TBI Flashcards
Most common cause of TBIs?
Civilians vs. veterans?
Civilians:
Falls (59%), MVC (29%), assaults (8%)….
Elderly - falls most common
Pediatric - MVC most common
Veterans: blast injury most common (33.1%), object hitting head (31.7%), falls (13.5%)
Diffuse axonal injury grading?
DAI = shearing of axons 2/2 acceleration/deceleration, rotational forces
Graded on MRI by location w/ associated petichial hemorrhages:
Grade 1 = cortical/subcortical
Grade 2 = corpus callosum
Grade 3 = Midbrain worst prognosis
Mechanism of injury typically seen for cerebral contusion injuries?
Coup-contrecoup injury involving rapid acceleration/deceleration
typically resolve over months - may impair executive function, behavior regulation, mood, and communication
Common brain locations for cerebral contusions?
orbital/inferior frontal lobe
anterior temporal lobe
due to sharp inner skull ridges (“horns” of the brain for PM&R recap)
What is the difference b/t primary and secondary injury in TBI?
Primary injury = immediate concussive force of impact causing disruptive shear forces, cerebral contusions, DAI, etc
Secondary injury = all the detrimental biochemical cascades that happen after the primary injury (inflammatory changes, ischemia, hypoxia, anoxia, vasogenic and cytotoxic edema)
Which neurotransmitter is responsible for excitatory toxicity in TBI/consussion?
Glutamate
Glutamate concentrations released into extracellular space d/t cellular lysis –> Ca++ activates second messenger pathways, exacerbated oxidative stress and initiates programmed cell death
Receptors implicated in excitatory toxicity enhancement?
NMDA receptors
GABA
Imaging to best appreciate DAI?
Diffusion-weighted MRI
Central white-matter damage (cortical/subcortial, corpus callosum, brainstem)
How is cerebral perfusion pressure (CPP) calculated?
CPP = mean arterial pressure (MAP) - intracranial pressure (ICP)
What is the rationale for monitoring ICP in acute TBI management?
Increased ICP causes decreased cerebral perfusion pressure (CPP)
CPP = MAP - ICP
Threshold for increased ICP?
> 20 mmHg (normal is < 15mm Hg, most people 2-5mm Hg)
Acute management methods for lowering ICP in TBI?
Elevating head
Diuretics (mannitol, acetazolamide)
Hypertonic saline
Barbituates/sedatives
Forced hyperventilation (temporarily, decreased PaCO2 causes cerebral vasoconstriction, lowering blood volume in brain)
Hypothermia - decreased metabolic demands of brain
Surgical decompression (burr holes, craniotomy/craniectomy)
Important exam finding in acute TBI management with prognostic value?
pupillary responsiveness
Unilateral blown pupil is an impending sign of what?
uncal herniation (surgical emergency)
What is diaschisis?
Lesions/damage to one region of CNS can produce altered function in other areas of the brain if there is a connection b/t the two sites (fiber tracts). Function is lost in both injured and in morphologically intact brain tissue (resolusion parallels recovery of focal lesion)
What is vicariation?
functions taken over by brain areas not originally managing that function (these areas alter their properties in order to subvert that function)
Plasticity consists of which two mechanisms?
Neuronal regeneration/neuronal collateral sprouting = intact axons establish synaptic connections through axon sprouting in areas where damage has occured
Functional reorganization/unmasking neural reorganization = healthy neural structures not formerly used for a given purpose are developed or reassigned to do functions performed by the lesioned area
Decorticate posturing
Arms flexed, legs extended
Lesion above midbrain (better prognosis)
Decerebrate posturing
Arms extended, legs extended
Lesion in midbrain (worse prognosis)
Most common bleed in TBI?
Subdural hematoma
Crescent shaped, 2/2 shearing of bridging veins or arterial vessel damage (increased risk w/ older age and brain atrophy; alcoholics)
Can cause midline shift
Lens-shaped brain bleed?
Epidural hematoma (EDH), 2/2 damage to middle meningeal artery/temporal bone fracture
Brain bleed from ruptured AVM or berry aneurysm?
Subarachnoid hemorrhage (SAH)
Aneurysm usually Acomm or Pcomm
Treatment for ruptured AVM/berry aneurysm w/ SAH?
nimodipine x 21 days to prevent cerebral vasospasm
most commonly injury cranial nerve in TBI?
