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Our Research

The Prevention of Cerebral Palsy

Cerebral palsy is a disorder of the motor (muscle) control areas of the developing brain, injury to which occurred in intrauterine life thru the second year of postnatal life. The brain injury is a one-time event, although several different events can occur; each injury is non-progressive. The brain injury results in dysfunctions of muscle coordination often causing muscle spasticity, muscle weakness and/or abnormal body movements (e.g. athetosis); these can change over time. Cerebral palsy is not a genetic disorder although it can sometimes “run in families”; this is probably due to a genetic susceptibility to an environmental factor or to the continuing presence in or near the family of an environmental risk factor. Cerebral palsy can be associated with other damage to the brain resulting in epilepsy, a visual or hearing disorder, mental retardation or a learning disability.

The overall objectives of the Foundation’s research program are (1) the prevention of cerebral palsy (damage to that part of the developing brain controlling muscle coordination) and (2) the development of more effective methods for diminishing disability in order to improve quality of life.

Prevention Research

Prevention of damage to the developing brain is a major goal of the Research Foundation’s program. Until recently, cerebral palsy (CP) was a “wastebasket” diagnosis describing the symptoms resulting from unspecified damage to the muscle control systems of the developing brain. However, in recent years the characteristics of the several different types of CP have been identified and have provided information about the specific brain pathologies that result in the different clinical manifestations of CP. Understanding the pathology supplies the research leads that help to identify the several possible causes; knowing the causes provides the insights needed for developing interventions to prevent damage to the developing brain. The brain damage that occurs is a result of either (1) disturbance of brain cell migration, (2) poor myelination (insulation) of developing nerve cell fibers, (3) the death of brain cells, or (4) non-functional or inappropriate connections (synapses) between brain cells.

At different times in fetal and infant development, specific areas of the brain are more vulnerable to damage. We now know that:

  • 70% of developmental brain damage occurs prior to birth, primarily in the second and third trimesters of pregnancy (prenatal).

  • 20% occurs in the birthing period (perinatal).

  • 10% occurs during the first two years of life (postnatal).

The causes of CP can be very different in each of these developmental periods, as is the susceptibility to injury of specific areas of the developing brain.

THE TARGETS OF THE FOUNDATION’S PREVENTION RESEARCH PROGRAM ARE:

PRENATAL BRAIN DAMAGE

  • Impaired migration of new brain cells to their destination in the developing brain is an important cause of cerebral palsy; major risk factors include infection, toxins, drugs and radiation exposure.

  • Poor myelination (insulation) of brain nerve cell fibers is an important cause of cerebral palsy; a major factor is hemorrhage in the developing brain.

  • Prematurity and low birth weight are major risk factors for cerebral palsy. Low grade infection of the mother’s urinary-genital tract is a very common cause and is receiving priority research attention.

  • The presence of multiple fetuses is an increasing reason for the occurrence of prematurity and developmental delay of the infant.

PERINATAL BRAIN DAMAGE

  • Increased pressure on the infant brain during delivery, impaired circulation to the fetal brain, and poor respiration can result in brain cell death and are potential causes of cerebral palsy.

  • A significant proportion of already existing prenatal brain damage is first recognized after delivery, but erroneously assigned to events in the perinatal period.

  • Low birth weight is a major risk factor for developmental brain damage. Survival of very low birth weight infants is a reason for the increased occurrence of cerebral palsy. This relationship is receiving focused research attention.

  • Improved neuroprotection of the threatened brain is also a principal research objective.

POSTNATAL BRAIN DAMAGE

  • Physical trauma, infection, respiratory distress and cerebrovascular disorders are the most common causes of postnatal damage of the developing brain.

  • Prevention of the complications associated with the disabilities resulting from cerebral palsy is of major importance to quality of life. This is an important Foundation research objective.

UCP FOUNDATION RESEARCH STRATEGY

In order to further its prevention research program, the Foundation’s strategy includes:

  • seeking and acting upon the continuing advice and assistance of research leaders in the field, particularly the Foundation’s Research Advisory Council.

  • interacting with and sometimes being part of the research advisory structure of other organizations such as government research agencies (e.g. NIH, CDC, NIDRR), academic institutions, research institutes (e.g. Burke, Kessler, Salk, Kennedy Krieger), foundations (e.g. Hearst Foundation), industry and other organizations.

  • sponsoring research workshops in which scientific leaders address a critical research question, share findings and problems, and agree to cooperate in answering the question.

  • providing risk venture financial support for pilot research projects exploring new approaches to the answer of important research questions.

  • funding the career development of young clinician-scientists to become the future academic leaders in cerebral palsy research, teaching and patient service.

  • informing the public of the continuing advances in research for the prevention of cerebral palsy and improving the quality of life of persons with disabilities due to developmental brain damage.

Copyright applied for by: UCP Research and Educational Foundation, 1025 Connecticut Avenue, Suite 701, Washington, DC 20036

UCP Research & Educational Foundation, July 2002

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