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PM&R Recap > TBI > Flashcards

TBI Flashcards

1
Q

Most common cause of TBIs?
Civilians vs. veterans?

A

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%)

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2
Q

Diffuse axonal injury grading?

A

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

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3
Q

Mechanism of injury typically seen for cerebral contusion injuries?

A

Coup-contrecoup injury involving rapid acceleration/deceleration

typically resolve over months - may impair executive function, behavior regulation, mood, and communication

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4
Q

Common brain locations for cerebral contusions?

A

orbital/inferior frontal lobe
anterior temporal lobe

due to sharp inner skull ridges (“horns” of the brain for PM&R recap)

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5
Q

What is the difference b/t primary and secondary injury in TBI?

A

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)

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6
Q

Which neurotransmitter is responsible for excitatory toxicity in TBI/consussion?

A

Glutamate

Glutamate concentrations released into extracellular space d/t cellular lysis –> Ca++ activates second messenger pathways, exacerbated oxidative stress and initiates programmed cell death

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7
Q

Receptors implicated in excitatory toxicity enhancement?

A

NMDA receptors
GABA

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8
Q

Imaging to best appreciate DAI?

A

Diffusion-weighted MRI

Central white-matter damage (cortical/subcortial, corpus callosum, brainstem)

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9
Q

How is cerebral perfusion pressure (CPP) calculated?

A

CPP = mean arterial pressure (MAP) - intracranial pressure (ICP)

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10
Q

What is the rationale for monitoring ICP in acute TBI management?

A

Increased ICP causes decreased cerebral perfusion pressure (CPP)

CPP = MAP - ICP

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11
Q

Threshold for increased ICP?

A

> 20 mmHg (normal is < 15mm Hg, most people 2-5mm Hg)

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12
Q

Acute management methods for lowering ICP in TBI?

A

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)

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13
Q

Important exam finding in acute TBI management with prognostic value?

A

pupillary responsiveness

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14
Q

Unilateral blown pupil is an impending sign of what?

A

uncal herniation (surgical emergency)

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15
Q

What is diaschisis?

A

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)

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16
Q

What is vicariation?

A

functions taken over by brain areas not originally managing that function (these areas alter their properties in order to subvert that function)

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17
Q

Plasticity consists of which two mechanisms?

A

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

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18
Q

Decorticate posturing

A

Arms flexed, legs extended

Lesion above midbrain (better prognosis)

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19
Q

Decerebrate posturing

A

Arms extended, legs extended

Lesion in midbrain (worse prognosis)

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20
Q

Most common bleed in TBI?

A

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

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21
Q

Lens-shaped brain bleed?

A

Epidural hematoma (EDH), 2/2 damage to middle meningeal artery/temporal bone fracture

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22
Q

Brain bleed from ruptured AVM or berry aneurysm?

A

Subarachnoid hemorrhage (SAH)

Aneurysm usually Acomm or Pcomm

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23
Q

Treatment for ruptured AVM/berry aneurysm w/ SAH?

A

nimodipine x 21 days to prevent cerebral vasospasm

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24
Q

most commonly injury cranial nerve in TBI?

A

CN 1 - olfactory; susceptible to shear injury

Altered smell/taste, lack of interest in eating, possible weight loss

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25
Q

Common cranial nerve injuries in TBI?

A

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

26
Q

Most common presentation of brain tumors?

A

HA w/ cognitive deficits

Order MRI w/ contrast

27
Q

Most common brain tumor in kids?

A

1 cerebellar astrocytoma

#2 medulloblastoma

28
Q

Most common primary brain tumor in adults?

A

glioblastoma multiforme

29
Q

Most common brain metastatic tumor?

A

Lung

30
Q

What brain structure is responsible for consciousness?

A

the reticular activating system

31
Q

Level of consciousness?
eyes closed, no sleep/wake cycle, no purposeful behavior

A

Coma

32
Q

Level of consciousness?
Eyes open, + sleep/wake cycle, no localization of objects, reflexive behaviors

A

Unresponsive Wakefulness Syndrome (Vegetative State)

33
Q

Difference between persistent and permanent Unresponsive Wakefulness Syndrome (UWS - Vegetative State)?

