Radiology Ischemia

Question 1

ACA supplies

Answer 1

supply medial portion of frontal lobe and anterior parietal, corpus callous, cingulate gyrus.

Question 2

ACA occlusion

Answer 2

tolerated if good collateral flow through anterior communicating A. infarct cause CL weakness and sensory loss. primarily of leg bc this part of motor homunulus is within inter hemispheric fissure. urinary incontinence due to disruption of micturition inhibition center. disinhibited or abulia. left sided lesion may cause transcortical motor aphasia. right lesion - hemineglect. hyper intensity and hypo density

Question 3

MCA stem infarct

Answer 3

infarcts of entire MCA. produce dense CL weakness, sensory loss, homonymous hemianopsia. left sided lesions- global aphasia. R-sided lesions- hemineglect. eyes deviate to side of lesion

Question 4

CT in ischemic bleeds

Answer 4

pt is to r/o intracranial bleeds or mass lesions that might mimic ischemic stroke. in hyper acute ischemic stroke, brian may be normal but might see hyper dense clot in artery: dense MCA sign, basilar sign.

Question 5

MRI v acute stroke

Answer 5

MRI are mores sensitive than CT. diffusion weighted seq reveal abn mvt of water in brain tissue. most sensitive seq for detecting acute ischemic events. corresponding hypointesity(drop-out) on apparent diffusion coefficient (ADC) MRI confirms infarct in appropriate clinical setting.

Question 6

diffusion positive changes

Answer 6

seen in acutes stroke, MS, tumors like primary lymphoma.

Question 7

inferior division of MCA

Answer 7

supplies posterior frontal lobe, anterior parietal lobe, lateral temporal lobe. infact on left- wernicke’s aphasea. right- hemineglect. either side- CL visual field deficit due to disruption of optic radiations. cortical sensory loss. min to no motor findings

Question 8

PCA supplies

Answer 8

inferior medial temporal lobe, occipital lobe. midbrain, thalamus.

Question 9

PCA infarct

Answer 9

CL homonymous hemianopsia. may have macular sparing due to collateral supply to occipital pole from MCA. left- alexia w/o agraphia if there is involvement of selenium of corpus callous. .involvement of midbrain may lead to motor deficit, upper CN palsies, cortical gaze impairment, coma

Question 10

cortical blindless

Answer 10

in pt who sustained damage to both occipital lobes. anton’s syndrome is denial of blindness due to damage in bilateral occipital lobes.

Question 11

Blaint syndrome

Answer 11

due to damage to both posterior parietal and lobes characterized by optic ataxia, oculomotor apraxia, simultananosis

Question 12

optic ataxia

Answer 12

incoordination of hand and eye tv

Question 13

optic ataxia

Answer 13

incoordination of hand and eye movment

Question 14

oculomotor apraxzia

Answer 14

inability to voluntarily guide eye mvt

Question 15

simultanagnosis

Answer 15

inability to perceive more than one obj at a time in some’s visual field

Question 16

PCA

Answer 16

fetal origin seen in 30%- atypical stroke syndrome- with pathology of ant circulation, there may be infarction in territories usually supplied by posterior circ. Post communicating A is larger and primary source

Question 17

cardioembolic infarct

Answer 17

20% ischemic strokes. most common cause- non rheumatic Afib. support by diffusion wt images with multi infarct in both hemisphere and dif age in dif vascular territories.

Question 18

non-rheumatic afib v stroke path

Answer 18

stasis in left atrial appendage –> thrombus

Question 19

cardioembolic infart workup

Answer 19

if suspect do TEE to see if there is an intracardiac thrombus. ekg if there is Afib. if have either, need lifelong anticoag with warfarin. maintain inr 2-3- 66% dear in stroke.

Question 20

Apixaban

Answer 20

direct factor Xa inhibitor. prevent 21% mores strokes than warfarin. 31% less bleeding. but no reversal

Question 21

remote PCA and MCA stroke sx

Answer 21

alexia without agraphia and expressive aphasia

Question 22

wallerian degeneration

Answer 22

deign of cortico spinal tract. damage to cortical motor tracts. seen in some PCA MCA infarcts

Question 23

hydrocephalus ex vacuo

Answer 23

often occur adj to old infarct due to destruction of adj tissue.

