Neurology - Walk 30min a day, most days of the wk (4-5days) to prevent dev’t

Neurovascular: Stroke Diagnosis of stroke, MI & peripheral arterial disease

and Management
December 7-10, 2007 Diagnosis
- 80% depend on history
Stroke
Sudden in onset
- Sudden occurrence of a nonconvulsive, focal neurologic
What kind of lesion
syndrome, specifically the type due to a cerebrovascular disease
Localize obstruction based on signs & symptoms
- Signs & symptoms of focal brain disease - Depends mostly on clinical assessment of the px
- Sudden loss of consciousness is NOT due to stroke
- CV disease means any abnormality of the brain resulting from a Vascular Anatomy
pathologic process of the blood vessels - Anterior circulation
- Pathologic process is given an inclusive meaning namely:
Carotid system

Occlusion of the lumen by embolus or thrombus
Consists of 3 major arteries

Rupture of a vessel 1. Common carotid

Altered permeability of the vessel wall  Right common carotid arises from the right

↑ viscosity of blood flow brachiocephalic artery

Change in the quality of the blood flowing thru the cerebral  Left arises directly from the aortic arch
vessels  Ascend in the neck to the C4 level, just below the
- The denotative feature in all forms of stroke is the temporal profile angle of the jaw, or sometimes at the level of the
of the neurologic events. It is the abruptness or rapidity with thyroid cartilage where each divides into the
which the neurologic deficit develops—a matter of sec or mins— external & internal branches
that stamps the disorder as vascular 2. Internal carotid – supply internal stream, inside the
- The vascular pathologic process may be considered not only in its cranial cavity
grosser aspects—embolism, thrombosis, dissection or rupture of 3. External carotid – supply external stream, outside the
vessel—but also in terms of the more basic or primary disorders: cranial cavity

Atherosclerosis
Syndromes caused by common carotid occlusion are

Hypertensive arteriosclerotic change identical to those of the internal carotid artery occlusion

Arteritis - Posterior circulation

Aneurysmal dilation
Vertebrobasilar system (the Circle of Willis & its branches)

Developmental malformation
Circle of Willis
- Signs & symptoms last for >24hrs: an impt qualifying event 1. Anterior cerebral artery
- As compared to “transient ischemic attack” (TIA) which reverses 2. Middle cerebral artery
itself (improves) dramatically over a period of minutes or hours 3. Posterior cerebral artery
- A medical emergency 4. Anterior communicating artery
5. Posterior communicating artery
Epidemiology of Stroke
Incidence: New Cases of Stroke THE BRAIN: Pathophysiology
- 0.2% per year - 2-3% of the body weight

1/3 die - 20% of all oxygen

1/3 disabled - 25% of all glucose

1/3 recover - 15% of CO or 45L/min of cardiac output (CO) [CO = SV x HR]
- Therefore, ~2/3 of cases recover from stroke
Respiratory quotient is zero. It means that for every amount
- Third most common cause of death, after heart disease & cancer of O2 entering the brain, none will come out
- The brain cannot reserve or store glucose & O2. That is why it
Prevalence has a high demand for these 2 most important substrates of brain
- 5,000/1,000,000 or 0.5% metabolism.
- Worldwide: in 100 acute cerebral infarctions, 7-10% will have - ATP for the brain:
recurrent stroke annually
Krebs cycle – aerobic glycolysis wherein 1 mol of glucose +
O2 generates 38 moles of ATP
Risk Factors
Anaerobic glycolysis (in cases of hypoxia), can generate 2
- Non-modifiable Risk Factors ATPs but its by-product, lactate, is toxic to the brain
1. Age: elderly at greater risk (particularly >65y/o) because it makes the brain acidic
2. Gender: males are at a greater risk, M:F = 2:1 - Also, the brain cannot tolerate a decreased amount of blood,
3. Hereditary glucose & O2. The ff parameters should be met, below which,
4. Race/ethnicity: no-white functional impairment can occur:
5. Prior strokes or MI
CBF of at least 500 mL/100g/min
6. Existing heart disease
500 mL of O2/min
- Modifiable Risk Factors
75-100mL of glucose/min
1. Lifestyle - CBF = Cerebral perfusion pressure/cerebral vascular resistance

Smoking
CPP is the pressure that drives the heart & the arterial

Less physical exercise system. Systolic pressure is mainly responsible.

