Ebook Diagnostic imaging - Emergency (2nd edition): Part 2

(BQ) Part 2 book Diagnostic imaging - Emergency presents the following contents: Nontraumac (central nervous system, abdomen/pelvis, chest/cardiovascular, musculoskeletal).

fragment and the medial condyle of the humerus This MR was obtained in a 13-year-old baseball pitcher with an acute injury (Right) Anteroposterior radiograph shows reduction and screw fixation of the medial epicondyle avulsion fracture

in the same patient

(Left) Anteroposterior radiograph shows avulsion of the tip of the medial epicondyle in a 12 year old who started pitching 3 weeks ago, now with elbow pain and presenting for radiographs (Right) Coronal T2WI MR in the same patient shows hyperintense signal throughout the medial epicondyle ossification center The small osseous fragment could not be identified This is an example of Little Leaguer's elbow

Part II - Nontrauma

Section 1 - Central Nervous System

Introduction to CNS Imaging, Nontrauma

> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Introduction to CNS Imaging, Nontrauma Introduction to CNS Imaging, Nontrauma

Anne G Osborn, MD, FACR

Overview

Patients with a number of different nontraumatic disorders of the brain, spine/spinal cord, and head and neck may present in the emergency department While virtually any disease in any body part can be seen in the emergency

department, some of the most common urgent entities are discussed in this section

Nontraumatic Brain Emergencies

Whom to Scan? When to Scan?

Head CT scans in nontraumatized patients with CNS-related complaints are commonly obtained in emergency settings and account for 70-80% of all CT requests from emergency departments Prospective studies have revealed that only 8% of such scans reveal clinically significant abnormalities Of these cases, over 95% have positive neurologic findings

Growing concerns about both the costs and the radiation exposure that occurs during CT acquisition have prompted attempts to identify clinical variables that are independent predictors of abnormal head CT findings in emergency

department patients Six such clinical variables have been identified:

(1) Age > 70 years

(2) Focal neurologic deficit

(3) Altered mental status

(4) History of malignancy

(5) Nausea &/or vomiting

(6) Derangements in coagulation profile

Recent studies do not support the routine use of brain CT in patients under the age of 70 years for the investigation of uncomplicated headache (i.e., in the absence of additional neurologic findings), migraine-like symptoms, vertigo,

dizziness, drug use, blood pressure abnormality, or generalized symptoms such as fatigue or diffuse weakness

Presentation at an emergency department with a known patient history of seizure is also not predictive of abnormal head

CT findings

Nontraumatic Hemorrhage and Vascular Lesions

Spontaneous (i.e., nontraumatic) intracranial hemorrhage and vascular brain disorders are second only to trauma as neurologic causes of death and disability When a patient with no history of trauma presents in the emergency

department with sudden onset of a neurologic deficit, NECT scans are the most appropriate initial imaging study

Challenging questions arise when screening NECT discloses parenchymal hemorrhage What are the potential causes? Is the patient at risk for hematoma expansion? Should further emergent imaging be performed?

The most recent American Heart Association/A merican Stroke Association guidelines recommend emergent CT or MR as the initial screening procedure to distinguish ischemic stroke from nontraumatic intracranial hemorrhage If the patient is older than 45 years and has preexisting systemic hypertension, a putaminal, thalamic, or posterior fossa intracranial hemorrhage is almost always hypertensive in origin and does not require additional imaging

In contrast, lobar or deep brain bleeds in younger patients or normotensive adults, regardless of age, usually require further investigation Contrast-enhanced CT/MR with angiography may be helpful in detecting underlying abnormalities, such as arteriovenous malformation, neoplasm, and cerebral sinovenous thrombosis

A CT angiogram (CTA) is indicated in patients with sudden clinical deterioration and a mixed-density parenchymal

hematoma (indicating rapid bleeding or coagulopathy) CTA is also an appropriate next step in children and aged adults with spontaneous intracranial hemorrhage detected on screening NECT Likewise, CTA is appropriate in patients with aneurysmal, perimesencephalic nonaneurysmal, or convexal subarachnoid hemorrhage

young/middle-If a CTA is negative, emergency MR is rarely necessary in patients with unexplained “spontaneous” intracranial

hemorrhage (sICH), although a follow-up nonemergent MR with and without contrast can be very useful Evidence for prior hemorrhage on T2* sequences (GRE or SWI) can be very helpful in narrowing the differential diagnosis Multifocal

“black dots” in elderly patients with sICH is typical for chronic hypertensive encephalopathy and amyloid angiopathy (CAA) Basal ganglia and cerebellar “black dots” are common in chronic hypertension but rare in CAA Conversely,

peripheral (cortical, meningeal) “blooming black dots” on T2* are more common in CAA

Strokes

“Stroke” is a generic term that describes a clinical event characterized by sudden onset of a neurologic deficit However, not all strokes are the same! Stroke syndromes have significant clinical and pathophysiological heterogeneity Arterial ischemia/infarction is by far the most common cause of stroke, accounting for 80% of all cases

The remaining 20% of strokes are mostly hemorrhagic, divided among primary “spontaneous” (nontraumatic) intracranial hemorrhage, nontraumatic subarachnoid hemorrhage, and venous occlusions

As the clinical diagnosis of acute stroke is inaccurate in 15-20% of cases, imaging has become an essential component of rapid stroke triage When and how to image patients with suspected acute stroke varies from institution to institution Protocols are based on elapsed time since symptom onset, availability of emergent imaging with appropriate software reconstructions, preferences of clinician (and radiologist), and availability of neurointervention

There are four “must know” questions in stroke triage that must be answered quickly and accurately:

(1) Is intracranial hemorrhage or a stroke “mimic” present?

(2) Is a large vessel occluded?

(3) Is part of the brain irreversibly injured?

(4) Is there a clinically relevant “penumbra” of ischemic but potentially salvageable tissue?

The primary goal of “brain attack” protocols is to distinguish “bland” or ischemic stroke from intracranial hemorrhage and

to select/triage patients for possible reperfusion therapies Most protocols begin with emergency NECT to answer the first

“must know” question: Is intracranial hemorrhage or a stroke mimic present? Once intracranial hemorrhage is excluded, presence or absence of a major vessel occlusion can be determined noninvasively with CTA The third and fourth

questions can be answered with either CT or MR perfusion

Meningitis is a clinical laboratory diagnosis, not a radiologic one NECT scans in meningitis can be normal or show only mild ventricular enlargement Large ventricles with blurred margins on NECT scans indicate acute obstructive

hydrocephalus with accumulation of extracellular fluid in the deep periventricular white matter Bone CT should be carefully evaluated for sinusitis and otomastoiditis

Encephalitis can be sporadic or epidemic NECT scans in the most common nonepidemic encephalitis, i.e., herpes simplex encephalitis, may be normal or show only hypodensity with mild mass effect in one or both temporal lobes Patients with suspected encephalitis are best evaluated with MR (including FLAIR and diffusion-weighted sequences)

Brain abscesses and empyemas are rare but potentially life-threatening CNS infections Intraventricular rupture of a brain abscess can be a catastrophic event All these are serious disorders that are best evaluated with contrast-enhanced MR (including FLAIR and diffusion-weighted sequences) Contrast-enhanced CT can also be performed if a screening NECT is suggestive of either diagnosis

Acute Toxic-Metabolic Derangements

A number of toxic and metabolic disorders present in the emergency department In the absence of focal neurologic deficit or altered mental status, emergent imaging is usually not indicated There are some notable exceptions, e.g., pregnant patients with preeclampsia or eclampsia or hypertensive patients on chemotherapy Posterior reversible encephalopathy syndrome (PRES) is common in both scenarios NECT scan is a good initial screening procedure If it's normal or equivocal, MR is more sensitive in subtle or atypical cases

Seizures

Patients with first-time seizures and no neurologic deficit usually do not require emergent neuroimaging A “screening” NECT scan is relatively useless as subtle abnormalities are easily overlooked Patients with recurrent, often drug-resistant epilepsy are common ER visitors Without trauma-associated brain injury, emergent neuroimaging is rarely indicated Complex febrile seizures are a common diagnosis in the pediatric emergency department Recent studies have shown a low likelihood of intracranial infections and abnormal neuroimaging findings

