STROKE SYMPOSIUM

Guide Questions:
1. What arteries supply the major parts of the brain?
Blood is supplied to the brain, face, and scalp via two major sets of vessels: the right and left
common carotid arteries and the right and left vertebral arteries.
The common carotid arteries have two divisions. The external carotid arteries supply the face and
scalp with blood. The internal carotid arteries supply blood to the anterior three-fifths of
cerebrum, except for parts of the temporal and occipital lobes. The vertebrobasilar arteries supply
the posterior two-fifths of the cerebrum, part of the cerebellum, and the brain stem.
Circle of Willis: At the base of the brain, the carotid and vertebrobasilar arteries form a circle of
communicating arteries known as the Circle of Willis. From this circle, other arteriesthe
anterior cerebral artery (ACA), the middle cerebral artery (MCA), the posterior cerebral artery
(PCA)arise and travel to all parts of the brain. Posterior Inferior Cerebellar Arteries (PICA),
which branch from the vertebral arteries, is also present.
Because the carotid and vertebrobasilar arteries form a circle, if one of the main arteries is
occluded, the distal smaller arteries that it supplies can receive blood from the other arteries
(collateral circulation).
Anterior Cerebral Artery: The anterior cerebral artery extends upward and forward from the
internal carotid artery. It supplies the frontal lobes, the parts of the brain that control logical
thought, personality, and voluntary movement, especially of the legs.
Middle Cerebral Artery: The middle cerebral artery is the largest branch of the internal carotid.
The artery supplies a portion of the frontal lobe and the lateral surface of the temporal and
parietal lobes, including the primary motor and sensory areas of the face, throat, hand and arm,
and in the dominant hemisphere, the areas for speech.
Posterior Cerebral Artery: The posterior cerebral arteries stem in most individuals from the
basilar artery but sometimes originate from the ipsilateral internal carotid artery. The posterior
arteries supply the temporal and occipital lobes of the left cerebral hemisphere and the right
hemisphere.
Lenticulostriate Arteries: Small, deep penetrating arteries known as the lenticulostriate arteries
branch from the middle cerebral artery.
2. What happens when the blood supply to a certain part is blocked?

Cellular Changes: Injury from ischemic stroke is the result of a complex series of cellular
metabolic events that occur rapidly after the interruption of nutrient blood flow to a region of the
brain. The duration, severity, and location of focal cerebral ischemia determine the extent of
brain function and thus the severity of stroke.

Inadequate Energy Supply: In ischemic brain tissue, the membrane that surrounds each affected
neuron becomes leaky, and the cell loses potassium and adenosine triphosphate (ATP), the
tissues medium for energy exchange.

Energy failure is not the immediate cause of cell death; however, since all brain cells tolerate loss
of ATP for several minutes. In humans, it appears that 5 to 10 minutes of complete occlusion is
required for irreversible brain damage. In actuality, most strokes do not involve a complete

occlusion of blood flow, but even a partial occlusion, if allowed to continue for a sufficient time,
may produce irreversible brain damage.
Once blood flow to cerebral neurons diminishes, one or more branching mechanisms may
independently lead to brain cell death. These mechanisms may involve deterioration of ion
gradients or the effects of anaerobic metabolism.
With respect to the latter, anaerobic glycotic pathways are utilized in the affected region to
compensate for the loss of oxygen and provide a source of energy. However, this produces
damaging byproducts, including lactic acid and hydrogen ions, which accumulate in tissue in
proportion to the carbohydrate stores present at the outset of ischemia. Toxicity of hydrogen ions,
especially their ability to facilitate ferrous-iron-mediated free-radical mechanisms, appears to
irreversibly affect neuronal integrity.
Deterioration of Ion Gradients
Inadequate energy supply leads to deterioration of ion gradients. Anoxic depolarization
(equilibration of intracellular and extracellular ions) causes potassium to leave the cell and
sodium, chloride, and calcium ions to enter. It also stimulates the massive release of the amino
acids glutamate and aspartate, excitatory neurotransmitters in the brain. Glutamate further
activates sodium and calcium ion channels in the neuron membrane.
As sodium and calcium ions rapidly accumulate within the cells, accompanied by an inflow of
water, cytotoxic edema causes rapid swelling of neurons and glia.
Activation of calcium channels results in further influx of calcium into the cell. One of the most
intensely studied calcium channels is the N-methyl-D aspartate (NMDA) channel.
Consequences of Calcium Overload
Entry of calcium through the NMDA (and similar channels) can be devastating. First, attempts to
get rid of the excess calcium use up already scarce supplies of ATP. Second, excessive calcium
influx causes the disordered activation of a wide range of enzyme systems (proteases, lipases,
and nucleases). These enzymes and their metabolic products, such as oxygen free radicals,
damage cell membranes, genetic material, and structural proteins in the neurons, ultimately
leading to cell death. This sequence of events has been termed excitotoxicity because of the
pivotal role of excitatory amino acids such as glutamate.
The Ischemic Penumbra: Within the ischemic cerebrovascular bed, there are two major zones of
injury: the core ischemic zone and the ischemic penumbra (the term generally used to define
ischemic but still viable cerebral tissue).

