STROKE

Dr. BHAWANI RANA

 INTRODUCTION
• Stroke (cerebrovascular accident [CVA]) is the sudden loss of
neurological function caused by an interruption of the blood flow
to the brain.
• According to WHO- It is defined as the sudden onset of
neurological deficits due to an abnormality in cerebral circulation
with the signs and symptoms lasting for more than 24 hours or
longer
• TIA(Transient ischemic attack)-It is defined as the sudden onset
of neurological deficits due to an abnormality in cerebral
circulation with the signs and symptoms lasting for less than 24
hours
• Ischemic stroke is the most common type, affecting about 80% of
individuals with stroke, and results when a clot blocks or impairs
blood flow, depriving the brain of essential oxygen and nutrients.
• Hemorrhagic stroke occurs when blood vessels rupture, causing
leakage of blood in or around the brain.
• Clinically, a variety of focal deficits are possible, including
changes in the level of consciousness and impairments of sensory,
motor, cognitive, perceptual, and language functions. To be
classified as stroke, neurological deficits must persist for at least
24 hours.
• Motor deficits are characterized by paralysis (hemiplegia) or
weakness (hemiparesis), typically on the side of the body opposite
the side of the lesion
 EPIDEMIOLOGY
Epidemiology of Stroke in India
 Incidence: ~119–145 per 100,000 people annually [1].
 Prevalence: ~84–262 per 100,000 population, varies by region [2].
 Mortality: High case fatality rate; stroke is a leading cause of death and disability.
 Age group: Increasing incidence in younger adults (<50 years), but most common in >60
years.
 Urban vs Rural: Higher incidence in urban areas, but rising in rural populations due to
lifestyle changes.
 Risk Factors: Hypertension, diabetes, smoking, alcohol, dyslipidemia, sedentary
lifestyle.
 Burden: Stroke is the second leading cause of death and a major cause of long-term
disability in India [3].
Let me know if you want this expanded with statistics or references in numbered format.
References :
[1] Pandian JD, Sudhan P. Stroke Epidemiology and Stroke Care Services in India. J Stroke 2013.
[2] Banerjee TK et al. Stroke in the urban population of Calcutta—an epidemiological study. Neuroepidemiology.
[3] Global Burden of Disease Study, India Report, ICMR 2020.
Atherosclerosis
ETIOLOGY
Cerebral Thrombus
Cerebral embolus
Embolism from the heart (cardiac origin)
Intracranial haemorrhage
Subarachnoid hemorrhage
Intracranial small vessel disease
Arterial aneurysms
Arterio-venous malformation
Haematological disorders (haemoglobinopathies, leukemia)
 R/F
NON MODIFIABLE MODIFIABLE
ž Ageing & gender  Smoking
ž Positive family history ž Obesity
ž Heart disease ž Lack of physical exercise or
ž Diabetes mellitus
- sedentary life style
ž Hypertension
ž Peripheral arterial disease ž Diet & excess alcohol
ž Blood pathology (increased consumption
hematocrit, clotting abnormalities, ž Oral contraceptives
sickle cell anemia etc.) ž Infection (meningeal infection)
ž Hyperlipidemia ž Psychological factors
ž TIA ž Vasectomy
 Warning sign of stroke
 Sudden numbness or weakness of face, arm, or leg, on one side of body
ž Sudden confusion, trouble speaking or understanding
ž Sudden blurring of vision
ž Sudden onset of dizziness, loss of balance or coordination
ž Sudden, severe headaches with no known cause
ž Other important but less common stroke symptoms include:
• Sudden nausea, fever, & vomiting distinguished from a viral illness by
speed of onset (minutes or hours vs several days)
• Brief loss of consciousness or a period of decreased consciousness
(fainting, confusion, convulsions, or coma)
 PATHO -PHYSIOLOGY
1. Ischemic Stroke (≈85% cases):

