* The views expressed herein are solely the views of the authors and do not necessarily represent those of Uniformed Services University of the Health Sciences, the Department of Defense (DoD), or the U.S. government.
Psychological stress is a normal human emotion associated with any disease. Most individuals confronting a diagnosis of a new disease are able to understand, accept, and move forward. Their ability to do this requires personal inner resources, as well as the support and understanding of their physicians, families, friends, and society. Musculoskeletal injuries often create a gamut of anxiety and fears related to future function and ability to remain active in everyday life. Among the many concerns are disabilities secondary to loss of a limb and unrepairable musculoskeletal injury, disfigurement secondary to the musculoskeletal injury, distress over finances and the ability to return to work, concerns about sexual function, and the ability to return to recreational activities. Patients frequently recover from the musculoskeletal injury uneventfully, but may never recover from the psychological comorbidity. Clinicians and researchers have considered psychological and physical injuries as distinct entities, but there is considerable evidence, both from military and civilian populations, that recovery from physical injuries is dramatically and adversely influenced by the presence of a variety of psychological and social comorbidities including depression, posttraumatic stress disorder (PTSD), or other psychiatric conditions.
It has become increasingly clear that as orthopaedic surgeons we must find a way to address the psychosocial needs of the patient and family so that we can do a better job of preventing a permanent disability and returning an individual to a fully functional member of society. Learning to actively seek out the concerns of our patients and families and validating and normalizing the common emotions associated with musculoskeletal injury creates a healthier psychological and social environment to assist recovery. Levin describes his daughter’s fear of being able to ski again after major musculoskeletal trauma. The fear, which was evident in his daughter’s mood, was only identified by inquiring why she appeared concerned. She expressed a fear that she would never be able to ski again and her mood immediately improved when it was predicted that she would definitely be able to ski. Active involvement of a patient’s family and friends during and after the hospitalization fills in the imperative psychosocial support that can only be supplied by an individual’s “loved ones,” and the orthopaedic surgeon should both encourage this involvement and guide the family in how they can be supportive.
The orthopaedic surgeon needs to be aware of numerous psychological and social sequelae associated with musculoskeletal injury, be able to recognize the symptoms and identify patients and family members in need of help from a professional mental health provider. This chapter will review our present understanding of the psychosocial comorbidities that are associated with musculoskeletal trauma and how these disorders can prevent a successful functional recovery from trauma. We will review the present state of our understanding of these common psychological comorbidities and strategies to treat these conditions, with particular attention paid to the role of the orthopaedic surgeon.
Biomedical Versus Biopsychosocial Model of Medicine
The biomedical model of disease is based on a generally accepted belief among both patients and physicians that symptomatology (pain, general malaise, fever, etc.) is related to an identifiable chemical, physiologic, or structural abnormality that may or may not be correctable. Initially, when a patient presents with acute orthopaedic trauma, this is a relatively straightforward exercise. The patient has a grade IIIB open tibia fracture and we are going to “cure” him or her by placing an intramedullary rod in his or her tibia and performing a gastrocnemius rotation flap and a split-thickness skin graft (STSG). Unfortunately, we have learned from the Lower Extremity Assessment Project (LEAP) and other studies, that individuals with seemingly similar musculoskeletal injuries can have very disparate recoveries. We see the potential for disparate recovery among individuals with both severe as well as less severe injuries.
This observed dichotomy of successful treatment of an individual’s disease (fracture) and recovery led Engel to the introduction of the biopsychosocial model and practice of medicine. Engel believed that the biomedical model failed to recognize each patient’s individuality and humanity. He observed that a patient’s personality (individuality) along with the patient’s social support structure dramatically affected recovery. We frequently discuss this philosophy when we acknowledge that the practice of medicine is “art not science.” Clearly, science and scientific discovery comprise a major component in our dramatic successes in caring for the multiply injured patient. Despite this success, the failure to recognize human emotion and individuality can have a devastating effect on a person’s recovery.
In the discussion that follows, we will focus on posttraumatic stress and depression, two common conditions that are associated with the aftermath of physical trauma. It is important to keep in mind, however, that most patients will not be diagnosed with either of these conditions, even in the face of significant physical injuries. However, studies have shown that even subclinical symptoms of emotional stress and anxiety, if not adequately addressed, can impact recovery. We will also review our rapidly expanding understanding of both mild traumatic brain injury (mTBI) and more extensive traumatic brain injury (TBI), which often accompany skeletal injury, especially in the military. It is important for the orthopaedic surgeon to understand how TBI can impact the functional recovery of their patients.
