10.7 Cerebral palsy: recommendation and future directions

The rate of CP has remained static for decades, at between 2 and 2.5 cases for every 1000 live births, due to abnormalities of the developing fetal or infantile brain resulting from a variety of causes. In a recent publication, however, Hollung et al. reported that the prevalence of CP declined for children born in Norway from 2.62 per 1000 in 1999 to 1.89 in 2010, and in addition a substantial improvement in the severity of clinical characteristics with a decrease in the proportion of children with severe motor impairments, epilepsy, intellectual disability, and difficult to understand or no speech was observed. They attributed this improvement to the better obstetric and neonatal care the first decade of the twenty-first century [43]. In general, however, methods that have been implemented, such as continuous electronic monitoring of the fetus in labor, have not had the anticipated benefits. Many neuroprotective strategies have failed. In premature infants, an increase in survival without a decrease in prevalence added more healthy citizens but also more disabled children to the population. As a consequence in recent years, efforts have focused on prevention, cure, early diagnosis, and early intervention in an attempt to reduce further CP prevalence.

Approximately one-half of all new cases of cerebral palsy arise from the group of neonates born prematurely (< 30 weeks gestation) that are at risk for long-term neurodevelopmental problems, with almost one-half having motor, cognitive, and/ or language impairments, a rate much higher than their term peers [44]. For many children, however, the cause of cerebral palsy is unclear. There are many known risk factors that affect the fetal and neonatal developing brain leading to cerebral palsy, and some of them can be prevented. Risk factors for congenital CP include infection during pregnancy (toxoplasmosis, rubella, cytomegalovirus, and herpes can infect the womb and placenta, leading to brain damage in the fetus), abuses of alcohol or drugs during pregnancy, smoking, exposure to toxic chemicals, multiple gestations, and infertility treatments that have an increased risk in preterm delivery and multiple gestations and certain medical conditions such as diabetes, high blood pressure, abnormal thyroid function, sexually transmitted infections, and eating disorders (anorexia nervosa, bulimia nervosa, binge eating disorder). Placental infarctions are most likely to be identified in the births of infants who will in the

atrophy and epilepsy is the fact that in many cases atrophy presents the end result

Intraventricular hemorrhage was identified as a significant risk factor for the development of neonatal seizures [41]. In patients with neonatal seizures, cerebral dysgenesis and intraventricular hemorrhage proved to be predictors for poor out-

Brain imaging in children with CP and epilepsy shows frequently abnormal findings. In children with CP and epilepsy, cerebral atrophy is more often reported [31, 40]. Atrophy is the consequence of prenatal and perinatal ischemia; this will lead to an extensive neuronal damage which may be the cause of the seizures. A significant risk factor for the development of neonatal seizures was found with intraventricular hemorrhage [41]. Cerebral dysgenesis and intraventricular hemorrhage were found to be predictors of poor outcome in patients with neonatal

The effect of imaging abnormalities in CP remains controversial. In one study, an MRI abnormality was noted in 86.7% of patients, and the abnormal finding variable in the MRI did not significantly affect the epilepsy development and sei-

In other studies the range of abnormal findings in MRI was reported as 84– 88% [42]. Cerebral infarct is found by neuroimaging to be an abnormality that significantly affects seizure outcome in epileptic patients with CP [4]. Table 5 shows the imaging findings in patients with CP and epilepsy and CP without

of prenatal or perinatal global ischemia with extensive neuronal damage.

Imaging findings in patients with cerebral palsy only and with cerebral palsy and epilepsy.

Neurodevelopment and Neurodevelopmental Disorder

come [29].

Table 5.

seizures [29].

zure outcome.

epilepsy.

62

future develop cerebral palsy, especially those with spastic quadriplegia, an early reliable biomarker.

double-blind, randomized control trials. However, identifying predictive biomarkers and developing preventive strategies phenotypically orientated to different subsyndromes, we can prevent or intervene early taking into consideration the

In general children with CP have epileptic seizures in about one-third that occur

, Dirk Deleu1,2, Hassan Al Hail1,2,

, Osama Alalamy1,2, Covanis Athanasios3

as a rule within the first 2 years of life. The most common seizure type is focal generalized seizures followed by focal, infantile spasms, and myoclonic seizures that are seen in one-fourth of cases. Seizures are most often seen in spastic hemiplegia and spastic quadriplegia. Children with CP and mental retardation have an early onset of seizures and more severe epilepsy. The response to antiseizure treatment in children with CP is generally difficult, and one-third to half of the cases is

3 Neurology and Neurophysiology Department, The Children's Hospital Agia

4 Department of Neurology, Thomas Jefferson University, Philadelphia, PA, USA

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

5 Department of Neurology, Shiraz University of Medical Sciences, Shiraz, Iran

\*Address all correspondence to: boulenouar.mesraoua@wanadoo.fr

receiving polytherapy and/or alternative therapies.

advantage of brain plasticity.

