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Traumatic Brain Injury and Pain

Traumatic Brain Injury and Pain. F.Antonio Luque, M.D. Ph.D. Neurology . Traumatic Brain Injury. TBI in the USA estimated 180-200 cases/100,000 Around 600,000 New TBI occur every year 10% of these Injuries are fatal.

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Traumatic Brain Injury and Pain

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  1. Traumatic Brain Injury and Pain F.Antonio Luque, M.D. Ph.D. Neurology

  2. Traumatic Brain Injury TBI in the USA estimated 180-200 cases/100,000 Around 600,000 New TBI occur every year 10% of these Injuries are fatal. NIH survey estimates in USA 1.9 million suffer skull fracture or intracranial injury, ½ have suboptimal outcome. Cost 40 Billion dollars/year

  3. TRAUMATIC BRAIN INJURY

  4. Military Fatalities: By Time PeriodAs of 2/20/07

  5. US Non Mortal Casualties: Including non-hostile and medical evacuations As of 2/3/07

  6. Traumatic Brain Injury Traumatic brain injury symptoms Inability to find wordsInability to perform tasksConfabulating (putting unrelated bits of conversation into conversation gaps)ImpulsivityAgitationPoor judgment and poor insightSexual inappropriateness, including a lack of sexual inhibitionsFor more information, call (800) 877-VETS, or visit www.va.gov.

  7. Frequency of PCS Symptoms following a MTBI • Poor concentration 71% • Irritability 66% • Tired a lot more 64% • Depression 63% • Memory problems 59% • Headaches 59% • Anxiety 58% • Trouble thinking 57% • Dizziness 52% • Blurry or double vision 45% • Sensitivity to bright light 40% Traumatic Brain Injury, VA Health Initiative

  8. Causes of TBI (CDC Data) • Transportation (MVA) 48.9% • Falls 25.8% • Firearms 9.7% • Other Assaults 7.5% • Others 7.4 % • Unknown 0.6% Traumatic Brain Injury, VA Health Initiative

  9. Severity Grades of TBI • Mild (Grade 1 ): altered or LOC <30 min with normal CT or MRI, GCS 13-15, PTA < 24 hours. • Moderate (Grade 2): LOC < 6 hours with abnormal CT and/or MRI, GCS 9-12, PTA < 7 days. • Severe (Grade 3 & 4): LOC > 6 hours with abnormal CT and/or MRI, GCS < 9, PTA > 7 days. Traumatic Brain Injury VA Health Initiative

  10. Functional Correlates of Injury Pathophysiology • Focal Cortical Contusion: ground level fall, assault, gunshot wound. They can have Hemiparesis, aphasia, Seizures, visuoperceptual. • Diffuse Axonal Injury: motor vehicle accident, non-ground level fall, geriatric ground level fall. They have confuse language, amnesia, apraxia, hypoarousal. • Hypoxic/Ischemic: anoxia, cardiac arrest, prolonged elevated ICP. They have quadriparesis, spasticity, confusion, amnesia, hypoaraousal. Traumatic Brain Injury VA Health Initiative

  11. Frequency of PCS Symptoms following a MTBI • Poor concentration 71% • Irritability 66% • Tired a lot more 64% • Depression 63% • Memory problems 59% • Headaches 59% • Anxiety 58% • Trouble thinking 57% • Dizziness 52% • Blurry or double vision 45% • Sensitivity to bright light 40% Traumatic Brain Injury, VA Health Initiative

  12. Specific or subjective PCS • Neurological or medical: Headaches, Dizziness/vertigo, Tinnitus, blurred or double vision, light and or noise sensitivity, Nausea and vomiting, Fatigue, sleep disturbances, Physical weakness. • Cognitive: Memory complaints, concentration complaints. • Psychological: Irritability, Increase aggression, Depression, Anxiety. Traumatic Brain Injury VA Health Initiative

  13. Referrals ( Team work) • Audiologist • Kinesiotherapist • Neuro-ophthalmologist • Occupational therapist • Recreational therapist • Speech and language pathologist • Case manager • Neurologist • Neuropsychologist (psychologist) • Physiatrist • Psychiatrist • Social worker (counselor) • Vocational rehabilitation counselor Traumatic Brain Injury VA Health Initiative

