John Peter Lovingski R. Esporlas b.

Chronic Stable Atrial Fibrillation

- 5 times
CVA c. Rheumatic Heart Disease + Atrial Fibrillation
- 17 times for embolic
- Non-traumatic, vascular cause, sudden neurologic
3. Diabetes Mellitus
deficit. - 3-6 times
Most Common Sign - 2 times as independent risk factor
- 2 times (De Lisa)
- Focal Weakness; it can produce a wide range of 4. Cigarette Smoking
symptoms such as sensory loss, speech & a. Heavy
language, disturbance, visual loss. - >40 cigarettes per day
- 2 times
Epidemiology b. Light
- <10 cigarettes per day
- Old>Young c. 5 years cessation
- >3 years from childhood stroke - Risk equal to normal
- <45 y/o for young stroke 5. Hypercholesterolemia
- Male>Female - Indirect risk factor for stroke
- Female>Male; if >85 y/o - Total for LDL & HDL: <200mg/dL
- Race a. Low-Density Lipoprotein
a. Black>White - <100 mg/dL
b. Asian>US b. High-Density Lipoprotein
- >60 mg/dL
Pathophysiology
6. Obesity
Process 7. Sedentary Lifestyle
8. Lack of Exercise
1. Focal Infarction & Ischemic Penumbra 9. Diet
- If the brain does not achieve blood flow at a 10. Heavy Alcohol Consumption
specific type; it will result to INFARCTION 11. Oral Contraception + Estrogen
2. Cerebral Edema
- Swelling of the brain TIA (Transient Ischemic Attack)
- Middle Cerebral artery has the largest cerebral - Asymptomatic carotid bruit
edema because it has 2 branches. - Carotid Bruit (Carotid Stenosis); Narrowing or
3. Increase Intracranial Pressure constricting of the carotid arteries.
4. Herniation
- (MC: Middle Cerebral Artery & Internal Carotid Risk Factors
Artery)
1. Hematocrit (Hct)
Signs & Symptoms - Faster blood clotting time
2. Serum Fibrinogen
Altered Level of Consciousness (coma, decreased - Faster coagulation
arousal levels) 3. Elevated C-Reactive Protein:
Widened pulse pressure - inflammatory marker due to endothelial injury
Increased HR 4. Elevated Homocysteine
Cheyne-Stokes Respiration - Can result from inherited or acquire enzyme
Vomiting deficiencies such as folate, B6, B12 and may
Unreacting pupils increase viscosity
Papilloedema
Metabolic Syndrome
Risk Factors (Modifiable)
- It is a cluster of interrelated metabolic risk factors
Lifestyle
for atherosclerotic disease.
1. Hypertension - 5 times risk if the following 5 are present
- Most significant risk factors 1. High Waist Circumference
- >165/95 mmHg (Braddom) 2. Increased Blood Pressure
- Parallel risk for Systolic Blood Pressure & Mean 3. Low HDL level
Arterial Pressure 4. Elevated serum triglyceride
2. Heart Disease 5. Elevated fasting glucose
- 2-6 times Non- Modifiable
a. Coronary Artery Disease
- 2 times - Race
 - Age
- Sex
- Previous Stroke;
Classification: (Temporal)
1. TIA
- A brief episode of neurologic dysfunction caused
by focal brain or retinal ischemia with clinical
symptoms typically lasting less than an hour and
without evidence of acute infarction as
determined by cranial imaging (Braddom)
- Within 24 hours, full resolution may show small
acute infarction in MRI
- No longer defined by time
- <1hr without evidence of acute infarction
- Infarction on imaging is considered a stroke
- Complete resolution, affects watershed zone
- CBF (Cerebral Blood Flow): <20-30 ml per 100
g/mL
Causes
Hemodynamic
- Hypoperfusion
- Insufficient of blood in one area, shift of blood
- Subclavian Steal Syndrome stenosis of the
proximal subclavian artery; one side may manifest
hypoxia; it may return to normal when rest; (-)
infarct when seen on MRI
- Retrograde from the Vertebral Artery
Embolic
- This is where usual embolus is found
- Most common cause; most common in anterior
circulation
- Faster occlusion but faster recovery
- (+) Dislodge of thrombus; not related in HTN
- Hemiplegic+ increase BP= severe stroke
Reversible Ischemic Neurologic Deficit
- TIA>24 hours, temporary impairments within 3
weeks
- Initial Symptom: Sudden fall weakness, after
few weeks faster recovery
- Some symptoms may still return, if infarct related
for more than 3 weeks; the area was perfused so it
will be on faster recovery
Stroke in Evolution
- Unstable, progressive
- Thrombus is a serious problem; it is starting to
occlude the arteries & multiple vessels
- 1 st Localized effect Increased symptoms per day
Completed Stroke
- Stable
- Neurological deficit must persist at least 24 hours
Cause:
Adults: Atherosclerosis; Thrombosis is the usual cause
Younger Patient: t/c inherited disease that cause
thrombophilia; probable inherited defects; abnormal
increase platelets coagulation disorder is inherited thats
why patient has thrombophilia
Children: Various (cerebrovascular anomalies, congenital
heart disease, carotid dissection, sickle cell disease,
inherited disorders of coagulation, and previous infection
with varicella zoster; hemorrhagic causes include
moyamoya disease & hemophilia)
Ischemic
