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

Table 2 outlines common neuro-psychiatric disorders seen following TBI. This author has delineated a medical model with evidence-based meth-odology for the assessment of TBI with comorbid medical, psychiatric, and neuropsychiatric conditions.⁷

TBI assessments in patients with PTSD

The history taken at the time of the psychiatric examination of a patient presenting to a psychiatrist with PTSD is the most telling. It is important to take not only a strong psychological history of traumatic events but also a careful history of physical injury that occurred at the time of the trauma that precipitated the PTSD.

For the child psychiatrist, a history of inflicted harm should arouse immediate suspicion of an underlying TBI. Clearly, a child injured in a motor vehicle accident or other accident by blunt force trauma should be historically evaluated to determine whether there was loss of consciousness or whether posttraumatic cognitive changes are present.

In adults, the most common scenarios for comorbid TBI and PTSD include assault and battery, blunt force trauma in motor vehicle or industrial accidents, suicide attempts associated with severe blunt force trauma (such as jumping from a building), and blunt force trauma or blast-overpressure trauma sustained from ordinance explosions during combat. In particular, psychiatrists should be suspicious when examining any returning combat veteran with PTSD symptoms that have resulted from an explosion (blast-overpressure trauma). Blast-overpressure brain injury is frequently underdiagnosed in soldiers returning from Iraq and Afghanistan who have sustained mild TBI or explosion-induced concussions. Among veterans who have been evaluated since April 2007, 15% have screened positive for mild TBI.¹⁰ Since the psychiatrist tends to see posttrauma victims well after the initial injury, it is important not to defer the diagnosis of comorbid PTSD and TBI to physicians who examined the victim at the time of injury. Often the physical trauma obviates the ability of physicians in the acute care setting to determine whether comorbid TBI and PTSD exist.

The assessment of potential TBI within the context of PTSD is no different from the assessment of potential TBI comorbid with any other medical or psychiatric condition. The procedures are fairly standard and comprehensive. The psychiatrist will have to determine whether he or she has the clinical experience and skills to perform the TBI assessment outlined in Table 3. If not, it may be wise to refer the patient to a colleague who practices neuropsychiatry or behavioral neurology. A comprehensive neuropsychiatric assessment is the most important single tool with which to determine whether a patient with PTSD has comorbid TBI.

Table 3 outlines the specific information that must be gathered to differentiate TBI from PTSD. If the neuropsychiatric history gathering is the most important variable in a quality TBI assessment, the second most important variable is a return to the scene of the accident. The psychiatrist should secure the original injury records-including the ambulance run sheet, police report, and emergency department records. These will help determine whether there was head trauma and its relationship to the onset of PTSD. For instance, if the emergency medical services (EMS) run sheet indicates a Glasgow Coma Scale below 15, the likelihood that the patient has sustained at least a mild TBI is increased. If the patient remained impaired based on the Glasgow Coma Scale (score below 15) after the emergency medical personnel released him to an emergency department, the likelihood of TBI is further increased, because it is obvious that the patient’s mental state did not improve during transit. Lastly, if the medical history from the emergency department and/or EMS observers and police indicates confusion, disorientation, inability to provide a history, or inability to be interviewed because of mental status changes, TBI is probable.

The neuropsychiatric history should focus on questions regarding alterations of attention, language, memory, constructional ability, executive function, affective and mood changes, thought processing, risk of injury to self or others, and inability to perform activities of daily living. The mental status examination should be focused on cognitive processing in addition to posttrauma psychological distress. The psychiatrist may defer the neurological examination to a neurologist, or if a quality neurological examination has been performed previously, it may be used in lieu of the psychiatrist performing a physical examination. However, the psychiatric portions of the examination should not be deferred.

With regard to structural imaging, the usual examination at the time of an acute head injury is CT of the head. For long-term outcome evaluation, however, CT is substantially inferior to MRI for detecting neurological tissue injury. The modern weightings on MRI sequences allow for the detection of traumatic signal changes (FLAIR), retained hemosiderin products (gradient echo), white matter tract injury (diffusion tensor), or loss of hippocampal volume (coronal T2). Consultation with a radiologist or a neuroradiologist will be required for most psychiatrists to analyze this information.

The standardized neurocognitive assessment is important because the commonly used mental status examination is incapable of detecting subtle neurocognitive changes. Moreover, frontal lobe disorders associated with executive dysfunction are difficult to detect on face-to-face mental examination. Apolipoprotein E examination may reveal an e4 allele. There is an association between the presence of 1 or 2 e4 alleles and a poorer prognosis for the patient with TBI. TBI has been convincingly implicated as a risk factor for Alzheimer disease in several epidemiological studies.⁸

Treatment and prognosis

Treating comorbid PTSD and TBI is a complex but rewarding process. It includes 3 major steps⁷:

• Pharmacological treatment aimed at improving cognitive symptoms.
• Pharmacological treatment aimed at suppressing PTSD symptoms.
• Psychotherapy directed at PTSD psychopathology.

Cognitive symptoms of PTSD are treated with either stimulants and/or cognitive enhancers of the acetylcholinesterase blockade type; psychiatric symptoms of PTSD are treated with SSRIs or dual-mechanism antidepressants. Psychotherapy directed at PTSD can include cognitive-behavioral therapy (CBT) or desensitization techniques.⁷ Prognosis varies with the severity of TBI; PTSD with comorbid TBI significantly reduces the likelihood of full recovery.⁷ However, CBT has been shown to be effective in treating acute stress disorder and PTSD comorbid with mild TBI.^11,12

References:

References

1. Kim E, Lauterbach EC, Reeve A, et al. Neuropsychiatric complications of traumatic brain injury: a critical review of the literature (a report by the ANPA Committee on Research). J Neuropsychiatry Clin Neurosci. 2007;19:106-127.
2. Bombardier CH, Fann JR, Temkin N, et al. Posttraumatic stress disorder symptoms during the first six months after traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2006;18:501-508.
3. Greenspan AI, Stringer AY, Phillips VL, et al. Symptoms of post-traumatic stress: intrusion and avoidance 6 and 12 months after TBI. Brain Inj. 2006;20: 733-742.
4. Hoge CW, McGurk D, Thomas JL, et al. Mild traumatic brain injury in US Soldiers returning from Iraq. N Engl J Med. 2008;358:453-463.
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7. Granacher RP Jr. Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment. 2nd ed. Boca Raton, FL: CRC Press; 2008.
8. Graham DI, Gennarelli TA, McIntosh TK. Trauma. In: Graham DI, Lantos PL, eds. Greenfield’s Neuropathology. 7th ed. London: Arnold; 2002:823.
9. Williams LM, Kemp AH, Felmingham K, et al. Trauma modulates amygdala and medial prefrontal responses to consciously attended fear. Neuroimage. 2006;29:347-357.
10. Alvarez L. War Veterans’ Concussions Are Often Overlooked. New York Times. August 25, 2008.
11. Bryant RA, Moulds M, Guthrie R, Nixon RD. Treating acute stress disorder following mild traumatic brain injury. Am J Psychiatry. 2003;160:585-587.
12. Nidiffer FD, Errico A, Trudell TM, Barth JT. Blast Injury Institute. Current trends in post traumatic stress disorder and traumatic brain injury.

http://www.blastinjuryinstitute.org/ node/52

. Accessed October 9, 2008.