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NEURORADIOLOGYInterhemispheric Fissure
Hugely deep (down to the corpus callosum Divides brain into 2 hemispheres
Sylvian fissure Hugely deep Mostly horizontal Insula is buried within it Separates tempral lobe from parietal and frontal lobes
Cingulate Sulcus Divides the gingulate gyrus from precuneus and
paracentral lobule
Central sulcusParacentral sulcusPost central sulcus
Notes:Diffusion weighted images (DWI): important in increasing density in areas with acute infarctMRI: depicts more of the brain anatomy (in that case, better than CT)Most common location of Hypertensive plane: area of thalamus
STROKE2 major types:
Hemorrhagic strokea. Intracerebral: due to drugs like Coumadin (warfarin)
or due to thrombocytopeniab. SAS: due to rupture of cerebral aneurysm as a result
of hypertension bleed (affects basal ganglia) and amyloid coagulopathy
Pathognomonic of Coagulopathy: fluid level with bloodSAS:
- MCC is trauma - In absence of trauma: due to cerebral aneurysm
- Manifestations: severe H/A, seizure, LOC - Increase in density in area of cistern
Ischemic stroke
**Serpiginous: AV Malformation
HEMORRRHAGIC STROKE Are due to a rupture of a cerebral blood vessel that causes
bleeding into or around the brain Accounts for 16% of all strokes 2 major categories of hemorrhagic stroke
o Intracerebral hemorrhage – the most common, accounts for 10% of all
strokes
o Subarachnoid hemorrhage – due to rupture of a cerebral aneurysm,
accounts for 6% of strokes overall
Intracerebral Hemorrhage Causes
o Hypertensive hemorrhage- most common cause of non traumatic intracerebral hematoma
o Other causes: amyloid angiopathy- a ruptured vascular malformation, coagulopathy, hemorrhage into a tumor, venous infection, and drug abuse
Hypertensive hemorrhage Often appears as a high density hemorrhage in the region
of the basal ganglia Blood may extend into the ventricular system Intraventricular extension of the hematoma is associated
with poor prognosis Commonly due to vasculopathy involving the deep
penetrating arteries of the brain Has a predilection for deep structures including the
thalamus, pons, cerebellum, and basal ganglia—particularly the putamen and external capsule
Coagulopathy related Intracerebral Hemorrhage Can be due to drugs such as Coumadin or a systemic
abnormality such as thrombocytopenia On imaging:
o Heterogeneous appearance due to completely clotted blood
o A fluid level within a hematoma suggests coagulopathy as an underlying mechanism
Hemorrhage due to Arteriovenous Malformation Underlying arteriovenous malformation (AVM) may or
may not be visible on a Ct scan. However, prominent vessels adjacent to the hematoma suggest an underlying AVM. In addition, some AVM contains dysplastic areas of calcifications and may be visible as serpentine enhancing structures
Subarachnoid hemorrhage Most common cause- ruptured cerebral aneurysm Cerebral aneurysms are frequently located around the
Circle of Willis
Common aneurysm locations: ACoA, PCoA, MCA bifurcation, tip of the basilar artery
Typically presents as the “worst headache of life” The re-hemorrhage rate of ruptured aneurysms is high and
often fatal On CT:
o Appears as high density within sulci and cisternso The insular regions and basilar cisternso May have associated intraventricular
hemorrhage and hydrocephalus
ISCHEMIC STROKE
Caused by blockage of flow in a major cerebral blood vessel due to a blood clot
Account for about 84% of all strokes Further subdivided based on their etiology:
o Thrombotic strokeo Embolic strokeo Lacunar strokeo Hypoperfusion infarction
Thrombotic Stroke Occurs when a blood clot forms in situ within a cerebral
artery and blocks and reduces the flow of blood through the artery
May be due to an underlying stenosis, rupture of an atherosclerotic plaque, hemorrhage within the wall of the blood vessel, or an underlying hypercoaguable state
May be preceded by a transient ischemic attack and often occurs at night or in the morning when the blood pressure is low.
