Injury may result from impairment orlocal declines in cerebral blood flow (CBF) after a TBI. Decreases in CBF are the result of local edema, hemorrhage,or increased intracranial pressure (ICP). As a result of inadequate perfusion, cellular ion pumps may fail, causing acascade involving intracellular calcium and sodium. Resultant calcium and sodium overload may contribute to cellulardestruction. Excessive release of excitatory amino acids, such as glutamate and aspartate, exacerbates failure of theion pumps. As the cascade continues, cells die, causing free radical formation, proteolysis, and lipid peroxidation.These factors can ultimately cause neuronal death.[9]

The exact role of the inflammatory response in secondary injury is not known. However, it is believed to contribute tocell damage.[9]

Clinical conditions associated with the risk of a decreased CBF are arterial hypotension, hypoxemia, intracranialhemorrhage and malignant brain edema, and hyperthermia.[9]


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Classification as Focal or Diffuse InjuryAnother injury classification based on clinical and neuroradiologic evaluation has been proposed. In this classification,TBI would be described as focal or diffuse. Focal injuries include scalp injury, skull fracture, and surface contusionsand are generally be caused by contact. Diffuse injuries include DAI, hypoxic-ischemic damage, meningitis, andvascular injury and are usually caused by acceleration-deceleration forces. These 2 forms of injury are commonlyfound together.

See also the following related Medscape Reference topic:Brain Contusion Imaging

Measures of SeverityThe classification of TBIs plays an important role in determining the patient's treatment, rehabilitation potential, andprognosis.

Glasgow Coma ScaleThe most common classification system for TBI severity is based on the Glasgow Coma Scale (GCS) scoredetermined at the time of injury. The GCS is a 3- to 15-point scale used to assess a patient's level of consciousnessand level of neurologic functioning.[10, 11] It consists of 3 sections, each of which is scored: best motor response, bestverbal response, and eye opening (Table 1). A total score of 3-8 for the 3 sections indicates severe TBI, a score of9-12 indicates moderate TBI, and a score of 13-15 indicates mild TBI.Table 1. Glasgow Coma Scale (Open Table in a new window)

Score Best Motor Response Best Verbal Response Eye Opening1 None None None2 Decorticate posturing Mutters unintelligibly Opens to pain3 Decerebrate posturing Inappropriate speech Opens to command4 Withdraws to pain Confused Opens spontaneously5 Localizing response to pain Alert and oriented NA6 Obeys commands NA NATotal* 1-6 1-5 1-4SourceTeasdale and Jennett, 1974.[11]

NoteNA = not applicable.

* The total of the motor, verbal, and eye-opening scores (range, 3-15) indicates the severity of a TBI, as follows: 3-8is severe TBI, 9-12 is moderate TBI, and 13-15 is mild TBI.

Loss of consciousnessThe duration of loss of consciousness (LOC) is another measure of the severity of a TBI (Table 2).[12]

Table 2. Severity of TBI Based on the Duration of LOC (Open Table in a new window)Severity of TBI FindingMild Mental status change or LOC < 30 minModerate Mental status change or LOC 30 min to 6 hSevere Mental status change or LOC > 6 hSourceGreenwald et al, 2003.[12]


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Other classifications of severityAs early as 1932, Russell introduced the concept of posttraumatic amnesia (PTA) and later defined it as the timeelapsed from injury to the moment when patients can demonstrate continuous memory of what is happening aroundthem.[13] Lack of accurate records may make this system difficult to use retrospectively. Zafonte found that the durationof PTA (as measured by using the Galveston Orientation and Amnesia Test) appeared to be a significant predictor offunctional outcome after a TBI and may best reflect the overall severity of injury.[14, 15]

