Cerebrovascular Diseases (II)

WU Qisi, MD, PhD

Department of Neurology
The First Affiliated Hospital Chongqing Medical University
 Outline
•Introduction
•Transient Ischemic Attacks (TIA)
•Ischemic stroke
•Intracerebral Hemorrhage
•Subarachnoid Hemorrhage
Intracerebral Hemorrhage (ICH)
 Intracerebral hemorrhage (ICH)

Spontaneous Intracerebral Hemorrhage (SICH)

ICH: Bleeding into the parenchyma, may extend into
the ventricles and subarachnoid space.
A devastating condition that accounts for 10–30% of
all strokes
The least treatable form of stroke associated with high
morbidity and mortality
 Etiology
Primary ICH
✓Hypertension
✓Cerebral amyloid angiopathy
Secondary ICH
✓Arteriovenous malformation
✓Aneurysm
✓Tumor
✓Hemorrhagic infarction
✓Anticoagulants
✓Cavernous angioma
 Pathology of Hypertensive ICH
Basal ganglia (50%)
Lobar regions (20-50%)
Thalamus (10-15%)
Pons (5-12%)
Cerebellum (1-5%)
Pathophysiology

Hemorrhage is dynamic; process continues for

several hours
Hemorrhage expansion: Hematoma growth
occurs within the first few hours (in the first 6
hours) and is rare after 24 hours
Edema: Peaks around 5 to 6 days and lasts up to
14 days
Ventricular hemorrhage and hydrocephalus:
disturbance of CSF circulation
Hematoma growth seen during 24 h from the initial presentation at 3·5 h
ICH Presentation
Hypertension (90%)
Altered mental status (50%)
Headache (40%)
Seizures (6-7%)
Focal neurological deficits depending on the
location of ICH
 Hypertensive ICH
Basal ganglia (50%)
◦ Contralateral hemiparesis, sensory loss, conjugate gaze

Lobar regions (20-50%)

◦ Contralateral hemiparesis or sensory loss, aphasia, neglect, or confusion

Thalamus (10-15%)
◦ Contralateral hemiparesis, sensory loss

Pons (5-12%)
◦ Quadriparesis, facial weakness, decreased level consciousness

Cerebellum (1-5%)
◦ Ataxia, dizziness
ICH Diagnosis
acute onset and focal
neurologic deficits;
CT shows hyperintense
signal

CT scan is excellent for

imaging blood
CT examples
Differencial Diagnosis
Subarachnoid hemorrhage
Infarction
hypertensive encephalopathy
Meningitis
Brain abscess

CT scan is excellent for

imaging blood
 Management principles
Airway support (Decreased level of consciousness)
Blood pressure control
Intracranial pressure control
Anticoagulation reversal
Surgery
Prevention of complications (urinary tract infection, upper
respiratory infection, bedsores etc)
Good nursing and care
Management of BP
In patients presenting with a systolic BP of 150 to
220 mmHg, acute lowering of systolic BP to 140
mm Hg is probably safe
Intracranial pressure control
20% Mannitol
Furosemide
Glycerol Fructose
hypertonic saline
Human Albumin Solution
Seizures
Clinical seizures should be treated with antiepileptic drugs
Continuous EEG monitoring is probably indicated in ICH
patients with depressed mental status out of proportion to the
degree of brain injury
 Prophylactic anticonvulsant medication should not be
used.
Anticoagulation associated ICH
ICH associated with Warfarin (Vit K antagonist)
Vitamin K
Anticoagulation associated ICH
ICH associated with IV heparin
Protamine sulfate
 Blood sugar control
Hyperglycemia
◦ Associated with poor outcome and  mortality
◦ Marker of outcome or contributor?
Surgical Hematoma Evacuation
For most patients with ICH, the usefulness of surgery is
uncertain.
Patients with cerebellar hemorrhage who are deteriorating
neurologically or who have brainstem compression and/or
hydrocephalus from ventricular obstruction should undergo
surgical removal of the hemorrhage ASAP
Surgery
For patients presenting with lobar clots >30 mL and within
1 cm of the surface, evacuation of supratentorial ICH by
standard craniotomy might be considered
Although theoretically attractive, no clear evidence at
present indicates that ultra-early removal of supratentorial
ICH improves functional outcome or mortality rate.
The City of Chongqing

Thank you for your attention!

