STROKE

 Stroke is an acute onset of neurological
dysfunction due to an abnormality in

cerebral circulation with resultant signs
& symptoms which corresponds to
involvement of focal areas of the brain
Dr. L. Surbala (MPT Neuro)

 Itis 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

 Itis 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

 Third leading cause of death
 The incidence of stroke is about 1.25
times greater for males than females
 Most common cause of disability among
adults

 Atherosclerosis
 Cerebral Thrombus Atherothromboembolism
 Cerebral embolus
 Embolism from the heart (cardiac origin)
 Intracranial hemorrhage
 Subarachnoid hemorrhage
 Intracranial small vessel disease
 Arterial aneurysms
 Arterio-venous malformation
 Haematological disorders (haemoglobinopathies,
leukemia)

 Infective endocarditis & HIV infection
 Tumour
 Perioperative stroke (due to hypotension and boundary
zone infarction, trauma to and dissection of neck arteries,
paradoxical embolism, fat embolism, infective endocarditis)
 Migraine
 Chronicmeningitis
 Inflammatory bowel disease (ulcerative and Crohn's
colitis)
 Hypoglycemia
 Snake bite, fat embolism

NON MODIFIABLE
 Ageing & gender
 Positive family history
 Circadian and seasonal
factors (peaks between 10 MODIFIABLE
am till noon)
 Smoking
 Heart disease
 Obesity
 Diabetes mellitus
 Lack of physical exercise
 Hypertension
or sedentary life style
 Peripheral arterial disease
 Diet & excess alcohol
 Blood pathology (increased
consumption
haematocrit, clotting
 Oral contraceptives
abnormalities, sickle cell
 Infection (meningeal
anaemia etc)
infection)
 Hyperlipidemia
 Psychological factors
 TIA
 Vasectomy

 Sudden numbness or weakness of face, arm, or leg,
on one side of body
 Sudden confusion, trouble speaking or
understanding
 Sudden blurring of vision
 Sudden onset of dizziness, loss of balance or
coordination
 Sudden, severe headaches with no known cause
 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)

 Ischemia results in irreversible cellular
damage with a core area of focal
infarction within minutes
• Transitional area surrounding core is termed
ischemic penumbra & consists of viable but
metabolically lethargic cells
 Ischemia produce cerebral edema, that
begins within minutes of insult &
reaches a maximum by 3 to 4 days.
 Swelling gradually subsides & generally
disappears by 2 to 3 weeks
 Oedema elevates ICP, leading to
intracranial HT & neurological
deterioration associated with
contralateral & caudal shifts of brain
structures
 Cerebral edema is the most frequent
cause of death in acute stroke & is
characteristic of large infarcts involving
MCA & ICA

 Depending on the cause
• Haemorrhagic stroke
 Intracranial haemorrhage
 Subarachnoid haemorrhage
 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. Characterised 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 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 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 symptoms
• MCA Syndrome
• ACA Syndrome
• PCA syndrome
• Vertebro basilar artery syndrome
 Vertebral artery
 Basilar artery
 Internal carotid artery
• Lacunar syndrome

• 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

 Contralateral hemiplegia (UL & face more
affected than LL)
 Contralateral hemisensory loss (UL & face
more affected than LL)
 Ideomotor apraxia
 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)

 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)
 Contralateral Hemiplegia or monoplegia
of LL (LL more affected than UL)
 Contralateral sensory loss of LL
 Urinary incontinence
 Problems with imitation & bimanual task
 Abulia (akinetic mutism)
 Apraxia
 Amnesia
 Contralateral grasp reflex, sucking
reflex
 Medial medullary syndrome (vertebral
artery)
 Lateral medullary (Wallenberg's) syndrome
(PICA)
 Complete basilar artery syndrome (locked-
in syndrome)
 Medial inferior pontine syndrome
 Lateral inferior pontine syndrome (AICA)
 Medial midpontine syndrome
 Lateral midpontine syndrome
 Medial superior pontine syndrome
 Lateral superior pontine syndrome

 Locked-in syndrome (LIS)
• Acute hemiparesis rapidly progressing to
tetraplegia & lower bulbar paralysis (CN V
through XII are involved)
• Initially patient is dysarthria & dysphonic &
progresses to mutism (anarthria)
• There is preserved consciousness & sensation
• Horizontal eye movements are impaired but
vertical eye movements & blinking remain
intact.
• Communication can be established via these eye
movements.
 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
 Dysarthria
 Clumsy hand syndrome
 Sensory/motor stroke
 Dystonia/involuntary movements

 1. Altered sensation
• Pain (central pain or thalamic pain syndrome
characterized by constant, severe burning pain
with intermittent sharp pains
• Hyperalgesia
• 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) is present immediately
after stroke
• Spasticity (hypertonicity) emerges in about 90
percent of cases

 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 (e.g.basilar 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.
• Apraxia is more evident with left hemisphere
damage than right and is commonly seen with
aphasia.
 Ideational apraxia
 Ideomotor apraxia

 9. Postural Control & Balance
• Impairments in steadiness, symmetry, & dynamic
stability
• Problems may exist when reacting to a
destabilizing external force (reactive postural
control) or during self-initiated movements
(anticipatory postural control).
• 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

Hemispheric Behavioral Differences.

