CV Disease and Trauma

1

• CV Disease and Trauma
• James A. Weyhenmeyer
• 515 Medical Sciences Bldg/346 Henry Admin Bldg
• 265-5440
• weyhen_at_uillinois.edu

2

• Cerebrovascular disease (CVD) most common
  adult neurologic disorder incidence increases
  with age
• - Stroke frequently results from
  atherosclerosis, hypertension, or
• both 25 of stroke victims gt65
  200,000 deaths/yr in US, significant
• neurologic disability
• - Clinical most present as abrupt onset
  of focal neurologic
• sign(s) deficit may
  remain fixed, rapidly improve or
• progressively worsen
  may be asymptomatic when partial or
• total arterial occlusion
  is compensated for by collateral flow or
• when infarct or
  hemorrhage in a silent region

3

• Focal brain dysfunction includes transient
  ischemic attack (TIA), reversible ischemic
  neurologic deficit (RIND) and stroke
• - TIA transient focal loss of brain function
  that can be
• attributed to a specific
  vascular supply
• - Usually lasts for 2-15 min (no more than 24
  hrs)
• - Pathology small infarct, usually no
  residual lesions
• - Pathogenesis attributed to
  platelet-fibrin emboli from ulcerative
  atherosclerotic plaques in carotids
• - RIND transient focal neurologic dysfunction
  (deficit) that persists for gt 24 hr but
  resolves by 1-3 wks

4

• - Stroke sudden or rapid onset of neurologic
  deficit caused by cerebral infarction,
  intraparenchymal hemorrhage, subarachnoid
  hemorrhage or mixed hemorrhage
• - Temporal profile either improving,
  worsening or stable
• - Infarcts (most common etiology, 85-90)
  caused by thrombi, emboli or hemodynamic
  alterations
• - Multiple infarcts occasionally cause
  dementia (vascular dementia, multi-infarct
  dementia) possible causes include vasculitis,
  intravascular lymphoma, hypertension, and
  emboli

5

• Intracerebral hemorrhage (10-15)
• - Intraparenchymal hemorrhage - resulting from
  hypertension,
• amyloid angiopathy, brain tumor,
  blood dyscrasias, vascular
• malformation and vasculitis
• - Subarachnoid hemorrhage - caused by rupture
  of saccular aneurysm in circle of Willis
  (clinical - sudden onset
• of severe headache,
  alterations of consciousness and
• vomiting)
• - Mixed hemorrhages involve both
  subarachnoid space and brain parenchyma
  usually related to arteriovenous
  malformation

6

• - Clinical focal neurologic signs
• - Carotid artery disease
• - Thrombosis of left ICA in cavernous sinus,
  massive
• infarction in distribution of MCAs and ACAs
  on left side
• - CT scan several days before death
•  

• Presentation contralateral
• weakness and numbness,
• dysphasia, dyspraxia, and confusion (dominant
  hemisphere), transient
• blurring of vision or blindness
• (ipsilateral eye), homonymous visual field
  loss ipsilateral headache

7

• Vertebral-basilar artery disease
• Arteriosclerosis of vertebral/basilar arteries
  results in dilation/lengthening of vessels -
  serpentine course (left)
• Thrombosis in vertebral and basilar arteries
  resulting in massive infarction of pons/midbrain
  pons/cerebellum along with basilar artery, pallor
  of nearly all tissue indicates extensiveness of
  infarction (right)

8
Vertebral-basilar artery disease (continued) -
Presentation PCA - cerebral hemisphere
(occipital lobes, temporal/parietal areas)
homonymous visual field loss temporal lobe
seizures transient global amnesia -
Presentation basilar - midbrain and pons (
infarcted pons) occipital headache
syncope mental confusion or coma diplopia
uni- or bilateral numbness or weakness
9
Vertebral-basilar artery disease
(continued) - Presentation internal auditory
- labyrinth and cochlea - vertigo, nausea,
vomiting tinnitus acute ipsilateral
deafness - Presentation PICA - lower
brainstem/upper spinal cord ipsilateral limb
incoordination (CBL peduncle) raspy,
breathy voice vocal cord paralysis (nucleus
ambiguous) loss of pain/temp on ipsilateral
face/contralateral body ipsilateral Horners
(Wallenbergs)
10