Anxiety Disorders and Posttraumatic Stress
Acute anxiety symptoms are common following a physical injury and acute stress disorder (ASD) is among the first forms of psychological pathology diagnosable postinjury. It is characterized by a sense of numbing or detachment, restlessness, anxiety, irritability, problems focusing or concentrating, flashbacks, and sleep disturbance. ASD is typically considered a short-term response to injury, with symptoms lasting between 2 and 30 days. A recent review of the literature found that signs and symptoms of ASD occurred in 23% to 45% of patents following physical trauma.
The anxiety disorder spectrum includes generalized anxiety disorder (GAD), panic disorder with and without agoraphobia, PTSD, obsessive-compulsive disorder (OCD), social anxiety disorder, and specific phobias. Of these, GAD, panic disorder, and PTSD are most likely to be related to physical injury. Overall, anxiety disorders are perhaps even more common than depression, and total direct and indirect costs are similar to those associated with depression.
Generalized Anxiety Disorder and Panic Disorder
GAD has a prevalence of 4% to 6%. The disorder features excessive anxiety and worry about a variety of events or activities over at least a 6-month period; difficulty exercising control over worrying; several symptoms associated with the anxiety, such as fatigue, irritability, restlessness, sleep disturbance, and difficulty concentrating; functional impairment; and the symptoms are not explained by the presence of another axis I disorder, another medical condition, or medication. GAD can be easily screened for, either by asking, “Are you bothered by nerves?,” which had 100% sensitivity and 59% specificity in a study of primary care patients, or with the two-item Generalized Anxiety Disorder scale (GAD-2). The GAD-2 had a sensitivity of 86% and specificity of 83% when using a cutoff score of 3, faring about as well as a GAD seven-item scale. Increasing its utility to the primary care physician, the GAD-2 is also effective at identifying other anxiety disorders: Using a cutoff of 2, its sensitivity was 91% for panic, 85% for social anxiety, 86% for PTSD, and 86% for any anxiety disorder. The GAD-2 was recently combined with the two highly sensitive screening questions for depression regarding anhedonia and feeling down, depressed, or hopeless. The composite instrument, the four-item Patient Health Questionnaire (PHQ-4), was validated in more than 2000 primary care patients, and demonstrated a strong correlation with functional status, disability days, and health care utilization ( Table 29-1 ).
|During the past month, have you been bothered a lot by:|
Panic disorder can be one of the most frustrating of all medical conditions, with the average patient having been seen by many physicians and having had extensive testing including repeated “rule outs” for myocardial infarctions, Holter monitors, and invasive assessments, such as cardiac catheterization and esophagogastroduodenoscopy. In fact, panic disorder is associated with the highest utilization rates of medical services of all mental health problems. However, on identification of the correct diagnosis and initiation of effective treatment, these patients are often most amenable to successful treatment. Panic disorder is characterized by recurrent, unexpected panic attacks, which feature the abrupt onset of numerous somatic symptoms such as palpitations, sweating, tremulousness, dyspnea, chest pain, nausea, dizziness, and numbness. Symptoms typically peak within 10 minutes of onset and attacks usually have duration from 15 to 60 minutes. While as many as 30% of Americans may experience a panic attack during their lifetime, the prevalence of panic disorder is only 1% to 2%, as its diagnosis also requires that one or more of the attacks be followed by at least a month of persistent worry about having another attack, about the implications of the attack or its consequences, or a significant change in behavior related to the attacks. Up to half of those with panic disorder also have agoraphobia, characterized by a fear of being in places from which escape might be difficult (e.g., in crowds, on a train or plane, on a bridge or in a tunnel). Individuals with agoraphobia either avoid such situations, or endure them with marked distress, even experiencing symptoms of panic.
Comorbid medical and/or psychiatric conditions are present in most patients with GAD. Panic disorder frequently coexists with major depression, GAD, PTSD, and/or other psychiatric disorders. GAD and panic disorders should be considered as primary diagnoses in the initial consideration of differential diagnoses, but the history and physical examination should also include consideration of hyperthyroidism, pheochromocytoma, Cushing syndrome, insulinoma, anemia, asthma or vocal cord dyskinesia, and cardiac conditions such as angina, mitral valve prolapse and atrial fibrillation or another arrhythmia, which all can mimic anxiety and panic disorders. Accordingly, symptoms that should be asked about, and carefully reviewed when present, include weight loss, heat intolerance, diaphoresis, headaches, lightheadedness, chest pain, palpitations, and dyspnea. Caffeine intake, as well as ingestion of drugs of abuse such as cocaine or amphetamines, should be assessed. Key physical examination elements include the vital signs, eye examination including an assessment of extrinsic ocular muscles and for exophthalmos, thyroid examination with a check for a bruit, cardiac and pulmonary examination, and assessment of the hair and skin. Laboratory testing need not be extensive—it should be guided by the findings on history and physical—but a complete blood count, serum chemistry panel, thyroid function tests, urinalysis, and electrocardiogram are prudent. Additional studies should not be routine, but may be necessary to rule out differential diagnoses depending on the presenting signs and symptoms.