 1. Musculoskeletal changes
• Loss of voluntary movement and immobility can
result in loss of ROM & contractures.
 Contractures are apparent in spastic muscles of
paretic limbs
• Disuse atrophy & muscle weakness results from
inactivity and immobility
• Osteoporosis, results from decreased physical
activity, changes in protein nutrition, hormonal
deficiency, & calcium deficiency.

 2. Neurological signs
• Seizures occur in a small % of patients - more
common in occlusive carotid disease than in
MCA disease
• Hydrocephalus is rare but can occur with
subarachnoid or intracerebral hemorrhage.

 3.Thrombophlebitis & deep venous
thrombosis (DVT)
• complications for all immobilized patients.

 4. Cardiac Function
• Stroke as a result of underlying coronary
artery disease (CAD) may demonstrate
impaired CO, cardiac decompensation, & rhythm
disorders.
• If these problems persist, they can alter
cerebral perfusion & produce additional focal
signs (e.g., mental confusion).
• Cardiac limitations in exercise tolerance

 5. Pulmonary Function
• Decreased lung volume, decreased pulmonary
perfusion & vital capacity & altered chest wall
excursion
• Aspiration, occurs in about one third of
patients with dysphagia.

 6. Integumentary
• The skin breaks down over bony prominences
from pressure, friction, shearing, and/or
maceration

 Urine analysis
 CBC count
 Blood sugar level
 Blood cholesterol & lipid profile
 Cardiac evaluation
 Lumbar puncture

 CT Scan
• In acute phase, CT scans are used to rule out
brain lesions such as tumor or abscess & to
identify hemorrhagic stroke
• In sub-acute phase, CT scans can identify
development of cerebral edema (within 3 days)
& cerebral infarction (within 3 to 5 days) by
showing areas of decreased density.

 Magnetic Resonance Imaging (MRI).
• MRI is more sensitive in diagnosis of acute
strokes, allowing detection of cerebral
infarction within 2 to 6 hours after stroke.
• It is also able to detail extent of infarction or
hemorrhage & can detect smaller lesions

 Cerebral Angiography.
• Involves injection of radiopaque dye into blood
vessels with subsequent radiography.
• It provides visualization of vascular system and
used when surgery is considered (carotid
stenosis, AVM).

 Fastest in first weeks after onset
 Measurable neurological & functional
recovery occurring in first month after
stroke.
 Continue to make measurable functional
gains for months or years after insult

 Laterecovery of function is also seen in
patients with chronic stroke who
undergo extensive functional training
• These changes are due to function-induced
plasticity

 Recovery also depends on severity of
stroke
 Depends on type of stroke –
hemorrhagic or ischemic
 Varies from individual to individual
 Depends on intensity of therapy
 Depends on age of the patient

A male patient with a known case of
hypertension came to emergency
department with history of sudden
collapse & LOC
 On examination there is decrease DTR
on right side of body with +ve Babinski’s
sign
 There is gradual regain of consciousness
but seems to be confused
 After a few days in hospital he regain
some of his LL movement but less
improvement in UL
 On careful examination he has right
Homonymous hemianopia & sensory loss
including two-point discrimination,
texture, & sense of weight
 He also has unilateral neglect & Broca’s
(expressive) aphasia
 What is the condition?
 What may be the cause?
 What emergency investigation is called
for ?
 Which artery may be involved?
 Which areas of the brain is involved?

 Abrupt onset with rapid coma is
suggestive of cerebral hemorrhage.
 Severe headache typically precedes LOC
 Embolus also occurs rapidly, with no
warning, & is frequently associated with
heart disease or heart complications.
 Uneven onset is typical with thrombosis.

