�The Rivers are Rising� Traumatic Brain Injury and Post-traumatic ...

―The Rivers are Rising:‖ Traumatic Brain Injury and Post-traumatic Stress Disorder Among Veterans Serving in OIF/OEF Stephen Jordan, PhD Summer Conference of National Association of Veteran’s Homes August 13, 2008 08/13/2008 1 Scope of the Problem • 1.6 million individuals deployed to Iraq/Afghanistan since October, 2001 • Unprecedented history for a volunteer force – – – – Highest proportion of forces in deployment Longer deployments Higher re-deployment rates Shorter breaks between deployment • Smaller forces, lower casualty rates • Body armor saving lives 08/13/2008 2 Prevalence of the Problem • ―Invisible‖ wounds: TBI & PTSD – 14% positive for PTSD (300,000 individuals) – 14% positive for depression – 19% probable TBI (320,000 individuals) • 1/3 of previously deployed have at least one of these problems • 20-40% troops enter subsequent deployment with post-concussion sx 08/13/2008 3 Access to Treatment • 47% of post-deployment veterans positive for PTSD or Major Depression, had NOT sought medical care • Of the 53% with PTSD, who received treatment, about half received minimally adequate treatment • 2004 VA Study: 90% of mental health providers not using ANY of the established treatments for PTSD; only handful had specialized training 08/13/2008 4 Access to Treatment • 53% positive for probable TBI had NOT been evaluated by a physician for brain injury • Dr. Jon Bowersox (COL, USAF Reserves), chief of surgery at Cincinnati VAMC: – ―No one knows how to treat it, how long it lasts, and whether it’s safe to leave someone deployed.‖ 08/13/2008 5 Traumatic Brain Injuries • CAPT Kevin ―Kit‖ Parker, US Army Res, Prof. of biomedical engineering at Harvard – ―With IEDs, the insurgents have by dumb luck developed a weapon system that targets our medical weakness: treating brain injury.‖ • TBI (30% of Walter Reed patients + up to 300,000 mild TBI) has no established treatment for resolution of symptoms 08/13/2008 6 Overview • • • • • • What happens in mild & severe TBI? What is Post-traumatic Stress Disorder? What happens in PTSD? How are mild TBI and PTSD related? Established Treatments Available Future System Needs 08/13/2008 7 What is Traumatic Brain Injury? • Constellation of symptoms associated with penetrating or blunt trauma OR from rapid acceleration/deceleration/rotation forces OR from blast injuries (air pressure/electromagnetic pulse) 08/13/2008 8 Severity Gradations • • • • Glasgow Coma Scale (coma to ―normal‖) Loss of consciousness Period of amnesia Ranges from ―mild‖ to ―severe‖ 08/13/2008 9 Mild TBI: Common Symptoms • • • • • • • • • • • Headache Nausea/vomiting Balance/coordination problems Fatigue Sensory changes/sensitivity Emotionality/irritability ―Fogginess‖/attention/concentration Short-term memory Slowed down Sleep changes/Drowsiness Word finding problems 10 08/13/2008 Severe TBI: Common Symptoms • Personality changes: labile moods/agitation, loss of initiative, impulsivity, perseveration, lack of emotional presentation, loss of empathy • Cognitive changes: dementia • Physical changes: spasticity, paralysis/paresis 08/13/2008 11 Pathophysiology of TBI • 1. Immediate indiscriminate release of neurotransmitters and disruption of the salt balance in neurons • 2. Glutamate (excitatory) binds to NMDA receptors (in fear centers and elsewhere) leading to K+ leaving neurons and Ca+ entering neurons 08/13/2008 12 Pathophysiology of TBI • 3. The Sodium-Potassium pump works overtime to recover the appropriate balance; burning high amounts of glucose in the process and leaving behind lactate. (Areas of emphasis are point of concussion and hippocampus, but eventually spread throughout the brain.) 08/13/2008 13 Pathophysiology of TBI • 4. While needing higher than normal levels of glucose, cerebral blood flow declines, creating an energy crisis and making brain vulnerable to further injury. • 5. Brain shuts down into period of depressed metabolism (5-10 days in animals) The ongoing excess of calcium in the neurons damages mitochondria (energy producers for the neurons). Unchecked Ca+ accumulation kills cells and damages future neural connections. In rats, Ca+ accumulation persists 2-4 days 08/13/2008 14 Pathophysiology of TBI • Post-injury depressed glucose metabolism does not correlate closely with level of consciousness! • The depressed metabolism is likely basis for some neurocognitive deficits after mild TBI. • The Ca+ accumulation, in combination with diffuse axonal injury, leads to axonal disconnection, which occurs over days and weeks after injury. • New MRI finding “white matter” disruption. 