Understanding Abnormal Motor Development and Cerebral Palsy

Abnormal Motor Development

What is the Diversion from Normal?

For direct CNS injury:

  • Development of pathological afferents by CNS injury
  • Musculoskeletal apparatus determines the functional abnormality
  • Insufficient differentiation of coordination

Primitive Reflexes

Maturation organization of progressive morphological structures

Classification

  • Cutaneospinal Reflexes
  • Tonic-Spinal Reflexes
  • Extensor Reflexes
  • Reactions: Moro, Galant

Latency Time

  • Babkin: 0-4 seconds
  • Rooting: 0-3 months
  • Doll’s Eyes (a sign of pathology): 0-4 seconds
  • Automatic March: 0-4 seconds
  • Primary Leg Extension: 0-4 seconds
  • Suprapubic: 0-4 seconds
  • Crossed Extension: 0-6 seconds
  • Plantar Heel: 0-4 seconds
  • Palmar Grasp Reflex: 2-8 weeks
  • Plantar Support Reflex
  • Heel-to-Palm: Indicates palsy
  • RAF since 10 days
  • ROF since 3 months

Postural Reactions

  • Vojta’s Reaction
  • Tensile Strength Reaction
  • Peiper-Isbert Vertical Suspension Reaction
  • Collis Vertical Reaction
  • Collis Horizontal Reaction
  • Landau Reaction
  • Axillary Suspension Reaction

First Quarter Warning Signs

  • Hand in hand, thumb included
  • Pelvis in anteversion
  • Impaired swallowing
  • RAF absent, isolated or accompanied by other signs
  • Lack of direction of gaze or identification of familiar faces
  • Abnormal posture reactions

Second Quarter Warning Signs

  • Lack of hand-hand coordination
  • Supine dystonic attacks
  • No limb muscle differentiation
  • Pathological motor patterns
  • Absent or blocked turning
  • Increased flexor or extensor tone
  • Altered postural reactions

Development of Spasticity

  • Spontaneous phasic motor activity
  • Increased phasic movement of facial EESS and better integration into the body schema
  • EESS affected (nuchal), outside the body schema
  • Underdevelopment of the function of straightening the EESS
  • Tendency to elbow flexion
  • Lack of coordination
  • Development of abnormal hand-eye-mouth coordination pattern
  • Lower limbs most affected, tending towards extension
  • Hypertonia of the forearm pronator
  • No lateral position
  • Rotation is always performed on the affected side
  • Affects balance in all positions
  • Positive palm-heel reflex
  • Intense neonatal palmar grasp reflex
  • Moro reaction of lower intensity on the affected side or with greater flexion
  • Plantar grasp reflex disappears early
  • Exacerbated plantar heel reflex
  • Negative Galant reflex

Development of Athetosis

  • Instability in any position
  • Positive Moro reaction (extension)
  • Mass movement with opisthotonos dystonic attacks
  • Hypotonia of the trunk and limb root at rest (changing tone)
  • Dorsal with ERIA scissor pattern
  • Asymmetrical head position when prone
  • Extends the neck in opisthotonos
  • Absent palmar grasp reflex
  • Intense neonatal plantar grasp reflex
  • Intense neonatal Galant reflex
  • Swallowing difficulties
  • Turning head with associated movements
  • No independent sitting

Congenital Cerebellar Syndrome

  • Hypotonia
  • Gastroesophageal reflux
  • Altered eye coordination
  • Convergent strabismus in 50% of cases
  • Intellectual deficit
  • Delay in motor development, lack of righting reactions
  • No independent sitting or presents with separate sitting
  • Limited hand-hand play
  • Dystonic attacks

Hypotonic Syndromes

  • Differential Diagnosis:
    • Congenital muscle hypoplasia
    • Congenital spinal myopathy
    • Congenital spinal amyotrophy
  • Increased proximal limb hypotonia
  • Intellectually normal
  • Turn their heads towards stimuli
  • Perform hand-mouth and mouth-body play
  • Do not turn over

Third Quarter

  • Not enough chewing or syllabic echolalia
  • Damage is clearly evident
  • Delayed and altered righting mechanisms
  • Establishment of disease patterns

Cerebral Palsy (CP)

CP does not include other causes of motor disorders or degenerative brain injuries that evolve into progressive irreversible motor impairment. The persistent nature is relevant in the approach to therapy.

