You are in: eMedicine Specialties > Physical Medicine and Rehabilitation > TRAUMATIC BRAIN INJURY Classification and Complications of Traumatic Brain InjuryArticle Last Updated: Apr 2, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: Percival H Pangilinan Jr, MD, Clinical Instructor and Consulting Staff, Department of Physical Medicine and Rehabilitation, University of Michigan Health System Percival H Pangilinan, Jr, is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists Coauthor(s): Brian M Kelly, DO, Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Michigan Medical School; Assistant Program Director, Residency Training Program, Consulting Staff, Service Chief 6A, Inpatient Rehabilitation Services, University of Michigan Health System; Joseph E Hornyak IV, MD, PhD, Assistant 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 Center; David E Smith, MD, Staff Physician, Department of Physical Medicine and Rehabilitation, JFK Rehabilitation Hospital Editors: Everett C Hills, MD, MS, Medical Director, Penn State Hershey Rehabilitation Hospital, Assistant Professor of Orthopaedics and Rehabilitation, Assistant Professor of Neurology, Penn State Milton S. Hershey Medical Center and Penn State University College of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Michael T Andary, MD, MS, Residency Program Director, Professor, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine; Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center; Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St. Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers, Phoenix Author and Editor Disclosure Synonyms and related keywords: traumatic brain injury, TBI, head injury, brain injury, acquired brain injury, concussion, mild traumatic brain injury, mild TBI, closed head injury, diffuse axonal injury, DAI, intracranial pressure, ICP, scalp injury, skull fracture, skull surface contusions, hypoxic-ischemic damage, meningitis, brain vascular injury, posttraumatic amnesia, PTA, posttraumatic seizure, PTS, hydrocephalus, deep venous thrombosis, DVT, heterotopic ossification, HO, spasticity, postconcussion syndrome, posttraumatic agitation, insomnia, posttraumatic headache, cognitive decline, posttraumatic depression EPIDEMIOLOGYSection 2 of 11
  Traumatic brain injury (TBI), also known as acquired brain injury, head injury, or brain injury, causes substantial disability and mortality. It occurs when a sudden trauma damages the brain and disrupts normal brain function. TBI may have profound physical, psychological, cognitive, emotional, and social effects. The diagnosis of mild TBI appears to be vastly 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, the following annual statistics apply in the United States2:
The following groups are at particular risk for TBI2:
A TBI is caused by an excessive force, blow, or penetrating injury to the head. The leading causes of TBI are as follows 2:
Mortality rates after brain injury are highest in people with a severe TBI. In the first year after a TBI, people who survive are more likely to die from seizures, septicemia, pneumonia, digestive conditions, and all external causes of injury than are other people of similar age, sex, and race.3 However, the mortality rate after severe TBI has decreased since the late 20th century.4 In one study, researchers estimated that the economic burden of TBI in the United States was approximately $37.8 billion in 1985.5 This estimate included $4.5 billion in direct expenditures for hospital care, extended care, and other medical care and services; $20.6 billion in work-related losses and disability; and $12.7 billion in lost income from premature death. PATHOPHYSIOLOGYSection 3 of 11
Classification as primary or secondary injuryTBI may be divided into primary injury and secondary injury. Primary injury is induced by mechanical force and occurs at 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 injury The 2 main mechanisms that cause primary injury are contact (eg, an object striking the head or the brain striking the inside of the skull) and acceleration-deceleration. Primary injury due to contact may result in injury to the scalp, fracture to the skull, and surface contusions. Primary injury due to acceleration-deceleration results from unrestricted movement of the head and leads to shear, tensile, and compressive strains. These forces can cause intracranial hematoma, 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, the inferior aspects of the frontal lobes, the cortex above and below the operculum of the sylvian fissures, and the lateral and inferior aspects of the temporal lobes. Intracranial hematoma is the most common cause of death and clinical deterioration after TBI. Hematomas are categorized as follows6:
Diffuse axonal injury (DAI) is one of the most common and important pathologic features of TBI. It constitutes mostly microscopic damage, and it is often not visible on imaging studies. The main mechanical force that causes DAI is rotational acceleration of the brain, resulting in unrestricted head movement. Rotational acceleration produces shearing and tensile forces, and axons can be pulled apart at the microscopic level. Microscopic evaluation of the brain tissue often shows numerous swollen and disconnected axons. Rapid stretching of axons is thought to damage the axonal cytoskeleton and, therefore, disrupt normal neuron function.8 Secondary injury Secondary injury may occur hours or even days after the inciting traumatic event. Injury may result from impairment or local 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 a cascade involving intracellular calcium and sodium. Resultant calcium and sodium overload may contribute to cellular destruction. Excessive release of excitatory amino acids, such as glutamate and aspartate, exacerbates failure of the ion 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 to cell damage.9 Clinical conditions associated with the risk of a decreased CBF are arterial hypotension, hypoxemia, intracranial hemorrhage and malignant brain edema, and hyperthermia.9 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 contusions and are generally be caused by contact. Diffuse injuries include DAI, hypoxic-ischemic damage, meningitis, and vascular injury and are usually caused by acceleration-deceleration forces. These 2 forms of injury are commonly found together. MEASURES OF SEVERITYSection 4 of 11