Morbid obesity
Average resting CBF = 55mL blood/100g of brain tissue/min

Excess alcohol consumption
Mean arterial BP (MABP) = 2S – D(1/3)

Diet (high salt & fat, low fiber)
Factors that affect CBF:
2. Pharmacotherapy 1. Extracerebral

HPN – most readily recognizable factor in the genesis - BP, CO, blood viscosity
of primary intracerebral hemorrhage 2. Intracerebral

Arterial disease - CV status

Heart failure - Neurogenic control

Risk of embolic-thrombotic phenomenon - Chemical factors

Certain blood disorders - Metabolic regulation (↑ PaCO2 – most potent)

High blood cholesterol - Autoregulation

DM - Cerebrovascular autoregulation
American Heart Association recommendations:

Over range of mean BP of ~50-150mmHg, the small pial
Or occlusion of the internal carotid in the neck, there
vessels are able to dilate & to constrict in order to maintain may be anastomotic flow from the external carotid via
CBF in a relatively narrow range the ophthalmic artery or small internal-external

This accommodation eventually fails at the extremes of BP, connections
after which CBF follows systemic pressure passively, falling 3. Resistance of the brain to ischemia
precipitously or rising to the levels that damage small vessel
walls Subtypes of Stroke
1. Ischemic Stroke
Levels of CBF & corresponding consequences: (mL/100g/min) a. By occlusion – atherothrombotic in origin; formed in the wall
40 Oligemia of the blood vessels
↑ O2 extraction b. Embolic stroke – clot formed mostly from the heart or the
May maintain normal major arteries
30 Mid-ischemia c. Hypoperfusion – may be due to blood pressure drop; areas
↑ glycolysis which are susceptible to ischemia will be affected
↓ protein synthesis 2. Hemorrhagic Stroke
20-23 Threshold of electrical deficit or critical a. HPN – Primary intracerebral hemorrhage
level of hypoperfusion b. Ruptured aneurysm (in >40y/o pxs) & arteriovenous
Moderate ischemia (PENUMBRA) malformation (in <40y/o pxs) – Primary subarachnoid
- In the region of marginal hemorrhage
perfusion where the tissues are - 5 common areas of hemorrhage:
still salvageable & neurons are - Basal ganglia – putamen, lentiform is the most common
still viable - Thalamus -- <10%
- 3 hrs is the golden period of - Cerebellum
Penumbra. After this period, - Pons
tissue are irreversibly damaged - Lobes of cerebral hemorrhage
<10 Severe ischemia
(Oxfordshire Community) Stroke Subtypes
- Anoxic depolarization (↑ K in the
1. Total anterior cerebral infarct (TACI)
ECF and ↓ Ca in the ECF)
2. partial anterior cerebral infarct (PACI)
3. Posterior circulation infarct (POCI)
Fissure & Rupture Plaque 4. Lacunar infarct (20%)
- Majority (75%) of blood vessel occlusion in the brain is secondary
to atherosclerosis or atherothrombosis Mechanisms of Infarct
- Atherosclerosis is a long standing process - 20% come from the heart: “cardioembolic infarct”; most of the
- Even in utero, some infants show fatty streak in their blood time associated with arrhythmia (especially atrial fibrillation)
vessels - Carotid artery developing plaque usually in the bifurcation: “artery-
- Fatty streak to-artery emboli

Initial step causing atherosclerosis
Example is the common carotid area where it bifurcates to

Risk factors predispose some individuals to develop become the int. & ext. carotid arteries
atherosclerosis - Atherothromboembolic infarct – 50%
 Food - Hypoperfusion area – most commonly at watershed areas (where
 Lifestyle 2 major blood vessels meet)
 Uncontrolled DM - Lacunar infarct
 HPN
Usually associated with atherothromboembolic infarct

Intracerebral hemorrhage in the basal ganglia, may develop
Plaque can come from
microinfarct (≤1.5cm)

Lipohyalinosis can develop occlusion & the area affected
gets infarcted
Rupture Fissure
CLINICAL MANIFESTATIONS
Collagen is exposed Focal Neurologic Deficits
A. Cerebral Dysfunction
Acted upon by platelet aggregates - Seizure
& other thrombogenic substrates - Language disorder – aphasia
- Organic mental, behavioral & personality changes
- Contralateral
Obstruct blood vessels
Hemiparesis with Babinski & CN deficits

