This document provides an overview of imaging for traumatic brain injury (TBI). It discusses the goals of imaging in TBI, including rapid diagnosis of life-threatening injuries. Computed tomography (CT) is emphasized as the initial important imaging modality due to its availability, speed, and sensitivity for injuries requiring surgery. CT findings of various primary and secondary brain lesions are reviewed in detail. The document also discusses indications for additional imaging with skull X-rays and magnetic resonance imaging (MRI) in certain clinical scenarios.
Summary and illustrations of various traumatic brain injury including primary and secondary lesions as well as limited information on indications of brain imaging in trauma
Definition of stroke and cerebrovascular disorders and pathophysiology of cerebral infarct and CT imaging overview of acute-subacute and chronic infarcts and penumbra.
causes of cerebral edema , Radiological signs of acute infarct and hemorrhagic infarct and comparison of MRI and CT in the diagnosis of acute infarct
Role of diffusion weighted imaging (DWI) and diffusion perfusion mismatch
Outlines of the presentation
- How to read a brain CT
- Gross CT brain anatomy
- Traumatic brain injury
- Ischemic and hemorrhagic strokes
- Type of intracranial hemorrhages
Summary and illustrations of various traumatic brain injury including primary and secondary lesions as well as limited information on indications of brain imaging in trauma
Definition of stroke and cerebrovascular disorders and pathophysiology of cerebral infarct and CT imaging overview of acute-subacute and chronic infarcts and penumbra.
causes of cerebral edema , Radiological signs of acute infarct and hemorrhagic infarct and comparison of MRI and CT in the diagnosis of acute infarct
Role of diffusion weighted imaging (DWI) and diffusion perfusion mismatch
Outlines of the presentation
- How to read a brain CT
- Gross CT brain anatomy
- Traumatic brain injury
- Ischemic and hemorrhagic strokes
- Type of intracranial hemorrhages
In this presentation we will dscuss the imp imaging features of Posterior fossa tumors in pediatric age group.
Medulloblastoma
Pilocytic Astrocytoma
Ependymoma
Brainstem Glioma
Schwanoma
Meningioma
Epidermoid Cyst
Arachnoid Cyst
This is a slideshow made essentially for undergraduate MBBS students to have a working knowledge about CT scan of brain in diagnosing common medical and surgical conditions. It includes detection of major anatomical structures in CT and prompt diagnosis of emergency conditions like head trauma and cerebrovascular accident. Last but not the least, I have also touched the areas where CT scan is not the first mode of diagnosis (like diagnosis of brain tumor and evaluation of headache).
In this presentation we will dscuss the imp imaging features of Posterior fossa tumors in pediatric age group.
Medulloblastoma
Pilocytic Astrocytoma
Ependymoma
Brainstem Glioma
Schwanoma
Meningioma
Epidermoid Cyst
Arachnoid Cyst
This is a slideshow made essentially for undergraduate MBBS students to have a working knowledge about CT scan of brain in diagnosing common medical and surgical conditions. It includes detection of major anatomical structures in CT and prompt diagnosis of emergency conditions like head trauma and cerebrovascular accident. Last but not the least, I have also touched the areas where CT scan is not the first mode of diagnosis (like diagnosis of brain tumor and evaluation of headache).
Five pearls and pitfalls in using head CT for diagnosis of traumatic brain injury. This was presented at the 51st Annual Scientific Meeting of the Royal College of Radiologists of Thailand (6 Aug 2014)
แนวทางการรักษาโรคลมชักสําหรับแพทย์
Clinical Practice Guidelines for epilepsy
ราชวิทยาลัยประสาทศัลยแพทย์แห่งประเทศไทย
แหล่งข้อมุล:
http://thaiepilepsysociety.com/wp-content/uploads/2013/07/Thai_CPG-for-epilepsy.pdf
pediatirc neuroimaging , primer for pediatricians interested in neuroimaging and basic stuff for radiologists.
included examples of normal and abnormal.
when to do what imaging
Imaging of the traumatic brain injury by Rathachai Kaewlai, MD
1. Rathachai Kaewlai, MD
Ramathibodi Hospital, Mahidol University, Bangkok
Emergency Radiology Minicourse 2013
Slides available at RiTradiology.com or Slideshare.net/rathachai
Imaging of Traumatic Brain Injury
www.RiTradiology.com
2. Disclaimer
All opinions expressed here are those of the authors and not of their
employers.