The classification of TBIs plays an important role in determining the patient's treatment, rehabilitation potential, and prognosis. Glasgow Coma Scale The most common classification system for TBI severity is based on the Glasgow Coma Scale (GCS) score determined at the time of injury. The GCS is a 3- to 15-point scale used to assess a patient's level of consciousness and level of neurologic functioning.10, 11 It consists of 3 sections, each of which is scored: best motor response, best verbal response, and eye opening (Table 1). A total score of 3-8 for the 3 sections indicates severe TBI, a score of 9-12 indicates moderate TBI, and a score of 13-15 indicates mild TBI. Table 1. Glasgow Coma Scale
Source—Teasdale and Jennett, 1974.11 Note—NA = not applicable. *The total of the motor, verbal, and eye-opening scores (range, 3-15) indicates the severity of a TBI, as follows: 3-8 is severe TBI, 9-12 is moderate TBI, and 13-15 is mild TBI. Loss of consciousness The 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
Source—Greenwald et al, 2003.12 Other classifications of severity As early as 1932, Russell introduced the concept of posttraumatic amnesia (PTA) and later defined it as the time elapsed from injury to the moment when patients can demonstrate continuous memory of what is happening around them.13 Lack of accurate records may make this system difficult to use retrospectively. Zafonte found that the duration of PTA (as measured by using the Galveston Orientation and Amnesia Test) appeared to be a significant predictor of functional 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 score of 15, the number of days that are needed to achieve a GCS motor score of 6, and the Abbreviated Injury Scale Head score. MEDICAL COMPLICATIONSSection 5 of 11
Posttraumatic seizures Posttraumatic 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 7 days. The incidence of late PTS is in the range of 5-18.9%. Risk factors include chronic alcoholism, older age at the time of injury, and a history of seizure disorder. Approximately one half to two thirds of patients with these risk factors develop late PTS within the first year after injury.16 If a patient with TBI has 1 PTS, his or her likelihood of having another is approximately 50%.17 Temkin showed that prophylactic use of phenytoin is effective during the first week after a TBI.18 However, the author recommended discontinuation after 1 week if no seizures develop because of its lack of effect in preventing late PTS and 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 with TBI have late seizure activity for which phenytoin may not be effective. Hydrocephalus 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 at which cerebrospinal fluid (CSF) exits the fourth ventricle. Communicating hydrocephalus is the most common form after TBI and occurs when the obstruction is in the subarachnoid space.19 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, and radio-isotope cisternography. Treatment usually consists of lumbar puncture or shunt placement. Deep vein thrombosis Deep vein thrombosis (DVT) is common in persons with TBI, with an incidence as high as 54%.20 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 DVT can result in PE, it can be critical. Given the rapid decline in pulmonary function when a PE has completely occluded the pulmonary capillary system, sudden death may be the first clinical sign.21 Other clinical signs of PE include shortness of breath, chest pain, and pulmonary crackles; these are usually present with small emboli. However, clinical signs and symptoms are often absent in the patient with DVT. Therefore, a high index of suspicion and timely medical intervention are of utmost importance. The most common modalities for detecting DVT are venous Doppler ultrasonography and contrast-enhanced venography. Venography remains the criterion standard for diagnosing DVT. Noninvasive Doppler ultrasonography is most commonly used because of its low risk of adverse effects compared with venography.22 Prophylaxis for DVT should be started as soon as possible. These measures include use of elastic compression stockings, intermittent pneumatic compression, vena cava filters, warfarin, unfractionated heparin (UH), and/or low–molecular weight heparin (LMWH). Mechanical methods of prophylaxis are generally used in patients with a high risk of bleeding or in combination with anticoagulation.22 The choice of prophylaxis should be patient specific and based 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 by chronic anticoagulation with warfarin (target international normalized ratio [INR], 2-3). Heparin or LMWH should be continued until the desired INR is achieved and stable. The duration of anticoagulation is specific to the indication and the patient.23 Use of anticoagulation in the patient with TBI could increase the risk for intracerebral hemorrhage. Each patient should be evaluated for his/her risk of intracerebral hemorrhage and of falling. Heterotopic ossification Heterotopic ossification is described as ectopic bone formation in the soft tissue surrounding the joints. In TBI, the incidence of heterotopic ossification is 11-76%, with a 10-20% incidence of clinically significant heterotopic ossification.24 Heterotopic ossification generally causes joint pain