Trauma

1. Dura Mater
a. Vessels running through the Dura:
i. Middle Meningeal Arteries (Posterior, Middle and Anterior)
2. Layers of ScalpBrain
a. SkinCTPeriosteumBoneDura mater Arachnoid mater Pia
mater
b. Epidural space: Between Bone and Dura
c. Subdural space: Between Dura and Arachnoid space/Pia Mater
i. CSF Drains from subdural space Arachnoid Granulations
Superior Sagittal Sinus (or other venous sinuses)
d. Middle Meningeal = in Subarachnoid Space itself (??? Probs misheard)
e. Hemorhhage can occur in subarachnoid space too
3. Parts of Dura Mater:
a. Falx = Between two hemispheres
b. Tentorium = Seperates Cerebrum from Cerbellum
i. Edge of tentorium as it comes around midbrain in center =
important for herniation reasons (will learn later why)
c. Sinuses:
i. Drain the brain
ii. Superior sagittal sinuses
iii. Transverse Sinuses
iv. Petrosal Sinuses
v. Straigh sinuses
vi. Vein of Galen
4. Uncus:
a. Inferior medial surface of the brain
b. Part o fhippocampal structures (Parahippocampal gyrus). Will be
important for herinations (learn more later)
5. Cerebellar Tonsil:
a. Important for hernation
b. Inferior, medial part of cerebellum. Will push down into foramen
magnum sometimes
6. Ventricular System
a. Have choroid plexus in them
b. Lateral Ventricles Third Ventricles Cerebral Aqeuduct 4th
ventricle
7. Blood Brain Barrier:
a. Blood Brain Neurovascular Unit
b. Site of BBB: Brain capillary endothelium
i. Tight, intercellular junctions (non permissive compared to
systemic endothelial cells) + Endothelial cels themselves
ii. Endothelium = Low pinocytotic rate and basement membrane
iii. Dynamic interaction of endothelium with astrocytes/pericytes
c. Small substances/small lipophilic molecules can still freely diffuse
through
d. Large substances/hydrophilic = Require Active Transport
8. Cerebral Edema:
 a. Accumulation of excess fluid in intracellular or extracellular spaces of
the brain
i. Major consequence = Increased intracranial pressure
ii. Cause: Variety of processes, and associated with significant
morbidity/mortality
b. Two Major Forms:
i. Vasogenic edema
ii. Cytotoix edema
9. Cebebral edema pictures:
a. Gyri/Sulci normally have space in between them
b. With Cerebral edema, you lose that space and have:
i. Widened, Flattened Gyri
ii. Narrowed Sulci
10.Vasogenic edema: Extracellular Edema
a. Disruption (increased permeability) of BBB
i. Results in shift of fluid from INTRAVASCULAR EXTRAVASCULAR
b. Predominantly involves White Matter
c. Most common causes: primary/secondary Brain tumors, abscesses,
contusions, intracerebral hematomas
d. Mechanisms:
i. Newly formed vessels in tumors deificent in tight junctions
ii. Production of VEGF in tumor cells increased endothelial
growth
iii. Production of inflame mediators/chemokines/cytokines/other
groft factors
1. Inflame leaky vessels
11.Vasogenic Edema Pictures:
a. Whole lobe looks big, gyri are flat/widened (Effaced), narrowed sulci,
compressed venricles, softened brain
b. Responds dramatically to corticosteroids (less inflame) and anti-vegf
antibody (Bevacizumab)
c. See Gliablastoma (Primary brain tumor) + edema around it (vasogenic
edema due to abnormal leaky vessels). Both lead to the increased size
of brain seen
12.Vasogenic Edema pictures slide #2:
a. Bacterial cerebral abscess on a contrast MRI image
i. Showns left occipital abscess/lesion with significant low signal
intensity around it
1. Bright = Tumor
2. Dark area around it = edema
ii. 2nd image: t2 weighted, and you can better see edema all
around the occipital lobe lesion/abscess
iii. 3rd image: see a right left shift due to marked vasogenic
edema around that abscess
13.Cytotoxic Edema: (Intracellular Edema)
a. Secondary to cellular energy failure (cells have died basically)
b. Results in a shift of water from extracellular Intracellular
compartment
 i. Intracellular swelling (Large amount of sodium enters cells
and water follows)
ii. Histologically: Brain tissue vacuolation/pallor
c. More pronounced in gray matter
d. Most common causes: Ischemia/Infarct (#1), meningitis, trauma,
seizures, hepatic cephelopathy
e. Mechanisms: Dysfunction of neuronal and astrocytic membrane pumps
(Due to excess glutamate, extracellular potassium or inflammatory
cytokines) (cells die and water goes into them)
14.Cytotoxic Edema Picture:
a. Acute infarct in left MCA territory, consistent in appearance with having
occurred 2-4 days before death. Early edema with hift of midline
