Cerebrovascular Accident

(Stroke)

JACQUELYN ARAO
I.Definition of Terms:

 Cerebrovascular Accident
- Also know as stroke and brain attacks
-is a sudden loss of neurological function
caused by an interruption of the blood flow to
the brain
I. Definition of terms

-It is a non-traumatic brain injury caused by

occlusion or rupture of cerebral blood vessel
that results in sudden neurological deficit
characterized by loss of motor control.
I. Definition of Terms

 Aneurysm

-It is a localized dilatation or bulging of the

blood vessels especially arteries
- It promotes rupture of the vessel as it
continues to bulge.
I. Definition of Terms

APOPLEXY – sudden strike of paralysis,

dumbness or fainting, from which victim is
frequently failed to recover
o Atherosclerosis

-Formation of multiple plaques within the

blood vessels.
I. Definition of Terms

 Embolus

- an object that migrates from one part of the

body to causes blockage or occlusion to
another part of the body.
I. Definition of terms

 Hematocrit

-Also know as Packed Cell Volume (PCV) or

Erythrocyte Volume Fraction (EVF)
-is the proportion of the blood volume, which
is occupied by red blood cell.
I. Definition of Terms

 Hemorrhage

-Is the loss of blood at the circulatory system

or excessive presence of blood outside the
circulation
- Can be internally or externally.
I. Definition of Terms
 Hypertension
– Also referred to as high blood pressure (HTN or
HPN.)
– It is a medical condition in which the blood
pressure is chronically elevated
 Infarction
-A process of anoxic death of tissue due to loss of
blood supply because of occlusion or blockage of the
artery
I. Definition of Terms

 Ischemic
-Insufficient blood flow to an organ cause by
the blockage of the artery.
 Transient Ischemic Attack
-(Mini Stroke) Caused by changes in blood
supply in the brain produces same
manifestation as stroke within 24 hours.
I. Definition of Terms

 Thrombus

- Is the final product of the blood coagulation

step in hemostasis It is achieved via the
aggregation of platelets that form a platelet
plug. It is physiologic in injury but pathologic
in case of thrombosis
II. Epidemiology

 Stroke is the third leading cause of death.

 The most common cause of disability among
adults at the United States
 It is approximately 700,000 individuals was
affected each year.
II. Epidemiology

 About 500,000 are new strokes and 200,000

are recurrent strokes (Usually people older
than 65 y/o).
 In United States, in 1960’s 200 per 100,000
are affected by stroke and it was decreased
as it reached to late 1960’s –1970’s.
II. Epidemiology

 In1980’s the stroke is flattened because of

the improvement of cranial computed
tomography (CT) and Magnetic Resonance
imaging (MRI).
 According to age, 28% higher possibilities in
people older than 65 y/o than younger ones
II. Epidemiology

 According to sex, having an incidence of

stroke, Men are 19% higher rather than
women.
 According to race, Black Americans are more
prone rather that White Americans.
 Asian Countries are more prone having
stroke compared to United States. (Cause by
intracranial hemorrhage)
II. Epidemiology

Causes Percentage
Large vessel 32
occlusion/infarction
Embolism 32
Small vessel occlusion/ 18
lacunar
Intracerebral hemorrhage 11
Subarachnoid hemorrhage 7

Table 77-2 Causes of stroke (Delisa)

II. Epidemiology

 Most of the patients who die from acute

stroke succumb in the first 30 days.
 Survival in the first 30 days of new stroke
reported to be 70- 85% dependent on the
stroke type.
II. Epidemiology

 InIntracerebral Hemorrhage is only 20-50%

, cause death usually occur in first 3 days.
 In Cerebral infraction is 85%.
 After 30 days of survival, the death rate
declines.
III. Epidemiology

 Stroke is most commonly cause of chronic

disability.
 Through the survivors, 1/3 of them are
dependent on ADL, ambulation and speech.
II. Etiology

 A. Atherosclerosis
-Major contributory factor of Cerebrovascular
Accident.
-accumulation of lipids, fibrins, complex
carbohydrates and calcium deposit on the arterial
walls that leads to progressive narrowing of blood
vessels.
 Found in the bifurcations of MCA and origin of ICA.
II. Etiology

 B. Ischemic Strokes
-Results from a thrombus, embolism or
conditions that produce low systemic
perfusions pressures.
II. Etiology

 C. Cerebral Thrombosis
– Refers to the formation of development of
a blood clot within the arteries and their
branches.
– Moving thrombus is called embolus.
II. Etiology

 Thrombosis  Ischemia  Infarction

 IntraCerebral Hemorrhage
– Is cause by the ruptured of cerebral vessel
with subsequent bleeding to brain
Types of IntraCerebral Hemorrhage
II. Etiology

-PrimaryCEREBRAL Hemorrhage
-occurs in small blood vessels weakened
by atherosclerosis produces aneurysm.
-SUBARACHNOID hemorrhage
-hemorrhage occurs at the sub arachnid
space typically from a saccular or berry
aneurysm affecting primary vessels.
II. Etiology

