Cath Lab Digest

Cerebral palsy (CP) is a non-progressive brain disorder characterized by insufficient development of postural reflexes (i.e. head control), prolonged retention of primitive patterns of activity, abnormal coordination and muscle patterning.
As a result, those with cerebral palsy have delayed motor development and impaired patterns of movement.”^1,2 It is a chronic disabling condition of childhood. It is occurs in 1.5/1,000 to 3/1,000 live births with spasticity as a prevalent disabling clinical symptom.³

When evaluating infants, physicians should be aware there are two signs that suggest the possibility of cerebral palsy as a diagnosis. One sign is the presence of hyperactive deep tendon reflexes in a hypertonic or hypotonic child. The other sign is a unilateral or bilateral persistence of neonatal reflexes beyond the time that they should have disappeared or been absorbed into a more sophisticated reflex.⁴

Spasticity is a form of cerebral palsy in which pyramidal system dysfunction leads to an inhibitory imbalance. This loss of inhibitory control contributes to an exaggerated spinal stretch reflex. As a result, patterns of voluntary movement are altered because this loss of inhibitory control leads to concurrent firing of muscle groups such as adductors and abductors.

Although cerebral palsy causes a variety of upper motor neuron dysfunctions, spasticity is the most common and typically results in asymptomatic foot dysfunction. As the child grows, longstanding imbalances between agonist and antagonist muscle groups can lead to fixed deformities of the foot such as muscle contractures and bony deformities, some of which may require surgery to correct.

It is typical of the spastic individual to have concomitant abnormalities in the superstructure such as the hip and knee that may have an impact on closed-chain foot position and function. Conversely, one must consider the retrograde role of abnormal foot postures on hip and knee position and function as well.

Keys To The Clinical Exam

In regard to the lower extremity assessment for these patients, it is important to correlate restricted joint range of motions with gait abnormalities. For example, one should take care during the clinical exam of ankle dorsiflexion to avoid a forceful slow stretch that tends to overestimate the functional range of motion actually available at the joint one is evaluating. Standing and walking tend to increase spasticity and the two-finger method of assessing joint range of motion offers a more approximate assessment of the motion actually available in gait.

Further complicating the assessment of ankle range of motion is that clinical assessment of the gastroc and soleus muscles as separate units can be difficult in this population. Traditional comparison of ankle dorsiflexion with the knee extended and knee flexed to distinguish the two muscles proves difficult as the position of adjacent joints affect spasticity.

However, examining ankle dorsiflexion in both knee positions is still valuable as children with increased dorsiflexion to 10 to 15 degrees with the knee flexed versus extended is suggestive of greater gastrocnemius involvement. These patients tend to have plantarflexion of the ankle in swing and early stance phase, but can achieve dorsiflexion in midstance.

There is growing enthusiasm for the role of instrumental gait analysis in evaluating patients with spasticity. It is helpful in determining exact information on abnormal muscle firing in such patients. It has been documented that preoperative gait analysis does alter surgical decision-making.⁵ One should seriously consider this when planning surgery.

Physical therapy, orthoses and/or manipulation are first line options for patients with spasticity. Even for those children who may eventually require surgery, the use of these modalities to delay surgery until the age of 6 to 8 years is considered advantageous.