Cerebral Palsy

Sorry for the long wait for this post. About 6 or 7 months ago I asked for input on different neurological and neuroscientific topics to talk about for the website. Cerebral Palsy (CP) was the first one I received and since then many life changes occurred and I was unable to commit proper time and energy to this website. Since finding a job after graduating college I have had a significant amount of time that I was able to devote to making this website a quality outlet for general education in science. Educating the people who do not have a science background is something that I have become very passionate about within the last year. With that said I would love to hear comments and critic from people pertaining to this website so that I can better serve you all.

It’s always great to start off a post by talking about Freud. Possibly one of the only theories that Freud created this hasn’t been proven wrong is one pertaining to CP, one of the most daunting and enigmatic diseases today. Freud’s theory was that Cerebral Palsy originates from underlying abnormalities in the brain structures that predate labor and delivery. An opposing theory of the origins of Cerebral Palsy is that of the surgeon James Little. Little believed that most cases of Cerebral Palsy are attributable to severe intrapartum (labor) asphyxia (a condition arising from inadequate oxygen levels). Both theories are helpful and both have served a purpose in modern CP research.

I would like to start this post about Cerebral Palsy (CP) by defining what the disease is and how it presents. A general description of CP is should be encompassing of the following criteria; has a broad range of expression, is a static condition, has origins within the central nervous system (CNS), is a disturbance of movement and/or posture, and originates during a time of the developing immature brain (Schaefer, 2008). To further our understanding it is beneficial to define all of the listed points. “Has a broad range of expression”, meaning that the disease phenotype (how the disease is expressed clinically) is variable. “Is a static condition” as opposed to progressive neurologic conditions, i.e. Alzheimer’s disease and Parkinson’s Disease, it seems that CP is caused by a single insult or trauma that occurs during the brain’s development and CP is thought to not become worse, this is not to say that the complications of CP cannot become worse but to mean that CP will not be the cause of the symptoms worsening. “Has origins within the CNS” this implies that the disease etiology starts in the CNS and can have implications for the rest of the body. “Is a disturbance of movement and/ or posture, and originates during a time of the developing of the immature brain” this definition implies that CP will manifest in movement and/or posture difficulties. Not only is CP a difficult disease to wrap your mind around in concern to all of the clinical manifestations, it is also prolific.

In 1994 the number per 1000 children born was two (2/100) and approximately 100 thousand people under the age of 18 were living in the United States (Schaefer, 2008). Today that number ranges anywhere from 2.3-3.6 per 1000 children born with approximately 500 thousand people under the age of 18 were living in the United States (Cerebralpalsy.org, 2015). CP has thus been considered a major developmental disease in America. Yet, CP seems to still be an unknown for many Americans, myself included.

Diagnostic Criteria

A diagnosis of CP is unfortunately not a concrete or exact science. One of the more telling observations that can be made for infants who are suspected of CP is that they must express the prolonged reflex called the Moro Reflex. The name is unimportant, however the presentation of the reflex is more hallmark and recognizable by most parents but after 6 months the presentation of the reflex should dissolve. The Moro reflex occurs when the infant feels like it is unsupported or falling. The infant will spread out its arms and then pull them close to their body and typically crying will occur as well. A video showing the Moro Reflex can be found here. In many cases the presence of the dominant hand becoming spastic at early age can be a diagnostic clue for diagnosing CP with spastic hemiplegia (the spastic contraction of muscles only present on one side of the body). It should also be noted that in order for CP to be diagnosed all other metabolic and neurological conditions must be ruled out (Taylor, 2001). In many ways it seems that most neurologists will try to rule out these other conditions to avoid a diagnosis of CP because of it’s incurable properties.