Hemisensory deficits

Homonymous hemianopsia/quadrantanopsia
Focal neurologic deficits
B. Cerebellar Dysfunction
- Hemisphere lesion
Note:

Ipsilateral limb ataxia
**The sudden onset of the platelet aggregation is the one that causes
 Intention tremor
the focal neurologic deficit.
 Dysmetria
**Turbulent blood flow is highest at bifurcations of a blood vessel.
 Dysdiadochokinesia
- Vermis lesion
Extent & Size of Ischemia

Truncal ataxia
- Depends on:

No limb ataxia
1. Rate of occlusion
C. Brainstem Dysfunction

Gradual narrowing allows time for collateral channels
- “Crossed motor/sensory syndrome
to open

Ipsilateral CN deficits
2. Adequacy of collateral channels

Contralateral hemiparesis with Babinski

Example, if obstruction lies proximal to the circle of
- Ipsilateral limb ataxia
Willis (toward the heart), the anterior & posterior
- Internuclear ophthalmoplegia – median longitudinal
communicating arteries of the circle are often
fasciculus syndrome
adequate to prevent infarction
ISCHEMIC STROKE
Quadriparesis (4 extremities paralyzed)
- 85% of strokes (60-80%)
Crossed paresis (Example, left half of the face & right half of
- Can be thrombotic or embolic the body)
- One month mortality = 15%
Dysarthria, hoarseness, dysphagia, ipsilateral ataxia, gait or
truncal instability
Middle Cerebral Artery - Sensory impairments
- Supplies most of the convex surface of the brain
Unilateral or bilateral sensory loss of face, & upper & lower
- Deep tissue: extremities

Basal ganglia
Dissociated sensory loss with difference in pin & vibratory

Putamen senses

Parts of globus pallidus
Facial pain or dysesthesia

Caudate nucleus
Absent or depressed corneal or gag reflex

Internal capsule - Abnormalities of extraocular mov’t
- Horner’s syndrome
Left Hemisphere – Dominant - Vertigo
- Right motor deficits - Nausea, vomiting

Face

Upper & lower extremities Signs & Symptoms Associated with the Posterior Circulation
- Right sensory loss More specific Less specific

All modalities Ataxia Dysarthria

Decreased stereognosis Diplopia Headache

Agraphesthesia Vertigo/disequilibrium Unilateral numbness or weakness
- Language deficits Bilateral numbness or weakness Nausea & vomiting

Dysarthria Visual field defects

Aphasia

Alexia Medial Midbrain Syndrome (Weber’s Syndrome)
- Right homonymous hemianopsia - Structure/s damaged
- Agraphia, acalculia, Apraxia of left limbs
Corticospinal fibers in crus cerebri

Oculomotor nerve
Dominant Hemisphere - Deficit
- Majority of right handed & most left-handed pxs have dominance
Contralateral hemiplegia of arm & leg
for speech & language located in the left hemisphere
Ipsilateral paralysis of eye mov’t; eye oriented down & out &
pupil dilated & fixed
Right Hemisphere – Non-dominant
- Left hemiparesis Central Midbrain Lesion (Claude Syndrome)
- Left sensory loss - Structure/s damaged
- Left homonymous hemianopia
Oculomotor nerve
- Neglect of left side of environment
Red nucleus & cerebellothalamic fibers
- Anosognosia - Deficit
- Asomatognosia
Ipsilateral paralysis of eye mov’t
- Loss of prosody of speech
Contralateral ataxia & tremor of cerebellar origin
- Flat affect
Pontine Syndromes
Anterior Cerebral Artery A. Lateral Pontine Syndrome (involves LONG CIRCUMFERENTIAL
- Supplies basal & medial aspects of the cerebral hemispheres branches of the basilar artery)
- Extends to anterior 2/3 of the parietal lobe Deficits:
- Perforating branches supply anterior caudate nucleus, parts of - Ataxia, unsteady gait, fall towards side of lesion – middle &
internal capsule, Putamen & anterior hypothalamus superior cerebellar peduncles
- Vertigo, nausea, nystagmus, deafness, tinnitus, vomiting –
Signs & Symptoms Associated with an Anterior Circulation vestibular & cochlear nerves & nuclei
More specific Less specific Uncommon - Ipsilateral paralysis of facial muscles – facial motor nucleus
Aphasia Unilateral numbness or Ataxia - Ipsilateral paralysis of masticatory muscles – trigeminal
weakness motor nucleus
Apraxia Visual field deficits Vertigo- - Ipsilateral Horner’s syndrome – descending
dysequilibrium hypothalamospinal fibers
Agnosia Dysarthria Nausea & vomiting - Ipsilateral loss of pain & thermal sense from face – spinal
Headache trigeminal tract & nucleus
- Contralateral loss of pain & thermal sense from the body –
ACA Stroke anterolateral system
- Weakness of the leg - Paralysis of conjugate horizontal gaze – paramedial pontine
- +/- proximal muscle weakness in the upper extremities reticular formation
- Affect frontal lobe; impaired judgment & insight, change in affect
- Presence of primitive grasp & suck reflexes B. Medial Pontine Syndrome (involves the PARAMEDIAN branches
of the basilar artery)
Vertebrobasilar System - Contralateral hemiplegia of arm * leg – corticospinal fibers in
- Supplies: basilar pons