Relatively uncommon measures of severity include the number of days that are required to achieve a total GCS scoreof 15, the number of days that are needed to achieve a GCS motor score of 6, and the Abbreviated Injury Scale Headscore.Another system for assessing TBI severity is the Simplified Motor Score (SMS). The SMS is a 3-point scaledeveloped to address the perceived limitations of the GCS, such as its complexity and poor interrater reliability.Table 3. Simplified Motor Score (Open Table in a new window)Score Best Motor Response0 Withdraws to pain or worse1 Localizes pain2 Obeys commandsA study by Thompson et al determined that in an out-of-hospital setting, the SMS was similar to the GCS score forpredicting TBI outcomes.[16]

Medical ComplicationsPosttraumatic seizuresPosttraumatic seizures (PTS) frequently occur after moderate or severe TBI. Seizures are usually general or partial,and absence seizures are uncommon. Seizures are classified according to the time elapsed after the initial injury:Immediate seizures occur in the first 24 hours. Early seizures occur in the first 2-7 days, and late seizures occur after 7days.The incidence of late PTS is in the range of 5-18.9%. Risk factors include chronic alcoholism, older age at the time ofinjury, and a history of seizure disorder. Approximately one half to two thirds of patients with these risk factors developlate PTS within the first year after injury.[17] If a patient with TBI has 1 PTS, his or her likelihood of having another isapproximately 50%.[18]

Temkin showed that prophylactic use of phenytoin is effective during the first week after a TBI.[19]However, the authorrecommended discontinuation after 1 week if no seizures develop because of its lack of effect in preventing late PTSand because of possible cognitive adverse effects.Although phenytoin maybe effective in preventing seizures in the first week after a TBI, at least 50% of patients withTBI have late seizure activity for which phenytoin may not be effective.

HydrocephalusHydrocephalus is characterized as communicating or noncommunicating on the basis of the causative obstruction.Noncommunicating hydrocephalus occurs secondary to an obstruction in the ventricular system before the point atwhich cerebrospinal fluid (CSF) exits the fourth ventricle. Communicating hydrocephalus is the most common formafter TBI and occurs when the obstruction is in the subarachnoid space.[20]

Patients with hydrocephalus can clinically present with nausea, vomiting, headache, papilledema, obtundation,dementia, ataxia, and/or urinary incontinence. The diagnosis is based on clinical suspicion, diagnostic imaging, andradio-isotope cisternography. Treatment usually consists of lumbar puncture or shunt placement.

Deep vein thrombosisDeep vein thrombosis (DVT) is common in persons with TBI, with an incidence as high as 54%.[21] In patients with TBI,risk factors for DVT include immobility, lower extremity fracture, paralysis, and disruption in coagulation and fibrinolysis.Complications of DVT include pulmonary embolism (PE), postthrombotic syndrome, and recurrence. Because DVTcan result in PE, it can be critical. Given the rapid decline in pulmonary function when a PE has completely occluded


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the pulmonary capillary system, sudden death may be the first clinical sign.[22]Other clinical signs of PE includeshortness of breath, chest pain, and pulmonary crackles; these are usually present with small emboli. However, clinicalsigns and symptoms are often absent in the patient with DVT. Therefore, a high index of suspicion and timely medicalintervention are of utmost importance.The most common modalities for detecting DVT are venous Doppler ultrasonography and contrast-enhancedvenography. Venography remains the criterion standard for diagnosing DVT. Noninvasive Doppler ultrasonography ismost commonly used because of its low risk of adverse effects compared with venography.[23]

Prophylaxis for DVT should be started as soon as possible. These measures include use of elastic compressionstockings, intermittent pneumatic compression, vena cava filters, warfarin, unfractionated heparin (UH), and/orlowmolecular weight heparin (LMWH). Mechanical methods of prophylaxis are generally used in patients with a highrisk of bleeding or in combination with anticoagulation.[23] The choice of prophylaxis should be patient specific andbased on his/her existing comorbidities.Treatment for DVT and/or PE in patients with TBI is similar to treatment for these conditions in the general population.Treatment generally consists of the administration of an immediate-acting anticoagulant (UH or LMWH), followed bychronic anticoagulation with warfarin (target international normalized ratio [INR], 2-3). Heparin or LMWH should becontinued until the desired INR is achieved and stable. The duration of anticoagulation is specific to the indication andthe patient.[24]Use of anticoagulation in the patient with TBI could increase the risk for intracerebral hemorrhage. Eachpatient should be evaluated for his/her risk of intracerebral hemorrhage and of falling.