  14. Comprehensive Assessment of Acquired Brain Injury History: Accident related facts Initial neurological presentation Pre injury information past medical history and surgical history substance abuse developmental history educational history. Military and legal records Vocational History Psychological history Life stressors Family history Post injury treatment interventions Current functional status Physical Examination: Neurological Cranial nerves 1-12 Deep tendon reflexes and pathological Sensory exam Cerebellar exam Motor exam Mental status exam Behavioral assessment Emotional/psychological status Musculoskeletal Head Face and temporomandibular joints Extremities Axial structures (neck, back, pelvis) Traumatic Brain Injury VA Health Initiative

  15. Chronic cognitive problems • Attention problems • New learning and memory problems • Executive control dysfunction • Others (orientation, communication, behavioral, bradyphrenia, etc) Traumatic Brain Injury VA Health Initiative

  16. Interplay of cognitive and emotional problems Psychogenic/Psychiatry symptoms Denial Anger and irritability Depression Rigid compulsive/hypervigilant Emotional lability Social withdrawl Sense of futurelessness Thought disorder Personality and conduct disorder Neurogenic symptoms Anasognosia (lack of awareness of impairment) Frustration, catastrophic reaction, reduce information Lack of initiative, impaired emotional expressiveness (Aprosodias), lower crying threshold, fatigue Distractability, inabilityto deal with more than one task at a time, dependence on external controls. Lability of emotional expressiveness (not the underlying feeling state) Lack of initiative Impaired planning Aphasia, anomia, or confusion Impulsivity, social disinhibition Traumatic Brain Injury VA Health Initiative

  17. Acute Pain:”Normal sensation triggered by the nervous system to alert you to possible injury.” • Chronic Pain:”Pain persists, signals keep firing in the nervous system for weeks, months, even years” NINDS Chronic Pain information page

  18. Pain • Tissue injury trigers an inflammatory cascade that will alter nociceptive function. • Plasticity and learning play a role in pain • Synaptic potentiation is facilitated by repetitive noxious stimulation and at the level of the brain,environmental influences alter the response to noxious stimulation. • The brain can generate pain in the absence of input from the peripheral nociceptors or the spinal cord. e.g. phantom limb pain • Therefore a Brain pattern generating mechanism or Neuromatrix has been proposed Pain: an overview, JD Loeser, R.Melzack . The Lancet 1999: 1607-1609

  19. International association for the Study of Pain: “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or describe in terms of such damage” JD Loeser, R Melzack, The Lancet 1999: 1607-1609 (Pain: an overview)

  20. Components of Pain • Nociception: detection of tissue damage by specialized transducers attached to A delta and C fibers. Aspirin can prevent inflammation and Local and regional anesthesia can prevent nociception. • Perception of Pain: triggerd by noxious stimulus, It can be generated by lesion in the peripheral or central nervous system.e.g. diabetic neuropathy, spinal cord injury or stroke. Pain can occur without nociception. The intensity of chronic pain has no relation to the extent of tissue injury or other pathology. • Suffering:negative response induce by pain and by fear, anxiety, stress, loss of loved objects and othr psychological states. Cassell:”Suffering occurs when the physcial and psychological integrity of the person is threatened”. • Pain Behaviors: results from pain and suffering and the things the person do or does not do. Examples:”ouch”, gramacing, limping, lying down , recourse to health care, refusing to work, etc. JD Loeser, R. Melzack, The Lancet 1999: 1607-1609 (Pain: an overview)

  21. The neurobiology of pain, Besson JM The Lancet,1999:353: 1610-1615

  22. Histamine, serotonin, bradykinin, prostaglandins, ATP, H+ ,NGF, TNF alpha, endothelins, interleukins

  23. Pain treatment options: TCA, anticonvulsants, Na+ channel blockers, NMDA receptor antagonists, opioids

  24. Molecular Events of PainPeripheral Transduction • TRPV1, TRPV2, TRPV3, TRPM8 • ASCI, DRASIC • MDEG, TREK-1 • BK1, BK2 • P2K3 Peripheral sensitization • NGF, TrkA • TRPV1 • Na, 1,8 • PKA, PKC isoforms, CalMK IV • Erk1/2, p38, JNK • IL-1β, cPLA2, COX2, EP1, EP3, EP4 • TNFα Membrane excitability of primary afferents • Nav 1.8, Nav 1.9 • K+ channel Synaptic transmission Presynaptic • VGCC • Adenosine-R • (mGlu-R) J.Scholz, CJ Woolf: Can we conquer pain? , Nature Neuroscience 2002: 10621067

