Moderate to Severe Brain Injury

CHAPTER 2

P. TYLER ROSKOS

LAUREN R. SCHWARZ

OVERVIEW

The Centers for Disease Control and Prevention (CDC) defines traumatic brain injury (TBI) as an injury to the head arising from blunt or penetrating trauma or from acceleration/deceleration forces resulting in one or more of the following: decreased level of consciousness, amnesia, objective neurological or neuropsychological abnormalities, skull fractures, diagnosed intracranial lesions, or head injury listed as a cause of death in the death certificate (Coronado, McGuire, Faul, Sugerman, & Pearson, 2013; National Center for Injury Prevention and Control, 2003; Thurman, Sniezek, Johnson, Greenspan, & Smith, 1995). TBI can result in multiple physical, cognitive, emotional/psychological, and social and functional symptoms and deficits. Injuries of greater severity (classified as moderate or severe TBI) tend to require more complex acute and postacute care, as well as result in greater long-term health care costs and morbidity (Draper & Ponsford, 2008; Finkelstein, Corso, & Miller, 2006).

As a resource for clinical professionals and trainees, the goal of this chapter is to provide a brief history of intervention for moderate and severe TBI, as well as a review of our current knowledge regarding the clinical features, intervention strategies, and prognosis for people with these injuries. We will also provide a case example of the theoretical and research-based concepts presented.

HISTORY

Early medical interventions for TBI were focused largely on acute injuries sustained on the battlefield in the context of warfare (Teasdale & Zitnay, 2013). It was not until the latter half of the 20th century and the development of the automobile, increased road traffic, and urban growth, that civilian TBI became more recognized. Most clinical care for TBI patients was within the domain of neurosurgery. The 1970s brought advances in medical technology, such as the computed tomography (CT) scanner (Ambrose, Gooding, & Uttley, 1976), that had a direct impact on the ability to evaluate and treat head injuries. Additionally, the Glasgow Coma Scale (GCS), which is still widely used today to assess injury severity, was developed by Graham Teasdale and Bryan Jennett in 1974. The 1980s and 1990s saw additional notable advancements in evaluation and intervention for acute head injury, including issues such as monitoring of intracranial pressure, use of neuroprotective pharmacological agents, and establishment of standard guidelines for clinical care. These advancements resulted in reduced mortality and improved outcomes from head injury (Teasdale & Zitnay, 2013).

Interdisciplinary brain injury rehabilitation programs began to develop during the 1940s during and after World War II, with the formal recognition of Physical Medicine and Rehabilitation as a medical specialty (Teasdale & Zitnay, 2013). Leaders in the field established early rehabilitation programs over several decades. Furthermore, the Vietnam War era resulted in improved legislation for individuals with disability, including support for community-based rehabilitation. During the 1980s, organizations focused on brain injury awareness, and specialized rehabilitation and advocacy also were established and grew (e.g., Brain Injury Association and the International Brain Injury Association). The TBI Model Systems programs were also established and funded by the National Institute of Disability and Rehabilitation Research (NIDRR), resulting in an increase in collaborative research involving clinical care and outcomes from TBI.

During the 1990s and early 2000s, there was an emphasis on demonstrating the effectiveness and efficacy of rehabilitation programs for TBI. This resulted in more rigorous scientific scrutiny of clinical strategies used by clinicians and the establishment of guidelines for acute care and rehabilitation for TBI (Neurotrauma Foundation, American Association of Neurological Surgeons). There was also increased emphasis on costs of care, lengths of rehabilitation stay, and insurance reimbursement issues during the early 2000s.

Currently, intervention for moderate and severe TBI can involve a complex continuum including the neurosurgical intensive care unit, shock trauma unit, a neurology or trauma floor, acute rehabilitation, nursing home, skilled nursing facility, long-term acute care, outpatient therapy, home health, day programs, residential rehabilitation and residential placement programs (Ivanhoe, Durand-Sanchez, & Spier, 2013). Rehabilitation programs often emphasize a multidisciplinary team approach to address the wide range of symptoms and problems that may develop over the course of acute and postacute rehabilitation care. The Functional Independence Measure (FIM) has also been established as the most widely used outcome measure in rehabilitation settings, and has been used as the gold standard to demonstrate the efficacy of rehabilitation programs for TBI patients across settings and providers (Granger, Cotter, Hamilton, & Fiedler, 1993; Granger, Divan, & Fiedler, 1995).