Information provided here is for medical education only. It is not intended as
and does not substitute for medical advice. If you are a patient, please see
your doctor for evaluation of your individual case. Under no circumstances
will the authors be liable to you for any direct or indirect damages arising in
connecting with the use of this website.
The presentation may contain links to third party web sites. This does not
constitute endorsement, guarantee, warrantee or recommendation by the
authors. We do not verify, endorse, or take responsibility for the accuracy,
currency, completeness or quality of the content contained in these sites.
There is no real life patient data on this presentation. We do not write about
patients. All case descriptions are fictional, similar to descriptions you can
find in a multiple choice questions textbook for examination preparation.
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4. Traumatic Brain Injury (TBI)
• Leading cause of death and disability
• Major risk factors: extreme age, male,
low socioeconomic status
• Mortality related to Glasgow Coma Scale
(GCS) score
www.RiTradiology.com
Head injury classified by GCS
13-15 = mild HI
8-12 = moderate HI
7 or less = severe HI
5. Traumatic Brain Injury (TBI)
• Closed or open? It depends on dura integrity
Closed Open
More common Less common
Dura intact Dura disrupted
Violent accelerations of
brain tissue (coup-contrecoup)
www.RiTradiology.com
Fracture or FB penetrating
dura
6. Traumatic Brain Injury (TBI)
• Primary or secondary brain lesions? It’s “how”
closely lesions are linked to traumatic event
Primary Secondary
Caused by trauma itself Processes arising from 1) brain’s
www.RiTradiology.com
responses to trauma 2)
compression of brain, CN, BV,
skull and dura
Less devastating More devastating
Skull fractures, extraaxial
hemorrhages, intraaxial lesions
(DAI, contusion, IVH)
Herniations, diffuse edema,
infarction and infarction
DAI = Diffuse axonal injury, IVH = intraventricular hemorrhage, CN = cranial nerves, BV = blood vessels
7. Goals of Imaging in TBI
Goals Answered by...
Rapid diagnosis of life-threatening
www.RiTradiology.com
injuries
Explanation of neurological
abnormality
Prognosis information
CT
CT (if not MRI)
Clinical findings, CT, MRI,
advanced MR techniques
8. CT in TBI: Why?
• Widely available
• Fast
• Sensitive for detection and evaluation of
injuries requiring acute neurosurgical
intervention
Deciding whether surgical or medical Rx
www.RiTradiology.com
Image from salvationist.ca
9. CT in TBI: When?
• Moderate & severe acute closed HI
• Minor acute closed head injury with…
– Risk factors* or
– Neurological deficit present
• Children <2 years old
• Penetrating injury
• Skull fracture
• R/O carotid or vertebral artery injury
www.RiTradiology.com
HI = head injury
10. CT in TBI: When?
• Patients with mild HI with
one of 7 clinical findings
need CT:
– Short-term memory deficit
– Drug/alcohol intoxication
– Physical evidence of trauma
above clavicles
– Age > 60
– Seizure
– Headache
– Vomiting
www.RiTradiology.com
New Orleans Criteria
Using this scheme, CT
positivity rate was about
NEJM 2000
7-10%
Sensitivity = 100%
11. CT in TBI
• Sensitivity for
predicting need for
neurosurgery
– High risk 100%
– Medium risk 98.4%
• Reduced the need
for CT in mild HI to
54%
• Positivity rate = 8%
(1% of cases
require
neurosurgical
intervention)
www.RiTradiology.com
Stiell IG, et al. Lancet 2001;357:1391-96. | Diagram from ohri.ca
12. CT in TBI: How?
• Non-contrast, axial scan with spiral technique
• At our hospital, we use 3 mm slice thickness and
alway do bone algorithm, coronal/sagittal
reformations
• If you see maxillary hemosinus do facial CT
• If you see skull base fracture consider CTA
and skull base reformation (thin slices with small
FOV)
• If suspect C-spine fracture do C-spine CT
www.RiTradiology.com
13. CT in TBI: Checklist
• Look at all three windows
Brain Subdural Bone
www.RiTradiology.com
14. CT in TBI: Checklist
• Look for primary lesions
• Don’t forget secondary lesions (they may
be more catastrophic)
• If the study looks near-normal
– Find coup injury look for contrecoup (can be
subtle)
– Check potential areas for contusions and DAI (esp if
low GCS)
• Recheck interpeduncular fossa for small
SAH
www.RiTradiology.com
15. Skull X-ray: Outdated Yet?
• No!
