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Joseph J Volpe - One of the best experts on this subject based on the ideXlab platform.

  • periventricular white matter injury in the Premature Infant is followed by reduced cerebral cortical gray matter volume at term
    Annals of Neurology, 1999
    Co-Authors: Terrie E. Inder, Joseph J Volpe, Petra Susan Hüppi, Simon K. Warfield, Ron Kikinis, Gary P. Zientara, Patrick D. Barnes, Ferenc A. Jolesz
    Abstract:

    Periventricular white matter injury, that is, periventricular leukomalacia (PVL), the dominant form of brain injury in the Premature Infant, is the major neuropathological substrate associated with the motor and cognitive deficits observed later in such Infants. The nature of the relationship of this lesion to the subsequent cognitive deficits is unclear, but such deficits raise the possibility of cerebral cortical neuronal dysfunction. Although cortical neuronal necrosis is not a prominent feature of brain injury in Premature Infants, the possibility of a deleterious effect of PVL on subsequent cerebral cortical development has not been investigated. An advanced quantitative volumetric three-dimensional magnetic resonance imaging technique was used to measure brain tissue volumes at term in Premature Infants with earlier ultrasonographic and magnetic resonance imaging evidence of PVL (mean gestational age at birth, 28.7 ± 2.0 weeks; n = 10), in Premature Infants with normal imaging studies (mean gestational age at birth, 29.0 ± 2.1 weeks; n = 10), and in control term Infants (n = 14). Premature Infants with PVL had a marked reduction in cerebral cortical gray matter at term compared with either Premature Infants without PVL or normal term Infants (mean ± SD: PVL, 157.5 ± 41.5 ml; no PVL, 211.7 ± 25.4 ml; normal term, 218.8 ± 21.3 ml). As expected, a reduction in the volume of total brain myelinated white matter was also noted (mean ± SD: PVL, 14.5 ± 4.6 ml; no PVL, 23.1 ± 6.9 ml; normal term, 27.6 ± 10.3 ml). An apparent compensatory increase in total cerebrospinal fluid volume also was found (mean ± SD: PVL, 64.5 ± 15.2 ml; no PVL, 52.0 ± 24.1 ml; normal term, 32.9 ± 13.5 ml). PVL in the Premature Infant is shown for the first time to be followed by impaired cerebral cortical development. These findings may provide insight into the anatomical correlate for the intellectual deficits associated with PVL in the Premature Infant.

  • Periventricular White Matter Injury in the Premature Infant Is Associated with a Reduction in Cerebral Cortical Gray Matter Volume at Term
    Pediatric Research, 1999
    Co-Authors: Terrie E. Inder, Petra Susan Hüppi, Simon K. Warfield, Ron Kikinis, Gary P. Zientara, Patrick D. Barnes, Ferenc A. Jolesz, Joseph J Volpe
    Abstract:

    Periventricular White Matter Injury in the Premature Infant Is Associated with a Reduction in Cerebral Cortical Gray Matter Volume at Term

  • brain injury in the Premature Infant overview of clinical aspects neuropathology and pathogenesis
    Seminars in Pediatric Neurology, 1998
    Co-Authors: Joseph J Volpe
    Abstract:

    Brain injury in the Premature Infant is an extremely important problem, in part because of the large absolute number of Infants affected yearly. The two principal brain lesions that underlie the neurological manifestations subsequently observed in Premature Infants are periventricular hemorrhagic infarction and perlventricular leukomalacia. The emphases of this article are the neurology, neuropathology, and pathogenesis of these two lesions. Recent work suggests that the ultimate goal, prevention of the lesions, is potentially achlevable. Periventricular hemorrhagic infarction may be preventable by prevention of germinal matrix/intraventricular hemorrhage, and periventricular leukomalacia, by detection of impaired cerebrovascular autoregulation, prevention of impaired cerebral blood flow, and interruption of the cascade to oligodendroglial cell death by such agents as free-radical scavengers.

  • brain injury in the Premature Infant from pathogenesis to prevention
    Brain & Development, 1997
    Co-Authors: Joseph J Volpe
    Abstract:

    Brain injury in the Premature Infant is an extremely important problem, in part because of the large absolute number of Infants affected yearly. The two principal brain lesions that underlie the neurological manifestations subsequently observed in Premature Infants are periventricular hemorrhagic infarction and periventricular leukomalacia. The emphases of this article are the neurology, neuropathology and pathogenesis of these two lesions. Recent work suggests that the ultimate goal, prevention of the lesions, is potentially achievable. Periventricular hemorrhagic infarction may be preventable by prevention of germinal matrix-intraventricular hemorrhage, and periventricular leukomalacia, by detection of impaired cerebrovascular autoregulation, prevention of impaired cerebral blood flow and interruption of the cascade to oligodendroglial cell death by such agents as free radical scavengers.

