Wendell Nakamura
LEARNING OBJECTIVES:
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| CASE STUDY: Remy Williamson is a 14-year old with moderate ataxic cerebral palsy. He lives with his parents and 10-year old, neurotypical sister in a single-level home with ramped entry in a small rural community. He has their own bathroom, which is modified with a roll-in shower, shower bench, grab bars, hand-held shower attachment, elevated toilet with toilet safety frame, and a wheelchair-height vanity and sink. He is unable to safely orally feed and has a PEG tube, for which he requires maximal assistance. He requires maximal assistance with grooming, dressing, bathing, and toileting. Remy will be starting high school soon and would like to explore options to improve communication. Read more about Remy by following this link to his EHR. |
Cerebral palsy is a broad category of non-progressive, permanent conditions that result from injury to the fetal or infant brain (Hallman-Cooper & Cabrero, 2022; Rogers, 2010). It is the most common cause of childhood disability, affecting 1.5 to 2.5 per 1000 live births in the U.S. (Hallmoan-Cooper & Cabrero, 2022). There are approximately one million people of all ages living with cerebral palsy in the U.S. (Cerebral Palsy Guide, n.d.). Life expectancy for people with cerebral palsy varies significantly, depending on the severity of disabillity (Cerebral Palsy Guidance, n.d.).
| ACTIVITY FOR CRITICAL THINKING: Consider the worldwide prevalence of children with cerebral palsy who are under the age of five years, as depicted in the map above. Areas colored with darker orange to red suggest a higher prevalence; areas colored with darker blue suggest lower prevalence. What factors do you think might account for this discrepancy? |
In the United States, there are disparities in various social groups in the prevalence of cerebral palsy. Boys are diagnosed with cerebral palsy more than girls (Flanagan et al., 2021). Black infants were 29% more likely than white infants to have cerebral palsy and with a greater severity of gross motor functioning (Wu et al., 2011). Women of all ethnicities who did not receive prenatal care were twice as likely to have an infant with cerebral palsy than women who did receive prenatal care (Wu et al., 2011). Mothers with low socioeconomic status (SES) who live in neighborhoods with higher exposure to environmental toxins are 67% more likely to have children with cerebral palsy than mothers with higher SES (Flanagan et al., 2021).
The healthcare costs associated with medical complications from cerebral palsy are estimated to be approximately $1.6 million per individual, approximately 10 times higher than for children without cerebral palsy (Warmbrodt, 2024b). The U.S. spends approximately $1 million in annual medications, physician visits, therapies, and long-term care for people with cerebral palsy and medical costs are estimated to be 26 times higher for children with cerebral palsy with intellectual disabilities than for children with cerebral palsy, but without intellectual disabilities (Warmbrodt, 2024b). Many families of children with cerebral palsy receive financial assistance through Social Security Disability Insurance (SSDI), state Medicaid programs, Children’s Health Insurance Program (CHIP), and Temporary Assistance for Needy Families (TANF).
Injury to the CNS during the prenatal and perinatal periods typically results in motor and postural deficits, but individuals can also experience impairments in visual, hearing, and cognitive systems (Hallman-Cooper & Cabrero, 2022; Rogers, 2010). The clinical presentations of people with cerebral palsy differ widely, depending on the location and severity of injury to the CNS. (Hallman-Cooper & Cabrero, 2022).
Causes of cerebral palsy
The many causes of cerebral palsy can be divided into one of three categories: prenatal causes, perinatal causes, and post-natal causes (Hallman-Cooper & Cabrero, 2022).