• Penetrating injury
• Radiopaque foreign bodies e.g. GSW
• Part of skeletal survey in cases suspecting
child abuse
• Caveats: Skull fractures...
– About 1/3 of cases with severe TBI do not
have skull fracture!
– Negative skull x-ray does not mean no CT
www.RiTradiology.com
16. Skull X-ray: How?
• Skull trauma series in adults should
include at least 3 views given complex
skull bones
– Frontal
– Lateral
– Towne’s
• Learn to find fractures and distinguish
them from mimics
www.RiTradiology.com
17. MRI in TBI: Pros
• More sensitive for 10 and 20 injuries than CT
• Better differentiation of hemorrhagic and
non-hemorrhagic lesions in acute phase
www.RiTradiology.com
Same-day MRI
Diffuse axonal injury
18. MRI in TBI: Cons
• Intrinsic limits:
– Absolute C/I: cardiac pacemaker, ferromagnetic foreign
bodies
– Lower sensitivity for bone fractures and hyperacute blood
• Difficult managing trauma patients in MRI suite:
metallic life support, monitoring device, time
T1 T2 FLAIR
CT Images from Scarabino, et al. Emergency Neuroradiology, 2006
www.RiTradiology.com
23. Types of Skull Fracture
• Linear fracture
– a/w EDH, SDH
• Depressed fracture
– a/w focal parenchymal
lesions
• Skull base fracture
• Open head injuries
– Knife, firearm
– Laceration of dura www.uchospitals.edu
www.RiTradiology.com
24. Significance of Skull Fracture
• Indicator of brain injuries?...Not quite
– Present in the majority of cases with severe
HI
– Absent in 1/4 of fatal injuries at autopsy
– Absent in 1/3 of severe brain injury cases
• Injuries to underlying brain structures
• Association
– 15% concomitant C-spine injury
– 10-15% concomitant facial injury
www.RiTradiology.com
25. Skull Fracture: Imaging
• Best = Helical CT scan with multiplanar
reformation (MPR)
www.RiTradiology.com
In-plane fracture easier to see on reformats
26. Skull Fracture: Imaging
• Bone window with edge enhancement algorithm
www.RiTradiology.com
Soft tissue algorithm Bone algorithm
28. Skull Fracture vs. Suture
FRACTURE SUTURE
Smooth or jagged edge Serrated edge
Straight line Curvilinear line
Angular turn Curvilinear turn
Greater in width Lesser in width
(X-ray) darker (X-ray) lighter
Any locations Specific anatomic location
www.RiTradiology.com
30. Skull Fracture: Diastatic
• Fracture along suture lines “traumatic sutural separation”
• Usually affected newborns and infants (unfused sutures)
• Commonly unilateral
• Most common location = lambdoid and sagittal sutures
• >2 mm separation that is asymmetric
www.RiTradiology.com
31. Skull Fracture: Depressed
• In adults, criteria to elevate:
– >8-10 mm depression or >1
thickness of skull
– Deficit related to underlying brain
– CSF leak
• In children, two types:
– Simple depressed: usually
remodelling occurs with growth,
surgery if dura penetrated or
persistent cosmetic defect
– Ping-pong ball fractures: Rx if
underlying brain injury or dura
penetrated
www.RiTradiology.com
32. Skull Fracture: Skull Base
• Most are extensions of
fracture of cranial vault
• Clinical clues:
– CSF otorrhea or rhinorrhea
– Hemotympanum or laceration of
EAC
– Postauricular ecchymoses
– Periorbital ecchymoses in
absence of direct orbital trauma
esp if bilateral
– Cranial nerve injury (I, VI, VII,
VIII)
www.RiTradiology.com
Longitudinal