Another piece of the diagnostic puzzle is simply surveillance of the child in a hospital setting while running various tests. These tests include measuring the following faculties

  • Hearing
  • Vision
  • Seizure induction
  • Perception
  • Over expressive nociceptive reactions (pain to the touch)
  • Cognition

Symptoms and etiology

Symptoms within the larger disease population of CP can vary and CP seems to be a larger collection of variable symptoms with many CP patients seeming to have a different mixture of clinical manifestations. Some of the clinical features are as follows, spastic limbs, tendon reflexes, muscular tremor, hypotonicity (abnormally low muscle tone), weakness, scissors gait/toe walking (Karen & Krigger, 2006). While physical disabilities must be present for a diagnosis other disabilities such as intellectual deficits can also be present and are so within 2/3 of the CP Population (Taylor, 2001).

CP can be further broken into subtypes by the clinical presentation of the number of limbs affected by the disease. The following list is compiled per type of motoric manifestation and the areas that are affected by CP within the clinical population.

  • Spastic quadriplegia (6%)- spasticity of the muscles found in all limbs (arms and legs)
  • Spastic diplegia (44%)- spasticity of the muscles found in only two limbs.
  • Spastic monoplegia/hemiplegia (33%) – affects only one limb with presentation of muscle spasticity.
  • Ataxic/ dyskinetic (12%)- Dyskinetic CP manifests with clinical features such as abnormally slow movements, writhing of hands, feet, arms, or legs which can also be exacerbated by sleep or stress (Karen, Krigger 2006).

Placental pathology (this image may be helpful in understanding some of the anatomy I am describing—–>

image courtesy of illustrationsource.com
image courtesy of illustrationsource.com

The placenta (main source of nutrients from the mother and air supply line) has been recently been the site of extensive Cerebral Palsy research. Disruption of normal placental processes has been said to contribute to hypoxic (deprived of adequate oxygen) derangements during the intrapartum (labor or birthing period) period during pregnancy (Adamson et al., 1995). In many cases neonatal encephalopathy (global brain dysfunction) are caused by hypoxic origins, which is subsequent of placental disruptions of major blood vessels.

Placental pathology is used to study how vasculature disruptions and supply lines are atrophied in a fetus with CP. There are two types of placental lesions (separations) that occur, uteroplacental vasculature (maternal supply line) and fetoplacental vasculature (fetal supply line). A specific type of lesion, Sentinel lesions, while uncommon are very dangerous to a fetus and can result in any of the following three disruptions; 1) total separation from the uterine vascular bed and placenta, 2) disruption of the fetal placental vasculature leading to major blood loss, 3) complete obstruction of the umbilical blood flow. All three of these possibilities would cause more than enough damage to result in hypoxia and subsequently, brain damage to the fetus. A more common type of vascular lesion that can occur leading to CP is a thromboinflammatory lesion. Thromboinflammatory lesions can lead to a number of different vascular disruptions including but not limited to vascular necrosis (cell death of the pulmonary system) (Redline, Patterson, 1994).

Sudden catastrophic events are also major contributors to a CP diagnosis. Such catastrophic events include traumatic injury to the mother, drug overdose, or cardiovascular compromise. It is obvious to see how any one of these scenarios would disrupt processes in a mother to fetus exchange of nutrients. A number of possible outcomes can occur in response to catastrophic events; 1) the placenta could become prematurely separated from the uterine vascular supply, 2) blood loss via fetal blood vessel ruptures, 3) umbilical blood flow disruptions sufficient enough in lapse of time leading to ischemic damage (lack of blood flow) (Redline, 2006).

In the review paper by Dr. Redline that I posted a while back, pertaining to placental pathology, Dr. Redline discussed the idea that genetic susceptibility to such lesions are major contributors to placental lesions. However, it is up for debate as to whether or not the placental lesions occur before the placental injury or after is a topic steeped in controversy.


While much evidence has been posed that hypoxic/ ischemic encephalopathies (HIE) is the cause of CP it has been shown by a study by Blair & Stanley (1988) that only between 7%-8% of CP cases can be traced back to HIE. It is also thought that even in the case of HIE that genetics are still implicated.