  25. Molecular Events of PainCentral Synaptic transmission Postsynaptic • AMPA/kainate-R, NMDA-R, mGlu-R • NK1 • Nav 1.3 • K+ channels Central inhibition • GABA, GABAA-R, GABAB-R • Glycine-R • NE, 5-HT • Opioid receptors • CB1 Signal transduction • PKA, PC isoforms • ERK, p38, JNK Gene expression • C-fos, c-jun, CREB • DREAM J.Scholz, CJ Woolf: Can we conquer pain? Nature Neuroscience 2002: 1062-1067

  26. The National Initiative on Pain Control, 2002

  27. The National Initiative on Pain Control, 2002

  28. The National Initiative on Pain Control, 2002

  29. The National Initiative on Pain Control, 2002

  30. The National Initiative on Pain Control, 2002

  31. The National Initiative on Pain Control, 2002

  32. The National Initiative on Pain Control, 2002

  33. The National Initiative on Pain Control, 2002

  34. BRAIN IMAGING TECHNIQUES PET Requires relatively long pain stimulation periods (40 – 60s). Different functional states (e.g., pain and rest) are always acquired in separate scans. Maximum number of scans that can be acquired is limited by radioactivity dose restraints. Usually requires multi-patient study designs. Potential to map neurotransmitter systems and drug uptake in vivo and molecular imaging. Provides a solution in cases where fMRI cannot be accomplished because of contraindications. fMRI Offers better temporal and spatial resolution than PET. Pain stimuli do not need to be applied over along period. The control state and the active pain condition are done in the same run. Better suited than PET for studying cognitive effects on pain processing. Unlimited amount of repetitions within a single patient, allowing single participant, and follow- up studies. Offers less comfort to the patient (noise, body constrained in the magnet bone). Requires expensive fMRI-compatible stimulation and monitoring equipment. MEG Allows mapping of the sequential activation of brain structures in pain processing. Provides a direct measure of neuronal activity. The most ecological technique with the highest comfort and least distress for participants. Allows conclusions from single trial and single participant studies (great clinical potential). Brain Imaging of clinical pain states..Kipers R, Kehlet H. The Lancet Neurology 2006: 5:1033-1044

  35. Kupers R, Kehlet H The Lancet Neurology 2006: 1033-1044

  36. Temporal Spatial Resolution Resolution Advantages Disadvantages_______________________________________________________________________Temporal Spatial Resolution Resolution Advantages Disadvantages_______________________________________________________________________ PET >49’s >4 mm Measures activity and Radioactivity. subcortical structures. Poor temporal resolution. Stimulus-independent Invasive technique. technique Limited amount of scans Allows receptor binding possible. studies fMRI 100 ms – 3’s >2 mm Measures activity in Poor patient comfort. cortical and structures. Requires non-magnetic Excellent spatial equipment. resolution. Stimulus-dependent technique. MEG Milliseconds >2 mm Excellent temporal Difficulties to measures resolution. subcortical activity. High patient comfort. Requires non-magnetic Ecological method. equipment. Stimulus-dependent technique. ____________________________________________________________________________________ Characteristics of different brain imaging techniques used in the study of pain. Kupers R, Kehlet H The Lancet Neurology 2006:1033-1044

  37. Kupers R, Kehlet H, The Lancet Neurology 2006:1033-1044

  38. METHODOLOGICAL DIFFICULTIES IN DESIGN OF BRAIN-IMAGING STUDIES IN CHRONONIC PAIN • Difficulty in finding a homogeneous population of chronic-pain patients. • Difficulty in discerning pain-related from psychological-related effects. • Possible confound by differences in genetic constitution. • Difficulty in dissociation of deafferentiation-related from pain-related changes in brain activation patterns. • Homologous contralateral area is not an unbiased site fro non-painful control stimulation. • Difficulty in switching pain on and off in a very precise and time-locked manner. • Effects of therapeutic interventions could be difficult to dissociate from pain-related effects. Kupers R, Kehlet H.The Lancet Neurology 2006:1033-1044

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