Pemicu 2

StevenOctavianus
405080098

Cerebrovascular Diseases
CVD any abnormality of the brain resulting
from a pathologic process of the blood vessels,
including occlusion of the lumen by
embolus/thrombus, rupture of a vessel, an
altered permeability of the vessel wall,
increased viscosity or other change in the
quality of the blood flow
Cerebrovascular diseases include some of the
most common and devastating disorders:
ischemic stroke
hemorrhagic stroke
cerebrovascular anomalies such as intracranial
aneurysms and arteriovenous malformations (AVMs).

Causes of cerebral abnormalities

Atherosclerothic
thrombosis
Transient ischemic
attacks
Embolism
Hypertensive
hemorrhage
Arteritis
Ruptured
Arteriovenousus
malformation

Hematologic
disorders
Trauma and
dissection of
carotid and basilar
arteries
Complications of
arteriography
Amyloid
angiopathy
Cerebral
thrombophlebitis

CVD Characteristic of each age period

Prenatal

Porencephaly
Hydranencephaly
Hipoxic-ischemic damage
Unilateral cerebral infarction

Perinatal and postnatal

Cardiorespiratory failure
Periventricular infarcts
Hemorrhagic disease of the
newborn

Infancy and childhood

Ischemic infarction
Congenital heart disease
Sickle cell anemia
Bacterial endocarditis
Rheumatic fever
SLE

Middle age
Atherosclerotic
thrombosis and embolism
Cardiogenic embolism
Hypertensive cerebral
hemorrhage
Ruptured saccular
aneurysm
Arterial dissection

Late adult life

Atherosclerotic thrombotic
acclusive disease
Embolic disease
Lacunar stroke
Brain hemorrhage

Risk factor for stroke

Hypertension
Atrial fibrilation
DM
Smoking
Hyperlipidemia
Hypercoagulable state

Stroke Symptoms
Sudden numbness or weakness of face, arm
or leg, especially on one side of the body
Sudden confusion, trouble understanding or
speaking
Sudden trouble seeing in one or both eyes
Sudden trouble walking, dizziness, loss of
balance or coordination
Sudden severe headache with no known
cause

Other Symptoms
Sudden nausea, fever and vomiting,
distinguished from a viral illness by rapid
onset (minutes or hours vs. days)
Brief loss of consciousness or period of
decreased consciousness
(fainting, confusion, convulsions or coma)

Anterior Cerebral Artery

The ACA is divided into two
segments: the precommunal (A1)
circle of Willis, or stem, which
connects the internal carotid artery
to the anterior communicating
artery, and the postcommunal (A2)
segment distal to the anterior
communicating artery

Middle cerebral artery

Signs and symptoms: Structures involved

Paralysis of the contralateral face, arm, and leg; sensory
impairment over the same
Motor aphasia:
Central aphasia, word deafness, anomia, jargon speech,
sensory agraphia, acalculia, alexia, finger agnosia, right-left
confusion (the last four comprise the Gerstmann syndrome):
Central, suprasylvian speech area and parietooccipital cortex of
the dominant hemisphere
Conduction aphasia: Central speech area (parietal operculum)
Apractognosia of the nondominant hemisphere, anosognosia,
hemiasomatognosia, unilateral neglect, agnosia for the left half
of external space, dressing "apraxia," constructional "apraxia,"
distortion of visual coordinates, inaccurate localization in the
half field, impaired ability to judge distance, upside-down
reading.
Homonymous hemianopia (often homonymous inferior
quadrantanopia):
Paralysis of conjugate gaze to the opposite side

Anterior cerebral artery

 Signs and symptoms:Structures involved

Paralysis of opposite foot and leg: Motor leg area
A lesser degree of paresis of opposite arm: Arm area of cortex or
fibers descending to corona radiata
Cortical sensory loss over toes, foot, and leg: Sensory area for foot
and leg
Urinary incontinence: Sensorimotor area in paracentral lobule
Contralateral grasp reflex, sucking reflex, gegenhalten (paratonic
rigidity): Medial surface of the posterior frontal lobe; likely
supplemental motor area
Abulia (akinetic mutism), slowness, delay, intermittent interruption,
lack of spontaneity, whispering, reflex distraction to sights and
sounds: Uncertain localizationprobably cingulate gyrus and
medial inferior portion of frontal, parietal, and temporal lobes
Impairment of gait and stance (gait apraxia): Frontal cortex near
leg motor area
Dyspraxia of left limbs, tactile aphasia in left limbs: Corpus
callosum

Posterior Cerebral Artery

In 75% of cases, both PCAs arise from the bifurcation
of the basilar artery; in 20%, one has its origin from
the ipsilateral internal carotid artery via the posterior
communicating artery; in 5%, both originate from the
respective ipsilateral internal carotid arteries
P1 Syndromes
Infarction usually occurs in the ipsilateral subthalamus and
medial thalamus and in the ipsilateral cerebral peduncle
and midbrain

P2 Syndromes
Occlusion of the distal PCA causes infarction of the medial
temporal and occipital lobes.