structures from left right
15.Increased intracranial pressure:
a. Brain is in a closed rigid box
b. Brain volume = Brain+blood+csf+lesion
c. Increased volume = increased pressure
d. Increased pressure decreaed perfusion and erniation syndromes
e. Rigid dural folds (the Falx/Tentorium) dictate what type of hernation
16.Subfalcine Herniation
a. Cingulate gyrus herniates under the falx cerebri
i. Cingulate gyrus is just above corpus collosum and underneat
falx cerebri
b. Caused by asymmetric expanding hemispheric lesion
c. May cause compression of anterior cerebral artery, leading to
infarction
i. ACA is right above corpus collosum
ii. Starts from circle of villus and travels alongside the top of the
corpus collosum posteriorly
17.Transtentorial uncal hernation:
a. Medial Temporal lobe is displaced through the tentorial opening due to
an asymmetric expanding lesion
b. Complications:
i. Isilateral CN3 compression Pupillary dilatation
ii. Brainstem compression (Midbrain peduncle containing
corticospinal tracts) again the tentorial edge opposite the
direction of the herniation:
1. Can lead to false localization of motor deificit-ipsilateral
hemiparesis (Kernohans notch)
iii. Posteiror ceberal artery compression (ipsilateral or bilateral)
iv. Duret Hemorrhage)
c. CN3 Compression inspilaterally:
i. Tentorium is firmly attached to skull and is taut
ii. When midbrain is pushed down from above it, it is pushed
against the tentorium, compressing CN3
iii. CN3 contains pupillary constrictor fibers, so compression
Pupillary dilation
d. Kernohans notch
 i. Compression of the midbrain (due to hernation from above) can
cause the opisite cerebral peduncle to get pushed against free
edge of opposite tentorium, compressing midbrain structures
1. Creasing of the cerebral peduncle = Kernohans notch
ii. Causes weakeness/Babinski sign ipsilateral to the cerebral
hemispheric lesion due to crossing of corticospinal tracts in the
distal medulla..
e. Posterior Cerebral Artery:
i. In same area, kinda runs along the lateral midbrain.
f. Duret Hemorrhage
i. Fatal brainstem hemorrhage
ii. Due to progression of uncal hernation which leads to tearing of
vessels in the midbrain/pons
18.Cerebellar tonsillar hernation:
a. Caused by
i. Symmetric expansion of supratentorial contents into posterior
fossa into posterior fossa
ii. OR
iii. Expanding mass lesion in posterior fossa (cerebellar tumor)
b. Caudal cerebellar structures (Tonsils) attempt to escape through
foramen magnum
c. Medullary compression Cardiorespiratory arrest
19.Review of Normal CSF Flow:
a. See Choroid plexus in alteral/third ventricles/4 th ventricle (Choroid
plexus makes CSF)
b. CSF Lateral Ventricles Foramen of Monroe 3rd ventricle
Cerebral Aqeuduct 4th ventricle
i. Foramena of Luschka Lateral Subarachnoid space
circulates around brain arachnoid grans sag sinus
ii. Foramen of Magendie MIDLINE --> Subarachnoid space
circulates around space arachnoid granulations sagittal
sinus
20.Hydrocephalus: Communicating (Non-Obstructive)
a. Enlargement of ventricles associated with increases in CSF volume
b. Ventricular system is patent
i. Increased size of ventricles due to:
1. Arachnoid villi obstruction due to decreased absorption at
arachnoid granulations
2. Decreased absorption causes: Meningitis, hemorrhage in
subarachnoid space, sinus thrombosis
ii. Or due to overproduction of CSF from choroid plexus papilloma
in the ventricles (the tumor can also block and have both
causes)
21.Non-communicating Hydrocephalus
a. Obstruction within ventricular system, preventing commmunicaiton
between ventricles proximal and distal to obstruction
b. Causes:
i. Tumors in ventricle blocking flow at foramen at Monroe (or other
locations)
 ii. Congenital malformations such as astresia of the aqeudut of
sylvius
iii. Thick meninges at base of the brain blocking flow (such as due
to fibrosis secondary to meningitis thick exduate)
22.Normal Pressure Hydrocephalus
a. Idiopathic condition associated with urinary incontinence, gait apraxia
and dementia (Wet, wobbly and wacky
b. Responds to shunt tx
23.Hydrocephalus ex vacuo
a. Loss of brain tissue due to stroke/trauma/degenative conditions
Hydrocephalus ex vacuo
b. No increased csf pressure or obstruction
24.Head Trauma:
a. #1 cause of death of people < 45 yo in developed countries (head
trauma accounts for 50% of deaths
i. 50% of deaths in road traffic accidents = head trauma