Dizziness

Adults triaged to the ED with complaints of dizziness, vertigo, or imbalance pose a challenge to physicians While dizziness

in the ED is generally benign, a substantial fraction of patients harbor serious neurologic disease such as stroke,

intracranial hemorrhage, transient ischemic attack, seizure, brain tumor, demyelinating disease, and CNS infection Older age, a chief complaint of imbalance, and focal neurologic abnormality are all independently associated with serious neurologic diagnoses and may deserve emergent imaging Imaging is usually negative in solated dizziness without other abnormalities

Head and Neck Emergencies

Patients may present to the emergency department with a wide variety of nontraumatic infectious, inflammatory, and neoplastic conditions affecting the head and neck Acute conditions that require emergent imaging are generally

restricted to trauma and suspected infections Some can be potentially life threatening

Oral cavity infections, tonsillitis and peritonsillar abscess, sialadenitis, parotiditis, thrombophlebitis, periorbital and orbital cellulitis, infectious cervical lymphadenopathy, epiglottitis, invasive fungal sinusitis, and deep neck abscess all require rapid diagnosis and treatment CT is the first-line imaging modality in the emergency setting, and MR plays an important secondary role

Nontraumatic Emergencies Involving the Spine/Spinal Cord

While patients with back pain are common ER visitors, they generally do not require emergent imaging unless a focal neurologic deficit is present

True nontraumatic spinal emergencies are rare but represent a potential loss of function if not treated promptly and properly Patients with acute myelopathy, suspected infection, or cord ischemia as well as individuals with a known malignancy and sudden onset of a neurologic deficit all require emergent imaging MR is generally the procedure of choice A new imaging sequence—diffusion tensor imaging—can be very helpful in early detection of cord ischemia Selected References

1 Balestrini S et al: Emergency room access for recurring seizures: when and why Eur J Neurol Epub ahead of print, 2013

2 Boyle DA et al: Clinical factors associated with invasive testing and imaging in patients with complex febrile seizures Pediatr Emerg Care 29(4):430-4, 2013

3 Wang X et al: Head CT for nontrauma patients in the emergency department: clinical predictors of abnormal findings Radiology 266(3):783-90, 2013

4 Kelley BC et al: Spinal emergencies J Neurosurg Sci 56(2):113-29, 2012

5 Navi BB et al: Rate and predictors of serious neurologic causes of dizziness in the emergency department Mayo Clin Proc 87(11):1080-8, 2012

6 Scheinfeld MH et al: Teeth: what radiologists should know Radiographics 32(7):1927-44, 2012

7 Capps EF et al: Emergency imaging assessment of acute, nontraumatic conditions of the head and neck Radiographics 30(5):1335-52, 2010 Erratum in: Radiographics 31(1):316, 2011

8 Crocker M et al: An extended role for CT in the emergency diagnosis of malignant spinal cord compression Clin Radiol 66(10):922-7, 2011

9 Jagoda A et al: The emergency department evaluation of the adult patient who presents with a first-time seizure Emerg Med Clin North Am 29(1):41-9, 2011

10 Ludwig BJ et al: Diagnostic imaging in nontraumatic pediatric head and neck emergencies Radiographics

30(3):781-99, 2010

11 Hardy JE et al: Computerized tomography of the brain for elderly patients presenting to the emergency department with acute confusion Emerg Med Australas 20(5):420-4, 2008

Brain

Aneurysmal Subarachnoid Hemorrhage

> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Aneurysmal Subarachnoid Hemorrhage

Aneurysmal Subarachnoid Hemorrhage

Perry P Ng, MBBS (Hons), FRANZCR

Anne G Osborn, MD, FACR

Key Facts

Terminology

SAH caused by ruptured aneurysm (aSAH)

Saccular (SA) > > dissecting aneurysm (DA)

Imaging

CT/CTA

Hyperdense sulci on NECT

Distribution varies with aneurysm location

Suprasellar cistern (IC-PCoA, ACoA aneurysms)

Sylvian fissure (MCA bifurcation)

Prepontine, CPA cisterns (PICA, BA bifurcation SA or vertebral DA)

CTA 90-95% positive if aneurysm ≥ 2 mm

MR/MRA

FLAIR hyperintense sulci, cisterns (nonspecific)

TOF MRA 85-95% sensitive for aneurysms ≥ 3 mm

Sudden onset severe headache

“Thunderclap/worst headache of life”

50% mortality

Vasospasm 1-3 weeks post aSAH

20% rebleed within 1st 2 weeks

(Left) Axial graphic through the midbrain depicts SAH in red throughout the basal cisterns Given the diffuse distribution of SAH without focal hematoma, statistically the most likely location of the ruptured aneurysm is the ACoA (Right) Series of axial NECT scans shows the typical appearance of aneurysmal SAH Acute subarachnoid blood is seen as hyperdensity

in the basal cisterns, sylvian fissures, perimesencephalic cisterns, and interhemispheric fissure Ruptured ACoA

aneurysm was found on CTA (not shown)

(Left) NECT scan shows diffuse basilar SAH with more focal clot in the right anteromedial temporal lobe and along the right side of the suprasellar cistern (Right) 3D SSD of the right ICA angiogram in the same patient shows a large trilobed IC-PCoA aneurysm

Extravasation of blood into subarachnoid space

Usually from ruptured saccular aneurysm

Less common: Intracranial dissecting aneurysm

IMAGING

General Features

Best diagnostic clue

Hyperdense basal cisterns, sulci on NECT

Location

Suprasellar, basal, sylvian, interhemispheric cisterns

± intraventricular hemorrhage (IVH) aSAH distribution depends on location of saccular aneurysm (SA)

aSAH highest near site of rupture

Anterior communicating artery (ACoA) aneurysm

→ anterior interhemispheric fissure

Middle cerebral artery (MCA) aneurysm → sylvian fissure Basilar tip, superior cerebellar artery (SCA), posterior inferior cerebellar artery (PICA) SA, or vertebral artery (VA) dissecting aneurysm (DA)

→ prepontine cistern, foramen magnum, 4th ventricle

“Culprit” aneurysm sometimes seen as filling defect within hyperdense aSAH

SAs typically located at bifurcation points along intradural ICA, circle of Willis (COW), MCA

90% located on anterior circulation: ACoA, posterior communicating artery (PCoA), MCA, carotid terminus, carotid-ophthalmic, superior hypophyseal

10% on posterior circulation: Basilar tip, PICA, anterior inferior cerebellar artery (AICA), SCA DAs: Intradural V4 VA segment most common

Blood-blister aneurysm (BBA)

Dorsal supraclinoid ICA Rarely MCA, basilar artery

CT Findings

NECT

95% positive in 1st 24 hours, < 50% by 1 week

“Effaced” sylvian fissure if subacute, filled with isodense SAH

Hydrocephalus common, may occur early

± intraparenchymal hemorrhage at site of ruptured aneurysm

CTA

90-95% positive if aneurysm ≥ 2 mm

MR Findings

T1WI

Acute aSAH is isointense to CSF

CSF may appear mildly hyperintense (“dirty”)

If > 1 aneurysm, then biggest, most irregular ± adjacent vasospasm is likely source of bleed

DA

Irregular ± dilated or stenotic V4 segment of VA BBA

Smooth/irregular bleb/dome-shaped outpouching Not associated with major vessel branch point Most common along supraclinoid ICA

DSA negative in 15% of aSAH; repeat positive < 5%

Evaluate ECAs (to exclude dural AV fistula [dAVF])

SA may not be seen on initial DSA if optimal projection not obtained, spontaneous partial or complete aneurysm thrombosis, &/or presence of vasospasm

Consider repeating DSA in 5-7 days Imaging Recommendations

Best imaging tool

NECT + multiplanar CTA

Protocol advice

Proceed to DSA if NECT consistent with aSAH but CTA negative

Consider MR if DSA + CTA negative

DIFFERENTIAL DIAGNOSIS

Nonaneurysmal SAH

Perimesencephalic SAH

Small SAH, localized to interpeduncular cistern

Presumed venous etiology with low recurrence rate

Traumatic subarachnoid hemorrhage

Adjacent to contusions, subdural hematomas

Rarely from intracranial dissection or rupture of traumatic pseudoaneurysm

Subarachnoid hemorrhage, NOS

Vascular malformation: Arteriovenous malformation (AVM), cavernous hemangioma

Reversible Cerebral Vasoconstriction Syndrome (RCVS)

