This document provides information about stroke including: - Definitions stroke as the sudden loss of neurological function caused by interrupted blood flow to the brain. - Descriptions of the types of strokes - haemorrhagic caused by blood vessels rupturing and ischemic caused by a blood clot blocking blood flow. - Details of assessments including reviewing systems like cardiovascular, respiratory and neurological systems. - Explanations of physiotherapy management which involves reducing impairments and improving functional ability.

1. STROKE
Dr. N.K.CHOUDHARY (PT)

2. CONTENTS
 DEFINITION
 TYPE OF STROKES
 ASSESSMENTS
 PHYSIOTHERAPY MANAGEMENT

3. DEFINITION
 Stroke (Cerebrovascular accident[CVA]) is the sudden
loss of neurological function caused by an interruption
of the blood flow to the brain.

4. CIRCLE OF WILLIS
ACA= ANTERIOR CEREBRAL
ARTERY
MCA= MIDDLE CEREBRAL ARTERY
PCA = POSTERIOR CEREBRAL
ARTERY
ICA = INTERNAL CAROTID ARTERY
CCA = COMMON CAROTID ARTERY

5. CIRCLE OF WILLIS cont..
 TWO arteries , called the
carotid arteries ,supply
blood to the brain. they
run along either side of
neck and provide collateral
flow between the anterior
and posterior circulations
of the brain.
 Each carotid artery
branches into an internal
and external carotid
artery.
 The internal carotid artery
then branches into an
cerebral arteries.
 Anterior circulation of the
brain derives from bilateral
ICAs

6. CIRCLE OF WILLIS
cont…
 Posterior communicating
artery is given off as a
branch of the internal
carotid artery just before it
divides into its terminal
branches - the anterior and
middle cerebral arteries.
The anterior cerebral artery
forms the anterolateral
portion of the circle of Willis,
while the middle cerebral
artery does not contribute to
the circle.
 The right and left posterior
cerebral arteries arise from
the basilar artery, which is
formed by the left and
right vertebral arteries.
The vertebral arteries arise
from the subclavian
arteries.

7. CIRCLE OF WILLIS
cont…
 The anterior communicating
artery connects the two
anterior cerebral arteries
and could be said to arise
from either the left or right
side.
 All arteries involved give off
cortical and central
branches. The central
branches supply the interior
of the circle of Willis, more
specifically, the
Interpeduncular fossa. The
cortical branches are
named for the area they
supply.

8. TYPES OF STROKE
HAEMORRHAGIC STROKE ISCHAEMIC STROKE
- Occurs when blood vessels
rupture, causing leakage of
blood in or around the brain.
-affecting about 80% of
individuals with stroke,
results when a clot blocks or
impairs blood flow,depriving
the brain of essential oxygen
and nutrients.
-80% of that type.

9. EPIDEMIOLOGY AND ETIOLOGY
 Stroke is the fifth leading cause of death and the
leading cause of long-term disability among adults in the
United States.
 The incidence of stroke increases dramatically with
age, effectively doubling in the decade after 65 years of
age. Approximately 10% of all strokes occur in
individuals 18 to 50 years of age. Between 5% and 8% of
persons who survive an initial stroke will experience
another one within 1 year; within 5 years, stroke will recur
in 16%.
 ischemic stroke survivors 65 or older, incidences of
disabilities observed at 6 months include hemiparesis
(50%), inability to walk without assistance (30%),
dependence in activities of daily living (ADL) (26%),
aphasia (19%), and depression (35%).

10. ISCHAEMIC STROKE
 thrombus(a blood clot within
the cerebral arteries or their
branches),
embolism(composed of bits
of matter (blood clot,
plaque) formed elsewhere
and released into the
bloodstream, traveling to
the cerebral arteries where
they lodge in a vessel,
producing occlusion and
infarction)

11. HAEMORRHAGIC STROKE
 abnormal bleeding into the extravascular
areas of the brain, are the result of rupture of a
cerebral vessel or trauma.
 increased intracranial pressures with injury to
brain tissues and restriction of distal blood
flow.
 Intracerebral hemorrhage (IH) is caused by
rupture of a cerebral vessel with subsequent
bleeding into the brain.
 Primary cerebral hemorrhage (nontraumatic
spontaneous hemorrhage) typically occurs in
small blood vessels weakened by
atherosclerosis producing an aneurysm.
 Subarachnoid hemorrhage (SH) occurs from
bleeding into the subarachnoid space typically
from a saccular or berry aneurysm affecting
primarily large blood vessels.

