Neuroradiology

NEURORADIOLOGY Interhemispheric Fissure • Hugely deep (down to the corpus callosum • Divides brain into 2 hemispheres

Sylvian • • • •

Central sulcus Paracentral sulcus Post central sulcus

fissure Hugely deep Mostly horizontal Insula is buried within it Separates tempral lobe from parietal and frontal lobes

Notes: Diffusion weighted images (DWI): important in increasing density in areas with acute infarct MRI: depicts more of the brain anatomy (in that case, better than CT) Most common location of Hypertensive plane: area of thalamus Cingulate Sulcus • Divides the gingulate gyrus from precuneus and paracentral lobule

STROKE 2 major types: • Hemorrhagic stroke a. Intracerebral: due to drugs like Coumadin (warfarin) or due to thrombocytopenia b. 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 blood SAS: MCC is trauma In absence of trauma: due to cerebral aneurysm

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Manifestations: seizure, LOC

severe

H/A,

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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

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2 major categories of hemorrhagic stroke

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Intracerebral hemorrhage – the most common, accounts for 10% of all strokes Subarachnoid hemorrhage – due to rupture of a cerebral aneurysm, accounts for 6% of strokes overall

Intracerebral Hemorrhage • Causes o Hypertensive hemorrhagemost 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

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Most common cause- ruptured cerebral aneurysm Cerebral aneurysms are frequently located around the Circle of Willis

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The detached clot often originates from the heart or from the walls of large vessels such as the carotid arteries

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Atrial fibrillation is also a common cause

Common aneurysm locations: ACoA, PCoA, MCA bifurcation, tip of the basilar artery Typically presents as the “worst headache of life”

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Account for 30% of all strokes

The re-hemorrhage rate of ruptured aneurysms is high and often fatal On CT: o Appears as high density within sulci and cisterns o The insular regions and basilar cisterns o 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 stroke o Embolic stroke o Lacunar stroke o Hypoperfusion infarction

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 nuclei o Loss of insular ribbon o Loss of gray white distinction o Sulcal effacement Notes: Plain CT: can visualize hemorrhage of infarction If shows dense basilar or MCA: signifies 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

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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

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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

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Embolic stroke • Occurs when a detached clot flows into and blocks a cerebral artery

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

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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

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Months to year

***SEE TABLE ON LAST PAGE (HYPERACUTE AND ACUTE INFARCT) INTRACRANIAL HEMORRHAGE

INTRACRANIAL VASCULAR MALFORMATION Arteriovenous Malformation

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MRI is the imaging study of choice for AVM detection

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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

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Arterial feeders o Arterial collaterals o Nidus o Venous outflow Causes

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Hemorrhage (50%) – most are parenchymal, although subarachnoid hemorrhage associated with ad=rterial aneurysms also occur Seizures (25%) Mass effect, steal phenomenon Venous hypertension headache

Acute Subdural Hematoma (white areas)

Subacute Subdural Hematoma (similar density as parenchyma)

Cavernous hemangiomas • lobulated collections of lined sinusoidal spaces

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dilated endothelial

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:

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Chronic Subdural Hematoma (hematoma is similar to CSF)

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

Subdural hematoma CT • Acute o Cresentric o Hyperdense • Subacute o Isodense

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Chronic o Hypodense o Rehemorrhage

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Hyperacute o T1- iso o T2- iso / hyper Acute o T1- iso / mod hypo o T2- hypo Subacute o T1 and T2- hyper Chronic o T1- iso / hypo o T2- hyper

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MRI

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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 NECT o Thin high density fluid collections within the superficial sulci and CSF cisterns o High density blood (fills the sulci over the right cerebral convexity)

Epidural • Associated with a skull fracture • Lacerated meningeal arteries • Between skull and dura • Cross dural attachments but not sutures • Temporoparietal area Secondary Effects of Craniocrebral Trauma

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Cerebral herniations

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Traumatic ischemia, infarction secondary (to) hemorrhage Diffuse cerebral edema Hypoxic injury

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On CT o o o o On MRI o o o

Biconvex Displaced gray-white matter 2/3 hyperdense 1/3 mixed hyper / hypo Biconvex T1- iso 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

CEREBRAL HERNIATIONS • Subfalcial (cingulate) herniation • Uncal herniations • Transtentorial herniation • External herniation • Tonsillar herniation

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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

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CT suggests DAI if petechial hemorrhages are found

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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

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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 common o After 24-48 hrs, hemorrhagic transformation or coalescence of petechial hemorrhages into a rounded hematoma

Subcortical white matter Posterior limb internal capsule Corpus callosum Dorsolateral midbrain The dorsolateral brain stem

Notes: Intracerebral hemorrhage 20 to trauma: 1. DAI 2. Cerebral contusion (MC location: lobe)

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Conforms to the shape hemisphere Chronic with rebleeding

Epidural Hematoma

Subdural Hematoma

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Biconvex Acute, contusion hematoma

of

the

temporal

cerebral

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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 spacessuprasellar and perimesencephalic (ambient, and quaadrigeminal plate) cisterns

Infarction

CT Scan

Hyperacute Infarct (<12hrs) normal (5060%)

hyperdense artery obscuration of the lentiform nucleus

1-3 days increasing mass effect

wedge shape low density hemorrhagi c transformati on

After 4-7 days gyral enhancem ent- due to the breakdown of the BBB, neovascular ity, reperfusion of the damaged brain tissue persistent mass effect

In 1-8 weeks mass effect resolves

4-7 days

In 1-8 weeks contrast enhancem ent persists mass effect resolves

Months - Year

enhance ment may persist

MRI on T1 wt

sulcal effacement gyral effacement loss of graywhite matter interface Acute Infarct (12hrs24 hrs) CT low density Scan basal ganglia loss of graywhite matter interface

sulcal effacement MRI

hyperdensity on T2

menigeal effacment adjacent to the infarct mass effect

1-3 days increase mass effect wedge shape low density area that involves the gray white matter hemorrhagi c transformati on intravascula r or meningeal enhanceme nt begins decreasing early parenchyma l CE hemorrhagi c transformati on

Months-Year volume loss

encephalomala cic change

contrast enhancem ent persists

encephalomala cic change

mass effect resolves

volume loss in affected vascular distribution hemorrhagic residua

decrease abnormal signal on T2 hemorrhagi c changes evolve and become chronic

Notes: In a 70 y/o man, the lateral ventricles and sulci are also prominent MRI: CSF – white on T2 weighted Black on T1 Enhancement of ________: T1 weighted with contrast DWTI: Blurred image Loss of gray and white matter interface:

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If white and without contrast enhancement – acute infarct

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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 nucleus b. 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, wedgeshaped, mass effect Chronic: No mass effect, density of infarct similar to CSF, rebleeding, meningeal enhancement Bright on DWTI (blurred image): acute or hyperacute 1. Presence of white areas: acute infarct 2. If dark: look at the contrast a. With enhancement of infarct: subacute b. Similar to CSF: chronic CT: blood is white; ischemia is similar to parenchyma 1. Look at the basal ganglia and thalamus 2. MCA