STROKE
PATHOPHYSIOLOGY
● Sudden cessation of cerebral blood flow
and oxygenglucose deprivation sets in
motion a series of pathological
events.Within minutes neurons die
PATHOPHYSIOLO within the ischemic core tissue, while
the majority of neurons in the
GY surrounding penumbra survive for a
(SULLIVAN) slightly longer time. Cell survival
depends largely on the severity and the
duration of the ischemic episode. For
cells to survive, 20% to 25% of regular
blood flow is required. Without timely
reperfusion, cells in the penumbra will
die, neuronal activity ceases, and the
infarct expands. Ischemia triggers a
number of damaging cellular events,
termed ischemic cascade.
● The release of excess
neurotransmitters (e.g., glutamate and
aspartate) produces a progressive
disturbance of energy metabolism and
anoxic depolarization. This results in
an inability of brain cells to
PATHOPHYSIOLO produce energy, particularly
adenosine triphosphate (ATP). This
GY is followed by excess influx of calcium
ions and pump failure of the neuronal
membrane. Excess calcium reacts
with intracellular phospholipids to
form free radicals.
● Calcium influx also stimulates the
release of nitric oxide and
cytokines. Both mechanisms further
damage brain cells. Research efforts
are ongoing toward development of
drugs that might promote
● Ischemic strokes produce cerebral edema, an
accumulation of fluids within the brain that begins
within minutes of the insult and reaches a
maximum by 3 to 4 days. It is the result of tissue
necrosis and widespread rupture of cell
membranes with movement of fluid from the
PATHOPHYSIOLO blood into brain tissues. The swelling gradually
subsides and generally disappears by 2 to 3
GY weeks. Significant edema can elevate intracranial
pressures, leading to intracranial hypertension
and neurological deterioration associated with
contralateral and caudal shifts of brain structures
(brainstem herniation). Clinical signs of
elevating intracranial pressure (ICP) include
decreasing level of consciousness (stupor and
coma), widened pulse pressure, increased heart
rate, irregular respirations (Cheyne-Stokes
respirations), vomiting, unreacting pupils (cranial
nerve [CN] III signs), and papilledema. Cerebral
ISCHEMIC
Ischemic stroke
1. Thrombosis
STROKE
According to DeLisa, thrombosis of the large extra- and
intracranial
vessels due to atherosclerotic cerebrovascular disease
PATHOPHYSIOLOGY accounts to
approximately 30-40%% of all stroke cases.
Classification of Atherosclerotic plaque formation occurs frequently at the
large vessels of
stroke according to the neck and at the major vascular branching sites at the
its origin base of the
brain, including the common carotid and vertebrobasilar
arteries. Sudden
occlusion to these vessels, without a good collateral
circulation, usually
results in a large brain infarction.
Atherosclerotic strokes, unlike embolic strokes, starts subtly
and affected
individuals may experience clinical deficits when they walk or
get out of
bed, which can worsen hours or sometimes days after onset,
followed by
2. Embolism
ISCHEMIC
According to DeLisa, embolism is responsible for about
30% of all stroke
cases.
STROKE
According to Braddom, majority of embolic strokes
have a cardiac origin.
Thrombus formation within the cardiac chambers is
caused by structural
PATHOPHYSIOLOGY or mechanical changes within the heart.
Cerebral emboli lodge within the arterial branches of
the major arteries,
causing an abrupt onset due to sudden loss of arterial
blood flow to a
focal part of the brain.
Many emboli are friable and can break into smaller
pieces as it travels
through the cerebral circulation, which can cause
multiple smaller infarcts affecting the distal branches of
a main arterial vessel.
Reperfusion of an occluded vessel can occur if the
embolus undergoes
lysis and fragmentation, causing the initial deficits to
change and fade rapidly.
the large
vessels that perfuse subcortical structures:
ISCHEMIC
Pure motor lacunar stroke: involves the posterior limb of
the
internal capsule, pons, and pyramid.
STROKE
Pure sensory lacunar stroke: involves the ventrolateral
thalamus
or thalamocortical projections.
Dysarthrial/Clumsy hand syndrome: involvement of the
base of
PATHOPHYSIOLOGY the pons, genu of the anterior limb, or the internal capsule.
Ataxic hemiparesis: involvement of the pons, genu of the
internal
capsule, corona radiata, or cerebellum.
Sensory/ motor stroke: involves the junction of the internal
capsule
and thalamus
Dystonial/Involuntary movements: choreoathetosis with
lacunar
infarction of the putamen or globuspallidus; hemiballismus
with
involvement of the subthalamic nucleus.
Deficits in consciousness, language, or visual fields are not
seen in
lacunar strokes because the higher cortical areas are
preserved.
Small lacunar infarcts may produce major neurologic
deficits if they occur
in a key region but they generally cause minor symptoms
than large
Hemorrhagic stroke
1. Intracerebral hemorrhage
Intracerebral hemorrhage accounts for
approximately 11% of all stroke
PATHOPHYSIOLOGY cases according to DeLisa.
According to Braddom, nearly one half of all ICHs
occur within the
putamen and the cerebral white matter.
The most common cause of cerebral hemorrhage is
hypertension.
Intracerebral hypertensive hemorrhage most
commonly occurs at the site of small, deep,
penetrating arteries. It is thought that hemorrhage
occurs through rupture of microaneurysms or the
Charcot-Bouchard aneurysms that develop in these
vessels in hypertensive patients. And according to
DeLisa, the majority of these lesions occur in the
putamen or thalamus, and in about 10% of patients,
2. Subarachnoid hemorrhage
About 7% of all stroke cases would be a subarachnoid
hemorrhage
according to DeLisa.