Brainstem - Contralateral loss or decrease of position & vibratory sense

Cerebellum & discriminative touch (arm & leg) – medial lemniscus

Thalamus - Ipsilateral lateral rectuses muscle paralysis – abducens

Visual occipital cortex nerve fibers of nucleus
- Level of consciousness - Paralysis of conjugate gaze towards side of lesion –

Ranges from alert to coma paramedian pontine reticular formation (pontine gaze

Confusion or agitation uncommon center)

No cognitive impairments
- Motor impairments

Contralateral paresis of upper & lower extremities
 C. Medial Medullary Syndrome (involves ANTERIOR SPINAL
ARTERY)
Deficits
- Contralateral hemiplegia of arm & leg – pyramid
- Contralateral loss of position sense, vibratory sense &
discriminative touch – medial lemniscus
- Deviation of tongue to ipsilateral side when protruded;
muscle atrophy & fasciculations – hypoglossal nerve in
medulla or hypoglossal nucleus
D. Lateral Medullary Syndrome (involves the POSTERIOR
INFERIOR CEREBELLAR ARTERY)
- Contralateral loss of pain & thermal sense ob body –
anterolateral system fibers
- Ipsilateral loss of pain & thermal sense on face – spinal
trigeminal tract & nucleus
- Dysphagia, soft palate, paralysis, hoarseness, diminished
gag reflex – nucleus ambiguous, roots of CN IX and X
- Ipsilateral Horner syndrome – descending
hypothalamospinal fibers
- Nausea, diplopia, tendency to fail to ipsilateral side,
nystagmus, vertigo – vestibular nuclei (inferior & medial)
- Ataxia to ipsilateral side – restiform body & spinocerebellar
fiber
INTRACEREBRAL HEMORRHAGE
- 20% of stroke
- Classic: sudden onset of headache, vomiting, elevated BP
- Focal neurologic deficits that progress over minutes
- May present with agitation & lethargy but progresses to stupor or
coma
- Often caused by hypertensive damage to small penetrating
vessels & has the same vascular distribution as lipohyalinosis
(stiff & breaks)
- Charcot & Bouchard originally described microaneurysms which
ruptured causing ICH
- Sudden ↑ in BP & blood flow can also cause these penetrating
arteries to break
- Other causes:

Trauma

Ruptured aneurysm

AV malformation

Anticoagulant intake

Thrombolytic agents

Cerebrovascular amyloidosis

Bleeding disorders
SUBARACHNOID HEMORRHAGE
- 10% of stroke
- At the surface of the brain
- Aneurysms related to cranial nerve have the tendency to
compress CN and lead to palsy
- May be secondary to ruptured aneurysm or AVM
- 3 major risks affect subsequent events:

Rebleeding

Vasoconstriction

Hydrocephalus
------Other Notes------
Clinical Presentation of Stroke
 Onset: Acute
- Stroke patients are not usually brought to the hospital
immediately (compared to MI patients) because symptoms
do not usually present as an emergency, e.g. weakness,
visual problems, etc.
- Primary intracerebral hemorrhage  usually one-sided
weakness/ numbness/ sensory loss/ language problems
(slurring of speech) / others
- Sudden onset of focal neurologic deficit
- Usually headache is not a presenting symptom
 Dysfunction in certain part of the brain: Localization:
1. Weakness
 Usually upper & lower extremity hemiparesis
 If upper extremity is more involved than lower extremity:
Middle cerebral artery involvement
 If lower extremities is more involved than upper
extremities: anterior cerebral artery involvement
2. Numbness
 “Pins & needles” (Like which occurs in crossing the legs:
Compression neuropathy)
 ½ of body
 Both weakness & sensory change occurs at the same ½
of body
3. Visual problem
 Blurring of vision
 Homonymous hemianopsia
- Can’t see on one side of the visual field
- If supratentorial lesion, hemiparesis is on the same
side of the homonymous hemianopsia. All the signs
& symptoms are on the opposite side of the lesion
 Transient Monocular blindness (TMB)
- Sudden blindness in one eye
- Associated with carotid artery disease on the same
side
- Ophthalmic artery is the 1st & only branch of the
internal carotid artery (before it bifurcates)
- Blind on one eye, hemiparesis on the opposite side
4. Speech problem
 Lesions are on cerebral hemispheres or on brainstem
 Most common: Slurring of the speech (Motor problem:
Dysarthria): Lesion maybe on the cerebellum or on the
brainstem medulla
 Language problems: Wernicke’s aphasia (sensory
aphasia; can’t understand) & Broca’s aphasia (motor
aphasia; telegraphic speech)
 Majority of lesions are on left cerebral hemisphere (the
dominant hemisphere if right-handed)
5. Hemineglect: can’t recognize half of body as own; usually
seen in parietal left-sided stroke
**NOT all presentations (weakness, numbness, visual & speech
problems) are seen at the same time; depends on location of the lesion
Neurovascular Syndrome (according to the blood vessel involved)
- Cerebral blood vessels
- Carotid system (anterior circulation) & vertebro-basilar system
(posterior circulation)
- Anatomy: Carotid artery (Right from the inominate artery, left from
the aorta)  Internal carotid artery  Enters cavernous sinus 
Branches into ophthalmic artery  Bifurcates into middle cerebral
artery & anterior cerebral artery
- 80% of strokes – anterior circulation, carotid system (40% each
CA), cerebral hemispheres
- 80% middle cerebral artery, contralateral hemiparesis & facial
weakness, sensory symptoms, visual symptoms
- 20%: posterior circulation, brainstem cranial nerves, “Complex
symptomatology”
Stroke Mimickers
- Malingerer
- Bell’s palsy: Frank weakness of 1 side of the face because of
cranial nerve 7 palsy, no numbness of the extremities
- Seizure
- Migraine: Migraine with focal signs (Weakness & numbness)
Establish Mechanism of Stroke
1. Hemorrhagic
- Primary intracerebral hemorrhage

Usually associated with uncontrolled hypertension

Bleeding into the substance of the brain

60% in basal ganglia, 10% in different lobes, 10% in
the cerebellum, 10% in the PONS
- Subarachnoid hemorrhage

Aneurysm, arteriovenous malformation

Between pia & arachnoid
- Cerebrospinal fluid
- Blood vessels
 2. Infarction - Acute Pulmonary edema
- Small vessel disease (Lacunar): 20% - Acute myocardial infarction

Perforating arteries obstruction

Perforating arteries develop microatheromas Neuroimaging

Perforating arteries develop microembolism - Non-contrast enhanced CT scan of the brain

Lipohyalinosis (Secondary to long-term uncontrolled - Early signs of infarction
hypertension) - Hyperdense MCA sign

Mostly in the basal ganglia - Loss of gray-white differentiation in the cortical ribbon

May develop pure motor or pure sensory stroke (particularly the lateral margins of the incula) or the
(Because of very isolated lesion) lentiform nucleus
- Intracranial atherosclerosis: 50% - Sulcal effacement
- Extracranial atherosclerosis

Hemodynamic Interventions
- At the bifurcation of the carotid arteries
- Primary prevention
- More common in the internal carotid artery
- Acute phase
- Hemodynamic/ hypoperfusion infarction
- Secondary prevention
- Decreased blood pressure: Area 1st
compromised is the area that is obstructed

Artery to artery embolism Treatment Approach
- Atherosclerotic plaques interact with platelets Hematoma evacuation
- Platelet debris Revascularization
- Cardioembolism Risk factor Neuroprotectants Recanalization

20% of cerebral infarction modification Thrombolytics Stroke unit

Atrial fibrillation (Most common), valvular heart
disease, congenital heart disease
- Other determined causes
3 hours
- Cryptogenic or unknown

