HEMIPLEGIA

Original Editor - Mandeepa Kumawat Top Contributors - Mandeepa Kumawat

Introduction

Paralysis of one side of the body due to Pyramidal Tract lesion at any point from its origin in the cerebral cortex down to the fifth Cervical segment ( beginning of origin of cervical plexus ) .

Etiology [1]

Vascular - Cerebral hemorrhage , Stroke , Diabetic Neuropathy.

Infective - Encephalitis , Meningitis , Brain abscess.

Neoplastic - Glioma - meningioma

Demylination - Disseminated sclerosis , lesions to the Internal capsule .

Traumatic - Cerebral lacerations , Subdural Hematoma . Rare cause of hemiplegia is due to local anaesthsia injections given intra arterially rapidly , instead of given in a nerve branch .

Congenital- Cerebral palsy

Disseminated - Multiple Sclerosis

Psychological - Parasomnia (Nocturnal hemiplegia ).

Mechanism -

Damage to the CorticospinalTract leads to the injury on the oppoSite side of the body. This happens because the motor fibres of the CorticospinalTract , which take origin from the motor cortex in brain , cross to the oppoSite side in the lower part of medulla oblongata and then descend down in spinal cord to supply their respective muscles.

Depending on the Site of lesion in brain , the severity of hemiplegia varies.[2]

Site of lesion Signs and symptoms
Internal capsule Dense and uniform Hemiplegia ( UMN Facial )

Hemisensory blunting

Homonymous hemianopia

Cortex Non dense non uniform weakness

Monoplegia

Cortical signs ( Dysphasia , Apraxia , Cortical sensory loss , Convulsions )

Subcortex Pattern of weakness similar to cortical
Brainstem Crossed hemiplegia

Ipsilateral LMN CN Palsy and contralateral hemiplegia

Cerebellar signs.

Midbrain Crossed cerebellar ataxia with Ipsilateral Third nerve palsy ( Claude `s Syndrome )

Weber`s Syndrome - Third nerve palsy and contralateral hemiplegia

Contralateral hemiplegia - Cerebral peduncle

Contralateral rhythmic , ataxic action tremor ; rhythmic postural or holding tremor (rubral tremor)

Pons LMN Facial and contralateral hemiplegia

Fifth nerve and contralateral hemiplegia

Lateral Gaze palsy and contralateral hemiplegia

Medulla- Lateral medullary Syndrome Same side ( Horner `s Syndrome , Loss of pain and touch on the face , Cerebellar signs , Palate weakness )

OppoSite side ( Loss of pain and temperature sensation on the body and limbs )

Medulla- Medial medullary Syndrome Same side ( wasting and weakness of the tongue )

OppoSite side ( hemiplegia without facial palsy )

Spinal cord Rare

No facial

Brown sequard Syndrome

Medical diagnosis

History and examination

An accurate history profiling the timing of neurological events is obtained from the patient or from family members in the case of the unconscious or noncommunicative patient . Of particular importance are the exact time and pattern of symptom occurs . The most common , slowest in hours , wakes up in the morning with weakness , history of TIA , old age is typical with thrombosis . An embolus occurs rapidly with no warning , history of heart disease , younger age group , no progression (maximum deficit occurs at onset) . An abrupt onset with worsening symptoms , history of prolonged hypertension , severe headache described as "worst headache of my life " , altered consciousness , convulsions , vomiting is suggestive of haemorrhage. The patient 's past history , including episodes of TIAs or head trauma , presence of major or minor risk factors and medications , pertinent family history and recent alterations in patient function ( either transient or permanent ) are thoroughly investigated.

The physical examination of the patient includes an investigation of vital signs ( heart rate , respiratory rate , blood pressure , clubbing ) , signs of cardiac decompensation, and function of the cerebral hemispheres , cerebellum , cranial nerves , eyes and sensorimotor system.

