Traumatic Brain Injury is more or less common than each of the following events/diseases?

Breast Cancer

HIV/AIDS

MS

Spinal Cord Injury

What age groups are at highest risk for TBI? How does mortality/disability from TBI differ amongst the groups?

M/F distribution?

Most common cause of TBI?

Increased risk for:

Adolescents/Young Adults

Greater than 75 y/o (falls)

elderly display higher mortality and disability

M/F is 2.5 to 1, men take more risks

Traffic related accidents

Pathophysiology of TBI's

Compare characteristics of Focal Injury vs. Diffuse Injury (4 types of focal injury vs. 5 diffuse injury types)

Focal:

• Contusions
• Lacerations
• Focal Hemorrhage
• Focal ischemia

Focal Injury: Contusions

What are 2 of the most common contusion sites in the brain? (he said potential test Q)

1. Anterior tip of the temporal lobe

2. Inferior portion of the frontal lobe

Focal Injury: Laceration

2 potential causes?

1. Depressed skull fracture

2. penetrating wound (gunshot, or even a knife!)

TBI: Hemorrhages

Name 4 possible brain-assoc hemorrhages

1. Basal ganglia hemorrhage (rupture of the deep penetrating arteries)

2. Epidural Hemorrhage

3. Subdural Hemorrhage

4. Subarachnoid Hemorrhage

Epidural hemorrhage

Where is the epidural space?

Are epidural hemorrhages usually venous or arterial?

Epidural hemorrhage is assoc w/ what type of TBI and injury to what artery?

Epidural space = potential space betweek the skull and dura

(dura is normally strongly adhered to skull at the sutures; hemorrhage will rip the dura off the skull up to the nearest suture line)

Epidural hemorrhages are usually arterial

Assoc w/ skull fracture and injury to the middle meningeal artery

Subdural Hemorrhage

Location? Venous/Arterial?

What is the cause, and why is a particular population at risk?

Located between the dura and arachnoid

usually venous

Usually caused by tearing of bridging veins;  (Cerebral atrophy results in increased tension of bridging veins)

Brains atrophy/shrink w/ age ---> increased incidence of SDH in elderly

Blood appearance on brain scans

Acute hemorrage would appear bright/dark on CT? Subacute hemorrhage? Why?

Subarachnoid Hemorrhage

Location?  Venous/arterial?

What is the typical cause (generally, and give a specific example)?

Describe the course/progression of the injury; Is this considered a focal or diffuse injury? And what category does this fall under within one of those groups?

Subarachnoid space is between arachnoid and pia;  usually arterial injury

 Typical cause: occluded artery (eg. compression of the PCA resulting from uncal herniation)

Course of Injury:  Occlusion of artery --> SAH --> Vasospasm leading to vasoconstriction --> Focal Ischemic Injury

Traumatic Axonal Injury (TAI)

aka?

Occurs as a result of what type of injury?

What are 3 areas of the brain typically affected?

Is white or gray matter generally more affected?

What sort of stress is placed on axons in TAI's, and what is the result?

aka Diffuse Axonal Injury (DAI)

Normally the result of an acceleration/deceleration injury

Areas affected:

Corpus callosum

Gray-white matter interface

Brain stem

(primarily white matter injuries)

Shearing stress to axons --> leads to axopathy (axon retraction balls seen histologically)

Axon retraction balls

Assoc w/ what type of TBI?

These histopath structures account for what 3 neurological changes in the patient?

What do brain scans reveal?

Are these seen in mild/moderate/severe/all TBI's?

Seen in Traumatic Axonal Injury TBI's

These account for impaired consciousness, cognition, and behavioral changes

Neuroimaging is often unremarkable (except for petechial hemorrhages)

Histo evidence of axon retraction balls seen following mild TBI (can be in mild or severe injury)

Originally thought TAI occurs at time of impact;

Now we think a more complex biochemical reaction is occuring, w/ interactions between axons at the injury site, resulting in delayed axonal disconnection

--> Involves cytoskeletal destruction, swelling/bursting of neurons, and apop, all due to Calcium imbalance

Cerebral Hypoxemia and Ischemia

What are 2 secondary consequences

Causes:

1. Diffuse secondary cerebral injury

2. Elevated ICP

Intracranial Pressure ICP

What is Cerebral Perfusion Pressure (CPP)?

What is our goal for CPP?

Which aspect of CPP do doctors attempt to alter in order the maintain adequate cerebral perfusion?

Is maintenance of systolic or diastolic BP more important following TBI?

Cerebral perfusion pressure is the difference between mean arterial pressure (MAP) and ICP

Goal is to maintain CPP at greater than 60mmHg

Used to maintain CPP by increasing MAP, but this is very damaging to the heart and kidneys over time, so now CPP is increased/maintained by decreasing ICP

Must maintain S-BP, increased incidence of death and vegetative state following TBI if S-BP falls below 90

1. Evacuation of mass lesions

2. Drainage of CSF

3. Osmotic Diuresis (increased urination)

4. Barbiturates

5. Hyperventilation  -- deacreased CO2 causes decreased ICP, but this is because it decreases bloodflow;  obviously this is just a quick fix for emergencies

Excitatory Amino Acids

How are these involved in TBI's? (specific AA?)

The role of Apoptosis in TBI

3 things that initiate apoptosis in neurons following TBI

Caused by:

1. Ca influx

2. oxidative stress

3. ATP depletion

Secondary injury

Assessing the patient following TBI

Describe the Glasgow Coma Scale;  what factor may cause this assessment to be misleading as to the actual patient prognosis?