13. RISK FACTORS
 Major risk factors for stroke are hypertension, diabetes
mellitus (DM), disorders of heart rhythm, high blood
cholesterol and other lipids, smoking/tobacco use, and
heart disease (HD).
 Cardiac disorders (e.g., rheumatic heart valvular disease,
endocarditis) and cardiac surgery (e.g., coronary artery
bypass graft [CABG]) increase the risk of embolic stroke.
 Cardiac disorders (e.g., rheumatic heart valvular disease,
endocarditis) and cardiac surgery (e.g., coronary artery
bypass graft [CABG]) increase the risk of embolic stroke.

14. WARNING SIGNS OF STROKE
 Early
warning
signs
identified
by the
America
n Heart
Associati
on and
National
Stroke
Asso-
ciation,
known
as FAST.

15.  Sudden cessation of CBF and oxygen-glucose
deprivation sets in motion a series of pathological events.
 Within minutes, neurons die in the ischemic core tissue,
while the majority of neurons in the surrounding
penumbra survive for a slightly longer time.
 Cell survival depends largely on the severity and the
duration of the ischemic episode.
 For cells to survive, 20% to 25% of regular blood flow is
required. Without timely reperfusion, cells in the
penumbra die, neuronal activity ceases, and the infarct
expands.
PATHOPHYSIOLOGY

16. PATHOPHYSIOLOGY

17. TRANSIENT ISCHEMIC
STROKE(TIA)
 It refers to the temporary interruption
of blood supply to the brain.
 The risk for recurrent stroke is 3.5%,
8%, and 9.2% at 2, 30, and 90 days
post-TIA respectively.
 Symptoms
 focal neurological deficit may last for
only a few minutes or for several
hours but by definition do not last
longer than 24 hours.
 After the attack, there may be
evidence of residual brain damage
or permanent neurological
dysfunction.

18.  CAUSES :
 occlusive episodes
 emboli
 reduced cerebral perfusion (arrhythmias, decreased
cardiac output, hypotension, overmedication with
antihypertensive medications, subclavian steal
syndrome),
 cerebrovascular spasm.

19. ASSESSMENT
SUBJECTIVE ASSESSMENT:
PERSONAL PROFILE
A) DATE OF ASSESSMENT
B) NAME OF PATIENT
C) AGE AND GENDER
D) HEIGHT
E) WEIGHT
F) BMI
G) HAND DOMINANCY
H) OCCUPATION OF PATIENT
I) ADDERESS
J) MARITAL STATUS
K) REFRENCE DOCTOR
L) PROVISIONAL DIAGNOSIS

20. ANTERIOR CEREBRAL ARTERY
SYNDROME
 FIRST AND SMALLER OF TWO TERMINAL BRANCHES OF
INTERNAL CAROTID ARTERY.
 SUPPLIES MEDIAL ASPECT OF CEREBRAL
HEMISPHERE(FRONTAL AND PARIETAL LOBES) AND
SUBCORTICAL STRUCTURES INCLUDING BASAL
GANGLIA ,ANTERIOR FORMIX AND ANTERIOR FOUR-
FIFTHS OF CORPUS CALLOSUM.
 AS ANTERIOR COMMUNICATING ARTERIES ALLOWS THE
PERFUSION OF PROXIMAL ACA ,OCCLUSION PROXIMAL TO
THIS POINT RESULTS IN MINIMAL DEFICIT, DISTAL
OCCLUSION CAUSE MORE SIGNIFICANT DAMAGE.

