Perinatal causes of cerebral palsy:
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
Philadelphia [u.a.]
Saunders
2006
|
| Schriftenreihe: | Clinics in perinatology
33,2 |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XVI S., S. 233 - 572 Ill. |
| ISBN: | 1416035435 |
Internformat
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| 245 | 1 | 0 | |a Perinatal causes of cerebral palsy |c guest ed.: Marcus C. Hermansen |
| 264 | 1 | |a Philadelphia [u.a.] |b Saunders |c 2006 | |
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| 490 | 1 | |a Clinics in perinatology |v 33,2 | |
| 650 | 4 | |a Cerebral Palsy |x etiology | |
| 650 | 4 | |a Cerebral palsy |x Etiology | |
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CONTENTS
Preface xv
Marcus C. Hermansen
Historical Perspectives on the Etiology of Cerebral Palsy 233
Tonse N.K. Raju
This essay presents the early history on the evolution of concepts
about the etiology of cerebral palsy, especially the contributions of
the early pioneers. Insight into how they derived their hypotheses,
including the errors they made, can help one understand the com¬
plex processes of deciphering etiologic associations.
The Descriptive Epidemiology of Cerebral Palsy 251
Nigel Paneth, Ting Hong, and Steven Korzeniewski
The prevalence of cerebral palsy (CP) ranges from 1.5 to 2.5 per
1000 live births with little or no variation among western nations,
although data from the Americas are sparse. Time trends in over¬
all CP prevalence for the past 40 years are most notable for their
stability, but a modest increase in prevalence probably occurred in
the last decades of the twentieth century. European countries have
pioneered the development of CP registries, and as a result, CP is
a condition that is enumerated regularly in several parts of the
world. The United States has no CP registries, although ongoing
surveillance of CP, along with other developmental disabilities, is
performed by the Centers for Disease Control and Prevention in
metropolitan Atlanta.
The Panorama of Cerebral Palsy After Very and Extremely
Preterm Birth: Evidence and Challenges 269
Michael E. Msall
During the past 2 decades, major advances in maternal fetal medi¬
cine and neonatology have resulted in unprecedented survival of
VOLUME 33 . NUMBER 2 • JUNE 2006 vii
very preterm ( 32 weeks) and extremely preterm ( 28 weeks)
babies. Despites these advances in prenatal care, neurodevelop
mental motor impairment remains a substantial sequela. This arti¬
cle describes the major progress and challenges in understanding
pathways of preterm children who go on to have one of the cere¬
bral palsy syndromes. The contributions of chronic lung disease,
intraventricular hemorrhage, retinopathy of prematurity, and post¬
natal steroids are analyzed. Management can then be directed to
limiting the comorbidities that are associated with threats to sur¬
vival and to improving protection of central nervous system func¬
tions that are involved in moving, manipulative skills, feeding,
communication, and learning.
Cerebral Palsy and Intrauterine Growth 285
Stephen Jarvis, Svetlana V. Glinianaia, and Eve Blair
When birth weight for gestation is used as a surrogate for intrauter¬
ine growth, the prevalence of cerebral palsy varies continuously in a
reversed I shape, with steep increases in the risk for infants lighter
and heavier than the optimum size. Patterns of size at birth specific
risk for cerebral palsy differ between male and female infants, as do
the patterns for more severe versus milder cases. Although these
excess risks with abnormal size at birth imply antenatal precursors, it
is not clear whether or how intrauterine growth is involved in any of
the suspected causal pathways resulting in cerebral palsy. The impli¬
cation for clinicians is that serial measures of in utero growth may
provide an important indicator of fetal health.
Risk of Cerebral Palsy in Multiple Pregnancies 301
Peter O.D. Pharoah
Multiple compared with singleton gestations have a five to ten¬
fold increased risk of CP. The increased risk associated with MC
placentation has been variously ascribed to transfer of thrombo
plastin or thromboemboli from the dead to the surviving fetus,
exsanguination of the surviving fetus into the low pressure reser¬
voir of the dead fetus, or hemodynamic instability with bidirec¬
tional shunting of blood between the two fetuses. An increased
risk of CP in assisted reproductive technology gestations is to be
expected because of the higher proportion of preterm births. The
increase in risk of CP associated with monochorionic placentation
will not be observed except for the minority of assisted reproduc¬
tive technology gestations that undergo monozygotic splitting.
