C. Douglas Phillips, MD FACR Director of Head and Neck Imaging

Weill Cornell Medical College NewYork-Presbyterian Hospital

I have no financial disclosures

Understand range of pathology that may present as an acute alteration in mental status or with focal neurologic symptoms

Guide and direct imaging evaluations of these patients

Recognize imaging appearance of these lesions

Venous sinus thrombosis

Aneurysmal and non-aneurysmal CNS hemorrhage

Vasculopathy

Reversible encephalopathy syndrome (PRES)

Osmotic myelinolysis

CNS masses which may present acutely

Thrombosis of cortical veins/dural sinuses

Cascade of pathology

Thrombosis leads to venous stasis/venous hypertension

Reduced perfusion pressures lead to decreased CBF

Infarction with hemorrhage

Potential Etiology Dehydration Pregnancy Drugs

Oral BCs, hormone therapy, etc.

Hypercoagulable states Certain disease states

Behcet’s, etc.

Contiguous inflammatory, infectious or neoplastic disease

Standard MRI sequences: T1/T2

Additional MRI sequences: T2*, SWI

DWI

Enhanced T1 SPGR

MR Venography TOF, PC, or enhanced

Dynamic evaluation

CT/CTV (=/- Dynamic evaluation)

Filling defects in venous structures

Fat in sinus

Arachnoid granulations

Asymmetric sigmoid/transverse sinus and/or IJV:

Confirm with source images

Central WM & deep nuclei drained by deep veins

ICV, subependymal & medullary veins, VOG, SS

MRV should suggest or confirm deep venous thrombosis

Rare cases may require other studies

•Typical bithalamic T2 hyperintensity for deep vein thrombosis •Blood in ventricle •“Flow voids” present in internal cerebral veins •MRV confirmed occluded deep venous system, including ICV

Susceptibility effects of thrombus helpful

Improved conspicuity of smaller structures:

Deep medullary veins

Small cortical veins

Improved visibility of parenchymal hemorrhage

Cautionary statement:

Not all stages of blood “bloom”

Dependent on enhancement; not flow

Advantages:

Sensitivity higher

Much faster

Disadvantages:

T1 bright clot may yield false negative appearance

Chronic thromboses enhance false negative

Too many veins

False negative MRV

Cortical vein thrombosis

Enhanced T1 SPGR using thin slices (<=1mm):

Better cortical & small vein detection

Better characterization in chronic thromboses

Excellent imaging of venous structures

Vary slab MPR thickness to advantage

Advantages: Fast

No susceptibility to IPH

High spatial resolution

Disadvantages: Parenchymal sequelae

less well characterized

Always obtain NCCT first

48 year old – headache, left hemiparesis

Lobar hemorrhage

Choice between CTA and MRI/MRA

Location was suspicious for venous hemorrhage MRI/MRA

NB – hemorrhage in atypical or non-vascular distribution THINK VENOUS

May propogate into dural sinus

1° consideration in “thunderclap” headache

CT + for SAH in 98% of patients within 24 hrs

Less than 50% at 48 hrs

No negative evaluation complete without LP

Typical aneurysm results from focal vascular wall weakening

Typical locations

PCOM, ACOM

Supraclinoid ICA

MCA bifurcation

Basilar tip

PICA

Increased density in subarachnoid space

Predominate in basilar cisterns

Accompanied by IVH or occasional SDH

Distribution is of little importance

Subacute SAH may be confusing picture

Acceptance of CTA in SAH

Good literature support, concordance with catheter angiography

May depict aneurysm to better advantage (neck, calcifications, etc.)

Contrary opinion holds that it only delays angiography

Good negative predictive value

MRA less commonly used acutely

Likely reliable for aneurysm greater than 2-3 mm in size

3T superior for aneurysm detection

Hypertension

AVM (lobar hemorrhage in an adult patient)

Vasculopathy

Inflammatory forms

Amyloid angiopathy in aged population

Coagulopathy

Non-aneurysmal SAH

Hemorrhage into existing CNS mass lesion

Venous sinus thrombosis

Determine location of hemorrhage

Subarachnoid, parenchymal, etc.

