Download MBBS Physical Medicine and Rehabilitation Presentations 8 Cerebral Palsy Rehabilitation Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Physical Medicine and Rehabilitation 8 Cerebral Palsy Rehabilitation PPT-Powerpoint Presentations and lecture notes




Cerebral Palsy

Rehabilitation

Department Of PMR

Team approach




Associate manifestations

& complications

Mental Retardation

Epilepsy

Feeding, Nutrition, and Growth

Bladder Dysfunction

Bowel Dysfunction

Sleep Disturbances

Drooling

Hearing Loss

Visual Abnormalities

Orthopaedic Abnormalities


Goals of Rehabilitation

Improve mobility level of child

Prevent deformity and contractures

Educate parents regarding home management of child

To train child in activities of daily living (ADL)

To improve social participation of affected child.

Rehabilitation plan

There is no single blue print

Each patient and his or her family provides

a separate chal enge


Prognosis

Bleck(1987) has described tests for prognosis of walking

in children over 1 year

Neck righting reflex, asymmetrical and symmetrical tonic

neck reflex, Moro reflex ? all should disappear by 1 yr

Children who retain more than two primitive reflexes after

1 year.

Cannot sit unsupported by 4 year.

Cannot walk unaided by 8 years are unlikely to ever walk

independently.

NON-PHARMACOLOGICAL

MANAGEMENT


Basic needs

9

Ability to communicate with others

Ability to cope with ADLs

Independent mobility

Basic needs for a non walking child is straight

spine with level pelvis, painless hip and knee and
plantigrade feet

Physical therapy

10

Passive ROM exercises

Stretching exercises

Strength training

Neurodevelopmental therapy (NDT)/ Bobath technique:

aims to improve gross motor function and postural control
by facilitating muscle activity through key points of control
assisted by the therapist.


Physical therapy

11

Constraint-induced movement therapy holds promise in

improvements of upper limb dysfunction

Involved placing a full arm cast on the unimpaired upper

limb for 21 consecutive days, accompanied by intensive
training of impaired hand for 6 hours each day.

Functional electrical stimulation and biofeedback can

be helpful in training specific muscles

Occupational therapy

12

The primary goal is to help patient gain more

independence

Children work on fine motor skills by grasping and releasing

toys

Practice handwriting skills and hand-eye coordination

Basic tasks such as bathing, dressing, brushing teeth, and

eating are also addressed

They also work on fitting the child for special devices that

help them function. This may include utensils, dressing
devices, wheelchairs, bathing seats




Orthosis

13

Goals include reduction of abnormal tone, avoidance of

deformity, and facilitation of normal movement patterns

AFOs are used in case of dynamic equinus setting the

ankle in neutral to slight dorsiflexion promotes heel strike
and limits knee recurvatum.

Hinged AFOs can be used with plantar flexion stop

Ankle Foot Orthosis

14


FLOOR REACTION

15

ORTHOSIS

Ankle set at neutral
dorsiflexion and molded
anteriorly to just below
the patella this limit
crouch gait secondary to
hamstring spasticity by
creating an extension
moment at knee

Orthosis

16

Posterior leaf spring orthoses are thinned posteriorly to

simulate push-off at the end of stance phase

KAFO & HKAFO do not improve gait and they add

weight to already weak muscles

But they prevent deformity and facilitate standing

Long leg Tone inhibiting orthosis (with abduction

mechanism in c/o adductor spasticity) and serial
casting help in cases of correctable deformities


Assistive technology

17

Power wheelchairs ? as young as 20 to 36 months can

learn to use

Posterior postural walkers

Ultrasonic detectors can be incorporated for cortical

blindness

Augmentative communication devices

NON-SURGICAL

MANAGEMENT OF

CEREBRAL PALSY


General consideration

Factors to be considered before spasticity treatment:

1.

Whether to treat at all

2.

Distribution (focal/ regional/global)

3.

Degree of spasticity

4.

Family support & ability

5.

Physical access to medical care

Treatment options

Oral antispasticity medications

Nerve & motor point block

Botulinum toxin

Intrathecal baclofen


Oral medications

Baclofen

Diazepam

Clonazepam

Dantrolene

Tizanidine

Baclofen

MOA: Activates GABA-B & decreases excitatory

neurotransmitter release.

Dose:- starting dose 1 mg/kg/d (bid). 2 to 7 yr: max 40

mg, 8 to 11: max 60 mg, >12 yr: max 80 mg (divided
doses).

S/E: sedation, confusion, paraesthesia, weakness.

Rapid withdrawal: rebound spasticity, fever,

hallucination, seizure.