21. CLINICAL MANISFESTATION OF
ACA
 CONTRALATERAL HEMIPARESIS
 SENSORY LOSS WITH GREATER INVOLVEMENT OF LOWER
EXTREMITY THAN UPPER EXTREMITY.
 URINARY INCONTINENCE
 PROBLEMS WITH IMITATION AND BIMANUAL TASKS
 ABULIA(INABILITY TO ACT DECISIVELY),SLOWNESS AND
DELAY IN MOTOR ACTION.

22. MIDDLE CEREBRAL ARTERY
SYNDROME
 IT IS SECOND OF THE TWO MAIN BRANCHES OF INTERNAL
CAROTID ARTERY AND SUPPLIES ENTIRE LATERAL
ASPECT OF CEREBRAL HEMISPHERE(
FRONTAL,TEMPORAL AND PARIETAL LOBE) AND
SUBCORTICAL STRUCTURES,INCLUDING INTERNAL
CAPSULE(POSTERIOR PORTION),CORONA
RADIATA,GLOBUS PALLIDUS,CAUDATE NUCLEUS AND
PUTAMEN.
 OCCLUSION OF PROXIMAL MCA PRODUCES EXTENSIVE
NEUROLOGICAL DAMAGE WITH SIGNIFICANT CEREBRAL
EDEMA.
 INCREASED INTRACRANIAL PRESSURES TYPICALLY LEAD
TO LOSS OF CONSCIOUSNESS , BRAIN HERNIATION AND
POSSIBLY DEATH.

23. CLINICAL MANISFESTATION OF
MCA
 CONTRALATERAL HEMIPARESIS INVOLVING MAINLY UE AND
FACE( LE IS MORE SPARED).
 CONTRALATERAL HEMISENSORY LOSS INVOLVING MAINLY
THE UE AND FACE(LE IS MORE SPARED)
 MOTOR SPEECH IMPAIRMENT : BROCA’S OR NONFLUENT
APHASIA WITH LIMITED VOCABULARY AND
SLOW,HESITANT SPEECH.
 RECEPTIVE SPEECH IMPAIRMENT: WERNICK’S OR FLUENT
APHASIA
 GLOBAL APHASIA:NON-FLUENT SPEECH WITH POOR
COMPREHENSION

24. CLINICAL MANISFESTATION OF
MCA CONT…
 CONTRA-LATERAL HOMONYMOUS HEMIANOPSIA.
 SENSORY ATAXIA OF CONTRALATERAL LIMBS
 PURE MOTOR HEMIPLEGIA.

25. POSTERIOR CEREBRAL ARTERY
 TWO POSTERIOR CEREBRAL ARTERIES ARISE AS TERMINAL
BRANCHES OF BASILAR ARTERY AND EACH SUPPLES THE
CORROSPONDING OCCIPITAL LOBE AND MEDIAL AND
INFERIOR TEMPORAL LOBE.
 IT ALSO SUPPLIES UPPER
BRAINSTEM,MIDBRAIN,POSTERIOR DICENPHALON AND
MOST OF THALAMUS.
 OCCLUSION OF POSTERIOR COMMUNICATING ARTERY-
SIMILAR TO ACA
 OCCLUSION OF THALAMIC BRANCHES-HEMIANESTHESIA
(CONTRALATERAL SENSORY LOSS) OR CENTRAL POST-
STROKE(THALAMIC)PAIN.

26. POSTERIOR CEREBRAL ARTERY
CONT…
 OCCIPITAL INFRACTION-HOMONYMOUS
HEMIANOPSIA,VISUAL AGNOSIA,PROSPOGNOSIA(INABILITY
TO RECOGNIZE FAMILIAR FACE)
 BILATERAL OCCIPITAL INFRACTION-CORTICAL BLINDNESS
 TEMPORAL LOBE ISCHEMIA-AMNESIA(MEMORY LOSS)

27. CLINICAL MANIFESTATION OF
PCA
 CONTRALATERAL HOMONYMOUS HEMIANOPSIA
 VISUAL AGNOSIA(INABILITY TO NAME AND DESCRIBE
OBJECT)
 PROSPOGNOSIA (DIFFICULTY IN NAMING PEOPLE ON
SIGHT)
 DYSLEXIA(DIFFICULTY READING)
 COLOR DISCRIMINATION PROBLEM
 MEMORY DEFECT
 DISORIENTATION

