abnormal development (CP)

  1. Who observed babies with mvmt disturbances and older children with CP?
    mary quinton
  2. What is a mvmt pattern or posture which inhibits normal motor development and normalmvmt?
    • block
    • begins as abnormal extensor activity
  3. What is the order of abnormal motor development?
    • original pattern
    • compensations
    • habit
    • contractures
    • deformities
    • surgery
  4. What are the areas where major blocks occur?
    • neck
    • shoulders
    • pelvis
    • hips
  5. What occurs when head and neck flexion is absent, therefore no midline head orientation, no chin tuck?
    neck hyperextension

    • if head is lifted in prone, it is done with neck hyperextension
    • throwing head up and catching it on their shoulders
  6. What are the typical compensations for a neck/head block?
    lack head control,so compensatin occurs by elevating the shoulders to stabilize the head (limits degree of freedom), therefore preventing normal head/neck mvmts and exaggerating neck hyperextension
  7. What are some consequences in sitting for a neck/head block?
    • increased shoulder elevation limits normal mobility of the scapulae resulting in decreased UE mvmt/control/development
    • (arms are stuck to the side and the shoulder girdle mm get tight)
    • neck hyperextension also causes an open mouth posture and forward jut of the chin (unopposed m control-should be out of jutting the chin at 4 months)
  8. What are some treatment options of a head/neck block?
    • stretch
    • elongate the neck mm while activating flexion and increase shoulder girdle mobility and UE function
    • work on head control and functional mobility
    • provide them with what is missing
  9. What is head/neck asymmetry?
    • lack of bilateral neck flexor activity, therefore lack midline control
    • tends to keeo the head to one side (becomes more and more asymmetric and push into a surface rather than pulling away like they should)
    • resulting inb decreased visual awareness (eyes pulling in direction of head)
    • decreased hands to midline
    • decreased body awareness (no experience with hands, hands to feet, or foot to foot contact
    • increased influence of ATNR
  10. What are some complications that occur during a head/neck asymmetry?
    • ATNR complicates with a lateral reach to swipe resulting in decreased bilateral and symmetrical UE use and ocular control (secondary to decreased midline convergence)
    • head is turned resulting in spinal rotation (at risk for scoliosis or extreme lordosis due to tight quadratus lumborum)
    • weight shift to the face side and increased spinal extension
  11. What are some consequences of head/neck asymmetry?
    • decreased bilateral symmetrical UE use
    • decreased body awareness
    • decreased ocular control
    • decreased hand to mouth play
    • increased oral sensitivity (they never desensitize by putting things in their mouth)
    • increased risk of scoliosis
    • increased risk of subluxation or dislocation (pelvis rotates toward face side, unsupported femur, and femoral IR)
  12. What are some treatment options for head/neck asymmetry?
    • increase head, neck, spinal mobility and midline control (need bilateral flexion and ext)
    • simulate UE symmetrical use
    • ocular convergence
    • body exploration
    • stretch
    • infant-carry
    • teen-bolster, ball
  13. What occurs when scapular stability does not develop therefre dissociated shoulder mvmts and independent humeral mvmts do not develop (no elongation)?
    • shoulder block (normally some degree of head block)
    • mm between the scapulae and humerus are not elongated and shoulder girdle control is hampered
  14. What are some compensations with a shoulder block?
    • decreased humeral ER, flex, and horiz abd
    • lack of shoulder girdle control/stability
    • decreased forearm WBing (therefore use prolonged primitive prone ext (arms close to body) and scapular add to reinforce spinal ext)
    • inhibits good shoulder development and use
    • may also stabilize humerus close to their side, increasing trunk elevation, and decreasing normal shoulder girdle use
  15. What are some consequences of a shoulder block?
    • m tightness between scapulae and humerus which blocks normal mvmt and devlopment of the shoulders so there is compensation at the elbows
    • decreased UE WBing in prone and quadraped and decreased reach, grasp, and manipulation skills
  16. What are some treatment options for a shoulder girdle block?
    • stretch
    • treat the head/neck block first if present
    • increase scapular stability
    • increase scapula-humeral mobility and active humeral mvmts such as ER, flexion, horiz add (hand to midline to mouth)
    • increase UE WBing and weight shifts (bc these kids have limited their mobility)
  17. What type of pelvic tilt block is most common?
  18. What are the characteristics of an anterior pelvic tilt block?
    • lower tone (block wider in W sit)
    • ant pelvic tilt with hip flex (iliopsoas), abd, ER is not balanced by antigravity flexion components (in supine- abdominal flexion, LE flexion, hip add, ER)
    • decreased post tilt and decreased elongation of lumbar extensors, decreased trunk, pelvic control PREVENTING LATERAL WEIGHT SHIFTS AND DECREASED RIGHTING REACTIONS
  19. What are some compensations for an ant pelvic tilt block?
    • frog leg position in prone is prolonged
    • increased hip flex/abd/ER mobility
    • increased lumbar ext
  20. What are some consequences of an ant pelvic tilt block?
    • attempt to weight shift causing lateral flexion on the nonWBing side (not normal)
    • decreased dissociation of lumbar, pelvic, and hip mvmts