Outcome measures

NIH Stroke Scale

Dynamic Gait Index, the 4-item Dynamic Gait Index, and the Functional Gait Assessment show sufficient validity, responsiveness, and reliability for assessment of walking function in patients with stroke undergoing rehabilitation, but the Functional Gait Assessment is recommended for its psychometric properties

Chedoke-McMaster Stroke Assessment

Chedoke Arm and Hand Activity Inventory

CRS-R Coma Recovery Scale Revised is used to assess patients with a disorder of consciousness, commonly coma.

Take a look at our Stroke Outcome Measures Overview for more information

Cerebrospinal imaging [3]

CerebroVascular imaging is the main tool to establish the diagnosis of suspected hemiplegia. Advanced neuroimaging can rapidly indentify the occluded artery and estimate the size of the core and the penumbra.

Computer tomography and MRI scans [4]

For acute care of stroke patients, a number of computed tomography (CT) and magnetic resonance (MR) techniques are essential. Noncontrast CT excludes other causes of acute neurologic defi cits and intracranial hemorrhage. CT and MR angiography can identify intraVascular clots, and the CT angiography source images improve detection of acute infarction over plain CT. Diffusion MRI estimates the size, location, and age of infarcted core more precisely, and perfusion imaging estimates the ischemic penumbra.CT and MR imaging techniques are used to provide four types of information that are essential to the care of acute stroke patients.

1. They establish the diagnosis of ischemic stroke and exclude other potential causes of an acute neurologic defi cit.

2. They identify intracranial hemorrhage.

3. They identify the Vascular lesion responsible for the ischemic event.

4. They provide additional characterization of brain tissue that may guide stroke therapy by determining the viability of different regions of the brain and distinguishing between irreversibly infarcted tissue and potentially salvageable tissue.

When a stroke has been diagnosed, determining the underlying aetiology is important with regard to secondary stroke prevention. Common techniques include:

• ultrasound of the carotid arteries to determine carotid stenosis

• electrocardiogram (ECG) to detect arrhythmias of the heart which may send clots in the heart to the blood vessels of the brain

• Holter monitor to identify intermittent arrhythmias

• angiogram of the blood vessels of the brain to detect possible aneurysms or arteriovenous malformations and

• blood test to examine the presence of hypercholesterolemia (high cholesterol).[5]

Examination

The selection of examination procedures will vary based on a number of factors including patient age , location and severity of stroke , stage of recovery , data from initial screenings , phase of rehabilitation and home /community / work situation , as well as other factors.

General examination

General appearance including posture , motor activity

Vital signs - Level of consciousness ,pulse , BP , look for pupil size , conjugate deviations of eyes , Meningeal signs.

Neurocutaneous markers-

  • Neurofibroma over the skin ( may have associated Tuberous sclerosis of brain )
  • Sebaceous adenoma
  • Sturge Weber Syndrome - facial nerve (port wine stain ) involving one half of face with upper eyelid - associated with atrophy and calcification of ipsilateral cerebral hemisphere.
  • Lymphadenopathy
  • Cyanosis
  • Clubbing
  • Shortening of hemiplegic limb - indicates it is dating from early childhood
  • Irregular pulse of atrial fibrillation

Higher examination[6]

A. Consciousness - Check level of altered sensorium . for this refer Glasgow Coma Scale

B. Orientation -In time , place , space , person are tested.

C. Memory-It includes Immediate memory , Recent memory , Remote memory.Check with relatives or friends of the patient if he is correct

D. Intelligence

E. Speech- Speech disturbances APHASIA may occur

F. Emotion - Anxious / depressed / elated / swings of mood.

G. Judgment

H. Behaviour

I. Presence of hallucination/dellusion/illusion

Gait

In hemiparesis, facial paresis may not be obvious. In mild cases, subtle features of facial paralysis (eg, flattening of the nasolabial fold on 1 side compared to the other, mild asymmetry of the palpebral fissures or of the face as the patient smiles) may be sought. The shoulder is adducted; the elbow is flexed; the forearm is pronated, and the wrist and fingers are flexed. In the lower extremities, the only indication of paresis may be that the ball of the patient's shoe may be worn more on the affected side.

