1. The document provides information about stroke, including its definition, risk factors, pathophysiology, early warning signs, and primary impairments. It notes that stroke is caused by either blockage or rupture of blood vessels in the brain. 2. High blood pressure, diabetes, heart disease, smoking, age, race, family history, and prior stroke or TIA are identified as major risk factors. Ischemic and hemorrhagic strokes are described in terms of pathophysiology. 3. Early warning signs include sudden numbness, confusion, vision problems, and difficulty walking or balancing. Primary impairments involve sensation, motor function, coordination, reflexes, and speech/language.

1. STROKE
Guide to physiotherapists
Dr Suraj B.Kanase
Associate professor
Krishna College Of Physiotherapy

2. Definition :
• Stroke is defined by the World Health Organization
as 'a clinical syndrome consisting of rapidly developing
clinical signs of focal (or global in case of coma)
disturbance of cerebral function lasting more than
24 hours or leading to death with no apparent
cause other than a vascular origin.

3. Risk factors for Stroke :
• High blood pressure.
High blood pressure is the main risk factor for stroke.
Blood pressure is considered high if it stays
at or above 140/90 millimeters of mercury (mmHg) over time.
If you have diabetes or chronic kidney disease,
high blood pressure is defined as
130/80 mmHg or higher.

4. • Diabetes.
Diabetes is a disease in which the blood sugar level
is high because the body doesn’t make enough insulin
or doesn’t use its insulin properly.
Insulin is a hormone that helps move blood sugar
into cells where it’s used for energy.

5. • Heart diseases. Coronary heart disease, cardiomyopathy, heart
failure, and atrial fibrillation can cause blood
clots that can lead to a stroke.
• Smoking. Smoking can damage blood vessels and raise
blood pressure. Smoking also may reduce the amount of
oxygen that reaches your body’s tissues.
Exposure to second hand smoke also can damage the blood vessels.

6. • Age and gender. Your risk of stroke increases as you get older. At
younger ages, men are more likely than women to have strokes.
However, women are more likely to die from strokes. Women who
take birth control pills also are at slightly higher risk of stroke.
• Race and ethnicity. Strokes occur more often in African American,
Alaska Native, and American Indian adults than in white, Hispanic, or
Asian American adults.

7. • Personal or family history of stroke or TIA. If you’ve had a stroke,
you’re at higher risk for another one. Your risk of having a repeat
stroke is the highest right after a stroke. A TIA also increases your risk
of having a stroke, as does having a family history of stroke.
• Brain aneurysms or arteriovenous malformations (AVMs).
Aneurysms are balloon-like bulges in an artery that can stretch and
burst. AVMs are tangles of faulty arteries and veins that can rupture
(break open) within the brain. AVMs may be present at birth, but often
aren’t diagnosed until they rupture.

8. Other risk factors for stroke, many of which of you can control,
include:
• Alcohol and illegal drug use, including cocaine,
amphetamines, and other drugs
• Certain medical conditions, such as sickle cell
disease, vasculitis (inflammation of the blood vessels),
and bleeding disorders.
• Lack of physical activity.

9. • Overweight and Obesity.
• Stress and depression
• Unhealthy cholesterol levels
• Unhealthy diet
• Use of nonsteroidal anti-inflammatory drugs (NSAIDs),
but not aspirin, may increase the risk of heart attack or stroke,
particularly in patients who have had a heart attack or cardiac bypass
surgery. The risk may increase the longer NSAIDs are used. Common
NSAIDs include ibuprofen and naproxen.

10. PATHOPHYSIOLOGY:
• The two major categories of stroke are ischaemic
(lack of blood and hence oxygen to an area of the brain)
and haemorrhagic (bleeding from a burst or leaking
blood vessel in the brain) stroke.
Ischaemic stroke:
• Ischemic stroke is lack of sufficient blood flow
to perfuse cerebral tissue, due to narrowed or
blocked arteries leading to or within the brain.