- mortality is higher in large lesions with edema and
brain shift, areas of reduced flow
- (gCBF in normal hemisphere d/t diachisis, if
rCBF <28 increase infarction) & increased flow
(luxury perfusion d/t arteriolar vasodilation)
- Diaschisis- sudden loss (or change) of function in
a portion of the brain connected to a distant, but
damaged, brain area.
LOOKUP IMPLICATION of CBF Values
1. Normal Cerebral Autoregulation
- 50 mL/100g cerebral tissue/min
2. Cerebrovascular Compromise
- 20 mL/ 100 g cerebral tissue/min
3. Cellular Death
- <10 mL / 100 g cerebral tissue/min
4. Sodium Potassium Pump Failed
- 10-20mL/ 100g cerebral tissue/min
Classification
Thrombotic (40%) Atherosclerosis
- Atherosclerotic plaque is most common in
Common Carotid Artery & Vertebrobasilar Artery
- Dependent on the length of time the vessel is
occluded, the rate of flow through the occluded
site and the effectiveness of the collateral
circulation
- Collateral Circulation can be less effective in
elderly, diffuse atherosclerotic disease and DM
Signs & Symptoms
- Subtle & Gradual Onset
Embolic (20%)
- Most common in Middle Cerebral Artery
- Majority are thromboembolism
Sources:
Cardiogenic
- (+) Atrial Fibrillation
 - Aysmptomatic, only one blood area, generally via
gravity, there is decrease of pressure blood will
pull downward, it will not flush down properly
that is why there is formation of blood clot in the
area.
- Arrhythmias; Atrial Fibrillation & Atrial Thrombus
- Valvular heart disease
- Mechanical/prosthetic valve, esp. if
anticoagulation is insufficient
VEGETATIONS
- verrucae (small warty vegetations along the lines
of closure of valve leaflets) in RHD
- septic emboli from infectious/infective (bacterial)
endocarditis
- Mural Thrombus: in recent MI, hypokinesis,
cardiomyopathy, cardiac surgery
- Paradoxical Emboli: Through (L) & cardiac
shunt (e.g patent foramen ovale)
- Atrial Myxoma: Primary Tumors of the heart
- Cholesterol emboli: atherosclerotic debris
- Air Emboli: neck, thoracic surgery it will go
straight to the brain
- Fat Emboli:
Signs & Symptoms
- Abrupt onset
- Some fragment may break to small pieces as they
travel through the cerebral circulation
- Multiple small infarcts affecting several distal
branches of the main vessel
- Lysis & Fragmentation
- Full Resolution
- Without previous or progressive symptoms
- Reperfusion can occur in response to endogenous
fibrinolysis, but may lead to 2 cerebral
hemorrhage since the capillaries become
incompetent due to ischemic damage
Lacunar: (20%)
- Area of lacune corresponds to vascular territory
supplied by one of the deep perforating branches
(Braddom)
- At most 1.5 cm diameter (De Lisa)
- Less than 1.5 cm (Braddom)
- Lacune: Refers to the small vessels found at the
deeper part of the brain.
- Areas: basal ganglia, internal capsule, pons,
cerebellum (Braddom)
- + thalamus, brainstem (De Lisa)
Signs & Symptoms
- May result to major neurologic deficits, minor
symptoms or even asymptomatic
Others
- Cerebral Vasculitis or cerebral hypoperfusion
Hemorrhagic
- Manifestation: Headache
1. Intracerebral (10%)
- Deep perforating arteries, but does not obey
anatomic distribution of vessel as compared to
lacunar stroke, but dissects through tissue
planes/parenchyma increase ICP, disruption of
neural tracts, ventricular compression, herniation
- Acute mortality is high, rapid recovery 2-3 months
after injury
- Areas: Putamen & White matter
- Causes
a. Hypertension
- Most common cause
- microvascular changes: lipohyalinosis, Charcot-
Bouchard aneurysms (pseudoaneurysms
microscopic ruptures)
- bleeding usually lasts for 1-2 hours, late
neurologic decline can be attributed to
posthemorrhagic edema or rebleeding
- Most common: Putamen & thalamus
b. Cerebral amyloid angiopathy
- Elderly, MC >65 y/o, usually lobar than deep, MRI
evidence of hemosiderin deposition indicative Hx
of microhemorrhage
- >55 y/o, with Hx of mild dementia, lobar
hemorrhage near cortex, amyloid deposits on
adventitia
c. Others
- Trauma, vasculitis, coagulation d/o, anticoagulant
therapy, bleeding into tumor
2. Intraventricular
- Loss of consciousness
Signs & Symptoms
- severe headache -> progressive neurologic
deficits -> coma, brain shift/displacement d/t
hematoma and cerebral edema and lead to
transtentorial herniation death; hematomas may
continue to expand, large posterior fossa lesions
(e.g. acute cerebellar hemorrhages) occlusion
of 4th ventricle acute hydrocephalus
- blood coagulum can block foramen of Sylvius or
4th ventricle -> acute obstructive hydrocephalus
Sub-arachnoid (5%)
Causes
- Saccular Aneurysm: 5th to 6th decade, MC
anterior portion of Circle of Willis, >10mm
greatest risk of bleeding, intervention is advised
- Arteriovenous Malformation: 2nd-3rd decade,
MC in MCA, tangle of dilated vessels
- Mycotic Vessels: Vessel wall infection
Signs