In the core zone, which is an area of severe ischemia (blood flow below 10% to 25%), the loss of
oxygen and glucose results in rapid depletion of energy stores. Severe ischemia can result in
necrosis of neurons and also of supporting cellular elements (glial cells) within the severely
ischemic area.
Brain cells within the penumbra, a rim of mild to moderately ischemic tissue lying between
tissue that is normally perfused and the area in which infarction is evolving, may remain viable
for several hours. That is because the penumbral zone is supplied with blood by collateral
arteries anastomosing with branches of the occluded vascular tree. However, even cells in this
region will die if reperfusion is not established during the early hours since collateral circulation
is inadequate to maintain the neuronal demand for oxygen and glucose indefinitely.
The penumbra is where pharmacologic interventions are most likely to be effective. However, it
may also be possible to salvage cells within the severely ischemic core zone. Although severe
ischemia kills selectively vulnerable neurons, glial cells may be spared if blood flow is restored
early. Therefore, timely recanalization of the occluded vessel should theoretically restore
perfusion in both the penumbra and in the severely ischemic core. Partial recanalization should
markedly reduce the size of the penumbra as well.
Cerebral Infarction/Effects of Edema: Following a stroke, blood flow to the region on the brain
is interrupted due to a thrombus or embolus. The lack of blood flow results in severe damage
(infarct) to some of the brain tissue. The infarcted tissue caused fluids to accumulate (edema) and
result in swelling. The center of the brain is shifted to the unaffected area due to swelling from
the affected area.
The rigid container of the cranium allows limited room for expansion, and any condition that
causes an increase in volume of one or more structures within this vault will cause an increase in
intracranial pressure (ICP) or will shift one compartment of the brain, thereby compressing
others. As the pressure increases, the brain shifts or is distorted, compressing neurons, nerve
tracts, and cerebral arteries. A sustained increase in pressure causes persistent ischemia,
irreversible damage to brain cells, and potentially death.
Edema Formation: Ischemic brain edema is a combination of two major types of edema:
cytotoxic (cellular) and vasogenic. Cytotoxic edema evolves over minutes to hours and may be
reversible, while the vasogenic phase occurs over hours to days, and is considered an irreversibly
damaging process.
Cytotoxic edema is characterized by swelling of all the cellular elements of the brain (shown). In
the presence of acute cerebral ischemia, neurons, glia (indicated by astrocytes), and endothelial
cells swell within minutes of hypoxia due to failure of ATP-dependent ion (sodium and calcium)
transport. With the rapid accumulation of sodium within cells, water follows to maintain osmotic

equilibrium. Increased intracellular calcium activates phospholipases and the release of