12. • Ischaemic strokes can be broadly subdivided into
thrombotic and embolic strokes.
• Narrowing is commonly the result of atherosclerosis .
• The occurrence of fatty plaques lining the blood vessels.
• As the plaques grow in size, the blood vessel
becomes narrowed and the blood flow to the
area beyond is reduced.

13. • Damaged areas of an atherosclerotic plaque can cause
a blood clot to form, which blocks the
blood vessel – a thrombotic stroke.
• In an embolic stroke, blood clots or debris from
elsewhere in the body, typically the heart valves,
travel through the circulatory system and block
narrower blood vessels.

14. • Based on the aetiology of ischaemic stroke, a
more accurate sub-classification is generally used
1. Large artery disease –
Atherosclerosis of large vessels, including the internal carotid
artery, vertebral artery, basilar artery, and other major
branches of the Circle of Willis.
2. Small vessel disease –
Changes due to chronic disease, such as diabetes, hypertension,
hyperlipidaemia, and smoking, that lead decreased compliance of the
arterial walls and/or narrowing and occlusion of the lumen of smaller
vessels.

15. 3. Embolic stroke –
The most common cause of an embolic stroke is atrial fibrillation.
4. Stroke of determined aetiology –
Such as inherited diseases, metabolic disorders, and
coagulopathies.
5. Stroke of undetermined aetiology –
After exclusion of all of the above.

16. • In the core area of a stroke, blood flow is
so drastically reduced that cells usually cannot recover
and subsequently undergo cellular death.
• The tissue in the region bordering the infarct core,
known as the ischaemic penumbra, is less severely affected
• This region is rendered functionally silent by reduced
blood flow but remains metabolically active.
• Cells in this area are endangered but not yet irreversibly damaged.

17. • They may undergo apoptosis after several hours or days
but if blood flow and oxygen delivery is restored shortly
after the onset of stroke, they are potentially recoverable .
Pathophysiology of haemorrhagic stroke:
• Haemorrhagic strokes are due to the rupture of a
blood vessels leading to compression of brain tissue
from an expanding haematoma.

18. • This can distort and injure tissue.
• In addition, the pressure may lead to a loss of blood
supply to affected tissue with resulting infarction,
and the blood released by brain haemorrhage appears
to have direct toxic effects on brain tissue
and vasculature.

19. Intracerebral haemorrhage –
• Caused by rupture of a blood vessel and accumulation
of blood within the brain.
• This is commonly the result of blood vessel damage from
chronic hypertension, vascular malformations, or the use
medications associated with increased bleeding rates, such
as anticoagulants, thrombolytics, and antiplatelet agents.

20. Subarachnoid haemorrhage
• Is the gradual collection of blood in the subarachnoid space
of the brain dura, typically caused by trauma to
the head or rupture of a cerebral aneurysm.

21. EARLY WARNING SIGNS OF STROKE :
1. Sudden numbness or weakness of face, arm or
leg especially on one side of the body.
2. Sudden confusion, trouble speaking or understanding.
3. Sudden trouble seeing in one or both eyes.
4. Sudden trouble walking, dizziness , loss of balance or coordination
Other important but less common symptoms:
1. Sudden nausea, fever, and vomiting distinguished from a viral illness
by the speed of onset.
2. Brief loss of consciousness or a period of decreased consciousness.

22. Transient ischemic attack (TIA) :
• It refers to temporary interruption of blood supply
to the brain.
• Symptoms may last for only few minutes or for several hours,
but does not last for longer than 24 hours.
• After the attack is over there is no evidence of
residual brain damage or permanent neurological dysfunction.

23. Primary impairments:
1. Sensation :
• Sensation is frequently impaired but rarely absent on
hemiplegic side.
• The type and extent of impairment is related to
location and size of vascular lesion.
• Common distribution of loss is face-UE-LE pattern.
• Proprioceptive losses are common.

24. • Patient may complaint of abnormal sensations like
numbness, hyperesthesia.
PAIN :
• Stroke can result in severe headache or neck and face pain.
• Lesions of PCA involving ventral posterolateral thalamus
can result in central post stroke ( thalamic) pain.
• There is constant, severe burning pain with intermittent
sharp pains.

