Cerebral Palsy Literature Review

Cerebral palsy is defined as a group of permanent disorders that develop in the fetal or infant brain that affect the development of movement and posture (Rosenbaum et al.

, 2006). These permanent disorders limit activity and thus are known as motor disorders. They also affect a wide range of functionality regarding disturbances in sensation, perception, cognition, communication, and behavior (Rosenbaum et al., 2006). Cerebral palsy can be classified or class. The classification system is based on four components: motor abnormalities, accompanying impairments, anatomical and neuroimaging findings, and causation and timing (Rosenbaum et al., 2006). Because cerebral palsy emerges in the early stages of development, many factors have been studied to find correlations between infants and the prevalence of cerebral palsy. The prevalence of cerebral palsy in normal birth weight infants is strongly associated with social class; the disorder is more prevalent in infants born into lower socioeconomic status (Odding et al., 2006). This paper will review the effects of cerebral palsy genetically, physiologically, neurologically, and behaviorally, and it will explore possible treatment methods.

Genetic

Cerebral palsy is a group of disorders, meaning that it is heterogeneous in types, causes, and now genetic variants (MacLennan et al.

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, 2015). According to MacLennan et al., epidemiological studies show that most origins of cerebral palsy are from before labor (2015). This is followed by associated risk factors in the labor and delivery process (MacLennan et al., 2015). Through new-generation exome sequencing, researchers have found 14% of cases to have single-gene mutations that likely cause cerebral palsy, and up to 31% of cases have clinically relevant copy number variations (MacLennan et al., 2015).

Physiological

Motor impairments are what characterize cerebral palsy. Many cases constitute spastic syndromes (Odding et al., 2006). These impairments lead to secondary issues in the musculoskeletal system (Odding et al., 2006). Lower physical fitness, low muscular endurance, and low anaerobic power are all common in patients in comparison to their able-bodied peers (Odding et al., 2006). Patients with cerebral palsy also experience symptoms affecting the endocrine system and urogenital impairments. Children with cerebral palsy have difficulty with feeding and other gastrointestinal problems; this could be due to trouble with sucking and swallowing (Odding et al., 2006). In 62% of cases of children with severe spastic cerebral palsy, patients have had significant silent aspiration (Odding et al., 2006). Many, close to a third, of children with cerebral palsy have suffered from pulmonary infection as well (Odding et al., 2006). Many children, close to one-fourth, experience stunted growth and more than half of children with cerebral palsy have problems with being underweight or overweight (Odding et al., 2006). Another symptom is low bone-mineral density. Although there is a lot of variation, on average children and adolescents with cerebral palsy have bone-mineral density one standard deviation below age norms (Odding et al., 2006). Regarding urogenital impairments, many patients experience primary urinary incontinence; the determinants of this occurrence are tetraplegia and low intellectual capacity (Odding et al., 2006). Chronic pain is very common in cerebral palsy patients; it is common in the back in all types of cerebral palsy (Odding et al., 2006).

Neurological

In most cases, patients with cerebral palsy exhibit cognitive impairment. Children and adolescents with tetraplegic cerebral palsy are severely intellectually impaired (Odding et al., 2006). Some symptoms include non-verbal learning impairments, shown by good language abilities and weak visual-spatial abilities, and fear of new situations (Odding et al., 2006). Epilepsy is commonly comorbid with cerebral palsy, although it varies with the type of motor impairment in cerebral palsy. Epilepsy is common in hemi- and tetraplegics, which leads to variance in onset and severity; tetraplegics have more generalized epilepsy and hemiplegics have more localized epilepsy (Odding et al., 2006). Sensation and sensory perception is also common symptom of cerebral palsy. Hemiplegic cerebral palsy patients experience sensory impairment the most (Odding et al., 2006).

Behavioral

Studies show that children with cerebral palsy have five times more likely the chance of exhibiting behavior problems compared to children with no health problems (Odding et al., 2006). Children with cerebral palsy display features of dependency, being headstrong and being hyperactive in general (Odding et al., 2006). Additionally, cerebral palsy patients commonly have attention deficit hyperactivity disorder (ADHD) (Odding et al., 2006).