• Infarct and hemorrhage Ischemic injury
• - Brain (major O2 consumer) receives 15 of
  resting
• cardiac output, accounts for 20 of O2
  consumption
• - Reduced O2
• - Anoxic anoxia low inspired pO2
• - CO poisoning multiple petechiae
  almost
• exclusively in white matter multiple
  perivascular
• zones of infarction blood vessels
  surrounded by
• extravasated red cells and
  intraluminal
• thrombosis
• - Anemic anoxia oxygen carrier hemoglobin
• reduced
• - Histotoxic anoxia cyanide poisoning
• - Stagnant (ischemic) anoxia no blood flow

11
- Severe hypoxia rapidly followed by severe
hypotension and cardiac arrest - Ischemia --
last common path for all forms of hypoxia -
Difference between hypoxia and ischemic
(stagnant) anoxia no blood flow in ischemia --
allows local accumulation of metabolic products
and pH changes - Metabolic failure within 10s
after blood flow ceases slowing of the EEG
focal neurologic signs - With restoration of
flow possible recovery of function, may take
mins to hrs no-reflow phenomenon due to
swelling of capillary endothelium - Selective
vulnerability - Neurons most vulnerable to
ischemia can tolerate 3-4 min w/o permanent
damage - Purkinje cells - Pyramidal cells
(CA1 region of the hippocampus) - If ischemia
is severe and prolonged, glial cells also die
complete necrosis
12
- Etiology - Occlusive thrombosis usually
arterial (atherothrombotic occlusion
most common in cervical segment of ICA and
basilar\artery) - Thrombotic (clot) occlusion
- absence of structural vascular
abnormalities in individuals with hypercoagulable
states (patients with pancreatic
adenocarcinoma) - Embolic (tissue, tumor,
fat, air bubbles, clumps of bacteria, etc)
occlusion of intracranial arteries -
Associated with cardiac disease or with artery to
artery embolism (detachment of
fragment of ulcerated plaque located at
origin of ICA and secondary occlusion of
intracranial arteries)
13
Etiology (continued) - Hemodynamic failure -
resulting from cardiac disease (MI) - Lower
brain perfusion pressure - resulting from
increased intracranial pressure (intracranial
bleed after closed head injury) - Arterial
vasospasm - most often associated with bleed into
subarachnoid space, but also occurs in
migraineurs and cocaine users
14
- Clinical sudden onset of a single, focal
neurologic deficit (e.g., monocular blindness,
difficulty with speech, limb weakness) - In
most instances, arterial occlusion manifests as
abrupt, painless event, with focal
neurologic signs in contrast, insidious, severe
headache (usually in the absence of focal
neurologic signs) is most common complaint
with intracranial sinus or venous thrombosis -
Most strokes (85) are attributed to brain
infarcts 15 result from hemorrhage into
brain or subarachnoid space
15
- Ischemic thresholds - Normal average CBF
is about 50 ml/100 g/min. - Response to
reduced blood flow vasodilation increase the
fraction of O2 extracted from
RBCs - Compensatory mechanisms are overwhelmed
when CBF falls below 20ml/100 g/min
slowing of the EEG - Unknown intrinsic factors
make some neurons stop firing at 23 ml/100 g/min,
while others continue functioning
with local blood flows at 8 ml/100 g/min may
explain selective vulnerability -
Factors influencing the outcome of an ischemic
crisis - Age child recovers faster and more
completely than adult (plasticity) -
Temperature lowering brain temperature (1o)
confers considerable protection
(neurosurgeons lower brain temp by 5o8o to
protect during periods of incomplete or
deficient CBF mechanism - ??)
16
- Excitatory transmitters - Glutamate and
aspartate - role in cell death - Glu promotes
ischemic cell necrosis by persistent opening
of Ca channels (NMDA receptors) uncontrolled
rise in intracellular
Ca leading to loss of mitochondrial respiratory
function and phospholipid metabolism
activation of Ca- dependent proteases and
lipo-oxygenases, caspases programmed cell
death - Block NMDA receptors protect
hippocampal neurons from effects of
forebrain ischemia??
17
Stages of ischemic injury - Acute within
sec of arterial occlusion - minimal changes in
neurons, neuropil and
microvasculature (reversible) progressively
worsens over next 6 hrs - Delayed after 6
hrs, presence of red (eosinophilic) neuron
(indicates irreversible neuronal
injury) - Possible mechanism contribution
of PMNs - Large stiff cells block brain
capillaries, aggravating local ischemia and
obstructing microcirculation no reflow -
Increased production and release of cytokines
(TNF and IL-1) stimulate expression of
ICAMs and cytotoxicity
18
- Pathology - First visible changes occur
after 12 hrs - Core of severe ischemia (the
"ischemic core") surrounded by an area of
reduced perfusion ("ischemic penumbra") - cells
may remain viable for several hrs - Affected
neurons eosinophilic cytoplasm, small pyknotic
nucleus (ischemic cell damage red
neurons) - Process can be widespread but not
uniform (damaged cells next to normal cells)
dead nerve cells replaced by fibrous astrocytes
(gliosis)
19
- Most severe ischemia in tissue supplied by
most distal branches wedge- shaped
areas of coagulation necrosis border zone or
watershed infarcts junctional zone
between major arterial territories (border zone
between ACA and MCA at most risk
linear parasagittal infarction) (border zone
infarcts almost invariably seen in
severe ischemic encephalopathy) -
Wedge-shaped border zone between the distribution
of MCA and PCA
20