Heterotopic ossificationHeterotopic ossification is described as ectopic bone formation in the soft tissue surrounding the joints. In TBI, theincidence of heterotopic ossification is 11-76%, with a 10-20% incidence of clinically significant heterotopicossification.[25]Heterotopic ossification generally causes joint pain and decreases range of motion (ROM). It is oftenassociated low-grade fever, peri-articular swelling, peri-articular warmth, and peri-articular erythema.In decreasing order of frequency, heterotopic ossification occurs in the hips, knees, elbows, shoulders, hands, andspine. Risk factors associated with the development of heterotopic ossification after TBI are a posttraumatic comalasting longer than 2 weeks, limb spasticity, and decreased mobility. The risk of heterotopic ossification is greatestduring the first 3-4 months after injury.[22]

The pathophysiology of heterotopic ossification remains unclear. However, inappropriate differentiation ofmesenchymal cells into osteoblasts is believed to be the basic defect. Autonomic dysregulation (due to increasedvascularity and venous hemostasis), humoral factors, and local inflammatory mediators contribute to the developmentof heterotopic ossification.Laboratory and radiologic data are critical in the diagnosis of heterotopic ossification. Although serum alkalinephosphatase levels and erythrocyte sedimentation rates are nonspecific markers, they are often elevated in the earlyphases of heterotopic ossification. Therefore, elevated levels might suggest additional evaluation.Three radiologic modes are useful for diagnosing heterotopic ossification: plain radiography, ultrasonography, andtriple-phase bone scanning. Triple-phase bone scanning reveals heterotopic ossification the earliest. Plainradiographic and ultrasonographic findings may lag behind results of bone scans because of lack of early calcificationin heterotopic ossification. Plain radiographic findings lag behind triple-phase bone scan results by 2-3 weeks.However, plain radiography can be used early to rule out an underlying fracture.The mainstay of preventing heterotopic ossification in patients with TBI is ROM exercise. The use of forceful ROM issomewhat controversial because it is thought to be a cause of heterotopic ossification, but data from human studieshave not demonstrated this mechanism.The prophylactic role of nonsteroidal anti-inflammatory drugs (NSAIDs), low-dose radiation, or bisphosphonatesremains unclear. NSAIDs and etidronate can help with pain management. The risks and benefits of these drugs inmanaging established heterotopic ossification should be assessed.Heterotopic ossification may result in functional impairment, and patients may require surgical excision. To minimizerisk of recurrence, surgical excision has traditionally been delayed 12-18 months to allow the heterotopic bone tomature. However, authors have questioned this delay.[25]

SpasticityTone is defined as resistance to stretch or movement across a joint during relaxation. Spasticity is defined as velocity-dependent increase in tone. Rigidity is also a function of tone, but it is defined as the nonvelocity-dependent increasein tone. These 3 terms are not interchangeable.


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In one inpatient rehabilitation unit, spasticity was found in an estimated 25% of patients with TBI.[26]

Spasticity is most often encountered in lesions of the upper motor neurons, whereas rigidity is most common indisorders of the basal ganglia. The morbidity associated with spasticity is variable, because in some people, spasticitymay assist in leg extension for walking or finger flexion for grasping. Prolonged low tone after TBI is generallypredictive of poor motor recovery.Guidelines for the treatment of spasticity are generally based on (1) any resulting limitation in function, (2) pain, (3)prevention of contracture, and (4) assistance with positioning.[26] First-line treatments for spasticity are correctpositioning of the involved body segment and ROM exercises. Second-line treatments include splinting, casting, andother modalities.Treatment varies according to whether the spasticity is generalized or local. Generalized spasticity is usually treatedsystemically. Dantrolene sodium is preferred in patients with TBI because of its lack of cognitive and sedative adverseeffects.Other drugs used to manage spasticity include baclofen, tizanidine, clonidine, and benzodiazepines. Their use may belimited because of their sedative and cognitive adverse effects. Local treatments for spasticity include chemicalneurolysis with phenol or alcohol injections and with botulinum toxin type A and type B injections.