In severe cases, the hand may be clenched; the knee is held in extension and the ankle is plantar flexed, making the paralyzed leg functionally longer than the other. The patient therefore has to circumduct the affected leg to ambulate.

In hemiplegic patients in whom all the paralysis is on the same side of the body, the lesion is of the contralateral upper motor neuron. In most cases, the lesion lies in the cortical, subcortical, or capsular region (therefore above the brainstem). In the alternating or crossed hemiplegias, CN paralysis is ipsilateral to the lesion, and body paralysis is contralateral. In such cases, CN paralysis is of the lower motor neuron type, and the location of the affected CN helps determine the level of the lesion in the brainstem. Therefore, paralysis of CN III on the right side and body paralysis on the left (Weber Syndrome) indicates a midbrain lesion, whereas a lesion of CN VII with crossed hemiplegia (Millard-Gubler Syndrome) indicates a pontine lesion, and CN XII paralysis with crossed hemiplegia (Jackson Syndrome) indicates a lower medullary lesion. [7]

Cranial nerve integrity

The therapist examines for facial sensation (CN 5) , facial movements (CN 5 and 7), and labrynthine / auditory function (CN 8 ) . The presence of swallowing and drooling necessitates an examination of the motor nuclei of the lower brainstem cranial nerves (CN 9 , 10 and 12) affecting the muscles of the face , tongue , pharynx and larynx. The visual system should be carefully investigated , including tests for visual field defects (CN 2 , optic radiation , visual cortex ), acuity (CN 2 ) ,Pupillary reflexes (CN 2 and 3 ) and extraocular movements (CN 3 , 4 and 6).

Cranial nerve Syndrome associated with hemiplegia [6]
Syndrome Site Tract Signs Usual cause
1.Weber's Base of midbrain CorticospinalTract +3rd Nerve nucleus Ipsilateral 3rd nerve palsy + contralateral hemiplegia Vascular,tumor
2. Benedikt's Midbrain CorticospinalTract , 3rd Nerve nucleus + Red nucleus Ipsilateral 3rd nerve palsy + contralateral hemiplegia + Tremors+ ataxia Vascular,tumor
3.Millard gubllar's Pons CorticospinalTract + 6th and 7th Nerve nucleus Ipsilateral LMN 6th and 7th nerve palsy + contralateral hemiplegia Vascular,tumor
4. Medial medullary Syndrome Medial medulla CorticospinalTract + 12th Nerve nucleus Ipsilateral tongue paralysis + contralateral hemiplegia Vascular

Sensation [8]

Sensory integration is the ability of the brain to organise , interpret , and use sensory information . Examination of sensory function involves testing patient's ability to interpret and discriminate among incoming sensory information.

Pattern of sensory loss Site of lesion
1.Mono-neural

2.Stock and glove

3.Maculo-anesthetic (leprosy)

Peripheral nerve
4.Radicular sensory loss Root
5.Saddle area loss Conus
6.Dissociated sensory loss (Brown-Sequard Syndrome)

joint position / vibration / light touch on same side and pain / temperature on oppoSite side

Unilateral cord lesion
7.Sensory level Extra-medullary lesion
8.Jacket sensory loss (dissociated) Intra-medullary lesion
9.Crossed hemihyposthesia Lateral medullary Syndrome
10.Hemi-hyposthesia Capsular & brain stem lesions
11.Corticalsensory loss

numbness , agnosia , loss of two point discrimination , astereognosis , graphanaesthesia ,sensory inattention

Area(1, 2, 3) of parietal lobe

Flexibility and joint integrity [3]

An examination of joint flexibility should include passive ROM using a goniometer , joint hypermobility/hypomobility , and soft tissue changes (swelling ,inflammation or restriction). The shoulder and wrist should be examined closely because joint malalignment problems are common. Edema of the wrist often produces malaligned carpal bones with resulting impingement during wrist extension. Active ROM may be limited or impossible for the patient in early or middle recovery in the presence of paresis , spasticity , or obligatory synergies that can preclude isolated voluntary movements.