Clinical: “Thunderclap” headache

SAH typically in cortical sulci vs basal cisterns with aSAH

“Pseudo-SAH”

Hypodense brain: Severe cerebral edema

Hyperdense CSF: Intrathecal contrast; meningitis

May be related to high-flow arteriopathy along feeding vessel of AVM or, less commonly, dAVF

↑ aneurysm rupture risk if female, smoker, HTN Fusiform aneurysms

Dissection from trauma, hypertension, ASVD Underlying arteriopathy including fibromuscular dysplasia (FMD), Marfan, Ehlers-Danlos, infection Mycotic

Blood-blister aneurysm: All layers absent (contained in fibrous cap)

30% have clinically apparent vasospasm Starts ˜ day 3-4 post SAH; peaks ˜ 7-9 days, lasts ˜ 12-16 days Cerebral salt-wasting syndrome

Excessive renal Na+ excretion → hyponatremia, hypovolemia Terson syndrome

Intraocular (retinal, vitreous) hemorrhage associated with SAH secondary to rapid ↑ intracranial pressure

Staging, Grading, & Classification

Clinical grading: Hunt and Hess (H&H) grade 0-5

0: No SAH (unruptured aneurysm)

1: No symptoms, minimal headache, slight nuchal rigidity

2: Moderate to severe headache, nuchal rigidity

No neurologic deficit except CN palsy 3: Drowsy, minimal neurologic deficit

4: Stuporous, moderate/severe hemiparesis

5: Coma, decerebrate rigidity, moribund appearance

WFNS clinical grading system: Based on GCS and presence/absence of major focal neurological deficit

Fisher CT grading

1: No SAH visible

2: Diffuse, thin layer (< 1 mm)

3: Localized clot or thick layer (> 1 mm)

4: Intraventricular blood

Gross Pathologic & Surgical Features

Blood in basal cisterns, sulci, and ventricles

CLINICAL ISSUES

Presentation

Most common signs/symptoms

Sudden “thunderclap/worst headache of life”

10% preceded by “sentinel hemorrhage” = self-limiting SAH + headache in preceding days/weeks

Aneurysms cause 85% of spontaneous SAHs

Incidence ˜ 9.9 per 100,000 population

Natural History & Prognosis

50% mortality; 20% rebleed within 1st 2 weeks

Clinical outcome inversely proportional to initial H&H or WFNS grade

Vasospasm + ischemia → delayed morbidity, mortality

Severity correlates with amount of SAH (Fisher CT grade); inverse correlation with patient age

Proven effective over decades but invasive, higher morbidity/mortality compared with coiling

1 study: Death or dependence at 1 year = 23.7% with coiling vs 30.7% with clipping Coil embolization (“coiling”), if anatomy favorable

Platinum coils ± bioactive coating to reduce recurrence rate Aneurysm recurrence > surgical clipping but low risk of recurrent SAH Vasospasm

Ca++ antagonists, “triple-H” therapy (hypervolemia, hemodilution, hypertension)

Endovascular: Intraarterial Ca++ antagonist (“chemical angioplasty”), balloon angioplasty

Hydrocephalus

Temporary or permanent CSF diversion

Cerebral salt-wasting syndrome

Na+ tablets or IV hypertonic saline

DIAGNOSTIC CHECKLIST

Consider

Nonaneurysmal SAH if characteristic blood distribution (e.g., perimesencephalic SAH, RCVS)

Look for multiple aneurysms and decide which most likely bled

Image Interpretation Pearls

Isodense SAH: Anterior 3rd ventricle and temporal horns are only CSF density structures at base of brain; absence of sylvian fissure(s)

(Left) Sagittal T1WI illustrates typical findings of acute aneurysmal SAH Note “dirty” CSF that appears isointense with adjacent brain The normal basilar artery “flow void” is surrounded by the SAH (Right) Axial T1WI in the same case shows a nice contrast between the isointense (with brain) “dirty” CSF and the more normal-appearing hypointense (“dark”) CSF in the cistern and temporal horns

(Left) T2WI in the same patient shows that the hyperintense SAH is difficult to distinguish from the normal “bright” CSF The SAH is very slightly less hyperintense than the adjacent CSF (Right) Normal CSF suppresses on FLAIR FLAIR scan in the same case shows CSF in the suprasellar cistern is abnormally hyperintense Sulcal-cisternal hyperintensity

is also seen in the left perimesencephalic and superior cerebellar cisterns as well as the parietooccipital subarachnoid spaces

Nonaneurysmal Perimesencephalic SAH

> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Nonaneurysmal

Terminology

Clinically benign SAH confined to perimesencephalic, prepontine cisterns

No source demonstrated at angiography

Imaging

CT: Hyperdense prepontine, perimesencephalic CSF

T1: Iso- to hyperintense

T2 variable (iso- to hyper-) intensity compared to CSF

FLAIR: Hyperintense prepontine, perimesencephalic CSF

May be mimicked by CSF pulsation artifact or in ventilated patients with > 50% O2 concentration

Normal DSA required to exclude aneurysm or other cause and confirm diagnosis

MR/MRA may confirm alternative diagnosis and negate need for repeat DSA

Pathology

Most likely cause: Ruptured perimesencephalic/prepontine vein

Other nonaneurysmal causes: Intracranial dissection, vasculitis, trauma, dural AV fistula, spinal vascular

malformation; have less benign course

Vertebrobasilar aneurysms, dissection may have pnSAH pattern

Clinical Issues

Benign course: Rebleed rare (< 1%); no vasospasm

Headache (usually Hunt/Hess grade 1 or 2), often intra-/post coitus

More extensive pnSAH may develop hydrocephalus or intraventricular blood

(Left) Axial graphic shows a classic pnSAH Hemorrhage is confined to the interpeduncular fossa and ambient

(perimesencephalic) cisterns The source is usually venous in pnSAHs, unlike in aneurysmal SAHs (Right) NECT scans in

a patient with pnSAH show blood in the prepontine, perimesencephalic/ambient cisterns but in the not anterior suprasellar cistern or sylvian fissures DSA was negative

(Left) NECT scan in a 39-year-old woman in the ER complaining of the “worst headache of my life” shows isolated subarachnoid hemorrhage in the interpeduncular fossa There is no blood in the suprasellar cistern or sylvian fissures The ventricles are normal with no evidence for hydrocephalus (Right) CTA with MIP axial projection in the same patient shows no evidence of aneurysm.

Clinically benign SAH confined to perimesencephalic, prepontine cisterns

No source demonstrated at angiography

IMAGING

General Features

Best diagnostic clue

Hyperdense prepontine, perimesencephalic CSF

Iso- to hyperintense CSF around midbrain

Focal clot around basilar artery

T2WI

Variable; iso- to hypointense blood in CSF

FLAIR

Hyperintense CSF is more extensive than on T1/T2

Mimicked by CSF pulsation artifact T2* GRE

Hypointense thrombus in CSF

Angiographic Findings

CTA/MRA/DSA

No source of hemorrhage identified

Normal DSA required to confirm diagnosis

Imaging Recommendations

Best imaging tool

NECT best screening for pnSAH

DSA to exclude aneurysm

MR/MRA may confirm SAH or cause; may negate need for repeat DSA

Protocol advice

NECT with CTA

MR/MRA may help confirm diagnosis

Consider cervical MR to exclude rare spinal vascular source

DIFFERENTIAL DIAGNOSIS

Aneurysmal SAH

More extensive hemorrhage

Vertebrobasilar aneurysms may have pnSAH pattern

Most likely cause: Ruptured perimesencephalic/prepontine vein

Other nonaneurysmal causes have less benign course

Intracranial dissection, vasculitis, trauma, dural AV fistula, spinal cord vascular malformation Vertebrobasilar aneurysms, dissection may have pnSAH pattern

Gross Pathologic & Surgical Features

Clotted blood in perimesencephalic cisterns

Similar to aneurysmal SAH

CLINICAL ISSUES

Presentation

Most common signs/symptoms

Headache (usually Hunt/Hess grade 1 or 2)