GI and GU complicationsGI and GU complications remain among the most common sequelae in patients with TBI. Some of the most frequentGI complications are stress ulcers, dysphagia, bowel incontinence, and elevated levels on liver function tests.Underlying constipation and/or impaired communication and mobility are often the causes of bowel incontinence. Theuse of oral stool softeners, laxatives, and rectal suppositories may facilitate full bowel evacuation and improveincontinence.GU complications include urethral strictures, urinary tract infections, and urinary incontinence. An appropriate workup toevaluate GU symptoms and rule out infection is indicated. When the causes of urinary incontinence are impairedcommunication and mobility, a trial of a timed voiding is indicated to manage overflow incontinence. Patients are takento the bathroom and given the opportunity to void without instrumentation every 2 hours during the day and every 4hours overnight.If the patient is unable to void or cannot evacuate the urinary bladder to completion, intermittent straight catheterizationmay be necessary in the acute recovery period. Although not preferred, diapers and condom catheters may beneeded if urinary incontinence does not improve.Voiding dysfunction and upper urinary tract status were studied in 57 survivors of coma resulting from TBI. Directstatistical links were found between urge incontinence, detrusor overactivity, and poor neurologic functional outcome,as well as between detrusor overactivity and right hemisphere injuries, and between impaired detrusor contractility andleft hemisphere damages.[27]

Gait abnormalitiesMartini et al performed gait analysis on subjects with and without a remote concussion history, measuring velocity, steplength, stride width, and time in single-leg versus double-leg stance. They found that subjects with a remoteconcussion history showed slowed walking velocity, greater time in double-leg stance, and less time in single-legstance, speculating that the patients with concussion histories are trying to limit injury risk from falls. They suggest thatpatients with even remote concussion histories may have prolonged risk for fall injuries.[28]

See also the following related Medscape Reference topic:Post Head Injury Autonomic ComplicationsPost Head Injury Endocrine Complications

AgitationPosttraumatic agitation is common after TBI. Baguley and colleagues found that 25% of patients with TBI wereclassified as being aggressive during the follow-up periods in their 5-year study.[29] Furthermore, aggression wasconsistently associated with depression or young age at the time of injury.Corrigan developed a 14-item instrument, the Agitated Behavior Scale (ABS), to quantify levels of agitation after TBI(see image below).[30]Bogner and colleagues found the ABS a reliable instrument for measuring agitation in patientsfollowing TBI.[31]


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Agitated Behavior Scale, developed by John D Corrigan, PhD, ABPP, Professor, Department of Physical Medicine and Rehabilitation,The Ohio State University. Permission for publication granted by Dr. Corrigan.Before posttraumatic agitation is treated, other medical conditions should be considered. After TBI, the patient may beuncomfortable, and impaired recognition and an inability to communicate are often agitating factors. Pain is a common(but often overlooked) cause of posttraumatic agitation. Combined with a diminished ability to communicate and/or aninability to cope with pain, agitation is not surprising. Furthermore, clinicians should consider the possibility of infection,electrolyte imbalance, adverse effects of drugs, psychosis, and insomnia.Environmental modifications are usually the first treatment. Minimizing unnecessary stimuli and assisting with tools fororientation may help to reduce the onset of agitation. External stimuli, such as noisy rooms, bright lights, and frequentvisitors, should be minimized. Use of centrally acting drugs that may exacerbate agitation should be minimized.Physical restraints often exacerbate posttraumatic agitation and should not be used routinely. Restraints should beused only as a last resort to secure patient, staff, and visitor safety. However, the use of less restrictive restraints, suchas net-covered beds (eg, Vail beds), has become acceptable and popular in the treatment of the agitated patient with abrain injury.In addition to environmental and behavioral modifications, various drugs, such as high-dose beta blockers,anticonvulsants, and antidepressants (particularly selective serotonin re-uptake inhibitors [SSRIs]), have had somesuccess in the management of posttraumatic agitation.[32] Brooke and colleagues found that the intensity of agitationwas significantly lower in patients with TBI who were treated with propranolol than in subjects who were treated withplacebo.[33] In addition, amantadine has shown some usefulness in reducing posttraumatic agitation.[34, 35]Casestudies support the use of lamotrigine[36] or divalproex[37] to manage posttraumatic agitation.The use of antipsychotics to treat posttraumatic agitation is controversial. Their effects on cognition and recovery arepoorly studied. Antipsychotics may cause excessive drowsiness, exacerbate cognitive deficits, and inhibit neuronalrecovery. Stanislav suggested that select areas of cognition may improve after thioridazine and haloperidol arediscontinued.[38]