Prenatal causes (approx. 80% of cases) include:
- Congenital brain malformations
- Intrauterine infections
- Intrauterine stroke
- Chromosomal abnormalities
- Premature birth (<28 weeks)
- Low birth weight
Perinatal causes (approx. 10% of cases) include:
- Hypoxic ischemic insults
- Central nervous system infections
- Stroke
- Kernicterus (liver-induced encephalopathy)
Postnatal causes (approx. 10% of cases) include:
- Accidental and non-accidental trauma
- Central nervous system infections
- Stroke
- Anoxic insults
The developmental milestones achieved by children with cerebral palsy varies greatly by the individual, depending on the severity and location of injury to the central nervous system and can have significant impact on occupational functioning. According to the Cerebral Palsy Alliance Research Foundation (n.d.b.), for people with cerebral palsy:
- 75% have chronic pain
- 33% are non-ambulatory
- 33% have hip displacement
- 25% are unable to communicate
- 25% are incontinent of bowel or bladder
- 20% require feeding through a tube
- 20% have severe intellectual disability
- 5% have hearing impairment
For a discussion of comorbidities that are often associated with cerebral palsy, follow this link
Clinical Presentations of Different Types of Cerebral Palsy
The Gross Motor Function Classification System – Expanded & Revised (GMFCS-E&R) is a scale that describes an individual’s gross motor abilities (e.g., sitting, walking, running, climbing, and jumping) during typical performance in home, school, and community settings. The GMFCS-E&R uses five different age bands (<2 years, 2-4 years, 4-6 years, 6-12 years, and 13-18 years) that correspond to developmentally appropriate skills to describe an individual's Level of Function between I (least severe) to V (most severe). Scoring may be completed through direct observation, a review of medical records, or by parent report. It provides a rough idea about what equipment or mobility aids (e.g., crutches, walker, wheelchair) a chid or adult may need. To read more about the GMFCS-E&R, follow this link. To download a copy of the GMFCS-E&R, follow this link. To view a brief video on the GMFCS-E&R, follow this link.
You’ll recall from Section 8.1 that there are three main areas of the brain that govern movement: the motor cortex, the basal ganglia, and the cerebellum. The areas of the brain that are injured result in the types of cerebral palsy with which the individual presents. The degree to which the areas are injured results in the severity of cerebral palsy.
Spastic Cerebral Palsy
Spastic cerebral palsy results from injury to the motor cortex and accounts for approximately 75% of cases (Cerebral Palsy Guide, n.d.). Presentations are typically characterized by muscle rigidity in the limbs, trunk, and/or face. You’ll recall from Section 8.1 that the motor cortex is generally responsible for the programming, organization, planning, and execution of motor acts. It’s made up of a three distinct areas of the frontal lobe: the primary motor cortex and the supplemental motor area, which itself is divided into two areas, the medial premotor cortex and the lateral premotor cortex.
- The primary motor cortex executes the sequences of complex movement that require the coordination of multiple muscle groups, such as during the movement patterns described in Chapters 11-13 of this Course Manual (e.g., developmental, fundamental, or performance patterns). The primary motor cortex also encodes the force, direction, distance, and speed of movement needed to generate an intended action.
- The medial premotor cortex programs the sequences of complex movement requiring multiple motor actions to perform. It’s involved with the mental rehearsal of movement patterns in the absence of actual movement.
- The lateral premotor cortex controls the planning and organization of voluntary movement patterns. It encodes the body’s preparation for movement, through adjustments of the body’s posture and proximal limbs. The lateral premotor cortex is active when motor routines are in response to external (auditory and visual) stimuli. Individuals with apraxia have difficulty performing motor acts in the absence of paralysis. Apraxia can have profound effects on speech production, feeding, tool use, design and construction, and walking. For a brief video on the different types of apraxia, follow this link.
You will recall the sensorimotor pathway that was covered in Section 8.2 of this Course Manual. The descending motor pathway is composed of an upper motor neuron and a lower motor neuron.
- The upper motor neuron connects the motor cortex to the spinal cord in what is called the corticospinal tract (see step 6 in the drawing below) or to the brainstem and cranial nerves in what is called the corticobulbar tracts. Damage to the corticospinal tracts results in muscle weakness, spasticity, or exaggerated tendon reflexes (hyperreflexia) in the limbs and trunk.
- The lower motor neuron connects the spinal cord (see step 7 in the drawing below) to the muscles of the limbs, connecting to the neuromuscular junction (see step 8 in the drawing below). Damage to the corticobulbar tracts results in visual dysfunction (CN-II, CN-III, CN-IV, & CN-VI), dysarthria (articulation dysfunction; CN-V, CN-VII, CN-XI, & CN-XII), hearing dysfunction (CN-VIII), and/or dysphagia (swallowing dysfunction; CN-IX).
So what exactly is spasticity in spastic cerebral palsy? Muscle tone can be defined as “a [muscle’s] state of preparedness to movement,” “tension in a relaxed muscle,” and “resistance felt by the examiner during passive stretching of a joint when muscles are at rest” (Ganguli et al., 2021). It is a constant state of fluctuation between relaxation and tension, moderated by muscle spindles and Golgi tendon organs. In short, it is a muscle’s readiness for movement. Dystonia is simply abnormal muscle tone. Spasticity is when there is a high degree of muscle tone (also called “hypertonicity“). A low degree of muscle tone is called “hypotonicity“.