Contractures can develop anywhere but are particular apparent in the paretic limbs. As contractures progress , edema and pain may develop and further restrict mobility . In the UE ,limitations in the shoulder motion of flexion , abduction and external rotation are common. Contractures are likely in the elbow and finger flexors , and forearm pronators. In the LE , plantarflexion contractures are common.

Motor function

Tone [9]

An examination of tone is essential . Passive motion testing can be done to determine the presence of hypertonicity or spasticity. Severity of spasticity can be graded on the basis of resistance to passive stretch using the Modified Asthworth Scale.

Stage of flaccid paralysis: It is also known as shock stage . It lasts from 2-6 weeks , the shorter the duration better the prognosis. On the paralysed side there is complete loss of muscle tone (flaccidity) , absence of deep reflexes and no plantar reflex.This stage is prolonged by general poor condition of the patients health , infections (e.g. chest or urinary tract infection ) and bed sores. During recovery from the shock stage , the muscle tone and deep reflexes reappear and gradually increase. Babinski sign becomes positive . The stage of spasticity sets in .If the onset is associated with coma , the paralysed side is determined by the following :

  1. The limb on the paralysed side are more flaccid and drop passively.
  2. The cheek on the paralysed side moves in and out with respiration.

Stage of flaccid paralysis : Stage of established hemiplegia where there is :

1.Paralysis of one side of the body . This paralysis shows a pyramidal distribution .

It affects the progravity more than the antigravity muscles as the former are normally weaker than the latter.

  • In upper limb , the extensors are weaker than the flexors.
  • In lower limb, the flexors are weaker than the extensors.

It affects the distal more than the proximal muscles.

  • The hand is weaker than the shoulders.
  • The foot is weaker than the hip

2. Hypertonia (spasticity) of the paralysed muscle of clasp knife:

It affects the antigravity more than the progravity muscles as the former normally have a stronger muscle tone :

  • In upper limb, the flexors are more spastic than the extensors.
  • In lower limb , the extensors are more spastic than the flexors.

Clonus - Series of rythmical contraction occuring in response to maintenance of tension in muscle tone . It is due to gamma neuronal discharge. Sustained clonus is a sign of pyramidal Tract lesion. [6]

Reflexes

Reflexes are altered and also vary according to the stage of recovery . Initially , stroke result in hyporeflexia with flaccidity . When spasticity and synergy emerges , hyperreflexia is seen . Deep tendon reflexes are hyperactive and patient may demonstrate clonus , claspknife response and positive Babinski , all consistent finding of upper motor neuron Syndrome.[3]There are certain pathological reflexes looked for in hemiplegia . In upper limb clinically significant - if markedly active and asymmetrical are Hoffmann's sign , Wartenberg's sign . Superficial reflexes in hemiplegia are loss of Abdominal reflex and cremastric reflex which is a sign of UMN Lesion .

Voluntary movements[3]

Abnormal and highly stereotyped obligatory synergies emerge with spasticity following stroke . Thus the patient is unable to perform an isolated movements of a single limb segment without producing movements in the remainder of the limb. Two distinct abnormal synergy patterns have been described for each extremity : flexion and extension synergy.

Obligatory Synergy Patterns Following Stroke[3]

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 dorsiflexion, inversion

Toe dorsiflexion

Hip extension, adduction,* internal rotation

Knee extension*

Ankle plantarflexion,* inversion

Toe plantarflexion

*Generally the strongest components.

File:Limb Synergies.png

Chedoke-McMaster Stroke Assessment

An inspection of synergy components reveals that certain muscles are not involved in either synergies . These muscles include the 1. latissimus dorsi 2. teres major 3. serratus anterior 4. finger extensors and 5. ankle evertors. These muscles are therefore generally difficult to activate while the patient are exhibiting these patterns.

For assessment Fugl-Meyer Assessment of Motor Recovery after Stroke

Co-ordination[3]

Proprioceptive loses can result in sensory ataxia . Strokes affecting the cerebellum typically produce cerebellar ataxia and motor weakness. The resulting problem with timing and sequencing of muscles can significantly impair function and limit adaptability to changing task and environmental demands.

