Types of Cerebral Palsy

1. Types of Cerebral Palsy Robyn Smith Department of Physiotherapy UFS 2012

2. 1. Spastic Group

4. Spastic Quadriplegia

5. Distribution • All four limbs similarly involved • UL sometimes to a greater degree than LL • Distribution of tone may be assymetrical with one side more involved • or with one side in flexion and the other in extension • Trunk often hypotonic or with increased extensor tone

6. Etiology • Asphyxia • Anoxia • Abruptio placenta • Merconium aspiration Usually indicative of severe cortical damage

7. Supine Asymmetrical ATNR Uses retraction of head roll side No segmental rotation Spasticity with IR hip may lead dislocation Sitting Flexed posture Strengthens TLR Grasp weak due IR pronation arm Lifts head extension and retraction shoulders “chin poke” Development

8. Prone Due to TLR battles lift head STNR with neck flexion and UL flexion with LL in extension Often don’t tolerate prone Mild – learns to lift head with extension and may even creep. Uses TLR and STNR constantly TLR/STNR used to get into M-sitting in mild cases Standing & walking Very mild cases –seldom realistic Uses extension spasticity LL - ??? No true active WB No rotation or dissociation AP weight shifts Shuffling gait As body weight increases loose ability to walk Development

9. Additional characteristics Associated with significant associated problems. • Microcephaly & cerebral atrophy • Mental retardation • Cortical blindness • Epilepsy • Feeding problems

10. Spastic Diplegia

11. Distribution • All four limbs involved • UL to a lesser degree than LL • ???? Terminology you will aslo hear refering to assymetrical diplegia or a hemiplegia superimposed on diplegia

12. Etiology Lesion lies near the para-ventricular region Forms part sub-cortical group lesions • Prematurity (PVL/ IVH) • Hydrocephalus

13. Supine Far better head and trunk control than quad Uses extension of head and retraction of head to roll Later as flexion improves uses arm and upper body to roll over No segmental rotation Kicking may notice scissoring legs Sitting No segmental rotation cannot come up into sitting through side lying Used STNR to get into M-sitting Pattern hip flexion and anterior pelvic tilt –becomes fixed deformity Often shortening hamstrings, long sitting difficult with poor balance and child uses arm support Development

14. Prone Creeps using arms to pull forward STNR to get into M-sitting “Bunny hops” or crawls asymmetrically due to poor rotation and dissociation On floor requires arm support in sitting Often sitting chair more comfortable and stable To get into kneeling pull up with arms, LL inactive Standing & walking Lumbar lordosis & hip flexion No segmental rotation or dissociation Lateral weight shifts Often up on toes High guard and poor balance Tries get foot flat Extension LL with scissoring Walking aid –swing through gait Development

15. Characteristics • Near normal IQ • Epilepsy • Feeding problems may occur

16. Spastic Hemiplegia

17. Distribution • Arm and leg on the same side of body involved • Arm usually to greater extent than leg BUT: • Arm more leg middle cerebral artery • Arm =leg anterior cerebral artery • “dense”(arm, leg and face) capsula interna

18. Etiology • Emboli • Thrombi • Artery malformations • Prematurity with anoxia

19. Initially may not appear asymmetric Start to become evident 6/12 Starts only using unaffected arm Orientate themselves only to unaffected side Retraction of hemi side Difficulty in rolling to unaffected side Dislikes prone Does not crawl Sitting falls over hemi-side to compensate shifts weight to normal side Associated reactions common Unable do bilateral hand activities Locomotes by bum shuffling Development

20. Standing no weight taken on hemi-leg Pelvis and hip in retraction, LL flexion up on toe Walk by 18/12 Under-development of hemi leg Postural deformities common e.g. scoliosis Development

21. Characteristics • Microcephaly • Sensory involvement • Epilepsy • Intelligence varies –left cerebral hemisphere poor prognosis Left vs. right hemiplegia: • Left hemi has speech, language and feeding problems • Right hemi has visual perceptual problems

23. Children with spasticity divided into 2 groups: Severe spasticty Moderate spsticity

24. Severe spasticity

25. Features • In a state of hypertonus • The hypertonia does not change • Little or no movement ability due to tone. • Only small movements are • Contractures tend to be more toward the mid- position • Balance reactions are absent • Problems e.g. respiration, feeding and speech • Emotionally child is fearful and cannot adjust to movement. • Children are often very passive