Effective therapies are available for both GAD and panic disorder. Cognitive behavioral therapy (CBT) is the best evidenced nonpharmacologic therapy for these conditions, supported by many randomized controlled trials and several meta-analyses. Several recent studies provide evidence that relatively brief courses of CBT, or even self-help CBT, is effective for GAD and panic disorder. CBT seems to have a more durable effect, with lower relapse rates than pharmacologic therapy, and use of CBT in patients who failed pharmacologic therapy also showed significant efficacy. However, there is good evidence that selective serotonin reuptake inhibitors (SSRIs) as well as venlafaxine are far superior to placebo in the treatment of both GAD and panic disorder, while pregabalin is also effective for GAD, and corresponding recommendations were recently made by an expert panel. Among the anxiety spectrum disorders, there is stronger evidence that the combination of CBT and pharmacotherapy is superior to either alone for panic disorder, although there has been more recent evidence to suggest this may be a worthwhile approach for GAD as well. Second-line therapies have been shown to have some utility but all have drawbacks, including tricyclic antidepressants such as imipramine (risk of fatal cardiac arrhythmias in overdose, as well as anticholinergic side effects), benzodiazepines (dependence and tolerance issues), and azaspirones such as buspirone (less compelling evidence, and relatively delayed onset of action).
Posttraumatic Stress Disorder (PTSD)
PTSD is unique among the anxiety disorders because it has a clear precipitant—exposure to a traumatic event, such as an industrial injury, motor vehicle or recreational accident, war, disaster, or an assault that involves an actual or threatened death or serious injury to one’s self or others. PTSD is sometimes, but not always, preceded by acute stress disorder (ASD). ASD is characterized by symptoms that occur within 30 days of a traumatic experience, and when present, is not surprisingly associated with a higher risk of subsequent PTSD, with one study indicating that 78% of persons with ASD following a motor vehicle crash (MVC) met criteria for PTSD within 6 months. The criteria for PTSD include disabling symptoms for at least 1 month in three different categories: reexperiencing the trauma (e.g., flashbacks, intrusive memories); avoiding thoughts, activities, people associated with the trauma (i.e., feeling emotionally “numb” about the traumatic event); and hyperarousal (e.g., irritability, difficulty concentrating, insomnia). PTSD was codified in the aftermath of the Vietnam War, but the symptoms and associated functional impairment it represents have been known for centuries. Homer depicts symptoms of this disorder in his account of Achilles in The Iliad, and hundreds of reports have appeared in the medical literature from the U.S. Civil War, both World Wars, and numerous other national and international conflicts. Most recently, PTSD has been well documented after the terrorist attacks of September 11, 2001, Hurricane Katrina, and the wars in Iraq and Afghanistan.
Although a majority of the general population has experienced trauma sufficient to induce PTSD, most of the exposed are resilient, so that the overall likelihood of developing PTSD after a traumatic event is estimated at 9% to 25%. Community surveys identify a 2% to 5% point prevalence and an 8% to 12% lifetime prevalence for PTSD. PTSD was documented in 39% of patients referred by their primary care providers for mental health services based on suspicion of depression or anxiety, but like most psychological disorders, PTSD often goes undiagnosed in primary care, and such patients often do not see mental health specialists.
