Department Of PMR
Team approach
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Associate manifestations
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& complications
Mental Retardation
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EpilepsyFeeding, Nutrition, and Growth
Bladder Dysfunction
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Bowel Dysfunction
Sleep Disturbances
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DroolingHearing Loss
Visual Abnormalities
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Orthopaedic Abnormalities
Goals of Rehabilitation
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Improve mobility level of child
Prevent deformity and contractures
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Educate parents regarding home management of childTo train child in activities of daily living (ADL)
To improve social participation of affected child.
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Rehabilitation plan
There is no single blue print
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Each patient and his or her family providesa separate chal enge
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PrognosisBleck(1987) has described tests for prognosis of walking
in children over 1 year
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Neck righting reflex, asymmetrical and symmetrical tonic
neck reflex, Moro reflex ? all should disappear by 1 yr
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Children who retain more than two primitive reflexes after1 year.
Cannot sit unsupported by 4 year.
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Cannot walk unaided by 8 years are unlikely to ever walk
independently.
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NON-PHARMACOLOGICALMANAGEMENT
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Basic needs9
Ability to communicate with others
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Ability to cope with ADLs
Independent mobility
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Basic needs for a non walking child is straightspine with level pelvis, painless hip and knee and
plantigrade feet
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Physical therapy10
Passive ROM exercises
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Stretching exercises
Strength training
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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.
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Physical therapy
11
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Constraint-induced movement therapy holds promise in
improvements of upper limb dysfunction
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Involved placing a full arm cast on the unimpaired upperlimb for 21 consecutive days, accompanied by intensive
training of impaired hand for 6 hours each day.
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Functional electrical stimulation and biofeedback canbe helpful in training specific muscles
Occupational therapy
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12
The primary goal is to help patient gain more
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independenceChildren work on fine motor skills by grasping and releasing
toys
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Practice handwriting skills and hand-eye coordination
Basic tasks such as bathing, dressing, brushing teeth, and
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eating are also addressedThey also work on fitting the child for special devices that
help them function. This may include utensils, dressing
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devices, wheelchairs, bathing seats--- Content provided by FirstRanker.com ---
Orthosis13
Goals include reduction of abnormal tone, avoidance of
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deformity, and facilitation of normal movement patterns
AFOs are used in case of dynamic equinus setting the
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ankle in neutral to slight dorsiflexion promotes heel strikeand limits knee recurvatum.
Hinged AFOs can be used with plantar flexion stop
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Ankle Foot Orthosis14
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FLOOR REACTION15
ORTHOSIS
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Ankle set at neutral
dorsiflexion and molded
anteriorly to just below
the patella this limit
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crouch gait secondary tohamstring spasticity by
creating an extension
moment at knee
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Orthosis16
Posterior leaf spring orthoses are thinned posteriorly to
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simulate push-off at the end of stance phase
KAFO & HKAFO do not improve gait and they add
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weight to already weak musclesBut they prevent deformity and facilitate standing
Long leg Tone inhibiting orthosis (with abduction
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mechanism in c/o adductor spasticity) and serial
casting help in cases of correctable deformities
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Assistive technology17
Power wheelchairs ? as young as 20 to 36 months can
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learn to use
Posterior postural walkers
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Ultrasonic detectors can be incorporated for corticalblindness
Augmentative communication devices
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NON-SURGICAL
MANAGEMENT OF
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CEREBRAL PALSYGeneral consideration
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Factors to be considered before spasticity treatment:1.
Whether to treat at all
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2.
Distribution (focal/ regional/global)
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3.Degree of spasticity
4.
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Family support & ability
5.
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Physical access to medical careTreatment options
Oral antispasticity medications
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Nerve & motor point block
Botulinum toxin
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Intrathecal baclofenOral medications
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BaclofenDiazepam
Clonazepam
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Dantrolene
Tizanidine
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BaclofenMOA: Activates GABA-B & decreases excitatory
neurotransmitter release.
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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).
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S/E: sedation, confusion, paraesthesia, weakness.
Rapid withdrawal: rebound spasticity, fever,
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hallucination, seizure.Caution: renal& hepatic compromise.
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DiazepamMOA: Acts centrally on GABA-A & facilitates GABA
mediated inhibition.
