Treating Mild Traumatic Brain Injury with EMDR
Posted on December 18th, 2013

Ruwan M Jayatunge M.D.

Abstract:  Mild Traumatic Brain Injury (m-TBI) has become one of the major public health problems. The Centers for Disease Control (CDC) estimates that more than 1.7 million Americans sustain TBI each year. The leading causes of m-TBI are falls, motor vehicle crashes, and sports injuries. The survivors with m-TBI often experience headaches, cervical pain, fatigue, anxiety, stress related physical symptoms and sometimes depression. Researches indicate that m-TBI can cause long lasting negative impact on mental and physical health. The survivors of m-TBI would be benefitted by an effective mode of psychotherapy such as Eye movement desensitization and reprocessing (EMDR). EMDR is a research proven   psychotherapeutic intervention that is effective in treating stress, anxiety, depression and psychogenic pain. The emotional, behavioral, and physical impairments associated with m-TBI can be successfully treated with EMDR. Therapeutic efficacy of EMDR is discussed with the clinical treatment of a sample of 3 individuals diagnosed with m-TBI. The interview-based assessments and self-evaluation psychometric scales indicate that EMDR is effective in treating survivors with m-TBI.

Key Words: Mild Traumatic Brain Injury (m-TBI) , Eye movement desensitization and reprocessing (EMDR)

Mild Traumatic Brain Injury (m-TBI) has become a significant public health concern over the past few years. Annually a large number of people sustain m-TBI following accidents and sports injuries. Majority of the mild traumatic brain injuries are undiagnosed and untreated. However m-TBI can cause long lasting impact on mental and physical health.

According to the American Congress of Rehabilitation Medicines (ACRM-1993) Mild Traumatic Brain Injury can cause physiological disruption of brain function. As a result of m-TBI there can be retrograde or anterograde amnesia (post traumatic amnesia not greater than 24 hours / loss of conscientiousness for approximately thirty minutes or less) with alteration in mental state and sometimes it can lead to long term focal neurologic deficits. This definition includes a head trauma after 30 minutes with an initial Glasgow Coma Scale (GCS) of 13-15.

The common symptoms of m-TBI include fatigue, headaches, nausea, visual disturbances, memory loss, impaired attention, impaired concentration, sleep disturbances, dizziness, loss of balance emotional disturbances and sometimes Seizures. Symptoms of mild traumatic brain injury typically resolve within days or weeks. However, a significant group of patients may report symptoms of Post-Concussional Syndrome (PCS) weeks, months and years post injury (Williams et al, 2010).

The National Center for Injury Prevention and Control (2004) indicate that nearly 235 000 people experience m-TBI in the United States annually. Based on epidemiological reports by Faul and colleagues (2010) the  leading cause of TBI is falls (35.2%), followed by motor vehicle crashes (17.3%), being struck by or falling against something (16.5%), and assaults (10%). Mild brain injury accounts for a substantial proportion of all persons admitted to a hospital for brain trauma, yet the amount of information on the epidemiology of this problem is quite sparse ( Kraus & Nourjah, 1988). According to the Armed Forces Health Surveillance Center (2012) in the United States armed forces, 233,425 traumatic brain injuries were reported between 2000 and 2011. Of these, approximately 76% were m-TBIs.

Although many physicians are familiar with severe TBI and its management, mild TBI comprises 70%”80% of all such injuries (Arciniegas et al ,2005; Jennett 1996, 1998 Kraus & Nourjah 1988). A significant number of people who sustained m-TBI do not get adequate treatment or seek medical help. Sosin and colleagues (1996) indicate that up to 25% of patients with a concussion do not seek medical care. In addition complications related to mild TBI are difficult to identify and it often remain subtle. There are instances; both in the sports literature and military arena, of individuals who were involved in a traumatic event without any alteration of consciousness, yet these patients have subsequently developed symptoms of concussion (Kay, et al., 1993).

Most patients with M-TBI recover quickly, with a predictable clinical course of recovery within the first one to two weeks following traumatic brain injury. Persistent physical, cognitive, or behavioral postconcussive symptoms may be noted in 5 to 20 percent of persons who have mild traumatic brain injury (Mott et al. 2012). Some individuals with m-TBI continue to experience persistent or intermittent headaches, fatigue, difficulties in concentration, sound intolerance, mood swings and sometimes changes in coordination. According to Dikmen and colleagues (2001) nearly 1% and 20%  of people who sustain m-TBI will continue to experience cognitive deficits (attention, memory, and executive dysfunction) , emotional and behavioral (irritability, anxiety, depression, affective lability, apathy,   impulsivity )  problems.