 E. Artriovenous malformation
– Is a congenital defect that can cause
stroke.
-The arteries and veins are tortuous tangled
with interposing capillaries system.
III. Risk Factors of Stroke

 Hypertension- Is the most important risk

factors
– It is define as a blood pressure higher
than 160/95 mmHg.
– Among the survivors of stroke, 67% of
them have chronic hypertension
– It gives risk in cerebral infarction,
thrombotic, lacunars and hemorrhagic
stroke.
III. Risk Factors of Stroke

2. Heart disease
– Is an important risk factor for stroke
– Atrial fibrillation and valvular heart disease
increase the risk of cerebral infarction
because of presence of cerebral emboli.
III. Risk Factors of Stroke

3.Diabetes Mellitus
 Independent risk factor that doubles
the risk of stroke.
 It increases the risk of ischemic stroke
to three to six times.
 The prevalence of diabetes among
stroke survivors is 20%.
III. Risk Factors of Stroke

 4. Hyperlipidemia
– Poses only small additional risk for strokes
mainly for individuals younger at age of
55.
– Increase in blood viscosity, hematocrit and
serum fibrinogen have been implied the
risk factor of stroke.
Risk Factors of stroke

 Smoking
– It is an important factor for cardiovascular
disease but influence for stroke is not
cleared.
– The risk for heavy smokers (>40
cigarettes) is twice than light smokers (<10
cigarettes).
III. Risk Factors Of Stroke

- Some studies that smoking to an increased

risk of hemorrhagic stroke in addition to
ischemic cerebral infarction.
III. Risk factor of stroke

6. Transient Ischemic Attack

-Is another important risk factor.
- An About 10 % of individuals with TIA will
go on to have a major stroke within 90 days
and 5 % will have a major stroke within 2
days.
III. Risk Factors of stroke

7. Obesity
– Hypertension and diabetes mellitus are in
common in obese and strong influences
risk of stroke.
– Some studies says that weight loss has
positive influences on blood pressure and
diabetic control and also helps in reduction
of risk of strokes.
IV. Stroke Prevention

 Active promotions of lifestyle changes by

physicians have the best potential to
decrease the annual rate of new stroke
occurrence.
IV. Stroke Prevention

 To the individuals who have a stroke in the

past history additional intervention and
medication was given like:
-Antiplatelet therapy
- Anticoagulation
-Carotid Endarterectomy.
IV. Stroke Prevention

 Antiplatelet Therapy
-Aspirin is the most frequently prescribe
antiplatelet agent.
-Aspirin achieves a significant anti platelet
effect at fairly low serum concentrations.
IV. Stroke Prevention

 Anticoagulation

-The use of Warfarin anticoagulation for

primary stroke prevention in non-valvular
atrial fibrillation.
-Warfarin reduces relative stroke risk by
58%to 86%over that in control subjects.
IV. Stroke Prevention

 Carotid Endarterectomy
– Is a surgical procedure that use to correct
the carotid stenosis
– It is the removal of material inside the
artery.
PATHOPHYSIOLOGY

PRINCESS PUNO
CEREBRAL BLOOD FLOW (CBF)

 Controlled by auto-regulatory mechanism

that modulates a constant rate of blood flow
through the brain.
 These mechanisms provide homeostatic
balance.
CEREBRAL BLOOD FLOW (CBF)

 Normal: 50-60 ml/100g/min

 Reversible: 20ml/100g/min
 Irreversible: 10ml/100g/min
CEREBRAL BLOOD FLOW (CBF)

 Factors Affecting CBF:

 Chemical regulation of CBF occurs in response to
changes in blood concentration of CO2 or O2.
 Increase
or decrease blood pH
 Changes in blood viscosity or intracranial pressure (ICP)
– CEREBRAL EDEMA
 Changes in blood pressure produces minor alterations
of CBF
 EXCITOTOXICITY

 The pathological process by which nerve

cells are damaged and killed by glutamate
and similar substances.
 ISCHEMIC CASCADE

 Within seconds to minutes of the loss of

perfusion to a portion of the brain, an
ischemic cascade is unleashed.
CLASSIFICATIONS OF STROKE

• Ischemic
 Thrombus
 Embolism
 Lacunar

• Hemorrhagic
 Subarachnoid
 Intracerebral
 ISCHEMIC STROKE

 Thrombus
Due to Atherosclerotic Plaque Formation
Occurs frequently at major vascular branching
sites including COMMON CAROTID and
VERTEBROBASILAR ARTERIES.
Occurs often in the presence of chronic
hypertension.
 ISCHEMIC STROKE

 Embolism
Major Source of cerebral emboli is the
heart.
– Atrial fibrillation
– Most emboli lodge in the middle
cerebral artery distribution because
80% of the blood carried by the large
neck arteries flow through the middle
cerebral arteries.
 ISCHEMIC STROKE

Most Frequent Target:

– Superficial branches of cerebral and
cerebellar arteries.
ISCHEMIC STROKE
ISCHEMIC STROKE
 ISCHEMIC STROKE