and decreases range of motion (ROM). It is often associated 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, and spine. Risk factors associated with the development of heterotopic ossification after TBI are a posttraumatic coma lasting longer than 2 weeks, limb spasticity, and decreased mobility. The risk of heterotopic ossification is greatest during the first 3-4 months after injury.21 The pathophysiology of heterotopic ossification remains unclear. However, inappropriate differentiation of mesenchymal cells into osteoblasts is believed to be the basic defect. Autonomic dysregulation (due to increased vascularity and venous hemostasis), humoral factors, and local inflammatory mediators contribute to the development of heterotopic ossification. Laboratory and radiologic data are critical in the diagnosis of heterotopic ossification. Although serum alkaline phosphatase levels and erythrocyte sedimentation rates are nonspecific markers, they are often elevated in the early phases of heterotopic ossification. Therefore, elevated levels might suggest additional evaluation. Three radiologic modes are useful for diagnosing heterotopic ossification: plain radiography, ultrasonography, and triple-phase bone scanning. Triple-phase bone scanning reveals heterotopic ossification the earliest. Plain radiographic and ultrasonographic findings may lag behind results of bone scans because of lack of early calcification in 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 is somewhat controversial because it is thought to be a cause of heterotopic ossification, but data from human studies have not demonstrated this mechanism. The prophylactic role of nonsteroidal anti-inflammatory drugs (NSAIDs), low-dose radiation, or bisphosphonates remains unclear. NSAIDs and etidronate can help with pain management. The risks and benefits of these drugs in managing established heterotopic ossification should be assessed. Heterotopic ossification may result in functional impairment, and patients may require surgical excision. To minimize risk of recurrence, surgical excision has traditionally been delayed 12-18 months to allow the heterotopic bone to mature. However, authors have questioned this delay.24 Spasticity Tone 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 non–velocity-dependent increase in tone. These 3 terms are not interchangeable. In one inpatient rehabilitation unit, spasticity was found in an estimated 25% of patients with TBI.25 Spasticity is most often encountered in lesions of the upper motor neurons, whereas rigidity is most common in disorders of the basal ganglia. The morbidity associated with spasticity is variable, because in some people, spasticity may assist in leg extension for walking or finger flexion for grasping. Prolonged low tone after TBI is generally predictive 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.25 First-line treatments for spasticity are correct positioning of the involved body segment and ROM exercises. Second-line treatments include splinting, casting, and other modalities. Treatment varies according to whether the spasticity is generalized or local. Generalized spasticity is usually treated systemically. Dantrolene sodium is preferred in patients with TBI because of its lack of cognitive and sedative adverse effects. Other drugs used to manage spasticity include baclofen, tizanidine, clonidine, and benzodiazepines. Their use may be limited because of their sedative and cognitive adverse effects. Local treatments for spasticity include chemical neurolysis with phenol or alcohol injections and with botulinum toxin type A and type B injections. GI and GU complications remain among the most common sequelae in patients with TBI. Some of the most frequent GI 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. The use of oral stool softeners, laxatives, and rectal suppositories may facilitate full bowel evacuation and improve incontinence. GU complications include urethral strictures, urinary tract infections, and urinary incontinence. An appropriate workup to evaluate GU symptoms and rule out infection is indicated. When the causes of urinary incontinence are impaired communication and mobility, a trial of a timed voiding is indicated to manage overflow incontinence. Patients are taken to the bathroom and given the opportunity to void without instrumentation every 2 hours during the day and every 4 hours overnight. AGITATIONSection 6 of 11
Posttraumatic agitation is common after TBI. Baguley and colleagues found that 25% of patients with TBI were classified as being aggressive during the follow-up periods in their 5-year study.26 Furthermore, aggression was consistently 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 (Image 2).27 Bogner and colleagues found the ABS a reliable instrument for measuring agitation in patients following TBI.28 Before posttraumatic agitation is treated, other medical conditions should be considered. After TBI, the patient may be uncomfortable, 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 an inability 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 for orientation may help to reduce the onset of agitation. External stimuli, such as noisy rooms, bright lights, and frequent visitors, 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 be used only as a last resort to secure patient, staff, and visitor safety. However, the use of less restrictive restraints, such as net-covered beds (eg, Vail beds), has become acceptable and popular in the treatment of the agitated patient with a brain 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 some success in the management of posttraumatic agitation.29 Brooke and colleagues found that the intensity of agitation was significantly lower in patients with TBI who were treated with propranolol than in subjects who were treated with placebo.30 In addition, amantadine has shown some usefulness in reducing posttraumatic agitation.31, 32 Case studies support the use of lamotrigine33 or divalproex34 to manage posttraumatic agitation. The use of antipsychotics to treat posttraumatic agitation is controversial. Their effects on cognition and recovery are poorly studied. Antipsychotics may cause excessive drowsiness, exacerbate cognitive deficits, and inhibit neuronal recovery. Stanislav suggested that select areas of cognition may improve after thioridazine and haloperidol are discontinued.35 SYMPTOMS OF TBISection 7 of 11