The gold standard instrument for the diagnosis of PTSD is the Clinician-Administered PTSD Scale (CAPS), but it is 17 pages long and must be administered by a professional, rendering it impractical for use in primary care. The PTSD Checklist (PCL) is a 17-item screen, which can be self-administered (see Appendix, available online ) and has had moderately good sensitivity and specificity, but a newer, 4-item screen, the Primary Care PTSD (PC-PTSD), has fared at least as well in some studies, using a cutoff of two or more positive replies ( Table 29-2 ).
|Have you ever had any experience that was so frightening, horrible, or upsetting, that in the past month you:|
|Over the Last 2 Weeks , How Often Have You Been Bothered by Any of the Following Problems? |
(Use “✓’” to Indicate Your Answer)
|Not at All||Several Days||More than Half the Days||Nearly Every Day|
|F or office coding 0 + ____ + ____ + ____ |
=Total Score: ____
|If you checked off any problems, how difficult have these problems made it for you to do your work, take care of things at home, or get along with other people?|
|Not difficult at all||Somewhat difficult||Very difficult||Extremely difficult|
There have been several reports describing the prevalence of PTSD among persons who suffered physical injuries, in both military and civilian trauma populations. Rates vary considerably because of differences in how PTSD is measured, when it is measured, and the population being studied. Among civilians, rates of PTSD following an MVC range from 6% to 54% (based on 51 prevalence estimates across 35 studies). The National Study on the Costs and Outcomes of Trauma (NSCOT) examined 1-year outcomes in 2707 trauma patients admitted to 69 hospitals across 12 states and found that 20.7% of patients with at least one injury with an Abbreviated Injury Scale (AIS) score of 3 or greater (associated with any injury mechanism) screened positive for PTSD (based on the PCL). Relatively few studies have focused specifically on the prevalence of PTSD associated with musculoskeletal trauma. In one of the more comprehensive of these studies, Starr reported that 51% of 580 orthopaedic trauma patients admitted to two level I trauma centers met the criteria for the diagnosis of PTSD based on the revised Civilian Mississippi Scale for PTSD (measured at an average of 12 months postinjury). The severity of injury does not appear to predict the development of PTSD. However, the type of trauma (e.g., physical assault vs. unintentional injury) as well as prior exposure to previous traumatic events has been shown to correlate with a higher likelihood of PTSD. Also, women are generally at higher risk of developing PTSD than men.
Recent data underscored the high prevalence of PTSD associated with combat duty in Iraq and Afghanistan. Hoge and colleagues used the military version of the PCL to estimate the prevalence of PTSD among U.S. Army infantry soldiers 3 to 4 months following their return from a year-long deployment to Iraq. They found that 36.2% and 16.2% of injured soldiers with and without mTBI, respectively screened positive for PTSD. Using the same criteria as Hoge, Doukas and colleagues found that 17.9% of 324 service members who sustained a limb-threatening injury to the lower extremity screened positive for PTSD at an average of 38.6 months postinjury. Rates of PTSD among service members and veterans are generally higher among those deployed versus not deployed, although there is evidence suggesting that exposure to specific combat experiences, rather than deployment alone, is more predictive of the development of PTSD symptoms.
The risk of developing PTSD after physical injury in the combat setting is controversial. Some have argued that physical injury decreases the risk of PTSD because the physical injuries provide a focus for anxious energy and garners greater sympathy from others (social and psychological support). Physical injury often leads to evacuation from the battlefield and removes the injured from further threat or traumatization. Studies that have found relatively low rates of PTSD in wounded service members have buttressed this perspective. However, the presence of a significant physical injury is also an incessant reminder of the life-threatening circumstances that the service members are exposed to and this physical reminder of their prior circumstances may be a constant reminder leading to PTSD. Pathophysiologically, Koren and coworkers hypothesized three potential mechanisms to explain why physical injury might increase the likelihood of PTSD. First, physical injury frequently increases activation of the hypothalamic-pituitary-adrenal (HPA) axis and related pathways. The HPA axis is altered in many PTSD patients, with studies documenting evidence such as lower baseline cortisol level, although results have been decidedly mixed with regard to cortisol and PTSD. Second, physical injury may activate other key mediators that contribute to the development of PTSD, in that physical injury might stimulate additional pathways other than those initially stimulated by the trauma. Substance P, endogenous opioids, and proinflammatory cytokines all might contribute to the impact of physical trauma on psychological well-being, but further research is needed to explore this possibility. Third, injury might interfere with the body’s attempts to recover from the trauma-induced alterations in such pathways. For example, physical injuries and PTSD-related nightmares interfere with sleep, thereby impairing both physical and psychological recovery.