33. Skull Fracture: Skull Base
• Thin slices, bone
algorithms and
coronal images
needed for Dx
• Indirect CT signs:
– Pneumocephalus
– Air-fluid level or
opacification of
mastoid or sinuses
Longitudinal Oblique
www.RiTradiology.com
34. Skull Fracture:
Missile Injuries
Depressed Penetrating Perforating
Missile not
penetrate skull
but produces
depressed fx
or brain
contusion
www.RiTradiology.com
Missile enters
cranial cavity
but does not
leave it
Missile enters
and exits
cranial cavity
Focal brain
damage
Injury depends
on damage to
vital structures
Most severe
injury due to
shockwaves
generated by
missiles
Foreign body,
meningitis,
abscesses
Foreign body,
meningitis,
abscesses
35. Skull Fracture: Pneumocephalus
• Gas within cranial cavity
• In acute trauma setting, this is
commonly due to fractures of
PNS and temporal bones (open
skull fracture is another cause)
• Most do not cause immediate
danger but rapid expansion can
lead to brain compression
(tension pneumocephalus)
– Mount Fuji sign
• Usually decreases by 10-15 days
and almost never present by 3
weeks
www.RiTradiology.com
37. Diffuse Axonal Injury (DAI)
• Traumatic acceleration/deceleration or violent
rotation
• LOC immediately at the time of trauma coma
• Most severe of all primary brain lesions
www.RiTradiology.com
Images from http://www.pathguy.com/bryanlee/dai.htm
38. Diffuse Axonal Injury (DAI)
• Frequent cause of
persistent vegetative
state / morbidity in
trauma patients
• Clinical symptoms
worse than CT findings
• Can be isolated with no
or little association with
SAH, SDH, fracture
www.RiTradiology.com
39. Diffuse Axonal Injury
• Non-hemorrhagic 80% of cases
• Common locations:
– Grey-white matter interface (m/c)
– Corpus callosum
– Dorsolateral midbrain
• Number and location of lesions
predict prognosis (worse if
multiple & supratentorial)
• MRI most sensitive imaging but
still underestimates real extent
www.RiTradiology.com
CT
Susceptibility-weighted MRI
40. Diffuse Axonal Injury
• When initial head CT is normal but the
patient is in vegetative state
– Do MRI with susceptibility sequence OR
– Follow up CT in 24 hours (1/6 of DAI will
evolve)
www.RiTradiology.com
Small interpeduncular SAH and petechial hemorrhage in dorsolateral midbrain on CT and susceptibility-weighted MRI
44. Cerebral Contusion
• Can be normal early; can be non-hemorrhagic
• Imaging worsened with time, most evident after 24 h
www.RiTradiology.com
Day 0 Day 1
45. Cerebral Contusion: MRI
www.RiTradiology.com
FLAIR T2W
MRI is the study of choice in patients with
• Acute TBI when neurological findins are unexplained by CT
• Subacute or chronic phases when there are TBI-related symptoms
46. OTHER INTRAAXIAL LESIONS
Traumatic intraparenchymal hematoma
Intraventricular hemorrhage
Traumatic lesions of deep grey structures and brainstem
www.RiTradiology.com
47. Intraparenchymal Hematoma
• Parenchymal vessel
rupture from blunt or
penetrating forces
• May not lose
consciousness (unlike
DAI, contusion)
• Hematoma at primary
trauma site (usually
frontal and temporal)
www.RiTradiology.com
48. Intraparenchymal Hematoma
• Well-circumscribed
hyperdense lesion w/wo
perilesional edema
• Up to 60% a/w SDH, EDH
• Not always easy to
distinguish IPH from DAI or
contusion
www.RiTradiology.com