28. B) CHIEF COMPLAINS AND ADL
DIFFICULTY:
 ON PATIENT’S WORD:
 TURNING
 SUPINE TO SIDELYING
 SUPINE TO SITTING
 DIFFICULTY IN EATING-
LIQUIDS,SEMISOLID,SOLID
 DRINKING DIFFICULTY
 BATHING DIFFICULTY
 DRESSING DIFFICULTY
 SITTING
 STANDING
 SIT TO STAND
 TOILETING
 STAIR CLIMBING
 SPEAKING

29. C) HISTORY
 A) HISTORY OF PRESENT
ILLNESS:
 B) HISTORY OF PAST
ILLNESS:
 C) PAIN HISTORY:
 ONSET OF PAIN
 DURATION OF PAIN
 SITE/LOCATION OF PAIN
 TYPE/QUALITY OF PAIN
 INTENSITY OF PAIN-
VAS,NPRS,MACGILL
QUESTIONNARIE
 AGGRAVATING/RELIEVING
FACTORS

30. D) SURGICAL HISTORY
 DETAILS OF ANY
SURGERY THE PATIENT
HAS UNDERWENT :
 A) DATE OF SURGERY:
 B)TYPE OF SURGERY
 C) OPERATIVE DETAILS
 D) POST-OPERATIVE
DETAILS
 CRANIOTOMY
 BURR-HOLE SURGERY

31. E) PERSONAL HISTORY
 BAD HABBITS LIKE
TOBACCO
CHEWING,ALCOHOL
INTAKE,DRUG ABUSE.ETC
 1) DURATION
 2)QUANTITY
 PACK OF YEAR:
 QUANTIFICATION OF
CIGARETTE SMOKING:
 NO.OF PACK-YEARS=
(NO.OF CIGRAETTES PER
DAY/20) .NUMBER OF
YEARS SMOKED.

32. F) DRUG/ PHARMACOLOGICAL
HISTORY
 LIST OF MEDICATIONS
 DURATION B/W TWO DOSAGE

33. G) FAMILY HISTORY
 HEREDITARY CONDITIONS LIKE HYPERTENSION, DIABETES
,ETC.
 1.H/O-PARENTS
 2.H/O-SIBLINGS
 3.H/O-GRANDPARENTS

34. H) OCCUPATIONAL HISORY
 1. NAME OF OCCUPATION
 2.DURATION OF
OCCUPATION
 3.TYPE OF OCCUPATION
 4. ENVIRONMENT OF
OCCUPATION
 5.ERGONOMICS OF
OCCUPATION
 TO RULL OUT ANY OF
RISK-FACTORS

35. G) ENVIRONMENTAL HISTORY
 TO RULLING OUT ANY ENVIRONMENTAL RELATED
CONDITION

36. J) SOCIO-ECONOMIC STATUS
 UPPER CLASS
 UPPER-MIDDLE CLASS
 LOWER-MIDDLE CLASS
 LOWER CLASS

37. K) PSYCHOLOGICAL HISTORY
 1. ANY EMOTIONAL DISTURBANCES
 2.ANXIETY OR DEPRESSION

38. I) INVESTIGATIONS
 RADIOLOGICAL
 X RAY,CT SCAN, MRI
 HEMATOLOGICAL
 CBC

39. OBJECTIVE ASSESSMENT:
 A) VITAL PARAMETERS:
 A. RESPIRATORY RATE:
 B.PULSE RATE:
 C.BLOOD PRESSURE:
 D.TEMPRATURE:

40. B) ON OBSERVATION
 A. BODY BUILT:
 BMI

41.  B. BREATHING PATTERN:
 THORACO-ABDOMINAL
 ABDOMINO-THORACIC
 C.I:E RATIO
 NORMAL=1:2

42. D. TROPHICAL CHANGES
 1) SWELLING/ODEMA:
 PRESENT ON UNUSED OR AFFECTED SITE.
 SITE OF SWELLING
 2) MUSCLE WASTING:
 ON AFFECTED SIDE BECAUSE OF IT’S UNUSED.
 3) SKIN CONDITIONS
 COLOR AND TEXTURE:
 DRY SKIN AND UNEVEN TEXTURE IF THERE IS AUTONOMIC
CHANGES.