Perception of a high degree of threat associated with the injury was an independent predictor of PTSD symptoms. A study of civilian MVC victims conducted diagnostic interviews at baseline as well as 1, 6, and 12 months later to assess independent predictors of the development of PTSD symptoms. In this study, those with PTSD symptoms at 1 month actually had less severe injuries than those without PTSD symptoms. Somewhat surprisingly, there was no relationship between injury severity and PTSD at 6 and 12 months; however, coping style was a key modulator of the physical injury–PTSD link. The strongest independent predictor of higher rates of PTSD symptoms was a coping style that relied on wishful thinking. Those engaging in wishful thinking tend to wish for a miracle, to want to change the circumstances or how they felt, or to pray that the situation would just go away. The researchers hypothesized that such individuals might get lost in such dreaming or fantasizing instead of developing more positive coping mechanisms. Coping mechanisms warrant study in other settings and with combat veterans to see if these findings can be replicated.
Traumatic Brain Injury and Posttraumatic Stress Disorder
Many skeletal trauma patients also sustain a concomitant injury to the brain, although precise rates of co-occurrence are largely unknown. TBI can range from severe brain injuries with prolonged coma to a mild injury with no loss of consciousness and transient dazed feeling or confusion in the aftermath of a blow to the head. Differentiation of TBI severity remains a matter of considerable debate, but the DoD considers mTBI to include those with no more than 30 minutes loss of consciousness (LOC), moderate TBI including those with more than 30 minutes LOC but no more than 24 hours, and severe TBI limited to those with more than 24 hours LOC. Some reports claim more than 280,000 service members have experienced TBI in Iraq or Afghanistan, at least 80% of which are believed to be mild. TBI is frequently labeled the “signature injury” of Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF). The clinical presentations of mTBI and PTSD are often indistinguishable from each other, featuring impaired sleep, decreased concentration, and other symptoms. There is also evidence that these two disorders have some shared pathophysiology. The frequent co-occurrence of mTBI and PTSD, as well as the overlap in symptoms, has resulted in a growing controversy regarding the relationship between the two disorders and the implications for diagnosis and treatment, especially among veterans returning from OEF and OIF. More research is clearly needed to better understand how mTBI impacts recovery from PTSD and how mTBI might influence the response to various therapies for PTSD.
A self-completed mail survey of 2235 U.S. military personnel returning from Iraq and Afghanistan reported that 12% had a history consistent with mTBI, while 11% were positive for PTSD. Even when overlapping symptoms were removed from the PTSD score, PTSD was more closely related to residual TBI symptoms than anything else. A similar pattern is found in survivors of MVCs, indicating that postconcussive symptoms of mTBI may be mediated by the interaction of neurologic and psychological factors. Another study of MVC-related TBI found that 14% met criteria for ASD in the immediate aftermath of the TBI, and most of them went on to develop chronic PTSD, suggesting it was the psychological rather than physical impact that led to chronic symptoms. Mild TBI spectrum is particularly difficult to define, as some of the persistent symptoms that have been attributed to mTBI, including headaches, dizziness, memory problems, irritability, and sleep problems, are often reported by those with PTSD and other psychological conditions, and those with persistent symptoms after TBI usually seem to meet criteria for a mood or anxiety disorder.
The diagnosis of mTBI is a clinical diagnosis that should be made by a neurologist or medical practitioner experienced with TBI. Evaluation should include a detailed history, physical and neurologic examination and, most importantly, an assessment of cognitive function. The decision to obtain neuroimaging is based on the level of suspicion of skull fracture or intracranial hemorrhage. Clinically available neuroimaging (computed tomography [CT] or magnetic resonance imaging [MRI]) is not adequate to rule out mTBI, which is a clinical diagnosis. If a patient has persistent altered mental status, LOC, abnormal Glasgow Coma Scale (GCS) score, focal neurologic deficit(s), or is clinically deteriorating, then neuroimaging should be obtained.
There is serious concern that reliance on self-reporting of symptoms to establish a diagnosis of mTBI is problematic and thus unreliable. This is both expected and obvious. After all, by definition, these patients are brain injured with alteration of consciousness and memory dysfunction. This is especially true of patients who suffer other severe injuries such as concomitant skeletal trauma. A recent report reviewed the reliability of mTBI diagnosis based on self-reported history of aberration of consciousness in patients suffering complex injuries requiring medical evacuation from the war theater. Patients diagnosed with mTBI had normal neuroimaging, higher Injury Severity Scale (ISS) scores, and longer lengths of stay than those without mTBI. Patients with higher ISS scores and longer lengths of stay are more likely at the time of injury to require pain medication and suffer from hypoxia, hypotension, metabolic derangement, and other conditions that could affect awareness and consciousness. As these disorders can alter consciousness in the absence of TBI, their impact on the diagnostic criteria in patients with severe injuries, especially extremity trauma, cannot be ruled out, which renders the TBI diagnosis unreliable. The paradoxical finding that further supports this conclusion is that patients who reported LOC actually had a lower incidence of abnormalities on neuroimaging.