 Lacunars Infarct
Lacunar infarcts occur as a result of an
occlusion of small, deep penetrating arteries
known as Lenticulostriate Arteries branch from
the MCA.
Occlusions of these vessels or penetrating
branches of the circle of Willis, including
vertebral or basilar arteries, are referred to as
lacunar strokes.
 ISCHEMIC STROKE

 Small arteriole becomes torturous and

develops subintimal dissection and micro-
aneuryms rendering the arteriole susceptible
to occlusion from micro-thrombi.
Fibrin Deposition
 HEMORRHAGIC STROKE

 Subarachnoid Hemorrhage
Bleeding that occurs between the Dura
and Pia Mater.
Commonly caused by:

3.ARTERIOVENOUS MALFORMATION
(AVM)
1.ANEURYSMS
 HEMORRHAGIC STROKE

2. AVM
• Tangled, dilated blood vessels in which arteries flow
directly into veins.
• Occur most often at the junction of cerebral arteries,
usually within the parenchyma of the frontal-parietal
region, frontal lobe, lateral cerebellum, or overlying
occipital lobe.
• Results to seizures.
HEMORRHAGIC STROKE

2. Aneurysms
• Focal dilations in the artery
• Found in the anterior region of the Circle of Willis,
particularly near branches of the Anterior Communicating
Artery, ICA, MCA and junctions of almost any branch site.
• Contributing factors include atherosclerosis and
hypertension.
 HEMORRHAGIC STROKE

 Intracerebral Hemorrhage
 Originates from deep penetrating vessels and causes
injury to the brain tissue by disrupting connecting
pathways and causing localized pressure injury.
 Bleeding in the surrounding brain tissue.
 Also caused by AVM and aneurysms.
OCCLUSIONS IN THE ARTERIES

• ANTERIOR CEREBRAL ARTERY (ACA)

 Firstof the two terminal branches of the internal carotid
artery (ICA). It supplies the medial aspect of the cerebral
hemispheres (frontal and parietal) and subcortical
structures, including basal ganglia.
 Proximal occlusion results to minimal defects since the
Anterior Communicating artery allows perfusion of the
proximal ant. cerebral artery.
 ACA occlusions are uncommon.
ACA
OCCLUSIONS IN THE ARTERIES
OCCLUSIONS IN THE ARTERIES

• INTERNAL CAROTID ARTERY (ICA)

 There is a complete occlusion if ICA produces massive
infarction in both MCA and ACA territories.
– Incomplete occlusions can produce mixture of MCA and
ACA symptoms.
 Extensivecerebral edema occurs and frequently leads
to coma and death.

ICA
OCCLUSIONS IN THE ARTERIES

• POSTERIOR CEREBRAL ARTERY (PCA)

 Two posterior arteries arise as terminal branches of the
basilar artery and each supplies corresponding occipital
and temporal lobes.
 Also supplies the brainstem, midbrain and posterior
diencephalons, including most of the thalamus.
 Occlusions proximal to the posterior communicating
artery (PICA) typically results in minimal deficits owing
to the collateral blood supply from the PICA.

PCA
OCCLUSIONS IN THE ARTERIES

• VERTEBROBASILAR ARTERY
Arise from the subclavian arteries and travel
into the brain along the medulla where they
merge at the inferior border of the pons to form
the basilar artery.
It supplies the pons, internal ear, and the
cerebellum.
The basilar artery terminates at the upper
border of the pons and gives rise to two PCA.
SIGN AND SYMPTOMS
COMPLICATION

MARIVIC CALINGA
DEFINITION OF TERMS

 DEEP VEIN THROMBOSIS(DVT)- is a blood clot

(thrombus) in a deep vein, usually in the legs.
 CARDIAC DECOMPENSATION- may refer to the
failure of the heart to maintain adequate blood
circulation, after long-standing (previously
compensated) vascular disease.
 PULMONARY ASPIRATION- the entry of secretions
or foreign material into the trachea and lungs
DEFINITION OF TERMS

 DYSPHAGIA- is the medical term for the symptom

of difficulty in swallowing
 HEMIPARESIS- is weakness on one side of the
body.
 ABULIA- refers to a lack of will or initiative. The
patient is unable to act or make decisions
independently. It may range in severity from subtle to
overwhelming
DEFINITION OF TERMS

 WEBER’S SYNDROME- (superior alternating

hemiplegia) is characterized by the presence of an
oculomotor nerve palsy and contralateral
hemiparesis or hemiplegia.
 MEDIAL MEDULLARY SYNDROME- also known as
inferior alternating syndrome, hyploglossal
alternating hemiplegia, or lower alternating
hemiplegia, is a set of clinical features resulting from
an infarct in the anterior spinal artery, which supplies
the medial part of the medulla oblongata.
DEFINITION OF TERMS