 Outline
•Introduction
•Transient Ischemic Attacks (TIA)
•Ischemic stroke
•Intracerebral Hemorrhage
•Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
(SAH)
Subarachnoid Hemorrhage
(SAH): Concept
Subarachnoid Hemorrhage
(SAH): Concept
Subarachnoid Hemorrhage
(SAH): Concept
 SAH: Concept
 Subarachnoid space—the area between the arachnoid membrane
and the pia mater surrounding the brain.
 Subarachnoid hemorrhage is an acute neurologic emergency that
follows rupture of a blood vessel in the subarachnoid space.
Epidemiology of SAH
Accounts for 2 to 7 percent of all new strokes
Worldwide incidence is about 10.5 cases per 100,000
person-years
The incidence increases with age and the risk for women is
1.6 times that of men
Case fatality rates for SAH
Population-based study in England with essentially
complete case ascertainment
◦ 24 hour mortality: 21%
◦ 7 days: 37%
◦ 30 days: 44%
◦ Relative risk for patients over 60 years vs. younger = 2.95

Pobereskin JNNP 2001;70:340-3

 Etiology
Subarachnoid hemorrhage can be spontaneous or traumatic
Traumatic subarachnoid hemorrhage is a type of bleeding that occurs
around the brain following some head injuries
 Spontaneous SAH
The most common cause of nontraumatic SAH is rupture of an
intracranial aneurysm.
Cerebral arteriovenous malformations (AVMs) cause approximately
10% of nontraumatic cases of SAH
Aneurysms: the leading cause of SAH
 A balloon-like bulge or
weakening of an artery wall that
ruptures
 1%–5% in the adult population
 The most common etiology of
nontraumatic SAH
 Accounts for about 80% of
cases
 Any aneurysm can rupture and
larger aneurysms are more
likely to do so

.
 Internal carotid artery

Posterior
communicating artery

aneurysm
Common sites of aneurysms
 Clinical features
History and Symptoms
Symptom onset: exercise, emotional stress, etc.
Sudden onset of severe headache described by patients as “the worst
headache of my life.” (15~60% warning headache ~2wks before aneurysms
rupture)
Associated symptoms : nausea, vomiting, seizure, photophobia, and focal or
generalized acute neurologic symptoms
Some patient may lose consciousness after the event
 Clinical features
Physical Exam
Meningeal irritation sign:
✓Nuchal rigidity occurs in 70% of
cases
✓Positive Kerning’s sign and
Bruzinskis sign
 Clinical features
Focal neurological deficits: 3rd nerve palsy

Third nerve palsy due to posterior

communicating artery aneurysm
 Clinical features
Fundoscopy

 Reveal retinal hemorrhage or papilledema suggestive of SAH and

increased intracranial pressure
Flame and dot hemorrhages Subhyaloid hemorrhage
 COMPLICATIONS
Rebleeding
Vasospasm
Hydrocephalus
 Rebleeding
•Associated with ~ 50% fatality rate
•~ 4% of re-bleeding occurs within the first 24 hours
• ~20-30% within the first month and ~ 3% per year thereafter
•Risk factors for re-bleeding:
– Higher initial blood pressure>170 mmHg
– Worse neurological status on admission (coma)

•Headache and symptoms occur one more time

or become worse, CT shows more bleeding
 Vasospasm
20~30% of patients, is associated with delayed ischemia and death
Signs of ischemia appear 4~14days, most often at 7 days
Potential mechanisms
◦ RBC hemolysis and subsequent release of oxygen, Hb, and other active
oxygen species
◦ Secondary effects -Vessel wall changes
Hydrocephalus
15~20% patients
May develops at any time: Acute, or over a few
days or weeks
Progressive drowsiness, gait difficulties, abulia
with incontinence
CT scanning shows enlarged ventricles
 Diagnostic approaches
CT
◦ Sensitivity 90~95% with in 24hrs
◦ intracerebral hemorrhage, mass effect, and hydrocephalus