Traumatic intraparenchymal hemorrhage with IVH
49. Intraventricular Hemorrhage
• Uncommon
• Consequence of severe trauma. a/w DAI and
trauma of deep grey and brainstem
• Poor prognosis
www.RiTradiology.com
50. Trauma of Deep Grey &
Brainstem
• Stretch and torsion causing ruptured perforators,
or direct impact on dorsolateral brainstem
against tentorial incisura
• Severe trauma, poor prognosis
• CT:
– Small hemorrhages in brainstem surrounding
aqueduct, basal grey nuclei
– Can be normal
www.RiTradiology.com
52. Epidural Hematoma (EDH)
• Hematoma between inner
table of the skull and dura
• Source of bleeding
– Most common = middle
meningeal artery (90%)
(squamous temporal bone)
– Venous EDH from dural
venous sinus
www.RiTradiology.com
www.practicalhospital.com
53. Epidural Hematoma (EDH)
• Most urgent of all cases of cranial trauma
– Requiring prompt Rx to relieve compression of
brainstem, tentorial herniation, acute hydrocephalus
– EDH in posterior fossa very worrisome
• 1-4% of head injury cases, 10% of fatal cases
• Young men (20s – 40s). Rare in patients >60 y
• Almost always with skull fracture
• Lucid interval in 40% of cases
www.RiTradiology.com
54. Epidural Hematoma (EDH)
• Delayed development in 10-25% of cases
(within 36 hrs)
– Arterial EDH: blood can flow into epidural
space only after resolution of arterial spasm
– Venous EDH bleeds slowly
www.RiTradiology.com
55. Epidural Hematoma:
CT Appearance
• Biconvex or lens shape
hyperdense lesion (rare to be
isodense)
• May cross midline and dural
attachment
• Do not cross suture (except
diastatic fracture, large EDH)
www.RiTradiology.com
56. Epidural Hematoma:
Potential Indications for Surgery
• Size > 2 cm
• Active bleeding
• Impending herniation
• Corresponding
neurologic deficit
www.RiTradiology.com
57. Epidural Hematoma: Swirl Sign
• First described by
Zimmerman in 1982
• Small rounded lesion
isodense to the brain,
representing active
extravasation of
unclotted blood
• Clotted component is
hyperdense (50-70
HU)
www.RiTradiology.com
58. Venous EDH
• Tear of venous sinus
(high flow, low pressure
system)
• More benign course,
subacute presentation,
usually not require
surgery
• Posterior fossa venous
sinus > sagittal sinus
www.RiTradiology.com
60. Subdural Hematoma (SDH)
• Blood collects between
dura and arachnoid
• Torn cortical bridging veins
• 10-20% of all cranial
trauma cases
• Demographics:
– Elderly (60-80y) with brain
atrophy,
– Large intracranial
subarachnoid spaces
– “Shaken baby syndrome”
www.RiTradiology.com
www.nucleusinc.com
61. Subdural Hematoma (SDH)
• Usually co-exist with
other brain injuries
– Esp. contusion-typed
injuries > skull fractures
• Acute: within 3 days
from trauma
• Subacute: within 3 mo
• Chronic: after 3 months
www.RiTradiology.com
Layer of acute blood on pre-existing CSF-like subdural
collection in the right cerebral convexity
62. Subdural Hematoma:
CT Appearance
• Crescentic hyperdense
collection
• Can cross suture
• Can extend to
interhemispheric
fissure, along tentorium
cerebelli
www.RiTradiology.com
Note coup (Rt.) and contrecoup (Lt.) pattern.
This SDH is a contrecoup injury.
64. Bilateral Subdural Hematomas
www.RiTradiology.com
Don’t feel “enough” with trauma findings. There’re almost always more to be discovered.
