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Disease Global Cerebral Ischemia

Mechanism/pathogenesi s Cardiac arrest, hypovolemic shock, chronic CO poisoning Histo changes: see FA pg.463 1.Earl changes 12-24hrs: red neurons 2.!ubacute changes 24-2 weeks: necrosis o tissue, in lu! o macrophages, vascular proli eration and reactive gliosis "."epair a ter 2weeks: removal o necrotic tissue, loss o organi#ed C$% structure with a pseudolaminar necrosis pattern in corte!

Clinical Presentation Con usion&uncons ciouness&coma&'r ain death

Course/complications Cere'ral atrophy due to apoptosis o neurons in layers ",(,) o corte!, hippocampus*C+1, and purkin-e cells o cere'ellum. called red neurons. in arcts occur ir at -unctions o arterial territories *+C+/0C+ -unction,. stroke&'rain death

Diagnostics/the rapeutics 1mmediate O2 ventilation. mechanical ventilation


Focal cerebral ischemia Atheroscler 2latelet throm'us develops 2receded 'y 2ale in arcts&li3ue active 4reatment: 5edge shaped pale

ipsilateral sensory loss o ace. tumor. contralateral sensory loss o trunk and lim's necrosis aspirin. ata!ia.otic #pale$ stro%e over a disrupted pla3ue. loss o white matter. H4$ and sickle cell disease transient ischemic attacks. usually at middle cere'ral artery or internal carotid artery near 'i urcation and ends o 'asilar artery. cervical carotid artery throm'us. at. due to vessel reper usion a ter lysis o em'oli C+4 scan . MCA stro%e& contralateral hemiparesis and sensory loss in ace and upper e!tremity and e!pressive aphasia ACA stro%e& contralateral hemiparesis and sensory loss o lower e!tremity 'asilar stro%e& vertigo. air. 78 1ntracere'ral hemorrhage. risk actors 6ia'etes. parado!ical em'oli. cere'ral edema. gliosis in-ury. septic em'oli *in ective endocarditis or 'urns. clopidigrel and ticlopidine in arct. li3ue active necrosis Embolic #hemorrhagi c$ !tro%e 0ost common causes: cardiac mural throm'i.

papilledema/visua l distur'ances. due to H4$. C+6+%19 or vasculitis. sie#ures.rie . i'rinoid necrosis/throm'osis o arterioles .Multi(in)arct Dementia 2nd most common cause o dementia. $otch" gene mutation&smooth muscle degeneration in vessel walls&notch receptor protein deposition in walls&thicken walls 9acunar-type in arcts or silent in arcts&multi-in arct dementia 0alignant Hypertension. reversi'le episodeo ocal neurological dys unction lasting <24hrs 0igraines and 41+s/C>+s. Coma&death Correct H4$ Cere'ral edema. herniation. atherosclerosis. high mortality rate %tepwise decline in cognitive a'ility over (-1: years 6ementia&death C+4 scan *ransient Ischemic Attac% 4ransient cere'ral artery occlusion . num'ness/weakn ess in e!tremities. mood/personality changes. Headache. pertensie Encephalop ath +6 inheritance. vision pro'lems High risk to develop ischemic stroke =ind source o occlusion CADA!I+ #cere'ral autosomal dominant arteriopathy with su'cortical in arcts and leukoenceph alopathy$ .

(cm !lit . nausea.emorrhage s 78 78 78 %lit like cavities surrounded 'y 'rownish discoloration and pigment laden macrophages . convulsions. coma +acunar in)arcts H4$/dia'etes&Hyaline arteriolosclerosis o lenticulostriate vessels&microin arcts in .asal ?anglia Hypertension&rupture o small vessels&hemorrhage. which is rea'sor'ed&slitlike cavitys %ymptoms could 'e silent. mood changes 78 78 Cystic areas o microin arction <1.con usion.

aneurysms *Charcot-. ACA Aupture can lead to su'arachnoid hemorrhage Cworst headache o my li eD and 'itemporal hemianopia %urgery to clamp vessel Cerebral Am loi. 4u'erous sclerosis. Communicating arter an. anticoagulants.. i'romuscular dysplasia. ehlers-6anlos syndrome and 0ar ans syndrome Most commonl occurs at /0n o) the ant.ouchard aneurysm. thalamus. Angiopath Conse3uence o aging. amyloid angiopathy. misc Chronic H4$&+neurysm o small vessels o the 'asal ganglia or thalamus @sually occurs in 'asal ganglia. Aneur sm 'err Aneur sm 6isruption o tunica media and internal elastic lamina Aisk actors +ssociated with +62B6. depositon o +. amilial orm associated with the +22 gene 1ntracere'ral hemorrhage . tumors. pons.. cere'ellar Charcot( 'ouchar. illicit drugs. $=-1. amyloid. pertensie Intracerebra l hemorrhage 0ost common causes in order: %ystemic Hypertension.

hemorrhage Aupture o 'erry aneurysm C5orst Headache o my li eD Aapid time course. located in su'aracnoid space Ca-ernous Mal)ormatio ns +6 inheritance sei#ures 4umor e ect&sei#ures and locali#ed symptoms 0ass o thin-walled a'normal veins with $O intervening .leeding into 'oth o 'rain Arterio-eno us Mal)ormatio ns congenital 1n ant with CH= and sei#ures High output Heart ailure in in ants. vasospasm and re'leed . sei#ures and neurological de icits 4angle mass o thickened. enlarged 'lood vessels with intervening gliotic 'rain tissue.Congo red stain !ubarachno i. 'lood in C%=.

alcohol. ata!ia. .ural .asilar*raccon eyes. lethargy. lucid interval&unresponsive 4ranstentorial herniation.ematoma Hemorrhage into space 'tw skull and dura. C$111 palsy @sually progress slowly&slow 'lood accumulation.ural .. shaken 'a'y.neural tissue Epi. 'lood rom ear.&rupture o middle meningeal artery Head in-ury&coma Aapid accumulation o 'lood.. whiplash Cresecent shaped hemorrhage !%ull )ractures " types: 9inear *involving sutures. con usion. C%= leakage . most due to skull ractures *temporal 'one. 6epressed *laceration o 'rain. sei#ures !ub.ematoma Aupture o 'ridging veins due to head trauma. headache.

amnesia Chronic *raumatic Encephalop ath #C*E$ Aepetitive 'rain in-ury rom concussions Aisk actors: 'o!ers.rom nose and meningitis. 6iagnosed postmortem. decreased 'alance coordination. 'ehavioral pro'lems %econd impact syndrome: death due to cere'ral edema a ter second concussion with 1: days %ensitive to light. poor-udgement 2: erratic 'ehavior. displacement o C1 rom its attachment to the occiput 2aralysis&death Concussion Head 'low&6isruption o reticular activating system 4ransient neurological dys unction ollowing head trauma 1ncreased risk o repeated concussion. sound. hippocampi and amydala . 2ostconcussive syndrome E headache. di##iness. 4reat with +l#heimer and parkinsons meds =rontal and temporal atrophy. poor concentration. oot'all players. Atlanto( occipital Dislocation 1nternal decapitation. soccer. +poF4 %ymptoms decades later %tage1:emotional disru'ances. military service.

+22 stain.aggression. 2arkinson symptoms ": overt dementia and 2arkinson disease Di))use a0onal in/ur %evere traumatic in-ury rom 0>+s or 'lows to the head. pathological -ealous. +ccumulation o 4au protien d amaged a!ons *. memory loss. paranoia. whiplash +!ons are stretched causing alterations in a!onal low&swelling 9oss o consciousness and coma atrophy. speech loss. +!onal swelling .