CT brain anatomy

Dr.P.Praveen Kumar.
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Ventricles of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
Anatomy of brain
 Anatomy of brain

Cerebellum Posterior fossa

 Anatomy of brain

High pons Cerebral peduncles

 Anatomy of brain

High mid brain Basal ganglia

 Anatomy of brain

Lateral ventricles Upper cortex

 CT brain anatomy-basal ganglia

BASAL GANGLIA

CORPUS STRIATUM AMYGDALA CLAUSTRUM

NEOSTRIATUM PALEOSTRIATUM

CAUDATE NUCLEUS PUTAMEN GLOBUS PALLIDUS

LENTIFORM NUCLEUS
CT brain anatomy
ACA segments
Vascular territories
Vascular anatomy of lacunar strokes
Anatomy of cavernous sinus
Major cerebellar arteries
Virchow robin spaces
Stroke and related vascular anatomy
Anatomy of extracranial vertebral arteries
Anatomy of venous drainage
Posterior circulation
Arterial supply of spinal cord
Respiratory patterns in CNS diseases
Cross sectional of cerebral hemisphere
NON INFECTIOUS PATHOLOGIES
Cerebral contusion
Extra dural hematoma
Le forts classification of facial fractures
Depressed skull fracture
Base of skull fracture
Acute – chronic –sub acute
CERVICAL SPINE CLEARING
C spine normal, tear drop fracture
C spine fractures
C spine normal alignment
Fracture spine
C SPINE CLEARING
Canadian c spine clearing criteria
Nexus criteria-c spine injury ruled out if
 Views of c spine

AP view lateral Open mouth view

Neck soft tissue shadow outline
C spine alignment
Important points related to c spine injuries
 C spine injuries

Atlanto occipital dislocation Tear drop injury

 C spine injuries

Uni facet injury Bifacet injury

INFECTIONS
Tuberculous meningitis
Neurocysticercosis
Toxoplasma encephalitis
Meningeal enhancement
 Encephalitis

Herpes encephalitis Varicella zoster vasculopathy

 Encephalitis

CMV vasculopathy Toga virus encephalitis

 Encephalitis

HIV cns infection JC encephalitis

AIDS with PML
Cerebral aspergillosis
Aspergillus lung infection
Aspergillus sinusitis
Mucormycosis
Allergic bronchopulmonary aspergillosis
 Pulmonary aspergillosis

Air crescent sign after neutrophil

Halo sign recovery
HIV encephalopathy
HSV encephalitis
Primary CNS lymphoma
Vasogenic edema
Cytotoxic edema
Global anoxic injury
Periventricular leukomalacia
Progressive multifocal leucoencephalopathy
ISCHEMIC STROKE
MRI BRAIN
Stroke protocol-time windows
T1 weighted MRI
T1 weighted with contrast
T2 weighted MRI
FLAIR
T2 * MRI
DWI
ADC MRI
MRI sequences
T1W T2W FLAIR
MRI ischemia T2W,Flair
Signal intensities in MRI
MRI sequences and abnormalities seen
MRI-ischemia
MRI various images
PWI-DWI mismatch
DWI-PWI mismatch
No mismatch DWI-PWI-no thrombolytic therapy
Mismatch DWI PWI-for thrombolysis
Stroke-MRI
Penumbra-mismatch
Maps of ischemic stroke
 Acute infarcts

PICA infarct Superior cerebellar artery infarct

 Acute infarcts

ACA infarct Ant.choroidal artery infarct

 Acute infarcts

MCA-lateral lenticulo strial MCA infarct-luxury perfusion

PCA infarct
Lacunar infarcts with normal perfusion
Water shed infarcts
Water shed infarcts
 Water shed infarcts

