Traumatic Brain Injury and Posttraumatic Stress Disorder
Traumatic Brain Injury and Posttraumatic Stress Disorder
Our returning military veterans remind us dramatically of the importance to consider traumatic brain injury (TBI) as a potential comorbid illness in cases of posttraumatic stress disorder (PTSD). The common causes of comorbid TBI and PTSD are assault and battery to the head, head trauma (personal or work-related injuries), civilian or military explosions, inflicted head trauma in children, motor vehicle accidents, and suicide attempts by jumping. Prevalence figures for comorbid TBI and PTSD historically have been lacking.
This article discusses the association between TBI and PTSD with a review of the possible mechanisms that link TBI and PTSD. Strategies for assessing and treating PTSD are also provided.
TBI and comorbid psychiatric disorders
The American Neuropsychiatric Association Committee on Research recently published a critical review of the literature and noted that psychiatric disorders frequently complicate recovery and rehabilitation from TBI.1 This study reviewed the literature from 1978 to 2006 on psychosis, depression, PTSD, mania, and aggression following nonpenetrating TBI. Studies included in that report were reviewed using the American Academy of Neurology’s criteria for classification of articles on diagnostic methods (I is the highest classification; IV, the lowest). Of the 66 studies reviewed, none was found to be class I or II; the majority were class IV. There are significant gaps in the literature on post-TBI psychiatric conditions with respect to nosology, epidemiology, and risk factors. Larger multicenter prospective studies using standardized diagnostic instruments are needed to further clarify these topics.1
Bombardier and colleagues2 studied the rate at which PTSD symptoms developed without other psychiatric illness during the first 6 months after TBI in a group of 124 civilians. The cumulative incidence of meeting partial DSM-IV-TR criteria for PTSD at 6 months was 11% and of meeting full criteria, 5.6%. Prevalence peaked at 1 month (10%). A large percentage of the participants (86%) had another psychiatric disorder; 29% had a history of PTSD.
A recent prevalence study from the CDC found that symptoms consistent with severe PTSD increased from 11% at 6 months to 16% at 12 months after the injury. The CDC concluded that regardless of severity, survivors with TBI are at risk for symptoms consistent with PTSD. Amnesia regarding the injury event did not protect against the development of these symptoms.3
Clearly, it is difficult to accrue large cohorts of civilians with comorbid TBI and PTSD to study prevalence of the disorders. However, findings from a comprehensive study of a large military population with comorbid TBI and PTSD were reported by Hoge and colleagues.4 In the study, 4618 soldiers in 2 brigades of the US Army were offered an anonymous neuropsychiatric questionnaire: 2714 soldiers (59%) completed the questionnaire. Of the 2525 soldiers who met inclusion criteria for the study, 124 (4.9%) reported an injury with loss of consciousness that lasted between a few seconds to 3 minutes after injury; 260 (10.3%) reported an injury with altered mental status not involving loss of consciousness; 253 soldiers said they had been dazed, confused, or saw stars after an injury. Four additional soldiers reported loss of consciousness lasting longer than 30 minutes. PTSD was strongly associated with mild TBI. Overall, 43.9% of soldiers who reported loss of consciousness following an injury met the criteria for PTSD, compared with 27.3% of those reporting altered mental status.
After complex statistical analysis, only loss of consciousness and combat intensity remained significantly associated with PTSD compared with other physical injuries at multiple anatomical locations (odds ratio for loss of consciousness, 2.98). Overall, nearly 15% reported an injury during deployment that involved loss of consciousness or altered mental status. These findings were defined as mild TBI. The soldiers who had mild TBI were significantly more likely to report high combat exposure and blast mechanism of injury than were the 17% of soldiers who reported other injuries. Those with mild TBI reported significantly higher rates of physical and mental health problems than did soldiers with other injuries. Mild TBI was significantly associated with psychiatric symptoms, notably PTSD. This association remained significant after combat experiences had been controlled for.4 The data indicate that a history of mild TBI in the combat environment, particularly when associated with loss of consciousness, reflects exposure to an intense traumatic event that threatens loss of life and significantly increases the risk of PTSD.5
The authors of that study concluded that the mechanisms between mild TBI and PTSD are complex.4 Studies have not confirmed any direct causative link between PTSD and injury to brain tissue from the concussion itself, although this is an important area of research. There is evidence that implicit processing of traumatic memories and fear conditioning, both mechanisms for the development of PTSD, occur even in persons with severe TBI who have amnesia about the traumatic event.6
Biomechanics and pathophysiology of TBI as it relates to PTSD
At the time of impact, the kinetic energy of blunt force trauma, or blast-overpressure trauma, produces a mechanical loading. This loading is dynamic to the head. Brain deformation caused by tissue strain is the proximate cause of injury whether induced by massive inertia or by contact. The strain to tissue is a result of compression, tension, and shear. Characteristically, the brain withstands strain better if the tissue is deformed slowly rather than quickly. Therefore, the velocity of mechanical loading covaries positively with the level of tissue injury.7 The 4 pillars of cellular damage that cause injury are presented in Table 1. Cellular brain damage is a dynamic and evolving process that occurs over several hours and may go on for a few days.8 The 4 pillars of cellular damage cause enzyme modulation and gene modulation in brain tissue, which results in apoptosis (programmed cellular death), necrosis, or if gene modulation is sufficient, repair. Either apoptosis or necrosis leads to cellular death.8
Many mechanisms are likely to underlie PTSD, but specific pathophysiology is not yet clear. Exposure to extreme stress activates the hypothalamic-pituitary-adrenal axis and increases autonomic reactivity, stress responses produce a reactive cell-mediated immune response, sleep physiology is disturbed, and perception of symptoms is psychologically altered.4 Functional MRI studies have shown that trauma modulates the amygdala and medial prefrontal areas as a response to consciously attended fear.9