Flashcards in Radiology Ischemia Deck (45):
supply medial portion of frontal lobe and anterior parietal, corpus callous, cingulate gyrus.
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
inferior medial temporal lobe, occipital lobe. midbrain, thalamus.
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
in pt who sustained damage to both occipital lobes. anton's syndrome is denial of blindness due to damage in bilateral occipital lobes.
due to damage to both posterior parietal and lobes characterized by optic ataxia, oculomotor apraxia, simultananosis
incoordination of hand and eye tv
incoordination of hand and eye movment
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
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
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.
blurring of GM/WM junction. hypo density of tentorium cerebelli
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.
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
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
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
cause by iC accumulation of Na and H2O due to dysfunction of Na/K pump in membrane of glial cells.