Often post coitus Demographics

Age: 40-60 years

Gender: M = F

Epidemiology

Majority of angiogram-negative SAH

Natural History & Prognosis

Benign course: Rebleed rare (< 1%); no vasospasm

More extensive pnSAH may develop hydrocephalus or intraventricular blood

Treatment

Monitoring and treatment of rare secondary hydrocephalus, vasospasm

DIAGNOSTIC CHECKLIST

Consider

Occult trauma, vertebral dissection, vasculitis, dural AV fistula, or spinal vascular malformation

Image Interpretation Pearls

DSA needed to exclude aneurysm, other vascular cause

Perimesencephalic thrombus and focal clot around basilar artery on MR

SELECTED REFERENCES

1 Kim YW et al: Nonaneurysmal subarachnoid hemorrhage: an update Curr Atheroscler Rep 14(4):328-34, 2012

2 Kong Y et al: Perimesencephalic subarachnoid hemorrhage: risk factors, clinical presentations, and outcome Acta Neurochir Suppl 110(Pt 1):197-201, 2011

Saccular Aneurysm

> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Saccular Aneurysm

Saccular Aneurysm

Perry P Ng, MBBS (Hons), FRANZCR

Anne G Osborn, MD, FACR

Key Facts

Terminology

Intracranial saccular aneurysm (SA)

Outpouching affecting only part of arterial circumference

Lacks internal elastic lamina ± tunica media

Imaging

Round/lobulated arterial outpouching

Usually arises from bifurcations of circle of Willis (COW), supraclinoid ICA, MCA, cerebellar arteries 90% occur in anterior circulation

10% posterior circulation: Basilar tip, cerebellar arteries (PICA most common)

Rare (< 1%): Trigeminal artery, vertebrobasilar junction fenestration

Ruptured SAs result in SAH

May have mural Ca++

Sensitivity of multislice CTA > 95% for SA > 2 mm

3D TOF: > 90% sensitive for aneurysms ≥ 3 mm

Top Differential Diagnoses

Vast majority of unruptured SAs are asymptomatic

2-6% incidental finding at autopsy, imaging

80-90% of nontraumatic SAH caused by ruptured SA

Treatment

Endovascular coiling vs surgical clipping

22.6% relative, 6.9% absolute risk ↓ for coiling vs surgery for ruptured aneurysms

↓ morbidity, mortality, and hospital costs; quicker recovery for unruptured aneurysms

(Left) Most common sites for SAs are ACoA and IC-PC junction MCA bifurcation and basilar tip are other

frequent sites (Right) Graphic illustrates rupture of an ACoA aneurysm with active extravasation from a superiorly directed bleb (Murphy teat) An additional posterior communicating artery SA and tiny bleb at the left MCA bifurcation are seen Patients with SAs have a 20% chance of having > 1 aneurysm.

(Left) Most intracranial SAs present with subarachnoid hemorrhage In this case, SAH is present in the basilar cisterns

A focal temporal lobe hematoma with a rounded “filling defect” is present (Right) CTA in the same case shows a right MCA trifurcation saccular aneurysm

Arterial outpouching affecting only part of arterial circumference

Lacks internal elastic lamina ± tunica media

IMAGING

General Features

Best diagnostic clue

Round/lobulated arterial outpouching

Usually arises from bifurcations of circle of Willis (COW), supraclinoid ICA, MCA, cerebellar arteries Location

90% occur in anterior circulation

ACoA, PCoA, MCA bifurcation, carotid terminus most common sites Other: Paraclinoid ICA, superior hypophyseal, anterior choroidal artery (AChA) 10% posterior circulation: Basilar tip, cerebellar arteries (PICA most common)

Rare (< 1%): Trigeminal artery, vertebrobasilar junction fenestration

Vessel bifurcation > side wall aneurysm (e.g., blood blister-like aneurysm)

Size

Small (< 3 mm) to giant (> 2.5 cm)

Morphology

Round, ovoid daughter lobe(s)

Narrow or wide necked

Branch vessel may be incorporated into aneurysm neck (can preclude coil embolization)

CT Findings

NECT

Ruptured SAs result in subarachnoid hemorrhage (SAH)

Pattern of SAH may help localize SA location

If SA contains thrombus → hyperdense to brain

May have mural Ca++

CECT

Lumen of patent SA enhances uniformly

Completely thrombosed SA may have rim enhancement

CTA

Sensitivity of multislice CTA > 95% for SA > 2 mm

Look for > 1 aneurysm, as SA is multiple in 20% of patients

Look for associated SAH vasospasm if ruptured SA

Alternative to DSA as first imaging technique in SAH

MR Findings

T1WI

Patent aneurysm (signal varies)

50% have flow void 50% iso-/heterogeneous signal (slow/turbulent flow, saturation effects, phase dispersion) Partially/completely thrombosed aneurysm

Signal depends on age of thrombus Common: Mixed signal, laminated thrombus Hypointense + “blooming” on susceptibility sequences (GRE, SWI) T2WI

Typically hypointense (flow void)

May be laminated with very hypointense rim

FLAIR

Acute SAH: High signal in sulci, cisterns

DWI

May see restricted diffusion secondary to ischemia from SAH vasospasm

Thromboembolic events from intraaneurysmal thrombus (rare)

T1WI C+

Slow flow in patent lumen may enhance

Increased phase artifact in patent SAs

MRA

3D TOF: > 90% sensitive for aneurysms ≥ 3 mm

Short T1 substances, such as subacute hemorrhage, may simulate flow on TOF MRA

Rare: Contrast extravasation with active SAH

Look for Murphy teat (bleb at site of recent rupture) vs daughter lobe (smaller outpouching from aneurysm fundus, likely indicating focal wall weakness, ↑ future rupture risk)

Imaging Recommendations

Best imaging tool

NECT + CTA for work-up of SAH

CTA or MRA for screening of high-risk groups

Protocol advice

Dual energy direct bone removal CT angiography for evaluation of skull base/paraclinoid SA

3D SSD reconstructions helpful to visualize ACoA and MCA bifurcation

DIFFERENTIAL DIAGNOSIS

Vessel Loop

Use multiple projections

Vessel Infundibulum

< 3 mm, conical, vessel arises directly from apex

Commonly at posterior communicating artery (PCoA) and anterior choroidal artery (AChA) origins

Fusiform Aneurysm

Sausage-shaped morphology with separate inflow, outflow pathways

Long segment, usually located distal to COW

Can be secondary to ASVD

Often pseudoaneurysm etiology

P.II(1):12

Trauma, mycotic, vasculitic, connective tissue disease

Flow Void (MR Mimic)

Aerated anterior clinoid or supraorbital cell

Abnormal vascular hemodynamics → ↑ wall stress

Flow-related “bioengineering fatigue” in vessel wall more likely with asymmetric COW → ↑ development of SA at site of anomaly

e.g., aplastic A1 segment, persistent trigeminal artery, vertebrobasilar fenestration Genetics

Familial intracranial aneurysms (FIAs)

No known heritable connective tissue disorder Occur in “clusters” (1st-order relatives) Younger patients, no female predominance compared to sporadic SAs Consider screening with CTA or MRA

Associated abnormalities

↑ SA incidence in patients with

Fibromuscular dysplasia (FMD): Autosomal dominant, sporadic Bicuspid aortic valve

Autosomal dominant polycystic kidney disease (10% have SA)

Intracranial AVM: Feeding pedicle (“flow-related”) aneurysms in 30%

May regress after treatment of AVM Gross Pathologic & Surgical Features

Round/lobulated sac, thin or thick wall, ± SAH

Microscopic Features

Disrupted/absent internal elastic lamina

Muscle layer absent

May have “teat” of fragile adventitia

CLINICAL ISSUES

Presentation

Most common signs/symptoms

Vast majority of unruptured SA are asymptomatic

Cranial neuropathy uncommon (e.g., pupil-involving CN3 palsy from PCoA aneurysm) TIA/stroke from thromboembolic events secondary to intraaneurysmal thrombus (rare) 80-90% of nontraumatic SAH caused by ruptured SA

