STROKE
Presentation by Krystel Escano
Brain Attack
Cerebrovascular Accident

Sudden loss of neurological function
secondary to interruption of blood flow
>24 hours manifestation
5th leading cause of death and severe
long-term disability
Stroke

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Nonmodifiable factors
•Age: >60
• Gender: M>F
• Ethnicity: African-
American
• History of previous
stroke
Risk factors
Modifiable factors
• HPN
• Heart Disease
• DM
• Smoking
• Hyperlipidemia
• Obesity
• Sedentary lifestyle

site and extent of the
affected area, or infarct,
commonly determine the loss
of function

Stroke is classified by:
Etiological classification
Ischemic Stroke
Hemorrhagic Stroke
Specific vascular territory (vascular
syndromes)
ACA
MCA
Management category
Transient Ischemic Attack
Deteriorating Stroke
Stroke in the young
ICA
PCA
Vertebrobasilar Artery Syndrome
Weber
Benedikt
Locked-in
Millard-Gubler
Wallenberg

01
Ischemic stroke
03
02
ISCHEMIA
clot blocks or impaired blood flow
80% of stroke cases
a.k.a. large vessels thrombosis
40% of stroke cases
due to atheroma --> atherosclerosis
Thrombotic
20% -25% of stroke cases
due to embolism: dislodged atheroma
Embolic
a.k.a. small vessels thrombosis
Secondary to hypertension
20% stroke cases
due to atheroma
affected sites:
Basal Ganglia
Cerebellum
Pons
Internal Capsule
Thalamus
Lacunar
Etiological classification

most common
occlusion: lenticulostriate artery
lesion site: posterior limb of internal capsule
weakness/ataxia, C/L hemiplegia
Occlusion: PCA
Lesion site: thalamus
sensory relay station
C/L hemianesthesia
tingling sensation of face and limbs
Pure motor
Pure sensory
Lacunar stroke

Parkinson's disease
of any movement
disorder
Involuntary
Movement
2nd most common
occlusion PCA and LSA
lesion site: junction of internal capsule and
thalamus
Least common type
Lesion site: anterior limb of
internal capsule
Sensory Motor
Dysarthria-
Clumsy Hand
Lacunar stroke
Lesion sites: PICC
Pons
Internal Capsule
Corona radiata
Cerebellum
I/L ataxia
C/L hemiplegia
Ataxic Hemiparesis

01
Hemorrhagic stroke
SH
02
Rupture of a cerebral blood vessel
20% of stroke cases
higher mortality rate than ischemic
stroke
bleeding directly into the brain
most commonly linked to hypertension
3% of all CVAs, most common to women
95% cause by leakage of blood from aneurysm
Etiological classification
Intracerebral
Subarachnoid
Types of Subarachnoid Hemorrhage
Saccular Aneurysm
also known as Berry Aneurysm
"worst headache of my life"
Arteriovenous malformation
congenital defect
blood vessels usually form incorrectly

01
Management Category
03
02
Temporary interruption of blood
supply to the brain
< 24 hours
+) residual brain damage/ permanent
neurological dysfunction
Transient Ischemic Attack (TIA)
Stroke in evolution
d/t cerebral or systemic causes
Deteriorating Stroke
< 45 years old
Most common cause:
Hemorrhage
Higher potential for better
recovery
Stroke in the young

Anterior Cerebral Artery
Stroke Syndrome
Specific Vasculary territory classifications (Vascular syndrome)
C/L hemiparesis
Sensory loss
(+) Frontal Gaze Pattern
(+) Urinary incontinence
(+) abulia (akinetic mutism)
MEDIAL ASPECT OF THE CEREBRAL HEMISPHERE
(FRONTAL AND PARIETAL LOBES)
LE > UE & Face

UE & Face > LE
C/L hemiplegia
Middle Cerebral Artery
Stroke Syndrome
largest branch and most commonly stroked artery
Specific Vasculary territory classifications (Vascular syndrome)

UE & Face > LE
C/L hemiplegia
Middle Cerebral Artery
Stroke Syndrome
Specific Vasculary territory classifications (Vascular syndrome)

Internal Carotid Artery
Stroke Syndrome
Specific Vasculary territory classifications (Vascular syndrome)
MCA stroke syndrome
features (UE > LE)
Distinct features:
Ophthalmic artery
Amaurosis Fugax
MCA
UE & face > LE
Supplies MCA and ACA

Posterior Cerebral Artery
Stroke Syndrome
Specific Vasculary territory classifications (Vascular syndrome)
Visual Problems
Supplies occipital lobe and medial and inferior temporal lobe
C/L homonymous hemianopsia (occipital infarction)
Visual agnosia
Prosopagnosia
Dyschromatopsia (color agnosia)
Simultanagnosia (aka: Balint’s syndrome)
Alexia without agraphia

Posterior Cerebral Artery
Stroke Syndrome
Specific Vasculary territory classifications (Vascular syndrome)
Memory
Impairment
Supplies occipital lobe and medial and inferior temporal lobe
Short-term memory
Long- term memory
Immediate recall
Amnesia (Temporal lobe ischemia)
C/L hemiballismus Subthalamic involvement