• M/63 with peripheral angiopathy due to
  hypertension border zone
• infarcts between distribution of ACA and MCA
  in both hemispheres (left)
• - M/49 with occlusion of right internal carotid
  numerous WMLs along the
• borders of ACA, MCA, and PCA (right)

21

• F/62 MRI "red" border zone infarct between
  middle and posterior
• cerebral distributions following carotid
  surgery acute phase - 3 days after
• stroke (left) subacute phase - day 27 (right)

22
Cerebral infarct well circumscribed area of
necrosis in the distribution of a specific
vascular territory resulting from occlusion or
severe hypoperfusion in feeding artery -
Cardiac emboli important cause of infarcts, arise
from mural thrombi or valvular heart
disease other sources of emboli     -
Atherosclerotic plaques from the ascending aorta
or carotids, rarely tumor or infectious
emboli from pulmonary lesions intravascular
lymphoma can produce infarcts by local
occlusion - Associated with multi-infarct
dementia
23
- Atheromatous plaques in leptomeningeal
arteries (left) histology (old
infarct in underlying cortex) (right)
24

• Isolated plaque distal to trifurcation of right
  MCA, plaque involves a
• bifurcation point that is swollen/white
  (left) longitudinal section shows significant
  atheroma involvement and thrombus (right)

25

• Longitudinal section of trunk arteries at base of
  brain, large
• atheromatous plaque in right MCA and a recent
  thrombosis at point
• of stenosis occluding the origin of ACA and
  distal ICA (left) histology of thrombus with
  platelet aggregates, red cells and PMNs
• trapped in strands of fibrin (right)

26

• Tandem emboli in lumen of a surface artery in
  left temporal lobe (upper right) large emboli
  occluding ICAs and MCAs on both sides (lower
  left) recent hemorrhagic infarct associated with
  embolic occlusion of right MCA at its
  trifurcation (lower right)

27

• Cross section of atheromatous embolus in right
  MCA trunk (left) extensive infarction resulting
  in swelling with mild discoloration
• of cortex (right)

28

• Lacunar infarct small cystic infarct (lt1.5 cm
  in dia) located in basal ganglia, thalamus or
  cortical white (internal capsule)
• - Etiology lipohyalinosis or ateriosclerosis
  of small penetration arteries
• - Multiple small bilateral old lacunar
  infarcts in basal ganglia (primarily
• neostriatum)

29

• Evolution and organization of cerebral infarcts
• - 24 hr well circumscribed area of necrosis,
  softening, and discoloration in arterial
  territory circumscribed pallor and acute
  nerve cell necrosis, often at edge of infarct
  (penumbral zone)
• - Days 1-2 minimal PMN infiltrate
• - Days 2-5 blood-brain-barrier breakdown and
  cerebral edema
• - Days 3-5 axonal retraction at edge of
  infarct Wallerian degeneration
• - Days 5-7 appearance of lipid-laden
  macrophages (gitter cells) at periphery
  hyperplastic blood vessels
• - Days 10-14 surrounding rim of astrocytes
• - Day 14 sheets of lipid-laden macrophages
• - gt3 months cystic space surrounded by
  fibrous astrocytes