arachidonic acid, leading to the release of oxygen-derived free radicals and infarction.
Vasogenic edema (not shown) is characterized by an increase in extracellular fluid volume due to
increased permeability of brain capillary endothelial cells to macromolecular serum proteins
(e.g., albumin). Normally, the entry of plasma protein-containing fluid into the extracellular
space is limited by tight endothelial cell junctions, but in the presence of massive injury, there is
increased permeability of brain capillary endothelial cells to large molecules. Vasogenic edema
can displace the brain hemisphere and, when severe, lead to cerebral herniation.
Acute hypoxia initially causes cytotoxic edema, followed within the next hours to days by the
development of vasogenic edema as infarction develops. The delayed onset of vasogenic edema
suggests that time is needed for the defects in endothelial cell function and permeability to
develop.
3. What function/s of the brain is/are lost?
The brain is an extremely complex organ that controls various body functions. If a stroke occurs
and blood flow can't reach the region that controls a particular body function that part of the
body won't work as it should. The effects of a stroke depend primarily on the location of the
obstruction and the extent of brain tissue affected.
Right Brain: The effects of a stroke depend on several factors, including the location of the
obstruction and how much brain tissue is affected. However, because one side of the brain
controls the opposite side of the body, a stroke affecting one side will result in neurological
complications on the side of the body it affects. For example, if stroke occurs in the brain's right
side, the left side of the body (and the left side of the face) will be affected, which could produce
any or all of the following: paralysis on the left side of the body, vision problems, quick,
inquisitive behavioral style, and memory loss
Left Brain: If stroke occurs in the left side of the brain, the right side of the body will be
affected, producing some or all of the following: paralysis on the right side of the body,
speech/language problems, slow and cautious behavioral style, and memory loss.
Brain Stem: When stroke occurs in the brain stem, depending on the severity of the injury, it can
affect both sides of the body and may leave someone in a locked-in state. When a locked-in
state occurs, the patient is generally unable to speak or achieve any movement below the neck.
Anterior Cerebral Artery (ACA) Occlusion

Weakness of foot and leg

Sensory loss of foot and leg
Ataxia

Incontinence
Slowness and lack of spontaneity
Occlusion proximal to ACOM is well tolerated
Distal Occlusion results in
o Weakness and cortical sensory loss in contralateral lower limb
o Incontinence
Bilateral ACA
o akinetic mutism
o Deterioration in conscious level

Middle Cerebral Artery (MCA) Occlusion

Contralateral lower face weakness

Contralateral hemiplegia
Contralateral hemianesthesia
Ataxia
Speech impairments (usually the left brain)
Perceptual deficits (usually the right brain)
Visual deficits

Posterior Cerebral Artery (PCA) Occlusion

Midbrain syndrome (Webers Syndrome)

o Third nerve palsy
o Contralateral hemiplegia
Thalamic Syndromes
o Chorea or hemiballismus
o Hemisensory disturbances
Visual field deficits (macular sparing)
Visual hallucinations
Memory problems

Brainstem Stroke

Double vision
Face weakness and sensation weakness
Taste disturbances
Hearing loss
Difficulties in balancing and dizziness
Difficulties in swallowing
Blood pressure and respiration dysfunction

Basilar Artery Occlusion

Complete Basilar Syndrome
o Impairment of consciousness
o Bilateral Sensory and Motor dysfunction
o Cerebellar signs
o Cranial nerve signs indicative of site
Top of Basilar Occlusion
o Lateral midbrain, thalamic, occipital and medial lobe infarction
o Hemiballismus
o Visual loss
o Pupillary abnormalities
o Gaze palsies
o Impairment of consciousness
Occlusion of Paramedian Perforating Vessels
o Locked-In Syndrome
Quadriplegia
Inability to speak
Intact cognition
May retain proprioception and sensation
Lack coordination between breathing and voice
Anterior Inferior Cerebellar Artery Syndrome (Lateral Pontine Syndrome)
Cerebellum
o Ipsilateral limb ataxia
Brainstem
o Ipsilateral Horners syndrome
o Ipsilateral sensory loss
o Ipsilateral facial weakness
o Contralateral sensory loss (pain/temperature)

Posterior Inferior Cerebellar Artery Syndrome (Lateral Medullary/Wallenberg Syndrome)

Cerebellum
o Dysarthria
o Ipsilateral limb ataxia
o Vertigo
o Nystagmus
Brainstem
o Ipsilateral Horners syndrome
o Ipsilateral sensory loss

