Cerebral Palsy Flashcards
Cause - during Pregnancy
- Multiple pregnancy (4.5 times in a twin; 18.2 times in triplets)
- Birth asphyxia/ hypoxia (10%)
- Low and very low birth weight (50%) (30 fold increase in risk)
- Vascular accidents
- Infection (toxoplasmosis, rubella- German Measles, Maternal diabetes, herpes simplex)
- Foetal malformation syndromes
- Iodine deficiency (i.e. maternal thyroid disorder)
- A damaged placenta which may interfere with foetal growth
<p>Definition</p>
<p>An umbrella term for a group of non-progressive movement and posture disorders caused by damage to the developing nervous system, before or during birth or in the early months of infanc</p>
Cause/risk factor - after birth
- Cerebral infection
- Infantile spasm
- Head injury
- Epilepsy
Epidemiology
- 2.0- 2.5/ 1000 live births in New Zealand
* Approximately 7000 people have some degree of CP (one third are under 21 years of age)
Lesion Location
Premotor- motor cortex- Spastic Cerebellum- Ataxic Basal Ganglia- Dyskinesia
Progression
Once primary cause(s) have been identified, they do not progress in nature. However, secondary impairments evolve during time
Clinical presentation- Spastic (70%-80%) - lesion location
primary and supplementary motor and sensory cortex
clinical presentation - Diplegia
Increased tone in the legs; little or no involvement in the arms
• Potential contractures of the hip flexors, hip adductors, hamstrings, internal rotators
• Femoral anteversion (internal rotation of the femoral shaft on the femoral neck). Normally at birth, have 40° and 25° hip flexion contraction; active extension and external rotation of the hip produce torsional stresses on the femur, thereby decreasing the anteversion to 15° by age 16. Children with CP do not have active WB and extension, therefore remain in anteversion)
• Tibial torsion (normal development includes the medial malleoli anterior to the lateral. Children with CP do not experience normal movement, so tibia remains in tibial torsion- malleoli are parallel)
• May have hyperextension (compensate for tight tendo-archilles)
• Kyphosis (balance mechanism)
clinical presentation - Hemiplegia
- Spasticity in the arm, leg and trunk on one side
- Underdevelopment of the affected side (smaller limbs and leg shortening)
- Equinus of foot, ankle, flexion of elbow, wrist and fingers
Clinical presentation - Quadriplegia
- All four limbs involved
- Deformities as above, with addition of possibility of dislocation/ subluxation of hip (60% of non-walkers by age 5)
- Spinal curvature
clinical presentation - Dyskinetic CP: characteristics
- Uncontrolled, purposeless, slow, writhing movements.
- Muscles which change from floppy to tense.
- May affect face or tongue (resulting in drooling)
clinical presentation - Ataxic CP: Cerebellum
Characteristics
- Affects about 5%-10% of the cases
- Characterised by low muscle tone and poor coordination of movements
- Affects the sense of balance and depth perception (resulting in poor co-ordination, unsteady, wide based gait)
Diagnosis
Based on patient history and physical examination
CT and MRI when aetiology of CP has not been established (suggest timing of initial insult)
Interdisciplinary management - Drugs
- Anticonvulsants
- Antispasmotics (Baclofen- inhibits gamma-amniobutyric acid (GABA)-B receptors in the spinal cord by blocking the excitatory effect of sensory input; Intrathecal baclofen; Botulinum toxin (Botox) (taken up at the cholinergic nerve terminals, blocking release of synaptic vesicles, thereby blocking the action of the synapse at the neuromuscular junction- lasts ~3 months)
Interdisciplinary Management - soft tissue surgery
Soft tissue surgery (release of tendon, muscle or connective tissue)
Multilevel surgery
Orthotics (maintain length, prevent further deformity, improve joint alignment, biomechanics and function) i.e. in diplegia- to pull knee back so that the PF and quads do not need to work as hard
Serial Casting (short periods, frequent reapplication over 6 weeks- effective in lengthening shortened muscles- Brouwer et al, 1998; Moseley, 1997)
Strength Training (ACSM guidelines- 3 x 8-12reps, 2 x/ week; light- mod load (30-60% 1RMà 70- 85% 1RM)- Scholte, et al., 2008)
Positioning- active, passive
Interdisciplinary Management- TRT
Has less specificity in its physiological effects since it addresses multiple impairments, but greater specificity in producing changes in activity since it often requires more than strength increases alone (Damiano, 2007). May improve muscle activation patterns and allow patients to learn improved motor control strategies (Rose & McGill, 1998)
interdisciplinary management : CIMT - Frequency
1- 6hrs during play/ day; 4- 7 weeks- Croker, et al., 1997; Taub, 1980; Willis, et al., 2002
Prognosis
Reduced life expectancy- 90% survival into teens and 20s (immobility and severe learning difficulties main influencing factor)
outcomeasures
• Gross Motor Function Classification System (GMFCS)- Palisano, et al., 1997
o Classification tool: Five levels based on the child’s ability to perform gross motor skills and assistance required when mobilising in a variety of conditions (stairs, distances, altered terrain, inclines)
• Functional Mobility Scale (FMS)- Graham, et al., 2004
o Considers the assistance the person’s requires over 5, 50 and 500 metres
• Manual Ability Classification System (MACS)- Eliasson, et al., 2006
• Gross Motor Function Measure (GMFM)- Russell, et al., 2002
• Gait Analysis (Spatial temporal gait parameters, Kinematics, Kinetics, EMG, energy consumption)
• Paediatric Balance Scale (PBS)- Knuckles et al., 2008; Franjoine, et al., 2003
• 6MWT- Maher et al., 2008
• 1MWT- McDowell et al., 2009