Symptoms Of TBILong-term physical, cognitive, and behavioral impairments are the factors that most commonly limit a patient'sre-integration into the community and his/her return to employment.In a study by Kraus and colleagues of 235 patients, the symptoms most commonly reported 6 months after mild TBIwere fatigue (43%), weakness (43%), memory deficits (40%), headache (36%), and dizziness (34%).[39]Otherinvestigators found similar complaints after mild TBI.[40, 41] The symptoms have collectively been referred to aspostconcussion syndrome. Kraus and co-authors found that approximately 83% of patients with mild TBI reported 1 ormore physical complaints at the end of their 6-month follow-up period.[39, 42]

InsomniaIn one study, patients with TBI reported higher rates of sleep changes than did sex-matched control subjects (80% vs23%).[20] The TBI group reported more nighttime awakenings and longer sleep-onset latency than did the other group.Increased levels of anxiety and depression were risk factors that may have partly accounted for increased complaintsof excessive daytime sleepiness.

Cognitive declineKhateb and colleagues found that patients with chronic TBI who were treated with donepezil had slight improvementsin neuropsychological test results, including in speed of processing, learning attention, and divided attention.[43]


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Posttraumatic headacheWalker and co-authors found that nearly 38% of patients with moderate or severe TBI had acute posttraumaticheadache, usually daily and most commonly in the frontal region.[44]Almost all of the patients who reportedposttraumatic headache at 6 months also reported symptoms at 12 months.Chronic posttraumatic headache is common, and the pathophysiology is not well understood. Tension-type headachesare the most common form, but exacerbations of migrainelike headaches are also frequent. Treatment ofposttraumatic headache is similar to that of primary headache if structural lesions or abnormalities are absent.[45]

Posttraumatic depressionMood disorders, particularly depression, are common sequelae of TBI. Major depression is found in about 40% ofpatients hospitalized for TBI.[46]Depression after TBI is further associated with cognitive decline,[47, 48] anxietydisorders, substance abuse, dysregulation of emotional expression, and aggressive outbursts.[49]Whitnall andcolleagues reported that persistent disability (5-7 y after TBI) was strongly associated with depression and anxiety, andthat it was more poorly associated with initial severity or persistent cognitive impairments.[50]

Dikmen and co-authors found that the following factors are predictive of posttraumatic depression: educational levelless than high school, unstable work history prior to injury, and alcohol abuse.[49]

Treatment options for posttraumatic depression include counseling, participation in support groups, andantidepressant medication. Early after TBI, a grief reaction is common, and this is better treated with supportivetherapies than with other approaches. If drugs are used, their profiles, including their adverse effects and interactions,must be carefully considered to prevent worsening sedation or cognitive impairment. Methylphenidate and sertralineare beneficial in treating posttraumatic depression.[51]

Methylphenidate is commonly used to treat patients with hypo-arousal, initiation, and attention problems associatedwith TBI. Methylphenidate may hasten recovery after TBI. The positive effects of methylphenidate are improved speedin processing and sustained attention.[52]By potentiating dopamine, amantadine may improve arousal, attention, andexecutive functions.[53]