Caused by thrombosis, embolism, or systemic

hypoperfusion.
•↓ Blood flow → ↓ Oxygen & glucose → Energy
failure
•ATP depletion → Na⁺/K⁺ pump failure → Cellular
depolarization
•↑ Intracellular calcium → Glutamate excitotoxicity
•Free radical formation → Oxidative damage
•Cell death (necrosis in core, apoptosis in penumbra)
•Inflammation worsens injury.
An ischemic penumbra is the area around the ischemic core
of a stroke. The ischemic core is the tissue that has been most
severely damaged by the stroke. The penumbra is viable
tissue (living and functioning)that can recover if perfusion
improves quickly.
 2. Hemorrhagic Stroke (≈15% cases):

Caused by rupture of a blood vessel (e.g., due to hypertension, aneurysm).

•Blood leaks into brain tissue → ↑ Intracranial pressure

•Mechanical tissue disruption + Toxic effects of blood
•Edema, inflammation, and vasospasm contribute to damage.
 CLASSIFICATION
Depending on the cause
Hemorrhagic stroke
– Intracranial hemorrhage
 Subarachnoid hemorrhage
 Signs of raised ICP will be evident with a history of a traumatic accident.

Ischemic stroke
 Thrombotic: more common. Usually occurs in the sleeping hours.
Characterized by gradual onset of symptoms
 Embolic: Occurs in the waking hours of the day. Sudden onset of
symptoms preceded by giddiness in most conditions.
 Depending on the duration
• Acute stroke: to a period of one week or until spasticity develops
• Sub acute stroke: after the development of spasticity & last for a
period of 3-12 months
• Chronic stroke: more than 12 months.
Depending on the severity
• Mild stroke: symptoms subside with no deficit in a week period
• Moderate stroke: symptoms recover in a period of 3 - 6 months
with minimal neurological deficit
• Severe stroke: there is no complete recovery of the symptoms even
after 1 years. Always ends up with severe neurological deficit.
 Depending on the symptoms

• MCA Syndrome
• ACA Syndrome
• PCA syndrome
• Vertebro- basilar artery syndrome
– Vertebral artery
 Basilar artery
 Internal carotid artery
 Lacunar syndrome
• A lacunar infarct, also known as a lacunar stroke, is a type of ischemic
stroke that occurs when an artery that supplies blood to the brain's
deeper parts becomes blocked.
• These strokes are the most common type of ischemic stroke,
accounting for 15% to 25% of all strokes.
Symptoms include:
Weakness on one side of the body
Impaired coordination.
Pure motor hemiparesis
Pure sensory stroke, Sensorimotor stroke.
Ataxic hemiparesis
 STAGE OF RECOVERY
• Stage 1: recovery occurs in a stereotyped sequence of events that begins with a
period of flaccidity immediately following acute episode. No movement of limbs
can be elicited
• Stage 2: basic limb synergies or some of their components may appear as
associated reactions. Minimal voluntary movement may be present. Spasticity
begins to develop.
• Stage 3: Gains voluntary control of movement synergy although full range is not
developed. Spasticity has further increased
• Stage 4: some movement combination that do not follow the synergy are
mastered first with difficulty & later with more ease. Spasticity begins to decline
• Stage 5: more difficult movement are learnt as the basic limb synergy lose their
dominance over motor roots. Spasticity further declines
• Stage 6: disappearance of spasticity, individual joint movement become possible
& coordination approaches normal. Normal motor function is restored
 The Brunnstrom stages of stroke
recovery
Stage 1: Flaccidity
Stage 2: Spasticity appears
Stage 3: Increased spasticity
Stage 4: Decreased spasticity
Stage 5: Complex movement combinations
Stage 6: Spasticity disappears
Stage 7: Normal function returns
In stage four, involuntary muscle movement begins to decline, and the brain becomes
more successful at sending signals to the muscles for voluntary movements.
In stage five, more signals from the brain to the muscles become successful, and
involuntary movements become minimal.
In stage six, there are no unexpected involuntary movements, and coordination
improves quickly
 MCA territory infarct

•  Contralateral hemiplegia (UL & face more affected than LL)

