CEREBROVASCULAR DISEASE
STROKE
- Cerebrovascular accident
- Either ischemic stroke / hemorrhagic
stroke
- Defined as the abrupt onset of a
neurologic deficit that is attributable
to a focal vascular cause
- Clinical manifestations are highly
variable d/t the complex anatomy of
the brain and its vasculature
- Symptoms last for >24 hours / brain
infarction is demonstrated on
imaging
CEREBRAL ISCHEMIA
- Caused by a reduction in blood flow
lasting for longer than several
seconds
- Usually caused by thrombosis of the
cerebral vessels or by emboli from a
proximal arterial source / the heart
- Thrombus can be
- Atheromatous
- Collagen disease (RA, SLE)
- Vasculitis
(polyarteritis
nodosa, temporal arteritis)
- Emboli
- Atheromatous plaque in the
intracranial / extracranial
arteries / from the aortic arch
/ from the heart (arrythmias,
endocarditis)
- Fat emboli, air emboli. Tumor
emboli
TRANSIENT ISCHEMIC ATTACK (TIA)
- Cerebral ischemia followed by quick
restoration of blood flow, resulting in
full recovery of the brain tissue and
therefore resolution of symptoms
- Complete resolution of neurologic
S/S within 24 hours
- Absence of brain infarction on
imaging
-
Risk of stroke after a TIA is ~10-15%
in the first 3 months, with most
events occurring in the first 2 days
INTRACRANIAL HEMORRHAGE
- Caused by bleeding directly into /
around the brain
- HPN
- Aneurysm
- AV malformation
- Coagulation disorders
- Anticoagulant therapy
- Produces neurologic symptoms by
- Mass
effect on neural
structures
- Toxic effects of the blood
itself
- Increased ICP
DIFFERENTIAL DIAGNOSIS
1. Seizure
2. Migraine
3. Intracranial tumor
4. Metabolic encephalopathy
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CEREBROVASCULAR DISEASE
STROKE SYNDROMES
- Neurologic symptoms / findings
correspond to a damage in a
particular region
- Can be classified:
1. Large vessel occlusion
2. Branch occlusion
3. Lacunar stroke
Large Vessel Occlusion (Middle Cerebral
Artery)
- Clinical picture depends on the site
of occlusion and whether dominant
or nondominant hemisphere is
affected
- Can either present with
- Contralateral hemiplegia
- Contralateral hemianesthesia
and hemianopia
- Aphasia
(dominant
hemisphere affected)
- Neglect of contralateral limbs
(nondominant hemisphere)
- Dressing
difficulty
(nondominant hemisphere)
Large
Vessel
Occlusion
(Anterior
Cerebral Artery)
- Clinical picture depends on site of
occlusion and anatomical variation
- Distal occlusion results in
weakness
and
cortical
sensory
loss
in
the
contralateral lower limb with
associated incontinence
- Proximal occlusion results in
cerebral
paraplegia
with
lower
limb
weakness,
sensory loss, incontinence
Large Vessel Occlusion (Posterior
Cerebral Artery)
- Midbrain syndrome
- CN III palsy with contralateral
hemiplegia
(Weber’s
syndrome)
- Thalamic syndrome
- Chorea / hemiballismus with
hemisensory disturbance
Large Vessel Occlusion (Internal Carotid
Artery)
- In the most extreme cases, there
may be
- Deterioration of conscious
level
- Homonymous hemianopia of
the contralateral side
- Contralateral hemiplegia
- Contralateral
hemisensory
disturbance
- Gaze palsy to the opposite
side (eyes deviated to the
side of the lesion)
Large Vessel Occlusion (Basilar Artery
Occlusion)
- Prodromal
symptoms
include
diplopia, visual field loss, intermittent
memory disturbance, vertigo, ataxia
- Complete basilar syndrome
- Impairment of consciousness
- Bilateral motor and sensory
dysfunction
- Cerebellar signs
- Cranial nerve signs indicative
of the level of occlusion
Lacunar Stroke
- Usually result from HPN
- Pure motor hemiplegia
- Equal
weakness
of
contralateral face, arm and
leg with dysarthria
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CEREBROVASCULAR DISEASE
-
Pure sensory stroke
- Numbness and tingling of
contralateral face and limbs
Dysarthria / clumsy hand
Ataxic hemiparesis
- Mild hemiparesis with more
marked ipsilateral limb ataxia
Severe
dysarthria
with
facial
weakness
- Dysarthria, dysphagia with
mild facial weakness and no
limb weakness or clumsiness
-
-
DIAGNOSIS
1. Complete neurologic examination
2. Imaging procedures
CT Scan
- Non-contrast CT scan is the
imaging modality of choice for
acute stroke
- Identify / exclude hemorrhage as
the cause of stroke
- Identify
extraparenchymal
hemorrhage,
neoplasms,
abscesses
- May not show an abnormality if
done during the first few hours of
onset of the infarction; need to
repeat in 24-48 hours
