Cerebrovascular Disease: Stroke most common Clinical DDX:

1. Hypoxia/Ischemia/Infarction: Impair CNS Tissue Oxygenation + BF so Brain

Embolism [Most common Cardiac Mural Thrombosis: Prone due MI Valvular
AFib] > 2nd Most Thromboembolism over AS Plaques in Carotid Arteries >
Paradoxical Fat/ Embolic w/ Cardiac Surgery/ Tumor-Fat-Air Embolism

Middle Cerebral Artery Territory Distribute Direct Extension of ICA More Freq by
Embolic Infarction w/ = Incidence in 2 Hemi/ Emboli tend to lodge where blood
vessels branch or in areas of preexisting luminal stenosis. “Shower
embolization,” as in fat embolism, may occur after fractures; affected individuals
manifest generalized cerebral dysfunction with disturbances of higher cortical
function and consciousness, often without localizing signs. Widespread
hemorrhagic lesions involving the white matter are characteristic of embolization
of bone marrow after trauma (Fig. 28-14)] more common >

Thrombosis [Lumen Progress Narrow = AS/Plaque Rupture May w/ Anterograde

Extension May to Fragmentation & Distal Embolization: Most at Carotid
Bifurcation/ In Situ MCA/ Basilar Artery Either End & COMMON ASSOC W/
DM/HTN] &

Vasculitis [Inflam may Luminal Narrow Occulsion Cerebral Infarcts]: Small/Large

w/ Syphilis/TB now more common in Immunosuppression + Opportunistic e.g.
Aspergillosis/ CMV Encephalitis & PAN + Other Noninf Vasculitides May Cerebral
Ve = 1/Mult Infarcts/ PRIMARY CNS ANGITIS [Granulomatous NS Angitis]: Mult
Small/Medium Paren/SAH Ve w/ Chronic Inflam Multinucl Giant: Affected
individuals manifest a diffuse encephalopathic or multifocal clinical picture, often
with cognitive dysfunction; patients improve with steroid and immunosuppressive
treatment. Other conditions that may cause thrombosis and infarction (and
intracranial hemorrhage) include hypercoagulable states, dissecting aneurysm of
extracranial arteries in the neck supplying the brain, and drug abuse
(amphetamines, heroin, cocaine)]: Brain Req Oxygen [Oxid Metab Gen ATP] +
Glucose [Circulation-Derived bc Min Use Glycolysis/E Substrates] as 20%
Consume Whole Body O2 + 15% Resting CO as Vascular R Autoregul to keep
CBF constant over wide BP + ICP:
Hypoxia: Due Dec PPO2 O2-Carry Capacity Inhibit O2 Tissue Use

Ischemia: Disrupt CBF Transient/Permanent [Here due Dec Perfusion P

[Hypotension]/ Small-Large Ve Obstruction/ Both] W/ ATP DEPLETION
NEURONAL CM LOSS INC CYTO CA [Ischemia: ATP Down = Inappropriate
Release Excitatory AA NT: Glutamate Excess Ca Influx via NMDA Glutamate
Rec: KEEP AN EYE OUT FOR PENUMBRA: AT-RISK TISSUE BETWEEN
[Necrotic & Normal] so can rescue via Anti-Apop:

GLOBAL CEREBRAL ISCHEMIA [Swollen Edema Brain w/ Wide Gyri + Narrow

SuLci: Poor Demarc Between White & Gray Matter: IRREV ISCHEMIC
INFARCTION EVOLVE OT: Early 12-24 Hrs Red Neurons + INSERT
Microvacuolization Later Pyknosis + Karyorrhexis Then 1st Neutro THEN
SUBACUTE 24 Hrs to 2 Wks: Necro Macro Vasc Prolif Rxn Gliosis THEN AFTER
2 Wks: Repair: In the cerebral neocortex the neuronal loss and gliosis are
uneven, with preservation of some layers and destruction of others, producing a
pattern of injury termed pseudolaminar necrosis]: Diffuse Ischemic/Hypoxic
Encephalopathy when Gen Dec Cerebral Perfusion AS IN CARDIAC ARREST/
SHOCK/ SEVERE HYPOTENSION: MILD [Transient Post-Ischemic Confusional
State w/ Complete Recovery No Irreversible CNS Tissue Damage yet still
possible Irrev in Mild/Transient & MOSTLY IN NEURONS [Hippocampus
Pyramidal Cell Layer esp CA1 Sommer Sector/ Cerebellar Purkinje/ Cerebral
Cortex Pyramidal Neurons] SINCE MORE SENSITIVE > BUT STILL Glia [Oligo
Astro]] to SEVERE GLOBAL CEREBRAL ISCHEMIA [Widespread so survive
remains in PVS & other meet brain death criteria: IRREVERSIBLE DIFFUSE
CORTICAL INJURY [[Isoelectric/Flat EEG] + BS Damage: Absent Reflex
Cerebral Perfusion Resp Drive: When individuals with this pervasive form of
injury are maintained on mechanical ventilation, the brain gradually undergoes an
autolytic process with gradual liquefaction producing the so-called “respirator
brain.”]. Focal Cerebral Ischemia: Arterial Occulsion/Hypoperfusion = Dec/Stop
CBF to local area [Infarction follows] AS GEN: MAJOR COLLAT FLOW: CIRCLE
OF WILLIS (Supplemented by External Carotid-Opthamlmic Pathway) Better >>
[Partial Inconstant] Cortical-Leptomeningeal for Ant/ Middle/ PCA & In contrast,
there is little if any collateral flow for the deep penetrating vessels supplying
structures such as the thalamus, basal ganglia, and deep white matter.