To better understand these concepts, let’s explore the anatomy of the neuromuscular junction and its underlying structures. A neuromuscular junction is the synapse where the axon terminal of the lower motor neuron connects with a muscle fiber that has acetylcholine (ACh) receptors. You will recall that ACh is an excitatory neurotransmitter. As an aside, botulinum toxin (aka, Botox) blocks the release of acetylcholine from the synaptic end bulb into the synaptic cleft and results in muscle paralysis. Botulinum toxin has been used extensively for cosmetic purposes, as well as for therapeutic purposes to reduce muscle spasticity.
In further trying to understand muscle tone and spasticity, we look at two sensory organs related to muscle tissue: muscle spindles and Golgi tendon organs.
- Muscle spindles are specialized sensory (Ia afferent) fibers that are located within the muscle belly that detect tissue length and the rate of change of the muscle fiber. Muscles that are responsible for fine movements (e.g., fingers) have greater number of muscle spindles than muscles responsible for more gross movements or for postural adjustments because fine movements require a greater threshold for detecting change. Muscle spindles contribute to one’s sense of proprioception (knowing where one’s body is in space) and kinesthesia (knowing how one’s body is moving in that space). When a muscle is loaded, the muscle spindle activates a stretch reflex (gamma efferent neurons), which contract agonist muscle tissue to modulate the amount of stretch, as a protective mechanism. Simply put, if you were to raise your forearm in front of you without a weight, then someone hands you a heavy box or dumbbell, the biceps brachii muscle would undergo a brief stretch to accommodate the additional weight and contract so as not to tear the muscle fibers. The muscle spindle also perform reciprocal inhibition of the antagonist muscles (e.g., relax the triceps brachii).
- The Golgi tendon organs (GTOs) are specialized sensory (Ib afferent) fibers that are located within the tendons attached to muscles that detect the amount of force/load being applied to muscle tissue. When a tendon is loaded with the maximum force it can sustain, GTOs activate an inverse stretch reflex through autogenic inhibition, meaning it inhibits the contraction of the agonist muscle as a protective mechanism. In our example above where your biceps brachii is maximally loaded and the tendons of the biceps brachii are at their maximum stretch, the GTOs inhibit biceps contraction so that the tendons don’t rupture or avulse off the bone.
So how does this all relate to spastic cerebral palsy? Muscle spasticity is sometimes inaccurately described as “muscle tightness” or “stiffness.” Rather, it is a motor disorder marked by a velocity-dependent increase in muscle tone (aka, hypertonia; Rivelis et al., 2023). When a muscle undergoes quick stretch, a hyper-excitability of the stretch reflex of muscle spindles (a contraction of the agonist muscles) occurs. To view a brief video of spasticity, follow this link. The degree of muscle spasticity may be measured using several different methods. One of the more common scales is the Modified Ashworth Scale (see Section 16.2 of this Course Manual).
While clinical presentations of spastic cerebral palsy differ depending on the location and severity of injury of the motor cortex, individuals with spastic cerebral palsy often present with (Cerebral Palsy Guide, n.d.):
- Muscle spasticity of one or more limbs, usually held in a flexed pattern
- Abnormal gait and/or limited mobility, often as scissored gait or toe-walking)
- Abnormal reaching patterns
- Joint contractures
- Abnormal reflexes
Depending on the number of limbs affected with spasticity, an individual may be classified as having either diplegia, hemiplegia, or quadriplegia (Cerebral Palsy Research Network, n.d.):
- Diplegia: greatest involvement of lower extremities
- Hemiplegia: mostly one side of the body is involved
- Quadriplegia: all four limbs and sometime trunk, and face are involved
To view a brief video of the presentation of spastic cerebral palsy, follow this link.
Dyskinetic Cerebral Palsy
Dyskinetic cerebral palsy results from injury to the basal ganglia and accounts for approximately 15% of cases (Cerebral Palsy Guide, n.d.). Presentations are typically characterized by random, writhing movements in the limbs, trunk, and/or face. You’ll recall from Section 8.1 that the basal ganglia are subcortical structures and consist of the caudate nucleus, putamen, and globus pallidus. The motor functions of the basal ganglia generally involved with the selection of appropriate movements from the library of motor plans stored in memory and the inhibition of competing motor plans. The basal ganglia are also implicated when attempting to establish a new motor plan.