•  Contralateral hemi sensory loss (UL & face more affected than LL)
•  Ideomotor apraxia(difficulty performing
skilled movements)
•  Ataxia of contralateral limb
•  Contralateral Homonymous hemianopia
•  Left hemisphere infarction
• Contralateral neglect
• Possible contralateral visual field deficit
• Aphasia: Broca’s (expressive) or Wernicke’s (receptive)
 PCA territory infarct

ž Coordination disorders such as tremor or

ataxia
 Contralateral homonymous field deficit
 Cortical blindness
 Cognitive impairment including memory impairment
 Contralateral sensory impairment
 Thalamic syndrome (abnormal sensation of severe pain from
light touch or temperature changes)
 Weber’s syndrome (contralateral hemiplegia & third nerve palsy).
 ACA territory infarct
•  Contralateral Hemiplegia or monoplegia of LL (LL more affected
than UL)
•  Contralateral sensory loss of LL
•  Urinary incontinence
•  Problems with imitation & bimanual task
•  Abulia (lack of will)
•  Apraxia (affects the brain's ability
• to plan and execute purposeful movements)
•  Amnesia (partial or complete loss of memory)
•  Contralateral grasp reflex, sucking reflex
 VARTIBRO-BASILARY ARTERY SYNDROME

•  Medial medullary syndrome (vertebral artery)- Dejerine syndrome

•  Lateral medullary (Wallenberg's) syndrome (PICA)
•  Complete basilar artery syndrome (locked- in syndrome)
•  Medial inferior pontine syndrome
•  Lateral inferior pontine syndrome (AICA)
•  Medial mid pontine syndrome
•  Lateral mid pontine syndrome
•  Medial superior pontine syndrome
•  Lateral superior pontine syndrome
 Medial Medullary Syndrome (Dejerine syndrome)
Caused by anterior spinal artery occlusion.
Triad:
[Link] tongue weakness (hypoglossal nerve).
[Link] hemiparesis (corticospinal tract).
[Link] loss of proprioception/vibration (medial lemniscus)
.
 Lateral Medullary Syndrome (Wallenberg’s Syndrome):

Caused by occlusion of the posterior inferior cerebellar artery

(PICA).
Key Features:

[Link] facial pain/temp loss (spinal trigeminal

nucleus).
[Link] body pain/temp loss (spinothalamic tract).
[Link] Horner’s syndrome.
[Link], hoarseness (nucleus ambiguus).
[Link], nystagmus, ataxia (vestibular nuclei, cerebellum).
Pontine Syndrome:
Results from infarction or lesion in the pons, often due to basilar artery occlusion.
Common Features (depending on level):
[Link] hemiparesis (corticospinal tract).
[Link] facial weakness (facial nerve nucleus).
[Link] gaze palsy (paramedian pontine reticular formation).
[Link] (middle cerebellar peduncle).
Locked-in Syndrome:
Caused by damage to the ventral pons (usually due to basilar
artery stroke).
Key Features:
[Link] – paralysis of all limbs.
[Link] – loss of speech.
[Link] consciousness and vertical eye movements
(midbrain intact).
[Link] via eye blinking or vertical gaze only.
 LACUNAR SYNDOME
 Caused by small vessel disease of deep white mater
Pure motor lacunar stroke: posterior limb of internal capsule,
pons, & pyramids
Pure sensory lacunar stroke: ventrolateral thalamus or
thalamocortical projections
 Ataxic hemiparesis
ž Dysarthria
 Clumsy hand syndrome
 Sensory/motor stroke
 Dystonia/involuntary movements
 PRIMERY IMPAIRMENTS
[Link] sensation
• Pain (central pain or thalamic pain syndrome characterized by
constant, severe burning pain with intermittent sharp pains
• Hyper analgesia
• Loud sound, bright light etc. may trigger pain
2. Vision
• Homonymous hemianopia, a visual field defect, occurs with
lesions involving the optic radiation (MCA) or to primary visual
cortex (PCA) • Visual neglect & problems with depth perception,
and spatial relationships
3. Weakness
•Usually seen in the contralateral side of the lesion
• MCA stroke are more common so weakness is largely seen in the UL in
clinical practice
• Distal muscle are more affected than proximal muscles
• Mild weakness of ipsilateral side
4. Alteration of tone
• Flaccidity (hypotonicity)
• Spasticity (hypertonicity)
5. Abnormal synergy
• Muscles not involved in either synergy • Latissimus dorsi • Teres major •
Serratus anterior • Finger extensors • Ankle evertors
6. Abnormal reflexes
• Initially, hyporeflexia with flaccidity & later hyperreflexia
• May demonstrate clonus, & +ve Babinski
• Movement of head or position of body may elicit a change in tone or
movement of extremities The most commonly seen is asymmetric tonic neck
reflex (ATNR).
• Associated reactions are also present in patients who exhibit strong spasticity
and synergies unintentional movements of hemiparetic limb caused by
voluntary action of another limb by stimulation of yawning, sneezing, or
coughing.
7. Altered co-ordination
• Proprioceptive losses can result in sensory ataxia
• Strokes affecting cerebellum typically produce cerebellar
ataxia ([Link] artery syndrome, pontine syndromes) &
motor weakness.
• Basal ganglia involvement (PCA syndrome) may lead to
bradykinesia or involuntary movements
8. Altered motor programing
• Motor praxis is ability to plan & execute coordinated movement
• Lesions of premotor frontal cortex of either hemisphere, left
inferior parietal lobe, & corpus callosum can produce apraxia.
9. Postural Control & Balance
• Impairments in steadiness, symmetry, & dynamic stability
• Problems may exist when reacting to a destabilizing external force
or during self-initiated movements .
• Pusher syndrome: characterized by active pushing with stronger
extremities toward affected side, leading to lateral postural
imbalance.
10. Speech, Language, and Swallowing
• Lesions involving cortex of dominant hemisphere
• Aphasia: impairment of language comprehension, formulation, and use.
• Dysarthria: motor speech disorders caused by lesions of CNS or PNS that
mediate speech production.
• Dysphagia, occurs with lesions affecting medullary brainstem (CN IX and
X), large vessel pontine lesions, as well as in acute MCA and PCA lesion.
11. Perception and Cognition • They are the result of lesions in right parietal
cortex & seen more with left hemiplegia than right. • These may include
disorders of body scheme/body image, spatial relations, and agnosias.
12. Emotional Status • Lesions of brain affecting frontal lobe, hypothalamus,
& limbic system • May demonstrate pseudobulbar affect (PBA), also known as
emotional lability or emotional dysregulation syndrome.  emotional outbursts
of uncontrolled or exaggerated laughing or crying that are inconsistent with
mood. • Depression is extremely common  persistent feelings of
sadness,feelings of hopelessness, worthlessness or helplessness.
13. Bladder and Bowel Function • Disturbances of bladder function are
common during acute phase • Urinary incontinence can result from bladder
hyperreflexia or hyporeflexia, disturbances of sphincter control, or sensory
loss. • Disturbances of bowel function can include incontinence & diarrhea or
constipation
FUNCTIONAL ASSESSMENT
Using FIM, Barthel index, FMA
There is compromised basic as well as instrumental ADL
Ambulatory capacity is compromised
BOWEL AND BLADDER
• Flaccid bowel & bladder during the acute stage
• Bowel & bladder function gradually regains
• Uninhibited bladder if frontal lobe is involved
• Constipation is frequently seen
 PROBLEM LIST
1) Tonal abnormalities
2) Muscular weakness
3) Synergistic pattern
4) Tightness & contracture
5) Imbalance & incoordination
6) Gait abnormalities
7) Postural abnormalities
8) Functional disability
 Physiotherapy Management of Stroke

• Reference: Susan B. O’Sullivan & Thomas J. Schmitz – Physical

Rehabilitation, 6th Edition
 I. Assessment (Evaluation Phase)
A thorough neurological and functional assessment
helps form a baseline and guides therapy:
Area Key Components