Evaluate for associated mass lesion or other positive findings

Calcifications

Arterial enlargement

CTA has shown strong predictive value

Diagnoses of exclusion typically more important than eventual diagnosis

Literature supports that patients with perimesencephalic pattern of SAH on CT and negative CTA need no further follow-up.

Ruigrok YM, Rinkel GJE, Buskens E, Velthuis BK, and van Gijn J. Perimesencephalic Hemorrhage and CT Angiography : A Decision Analysis. Stroke, Dec 2000; 31: 2976 - 2983.

Grade I or Grade II on presentation Middle aged male

Blood confined to perimesencephalic cisterns, proximal interhemispheric fissure, or proximal sylvian fissure

No ventricular penetration, no hydrocephalus

Presumed venous hemorrhage

Striatocapsular (60-65%)

Thalamus (15%)

Most common cause of ICH in 45–70 yr

Fibrinoid necrosis of vessel wall

Microbleeds are very common on GRE MR

“Spot sign” on CTA thought highly useful

Presentation CT exam – 46 year old male with BP 180/105

Prior external capsule hemorrhage

“Lenticular Crescent”

Hypertensive “hit list”

External Capsule

Thalamus

Dentate Nucleus

Pons

Lobar

* *

Suspicious enhancement noted on post-Gd images

Potentially tumor? Vascular?

Lobar hemorrhage in adult patient is always potential AVM

CTA and/or MRI/MRA should be performed

Gadolinium recommended for MRI

Wide range of clinical presentations

Acute presentations

Intracranial hemorrhage

ICH, SAH, IVH

Infarctions

Altered mental status, headaches and white matter changes

Diagnosis often delayed or unsuspected

Inflammatory disease affects walls of cerebral arteries

Weakens muscle Vessel dilatation

Fibrotic or inflammatory thickening Vessel narrowing

“String of beads” or “string of pearls” sign

Differential considerations – vasospasm, intracranial atherosclerotic disease

Drugs (sympathomimetics), toxins

Post-partum

Inflammatory or collagen-vascular diseases

Infections

Basilar meningitides

Diffuse meningitis

“The more you look, the more you see”

Encephalopathy accompanying transient loss of normal BBB functions

Predominant involvement of posterior circulation vessels

Affect all territories in advanced cases

Leaky capillaries lead to vasogenic edema, occasional hemorrhage

Large number of potential etiologies

Common thread is likely hypertension

Symmetric, often confluent WM lesions

Can involve cortex

Parieto-occipital predominance

Hyperintense on T2

Normal DWI

Patchy enhancement common

Occasional hemorrhage

Hypertensive 42 year old with cortical blindness, seizures

Common in alcoholics

Always associated with electrolyte abnormalities

Classic - rapidly corrected hyponatremia

Involvement of oligodendroglial cells (transverse pontocerebellar fibers)

Symmetric demyelination in brain stem and pons

Clinical Picture

Confusion

Horizontal gaze paralysis

Spastic quadriplegia

Demyelination leads to significant dysfunction and cell loss

DWI abnormality is nearly always seen

Can help distinguish OM from PRES

Unsuspected/undiagnosed CNS lesions may have acute presentations

Seizures as initial presentation

Complication arising from an existing lesion

Hemorrhage

Development of acute hydrocephalus

Vascular occlusions

White matter inflammatory disease

TDL

Glioblastoma Multiforme

“Incomplete Ring” of Enhancement

Large number of diseases may present with acute CNS symptoms

Knowledge of disease patterns may provide specific diagnoses

Correlation of imaging studies with known clinical findings improve diagnostic accuracy

Rapid evaluation can provide improved outcomes