ACA & MCA infarcts MCA-PCA

Lacunar infarcts
CT FINDINGS OF ISCHEMIC INFARCTS
Ischemic stroke
Ischemic stroke-early findings
Sulcal effacement
Acute-sub acute stroke(hours to days).
Chronic infarct(months to years).
Hemorrhagic infarcts-seen on gradient echo
CTAngio normal, abnormal,Hyperdense MCA sign
CT perfusion
CT initially normal, later perfusion defect,CTAngio
dissection
CLINICAL COURSE OF VARIOUS STROKES
Course of hemorrhagic stroke
Course of embolic stroke
Course of lacunar stroke
Course of thrombotic course
CNS PATHOLOGIES
PRES
Sub arachnoid haemorrhage
VENOUS THROMBOSIS
Deep cerebral vein thrombosis
Venous thrombosis
Thrombosis in brain
MR venography
Thrombosis and increased CSF pressure
Dense clot sign and empty delta sign
Superior sagittal sinus thrombosis
Thrombosed transverse sinus and deep cerebral
thrombosis
Venous infarct of labbe
Venous thrombosis of straight sinus
 Ct scan brain

 Center out approach.

 Problem oriented approach.
 Blood Can Be Very Bad.
Haemorrhage vs infarction in CT & MRI
Haemorrhages
 IC Bleeding

Epidural hematomas Subdural hematomas

Don`t cross the suture line.

Sickle shaped.
Biconvex in shape.
Cross suture lines.
Arise from arterial laceration.
Poor prognosis than epidural hematoma.
Mostly middle meningeal artery.
Venous bleed.
Can be venous also.
Hematomas
 IC bleeding

Intra parenchymal bleed Sub arachnoid bleed

 Cisterns

 Circumesencephalic cistern:
1. CSF ring around the mid brain.
2. Most sensitive marker for raised ICP,herniation syndromes.
 Supra sellar cistern:
1. star shaped space above sella and pitutary.
2. Location of circle of willis.
3. Identifying aneurysmal bleeding.
 Quadrigeminal cistern:
1. W shaped cistern above mid brain.
2. Identifying traumatic SAH,raised ICP,rostrocaudal herniation.
 Supra sellar cistern:
1. located between frontal and temporal lobes.
2. Identify traumatic and aneurysmal SAH (distal MCA aneurysm)
 High pontine level.

Cerebral peduncle level. High mid brain level

 Brain window

Gray white differentiation.

Shift-
1. falx should be midline.
2. Rostrocaudal herniation-midline will
be preserved.
3. Unilateral effacement/bilateral
effacement.
Hypo/hyperdensity.
 Blood window

Epidural hematoma.
Sub dural hematoma.
Intraparenchymal hemorrhage.
Intraventricular hemmorrhage.
Sub arachnoid hemmorrhage.
Extracranial hemorrhage.
 Abnormal ventricles

First evidence of hydrocephalus-temporal horn dilatation.

Differentiate between atrophy of brain & dilated ventricles.
 Abnormal findings

 Tumors and abscess hypodense on non contrast CT,but

enhanced with contrast.
 Edema due to leaky BBB-Hypodense.
 Infarct:
1. Acute-hypodense area.
2. Early findings-loss of grey white differentiation.
3. Loss of insular ribbon.
4. Effacement of sulci.
5. Vascular territory.
Bone window
 Linear, Depressed & Basilar skull fractures

Any fluid or blood in mastoid,sphenoid,ethmoid,maxillary sinuses in setting of

trauma should suspect skull fracture.
Normal and raised Intracranial pressure
CT appearence of intracranial air
Motion artifact
WHITE MATTER LESIONS
White matter lesions
 cerebellum

vascular Multiple sclerosis

Multiple sclerosis
Multiple sclerosis
Multiple sclerosis-Dawson fingers
ADEM
Difference between ADEM & MS
D/d of white matter lesions
Dissemination in TIME & SPACE
Multiple patchy lesions
Multiple enhancing lesions
Vascular disease
Vascular disease
Sarcoid
MS vs PML
ADEM
PML
Normal aging
HERNIATION SYNDROMES
 Brain herniation

1.Cingulate herniation
2.Central transtentorial
herniation
3.Uncal herniation
4.Tonsilar herniation

Resulting in strangulation, compression of vital structures and blood vessels.