In Aneurysm

- Localized CN lesion can develop from direct

pressure of expanding aneurysm, headache can
occur from small bleed prior to major rupture
- major rupture will result to severe headache ->
meningism
- worst headache in my life
- Focal neurologic signs does not occur initially but
may develop due to intracerebral bleeding or
infarction (d/t arterial vasospasm caused by blood
in subarachnoid space)
- coma, acute death and rebleeding is more
common in aneurysm than AVM
- acute LOC is due to sudden decrease cerebral
perfusion pressure
- Hydrocephalus: immediate after intraventricular
hemorrhage, or a later complication of
arachnoiditis (d/t blood in CSF)
- poor prognosis for proximate survival: coma,
stupor, severe hemiplegia

IN AVM

- Can grow large and displace neural structures

without disruption of function
- MC initial indication of lesion hemorrhage (most
patients survive a single hemorrhagic event)
- Seizure, migraine & hemorrhage
- Hypertensive: >170/90 mmHg

Others: vasculitis, hypoperfusion

Neuroanatomical:

ICA: manifestation ACA + MCA

Can manifest ACA if ACOM problem; if wala symps
niya is usually MCA
Tagal madevelop thrombus; extend ng collateral
circulation -> neurological symp
Some cases: Walang nangyayari sobrang tagal ->
gawa sariling circulation
-Pre existing stenosis + nabara sa kabila
BICORTICAL presentation

1st Branch: Opthalmic artery: supplies retina

(globe of eyes)
-monocular blindness
-field of vision loss; unilat
BRACHIOCEPHALIC TRUNK
-symptoms of ICA; extremity circulation affected
(cyanosis); hemiplegia of kabila LE
-very rare
HYPOTENSION: WATERSHED ZONE watershed
infarcts
-area kung saan ambon lang yung circulation
CARDIAC ARREST: bilat symmetric
Nagsisimula na watershed din, dec blood supply
CRESCENT SHAPED INFARCRTS bilat.