CEREBROVASCULAR DISORDERS:

Blood supply to the Brain

-many arteries and their branches carry blood to the brain
-each artery supplies specific areas of the brain, but some brain areas are supplied by more than one artery
ie: anterior cerebral artery

HEART--------- Brain ---- motor, speech and vision

What is a stroke:
-acute cerebral circulatory disturbance
-cerebrovascular accident (CVA)
-cerebral infarction
-cerebral insufficiency
-cerebral apoplexy

CVA ----- CVD --- Brain attack

“stroke should be treated as an EMERGENCY BASIS as a BRAIN ATTACK analaogouys to the treatment of
CORONARY HEART DISEASES”

Incidence: -most common neurologic disorder

-3rd in the US
-1000- 2000/ million in Europe
-1.2 million death in years 2000- Asia
-common after age of 50
-63 yo mean age -58% in males
-95% with CT scan -74% infarct
-23% ICH -3% SAH

Prevalence of Stroke: -worldwide: 600/ 100,000

-community survey: Morong Riza 480/ 100,000
-hospital base JRRMMC 100- 150/ month
USTH: 100

Stroke: Clinical Definition

1. SUDDEN
-non abulsive: initial approach is not seizure

2. FOCAL NEUROLOGIC ACTIVITY

-w/wo change in consciousness/ reason

3. DUE TO A PATHOLOGIC PROCESS OF THE BLOOD VESSEL

-neurological impairment caused by disruption in bld supply to a region in the brain (20% of CO to brain)
-sudden brain disorder caused by the temporary or protracted circulatory displacement in certain areas of
the brain
-caused by a clot that blocks blood vessel in the brain
ISCHEMIC: bleeding within
HEMATIC: or hemorrhage

Consequences: -leads to reduced supply of OXYGEN and GLUCOSE - destruction of neurons

- affected areas cease o function  sometimes permanently

Different Terms: -hemiplegia, hemiparesis

-hemianesthesia, hemihype
-lethargic or drowsy
-stuporous coma
-light coma
-deep coma

Patophysiology: any lesion of the brain area resulting from a pathologic process of the blood vessel wall

Occlusion: by a thrombus, emboli

Rupture: blood vessel wall
 -any tension or altered permeability of the blood vessel wall
-increased viscosity or other changes in frequency of the blood vessel wall

Etiologic Classification:
ISCHEMIC HEMORRHAGIC-intercerebral bleed
Types: Lacunar 29% Types: Hypertensive Intercerebral
Thrombotic Infarct –60% SAH
Embolic- 15% Ruptured Sacular Aneurysm
Others- 5% AV Malformation—Primary Parenchymal

Incidence: 80% Incidence: 2%

- AV aneurysms, usu in bifurcation
LACUNAR: transient Ischemic Attack, small infarct - LENTICUSTRIATE can also rupture ; like in lacunar; more BV in BASAL
EMBOLUS: dislodged Ganglia
Hypohyalinoma can laso be due to DM - Chronic HPN can lead to this
Right innominate artery: more than L - MC location of bleed is PUTAMEN (Basal Ganglia)
MC caused by atrial fibrillation - Aneurysm- can rupture right away
-rupture vasospasm 2-10th day  chemical neuritis and parenchymal
Carotid Artery Syndrome: MCA, ACA, PCA insufficiency
Posterior Artery: acts as collaterals
hypodense hyperdense

PATOPHYSIOLOGY OF CEREBROVASCULAR STROKE:

CONCEPTS:
1. Ischemic (Geographic ) Pinumbra –most of the Tx is directed
Whire- if treated
4x bigger than core
2. Therapeutic Window

MCA: MC area of Ischemic stroke

MCA Syndrome: Parietal Lobe Syndrome
Frontal Lobe Syndrome

-Clinical signs would be made by area destroyed by the infarct and area of penumbra
-if Tx is delayed; half

“the concept of Ischemic penumbra “
-at the periphery of one of the infarct
-blood flow is reduced (moderately decreased)
-inherent restorative mechof brain are most active & where cell death occurs late
-15 – 20% in 48-72 hrs (therapeutic window)
-3-4 x larger than infarct
-where neuroprotectors are most effective
-any form of management that protect brain from dying
-the core infarct = dead neurons and ganglia
-infarction: can determine why patient have residua

“concept of therapeutic window” - “window of therapeutic opportunity”

-“duration of TIME during which the ISCHEMIC PENUMBRA” can survive before either
getting infracted returning to normal haemodynamic and metabolic status”
-time for the neuroprotectors to be effective

ISCHEMIC CASCADE: -only in ischemic stroke

Reduction of blood flow

Depletion of cellular stores

NA/ K pump failure Acidosis

Free Radical Formation
Membrane Depolarization (Open channel)
Death (apoptosis)

Opening of Voltage-operated Ca channels Release of Glutamate (toxic)