    • bunny hop instead of creep (decreased ability to weight shift) and have bigger excursions of mvmt
    • tailor sit (indian sit) if placed but still have an pelvic tilt, flexed hips, abduction, and ER and will still demonstrate decreased weight shifts
  21. In a pt with an APT, how do they kneel or stand?
    • APT
    • hip flexion
    • wide BOS
    • lower their COG (crouch)
    • adduct hips for added stability
    • may have ankle pronation/eversion
  22. What are some treatment options for an APT?
    • stretch the back out
    • have weak abs, so increase abd m. activity (lateral righting and equilibrium reactions)
    • increase hip mobility and control
    • increase proper weight shifts
    • treat secondary compensations such as ankle and knee alignment, control and mobility
    • work in ALL positions
  23. What are the characteristics of a post pelvic tilt?
    • very stong extension
    • in prone, very strong lumbar ext with weak hip ext and add and decreased antigravity mvmt
    • if you put a pt into sit, they look like they are struggling (reaching for knees for stability)
    • HS's are active and tight
    • glutes are very inactive
    • sacral sit
  24. What are some compensations of a post pelvic tilt?
    • very limited function, therefore compensations are result of positions theyre placed in
    • decreased joint mobility and tight mm, so they usually obtain mobility from the point of least resistance
  25. What are some secondary compensations of a post pelvic tilt?
    • cant tailor sit without falling over
    • W sit at times with a PPT and trunk flexion
    • if they creep, usually also bunny hop
    • decreased ability to stand
    • decreased BOS, weight shift, control
    • look likes knees are touching
  26. What are some consequences of a PPT?
    • in sitting: tight HS's so dont allow for full hip flexion or ext of the knees
    • have posterior tilt
    • rounded trunk
    • sacral sit (hang on rectus abdominus)
    • knees are flexed to decrease the HS stretch
  27. What are some treatment options for a PPT?
    • treat all other blocks and elongate short mm (HS's)
    • increase jt mobility
    • increase antigravity flexion balanced with ext
    • perform weight shifts and LE dissociation (half kneel, sidelying, etc)
  28. What is cerebral palsy?
    • come from cerebrum
    • loss of ability to move or control mvmt
    • results from injury to the developing brain up to 2 yrs of age causing a disturbance in normal motor abilites of a person
  29. What are some associated causes of CP in the prenatal stage?
    • problems experienced during intrauterine
    • development, maternal metabolic diseases
    • maternal nutritional deficiencies
    • twins or multiple births
    • maternal bleeding
    • toxemia
    • mother is RH positive, develops antibodies
    • infextion, exposure to radiation
  30. What are some associated causes of CP in the perinatal stage?
    • prematurity, low birth weight, anoxia (lack of oxygen during labor and delivery)
    • mechanical trauma during delivery
    • electrolyte disturbances
  31. What are some associated causes of CP in the postnatal stage?
    trauma,infections, anoxia, cerebral hemmorhage related to MVA, child abuse
  32. What are some postnatal factors of CP?
    • traumatic injuries (MVA)
    • infections- encephalitis, meningitis
    • toxic exposure-lead poisoning
    • vascular accidents-congenital aneurysms
    • cerebral anoxia
    • brain tumors
  33. What are some early signs and symptoms of CP?
    • abnormally still and quiet-unreactive to environment
    • overactive with irritable cry
    • failure to suck or root properly
    • motor skills not developing on schedule- poor head control, hands remain fisted, abnormal reflexes persist
  34. What are some later signs and symptoms of CP?
    • abnormal patterns of posture and mvmt
    • disturbed muscle tone
    • muscle weakness
    • defective proprioceptive and cutaneous sensation
    • deafness, blindness
    • epilepsy- disturbances in elextrical activity of the brain
  35. What are the 2 most common encountered lesions?
    • UMN- occurs in CNS
    • LMN- innervates skeletal mm
  36. quadriplegia
    • entire body involved
    • UE>LE
    • have difficulty with head and trunk control and may or may not walk (bilateral brain damage)
  37. hemiplegia
    • one side of the body affected
    • trunk ism ost likely affected as well due to compensations for lack of controlled mvmt (unilateral brain damage)
  38. diplegia
    • mostly lower body involvement, but trunk is almost always affected
    • can be UEs
  39. paraplegia
    bilateral LE involvement
  40. monoplegia
    unilateral UE involvement
  41. triplegia
    • both LEs and 1 UE involved
    • aka hemi-di
  42. What is the resistance to a stretch?
    • spastic
    • stiff, hypertonic
    • clasped knife phenomenon (when you resist a body part then let it go, it shoots back at them)
    • syngergist mvmt patterns (abnormal-group of mm that work together to provide mvmt patterns) with weakness in the antagonist
    • isolated mvmts are difficult/impossible so your tx would involve dissociation
    • increased deep tendon reflexes (stretch reflexes that can be elicited by striking the m tendon, such as the knee using a hand or reflex hammer
    • may have clonus
    • may have toe signs such as babinski or chaddock (ext of big toe to irritation of the skin covering the malleolus)
    • loss of control of volitional mvmts
  43. What procedures may be performed to decrease spasticity?
    dorsal rhizotomy - dorsal roots of spinal cord are selectively cut to decrease synaptic, afferent activity within the spinal cord which in turn decreases spasticity

