Trauma

Question 1

blood brain barrier bbb

Answer 1

Also called BB neurovascular unit
Site of BBB- brain capillary endothelium
Tight intracellular junctions (non-permissive compared to systemic endothelial cells)

Endothelium has low pinocytotic rate and basement membrane, Dynamic interaction of endothelium with astrocytes and pericytes

Small substances and small lipophilic molecules freely diffuse through membrane

Large substances and hydrophilic molecules require active transport

Question 2

Cerebral edema

Answer 2

Defined as an accumulation of excess fluid in intracellular or extracellular spaces of the brain–> increased intracranial pressure, results from a variety of processes and associated with significant morbidity and mortality

2 forms: Vasogenic edema and cytotoxic edema

The gyri and sulci go awau

Question 3

Vasogenic edema– extracellular edema

Answer 3

Disruption (increased permeability) of BBB
Results in a shift of fluid from the intravascular to the extravascular compartment

Predominant invloves white matter

Causes- primary or secondary brain tumors, abcesses, contusions, intracerebral hematomas

Machanisms- Newly formed vessels in tumors (deficient in tight junctions), production of vascular endothelial growth factor VEGF by tumor cells, production of inflammatory mediators, chemokines, cytokines, and other growth factor

Often responds dramatically to corticosteroids and to anti vegf antibody (Bevacizumab), flattened gyri, narrow sulci compressed ventricles, brain softening

Question 4

Cytotoxic edema- intracellular edema

Answer 4

Occurs secondary to cellular energy failure
Results in a shift of water from the extracellular to intracellular compartment
Intracellular sweilling- large amounts of Na enter cells, water follows,
histologically brain tissue vacuolation

More pronounced in gray matter

Most common causes- ischemia/infarct, meningitis, trauma, seizures, hepatic encephalopathy

MOA- dysfunction of neuronal and astrocytic membrane pumps (caused by excess glutamate, extracellular potassium, inflammatory cytokines)

Question 5

Edema leads to increased intracranial pressure

Answer 5

The brain is in a closed rigid box
Brain volume= Brain and blood and csf (with possible lesions)
Increased volume=increased pressure
Increased pressure leads to decreased perfusion and or herniation syndrome

Rigid dural folds (falx, tentorium) dictate what type of herniation

Question 6

Subfalcine herniation

Answer 6

Cingulate gyrus herniates under the falx
Caused by asymmetric expanding hemispheric lesions
May cause compression of anterial cerebral artery –> infarct (messes with the leg of homonculus)

Question 7

Transtentorial uncal herniation

Answer 7

Medial temporal lobe (spc- the uncus) displaced thru the tentorial opening because of asymmetric expanding lesion

Complications- Ipsilateral CN3 nerve compression with pupillary dilatation, compression of brainstem (midbrain peduncle containing corticospinal tracts) against the tentorial edge opposite the direction of herniation (can lead to false localization of motor deficit -ipsilateral hemiparesis (kernohans notch)– Pupillary contrictor fibers (dilatation
Posterior cerbral artery compression (ipsi-bilateral )
Duret hemorrhage

Question 8

Kernohans notch

Answer 8

With compression of midbrain due to herniation from above the opposite cerebral peduncle is pushed against the opposite free edge of the tentorium (the creasing of the peduncle is called kernohans notch)

Causes weakness and a babinski sign ipsilateral to the cerebral hemispheric lesion (bc of crossing of the corticospinal tracts in distal medulla)

Question 9

Duret hemorrhage

Answer 9

Fatal brainstem hemorrhage

Secondary to pregression of uncal herniation and resultant tearing of vessels in midbrains and pons

Question 10

Cerebellar tonsillar herniation

Answer 10

Caused by symmetric expansion of supratentorial contents into posterior fossa OR expanding mass lesion in posterior fossa
Caudal cerebellar structures- tonsils attempt to escape thru the foramen magnum
Medullary compression results in cardiorespiratory arrest

Question 11

CSF flow

Answer 11

Choroid plexu of the lateral and third ventricles make the CSF, it flows in the lateral ventricles

Then to the third venricle
Cerbral Aqueduct: 3rd ventricle to 4th ventricle

Foramen of luschka: 4th ventricle to subarachnoid space (lateral L for lateral)

Foramen of magendie: 4th ventricle to subarachnoid space (medial)

