Traumatic Brain Injury




Abstract


Traumatic brain injuries are defined as an insult to the brain from external forces resulting in temporary or permanent impairment, functional disability, or psychosocial maladjustment. The World Health Organization now suggests that traumatic brain injury will soon be the third leading cause of death and disability in the world. This chapter reviews the associated demographics and pathophysiology of brain injury, identifying early and late sequelae. Medical complications are reviewed, with symptoms common to both early and late recovery discussed. Outlined are the essential elements of the physical examination including diagnostic studies, and assessment tools that may be of help to the practitioner. Reviewed are the treatment issues of the patient with brain injury including early stabilization, and intervention into common issues including arousal, attention, agitation, seizures, spasticity, and autonomic nervous system dysfunction. We then review a focus of the treatment team including that of physical therapy, occupational therapy, speech therapy, vocational rehabilitation, physicians, and the use of technology. Finally, we discuss surgery, potential disease complications, and potential complications of the treatment itself.




Keywords

Brain Injury, Closed Head Injury, Concussion, TBI

 


























Synonyms



  • Head injury



  • Acquired brain injury



  • Concussion



  • Diffuse axonal injury

ICD-10 Codes
S06.2X0-8 Diffuse traumatic brain injury (sixth digit will define the level of consciousness)
S06.2X9 Diffuse traumatic brain injury with loss of consciousness of unspecified duration
S06.300-389 Focal traumatic brain injury (fifth digit will define the location of injury, sixth digit will define the level of consciousness)
S06.309 Unspecified focal traumatic brain injury with loss of consciousness of unspecified duration
Add seventh character for episode of code; S—late effect




Definition


Traumatic brain injury (TBI) is an insult to the brain from an external physical force that results in temporary or permanent impairment, functional disability, or psychosocial maladjustment. In the United States, recent data estimated an annual incidence of 2.8 million TBI-related emergency department (ED) visits, hospitalizations, and deaths. This estimate is likely low, as the data do not include persons treated for TBI in other settings such as outpatient clinics and physicians’ offices nor those who served in the military. Current estimates from the World Health Organization suggest that TBI will be the third leading cause of death and disability by the year 2020. The financial burden of TBI has been estimated at more than US $76 billion per year.


Epidemiology and Pathophysiology


By age range, the incidence of ED visits, hospitalizations, and death secondary to TBI is greatest among those 75 years and older (2232 per 100,000), 0 to 4 years old (1591 per 100,000), and those 15 to 24 years old (1080 per 100,000). TBI occurs more frequently among males than females. By etiology, TBI most commonly results from falls, followed by being struck by or against an object, and then motor vehicle crashes. ED visits for TBI have recently been increasing despite a reduction in TBI due to motor vehicle accidents (MVAs). The age-adjusted rate of ED visits was higher in 2013 compared with 2007, with fall-related TBIs among persons aged ≥75 years accounting for 17.9% of the increase. Falls are the most likely cause of TBI among those 0 to 14 years of age and those greater than 75 years of age, while MVAs are the most common among those 15 to 44 years of age. These can be reduced through traffic law enforcement. These trends have consequences for the type of brain damage seen; contusion injury tends to be associated with falls, and diffuse injuries are more often seen in high-velocity traffic accidents.


The pathophysiologic process of TBI is usually divided into primary injury, which is the injury to the brain that results at the time of the insult, and secondary injury, which can be thought of as the summation of the biochemical or physiologic damage that develops during a period of hours, days, weeks, and perhaps months after the primary injury. The primary injury is sustained from external forces as a result of direct impact, rapid velocity changes, penetrating injuries, or blast injuries. The resulting injuries include contusion, hematomas, and diffuse axonal injuries (DAIs). DAI can best be thought of as a disorder of diffuse circuit disruption, which impairs excitatory and inhibitory networks. These are frequently associated with superimposed hypoxic or ischemic injury, often as a result of systemic insult. In patients with mild TBI, there is often a disruption of the sodium channels of the axons, which can result in a transient disruption in function and, with it, an increased state of vulnerability to additional trauma. Secondary injury may include impaired regulation of cerebral blood flow (CBF) and metabolism, and an ischemic-like response with accumulated lactic acid due to anaerobic metabolism, increased membrane permeability, and edema formation. Although many of the mechanisms of secondary TBI have yet to be identified, they are thought to include terminal membrane depolarization, excessive release of excitatory neurotransmitters, mitochondrial dysfunction, inflammatory responses, and disruption of calcium and sodium channels, resulting in an increase in intracellular concentration of free fatty acids and free radicals with progressive structural changes of biological membranes and DNA. To minimize the secondary effects of brain injury, the Brain Trauma Foundation has 28 evidence-based guidelines for treatment.




