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Mild Traumatic Brain Injury: Current Diagnosis and Management

Mild Traumatic Brain Injury: Current Diagnosis and Management. Kathleen R. Bell, MD Department of Rehabilitation Medicine University of Washington May 6, 2004. Overview . Why do we care about mild TBI? TBI overview and spectrum Mild traumatic brain injury Mechanism of injury

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Mild Traumatic Brain Injury: Current Diagnosis and Management

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  1. Mild Traumatic Brain Injury: Current Diagnosis and Management Kathleen R. Bell, MD Department of Rehabilitation Medicine University of Washington May 6, 2004

  2. Overview • Why do we care about mild TBI? • TBI overview and spectrum • Mild traumatic brain injury • Mechanism of injury • Presentation • Dilemmas in diagnosis and definition • Medical issues and management

  3. Mild Traumatic Brain Injury • Why do we care?

  4. What is concussion? • Mild Traumatic Brain Injury (MTBI) • Defined by symptoms (1 or more) • Any period of observed or self-reported • Transient confusion, disorientation or impaired consciousness • Dysfunction of memory around the time of the injury • Loss of consciousness lasting less than 30 minutes

  5. Observed signs of neurological or neuropsychological problem • Seizures right afterwards • Young children – irritability, lethargy, vomiting • Symptoms like headache, dizziness, irritability, fatigue or poor concentration soon after injury

  6. Traumatic Brain Injury • 1. Incidence - 500,000 admitted cases per year • estimated 1.5 million sustain non-fatal brain injury never admitted • 2. Severity - 80% mild TBI, remaining 20% • 3. Gender - male preponderance in more severe TBI, possible female preponderance in mild TBI • 4. Age - young adults 15-24 years (infants, children, elderly); wider ranger for mild

  7. How often does it happen? • Centers for Disease Control estimates: • 1.5 million people a year have a TBI • About 75% of these are mild (like concussions) • Don’t really know how many because: • No one keeps track outside of hospitals • Lots of concussions aren’t reported to anyone

  8. Etiology of TBI • 1. No study has specifically focussed on mild TBI • 2. Leading Cause - MVA approx. 28-50% • 3. Falls 20-30% (infants, children, elderly) • 4. Assaults 9-10% • 5. Sports and recreational - 10-20%

  9. Costs of TBI • For TBI associated with hospitalization and rehabilitation: $37 billion dollars in direct and indirect costs • For mild TBI: ?

  10. Mechanisms of Severe TBI • Penetrating (hi velocity, more damage) • Closed/Moderate-Severe • High velocity translational (inferior frontal and temporal lobes) • High velocity rotational (shearing at grey-white interface) • Blunt Force • skull fracture • contusion at point of impact • contrecoup injury (fall)

  11. Space occupying lesions • epidural hematomas 6% - good recovery • subdural hematomas 24% • intracerebral hemorrhage/intraventricular hemorrhage • temporal lobe contusion/bleed - transtentorial herniation • Basilar skull fractures • infection, CSF leaks

  12. Secondary Brain Injury • altered cerebral blood flow • hypotension (relationship to ICP and CPP) • release of neurotoxic compounds • cellular inflammatory response • cytokines • calcium influx • oxygen free radicals

  13. What Happens in Mild TBI? • Because full recovery often occurs, must be temporary neuronal dysfunction rather than cell death • Ionic shifts • Altered metabolism • Impaired connectivity • Changes in neurotransmission

  14. Acute Metabolic/Ionic Changes • Disruption of neuronal membranes and axonal stretching • Increase in extracellular potassium • Release of excitatory amino acid (EAA) glutamate • Increases kainate, NMDA, D-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) • Increases extracellular potassium and so on

  15. “Spreading depression” • This cascade results in neuronal depression • May be the cause of early loss of consciousness, amnesia, and other cognitive dysvunction

  16. Manning the pumps • To head off further ionic fluxes: • Activation of membrane pumps • Increase in glucose use • Results in glycolysis • Glyocolysis and poor mitochondrial function • Results in increased lactate production • Results in neuronal dysfunction: acidosis, membrane damage, altered blood brain barrier permeability, and edema

  17. Further disruptions • Cerebral blood flow usually matches up to glucose metabolism • BUT after a percussion injury to the brain, the cerebral blood flow drops • Now have a mismatch in supply (blood) and demand (increased neuronal metabolism)

  18. Other Ion Malfunctions • Calcium accumulation in the cells because of EAA • Calcium gums up the mitochondria, impairing energy production in the cerebral cortex and the hippocampus • Global decreases in cerebral glucose metabolism lasting 2-4 weeks after injury (present regardless of severity of injury)

  19. Still more problems • Reduced intracellular magnesium levels (correlated with neurologic deficits) • Results in reduced glyocolytic and oxidative energy production, disordered membrane function, and decreased protein synthesis • Higher flux of calcium

  20. Mechanical axonal disruption • Stretching of axons can occur immediately and axonal disconnection can persist for days or weeks • Blocks neuronal transmission by treakdown of the microtubules

  21. Neurotransmitter alterations • Postconcussive alterations in • Glutamatergic (NMDA) systems • Adrenergic systems • Cholinergic systems • Impaired long-term potentiation (NMDA dependent) in hippocampus • Changes in choline acetyltransferase activity and loss of forebrain cholinergic neurons – learning and memory

  22. Other Mechanisms of Mild TBI • Acceleration-deceleration mechanism • Mild diffuse axonal injury without shear • “strain” to neural tissue - affecting intra-axonal neurofilament organization • Focal contusions in white matter • Labyrinth injury • Subtle changes in blood-brain barrier inducing neurotransmitter release

  23. Diagnostic dilemma • Defining the lower and upper limits of mild TBI • Insensitivity of GCS to mild injury • Ineffectiveness of imaging studies for detecting mild injury • Reporting of PTA highly unreliable (even reporting LOC!)