Arachnoid granulations spit out the excess CSF into the venous sinuses–> circulated in th body and peed out

Question 12

hydrocephalus: communicating (non obstructive

Answer 12

Enlargement of ventricles associated with increas in CSF volume
Ventricular system is patent- increased size of ventricles may be due to: arachnoid villi obstruction due to decreased absorption at arachnoid granulation, causes of decreased absorption: meningitis, hemorrhage in subarachnoid space, or sinus thrombosis

OR over production of CSF from a choroid plexus papilloma

Question 13

non- communicating hydrocephalus

Answer 13

Obstruction within ventricular system
Prevents Communication between the ventricles proximal and distal to obstruction
Examples of causes- tumor in ventricle blocking flow (at the foramen of monro), congenital malformation (atresia of aquduct of sylvius)
Thick meninges at base of brain blocking flow (fibrosis secondary to meningitis)

Question 14

Normal pressure hydrocephalus and hydrocephalus ex vacuo

Answer 14

Normal pressure hydrocephalus: idiopathic condition associated with urinary incontinence, gait apraxia, and dementia (wet, wobbly, wacky), responds to shunt placement

Hydrocephalus ex vacuo- Occurs when there is loss of brain tissue due to stroke, trauma, or degenerative contions, no increase in CSF pressure and no obstruciton

Question 15

head trauma

Answer 15

Leading cause of death of people<45
2 types: Blent and penetrating
Blunt- most common, associated with acceleration or deceleration forces to the head, Results in skull fractures, parenchymal injury, vascular injury
Penetrating missle- penetration by external object bullet

Characterization of trauma- open vs closed (referring to skull), focal vs diffuse, primary damage vs secondary damage

Question 16

Primary vs Secondary damage related to non missle head injury

Answer 16

Primary damage- scalp laceration, skull fracture, cerebral contusions, cerebral laceration, intracranial hemorrhage, diffuse axonal injury

Secondary damage- ischemia, hypoxia, cerebral swelling, infection

Question 17

Skull fractures

Answer 17

3 patterns-
linear :single fracture line, through entire thickness of skull
Comminuted- multiple linar fractures radiate from point of impact
Depressed: bone fragments displaced inward

Occur over convexity or base
Skin may be open or closed

Question 18

Parenchymal damage- focal (concussions)

Answer 18

Concussion- pathophysiologic process induced by traumatic biomechanical forces (mild tramatic brain injury)

Caused by direct or indirect forces to head: biochemical and physiologic abnormalities occur, usually no structural abnormalities on imaging acutely, immediate transient neurologic impairment, constellation of physical, cognitive, emotional, and or sleep related symptoms that may or may not involve loss of consiousness, duration is highly variable- several minutes to days weeks, months or longer

Question 19

Parenchymal damage- focal (contusions)

Answer 19

Wedge shaped superficial bruises of the brain, occur at any point of impact from fall or from direct blow to head
Usually at crests of gyri overlying rough area of inner skull
(oribital surfaces, tips of temporal lobes, occipital poles)

Small blood vessels, neurons, and glia are damaged
(Grossly- hemorrhage in meninges and superficial cortex), microscopically corresponds to subarachnoid space blood, perivascular accumulation of blood, after hours, necrosis, brain edema

Clinical correlations- deficits correlate with size and location of injury

Question 20

coup vs contrecoup contusion

Answer 20

coup contusion- contusion occurs at at point of impact, usually secondary to blow to stationary head, may occur at point of impact from fall

Contrecoup contusion- contusion directly opposite the point of impact (usually occur with fall, as head hits groud a sudden decelration occurs that causes brain to bounce back and hit skull 180 opposite the point of imapct with ground
Another theory is brain in motion lags behind skull and with deceleration or impact of skull, it keeps moving the tensile strength of vessels at the site opposite of impact is exceeded producing damage

Question 21

Parenchymal damage- diffuce

Answer 21

Diffuse axonal injury (DAI)- deceleration/acceleration injury and or angular acceleration, loss of consciousness at onset without lucid interval, unconscious or disabled till death, lesser degrees may be compatible with varying severity of neurologic deficits, axons are disrupted axonal transport continues and causes axonal swellings (acute and subacute - axonal swellings reactive macrophages, chronic degeneration of involved fiber tracts

Damage to white matter mostly