Outcome MeasuresTools to effectively measure outcome are needed to quantify results.[54]Outcome measures can be used to assessthe effectiveness of different treatments.Three tools commonly used to measure outcome after TBI are the Functional Independence Measure (FIM),[55] theGlasgow Outcome Scale (GOS),[56] and the Disability Rating Scale (DRS).The FIM is one of the most widely used measures of function in rehabilitation (Table 3). It is an 18-item scale used toassess the patient's level of independence in mobility, self-care, and cognition. However, it may lack sensitivity inpatients with very low or very high levels of function. Therefore, the FIM may be an inadequate outcome measure forpatients at either extreme of TBI recovery.Table 4. Functional Independence Measure (Open Table in a new window)

Clinical AreaSelf-care A. Eating

B. GroomingC. BathingD. Dressing - upper bodyE. Dressing - lower bodyF. Toileting

Sphincter control G. Bladder managementH. Bowel management

Transfers I. Bed, chair, wheelchairJ. ToiletK. Tub, shower

Locomotion L. Walking, wheelchair


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M. StairsMotor subtotal score:

Communication N. ComprehensionO. Expression

Social interaction P. ExpressionQ. Problem solvingR. Memory

Cognitive subtotal score:TOTAL FIM SCORE:

SourceKeith et al, 1987.[55]

The GOS is a scoring system commonly used to rate outcomes after TBI (Table 4).[56]

Table 5. Glasgow Outcome Scale (Open Table in a new window)Score Rating Definition1 Dead Nonsurvival2 Persistent vegetative Minimal responsiveness3 Severe disability Conscious but disabled; dependent on others for daily support4 Moderate disability Disabled but independent; can work in sheltered setting5 Good recovery Resumption of normal life despite minor deficitsSourceJennett and Bond, 1975.[56]

The DRS (see the image below) is intended to accurately measure general functional changes over the course ofrecovery after TBI, where a score of 0 indicates no disability and 29 indicates an extreme vegetative state.[57] TheDRS includes 8 items, including the GCS score and disability and return-to-work measures.

Disability Rating Scale (DRS).

PrognosisDetermining the patient's prognosis after TBI remains difficult and complex. The heterogeneity of patients' premorbidhealth status, the natures and severities of injury, the intervals from injury to initial treatment, the acute interventions,and the differences in follow-up create difficulty in developing a simple and accurate scoring system.Brown and co-authors found the following variables to be predictive of outcome[58] :

Initial GCS scoreDuration of PTAAmnesia[59]SexAgeYears of education

Cuthbert et al investigated injury severity and sociobiological and socioeconomic factors to predict discharge location(home vs not to home) in adults with moderate to severe TBI. They found GCS and acute hospital length of stay to bethe most predictive in discharges to home versus not to home (ie, higher GSC and shorter LOS were more likely to be


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discharged to home). They also found that old age was associated with a decreased likelihood of discharge torehabilitation and more likely to be discharged to subacute rehabilitation.[60]

Bogner and colleagues found that substance abuse contributed to the prediction of life satisfaction and productivity,while violent etiology was not a significant contributor to prediction.[61]Corrigan and co-authors found that a lack ofpre-injury history of substance abuse and the possession, at the time of follow-up, of gainful employment wereassociated with higher life satisfaction 1-2 years after TBI.[62]An evaluation of the employment outcome in patientswith moderate to severe TBI found that patients with comorbid psychiatric symptoms and impaired cognitivefunctioning are at the highest risk of long-term unemployment.[63]

Three-month GOS scores are powerful independent predictors of long-term outcome after severe TBI.[64, 65]Davisand colleagues found that GCS scores in the field and on the patient's arrival in the emergency department are highlypredictive of mortality and of a need for neurosurgical care.[66]Davis's study also found that an increase in the GCSscore from the field to the emergency department is highly predictive of survival. Studies have shown that the level ofabnormality on brain computed tomography (CT) scans and the early loss of autoregulation of ICP are predictive of theoutcome.[67, 68, 69]