25. • Patients experience an exaggerated response to stimuli
affecting the contra lateral half of the body.
• Paroxysmal spasms pain may be triggered by simply
stroking the skin, pinprick, contact with heat or cold,
and pressure ( hyperalgesia).
• Loud noises , bright lights, or mild irritants may
also trigger pain.

26. Visual changes :
• Homonymous hemianopsia , a visual field defect occurs with
lesions involving then optic radiation in the internal
capsule (MCA distribution) or in primary visual
cortex (PCA territory).
• It occurs in 26 percent of patients with stroke.
• There is loss of vision in contra lateral half
of each visual field.

27. • Patients may also experience visual neglect ( visual inattention)
and problems with depth perception.
Forced gaze deviation :
• Paralysis of conjugate gaze from involvement of frontal
lobe eye field area, CN III, or gaze centers in
the pontine reticular formation.
Brainstem strokes may lead to signs of diplopia, oscillopsia or visual
distortions.

28. MOTOR FUNCTION :
• Initially flaccid paralysis is present.
• This is replaced by development of spasticity, hyperreflexia,
and mass patterns of movement termed as “obligatory synergies”.

30. Alterations in tone :
• Flaccidity is present immediately after stroke and is due
primarily to effects of cerebral shock.
• It is generally short lived, lasting a few days or weeks.
• Spasticity emerges in about 90 percent of cases and
occurs in antigravity muscles.

31. • Spasticity results in tight muscle that restrict
voluntary movement.
• Posturing of limbs is common in moderate to severe spasticity.
• It can lead to painful spasms similar to
muscle cramping, degenerative changes, and fixed contractures.
• Automatic postural tone is also impaired.
• Pts with stroke lack the ability to adjust proximal limbs and trunk
during movement.

32. Extremity Flexion synergy components Extension synergy
components
upper extremity Scapular retraction/ elevation
or hyperextension.
Shoulder abduction, external
rotation
Elbow flexion
Forearm supination
Wrist and finger flexion.
Scapular protraction
Shoulder adduction, internal
rotation
Elbow extension
Forearm pronation
Wrist and finger flexion.
Lower extremity Hip flexion, abduction,
external rotation
Knee flexion
Ankle dorsifelxion, inversion
Toe dorsiflexion.
Hip extension, adduction,
internal rotation
Knee extension
Ankle plantarflexion, inversion
Toe plantarflexion

33. Muscles not involved in any synergy patterns:
1. Latissimus dorsi.
2. Teres major
3. Serratus anterior
4. Finger extensors
5. Ankle evertors.

34. Abnormal reflexes :
• Reflexes are altered and also vary according to
the stage of recovery.
• Initially, there is hyporeflexia with flaccidity.
• when spasticity and synergies emerges, hyperflexia is seen
• The most common seen is ATNR, in which head
rotation causes elbow extension of the UE on the
jaw side with elbow flexion of the opposite skull limb.

35. • Associated reactions are also present in patients with
stroke who exhibit strong spasticity and synergies.
• It consists of unintentional movements of hemiparetic limbs
caused by voluntary action of another limb or by
stimulation of yawing, sneezing, or coughing.
Altered coordination:
• Proprioceptive losses can result in sensory ataxia.

36. • The resulting problems with timing and sequencing of
muscles can significantly impair function and limit adaptability
to changing task and environmental demands ( CEREBELLAR)
• Few may have slow movements or involuntary movements (BASAL
GANGLIA)
Altered motor planning:
• Motor praxis is the ability to plan and execute coordinated movement.
• Lesions of the premotor frontal cortex of either hemisphere,
left inferior parietal lobe and corpus collosum can
produce apraxia.

37. • Apraxia is more evident with left hemisphere damage
that right and is commonly seen with aphasia.
• Patient demonstrate difficulty planning and executing purposeful
movements that cannot be accounted by any other reason.
Ideational apraxia:
• Refers to inability to produce movement either on command
or automatically and represents a complete breakdown in
the conceptualization of the task.

