CEREBRAL PALSY

Dr. NAVEEN RATHOR Dept. of Orthopaedics RNTMC , UDAIPUR

CEREBRAL PALSY

• A motor function disorder – caused by permanent, non-progressive brain lesion – present at birth or shortly thereafter. (Mosby, 2006)

• Non-curable, life-long condition• Damage doesn’t worsen• May be congenital or acquired

In all cases, the following mustbe true:

1. CP is the result of a brain lesion; therefore, the spinal cord and muscles are structurally and biochemically normal.

2. The brain lesion must be fixed and nonprogressive. Thus, all the progressive neurodegenerative disorders are excluded from the definition.

3. Although brain lesions that result in CP are not progressive, clinical picture of CP may change with time due to devlopment of muscle and joint contracture.

EPIDEMIOLOGY

• The incidence of CP is increasing slightly.

• 2.4 and 2.7 per 1000 live births.

• increased survival of low birth weight babies.

• whereas the rate of CP in infants of a given birth weight has remained stable.

• Economic impact

ETIOLOGY-Severe deprivation of oxygen or blood flow to the brain A. Prenatal ( 70 % )

1.INFECTIONS-The TORCHES group of infections2.Rhesus blood group incompatibility3.Kericterus.etc B. Perinatal (5-10 % )1. FETAL Anoxia2. Premature delivery3. Sepsis 4. Cardiac conditions. C. Postnatal5. Infections such as meningitis in early childhood.6. Hypoxia 7. Trauma

CLASSIFICATIONS

i. Physiologic

ii. Geographical.

iii. Functional.

I. Physiologic

• TYPE of movement disorder present.1. Spasticity.2. Dystonia.3. Athetosis.4. Ataxic

1. SPASTICITY• Most common • damage to the pyramidal system, particularly the motor

cortex (corticospinal tract ) in the brain. • Disinhibition of pathologic reflex arcs.• increased tone in the extremities. • The tone is dependent on velocity, which means that if a

muscle is stretched rapidly, tone increases more than if the same muscle group were stretched gradually and gently.

• ‘CLASPED KNIFE DEFORMITY’-decerase in resistence when it is passively flexed.

2. DYSTONIA

• is described as increased tone, • Due to lesion in basal ganglia.

• which is not dependent on velocity.

• tone in dystonic CP is described as “LEAD PIPE” which means that tone does not decrease with gentle prolonged stretching.

3. ATHETOSIS• is characterized by abnormal writhing movements that

the patient cannot control.

• exaggerated as the patient tries to complete a purposeful motion.

• Lesion in basal ganglia.

• Speech - difficult to understand

• neonatal kernicterus.

4. ATAXIC

• Cerebellar lesions lead to ataxic CP.

• wide-based and clumsy gait.

• rare.

“It is important to correctly classify the

movement disorder of a patient with CP because the results of surgical treatment are unpredictable for all but purely spastic patients.”

II. GEOGRAPHIC

• Part of the body affected, 1. Hemiplegia2. Diplegia –

- With both lower extremities being involved (though not always symmetrically) and lesser involvement of the upper extremities

-m/c form of cerebral palsy3. Double hemiplegia4. Quadriplegia5. Monoplegia-rare

III. FUNCTIONAL

• Current emphasis.

• The Gross Motor and Functional Classification System (GMFCS)

• Five levels.

level 1 - 34.2%

level 2 - 25.6% level 3- 11.5% level 4- 13.7%

level 5- 15.6%

EVALUATION - HISTORY• Birth history – Birth weight, gestational age,

complications, NICU etc.• Motor Mile stones- Delayed.

• Preferential use of one hand or leg.• strabismus, difficulty swallowing, frequent choking,

delayed speech development, poor eyesight, and seizures ( 20 to 40 %).

Head control 3 to 6 months

Sitting 6 to 9 months

Crawling 9 months

Standing and cruising 10 to 12 months

Walking 12 and 18 months

PHYSICAL EXAMINATION

1. Muscle tone – • Spasticity feels like tightness in the muscles,

which become tighter the quicker the limbs are passively moved.

• Greater range of motion can be gained by slowly and gently stretching the joints in question.

• Tardieu test is a measure of spasticity.

• For example, if the examiner is assessing hamstring spasticity, the angle at which a “grab” of resistance occurs when quickly extending the knee with the hip in flexion is compared with the amount of extension possible when the knee is stretched.