Perinatal Infections and Cerebral Palsy 315
Marcus C. Hermansen and Mary Goetz Hermansen
Infections of the mother, the intrauterine environment, the fetus,
and the neonate can cause cerebral palsy through a variety of
mechanisms. Each of these processes is reviewed. The recently
viii CONTENTS
proposed theory of cytokine induced white matter brain injury
and the systemic inflammatory response syndrome with multiple
organ dysfunction syndrome is critically evaluated.
Intrapartum Asphyxia and Cerebral Palsy: Is There a Link? 335
Jeffrey M. Perlman
Perinatal hypoxic ischemic cerebral injury, secondary to interruption
of placental blood flow that results in cerebral palsy (CP), is a rare
event. The ability to link an intrapartum event to subsequent CP
should include a history of a sentinel event during labor, followed by
the delivery of a depressed acidemic infant, and the subsequent evo¬
lution of neonatal encephalopathy, systemic organ injury, and acute
neuroimaging abnormalities.
Perinatal Trauma and Cerebral Palsy 355
Michael J. Noetzel
In this article perinatal trauma is restricted to injuries that are
sustained by the infant during the labor and delivery primarily as
a result of mechanical factors, with the understanding that even
under optimal circumstances, the process of birth is traumatic.
Mechanical insults to the perinatal brain may result in primarily a
hypoxic or ischemic injury to the cerebral tissues; those conditions
are not discussed in this article. Although there are multiple types of
perinatal trauma, this article is restricted mainly to those types
that impact upon the subsequent development of cerebral palsy,
although when applicable, other adverse developmental outcomes
are mentioned.
Cerebral Palsy Secondary to Perinatal Ischemic Stroke 367
Adam Kirton and Gabrielle deVeber
Congenital hemiplegia is the most common form of cerebral palsy in
children born at term, and stroke is the number one cause. Neonatal
ischemic stroke includes perinatal arterial ischemic stroke, presumed
pre or perinatal stroke, and cerebral sinovenous thrombosis, all of
which have emerged as important contributors to cerebral palsy. Of
increasing interest is how the overlapping list of associations and
risks for stroke and cerebral palsy relate to each other. Stroke induced
injury is focal, and the preservation of normal areas of brain may
afford unique opportunities for plastic adaptation. The implications
of this essential difference are stressed in a discussion of how the epi¬
demiology, pathophysiology, diagnosis, and therapeutic advance¬
ments in perinatal stroke relate to the outcome of cerebral palsy.
CONTENTS ix
Hyperbilirubinemia and Kernicterus 387
Steven M. Shapiro, Vinod K. Bhutani, and Lois Johnson
This article describes new findings concerning the basic science of
bilirubin neurotoxicity, new considerations of the definition of clin¬
ical kernicterus, and new and useful tools to diagnose kernicterus
in older children, and discusses treatments for kernicterus beyond
the newborn period and why proper diagnosis is important.
Neurometabolic Diseases in the Newborn 411
James J. Filiano
This article is designed to be a basic introduction to neurometabolic
diseases (ie, inheritable inborn errors of metabolism, genetic dis¬
orders of developmental neural topography, and degenerative
disorders of neural function) that present in the neonate. It is
intended to assist those who provide primary care for newborns to
help them recognize signs and symptoms that signify neurometa¬
bolic disease; to teach how and when to initiate a neurometabolic
diagnostic sequence; and to help neurologists and pediatricians
interface with geneticists and metabolists. This article is intended
to inform general newborn care practitioners, not metabolists.
Therefore, pathways and concepts are presented in a simplified
manner for deliberate educational purposes.