38. • Ideomotor apraxia is when patient is unable to
produce a movement on command but is able to
move automatically.
• Thus patient can perform habitual tasks when not commanded
to do so and often repeats the activity again
and again.

39. Postural control and balance:
• Disruptions of central sensorimotor processing lead to an inability
to adapt postural movements to changing task and
environmental demands and impair motor learning.
• There is asymmetry while weight distribution.
• There is increased postural sway in standing.
• Delay in onset of motor activity, abnormal timing and
sequencing of muscular activity, abnormal co-contraction results
in disorganization of postural synergies.

40. IPSILATERAL PUSHING:
• Also known as pusher syndrome or contraversive pushing.
• There is active pushing with the stronger extremities toward
the hemi paretic side, leading to a lateral
postural imbalance.
• The end result is tendency to fall towards the
hemiparetic side.

41. SPEECH
LANGUAGE
SWALLOWING

43. • Language is the ability to acquire and use
complex systems of communication, particularly the human
ability to do so, and a language is any specific example
of such a system.
• Human language has the properties of productivity,
Recursivity ( determining sequence), and displacement, and relies
entirely on social convention and learning.

45. • Aphasia is a communication disorder that results from damage to the
parts of the brain that contain language (typically in the left half of the
brain).
• Individuals who experience damage to the right side of the brain may
have additional difficulties beyond speech and language issues.
• Aphasia may causes difficulties in speaking, listening, reading, and
writing, but does not affect intelligence.
• Individuals with aphasia may also have other problems, such as
dysarthria, apraxia, or swallowing problems.

46. • Aphasia is most often caused by stroke.
• However, any disease or damage to the
parts of the brain that control language
can cause aphasia.
• These include brain tumors, traumatic brain injury,
and progressive neurological disorders.

48.  Types of aphasia :
1. Broca’s Aphasia / Expressive aphasia/ nonfluent aphasia
• The term, Anomic Aphasia, usually refers to
patients whose only prevalent symptom is impaired
word retrieval in speech and writing.
• Typically, the spontaneous speech of a person with anomic aphasia
is fluent and grammatically correct but contains many
word retrieval failures. These failures lead to unusual pauses,
talking around the intended word, or substituting the
intended word for a different word.

49. • Anomic aphasia is the mildest form of aphasia,
indicating a likely possibility for better recovery.
• Patients with Broca’s aphasia may also have difficulty
with word retrieval.
2. Wernicke’s aphasia / sensory/ receptive aphasia:
• Receptive aphasia, also known as Wernicke's aphasia,
fluent aphasia, or sensory aphasia, is a type
of aphasia in which an individual is unable
to understand language in its written or spoken form.

50. • Even though they can speak using grammar,
syntax, rate, and intonation, they typically have
difficulty expressing themselves meaningfully through speech.
• Receptive aphasia was named after Carl Wernicke who
recognized this condition.
• People with receptive aphasia are typically unaware
of how they are speaking and do not
realize their speech may lack meaning.

51. • Receptive aphasia is traditionally associated with neurological damage
to Wernicke's area in the brain.
(Brodmann area 22, in the posterior part of the superior temporal
gyrusof the dominant hemisphere).
3. Global aphasia :
• Global aphasia is a severe form of nonfluent aphasia
that affects bothreceptive and expressive language skills.
• symptoms of global aphasia include the inability to
comprehend speech, the inability to form speech,
and the inability to repeat the speech one has heard.

52. • Global aphasia typically results from an occlusion to
the trunk of the middle cerebral artery (MCA),
which affects a large portion of the perisylvian region
of the left cortex. The large areas in the anterior (Broca’s)
and posterior (Wernicke’s) area of the brain
are either destroyed or impaired because they
are separate branches of the MCA that are supplied
by its arterial trunk.