Question 24

ant inf cerebellar A (AICA) supplies

Answer 24

basilar. inf, lateral pon.middle cerebellare peduncle. part of ant cerebellum

Question 25

PICA

Answer 25

from vertebral A. supplies lateral medulla. most of inf cerebellar hemisphere and vermis

Question 26

SCA

Answer 26

upper lateral pons. sup cerebellar peduncle. sup ppart of vermis. each cerebellar hemisphere

Question 27

locked in syndrome

Answer 27

preserve consciousness wo voluntary mvt besides vertical eye controlled by vertical gaze centers in midbrain. embolism of basilar A - can infarct entire pons

Question 28

lipohyalinosis

Answer 28

change in small A that lead to lacunar infarcts=20% of all ischemic strokes

Question 29

lacunar stroke prsent w/

Answer 29

pure motor hemiparesis- localizes to posterior limb of internal capsule, cubcortical WM or pons. pure sensory- thalamus. ataxic-hemiparesis- base of pons. clumsy hand/ dysarthria- base of pons of menu of posterior limb of internal capsule. not associated with higher cortical fun abn like aphasia, neglect unless in thalamus.

Question 30

lateral medullary stroke

Answer 30

dysphonia, facial numbness/ loss of T in CL side of body and IL side of face, horner’s, N/V, nystagmus, gait/balance prob. occlusion of vertebral or PICA lateral medullary (wallenberg) syndrome.

Question 31

medial medullary infacrt

Answer 31

ipsilateral paralysis of tongue due to hypoglossal N and nut damage. CL weakness of arm, leg due to corticospinal damage.

Question 32

medial lemiscus damage

Answer 32

CL impairment of proprioception and light touch

Question 33

global hypoxic -ischemia injury

Answer 33

cause: decr perfusion to brain in cardiac arrest or respiratory arrest, near drowning, asphyxia, CO poisoning. BG especially sensitive- memory and attention prob. mvt disorder- parkinson, dystonia see cortical laminar necrosis and infarct in watershed distribution.

Question 34

MRI in global hypoxic ischemic injury

Answer 34

hyperintensity in BG, diffusely bright T2-laminar necrosis. sulcal effacement, diffuse loss of GM/WM junction.

Question 35

reversal sign

Answer 35

blurring of GM/WM junction. hypo density of tentorium cerebelli

Question 36

brain death

Answer 36

irreversible/ promimate cause of coma. exclude presence of CNS-depressant drug. achieve normal SBP, perform 2 euro exam confirm no brainstem reflexes. apnea test. others: no pupillary response to light in both eyes, no CN3 mV, no corneal reflex, no mvt to noxious stimulus, no trachea/ pharyngeal reflex.

Question 37

venous infarction

Answer 37

no specific patter. can have focal near deficits. more indolent than arterial infarct. may present with seizure, HA, incr ICP. often see hemorrhagic component. tx: oral anticoag for 3-4m.

Question 38

SVT

Answer 38

sinus, venous thrombosis. RF: hypercoag states, reg, postpartum, infection, some meds. OCP+ smoking.

Question 39

microvascular disease (MVD)

Answer 39

unlike MS, scattered in WM. usually not in corpus callous or below tentorium as in MS. non-enhancingg with contrast. RF: smoking, DM, dyslipdemia

Question 40

watershed stroke

Answer 40

located at brain areas bordered by ACA and MCA or MCA and PCA. due to hypo perfusion from systemic hypotension, CHF, high grade carotid stenosis. present with weakness of proximal arm, leg M, preservation of distal strength. man in a barrel presentation

Question 41

carotid endarectomy

Answer 41

done as soon as stroke pt is medically stable bc highest risk for 2nd stroke is within 72hr of the 1st. can cause reperfusion injury- gyro enhancement on mri (HA, seizure, or focal deficit) 2nd ischemic stroke is most common complication

Question 42

vertebral A dissection

Answer 42

present ~ to CA dissection. neck pain, infarction of posterior circ. hornet’s if SNS affected. spontaneous or in pt with CT disorder. or rom neck trauma. tx: anti coat or anti plt. or stent

Question 43

massive MCA infarct

Answer 43

swelling= cytoxic edema= BBB intact so don’t need glucocorticoids, transtenorial herniation, death. swelling peaks on d 3-5. younger pt with less brain atrophy are at highest risk for herniation and deathtx with hemicraniectomy

Question 44

cytoxic edema

Answer 44

cause by iC accumulation of Na and H2O due to dysfunction of Na/K pump in membrane of glial cells.

Question 45

cerebral autosomal dom arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)

Answer 45

most common hereditary stroke disorder. must on NOTCH 3on chromosome 19. lead to degeneration of SMC in vessels. arteriopathy not limited to CNS, skin biopsies confirm dx. clinic: history of confusional migraine that dev in adulthood and multiple lacunar strokes. middle age- absence of other stroke RF. become demented. tx: antiplt