• Difference in angle is the spasticity.

2. Deep tendon reflexes – are increased in patients with CP– Clonus– Asymmetric in hemiparesis.– Infantile reflexes will be retained.

3. Balance, Sitting, and GaitGait analysis-observational computerised instrumental– Crouched gait– Jumping gait– High stpping gait– Scissoring gait– True and apperent equinus

HPE + IMAGING

1. periventricular leukomalacia2. intraventricular and periventricular

hemorrhage.

Patchy areas of necrosis secondary to vascular insult

MANAGMENT• Childhood is the optimal time for intervention to

maximize the function of a patient with CP.

• duty to ensure that the musculoskeletal treatment of the child prevents future problems with pain and deformity as an adult.

• Patients with CP do not usually have severely shortened life spans.

NON SURGICAL TREATMENT-1.PHYSICAL THERAPY.

• Frequently the first treatment.• Passive stretching.• Strenghtening of the muscles.• Wheel chair transfers

2. ORTHOSIS -Improving gait in ambulatory -AFOs are helpful in positioning the ankle and foot

during gait.

Indications for bracing

1. To obtain a plantigrade foot position and reduce genu recurvatum in patients with dynamic equinus.

• 2. To support the foot in dorsiflexion during swing phase when footdrop is present

• 3. To assist the foot postoperatively while weakness is being treated by physical therapy.

• 4. To improve mild crouch

CONTRAINDICATIONS

• Nonambulatory patients who are able to wear shoes with orthoses- Level 4 and 5.

• Preambulatory– they interfere with the child’s ability to crawl and move

about the floor.

3. MEDICAL THERAPY

• Dantrolene sodium-peripheral acting muscle relexent

-act by inhibiting calcium ion release during muscle contraction.

-Diazepam , Baclofen, Tizanidine– reduce tone, relieve spasticity

Intrathecal Baclofena -aminobutyric acid agonist, acts at the spinal cord level to impede release of the excitatory

( GABA) neurotransmitters that cause spasticity

Botulinum Toxin• Botulinum toxin type A commonly marketed at BOTOX.

• blocking the release of acetylcholine at the NMJ

• The targeted muscle becomes weak because of lack of innervation until the neuromuscular junction sprouts new endings.

• dynamic deformities in the absence of fixed contracture.

• begins taking effect after 2 to 3 days

• wears off after approximately 3 months

Indications1. A child with a dynamic equinus deformity and no

fixed plantar flexion contracture

2. A child with equinus gait without multilevel crouch

3. A child younger than 4 years who cannot tolerate AFOs because of dynamic equinus

4. Parents’ desire for injections and refusal of tendon lengthening surgery.

SURGERY- GENERAL PRINCIPLES

• Goals of the surgery – defined and discussed.

• Once other modalities fail.

• Expected Post operative course.

• NO CURE.

• “Walk differently hopefully better but no normal “.

SURGERY – TIMING.• combining multiple tendon surgeries and

osteotomies into a single surgical event, Single Event Multi Level surgery (SEMLS).

• Avoid ‘ birthday surgery ‘- correcting all concomitant contractures simultaneously during one surgery is important to avoid recurrence or overcorrection. Because gait changes and matures until approximately 7 years of age.

Selective Dorsal Rhizotomy• Neurosurgical intervention• A technique to reduce spasticity and balance muscle tone

in carefully selected patients.• The goal of selective dorsal rhizotomy is to identify the

rootlets carrying excessive stimulatory information and section them to reduce the stimulatory input from the dorsal sensory fibers.

• The ideal patient for this procedure is a child 3 to 8 yr old with spastic diplegia , voluntary motor and trunk control, pure spasticity, and no fixed contractures.

• Majority of patients can be expected to improve one GMFCS level.

INDICATIONS--The ideal patient for this procedure is a child 3 to 8 yr

old with spastic diplegia , voluntary motor and trunk control, pure spasticity, and no fixed contractures.

Complication--hip subluxation and dislocation-lumber lordosis , scoliosis ,spondylosis and

spondylolisthesis-paraparesis

MANAGEMENT OF FOOT

1. EQUINUS2. EQUINOVARUS3. PES VALGUS4. ANKLE VALGUS5. BUNIONS

1. EQUINUS-One of the m/c deformity.

-m/c due to calf muscle spasticity (hamstring contracture).-should be deferentiated from apperent equinus.