- Contrast-enhanced
CT
scan:
visualize the venous structures
- CT angiography: visualize the
cervical and intracranial arteries,
intracranial veins, aortic arch, etc
MRI
-
Cerebral angiography
- Gold standard for identifying and
quantifying
atherosclerotic
stenoses of the cerebral arteries
and
for
identifying
and
characterizing other pathologies
(aneurysm,
vasospasm,
intraluminal thrombi, fibromuscular
dysplasia, AV fistulae, vasculitis,
and collateral channels of blood
flow
UTZ
-
Identifies and quantifies stenosis
at the origin of the internal carotid
artery
ISCHEMIC STROKE
- The magnitude of flow reduction is a
function of collateral blood flow, and
this depends on individual vascular
anatomy (which may be altered by
disease), the site of occlusion, and
systemic blood pressure
- Zero blood flow to brain tissue
causes brain infarction within 4-10
minutes
- Blood flow of < 16-18 mL/100 gm
tissue per minute causes infarct
within an hour
- Blood flow of < 20 ml/100 gm tissue
per minute causes ischemia without
infarction unless prolonged for
several hours / days
- Treatment goals is rapid reversal of
ischemia
Allows visualization of possible
injuries in the posterior fossa and
cortical surface
Able to visualize an estimate of
the ischemic penumbra
MR angiography: highly sensitive
for stenosis of extracranial internal
carotid arteries and of large vessel
arteries
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CEREBROVASCULAR DISEASE
Darkened portion = ischemic area
Brightened portion = clot
-
Risk factors
- HPN
- Atrial fibrillation
- Carotid stenosis
- Diabetes
- Hyperlipidemia
- smoking
ETIOLOGY OF ISCHEMIC STROKE
1. Occlusion of an intracranial vessel
by an embolus (ie cardiogenic
sources such as atrial fibrillation /
artery to artery emboli from carotid
atherosclerotic
plaque),
often
affecting the large intracranial
vessels
2. In situ thrombosis of an intracranial
vessel, typically affecting the small
penetrating arteries that arise from
the major intracranial arteries
3. Hypoperfusion
caused
by
flow-limiting stenosis of a major
extracranial (ie internal carotid) or
intracranial vessel, often producing
“watershed” ischemia
ISCHEMIC PENUMBRA
- The
ischemic
but
reversibly
dysfunctional tissue surrounding a
core area of infarction
- Can progress to infarction if no
reversal of blood flow occlusion
occurs
- Is reversible and thus should be
treated immediately
Less common causes of ischemic stroke
- Hypercoagulable disorders
- Venous sinus thrombosis
- Sickle cell anemia
- Fibromuscular dysplasia
- Temporal (giant cell) arteritis
- Necrotizing (granulomatous) arteritis
- Amphetamine and cocaine
DIAGNOSTIC TESTS
1. CT brain +/- CT or MR Angiography
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CEREBROVASCULAR DISEASE
2. CXR, ECG, UA, CBC, ESR, serum
electrolytes, BUN, creatinine, blood
glucose, serum lipid profile, PT, PTT
TREATMENT OF ISCHEMIC STROKE
1. Medical support
→ to ensure collateral blood flow
→lower BP if > 220 mmHg, if there
is malignant HPN / concomitant MI /
if > 185/110 and thrombolytic
therapy is anticipated
→use B blockers to decrease CO
and maintain BP
→address fever and hyperglycemia
since both worsen brain injury
→give IV mannitol and/or water
restriction if with brain edema
2. IV thrombolysis
→ recombinant tissue plasminogen
activator (rtPA)
→ dose: 0.9 mg/kg to a 90 mg
maximum; 10% as a bolus, then the
remainder over 60 mins
→ improves clinical outcome if given
within 3 hours from symptom onset
→ risk: intracranial hemorrhage
→ indication for rtPA
a. Clinical dx of stroke
b. Onset of symptoms to time of
drug administration ≤4.5h
c. CT
scan
showing
no
hemorrhage or edema of >⅓
of the MCA territory
d. Age ≥18 y/o
→ contraindication
a. Sustained
BP
>185/110
mmHg despite treatment
b. Bleeding diathesis
c. Recent
head
injury
/
intracranial hemorrhage
d. Major surgery in preceding
14d
e. GIT bleeding in preceding
21d
f. Recent myocardial infarction
3. Endovascular revascularization
→ occlusions in such large vessels
(MCA, ICA, and basilar artery)
generally involve a large clot volume
and often fail to open with IV rtPA
alone
→ alternative / adjunct to IV
thrombolysis
→ improved clinical outcome if done
within 6 hrs from onset
4. Anti-thrombotic treatment
→ aspirin - reduces stroke
recurrence risk and mortality if given
within 48 hrs from onset
-can be combined with
Clopidogrel / Ticagrelor
→ anticoagulation
-heparin
-no proven benefit except for
