☺Components of cerebral palsy

• Abnormal control of motor function
• Nonprogressive disorder of movement and/or posture
• Damage to Immature Brain

☺ Detection of CP

• Most patients with cerebral palsy are simply hypotonic and physically and developmentally delayed during the first year of life.
• Frequently, the child is older than 1 year of age before he is referred to a specialist because the child appears to be developmentally delayed and the only physical sign of cerebral palsy may be persistent infantile reflexes.
• Probably the greatest predictor of cerebral palsy in the first year of life is an abnormal perinatal history.

☺ Average age at detection

• Spastic diplegia 8 to 10 mths
• Hemiplegia 20 to 24 mths
• Athetosis 24 mths

Etiology of CP

• In most cases of cerebral palsy only risk factors can be identified, and not specific causes. Only approximately 10 to 15% of patients in one large group had documented perinatal hypoxia or other problems
• 60 to 65% of afflicted children were born at full term
• 10% of cerebral palsy patients weigh less than 1,500 grams at birth
• The risk of having cerebral palsy is 90 per 1,000 for premature SGA child compared with 3 per 1,000 if weighing more than 2,500 grams and appropriate for gestational age

☺ Risk Factors for CP

Classification

☺ Neuropathic

• Spastic: Hyperreflexia and Hyperre
  flexia, Weakness, Loss of muscle,control Dexterity, Interference with balance, Fatigability, Simultaneous contracting of antagonistic muscles

• Athetoid: Purposeless writhing movements which become intensified when the child is frightened or excited.Associated with Kernicterus
• Dystonia; Increased general muscle tone, Distorted postures, Abnormal positions that are induced by voluntary movements
• Ataxic: Disturbance of coordinated movement, most noticed when walking, Cerebellar dysfunction, Intention tremor
• Hypotonic: Transient Phase,The brain lesion is present but masked by lack of myelination of the pathways that will carry its abnormal messages,Mixed

☺ Anatomical types

• Diplegia:

  • Lower limb > Upper limb

  • Periventricular haemorrahage

  • Hypoxia

• Hemiplegia:

  • Upper limb > Lower limb
  • Focal brain lesion: Trauma, vascular, infection
  • Homonymous hemianopia
  • Asteriognosis
  • Epilepsy

• Whole body (quadriplegia)

  • Global involvement with mental retardation
  • The usual cause is severe hypoxia.
  • Initially presenting as a floppy babyBulbar dysfunction ( drooling, dysarthria, and dysphagia)
  • Seizures
• Monoplegia
• Double hemiplegia
• Triplegia

History

☺Purpose

History will provide knowledge about

• Etiology/ Risk factors
• Milestones
• Ability/ disability
• Associated problems
• Treatment
• Family’s resourses

☺ Presentations

• Follow up of “at risk” infants, such as those born prematurely
• Delayed motor milestones, particularly learning to sit, stand and walk
• Asymmetric movement patterns, for example, strong hand preference early in life
• Abnormalities of muscle tone particularly spasticity or hypotonia
• Management problems, for example, severe feeding difficulties and unexplained irritability. Many other conditions present with these features.

☺ Key points in history

Examination

☺ Neurological examination

• Skull circumferance ( Hydrocephalus/ microcephaly)
• Mental status
• Cranial nerves
• Vision/ Hearing/ speech
• Motor System
• Muscle strength and selective control
• Muscle tone
• Reflexes and sensory function

☺Degree of deformity or muscle contracture

• Range of motion
• Deformity (linear, angular, and torsional deformation of the spine and long bones, and fixed hand or foot deformities)
• Balance, equilibrium, and standing or walking postures

☺ Functional Examination

• Dynamic examination evaluate the head control, sitting balance, the ability to crawl, the ability to pull up to stand, standing posture and balance, and the ability to walk.
• Observational gait assessment is imperative in those who can walk.

☺Orthopaedic Evaluation of the lower limb

These tests are described in standard orthopaedic examination text books

☺ Measurements in spasticity

Tardieu Scale

This test is performed with patient in the supine position, with head in midline.

Measurements take place at 3 velocities (V1, V2, and V3). Responses are recorded at each velocity as X/Y, with X indicating the 0 to 5 rating, and Y indicating the degree of angle at which the muscle reaction occurs. By moving the limb at different velocities, the response to stretch can be more easily gauged since the stretch reflex responds differently to velocity.

Velocities:

V1: As slow as possible, slower than the natural drop of the limb segment under gravity

V2: Speed of limb segment falling under gravity

V3: As fast as possible, faster than the rate of the natural drop of the limb segment under gravity

Angles

R1, the angle of catch following a fast velocity stretch at either V2 or V3; and R2, the passive range of movement achieved following a slow velocity stretch at V1

Scoring:

0 No resistance throughout the course of the passive movement

1 Slight resistance throughout the course of passive movement, no clear

catch at a precise angle

2 Clear catch at a precise angle, interrupting the passive movement, followed

by release

3 Fatigable clonus with less than 10 seconds when maintaining the pressure

and appearing at the precise angle

4 Unfatigable clonus with more than 10 seconds when maintaining the

pressure and appearing at a precise angle

5 Joint is immovable

Modified Ashworth Scale

0 No increase in muscle tone

1 Slight increase in muscle tone, manifested by a catch and release

or by minimal resistance at the end range of motion when the part is

moved in flexion or extension/abduction or adduction, etc.