43.  4) NAILS:
 1.COLOR-
 2.SHAPE-

45.  E) SCAR/PRESENCE OF PRESSURE SORES:
 1) SITE OF SCAR
 2) SIZE OF SCAR
 3)INFECTIVE/NON-INFECTIVE
 4) HEALING/NON-HEALING

47. F) ATTITUDE OF LIMB

48. G) DEFORMITIES
 1. NAME OF DEFORMITY
 2. SITE OF DEFORMITY
 3. SIDE OF LIMB WHERE
DEFORMITY IS PRESENT
 DUE TO STIFFNESS THAT
LEADS TO RESTRICT
MOTION LEADS TO
DEFORMITY .

49. H) EXTERNAL AIDS
/APPLIANCES

50. I)POSTURE
 ACCORDING TO SYNERGY.
 EXAMINE POSTURE
 LATERAL , ANTERIOR AND POSTERIOR VIEW
 DURING SUPINE,SITTING AND STANDING POSITIONS.

51. J) GAIT
 EQUINUS GAIT:
 HEEL DOESN’T TOUCH THE GROUND
 DUE TO CONTRACTURE OF GASTROCNEMIUS AND SOLEUS
 VARUS FOOT:
 PATIENT BEARS MORE WEIGHT ON THE LATERAL SIDE OF
FOOT
 DUE TO SPASTIC ANTERIOR TIBIALIS,SOLEUS AND TOE
FLEXORS
 LACK OF DORSIFLEXION IN STANCE PHASE AND
EXAGGERATED DF IN SWING PHASE
 UNEQUAL STEP LENGTH
 WIDE BASE OF SUPPORT

52. C) ON PALPATION
 A) TENDERNESS:

53.  B) WARMTH:
 SIDE AND SITE
 PRESENT IF SWELLING IS PRESENT.
 C)LOCAL SWELLING OR ODEMA:
 D)MUSCLE TONE:
 SITE AND SIDE
 INCREASED/DECREASE
 SPASTICITY IN SUB-ACUTE AND CHRONIC STAGE,
FLACCIDITY IN ACUTE STAGE
 E) SCAR: MOBILE/NON-MOBILE

54. D) ON EXAMINATION
 A. HIGHER MENTAL FUNCTION EXAMINATION:
 1) LEVEL OF CONSCIOUSNESS:
 GCS/MMSE

55. GCS

56. MMSE

57. INTERPRETATION OF MMSE

58.  B) BEHAVIOUR:
 DEPRESSED
 IRRITATED
 NOT RESPONDENT
 E) ATTENTION
 SUSTAINED ATTENTION
 SELECTIVE ATTENTION
 DIVIDED ATTENTION
 ALTERNATING ATTENTION

59.  F) MEMORY:

60.  4) VISION
 HEMIANOPIA: partial blindness or a loss of sight in
half of your visual field.

61.  5) SPEECH:
 DYSARTHRIA:
 APHASIA:
 DYSPHONIA:

62.  6) DYSPHAGIA
 7) HEARING:
 8) PERCEPTION EXAMINATION
 9) CRANIAL NERVE EXAMINATION

63. CRANIAL NERVE INTEGRITY
 CN V: FACIAL SENSATION
 CV V AND VII:FACIAL MOVEMENTS
 CN VIII: AUDITORY FUNCTION
 CN IX,X,XII: DETERMINATION OF MOTOR FUNCTION AS
WELL GAG REFLEX .
 IF GAG REFLEX IS NEGATIVE –POSSIBILITY OF ASPIRATION.
 CN II: VISUAL FIELD DEFECTS
 CN II AND III: ABSENT PUPILLARY REFLEX
 CN III,IV AND IX: ABSENCE OF EXTRAOCULAR MOVEMENT