Silfverskiöld test –for hamstring contracture

• If the ankle can be passively dorsiflexed with the knee bent to 90 degrees but cannot be dorsiflexed with the knee extended,

• it is believed that the gastrocnemius is tight but the soleus is not contracted.

Gastrocnemius recession- Strayer, Baker, or Vulpius

• Strayer procedure-– The cut in the gastrocnemius is transverse and more proximal– not lengthen the soleus whatsever

• Baker technique –– the gastrosoleus aponeurosis is cut in tongue-in-groove fashion

and– dissected free from the underlying soleus muscle. – The fascia is allowed to slide on the underlying muscle, thereby

increasing the overall length of the muscle, – and the four corners of the aponeurosis are sutured in the lengthened position

Vulpius procedure –the aponeurosis of the gastrocsoleus is divided in chevron fashion the midline fibrous septum of the gastronemius is transected, but the soleus muscle fibers are not disturbed .

1. Isoloated Gastrocnemius – Aponeurotic lenghtening.

2. Gastocnemius + Soleus – TA Lenghtening3. Don’t over lengthen – calcaneal deformity.4. Aponeurotic lengthening is preferred over TA

2. EQUINOVARUS DEFORMITY• Muscle imbalance in which the invertors of the foot,

specifically the, posterior and anterior tibialis muscles, overpower the evertors (the peroneals).

• The gastronemius contributes equinus to the deformity.

• Patients walk on the lateral border of the inverted foot,

• painful calluses may develop laterally over the fifth metatarsal.

If supination of theforefoot is seen, the anterior tibialis is most likely contributingto the equinovarus deformity.

Next, feels for spasticity in the posteriortibialis muscle.

Passive manipulation of the hindfoot into valgus while feeling the posterior tibialis tendon can help

the physician appreciate tightness in the posterior tibialis

Surgery • Split Tibialis anterior transfer.• Split tibialis posterior transfer.• Tenotomy of tibialis posterior.

Management of knee-Problems

• Hamstring spasticity or contracture

• Quadriceps weakness

• Lengthening of the patellar tendon and patella alta

• Flexion deformity

HARMSTRING SPASTICITY

Treatment• PT (hamstring + quadriceps strengthening)• Myoneural block of hamstring muscles.• Hamstring release.• Hamstring transfer.• Femoral supracondylar extension osteotomy.• Correcting patella alta– Plication of the patellar tendon– Distal transfer of the tibial tuberosity

HARMSTRING RELEASE

• The most widely recommended• fractional lengthening technique.• aponeurotic lengthening of the

semimembranosus and biceps femoris and Z-plasty of the semitendinosus.

MANAGEMENT OF HIP

1. Adduction deformity2. Flexion deformity3. internal rotation gait 4. Hip subluxation and dislocation.

Problems – Adduction deformity

• Scissor gait• Tendency for hip subluxation and dislocation• Recurrence of deformity• Overcorrection of deformity

Treatment options for dealing withadduction deformity and scissoring

• Stretching exercises and modification of sitting and lying posture.

• Myoneural blocks.• Adductor tenotomy and obturator neurectomy.• Adductor transfer

Adductor tenotomyidentify the adductor longus by palpation, and make a 3 cm

transverse incision over the adductor longus tendon approximately 1 cm distal from its origin.

Problems – Flexion deformity

• Abnormal posture and gait.– hip flexion and compensatory knee flexion or– with the knee straight and compensatory lumbar

lordosis• Tendency for hip instability.• Excessive weakening of the hip flexor

Treatment

• Stretching exercises- Hip flexors.• Iliopsoas tenotomy.– Division of the iliopsoas tendon close to its

insertion into the lesser trochanter.• Intramuscular release of psoas at the pelvic

brim.• Rectus femoris release

Iliopsoas recession

make a 5cm incision medial to and 2 cm below the

ASIS.Develop the interval

between the tensor fascia lata and sartorius.

Palpate the pelvic brim just medial and inferior to the

rectus femoris origin to locate the iliopsoas tendon

in a shallow groove.

Treatment options - hip subluxation and dislocation (Internal rotation gait)

• Femoral varus and derotation osteotomy.• Medial hamstring release• Anterior and medial transfer of gluteus

medius.• Selective internal rotator release

Varus femoral derotation osteotomy of hip

THANK YOU FOR PATIENTLY LISTENING!!!

"Time and gravity are enemies of very aging body, especially mine." - Adult with CP