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

Images/histo

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

otic #pale$ stro%e

over a disrupted pla3ue, usually at middle cere'ral artery or internal carotid artery near 'i urcation and ends o 'asilar artery. risk actors 6ia'etes, H4$ and sickle cell disease

transient ischemic attacks, 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, ata!ia, ipsilateral sensory loss o ace, contralateral sensory loss o trunk and lim's

necrosis

aspirin, clopidigrel and ticlopidine

in arct, cere'ral edema, loss o white matter, gliosis in-ury, li3ue active necrosis

Embolic #hemorrhagi c$ !tro%e

0ost common causes: cardiac mural throm'i, cervical carotid artery throm'us, parado!ical em'oli, tumor, at, air, septic em'oli *in ective endocarditis or 'urns,

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1ntracere'ral hemorrhage, due to vessel reper usion a ter lysis o em'oli

C+4 scan

Multi(in)arct Dementia

2nd most common cause o dementia. due to H4$, atherosclerosis, C+6+%19 or vasculitis. 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

;rie , reversi'le episodeo ocal neurological dys unction lasting <24hrs 0igraines and 41+s/C>+s, mood/personality changes, sie#ures, 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$ , pertensie Encephalop ath

+6 inheritance, $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,

Headache, papilledema/visua l distur'ances, num'ness/weakn ess in e!tremities,

Coma&death

Correct H4$

Cere'ral edema, herniation, i'rinoid necrosis/throm'osis o arterioles

con usion, convulsions, nausea, 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

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Cystic areas o microin arction <1.(cm

!lit ,emorrhage s

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%lit like cavities surrounded 'y 'rownish discoloration and pigment laden macrophages

, pertensie Intracerebra l hemorrhage

0ost common causes in order: %ystemic Hypertension, amyloid angiopathy, anticoagulants, aneurysms *Charcot-;ouchard aneurysm,, tumors, illicit drugs, misc Chronic H4$&+neurysm o small vessels o the 'asal ganglia or thalamus

@sually occurs in 'asal ganglia, thalamus, pons, cere'ellar

Charcot( 'ouchar. Aneur sm

'err Aneur sm

6isruption o tunica media and internal elastic lamina Aisk actors +ssociated with +62B6, i'romuscular dysplasia, $=-1, 4u'erous sclerosis, ehlers-6anlos syndrome and 0ar ans syndrome

Most commonl occurs at /0n o) the ant. Communicating arter an. ACA

Aupture can lead to su'arachnoid hemorrhage Cworst headache o my li eD and 'itemporal hemianopia

%urgery to clamp vessel

Cerebral Am loi. Angiopath

Conse3uence o aging, depositon o +; amyloid. amilial orm associated with the +22 gene

1ntracere'ral hemorrhage

Congo red stain !ubarachno i. hemorrhage Aupture o 'erry aneurysm C5orst Headache o my li eD Aapid time course, 'lood in C%=, vasospasm and re'leed

;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, sei#ures and neurological de icits 4angle mass o thickened, enlarged 'lood vessels with intervening gliotic 'rain tissue, 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

neural tissue

Epi.ural ,ematoma

Hemorrhage into space 'tw skull and dura. most due to skull ractures *temporal 'one,&rupture o middle meningeal artery

Head in-ury&coma

Aapid accumulation o 'lood, lucid interval&unresponsive 4ranstentorial herniation, C$111 palsy @sually progress slowly&slow 'lood accumulation, lethargy, con usion, headache, ata!ia, sei#ures

!ub.ural ,ematoma

Aupture o 'ridging veins due to head trauma, alcohol, shaken 'a'y, whiplash

Cresecent shaped hemorrhage !%ull )ractures " types: 9inear *involving sutures,, 6epressed *laceration o 'rain,, ;asilar*raccon eyes, 'lood rom ear, C%= leakage

rom nose and meningitis, Atlanto( occipital Dislocation 1nternal decapitation. 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, 2ostconcussive syndrome E headache, di##iness, poor concentration, 'ehavioral pro'lems %econd impact syndrome: death due to cere'ral edema a ter second concussion with 1: days

%ensitive to light, sound, decreased 'alance coordination, amnesia

Chronic *raumatic Encephalop ath #C*E$

Aepetitive 'rain in-ury rom concussions Aisk actors: 'o!ers, oot'all players, soccer, military service, +poF4

%ymptoms decades later %tage1:emotional disru'ances, poor-udgement 2: erratic 'ehavior,

6iagnosed postmortem. 4reat with +l#heimer and parkinsons meds

=rontal and temporal atrophy, hippocampi and amydala

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

atrophy, +ccumulation o 4au protien

d amaged a!ons *;+22 stain,

+!onal swelling