The therapist focuses on elements of speed / rate control , steadiness , response orientation , and reaction and movement times.Fine motor control and dexterity should be examined using writing , dressing and feeding tasks .

Management

General[9]

In acute (shock ) stage of hemiplegia and in the comatosed patient

Treatment of the adult with Hemiplegia, following stroke starts from the very acute stage, when the patient in the ICU or Hospital bed. Treatment should be based on assessment by the relevant health professionals, including physiotherapists, Physicians and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercises.

Aims :[10]

1) Prevent recurrent stroke

2) Monitor vital signs, dysphasia adequate nutrition, bladder & bowel function.

3) Prevent complications

4) Mobilize the patient

5) Encourage resumption of self-care activities

6) Provide emotional support & education for patient & family

7)Screen for rehabilitation and choice of settings

Treatment

1.Care of the skin

  • Frequent changes of the patient's position (every 2 hours) and of the bed sheets.
  • Frequent wash of the skin of the back and pressure points by alcohol followed by talc powder.

2. Care of respiration

  • Suction of nasal and pharyngeal secretions.
  • Oxygen inhalation via catheter or mask specially in cases of coma.
  • Tracheostomy in urgent cases.
  • Breathing exercise
  • Chest expansion exercise
  • Huffing and coughing technique
  • Postural drainage

3.Care of nutrition and fluid balance

  • Tube feeding giving fruit juices , milk and pureed food , besides I.V. Fluids , in comatosed patients.

4. Care of urinary bladder

  • Foley's self retaining catheter in case of retention or incontinence.
  • Urinary antiseptics : Gentamycin 80 mg I.M . every 12 hours.
  • Care of bowels : Daily enema.

5.Prevent from deconditioning[11]

  • Early mobilization in the bed (activeturning, supine to sit, sit to supine, sitting, sitto stand)
  • Pelvic bridging exercise
  • Early propped up positioning, sitting & thenlater to standing
  • Moving around the bed
  • Facilitate movement of functioning limbs
Rehabilitation-of-neurological-patients-34-638.jpg

Once the patient’s condition is stable he is made to move out of the hospital bed and attends the Rehabilitation therapy clinic of the concerned Hospital or is referred to such clinics outside..

Rehabilitation

Stroke rehabilitation begins almost immediately, preferably within 24-36 hours once a patient is found medically stable.

The Physiotherapist focuses on joint range of motion and strength by performing exercises and re-learning functional tasks such as bed mobility, transferring, walking and other gross motor functions. Physiotherapists can also work with patients to improve awareness and use of the hemiplegic side. Rehabilitation involves working on the ability to produce strong movements or the ability to perform tasks using normal patterns. Emphasis is often concentrated on functional tasks and patient’s goals. One example physiotherapists employ to promote motor learning involves constraint-induced movement therapy. Through continuous practice the patient relearns to use and adapt the hemiplegic limb during functional activities to create lasting permanent changes.

Physiotherapy protocol

a. Conventional therapies (Therapeutic Exercises,Traditional Functional Retraining)

  • Range Of Motion (ROM) Exercises
  • Muscle Strengthening Exercises
  • Mobilization activities
  • Fitness training
  • Compensatory Techniques

b. Neurophysiological Approaches:

1. Muscle Re-education Approach.

2. Neurodevelopmental Approaches :Neurology Treatment Techniques

  • Sensorimotor Approach (Rood, 1940S)
  • Movement Therapy Approach (Brunnstrom, 1950S)
  • NDT Approach (Bobath, 1960-70S)
  • PNF Approach (Knot and Voss,1960-70S)

3. Motor Relearning Program for Stroke (1980S)

4. Contemporary Task Oriented Approach (1990S)

Posture : Primary focus, Potential Treatment, Benefits , Activities[12]