 1. Cingulate herniation:
(subfalcian herniation)

 The cingulate gyrus in one

hemisphere is pushed under the
falx towards the other
hemisphere.
 compress the internal cerebral
veins and the anterior cerebral
artery.
 2.Central Herniation

 Transtentorial herniation.
 Caused by diffuse cerebral
edema as seen in patients with
severe traumatic brain injury
 CT Scan shows effacement of
the perimesencephalic cisterns
and loss of gray-white matter
differentiation
 Central Herniation

 In the first phase of central herniation, the

diencephalon (the thalamus and
hypothalamus) and the medial parts of
both temporal lobes are forced through a
notch in the tentorioum cerebelli
 Central Herniation
Early diencephalic stage
• (reversible) Decreasing level of
consciousness with difflculty
concentating, agitation and Late diencephalic stage
drowsiness
• Patient becomes more difficult to
• Pupils are small (1-3 mm) but arouse
reactive
• Localizing motor responses to pain
• Pupils dilate briskly in response disappear and decorticate posturing
to a pinch of the skin on the neck appears with eventual progression to
(ciliospinal reflex) decerebrate posturing
• Oculocephalic reflexes are intact Progressive diencephalic impairment is
(Doll’s eyes) thought to be the result of stretching
• Plantar responses are flexor of the small penetrating vessels of the
• Respirations contain deep sighs, posterior cerebral and communicating
yawns and occasional pauses then arteries which supply the
progress to Cheyne-Stokes hypothalamus and thalamus
 Central Herniation
Midbrain stage

 As herniation progresses to the

midbrain stage signs of oculomotor
failure appears
The pupils become irregular and then fixed at
midposition The progression of
 Oculocephalic movements become symptoms indicates
more difficult to elicit irreversible ischemia and
 Extensor posturing appears therefore intervention must
spontaneously occur before the midbrain
stage to prevent permanent
 Motor tone is increased and plantar deficits from central
responses are extensor herniation
 Uncal Herniation

 Subset of transtentorial herniations

 The uncus, the medial part of the
temporal lobe, is displaced into the
suprasellar cistern
 As the herniation progresses the uncus
puts pressure on the midbrain
 As the uncus herniates it squeezes the
third cranial nerve affecting the
parasympathetic input to the eye causing
pupillary dilation and a lack of pupillary
constriction to light
Uncal herniation
 Kernohan’s Notch

 In some cases of uncal herniation the

lateral translation of the brainstem is
so severe that the midbrain is is
pushed against the opposite edge of
the tentorium
 A false localizing sign occurs as the
shift of the midbrain causes
compression of the contra-lateral
cortico-spinal tract and less
frequently, the contra-lateral third
nerve
 The side of the dilated pupil is a
much more reliable sign (90%) of the
side of the lesion than the side of the
hemiparesis
 Uncal Herniation

Clinical Findings Imaging Findings Complications

Ipsilateral dilated Contralateral temporal horn Occipital infarct
pupilContralateral widening from posterior cerebral
hemiparesis Uncus extending into the artery compression
Ipsilateral hemiparesis suprasellar cistern
if Kernohan s Notch
is present (false
localizer)

In addition to pupillary dilatation, a second key feature of uncal herniation is a

decreasing level of consciousness (LOC) due to distortion of the ascending arousal
systems as they pass through the midbrain

A dilated pupil in the absence of a LOC is not due to uncal herniation

 Tonsillar Herniation

 The cerebellar tonsils move downward

through the foramen magnum causing
compression of the medulla oblongata
and upper cervical spinal cord
 May cause cardiac and respiratory
dysfunction
Tonsillar herniation
Basilar artery thrombosis
Locations of cerebro vascular complications
External ventricular drain
Wernicke encephalopathy
wer
Hypoxic brain injury
Hypoglycemic injury
ods
ods
pres
cjd
Vascular dementia
caa
Alzhemeirs disease
ods
eernicke