 Medial medullary syndrome

(occlusion of vertebral artery or of
branch of vertebral or lower basilar
artery)
On side of lesion
Paralysis with atrophy of half the
tongue: Ipsilateral twelfth nerve
On side opposite lesion
Paralysis of arm and leg, sparing face;
impaired tactile and proprioceptive
sense over half the body: Contralateral
pyramidal tract and medial lemniscus

 2. Lateral medullary syndrome (occlusion of any of five vessels

may be responsiblevertebral, posterior inferior cerebellar,
superior, middle, or inferior lateral medullary arteries)
On side of lesion
Pain, numbness, impaired sensation over half the face: Descending
tract and nucleus fifth nerve
Ataxia of limbs, falling to side of lesion: Uncertainrestiform body,
cerebellar hemisphere, cerebellar fibers, spinocerebellar tract (?)
Nystagmus, diplopia, oscillopsia, vertigo, nausea, vomiting: Vestibular
nucleus
Horner's syndrome (miosis, ptosis, decreased sweating): Descending
sympathetic tract
Dysphagia, hoarseness, paralysis of palate, paralysis of vocal cord,
diminished gag reflex: Issuing fibers ninth and tenth nerves
Loss of taste: Nucleus and tractus solitarius
Numbness of ipsilateral arm, trunk, or leg: Cuneate and gracile nuclei
Weakness of lower face: Genuflected upper motor neuron fibers to
ipsilateral facial nucleus

On side opposite lesion

Impaired pain and thermal sense over half the body, sometimes face:
Spinothalamic tract

 3. Total unilateral medullary syndrome (occlusion of

vertebral artery): Combination of medial and lateral
syndromes
4. Lateral pontomedullary syndrome (occlusion of
vertebral artery): Combination of lateral medullary and
lateral inferior pontine syndrome
5. Basilar artery syndrome (the syndrome of the lone
vertebral artery is equivalent): A combination of the
various brainstem syndromes plus those arising in the
posterior cerebral artery distribution.
Bilateral long tract signs (sensory and motor; cerebellar
and peripheral cranial nerve abnormalities): Bilateral
long tract; cerebellar and peripheral cranial nerves
Paralysis or weakness of all extremities, plus all bulbar
musculature: Corticobulbar and corticospinal tracts
bilaterally

 Signs and symptoms:Structures involved

1. Medial inferior pontine syndrome (occlusion of
paramedian branch of basilar artery)
On side of lesion
Paralysis of conjugate gaze to side of lesion (preservation
of convergence): Center for conjugate lateral gaze
Nystagmus: Vestibular nucleus
Ataxia of limbs and gait: Likely middle cerebellar peduncle
Diplopia on lateral gaze: Abducens nerve

On side opposite lesion

Paralysis of face, arm, and leg: Corticobulbar and
corticospinal tract in lower pons
Impaired tactile and proprioceptive sense over half of the
body: Medial lemniscus

 2. Lateral inferior pontine syndrome (occlusion of

anterior inferior cerebellar artery)
On side of lesion
Horizontal and vertical nystagmus, vertigo, nausea,
vomiting, oscillopia: Vestibular nerve or nucleus
Facial paralysis: Seventh nerve
Paralysis of conjugate gaze to side of lesion: Center for
conjugate lateral gaze
Deafness, tinnitus: Auditory nerve or cochlear nucleus
Ataxia: Middle cerebellar peduncle and cerebellar
hemisphere
Impaired sensation over face: Descending tract and
nucleus fifth nerve

On side opposite lesion

Impaired pain and thermal sense over half the body
(may include face): Spinothalamic tract

Clinical Presentations of Stroke

Focal ischemia (85%)
Embolism
Thrombosis

Hemorrhage (15%)
Epidural
Subdural
Intraparenchymal

Cerebral Ischemia
Embolism
Abrupt onset
Small vascular area
Focal deficit
Pure aphasia
Pure hemianopia

Acute CT normal
High recurrence
risk

Thrombosis
Preceded by TIAs
Abrupt onset
Large vascular area
More complex
symptoms

