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Flashcards in Radiology Ischemia Deck (45)

ACA supplies

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


ACA occlusion

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


MCA stem infarct

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


CT in ischemic bleeds

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.


MRI v acute stroke

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.


diffusion positive changes

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


inferior division of MCA

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


PCA supplies

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


PCA infarct

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


cortical blindless

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


Blaint syndrome

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


optic ataxia

incoordination of hand and eye tv


optic ataxia

incoordination of hand and eye movment


oculomotor apraxzia

inability to voluntarily guide eye mvt



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



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


cardioembolic infarct

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.


non-rheumatic afib v stroke path

stasis in left atrial appendage --> thrombus


cardioembolic infart workup

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.



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


remote PCA and MCA stroke sx

alexia without agraphia and expressive aphasia


wallerian degeneration

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


hydrocephalus ex vacuo

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


ant inf cerebellar A (AICA) supplies

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



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



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


locked in syndrome

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



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


lacunar stroke prsent w/

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.


lateral medullary stroke

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.


medial medullary infacrt

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


medial lemiscus damage

CL impairment of proprioception and light touch


global hypoxic -ischemia injury

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.


MRI in global hypoxic ischemic injury

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


reversal sign

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


brain death

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.


venous infarction

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.



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


microvascular disease (MVD)

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


watershed stroke

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


carotid endarectomy

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


vertebral A dissection

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


massive MCA infarct

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


cytoxic edema

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


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

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