Cerebral palsy (CP) refers to a collection of manifestations of a psychological disorder that affects about 2.1 for every 1000 children globally (Braun et al., 2015). This is a high proportion, making CP a major predicament both as a psychological and a physiological problem due to the resultant effects and complications. It is worthy of notice that CP is caused by a singular occurrence and makes a singular psychological damage to an aspect or aspects of the brain (Braun et al., 2015). Once this damage takes place, it neither progresses nor can it be reversed. However, it triggers a series of physiological problems, weaknesses, effects and complications that will be prevalent throughout the life of the individual. CP results in a continuous fight throughout the life of the individual as a struggle is made against an underlying problem that cannot be treated. It is on this premise that this research paper delves into the continuous fight entailed in the lives of CP sufferers, even as it looks at CP from a general perspective.
History of the Discovery of CP
Due to the diversity of causes of CP, it must have existed as long as human beings have. The first recorded instances of diagnosis of a disorder as CP dates back to the 5th century BCE and is credited to Hippocrates (Braun et al., 2015; Linsell et al., 2016). It is however, in the 19th century that intense research on the condition was rejuvenated courtesy of William John Little. Canadian Physician Sir William Osler made major breakthroughs in understanding the disorder and is even credited for coining the term ‘cerebral palsy’. This was derived from the word "zerebrale Kinderlähmung" which means cerebral child-paralysis (Linsell et al., 2016). This understanding has been crucial as it ended the mystery and even mythology of CP due to its complicated nature and diversity. The understanding that all the physical attributes are premised on a singular mental problem was essential for the management of patients and mitigation of effects to create a better life for patients (Linsell et al., 2016).
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Causes
From a very general and elementary perspective, CP is caused by poor development of the brain, abnormal development of the brain or damage to the brain during the process of development (Linsell et al., 2016). This can happen during pregnancy which accounts to 75% of the cases or in early childhood, mostly during the 1st month of life. In an overwhelming majority of the case, the damage to the brain is structural in nature and therefore can be discerned physically. Research is still ongoing on what actually causes the damage (Linsell et al., 2016). Credible causes however, include exposure to radiation during pregnancy, infections during pregnancy, and fetal growth restrictions especially in the event of twins. Hypoxia caused by thrombotic events, and birth complications that distress the baby have also been credibly associated with CP (Linsell et al, 2016).
Further, as there is great diversity in CP specifically from the perspective of causes, research is still ongoing to establish many of the factors that contribute to the onset of CP. It is however, settled that CP begins before birth and at infancy (Linsell et al., 2016). Further, CP is caused by a singular occurrence that creates an actual physical damage to the brain. It is on this premise that CP is before all else a psychiatric problem and of major interest to psychology. One of the major areas of research has been on the correlation between premature birth and CP (Linsell et al., 2016). Among the most recent such research have been reported by Linsell et al. (2016) after an intensive research on the relationship between CP, premature birth, and the condition of the baby upon birth (Linsell et al., 2016).
The intensive literature review regarding CP shows that the nature of birth is a major bearing factor towards the prognosis of CP. About 50% of all CP cases involve children born prematurely (Linsell et al., 2016). However, it is mainly the process of birth and what happens immediately after birth, as opposed to what causes the early birth itself that is mainly to blame for the cause of CP. Further, a close correlation between multiple births and CP was also seen which was mainly credited to extra low birth weight and general weakness of the new born (Linsell et al., 2016). Three main trends were therefore marked. The first is multiple birth, the second is low weight with the third being how early the premature birth occurred.
Research on prognosis of CP on term infants has also been carried out recently with the article by Nelson and Blair (2015) giving an analysis of recent findings. Among the problems associated with a high prevalence of CP on children either born at term or reasonably close to term include cases where the placenta had problems. This creates a correlation between CP and poor nourishment and asphyxia. Children with birth defects and below normal birth weight have also been reported to be highly susceptible. If meconium finds its way into a child’s lungs, instrumentation used during a difficult birth or even a caesarean birth are also reported culprits (Nelson & Blair, 2015).