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Dose:- <12 yr: 0.1--0.8 mg/kg/d,
>12 yr: 6--30 mg/d. (divided tid or qid)
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S/E: sedation, memory loss.Rapid withdrawal: anxiety, insomnia, seizures.
Caution: Hepatic compromise
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Clonazepam
MOA: Same as Diazepam
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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.
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Tizanidine
MOA: Alpha 2 agonist, facilitates action of glycine
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spinally & supraspinally.Dose: 0.2--0.3 mg/kg/d (tid/qid).
Advantage: Reduces spasm at night, helpful for sleep
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S/E: hypotension, drowsiness.
Caution: Ciprofloxacin, hepatic compromise.
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Nerve & motor point blockNerve block: Peri-neural injection targeting a
motor/mixed nerve to impair its function.
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Motor point block: Intramuscular injection lower down
the nerve trunk (below sensory branches) to create a
motor block with minimum sensory involvement.
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Chemical denervation
agents
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Phenol (5-7%): Denature protein of nerve tissue.
Alcohol (45-100%): Dehydrates nerve tissue & causes
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sclerosis of myelin sheath.Site: Motor nerve/point located by electrical nerve
stimulator.
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Disadvantage of
phenol/alcohol
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Needs precise location of injection.Pain & dysesthesia very common.
Overdose & accidental i.v injection may lead to
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depression, convulsion, cardiovascular collapse.
Botulinum toxin
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A protein and neurotoxin produced by the anaerobic
bacteria Clostridium botulinum.
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MOA: Blocks neurotransmitter (Ach) release at theperipheral cholinergic nerve terminals
Reduction in muscle tension improved passive and active
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range of motion, facilitates stretching techniques (casting
and splinting).
Dosing is based on amount of tone present, patient's prior
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response to injections, residual function of the spastic
muscles, and potential impact of excessive tonal reduction
Intrathecal baclofen
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ITB therapy significantly reduced severe spasticity which
did not respond to oral medications and botulinum
toxin treatment.
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It might have reversible adverse effects or catheter-
related complications and spasticity reduction did not
always induce functional improvements.
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SURGICAL MANAGEMENT
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Four basic principlesAlthough the central nervous system injury, by definition, is non-
progressive, the deformities caused by abnormal muscle forces
and contractures are progressive.
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The treatments currently available correct the secondary
deformities only and not the primary problem.
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The deformities typically become worse during times of rapidgrowth. For some patients, it may be beneficial to delay surgery
until after a significant growth spurt to decrease the risk of
recurrence.
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Operative or non-operative treatment should be done to
minimize the impact it has on the patient's socialization and
education.
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Operative Treatment
Operative treatment of deformities:
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(1) correct static or dynamic deformity(2) balance muscle power across a joint
(3) reduce spasticity (neurectomy)
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(4) stabilize uncontrollable joints
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Often, procedures can be combined--an adductor tendonrelease can be done at the time of pelvic osteotomy for hip
subluxation.
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Procedure
Indication
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Possiblecomplications
Hip
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Z-lengthening ofFlexion deformity
1. Decrease in hip
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Psoas tendon
of the hip over 20
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flexion pulldegree, shifting
the centre of
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2. Compensatory
gravity forwards if
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caliper gait withprimarily due to
increased pelvic
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Psoas
rotation
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AdductorScissoring gait
Asymmetrical
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tenotomy
causing instability
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abduction deformitywith pelvic tilt
Adductor tenotomy
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---- do ---
---- do ----
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with Obturatorneurectomy
Procedure
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Indication
Possible
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complicationsKnee surgery
Medial hamstring
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Flexion deformityPatella alta, Knee
lengthenig
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of the hip over 30
recurvatum and
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degree during theSecondary rotation of
gait
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tibia
Lateral hamstring
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Insufficient correction Patella alta & Kneelengthening
after medial release
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recurvatum
(Biceps)
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(over 30 degree)Distal rectus
Caliper gait (lack
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Decrease of
release
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of flexion at swingextension pull
phase)
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inducing relapse of
flexion at stance
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phaseProcedure
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IndicationPossible
complications
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Ankle & Foot
Surgery
Tendo Achilles (Z-
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Equinus Deformity
Progressive crouch
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lengthening)gait
Selective
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------ do -------
gastrocnemius
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fascial lengtheningusing the Strayer or
Baker surgical
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techniques
Thank you
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