Subarachnoid hemorrhage is a lesion that occurs when
an arterial
Pathophysiolog aneurysm ruptures at the base of the brain with bleeding
in the
y subarachnoid space. According to Braddom, SAH is most
commonly
caused by a rupture of a saccular aneurysm or an
arteriovenous
malformation (AVM).
Saccular aneurysms develop from a congenital defect in
an arterial wall
followed by progressive degeneration of the adventitia,
causing the
ballooning or outpouching of the vessel. These types of
aneurysm often
rupture during the 5th or 6th decade of life. When rupture
occurs,
extravasation of blood into the subarachnoid space is
irritating to the dura
● Transient Ischemic Attack (TIA)
-According to the American Stroke Association, it is a brief episode of
neurologic
-dysfunction caused by focal brain or retinal ischemia, with clinical
symptoms typically
-lasting less than an hour, and without the evidence of acute infarction,
as determined by
PATHOPHYSIOLO -cranial imaging.
-Brief episodes of focal neurologic deficits occurring up to 15-30 minutes
GY
and disappears completely in 24 hours, as defined by Abiog.
- It is the sudden decrease of blood supply to specific portions of the
brain.
- According to DeLisa, ~15% of all strokes are preceded by a TIA, with the
greatest risk of occurrence within 90 days.
-Reversible Ischemic Neurological Deficit (RIND) Follows the same
course but with residual deficit after 24 hours
- Returns to normal after 2 weeks
● Transient Ischemic Attack-Irreversible recovery (TIA-IR)
-After 2 weeks, focal neurologic deficit persists.
● Stroke-in-evolution
- Progressing stroke with deterioration that can result to:
o Completed stroke
o TIA-RIND
● Completed stroke
CLINICAL
MANIFESTATIONS
Middle Cerebra Artery (MCA)
STROKE Syndromes
SYNDROMES Anterior Cerebral Artery (ACA)
AND THEIR Syndromes
CLINICAL Internal Carotid Artery (ICA)
MANIFESTATION Syndromes
Posterior Cerebral Artery (PCA)
Syndromes
Basilar Artery Syndromes
Vertebral Artery Syndromes
MIDDLE CEREBRAL ARTERY (MCA) SYNDROMES
● MCA supply the part of the lateral side of frontal
lobe, lateral parietal lobe, and temporal lobe
- 1. Primary Motor Cortex= Contralateral
Hemiplegia more on Face and U.
Extremities than L. Extremities.
- 2. Primary Somatosensory Cortex=
Contralateral Sensory loss
(Hemianesthesia) more on Face and UE
than LE.
- 3. Frontal Eyefields = Ipsilateral Gaze
Deviation/ Preference
- 4. Wernickes Area= Wernicke’s Aphasia
- 5. Brocas Area= Brocas Aphasia
- 6. Apraxia – Ideomotor and Ideational
Anterior Cerebral Artery (ACA)
Syndrome
● Supplies primarily the medial frontal lobe and
medial parietal lobe and basal ganglia.
- 1. Primary Motor Cortex and
Primary Somatosensory Cortex =
Contralateral Hemiplegia more
on Lower extremity than
Upper Extremity and Face.
- 2. Paracentral Lobule= Urinary
Incontinence and Fecal
Incontinence
- 3. Prefrontal Cortex and Ant.
Cingulate Cortex= Abulia and
Posterior Cerebral (PCA)
Syndrome
- It supplies the midbrain,
occipital lobe, thalamus
Occipital lobe:
1. Primary Visual Cortex and Association
Cortex= Contralateral
Homonymous Hemianopia, Alexia
without Agraphia, Anomia
Midbrain:
2. Weber Syndrome- ipsilateral third
nerve palsy and contralateral
hemiplegia
3. CLAUDE SYNDROME= Ipsilateral
third nerve palsy, contralateral ataxia
4. Benedict Syndrome- Combination of
Internal Carotid Artery (ICA)
Syndromes
● Feeds the ACA and MCA.
● Take note that PCA also
comes to ICA besides
coming from vertebral
artery
● Any lesion in ICA=
decrease blood flow to
ACA,MCA, and some PCA=
ACA, MCA, AND SOME PCA
SYMPTOMS
BASILAR ARTERY SYNDROMES
● Basilar artery supplies the medial and
lateral pons and the superior, inferior,
anterior part of Cerebellum.
- 1. Medial Pons
CNVI nucleus= Ipsilateral CN VI
palsy
Medial longtitudinal fasciculus=
internuclear opthalmoplegia
Paramedian Pontine Reticular
Formation= Contralateral gaze
deviation
Medial Meniscus= loss of
sensation in Contralateral side
Cortico Spinal Tract=
Contralateral Hemiplegia
2. Lateral pons
● Middle cerebellar Peduncle= Ipsilateral ataxia
● Vestibular and Cochlear nuclei= loss of equilibrium
(Vertigo), Vertigo ,nausea vomiting, Nystagmus.
Deafness and Tinnitus.
● Descending sympathetic fibers = Horner’s
Syndrome, anhidrosis, constriction/miosis of
Pupil
● Motor nuclei of Trigeminal Nerve and trigeminal tract=
Less effective muscles of mastication and
Ipsilateral loss of sensation from the face.
● Spinal Thalamic Tract= Contralateral loss of
3. Cerebellum
Ataxia, loss of coordination,
dysmetria
DIFFERENTIAL
DIAGNOSIS
● Bell’s Palsy
● Guillain-Barre Syndrome
● Poliomyelitis
Thank
you!