Symptoms


Symptoms may vary according to the severity of the injury and the stage of recovery. The patient’s history should include a detailed summary of the mechanism of injury, comorbid conditions, initial Glasgow Coma Scale score ( Table 163.1 ), length of the coma (if any), and length of post-traumatic amnesia. Glasgow Coma Scale scores, however, can be obscured by confounders such as concurrent spinal cord injury, sedation, intubation, or other related injuries. Extracranial injuries (such as extremity fractures, thoracic or abdominal traumas), which have been reported to occur in about 35% of the cases, are associated with a higher incidence of secondary brain injuries.



Table 163.1

The Glasgow Coma Scale


























































Patient Response Score
Eye Opening
Eyes open spontaneously 4
Eyes open when spoken to 3
Eyes open to painful stimuli 2
Eyes do not open 1
Motor
Follows commands 6
Makes localized movements to painful stimuli 5
Makes withdrawal movements to painful stimuli 4
Demonstrates flexor posturing to painful stimuli 3
Demonstrates extensor posturing to painful stimuli 2
No motor response to pain 1
Verbal
Oriented to place and date 5
Converses but is disoriented 4
Utters inappropriate words, though not conversing 3
Makes incomprehensible nonverbal sounds 2
Not vocalizing 1


Those with concussions (defined as “a clinical syndrome characterized by immediate and transient alteration in brain function, including alteration of mental status and level of consciousness, resulting from mechanical force or trauma”) most often complain of cognitive issues (difficulty thinking clearly, feeling slowed down, difficulty concentrating), physical issues (headache, altered vision, nausea and vomiting, dizziness, sensitivity to light or noise, balance problems, and feeling tired), emotional issues (irritability, sadness, emotional lability, anxiety), and sleep disturbances. Patients with severe injury and dramatically altered levels of arousal often can offer no subjective symptoms. After the acute phase of recovery, the clinician may expect those with moderate or severe TBIs to have symptoms including seizures, contractures, spasticity, altered vision, vertigo or dizziness, and altered sense of smell. These may be the result of cranial nerve injuries or of central processing dysfunction. Symptoms of dysautonomia, a disorder of the autonomic nervous system, may still be seen at outpatient follow-up. This syndrome is characterized by increased body temperatures, tachycardia, tachypnea, increased posturing or tone, and profuse sweating. Common late symptoms may include memory deficits, higher level executive dysfunction, headaches, difficulty with sleep-wake cycles, labile mood, depression, apathy, difficulty with attention, social disinhibition, sexual dysfunction, anxiety, impulsivity, fatigue, and difficulties with fine and gross motor control.




Physical Examination


A thorough neurologic examination, including a neuropsychological evaluation, is important to assess the consequences of a brain injury. The neurologic examination evaluates mental status, cranial nerve function, vision, hearing, and deep tendon and other reflexes. The examination should also evaluate muscle strength, tone, and coordination and assess gait or mobility in a wheelchair. It may be important to create a thorough neuropsychological profile with the assistance of a neuropsychologist. This should be done to determine both physical abilities and the cognitive and emotional issues that will affect the patient’s function. Cervical injury can be associated with TBI, especially in patients with a Glasgow Coma Scale score below 8, and may be central to some of the patient’s symptoms. This must be recognized early to accurately assess injury severity and to determine treatment course.




Functional Limitations


Motor


Patients may have difficulty with mobility and self-care as a result of isolated motor weakness or coordination of either the upper or the lower extremities. Safe mobility may also be impeded by poor cognition, including deficits with planning and poor impulse control.


Behavior


Individuals often experience subtle or dramatic personality changes that alter relationships with others. These may include problems with the initiation of responses, verbal or physical aggression, altered emotional control, social disinhibition, depression, apathy, decreased sense of self-worth, and altered sexual function.


Social


Patients often are unable to return to work at their previous level of function. As a consequence, they may suffer significant economic strain and may have difficulty with their relationships, including their marriage. Studies have failed, however, to consistently show a significantly higher rate of divorce among those married at the time of injury. Family members may be helpful in identifying issues of social isolation, depression, and anger.




