James F. Malec, PhD, ABPP-Cn, Rp Professor & Research Director PM&R, Indiana University School of Medicine & Rehabilitation Hospital of Indiana Emeritus Professor of Psychology, Mayo Clinic

Overview 1. What is traumatic brain injury? 2. What sorts of injuries or events can cause TBI? 3. What behaviors should lawyers be looking for that might be red flags for TBI? 4. What questions should we be asking our clients to verify TBI (other than seeking medical records)? 5. How is TBI diagnosed? Is imaging necessary or helpful? Are there other ways to diagnose? 6. What are the symptoms of TBI? 7. How can TBI impact cognition? 8. Can TBI be cured or ameliorated and if so, how? What is the long term prognosis for persons with TBI?

Definitions  TBI Model System (moderate-severe): TBI is defined as damage to brain tissue caused by an external mechanical force as evidenced by medically documented loss of consciousness or post traumatic amnesia (PTA) due to brain trauma or by objective neurological findings that can be reasonably attributed to TBI on physical examination or mental status examination.  CDC: A TBI is caused by a bump, blow, or jolt to the head or a penetrating head injury that disrupts the normal function of the brain. Not all blows or jolts to the head result in a TBI.

TBI Severity  Ranges from “mild” (i.e., a brief change in mental status or consciousness) to “severe” (i.e., an extended period of unconsciousness or memory loss after the injury)  Concussion = mild TBI  Severity based on initial injury NOT severity of sequelae These are associated but not perfectly

TBI Severity  Severity based on initial injury Glasgow Coma Scale (GCS) Duration of loss of consciousness (LOC) Duration of post-traumatic amnesia (PTA) Time to follow commands  Severity NOT based on severity of sequelae or symptoms  Severity of injury and sequelae are associated but not perfectly

Glasgow Coma Scale  Eye Opening Response Spontaneous; eyes open with blinking at baseline: 4 points To verbal stimuli, command, speech: 3 points To pain only (not applied to face): 2 points No response: 1 point

Glasgow Coma Scale  Motor Response Obeys commands for movement: 6 points Purposeful movement to painful stimulus: 5 points Withdraws in response to pain: 4 points Flexion in response to pain (decorticate posturing): 3 points Extension response in response to pain (decerebrate posturing): 2 points No response: 1 point

Glasgow Coma Scale  Verbal Response Oriented: 5 points Confused conversation, but able to answer questions: 4 points Inappropriate words: 3 points Incomprehensible speech: 2 points No response: 1 point

Glasgow Coma Scale  GCS = sum of three components  Usually worst within first 24 hours  Motor score alone is good proxy for entire scale  In current practice, often invalidated by emergency intubation/sedation

Post-traumatic Amnesia (PTA)  Time between injury and recovery of continuous anterograde memory Usually signified by orientation to person, time, place Scales used in research, eg, O-LOG, Galveston Orientation and Amnesia Test (GOAT)  Memory loss may also be retrograde Retrograde < anterograde

Post-traumatic Confusional State (Delirium)  PTA or memory loss is one component  Disturbance of awareness/attention  Behavior disturbance Agitation vs. abulia  Sleep cycle disturbance

TBI severity  Mild (Concussion) GCS >13 LOC < 30 min PTA <24 hrs may include no LOC or PTA and normal GCS (15) with disruption of consciousness, ie, dazed or confused  Complicated mild Above criteria + positive neuroimaging Sequelae similar to moderate

TBI severity  Moderate GCS = 9-12 LOC = 30 min-24 hrs PTA = 24 hrs-1 wk  Severe GCS < 9 LOC > 24 hrs PTA > 1 wk  Systems with finer grades exist  Others differentiate only mild vs. moderate/severe

ABI: Acquired brain injury  Brain damage from other causes, eg, anoxia, cerebrovascular event, electrocution, poisoning or metabolic imbalance  Not congenital or developmental  Not progressive (eg, dementia, MS, Huntingtons, Parkinsons)  Stroke With vs. without hemiplegia