Note: Antithrombotic
 Risk factors may sometimes not help in the diagnosis: Stroke event Hospital Anticoagulant
Hypertension, diabetes, hypercholesterolemia are risk factors for
both infarct & hemorrhagic stroke
 Clinically, one may be able to determine the mechanism of stroke Beyond 3 hours → permanent damage
- Hx of transient ischemic attack: Infarction
- Depressed/ alteration of consciousness: Hemorrhagic Acute Ischemic Stroke Treatment in 2007
- Neck rigidity (Because of presence of blood in the
Local Cerebral Blood Flow

subarachnoid space): Hemorrhage 30

- Hemorrhages in the optic fundi: Hemorrhagic
20 Paralysis
Management Goals
- Goals of immediate diagnosis and evaluation: Infarction
- Determine the symptoms are due to stroke 10
- Determine advisability for acute treatment with thrombolytic
therapy
- Screen for acute medical or neurological complications of 0
stroke 1 2 3 hours Permanent
- Provide historical data to establish the vascular distribution Time
of stoke and provide clues about pathophysiology and
etiology Treatment Options – Acute Phase
- History and Physical Examination - Stroke Units
- Note vital signs - Thrombolysis
- Cardiac examination - Neuroprotection
- Check for carotid bruit - Aspirin and Heparin
- Use of validated scoring systems e.g. NIHSS, to determine - Surgery for Intra-cerebral Hemorrhage
stroke severity - Early Secondary Prevention
- Immediate diagnostic studies
- Cranial CT scan or MRI Treatment Options – Secondary Prevention
- ECG
- Antiplatelet & Antocoagulant treatment
- Blood glucose
- Antihypertensive treatment post-stroke
- Serum electrolytes
- Statin Therapy
- Renal function tests
- Carotid artery disease
- CBC, including platelet count
Intervention Outcome OR (95%C.I) NNT
General supportive care Death 0.81 (0.68-0.96) 21
- ABCs Stroke Unit Death or 0.75 (0.65-0.87) 14
- Control of fever Institutionalization
- Cardiac rhythm Death or dependency 0.71 (0.60-0.84) 15
- Hypoglycemic/hyperglycemia ASA Death or dependency 0.95 (0.91-0.99) 83
- Hypertension
Early death (2 weeks) 1.99 (1.56-2.55) -
- No clinically proven benefit for lowering BP among patients
Early ICH (2 weeks) 3.6 (2.7-4.8) -
with acute ischemic stroke
Thrombolysis Death 1.36 (1.1-1.6) -
- Antihypertensive agents should be withheld unless
- DBP >120 or SBP >220 Death or dependency 0.75 (0.6-0.9) 15
- Hypertensive encephalopathy The lower the NNT number the better → therefore according to the
- Aortic dissection table: Stroke unit is the best
- Acute renal failure High ARR and High RRR → better
 Goals for Management of Patients with Suspected Stroke Prevention of Vascular Events in Stroke/TIA patients
Algorithm - Aspirin better than placebo
- 30% relative risk reduction
Identify signs of possible stroke

Aspirin in Secondary Prevention of Stroke

- In stroke trials, aspirin effect is independent of doses between
Critical EMS assessments and actions: 50 – 1,500mg/day
- Support ABCs, give oxygen if needed - FDA: professional labelling for aspirin recommends 50 to
- Perform prehospital stroke assessment 325mg/day
- Establish time when patient last known normal (note: - ACCP: aspirin recommended at 50 to 325 mg/day
therapies may be available beyond 3 hours from onset
- Transport, consider triage to a center with stroke unit, if CARPIE Results by Subgroup Analysis Combined Endpoint
appropriate, consider bringing a witness, family member or
caregiver - Clopidogrel better than aspirin in stroke, PAD, AI; Aspirin better
- Alert hospital in MI
- Check glucose if possible
Indirect Comparison of Stroke Prevention Therapy
Immediate general assessment and stabilization
Therapy (vs. ASA) NNT Mean follow-up time years
- Assess ABCs, vital signs
- Provide oxygen if hypoxemic Aggrenox 33 2
- Obtain IV access and blood samples Plavix 121 1.91
10 min - Check glucose, treat if indicated
ED arrival
Ticlid 40 3
- Perform neurologic screening assessment Endpoint → stroke
- Activate stroke team
- Order emergent CT scan of brain
- Obtain 12-lead ECG Neuroprotection
- No clinical trials have yet demonstrated benefit for
neuroprotective agents
- IMAGES trial
Immediate neurologic assessment by stroke team or
- IV magnesium given within 24 hours of stroke onset
designee
25 min - 2589 patients were recruited
- Review patient history - There was no overall benefit although there was a possible
ED arrival - Establish symptom onset trend in patients with lacunar stroke
- Perform neurologic examination (NIH Stroke scale or
Canadian neurologic scale)
Hypertension and Secondary Prevention for Stroke