Glasgow Coma scale assesses 3 patient features on a numbered scale - Motor, Verbal, and Eye

lower Glaslow score indicates more severe TBI

**Motor score is the most prognostic measure of early death following TBI

This assessment can be misleading in intoxicated patients

Post Traumatic Amnesia

Def

How is it assessed?

Longer PTA implies...?

PTA = a length of time that there is no recollection of ongoing events

Assessed w/ the Galveston Orientation and Amnestic Test (GOAT)

or

Orientation log (O-log)

Longer PTA --> more severe injury

1. Glaslow coma scale (good for early assessment)

2. Age

3. Presence of SAH

4. PTA status

5. Pupil Response

6. Hypoxemia

7. hypoTension

(Glad Agnus Sat Patiently Pooping Hard Turds)

Glaslow Outcome Scale

What are the 5 rungs/outcomes on the scale?

Disadvantages?

What is different about the GOS extended? How is it determined?

1. Death

2. Vegetative

3. Severe Disability - dependent on someone else in Activities of Daily Living (ADLs)

4. Moderate disability - impaired vocationally and socially

5. Good outcome 

Its terribly non-specific, not sensitive to differentiate many clinically significant differences; most patients can never move from one category to another

GOS-Extended: Subdivides top 3 categories into upper and lower levels; determined by a structured interview

Disability Rating Scale

What is the focus of this assessment?

2 Behavioral Disorders assoc w/ TBI

How can these be treated/handled?

1. Depression

Treatments:

• Psychotherapy for those w/ preserved insight/cognitive skills
• Pharm:  SSRI's (avoid tricyclics), psychostimulants (they energize the patient, more likely to go outpatient and rehab properly)

2. Agitation/Aggression 

First, identify the cause

Internal: Pain, Impaired cognition causing frustration

External:  Excessive sensory stim (wife puts up christmas lights in your hospital room)

Treat: Pharmacologic intervention

Pharmacologic Intervention to treat TBI patients w/ Agitation/Aggression

List 4 pharmacologic options; what drug category should be avoided and why (several reasons)?

Options:

1. Beta-blockers

2. Anticonvulsants (carbamazepine, valproic acid, lamictal) --> tends to 'lengthen their fuses'

3. Dopaminergic agonists (amantadine)

4. The newer antipsychotics

Don't give neuroleptics! Results in:

Lower seizure threshold

Impaired cognition and motor recovery

Extra-pyramidal symptoms

potential Neuroleptic Malignant syndrom

Cognition and Synaptic NT Concentration

explain how NT conc mediated cognition

What are 3 general NT agonists that can enhance cognition in TBI patients?

Moderate levels of catecholamines = optimal function

Too little OR too much = impaired function; so ppl w/ normal cognition don't increase their cognition by taking a dopamine agonist

1. Noradrenergic agonists

2. Dopaminergic agonists

3. acetylcholinergic agonists

Post Traumatic Seizures

Describe early vs. late PTS's;  What type of injuries increase the risk of experiencing a PTS?

How, if at all, can you prevent PTS?

Why is it better to use a single agent to treat then multiple drugs?

Early occurs within 1 week of trauma, late occurs greater than 1 week after

Increased risk for PTS following:

Intracranial hemorrhage

Penetrating injury

Depressed skull fracture w/ focal neurological impairment

Phenytoin (an anti-epileptic) was shown to prevent early PTS, but not late PTS

Phenobarbitol is another option, but not as good

Should try to only use 1 agent; adding another anticonvulsant will make the patient extremely fatigued, other side effects can be additive as well

Hydrocephalus

What is the classic triad of symptoms?

When do you suspect TBI-related hydrocephalus? (patient presentation and history)

Classic triad:

1. Urinary incontinence

2. Dementia

3. Ataxia

(Wet, wacky, wobbly)

Suspect TBI-related hydrocephalus when

1. patients dont progress as expected

2. often assoc w/ history of SAH, Intraventricular Hemorrhage, or meningitis

Diagnosing Hydrocephalus

Neuroimaging --> 3 findings?

What is another test you can do?

Neuroimaging findings:

Enlarged ventricles

Periventricular edema

Effaced (shorter) sulci

Can perform a CSF tap and remove some fluid to see if shunting will help

Hydrocephalus exvacuo

How can it be assessed thru brain scans?

Brain injury causes brain tissue loss, ventricles expand to fill the space

Use brain scans to compare ventricle size to the relative sulci sizes; if they are properly proportional, you are looking at Hydrocephalus evacuo; if not, you're looking at a different type of hydrocephalus

2 non-neuronal side effects of TBI (one endocrine, one bone)

How do you treat HO?

1. Pituitary Dysfunction

2. Heterotopic ossification

• caused by metaplasia of mesenchymal cells
• normally occurs at the elbow, hip, shoulder, or knee
• makes rehab very difficult

Disorders of Conciousness

Describe 4

1. Coma - eyes closed, no sleep/wake cycles

Generally short-lived, patient either dies or emerges into another level of conciousness

2. Vegetative State - eyes are open

body temp and breathing regulation is maintained

No voluntary responses to internal/external simuli, apparently no self-awareness

3. Minimally concious state - display evidence of voluntary activity

*effective communication increases likelyhood of emergence from a minimally conscious state

4. Locked in syndrome - NOT a true disorder of consciousness

Due to injury to bilateral corticospinal and corticobulbar tracts

Relatively spared cognition (can often move eyes but not face or body) -- superficially resembles a vegetative state