08/13/2008 15 Pathophysiology of TBI • Long-term cognitive deficits appear to result from neuronal damage (particularly to the vulnerable hippocampal region) as well as from neurotransmitter changes. • Post-concussive changes in NMDA, adrenergic (noradrenaline, adrenaline), and cholinergic (acetylcholine) systems have been documented. • The hippocampus suffers from changes in acetylcholine (memory storage), NMDA (long-term potentiation/consolidation), and GABA (leading to development of seizures). 08/13/2008 16 Recovery from Mild TBI • We are told that first 72 hours are period of vulnerability due to physiological cascade noted above. • Post-concussive research suggests a typical window of vulnerability to second-impact syndrome of one to several weeks due to unstable autoregulation systems. • Neuropsychological research shows most people recover in three months. • Individuals not recovered are typically thought to have psychiatric disorder or secondary gain issues. 08/13/2008 17 Post-Traumatic Stress Disorder • Exposed to a traumatic event that resulted in intense fear, helplessness or horror • Re-experiencing of trauma • Persistent avoidance of reminders and numbing • Symptoms of autonomic arousal 08/13/2008 18 Autonomic Hyperarousal • • • • • • • • Insomnia Irritability/outbursts Difficulty concentrating Hypervigilance/exaggerated startle Nightmares Shaking Easy fatigue Heart racing, dizziness, nausea/vomiting, sweating 19 08/13/2008 PTSD: Acute Predictors • Single best predictor of development of PTSD after a traumatic exposure is heart rate. • Second best predictor is electrodermal response (hand perspiration) • Dissociation, avoidance coping, rumination are subacute (1 month) predictors • Chronic pain, severity of physical problems subacute predictors 08/13/2008 20 Physiology of Stress & PTSD • Evaluation of threat is monitored by the amygdala and hippocampus • Under perceived threat, the amygdala-hippocampal region activates the sympathetic nervous system through the hypothalamic-pituitary-adrenal axis through the use of noradrenaline, adrenaline, and cortisol • Core of trauma is: (1) inability to move or escape; and (2) sense of abandonment from protection. • Do not have to actually be directly exposed to trauma or even remember trauma to generate the cortisol—role of beliefs and expectations. 08/13/2008 21 Stress Neurotransmitters & Memory • Adrenaline/noradrenaline has U-shaped relationship to memory; extreme levels impair memory functioning. Moderate levels enhance formation of memory traces. • Cortisol speeds up extinction of memory • GABA (benzodiazepines) impairs memory but also extinguishes fear conditioning • NMDA/Glutamate changes impair memory 08/13/2008 22 Effects of Chronic Stress on Brain • Hippocampus is damaged by high concentrations of cortisol, impacting memory at the levels of attention, storage/consolidation, and retrieval. • Chronic stress leads through a number of mechanisms to hippocampal atrophy as well as damage to emotional centers of the frontal lobe. 08/13/2008 23 PTSD & the Brain • Individuals with PTSD, through learning, have over-reactive amygdala and hippocampal systems. • The feedback loop becomes self-destructive. High stress levels damage hippocampal function, while creating sensitization effects that lead to higher than normal stress responses to perceived future threats. 08/13/2008 24 PTSD & the Brain • Evidence of decreased blood flow to Broca’s leading to word finding problems and “blocking” • Decreased blood flow to the anterior cingulate gyrus during traumatic recall leading to disrupted processing and modulation of emotional nuances, emotional learning, formation of emotional attachments, pain processing and autonomic regulation, emotional numbing 08/13/2008 25 PTSD & the Body • Cardiac: Chronic PTSD raises odds of abnormal EKG with atrioventricular conduction defects or infarctions • Auto-immune: Chronic PTSD raises leukocyte and T-cell counts with evidence of highly sensitized T-cell lymphocytes. There is evidence of greater cell-mediated inflammatory reactions with PTSD. 08/13/2008 26 Mild TBI versus PTSD • Structures sensitive to TBI include the amygdala/hippocampal region in the temporal poles as well as the frontal lobe due to proximity to bone as well as sensitivity to physiological changes. • Structures sensitive to PTSD include the amygdala/hippocampal region and the anterior cingulate gyrus of the frontal lobe • Both cause similar disruptions of certain neurotransmitters 08/13/2008 27 Mild TBI in U.S. Soldiers Returning from Iraq (Hoge et al, 2008) • Surveyed 2525 soldiers – 5% with loss of consciousness – 10% with altered mental status – 17% with other injuries • • • • • If loss of consciousness, 44% met criteria for PTSD If altered mental status, 