64.  10) SENSORY EXAMINATION
SUPERFICIAL DEEP COMBINED
CORTICAL
PAIN
TOUCH
TEMPRATURE
LIGHT PRESSURE
CRUDE TOUCH
PROPRIOCEPTION
KINESTHETIC
SENSATION
VIBRATION
CRUDE PRESSURE
STEREOGNOSIS
TACTILE
LOCALIZATION
TWO POINT
DISCRIMINATION
GRAPHESTHESIA
BAROGNOSIS

65. INTERPRETATION OF SENSORY
 TOUCH(64-94%), PAIN, TEMPRATURE, VIBRATION(44%)
PROPRIOCEPTION(17-52%) ARE MOST COMMONLY
AFFECTED.
 KEY TO GRADING
INTACT NORMAL ACCURATE RESPONSE
DECRESED DELAYED RESPONSE
EXAGGERATED INCREASED SENSITIVITY
INACCURATE INAPPROPRIATE PERCEPTION OF STIMULUS
ABSENT NO RESPONSE
INCONSISTENT RESPONSE INADEQUATE TO DETERMINE
FUNCTION

66. D. MOTOR EXAMINATION
 1. MUSCLE TONE
 SPASTICITY GRADING BY MAS

67. 2.REFLEXS
SUPERFICIAL REFLEXES DEEP REFLEXES
CORNEAL
CONJUCTIVAL
ABDOMINAL
PLANTAR
BICESPS JERK
TRICEPS JERK
PATELLAR JERK
ANKLE JERK
0 NO RESPONSE
1+ PRESENT BUT DEPRESSED,LOW NORMAL
2+ AVERAGE,NORMAL
3+ INCREASE,BRISKER THAN AVERAGE
4+ VERY BRISK,WITH CLONUS;ABNORMAL

68. INTERPRETATION
 INITIALLY,HYPOREFLEXIA WITH FLACCIDITY.
 WHEN SPASTICITY AND SYNERGY
EMERGES,HYPERREFLEXIA IS SEEN.
 DEEP TENDON REFLEXES ARE HYPERACTIVE AND
PATIENTS DEMONSTRATES CLONUS AND +VE BABINSKI
SIGN.
 ATNR-HEAD ROTATION CAUSES ELBOW EXTENSION OF
UPPER EXTREMITY WITH ELBOW FLEXION OF OPPOSITE
LIMB.-COMMONLY SEEN

69.  3) TIGHTNESS/CONTRACTURE/DEFORMITY;
 ACCORDING TO PATIENT
 CONTRACTURES ARE LIKELY IN ELBOW FLEXORS,WRIST
AND FINGER FLEXORS AND FOREARM PRONATORS.
 4)CHEST EXPANSION
 MAY OR MAY NOT REDUCED
 5)ROM:AFFECTED
 AROM IS LIMITED DUE TO TONAL ABNORMALITIES

70. VOLUNTARY CONTROL
GRADING

71.  8) ODEMA ASSESSMENT AND MUSCLE WASTING
 SEEN IN UNUSED LIMB.
 9)BALANCE ASSESSMENT
 STATIC BALANCE
 DYNAMIC BALANCE
 SCALES :
 1.BBS
 2.POMA
 3.TUG
 4.FUNCTIONAL REACH TEST

72.  10) COORDINATION ASSESSMENT:
 PROPRIOCEPTIVE LOSSES CAN RESULT IN SENSORY
ATAXIA.
 SLOWED MOVEMENTS-BRADYKINESIA
 INVOLUNTARY MOVEMENTS
 YOU CAN ASSESS FINGER TO NOSE, HEEL DRAG
 11)BOWEL BLADDER EXAMINATION:
 INCONTIENCE ASSESSMENT
 CHECK PELVIC FLOOR STRENGTH