o Ipsilateral pharyngeal and layngeal paralysis

o Contralateral sensory loss (pain/temperature)
4. How will the lost of blood supply be clinically manifested? (Clinical history and physical
examination, neurologic examination findings)
Initially, the doctor takes a medical history from the patient if he/she is alert or others familiar
with the patient if they are available, and performs a physical examination. A neurologist will
often assist in the diagnosis and management of stroke patients. Just because a person has slurred
speech or weakness on one side of the body does not necessarily signal the occurrence of a
stroke. There are many other possibilities that can be responsible for these symptoms. Other
conditions that can mimic a stroke include: brain tumors, a brain abscess (a collection of pus in
the brain caused by bacteria or a fungus), migraine headache, bleeding in the brain either
spontaneously or from trauma, meningitis or encephalitis, an overdose of certain medications, or
an imbalance of sodium, calcium, or glucose in the body can also cause changes in the nervous
system that can mimic a stroke.
In the acute stroke evaluation, many things will occur at the same time. As the physician is
taking the history and performing the physical examination, nursing staff will begin monitoring
the patient's vital signs, getting blood tests, and performing an electrocardiogram (EKG or ECG).
Part of the physical examination that is becoming standardized is the use of a stroke scale. There
is a narrow time frame to intervene in an acute stroke with medications to reverse the loss of
blood supply to part of the brain. The patient needs to be appropriately evaluated and stabilized
before any clot-busting drugs can be potentially utilized.
Medical/clinical history:
Time of onset of symptoms. This is very important in determining if patient is a candidate
for some new therapies that are most effective when used within a certain timeframe.
Stroke Warning Signs: Stroke should be suspected when any of the following symptoms
occur. Even if they are temporary - lasting less than an hour - they must be taken very
seriously.
o Sudden numbness or weakness of the face, arm or leg, especially on one side of the
body.
o Sudden confusion, trouble speaking or understanding.
o Sudden trouble seeing in one or both eyes.
o Sudden trouble walking, dizziness, loss of balance or coordination.
o Sudden, severe headache with no known cause.

 Medications the patient is taking. Certain medications can thicken the blood so it clots
more (a problem in ischemic strokes), while others have the opposite effect (which can
exacerbate a hemorraghic stroke).
Patients medical history in order to determine if he/she is affected by the following
common risk factors for stroke:
Manageable or Preventable Risk Factors:

Diet and Nutrition

Physical Inactivity
Smoking
Substance Abuse
Alcohol Consumption
Certain medical conditions, including:
o Abnormal blood vessel connections (arteriovenous malformations and arteriovenous
fistulas)
o Cerebral aneurysms (unruptured)
o Cholesterol level (high levels of bad and/or low levels of good cholesterol)
o Diabetes
o Hardening of the arteries (atherosclerosis/arteriosclerosis)
o Heart (cardiovascular) disease
o High blood pressure (hypertension)
o Obesity
o Transient ischemic attacks (TIAs)

Unalterable Risk Factors

Age
Ethnicity
Heredity/family history of stroke
Prior stroke
Gender

Physical examination
There are several tests/scales for quickly assessing a patients responses in key functional areas
such as the Glasgow Coma Scale (GCS), Barthel Index, Modified Rankin Scale (MRS), NIH
Stroke Scale (NIHSS) and others.
Diagnostic tests to determine the type of stroke and its location.
Computed Axial Tomography (CT scan, CAT scan): An initial CT scan can quickly rule
out hemorrhage or a brain tumor causing stroke-like symptoms. It may even show areas
of the brain that are in danger of dying but still salvageable.

Magnetic Resonance Imaging (MRI scan, MR scan): MRI can be used to diagnose
ischemic stroke, hemorrhagic stroke, and other problems involving the brain, brainstem,
and spinal cord.
Carotid Ultrasound (Carotid duplex, Carotid doppler): It can show if the patients carotid
artery is narrowed or blocked by atherosclerosis.
Cerebral Angiography: (Cerebral arteriogram) X-ray images show any abnormalities of
the blood vessels, including narrowing, blockage or malformations.
Computed Tomographic Angiography: (CT-angiography): It can also catch aneurysms
that cerebral angiography may miss.
Magnetic Resonance Angiography (MRA): It can help determine the extent of damage.
5. Can the brain recover after a stroke? Through what mechanisms will brain cells
regenerate?
Following stroke, the neuronal circuitries that support cognitive and sensory-motor functions are
lost due to neuronal death and dysfunction. Still, over a 3 to 6 months period, stroke patients
regain some neurological functions, albeit a majority remains disabled to a significant degree. In
man, recovery processes primarily engage ipsilateral brain regions, and if damage is severe,
contralateral brain areas are involved as well.
From experimental studies it is evident that within hours after ischemia regenerative mechanisms
are activated in the brain and develop along with tissue demise. In later stages, tissue edema is
resolved, inflammation ceases, injured neurons are partially repaired, neuronal pathways
activated, and glia cells and neuroblasts migrate into peri-infarct areas. In surviving tissue,
growth-promoting as well as growth-inhibitory genes are activated. Still, recovery is limited
because of the restricted capacity for anatomical reorganization of the brain. During the first four
weeks of recovery after experimental stroke axonal sprouting and spine growth is stimulated and
some neuroblasts resume a neuronal phenotype, accompanied by angiogenesis in the peri-infarct
areas. The established novel neural networks are stabilized by an experience-driven process.
Hence, spontaneous functional recovery appears to involve four distinct phases of cellular
response: (1) reactivation of existing neural pathways, (2) activation of alternative existing
pathways (3) formation of new connections by axonal sprouting or neurogenesis and (4)
consolidation of new neural networks.
During recent years novel therapies that enhance recovery of function during the first month
following stroke have been proposed, including measures to activate brain plasticity, attenuate
axonal growth inhibition, and cortical stimulation and physical therapy. In the experimental
setting, changing housing environment or training is a strong stimulus of recovery of function.
Housing injured animals in an enriched environment (EE), starting 2-5 days after stroke
stimulate functional recovery, activates specific gene programs, enhances dendritic arborization
and spine density on the contralateral pyramidal neurons, and activates cell genesis. The relative