26. Moderate spasticity

27. Features • Tone moderate at rest increases activity • More able to move due to changeability in tone • Inconsistent performance during execution task • Contractures more dangerous in this group • Associated reactions • Balance reactions present but underdeveloped • Emotionally these children are often frustrated and insecure

28. Principles to use when treating a spastic child • Reducing the spasticity in itself will not make the child more functional • Therapist should always have a functional goal in mind. • Analyse the patterns of hypertonia and the way in which it interferes with postural control and the performance of functional tasks. • Asses the degree of compensation

29. Principles to use when treating a spastic child Use of tone influencing patterns, postures and techniques • Facilitate large range movements, free and rhythmical • Dissociation/ rotation • Mobile weight bearing in elongation • Elongation of muscles • Correct biomechanical alignment • Reciprocal patterns • Shaking and vibrating

30. Principles to use when treating a spastic child • Use patterns of activity that lead to function. • Facilitate active movements  • Facilitate balance reactions • Prevent and minimize contracturing • Grade stimulation

31. 2. Hypotonic Group

32. Aetiology • Most children with CP start out hypotonic • Premature babies are hypotonic • Hypotonia usually transient • True hypotonia is rare

33. Complex differential diagnosis • The following other possible conditions need to be excluded: • PNL e.g. GBS • SC lesion • Neuromuscular junction diseases e.g. Myasthenia Gravis • Muscle diseases e.g. SMA, DMD • UMN = CP NB: valuable clinical tool is to test reflexes as hypotonic CP reflexes will still be present

34. Long term outcome for intial hypotonia • 45 % Hypertonic • 10% Diplegia • 45% Dyskinetic • ? % Ataxic • ?? % True hypotonia

35. Features • Little or no postural control against gravity • Body takes up all the available support • Move with difficulty • Uses limbs as post of postural control i.e. Wide base • Hyper mobility of all joints • Apathetic/ passive. Reduced state of alertness. Possible lack of motivation due to their inability to respond . Placid, often describes as “good” baby • Delayed intellectual development • Usually problems with breathing, feeding and drinking • Respiration often shallow with recession of the chest wall evident. Aspiration common. Children also usually have a depressed cough reflex with ineffective cough

36. Principles to use when treating a hypotonic child • Be careful of how stimulate child often hard to arouse • Increase postural tone by stimulation techniques: • Compression • Symmetrical patterns • Static weight bearing • Rhythmical stabilization • All forms of tapping • Movements to be fast and resisted • Work for head and trunk control and alignment • Address associated problems of breathing, eating and drinking • Maximize positioning and handling to ensure the preservation of joint integrity and to prevent aspiration. • Prevent contractures especially postural deformities

37. 3. Athetoid Group

38. Athetoid group Characterised by: • Involuntary movements • Abnormal or fluctuating postural tone

39. Athetoid group Classified according to type of involuntary movement into 4 groups • Pure athetosis • Choreoathetosis • Athetosis with dystonic spasms • Athetosis with spasticity

40. Distribution tone

41. Pure athetosis • Tone varies very low normal • Distal > proximal • Slow wreathing movements

42. Choreoathetoid • Tone varies very low high • Proximal > distal • Large wreathing movements • Poor grading of movement

43. Athetoid with dystonic spasms • Hypotonic OR hypertonic

44. Athetoid with spasticity • Moderate spasticity • Proximal > distal • Poor grading of movement

45. Etiology • Kericterus hyperbilirubinaemia (severe jaundice) • Rh incompatability • Prematurity • Asphyxia • Metabolic disorders • Encephalitis/ meningitis • Heavy metal poisoning • Rhumatic fever • Degenerative disorders brain

46. Management of jaundice

47. Etiology = damage to the basal ganglia Basal ganglia are NB for: • Control of movement • Scale and amplitude determination of movement • Important in the control of eye movements

48. Characteristics • High IQ –cortex not involved • However usually severely disabled • Abnormal fluctuating tone • Lack of proximal stability • Poor grading movement • Poor balance • Contracturing usually not a concern • Repetitive assymetrical movement patterns may lead to deformities • Joint hypermobility • Emotionally volatile • Often frustrated –temper tantrums

49. Speech Vocalization & speech problem –speech poor and indistinct Hearing loss Can hear but does not listen Feeding Difficulty in swallowing Battle especially with liquids Associated problems

50. Vision Battle to focus May have nystagmus = rapid, rhythmic, involuntary eye movements caused by damage brain Eyes unable move independently head Lack of stability of head affects vision Associated problems