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21 Cards in this Set

  • Front
  • Back
How many days after an infarct does edema reach maximum?
3 days
By when do you see cystic encephalomalacia?
6 –8 weeks
3 signs of significant stenosis on Doppler?
1. high velocity flow
2. turbulent flow
3. luminal narrowing
Intraparenchymal hemorrhage – DDx
1. Hypertension
2. Trauma
3. amyloid angiopathy
4. venous hypertension/venous sinous occlusion/venous infarct
5. coagulopathy
6. Large infarct territory/reperfusion
7. hemorrhagic metastasis
8. AVM
9. anuerysm dissecting into tissue
Most common sites of spontaneous intraparenchymal hemorrhage
1. External capsule/basal ganglia
2. cerebellum
3. thalamus
4. pons
Intraparenchymal Hematoma
1. How long until isodense to CSF?
2. How long until ring-enhancing?
3. How long remains ring-enhancing?
1. 2-3 months
2. 7-10 days
3. 3-4 months
SAH
1. 2 most common causes?
2. 5 rarer causes
1. Trauma, ruptured anuerysm
2. AVM (dural), pituitary apoplexy, idiopathic mesencephalic hemorrhge, coagulopathy, neoplasm,
Aneurysm rupture – major causes of morbidity? (4)
1. rerupture
2. vasospasm, infarction
3. hydrocephalus
4. herniation
AVM
1. 2 most common clinical presentations?
2. What is common in adjacent brain tissue?
1. seizure, intraparenchymal bleed
2. atrophy
Carotid-Cavernous Fistula – 2 types
1. Direct connection in cavernous sinus
2. Parasellar AVM
Birth Trauma – DDx
1. Caput succedaneum – soft superficial pitting edema, crosses suture lines
2. Subgaleal hemorrhage – firm fluctuant mass, can dissect into neck, deep to aponeurosis
3. Cephalohematoma – hematoma between outer layer of periosteum, most commonly parietal, firm tense mass, may calcify, thicken diploe, does NOT cross suture line
4. Skull fracture
5. Subdural Hemorrhage
6. Benign subdural effusion
Increased Intracranial Pressure
1. Intracranial mass
2. Hydrocephalus
3. Malignant hypertension
4. Diffuse cerebral edema
5. Increased Venous Pressure
6. Elevated CSF protein
7. Pseudotumor cerebra – papilledema, enlargement of perioptic nerve subarachnoid space
Strokes – Vascular Etiologies/categories
Brain Infarction – 80%
a. Occlusive atheromatous disease
i. Extracranial aa. 35%
ii. Intracranial aa – 10%
b. Small vessel dz – lacunar infarct (25%)
c. Cardiogenic emboli
i. Ischemic HD with mural thrombus (AMI, arrhythmia)
ii. Valvular HD – postinflammtory (rheumatic) valvulitis, infective endocarditis, nonbacterial thrombotic endocarditis, MVP, MS, prosthetic valves
iii. A-fib
iv. Left Atrial Myxoma
Strokes – Vascular Etiologies/categories
Non-atheromatous Disease
i. Elongation, coils, kinks
ii. FMD
iii. Aneurysm
iv. Dissection
v. Cerebral arteritis (takayasu, collagen disease/SLE, lymphoid granulomatosis, termpoal arteritis, behcet dz)
vi. Postenarterectomy thrombosis/embolism, restenosis
e. Coagulation disorder
2. Primary Intracranial Hemorrhage – 15%
f. Hypertensive hemorrhage – 40-60%
g. Amyloid angiopathy – 15-25%
h. Vascular malformation – 10-15%
i. Drugs: eg anticoagulants 1-2%
j. Bleeding diathesis (<1%)
3. Vasospasm due to nontraumatic SAH
k. Ruptured aneurysm 75-80%
l. Vascular malformation 10-15%
m. Nonaneurysmal SAH5
CAUSES OF EARLY DRAINING VEIN - (rapid or short "transit time")
1. Neoplasms - primary or secondary
2. AVM
3. Inflammatory lesion
4. Trauma (hyperemia)
5. Ischemia
6. Epileptic focus
7. Toxic encephalopathy
COMMENT: Definition is vein seen < 3 sec after beginning of intracerebral contrast - usually veins drain into Sup Sinus from anterior to posterior
DEEP VENOUS DRAINAGE
1. Anterior septal
2. Thalamostriate
3. Internal cerebral veins (paired)
4. Basal vein(s) of Rosenthal (medial temporal lobe)
5. Great vein of Galen
6. Inferior sagittal sinus (free edge of Falx)
7. Straight sinus
8. Superior sagittal
9. Transverse sinus
10. Sigmoid sinus
11. Internal jugular
COMMENT: Superficial drainage is superficial middle cerebral vein, vein of Trolard and vein of Labbe to superior sagittal sinus
Moya Moya – DDx
1. Primary (inherited)
2. Secondary
a. Down
b. TS
c. SCD
d. CTD
e. Progeria
f. Midline anomalies (morning glory syndrome)
g. NF1
h. Irradiation
i. Inflammatory: CNS angiitis (of childhood) basal meningitis (TB), leptospirosis, atherosclerosis, local infection (tonsillitis/otitis)
j. Vasculopathies and prothrombotic states: Kawasaki disease, anticardiolipin antibody, Factor V leiden, polyarteritis nodosa, behcet’s, SLE
IVY sign (FLAIR) – DDx
1. Moya Moya
2. Leptomeningeal mets
3. meningitis
4. Hyperoxygenation
Severely Attenuated Circle Of Willis
1. Moya Moya
2. SAH
3. Meningitis (basilar)
4. Tumor Encasement
DDx of Puctate T2-bright fFoci in basal ganglia
1. Moya moya – engorged vessels in punctate foci enhance
2. Cribriform lacunar state: no enhancement
Dural Venous Occlusion – DDx (mimics)
1. Normal – blood in vessels normal slightly hyperdense on NECT, especially newborn (dense fetal hgb in 1st 14 days
2. Anatomic Variant
a. congenital hypoplastic/absent transverse sinus
b. High-splitting tentorium (low density fluid in superior vermian fissure between leaves of high tentorium)
3. Giant Arachnoid Granulation
4. False “Empty Delta” Sign
c. Subdural hematoma/empyema
d. Empty delta sign requires contrast!