27% with PTSD If other injury, 16% with PTSD If no injury, 9% with PTSD Conclusion: PTSD/Depression generally explains relationship between mild TBI and health problems 28 08/13/2008 Treatment of Severe TBI • Well-established protocols for initial stabilization; good acute care ―care paths‖ • Despite considerable research, no clear ―care paths‖ for rehabilitation even though structured programs with interdisciplinary approaches do result in overall better outcomes 08/13/2008 29 Residential Treatment for Severe TBI • Many of characteristics of ―Alzheimer’s‖ programs will carry over to address long-term care needs for vets with chronic severe TBI – Secured environment – Highly structured routine 24/7; often younger, more active population – Agitation management protocols – Often increased PT needs for spasticity – Increased role of psychiatry/neurology for behavior problems 08/13/2008 30 Mild TBI/Concussion Treatments • Not established for blast injuries; at this time, using civilian/sports protocols • Removal from stressful activities: cognitive, physical, and emotional until symptom-free • Withdrawal from provoking activities • Graduated re-entry into physical activity • Symptom management 08/13/2008 31 Concussion Symptom Management • Insomnia – SSRI – Cranial electrotherapy stimulation (CES) • Headache – SSRI, muscle relaxants, analgesics – Physical therapy (neck) – CES 08/13/2008 32 Established Treatments for PTSD: Institute of Medicine (October, 2007) • Pharmacotherapies: ―Inadequate evidence to determine efficacy for‖ – – – – – 08/13/2008 All antidepressants Benzodiazepines Seroquel or Risperdal Anticonvulsants Alpha-blockers (blood pressure medications) 33 Established Treatments for PTSD: Institute of Medicine (October, 2007) • Psychotherapies: ―Sufficient efficacy for‖ – Exposure therapies: Helps reduce fear through repetitive, therapist-guided confrontation of feared memories/situations/feelings; critical to induce fear in a controlled setting 08/13/2008 34 Established Treatments for PTSD: Institute of Medicine (October, 2007) • Psychotherapies: ―Insufficient efficacy for‖ – – – – Eye Movement Desensitization & Reprocessing Cognitive restructuring Coping skills training Group format psychotherapy 08/13/2008 35 VA’s Findings for PTSD Treatment • Exposure Treatment – Good versus no treatment – Good versus alternative psych treatments • Cognitive Therapy – Good among civilians exposed to combat – Poor among veterans – Good among sexual assault victims 08/13/2008 36 VA’s Findings for PTSD Treatment • Eye Movement Desensitization & Reprocessing (EMDR) – Good versus no treatment – Fair versus Exposure Tx & Cognitive Tx – Eye movements not critical for success • Dialectical Behavior Therapy – Fair with borderline personalities and parasuicidal populations 08/13/2008 37 VA’s Findings for PTSD Treatment • Pharmacotherapy – SSRI antidepressants: Significant benefit – Other antidepressants/Alpha blockers (antihypertensives): Some benefit – Anticonvulsants/Atypical antipsychotics/Hypnotics: Unknown benefit – Benzodiazepines/Typical antipsychotics: No benefit 08/13/2008 38 One Promising Treatment • Cranial electrotherapy stimulation uses microampere electrical current with ear clips to induce relaxed state and to induce physiological changes leading to pain control, sleep stabilization, anxiety reduction, and improved depression • Alpha-Stim produced by Electromedical Products International is FDA approved for insomnia, anxiety, depression, and pain • www.alpha-stim.com • VA/DoD contracts 08/13/2008 39 Alpha-Stim Outcomes • 125 research studies, including double-blind controlled studies for pain, anxiety, insomnia and depression • Outcomes: – Anxiety: 83% > 50% improvement – Insomnia: 75% > 50% improvement – Depression: 60% improvement versus 20-30% for SSRI’s 08/13/2008 40 System Needs • Marked increase in budget allocations at federal and state levels for treatment, rehabilitation, and social impact (disability, housing, etc). • Educating warriors/reducing real and perceived barriers to treatment • VA/Armed Forces/Guard needs specialty training in concussion and PTSD specialty treatments; need to reach out to private sector • Increased coordination across levels of care; excellent acute care/acute rehabilitation, but poor post-acute coordination 08/13/2008 41 System Needs • Domiciliaries/veteran’s homes need to ramp up skills for severe TBI housing/treatment – American Academy for the Certification of Brain injury Specialists • Certified Brain Injury Specialist/Trainer – Increased role for psychiatry, neuropsychology, behavioral management specialists • Residential treatment for chronic PTSD to address homeless veteran problem? 08/13/2008 42