Causes of TBI  Any injury to the brain resulting from an external force Most common: car accidents, falls, fights, blast injuries  Penetrating or nonpenetating  Usually results from a blow to the head  May result from acceleration- deceleration or blast injury without direct head trauma

Most Common TBI/ABI Sequelae  Impaired attention or memory  Limited behavioral or emotional control Impulsivity vs. lack of initiation  Above may also result from many other causes including personality, psychiatric disorder, sleep disorder, other medical illness  TBI/ABI requires documentation of an event that abruptly disrupted consciousness and resulted in identifiable brain damage or sequelae attributable to brain damage

OSU-TBI-ID  Systematic method for discovering a history of significant TBI as suggested by: Hospitalization, ER visits, car accident, falls, fights, blast injuries Loss or alteration of consciousness Multiple injuries  Only for TBI  Form, information and training at:

Mayo Criteria: Moderate-Severe (DEFINITE) One or more of the following criteria apply: 1. Death due to this TBI 2. Loss of consciousness of 30 minutes or more 3. Post-traumatic anterograde amnesia of 24 hours or more 4. Worst Glasgow Coma Scale full score in first 24 hours (unless invalidataed upon review, e.g., attributable to intoxication, sedation, systemic shock) 5. One or more of the following present: intracerebral, subdural, or epidural hematoma, cerebral contusion, hemorrhagic contusion, penetrating TBI (dura penetrated), subarachnoid hemorrhage, brain stem injury

Mayo Criteria: Mild (PROBABLE) Not moderate-severe and one or more of the following criteria apply: 1. Loss of consciousness of momentary to less than 30minutes 2. Post-traumatic anterograde amnesia of momentary to less than 24 hours 3. Depressed, basilar or linear skull fracture (dura intact)

Mayo Criteria: Symptomatic (POSSIBLE) Not moderate-severe or mild and one or more of the following symptoms are present:  Blurred vision  Confusion (mental state changes)  Dazed  Dizziness  Focal neurologic symptoms  Headache  Nausea

Imaging  Intracranial damage attributable to trauma is clear evidence of TBI Although subdural hematoma will be challenged  MRI more sensitive than CT  TBI can also be present with normal neuroimaging

Diagnosis with normal imaging  History of injury and sequelae are critical  Medical diagnosis by brain injury specialist, ie, neurosurgeon, neurologist, neuropsychiatrist, physiatrist (PM&R) Not all in these specialties are brain injury experts  Neuropsychology evaluation and testing “consistent with” TBI/ABI Neuropsychologists = clinical psychologists ○ May diagnose within DSM

Symptoms of Mild TBI Symptoms of Mild TBI [from Rivermead Postconcussion Symptoms Questionnaire]  Headaches  Dizziness  Nausea and/or Vomiting  Noise Sensitivity, easily upset by loud noise  Sleep Disturbance  Fatigue, tiring more easily  Being Irritable, easily angered  Feeling Depressed or Tearful  Feeling Frustrated or Impatient  Forgetfulness, poor memory  Poor Concentration  Taking Longer to Think  Blurred Vision  Light Sensitivity, Easily upset by bright light  Double Vision  Restlessness

Symptoms of Moderate-Severe TBI  Similar to mild but more severe  More often include impairments of higher order abilities Reasoning and judgment Planning Self-awareness  No symptoms are specific to TBI or ABI

Effects on Cognition  Neurotransmitter disruption Often transient in mild TBI  Structural damage Neural damage to brain areas that are critical for specific types of cognition ○ Frontal lobes: reasoning, judgment, self-regulation ○ Left hemisphere: language ○ Right hemisphere: spatial abilities ○ Temporal lobe, hippocampus: memory Diffuse axonal injury: disconnection syndromes, impaired attention

Only Cure is Prevention And prevention of secondary complications/ injuries

Rehab Works Inpatient Outpatient/ Community-based Medical and behavioral interventions Ideally: early, focused, lifelong follow-along

Long term Prognosis Much better than it is…