    pt is very weak after surgery...important to stretch
  44. What is the area of damage for spasticity?
    hemispheric lesion, cerebral cortex (hemisphere)
  45. What are some treatment ideas for spastic pts?
    techniques to inhibit spasticity include WBing, weight shifting, slow and rhythmic rocking, rythmic rotation, dissociation

    be slow and gentle!!!!
  46. What is athetoid?
    • purposeless mvmts
    • can be fast or slow
    • patterned or unpatterned
    • may be at rest or only with mvmt
    • difficulty grading mvmts
    • choroid mvmts possible

    • worm like mvmts, jerky, swiping mvmts, tremors, rotary mvmts may be present in all or some body parts, uncontrollable, unpredicatable
    • hypertonic or hypotonic - may fluctuate
    • may have sudden spasms, bad fine motor mvmts, weakness, voluntary mvmts are disruppted, extremes with range, problems with midline control
  47. What is the area of damage with athetoid?
    basal ganglia (regulates posture and m tone)
  48. What are abnormal/absent postural reactions, loss of balance/control that can be in trunk, limbs or both, and the child is moving all the time?
    ataxia (drunken soldier)

    • clumsy, uncoordinated mvmts
    • hypertonia
    • trunk or limb ataxia or both
    • tremors - nystagmus (eye tremor)
    • dysmetria (over/under shoot)
    • delays in initiating mvmt
    • weakness
    • joint laxity
    • decreased resistance to passive mvmt
    • increased fatigueability
  49. Where is the area of damage with ataxia?
    cerebellum (controls balance and muscular mvmts)
  50. What helps children with ataxia?
    putting weights on their arms/ankles to help control mvmts
  51. What is rigidity, and where is the damage area?
    • uncommon with CP
    • m tone is increased to the point of rigid postures and any directional mvmt is impeded

    damage at the cerebellum (severe)
  52. What is a tremor and where is the area of damage?
    • slow, regular reciprocal mvmts (alternating agonist/antagonist contractions)
    • normally occur with concentration

    damage at the basal ganglia
  53. What is lack of tone, failure of muscles to respond to volitional stimulation, muscles lack normal firmness?
  54. What % of individuals with CP have mental retardation?
  55. What is the sequence of abnormal mvmt?
    abnormal muscle tone> abnormal mvmt> abnormal sensory feedback> reinforcement of abnormal mvmt
  56. What is considered mild severity?
    pt needs no tx as only minimal interference with normal ADLs or amb
  57. What is considered moderate severity?
    • needs specialized tx, is inadequate in self care, amb or ADLs
    • braces such as ankle-foot orthoses (AFO) and self help devices are required
  58. What is considered severe severity?
    • needs tx to such a degree that the prognosis for improvement/function is very poor
    • may need specialized w/c for positioning-normally w/c bound
  59. What are the 4 stages of tx?
    • early intervention
    • preschool
    • school age and adolescence
    • adulthood
  60. What are some therapy goals and treatments used?
    • suppress abnormal reflex activity by training inhibitory function of the nervous system and thus improve the pattern of posture and mvmt. practicing postural control within socially an cognitively appropriate functional tasks
    • stimulate and train the sensory nervous system in proprioception-sensorimotor development
    • maintain full ROM at all joints
    • facilitate or inhibit tone
    • developmental activities and play
    • train perception such as body image, spatial appreciation, and size/shape recognition
    • attain and sustain upright orientation
Card Set
abnormal development (CP)
abnormal development