• CBC, BP monitoring LEGEND:

ACUTE ISCHEMIC STROKE
 • FBS, Lipid Profile

• Cardiac Biomarkers, ECG
• Coagulation Studies, Pregnancy RISK FACTORS
MODIFIABLE RF Test, Toxicology Screening
NONMODIFIABLE RF Hypertension
Age Diabetes Mellitus MECHANISM
Gender Cardiac
Race Disorders
Hx of Migraine Hyperlipidemia DIAGNOSTIC TESTS
Headaches Carotid Stenosis
Prior stroke/TIA Hyper Lifestyle
Heredity coagulability modification
TREATMENT
Oral Antihypertensive
Direct damage to arterial endothelium
contraceptive Drugs
use/ Hypoglycemic CLINICAL
Abbreviations:
RF - RisK factors postmenopausal Agents MANIFESTATIONS
LDL - low density lipoprotein hormone use Lipid Lowering
CRP- C-reactive protein
Lifestyle RF Agents
CT- Computed Tomography More LDL diffuses across damaged RED TEXTS SEEN IN
Antithrombotic PATIENT
TNFa,- Tissue necrosis endothelium & accumulate in the intimate
Factor a Therapy
layer of the artery wall
IFy,- interferon gamma
IL-1B- Interleukin 1B
ACA- Anterior Cerebral Artery
MCA- Middle Cerebral Artery
PCA- Posterior Cerebral
Artery LDL in the intimate is oxidized into lipids Elevation of
VBA- Vertebrobasilar Artery that trigger chronic inflammation in the systemic markers Elevated serum CRP
L - left vessel wall of inflammation
Ca- Calcium
Na- sodium
K- Potassium
BBB- Blood brain barrier
Inflammation recruits monocytes into the Streaks of fatty tissue can be observed
vessel wall, which then differentiate into Fatty streaks
between the endothelium and the
macrophages (seen on pathological specimen, early
smooth muscle layer (media) of the
indicator of developing atherosclerosis)
artery

Macrophages phagocytose the oxidized

LDL and become filled with fat
(henceforth, these cells are termed “foam
cells”)
 Overtime, foam cells accumulate in the
intimate to form an enlarging lipid core.
Fibrous connective tissue accumulates
around the lipid core forming a “fibrous
cap”



Development of an atheroma (lipid-filled

plaque that can enlarge and eventually
impinge on vessel lumen) in the artery
wall

The atheroma can calcify and further

enlarge and can either remain stable
( not rupture) or rupture

SMALL ARTERY LARGE ARTERY CARDIO AORTIC

OCCLUSION ATHEROSCLEROSIS EMBOLISM

• Anti platelet/
Anticoagulant
• Fibrinolytic
agents • Anti thrombotic
• Endovascular Thrombolysis
Acute Infarction Atherosclerotic plaque Revascularization
Thrombus forms in the •
decreases diameter of • Anti platelet / heart and travels to the • Thrombectomy
intra or extra cranial Anticoagulant brain • Beta Blockers,Ca
vessel therapy Channel Blockers
• Lipid-lowering
therapy
• BP control

CT: Hyperdense
segment of a vessel
 Decreased cerebral blood
flow


 • CT Perfusion
Decreased O2 and glucose • prolonged (increased) T-max, ↑ glucose metabolism in
in infarct location typically >6 seconds (or other
penumbra
measures of delayed arrival of
contrast such as mean transit
time (MTT) or time to peak
(TTP))
Increased Anaerobic • normal or increased cerebral
blood volume (CBV) due to • Revascularization Peri-Infarct depression like
Metabolism autoregulation Therapies depolarization

↑ volume of Infarct
↓ ATP ↑ Lactate

Microglia clear
Astrocytes death
debris
Dysfunction of Sodium/ Astrocytes release
Potassium ATPase pump CITICOLINE Glutamate
on neurons

Excitotoxicity
Release TNFa, IFy, IL-1B

Water influx with ↑ Na, Ca influx, Activate postsynaptic CT

sodium K outflow glutamate receptors • loss of grey–white
matter differentiation
• hemispheric sulcal
INFLAMMATION effacement,
• loss of integrity of the
lentiform nucleus or
Neurons release ↑ Ca influx hyperdensity within an
Cerebral Edema Depolarization Glutamate MANNITOL intracranial artery (the
‘dense artery sign’)
•
 Compression of
vessels and tissues • Water
Restriction

 Activate catabolic
• IV Mannitol Oxidative and
CITICOLINE
proteases, lipase, nitrosative injury
nucleases
Breakdown BBB
CT
• loss of grey–white matter
differentiation
• hemispheric sulcal effacement,
Secondary • loss of integrity of the lentiform
inflammation nucleus or hyperdensity within an Apoptosis
intracranial artery (the ‘dense Necrosis
artery sign’)

↓ blood flow in ↓ blood flow in ↓ blood flow in ↓ blood flow in

the ACA the MCA the PCA the VBA

• Disinhibition and
• Contralateral • Vertigo
speech
homonymous • Nystagmus
perseveration
R hemisphere hemianopsia • Diplopia
• Primitive reflexes L hemisphere
damage • Cortical blindness • V i s u a l fi e l d
(eg, grasping, damage • Visual agnosia deficits
sucking reflexes)
• Altered mental • Dysphagia
• Altered mental status
status • Dysarthria
• Impaired judgment
• Impaired memory • Facial
• Contralateral
Visual perceptual hypesthesia
weakness (greater in
legs than arms) APHASIA deficits & neglect (L • Syncope
• Ataxia

• Contralateral hemiparesis & sensory deficits, Dysphagia,

dysrthria, visual field deficits, aphasia, agnosia, apraxia,
agraphia-
• Weakness of the arm and face is usually worse than that of
the lower limb.
 • Oxygen supplementation
• Fibrinolytic Therapy
• Intraarterial Reperfusion
• Anti platelet agents
• Blood Pressure control
• Glucose Control
• Mechanical Thrombectomy
• Cerebral Edema Control
• Seizure Control
• Anticoagulation and prophylaxis
• Neuroprotective Agents
• Lifestyle Modification
• Physical, Occupational and Speech Therapy

References:
• Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease (Ninth edition.). Philadelphia, PA: Elsevier/
Saunders.
• Dennis L.,, et al. Harrison's Principles of Internal Medicine. 19th edition. New York: McGraw Hill Education,
2015.
• Merrit’s NeurologyKumar, V., Abbas, A. K., &
• Snell, Richard S. Clinical Neuroanatomy. Philadelphia : Wolters Kluwer Health/Lippincott Williams & Wilkins,
2010.
• https://radiopaedia.org/articles/ischaemic-stroke?fbclid=IwAR2OtDEJX4VlRK9tqxClLshGwd5ozc76x-
d5ih0DVpOUJapyqFq9hd9DHmw
• https://neuropathology-web.org/chapter2/chapter2bCerebralinfarcts.html?
fbclid=IwAR2_DrDANYk2yPJwdHZgS8f90bLmJofaD8CkT5fnHxzGdj69iDCtEOYLcYg
•

ALFONSO, LOURADEL/ LEGION, NATHALIE

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