Types According to Topographical Involvement

  • Tetraparesis
  • Diparesis
  • Paraparesis
  • Hemiparesis
  • Double Hemiparesis
  • Monoparesis

Types According to Clinical Manifestation

  • Spastic
  • Spastic Tetraparesis
  • Spastic Diplegia
  • Spastic Paraparesis
  • Spastic Hemiplegia
  • Spastic Double Hemiplegia
  • Dystonic or Athetoid
  • Hypotonic
  • Ataxic
  • Mixed

Spastic Hemiparesis

  • Spastic posture of the affected EESS
  • Establishment of the first metacarpal in adduction
  • Independent sitting is achieved on the affected side only
  • May not achieve separate sitting
  • Sitting with extension of the affected lower limbs with equinus foot, elbow flexion, and head tilt towards the healthy side

Spastic Hemiparesis

  • Premature disappearance of plantar grip on the affected side
  • Mouth-body play with the sound side only
  • Primitive extension reflex
  • No four-point support
  • No support on the open paretic hand
  • When hand or knee support is achieved, it is not stable
  • Slows the growth of the paretic side (hemihypogenesis)

Spastic Diparesis in Children

  • Do not perform active sitting
  • Back curved and lower limbs in flexion when sitting
  • In the supine position, maximum flexion, abduction, and external rotation of the head in flexion or extension, and adduction of lower limbs with clubfoot
  • In prone, extension and adduction of the lower limbs; can draw on the elbows

Spastic Diparesis in Children

  • Positive plantar heel, suprapubic heel, and palmar extension reflexes
  • Poor spontaneous movements in lower limbs (simultaneous or alternating gooseneck extension)
  • Extension of limbs, dystonic attacks with mood swings
  • In dystonic attacks, prone to lower limbs in a scissor pattern when trying to catch an object
  • Unstable lateral recumbency

Spastic Diparesis in Children

  • Impulse to standing
  • No crawling
  • Unstable pelvic girdle without antigravity components
  • Increased anteroposterior spinal curvature
  • If standing is achieved, it is without a stabilizing role of the pelvis, with exaggerated swaying of the trunk and EESS separated from the trunk
  • Some righting of the scapular girdle
  • Similar to spastic tetraparesis
  • Even prone dystonic attacks
  • Opisthotonos
  • Hands in ulnar deviation
  • Pronated feet
  • Positive grasp reflex

Spastic Tetraparesis

  • In the supine position, EESS remain in flexion, ulnar deviation of hands, hips and knees flexed, and feet in equinus
  • Hands in a fist with thumb included
  • Increased deep tendon reflexes
  • Exacerbated reflex and palmar plantar heel (clonus)
  • Positive palmar and plantar grasp reflex
  • Positive Galant reflex
  • In prone, does not freely rotate the head
  • Risk of hip dislocation

Athetosis

  • Massive dystonic attacks
  • Most develop hypotonia from the neonatal period
  • Instability of the trunk (moves like a snake and leans towards the facial side)
  • Positive Galant reflex
  • Absent palmar grasp reflex without layers to support the hand
  • Exacerbated plantar grasp reflex
  • In prone, may try to catch objects in an uncoordinated manner with exaggerated finger extension, wrist flexion, and ulnar deviation
  • Eye-hand-mouth and mouth-body play with associated movements of limbs and open mouth
  • Tries to turn with opisthotonos
  • Absent plantar heel, crossed extension, and suprapubic reflexes

Spastic Atonia

  • Presents with great mental disturbance
  • Very poor spontaneous mobility
  • Unobvious dystonic attacks against strong external stimuli
  • Does not achieve turning over
  • In prone, adopts the frog position
  • Increased deep tendon reflexes
  • In supine, lower limbs are in high abduction
  • Positive grasp reflexes
  • Positive search and suction reflexes

Congenital Cerebellar Syndrome

  • Hypotonia and ataxia
  • Mental retardation
  • Can move to side-lying
  • Does not achieve active sitting
  • Attempts to sit with oscillation
  • Inaccurate movements when trying to grasp an object
  • Without treatment, survival beyond 5 years is unlikely