1+ Slight increase in muscle tone, manifested by a catch, followed by

minimal resistance throughout the remainder (less than half) of the

ROM

2 More marked increase in muscle tone through most of the ROM, but

the affected part is easily moved

3 Considerable increase in muscle tone, passive movement is difficult

4 Affected part is rigid in flexion or extension (abduction ,adduction, etc.)

Associated Problems

• CNS:
• Mental retardation (30 to 65%) behavioral and emotional difficulties perceptual disorders
• Learning disorders
• Bulbar involvement
• Sensory deafness
• Visual difficulties (50%) perceptual problems, strabismus, nystagmus, and cortical blindness
• Gastrointestinal
• Constipation and fecal impaction
• Impaired swallowing, vomiting, esophageal reflux, and hiatal hernia
• Aspiration and the risk of severe pneumonia, epigastric pain, profound feeding problems, and poor nutrition
• Genitourinary
• Bladder dysfunction (28 %)
• Urinary incontinence (26 %)
• Urinary tract infections

Functional Assessment

☺Gross Motor Function Classification System (GMFCS)

Class Goal of treatment

1- Walks independently, speed, balance & coordination reduced

2- Walks without assistive devices but limitations in community Diminish energy expenditure, decrease level of support, improve appearance

3- Walks with assistive devices Improve gait, position for sitting, transfers, supported standing

4- Transported or uses powered mobility Decrease pain, improve sitting & standing

5- Severely limited, dependent on wheelchair Better positioning, decrease pain, improve hygiene

Gaits in cerebral palsy

Hemiplegic gait

Hemiplegic gait is characterised by pes equinus, genu recurvatum,

internal femoral rotation and hip adduction.

There are four types of hemiplegic gait

Type 1: There is weakness of the tibialis anterior and an adequate

gastrocnemius-soleus length.

Type 2: Gastrocnemius-soleus muscle is short in addition to tibialis anteriorweakness. The child compensates with knee hyperextension in midstance

Type 3: There is persistent knee flexion in stance phase and decreased knee motion in swing phase in addition to the above findings. This is defined as stiff knee gait.

Type 4: There is adduction and flexion of the hip in addition to the findings above  Bony deformities such as excessive internal femoral rotation and tibial torsion may also be seen

Diplegia gait patterns.

Scissoring

Scissoring is a frontal plane pathology also called crossing over.

Cause-hip adductor and/or medial hamstring spasticity.

Persistent femoral anteversion

The child walks with legs crossing one another. The hip is in flexion, adduction and internal rotation. The knees are turned inward.

Jump gait

most common sagittal plane pathology in young diplegic children. Almost all diplegic children begin walking with a jump knee gait pattern.

Jump gait is defined as excessive hip flexion, knee flexion and equinus in stance Cause- lower extremity flexor muscle spasticity.

The child walks with hips and knees in flexion and ankles in plantar flexion looking like an athlete getting ready to jump.

Crouch gait

The second most common sagittal plane pathology and it occurs in the older diplegic.

It is defined as excessive knee flexion throughout the stance phase with dorsiflexion of the ankle joint.

Causes-short or spastic hamstrings, hip flexor tightness and excessive ankle

dorsiflexion. Excessive ankle dorsiflexion may result from isolated triceps surae lengthening without addressing the spastic hamstrings.

Hamstring tightness causes crouch and a short step length when walking. When sitting, tight hamstrings pull the ischial tuberosities and tilt pelvis posteriorly causing kyphosis and sacral sitting.

Stiff knee

This is a sagittal plane pathology characterized by limited range of motion in the knee joint, especially a lack of flexion in swing

Cause- spasticity of rectus femoris muscle or unopposed rectus femoris function after hamstring lengthening.Compensatory movements of hip external rotation and circumduction are observed. The patient experiences difficulty going up steps. Step length is shortened, foot clearance is poor, shoes wear out rapidly.

Genu recurvatum

Genu recurvatum occurs in the stance phase of walking and is generally  associated with mild equinus caused by triceps surae spasticity, excessive spasticity in the quadriceps, and may be related to weakness of the hamstring muscles or contracture of the hip flexors.

Investigations

• Urine / plasma metabolic screen if a metabolic disorder is suspected
• TORCH titer if congenital infections suspected
• Chromosomal analysis if genetic disorder suspected
• MRI
  ? vascular lesion
  ? malformation
  ? periventricular leucomalacia