Posture/description Primary focus/benefits/activities
Prone on elbow

Prone ,weight bearing on elbows

Stable posture

Wide BOS

Low COM

Focus on improving upper trunk, UE and neck/head control

Improve ROM in hip extension

Improve shoulder stabilizers

Activities in posture : holding , weight shifting , UE reaching , assumption of posture

Modified prone on elbows can be achieved in sitting and plantigrade positions

Quadruped

All four positions (hands and knees)

Weight bearing at knees through extended elbows and hands

Stable posture

Wide BOS

Low COM

Focus on improving trunk , LE , UE and neck/head control

Improve trunk , hip , shoulder and elbow stabilizers

Decrease extensor tone at knees by prolonged weight bearing

Decrease flexor tone at wrist , elbows and hands by prolonged weightbearing

Promote extensor ROM at elbows, wrist and fingers

Lead up for I plantigrade activities , floor to standing transfers , antigravity balance control

Activities in posture : holding , weight shifting , UE reaching , LE lifts , assumption of posture , locomotion on all fours.

Bridging

Weight bearing at feet and ankles , upper trunk

Stable posture

Wide BOS

Low COM

Focus on improving lower trunk and LE control

Improve hip and ankle stratergies

Weight bearing at feet and ankles

Lead up for bed mobility , sit to stand transfers , standing and stair climbing

Activities in posture : holding weight shifting , assumption of postures , LE lifts

Sitting

Weight bearing through trunk and at buttocks , feet

Can include weightbearing through extended elbows and on hands

Intermediate BOS

Intermediate height COM

Focus on improving upper trunk , lower trunk , LE and head/neck control

Important for upright balance control

Lead up for UE ADL skills ; wheelchair locomotion

Activities in posture : holding , weight shifting , UE reaching , assumption of posture

Kneeling and half kneeling Focus on improving upper trunk , lower trunk , LE and head/neck control

Weightbearing through hips and at knees ; upright antigrade postion

Decrease extensor tone at knee by prolonged weightbearing

Improve hip and trunk stabilizers

Weightbearing through ankle in half kneeling

Lead up for upright balance control , standing and stepping , floor to standing transfers

Activities in posture ; holding , weight shifting , UE reaching ,assumption of posture , knee walking

Modified plantigrade

Standing with weightbearing on hands through

extended elbows (on support surface) and through

trunk, LEs

Modified upright antigravity position

Stable posture

Wide BOS

High COM

• Focus on improving head/neck, trunk, and UE/LE

control in supported, modified upright posture

• Decrease tone in elbow, wrist, and finger flexors by

prolonged weightbearing

• Increase extensor ROM at elbows, wrists, and fingers

• Hips flexed, COM forward of weight bearing line

creating an extension moment at the knee

• Increased safety for early standing (four-limb posture)

• Lead-up for upright balance control, standing and

stepping; standing UE ADL tasks

• Activities in posture: holding, weight shifting, UE

reaching, LE stepping, assumption of posture

Standing

Weightbearing through trunk and LEs

Full upright, antigravity position

Narrow BOS

High COM

• Focus on improving head/neck, trunk, and LE control in

fully upright posture

• Hips and knees fully extended

• Lead-up for upright balance control, stepping,

locomotion, stair climbing; standing UE ADL skills

• Activities in posture: holding, weight shifting, UE

reaching, LE stepping, assumption of posture

Programming variables[13]

Duration

The overall duration of the session will be one hour. The total duration of the aerobic/cardiac exercise training should increase from 15 minutes (week one) to 40 minutes by week 12.

Intensity

The intensity of exercise should aim to be moderate as opposed to low. This effort level is required for all components but will be adjusted for each individual according to health status on a session-by-session basis.

Frequency

The frequency of the session should be three times per week wherever possible.

Functional electrical stimulation (FES):

  • FES is a modality that applied a short burst of electrical current to the hemiplegic muscle or nerve.
  • In Hemiplegia Physical Therapy, FES has been demonstrated to be beneficial to restore motor control, spasticity, and reduction of hemiplegic shoulder pain and subluxation. It is concluded that FES can enhance the upper extremity motor recovery of acute stroke patient.
  • FES could reduce spasticity in stroke patient. A recent meta- analysis of randomized controlled trial study showed that FES improves motor strength.
  • FES can significantly improve arm function, electromygraphic activity of posterior deltoid, range of motion and reduction of severity of subluxation and pain of hemiplegic shoulder.