CN 1 - olfactory; susceptible to shear injury
Altered smell/taste, lack of interest in eating, possible weight loss
Common cranial nerve injuries in TBI?
CN1 - olfactory
CN2 - visual field deficits
CN7 - facial n; deficits in 2/3 tongue taste, facial expression, salivation, tears
CN8 - vestibulocochlear; hearing and balance loss (BBPV is common in TBI, however - if patient complaining of dizziness)
*often associated w/ temporal and skull base fractures
Most common presentation of brain tumors?
HA w/ cognitive deficits
Order MRI w/ contrast
Most common brain tumor in kids?
1 cerebellar astrocytoma
#2 medulloblastoma
Most common primary brain tumor in adults?
glioblastoma multiforme
Most common brain metastatic tumor?
Lung
What brain structure is responsible for consciousness?
the reticular activating system
Level of consciousness?
eyes closed, no sleep/wake cycle, no purposeful behavior
Coma
Level of consciousness?
Eyes open, + sleep/wake cycle, no localization of objects, reflexive behaviors
Unresponsive Wakefulness Syndrome (Vegetative State)
Difference between persistent and permanent Unresponsive Wakefulness Syndrome (UWS - Vegetative State)?
Persistent = lasting for over 1 month
Permanent = lasting for over 1 year after TBI (over 3 months if non-traumatic brain injury, such as anoxic)
Level of consciousness?
Evidence of self or environmental w/ inconsistent purposeful behaviors and crossing midline
Minimally conscious state
What is the standardized assessment used to distinguish between unresponsive wakefulness syndrome (vegetative state) and minimally conscious state?
The JFK Coma Recovery Scale -Revised (CRS-R) = standardized neurobehavioral assessment designed to help differentiate between unresponsive wakefulness syndrome and minimally conscious state
Current practice guidelines for pharmacologic interventions in DOC?
MOA of neurostimulation?
Practice guidelines recommend trialing amantadine for traumatic vegetative state/unresponsive wakefulness between 4 and 16 weeks post-injury to hasten functional recovery
MOA: increase dopamine in the brain
Which component of the glascow coma scale is the most important predictor of outcome in TBI?
Motor response
Motor response 1-6
Verbal Response 1-5
Eye Opening 1-4
What indicates that a patient is out of post-traumatic amnesia (PTA)?
Galveston Orientation and Amnesia Test score of 75 or more for 2 consecutive days
(technically PTA is over once you’ve scored 75 or higher on the first of the two days)
Orientation Log (O-log)
Score of 25 or higher for two straight days
Classification of TBI Severity?
LOC < 30min, CGS 13-15, PTA 0-1 day
Mild TBI
Classification of TBI Severity?
LOC 30min - 24hr, GCS 8-12, PTA 1-7 days
Moderate TBI
Classification of TBI Severity?
LOC > 24hr, GCS 3-8, PTA > 7 days
Severe TBI
Prognosis for severe disability is PTA < 2 months?
Severe disability unlikely
Prognosis if PTA is > 3 months?
Good recovery unlikely
Difference b/t immediate, early, and late post-traumatic seizures?
Immediate < 24hrs
Early: 1-7 days
Late: > 7 days
*Check prolactin level if seizure suspected, will be increased
*keppra/phenytoin recommended ppx x 7 days to prevent early post-traumatic seizures
Risk factors for post-traumatic epilepsy?
Having things in the brain that shouldn’t be there
- Foreign bodies (bullets, knife)
- Blood (EDH, SDH, SAH, IPH)
- Bony fracture (depressed)
- abnormal neuronal discharge (early seizure)
B/l contusions (esp parietal and temporal lobes)
Dural tear
Midline shift > 5mm
Severe TBI as measured by GCS
minimum AED treatment time for a late post-traumatic seizure?
2 years (can consider discontinuing if seizure-free after 2 years)
Valproic acid and carbamazepine recommended for preferable side effect and mood-stabilizing effects in TBI. EEG often performed prior to cessation of AEDs.
Management of immediate post-traumatic seizures?
cont standard prophylaxis x 7 days (keppra/phenytoin), not predictive of future seizures
Management of early posttraumatic seizures?