Account for 53% of all strokes
Embolic stroke Occurs when a detached clot flows into and blocks a
cerebral artery The detached clot often originates from the heart or from
the walls of large vessels such as the carotid arteries Atrial fibrillation is also a common cause Account for 30% of all strokes
Lacunar infarction Occurs when the walls of the small arteries thicken Cause the occlusion of the artery
Typically involve the small perforating vessels of the brain and result in lesions that are less than 1.5 cm in size
Hypoperfusion Infarction Occur under two circumstances
o Global anoxia may occur from cardiac or respiratory failure
o Presents an ischemic challenge to the brain Tissue downstream from a severe proximal stenosis of a
cerebral artery may undergo a localized hypoperfusion infarction
CT findings of Stroke Presence or absence of hemorrhage Dense MCA or dense basilar artery Subtle changes of acute ischemia
o Obscuration of the lentiform nucleio Loss of insular ribbono Loss of gray white distinction o Sulcal effacement
Notes: Plain CT: can visualize hemorrhage of infarction If shows dense basilar or MCA: signifies infarction
Lentiform Nucleus Obscuration Due to cytotoxic edema in the basal ganglia This sign indicates proximal MCA occlusion, which results
in limited flow to the lenticulostriate arteries Lentiform nucleus obscuration can be seen as early as one
hour post
Diffuse Hypodensity and Sulcal Effacement
Most consistent sign of infarction Extensive parenchymal hypodensity is associated with
poor outcome If this sign is present in greater than 50% of the MCA
territory there is, on average, an 85% mortality rate
CERBRAL INFARCTION Hyperacute Acute 1-3 days 4-7 days 1-8 weeks Months to year
***SEE TABLE ON LAST PAGE (HYPERACUTE AND ACUTE INFARCT)
INTRACRANIAL HEMORRHAGE
INTRACRANIAL VASCULAR MALFORMATIONArteriovenous Malformation
MRI is the imaging study of choice for AVM detection Serpiginous high and low signal within feeding and
containing areas (depending on flow rates) is seen in all on MR/ MRA
Adjacent parenchymal atrophy may be present secondary to vascular steal and ischemia
Brain parenchymal is replaced, but not displaced Edema is present only with recent hemorrhage or venous
thrombosis and infarction Four anatomic components
o Arterial feederso Arterial collateralso Niduso Venous outflow
Causes o Hemorrhage (50%) – most are parenchymal, although
subarachnoid hemorrhage associated with ad=rterial aneurysms also occur
o Seizures (25%)o Mass effect, steal phenomenono Venous hypertensiono headache
Cavernous hemangiomas lobulated collections of dilated endothelial lined sinusoidal
spaces the most common vascular malformation in the brain 90% are supratentorial with the frontal and temporal lobes
(deep white matter, corticomedullary junction and basal ganglia) being the most frequently involved sinus
Presentation is usually between 20 and 40 years of age and more than 50% of the time, the lesions are multiple
On CT:o Non contrast – isodense to moderately
hyperdense lesions with calcifications being fairly common
o Contrast – enhancement of lesions is variable On MRI:
o On T1 wt – the classic lesion has mixed signal or “popcorn-like” core that is surrounded by a low signal hemosiderin rim. The mixed signal of “popcorn-like” core is the result of hemorrhage in different stages of evolution
CRANIOCEREBRAL TRAUMA
Subdural Stretching or tearing of cortical veins Between dura and arachnoid Cross sutures but not dural attachments Frontoparietal convexities in the middle cranial fossa
Acute Subdural Hematoma (white areas)
Subacute Subdural Hematoma (similar density as parenchyma)
Chronic Subdural Hematoma (hematoma is similar to CSF)
Subdural hematomaCT
Acuteo Cresentrico Hyperdense
Subacuteo Isodense
Chronico Hypodenseo Rehemorrhage
MRI Hyperacute
o T1- isoo T2- iso / hyper
Acuteo T1- iso / mod hypoo T2- hypo
Subacuteo T1 and T2- hyper
Chronico T1- iso / hypoo T2- hyper
Epidural Associated with a skull fracture Lacerated meningeal arteries Between skull and dura Cross dural attachments but not sutures Temporoparietal area
On CTo Biconvexo Displaced gray-white mattero 2/3 hyperdenseo 1/3 mixed hyper / hypo
On MRIo Biconvexo T1- isoo Displaced dura seen as thin, low signal line
between hematoma and brain
Subarachnoid hemorrhage (ang gulo ng arrangement ni dra.) Occurs with injury of small arteries or veins on the surface
of the brain The ruptured vessel bleeds into the space between the pia
and arachnoid matter Trauma- most common cause
o Occurs most commonly over the cerebral convexities or adjacent to otherwise injured brain
Rupture of a cerebral aneurysm – most common cause in the absence of trauma
o A large amount of subarachnoid hemorrhage. Particularly in the basilar cisterns
On NECTo Thin high density fluid collections within the