Experimental injury models demonstrate that mild brain injuries are capable of producing diffuse axonal injury, both as a function of biomechanical forces and a host of injury-mediated cytotoxic processes (ie, calcium and magnesium regulation, free radical formation, neurotransmitter excitotoxicity, inflammatory responses, disruption of vascular homeostasis) (Arciniegas et al,2005; Povlishock et al 1979, 1983; Povlishock 1992; Povlishock and Christman 1995). Maxwell, Povlishock & Graham (1997) hypothesize that m-TBI could produce structural neuronal damage and sometimes diffuse neuronal dysfunction.

EMDR as one of the Potential Treatment Options for m-TBI

Although symptoms following m-TBI generally resolve with time, active treatment is centered on symptom management, supervised rest, recovery, and patient education (Marshall et al., 2012).  The cognitive, emotional, behavioral, and physical impairments experienced by mild TBI survivors are often treated with Cognitive rehabilitation and pharmacotherapy. In addition to these major treatment methods Eye movement desensitization and reprocessing (EMDR) can be successfully used to treat individuals with m-TBI.

EMDR is a relatively new psychological intervention that has been used to treat PTSD. However recent researches show that EMDR is now a full-scale protocol that is being used to treat a wide-range of disorders (Gallagher, 2002).  Sack,   Lempa,   & Lamprecht (2007) specify that EMDR may be beneficial in the treatment of a wide range of stress-mediated symptoms. Although the complete mechanism of EMDR is still unknown a large body of researches indicates that EMDR stimulates the brain’s information processing system. In addition some experts believe that EMDR stimulates natural benzodiazepine receptors in the brain (Jayatunge, 2008).

A study reported by Oh & Choi,  (2007) show changes in the resting regional cerebral blood flow after successful EMDR treatment in 2 patients with PTSD. As the researchers report ” Brain 99mTc-ECD-SPECT (Technetium 99m-ethyl cysteinate dimmer-single photon emission computerized tomography) was performed before and after EMDR, and, in addition, a pre- and posttreatment comparison was made with 10 non-PTSD participants as a control group. After EMDR, cerebral perfusion increased in bilateral dorsolateral prefrontal cortex and decreased in the temporal association cortex. The differences between participants and normal controls also decreased. Changes appeared mainly in the limbic area and the prefrontal cortex” According to the researchers these results are in line with current understanding of neurobiology of PTSD and EMDR treatment appears to reverse the functional imbalance between the limbic area and the prefrontal cortex.

Traumatic Memory linked with m-TBI

Mild TBI is often associated with traumatic events such as motor vehicle crashes, violent personal attacks, military combat etc. that can cause profound psychological distress among the survivors. Apart from the m-TBI symptoms underlying psychological distress can have a long term impact sometimes interfering with m-TBI related physical symptoms. Therefore psychological interventions are required to minimize the psychological distress connected with    m-TBI. In this context EMDR can be viewed as one of the effective mode of psychotherapies to treat traumatic memories associated with m-TBI.

de Jongh   & ten Broeke   (2007) indicate that  Eye movement desensitization and reprocessing (EMDR) has been shown to be a structured, noninvasive, time-limited, and evidence-based treatment for unprocessed memories and related conditions.  Studies conducted by van der Kolk and colleagues (2007) concur that the efficacy of brief EMDR treatment to produce substantial and sustained reduction of PTSD and depression in most victims of adult-onset trauma.

Posttraumatic Headache Following m-TBI

Headache after m-TBI is very common and persistent across the first year after injury (Lucas et al. 2013). Posttraumatic headache (PTH) appears to be more likely to develop following mild TBI (concussion) compared with moderate or severe TBI. Posttraumatic headache often clinically resembles primary headache disorders, usually migraine (Theeler et al., 2013). Posttraumatic Headache has detrimental effect on survives life interfering his/her day-to-day activities.  According to Lew and colleagues (2006)   18”22% of PTH lasted longer than 1 year.

A study done among the  U.S. Soldiers returning from Iraq  Hoge and colleagues (2008)  found that 32% of soldiers with mild TBI that included a loss of consciousness described having headaches in the past month. In addition they found that Headache was the only physical symptom that remained related to mild TBI after controlling for mental disorders.