APOE polymorphisms have been recently implicated in HIE (Kuroda et. al, 2007). APOE may sound familiar to you because this gene, more specifically the E4 mutation, is thought to be the main contributor to Alzheimer’s disease is called. APOE is a main catabolic (process that breaks down molecules) component of cholesterol/ triglycerides. In lay terms, APOE breaks down cholesterol/ triglycerides into smaller components to be further metabolized (broken down) by various cellular components.

Prematurity within the Cerebral Palsy population is also much more common. Recent genetic studies have shown links between specific gene markers, linkage, and polymorphisms that could possibly predispose a fetus to a premature birth (Towson, 2001, Gibson et al., 2007, Nelson et al., 2005). Scientists have since proposed that possibly, premature births are genetically linked and that Cerebral Palsy is just a secondary effect of the said premature birth. This idea is called genetic sequencing.

A somewhat new idea only present within the past 10 years is that of expanded genetic phenotypes (clinical presentation). Expanded genetic phenotypes imply that a single genetic mutation can have a plethora of phenotypic expressions. The idea of expanded genetic phenotypes would help to then explain the high rate of co-morbidities (having more than one disease) that are often expressed in patients with Cerebral Palsy. Some of the specific genes that are thought to be associated in the expanded genetic phenotypes are (ataxia within Cerebral Palsy) 9p12q12 and (muscle spasticity within Cerebral Palsy) 2q24 to q25 (McHale et al., 2000, McHale et al., 1999).


While Cerebral Palsy remains an enigmatic disease, science is moving forward to combat this disease. Cerebral Palsy seems to be growing as the population is growing and in part that may be due to the technology that allows premature infants to live. As time progresses this disease will become more present and it is going to be a disquiet situation medically, economically and emotionally.

If you would like me to expound upon any of the points made above please feel free to comment below. Also feel free to share this website with family and friends. From this point onwards, I will be posting an article every month. I hope to hear from you all.




Blair, E., & Stanley, F. J. (1988). Cerebral Palsy in Low‐birthweight Infants. Developmental Medicine & Child Neurology, 30(4), 550-552.

Dizon-Townson DS: Preterm labour and delivery: A genetic predispo- sition. Paediatr Perinat Epidemiol 15:57-62, 2001 (suppl 2)

Gibson CS, MacLennan AH, Dekker GA, et al: Genetic polymorphisms and spontaneous preterm birth. Obstet Gynecol 109:384-391, 2007

Krigger, K. W. (2006). Cerebral palsy: an overview. American Family Physician, 73(1), 91–100.

KurodaMM,Weck ME, Sarwark JF, et al: Association of apolipoprotein E genotype and cerebral palsy in children. Pediatrics 119:306-313, 2007

McHale DP, Mitchell S, Bundey S, et al: A gene for autosomal recessive symmetrical spastic cerebral palsy maps to chromosome 2q24-25.AmJ Hum Genet 64:526-532, 1999

McHale DP, Jackson AP, Campbell, et al: A gene for ataxic cerebral palsy maps to chromosome 9p12-q12. Eur J Hum Genet 8:267-272, 2000

Nelson KB, Dambrosia JM, Iovannisci DM, et al: Genetic polymor- phisms and cerebral palsy in very preterm infants. Pediatr Res 57:494- 499, 2005

Redline, R. W. (2006). Placental pathology and cerebral palsy. Clinics in Perinatology, 33(2), 503–16. doi:10.1016/j.clp.2006.03.007

Redline, R. W., & Patterson, P. (1994). Patterns of placental injury. Correlations with gestational age, placental weight, and clinical diagnoses. Archives of pathology & laboratory medicine, 118(7), 698-701.

Redline, R. W. (2006). Placental pathology and cerebral palsy. Clinics in Perinatology, 33(2), 503–16. doi:10.1016/j.clp.2006.03.007

Taylor, F. (2006). National Institute of Neurological Disorders and Stroke (US), Office of Science and Health Reports. Cerebral palsy: hope through research. Bethesda, Md.: The Institute, 2001. Accessed online September 28, 2005.


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