Motor Function Muscle tone (Modified Ashworth Scale), synergy patterns

Sensory Function Light touch, proprioception, stereognosis

Balance & Posture Sitting and standing balance (Berg Balance Scale)
Gait Analysis Observational gait analysis or Tinetti Gait Assessment
Coordination Finger-to-nose, heel-to-shin

Functional Independence Functional Independence Measure (FIM), Barthel Index

Cognition & Perception MMSE, neglect tests, problem-solving

Pain Shoulder subluxation, central post-stroke pain
Spasticity Using tools like the Modified Tardieu Scale, MAS
II. Acute Stage (0–7 days post-stroke) Key Interventions:
Goals: Prevent complications, Stabilize vital functions, Initiate early mobilization

Treatment Rationale

Prevent pressure sores & contractures; support flaccid

Positioning
limbs
PROM & AAROM Maintain joint range, prevent stiffness
Chest physiotherapy Prevent chest infection, especially in hemiparetic patients
Sit at edge of bed, stand with support (if medically
Early Mobilization
stable)
Bed Mobility &
Roll, sit, stand with assistance
Transfers
Education Teach caregivers about handling limbs properly
 III. Subacute Phase (1 week to 6 months) Goals: Restore functional independence,
Promote recovery of motor function, Begin gait and balance training
Interventions:
Focus Techniques
Neurodevelopmental Techniques (NDT), PNF, Brunnstrom
Motor Recovery
approach
Balance Training Static & dynamic tasks, reaching in sitting/standing
Gait Training Parallel bars → walker → cane → independent
Strengthening Focus on both affected and unaffected limbs
ADLs Training Dressing, grooming, toileting with or without aids
Spasticity Management Weight-bearing, stretching, FES, splints
Constraint-Induced Movement
For upper limb use in patients with residual voluntary control
Therapy (CIMT)
Mirror Therapy / Mental
Activate motor areas with limited movement
Practice
IV. Chronic Phase (After 6 months)
Goals: Maximize independence, Community reintegration , Long-term wellness and
maintenance
Interventions:
Focus Activities
Aerobic Fitness Walking, cycling, aquatic therapy
Fine Motor Skills Pegboards, coin manipulation, object sorting
Vocational
Job-specific retraining if applicable
Rehabilitation
Community Mobility Public transport, driving simulation (if safe)
Home Modifications Ramps, handrails, adaptive equipment
Support Groups Psychosocial support to reduce isolation
 V. 🎯 Goals of Physiotherapy
Short-term Goals (Days to Weeks)
1. Prevent complications (DVT, pneumonia, contractures)
2. Normalize tone and reduce spasticity
3. Improve trunk control and sitting balance
4. Initiate controlled movement in limbs
5. Improve bed mobility and transfers
6. Begin ambulation (with or without aids)
7. Enhance independence in basic ADLs
8. Educate patient and caregiver on safety and self-care
 Long-term Goals (Weeks to Months+)

1. Maximize motor recovery and function

2. Improve balance and postural control
3. Achieve independent or assisted ambulation
4. Improve upper limb dexterity and coordination
5. Achieve independence in complex ADLs.
6. Reintegration into community or workplace
7. Maintain musculoskeletal and cardiopulmonary health
8. Reduce risk of secondary stroke or falls
9. Improve quality of life and participation
 list of commonly used stroke outcome scales :

• Modified Rankin Scale (mRS)-degree of disability

• National Institutes of Health Stroke Scale (NIHSS)-to assess the severity of stroke-related neurological deficits
• Barthel Index (BI)-To measure a person's ability to perform basic activities of daily living (ADLs)
• Functional Independence Measure (FIM)-
• Berg Balance Scale (BBS)-
• Fugl-Meyer Assessment (FMA)-to assess motor recovery in individuals with stroke
• Stroke Impact Scale (SIS)-to assess the biopsychosocial impact of stroke
• Motor Assessment Scale (MAS)-to assess motor function
• Ashworth Scale / Modified Ashworth Scale (MAS)
• Glasgow Coma Scale (GCS)
• Timed Up and Go Test (TUG)-
• Mini-Mental State Examination (MMSE),
• Rivermead Mobility Index (RMI)-to assess functional mobility in patients
• Postural Assessment Scale for Stroke Patients (PASS)-to evaluate and monitor postural control in stroke
• Trunk Impairment Scale (TIS)-to assess trunk motor impairment
 VI. 🧠 Principles of Stroke Rehab (as per
O’Sullivan)