  24. Mild Traumatic Brain Injury • ACRM Brain Injury Special Interest Group: • Any period of LOC <30 minutes and GCS of 13-15 after this period of LOC • Any loss of memory for events immediately before or after the accident, with PTA of <24 hours • Any alteration in mental state at the time of the accident • Focal neurological deficit(s) that may or may not be transient

  25. DSM-IV Post-concussional disorder • 1. LOC > 5 minutes • 2. PTA > 12 hours • 3. New onset of seizures or marked worsening of pre-existing seizure disorder occurring in the first 6 months • 4. Rec: abnormal neuropsychological exam • 5. Persisting symptoms

  26. AAN Practice Parameter Sports Concussion • Grade 1: Transient confusion, no LOC, resolution in <15 minutes • Grade 2: Transient confusion, no LOC, lasts >15 minutes • Grade 3: Any LOC, brief or prolonged

  27. Sports-Related Concussion • (Cantu) Grade I - no LOC, PTA <30 minutes • Grade 2 - LOC <5 min • Grade 3 - LOC >5 min, PTA >24 hrs

  28. Scales of Severity of TBI • Confusion Normal consciousness, no amnesia • Confusion Normal consciousness, PTA • Confusion Normal consciousness, PTA, RGA • Coma (paralytic) Level III: Normal consciousness, PTA, RGA • Coma Vegetative state or death • Death

  29. Glasgow Coma Scale Severe 3-8 Moderate 9-12 Mild 13-15

  30. What the heck is Post-Concussion Syndrome? • Constellation of symptoms: • Headache, sleep disturbance, dizziness/vertigo, nausea, fatigue, oversensitivity to noise/light, attention/concentration problems, decreased memory, irritability, anxiety, depression, emotional lability

  31. Physical complaints • Headache - usually mixed • Neck pain - often associated with HA • Tinnitus • Dizziness - BPPV vs. central vs. possible other otologic problems • Fatigue/drowsiness

  32. Cognitive Sequelae • Memory difficulties (consolidation and retrieval • Diminished attention and concentration (especially divided and alternating attn) • Slowed information processing • Decreased cognitive endurance and judgment

  33. Depression Loss of emotional control Anxiety Irritability Sleep disturbances Sexual disturbances Hypochondriacal concern Hypersensitivity to noise Photophobia Behavioral/affective sequelae

  34. Duration of symptoms in Mild TBI • Most report resolution of symptoms within the first 3 months after injury • Perhaps 12% of all have symptoms persisting into one year • Does persistence reflect interplay of organic and psychologic factors?

  35. Diagnostic dilemma • No strict rule ins/outs for the diagnosis of mild TBI • Head CT, MRI, SPECT - none are entirely reliable for diagnosis • Presence of lesions on CT/MRI indicate a “complicated” mild TBI • PET scans can measure metabolic derangements but no difference between those with a LOC and those without • Abnormalities require about 10 days to resolve

  36. Diagnostic dilemma • Neuropsychological testing • No consensus on which tests to use • Impairments generally resolve 3-6 months • Must be paired with an interview to avoid “faking” results • Heavily dependent on the diagnostic interpretation of the examiner • PASAT, Wechsler Memory Scale

  37. Contribution from Sports Medicine • Observed concussions • Disturbances in mental function measured immediately after concussion can determine the severity of injury • Players with a LOC (brief) do not recover to baseline in 15 minute but did within 48 hours (small study 91 participants, Kelly)

  38. Catastrophic outcomes • 1. Really not a mild injury • 2. Unrecognized posttraumatic depression • 3. Premorbid psychiatric condition is organized around the mild TBI as a focal event • 4. Signs of a “functional” event

  39. Cerebral reserve • Effects of cumulative brain injuries (dementia pugilistica) • Persons with lower initial “reserve” for other reasons • Premorbid psychiatric coditions

  40. Doctor/Attorney dilemma • Role of litigation • conflicting studies • comparison of 2 groups, one with and one without litigation: equivalent cognitive performance, similar family reports • Canadian study 2000: amending tort law regarding MVA resulted in significant decrease of claims for mild TBI • “Compensation neurosis”

  41. Rehabilitation of Mild TBI • Most cases: reassurance • Persistent symptoms • reassurance, education, support, and regular monitoring • teaching effective coping • cognitive remediation • Medical management: avoid prolonged passive treatments, reconditioning

  42. “I don’t know what it is, but there’s something out there, Mr. Jones.” • Bob Dylan

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