superficial sulci and CSF cisternso High density blood (fills the sulci over the right
cerebral convexity)
Secondary Effects of Craniocrebral Trauma Cerebral herniations Traumatic ischemia, infarction secondary (to) hemorrhage Diffuse cerebral edema Hypoxic injury
CEREBRAL HERNIATIONS Subfalcial (cingulate) herniation Uncal herniations Transtentorial herniation External herniation Tonsillar herniation
Diffuse Axonal Injury Is often referred to as “shear injury” Most common cause of significant morbidity in CNS
trauma 50% of all primary, intra-axial injuries are diffuse axonal
injuries Mechanism: sudden deceleration or angular acceleration
causing shear strain injuries Marked neurological impairment disproportional with CT
finding with a normal CT is typical CT suggests DAI if petechial hemorrhages are found MRI can be useful in demonstrating the extent of injury T1 wt images will show hemorrhages as hyperintensities Non hemorrhagic injuries are better shown on T2
weighted images as hyperintensities Most common locations
o Subcortical white mattero Posterior limb internal capsuleo Corpus callosumo Dorsolateral midbraino The dorsolateral brain stem
Notes:Intracerebral hemorrhage 20 to trauma:
1. DAI2. Cerebral contusion (MC location: temporal lobe)
Cerebral Contusion The most common primary intra-axial injury Often occur when the brain impacts an osseous ridge or a
dural fold The foci of punctuate hemorrhage or edema are located
along the gyral crests On CT:
o An ill defined hypodense area mixed with foci of hemorrhage
o Adjacent subarachnoid hemorrhage is commono After 24-48 hrs, hemorrhagic transformation or
coalescence of petechial hemorrhages into a rounded hematoma
Multiple Petechial Hemorrhage in Diffuse Axonal Injury
Similar to MS (has on and off sxs); the difference is there is a history of trauma in DAI
Cerebral Edema Most life threatening Most reliable early imaging finding:
o Effacement of the surface sulci and basilar subarachnoid spaces- suprasellar and perimesencephalic (ambient, and quaadrigeminal plate) cisterns
Infarction
Hyperacute Infarct (<12hrs) 1-3 days After 4-7 days In 1-8 weeks Months - Year
CT Scan normal (50- 60%) increasing mass effect
gyral enhancement- due to the breakdown of the BBB, neovascularity, reperfusion of the damaged brain tissue
mass effect resolves
hyperdense artery
wedge shape low density
persistent mass effect
enhancement may persist
obscuration of the lentiform nucleus
hemorrhagic transformation
MRI on T1 wt
sulcal effacement
gyral effacement loss of gray-white
matter interface
Acute Infarct (12hrs-24 hrs) 1-3 days 4-7 days In 1-8 weeks Months-Year
CT Scan low density basal ganglia
increase mass effect
contrast enhancement persists
volume loss
loss of gray-white matter interface
wedge shape low density area that involves the gray white matter
mass effect resolves
encephalomalacic change
sulcal effacement hemorrhagic transformation
MRI hyperdensity on T2
intravascular or meningeal enhancement begins decreasing
contrast enhancement persists
encephalomalacic change
menigeal effacment adjacent to the infarct
early parenchymal CE
mass effect resolves
volume loss in affected vascular distribution
mass effect hemorrhagic transformation
decrease abnormal signal on T2
hemorrhagic residua
hemorrhagic changes evolve and become chronic
Notes: In a 70 y/o man, the lateral ventricles and sulci are also prominentMRI: CSF – white on T2 weighted Black on T1Enhancement of ________: T1 weighted with contrastDWTI: Blurred image Loss of gray and white matter interface:
If white and without contrast enhancement – acute infarct
With contrast enhancement – subacute infarct Review by Dra:
1. With presentation of LOC, the first modality to order is CT scan to rule out infarct or hemorrhage
2. In acute infarct, common finding is a dense basilar or MCA (most common)
3. Observe the lentiform nucleus- If there is obliteration, then it is acute infarct- If it has a normal finding, it is a hyperacute infarct.
Repeat CT scan after 1 day.
In hyperacute infarct:a. aside from the normal CT, you also see a hyperdense
artery and obliteration of the lentiform nucleusb. MRI (T1 weighted): gyral edema and loss of gray-white
matter interface After 1-3 days: CT shows increase mass effect and wedge-shaped
Subacute: hypodense (darker than adjacent brain parenchyma), meningeal enhancement, wedge-shaped, mass effect
Chronic: No mass effect, density of infarct similar to CSF, rebleeding, meningeal enhancement
Bright on DWTI (blurred image): acute or hyperacute1. Presence of white areas: acute infarct2. If dark: look at the contrast
a. With enhancement of infarct: subacuteb. Similar to CSF: chronic
CT: blood is white; ischemia is similar to parenchyma1. Look at the basal ganglia and thalamus2. MCA