 LATERAL MEDULLARY SYNDROME- (also called

Wallenberg's syndrome and posterior inferior
cerebellar artery syndrome) is a disease in which the
patient has difficulty with swallowing or speaking or
both owing to one or more patches of dead tissue
(known as an infarct) caused by interrupted blood
supply to parts of the brain.
 MEDIAL PONTINE SYNDROME- results from
occlusion of paramedian branches of the basilar
artery.
 LATERAL PONTINE SYNDROME- It can be caused
by an interruption to the blood supply of the
anterior inferior cerebellar artery.
 COMPLETE BASILAR SYNDROME- The cause of
VD is atherosclerosis and vertebrobasilar
insufficiency in the brain caused by blockage
(occlusion).
SIGN AND SYMPTOMS

MARIVIC R. CALINGA
SIGN AND SYMPTOMS…

 Symptoms of stroke depend on the type and

which area of the brain is affected. Signs of
ischemic stroke usually occur suddenly, and
signs of hemorrhagic stroke usually develop
gradually. Symptoms include the following:
SIGN AND SYMPTOMS…

 Difficulty speaking or understanding speech

(aphasia)
 Difficulty walking
 Dizziness or lightheadedness (vertigo)
 Numbness, paralysis, or weakness, usually
on one side of the body
 Seizure (relatively rare)
 Severe headache with no known cause
 Sudden confusion
SIGN AND SYMPTOMS…

 Sudden decrease in the level of

consciousness
 Sudden loss of balance or coordination
 Sudden vision problems (e.g., blurry vision,
blindness in one eye)
 Vomiting
Clinical Manifestations of Anterior
Cerebral Syndrome

 The most common characteristic of ACA

syndrome is contralateral hemiparesis and
sensory loss with greater involvement of the
lower extremity because the somatotopic
organization of the medial aspect of the
cortex includes the functional area for the
extremity.
 Clinical Manifestations of Anterior
Cerebral Syndrome
Sign and Symptoms
Contralateral hemiparesis
involving mainly the LE
Contralateral hemisensory loss
involving mainly the LE
Urinary Incontinence
Problems with imitation and
bimanual tasks, apraxia
Structures involved
Primary Motor Area, medial
aspect of cortex, internal
capsule
Primary Motor Area, medial
aspect of cortex
Posteromedial aspect of superior
frontal gyrus
corpus callosum
 Clinical Manifestations of Anterior
Cerebral Syndrome

Abulia (akinetic mutism), Uncertain localization

slowness, delay, lack of
spontaneity, motor inaction

Contralateral grasp reflex, Uncertain localization

sucking reflex Can be
asymptomatic if circle of Willis
is competent
Clinical Manifestations of Middle
Cerebral Artery Syndrome

 The most common characteristic of MCA syndrome

are contralateral spastic hemiparesis and sensory
loss of the face, upper extremity, and lower
extremity, with the face and UE more involved than
the LE. Lesions of the parieto-occipital cortex of the
dominant hemisphere typically produced aphasia.
Lesions of the right parietal lobe of the nondominant
hemisphere typically produce perceptual deficits.
Homonymous hemianopsia is also a common
finding. The MCA is the most common site of
occlusion in stroke.
 Clinical Manifestations of Middle
Cerebral Artery Syndrome

Sign and Symptoms Structures Involved

Contralateral hemiparesis Primary motor cortex and
involving mainly the UE and internal capsule
face
Contra;ateral hemisensory loss Primary sensory cortex and
involving mainly the UE and internal capsule
face
Motor speech impairment: Wernicke’s cortical area
Wernicke’s or fluent aphasia (posterior portion of the
with impaired auditory temporal gyrus)
comprehension and fluent
speech with normal rate and
melody
 Clinical Manifestations of Middle
Cerebral Artery Syndrome

Global Aphasia: nonfluent speech Both third convolution and

with poor comprehension
Perceptual deficits: unilateral
neglect, depth perception, spatial
relations, agnosia
Limb-kinetic apraxia
Contralateral homonymous
hemianopsia
Loss of conjugate gaze to the
opposite side
posterior portion of the superior
temporal gyrus
Parietal sensory association,
cortex in the nondominant
hemisphere
Premotor or parietal cortex
Optic radiation in internal capsule
Frontal eye fields on their
descending tracts
 Clinical Manifestations of Middle
Cerebral Artery Syndrome

Ataxia of contralateral limb(s) Parietal lobe

(sensory ataxia)

Pure motor hemiplegia (lacunar Upper portion of posterior limb of

stroke) internal capsule
Clinical Manifestations of Posterior
Cerebral Artery Syndrome

 Occlusion of thalamic branches may produce

hemianesthesia or central post-stroke pain.
Occipital infarction produces homonymous
hemianopsia, visual agnosia, prosopagnosia,
or bilateral, cortical blindness. Temporal lobe
ischemia results in amnesia. Contralateral
hemiplegia occurs with involvement of the
cerebral peduncle.
 Clinical Manifestations of Posterior
Cerebral Artery Syndrome