Headache (typical = “thunderclap”) Clinical profile

2 common scenarios

Middle-aged patient with “worst headache of my life” from ruptured SA → SAH Incidental finding on imaging performed for unrelated symptoms in patient of any age

2-6% incidental finding of unruptured SA at autopsy

Annual risk of de novo aneurysm formation = 0.8% in patients with previous SA

Natural History & Prognosis

Rupture risk

Size: Low risk of SA rupture if < 7 mm

Growth, rupture risk for unruptured aneurysms

Growth rate = 3.9% per year 1.8% per year rupture risk

˜ 20% of ruptured unsecured SA rebleed within 2 weeks, 50% in 6 months

Shape: Daughter lobe likely ↑ risk of future SAH; Murphy teat = site of recent rupture and possible rebleed if untreated

↑ in females with history of HTN, smoking

Treatment

Endovascular coiling

Ruptured SA: 22.6% relative, 6.9% absolute risk ↓ for coiling vs surgery (1 study)

Unruptured SA: Coiling vs clipping

↓ morbidity, mortality, and hospital costs; shorter hospital stay; quicker recovery Surgical clipping

Lower SA recurrence risk compared with coiling, although rebleeding risk is low with either Rx

May have advantage in MCA and other SA where branch vessel arising from SA must be preserved

DIAGNOSTIC CHECKLIST

Consider

Blood blister-like aneurysm if negative CTA in patient with SAH → perform DSA

Perimesencephalic bleed in patient with blood localized to interpeduncular cistern

Image Interpretation Pearls

Diffuse SAH without focal hematoma → ACoA is most likely site of ruptured SA

Absence of sylvian fissures may be clue to subacute (isodense) SAH

SELECTED REFERENCES

1 Matsumoto K et al: Incidence of growth and rupture of unruptured intracranial aneurysms followed by serial MRA Acta Neurochir (Wien) 155(2):211-6, 2013

2 Rabinstein AA: Subarachnoid hemorrhage Neurology 80(5):e56-9, 2013

3 Vasan R et al: Pediatric intracranial aneurysms: current national trends in patient management and treatment Childs Nerv Syst 29(3):451-6, 2013

4 Wang H et al: 320-detector row CT angiography for detection and evaluation of intracranial aneurysms: comparison with conventional digital subtraction angiography Clin Radiol 68(1):e15-20, 2013

5 Cianfoni A et al: Clinical presentation of cerebral aneurysms Eur J Radiol Epub ahead of print, 2012

P.II(1):13

Image Gallery

(Left) Patent saccular aneurysms are seen as rounded hypointense “flow voids” on MR This saccular aneurysm at the distal ICA bifurcation was found incidentally on the T2WI of this elderly patient (Right) Thrombosed SAs can appear very hyperdense This patient presented in the ER with sudden onset of right hemiparesis NECT scan, obtained as the initial study in the standard stroke protocol, shows an ovoid hyperdensity with what appears to be thrombus in the left proximal MCA

(Left) Source image from the CTA in the same patient shows abrupt “cut-off” of the left MCA and non-filling of a large, completely thrombosed saccular aneurysm (Right) CT perfusion study in the same case shows markedly decreased cerebral blood flow in the left MCA distribution The basal ganglia (supplied by lenticulostriate branches from the unoccluded proximal MCA) are spared Cerebral infarction can be caused by distal migration of clot from a thrombosed SA

(Left) Some aneurysms exhibit mural calcification NECT scan shows an incidentally discovered SA, seen here as a demarcated rounded hyperdensity with a peripheral rim of calcification (Right) CTA was subsequently performed

well-in the same case Coronal MIP shows a patent saccular aneurysm at the terminal bifurcation of the left ICA

Spontaneous Intracranial Hemorrhage

> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Spontaneous Intracranial

Primary intraparenchymal hemorrhage

Acute nontraumatic intracranial hemorrhage (ICH)

Imaging

Tiny “microbleeds” to massive lobar hematoma

Peripheral edema

Hematoma location vs common causes of pICH

HTN: Basal ganglia, thalamus, pons, cerebellum

Amyloid angiopathy: Microbleeds, lobar hemorrhages

Arteriovenous malformation: Any location

Cavernous malformation: Any location

Venous sinus thrombosis: Subcortical white matter

Neoplasm: Any location

May have fluid-fluid level: Coagulopathy, brisk bleeding, underlying cystic mass

Recommended imaging protocol

Start with NECT

If HTN with striatocapsular hematoma, no further imaging necessary

If unclear history, CTA

Atypical hematoma: MR (T2*, DWI, T1 C+)

Follow-up: Repeat MR if etiology unclear ± DSA if initial MRA/CTA negative

Pathology

Child < 15? Think AVM!

Young adult? Vascular malformation, drug abuse, venous thrombosis, vasculitis

Patient > 45 years old? HTN, amyloid, venous infarct, neoplasm (primary or metastatic), coagulopathy

Clinical Issues

sICH causes 15-20% of acute strokes

Control of ICP, hydrocephalus critical

Surgical evacuation when clinically indicated

(Left) A 15-year-old male presented in the ER with sudden-onset severe headache and right-sided weakness NECT scan shows an acute temporal lobe hematoma (Right) Lateral view of the left internal carotid angiogram in the same case shows a large left temporal lobe mass effect with a tightly packed “tangle” of vessels and an “early draining vein” consistent with hemorrhagic, partially-thrombosed AVM

(Left) A 23-year-old male with a cocaine overdose presented in the ER with severe headache and left-sided weakness Blood pressure was 220/120 on admission NECT scan shows a classic hypertensive right putamen-external capsule hemorrhage (Right) A 34-year-old male with headache and right-sided weakness was sent from the ER for emergent imaging NECT scan shows a right parietal hematoma The superior sagittal sinus appears more dense than normal Thrombosed SSS, cortical vein caused this sICH

Definitions

Spontaneous (nontraumatic) intracranial hemorrhage (sICH)

Etiology often initially unknown

IMAGING

General Features

Best diagnostic clue

Acute nontraumatic intracerebral hematoma

Location

Varies with etiology

Hypertension (HTN): Deep gray matter (basal ganglia, thalamus), pons, cerebellar hemisphere Amyloid angiopathy: Lobar

Arteriovenous malformation (AVM): Any location Cavernous malformation: Any location, common in brainstem Venous sinus thrombosis: Subcortical white matter adjacent to occluded sinus Neoplasm: Any location

Size

Subcentimeter “microbleeds” to massive hemorrhage

Morphology

Typically round or oval; often irregular when large

Patterns with HTN and amyloid angiopathy

Acute parenchymal hematoma Multiple subacute/chronic “microbleeds” in deep gray matter (HTN > amyloid) &/or subcortical white matter (amyloid > HTN)

Microbleeds often seen only on GRE MR

CT Findings

NECT

Acute hyperdense round/elliptical mass

May be mixed iso-/hyperdense

May have fluid-fluid level

Coagulopathy Brisk bleeding Bleed into cystic mass Peripheral low density (edema)

Deep (ganglionic) ICH may rupture into lateral ventricle

CTA

Look for “spot sign” (contrast extravasation in hematoma)

Predicts subsequent hematoma expansion Associated with increased morbidity/mortality Look for dural sinus venous thrombosis

Multifocal hypointense lesions (“black dots”)

Basal ganglionic suggests HTN Subcortical WM suggests amyloid angiopathy

DSA, often negative

Look for dural sinus occlusion, “stagnating vessels” (thrombosed AVM)

Imaging Recommendations

Best imaging tool

Start with NECT

If patient with HTN and striatocapsular hematoma, no further imaging necessary

If unclear history, add CTA Standard MR (include T2*, DWI)

If no clear cause of hemorrhage, or atypical appearance on CT T1WI C+ to assess for underlying tumor

If standard study suggests vascular etiology → MRA Consider DSA if initial MRA/CTA negative

Follow-up: Repeat MR if etiology remains unclear

Protocol advice

Add CTA to NECT if unclear history

If atypical/unexplained hematoma, consider adding MR (with T2*, DWI, T1WI C+)

DIFFERENTIAL DIAGNOSIS

Hypertensive Intracranial Hemorrhage

Patients usually older

Basal ganglionic hematoma most common

Cerebral Amyloid Angiopathy

Older patients (70 years old, normotensive)

Usually lobar

Microbleeds (“black dots”) on T2*

Underlying Neoplasm

Causes 2-15% of nontraumatic ICHs

Primary (glioblastoma multiforme) or metastasis

May show enhancement

Vascular Malformation

AVM, cavernous malformation most common

ICH rate in AVMs of basal ganglia or thalamus (9.8% per year) much higher than AVMs in other locations Cortical Venous Thrombosis

Adjacent dural sinus often thrombosed

May have hypertensive striatocapsular hemorrhage

Uncommon = pseudoaneurysm rupture into cerebrum

Vasculitis

Less common cause of spontaneous ICH

Patients usually younger

Dural AVF (With Cortical Venous Drainage)

Dilated venous “flow voids”

Child < 15? Think AVM!