30
- Cerebellar infarct patient died 2 days
post- infarct loss of staining in
necrotic tissue (N) extravasation
of RBCs (E) infarct appears pale
(anemic) or hemorrhagic (caused by
blood flowing back into capillaries damaged
by initial anoxia) - Cortical infarct
- 7-10 days post-infarct (autolysis
and liquefaction), infarct becomes
soft and cystic area of homogenous stained
mass of necrotic neurons (I) surrounded
by area of compound granular cells
(C) and zone of proliferating glial
cells (G) - glial scar formation
31

• Cystic infarct in internal capsule (old)
  gliosis unable to completely fill
• defect (cyst-like cavity (C) lined by glial (G)

32

• Old infarction in the distribution of left MCA,
• necrotic brain has liquefied leaving a cyst
• Although most infarcts are pale, "red
• infarcts" are occasionally seen following a
• local hemorrhage into necrotic tissue gray
• matter tends to have petechial hemorrhages
• and white matter tends to have pale (ischemic)
• infarcts

33
- Clinical - Acute onset of focal neurologic
signs (e.g., hemiparesis) secondary to vascular
event - Most vascular occlusions either
thrombotic or embolic - Thrombotic
predisposing - atherosclerosis occur at
bifurcations in carotid or vertebrobasilar
system - Carotid occlusion asymptomatic if
Circle is patent. - Circle's capacity reduced
by atherosclerosis or abnormal pattern of
circulation infarction may range from small
distal lesion to whole hemisphere -
Posterior circulation does not have same
anastomotic protection atherosclerosis of
basilar often fatal - Before total occlusion
TIAs - suggest significant atherosclerotic
disease
34

• Patient with seizures and progressive loss of
  consciousness, died 12 hr after admission
  hemorrhagic microinfarcts in right inferior
  colliculus (level of midbrain/upper pons) (left)
  occipital cortex of same patient showing
  multiple, pinpoint infarcts (right)

35
Embolic usually occlude intracerebral
arteries, often producing infarct in only part of
a major cerebral artery territory - Cardiac
and carotid emboli usually affect MCA
territory - Small emboli tend to affect most
distal branches in border zone between MCA
and ACA watershed infarct - Most emboli
are sterile, but some may contain bacteria
(secondary to acute or
subacute endocarditis, lung infection)
36
Clinical (continued) - M/13 with bacterial
endocarditis mycotic embolus occluding the right
MCA intracerebral hemorrhage following rupture
of mycotic aneurysm
37

• Septic infarct creamy central spot surrounded
  by zone of hemorrhage
• microscopic, focal collections of bacterial
  colonies within infarcted area,
• proximal border of superficial septic infarct
• Air embolus usually follows trauma or
  surgical procedures involving the
• lungs, dural sinuses, or jugular veins may
  also result from a release of
• nitrogen bubbles into general circulation
  following a rapid reduction in
• barometric pressure (bends)

38
Fat embolus rare, may follow a bone
fracture - M/45 admitted to hospital 5 days
previously with multiple injuries, including
fractures, following a car accident became
comatose, jaundiced and died numerous small
petechial hemorrhages scattered throughout white
matter (relative sparing of gray)
39

• Histology
• Small (2-3 mm dia) hemorrhagic areas in
  brainstem each has a circular (ring) hemorrhage
  around a dilated small blood vessel blocked by
  RBCs and PMNs
• Ttissue between vessel and extravasated blood is
  necrotic
• Macrophages have infiltrated blood clot and
  necrotic tissue

40
- Course - Arterial bed that contains lodged
embolus may initially spasm -
Tissue becomes ischemic infarction - If
embolus is lysed, blood flow is restored,
resulting in hemorrhagic infarction -
Clinical - Focal neurologic signs -
F/78 with infarction area at posterior
-inferior end of left frontal lobe aphasia
(upper) - F/69 with recent infarction of
medial right occipital lobe
(occlusion of right posterior
cerebral) - blurred vision (lower left)
41

