Progression of atypical movement patterns

Children who have CP demonstrate difficulty in achieving and maintaining normal posture while lying down, sitting, and standing because of impaired patterns of muscle activation.^3,19 These abnormal patterns result from the decreased ability of the CNS to control coactivation and reciprocal innervation of select muscle groups. Coactivation of muscle is the result of a co-contraction of agonist and antagonist muscle groups around a joint. Simultaneous contraction of agonist and antagonist muscle groups provide stability around a joint and also affect overall body posture. Reciprocal innervations in muscle groups occur when excitatory input directs the agonist muscle to contract while inhibitory input directs the antagonist muscle to remain inactive.^12,19 These reciprocal innervations allow for movement to occur around a joint and in the body. Children who have CP may develop abnormal movement compensations and body postures as they try to overcome these motor deficits to function within their environments. Over time, movement compensations and atypical motor patterns create barriers to ongoing motor skill development. Instead of freely moving and exploring the world, as children with a normally developing sensorimotor system do, children who have CP may rely on early automatic reflex movement patterns as their primary means of mobility. These early automatic reflexive movements occur without conscious control of the child and are typically elicited by a specific sensory motor action.

Primary and secondary impairments

Children with CP manifest primary impairments that are the direct result of the lesion in the CNS. Primary impairments are an immediate and direct result of the cortical lesion in the brain. The nervous system damage that causes CP can occur before or during birth or before a child’s second year, the time when myelination of the child’s sensory and motor tracts and CNS structures rapidly occurs. CP is described as nonprogressive, nonhereditary, and noncontagious.¹² As a nonprogressive condition, the original defect or lesion occurring in the CNS typically does not worsen or change over time. However, because the lesion occurs in immature brain structures, the progression of the child’s motor development may appear to change. Normal nervous system maturation shifts control of voluntary movement to increasingly higher and more complex areas of the brain. The child who has CP exhibits some changes in movement ability that results from the expected progression of motor development skills, but these changes tend to be delayed relative to age and often show much less variety than those seen on the normally developing child.

Children with CP develop secondary impairments in systems or organs over time due to the effects of one or more of the primary impairments.^3,20 These secondary impairments may become just as debilitating as the primary impairments. For example, a child with CP may have a primary impairment such as hypertonia and a muscle imbalance across a joint. This abnormal muscle tone may cause poor alignment across a joint, further muscle weakness, and eventually a contracture in the joint. The resulting muscle contractures, poor body alignment, and poor ability to initiate movement would be considered secondary impairments. It is important to understand this, since the diagnosis of CP means that a child has a static nonprogressive lesion in the brain. Although the initial brain injury remains unchanged, the results or the secondary impairments are not static and change over time with body growth and attempts to move against gravity. Children with CP may continue to rely on automatic movement patterns because they are unable to direct their muscles to move successfully in more typical motor patterns (Figure 16-1). The atypical patterns used to play or complete functional activities may become repetitive and fixed. The repetition of the atypical movement patterns prevent children with CP from gaining independent voluntary control of their own movements and can lead to diminished strength and musculoskeletal problems. The combination of impaired muscle coactivation and the use of reflexively controlled postures may lead to future contractures in muscles, tendons, and ligamentous tissues, causing the tissues to become permanently shortened. Bone deformities and alterations of typical posture or spinal and joint alignment may also occur.

Frequency and causes

CP is the leading cause of childhood disability, and the reported incidence varies from 2 to 3 per 1000 live births.¹² The prevalence rate of CP has remained stable since the 1950s, in spite of dramatic improvements in prenatal and perinatal care over the last four decades.²⁰ According to the United Cerebral Palsy (UCP) Foundation, there are nearly 800,000 children and adults in the United States living with one or more symptoms of cerebral palsy.²¹ The accident that causes brain injury may occur during the prenatal, perinatal, or postnatal period, but evidence suggests that 70% to 80% of the causes of brain injury are prenatal in origin (Box 16-2).³ Prenatal maternal infection and multiple pregnancies have also been associated with cerebral palsy.¹² Other prenatal factors include genetic abnormalities and maternal health factors such as stress, malnutrition, exposure to damaging drugs, and pregnancy-induced hypertension. Some gestational conditions of the mother, such as diabetes, may cause perinatal risks to the developing fetus; prematurity and low birth weight significantly increase an infant’s risk of developing cerebral palsy.¹⁹ Medical problems associated with premature birth may directly or indirectly damage the developing sensorimotor areas of the CNS. In particular, respiratory disorders can cause the premature newborn to experience anoxia, which deprives cells of oxygen that cells need to function and survive. Typical postnatal causes of CP could include conditions that result in significant damage to the developing CNS, such as malnutrition or hypoxic ischemia resulting from lack of oxygen to the brain. Hypoxic ischemic encephalopathy is defined as damage to cells in the CNS (brain and spinal cord) caused by inadequate oxygen. Other postnatal causes include infections and exposure to environmental toxins.