65. “Isodense” Subdural Hematoma
• Usually takes 2-6
weeks for acute SDH
to become isodense
• At Hb 8-10 g/dL, blood
will be isodense to
grey matter
• Anemic patients can
present with acute
isodense SDH
www.RiTradiology.com
66. Acute On Chronic SDH
• New hemorrhage
superimposed on
chronic SDH
• Recurrent trauma
• Can be spontaneous
• Blood-fluid level , blood
clot organization,
membranes
www.RiTradiology.com
67. Comparison of EDH and SDH
www.RiTradiology.com
EDH SDH
Incidence 1-4% of trauma cases;
10% of fatal trauma cases
10-20% of all trauma cases;
30% of fatal trauma cases
Etiology a/w fractures in 90% of cases
Laceration of MMA/venous sinus
Tearing of cortical veins
Site Between skull and dura
95% supratentorial
Between dura and arachnoid
95% supratentorial
Crosses dura but not sutures Crosses suture but not dura
CT findings Biconvex (lens) shape
Shift grey-white matter interface
Crescentic shape
Diagram from Kumar et al. Basic Pathology 7E
68. Subdural Hygroma
• Extraaxial collection of
CSF caused by
extravasation of CSF
from SA space
through a traumatic
tear in arachnoid
mater
• Acute: Children >> adults
• Subacute and chronic:
Following surgery for head
injuries in operative bed or
opposite site
www.RiTradiology.com
Day of injury
1 week after injury
70. Subarachnoid Hemorrhage
(SAH)
• Blood collects beneath
arachnoid
• Tear of veins in SA space
• Usually associated with
other brain injuries
(common with contusions)
• ‘Nearly all cases of
traumatic SAH have other
lesions to suggest
traumatic cause’
– Isolated SAH in trauma
patients – possible ruptured
aneurysm causing trauma
www.RiTradiology.com
SAH with SDH
71. Subarachnoid Hemorrhage
• Site
– Next to brain contusion,
under SDH/fracture/
scalp lac
– Can be distant because
blood diffuses in SA
space
• IVH may co-exist due to
retrograde flow through
foramen of Luschka
and Magendie
www.RiTradiology.com
SAH with contusion
74. Traumatic Vascular Lesions
• Rare
• Can be overlooked initially
• ICA injury (dissection, aneurysm, occlusion)
– Base of skull fracture
• Traumatic carotid-cavernous fistula (TCCF)
www.RiTradiology.com
75. Traumatic ICA Injury
• Common cause of
ischemic stroke in the
young
• Extracranial ICA much
more common (esp
just proximal to
petrous bone)
• Dissection
occlusion or
thromboembolism
www.RiTradiology.com
At initial trauma, there were diffuse subarachnoid hemorrhage, pneumocephalus, facial fractures
and C-spine injury. Days after the injury (image C) , the patient developed left ICA territory
infarction. Angiiography (D) confirmed occlusion of the cervical ICA.
Images from Yang S, et al. J Clin Neurosci 2006;13:123
76. Traumatic CCF
• Most common traumatic AV fistula = CCF
– Clues on CT: proptosis, bulging cavernous sinus, enlarged-arterialized
www.RiTradiology.com
ophthalmic vein
A vividly enhancing structure in the right cavernous sinus with a dilated superior ophthalmic vein.
Note right proptosis
77. SECONDARY LESIONS
Herniation
Cerebral edema
Ischemia and infarction
Secondary hemorrhage
Hydrocephalus
Brain death
www.RiTradiology.com
78. Herniation
• Supra- and
infratentorial cranial
compartments by dura
and bones
• Expanding lesion
mechanical shift of
cerebral parenchyma,
CSF and attached BV
from one compartment
to another Wikipedia.org
www.RiTradiology.com
79. Herniation
Herniation Clinical Findings Imaging Findings Where to
www.RiTradiology.com
Look?
Complications
Descending
transtentorial
• Ipsilated dilated pupil
• Contralateral hemiparesis
• Ipsilateral hemiparesis (if
Kernohan notch is present)
• Uncus extending into suprasellar
cistern
• Widening of ipsilateral ambient and
prepontine cisterns
• Widening of contralateral temporal
horn
Midbrain Occipital infarct
from PCA
compression
Ascending
transtentorial
• Nausea
• Vomitting
• Obtundation
• Spinning top appearance of midbrain
• Narrow bilateral ambient cisterns
• Filling of quadrigeminal plate cistern
Midbrain and
associated
cisterns
Hydrocephalus
Rapid onset
obtundation and
possible death
Alar
(sphenoid)
• None • Displacement of MCA on axial views
• Distorted insular cortex on sagittal
views
MCA None
Subfalcine • Headache
• Contralateral leg weakness
• Asymmetric anterior falx
• Obliterated ipsilateral frontal horn
and atrium of lateral ventricle
• Septum pellucidum shift
Septum
pellucidum at
level of foramen
of Monro
Ipsilateral ACA
infarction