Cerebral Palsy due to Chromosomal Anomalies and
Continuous Gene Syndromes 481
John H. Menkes and Laura Flores Sarnat
When cerebral palsy is defined as a disorder of movement and pos¬
ture that is due to nonprogressive disturbances that occur in the
developing fetal and infant brain, a significant proportion—up to
10%—is the consequence of chromosomal anomalies and continu¬
ous gene syndromes. Abnormalities of chromosomes are constitu¬
tional or acquired. Acquired chromosomal abnormalities develop
postnatally, affect only one clone of cells, and are implicated in the
evolution of neoplasia. Constitutional abnormalities develop dur¬
ing gametogenesis or early embryogenesis and affect a significant
portion of the subject s cells.
Placental Pathology and Cerebral Palsy 503
Raymond W. Redline
Recent classification systems of cerebral palsy call for an assess¬
ment of the timing and etiology of brain injury. The placenta is an
underused resource for addressing these important questions. An
expert assessment of the placental pathology can provide tempo¬
rally and mechanistically specific data not available from any other
source. Key concepts for an understanding of the role of placental
v CONTENTS
pathology are the sentinel lesion, the high prevalence of throm
boinflammatory lesions affecting large fetal placental vessels, the
significance of underlying placental reserve, and the realization
that placental findings can serve as markers for processes occur¬
ring in the mother or fetus.
Neuroimaging Evaluation of Cerebral Palsy 517
Robert A. Zimmerman and Larissa T. Bilaniuk
MRI can demonstrate and differentiate the various insults and anom¬
alies that can be responsible for cerebral palsy. Recent advances have
resulted in techniques and sequences that allow prompt detection of
cytotoxic edema and evaluation of brain perfusion. MRI precisely
demonstrates the various patterns of injury, distinguishing insults
owing to profound asphyxia, partial prolonged asphyxia, and
mixed partial prolonged and profound asphyxia. Infants and chil¬
dren can be studied with MRI, and ultrafast MRI permits evalua¬
tion of the fetal central nervous system. In the fetus, the cause of
ventriculomegaly can be determined, such as cerebrospinal fluid
flow obstruction, brain malformation, or brain destruction with or
without hemorrhage. Results from fetal MRI have led to better
understanding of many brain abnormalities.
Cerebral Palsy Life Expectancy 545
J.L. Hutton
The life expectancy of people who have perinatally acquired cere¬
bral palsy can be similar to that of the general population, or it can
be reduced substantially. The most important factors that are asso¬
ciated with reduced survival are disabilities of motor, cognitive, or
visual functions. Prematurity and low birth weight are associated
with lower rates of disability, and better survival. A 2 year old who
has severe cerebral palsy has about a 40% chance of living to age
20, in contrast to a child who has mild cerebral palsy, for whom the
chance is 99%. Cerebral palsy, respiratory diseases, epilepsy, and
congenital malformation are the most commonly recorded causes
of early death.
Erratum 557
Index 559
CONTENTS xi
|
| adam_txt |
Pf mATALCAbSJAOI LfcREBRM PAI^
CONTENTS
Preface xv
Marcus C. Hermansen
Historical Perspectives on the Etiology of Cerebral Palsy 233
Tonse N.K. Raju
This essay presents the early history on the evolution of concepts
about the etiology of cerebral palsy, especially the contributions of
the early pioneers. Insight into how they derived their hypotheses,
including the errors they made, can help one understand the com¬
plex processes of deciphering etiologic associations.
The Descriptive Epidemiology of Cerebral Palsy 251
Nigel Paneth, Ting Hong, and Steven Korzeniewski
The prevalence of cerebral palsy (CP) ranges from 1.5 to 2.5 per
1000 live births with little or no variation among western nations,
although data from the Americas are sparse. Time trends in over¬
all CP prevalence for the past 40 years are most notable for their
stability, but a modest increase in prevalence probably occurred in
the last decades of the twentieth century. European countries have
pioneered the development of CP registries, and as a result, CP is
a condition that is enumerated regularly in several parts of the
world. The United States has no CP registries, although ongoing
surveillance of CP, along with other developmental disabilities, is
performed by the Centers for Disease Control and Prevention in
metropolitan Atlanta.