•Neuroplasticity: Use repetitive, meaningful tasks to stimulate

brain reorganization.
•Motor learning: Emphasize task-specific practice and feedback.
•Compensation vs Recovery: Balance between restoring lost
function and adapting for independence.
•Patient-centered care: Goal setting should be collaborative and
functional.
REFRENCES
• O’ Sullivan SB, Schmitz TJ. Stroke. Physical rehabilitation. 5th ed.,
New Delhi: Jaypee Brothers, 2007.
• Darcy A. Umphred. Neurological Rehabilitation, 5th ed.
 Write down question
Q. A 64-year-old male, is in the subacute phase following a left MCA
ischemic stroke. He presents with right-sided hemiparesis (arm more
affected than leg), mild expressive aphasia, poor trunk control, increased
tone in the right upper limb, and dependency in ADLs. As a physiotherapy
student, outline a detailed physiotherapy management plan including:

• A problem list (based on assessment findings) 3 Mark

• Short-term and two long-term physiotherapy goals 5 Mark
• Physiotherapy interventions for improving motor control, balance, and
functional independence. 7 Mark
 ANSWER
Problem List
Based on the case, identify the key physiotherapy problems:
• Right-sided hemiparesis (especially upper limb)
• Increased tone in right upper limb (spasticity)
• Poor trunk control and postural instability
• Impaired balance (sitting and standing)
• Reduced mobility and ambulation
• Dependency in ADLs
• Communication difficulty due to expressive aphasia
• Risk of complications (e.g., shoulder subluxation, falls, contractures)
 Goals of Treatment
🔹 Short-Term Goals (1–2 weeks)

• Improve trunk control and sitting balance

• Reduce spasticity in right upper limb
• Maintain joint ROM to prevent contractures
• Achieve independent bed mobility and transfers with
supervision
• Begin standing and stepping with support
• Improve participation in basic ADLs (feeding, grooming)
 Long-Term Goals (4–12 weeks)

• Achieve independent ambulation with or without aids

• Restore functional use of right upper limb
• Improve independence in ADLs (dressing, toileting, bathing)
• Enhance balance and prevent falls
• Achieve community-level mobility
• Maximize functional communication strategies (in
coordination with SLP)
• Improve quality of life and social participation
 Physiotherapy Management Plan
🔸 1. Positioning and Early Mobility
• Proper limb positioning to prevent shoulder subluxation and pressure sores
• Frequent bed turning and upright positioning
🔸 2. Range of Motion and Spasticity Management
• Passive and active-assisted ROM exercises
• Stretching of spastic muscles (especially biceps, wrist flexors)
• Weight-bearing and functional activities for tone reduction
• Splinting if needed
🔸 3. Motor Relearning & Strengthening
• Neurodevelopmental techniques (NDT)
• Task-oriented training: reaching, grasp-release tasks
• Functional strengthening of trunk and unaffected side
🔸 4. Balance and Postural Control
• Sitting balance training (reaching outside BOS)
• Trunk activation and core exercises
• Progress to standing and dynamic balance
🔸 5. Gait and Mobility Training
• Parallel bars → walker → stick
• Emphasize weight shifting and symmetry in stance
🔸 6. ADL Training and Functional Skills
• Bed mobility, transfers, toilet training
• Use of adaptive equipment (dressing aids, grab bars)
🔸 7. Communication Support
• Use of gestures, picture boards
• Collaborate with speech therapist
🔸 8. Education
• Educate family/caregiver on home program, handling, and safety
• Stroke risk factor management (refer to interdisciplinary team)

Reference
• O’Sullivan, S. B., & Schmitz, T. J. (2013). Physical Rehabilitation, 6th
Edition. F.A. Davis Company.