Findings from studies conducted at Walter Reed National Military Medical Center, have led to similar conclusions. In these investigations, self-report of feeling dazed or confused at the time of injury captures large numbers of individuals who experience PTSD and depression related to blast exposure regardless of whether there is any physical injury or PTSD. This is true also in civilian clinical practice. A study of hospitalized civilian trauma victims that compared 90 patients initially diagnosed with mTBI to 85 non–brain-injured trauma patients found identical rates of postconcussional syndrome (PCS) in both groups. These results suggest no relationship between the diagnosis of mTBI and subsequent PCS symptomatology; moreover, the strongest predictor of PCS was in fact a prior mood or anxiety disorder, with an odds ratio of 5.76.
Although many patients will recover fully following mTBI, some may develop postconcussional disorder (PCD) or PCS. These have persistent symptoms analogous to psychological disorders. PCD was initially codified in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) as an area requiring further research, with insufficient data to fully support it as a diagnostic entity. PCD criteria require the history of a head trauma, followed by the onset of at least three of the following symptoms, which were not present prior to the trauma and have persisted at least 3 months: fatigue, headache, sleep disturbance, dizziness, irritability, anxiety or depression, personality changes, or apathy. By comparison, the World Health Organization’s (WHO) International Classification of Diseases, Tenth Edition (ICD-10) includes criteria for PCS that are less restrictive, only requiring a history of TBI and three or more of the following eight symptoms: (1) headache, (2) dizziness, (3) fatigue, (4) irritability, (5) insomnia, (6) difficulty with concentration, (7) memory problems, and (8) intolerance of stress, emotion, or alcohol. Because PCD criteria require that the head trauma cause significant cerebral concussion, along with quantifiable impairment in memory or attention, it is not surprising that a study directly comparing the two sets of criteria in mTBI found that the ICD-10 criteria were met three times more frequently. However, neither set of criteria is ready for clinical use without further research. In fact, WHO acknowledges in the description of PCS that
These symptoms may be accompanied by feelings of depression or anxiety, resulting from some loss of self-esteem and fear of permanent brain damage. Such feelings enhance the original symptoms and a vicious circle results. Some patients become hypochondriacal, embark on a search for diagnosis and cure, and may adopt a permanent sick role. The etiology of these symptoms is not always clear, and both organic and psychological factors have been proposed to account for them. The nosological status of this condition is thus somewhat uncertain. There is little doubt, however, that this syndrome is common and distressing to the patient. (p. 67)
Perhaps as a result, most researchers continue to simply refer to the overall, albeit ill-defined, category of TBI, rather than using either PCS or PCD.
As the diagnosis of mTBI based on self-report is problematic, there is a broad effort to employ point-of-care screening tools. For these to be effective, it must first be recognized that most TBI patients are typically unaware that they are injured and thus do not seek medical attention. For this reason, it is incumbent on colleagues, leaders, coaches, and sideline officials to have heightened sensitivity that an individual may be at risk of having suffered an mTBI or concussion and to then institute screening, sometimes in the face of protestations by the victim that he or she is uninjured. There are a number of available point-of-injury clinical screening tools, such as the Standardized Assessment of Concussion (SAC) and Sports Concussion Assessment Tool, version 3 (SCAT3). The military uses the Defense and Veterans Brain Injury Center’s (DVBIC) Military Acute Concussion Evaluation (MACE). Embedded in the MACE is the SAC. The MACE collects history and symptoms and uses the SAC to test four cognitive domains: orientation, immediate recall, concentration, and memory. By regulation through the DoD Directive-Type Memorandum (DTM) 09-033, which is a general order that affects all service members, the MACE is administered to any service member to be at risk of having suffered an mTBI. “At risk” is defined as involvement in a vehicle blast event, collision, or rollover, presence within 50 meters of a blast (inside or outside of a vehicle), a direct blow to the head, or witnessed LOC. If screening is positive, the victim is referred to an advanced medical provider for further evaluation and diagnosis.
Moderate to severe TBI is a life-threatening medical condition. Point-of-injury care is focused on the “ABCs” of airway, breathing, and circulation. A GCS score determination should be made. In the field, care focuses on maintaining oxygen saturation higher than 92%, partial pressure of oxygen (PO 2 ) higher than 60 mm Hg, partial pressure of carbon dioxide (PCO 2 ) at 40 mm Hg, and systolic blood pressure higher than 90 mm Hg. Hyperventilation is reserved for those patients who are exhibiting clinical signs of cerebral herniation. Rapid transport to the nearest level 1 trauma center with neurosurgical and neurology critical care is essential. There, care is primarily dictated by neurology specialists if there is isolated TBI or with the general trauma surgery service if there are also complex injuries, including skeletal.