halting progression of dural sinus
thrombosis
5. Neuroprotection
→ prolongs the brain’s tolerance to
ischemia
6. Stroke centers and rehabilitation
→provide emergency 24h evaluation
of acute stroke px for acute medical
management and consideration of
thrombolysis
/
endovascular
treatments
→rehabilitation includes physical,
occupational, and speech therapy
-directed toward educating
the patient and family about the px’s
neurologic deficit, preventing the
complications of immobility (ie
pneumonia, DVT and pulmonary
embolism, pressure sores of the
skin, and muscle contractures), and
providing
encouragement
and
instruction in overcoming the deficit
___________________________________
Maille
CEREBROVASCULAR DISEASE
INTRACRANIAL HEMORRHAGE
→ hemorrhage directly into the brain
parenchyma (either in the subdural, epidural
space, or subarachnoid hemorrhage)
-intracerebral hemorrhage
-AV malformations of the brain
→ hemorrhage into the subdural and
epidural space
→ subarachnoid hemorrhage
→ causes
1. Hypertensive hemorrhage - most
common in the hospital
2. Head trauma
3. Metastatic brain tumor
4. Coagulopathy
5. drug
INTRACEREBRAL HEMORRHAGE (ICH)
→ causes
- HPN (hypertensive ICH)
- Coagulopathy
- Cocaine, methamphetamine
- Cerebral amyloid angiography
→ aggravated by advanced age, heavy
alcohol use, low-dose aspirin
HYPERTENSIVE ICH
→ usually results from spontaneous rupture
of a small penetrating artery deep in the
brain
→ most common sites are the basal ganglia
(esp putamen), thalamus, cerebellum, and
pons
→ presents as the abrupt onset of a focal
neurologic deficit
→ clinical symptoms may be maximal at
onset more commonly / the focal deficit
worsens over 30-90 mins and is associated
with a diminishing level of consciousness
and signs of increased ICP (headache and
vomiting)
→ initial BP should be maintained until the
results of the CT scan are reviewed and
demonstrate ICH
→ consider lowering SBP to <140 mmHg in
px with spontaneous ICH whose initial SBP
was 150-220 mmHg
→ nicardipine, labetalol, esmolol
Avoid elevated ICP
→ may manifest as decreased sensorium,
inability to maintain patent airway
→ evidenced by marked midline shift of
brain structures
→ may lead to brain herniation
→ management
1. Tracheal intubation and sedation
2. Administration of osmotic diuretics
(mannitol / hypertonic saline)
3. Surgical evacuation for cerebellar
hematomas >3cm or if there is
midline shift or brain structures
SUBARACHNOID HEMORRHAGE (SAH)
→ causes
1. Head trauma
2. Rupture of saccular aneurysm
3. Bleeding
from
a
vascular
malformation
4. Extension into the subarachnoid
space from a primary intracerebral
hemorrhage
To prevent hematoma expansion
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CEREBROVASCULAR DISEASE
ANEURYSMAL SAH
→ 3 most common locations
1. Terminal ICA
2. MCA bifurcation
3. Top of basilar artery
→ aneurysm size and site are important in
predicting risk of rupture
- >7mm dm
- Top of basilar artery
- Origin
of
the
posterior
communicating artery
→ overall mortality: 35%
→ presentation:
- Loss of consciousness
- Headache (“worst headache of my
life”)
- Sudden onset
- Generalized
- Neck stiffness
- vomiting
4 causes of delayed neurologic deficits
1. Rerupture
a. >20% risk of rebleeding in
the first 2 weeks
b. 30% in the first month
c. 3% in the succeeding years
2. Hydrocephalus
a. Decrease in sensorium
b. Treated by placement of
external ventricular drain
3. Delayed cerebral ischemia (DCI)
a. d/t vasospasm at the base of
the arteries of the brain
b. May be observed between
days 4-14
c. Major cause of delayed
morbidity and death
4. Hyponatremia
a. Cerebral
salt-wasting
syndrome
b. d/t natriuresis and volume
depletion
c. Usually seen during the first
2 weeks
DIAGNOSIS OF SAH
1. CT scan
2. Lumbar puncture
3. 4
vessel
conventional
xray
angiography (both carotids and both
vertebrals)
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CEREBROVASCULAR DISEASE
-
To localize and define the
anatomic details of the
aneurysm and to determine if
other unruptured aneurysms
exist
MANAGEMENT OF SAH
→ definitive: repair of aneurysm
→ supportive:
1. Protect airway
2. Mild sedation and analgesia for
headache
3. Adequate hydration to prevent
ischemia
4. Nimodipine to prevent DCI
5. BP management
a. Lower SBP <160 mmHg with
Nicardipine,
Labetalol,
Esmolol
6. DVT prophylaxis by pneumatic
compression
stockings
and/or
unfractionated heparin (provided that
the aneurysm has been treated)
Maille