53. DYSARTHRIA :
• Definintion : Dysarthria is indistinct speech due to
weakness or impaired co-ordination of the orolingual
muscles concerned with the production of consonants
( basic speech sound).
Types of dysarthria :
1. Spastic :
• Results from bilateral upper motor neuron lesion .
• The tongue is small and spastic.
• Difficulty in pronouncing “b” “p” and “t”.

54. 2. Monotonus :
• Results from extrapyramidal lesions.
• Speech is slow, monotonus and lacking acents.
3. Ataxic:
• Results from cerebellar leisons.
• Speech is slurred and irregular in rhythm, tone and volume.
• Its is due to incoordination of musles of respiration.

55. 4. Lower motor neurone :
• Results from paralysis of soft palate giving
rise to nasal speech.
• Failure to produce “b” and “g” . E.g Egg is pronouced as eng.

56. DYSPHAGIA :
• Lesions affecting medullary brainstem ( CN IX and X),
large vessel pontine lesions.
• Dysfunction of lips, mouth, tongue, palate, pharynx,
larynx or proximal oesophagus all contribute to dysphagia.
• Commonest problem seen is delay in triggering of the swallowing
reflex.

57. Recovery And OPD Management Of
Stroke
a conventional approach

58. Neurological Complications And Associated
Conditions With Stroke.
• Altered Consciousness
• Disorders of Speech and Language
• Dysphagia.
• Cognitive Dysfunction.
• Altered Emotional Status.
• Perceptual Dysfunction
• Seizures
• Bladder and Bowel Dysfunction
• Cardiovascular and Pulmonary Dysfunction
• Deep Venous Thrombosis and Pulmonary Embolus.
• Osteoporosis and Fracture Risk.
(PHYSICAL REHABILITATION – SUSAN B O’SULLIVAN)

59. SEQUENTIAL RECOVERY STAGES OF STROKE
• 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.

60. Recovery and prognosis :
• Recovery is faster in first weeks after the onset.
• Measurable neurological and functional recovery occurs in first month
after stroke.
• There is measurable functional gains for months or years after insult.
• Late recovery is seen in chronic stroke who has to undergo extensive
functional training.
Variation of recovery:
1. Type of stroke.- hemorrhagic or ischemic
2. Site of lesion.
3. Timing of intervention.
4. Assessment strategies.
5. Treatment strategies.

61. FRAMEWORK FOR REHABILITATION
• Rehabilitation has an important role in reducing disability and
promoting independence.
• Optimal management involves a coordinated interdisciplinary team to
oversee a comprehensive plan of care (POC).
• The team of rehabilitation specialists includes the physician, nurse,
physiotherapist , occupational therapist, speech-language pathologist,
and social worker.
• Additional disciplines may include a neuropsychologist, nutritionist,
and recreational therapist or vocational counselor.

62. • For patients with stroke, the care continuum is based on two important
factors: (1) stage of recovery; and (2) degree of disability resulting from
stroke.
 Acute Phase
• Low-intensity rehabilitation is begun in the acute care facility as soon as the
patient is medically stabilized, typically within 72 hours.
 Subacute Phase
• Patients with moderate or severe residual impairments or activity limitations
may benefit from intensive inpatient rehabilitation provided in a
freestanding rehabilitation facility or in a rehabilitation unit within the acute
care hospital.
• Patients are referred to inpatient rehabilitation if they can tolerate an
intensity of services consisting of two or more rehabilitation disciplines, 6
days a week for a minimum of 3 hours of active rehabilitation per day.

63.  Chronic phase:
• Rehabilitation services during the chronic phase, generally defined to
be more than 6 months post-stroke, are typically delivered in an
outpatient rehabilitation facility, in a community setting, or at home.
• Many of the interventions begun at the acute phase are progressed in
order to sustain the gains made and improve functional performance.