Treatment

Many medications and therapeutic routes alleviate the spasticity of cerebral palsy, but they do not reverse the effects of the disorders. Many other medications focus on dystonia or pain; however, there should be more focus on treating the root of cerebral palsy as a whole. There is no cure for cerebral palsy; however, McDonald et al. propose umbilical cord blood (UCB) cell therapy and have conducted clinical trials. The use of UCB cell therapy would be for neuroprotection and neuroregeneration. This stem cell research is still being developed and would be administered at the optimal time as early intervention (McDonald et al., 2017). Although this seems promising, it would not have potential benefits for patients with existing cerebral palsy. In a study done by Fleiss and Gressens, tertiary mechanisms of damage from cerebral palsy may include persistent inflammation and epigenetic changes (Fleiss and Gressens, 2012). They propose these mechanisms are essential to endogenous repair and regeneration (Fleiss and Gressens, 2012). Treatment would involve repressing the effects of microglia and astrocyte over-activation (Fleiss and Gressens, 2012). They state that aberrant gliosis can cause tertiary brain damage, despite the positive effects of glial responses (Fleiss and Gressens, 2012). Tertiary brain damage is detrimental because they worsen the outcome of the disorder and they predispose the patient to further injury and prevents repair or regeneration (Fleiss and Gressens, 2012). This study uses neonatal and adult data to assess the treatment efficacy. The confirmation of glial activation states and the mechanisms that underpin white matter allow treatment in the tertiary phase (Fleiss and Gressens, 2012). While these two therapeutic options show great potential, some might give more immediate outcomes. Jantzen et al. tested a postnatal treatment regimen that combines endogenous neuroreparative agents, erythropoietin (EPO), and melatonin (MLT). They hypothesized that it would alleviate abnormalities on the molecular, sensorimotor, and cognitive levels (Jantzie et al., 2018). They showed that the EPO + MLT treatment repaired disinhibition in injured rats and normalized hindlimb deficits (Jantzie et al., 2018). It also alleviated behavioral effects by normalizing social drive (Jantzie et al., 2018). Neurologically, the EPO + MLT treatment normalized the complex cognitive tasks of visual discrimination and reversal (Jantzie et al., 2018). Therefore, the EPO + MLT treatment seems like a viable, realistic option for treatment to repair a wide range of the effects of cerebral palsy on cognitive, behavioral, and sensorimotor levels.

Works Cited

1. A report: The definition and classification of cerebral palsy April 2006. (2007). Developmental Medicine & Child Neurology, 49, 8-14. doi:10.1111/j.1469-8749.2007.tb12610.x
2. Fleiss, B., & Gressens, P. (2012). Tertiary mechanisms of brain damage: A new hope for treatment of cerebral palsy? The Lancet Neurology, 11(6), 556-566. doi:10.1016/s1474-4422(12)70058-3
3. Jantzie, L. L., Oppong, A. Y., Conteh, F. S., Yellowhair, T. R., Kim, J., Fink, G., … Robinson, S. (2018). Repetitive neonatal erythropoietin and melatonin combinatorial treatment provide a sustained repair of functional deficits in a rat model of cerebral palsy. Frontiers in Neurology, 9. https://doi.org/10.3389/fneur.2018.00233
4. Mcdonald, C. A., Fahey, M. C., Jenkin, G., & Miller, S. L. (2017). Umbilical cord blood cells for the treatment of cerebral palsy; timing and treatment options. Pediatric Research, 83(1-2), 333-344. doi:10.1038/pr.2017.236
5. Maclennan, A. H., Thompson, S. C., & Gecz, J. (2015). Cerebral palsy: Causes, pathways, and the role of genetic variants. American Journal of Obstetrics and Gynecology, 213(6), 779-788. doi:10.1016/j.ajog.2015.05.034
6. Odding, E., Roebroeck, M. E., & Stam, H. J. (2006). The epidemiology of cerebral palsy: Incidence, impairments, and risk factors. Disability and Rehabilitation, 28(4), 183-191. doi:10.1080/09638280500158422