• Intracranial hemorrhage may result from
  rupture of a vessel anywhere in the cranial
  cavity classified according to location
  (extradural, subdural, subarachnoid, parenchymal,
  intraventricular), type of ruptured vessel, or
  cause (trauma, coagulation defect, degeneration,
  hypertension, infection)
• - Spontaneous (non-traumatic) 3 general
  categories
• - Intracerebral hemorrhage most often
  associated with history of hypertension
• - Hypertensive hemorrhage results from
  microaneurysm (Charcot-Bouchard aneurysm)
  that forms at bifurcation of small
  intraparenchymal arteries rupture destroys
  aneurysm and surrounding brain
  tissue
• - Most affected sites putamen (55),
  cortical white matter (15),
  thalamus (10), pons (10), cerebellum (10).
• - Subarachnoid hemorrhage usually
  associated with aneurysm
• - Mixed brain/subarachnoid hemorrhage

42
- Pathology - Swelling of affected cortex
and flattening of gyri (uncinate
herniation) - If vessel ruptures into the
ventricle, blood clots can lodge in
foramina hydrocephalus mass effect of clot
causes distortion of ventricles
(ipsilateral ventricle compressed) -
Resolution begins with appearance of macrophages
digest the clot (takes mos)
leaving slit-like cavity surrounded by fibrillary
astrocytosis containing
hemosiderin-laden macrophages
43
- Clinical - Initial mortality - 40 -
If hemorrhage into lateral ventricle spreads
through the ventricular system into
subarachnoid space almost always fatal -
Relatively good prognosis for initial survivors
resolution of hematoma may be
accompanied by a return of function -
Supratentorial hemorrhages progressive
hemiplegias
44

• F/73 suffered a CVA with left-sided hemiparesis
  (5 yrs earlier) organized,
• partly cystic area of hemorrhage located in
  region of basal ganglia
• (adjacent to the internal capsule) vascular
  rupture occurred at site of a
• Charot-Bouchard microaneurysm (classical
  feature of CVA hypertensive
• disease) (left)
• F/16 had acute myeloblastic leukemia died from
  bleeding diathesis
• multiple hemorrhages indicate bleeding
  disorder rather than vessel rupture (right)

45
- Cerebellar hematomas ataxia, eye movement
abnormalities, and intractable
vomiting - No matter where the location,
raised ICP, coma, and herniation
rapidly become dominant picture
- Effects of increased ICP -
Cerebellar tonsil herniation through
foramen magnum - pressure on brainstem. -
Uncal herniation - compression of
brainstem and stretching of
posterior communicating artery -
Diagnosis CT scan/MRI reveals increased
density (fresh blood)
46
Subarachnoid hemorrhage usually results from
aneurysm (berry, congenital), atherosclerosis,
infection, trauma, or rarely AV malformation
primary ruptured vessel hemorrhages into
subarachnoid space (arterial aneurysm of the
Circle of Willis) secondary hemorrhage into
the brain - Saccular (berry) aneurysm most
common aneurysm (95) most common sites are at
junction of carotid and posterior communicating
arteries, anterior communicating artery, major
bifurcation of MCA in Sylvian fissure
47
- Pathogenesis - Defective arterial elastic
lamina wall bulges to form saccular fundus
composed of fibrous tissue -
Laminated blood clot and fibrin may be deposited
on wall - Rupture often associated with
activities that acutely raise ICP (straining at
stool, lifting heavy weights, sex) most
ruptures are sporadic likelihood of
rupture increased when dia gt10 mm - Lab -
CSF - usually bloody with xanthrochromic
supernatant - Increased ICP - Increased
protein, glucose may be abnormally low -
Reactive pleocytosis (late) - CT shows
intra-extraparenchymal hematoma angiography is
definitive
48
- Clinical - Compression of cranial nerves,
thrombosis in aneurysm and dispersing of
emboli to distal branches, bleeding focal
neurologic signs - Usually complain of sudden
severe headache ("the worst headache I've ever
had") lower back pain sometimes more
prominent than headache - Alert and lucid to
confused, delirious, amnestic, lethargic, or
comatose loss of consciousness - grave
prognosis - Stiff neck and Kernig's -
hallmarks of subarachnoid hemorrhage -
Mortality 25-50 with first rupture most
survivors improve and recover
consciousness in mins rebleeding is common
grave prognosis
49