64. PHYSIOTHERAPY ASSESSMENT :
The purposes of the assessment are to
• Determine the diagnosis and classification within a specific practice pattern.
• Monitor recovery from stroke.
• Identify patients who are most likely to benefit from rehabilitation services
and the most appropriate choice of a care setting.
• Develop a specific POC, including anticipated goals, expected outcomes,
prognosis, and interventions.
• Monitor progress toward projected goals and outcomes through periodic
reevaluation.
• Determine if referral to another practitioner is indicated.
• Plan for discharge.

65. The following points should be given special consideration while
assessing a stroke patient:
1. Higher function examination
2. Cranial nerve examination
3. Motor examination
4. Reflex testing
5. Coordination testing
6. Sensory evaluation
7. Flexibility and joint integrity
8. Postural control and balance.
9. Gait and locomotion evaluation.
10. Integumentary integrity
11. Aerobic capacity and endurance
12. Functional status : FIM, Barthal index

66. Common problem list :
• When the patients are transferred to wards followed by OPD following
problems are commonly seen:
1. Tonal abnormalities.
2. Muscular weakness.
3. Synergistic patterns.
4. Tightness and contractures.
5. Gait abnormalities.
6. Postural abnormalities.
7. Functional disability.

67. Physiotherapy management:
Goals of the treatment are:
• Prevent ignorance or unawareness of the hemiplegic side.
• Decrease tendency to develop synergy in the chronic stage
• Prevention of any joint restriction or stiffness
• Prevention of complications like chest complications,
deconditioning of bone and muscles.
• Early weight bearing
• Psychological counseling
• Education to family.

68. 1. Positioning strategies:
• Due to lesion the patient suffers from sensory deprivation that leads to
neglect of hemiplegic side which can be greatly influenced by patients
head position.
• Hence all forms of the stimulus like entrance to the room, the
relatives, television etc should be present on hemiplegic side so that
patient is forced to turn to that side which will stimulate awareness of
the hemiplegic side.

70. 2. Improve respiratory and circulatory function:
• Breathing exercises.
• Chest expansion exercises
• Postural drainage
• Huffing and coughing techniques
• Passive and active ankle toe exercises ( after careful and thorough
examination of cardiopulmonary system)

71. 3. Prevent pressure sores:
• Proper positioning
• Relive pressure points by padding and cushion
• Frequent turning and changing position
• Prevent from moisture
• Use cotton clothing
• Tight fitting cloth is prevented
• Use of water bed, air bed and foam mattress.

72. 4. Prevent from deconditioning :
• Early mobilization in the bed ( active turning, supine to sit, sit to
supine, sitting, sit to stand)
• Pelvic bridging exercises.
• Early propped up positioning , sitting and then later to standing.
• Moving around the bed
• Facilitate movement of functioning limbs.

73. 5. Improve sensory function:
• Presentation of repeated sensory stimuli from distal to proximal .
• Stretching, stroking, superficial and deep pressure, icing , vibration etc
can be used to improve sensory awareness and integrity.
• Weight bearing exercises and joint approximation techniques can
enhance joint receptors which in turn can facilitate sensory retraining.
• Stroking with different textures, fabrics can be used.
• Improvement of other senses like visual, auditory should be done to
improve sensory functioning.

74. 6. Flexibility and joint integrity:
• Initially passive movements can be done in order to maintain the
muscle flexibility , sensory awareness through proper manual grip.
• Active range of motion and passive range of motion with end range
stretch.
• Effective positioning and edema reduction.
• Stretching program and splinting.

75. 7. Manage spasticity:
Aims:
1. Normalize the tone.
2. Development of normal functional pattern.
3. Prevention of contracture and deformity
4. Train the patient to be functionally independent.
5. Achieve highest possible physical security to the patient.
Methods:
• Gentle rhythmic passive movement.
• Sustained gradual stretching.
• Prolonged icing over the spastic muscles for about 15-20 minutes.
• Faradic stimulation to the weak antagonist muscle can reduce the
spasticity of agonist muscle by the principle of reciprocal inhibition.
• Reflex inhibiting postures or pattern
• Biofeedback can be used to relax spastic muscle as well as activate
anatagonist

76. 8. Improve motor control:
• Dissociation and selection of desired movement patterns.
• Select postures that assist desired movements through optimal
biomechanical stabilization and use of optimal point in range.
• Start with assisted movement, followed by active and resisted movements.
• Task oriented exercises.
9. Postural control and functional mobility:
• Sequence of “ontogenic developmental pattern” are to be practiced in OPD
as well as at home to achieve functional mobility.
• Supine, rolling to side, prone on hands, prone on elbows, crawling,
kneeling, half kneeling, standing.
• Transfer training needs to be evaluated and trained.