Sign and Symptoms Structures Involved

Peripheral territory
Contralateral homonymous Primary visual cortex or optic
hemianopsia radiation
Bilateral homonymous Calcarine cortex (macular sparing
hemianopsia with some degree of is due to occipital pole receiving
macular sparing collateral blood supply from MCA)
Visual agnosia Left occipital lobe
Prosopagnosia (difficulty naming Visual association cortex
people on sight)
 Clinical Manifestations of Posterior
Cerebral Artery Syndrome
Dyslexia (difficulty reading)
without agraphia (difficulty
writing), color naming
(anomia), and color
discrimination problems.
Memory defect
Topographic disorientation
Dominant calcarine lesion and
posterior part of corpus
callosum
Lesion of inferomedial portions
of temporal lobe bilaterally or
on the dominant side only
Nondominant primary visual
area, usually bilaterally
 Clinical Manifestations of Posterior
Cerebral Artery Syndrome

Central territory
Central post-stroke (thalamic) Ventral posterolateral nucleus of
pain thalamus
Spontaneous pain and
dysenthesias; sensory
impairments (all modalities)
Involuntary movements; Subthalamic nucleus or its
choreoathetosis, intention tremor, pallidal connections
hemiballismus
Contralateral hemiplegia Cerebral peduncle of midbrain
 Clinical Manifestations of Posterior
Cerebral Artery Syndrome

Weber’s syndrome Third nerve and cerebral

Oculomotor nerve palsy and peduncle of midbrain
contralateral hemiplegia
Paresis of vertical eye Supranuclear fibers to third
movements, slight miosis and cranial nerve
ptosis, and sluggish papillary
light response
Clinical Manifestations of
Vertebrobasilar Artery Syndromes

 Patient develops acute hemiparesis rapidly

progressing to tetraplegia and lower bulbar
paralysis. Initially the patient is dysarthric and
dysphonic but rapidly progress to mutism.
There is preserved consciousness and
sensation. Thus the patient cannot move or
speak but remains alert and oriented.
Horizontal eye movements are impaired but
vertical eye movements and blinking remain
intact.
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes

Signs and Symptoms Structure Involved

Medial medullary syndrome Occlusion vertebral artery,
medullary branch
Ipsilateral to lesion CN XII, hypoglossal, or nucleus
Paralysis with atrophy of half the
tongue with deviation to the
paralyzed side when tongue is
protruded
Contralateral to lesion Corticospinal tract
Paralysis of UE and LE
Impaired tactile and Medial lemniscus
propricoceptive sense
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes
Lateral medullary
(Wallenburg’s) syndrome
Ipsilateral to lesion
Decreased pain and temperature
sensation in face
Cerebellar ataxia: gait and limbs
ataxia
Vertigo, nausea, vomiting
Nystagmus
Horner’s syndrome: miosis,
ptosis, decreased sweating
Occlusion of posterior inferior
cerebellar artery or vertebral
artery
Descending tract and nucleus of
CN V, Trigeminal
Cerebellum of inferior cerebellar
peduncle
Vestibular nuclei and connections
Vestibular nuclei and connections
Descending sympathetic tract
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes

Dysphagia and dysphonia: CN IX, glossophraryngeal, and

paralysis of palatal and laryngeal CN X, vargus, or nuclei
muscles, diminished gag reflex
Sensory impairment of UE, trunk, Cuneate and gracile nuclei
or LE
Contralateral to lesion Spinal lemniscus-spinothalamic
Impaired pain and thermal sense tract
over 50% of body, sometimes
face
Complete basilar artery Basilar artery, ventral pons
syndrome (locked-in
syndrome)
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes
Tetraplegia (Quadriplegia)
Bilateral cranial nerve palsy:
upward gazed spared
Coma
Cognition spared
Medial Inferior pontine
syndrome
Ipsilateral to lesion
Paralysis of conjugate gaze to
side of lesion (preservation of
convergence)
Corticospinal tracts bilaterally
Long tracts to cranial nerve
nuclei bilaterally
Relicular activating system
Occlusion of paramedian branch
of basilar artery
Pontine center for lateral gaze
paramedian pentine reticular
formation (PPRF)
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes
Nystagmus
Ataxia of limbs and gait
Diplopia on lateral gaze
Contralateral to lesion
Paresis of face, UE, and LE
Impaired tactile and
proprioceptive sense over 50%
of the body
Vestibular nuclei and
connections
Middle cerebellar peduncle
CN VI, abduncens, or nucleus
Corticobulbar and corticospinal
tract in lower pons
Medial lemniscus
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes
Signs and Symptoms
Lateral inferior pontine
syndrome
Ipsilateral to lesion
Horizontal and vertical
nystagmus, vertigo, nausea,
vomiting
Facial paralysis
Paralysis of conjugate gaze to
side of lesion
Deafness, tinnitus
Structure Involved
Occlusion of the anterior inferior
cerebellar artery, a branch of the
basilar artery
CN VIII, vestibular, or nucleus
CN VII, facial or nucleus
Pontine center of lateral gaze
(PPRF)
CN VIII, cochlear, or nucleus
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes

Ataxia Middle cerebellar peduncle amd

cerebellar hemisphere
Impaired sensation over face Man sensory nucleus and
descending tract of fifth nerve
Contralateral to lesion Spinothalamic tract
Impaired pain and thermal sense
over half body (may include face)
Medial midpontine syndrome Occlusion of paramedian branch
of mid-basilar artery
Ipsilateral lesion Middle cerebellar peduncle
Ataxia of limbs and gait (more
prominent in bilateral
involvement)
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes

Contralateral lesion Corticobulbar and corticospinal

Paralysis on face, UE and LE tract
Deviation of eyes PPRF
Lateral midpontine syndrome Occlusion of short circumferential
artery
Ipsilateral lesion Middle cerebellar peduncle
Atacia of limbs
Paralysis of muscles on Motor fibers of nucleus of CN V,
mastification trigeminal
Impaired sensation over side of Sensory fibers or nucleus of CN
face V, trigeminal
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes

Medial superior pontine Occlusion of paramedian

syndrome
Cerebellar ataxia
Internuclear ophthalmoplegia
Contralateral lesion
Paralysis of face, UE, and LE
branches of upper basilar artery
Superior or middle cerebellar
peduncle
Medial longitudinal fasciculus
Corticobulbar and corticospinal
tract
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes

Signs and Symptoms Structure Involved

Lateral superior pontine
syndrome (occlusion of superior
cerebellar artery, a branch of the
basilar artery)
Ipsilateral lesion Middle and superior cerebellar
Cerebellar ataxia of limbs and peduncles, superior surface of
gait, falling aside of lesion cerebellum, dentate nucleus
Dizziness, nausea, vomiting Vestibular nuclei
Horizontal nystagmus Vestibular nuclei
Paresis of conjugate gaze Uncertain
(ipsilateral)
 Clinical Manifestations of
Vertebrobasilar Artery Syndromes

Loss of optokenetic nystagmus Uncertain

Horner’s syndrome: miosis, Descending sympathetic fibers
ptosis, decreased sweating on
opposite side face
Contralateral lesion Spinothalamic tract
Impaired pain and thermal sense
of face, limbs, and trunk
Impared touch, vibration, and Medial lemniscus (lateral portion)
position sense, more in LE than
UE (tendency to incongruity of
pain and touch deficits)
COMPLICATION
COMPLICATION…

 Complicationsmay result from ischemic

cascade or develop as a result of the patient
becoming immobile or bedridden.
COMPLICATION…

Complications that may occur within 72 hours

of stroke include the following:
 Cerebral swelling (edema)
 Increased intracranial pressure (ICP)
 Intracerebral hemorrhage
 Seizures
COMPLICATION…

Complications that may develop gradually as a

result of immobility include the following:
 Bedsores
 Blood clots
 Fibrosis of connective tissue resulting in
decreased mobility
 Malnutrition
 Pneumonia
 Urinary tract infections (UTIs; if a catheter is
required
MUSCULOSKELETAL

 loss of voluntary movement and immobility

result in loss of range of movement and
contractures.
 UE: limitations in shoulder motions of flexion,
abduction, and external rotation
 Contructure
 Disuse atrophy and muscle weakness
 Impairments in gait, balance, falls
 Osteoporosis
NEUROLOGICAL

 SEIZURES- common right after stroke during

the acute phase and late-onset seizures can
also occur several month after stroke
 Common in occlusive carotid disease (17%)
 HYDROCEPHALUS- may experience
headache, nausea, vomiting, ↑ lethargy, and
ataxia.
CARDIOVASCULAR/PULMONARY

 THROMBOPHLEBITIS/DVT

-complication for all immobilized patients

DVT signs:
- rapid onset of unilateral leg swelling
with dependent edema
- tenderness, dull ache, or tight
feeling in calf; not severe pain
CARDIOVASCULAR/PULMONARY
 CARDIAC FUNCTION

- impaired cardiac output

- cardiac decompensation
- serious rhythm disorders
- directly alter cerebral perfusion and produce
additional focal signs
- exhibit low work capacities result acute illness,
bedrest, and limited activities level.
- ↓ activity levels may also related to depression
CARDIOVASCULAR/PULMONARY

 PULMONARY FUNCTION
- ↓lung volume
- ↓pulmonary perfusion
- ↓vital signs
- altered chest wall excursion
- ↑fatigue
- ↓endurance
CARDIOVASCULAR/PULMONARY

 ASPIRATION- more common during any

phase of recovery and can occur during any
phase of swallowing
 DYSPHAGIA- lead to dehydration and
compromised nutrition
INTEGUMENTARY

 Ischemic damage and subsequent necrosis

of the skin results in skin breakdown and
decubitus ulcer
 Skin breakdown typically over bony
prominence from pressure, friction, shearing
and/or maceration
INTEGUMENTARY

 FRICTION- skin rubs or dragged against the

supporting surface
 SHEARING- sliding of adjacent structures in
opposite directions
 MACERATION- caused by excess moisture
Differential Diagnosis

KAREN BARRACA
Differential Diagnosis

 Paralysis of one side of the body

 Hemiplegia
 Numbness
 Confusion
 Vision complications
 Fatigue
 Aphasia
 Vomiting
 Decrease level of consciousness
Differential Diagnosis

 Lethargy
 Dizziness/Vertigo
 Slurred speech
 Loss of coordination
 Uncontrollable eye movements
 Behavioral changes
 Differential Diagnosis