Finally, other causes may include an infection immediately after birth, asphyxia at birth, seizures immediately after birth, any form of respiratory distress syndrome, and low blood sugar. Among the minor causes within the literature review conducted in the article is genetic causes, which account to about 2% of the cases (Nelson & Blair, 2015). In this instance, both parents must be carriers of the gene that increases susceptibility. Issues relating to early childhood have also been seen to result in an advent of CP albeit in a very small scope. This may include exposure to toxins, lead or mercury poisoning, strokes, shaken baby syndrome, hypoxia, meningitis or an actual physical injury to the brain (Nelson & Blair, 2015). An infection to the mother during birth was also detected as a minor bearing factor encouraging the occurrence of CP.
Signs and Symptoms
In almost all cases, CP is determined not by the actual damage to the brain but by the resultant physiological manifestations thereof (Maher, 2015). This physiological manifestation is mainly determined by which part of the brain has been interfered with or damaged. As indicated above, the damage is a one instance occurrence and does not increase or reduce. The manifestation however, will change with time depending on the nature, extent and extenuation measures (Maher, 2015). Noticeability and disability are key factors in the symptom of CP. With this regard, symptoms relating to movement are the most noticed and recognized. Indeed, in looking at CP as a continuous fight, physical disability which mainly involves the strengths of limbs is a major factor. Over and above movement, CP is also known to manifest through intellectual disability, communication problems, irrational behavior, and emotional challenges. Secondary problems include epilepsy in almost 30% of the cases, impaired communication at about 57%, vision impairments at about 42%, and intellectual disability at about 40%. According to Braun et al. (2015), due to communication problems, speech impairment is also common and can be controlled through breathing and relaxation training. It is the combination of all these factors, the physical and emotional that result in intellectual incapacitation or impairment for individuals with CP (Braun et al., 2015). In several instances, through intervention and extenuation, the intellectual impairments have been overcome. This is however the exception, not the norm.
According to Maher (2015), physical inabilities as a manifestation of CP has a cause and effect perspective and in many cases the actual damage to the brain is only a trigger. The physical growth of limbs and the development of capabilities involve nerves, muscles, and bones. The nervous system coordinates several movements before birth, in early infancy, and indeed through life to enable proper development of limbs and maintenance of proper shape to enable proper structure and movement. This is mainly how CP causes physical disability or impairments. The part of the brains that controls physical movement gets damaged by the occurrence that creates the CP (Maher, 2015).
The brain is, therefore, unable to initiate the right movements to the muscles in order to occasion their proper development. Similarly, bones grow due to the way the muscles control and handle them (Maher, 2015). Once the development of muscles is interfered with, even the development of bones will be interfered with. Depending on the severity of the brain damage, limbs will either under-grow or grow disproportionately leading to movement impairment or even disability. Expert physiotherapy based on the understanding of exactly how to enable different limbs, muscles, and bones to grow properly coupled with early diagnosis can extenuate the limb impairment as it is purely a physical manifestation (Maher, 2015).
Diagnosis
The current trends in the diagnosis and intervention in CP have been outlined in Hubermann et al. (2016). There are generally two phases of CP diagnosis. The first involves the establishment of whether or not the individual indeed has CP while the second involves seeking to establish the nature and extent of the CP itself. Establishing the existence of CP is currently being done through the general movement assessment test (Hubermann et al., 2016). This requires medical expertise and is best done at the age of 4 months. At this age, the onset of movement impairments as a manifestation of CP will have begun but is not easily recognizable. A diagnosis at this stage creates great room and probability for more successful extenuation. By the age of 2 years, most movement based signs of CP will have manifested and movement impairments will already have set in. This makes successful extenuation much difficult (Hubermann et al., 2016).
The second part of the diagnosis, as with all psychological testing is the subject of informed consent mostly by the guardian or parent. This is because many of these processes can be incisive, expensive and perhaps adverse to the general health of the infant, yet when CP is confirmed, the issue of cure is no longer canvassed as only control of symptoms and mitigation of physical manifestations can be done. This includes CT or MRI tests for the purposes of prognosis (Hubermann et al., 2016). Further, CT and MRI can also in some instances be able to show the nature of damage to the brain and create an ability to predict the nature of manifestation that the version of CP will result in. This is critical to the development of mitigation regimens. However, CT and MRI tests carry with them the risks associated with gamma rays, hence the need for an informed consent (Hubermann et al, 2016).
