C. Douglas Phillips, MD FACR Director of Head and Neck Imaging Weill Cornell Medical College NewYork-Presbyterian Hospital

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

Lenticular Crescent Prior external capsule hemorrhage

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