Abstract

Cerebral palsy (CP) is the most common motor disability in childhood. This syndrome is the manifestation of intrauterine pathologies, intrapartum complications, and the postnatal sequel, especially among preterm neonates. A double hit model theory is proposed suggesting that an intrauterine condition along with intrapartum or postnatal insult lead to the development of CP. Recent reports demonstrated that treatment during the process of preterm birth such as magnesium sulfate and postnatal modalities such as cooling may prevent or reduce the prevalence of this syndrome. Moreover, animal models demonstrated that postnatal treatment with anti-inflammatory drugs coupled with nanoparticles may affect the course of the disease in pups with neuroinflammation. This review will describe the changes in the epidemiology of this disease, the underlying prenatal mechanisms, and possible treatments that may reduce the prevalence of CP and alter the course of the disease.

Highlights

  • INTRODUCTIONCerebral palsy (CP) is a heterogeneous group of clinical syndromes that describe permanent disorders of movement and posture

  • Cerebral palsy (CP) is the most common motor disability in childhood [1]

  • A recent population-based cohort study demonstrated that early-onset preeclampsia is an independent risk factor for CP after adjustment for fetal growth restriction and gestational age at delivery

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Summary

INTRODUCTION

CP is a heterogeneous group of clinical syndromes that describe permanent disorders of movement and posture. The motor disorders of CP are often accompanied by disturbances of sensation, perception, cognition, communication and behavior, epilepsy, and secondary musculoskeletal problems [2]. These disorders are attributed to non-progressive disturbances in the developing fetal brain [2], alteration in fetal development [2], pathologic intrauterine processes [3,4,5,6,7,8], or considered as prematurity complication [9]. Update on Cerebral Palsy clinical expression may change over time as the brain matures. We describe the changes in the epidemiology of this disease and the underlying prenatal mechanisms as well as possible treatments that may reduce its prevalence and alter the course of the disease

EPIDEMIOLOGY OF CP
RISK FACTORS FOR CP
Congenital Malformations
Multiple Gestations
Perinatal Stroke
GENETICS CONTRIBUTIONS TO CP
MECHANISMS LEADING TO CP
Placental Lesions and Their Association with CP
CAN WE PREVENT OR REDUCE THE RATE OF CP?
Prevention of Risk Factors
Affecting the Disease Process
Postexposure Treatment of the Affected
Findings
CONCLUSION
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