The Panorama of Cerebral Palsy After Very and Extremely
Preterm Birth: Evidence and Challenges 269
Michael E. Msall
During the past 2 decades, major advances in maternal fetal medi¬
cine and neonatology have resulted in unprecedented survival of
VOLUME 33 . NUMBER 2 • JUNE 2006 vii
very preterm ( 32 weeks) and extremely preterm ( 28 weeks)
babies. Despites these advances in prenatal care, neurodevelop
mental motor impairment remains a substantial sequela. This arti¬
cle describes the major progress and challenges in understanding
pathways of preterm children who go on to have one of the cere¬
bral palsy syndromes. The contributions of chronic lung disease,
intraventricular hemorrhage, retinopathy of prematurity, and post¬
natal steroids are analyzed. Management can then be directed to
limiting the comorbidities that are associated with threats to sur¬
vival and to improving protection of central nervous system func¬
tions that are involved in moving, manipulative skills, feeding,
communication, and learning.
Cerebral Palsy and Intrauterine Growth 285
Stephen Jarvis, Svetlana V. Glinianaia, and Eve Blair
When birth weight for gestation is used as a surrogate for intrauter¬
ine growth, the prevalence of cerebral palsy varies continuously in a
reversed I shape, with steep increases in the risk for infants lighter
and heavier than the optimum size. Patterns of size at birth specific
risk for cerebral palsy differ between male and female infants, as do
the patterns for more severe versus milder cases. Although these
excess risks with abnormal size at birth imply antenatal precursors, it
is not clear whether or how intrauterine growth is involved in any of
the suspected causal pathways resulting in cerebral palsy. The impli¬
cation for clinicians is that serial measures of in utero growth may
provide an important indicator of fetal health.
Risk of Cerebral Palsy in Multiple Pregnancies 301
Peter O.D. Pharoah
Multiple compared with singleton gestations have a five to ten¬
fold increased risk of CP. The increased risk associated with MC
placentation has been variously ascribed to transfer of thrombo
plastin or thromboemboli from the dead to the surviving fetus,
exsanguination of the surviving fetus into the low pressure reser¬
voir of the dead fetus, or hemodynamic instability with bidirec¬
tional shunting of blood between the two fetuses. An increased
risk of CP in assisted reproductive technology gestations is to be
expected because of the higher proportion of preterm births. The
increase in risk of CP associated with monochorionic placentation
will not be observed except for the minority of assisted reproduc¬
tive technology gestations that undergo monozygotic splitting.
Perinatal Infections and Cerebral Palsy 315
Marcus C. Hermansen and Mary Goetz Hermansen
Infections of the mother, the intrauterine environment, the fetus,
and the neonate can cause cerebral palsy through a variety of
mechanisms. Each of these processes is reviewed. The recently
viii CONTENTS
proposed theory of cytokine induced white matter brain injury
and the systemic inflammatory response syndrome with multiple
organ dysfunction syndrome is critically evaluated.
Intrapartum Asphyxia and Cerebral Palsy: Is There a Link? 335
Jeffrey M. Perlman
Perinatal hypoxic ischemic cerebral injury, secondary to interruption
of placental blood flow that results in cerebral palsy (CP), is a rare
event. The ability to link an intrapartum event to subsequent CP
should include a history of a sentinel event during labor, followed by
the delivery of a depressed acidemic infant, and the subsequent evo¬
lution of neonatal encephalopathy, systemic organ injury, and acute
neuroimaging abnormalities.
Perinatal Trauma and Cerebral Palsy 355
Michael J. Noetzel
In this article "perinatal trauma" is restricted to injuries that are
sustained by the infant during the labor and delivery primarily as
a result of mechanical factors, with the understanding that even
under optimal circumstances, the process of birth is traumatic.
Mechanical insults to the perinatal brain may result in primarily a
hypoxic or ischemic injury to the cerebral tissues; those conditions
are not discussed in this article. Although there are multiple types of
perinatal trauma, this article is restricted mainly to those types
that impact upon the subsequent development of cerebral palsy,
although when applicable, other adverse developmental outcomes
are mentioned.