• M/48 with a berry aneurysm on anterior
  communicating artery
• bleed caused a subarachnoid hemorrhage (left)
• F/57 with a ruptured aneurysm on internal
  carotid (right) at origin of
• middle cerebral hemorrhage in subarachnoid
  space that extends
• into optic nerve (upper right)
• - F/61 with a large, unruptured aneurysm of
  basilar artery (lower right)
• - Treatment surgical

50
Mixed CNS and subarachnoid hemorrhage - AV
malformation tangles of abnormal vessels with
characteristics of both arteries and veins 90
of AVM's found in the cerebral hemispheres -
Abnormal vessels separated by gliotic scar
(evidence of repeated bleeds) -
Bleeds into brain and subarachnoid space (70)
bleeds into subarachnoid space alone (25)
51

• F/20 - large AVM in left basal ganglia
  following repeated
• headaches after a normal pregnancy and
  delivery AVM is fed by all
• three cerebrals, lenticulostriate and
  choroidal arteries (left)
• M/23 with a large AVM in temporal lobe
  extending into subarachnoid
• space bleeding caused subarachnoid and
  intracerebral hemorrhage
• - Seizures common

52
Hypertensive vascular disease associated with
intracerebral hemorrhage, occlusive
atherosclerotic vascular disease, atheroembolic
infarcts, lacunae, subcortical leukoencephalopathy
, hypertensive encephalopathy - Lacunae (little
lakes) - Small necrotic foci (2-15 mm dia)
most common in deep areas of brain (basal
ganglia, thalamus, internal capsule, cerebral
white matter, pons) - F/70 developed
left-sided hemiplegia (3 yrs ago) severe
atheroma of ACA and MCA small areas of
cystic softening in basal ganglia (globus
pallidus (left and right), caudate nuclei, and
left claustrum
53

• Most result from occlusion of deep penetrating
  arterioles (due to
• emboli or atherosclerosis) usually follows
  long-term hypertension
• Pigmented macrophages present suggests a
  hemorrhagic
• component
• Often asymptomatic, but if there is a
  vulnerable spot (e.g., internal
• capsule) may produce symptoms (pure motor
  hemiplegia, pure
• hemisensory stroke, sensorimotor pseudobulbar
  palsy, ipsilateral
• ataxia and hemiparesis, dysarthia, clumsy
  hand syndrome)

54
Hypertensive encephalopathy associated with
malignant hypertension and acute hypertension
seen in eclampsia and acute nephritis -
Clinical headache, drowsiness, vomiting,
convulsions, progressing to stupor
and coma - If diastolic pressure rises above
130 mm Hg retinal exudate and
hemorrhage with papilledema - Symptoms
reversed when blood pressure is reduced - Rx
hypotensive agents (nitroprusside) -
Pathology cerebral edema, petechial
hemorrhages, fibrinoid necrosis of
small artery walls - Associated with failure
of auto-regulation (generalized arterial
dilation), increased CBF, and
breakdown of blood-brain barrier with development
of cerebral edema
55
Trauma - Single largest contributor to death
in the emergency department major
cause of persisting neurologic handicap affects
mostly young (ages 15 to 24 MF
31) - Effect of trauma on skull and brain
depend on shape of object, force of
impact, and whether head is in motion at time of
impact - Severe brain damage can occur
without external injury severe external
lacerations (even skull fractures) do not
necessarily indicate brain injury
56
Skull fractures common complications of head
trauma - Closed head injury - No injury to
skull or a linear fracture (subdivided into - no
significant structural damage to
brain (concussion) and destruction
of brain tissue (related to edema, contusion,
laceration, or hemorrhage) - Linear
fractures commonly produced by broad-based forces
(impacts that occur in traffic accidents
and falls)
57
- Depressed fracture - Pericranium
intact but a fragment of fractured bone is
depressed inward either compressing or
injuring brain - Possible causes
assaults, impacts with protruding pointed
objects in auto collisions leading
mechanisms for depressed fractures in
children are home accidents and traffic
accidents - Compound fracture - Direct
communication between scalp and brain through
depressed or comminuted (splintered)
fragments of bone and lacerated dura
simple concussion less likely and severe brain
damage more likely
58
- Complications of head injury - Vascular
lesion (hemorrhage, thrombosis,
aneurysm) - Infection (osteomyelitis,
meningitis, abscess, rhinorrhea, otorrhea,
pneumocele) - Leptomeningeal cysts
(kids) - Injury to cranial nerves and focal
cerebral lesions - Sequelae - Convulsive
seizures - Psychosis (and other psychiatric
disorders) - Post-traumatic syndrome
59
Epidural hematoma - Localized collections of
blood between skull and
dura - M/16 with epidural hemorrhage resulting
from rupture of right middle
meningeal artery following head injury
(upper left)   Subdural hematoma - Rupture
of bridging veins that connect venous
system to large dural sinuses, bleeding into
subdural space between dura and
arachnoid - Almost always secondary to head
injury, may be mild or unnoticed   -
Subdural hemorrhage - rupture of veins
following head injury (upper right)
60