PATHOPHYSIOLOGY

The acute pathophysiology of moderate and severe TBI is typically viewed as a process involving both primary and secondary focal and diffuse brain injury that results from the initial blunt trauma event (Yokobori & Bullock, 2013). Acceleration and deceleration during blunt trauma can lead to both translational and rotational forces that impact the head, leading to brain injury (Viano, 2013). Additionally, there can be more chronic complications of TBI, resulting in potentially greater morbidity in these patients. These pathophysiological components of TBI are discussed in greater detail in the following subsections.

Primary Injury

Contusions are hemorrhages caused by acceleration–deceleration forces, leading to differential movement between brain and skull or brain matter at gray–white interfaces (Ponsford, Sloan, & Snow, 2013). Often referred to as “coup–contrecoup” injuries, contusions can be seen at the site of impact and at the opposite side of the impact (Gaetz, 2004). The bony skull protuberances located on the frontal bone, sphenoidal ridge, temporal bone, and the edges of the falces often result in contusive injury on the poles of the frontal and temporal lobes (Le & Gean, 2009). Contusions can lead to necrosis and apoptosis (i.e., cell death) owing to reduced supply of blood, oxygen, and glucose.

Tearing of blood vessels as a result of external impact to the head can cause bleeding inside of the skull (i.e., hematomas) and the formation of clots that can compress brain tissue (Gennarelli & Graham, 2005; Ponsford et al., 2013). Subdural hematoma (SDH) results from bleeding between the dura and arachnoid layers of the meninges, and subarachnoid hemorrhage (SAH) refers to bleeding between the arachnoid and pia layers. An intracerebral hematoma (ICH) forms within the brain parenchyma as a result of a tear in deep brain vasculature. Hematomas within the meninges or brain tissue can result in increased intracranial pressure, ischemic brain damage, and obstruction of the flow of cerebrospinal fluid, often requiring neurosurgical intervention.

Diffuse axonal injury (DAI), also known as “traumatic axonal injury” (TAI), is the primary mechanism of injury in a large number of moderate and severe TBIs, and can result in micropathological injury to axons in multiple brain regions (Gaetz, 2004; Meythaler, Peduzzi, Eleftheriou, & Novack, 2001). In DAI, deformation of brain tissue caused by acceleration–deceleration forces during blunt head trauma results in shearing, tearing, and twisting of neuronal axons, as well as local cell death and downstream denervation and wallerian degeneration (a process that occurs when nerve fiber is damaged, in which the part of the axon separated from the neuron’s cell body degenerates) over time following injury (Ponsford et al., 2013). Petechial hemorrhage, as well as SAH and intraparenchymal hemorrhage (IPH), can also be associated with DAI because of rotational forces, causing further white matter damage (Povlishock & Katz, 2005). The most common sites of DAI include the subcortical white matter, corpus callosum, gray–white matter junctions, and brain stem.

Secondary Injury

Increased intracranial pressure (ICP) is a common consequence of intracranial injury that can result in reduced cerebral perfusion pressure and blood flow (Gennarelli & Graham, 2005). Disruption in blood flow due to increased ICP can cause diffuse ischemic injury, increases in inflammation, and metabolic dysfunction, leading to neuronal death. Additionally, increased ICP can lead to shifting of brain tissues and/or downward herniation. If not addressed, herniation can result in compression of the brain stem, leading to respiratory arrest and eventual death (Gennarelli & Graham, 2005). Decompressive craniotomy is the most common neurosurgical intervention involving removal of a portion of the skull to allow for reduction in pressure to reverse the process of herniation. Other secondary factors that can lead to greater brain injury include hypoxia, cerebral edema, and infection (i.e., meningitis or cerebral abscess; Long, 2013; Ponsford et al., 2013).

Chronic Complications of TBI

Individuals with moderate or severe TBI are also at risk for a number of neurological complications that can affect functioning and recovery. Hydrocephalus can be caused by disruptions in the flow of cerebrospinal fluid (CSF) in the ventricles (noncommunicating), or can result from blood within the subarachnoid space, preventing proper absorption of CSF (communicating). This can be difficult to diagnose using radiological studies alone because of the presence of ex vacuo dilation of the ventricles in many moderate and severe TBI patients (Long, 2013). Aspects of clinical presentation (e.g., behavioral or cognitive worsening) can be diagnostically useful in determining patients who need treatment, which usually involves neurosurgical placement of a ventriculoperitoneal shunt.

Posttraumatic epilepsy is also a common chronic complication of moderate and severe TBI. When looking over a 5-year period, Annegers, Hauser, Coan, and Rocca (1998) found the following prevalence rates of seizures following TBI: 0.5% for mild injuries, 1.2% for moderate injuries, and 10% for severe injuries. Many patients are treated prophylactically with antiepileptic medications within the first week postinjury to reduce early-onset seizures, but this has not been shown to reduce the risk of late-onset seizure disorder (Ponsford et al., 2013).