Acute CT normal

Cerebral Hemorrhage
Epidural
hemorrhage
Smooth onset
Arterial origin
Mass effect
causes coma
over hours
Similar (but
slower in
evolution) to

Subdural hemorrhage
Smooth onset
Venous origin
May be recurrent
Fluctuating, falsely
localizing signs

Embolic infarction
The most common cause of stroke
Embolic materials consist of a fragment that has
broken away from a thrombus within the heart
cardioembolic
Atrial fibrilation predispose to this type of stroke
The infarction is pale, hemorrhagic, or mixed
Large embolic clots can block large vessel
Embolic material more often it breaks into
fragment that enter smaller vessels reveal
their final location

Causes of cerebral
embolism
Cardiac origin
Atrial fibrilation
Myocardial
infarction
Acute and subacute
bacterial
endocarditis
Heart disease
Complication of
cardiac surgery
Valve prostheses

Non cardiac origin

Atherosclerotis of
aorta and carotid
arteries
Thrombus in
pulmonary veins
Fat,tumor, air
Complication of
neck and thoracic
surgery

Clinical syndrome of
embolic stroke
Develop most rapidly like a bolt out of
the blue
Depend on the artery involved and the
site of obstruction in the vessel
Large embolus distal internal carotid artery
Full blown syndromes

Branches of the midle cerebral artery

Motor or sensory aphasia
Monoplegia
Brachiofacial weakness with dysarthria

 Posterior cerebral artery

Homonymous Hemianopias

Basilar artery
Upper basilar bifurcation coma

Medial temporal lobe of thalamus and

subthalamus
Complex disorders of memory, sensation,
movement

Lateral medullary
Ataxia

Treatment and prevention

Three phases of therapy
1. Measures directed to restoring
ciirculation
1. Thrombolysis
2. embolectomy

2. Prevent recurrent embolus

1. Long terms of anticoagulants
2. Antiarrhytmic drugs

3. Physical therapy and rehabilitation

Presentation of Lacunar Stroke

Risk factors
Diabetes
Hypertension
Polycythemia

Variable course progressing over days

Fluctuating; progressing in steps; or
remitting
Preceded by TIAs in 25%
Without headache or vomiting

Lacunar Stroke Syndromes

Well-defined syndromes
Pure motor hemiparesis (with
dysarthria)
Pure sensory stroke (loss or
paresthesias)
Dysarthria-clumsy hand (with
contralateral face and tongue
weakness)
Ataxia-hemiparesis (contralateral face
and leg weakness)

Lacunar Stroke Outcome

Management
Long-term blood pressure control
Empiric anti-platelet therapy
Omega-3 oil 1 gm TID to improve
viscosity

Prognosis
Good recovery of function
Other lacunes develop

Prevention Pearls

Reducing Primary Risk - 1

Obstructive sleep apnea

Homocysteine folate, B6, B12
Hypertension morning BP surge
Smoking 50% risk reduction in 1 yr
Hyperlipidemia statins
Migraine triptans
Drugs cocaine, ephedra, PPA

Reducing Primary Risk - 2

Asymptomatic carotid stenosis
Endarterectomy for > 60% stenosis
Risk reduction for 3% to 1% per year
Benefit related to surgical risk

Nonvalvular atrial fibrillation

Aspirin for patients < 65 years,
healthy
Warfarin for patients > 65 years or
having other stroke risk factors

Reducing Secondary Risk

Reducing risk of recurrence
TIA with ipsilateral carotid stenosis
endarterectomy for > 70%
stenosis
Cardiogenic embolism warfarin
Lacunar infarcts aspirin,
dipyridamole
Cryptogenic infarcts (40% embolic)

Reducing Risk in Children

Sickle cell disease
Screen with transcranial doppler q 6
mo
Transfusion therapy for 2 abnormal
studies

Congenital heart disease

Arterial dissections (trauma)
Prothrombotic disorders
Mitochondria disorders (MELAS)

Decreasing Salt Intake

Reducing salt intake by 3 g per day
lowers blood pressure; the effect is
doubled with a 6 gm/day reduction
and tripled with a 9 gm/d reduction.
Reduction in stroke risk parallels
reduction in salt intake.

Using Statins
Pooled results after 5 years
Pravastatin or Simvastatin 40 mg/day
Changes in cholesterol levels
Total cholesterol decreased 20%
LDL cholesterol decreased 28%
HDL cholesterol increased 5%
Triglycerides decreased 13%

Using Statins
Reducing LDL cholesterol by 1
mmol/L
22% stroke reduction in patients with
known vascular disease
6% stroke reduction in patients without
known vascular disease
28% reduction in thromboembolic stroke