According to the empirical findings of the EMDR developer- Shapiro, physical sensations can be activated by attending to a traumatic memory, may be a component of the sensory experience of the target trauma itself (i.e. an accident or an attack) and are additionally elicited by the resonance of the negative cognition. Accordingly, body sensations are invaluable focal points for EMDR processing. The clear body scan is a fundamental criterion used to determine the completion of a treatment protocol. Significant somatic involvement in EMDR is also demonstrated by the use of hand tapping as an alternative to eye movements as a method of bi-hemispheric activation (Grand, 1996).

EMDR uses the pain protocol to ease painful sensations and it is based on the Adaptive Information Processing model (Shapiro 1995).  The overlap between the experience of pain and traumatic experiences are often interconnected and EMDR Pain Protocol can be successfully used to minimize headaches and somatic pains associated with m-TBI. According to McDonald (2010) the EMDR Pain Protocol can be effective in three main ways: ”¢ Reducing the experience of pain; ”¢ Targeting pain memories and ”¢ Overcoming the impact of pain on the individual. McDonald (2010) further elucidate that the application of the protocol assumes that it is possible to influence neurological pathways involved in maintaining persistent pain messages.

EMDR combines a range of therapeutic approaches with eye movements or other forms of rhythmical stimulation (e.g., audio sound and touch) in ways that stimulate the brain’s information processing system. Some individuals with m-TBI experience intensified headaches with bilateral eye moments. In such clients using tactile desensitization and reprocessing would be advisable.

Other Somatic Symptoms in m-TBI

In addition to headaches, chronic cervical pain, body pain and fatigue are common complaints in m-TBI. Psychosomatic conditions associated with m-TBI are well known to the researchers. There is a strong link between somatic symptoms and m-TBI. These symptoms are long lasting and it can cause irritability, insomnia and occupational difficulty. Sleep difficulties could lead to tiredness, exhaustion and somatic pain. According to Buffett-Jerrott & Stewart (2002) for TBI related sleep disturbances benzodiazepines may not be suitable and as they indicate Benzodiazepines impair cognition, and exacerbating motor impairments. Sometimes stress and anxiety amplify somatic pain. On most occasions patients are poorly responding to analgesic and to pain medication. Some patients have a risk of addiction to prescription drugs. In such circumstance psychotherapy would be the perfect solution. Klaus (2008) underlines successful use of EMDR in somatic problems.

 Cognitive and Emotional Difficulties and m-TBI

The survivors with M-TBI often have affective complaints of irritability, anxiety, and depression which have negative consequences on psychosocial health. As indicated by Goodrich and colleagues (2013) many physical, psychological, and social problems are associated with m-TBI. Mild traumatic brain injury (m-TBI) leads to long-term cognitive and emotional difficulties and behavioral disturbances (Gao, & Chen, 2011). Anxiety and depression impacts the survivor’s functionality. To combat such symptoms psychotherapy is indicated.

EMDR has been recognized as an imperative psychotherapeutic method. EMDR   has proven to be effective and it brings together elements of well established approaches such as psychodynamic, cognitive, behavioral and client-centered approaches (Balibey & Balik§i ,2013). Treating anxiety and depression related symptoms EMDR has shown a remarkable effectiveness. EMDR is regarded as an evidence-based practice for treatment of anxiety and depression symptoms. EMDR can be used to relief pain, fatigue and anxiety and depression that are experienced by the survivors with M-TBI.

Case Discussion

1)       Corporal BXVX486 served in an artillery battery for over 9 years. During this time period his team had fired a large number of artillery rounds.  After serving a long period in the artillery battery Corporal BXVX486 complained of tremors in both hands, frequent headaches and myalgia. The physicians who examined him found no any organic factor associated with his condition. There were no Electroencephalography (EEG) changes and his brain scan and other reports were normal. He was suspected as a malingerer at one point but later found that his symptoms were real. Corporal BXVX486 poorly responded to the pain killers. His condition started to improve with relaxation therapy and EMDR. After a 6 sessions of EMDR Corporal BXVX486 showed a dramatic improvement. The follow up in 6 , 12 and 18 months revealed that his headache and other somatic symptoms  did not interfere with his functionality. The self-report questionnaires were compared with pre-treatment scores and it indicated that   Corporal BXVX486 was able to gain a successful therapeutic outcome as a result of EMDR.