Disease History Distinguishing

Features
Blood sugar is too Hunger,
Hypoglycemia
low Nervousness, Cold
sweat, Convulsion

Mass Lesions Cerebral Abscess Progressive

syndrome,
Subdural
Rigorous
Hematoma headache,
Metastatic Tumor
Stiff/aching at the
neck, shoulders
and back
 Differential Diagnosis

Disease History Distinguishing

Features
Autoimmune Decrease attention
Multiple
disease that span, urinary
Sclerosis frequency, hearing
affects the CNS
loss

Epilepsy Electric shock

Abnormal
electrical activity feeling, drooling,
in the brain twitching
movements
Encephalitis
Fever, , delirium,
LABORATORY TEST AND
DIAGNOSTIC TOOLS

NEEMA ESTORES
NEUROVASCULAR TEST

- Neck Flexion
- Palpation of arteries
- superficial and deep
- Auscultation of heart and blood vessel
-Ophthalmic pressure
TEST AND MEASURES

1. Urinalysis
-Detects infection, diabetes, renal
failure, dehydration
-can reveal diseases that have gone
unnoticed because they do not
produce striking signs or symptoms.
TEST AND MEASURES

2. Blood analysis
-Provides complete blood count,
platelet count, prothrombin time,
partial thromboplastin time, and
erythrocyte sedimentation rate.
TEST AND MEASURES

3. Fasting blood glucose level

-Is used to screen for and diagnose
diabetes and pre-diabetes.
-Collected after an 8 to 10 hr fast
4. Blood chemistry profile
-Test measures the value of a different
substance in the blood. These values
provide information on the function of different
organ systems (kidney, liver, etc.) or the risk
for
TEST AND MEASURES

5. Blood cholesterol and lipid profile

-Is a group of simple blood tests that
reveal important information about the types,
amount and distribution of the various types
of fats (lipids) in the bloodstream.
6. Thyroid function tests
-A collective term for blood tests used to
check the function of the thyroid
TEST AND MEASURES

7. Full cardiac evaluation

-Includes electrocardiograph to detect
arrhythmias as source of emboli or
coincidental heart disease.
8. Echocardiography
-Also known as a cardiac
ultrasound
-It uses standard ultrasound techniques
to image two-dimensional slices of the heart.
The latest ultrasound systems now employ
3D real-time imaging.
TEST AND MEASURES

9. Lumbar puncture
-diagnostic and at times therapeutic
procedure that is performed in order to
collect a sample of cerebrospinal fluid
(CSF) for biochemical, microbiological,
and cytological analysis, or occasionally
as a treatment ("therapeutic lumbar
puncture") to relieve increased
intracranial pressure.
IMAGING

1. Computerized Tomography
-Commonly used imaging technique
-Allows identification of large arteries
and vein, and venous sinuses
-Used to rule out other brain lesions
Hemorrhagic stroke Ischemic stroke
IMAGING

2. Magnetic Resonance Imaging

-Measures nuclear particles as
they interact with powerful
magnetic field
IMAGING

3. Positron Emission Tomography

-Allows imaging of regional blood
flow and localized cerebral
metabolism
4. Transcranial and Carotid Doppler
-Used for noninvasive imaging of
the neck and chest level.
Transcranial Doppler
IMAGING

5. Cerebral Angiography
-Invasive and involves the
injection of radiopaque dye into
blood vessels with subsequent
radiography
Cerebral Angiogram showing a transverse projection of
vertebrobasilar and posterior cerebral circulation
PT Management

JENNYLYN C. PASSILAN
• Recovery begins as people get better from the
immediate effects of a stroke. Over months and even
years, other areas of the brain might learn to take
over from the dead areas.

• Rehabilitation is the process of overcoming

or learning to cope with the damage the stroke has
caused.

• Stroke can cause weakness or paralysis in one

side of the body and problem with balance or
coordination.
 
• Helps regain as much mobility and muscle
control as possible.

Assess the stroke survivor’s strength,

endurance, ROM, gait abnormalities and
sensory deficits to design individualized
rehabilitation program.
• Work at patient bedside assuring adequate
ROM and teaching bed mobilities, rolling and
sitting.

• Helps survivors regain the use of stroke

impaired limbs, teach compensatory strategies
to reduce the effect of remaining deficits and
establish ongoing program to help people
retain their newly learned skills.
 MENTAL STATUS EXAMINATION
LEVEL OF CONCIOUSNESS
Alertness, response to stimulation
Attention
Memory
Orientation, new learning, remote memory
Cognition
Fund of knowledge, calculation, problem solving,
Abstract thinking, judgment
Perception, Constructional Ability, Apraxia
Affect and Behavior
 BEDSIDE TEST

Does the patient understand?

Give verbal commands, ask patient to point objects

Is the patient able to talk?

Ask the patient to name objects, describe them, and
count. Listen for spontaneous speech.

Can the patient repeat?

Ask the patient to repeat words.
 BEDSIDE TEST

Can the patient read?

Give commands in writing.

Can the patient write?