77. 10. Improving upper extremity functions:
• Early mobilization, range of motion and positioning strategies.
• Relearning of movement pattern and retraining of missing component.
• Upper limb weight bearing exercises.
• Dynamic stabilization exercises.
• Picking up of objects and reaching activites.
• Manipulation of common objects to achieve muscular control.
• NMES to reduce spasticity to anatagonist muscle.
• Activities of daily living training with ADL table, peg boards, writing
activites, towel exercises.

78. 11. Managing shoulder pain:
• Proper handling and positioning of shoulder joint.
• Neuromuscular electrical stimulation, TENS for reducing pain .
• Proximal joint control exercises in bed
• Use of slings in order to maintain the normal anatomical position of
shoulder.
• Active assisted exercises to improve shoulder control.
12. Improving lower limb function:
• Active assisted close chain exercises to gain voluntary control.
• Facilitation of hip abductors, knee flexors and ankle dorsiflexors in
order to achieve good voluntary control.
• Cycling and treadmill training.

79. 13. Improve balance:
• Facilitate symmetrical weight bearing on both sides
• Postural perturbations can be induced in different positions.
• Sit or stand on moving surface to increase challenge .
• Reaching activites.
• Dual task training like walking, standing, throwing activities, carrying
a object while walking.
• Divert attention.
• Single limb stance.
• Exercise on trampoline.

80. 14. Improve locomotion:
• Initial gait training in parallel bar with mirrors.
• Activities in parallel bar like forward walking. Backward walk, side
walk, marching, walking over wooden blocks can be used in gait
training.
• Proceed outside the bar with aids and then without aids.
• Training on stair case, inclined surfaces, field training.
15. Improve aerobic function:
• Early mobilization and functional activity training
• Treadmill training and cycle ergo meter
• Symptom limited graded exercise training.
• Proper rest should to be given
• Gradually progress to 30 minutes continuous program.

81. 16. Improve motor learning :
• Strategy development:
 Patient as an active explorer of activity
 Modify strategy of activity in correct patterns.
• Feedback :
 intrinsic or extrinsic feedback
 Positive and negative feedback
• Practice:
 Repeated practice of functional activity
 Practice in different environment.

82. 17. Patient And Family Education:
• Give factual information, counsel family members about patients
capabilities and limitations.
• Give information as much as patient or family can assimilate.
• Provide open discussion and communication.
• Be supportive, sensitive and maintain a positive supporting nature.
• Give psychological support.
• Refer to help groups.

83. Home exercises

84. Discharge planning:
• Family member should participate daily in therapy session and learn
exercises.
• Home visits to be made.
• Architectural modifications, assistive devices or orthotics should be
ready before discharge.

85. Summary
Conventional training:
1. Proper assessment strategies.
2. Deriving correct problem list.
3. Intensive care unit:
• Correct positioning , passive movements, sensory retraining
exercises, limb mobility exercises ( considering vitals, stage of
recovery)
4. Wards :
• Tone normalization exercises, trunk control exercises, bed mobility
exercises, functional reeducation activities, electrotherapy modalities.
5. OPD:
• Functional reeducation, spasticity management, functional training
exercises, gait training, activities of daily living training, close chain
exercises with help of gymnasium, community based training.
6. Home exercises

86. Neurophysiological approaches
1. Brunstroom therapy
2. Bobath therapy
3. Proprioceptive neuromuscular facilitation therapy
4. Roods approach
5. Motor imagery therapy.

87. References
• 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.

88. THANK YOU.