 Pasthistory include TIAs or head
trauma, presence of major or minor risk
factors, medications, positive family
history, & recent alterations in patient
function

 May have abnormal posturing of limbs
 Synergistic patterns in the UL & LL
 Facial asymmetry
 May use a walking aid E.g. cane
 Abnormal gait pattern may also be
observed

 May present with hypertension
 Pain
 Shoulder pain, secondary to subluxation, is a common
issue
 Shoulder-hand syndrome involves swelling &
tenderness in hand and pain in entire limb
 Complex Regional Pain Syndrome involves pain &
swelling of hand

 Expressive and/or receptive aphasia
 Attention disorders
 Memory deficits, including declarative
and procedural memory
 Executive function deficits

 Visualfield deficits
 Weakness & sensory loss in facial
musculature
 Deficits in laryngeal & pharyngeal function
 Hypoactive gag reflex
 Diminished, but perceived, superficial
sensations

 Hemi sensory loss (dysesthesia, or hyperesthesia,
joint position & movement sense)
 May be able to identify sensations but difficulty
in localizing
 Cortical sensations s/a 2 point discrimination,
stereognosis & graphaesthesia are affected
secondary to loss of grip function
 Agnosia
 Perceptual problems
 Unilateral spatial neglect
 Pusher syndrome

 Glenohumeral subluxation
 Shoulder impingement syndrome
 Adhesive capsulitis
 Complex Regional Pain Syndrome and
Shoulder-Hand Syndrome

 Soft tissue shortening and contractures
 Increased muscle stiffness
 Joint immobility
 Disuse-provoked soft tissue changes
 Over extensibility of capsular
structures of Glenohumeral joint

 Synergistic patterns of movement
 Hypertonicity
 Weakness
 Associated movements or synkinesis
 Apraxia including motor & verbal apraxia

 Exaggerated deep tendon reflexes
 Diminished superficial reflexes
 Positive Babinski’s reflex
 Impaired Righting, equilibrium, and
protective reactions
 Abnormal primitive reflex (ATNR) may
be present

A sling for Glenohumeral support
 AFO
 Cane

 BP, RR, & HR at rest & during exercise
may have a sudden rise
 Review pulse oximetry, blood gas, tidal
volume, & vital capacity
 Administer a 2 or 6-minute walk test
 Administer Borg RPE after walk test or
other physical activity

 Edema may occur in affected limbs
 May be associated with shoulder hand
syndrome

• Decrease Tidal volume & vital capacity
• Decrease Respiratory muscle strength
• Ability to cough & strength of cough is
decreases
• Dyspnea during exercise

 Decreased extension of hip &
hyperextension of knee
 Decreased flexion of knee & hip during
swing phase
 Decreased ankle DF at initial contact &
during stance resulting in hip
circumduction
 Trendelenburg

 Compromised static as well as dynamic
balance
 Pusher’s syndrome may be present
resulting in fall on the affected side

 Spastic patterns can involve flexion &
abduction of arm, flexion of elbow, &
supination of elbow with finger flexion
 Hip & knee extension with ankle
plantarflexion & inversion
 Protracted & depressed shoulder,
scoliosis & hip hiking

 Using FIM, Barthel index, FMA
 There is compromised basic as well as
instrumental ADL
 Ambulatory capacity is compromised

 Flaccid bowel & bladder during the acute
stage
 Bowel & bladder function gradually
regains
 Uninhibited bladder if frontal lobe is
involved
 Constipation is frequently seen

 Tonal abnormalities
 Muscular weakness
 Synergistic pattern
 Tightness & contracture
 Imbalance & incoordination
 Gait abnormalities
 Postural abnormalities
 Functional disability

 Positioningstrategies
 Improve respiratory & circulatory
function
 Prevent pressure sores
 Prevent from deconditioning

 Positioning strategies
• In supine
• In side lying on normal side
• In side lying on affected side

 Improve respiratory & circulatory
function
• Breathing exercise
• Chest expansion exercise
• Postural drainage
• Huffing & Coughing techniques
• Passive & active ankle & toe exercise
 (after careful & thorough examination of
cardiopulmonary system)

 Prevent pressure sores
• Proper positioning
• Relieve pressure points by padding & cushion
• Frequent turning & changing position
• Prevent from moisture
• Use cotton clothing
• Tight fitting cloth is prevented
• Use of water bed, air bed & foam mattress

 Prevent from deconditioning
• Early mobilization in the bed (active turning,
supine to sit, sit to supine, sitting, sit to stand)
• Pelvic bridging exercise
• Early propped up positioning, sitting & then
later to standing
• Moving around the bed
• Facilitate movement of functioning limbs

5 days a week for a minimum of 3 hours
of active rehabilitation per day
 Intensive rehabilitation if vitals are
stable

 Positioning hemiplegic side towards door or
main part of room
 Presentation of repeated sensory stimuli
 Stretching, stroking, superficial & deep
pressure, iceing, vibration etc.
 Wt bearing ex & Joint approximation tech
 Stoking with different texture fabrics
 Pressure application
 Improve other senses like use of visual &
auditory
 PNF tech., use of bilateral UE

 Soft tissue, joint mobilization & ROM
exercise
 AROM & PROM with end range stretch
 Effective positioning & edema reduction
 Stretching program & splinting
 Suggested activities
• Arm cradling
• Table top polishing
• Self overhead activities in supine & sitting &
reaching to the floor