DOI: http://dx.doi.org/10.5772/intechopen.82804

Epilepsy and Cerebral Palsy

11. Conclusions

Author details

Boulenouar Mesraoua1,2\*, Musab Ali1

1 Hamad Medical Corporation, Doha, Qatar

2 Weill Cornell Medical College, Doha, Qatar

provided the original work is properly cited.

Gayane Melikyan1,2, Naim Haddad2

and Ali A. Asadi-Pooya4,5

Sophia, Athens, Greece

65

Before pregnancy we have to make sure that the woman is protected against certain diseases such as rubella with vaccination and certain preventable infections or cytomegalovirus (CMV). CMV in particular, is transmitted through close personto-person contact with infected secretions such as in urine and saliva. The infection is transmitted from the mother to the fetus during pregnancy and can sometimes cause stillbirth, premature birth, and neurological conditions such as cerebral palsy. Children with cerebral palsy infected with CMV are more likely to have spastic quadriplegia, severe functional mobility limitations and a range of associated impairments including epilepsy, deafness, vision impairment, and moderate-tosevere intellectual disabilities, than children born with cerebral palsy but without CMV. There is evidence that public health approaches based on hygiene can dramatically reduce the rate of primary maternal cytomegalovirus infections during pregnancy. Formulated consensus recommendations on the diagnosis, prevention, and treatment of maternal and congenital CMV infection are found in the publication of Rawlinson et al. [45].

Our primary aim, therefore, is to provide a healthy pregnancy by advising and treating appropriately treatable conditions and introduce current preventable strategies and interventions that hold promise for reducing the prevalence of cerebral palsy. Such interventions include strategies to decrease the risk of premature birth (e.g., 17α-progesterone), limit the number of multiple gestations related to assisted reproductive technology, treat mothers who are expected to deliver prior to 30 weeks gestation with magnesium sulfate for fetal neuroprotection that can prevent cerebral palsy, give antenatal steroids for mothers expected to deliver prematurely, caffeine for extremely low-birth-weight neonates, and induce hypothermia for a subgroup of neonates diagnosed with intrapartum hypoxic-ischemic encephalopathy [46]. Hypothermia, either selectively applied to the head or total body, appears to decrease the risk of cerebral palsy [47]. Interventions which either prolong gestation or decrease the risk of preterm delivery will also decrease the risk of cerebral palsy.

Although 50% of very preterm children has neurodevelopmental impairments, an early prediction of infants who will experience problems later in life still remains an early diagnostic challenge. White matter abnormalities (WMA) at term have been associated with CP in very preterm children and can be used as a biomarker for early multidisciplinary approach. Very preterm children with any WMA at term require follow-up throughout childhood [48]. Abnormal general movements in very preterm infants born <30 weeks gestation, particularly at 3 months post term, are predictive of worse neurodevelopment at ages 2 and 4 years and need multidisciplinary approach. The accuracy for predicting moderate to severe cognitive impairment was good at 83% and 77% for 2 and 4 years, respectively [49].

Recent research on neuroplasticity supports intensive, repetitive, task-specific intervention for CP that should commence early while the brain is most plastic. Early postnatal recognition is important for a prompt referral to diagnostic-specific early intervention setting to optimize infant's motor and cognitive plasticity, prevent secondary complications, and enhance caregiver's well-being [50].

Beside traditional conventional therapies, physical therapy, occupational therapy, and speech-language therapy, a number of other approaches have been used such as the use of Botox, selective dorsal rhizotomy, functional vision assessment and intervention programs, developmental optometry, biofeedback, hippotherapy, hyperbaric oxygen therapy, deep brain stimulation for dyskinetic forms of cerebral palsy, stem cell applications, and even yoga. It is very difficult to decide which method is "gold standard" type of therapy for CP because it is impossible to conduct