Cerebral Palsy Secondary to Perinatal Ischemic Stroke 367
Adam Kirton and Gabrielle deVeber
Congenital hemiplegia is the most common form of cerebral palsy in
children born at term, and stroke is the number one cause. Neonatal
ischemic stroke includes perinatal arterial ischemic stroke, presumed
pre or perinatal stroke, and cerebral sinovenous thrombosis, all of
which have emerged as important contributors to cerebral palsy. Of
increasing interest is how the overlapping list of associations and
risks for stroke and cerebral palsy relate to each other. Stroke induced
injury is focal, and the preservation of normal areas of brain may
afford unique opportunities for plastic adaptation. The implications
of this essential difference are stressed in a discussion of how the epi¬
demiology, pathophysiology, diagnosis, and therapeutic advance¬
ments in perinatal stroke relate to the outcome of cerebral palsy.
CONTENTS ix
Hyperbilirubinemia and Kernicterus 387
Steven M. Shapiro, Vinod K. Bhutani, and Lois Johnson
This article describes new findings concerning the basic science of
bilirubin neurotoxicity, new considerations of the definition of clin¬
ical kernicterus, and new and useful tools to diagnose kernicterus
in older children, and discusses treatments for kernicterus beyond
the newborn period and why proper diagnosis is important.
Neurometabolic Diseases in the Newborn 411
James J. Filiano
This article is designed to be a basic introduction to neurometabolic
diseases (ie, inheritable inborn errors of metabolism, genetic dis¬
orders of developmental neural topography, and degenerative
disorders of neural function) that present in the neonate. It is
intended to assist those who provide primary care for newborns to
help them recognize signs and symptoms that signify neurometa¬
bolic disease; to teach how and when to initiate a neurometabolic
diagnostic sequence; and to help neurologists and pediatricians
interface with geneticists and metabolists. This article is intended
to inform general newborn care practitioners, not metabolists.
Therefore, pathways and concepts are presented in a simplified
manner for deliberate educational purposes.
Cerebral Palsy due to Chromosomal Anomalies and
Continuous Gene Syndromes 481
John H. Menkes and Laura Flores Sarnat
When cerebral palsy is defined as a disorder of movement and pos¬
ture that is due to nonprogressive disturbances that occur in the
developing fetal and infant brain, a significant proportion—up to
10%—is the consequence of chromosomal anomalies and continu¬
ous gene syndromes. Abnormalities of chromosomes are constitu¬
tional or acquired. Acquired chromosomal abnormalities develop
postnatally, affect only one clone of cells, and are implicated in the
evolution of neoplasia. Constitutional abnormalities develop dur¬
ing gametogenesis or early embryogenesis and affect a significant
portion of the subject's cells.
Placental Pathology and Cerebral Palsy 503
Raymond W. Redline
Recent classification systems of cerebral palsy call for an assess¬
ment of the timing and etiology of brain injury. The placenta is an
underused resource for addressing these important questions. An
expert assessment of the placental pathology can provide tempo¬
rally and mechanistically specific data not available from any other
source. Key concepts for an understanding of the role of placental
v CONTENTS
pathology are the "sentinel lesion," the high prevalence of throm
boinflammatory lesions affecting large fetal placental vessels, the
significance of underlying placental reserve, and the realization
that placental findings can serve as markers for processes occur¬
ring in the mother or fetus.
Neuroimaging Evaluation of Cerebral Palsy 517
Robert A. Zimmerman and Larissa T. Bilaniuk
MRI can demonstrate and differentiate the various insults and anom¬
alies that can be responsible for cerebral palsy. Recent advances have
resulted in techniques and sequences that allow prompt detection of
cytotoxic edema and evaluation of brain perfusion. MRI precisely
demonstrates the various patterns of injury, distinguishing insults
owing to profound asphyxia, partial prolonged asphyxia, and
mixed partial prolonged and profound asphyxia. Infants and chil¬
dren can be studied with MRI, and ultrafast MRI permits evalua¬
tion of the fetal central nervous system. In the fetus, the cause of
ventriculomegaly can be determined, such as cerebrospinal fluid
flow obstruction, brain malformation, or brain destruction with or
without hemorrhage. Results from fetal MRI have led to better
understanding of many brain abnormalities.
