Cerebral Palsy Research Network Blog

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Cerebral Palsy Causes and Risk Factors – Part 2

[This post is part of our Knowledge Translation/Education Tuesday series. Guest author Lily Collison, author of Spastic Diplegia–Bilateral Cerebral Palsy, continues the series.]

Our home is in Sligo, on the north west coast of Ireland. It’s known for its scenery and also its association with the poet, WB Yeats. Sligo has special mountains–Knocknarea (really only a hill, included in a previous post) and Ben Bulben above (elevation 1,726 feet).

In my last post I gave a typical list of causes of and risk factors for CP. This week I will look at some studies that give us further insight.

  • Although any one risk factor, if severe, may be sufficient to cause CP, more often it is the presence of multiple risk factors that leads to CP. One factor may interact with another to cause the brain injury, such as an event (or events) during pregnancy combined with the stress of birth combined with a genetic vulnerability1.
  • The literature suggests that events during pregnancy are more likely to cause CP than events during labor or delivery. More specifically:
  • A major US study, called the Collaborative Perinatal Project, conducted between 1959 and 1974 followed approximately 50,000 women and their children from the first prenatal visit until the children were seven years old. It found that events during labor and delivery were not major contributors to the occurrence of CP; most cases had their origins before labor began. A second finding was that intrauterine inflammation was a major cause of adverse pregnancy outcome2.
  • At least 70 percent of cases of CP have antecedents* during pregnancy, and only 10 to 20 percent of cases are related to the child’s birth3. Neither the routine use of fetal monitoring during labor nor the increased incidence of caesarean births (factors which reduce risk during labor and delivery) have reduced the number of cases of CP3.
  • Most brain injuries which cause CP occur in the second half of pregnancy, a period when the rate of brain development is fastest4.
  • Some risk factors are on the decline, but others are increasing3,5. Advances in neonatal care have reduced the risk of birth injury. However, with these advances more preterm infants and infants with low birth weight are surviving, some of whom may develop CP. In vitro fertilization has led to more multiple births, and multiple births is a risk factor for CP. The fact that some risk factors are decreasing while others are increasing is leading to a change in the type of CP that develops. For example, an injury to a brain at 24 weeks can have a different effect than one at 28 weeks or 36 weeks. Until recently, babies born at 24 weeks would not have survived. Now, thankfully, many of these babies survive; however, some may develop CP. The most common types of CP differ in different parts of the world, depending on risk factors.
  • In approximately 90 percent of cases, CP results from healthy brain tissue becoming damaged rather than from abnormalities in brain development5.
  • Confirmation of the presence of a brain injury by magnetic resonance imaging (MRI) occurs in many but not all cases. Up to 17 percent of people with CP have normal MRI brain scans5. Imaging may also help determine when the brain injury occurred5.
  • The cause of CP in an individual child is very often unknown6.

Though I did not know what caused Tommy’s CP, in the early days I wasted a lot of time feeling guilty. I had worked very hard and was stressed during his pregnancy, and I felt responsible. Today I no longer feel that sense of guilt. I didn’t knowingly do anything wrong: my life circumstances were such that I was very busy, and besides, there are multiple possible causes of brain injury. I encourage parents to waste no time on guilt—we are where we are and we must move forward.

* Things that existed before or that logically preceded another event.

1Nelson KB (2008) Causative factors in cerebral palsy. Clin Obstet Gynecol 51: 749–762.
2Klebanoff MA (2009) The collaborative perinatal project: a 50-year prospective. Pediatr Perinat Epidemiol 23: 2–8.
3Graham HK, Thomason P, Novacheck TF (2014) Cerebral palsy. In: Weinstein SL, Flynn JM, editors, Lovell and Winter’s Pediatric Orthopedics, Level 1 and 2. Philadelphia: Lippincott Williams & Wilkins, pp 484–554.
4Hadders-Algra M (2014) Early diagnosis and early intervention in cerebral palsy. Front Neurol 5(185): 1–13.
5Graham HK, Rosenbaum P, Paneth N, et al. (2016) Cerebral palsy. Nat Rev Dis Primers 2: 1–24.
6Rosenbaum P, Rosenbloom L (2012) Cerebral Palsy: From Diagnosis to Adulthood. London: Mac Keith Press.

Cerebral Palsy Causes and Risk Factors – Part 1

[This post is part of our Knowledge Translation Tuesday series. Guest author Lily Collison, author of Spastic Diplegia — Bilateral Cerebral Palsy, continues the series on her journey with her son and cerebral palsy (CP). Author note: The is the view out over the Atlantic on Sunday as we climbed Knocknarea–the hill I pointed out in last week’s post.]

In coming to terms with our child’s CP diagnosis, we almost always ask the question why? This week I will write about cerebral palsy causes and risk factors. As we will see below, very often no specific cause is identified. This was the case with our son.

The term cause is self-explanatory. The term risk factor can be defined as any attribute, characteristic, or exposure of an individual that increases the likelihood of developing a disease or injury. Causes thus have a stronger relationship with CP than risk factors. Significant deprivation of oxygen to the infant’s brain, for example, is a cause of CP. Preterm birth is a risk factor but not a cause of CP—in other words, not every preterm baby is found to have CP. There are many possible causes of brain injury, including events before and during pregnancy, during birth, or in early infant life. Much is known about the causes and risk factors for CP, but much remains unknown as well. Depending on what you read, you may come across different lists of causes and risk factors for CP.