  • brain injury in the Premature Infant neuropathology clinical aspects pathogenesis and prevention
    Clinics in Perinatology, 1997
    Co-Authors: Joseph J Volpe
    Abstract:

    Brain injury in the Premature Infant is an extremely important problem, in part because of the large absolute number of Infants affected yearly. The two principle brain lesions that underlie the neurologic manifestations subsequently observed in Premature Infants are periventricular hemorrhagic infarction and periventricular leukomalacia. The emphases of this article are the neuropathology, clinical aspects, pathogenesis, and prevention of these two lesions. Recent work suggests that the ultimate goal, prevention of the lesions, is potentially achievable. Periventricular hemorrhagic infarction may be preventable by prevention of germinal matrix-intraventricular hemorrhage and periventricular leukomalacia, by detection of impaired cerebrovascular autoregulation, prevention of impaired cerebral blood flow, and interruption of the cascade to oligodendroglial cell death by such agents as free radical scavengers.

Anna Taddio - One of the best experts on this subject based on the ideXlab platform.

Bonnie Stevens - One of the best experts on this subject based on the ideXlab platform.

  • validation of the Premature Infant pain profile revised pipp r
    Early Human Development, 2014
    Co-Authors: Bonnie Stevens, Sharyn Gibbins, Janet Yamada, Kimberley Dionne, Grace Lee, Marsha Campbellyeo, Kim Caddell, Celeste Johnston
    Abstract:

    Abstract Objectives To examine the construct validity, inter-rater reliability, and feasibility of the Premature Infant Pain Profile-Revised in Infants of varying gestational ages, diagnoses, and procedures. Methods A prospective cross-over study with Infants in three gestational age groups (26–31, 32–36, and ≥ 37 weeks) at three university-affiliated Neonatal Intensive Care Units in Canada. One hundred and ninety five bedside nurses and expert raters rated 202 hospitalized Infants' pain during scheduled procedures using the measure. An expert rater and a nurse independently assessed Infants' pain scores, using the Premature Infant Pain Profile-Revised, during 246 scheduled pairs of painful and non-painful procedures in the 202 Infants. Nurses also completed a feasibility survey on using the measure in a clinical setting. To establish construct validity, pain scores were computed during painful and non-painful procedures. Inter-rater reliability between pain experts and nurses was calculated. A 5-point Likert scale was used to measure feasibility in terms of clarity, ease of use, and time to complete. Results Irrespective of gestational age, Premature Infant Pain Profile-Revised scores were significantly higher during painful procedures (mean 6.7 [SD 3.0]) compared to non-painful procedures (mean 4.8 [SD 2.9]). There was a high degree of correlation between nurses' and experts' ratings for painful (all R2 = 0.92, p  Discussion The Premature Infant Pain Profile Revised has beginning construct validation, inter-rater reliability, and is considered feasible by clinicians. Concurrent validation studies should be considered.

  • the Premature Infant pain profile revised pipp r initial validation and feasibility
    The Clinical Journal of Pain, 2014
    Co-Authors: Bonnie Stevens, Sharyn Gibbins, Janet Yamada, Kimberley Dionne, Grace Lee, Celeste Johnston, Anna Taddio
    Abstract:

    Objectives:To describe revisions to the Premature Infant Pain Profile (PIPP) and initial construct validation and feasibility of the Premature Infant Pain Profile-Revised (PIPP-R).Methods:The PIPP was revised to enhance validity and feasibility. To validate the PIPP-R, data from 2 randomized cross-o

  • validation of the Premature Infant pain profile in the clinical setting
    The Clinical Journal of Pain, 1999
    Co-Authors: Marilyn Ballantyne, Bonnie Stevens, Mary Mcallister, Kim Dionne, Anne Jack
    Abstract:

    Abstract:Objective:The Premature Infant Pain Profile (PIPP) is a 7-indicator composite measure developed to assess acute pain in preterm and term neonates. It has been validated in studies using synchronized videotaping of Infants undergoing procedures. The purpose of this study was to establish (a)

  • Premature Infant Pain Profile: Development and Initial Validation
    The Clinical journal of pain, 1996
    Co-Authors: Bonnie Stevens, C. Celeste Johnston, Patricia Petryshen, Anna Taddio
    Abstract:

    Objective:Inadequate assessment of pain in Premature Infants is a persistent clinical problem. The objective of this research was to develop and validate a measure for assessing pain in Premature Infants that could be used by both clinicians and researchers.Design:The Premature Infant Pain Profile (

Paul A Rosenberg - One of the best experts on this subject based on the ideXlab platform.