Long-term physical, cognitive, and behavioral impairments are the factors that most commonly limit a patient's re-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 TBI were fatigue (43%), weakness (43%), memory deficits (40%), headache (36%), and dizziness (34%).36 Other investigators found similar complaints after mild TBI.37, 38 The symptoms have collectively been referred to as postconcussion syndrome. Kraus and co-authors found that approximately 83% of patients with mild TBI reported 1 or more physical complaints at the end of their 6-month follow-up period.36, 39 Insomnia In one study, patients with TBI reported higher rates of sleep changes than did sex-matched control subjects (80% vs 23%).19 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 complaints of excessive daytime sleepiness. Cognitive decline Khateb and colleagues found that patients with chronic TBI who were treated with donepezil had slight improvements in neuropsychological test results, including in speed of processing, learning attention, and divided attention.40 Posttraumatic headache Walker and co-authors found that nearly 38% of patients with moderate or severe TBI had acute posttraumatic headache, usually daily and most commonly in the frontal region.41 Almost all of the patients who reported posttraumatic headache at 6 months also reported symptoms at 12 months. Chronic posttraumatic headache is common, and the pathophysiology is not well understood. Tension-type headaches are the most common form, but exacerbations of migrainelike headaches are also frequent. Treatment of posttraumatic headache is similar to that of primary headache if structural lesions or abnormalities are absent.42 Posttraumatic depression Mood disorders, particularly depression, are common sequelae of TBI. Major depression is found in about 40% of patients hospitalized for TBI.43 Depression after TBI is further associated with cognitive decline,44, 45 anxiety disorders, substance abuse, dysregulation of emotional expression, and aggressive outbursts.46 Whitnall and colleagues reported that persistent disability (5-7 y after TBI) was strongly associated with depression and anxiety, and that it was more poorly associated with initial severity or persistent cognitive impairments.47 Dikmen and co-authors found that the following factors are predictive of posttraumatic depression: educational level less than high school, unstable work history prior to injury, and alcohol abuse.46 Treatment options for posttraumatic depression include counseling, participation in support groups, and antidepressant medication. Early after TBI, a grief reaction is common, and this is better treated with supportive therapies 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 sertraline are beneficial in treating posttraumatic depression.48 Methylphenidate is commonly used to treat patients with hypo-arousal, initiation, and attention problems associated with TBI. Methylphenidate may hasten recovery after TBI. The positive effects of methylphenidate are improved speed in processing and sustained attention.49 By potentiating dopamine, amantadine may improve arousal, attention, and executive functions.50 OUTCOME MEASURESSection 8 of 11
Tools to effectively measure outcome are needed to quantify results.51 Outcome measures can be used to assess the effectiveness of different treatments. Three tools commonly used to measure outcome after TBI are the Functional Independence Measure (FIM),52 the Glasgow Outcome Scale (GOS),53 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 to assess the patient's level of independence in mobility, self-care, and cognition. However, it may lack sensitivity in patients with very low or very high levels of function. Therefore, the FIM may be an inadequate outcome measure for patients at either extreme of TBI recovery. Table 3. Functional Independence Measure
Source—Keith et al, 1987.52 The GOS is a scoring system commonly used to rate outcomes after TBI (Table 4).53 Table 4. Glasgow Outcome Scale
Source—Jennett and Bond, 1975.53 The DRS is intended to accurately measure general functional changes over the course of recovery after TBI, where a score of 0 indicates no disability and 29 indicates an extreme vegetative state.54 The DRS includes 8 items, including the GCS score and disability and return-to-work measures (see Image 1). PROGNOSISSection 9 of 11
Determining the patient's prognosis after TBI remains difficult and complex. The heterogeneity of patients' premorbid health 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 outcome55:
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.57 Corrigan and co-authors found that a lack of pre-injury history of substance abuse and the possession, at the time of follow-up, of gainful employment were associated with higher life satisfaction 1-2 years after TBI.58 Further research is needed to develop simple prognostic tools. Improved prognostic tools, if available, would assist clinicians in planning for patients' long-term care and needs. MULTIMEDIASection 10 of 11
REFERENCESSection 11 of 11
Classification and Complications of Traumatic Brain Injury excerpt Article Last Updated: Apr 2, 2008 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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