A

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)

34
Q

Level of consciousness?
Evidence of self or environmental w/ inconsistent purposeful behaviors and crossing midline

A

Minimally conscious state

35
Q

What is the standardized assessment used to distinguish between unresponsive wakefulness syndrome (vegetative state) and minimally conscious state?

A

The JFK Coma Recovery Scale -Revised (CRS-R) = standardized neurobehavioral assessment designed to help differentiate between unresponsive wakefulness syndrome and minimally conscious state

36
Q

Current practice guidelines for pharmacologic interventions in DOC?

MOA of neurostimulation?

A

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

37
Q

Which component of the glascow coma scale is the most important predictor of outcome in TBI?

A

Motor response

Motor response 1-6
Verbal Response 1-5
Eye Opening 1-4

38
Q

What indicates that a patient is out of post-traumatic amnesia (PTA)?

A

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

39
Q

Classification of TBI Severity?
LOC < 30min, CGS 13-15, PTA 0-1 day

A

Mild TBI

40
Q

Classification of TBI Severity?
LOC 30min - 24hr, GCS 8-12, PTA 1-7 days

A

Moderate TBI

41
Q

Classification of TBI Severity?
LOC > 24hr, GCS 3-8, PTA > 7 days

A

Severe TBI

42
Q

Prognosis for severe disability is PTA < 2 months?

A

Severe disability unlikely

43
Q

Prognosis if PTA is > 3 months?

A

Good recovery unlikely

44
Q

Difference b/t immediate, early, and late post-traumatic seizures?

A

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

45
Q

Risk factors for post-traumatic epilepsy?

A

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

46
Q

minimum AED treatment time for a late post-traumatic seizure?

A

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.

47
Q

Management of immediate post-traumatic seizures?

A

cont standard prophylaxis x 7 days (keppra/phenytoin), not predictive of future seizures

48
Q

Management of early posttraumatic seizures?

A

Typically treat w/ AEDs for 6 months

25% of pts w/ early posttraumatic seizure will have a subsequent seizure

49
Q

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?

A

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

50
Q

Threshold for severe agitation on the Agitation Behavioral Scale?

A

> 34 = severe agitation
< 21 is normal

51
Q

TBI pt w/ cyclical tachycardia, HTN, tachypnea, fever, diaphoresis, and dystonia - diagnosis and treatment?

A

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)

52
Q

Most common site for HO formation in TBI?
Common risk factors?

A

Hip (other common sites = knees, elbows, shoulders)

Risk factors: long bone fractures, coma > 2 months, immobility

53
Q

Recommendations for neuroendocrine screening following TBI?

A

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

54
Q

Sodium abnormality in TBI?
hyponatremia, low serum osmolality, high urine osmolality, increased urine output

A

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)

55
Q

Sodium abnormality in TBI?
hyponatremia, low serum osmolality, normal urine osmolality; signs of hypovolemia

A

Cerebral Salt Wasting - hypovolemic hyponatremia; ADH appropriately elevated

Tx: IVF, isotonic saline, fludrocortisone

56
Q

Sodium abnormality in TBI?
Hypernatremia, high serum osmololality, low urine osm

A

Diabetes Insipidus - hypernatremia due to excessive volume depletion

Tx: fluid replacement, DDAVP/vasopressin

57
Q

Assessment tools for concussion symptoms?

A

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)

58
Q

Poor prognostic factors on exam for concussion recovery?

A

Abnormalities in saccades, smooth pursuits, convergence insufficiency, nystagmus

Fiber tracts that connect frontal cortex w/ cerebellum sensitive to shear injury

59
Q

General management of concussion?

A

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

60
Q

Supplements shown to be beneficial for posttraumatic headaches?

A

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)

61
Q

Return to Play Protocol for Concussion?

A

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

62
Q

Role of S-100B in concussion?

A

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

PM&R Recap (10 decks)

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