Posterior Cerebral Artery
Stroke Syndrome
Specific Vasculary territory classifications (Vascular syndrome)
Midbrain
involvement
Supplies occipital lobe and medial and inferior temporal lobe
C/L hemiplegia (CST involvement ->motor)
CN 3 palsy
Weber syndrome
Benedikt syndrome
Thalamic Pain
Syndrome
a.k.a central post-stroke sydnrome
Dejerine-Roussy Syndrome

Vertebrobasilar Artery Syndrome
Specific Vasculary territory classifications (Vascular syndrome)

large proximal MCA occlusion --> coma,
decreased arousal level
involuntary increase in muscle tone
velocity-dependent resistance
90% of stroke cases
Altered Consciousness
Cognitive Deficits
Neurological and Functional Complications
• Difficulty with Alertness
• Attention
•Orientation
• Memory
• Executive functions
Spasticity
Modified Ashworth Scale (MAS)

delayed triggering of the swallowing
reflex
reduced pharyngeal peristalsis
reduced lingual control.
Ideomotor apraxia
Ideational apraxia
oral apraxia
dressing apraxia
constructional apraxia
gait apraxia
limb-kinetic apraxia
Dysphagia
Aphasia
Neurological and Functional Complications
an acquired communication disorder caused by brain damage
Apraxia
IDEATIONAL VS IDEOMOTOR

Gaze Impairments
Neurological and Functional Complications
01
02
Pontine Gaze Pattern
•due to anterior circulation stroke
•looks toward the lesion site
•looks away from the hemiplegic side
•lesion site: area 8 or the frontal eye field of frontal lobe
•due to posterior circulation stroke
•looks away from the lesion
•towards the hemiplegic side
•lesion site: pontine nuclei
Frontal Gaze Pattern

depends on the type and location of the vascular lesion, as well as the severity of the clinical deficits.
Medical Management
aspirin and heparin
to improve flow through occluded vessels
and prevent further clotting or thrombosis
Anti-platelet and anti-coagulation drugs
01 Tissue plasminogen activator (t-PA): open
occluded cerebral vessels and immediately
restore circulation.
Limited, 3-6 hours after stroke onset
Thrombolytic drugs
02

Intervention Principles for
Stroke
Intrinsic Recovery
refers to the
remediation of
neurological
impairments
Adaptive Recovery entails
regaining the ability to
perform meaningful
activities, tasks, and roles
without full restoration of
neurological function
ACTIVE USE OF TASK-ORIENTED TRAINING
(Pendleton and Schultz-Krohn, 2018)
Help clients adjust to role and task performance
limitations by exploring new roles and tasks.
Create an environment that includes the common
challenges of everyday life.
Practice functional tasks or close simulations that have
been identified as important by participants to find
effective and efficient strategies for performance.
Provide opportunities for practice outside therapy time.
Minimize ineffective and inefficient movement patterns.

Utilization
Individuals with stroke are among one of the primary clients of occupational therapy
facilitate the client’s performance of needed or
meaningful occupations within realistic context
Working collaboratively with the members
of the rehabilitation team
provides healthcare professionals in
various practices with the fundamental
knowledge necessary to work with the
stroke population
focus the evaluation procedures and begin to
reflect on the client factors that may have been
impaired and that affect the client’s occupational
performance based on the brain lesions

Reflection
I was anxious as I prepared for this topic because stroke is one of the conditions I
consider complicated. Many terminologies must be discussed, including
anatomical structures and their physiological activities, as well as the
accompanying conditions that I find intimidating. For me, it is one of those
conditions that has been discussed numerous times but is still difficult to recall.
Still, I was thrilled to be assigned this topic because I see it as an opportunity to
go over everything that had been previously covered with us. I am not confident
enough to say that I have already improved in terms of application but I know that
using this fundamental knowledge is essential to understand the symptoms,
diagnosis, and management of stroke.

Thank You
So Much!
Presentation by Krystel Camille Escano
Noted by Miss Ma. Alessandra Elisabeth Könst, OTRP and Sir Jace Devin Lapus, OTRP

Atchison, B., & Dirette, D. (2016). Conditions in Occupational Therapy: Effect on
Occupational Performance. Lippincott Williams & Wilkins.
O’Sullivan, S. B., Schmitz, T. J., & Fulk, G. (2019). Physical Rehabilitation (7th ed.). F.A.
Davis.
Pendleton, H. M., & Schultz-Krohn, W. (2013). Pedretti’s Occupational Therapy - E-
Book: Practice Skills for Physical Dysfunction. Elsevier Health Sciences.
Pendleton, H. M., & Schultz-Krohn, W. (2018). Pedretti’s Occupational Therapy: Practice
Skills for Physical Dysfunction. Mosby.
Radomski, M. V., & Latham, C. a. T. (2008). Occupational Therapy for Physical
Dysfunction. Lippincott Williams & Wilkins.
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REFERENCES