Caution: renal& hepatic compromise.


Diazepam

MOA: Acts centrally on GABA-A & facilitates GABA

mediated inhibition.

Dose:- <12 yr: 0.1--0.8 mg/kg/d,

>12 yr: 6--30 mg/d. (divided tid or qid)

S/E: sedation, memory loss.

Rapid withdrawal: anxiety, insomnia, seizures.

Caution: Hepatic compromise

Clonazepam

MOA: Same as Diazepam

Dose:- <10 yr: 0.1--0.2 mg/kg/d,

>10 yr: max 20 mg/d. (divided bid/tid)

S/E: more sedation than Diazepam.


Tizanidine

MOA: Alpha 2 agonist, facilitates action of glycine
spinally & supraspinally.

Dose: 0.2--0.3 mg/kg/d (tid/qid).

Advantage: Reduces spasm at night, helpful for sleep

S/E: hypotension, drowsiness.

Caution: Ciprofloxacin, hepatic compromise.

Nerve & motor point block

Nerve block: Peri-neural injection targeting a

motor/mixed nerve to impair its function.

Motor point block: Intramuscular injection lower down

the nerve trunk (below sensory branches) to create a
motor block with minimum sensory involvement.


Chemical denervation

agents

Phenol (5-7%): Denature protein of nerve tissue.

Alcohol (45-100%): Dehydrates nerve tissue & causes

sclerosis of myelin sheath.

Site: Motor nerve/point located by electrical nerve

stimulator.

Disadvantage of

phenol/alcohol

Needs precise location of injection.

Pain & dysesthesia very common.

Overdose & accidental i.v injection may lead to

depression, convulsion, cardiovascular collapse.


Botulinum toxin

A protein and neurotoxin produced by the anaerobic

bacteria Clostridium botulinum.

MOA: Blocks neurotransmitter (Ach) release at the

peripheral cholinergic nerve terminals

Reduction in muscle tension improved passive and active

range of motion, facilitates stretching techniques (casting
and splinting).

Dosing is based on amount of tone present, patient's prior

response to injections, residual function of the spastic
muscles, and potential impact of excessive tonal reduction

Intrathecal baclofen

ITB therapy significantly reduced severe spasticity which

did not respond to oral medications and botulinum
toxin treatment.

It might have reversible adverse effects or catheter-

related complications and spasticity reduction did not
always induce functional improvements.


SURGICAL MANAGEMENT


Four basic principles
Although the central nervous system injury, by definition, is non-

progressive, the deformities caused by abnormal muscle forces
and contractures are progressive.

The treatments currently available correct the secondary

deformities only and not the primary problem.

The deformities typically become worse during times of rapid

growth. For some patients, it may be beneficial to delay surgery
until after a significant growth spurt to decrease the risk of
recurrence.

Operative or non-operative treatment should be done to

minimize the impact it has on the patient's socialization and
education.

Operative Treatment

Operative treatment of deformities:

(1) correct static or dynamic deformity

(2) balance muscle power across a joint

(3) reduce spasticity (neurectomy)

(4) stabilize uncontrollable joints



Often, procedures can be combined--an adductor tendon

release can be done at the time of pelvic osteotomy for hip
subluxation.


Procedure

Indication

Possible

complications

Hip
Z-lengthening of

Flexion deformity

1. Decrease in hip

Psoas tendon

of the hip over 20

flexion pull

degree, shifting

the centre of

2. Compensatory

gravity forwards if

caliper gait with

primarily due to

increased pelvic

Psoas

rotation

Adductor

Scissoring gait

Asymmetrical

tenotomy

causing instability

abduction deformity

with pelvic tilt

Adductor tenotomy

---- do ---

---- do ----

with Obturator

neurectomy

Procedure

Indication

Possible

complications

Knee surgery
Medial hamstring

Flexion deformity

Patella alta, Knee

lengthenig

of the hip over 30

recurvatum and

degree during the

Secondary rotation of

gait

tibia

Lateral hamstring

Insufficient correction Patella alta & Knee

lengthening

after medial release

recurvatum

(Biceps)

(over 30 degree)

Distal rectus

Caliper gait (lack

Decrease of

release

of flexion at swing

extension pull

phase)

inducing relapse of

flexion at stance

phase


Procedure

Indication

Possible

complications

Ankle & Foot

Surgery
Tendo Achilles (Z-

Equinus Deformity

Progressive crouch

lengthening)

gait

Selective

------ do -------

gastrocnemius

fascial lengthening

using the Strayer or

Baker surgical

techniques

Thank you

This post was last modified on 08 April 2022