Treatment and Control
As well reflected in Dewar et al. (2016), there are many treatment regimens for CP currently being experimented on from a pharmacological perspective. Most of them are however, facing the mammoth challenges of safety, especially in children. The most recommended approach to CP is the control of psychical manifestation which in a majority of cases involves movement. Physiotherapy to encourage the growth of muscles and bones has been done with a lot of success according to Kirkpatrick et al. (2016). This research also involved the innovative use of equipment to assist in physiotherapy, and encouraging levels of success was realized. This is because in most instances, CP does not create movement impairment directly. Instead, it reduces the capacity for limbs and muscles to develop properly in order to support movement. This can be corrected through physiotherapy, more so if it is done early and done right.
In developed countries such as the US, this capacity has been developed with overwhelming success albeit at a very high cost (Kirkpatrick et al., 2016). In some instances, pharmacological manifestation interventions have been done with some level of success. This is mainly when CP manifestations are painful as evident in muscle hypertonus. Botulinum injections into the spastic or dynastic muscles have been recorded to work in these instances. It should however, be noted that the use of Botulinum is limited and cannot be used in some muscles. Further, a repeat treatment is necessary either quarterly or biannually (Dewar et al, 2016). However, the effects of the toxins in the body are reversible, making it relatively safe. Surgery to loosen tight muscle or severe extremely sensitive nerves has also been tried with success in some instances.
Conclusion
The totality of the foregoing reflects two major avenues of the continuing fight against CP. The first is the fight to understand better its prognosis to enable better prevention thereof. The second fight is to understand its effects better, to enable better mitigation of its manifestation in patients. CP is a major global concern that affects millions of people. However, it is so diverse in nature and scope, thus making it very difficult to understand and manage. Major strides have been made in different areas of this fight, strengthening the capacity to manage it. Further, research is still ongoing towards the development of stronger and better means of handling it. Perhaps in the future, an actual cure for the problem will be discovered. Until then, every step must be made to reduce the number of occurrences as well as mitigate on manifestations and their kindred adverse effects.
References
Braun, K. V. N., Christensen, D., Doernberg, N., Schieve, L., Rice, C., Wiggins, L., ... & Yeargin-Allsopp, M. (2015). Trends in the prevalence of autism spectrum disorder, cerebral palsy, hearing loss, intellectual disability, and vision impairment, metropolitan Atlanta, 1991–2010. PLoS One , 10 (4), e0124120.
Dewar, R., Claus, A. P., Tucker, K., & Johnston, L. M. (2016). Perspectives on postural control dysfunction to inform future research: A Delphi study for children with cerebral palsy. Archives of Physical Medicine and Rehabilitation . http://dx.doi.org/10.1016/j.apmr.2016.07.021
Hubermann, L., Boychuck, Z., Shevell, M., & Majnemer, A. (2016). Age at referral of children for initial diagnosis of cerebral palsy and rehabilitation current practices. Journal of Child Neurology , 31 (3), 364-369.
Kirkpatrick, E., Pearse, J., James, P., & Basu, A. (2016). Effect of parent‐delivered action observation therapy on upper limb function in unilateral cerebral palsy: a randomized controlled trial. Developmental Medicine & Child Neurology, 58(10), 1049-1056
Linsell, L., Malouf, R., Morris, J., Kurinczuk, J. J., & Marlow, N. (2016). Prognostic factors for cerebral palsy and motor impairment in children born very preterm or very low birth weight: a systematic review. Developmental Medicine & Child Neurology , 58(6), 554-69. doi: 10.1111/dmcn.12972
Maher, C. (2015). Heavy going but making progress: challenges for increasing physical activity in young people with cerebral palsy. Developmental Medicine & Child Neurology , 57 (2), 113-114.
Nelson, K. B., & Blair, E. (2015). Prenatal factors in singletons with cerebral palsy born at or near term. New England Journal of Medicine , 373 (10), 946-953.