Tonsillar • Bilateral arm dysesthesia
• Obtundation
• Tonsils at level of dens on axial
• Tonsils on sagittal 5mm below
foramen magnum (adult); 7mm below
(children)
Foramen
magnum on
axials and
sagittals
Obtundation
Death
80. Herniation: Tonsillar
• Downward displacement of tonsils through
foramen magnum
• Seen with
– Up to ½ of all descending transtentorial herniation
– Up to 2/3 of ascending transtentorial herniation
www.RiTradiology.com
81. Herniation: Subfalcine and
Midline Shift
• Shift of cingulate gyrus across midline below falx
• Thinner ipsilateral ventricle, dilated opposite
ventricle (CSF obstruction at foramen of Monro)
www.RiTradiology.com
82. Herniation: Subfalcine and
Midline Shift
• Measured at level of foramen of Monro
• Distal ACA may be compressed against falx
www.RiTradiology.com
83. Herniation:
Descending Transtentorial
• Medial and caudal shift
of uncus and
parahippocampal gyrus
of temporal lobe beyond
tentorium cerebelli
• Asymmetric prepontine
cisterns and CP angle
(wider on side of lesion)
• AchA, PCoA, PCA may
be compressed against
tentorium
www.RiTradiology.com
85. Herniation:
Ascending Transtentorial
• Cranial shift of vermis and
parts of superomedial
cerebellar hemisphere
through tentorium incisura
• Compressed superior
cerebellar, vermian
cisterns and forth ventricle
www.RiTradiology.com
86. Posttraumatic Cerebral Edema
• Increased water content of brain and/or
increased intravascular blood volume
• Severe condition. Can be fatal
• Can be unilateral or bilateral
• Vasogenic and cytotoxic edema coexist
(vasogenic immediately, then cytotoxic)
• Evolves over 24-48 hours
• Generally resolved in 2 weeks
www.RiTradiology.com
87. Posttraumatic Cerebral Edema
• Generalized obliteration of
cortical sulci and SA
spaces of suprasellar,
perimesencephalic and
compressed/thin ventricles
• Diffuse hypodensity, loss of
grey-white matter interface
• Hyperdense cerebellum
• Often w/ transtentorial
herniation
www.RiTradiology.com
88. Posttraumatic Ischemia/Infarct
• m/c cause = herniation
• m/c location = occipital
(PCA infarct from
descending transten)
• 2nd m/c location = frontal
(ACA infarct from
subfalcine h)
• Rare = basal ganglia
(perforator/choroidal
infarct against base skull)
www.RiTradiology.com
At time of trauma
3 months later
89. Posttraumatic
Secondary Hemorrhages
• Small hemorrhagic foci in
tegmen = Duret hemorrhage
– Classic in midline of
pontomesencephalic junction
– May be multiple or extending
into cerebellar peduncles
• Necrosis/hemorrhage of
contralateral cerebral
peduncle = Kernohan’s notch
“false localizing sign”
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Hemorrhage in the midline near
pontomesencephalic junction. Also note
intraventricular hemorrhage in the 4th
ventricle
90. Hydrocephalus
• Acute hydrocephalus can
occur 2/2 brain herniation
or IVH
• Delayed hydrocephalus
usually 2/2 adherence of
meninges over cerebral
convexity, basal cisterns
or aqueduct resulting in
obstruction at level of
ventricles and arachnoid
granulations
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Look for “early sign” of hydrocephalus at temporal horns of lateral ventricles.
When acute with high ICP, there may be hypodensity around the frontal horns of lateral ventricles
91. Brain Death
• Severe increased ICP
decreases cerebral blood
flow, then irreversible loss
of brain function
• Clinical criteria: coma +
absent brainstem reflexes
+ apnea test
• No flow in intracranial
arteries/venous sinuses
• Diffuse cerebral edema,
hyperdense cerebellum
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Pseudo-SAH with non-visualization of contrast enhancement of intracranial vessels.
Only external carotid arterial branches are enhanced
92. Conclusions
• CT = primary modality for head trauma,
enough for most parts
– Skull x-rays still used in penetrating trauma,
suspected child abuse
– MR to help predicting prognosis by detection
of subtle injuries i.e., contusion and DAI
• Primary vs secondary lesion. Often,
secondary lesion more important
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93. Conclusions
• While checking the scan, make sure to
think if the patient needs CTA or other CTs
(C-spine, facial bones, etc)
• Coup-contrecoup mechanism helps
confirm acute trauma nature and search
for subtle lesions
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