ETIOLOGY

The etiology of TBI typically involves an external force (i.e., injury mechanism) that causes injury to the brain. Falls are the most common injury mechanism of TBI overall, especially in children and older adults (Coronado et al., 2013). The CDC reported that from 2006 to 2010, falls accounted for 40% of all TBIs that led to emergency department (ED) visits, hospitalizations, or deaths. Unintentional blunt trauma and motor vehicle accidents (MVAs) account for 15% and 14%, respectively, of all TBI-associated ED encounters (Centers for Disease Control and Prevention [CDC], 2016). MVAs are the most common mechanism of injury in teenagers and younger adults (ages 15–34; Coronado et al., 2013).

Sports-related TBI has also emerged as a public health issue in the United States, with an estimated 1.6 to 3.8 million sports-related TBIs per year. However, moderate or severe TBI cases are a minority of sports-related injuries, with most patients being treated in the emergency department and released (Coronado et al., 2013). TBI has also been a critical health issue in military combat veterans, moderate and severe TBI representing about 10% of cases from 2000 to 2015 (Center for Defense and Veterans Brain Injury, 2015).

EPIDEMIOLOGY

Despite the growing awareness of TBI as a public health concern, the determination of incidence rates has been complicated by factors such as accuracy of diagnosis, cost related to these medical workups, and timeliness of diagnosis (Korley, Kelen, Jones, & Diaz-Arrastia, 2015). To further complicate the matter, many individuals with mild injuries never come to the attention of medical providers. Much of what is known about prevalence rates comes from investigations of EDs. The CDC (2016) reported that in 2010, TBI accounted for 2.5 million ED visits, hospitalizations, or deaths. Specifically, TBI resulted in more than 280,000 hospitalizations and was related to the cause of death in more than 50,000 individuals. In the last decade, the number of individuals seen in the ED for TBI increased by 70%, hospitalization rate increased by 11%, but the rate of death fell by 7%.

Of those individuals hospitalized with TBI, discharge rates vary by severity of injury. More specifically, most patients with mild and moderate injuries are discharged from the hospital and return home; however, those with more severe injuries may be sent from the acute setting into a skilled care facility. The discharge diagnoses include, for example, intracranial injury with and without fracture, concussion, intracranial hemorrhage, contusion, and so forth. Despite discharge, TBI can be a lifelong injury for patients. It is estimated that 80,000 to 90,000 individuals have new onset of disability due to TBI each year, with more than 1 million individuals disabled secondary to TBI (Thurman, 1999; Thurman, Alverson, Dunn, Guerrero, & Sniezek, 1999). It is estimated that the annual economic cost of TBI in the United States is at least $76 billion (Coronado et al., 2013).

Certain members of the population have been found to be at greater risk for experiencing TBI. More specifically, age has been identified as a risk factor, with those between 15 and 24 years old and those over the age of 65 having the highest rates of brain injury (Kraus & Chu, 2005; Sosin, Sniezek, & Thurman, 1996). Children under the age of 5 also have a higher reported incidence rate of TBI (Jager, Weiss, Coben, & Pepe, 2000). An additional risk factor appears to be gender, with males having a 1.6 to 2.8 times greater rate compared with females (Kraus & Chu, 2005). Individuals with a prior history of TBI are also at a 2.8 to 3.0 times increased risk of additional injury (Salcido & Costich, 1992). Several investigations have found higher rates of TBI in individuals of lower socioeconomic status (SES) (Roebuck-Spencer & Sherer, 2008). Finally, alcohol consumption has also been implicated as a risk factor for TBI (Smith & Kraus, 1988).