Elevation of Intracellular Ca Activation of NMDA/ AMPA and metabolic receptors

Activation of: lipase
NO synthetase---------- NO --------------------- FREE RADICAL FORMATION
Proteases
Endonucleases DEath

Activates INFLAMMATION---------------------------- Reperfusion

Risk Factors of CVD (Stroke)

Asian Acute Stroke Advisory Panel (AASAP) 66% w/ HPN
39% are smokers
27% previos TIA/ stroke
22% w/ DM
17% hx of ischemic heart disease
10% has AF

Major: HPN, Heart Disease, DM (123 punch) Cig smoking, Hyperlipidemia

Minor: Obesity, polycythemia, Alcohol, Contraceptive Pills. Family history
Migraine, hct elevation, change weather, hypoxia

WHO
Modifiable risk factors: high BP, TIA, heart disease, DM, cig smoking, hypercoagulability high rBc

DEFINITIONS:
TRANSIENT ISCHEMIC ATTACK: neurological deficits that usually last 30 sec to 30 mins or a maximum of 3 hrs,
reverting completely to normal thereafter

a reversible episode of focal dysfunction of the brain or eye that is secondary to t

transient occlusion of an artery whose signs and symptoms are similar to
stroke but usually lasts a few minutes to hours before resolving

if an artery inside the brain or leading to the brain becomes blocked temporarily, t
he flow of blood to an area of brain shows

the lack of blood can cause temporary syndromes such as weakness, speech
impairment, dizziness and loss of vision (MONOCOLAR LOSS OF
VISION= Fugax)

The symptoms of TIA usually lasts a few minutes

CLASSIC MECHANISMS OF TIA Cerebral seizures

Syncopal Attacks
Migraine
Hypoglycemia
Labyrinthine Vertigo

Hospitalization for TIA probable heart source of emboli

deficit associated with the ischemic event if severe
crescendo TIA

Apprpriate TIA tx for RR Carotid Endarterectomy

Antiplatelts
Anticoagulants – for AF PX

Common Clinical Manifestations of CVD: (STRoke) weakness, paresis, plegia, paralysis, numbness, hypoesthesia,
anesthesia, headache w/ w/o vomiting, altered level of
consciousness, seizures, convulsions,at onset: no stroke

SYMTOMS OF ACUTE STROKE: paralysis on one side of body paralysis of ½ of face

Speech d/o: aphasia visual field defect
Blindness on one side gaze palsy and blurred vision
Neglect: ANOSOGNOSIA

TYPICAL S: paralysis on one side double vision

 Speech disorder impaired coordination/ ataxia
Numbness Diziness

Headache Decreased LOC Focal deficit

Infarction ++ + +++
ICH Intercereb he +++ +++ +++
Subarachnoid he +++ ++ +

-absence of headache, change in sensorium but r/o bleed

COMMON CLINICAL MANIFESTATIONS OF TIA and STROKE:

CAROTID ARTERY (ANT) CIRC unilateral paralysis language disturbance
Numbness visual disturbance
Monocular blindness

EVALUATION FORMS: Glasscow coma scale- changes in sensorium

Hunt and Hess Scale- for aneurysm
Cincinnati Prehospital Stroke Scale – for EMS
Diaz Stroke Scale
Hatchinski Ischemic Scale
National Institute of Health Stroke Scale (HIHSS) –most extensive

CINCINNATI PRE-HOSPITAL STROKE SCORE

FACIAL DROP- hav px show teeth or smile
ARM DRIFT- close eyes and hold both arms out, max lose
SPEECH- have ptient say a phase

EMERGENCY NEUROLOGICAL STROKE ASSESSMENT: Level of consciousness

Type of stroke
Location of stroke
Severity of Stroke

DDx of STROKE: hGic stroke Ischemic Stroke

Cervical Trauma/ Craniocerebral – Seizures, Migraine, Metabolism Meningitis
Encephalitis
Intracranial Mass (+) hematoma

MANAGEMENT: ISHEMIC ATTACK: CBC, Blood Chem, Sensorium Elec, EKG, CXr, Angigraphy, Doppler UTZ and
Doppler Scanning, Echocardiogram, CT Scan or MRI (w/r ischemic, hgIC,
SPECT or PET

EMERGENCY Dxic STUDIES: CT SCAn- seizure CXR, Cervical Xray

CSF analysis- subarach hge Blood Studies : assess RF hyperlipidemia..
EKG, ECG- see AF Doppler
Angiogram- see aneurysm

CT SCAN Stroke in first 12 hrs seem Normal

Embolic infarct: “red infarct” due to Microghes

Or a result of sudden Reperfusion: hgic conversion
Antiplatelet, anticoagulants, anti thrombolytics
Occlusion of L MCA stick needle angiograph
4 vessel
Digital Subtractionagraphy