Young adult? Vascular malformation, drug abuse, venous thrombosis, vasculitis

Patient > 45 years old? HTN, amyloid, venous infarct, neoplasm (primary or metastatic), coagulopathy Genetics

MMP-9, cytokine gene expression ↑ after acute spontaneous ICH

Staging, Grading, & Classification

Clinical “ICH score” correlates with 30-day mortality

Admission GCS

> 80 years old, ICH volume

Infratentorial

Presence of intraventricular hemorrhage

Gross Pathologic & Surgical Features

Findings range from petechial “microbleeds” to gross parenchymal hematoma

Microscopic Features

Coexisting microangiopathy common in amyloid, HTN

CLINICAL ISSUES

Presentation

Most common signs/symptoms

90% of patients with recurrent pICH are hypertensive

Large ICHs present with sensorimotor deficits, impaired consciousness

Demographics

Age

Perinatal through elderly

Epidemiology

Causes 15-20% of acute strokes

Natural History & Prognosis

Prognosis related to location, size of ICH

Hematoma enlargement common in 1st 24-48 hours

Risk factors: EtOH, low fibrinogen, coagulopathy, irregularly shaped hematoma

Edema associated with poor outcome

Mortality: 30-55% in 1st month

30% rebleed within 1 year

Most survivors have significant deficits

Treatment

Control of ICP, hydrocephalus

Surgical evacuation when clinically indicated

DIAGNOSTIC CHECKLIST

Consider

Underlying etiology for hemorrhage (AVM, amyloid, neoplasm, drug use, etc.)

Image Interpretation Pearls

Unexplained ICH → search for microbleeds on T2* MR

Fluid-fluid level, iso-/mildly hyperdense clot may indicate coagulopathy

SELECTED REFERENCES

1 Freeman WD et al: Intracranial hemorrhage: diagnosis and management Neurol Clin 30(1):211-40, ix, 2012

2 Khosravani H et al: Emergency noninvasive angiography for acute intracerebral hemorrhage AJNR Am J Neuroradiol Epub ahead of print, 2012

3 Thanvi BR et al: Advances in spontaneous intracerebral haemorrhage Int J Clin Pract 66(6):556-64, 2012

4 Fischbein NJ et al: Nontraumatic intracranial hemorrhage Neuroimaging Clin N Am 20(4):469-92, 2010

5 Hanley DF: Intraventricular hemorrhage: severity factor and treatment target in spontaneous intracerebral hemorrhage Stroke 40(4):1533-8, 2009

6 Jeffree RL et al: Warfarin related intracranial haemorrhage: a case-controlled study of anticoagulation monitoring prior

to spontaneous subdural or intracerebral haemorrhage J Clin Neurosci 16(7):882-5, 2009

7 Kumar R et al: Spontaneous intracranial hemorrhage in children Pediatr Neurosurg 45(1):37-45, 2009

8 Tejero MA et al: [Multiple spontaneous cerebral haemorrhages Description of a series and review of the literature.] Rev Neurol 48(7):346-8, 2009

9 Walsh M et al: Developmental venous anomaly with symptomatic thrombosis of the draining vein J Neurosurg

109(6):1119-22, 2008

10 Harden SP et al: Cranial CT of the unconscious adult patient Clin Radiol 62(5):404-15, 2007

11 Chao CP et al: Cerebral amyloid angiopathy: CT and MR imaging findings Radiographics 26(5):1517-31, 2006

12 Finelli PF: A diagnostic approach to multiple simultaneous intracerebral hemorrhages Neurocrit Care 4(3):267-71,

(Left) Coronal T1 C+ MR shows an “empty delta” sign with dura enhancing around a thrombosed right transverse sinus Bizarre enhancement in the adjacent occipital lobe and along the tentorium represent venous stasis and retrograde venous drainage Enlarged, intensely enhancing choroid plexus provides collateral venous drainage (Right) Lateral DSA shows a dAVF in the wall of the thrombosed TS Acute hemorrhage was caused by thrombosis of the outlet draining vein.

(Left) An elderly female presented in the ER with headache and visual field problems NECT scan shows a right occipital hematoma Bone CT (not shown) demonstrated lytic foci from a previously undiagnosed renal cell carcinoma (Right) Emergency NECT scan in an over-anticoagulated patient shows multiple hemorrhagic foci with fluid-fluid levels

Hypertensive Intracranial Hemorrhage

> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Hypertensive Intracranial

Hypertensive intracranial hemorrhage (hICH)

Acute nontraumatic ICH 2° to systemic hypertension

2nd most common cause of stroke

Imaging

Initial screen = NECT in patients with HTN

CT: Acute round or oval hyperdense mass

Striatocapsular: Putamen/external capsule (60-65%)

Mass effect: Hydrocephalus, herniation

MR signal intensity (varies with age of clot)

Hyperacute (< 6 hours): T1WI iso-hypo/T2WI hyper

Acute (7 hours-3 days): T1WI iso-hyper/T2WI hypo

Subacute (days): T1WI hyper/T2WI hypo-hyper

Chronic (weeks-months): T1WI hyper/T2WI hypo

Top Differential Diagnoses

Cerebral amyloid angiopathy

Hemorrhagic neoplasm

Coagulopathy

Deep cerebral venous thrombosis

Drug abuse (especially in young patient)

Vascular malformation (rare in elderly)

Clinical Issues

HTN single most important risk factor for all types of stroke!

10-20% of stroke patients have hICH

50% of nontraumatic ICHs caused by hICH

HTN most common cause of spontaneous ICH in patients 45-70 years old

(Left) Axial graphic shows acute hypertensive basal ganglionic/external capsule hemorrhage with dissection into the lateral ventricle Hemorrhage extends through the foramen of Monro to the 3rd ventricle (Right) NECT scan shows classic hypertensive basal ganglionic hemorrhage Intraventricular rupture is common with large bleeds

(Left) NECT scan in a 57-year-old woman with “stroke” shows a typical putamen-external capsule hypertensive hemorrhage (Right) Because of the patient's young age and previously undiagnosed hypertension, CTA was performed Coronal image shows that the focal basal ganglionic hematoma displaces the lenticulostriate arteries medially (compare to the normal left side ) No “spot sign” that would indicate active bleeding is identified.P.II(1):19

Best diagnostic clue

Round or oval hyperdense mass in putamen/external capsule or thalamus in patients with hypertension Location

Striatocapsular: Putamen/external capsule (60-65%)

Typically rounded or oval

2 distinct patterns seen with hICH

Acute focal hematoma Multiple subacute/chronic “microbleeds” (1-5%)

CT Findings

NECT

Round or oval hyperdense parenchymal mass

Heterogeneous density if coagulopathy or active bleeding

Other: Intraventricular extension

Mass effect: Hydrocephalus, herniation

Varies with age of clot

Hyperacute hematoma (< 6 hours)

Oxyhemoglobin (Hgb) (iso-/hypointense) Acute hematoma (7 hours to 3 days)

DeoxyHgb (iso-/hyperintense) Early subacute hematoma (several days)

Intracellular metHgb (hyperintense) Late subacute hematoma (week to months)

Extracellular metHgb (hyperintense) Chronic hematoma

Hypointense (± hyperintense center) T2WI

Appearance of hematoma varies with stage

Hyperacute hematoma (< 6 hours)

OxyHgb (hyperintense) Acute hematoma (7 hours to 3 days)

DeoxyHgb (hypointense) Subacute hematoma (3-7 days)