b. Two primary types:
i. Blunt (nonmissle): Most Common
1. Associated with acceleration/deceleration forces to head
a. Skull Fractures, Parenchymal injuries, Vascular
injuries
ii. Penetrating (missle): Penetration by external object (Bullet)
c. Trauma Characterizations:
i. Open vs closed (referring to skull) (skull fracture or not)
ii. Focal vs diffuse
iii. Primary vs secondary dmg (For non-missle head injury)
1. Primary = skull laceration/fracture/contusions/ceberal
lacerations/intracranial hemorrhage/diffuse axoal injury
2. Secondary = ischemia,hypoxia, cerebral swelling,
infection
25.Skull Fractures:
a. Three patterns:
i. Linear: Single fracture line, through entire skull thickness
ii. Comminuted: Multiple linear fractures radiate from point of
impact
iii. Depressed: Bone fragments displaced inward
b. Occurs over convexity or base and skin may be open or closed
26.Basilar skull fracture:
a. Motor vehicle crash victim
b. Hinge fracture extending transversely across base of the skull anterior
to petrous ridges
c. Displaced circular fracture extending through occipital bones
d. Results in a ring fracture rencricling foramen magnum
27.Parenchymal Damage: [FOCAL]
a. Concussion
i. Pathophysiologic process induced by biomechanical forces (also
called mild traumatic brain injury)
ii. Direct/Indirect forces to the head
 iii. Biochemical/physiological abnormalities, but no structural
abnormalities on acute imaging
iv. Immediate transient neurologic impairment
v. Constellation of physical, cognitive, emotional and sleep related
symptoms that may or may not include loss of consciousness
1. Duration = Highly variable, minutes to months
2. Additional information: Joining forces day at end of unit
b. Contusions:
i. Wedge shaped superficial bruises of brain
ii. Occur at point of impact from fall/direct blwo to had
iii. Usually at crests of gyri overlying rough area of inner skull (such
as orbital surfaces, tip of temporal lobes, occipital poles, and
frontal tips)
iv. Damage to small blood vessels, neurons and glia
1. Gross: Hemorrhage in meninges/superficial cortex
2. Microscopically:
a. Subarachnoid space blood
b. Perivascular blood accumulation
c. After hours, necrosis, brain edema
v. Clincail correlations: Deficits correlate with size/location of injury
vi. Old Contusions:
1. Brain repairs itself poorly, so it kinda ends up as a
brownish/orange damaged area with a hole/cavity left in
that area. (brown/orange = from old blood).
2. Astrocytes make fibrillary cytoplasm glial scars in
these areas
3. Gross: Gyri idented, cavitated, brown orange discoloration
4. Microscopic: Tissue losss, m0s with hemosiderin, fibrillary
astrocytes
vii. Coup Contusion:
1. Contusion occurs at point of impact:
a. Usually secondary to blow ot stationary head (or at
point of impact from fall)
viii. Contrecoup Contusion:
1. Contusion directly opposite the point of impact
a. Usually from Falling
b. As head hits ground, a sudden deceleration occurs
causing brain to bounce back and hit skull 180
opposite point of impact with ground
i. 2nd theory is that brain in motion lags behind
skull and keeps moving after deceleration
occurs and tensile strength of vessels at site
opposite to impact is exceeded, producing
damage
28.Parenchymal damage Diffuse:
a. Diffuse axonal injury (DAI)
b. Deceleration/Acceleration injury and/or angular acceleration
c. Loss of consciousness at onset WITHOUT lucid interval before hand
d. Unconscious/disabled until death
 e. Lesser degrees may be compatible with carrying severity of neurologic
deficits
f. Axon disruption; axon transport continues Axonal swelling
i. Acute/subacute: Axonal swelling, reactives m0s
ii. Chronic: degeneration on involved fiber tracts
g. Damage of white matter (predominantly)
i. Corpus callosum, paraventricular white matter, superior
cerebellar pedunce, superior colliculi
h. Acute changes
i. Clusters of petechial hemorrhages/soft hemorrhagic foci
i. Chronic Changes
i. Hydrocephalus ex vacuo, thinned corpus callosum, gray
discoloration of white matter
29.Vascular injury
a. Epidural hematoma
b. Subdural hematoma
c. Subarachnoid space hemorrhage
d. Intracerebral hemorrhage (discuseed later)
30.Epidural and subdural hematoma (MMA is on surface eof dura)
a. Epidural hematoma:
i. Secondary to trauma at side of the head where temporal skull is
thinner
ii. Skull fracture occurs and middle meningeal artery ruptures
iii. Lucid interval may occur before signs as blood slowly