Cerebral Palsy Life Expectancy 545
J.L. Hutton
The life expectancy of people who have perinatally acquired cere¬
bral palsy can be similar to that of the general population, or it can
be reduced substantially. The most important factors that are asso¬
ciated with reduced survival are disabilities of motor, cognitive, or
visual functions. Prematurity and low birth weight are associated
with lower rates of disability, and better survival. A 2 year old who
has severe cerebral palsy has about a 40% chance of living to age
20, in contrast to a child who has mild cerebral palsy, for whom the
chance is 99%. Cerebral palsy, respiratory diseases, epilepsy, and
congenital malformation are the most commonly recorded causes
of early death.
Erratum 557
Index 559
CONTENTS xi |
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| genre | (DE-588)4143413-4 Aufsatzsammlung gnd-content |
| genre_facet | Aufsatzsammlung |
| id | DE-604.BV021671156 |
| illustrated | Illustrated |
| index_date | 2024-07-02T15:08:50Z |
| indexdate | 2024-07-09T20:41:17Z |
| institution | BVB |
| isbn | 1416035435 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-014885514 |
| oclc_num | 70881545 |
| open_access_boolean | |
| owner | DE-355 DE-BY-UBR DE-19 DE-BY-UBM DE-20 |
| owner_facet | DE-355 DE-BY-UBR DE-19 DE-BY-UBM DE-20 |
| physical | XVI S., S. 233 - 572 Ill. |
| publishDate | 2006 |
| publishDateSearch | 2006 |
| publishDateSort | 2006 |
| publisher | Saunders |
| record_format | marc |
| series | Clinics in perinatology |
| series2 | Clinics in perinatology |
| spelling | Perinatal causes of cerebral palsy guest ed.: Marcus C. Hermansen Philadelphia [u.a.] Saunders 2006 XVI S., S. 233 - 572 Ill. txt rdacontent n rdamedia nc rdacarrier Clinics in perinatology 33,2 Cerebral Palsy etiology Cerebral palsy Etiology Perinatology Perinatale Medizin (DE-588)4045170-7 gnd rswk-swf Cerebrale Kinderlähmung (DE-588)4147490-9 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Cerebrale Kinderlähmung (DE-588)4147490-9 s Perinatale Medizin (DE-588)4045170-7 s b DE-604 Hermansen, Marcus C. Sonstige oth Clinics in perinatology 33,2 (DE-604)BV000003382 33,2 HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=014885514&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Perinatal causes of cerebral palsy Clinics in perinatology Cerebral Palsy etiology Cerebral palsy Etiology Perinatology Perinatale Medizin (DE-588)4045170-7 gnd Cerebrale Kinderlähmung (DE-588)4147490-9 gnd |
| subject_GND | (DE-588)4045170-7 (DE-588)4147490-9 (DE-588)4143413-4 |
| title | Perinatal causes of cerebral palsy |
| title_auth | Perinatal causes of cerebral palsy |
| title_exact_search | Perinatal causes of cerebral palsy |
| title_exact_search_txtP | Perinatal causes of cerebral palsy |
| title_full | Perinatal causes of cerebral palsy guest ed.: Marcus C. Hermansen |
| title_fullStr | Perinatal causes of cerebral palsy guest ed.: Marcus C. Hermansen |
| title_full_unstemmed | Perinatal causes of cerebral palsy guest ed.: Marcus C. Hermansen |
| title_short | Perinatal causes of cerebral palsy |
| title_sort | perinatal causes of cerebral palsy |
| topic | Cerebral Palsy etiology Cerebral palsy Etiology Perinatology Perinatale Medizin (DE-588)4045170-7 gnd Cerebrale Kinderlähmung (DE-588)4147490-9 gnd |
| topic_facet | Cerebral Palsy etiology Cerebral palsy Etiology Perinatology Perinatale Medizin Cerebrale Kinderlähmung Aufsatzsammlung |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=014885514&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
| volume_link | (DE-604)BV000003382 |
| work_keys_str_mv | AT hermansenmarcusc perinatalcausesofcerebralpalsy |