Intracellular metHgb (hypointense) Late subacute hematoma (7 days to 3 weeks)

Extracellular metHgb (hyperintense) Chronic hematoma (> 3 weeks to months)

Hemosiderin (hypointense) Remote hematoma (months to years)

Hypointense hemosiderin scar ± central hyperintense cavity

“White matter hyperintensities” are hICH risk markers

T2* GRE

Multifocal hypointense lesions (“black dots”) on T2*

Common with longstanding HTN

Also commonly seen with amyloid angiopathy

DWI

Hypo- or mixed hypo-/hyperintense (early hematoma)

T1WI C+

Typically no enhancement with acute hematoma

Contrast extravasation = active hemorrhage

MRA

Negative

Angiographic Findings

Conventional

DSA usually normal if history of HTN + deep ganglionic hemorrhage

May show avascular mass effect Rare: “Bleeding globe” microaneurysm on lenticulostriate artery (LSA) Coexisting vascular abnormalities

Increased prevalence of unruptured intracranial aneurysms More common in females

Imaging Recommendations

Best imaging tool

If older patient with HTN and suspected hICH, NECT

If hyperacute ischemic “stroke” suspected, MR + T2* and DWI

If MR shows classic hematoma + coexisting multifocal “black dots,” most likely amyloid angiopathy or chronic HTN

If MR shows atypical hematoma, MRA or CTA

If MRA or CTA inconclusive, consider DSA

DIFFERENTIAL DIAGNOSIS

Cerebral Amyloid Angiopathy

Lobar > > basal ganglionic

Usually elderly, often normotensive

Only 5-10% of hICHs are lobar, but HTN is so common that it is always a consideration

Hemorrhagic Neoplasm

Secondary (metastasis) and primary (GBM)

Venous Thrombosis

May have history of dehydration, “flu,” pregnancy/birth control pills

Cause lobar hematomas

Look for hyperdense dural sinus (not always present)

Deep Cerebral Venous Thrombosis

Less common than dural sinus or cortical vein thrombosis

Look for hypodense bilateral thalami

Look for hyperdense internal cerebral veins, intraventricular hemorrhage

P.II(1):20

Coagulopathy

Elderly patients on anticoagulant therapy

Drug Abuse

Cocaine may cause sudden ↑ ↑ HTN

Be suspicious if unexplained basal ganglionic bleed in young patient

Vascular Malformation

Patients usually normotensive, younger

Most common = cavernous malformation

Look for “black dots” (multiple lesions) on T2* (GRE, SWI) scans

Less common = thrombosed hemorrhagic AVM or dAVF

PATHOLOGY

General Features

Etiology

Chronic HTN with atherosclerosis, fibrinoid necrosis, abrupt wall rupture ± pseudoaneurysm formation

“Bleeding globe” (penetrating LSA aneurysm)

Diffuse “microbleeds” common

Striatocapsular hematoma most common autopsy finding

Gross Pathologic & Surgical Features

Large ganglionic hematoma ± IVH

Subfalcine herniation, hydrocephalus (common)

Coexisting small chronic hemorrhages, ischemic lesions (common)

Microscopic Features

Fibrous balls (fibrosed miliary aneurysm)

Severe arteriosclerosis with hyalinization, pseudoaneurysm (lacks media/IEL)

CLINICAL ISSUES

Presentation

Most common signs/symptoms

10-20% of stroke patients have hICH

Large ICHs present with sensorimotor deficits, impaired consciousness

Clinical profile

HTN single most important risk factor for all types of stroke!

Major risk factor = HTN (increases risk of ICH 4x)

Demographics

50% of primary nontraumatic ICHs caused by hypertensive hemorrhage

HTN most common cause of spontaneous ICH in patients 45-70 years

10-15% of all stroke cases; associated with highest mortality rate

10-15% of hypertensive patients with spontaneous ICH have underlying aneurysm or AVM

Natural History & Prognosis

Bleeding can persist for up to 6 hours following ictus

Neurologic deterioration common within 48 hours

Increasing hematoma, edema

Hydrocephalus

Herniation syndromes

Recurrent hICH in 5-10% of cases, usually different location

Prognosis related to location, size of hICH

80% mortality in massive hICH with IVH

1/3 of survivors are severely disabled

Treatment

Control of ICP and hydrocephalus

DIAGNOSTIC CHECKLIST

Consider

Does patient have history of poorly controlled systemic HTN?

Could there be underlying coagulopathy, hemorrhagic neoplasm, or vascular malformation?

Substance abuse in young patients with unexplained hICH

Image Interpretation Pearls

Underlying cause of lobar intracerebral hemorrhage (ICH) is often difficult to determine

Subarachnoid extension of hematoma on CT is usually indicative of nonhypertensive etiology; consider lobar ICH caused by vascular abnormality

3 Dubow J et al: Impact of hypertension on stroke Curr Atheroscler Rep 13(4):298-305, 2011

4 Shinohara Y et al: III Intracerebral hemorrhage J Stroke Cerebrovasc Dis 20(4 Suppl):S74-99, 2011

5 Bogucki J et al: A new CT-based classification of spontaneous supratentorial intracerebral haematomas Neurol

Neurochir Pol 43(3):236-44, 2009

6 Waran V et al: A new expandable cannula system for endoscopic evacuation of intraparenchymal hemorrhages J Neurosurg 111(6):1127-30, 2009

7 Narotam PK et al: Management of hypertensive emergencies in acute brain disease: evaluation of the treatment effects

of intravenous nicardipine on cerebral oxygenation J Neurosurg 109(6):1065-74, 2008

8 Lee GY et al: Hypertensive intracerebral hematoma after aneurysmal subarachnoid hemorrhage J Clin Neurosci 14(12):1233-5, 2007

9 Shah QA et al: Acute hypertension in intracerebral hemorrhage: pathophysiology and treatment J Neurol Sci 2):74-9, 2007

261(1-P.II(1):21

Image Gallery

(Left) NECT scan in a 52-year-old hypertensive man with sudden onset of multiple cranial neuropathies shows a pontine hemorrhage (Right) NECT scan in an elderly hypertensive man shows a right cerebellar hemorrhage The posterior fossa (pons, cerebellum) is a relatively uncommon location for hypertensive hemorrhages, yet it is the 3rd most common overall site (after the basal ganglia and thalami).

(Left) Axial T2* GRE MR in a patient with a remote history of hypertensive hemorrhage in the left putamen & external capsule shows multifocal “black dots” in the basal ganglia & thalami with only a few lesions in the cortex (Right) SWI in the same case shows the old hemorrhage Multiple “black dots” (microbleeds) are even more apparent Basal ganglia microhemorrhages are more common in hypertension than cerebral amyloid-associated microangiopathy, a helpful distinguishing feature

(Left) NECT scan in an 80-year-old man in the ER with a “brain attack” shows a heterogeneous-appearing acute left occipital hematoma Lobar hemorrhages account for just 5-10% of hypertensive bleeds (Right) Because of the unusual appearance and location of the hematoma, emergent CTA was performed Contrast extravasation into the hematoma (“spot” sign) indicates active bleeding Surgery disclosed an actively bleeding hemorrhagic metastasis (adenocarcinoma, primary unknown).

Acute Hypertensive Encephalopathy, PRES

> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Acute Hypertensive Encephalopathy, PRES

Acute Hypertensive Encephalopathy, PRES

Anne G Osborn, MD, FACR

Key Facts

Terminology

Cerebrovascular autoregulatory disorder

Many etiologies with HTN as common component

Predilection for posterior circulation

Occipital lobes, cortical watershed zones

CT

Bilateral nonconfluent hypodense foci

± symmetric lesions in basal ganglia

MR

Parietooccipital T2/FLAIR hyperintensities in 95%

± basal ganglia, pontine, cerebellar involvement

“Blooming” on T2* if hemorrhagic (uncommon)

Generally no restriction on DWI

Variable patchy enhancement

Top Differential Diagnoses

Acute cerebral ischemia-infarction

Status epilepticus

Hypoglycemia

Thrombotic microangiopathies (DIC, TTP, mHTN)

Pathology

Acute HTN damages vascular endothelium

Breakthrough of autoregulation causes hyperperfusion, blood-brain barrier disruption

Result = vasogenic (not cytotoxic) edema

Clinical Issues

Headache, seizure, ↓ mental status, visual symptoms

Caution: Some patients, especially children, may be normotensive or have only minimally elevated BP!