In a secondary analysis of data on 365 patients with moderate or severe TBI from a randomized trial, Badri et al foundthat average ICP in the first 48 hours of monitoring independently predicted mortality as well as a composite endpointof functional and neuropsychological outcome at 6 months. Average ICP, however, was not independently associatedwith neuropsychological functioning.[70] In patients with severe TBI due to acute subdural hematoma, TBI severity, ageand neurological status are the primary factors influencing outcomes, and nonoperative management is associatedwith a significantly increased mortality risk.[71]

Further research is needed to develop simple prognostic tools. Improved prognostic tools, if available, would assistclinicians in planning for patients' long-term care and needs.

Contributor Information and DisclosuresAuthorPercival H Pangilinan Jr, MD Assistant Professor, Department of Physical Medicine and Rehabilitation,University of Michigan Health SystemPercival H Pangilinan Jr, MD is a member of the following medical societies: American Academy of PhysicalMedicine and Rehabilitation and Association of Academic PhysiatristsDisclosure: Nothing to disclose.Coauthor(s)Brian M Kelly, DO Associate Professor, Department of Physical Medicine and Rehabilitation, University ofMichigan Medical School; Assistant Program Director, Residency Training Program, Consulting Staff, Service Chief6A, Inpatient Rehabilitation Services, University of Michigan Health SystemBrian M Kelly, DO is a member of the following medical societies: American Academy of Physical Medicine andRehabilitation, American Osteopathic Association, American Osteopathic College of Physical Medicine andRehabilitation, and Association of Academic PhysiatristsDisclosure: Nothing to disclose.Joseph E Hornyak IV, MD, PhD Associate Professor, Department of Physical Medicine and Rehabilitation,University of Michigan Medical School; Consulting Staff, Medical Director of Human Performance Laboratory,Department of Physical Medicine and Rehabilitation, University of Michigan Medical CenterJoseph E Hornyak IV, MD, PhD is a member of the following medical societies: American Academy of CerebralPalsy and Developmental Medicine, American Academy of Physical Medicine and Rehabilitation, American Collegeof Sports Medicine, and Association of Academic Physiatrists


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Disclosure: Nothing to disclose.Specialty Editor BoardEverett C Hills, MD, MS Assistant Professor of Physical Medicine and Rehabilitation, Assistant Professor ofOrthopaedics and Rehabilitation, Penn State Milton S Hershey Medical Center and Pennsylvania State UniversityCollege of MedicineEverett C Hills, MD, MS is a member of the following medical societies: American Academy of Disability EvaluatingPhysicians, American Academy of Physical Medicine and Rehabilitation, American College of PhysicianExecutives, American Congress of Rehabilitation Medicine, American Medical Association, American Society ofNeurorehabilitation, Association of Academic Physiatrists, and Pennsylvania Medical SocietyDisclosure: Nothing to disclose.Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center Collegeof Pharmacy; Editor-in-Chief, Medscape Drug ReferenceDisclosure: Medscape Salary EmploymentMichael T Andary, MD, MS Professor, Residency Program Director, Department of Physical Medicine andRehabilitation, Michigan State University College of Osteopathic MedicineMichael T Andary, MD, MS is a member of the following medical societies: American Academy of PhysicalMedicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, AmericanMedical Association, and Association of Academic PhysiatristsDisclosure: Allergan Honoraria Speaking and teachingKelly L Allen, MD Medical Director, MedevalsDisclosure: Nothing to disclose.Chief EditorDenise I Campagnolo, MD, MS Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, BarrowNeurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director,NARCOMS Project for Consortium of MS CentersDenise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, AmericanAssociation of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association ofAcademic Physiatrists, and Consortium of Multiple Sclerosis CentersDisclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching;Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator;Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds investigator; Novartisinvestigator; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research fundsinvestigator; Avanir Pharmaceuticals Grant/research funds investigator

ReferencesChambers J, Cohen SS, Hemminger L, et al. Mild traumatic brain injuries in low-risk trauma patients. JTrauma. Dec 1996;41(6):976-80. [Medline].

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