Mild Traumatic Brain Injury amnesia

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					Mild Traumatic Brain Injury: Current
Diagnosis and Management

               Kathleen R. Bell, MD
               Department of
                 Rehabilitation Medicine
               University of Washington
               May 6, 2004

   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
Mild Traumatic Brain Injury

                  Why  do we
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
            Dysfunction of memory around the time of the injury
            Loss of consciousness lasting less than 30 minutes
   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
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
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
Etiology of TBI

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

   For TBI associated with hospitalization and
    rehabilitation: $37 billion dollars in direct and
    indirect costs

   For mild TBI: ?
    Mechanisms of Severe TBI
   Penetrating (hi velocity, more damage)
   Closed/Moderate-Severe
           High velocity translational (inferior frontal and temporal
           High velocity rotational (shearing at grey-white interface)
   Blunt Force
           skull fracture
           contusion at point of impact
           contrecoup injury (fall)
–   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
   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
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
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
“Spreading depression”

   This cascade results in neuronal depression
   May be the cause of early loss of
    consciousness, amnesia, and other cognitive
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
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)
Other Ion Malfunctions

   Calcium accumulation in the cells because of
   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)
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
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
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
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
Diagnostic dilemma

   Defining the lower and upper limits of mild
   Insensitivity of GCS to mild injury
   Ineffectiveness of imaging studies for
    detecting mild injury
   Reporting of PTA highly unreliable (even
    reporting LOC!)
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
DSM-IV Post-concussional

   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
   4. Rec: abnormal neuropsychological exam
   5. Persisting symptoms
AAN Practice Parameter Sports

   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
Sports-Related Concussion

   (Cantu) Grade I - no LOC, PTA <30 minutes
   Grade 2 - LOC <5 min
   Grade 3 - LOC >5 min, PTA >24 hrs
Scales of Severity of TBI

I.     Confusion     Normal consciousness, no
II.    Confusion     Normal consciousness, PTA
III.   Confusion     Normal consciousness, PTA, RGA
IV.    Coma (paralytic)    Level III: Normal
                     consciousness, PTA, RGA
V.     Coma          Vegetative state or death
VI.    Death
Glasgow Coma Scale
   Eyes       Open         Spontaneously             4
                           To verbal command         3
                           To pain                   2
                           No response               1
   Best       To verbal    Obeys                     6
   motor      command
              To painful   Localizes pain            5
                           Flexion-withdrawal        4
                           Flexion-abnormal          3
                           Extension                 2
                           No response               1
   Best                    Oriented, converses       5
                           Disoriented, converses    4
                           Inappropriate             3
                           Incomprehensible sounds   2
                           No response               1

  Severe 3-8
  Moderate 9-12
  Mild        13-15
What the heck is Post-Concussion

   Constellation of symptoms:
    –   Headache, sleep disturbance, dizziness/vertigo,
        nausea, fatigue, oversensitivity to noise/light,
        attention/concentration problems, decreased
        memory, irritability, anxiety, depression, emotional
Physical complaints

   Headache - usually mixed
   Neck pain - often associated with HA
   Tinnitus
   Dizziness - BPPV vs. central vs. possible
    other otologic problems
   Fatigue/drowsiness
Cognitive Sequelae

   Memory difficulties (consolidation and
   Diminished attention and concentration
    (especially divided and alternating attn)
   Slowed information processing
   Decreased cognitive endurance and
Behavioral/affective sequelae

   Depression              Sexual disturbances
   Loss of emotional       Hypochondriacal
    control                  concern
   Anxiety                 Hypersensitivity to
   Irritability             noise
   Sleep disturbances      Photophobia
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?
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
           –   Abnormalities require about 10 days to resolve
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”
    –   Heavily dependent on the diagnostic
        interpretation of the examiner
            PASAT, Wechsler Memory Scale
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)
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
   4. Signs of a “functional” event
Cerebral reserve

   Effects of cumulative brain injuries (dementia
   Persons with lower initial “reserve” for other
   Premorbid psychiatric coditions
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”
Rehabilitation of Mild TBI

   Most cases: reassurance
   Persistent symptoms
    –   reassurance, education, support, and regular
    –   teaching effective coping
    –   cognitive remediation
   Medical management: avoid prolonged passive
    treatments, reconditioning
   “I don’t know what it is, but there’s
    something out there, Mr. Jones.”

        Bob   Dylan