(Left) Axial graphic shows the classic posterior circulation cortical/subcortical vasogenic edema characteristic of PRES Petechial hemorrhage occurs in some cases but is unusual (Right) Gross pathology of a patient with complicated PRES demonstrates diffuse cerebral edema with swollen gyri Multifocal petechial microhemorrhages are present in the occipital cortex together with several areas of focal encephalomalacia secondary to infarction (Courtesy R Hewlett, PhD.)

(Left) Axial NECT scan in a 26-year-old pregnant patient with eclampsia was initially read as normal; however, it shows subtle but definite hypodensities in the cortex and subcortical white matter of both occipital lobes (Right) Axial T2WI

MR in the same patient shows hyperintensities in both occipital lobes corresponding to the hypodensities noted on NECT DWI (not shown) was normal If clinical suspicion of PRES is high and NECT is scan normal/subtly abnormal, MR with T2WI, FLAIR, and DWI is helpful

P.II(1):23

Best diagnostic clue

Patchy cortical/subcortical PCA territory lesions in patient with severe acute/subacute HTN

Location

Most common: Cortex, subcortical white matter

Predilection for posterior circulation (parietal, occipital lobes, cerebellum)

At junctions of vascular watershed zones Usually bilateral, often somewhat asymmetric Less common: Basal ganglia

Rare: Predominant/exclusive brainstem involvement

May be normal or subtly abnormal

If PRES suspected, do MR to confirm!

Common: Bilateral nonconfluent hypodense foci

Posterior parietal, occipital lobes Cortical watershed zones Less common: Petechial cortical/subcortical or basal ganglionic hemorrhages

Uncommon: Thalamic, basal ganglia, brainstem, cerebellar hypodensities

Hyperintense cortical/subcortical lesions

Occipital lobes, cortical watershed zones Less common

Basal ganglia involvement Extensive brainstem, cerebellar hyperintensity Generalized white matter edema

FLAIR

Parietooccipital hyperintense cortical lesions in 95%

± symmetric lesions in basal ganglia

Variable pontine, cerebellar involvement

“Leaky” blood-brain barrier may cause gadolinium accumulation in CSF, FLAIR hyperintensity T2* GRE

Blooms if hemorrhage present

DWI

Most common: No restriction

Less common: Hyperintense on DWI with “pseudonormalized” ADC

May indicate irreversible infarction ADC map: Markedly elevated (bright areas)

Shows foci of increased diffusion representing anisotropy loss

Vasogenic edema due to cerebrovascular autoregulatory dysfunction

Nuclear Medicine Findings

Acute Cerebral Ischemia-Infarction

MCA distribution > > PCA

Infarcts restrict on DWI; PRES usually does not

Status Epilepticus

May cause transient gyral edema, enhancement

Can mimic PRES, stroke, infiltrating neoplasm

Unilateral (PRES often bilateral)

Hypoglycemia

Severe parietooccipital edema

Can resemble PRES, so history important

Thrombotic Microangiopathies

Malignant hypertension, DIC, HUS, TTP

Significant overlap as PRES is common imaging manifestation

Cerebral Hyperperfusion Syndrome

Postcarotid endarterectomy, angioplasty, or stenting

Hyperperfusion syndrome occurs in 5-9% of cases

Perfusion MR or CT scans show elevated rCBF

P.II(1):24

Aggressive control of blood pressure associated with clinical, radiological improvement Gliomatosis Cerebri

Entire lobe(s) involved rather than patchy cortical/subcortical

Occipital lobe involvement less common

Can mimic brainstem PRES

PATHOLOGY

General Features

Etiology

Diverse causes and clinical entities with HTN as common component

Acute HTN damages vascular endothelium

Breakthrough of autoregulation causes blood-brain barrier disruption

Result = vasogenic (not cytotoxic) edema

Arteriolar dilatation with cerebral hyperperfusion Hydrostatic leakage (extravasation, transudation of fluid/macromolecules through arteriolar walls) Interstitial fluid accumulates in cortex, subcortical white matter

Posterior circulation sparsely innervated by sympathetic nerves

Predilection for parietal, occipital lobes Frank infarction with cytotoxic edema rare in PRES

Common

Cortical/subcortical edema

± petechial hemorrhage in parietal, occipital lobes

Less common: Basal ganglia, cerebellum, brainstem, anterior frontal lobes

Rare: Gross hemorrhage, frank infarction

Microscopic Features

Autopsy in severe cases shows microvascular fibrinoid necrosis, ischemic microinfarcts, variable hemorrhage Chronic HTN associated with mural thickening, deposition of collagen, laminin, fibronectin in cerebral arterioles CLINICAL ISSUES

Presentation

Most common signs/symptoms

Headache, seizure, ↓ mental status, visual disturbances

Caution: Some patients, especially children, may be normotensive or have only minimally elevated BP! Clinical profile

Pregnant female with acute systemic HTN, headache ± seizure

Middle-aged, older adult on chemotherapy

Child with kidney disease or transplant

Eclampsia lower rate (< 1%)

Natural History & Prognosis

Usually no residual abnormalities after HTN corrected

Reversibility related to blood pressure normalization

Brainstem, deep white matter lesions less reversible than cortical/subcortical

Eclampsia more reversible than drug-related PRES

In rare cases may be life threatening

Permanent infarction rare

4% of patients develop recurrent PRES

Treatment

Control blood pressure, remove precipitating factors

Delayed diagnosis/therapy can result in chronic neurologic sequelae

DIAGNOSTIC CHECKLIST

Consider

Patchy bilateral occipital lobe hypodensities may be earliest NECT manifestation of PRES

Image Interpretation Pearls

Major DDx of PRES is cerebral ischemia; DWI is positive in latter, usually negative in former

(Left) Axial T2WI MR in a patient on cyclosporine who developed acute onset of extreme hypertension shows symmetric hyperintensities in both cerebellar hemispheres (Right) Axial T2WI MR in the same patient shows striking

hyperintensity in both basal ganglia with relatively subtle findings in the occipital poles

(Left) Axial T2WI MR in the same patient shows florid changes in the cortical watershed zones DWI showed no restriction, which is typical even in severe cases of PRES All findings resolved when the patient was taken off

chemotherapy and blood pressure normalized (Right) Axial T2WI MR in a patient with PRES shows pontine-predominant pattern with only subtle change in the occipital lobe Sometimes pontine or cerebellar abnormalities can be found without other imaging evidence of PRES

Acute Cerebral Ischemia-Infarction

> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Acute Cerebral Infarction

Ischemia-Acute Cerebral Ischemia-Infarction

Edward P Quigley, III, MD, PhD

Anne G Osborn, MD, FACR

Key Facts

Terminology

Interrupted blood flow to brain resulting in cerebral ischemia/infarction with variable neurologic deficit

Imaging

Major artery (territorial) infarct

Generally wedge-shaped; both GM, WM involved

Embolic infarcts

Often focal/small, at GM-WM interface

NECT

Hyperdense vessel = clot (“dense MCA” sign)

Loss of GM-WM distinction in 1st 3 hours (50-70%)

“Insular ribbon” sign: Insular cortex GM-WM interface lost

“Disappearing basal ganglia” sign

Parenchymal ± intraarterial FLAIR hyperintensity

↑ intensity on DWI + corresponding ↓ on ADC

↓ CBF, CBV on perfusion MR

Top Differential Diagnoses

Hyperdense vessel mimics

Parenchymal hypodensity (nonvascular causes)

2nd most common cause of death worldwide

#1 cause of morbidity in USA

IV thrombolysis (< 3 hours of symptom onset)

(Left) Graphic illustrates left M1 occlusion Proximal occlusion affects the entire MCA territory, including the basal ganglia (perfused by lenticulostriate arteries ) Acute ischemia is often identified by subtle loss of the gray-white interfaces with blurring of the basal ganglia and an “insular ribbon” sign on the initial CT (Right) NECT scan in a 46-year-old man shows a very “dense” left MCA compared to the normal minimally hyperdense right MCA