MRI
◦ 4 days ~2wks, detects deoxygenated hemoglobin

DSA
◦ Useful for aneurysm location and vasospasm
◦ Within 3 d or after 4 wks to avoid rebleeding and vasospasm
Interhemispheric
fissure

Sylvian fissure
SAH with
early hydrocephalus

(ACLS text)
Vasospasm in acute SAH
Repeat angiogram
Initial angiogram showing vasospasm
(small arrows)
 Diagnostic approaches
Lumbar puncture (LP)

◦ Suspected SAH with negative CT

 Diagnosis
Sudden onset of severe headache
Meningeal irritation sign(stiff-neck, kernig`s sign)
CT scan (head CT scanning should be the first study performed)
Examination of CSF (in patient with suspected SAH and negative
CT scanning)
CTA, MRA or DSA (careful evaluation of all cerebral vessels
should be undertaken )
Differential diagnosis
SAH vs. other strokes
SAH in older patients: no obvious headache
Meningitis
Metastatic brain tumor
History, symptom onset, CSF profiles, CT fails to show positive signs of hemorrhage
Treatment principles
General management
Treating cerebral hypertension
Dealing with complications
◦ Rebleeding
◦ Vasospasm
◦ Hydrocephalus
◦ Epilepsy
◦ Hyponatremia (low blood sodium)
Management of SAH
2 major objectives must be addressed:
Identification of the bleeding source with possible
procedural intervention
Management of subsequent complications
General treatment: absolute bed rest, reduce ICP
Management of bleeding source
Aneurysms: The most common cause
How to treat? (clipping or coiling)
Basilar artery aneurysm before coiling
Basilar artery aneurysm after coiling
Management of Complications
 Vasospasm
 Vasospasm is characterized by mental status changes with focal
neurologic deficit.

 Develops between days 4 and 12 after subarachnoid hemorrhage

 Maintain hypervolemia or induced hypertension

 Calcium channel blocker: Nimodipine/Nicardipine

 Endovascular treatment
Management of Complications
Management of Complications
 Rebleeding
 Rebleeding has a mortality rate of 70 and it is associated with a
marked reduction in chance of survival

 Absolute bed rest

 To reduce the risk of rebleeding prior to aneurysm repair, blood

pressure must be carefully managed

 Provide supportive care and emergency treatment of aneurysm

Management of Complications
◼Hydrocephalus

◼Occurs in approximately 5%-50% of patients after initial SAH

◼Diversion of cerebrospinal fluid:
✓Lumbar drainage or external ventricular drainage (EVD)
✓CSF shunt
◼Dehydrattion: manitol, ferosimide
A 69-y/o woman
a 69-Year-Old Woman who had a long-standing history
of smoking and hypertension, presented to the
emergency room with severe headache with nausea and
vomiting for four hours and had meningismus on
physical examination.

What’s next?
Initial computed
tomography (CT) of the
head revealed a
subarachnoid hemorrhage, a
right frontal hematoma
suggestive of an anterior
communicating artery
aneurysm, and
hydrocephalus (Panel A).
What’s next? 
Digital-subtraction cerebral
angiography (oblique view)
showed an aneurysm
stemming from the anterior
communicating artery
(Panel B, arrow). Three-
dimensional digital-
subtraction angiography
clearly showed the bilobed,
irregular nature of the 
aneurysm (Panel C, arrow).
 How to treat?
 Clipping or coiling of the aneurysm

 What if the patient developed vasospasm?

 Angiography showed considerable vasospasm (Panel D) in the proximal

segments of the left anterior arteries (arrowhead) and middle cerebral arteries
(arrow).
 Treatment of complications

The patient underwent transluminal balloon angioplasty of the left middle cerebral artery,
and direct vasodilators (papaverine and verapamil) were infused into the left anterior
cerebral artery with good resolution of the vasospasm (Panel E).
Merci!