2)      Mrs.WXXBX52 met with an automobile accident in LA and she was unconscious for about 20 minutes. She was admitted to the hospital immediately and then had a fast recovery. According to the Glasgow Coma Scale (GCS) her head injury was recorded as a mild traumatic brain injury. After the accident Mrs.WXXBX52 had intrusions about the accident, headache that did not subside for analgesics and was troubled by insomnia. In addition she had a fear of driving vehicles. Mrs.WXXBX52 underwent (each 90 minutes) 8 sessions of EMDR for a period of 12 weeks. In the first session her headache intensified with eye movements and soon eye movements were change in to hand tapping (tactile desensitization). In subsequent sessions headache did not interfere. With EMDR her sleep improved and fear decreased. After 3 months of the accident Mrs.WXXBX52 was able to overcome her fear of driving and her headache decreased significantly.

3)       Mr. RXXNX38 experienced an interpersonal violent attack in which he sustained a laceration to the occipital region of the skull. Following the blow to the head he became dizzy but did not lose his consciousness. Mr. RXXNX38 was able to escape from the violent situation and then cried for help. He was admitted to the hospital and monitored for 48 hours and then discharged. After a few weeks of the incident he experienced transient headaches and sleep difficulties. He was referred to a Neurologist. His EEG and brain scan did not indicate any neurological pathology. Mr. RXXNX38 was treated with a small dose of Sodium valproate and Imipramine (Tofranil). Despite the medication his headache recurred. The transient headache aggravated with sleep difficulty interfered his occupational and family life. Mr. RXXNX38 agreed to undergo EMDR treatment and he was administered 6 sessions of EMDR. Upon interventions made by EMDR his transient headaches and sleep difficulties subsided. His follow up was uneventful.

Conclusion

Annually a large number of people sustain mild head injuries and it has become a growing public health concern. The cognitive, emotional, behavioral, and physical deficits produced by mild TBI are frequently more subtle and could last for a long period affecting survivor’s psychosocial health. The survivors of m-TBI would be benefitted by psychotherapy. The American Psychiatric Association (APA) has recognized Eye movement desensitization and reprocessing (EMDR) as one of the principal modes of psychotherapeutic interventions. A large body of research has proven the efficacy of EMDR in anxiety management, combating depression and in pain management.  EMDR) seems to be effective in treating patients with mild traumatic brain injury. Future research is needed to determine the therapeutic significance of EMDR in treating survivors with m-TBI.

References

 American Congress of Rehabilitation Medicine. Definition of mild traumatic brain injury. J Head Trauma Rehabil. 1993;8:86”7.

Arciniegas, D.B., Anderson,C.A., Topkoff,J., McAllister ,T.W. (2005).Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat.  ; 1(4): 311”327.

Armed Forces Health Surveillance Center, (2012). TBI numbers by severity. Retrieved from www.dvbic.org/TBI-Numbers.aspx.

Balibey, H., & Balik§i, A. (2013). Eye movement desensitization and reprocessing (EMDR) treatment at a patient diagnosed with post-traumatic stress disorder: Case report. D¼ÅŸ¼nen Adam: The Journal of Psychiatry and Neurological Sciences, 26(1), 96-101.

Buffett-Jerrott, S.E., Stewart, S.H. (2002). Cognitive and sedative effects of benzodiazepine use. Curr Pharm Des.8:45”58

de Jongh, A., ten Broeke, E. (2007). Treatment of specific phobias with EMDR: Conceptualization and strategies for the selection of appropriate memories. Journal of EMDR Practice and Research, 1(1), 46-56. doi:10.1891/1933-3196.1.1.46.

Dikmen S, Machamer J, Temkin N. (2001). Mild head injury: facts and artifacts. J Clin Exp Neuropsychol.  23:729”38.

Faul, M., Xu, L,. Wald, M, M.,Coronado, V,G., (2010). Traumatic Brain Injury In the United States Emergency Department Visits, Hospitalizations and Deaths 2002”2006. Retrieved from http://www.cdc.gov/traumaticbraininjury/pdf/blue_book.pdf

Gallagher, C. (2002). Making sense of EMDR: Efficacy of EMDR and the application of Horowitz’s control process theory to a psychological analysis of EMDR psychotherapy. Dissertation Abstracts International, Section B. Sciences and Engineering, 65(5), 2625.

Goodrich, G.L., Martinsen, G.L., Flyg, H.M., Kirby, J., Asch, S.M., Brahm, K.D., Brand, J.M., Cajamarca, D., Cantrell, J.L., Chong, T., Dziadul, .JA., Hetrick, B.J., Huang, M.A., Ihrig, C., Ingalla ,S.P., Meltzer, B.R., Rakoczy, C.M., Rone, A., Schwartz, E., Shea, J.E. (2013).  Development of a mild traumatic brain injury-specific vision screening protocol: A Delphi study.J Rehabil Res Dev.50(6):757-68.