There is an elevated risk of developing depression or other psychiatric disorders among moderate to severe TBI survivors similar to that of other serious medical conditions, such as stroke or myocardial infarction. Several studies demonstrate that at least one-quarter to one-half of those with TBI have major depression. However, moderate to severe TBI may, at least initially, provide some “protection” against the development of PTSD by obscuring the memory of the traumatic event. Further evaluation is necessary to better delineate the relationship between the severity of TBI and the risk of PTSD. In addition, it is important to emphasize the need for close attention to, and repeated formal assessment for, the potential evolution of PTSD symptoms as rehabilitation progresses and memory improves in individuals with moderate to severe TBI. A combination of serial neuropsychological testing, along with the use of validated instruments such as CAPS for PTSD, and Beck Depression Inventory or PHQ for depression, is advisable to best sort out improvement in TBI and potential onset of psychological disorders.
TBI and PTSD commonly occur together. Explosive blast patients who experience significant persistent and recalcitrant symptoms should have a thorough evaluation for PTSD and other psychological sequelae. This may be particularly beneficial to the individual patient, because there are specific treatments for PTSD, depression, and related conditions. Hoge and colleagues identified a significant association between mTBI and psychiatric symptoms, including PTSD in more than 40% of those who had LOC. These investigators noted that the high rates of physical symptoms reported by soldiers could be attributed to PTSD and depression. When these conditions were included in the analyses, there was no direct relationship between mTBI and physical health problems except for headache. It should be noted that the diagnosis for mTBI in this study was based on self-reporting of alteration of consciousness.
Magnetic resonance spectroscopy (MRS) may be better than traditional MRI for identifying mTBI and differentiating it from PTSD. A study by Hetherington and colleagues of veterans exposed to explosive blast and suffering persistent memory impairment associated with mTBI revealed decreased N-acetylaspartate (NAA)/choline (Ch) and NAA/creatinine (Cr) ratios in the anterior hippocampus when compared to patients exposed to blast but did not have these impairments. The hippocampus in affected TBI patients was also reduced in size. When compared to patients with PTSD, TBI patients had anterior hippocampus metabolic ratios that were significantly lower. PTSD patients exposed to blast had no difference in their anterior hippocampus NAA : Ch and NAA : Cr ratios when compared to blast-exposed patients who did not have PTSD. The metabolic ratios in the anterior hippocampus were also not different between blast patients with PTSD and PTSD patients who had no blast exposure. Furthermore, these metabolic ratios did not vary with patients diagnosed with depression or anxiety.
Proper clinical management for mTBI begins with immediately removing the victim from further play or activity. This is to avoid reinjury before the brain has adequately recovered. An injury during the vulnerable period results in further compromised autoregulation of cerebral blood flow, rapid development of cerebral edema, intracranial hypertension (elevated intracranial pressure), and neurologic deterioration to coma and, possibly, death.
Mild TBI treatment begins by allowing the patient to rest with minimal cognitive burden. Symptoms are managed using evidence-based clinical practice guidelines. Unfortunately, there is presently no clinically available pharmacologic agent that will facilitate or hasten the brain’s recovery from TBI.
Return to work and type of work is guided by clinical improvement. The DoD DTM 09-033 and the American Academy of Neurology’s 2013 sports concussion guidelines each recommend that patients be prescribed rest without exposure to excess cognitive stimulation. Both physical and cognitive activities should be gradually increased as the patient tolerates, that is, without exacerbation of symptoms. When the patient can tolerate normal activities, then a provocative test can be performed. This provocative test is exertional physical activity (e.g., run) followed by cognitive testing. If the patient does not have symptoms recurrence and performs well on testing, then he or she may return to full play or work. Many states now have laws that require at least 24 hours’ recovery and written permission from a neurologist or other medical practitioner skilled in managing concussion before return to play or work.