Ischemic stroke: lacunar/ mild/ small

Regional/ moderate/ medium
Malignan/ severe/ large

MRI- opposite ng CT
Diffusion- Weighed MRI: Px after 4 hours of onset of symptoms

SPECT:
 DOPPLER: Carotid Doppler
Transcranial Doppler
Transesophageal Doppler
Cardiac Ultrasound

BLOOD STUDIES: CBC, plt ct Electrolytes. Glu (see acidosis) can obstruct bld flow
INR, perfusion time, PTT Drug or alcohol levels
O2 saturation, ABG’s

CORRECT DIAGNOSIS: complete history

Complete neuro exam]
Clinical Dx (tentative or final)
Any further studies req’d

BASIS FOR CHOOSING THE BEST: Safest Least Invasive Most Invasive

Reminders: Do not order every conceivable or available test to cover every Dx personality
If fail to establish the Dx, only then u select other test “logically”

THE HILSINBORG DECLARATION OF US

-all current and future treament of stroke with drugs should be bsed on SCIENTIFIC EVIDENCE
-tx of unproven value should not be used ROUTINELY in patient with stroke

THE ABSENCE OF EVIDENCE IS NO ABSENCE OF ITS ABSENCE

Once Stroke is diagnosed, prehospital treatment includes:

1. ABC’s of Critical Care
2. Close monitoring of Vital Signs
3. other Supportive measures
IV line
Control of Seizures
Correction of hyperglycemia/ hypoglycemia
Correction of hypererthermia- increase size stoke area

Management: Therapeutic: Definitive

1. anti HPN nad for other risk factors
2. anti edema or decompenssants
3. anti vasoconstrictors or vasodilators
4. anti platelts and anticoagulants
5. antifibrinolytic

Specific Stroke Therapy:

1. General care
2. Mgmt of increased BP
3. Mgmt of Seizures
4. Mgmt of increased ICP

Management of Elevated BP: SBP > 220 mm Hg

DBP > 120 mm Hg
*MAP > 130 mm Hg
-preferred drugs: B-blockers or ACE inhibitor
-drop by 15-20% (20% of last BP recording)

-systolic BP : 110- 220 mm Hg

-diastolic BP: 90- 120 mm Hg
-MAP= 130 mm or systolic + 2 (DP)/ 3

in Chronic HPN- higher autoregulatory limit due to elevated BP

-tolerance to acute decrease in BP is impaied
-tolerance to acute increase in arterial pressure is impaired

BP lowering in Ischemic Strokes: BP outside the upper limit of autoregulation

Malignant hypertension with end-organ damage
 Aortic dissection
Severe symptomatic heart disease requiring after-load reduction

Management of Seizures: airway, O2 inhalation, control fever

IV AED drugs: BENZODIAZEPINES: Diazeoam, Lorazepam
PHENYTOIN
PHENOBARBITAL

Status epilepticus: Phenytoin and Phjenobarbital

Phenobarbital – produces hyperactivity in children, drowsiness
- 3-6 mg/ kg mtnce dose
Dilantin- 5-8 mg/ kg : 3x maintainance

Management of Increase ICP control fever; hyperglycemia; hyponatremia, seizures

Avoid hypotonic fluids
Keep head elevated to 30 degrees
Reduce PaCO2
Use drugs like thiopental, lidocaine, mannitol, furosemide, acetazolamine
Neurosurgical treatment
-evacuate blood clot, only done in Malignant Infarct
CO2 most potent VD known to man
Mannitol- should not be used for long time because of rebound
Furosemide- may diurese the patient and loss of Na and K; loop diuretic; excret Na-K
Hemicranionectomy- not for ischemic stroke

Major Treatment Strategies for Stroke: control risk factors

“The identificationof stroke precursor is the first stepin instituting a program for
stroke prevention”

WHY DO WE WANT TO PREVENT STROKE: high prevalence

Burden of illness
Economic cost

RISK FACTORS and PREVENTION: anyone can suffer a stroke

There exist stroke risk factor
The Rf can be controlled
Strokes can be avoided

TYPES OF STROKE PREVENTION PRIMORDIAL PREVENTION –controversial, hypochondriacs

PRIMARY PREVENTION – w/ RF and not stroke
SECONDARY PREVENTION – w/ attack; 35-40% chance of another stroke

PRIMORDIAL PREVENTION – before RF has been established

-use of anti-plt
-use of anti-oxidants
-avoidance of known causes of modifiable RF

PRIMARY PREVENTION- to avoid INITIAL stroke

- at risk ASYMPTOMATIC Patients
-control the existing RF
- use of anti- aggressants

SECONDARY PREVENTION- to avoid RECURRENCE of Stroke

-SYMPTOMATIC px
-control RF
-use anti plt
-use neuroprotectors

Modifiable RF: hypercholesterolemia

HPN: 5x risk of inc stroke
DM: 3x rsik
Smoking polychtemia