Ask the patient to copy of to write dictated words.
unnstrom stages of Motor Recovery
Stage Characteristics

1 No activation of the Limb

2 Spasticity appears, and weak basic flexor and extensor synergies

are present
3 Spasticity is prominent; the patient voluntarily moves the limb, but
muscle activation is all within the synergy patterns

4 The patient begins to activate muscles selectively outside the

flexor and extensor synergies
5 Spasticity decreases; most muscle activation is selective and
independent from the limb synergies
6 Isolated movements are performed in smooth , phasic, well
coordinated manner
 Maintain ROM and prevent deformity

Promote awareness, AROM, and use of

hemiplegic side

Improve trunk control, symmetry, and

balance

Improve functional mobility

Initiate self care activities

Improve respiratory function

Monitor changes associated with recovery.

Positioning
The room should be arranged to maximize
patient awareness of the hemiplegic side.
Affected side should be towards the main part
of the room.
Since patient spends significant time on
bed, we have to prevent undesirable posture
which can lead to contractures or pressure
Passive Range of Motion Exercises
 
• maintain good blood flow

• keep the muscles and tendons flexible

• preventing the joints from tightening

passive range of motion exercises are done for the shoulder, elbow, wrist,
fingers, hip, knee, ankle, foot, and toes
Active Range of Motion Exercises

• help to strengthen the muscles on the weak side,

but also should be done on the good side.

 
Balance and Transfer Exercises

• The patient will practice moving from lying to sitting

position and then practice sitting balance. Next they
will learn to transfer from bed to wheelchair and back
to bed sometimes using a sliding board if necessary.
 
Gait (Walking) Training Exercise

Starts practicing standing up in the parallel bars.

Next the patient learns to shift weight from one leg to the
other, shifting both from side to side and from front to
back. After this the patient walks a short distance betwee
the parallel bars using the bars for support. Next, the
patient will walk outside the bars using a quad cane or
walker
Bobath approach /neurodevelopmental
technique (NDT)

The goal of NDT is to normalize tone, to inhibit primitive

patterns of movement, and to facilitate automatic, voluntary
reactions and subsequent normal movement patterns.

inhibits abnormal patterns of movement

Brunnstrom approach/Movement therapy (
Brunnstrom, 1970)

Uses primitive synergistic patterns in training in attemptin

to improve motor control through central facilitation

encourages the use of abnormal movements

Sensorimotor approach/Rood approach (
Noll, Bender, and Nelson, 1996)

Facilitatory or inhibitory inputs through the use of

sensorimotor stimuli, including, quick stretch, icing
fast brushing, slow stroking, tendon tapping,
vibration, and joint compression to promote
contraction of proximal muscles
Motor relearning program/Carr and Shepard
approach (Carr et al., 1985)

Based on cognitive motor relearning theory and influenced

by Bobath's approach
Goal is for the patient to relearn how to move functionally
and how to problem solve during attempts at new tasks
Proprioceptive (or peripheral) Neuromuscular
Facilitation (PNF) (Knott and Voss, 1968)

Uses spiral and diagonal components of movement

rather than the traditional movements in cardinal
planes of motion with the goal of facilitating movement
patterns that will have more functional relevance than
the traditional technique of strengthening individual
group muscles
 ADJUNCT THERAPIES
TRANSCUTANEOUS ELECTRICAL NERVE
STIMULATION (TENS)
 
Encourages brain reorganization and recovery of function.
It involves using a small probe that generates an electrical
current to stimulate nerve activity in stroke- impaired limbs.
The mild electrical current generates heat that serves to
relieve stiffness, improve mobility, and relieve pain.
 
 ADJUNCT THERAPIES
TRANSCUTANEOUS ELECTRICAL NERVE
STIMULATION (TENS)
 
 ADJUNCT THERAPIES
FUNCTIONAL ELECTRICAL STIMULATION (FES)
 

Used to promote and improve muscle function,

prevent atrophy, increase strength, maintain ROM
and increase circulation and blood flow to the muscles
 ADJUNCT THERAPIES
FUNCTIONAL ELECTRICAL STIMULATION (FES)
 
 ADJUNCT THERAPIES
ELECTROMYOGRAPHIC BIOFEEDBACK
 

Another method designed to promote recovery and when used

along with FES can result in greater improvement. EMG is the
practice of measuring the electrical signal produced by a
contracting muscle.
 
ELECTROMYOGRAPHIC BIOFEEDBACK
 
BE PATIENT. REHABILITATION IS A
SLOW AND OFTEN FRUSTRATING PROCESS.
DON’T WORRY IF THERE ARE DAYS WHEN
LITTLE PROGRESS SEEMS TO BE MADE.
BE POSITIVE. CONSTANT
ENCOURAGEMENT AND PRAISE ARE
NEEDED TO KEEP UP EVRYONE’S
SPIRITS.
 
 
NO PROGRAM CAN SUCCEED WITHOUT
A STRONG DESIRE BY THE
PATIENT TO BE
INDEPENDENT.NEVERTHELESS;
FAMILY INVOLVEMENT IS ALSO A KEY
INGREDIENT IN A SUCCESSFUL