Typically treat w/ AEDs for 6 months
25% of pts w/ early posttraumatic seizure will have a subsequent seizure
What potential complication should be considered if a TBI patient has an unexpected functional plateau or deterioration during rehabilitation? N/V, HA, confusion w/ dilated ventricles on imaging?
Posttraumatic hydrocephalus (occurs in up to 45% of TBI patients). Usually caused by impaired resorption of CSF (particularly w/ subarachnoid hemorrhages).
Tx: VP shunt placement
Threshold for severe agitation on the Agitation Behavioral Scale?
> 34 = severe agitation
< 21 is normal
TBI pt w/ cyclical tachycardia, HTN, tachypnea, fever, diaphoresis, and dystonia - diagnosis and treatment?
Paroxysmal Sympathetic Hyperactivity (PSH)
Mechanism: thought to be loss of cortical inhibition on sensory afferent information activating the sympathetic nervous system. Occurs in approx 1/3 of TBI patients.
Tx: minimizing stressors (pain/noise), environmental measures (cooling blanket), pharmacologic interventions (propranolol, clonidine, benzodiazepines, bromocriptime, morphine, gabapentin, dantrolene, ITB)
Most common site for HO formation in TBI?
Common risk factors?
Hip (other common sites = knees, elbows, shoulders)
Risk factors: long bone fractures, coma > 2 months, immobility
Recommendations for neuroendocrine screening following TBI?
3-6 months, and then 1 year post injury
Test: morning cortisol, FSH, LH, testosterone, prolactin, insulin-like growth factor 1 [IGF-1], estradiol, thyroid panel
30-50% of pts who survive TBI have endocrine abnormalities
Sodium abnormality in TBI?
hyponatremia, low serum osmolality, high urine osmolality, increased urine output
Syndrome of Inappropriate antidiuretic hormone (SIADH) - euvolemic hyponatremia
Tx: free water restriction (do not correct Na faster than 10mEq/L over 24hrs until Na reaches 125 due to risk of pontine myelinolysis)
Chronic SIADH: can treat w/ democlocycline (inhibits ADH action in the kidney)
Sodium abnormality in TBI?
hyponatremia, low serum osmolality, normal urine osmolality; signs of hypovolemia
Cerebral Salt Wasting - hypovolemic hyponatremia; ADH appropriately elevated
Tx: IVF, isotonic saline, fludrocortisone
Sodium abnormality in TBI?
Hypernatremia, high serum osmololality, low urine osm
Diabetes Insipidus - hypernatremia due to excessive volume depletion
Tx: fluid replacement, DDAVP/vasopressin
Assessment tools for concussion symptoms?
Neurobehavioral Symptom Inventory (NSI): 22-item self resport questionnaire (measures somatic, affective and cognitive symptoms) - adopted by Dept of Defense and VA
Post-Concussion Symptom Scale (PCSS): 21 item self-report measure that identifies concussion in athletes w/ high specificity, shown to discriminate b/t concussed and non-concussed athletes
Graded Symptom Checklist (GSC)
Poor prognostic factors on exam for concussion recovery?
Abnormalities in saccades, smooth pursuits, convergence insufficiency, nystagmus
Fiber tracts that connect frontal cortex w/ cerebellum sensitive to shear injury
General management of concussion?
Relative rest for first 24-48 hours, then exercise can improve brain function through favorable effects on brain neuroplasticity
Moderate aerobic exercise (60% of max HR) performed for 150min/week is cognitively protective
Supplements shown to be beneficial for posttraumatic headaches?
Riboflavin 400mg
Magnesium oxide
(have a role in mitochondrial energy production and electron transport in mitochondrial membrane. Decreased levels of micronutrients have been found in plasma and brains of migraine patients)
Return to Play Protocol for Concussion?
Each stage lasts at minimum 24hrs
Stage 1 - do nothing (relative rest)
Stage 2 - light cardio
Stage 3 - directional cardio (cardio + directional movement)
Stage 4 - Sport-specific cardio (drills)
Stage 5 - full practice
Stage 6 - cleared to play
Role of S-100B in concussion?
Scandinavian Neurotrauma Committee guidelines for adults recommend S-100B values < 0.10ug/L, if sampled within 6hrs of injury, can help rule out need for head CT in pts < 65yo with a GCS of 14, or GCS of 15 w/ + LOC and N/V
