Neurological complications

of acute ischemic stroke

Neurology
R5 林念穎
2012/03/22
 原由
• 在神經內科病房有好多中風病人唷, 中風病人除
了吊吊IVF, 吃aspirin, 做復健之外, 好像就沒
再幹嘛了…
住院就是在 「觀察」…
那那那…到底是在觀察些什麼呢????

喔天那…那個中風病人怎麼突然
consciousness change了…我是值班
醫師/主護,我要想什麼呢?
 Introduction
• Mortality after stroke still high
– 3nd most common, after ischemic heart
disease and all neoplastic diseases
• Post-stroke complications account for
23~50% of deaths
• Neurological and medical complications
 Introduction
• Neurological complications
(1) brain edema
(2) haemorrhagic transformation
(3) seizures and epilepsy
(4) recurrent stroke
(5) sleep disorders & sleep-disordered
breathing…etc.
• Less frequent than medical complications, but
occur earlier
– Within 48~72 hours of stroke onset
 (1) Brain Edema
• Brain edema: leading cause of death after stroke, in
the first week
• Ionic imbalance due to energy depletion
• Two types:
– Cytotoxic:
• Occurs early, blood-brain barrier intact
• High signal in diffusion-weighted MRI (DWI), low
signal in apparent diffusion coefficient (ADC)
– Vasogenic:
• Late; blood-brain barrier compromised
• High signal in T2-weighted and T2-FLAIR
• Increased intracranial pressure, herniation, additional
ischemic injuries
Brain edema

www.thelancet.com/neurology Vol 10 April 2011

 (1) Brain Edema
• Younger patients fatal brain edema, malignant MCA
syndrome
• Overall risk of cerebral edema in anterior circulation
ischemic stroke: 10~20%
• Occurs within first 4 days
• Brain edema increased intracranial hypertension
(IICP)
– Headache, vomiting
– Herniations （腦疝脫）

• Brainstem compression is major cause of

mortality!!!!
Herniation:
-Pressure against
reticular formation in
midbrain
consciousness
deterioration
- Compression of CN3
pupil dilatation
 Malignant MCA Infarction
• MCA territory completely infarction
rapidly developing massive swelling
brain herniation as near as 20 hour after onset

• 1~10% of all supratentorial ischemic strokes

• Overall mortality rate estimated 40~80% (compare to

7~23% for acute MCA infarctions)

• Predicted by large hypoattenuation (>2/3 of MCA territory) on

brain CT– sensitivity 91%; specificity 94%
Figure 2: CT scans showing cerebral
edema after ischemic infarct.
(A) CT scan showing cerebral
edema (green arrow) with
compression of the left ventricle
(red arrow) after infarct of the left
middle cerebral artery territory.
 Cerebellar Edema
• Common in cerebellar infarctions;
17~54% of cerebellar
• Posterior fossa provides little space for
compensation of mass effect
• Usually peaks on the 3rd day
• CT scans displacement of 4th ventricle,
obstructive hydrocephalus, obliteration of
basal cisterns
 Cerebellar Edema
• Induce brainstem compression & obstructive
hydrocephalus
– Gaze palsy
– Decline in consciousness level
– Sudden apnea, cardiac arrhythmias
– Hiccups lesions of lateral medulla,
pontomedullary area of brainstem
(B) CT scan showing posterior
circulation stroke (left-sided
posterior inferior cerebellar
artery infarct) with involvement
of the pons 10 h after onset of
stroke (green arrows).
 (1) Brain Edema
• Treatment- medical
– General: close monitor for neurological worsening

– Osmotherapy:
• Glycerol, mannitol, hyperosmolar saline solutions,
corticosteroids, barbiturates; unproven (level 3C)
• May be harmfal in CVST

– Hypothermia (32~35℃):
• in small RCT (n=25), in addition to decompressive
surgery led to better outcome than surgery alone (level
3C)
 (1) Brain Edema
• Surgical
– Decompressive surgery
• Early decompressive hemicraniectomy (<48hr) improves
survival and functional outcome in patients (aged < 60 years)
with malignant cerebral artery infarction (level 1B)

• Suboccipital decompressive craniectomy-- recommended as

therapy of choice in malignant cerebellar infarction (level 1B)

– External ventricular drainage (EVD)–

• for patients with worsening levels of consciousness and
obstructive hydrocephalus secondary to cerebellar infarction
(2) Hemorrhagic Transformation
• Common; 30~40% of acute ischemic stroke
– Symptomatic:
• 0.6% in those with supportive care
– Aspirin: small increase in bleeding risk, but non-
significant
• 6% of intravenous alteplase
• 7% of intra-arterial fibrinolytics and mechanical
embolectomy
(2) Hemorrhagic Transformation
• Risk factors of thrombolysis-related ICH
– Old age (>65y/o):
• impaired rate of alteplase clearance, high frequency of
cardioembolic stroke, age-associated microangiopathy (cerebral
amyloid angiopathy or hypertensive microangiopathy)
– Larger infarct size  mass effect on pre-treatment
imaging
– High baseline systolic blood pressure
– Congestive heart failure
– High glucose concentrations/diabetes mellitus
• Expands brain edema, increase ICP higher mortality
 Haemorrhagic
transformation

ECASS classification of hemorrhagic transformation:

Hemorrhagic infarction (HI)
• HI-1: small petechiae along margins of infarcted area
• HI-2: conflent petechiae within infarcted area; no mass effect
Parenchymal hemorrhages (PH)
• PH-1: hematoma less than 30% of infarcted area, with mild mass effect
• PH-2: hematoma in more than 30% of infarcted area with notable mass
effect

www.thelancet.com/neurology Vol 10 April 2011

(2) Hemorrhagic Transformation
• No intervention to reduce risk of hemorrhagic
transformation
• Careful selection of suitable patients for
thrombolytic therapy
• Antithrombotics not recommended for use in
first 24hrs after thrombolytic treatment
• Management
– Asymptomatic: no specific intervention
– Symptomatic
• Medical
• Surgical
(2) Hemorrhagic Transformation
• Medical:
– Stop anti-thrombotic medication
– Secondary to thrombolytic therapy
platelet and cryoprecipitate infusion to correct
systemic fibrinolytic state created by alteplase
(level 2BC)
– Intravenous vitamin K to reverse effects of warfarin
(level 1B)
• Surgical:
– Supratentorial: lobar clots >30 mL and within 1 cm
of surface (level 2B)
– Cerebellar hemorrhage > 3cm (level 1B)
(2) Hemorrhagic Transformation
• Management
– Antithrombotic therapy after hemorrhagic
transformation
• Depends on risk of subsequent arterial or venous thromboembolism, risk of
recurrent intracerebral hemorrhage and clinical state of patient
• Antiplatelet:
– safer choice than warfarin for patients with lower risk of
cerebral infarction (eg non-valvular Af), but with higher
risk of rebleeding (eg elderly with lobar ICH, possible
amyloid angiopathy)
• Warfarin:
– In patients with high risk of thromboembolism (Level 2B)
– Can be restarted 7~10 days after onset of
ICH
 (3) Seizure
• Early seizures: within 1~2 weeks
– Frequency: 2~23%
– Cellular biochemical dysfunction electrically excitable
tissue
– Recurrence rate 16%

• Delayed: > 2 weeks

– Frequency: 3%~67%
– Mechanism: gliosis, meningocerebral cicatrices (scar)
– Recurrence rate more than 50%

• Prognosis:
– Recurrent seizure in post-stroke seizures increase
disability, vascular cognitive impairment
 (3) Seizure
• Risk factors:
– Venous sinus thrombosis (more than
arterial stroke)
• In one study, 40% CVST had seizure at
presentation, additional 7% within 2 weeks of
diagnosis
– Large cortical infarcts, multiple infarcts,
embolic stroke, hemodynamic and metabolic
disturbances
 (3) Seizure
• Management
– No clear guideline for when to initiate
anticonvulsant therapy, choice of therapy, or for
duration of therapy
– Prophylactic use not recommended
– Early seizures short-term AED for 3~6 months
– Late seizures require long-term treatment
 (4) Recurrent Stroke
• Risk of early stroke recurrence: 10% at 1 week,
2~4% at 1 month, 5% yearly thereafter

• Major risk factors of recurrence:

– Old age,
– previous stroke,
– diabetes,
– hypertension,
– atrial fibrillation, cardiac diseases,
– smoking,
– carotid/vertebrobasilar stenosis (large artery
atherosclerosis)
 (4) Recurrent Stroke
• Management
– Antiplatelet therapy
• First line for non-cardioembolic ischemic stroke or TIA
(level 1A)

– Anticoagulation for atrial fibrillation

• 68% RRR with warfarin vs 19% with aspirin (level 1A)

– Carotid endarterectomy and endovascular

interventions
• Early carotid endarterectomy (first 2 weeks) more
beneficial (level 1A)
• Carotid angioplasty reserved for those contraindicated to
carotid endarterectomy (level 2B)
 (4) Recurrent Stroke

– Treatment of hypertension
• Controversial

– Reduction of elevated cholesterol (level 1A)

– Blood sugar control

• Hyperglycemia (> 140 mg/dL)  insulin therapy in acute
ischemic stroke (level 2C)
 (5) Sleep disorders
• Frequent in initial stages after stroke
– 10~50% of stroke patients
– Hypersomnia (increased sleep need), excessive daytime
sleepiness, insomnia

• Bilateral paramedian thalamus, brainstem, large

hemispheric stroke with mass effect

• Associated with depression, anxiety, sleep-disordered

breathing, drugs, post-stroke pain, medical complications
(UTI, respiratory infections, nocturia), environmental factors
(noise, light)
 (5) Sleep-disordered Breathing
• Obstructive apnea
– Most common form, over 50% of patients
– Share same risk factors as stroke: age, obesity, hypertension
– Collapse of upper airway
– Treat with continuous positive airway pressure breathing

• Central apnea= Ondine’s curse

• Mixed apnea

• 50~72% of stroke patients

 Ondine’s curse
Ondine is a water nymph and falls in love with a
handsome knight, Sir Lawrence, and they are
married.
One afternoon, she sees Lawrence lying in the arms of
another woman.
Ondine curses him, “You swore faithfulness to me with
every waking breath. As long as you are awake, you
shall have your breath, but should you ever fall
asleep, then that breath will be taken from you and
you will die!"
 Ondine’s curse
• Respiratory control:
– Voluntary: supramedullary respiratory control;
cerebral cortex corticospinal tract

– Automatic:
• Regulates breathing automatically in response to the
changes in oxygen and carbon dioxide in the blood
• Respiratory center in medulla and pons
 Ondine’s curse
• Ondine’s curse
– impairment of the automatic respiration
– no damage to the voluntary respiration

• Lateral medullary infarction in distal vertebral

artery occlusion

• Central apnea during sleep

• Progress to fatal respiratory failure need mechanical

ventilation
 Take home message
• Neurological complications occur early after
ischemic stroke lead to death within first few
days (high mortality rate)
• Improved detection and management is
important
• Neurological complications include:
– Brain edema
– Hemorrhagic transformation
– Post-stroke seizures
– Recurrent stroke
– Sleep disorder and sleep-disordered breathing
– Delirium
下課囉~