Stroke Unit Scare vs. Conventional Care Proven for Proven for
- Stroke units show to be better in outcome in 20 trials when it Primary Prevention Secondary Prevention
comes to death, dependency or in-hospital stay Beta-Blockers ACE-I +
Diuretics Diuretics
Thrombolysis Ca2+ Antagonist ARBs
- IV rtPA ACE-I
- The only FDA approved therapy for treatment of patients ARBs
with acute ischemic stroke
- For patients with acute ischemic stroke <3hours
- IA rtPA AntiHPN trials with Stroke Outcome
- Experimental
- Option for treatment for selected patients with major stroke Trials Year Drug Primary Secondary RR
<6 hours duration due to large vessel occlusion of the Prevention Prevention
middle cerebral artery HOPE 2000 Ramipril vs. X 22%
- Established as a treatment in acute ischemic stroke for patients Placebo
seen within 3 hours of stroke onset PROGRESS 2001 Perindopril X 43%
- The first evidence of benefit from RCTs was provided by the +
NINDS rt-PA stroke study published in 1995 Indapamide
- A meta-analysis of randomized studies has shown that t-PA vs. Placebo
reduces the chance of an unfavourable outcome with an odds LIFE 2002 Losartan X 25%
ratio of 0.66 (95% Cl 0.53 to 0.83) when given within 3 hours of vs. Atenolol
stroke onset MOSES 2005 Eprosartan X 25%
vs. *IDR
Thrombolysis in acute ischemic stroke: Nitrendipine
Controlled trials and clinical experience ONTARGET 2008 Teimisartan X
- rtPA better than placebo TRANSCEND Nitrendipine
combination
Thrombolysis
- Thrombolysis provide benefit only if there is persisting arterial New Treatment for Intracerebral Hemorrhage
occlusion, and there is persisting “ischemic penumbra” - Recombinant activated factor VIIa (rFVIIa)
- A series of careful PET studies has demonstrated that - Hemostatic agent approved for hemophilia (NovoSeven)
penumbral tissue may persist many hours after acute stroke - 3-hour time window
onset, and sometimes even beyond 10 hours - Decrease enlargement of the hematoma
- Improve survival and favourable clinical outcomes
- Potential thrombotic complications (arterial thromboembolic
events) – 7%
- FDA approval pending due to this safety issue
TREATMENT STRATEGIES
- Stroke unit: decrease morbidity & mortality
- Stroke team – mostly neurologists
- Hyperacute

Onset of stroke → 3hrs

Golden period ≤ 3hrs
- Acute: within the first 48hrs
- Prevention:

10% will develop recurrence

An average of 15hrs before pxs are brought to the hospital

75% will be given water in case of acute stroke
- This is bad because 60% of acute stroke has
dysphagia & which may develop aspiration pneumonia

Massage – given next after water

Thrombolytics
- Recombinant tPA: the only FDA approved tx for acute ischemic
stroke
- Must be given within 3hrs (IV)
- > 3hrs - ≤ 6hrs (intraarterial catheterization)
- Disadvatages:

Time: should be given within a specified time

Cost: 1 vial = 48T

6% has a complication of bleed in the brain: “hemorrhagic
conversion from infarct”

Neuroprotectants (5H): protects from the ff

- Hypotension
- Hypoglycemia
- Hypeglycemia
- Hypernatremia
- Hyperpyrexia

Mainstay of Tx: ANTI-PLATELET DRUGS

- Aspirin
- Aggrinox: Dypyrimadole + aspirin
- Clopidogrel
- Cilostazol

**You can give Mannitol to decrease ICP

**Warfarin, heparin
**Rehabilitation

Transcribed by Denise Zaballero & Fred Monteverde

Additional Notes from: Abi Uy
Cecile Ong
Ria Yulo
Joana Nayal
Angge Munoz
Mitzel Mata
Brian Yu

Thanks for the pictures: JB Villegas