Treatment of mTBI is symptoms focused. In 2009, the U.S. Department of Veterans Affairs in conjunction with the DoD published a set of clinical practice guidelines for the management of concussion and mTBI. These are evidence-based recommendations for which pharmacologic and nonpharmacologic options are provided for each major symptom. For example, headache is to be treated with acetaminophen or nonsteroidal antiinflammatory agents, insomnia with sleep hygiene and nonbenzodiazepine soporific agents acutely, dizziness with physical therapy, and so forth. The American Academy of Neurology’s guidelines note that there is no specific treatment for accelerating or improving recovery from mTBI. The goals are to allow sufficient time for the brain to heal, to minimize risk of reinjury, and treat symptoms.
Recovery from mTBI is a gradual process with the majority of the cognitive recovery occurring in the first 6 months, and approximately 70% to 80% of individuals having few postinjury problems. However, the remaining 20% to 30% have impaired function from residual symptoms that are usually psychiatric. While depression, anxiety, and behavioral problems are commonly identified following TBI, it is exceedingly difficult to discern whether persistent emotional and behavioral symptoms are directly related to the neurologic damage, a secondary reaction to the cognitive deficits of the injury, or a comorbid psychological complication of the trauma itself.
Belanger and colleagues conducted a meta-analysis that raises doubts that persistent postconcussive syndrome symptoms are attributable solely to the injury. This work revealed greater cognitive sequelae of mTBI in “convenience samples,” that is, those seeking medical care for their symptoms, and those involved in litigation, as opposed to unselected or prospective samples. Litigation in particular was associated with stable or worsening cognitive function over time, which is perhaps not surprising; whether subconscious or not, functional improvement would presumably lessen reimbursement from pending litigation, serving as a disincentive to recovery.
In contrast, the investigators also found that studies with unselected populations or prospective designs had no evidence of residual neuropsychological impairment 3 months after their injury. In an exception, one longitudinal study of veterans compared long-term neuropsychological outcomes in those with self-reported mTBI after a motor vehicle accident, to those who had a motor vehicle accident without TBI, and another group who had not had an accident, at an average of 8 years after the accident. Comprehensive neuropsychological testing identified no significant differences between the three groups, although the authors argued that minor, borderline differences on the Paced Auditory Serial Addition Test (PASAT) and California Verbal Learning Test (CVLT) suggested potential subtle attentional problems in the mTBI population. While this finding might indicate potential long-term adverse neuropsychological effects of mTBI, it is quite conceivable that such differences are entirely due to psychiatric comorbidity, which should be carefully assessed in any studies that evaluate the impact of mTBI. Regardless of the pathogenesis, it is clear that the residual emotional and behavioral changes have a significant impact on adjustment, including employment and social relationships. Several factors influence this adjustment such as injury severity, social support, premorbid functioning, and coping styles. For example, coping strategies, such as avoidance, wishful thinking, worry, and self-blame, are associated with higher levels of depression and anxiety in TBI patients. Coping strategies are an area that can be targeted for treatment intervention.
There is an expectation that the military’s social structure can assist soldiers who are struggling with poor concentration, attention, and memory. Having clear responsibilities, belonging to a group and a defined chain of command can provide needed support and structure to a recovering mTBI patient. However, the military can also be relatively unforgiving of mistakes, forgetfulness, or poor attention to detail, leading to soldiers receiving a counseling statement (i.e., an administrative warning) or an Article 15 (i.e., nonjudicial military discipline) for infractions related to their symptoms. This punitive response can lead to increased psychosocial stress, which exacerbates existing symptoms and may contribute to further maintenance of TBI symptoms. Rank structure can be an additional complication as military hierarchy demands more from those of higher rank. Anecdotally, some higher ranking soldiers have reported trying to “pass” as if they are not having difficulties in order to preserve pride and to meet expectations they believe are being placed on them. Intervention research may also need to include specific education for military leaders in how to handle TBI symptoms in the workplace as more soldiers resume their military duties.
Traumatic Brain Injury and Suicide
Suicide is tragic and represents a significant concern among TBI survivors. One study identified that 6.9% of patients who had a single TBI had suicidal ideation, a figure that rose to 21.7% among those who had sustained multiple TBIs. This is in contrast to the non-TBI control group who had no suicidal thoughts. The multiple TBI group had higher rates of PTSD and depression, and depression severity was strongly associated with suicide risk. In contrast, however, another study of veterans with mTBI did not identify an association between PTSD and suicide risk. Moreover, severe TBI was associated with lower suicide risk, as the duration of LOC was inversely correlated with suicidality, presumably contributed to by both less memory of the trauma as well as less physical wherewithal to carry out a suicide attempt. Nevertheless, it is judicious to screen those with TBI, especially those with mTBI and/or symptoms of depression, and refer those with suicidal ideation to mental health professionals.