Causes of CP
Developing fetuses and infants (up to age two to three) can develop CP if they experience brain injury or disruptions in brain development caused by1:

  • Bleeding in the brain before, during, or after birth.
  • Infections of the brain, including meningitis or encephalitis.
  • Shock—a state in which organs and tissues do not receive adequate blood flow.
  • Traumatic brain injuries, such as from a serious car accident.
  • Seizures at birth or in the first month following birth.
  • Certain genetic conditions.

Risk factors for CP
Risk factors for CP include1:

  • Preterm birth and low birth weight. A typical pregnancy lasts 40 weeks. Babies born before 37 weeks have a greater risk of having CP. The risk increases the earlier a baby is born and the lower the baby’s birth weight. Twins and other multiple-birth siblings are at particular risk because they tend to be born earlier and at lower birth weights.
  • Serious illness, stroke, or infection in the mother. CP is more common in children whose mothers:
    – Experience certain viral and bacterial infections and/or high fevers during pregnancy.
    – Have coagulation (clotting) disorders or experience blood clots during pregnancy.
    – Receive excessive exposure to harmful substances during pregnancy.
    – Have thyroid problems, seizure disorders, or other serious health concerns.
  • Serious illness, stroke, or infection in the baby. Infants who experience serious illnesses, strokes, or seizures around the time of birth are at greater risk of having CP. Such illnesses might include:
    – Severe jaundice. (Kernicterus is a rare kind of preventable brain damage that can happen in newborns with jaundice.)
    – Seizures during the first 48 hours after birth.
    – Infections of the brain, such as meningitis or encephalitis.
    – Strokes caused by broken or clogged blood vessels or abnormal blood cells.
  • Pregnancy and birth complications. For example, not enough nutrition through the placenta or a lack of oxygen during labor and birth. Incompatible blood types between mother and baby.
  • Genetic issues.

I will continue with part 2 next week.

1Gillette Children’s Specialty Healthcare (2019) What Is Cerebral Palsy? [online].

Defining Cerebral Palsy

[This post is the continuation of our Knowledge Translation Tuesday. Guest author Lily Collison, author of Spastic Diplegia — Bilateral Cerebral Palsy, continues the series on her journey with her son and cerebral palsy (CP).]

For a multitude of reasons, I believe it is very important for parents of young children and adolescents and adults with CP to fully understand the condition. I was that mom who didn’t understand my son’s diagnosis and therefore didn’t know how best to help him. My adult son now needs to have a good understanding to best help himself. When I was invited to write for CPRN to expand its knowledge translation objective, Paul (Gross) asked me to first write about SDR in adulthood because my son, Tommy had just undergone this procedure. Once I’d finished that series of posts, I debated whether it was best to work back to childhood or start from childhood. I was also conscious of recent data which showed that people who themselves have CP–adolescents/adults with CP are the biggest single group (58%) in MyCP. In the end, I decided to go back to the start and follow a logical sequence of subjects from childhood to adulthood. Issues in adulthood to some extent build on issues in childhood. It’s like the Wordsworth quotation “The Child is father of the Man.

Let’s start with the actual definition of CP. Over the years there has been much discussion of the definition of CP, and different definitions have been adopted and later discarded. The most recently adopted definition, published in 2007, is as follows:1

Cerebral palsy (CP) describes a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain. The motor disorders of cerebral palsy are often accompanied by disturbances of sensation, perception, cognition, communication, and behavior, by epilepsy, and by secondary musculoskeletal problems.

(Here is a link to a table explaining each term in that definition.)

CP is a lifelong condition and there is currently no cure, nor is one imminent, but good management and treatment can help alleviate some or many of the effects of the brain injury. When the brain injury occurs is important. The consequences of a brain injury to a fetus developing in the womb are generally different from those of a brain injury sustained at birth, which in turn are different from those of a brain injury acquired during infancy. It is generally accepted that only brain injuries occurring before the age of two or three fit the definition of CP. A brain injury occurring after that age is called an acquired brain injury. This cutoff is due to the differences in brain maturity when the injury occurs. In my son’s case I’m not certain when his brain injury occurred–he was born after an uneventful pregnancy and delivery–most likely it occurred during pregnancy.

Returning to the definition of CP, although this definition is very useful, I’m not sure it sufficiently alerts us to the secondary conditions that may arise in adulthood. As O’Brien, Bass, and Rosenbloom (2009) explained, the definition was developed to be used in childhood—it was not intended to infer that progressive problems might not appear in adult life.2

(The photo is one I took yesterday evening at Rosses Point, Sligo, Ireland, where I live. Yeats had close connections with Sligo. The hill in the left background is Knocknarea at 1,073 ft. Tommy was very proud when he first climbed it as a child.)

1Rosenbaum P, Paneth N, Leviton A, Goldstein M, Bax M (2007) A report: the definition and classification of cerebral palsy April 2006. Dev Med Child Neurol 49 Suppl 2: 8–14.

2O’Brien G, Bass A, Rosenbloom L (2009) Cerebral palsy and aging. In: O’Brien G, Rosenbloom L, editors, Developmental Disability and Aging. London: Mac Keith Press, pp 39–52.