 Strengthening of agonist & antagonistic
muscle
 Graded ex program using free weights,
therabands, sand bags & isokinetic
devices
 For weak patients (<3/5), gravity-
eliminated ex using powder boards, sling
suspension, or aquatic ex is indicated
 Gravity-resisted active movts are
indicated (>3/5 strength)
 Sustained stretch & slow iceing of spastic
muscle
 Rhythmic rotations
 Weight bearing exercise
 Prolonged & firm pressure application
 Slow rocking movement
 Positioning in anti synergistic pattern
 Rhythmic initiation
 Air splints
 Neural warmth
 Electrical stimulation

 Dissociation & selection of desired movt
patterns
 Select postures that assist desired
movements through optimal biomechanical
stabilization & use of optimal point in
range
 Start with assisted movt, followed by
active & resisted movt
 Task oriented exercise

 Suggested exercise
• Rolling
• Supine to sit & sit to supine
• Sitting
• Bridging
• Sit to stand & Sit down
• Modified plantigrade
• Standing
• Transfer

 In pusher syndrome
• Passive correction often fails
• Use visual stimuli to correct
• Sit on the normal side & ask patient to lean on
you
• Sitting on swiss ball
• Environmental boundary can be used e.g. corner
or doorway

• Early mobilization, ROM, & positioning strategies
• Relearning of movt pattern & retraining of missing
component
• UL weight bearing exercise
• Dynamic stabilization exercise
• Picking up objects, Reaching activities
• Lifting activities
• Manipulation of common objects
• Push up ex. in various position
• Kitchen sink exercise
• Functional movement like hand to mouth & hand to
opposite shoulder
• Advance training – CIMT, biofeedback, NMES, FES
 Proper handling & positioning of shoulder
joint
 Reducing subluxation, NMES, gentle
mobilization (grade 1 & 2)
 Use of supportive devices & slings
 Use of overhead pulley is contraindicated
 TENS & heat therapy

 Strengthening muscles in appropriate
pattern
 Suggested activities
• PNF pattern of LL
• Holding against elastic band resistance around
upper thighs in supine or standing positions
• Standing, lateral side-steps
• Exercise to improve pelvic control
 Facilitationof DF
 Cycling & treadmill training

 Facilitate symmetrical wt bearing on both side
 Postural perturbations can be induced in
different positions
 Sit or stand on movable surface to increase
challenge
 Reaching activities
 Dual task training s/a kicking ball in standing,
throwing activities, carrying an object while
walking
 Divert attention
 Single limb stance
 Exercise on trampoline

 Initial gait training between parallel
bars
 Proceed outside bars with aids & then
without aids
 Walking forward, backward, sideways &
in cross patterns
 PBWSTT with higher speed improve
overall locomotor activity & overground
speed
 Proper use of orthotics & wheelchair

• Early mobilization & functional activity
• Treadmill training & cycle ergometer
• Symptom limited graded ex. training
• Ex at 40- 70 % of VO2max, 3 times a week for
20-60 minutes
• Proper rest should be given
• Gradually progressed to 30 minutes continous
program
• Regular ex reduces risk of recurrent stroke

 Proper head position in chin down position
 Movements of lips, tongue, cheeks, & jaw
 Firm pressure to anterior 3rd of tongue
with tongue depressor to stimulate
posterior elevation of tongue,
 Puffing, blowing bubbles, & drinking thick
liquids through straw
 Food presentation in proper position
 Texture of food should be smooth
 Tasty food should be given to facilitate
swallowing reflex
 Stroking the neck during swallowing

 Strategy development
• Patient as an active explorer of activity
• Modify strategy of activity in correct patterns
 Feedback
• Intrinsic or extrinsic feedback
• Positive & negative feedbacks
 Practice
• Repeated practice of functional activity
• Practice in different environment

 Give factual information, counsel family
members about patient’s capabilities &
limitations
 Give information as much as Pt or family
can assimilate
 Provide open discussion & communication
 Be supportive, sensitive & maintain a
positive supporting nature
 Give psychological support
 Refer to help groups

 Family member should participate daily
in the therapy session & learn exercises
 Home visits should be made prior to
discharge
 Architectural modifications, assistive
devices or orthotics should be ready
before discharge
 Identify community service & provide
information to the patient
 O’Sullivan SB, Schmitz TJ. Stroke.
Physical rehabilitation. 5th ed., New
Delhi: Jaypee Brothers, 2007.
 Darcy A. Umphred. Neurological
Rehabilitation, 5th ed., Mosby Elsevier,
Missouri, 2007.

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 Stroke is an acute onset of neurological

dysfunction due to an abnormality in

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

• Stage 2: basic limb synergies or some of their

Dr. L. Surbala (MPT Neuro)

• Stage 4: some movement combination that do not

Dr. L. Surbala (MPT Neuro)

• Stage 6: disappearance of spasticity, individual

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)

Dr. L. Surbala (MPT Neuro)