Diagnostic Studies


Initial diagnostic studies can provide clues to the severity of the injury and will have prognostic implications. Independent prognostic factors for patient outcome in moderate to severe TBI include age, Glasgow Coma Scale motor scores, pupillary response, computed tomography characteristics, and the presence of a subarachnoid hemorrhage. Other prognostic factors include hypotension, hypoxia, eye and verbal components of the Glasgow Coma Scale, hyperglycemia, low platelet number, low hemoglobin concentration, and early CT findings.


Imaging Studies


The initial computed tomography scan has been shown to be useful as an outcome predictor with use of the Traumatic Coma Data Bank classification or the Rotterdam CT score. Previous studies and guidelines have recommended computed tomography scans for all TBI patients with a Glasgow Coma Scale score of 14 and of 15 in the presence of risk factors, such as emesis, advanced age, duration of amnesia, injury mechanism, neurologic deficits, or anticoagulation ( Table 163.2 ). More sophisticated testing has been introduced, including single-photon emission computed tomography, functional magnetic resonance imaging, and positron emission tomography, but for the most part, these are of little clinical use in assessing the functional limitations caused by the injury. In patients with otherwise normal findings on neuroimaging, diffusion tensor imaging is emerging as a potential diagnostic tool for mild brain injury, as it can detect white matter microstructure changes ( Fig. 163.1 ). Despite the potential of new imaging techniques, TBI remains primarily a clinical diagnosis.



Table 163.2

Risk Factors for Intracranial Complications

















Vomiting
Severe headaches
Age > 60 years
Coagulation disorder or anticoagulation
Trauma above the clavicle with clinical signs of skull fracture
Continued post-traumatic amnesia or retrograde amnesia longer than 30 min
Unclear mechanism of injury or intoxication with drug or alcohol



FIG. 163.1


Diffusion tensor imaging in traumatic brain injury: loss of white matter tract fibers after traumatic brain injury (right) compared with an age-matched control (left) .

From Maas AI, Menon DK. Traumatic brain injury: rethinking ideas and approaches. Lancet Neurol. 2012;11:12–13.


At the time of outpatient follow-up, it may be necessary to remind the patient and his or her caregivers of the extreme limitations of these diagnostic studies and to focus on that patient’s functional abilities as the more important measure of the extent of the injury. In general, follow-up radiologic examinations are useful tools only if the patient has excessively slow progress or has demonstrated a decline in function. These may be helpful in determining new or expanding lesions. Otherwise, these are generally of limited utility.


Biomarkers


The use of biomarkers to assess the magnitude of total brain injury and to localize brain injury is promising, though with little routine clinical use. These markers may prove to be useful in patients with mild TBI with otherwise normal imaging findings, as well as in patients whose injury severity cannot be accurately assessed because of confounders mentioned previously.


Important cognition-related biomarkers include acetylcholine, glutamate, dopamine, serotonin (5-HT), gamma-aminobutyric acid, substance P (SP), amyloid-β (Aβ), and neurotrophic protein S100B. These may soon be of clinical use as an adjunct to neuroimaging in the early assessment of primary and evolving damage in traumatic and ischemic brain injury.


Functional Assessment Tools


One of the best diagnostic tools is the Glasgow Coma Scale, which is used for the initial evaluation of the severity of the patient’s injury (see Table 163.1 ). A review of this initial score will help in the determination of the extent of the injury and thus with prognostication. Later, as a review of function in the outpatient setting, progress can be measured by the Disability Rating Scale. Post-traumatic amnesia is important for prognostication as well and can be assessed by the Galveston Orientation and Amnesia Test. For the current level of functional recovery to be characterized, the Rancho Los Amigos Scale is helpful in the assessment of the patient’s awareness and interaction with the environment.


Neuropsychological Testing


This battery of tests, performed by a neuropsychologist, is the best means of determining the full spectrum of cognitive, affective, and emotional function of the individual. This may be completed before discharge from inpatient rehabilitation and should be repeated when a change in function needs to be documented. This testing may provide the clinician with critical information needed to understand the ability of the patient to progress toward more independence or responsibility at home or at work. This also may be a critical assessment tool for the documentation of the injury for insurance and/or legal purposes.


Jul 6, 2019 | Posted by in PHYSICAL MEDICINE & REHABILITATION | Comments Off on Traumatic Brain Injury
Premium Wordpress Themes by UFO Themes