Grand, D. (1996, June). Body processing:  Innovative applications of EMDR to the somatic experience. Presentation at the 1st EMDR International Association Conference, Denver, CO.

Hoge, C., McGurk, D., Thomas, J., Cox, A., Engel, C., Castro, C. (2008).Mild traumatic brain injury in U.S. soldiers returning from Iraq. N. Engl. J. Med. 358:453”463.

Jayatunge, R. (2008) . EMDR Sri Lanka experience: (Psychological trauma management through EMDR in Sri Lanka , Sarasavi Publishers Colombo.

Jennett, B. (1998).Epidemiology of head injury. Arch Dis Child.78:403”6.

Kay, T., Harrington, D.E., Adams, R., Anderson, T., Berrol, S., Cicerone, K., Dahlberg, C., Gerber, D., Goka, R., Harley, P., Hilt, J., Horn, L., Lehmkuhl, D., Malec, J. (1993). Definition of mild traumatic brain injury. J Head Trauma Rehabil.8:86-87.

Klaus, P. (2008, June). The use of EMDR in somatic & medical problems: Special emphasis on early life interventions. Presentation at the annual meeting of the EMDR Europe Association, London, England.

Kraus, J.F., Nourjah, P.(1988). The epidemiology of mild, uncomplicated brain injury. J Trauma. 28:1637”43.

Lew, H..L., Lin, P.H,. Fuh, J.L., Wang, S.J., Clark, D.J., Walker, W.C. (2006). Characteristics and treatment of headache after traumatic brain injury: a focused review. Am. J. Phys. Med. Rehabil. 85:619”627.

Lucas, S., Hoffman, J.M., Bell, K.R, Dikmen, S.(2013).A prospective study of prevalence and characterization of headache following mild traumatic brain injury. Cephalalgia.  0333102413499645.

Marshall, K.R., Holland, S.L., Meyer, K.S., Martin, E.M., Wilmore, M., Grimes, J.B.(2012). Mil Med. 177(8 Suppl):67-75.

McDonald, H. (2010, March). EMDR chronic pain protocol. Presentation at the 8th EMDR Association UK & Ireland Annual Conference & AGM, Dublin, Ireland.

Maxwell, WL, Povlishock, J.T, Graham, D.L. (1997). A mechanistic analysis of nondisruptive axonal injury: a review. J Neurotrauma. 14:419”40.

Mott, T.F., McConnon, M.L., Rieger, B.P (2012). Subacute to Chronic Mild Traumatic Brain Injury.Am Fam Physician.86(11):1045-51.

National Center for Injury Prevention and Control. (2004). Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths.

Oh, D. H., & Choi, J. (2007). Changes in the regional cerebral perfusion after eye movement desensitization and reprocessing:  A SPECT study of two cases. Journal of EMDR Practice and Research, 1(1), 24-30. doi:10.1891/1933-3196.1.1.24.

Sack, M., Lempa, W., & Lamprecht, W. (2007). Assessment of psychophysiological stress reactions during a traumatic reminder in patients treated with EMDR. Journal of EMDR Practice and Research, 1(1), 15-23. doi:10.1891/1933-3196.1.1.15.

Shapiro, F. (1995).  Eye Movement Desensitization and Reprocessing:  Basic Principles, Protocols, and Procedures.  New York:  Guilford Press.

Sosin, D.M., Sniezek, J.E., Thurman, D.J.(1996). Incidence of mild and moderate brain injury in the United States, 1991. Brain Injury.10:47-54.

Theeler, B., Lucas, S., Riechers, R.G.,  Ruff, R.L.(2013). Headache. .53(6):881-900. doi: 10.1111/head.12123.

van der Kolk, B.A., Spinazzola, J., Blaustein, M.E., Hopper, J.W., Hopper, E.K., Korn, D.L, Simpson, W.B. (2007).A randomized clinical trial of eye movement desensitization and reprocessing (EMDR), fluoxetine, and pill placebo in the treatment of posttraumatic stress disorder: treatment effects and long-term maintenance. J Clin Psychiatry. 2007 Jan;68(1):37-46.

Williams, W.H., Potte, S., Ryland, H. (2010).  Mild traumatic brain injury and Postconcussion Syndrome: a neuropsychological perspective.J Neurol Neurosurg Psychiatry. 81(10):1116-22.

 

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