Neuroradiology

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