Biofeedback:

  • Biofeedback is a modality that facilitates the cognizant of electromyographic activity in selected muscle or awareness of joint position sense via visual or auditory cues. In Hemiplegia Physical Therapy the result of studies in biofeedback is controversial.
  • A meta-analysis of 8 randomized controlled trials of biofeedback therapy demonstrated that electromyographic biofeedback could improve motor function in hemiplegic patient.
  • Another meta-analysis study on EMG has showed that EMG biofeedbcak is superior to conventional therapy alone for improving ankle dorsiflexion muscle strengthbshowed that biofeedback could improve earlier postural control to improve impaired sitting balance.

Conventional gait training:

Conventional gait training has focused on part-practice of components of gait in preparation for walking. It includes

  • Symetrical Weight bearing training
  • Weight shifting
  • Stepping training (swinging / clearance )
  • Heel strike
  • Single leg standing
  • Push off / Calf rise.  Followed by,

Circuit training (reaching in sitting and standing, sit-to-stand, step-ups, heel lifts, isokinetic strengthening, walking over obstacles, up and down slopes).

Traditional approaches to stroke recovery have a focus on neuro facilitation or neuro developmental techniques (NDT) to inhibit excessive tone, stimulate muscle activity if hypotonia is present and to facilitate normal movement patterns through hands-on techniques. Practice based on the framework advocated by Berta Bobath remains the predominant physical therapy approach to stroke patients in the UK and is also common in many other parts of the world, including Canada, United States, Europe, Australia, Hong Kong and Taiwan. The Bobath framework has evolved from its original foundations, however, therapists surveyed on the core Bobath elements still emphasize normal tone and the necessity of normal movement patterns to perform functional tasks. Strength training to improve walking ability Task-specific training to improve walking ability.

References

  1. Hemiplegia Dr. V.S.Nandakumarhttps://www.slideshare.net/danny14871/hemiplegia-43636165 (accessed 29 June 2018)
  2. Hemiplegia bilisi State Medical Universityhttps://www.slideshare.net/jinujvarghese/hemiplegia-1 (accessed 29 June 2018)
  3. 3.0 3.1 3.2 3.3 3.4 3.5 O’ Sullivan SB, Schmitz TJ. Stroke.Physical rehabilitation. 5th ed., NewDelhi: Jaypee Brothers, 2007.
  4. Boulter DJ, Mukundan G, Schaefer PW. Neuroimaging of Acute Stroke. Stroke Recovery and Rehabilitation. 2014 Sep 18.
  5. Maria Stokes,Emma Stack Physical Management for Neurological Conditions 3rd edition ,25th April 2011
  6. 6.0 6.1 6.2 CLINICAL EXAMINATION IN HEMIPLEGIA.pdf - Google Drive (accessed 29 June 2018)
  7. Oommen, Kalarickal J. "Neurological history and physical examination." (2013).
  8. DR. WILLIAM P. HOWLETT ,PART I CLINICAL SKILLS ,CHAPTER 2 - LOCALIZATION , 2012
  9. 9.0 9.1 Dr. Hassan Elwan ,principles of neurology ,page no.39 ,2007
  10. Physiotherapy Treatment Approach https://www.physiotherapy-treatment.com  (accessed 28 June 2018)
  11. Stroke: PT Assessment and Management http://www.slideshare.net/surbaladevi/stroke-pt-assessment-and-management-22968324/ (accessed 29 June 2018)
  12. O'Sullivan SB, Schmitz TJ. Improving functional outcomes in physical rehabilitation. FA Davis; 2016 Feb 17.
  13. Best C, van Wijck F, Dinan-Young S, Dennis J, Smith M, Fraser H, Donaghy M, Mead G. Exercise after Stroke Services.(accessed 29 June 2018)