Posture, postural control, and movement

To understand the functional movement problems that develop in children who have CP, the occupational therapy (OT) practitioner must be familiar with the ways that people normally control their bodies and execute skilled movements. The term posture describes the alignment of the body’s parts in relation to each other and the environment. The ability to develop a large repertoire of postures and change them easily during an activity depends on the integration of several automatic, involuntary movement actions referred to as the postural mechanism, which includes several key components:

Disruption in the postural mechanism and the movement problems seen in children with CP are considered secondary impairments, which may be significantly reduced by OT interventions.

Postural development and motor control

As newborns grow, they are continually developing and refining postural control. As with motor skills, the characteristics of posture vary with age. In the past 20 years, much research has been devoted to understanding motor control so that OT practitioners may provide effective neurologic rehabilitation to persons who have CP and other neurologic disorders. Motor control theory is complex, and detailed explanations of this theory are beyond the scope of this text. However, the OTA should be aware of the two main schools of thought on motor control. This knowledge can guide the OT practitioner in seeking information that can contribute to implementing effective therapeutic approaches. The theories can be grouped into two models of motor control: (1) the traditional reflex–hierarchical models, and (2) the more recent systems models.

Reflex–hierarchical models

Reflex–hierarchical models propose that purposeful movement is initiated only when the individual experiences a need to move.¹⁹ When the desire to move is stimulated, the person searches his or her long-term memory for a pattern of movement that will accomplish the desired task. The movement patterns that the person has practiced the most are the most likely to be used again because they are embedded in memory. The person prepares to execute the movement, incorporating additional information from the environment to make the movements meet the demands of the task. For example, when a child is thirsty or hungry and sees food or drink, the child will become motivated to reach for or move to the desired food or drink. Long-term memory is searched for a pattern of movement that will enable the child to achieve the desired goal, that is, to reach the food or drink. Because all previous efforts to reach a bottle were stored in a generalized movement program, the child has a general history of the motor skills necessary for proper sequence, timing, and force of motor actions. Environmental factors, such as the sizes and weights of the objects, are also considerations used to determine the appropriate movement patterns. Sensory feedback determines whether the child’s movement efforts have been successful (i.e., have met the task demands). The agonist muscles help lift the food or drink to the mouth, while the antagonist muscles are programmed to relax, allowing the movement of the agonist muscle to occur. Coactivation occurs when both the agonist and antagonist muscle groups work together to stabilize the container of the food or drink at the mouth in order to actually eat or drink. With continual repetition, these movement patterns can develop into motor skills. Reflex–hierarchical models support the idea that motor learning optimally occurs when a person engages in repeating the same task during frequent, regular practice; breaking down a task during frequent, regular practice into small parts is the most effective way to learn the entire task.

According to reflex models, many children with CP use tonic reflexes controlled by the lower levels of the CNS for managing most of their movements. These movement patterns are “hard wired” into the human nervous system and do not depend on the application of learned patterns for performing tasks. According to this model, children with CP lack the ability to independently learn to control movement from higher-level brain centers. Their abnormal postural mechanisms and disordered muscle tone cause them to repeatedly use and store in memory those movement patterns that are governed predominantly by the early tonic reflex patterns; these patterns inhibit the functional use of agonist and antagonist muscles during daily tasks (reciprocal innervations and coactivation). The reflex–hierarchical model has been challenged by motor theorists on several issues, including the impact of the environment on learning new motor patterns and the ability of the brain to actually store all the motor programs necessary to perform the infinite number of tasks an individual completes in his or her lifetime.

CLINICAL Pearl

The movement patterns of children with cerebral palsy may be influenced by primitive reflex activity, including the asymmetric tonic neck reflex, symmetric tonic neck reflex, and the tonic labyrinthine reflex affecting the acquisition of normal developmental milestones such as the ability to roll, sit unsupported, stand, and walk (Figure 16-2).