importance of the different mechanisms for recovery of function will be studied within the frame
of the application.
Certain motor skills recover within a few days after the lesion, suggesting that for such rapid
recovery of neuronal function the unmasking or activation of silent pathways or silent synapses
must be considered. At the cellular level, adaptive changes in neuronal morphology (axonal
growth, dendritic arborization, and spine remodeling) are seen in the contralateral cortex. These
most certainly involve recovery of spine function, since ischemia causes spine collapse and actin
aggregation. Axonal outgrowth is limited by growth-inhibitors such as Nogo A. This inhibition
can be overcome by Nogo A antibodies or by blocking peptides or mutations. Intrathecal delivery
of Nogo A antibody for one month, starting as late as seven days after ischemia, dramatically
enhances functional recovery after stroke, and is associated with increased sprouting of corticorubral projections. The contribution of the individual hemispheres for the recovery process will
be explored within this project.
Cell genesis in neurogenic zones is stimulated following stroke. Neuroblasts are continuously
generated up to 4 month after injury, providing a pool of cells that potentially can develop into
mature neurons. Neurogenesis is depressed by inflammation occurring during recovery after
stroke. Neuronal, glial, and endothelial progenitor cells support plasticity of surviving neurons
by releasing growth factors, or providing cellular components. In addition, angiogenesis is
prominent and may enhance vascularization of the surviving penumbra area as well as
stimulating neurogenesis.
6. Name the three most important lessons you learned from the symposium?
Stroke is the 2nd most common cause of death and is a leading cause of adult disability.
Healthcare costs associated with the treatment of stroke are high and burdensome especially
in lower income countries such as our country. Keeping our population healthy is one of the
most effective ways in reducing the healthcare burden of our government and its people.
Early action is the key and we need to identify the symptoms of a stroke and the high risk
population so that when we see signs of stroke act FAST and call emergency services (e.g.
911) immediately! Every minute counts. The longer blood flow is cut off to the brain, the
greater the damage. The window of opportunity to start treating stroke patients is three hours.
But a person needs to be at the hospital within 60 minutes of having a stroke to be evaluated
and receive treatment.
Well-staffed and organized stroke units have been shown to reduce death, dependency and
length of inpatient stay after stroke. All healthcare workers in the multidisciplinary team have
a contribution to make to ensure the team works towards agreed goals in a consistent and
supportive manner.
The physician has the major responsibility to provide acute efficient stroke management
because time is brain and early medical treatment can reduce the risk of death or disability

from stroke. Also, he/she must also be continuously learning on the updates on the
management of stroke.
Nurses not only have a care management role, but also take responsibility for promoting
recovery and preventing complications. Their role is central to stroke rehabilitation and
nursing intervention is significant in terms of improving outcomes for stroke survivors and
their carers, and reducing the costs associated with inpatient stay, and promotes survivors
return towards independent living. This role is diffuse and complex and has been described as
comprising three main domains of care - provider, facilitator and manager.
The Stroke Society of the Philippines (SSP) advocacy of increasing public awareness about
stroke is very important because there is still poor knowledge and misconceptions regarding
stroke. Many people do not recognize the common symptoms of stroke - weakness on one
side of the body, difficulty speaking, drooping on one side of the face, difficulty walking and this can cause a delay in receiving treatment. It turns out that the time that lapses from
the onset of symptoms to the treatment for stroke is a huge factor in determining how
significant its effect will be. The time between a stroke patients arrival in the emergency
department and the time they receive treatment with tPA - a medication that dissolves blood
clots - is referred to as door-to-needle time.