73. E) SPECIAL TESTS:
 1. FUGL-MEYER ASSESSMENT(FMA)
 2.POSTURAL ASSESSMENT SCALE
 3.STROKE REHABILITATION ASSESSMENT OF
MOVEMENT(STREAM)
 4.STROKE IMPACT SCALE(SIS)
 5.CHEDOKE-MCMASTER STROKE ASSESSMENT

74.  F) PHYSICAL AND FUNCTIONAL DIAGNOSIS:ICF
 G)CLINICAL CONCLUSION AND PT DIAGNOSIS

75. MANAGEMENT
ACUTE STAGE SUB-ACUTE STAGE CHRONIC STAGE
WITHIN 72 HOURS
SEEN IN ICU OR
SPECIALIZED STROKE
CARE UNIT
AVERAGE STAY IS ABOUT
5 DAYS
LEARNED NONUSE OF
HEMIPARETIC
EXTREMITIES AND
MALADAPTIVE
PATTERNS OF
MOVEMENT ARE
MINIMIZED.
DAY 4 UPTO 6 MONTHS
TRANSFFERED IN
TRANSITIONAL UNIT.
60-90 MINUTES OF
THERAPY 5 DAYS/WEEK
MORE THAN 6 MONTHS
OUT-PATIENT
INTERVENTION IS
NECESSARY.

76. IMPROVE MOTOR LEARNING
 MOTOR SKILL LEARNING IS BASED ON BRAIN’S CAPACITY
FOR RECOVERY THROUGH MECHANISM OF
REORGANIZATION AND ADAPTATION.
 AN EFFECTIVE REHAB PLAN CAPITALIZES ON THIS
POTENTIAL AND ENCOURAGES ACTIVE PARTICIPATION.
 ACTIVITY> SELECTIVE,MEANINGFUL AND IMPORTANT
 OPTIMAL MOTOR LEARNING>STRATEGY
DEVELOPMENT,FEEDBACK AND PRACTICE

77. IMPROVE MOTOR LEARNING
CONT…
 STRATEGY DEVELOPMENT:
 THERAPIST ASSIST PATIENT IN LEARNING DESIRED TASK-
COGNITIVE STAGE
 VERBAL CUES AND MORE ATTENTION IS REQUIRED.
 TASK-ANALYSIS
 FEEDBACK:
 MIRROR THERAPY : IMPROVE DORSIFLEXION AND UE
FUNCTION.
 IMPROVING DETECTION OF LIGHT,TOUCH
,PRESSURE,PAIN AND TEMPRATURE
 INTRINSIC- OCCURING AS PART OF MOVEMENT
 EXTRINSIC-PROVIDED BY THERAPIST
 EXP: VERBAL CUEING

78. IMPROVE MOTOR LEARNING
CONT…
 PRACTICE:
 PRACTICE IS MORE IMPORTANT.
 MOTIVATION IS KEY TO SUCCESS.
 SUPPORTIVE STRATERGIES ARE USED TO CLOSED
ENVIORNMENT > OPEN ENVIORNMENT
 ENVIORNMENT-MINIMUM DISTRACTIONS
 MOTIVATION IS KEY TO SUCCESSFUL LEARNING.

79. INTERVENTIONS TO IMPROVE
SENSORY FUNCTION
 MORE PATIENT USED AFFECTED SIDE> GREATER CHANCES
OF INCREASED AWARENESS AND FUNCTION.
 SENSORY RETRAINING PROGRAMME-
 1.MIRROR THERAPY
 2.REPETITIVE SENSORY DISCRIMINATION ACTIVITIES
 3.REPETITIVE TASK PRACTICE
 SENSORY STIMULATION ACTIVITIES:
 1.COMPRESSION TECHNIQUE-WEIGHT BEARING,MANUAL
COMPRESSION,INFLATABLE PRESSURE
SPLINTS,INTERMITTENT PNEUMATIC COMPRESSION.

80. INTERVENTIONS TO IMPROVE
HEMIANOPSIA AND UNILATERAL
NEGLECT
 PATIENTS WITH HEMIANOPSIA OR UNILATERAL NEGLECT
DEMONSTRATES THE STATE OF LACK OF AWARENESS OF
CONTRALATERAL SIDE.