CLINICAL PRESENTATION AND DIAGNOSTIC CONSIDERATIONS

Severity of Injury

In the evaluation of patients with TBI, severity of injury is one of the most important factors to consider, as this has implications for predictions concerning symptoms, course of recovery, and, ultimately, outcome. Several sources of information are often used to determine severity, including duration of loss of consciousness (LOC)/coma, time to follow commands, length of posttraumatic amnesia (PTA), GCS (Teasdale & Jennett, 1974), and the presence of neuroimaging findings. Concerning LOC, Lezak and colleagues developed a classification index for severity as follows: ≤20 minutes = mild, ≤6 hours = moderate, and greater than 6 hours = severe (Lezak, 1995; Lezak, Howieson, Loring, Hannay, & Fischer, 2004). PTA refers to the time period during which individuals are responsive, but disoriented, confused, and unable to form new memories. Russell and Smith (1961) developed the most frequently used classification ranges, which are as follows: less than 1 hour = mild, 1 to 24 hours = moderate, 1 to 7 days = severe, and greater than 7 days = very severe. This time period can be assessed by asking patients their first and last memory surrounding the injury or more formal measures of orientation such as the Orientation Log (Jackson, Novack, & Dowler, 1998) and the Galveston Orientation and Amnesia Scale (GOAT) (Levin, O’Donnell, & Grossman, 1979). The GCS is tabulated by assessing patients’ eye opening, motor movements, and verbal communication. Scores range from 3 to 15; higher numbers are associated with greater levels of functioning. GCS classification ranges are as follows: 13 to 15 = mild, 9 to 12 = moderate, 6 to 8 = severe, and 3 to 5 = very severe. Numerous studies have investigated the distributions of severity of injury. This data has varied significantly according to the severity parameters utilized (Roebuck-Spencer & Sherer, 2008). In general, about 80% of injuries are mild in nature, whereas 10% are moderate, and 10% are severe.

Typical Cognitive Deficits

The deficits patients experience acutely following injury depend largely on severity of injury. In the case of mild TBI (mTBI), typical acute deficits include slowed speed of thought processes, reduced attention span, and memory inefficiency. In a meta-analysis, Schretlen and Shapiro (2003) found that 96% of mTBI patients were asymptomatic at 3 months. Although there is some variability in recovery rate after mTBI, the overall consensus is that barring any complicating factors, individuals who suffer mTBI typically make a good recovery. In contrast, the severity and pattern of deficits in patients with moderate to severe TBI are quite variable and depend not only upon the injury itself, but also on factors such as premorbid level of functioning. In general, patients with moderate to severe TBI often experience deficits in attention, expressive language, speed of processing, memory, and reasoning skills (Roebuck-Spencer & Sherer, 2008).

Physical and Emotional Symptoms

Physical symptoms are commonly associated with TBI. Typical symptoms include headache, dizziness, double vision, light sensitivity (i.e., photophobia), smell and taste changes, and motoric slowing and incoordination. Other motor-related symptoms can arise and are typically associated with brain bleeds/contusions and include dysarthria, dysphagia, imbalance, spasticity, and hemiparesis. Sleep quality is also an area of concern; about 67% of TBI patients have some form of sleep disturbance (including hypersomnia or insomnia) (Kempf, Werth, Kaiser, Bassetti, & Baumann, 2010).

Neurobehavioral symptoms are also quite common in patients with moderate to severe TBI. Oftentimes, patients and family members report these symptoms to be the most distressing. Symptoms can include depression, fatigue, anxiety, irritability, and personality change (Roebuck-Spencer & Sherer, 2008). Impaired awareness of deficits is common in patients with moderate to severe TBI.

Course of Recovery

Patients who have suffered moderate to severe TBIs typically experience recovery in stages. However, there is a significant amount of interindividual variability in progression of recovery. TBI is often associated with impairment in the level of alertness/consciousness. On the severe end of the spectrum, coma represents a time in which patients are completely nonresponsive. Level of alertness/coma is often the first state to improve. It is rare for patients who recover from coma to remain in a persistent vegetative status (<1%, Jiang, Gao, Li, Yu, & Zhu, 2002). Once alertness has improved, individuals may be in a period of confusion. During this time, individuals may have marked impairments in cognition, as mentioned previously. This period is typically referred to as “PTA.” The skills of orientation, attention, expressive language, memory, and executive functioning typically recover in the order in which they were listed. The research has been mixed with regard to duration of time for cognitive recovery. Some studies have cited up to 18 months (Levin, 1995); however, more recent investigations have indicated recovery can occur significantly beyond that time frame. With respect to motoric recovery, Walker and Pickett (2007) found that in general, motoric improvements in severely brain-injured patients plateaued at 12 months and that over one third of them continued to manifest impairment at 2 years.

Complication Factors in Recovery

There are certain patient characteristics that have been associated with less than optimal injury recovery. One uncontrollable factor is age. Being over the age of 65 at the time of injury is associated with higher TBI-related mortality and morbidity (Gomez et al., 2000). History of experiencing more than one TBI, even if they are mild in nature, has a tendency to be related to poorer outcome. Other factors related to psychiatric status have been linked with complicating TBI recovery. Alcohol abuse, in particular, has been linked with less than optimal recovery. The development of conditions such as depression, anxiety, and posttraumatic stress disorder (PTSD) has also been linked to suboptimal or prolonged recovery in brain-injured patients. Thus, treatment for TBI must ensure that all aspects of patients are being treated, which include appropriate referrals for mental health interventions.

Only gold members can continue reading. Log In or Register to continue