• Subdural hemorrhage - rupture of dorsal
  bridging veins acute
• subdural in elderly woman taking
  anticoagulants for TIAs following minor
• head injury in car accident, died 1-day
  later (left)
• M/87 Chronic left subdural, trichrome shows
  neomembranes
• staining pale blue when compared to denser
  collagen of the dura
• compressive effects shown in MRI 3 mo later,
  patient died of acute
• myocardial infarction, blood clot almost
  completely organized (no
• compression effect) (right)

61
Parenchymal injuries - Concussion transient
loss of consciousness following head
trauma duration usually short, may last for hrs
recovery almost always
complete - Angular (rotational)
acceleration of head is more potent than
translational (anteroposterior) movement in
producing concussion (left hook) -
Hypothesis torsion of the midbrain may
temporarily disrupt function of the RAS
62
Contusions - Bruise (cortical surface) -
hemorrhage from torn vessels within cortex -
Related to site of impact (coup, least common) or
opposite the impact (contrecoup,
most common occurs with falls/traffic
accidents), or indirectly as brain strikes
irregularities on inner surface of skull
(lesser wing of sphenoid/orbital ridges
producing contusions on frontal/temporal
poles) - Focal damage, even in severe cases
there may be complete recovery if no diffuse
axonal injury - Larger and more
hemorrhagic in alcoholics, hypertensives or
patients with bleeding disorders -
As contusion matures, necrotic tissue removed,
leaving a sunken orange-brown scar
with a reactive glial tissue floor ("plaques
jaunes")
63

• Patient struck by a protruding object from a
  moving train died 8 days later
• multiple contusions in brain sections (upper
  left), petechial hemorrhages diffusely
• distributed (upper right)

64
Lacerations - Tear in brain tissue resulting
from severe blunt trauma, often accompanied
by other damage (fracture, local hemorrhage,
necrosis) resolution results in a
yellow-brown gliotic scar that involves cortex
and deeper structures   Traumatic
intracerebral hemorrhage - Contained within
brain (does not extend to surface) often
multiple, involving frontal and temporal
lobes as well as deep structures results
from rupture of intracerebral vessels at time of
trauma
65
Diffuse axonal injury - Severe neurologic
impairment after trauma without grossly visible
brain damage - Clinical deeply comatose, may
recover only to point of persistent vegetative
state - Shaken baby syndrome newborn to 4
yrs - Mechanism shearing forces that occur
during acceleration and deceleration of
brain cause rupture of axons -
Pathology - Widespread white matter damage
in form of ruptured axons and spheroids
(circular or elongated granular bodies containing
cell organelles) - Brain with most
severe diffuse axonal injury has focal lesions in
corpus callosum and in one or both
quadrants of rostral brainstem similar
hemorrhagic lesions in subcortical white matter,
fornix, tela choroidea, walls of third
ventricle, basal ganglia and hippocampus - Diagn
osis history, CT scan or MRI
66
Complications of trauma - Post-traumatic
brain edema herniation, brainstem
compression. - Skull fractures conduit for
infection - Hydrocephalus secondary to blood
or infection in the ventricle,
aqueduct, or subarachnoid space - Death may
occur even though there is no apparent physical
disruption of tissue - Delayed
sequelae post-traumatic epilepsy (usually with
cortical contusion or laceration)
delayed intracerebral hemorrhage