Where muscle tone is high in spastic cerebral palsy, muscle tone in dyskinetic cerebral palsy may fluctuate between high and low, making it very difficult to control voluntary movement. There are subtypes of dyskinetic cerebral palsy; these include athetoid, choreoathetoid, and dystonic cerebral palsy. While clinical presentations differ depending on the location and severity of injury, clinical presentation of dyskinetic cerebral paly is generally characterized by slow, writhing movements of the face, trunk, and distal limbs). To view a short video of a child with a combination of both spastic and dyskinetic cerebral palsy, follow this link.
Ataxic Cerebral Palsy
Ataxic cerebral palsy results from injury to the cerebellum and accounts for approximately 6% of cases. Presentations are typically characterized by shaky or unsteady movements of the limbs, trunk, and/or face. You will recall from Section 8.1 that the cerebellum’s motor functions are to regulate and refine balance and posture, muscle tone, and motor control. It is also involved with establishing new motor plans during motor learning. The upper motor neurons in the descending corticospinal tracts have branches that extend to the pons and cerebellum, providing the cerebellum with a copy of the motor plan. When sensory feedback about a motor command ascends from the trunk and limbs to the somatosensory cortex, the cerebellum compares what actually happened to what was intended to happen. If the motor plan needs correcting, the cerebellum initiates those corrections. Ataxia is a disturbance of voluntary movement that results in tremors and shakiness because of the cerebellum’s constant attempts to correct movement (Jimsheleishvili & Dididze, 2023).
While clinical presentation differs depending on the location and severity of the injury to the cerebellum, general characteristics of someone with ataxic cerebral palsy include imprecise motor skills, trouble walking and balancing, tremors and shakiness, hypotonia with lack of stability in proximal joints, walking with a wide base of support, over-correction of movements, struggles with speech production, and trouble bringing hands together at midlline. To view a short video of a child with ataxic cerebral palsy, follow this link.
Medical Management & Alternative Therapies
Because cerebral palsy is permanent and nonreversible, interventions directed toward the management of cerebral palsy generally focus on reducing secondary complications (e.g., muscle spasticity, joint contractures, skin breakdown, decubitus ulcers, and pain management) and maximizing function. Interdisciplinary services may include neurology, ophthalmology, pharmaceutics, surgery, orthotics, occupational therapy, physical therapy, speech therapy, vocational rehabilitation specialists, and recreational therapists (Centers for Disease Control and Prevention, 2023; National Institutes of Neurological Disorders and Stroke [NINDS], 2023).
Medications may include:
- Anti-seizure medications (benzodiazepines [Diazepam])
- Muscle relaxants (baclofen [Lioreseal], dantrolene sodium)
- Anti-spasticity medications (botulinum toxin A [Botox])
Surgeries may include:
- Orthopedic surgery to release joint contractures
- Selective dorsal rhizotomy to sever hyperactive nerves
Assistive technologies may include:
- Wheelchair seating and positioning
- Vision and hearing aids
- Augmentative and alternative communication devices
Complementary & Alternative Therapies
While not yet approved by the Federal Food and Drug Administration for the treatment of cerebral palsy, some families find relief with hyperbaric oxygen treatment, compression garments, neuromuscular electrical stimulation (NMES) of antagonist muscles, transcutaneous electrical nerve stimulation (TENS) for spasticity reduction, and acupuncture for global relief of symptoms (Battibugli et al., 2017; Laureau at el., 2022; NINDS, 2023; Warmbrodt, 2024a).
Summary
Cerebral palsy is a broad category of non-progressive, developmental conditions that result from prenatal, perinatal, or post-natal insult to the brain. Three primary areas of the brain that govern movement: the motor cortex, basal ganglia, and cerebellum. The different types of cerebral palsy are governed by which of the three areas of the brain are damaged. Spastic cerebral palsy is a result of damage to the motor cortex, dyskinetic cerebral palsy is a result of damage to the basal ganglia, and ataxic cerebral palsy is a result of damage to the cerebellum. By far, most (80%) cases of cerebral palsy are of the spastic type. Spastic cerebral palsy can affect one limb to all four limbs, the trunk, and face. Muscle spasticity is the hallmark of spastic cerebral palsy and is characterized by hyper-reactivity of the muscle spindles to quick stretch. The Gross Motor Function Classification System – Expanded & Revised (GMFCS-E&R) is a tool that clinicians can use to describe the functional abilities of people with cerebral palsy. There are many pharmacological interventions (mostly aimed at reducing muscle spasticity and controlling seizures), as well as complementary and alternative therapies that are available for people with cerebral palsy.
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