accumulates due to strong adherence of dura to undersurface of
the sull
1. However, still shorter interval than subdural hematoma as
its an arterial rupture and subdural hematomas are from
venous ruptures
iv. Compression of underlying brain may require emergency
drainage to prevent death
v. Biconvex disc on imaging
b. Subdural hematoma
i. Also from trauma
ii. Tear of bridging veins extending from subarachnoid space to
dura, usually over cerebral hemispheres (may be bilateral)
iii. Symptoms typically occur within 48 hours of events (slower than
epidural hematoma due to venous rupure)
iv. Most often non-localizing signs such as headache/confusion
v. More common in elderly people as brain atrophy makes those
bridging veins more stretched
vi. Crescent shaped hematoma
vii. Chronoic subdural hematoma well organized membrane,
composed of fibroblasts encloses hematoma after a long period
of time, and the friable vessels in this granulation tissue are
susceptible to recurrent bleeds
c. Subarachnoid space hemorrhage:
i. Under the meninges, occurs from contusions, lacerations, skull
base fractures
 ii. Escape of blood fom ventricular system
31.Sequelae of brain trauma
a. Post traumatic hydrocephalus (communicating hydrohcephalus)
i. Subarachnoid space hemorrhage plugs up arachnoid
granulations obstruction of CSF resorption
b. Post-traumatic epilepsy or seizures
c. Chronic traumatic encephalopathy
i. Associated with mild repetitive traumatic brain injury
1. Athlets(football, hockY) and veterans
ii. Initially impulsivity, aggression, depression, short term memory
loss
iii. Eventually dementia, gait, speech abnormalities, parkinsonism
iv. Pathology: Extensive depositions of tau in form of neurofibrillary
and glial tangles and TDP-43 inclusions
1. (Tau is a normal protein in axons (microtubule associated
protein) that becomes abnormal in alzheimers disease.
Same with tdp-43
v. More later
d. See key concepts slide at end
32.From cases:
a. Brain Death
i. Unresponsive to pain/central stimulation
ii. Absence of reflexes (pupillary, corneal, cough, gags, dolls eye
reflex (oculocephalic), cold caloric (oculovestibular) reflex,
iii. Absense of respirations (positive apnea test and pCO2 >60
iv. T > 32.2c (90 F)
v. SBP > 90
vi. No sedatives/paralytics/metabolic imbalances
b. Case #2
i. 80yo female, afib on Rivaroxaban (10a inhibitor anticoagulant
with no current reversible agent)
ii. Fell in yard with no loss oc consciousness
iii. At 4 hours: Subdural huemorrhage seen, braindead by 36 hours
iv. Most likely cause: Tentorial Hernation
v. Wrong answers:
1. Subfalcine hernation
a. On imaging: Braindead is ually talking about
brainstem death, which would be from a
transtentorial herination (even though pt has
some subfalcine hernation)
2. Anoxia brain injury
a. Not likely reason of brain death: probably on
ventilator, and she wasnt unconscious, so
respirations were maintained
b. Not same as hypoxic-ischemic (with lack ofblood
flow)
3. Diffuse axonal injury
a. Not likely to cause edema or brain death
 b. Either you die immediately or you dont (as
severing of axons is immediate)
c. No edema seen
d. High speed injury (car/motorcycle injury requiring
torque usually)
c. Case #6
i. Subdural vs. Epidural bleeding
ii. Subdural: Venous bleeding that tracks around the brain
iii. Epidural: Pounds: that pushes into brain into a potential space
that is more localized as its arterial bleeding
d. Case #7 Diffuse Axonal Injury
i. Not a lot of sweeling/edema/findings:
ii. No contusions seen at frontal/temporal/occipital lobe tips.
Normalish looking brain
iii. High speed injury/impact w/ no hernation Diffuse axonal injury
iv. Not concussion because pt isnt back to normalish
v. No subdural hemorrhage seen
vi. Have to do special scan to see DAI damage (but still no eema)
e. Case #8
i. Chronic/Subacute hematoma
ii. 2 weeks after fall: not a ton of hernation due to subdural
hematomas on both side, so all that we really see is compress
dilated ventricles.
iii. Blood separting into components on right sie of brain in the
subdural hematoma because its chornic
iv. Not contusions as outside brain parenchyma
v. Not duret as those are in brainstem due to brainstem being
curshed aginst foramen magnem
vi. Epidural hematoma: wwould not live for 2 week, much more
lethal. Does not present subactuely
vii. The left lateral ventricle is compressed and there is no blood it in
as seen on imag