  • the challenge of understanding cerebral white matter injury in the Premature Infant
    Neuroscience, 2014
    Co-Authors: Christopher M Elitt, Paul A Rosenberg
    Abstract:

    White matter injury in the Premature Infant leads to motor and more commonly behavioral and cognitive problems that are a tremendous burden to society. While there has been much progress in understanding unique vulnerabilities of developing oligodendrocytes over the past 30years, there remain no proven therapies for the Premature Infant beyond supportive care. The lack of translational progress may be partially explained by the challenge of developing relevant animal models when the etiology remains unclear, as is the case in this disorder. There has been an emphasis on hypoxia-ischemia and infection/inflammation as upstream etiologies, but less consideration of other contributory factors. This review highlights the evolution of white matter pathology in the Premature Infant, discusses the prevailing proposed etiologies, critically analyzes a sampling of common animal models and provides detailed support for our hypothesis that nutritional and hormonal deprivation may be additional factors playing critical and overlooked roles in white matter pathology in the Premature Infant.

Terrie E. Inder - One of the best experts on this subject based on the ideXlab platform.

  • periventricular white matter injury in the Premature Infant is followed by reduced cerebral cortical gray matter volume at term
    Annals of Neurology, 1999
    Co-Authors: Terrie E. Inder, Joseph J Volpe, Petra Susan Hüppi, Simon K. Warfield, Ron Kikinis, Gary P. Zientara, Patrick D. Barnes, Ferenc A. Jolesz
    Abstract:

    Periventricular white matter injury, that is, periventricular leukomalacia (PVL), the dominant form of brain injury in the Premature Infant, is the major neuropathological substrate associated with the motor and cognitive deficits observed later in such Infants. The nature of the relationship of this lesion to the subsequent cognitive deficits is unclear, but such deficits raise the possibility of cerebral cortical neuronal dysfunction. Although cortical neuronal necrosis is not a prominent feature of brain injury in Premature Infants, the possibility of a deleterious effect of PVL on subsequent cerebral cortical development has not been investigated. An advanced quantitative volumetric three-dimensional magnetic resonance imaging technique was used to measure brain tissue volumes at term in Premature Infants with earlier ultrasonographic and magnetic resonance imaging evidence of PVL (mean gestational age at birth, 28.7 ± 2.0 weeks; n = 10), in Premature Infants with normal imaging studies (mean gestational age at birth, 29.0 ± 2.1 weeks; n = 10), and in control term Infants (n = 14). Premature Infants with PVL had a marked reduction in cerebral cortical gray matter at term compared with either Premature Infants without PVL or normal term Infants (mean ± SD: PVL, 157.5 ± 41.5 ml; no PVL, 211.7 ± 25.4 ml; normal term, 218.8 ± 21.3 ml). As expected, a reduction in the volume of total brain myelinated white matter was also noted (mean ± SD: PVL, 14.5 ± 4.6 ml; no PVL, 23.1 ± 6.9 ml; normal term, 27.6 ± 10.3 ml). An apparent compensatory increase in total cerebrospinal fluid volume also was found (mean ± SD: PVL, 64.5 ± 15.2 ml; no PVL, 52.0 ± 24.1 ml; normal term, 32.9 ± 13.5 ml). PVL in the Premature Infant is shown for the first time to be followed by impaired cerebral cortical development. These findings may provide insight into the anatomical correlate for the intellectual deficits associated with PVL in the Premature Infant.

  • Periventricular White Matter Injury in the Premature Infant Is Associated with a Reduction in Cerebral Cortical Gray Matter Volume at Term
    Pediatric Research, 1999
    Co-Authors: Terrie E. Inder, Petra Susan Hüppi, Simon K. Warfield, Ron Kikinis, Gary P. Zientara, Patrick D. Barnes, Ferenc A. Jolesz, Joseph J Volpe
    Abstract:

    Periventricular White Matter Injury in the Premature Infant Is Associated with a Reduction in Cerebral Cortical Gray Matter Volume at Term