A Critical Review of Models of Perinatal Infection

2015 ◽  
Vol 37 (4-5) ◽  
pp. 289-304 ◽  
Author(s):  
Justin M. Dean ◽  
Zhongjie Shi ◽  
Bobbi Fleiss ◽  
Katherine C. Gunn ◽  
Floris Groenendaal ◽  
...  
Keyword(s):  
Brain Injury ◽  
Time Course ◽  
Clinical Evidence ◽  
Postnatal Life ◽  
Perinatal Brain Injury ◽  
Neuroprotective Strategies ◽  
Infection And Inflammation ◽  
Precise Time ◽  
Nonspecific Inflammation

One of the central, unanswered questions in perinatology is why preterm infants continue to have such poor long-term neurodevelopmental, cognitive and learning outcomes, even though severe brain injury is now rare. There is now strong clinical evidence that one factor underlying disability may be infection, as well as nonspecific inflammation, during fetal and early postnatal life. In this review, we examine the experimental evidence linking both acute and chronic infection/inflammation with perinatal brain injury and consider key experimental determinants, including the microglia response, relative brain and immune maturity and the pattern of exposure to infection. We highlight the importance of the origin and derivation of the bacterial cell wall component lipopolysaccharide. Such experimental paradigms are essential to determine the precise time course of the inflammatory reaction and to design targeted neuroprotective strategies to protect the perinatal brain from infection and inflammation.

scholarly journals Anti-Inflammatory Therapies for Treatment of Inflammation-Related Preterm Brain Injury

2021 ◽  
Vol 22 (8) ◽  
pp. 4008
Author(s):  
Jaya D. Prasad ◽  
Katherine C. Gunn ◽  
Joanne O. Davidson ◽  
Robert Galinsky ◽  
Scott E. Graham ◽  
...  
Keyword(s):  
Brain Injury ◽  
Immune Responses ◽  
Therapeutic Strategy ◽  
Brain Cell ◽  
Neonatal Immunity ◽  
Neuroprotective Strategies ◽  
Infection And Inflammation ◽  
Anti Inflammatory ◽  
Neurobehavioral Deficits ◽  
Nonspecific Inflammation

Despite the prevalence of preterm brain injury, there are no established neuroprotective strategies to prevent or alleviate mild-to-moderate inflammation-related brain injury. Perinatal infection and inflammation have been shown to trigger acute neuroinflammation, including proinflammatory cytokine release and gliosis, which are associated with acute and chronic disturbances in brain cell survival and maturation. These findings suggest the hypothesis that the inhibition of peripheral immune responses following infection or nonspecific inflammation may be a therapeutic strategy to reduce the associated brain injury and neurobehavioral deficits. This review provides an overview of the neonatal immunity, neuroinflammation, and mechanisms of inflammation-related brain injury in preterm infants and explores the safety and efficacy of anti-inflammatory agents as potentially neurotherapeutics.

scholarly journals Post-Insult Hypothermia and Long-Term Learning and Memory Functions in a Rat Model of Perinatal Brain Injury

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 343A-343A
Author(s):  
Manhal Khilfeh ◽  
Tonse Raju ◽  
Michael Bunting ◽  
Holley Rice ◽  
Shankar Navale
Keyword(s):  
Brain Injury ◽  
Learning And Memory ◽  
Rat Model ◽  
Perinatal Brain Injury ◽  
Memory Functions

scholarly journals The Role of Cytokines and Inflammatory Cells in Perinatal Brain Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Ryan M. McAdams ◽  
Sandra E. Juul
Keyword(s):  
Preterm Birth ◽  
Brain Injury ◽  
Reperfusion Injury ◽  
Current Knowledge ◽  
Inflammatory Cells ◽  
Perinatal Brain Injury ◽  
The Common ◽  
Hypoxic Ischemic Injury

Perinatal brain injury frequently complicates preterm birth and leads to significant long-term morbidity. Cytokines and inflammatory cells are mediators in the common pathways associated with perinatal brain injury induced by a variety of insults, such as hypoxic-ischemic injury, reperfusion injury, toxin-mediated injury, and infection. This paper examines our current knowledge regarding cytokine-related perinatal brain injury and specifically discusses strategies for attenuating cytokine-mediated brain damage.

scholarly journals Intranasally Administered Exosomes from Umbilical Cord Stem Cells Have Preventive Neuroprotective Effects and Contribute to Functional Recovery after Perinatal Brain Injury

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 855 ◽  
Author(s):  
Thomi ◽  
Joerger-Messerli ◽  
Haesler ◽  
Muri ◽  
Surbek ◽  
...  
Keyword(s):  
Cell Death ◽  
Brain Injury ◽  
Neurodevelopmental Outcome ◽  
Neuronal Cell ◽  
Learning Ability ◽  
Specific Cell ◽  
Perinatal Brain Injury ◽  
Neuroprotective Effects ◽  
Cell Counts

Perinatal brain injury (PBI) in preterm birth is associated with substantial injury and dysmaturation of white and gray matter, and can lead to severe neurodevelopmental deficits. Mesenchymal stromal cells (MSC) have been suggested to have neuroprotective effects in perinatal brain injury, in part through the release of extracellular vesicles like exosomes. We aimed to evaluate the neuroprotective effects of intranasally administered MSC-derived exosomes and their potential to improve neurodevelopmental outcome after PBI. Exosomes were isolated from human Wharton’s jelly MSC supernatant using ultracentrifugation. Two days old Wistar rat pups were subjected to PBI by a combination of inflammation and hypoxia-ischemia. Exosomes were intranasally administered after the induction of inflammation and prior to ischemia, which was followed by hypoxia. Infrared-labeled exosomes were intranasally administered to track their distribution with a LI-COR scanner. Acute oligodendrocyte- and neuron-specific cell death was analyzed 24 h after injury in animals with or without MSC exosome application using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and immunohistochemical counterstaining. Myelination, mature oligodendroglial and neuronal cell counts were assessed on postnatal day 11 using immunohistochemistry, Western blot or RT-PCR. Morris water maze assay was used to evaluate the effect of MSC exosomes on long-term neurodevelopmental outcome 4 weeks after injury. We found that intranasally administered exosomes reached the frontal part of the brain within 30 min after administration and distributed throughout the whole brain after 3 h. While PBI was not associated with oligodendrocyte-specific cell death, it induced significant neuron-specific cell death which was substantially reduced upon MSC exosome application prior to ischemia. MSC exosomes rescued normal myelination, mature oligodendroglial and neuronal cell counts which were impaired after PBI. Finally, the application of MSC exosomes significantly improved learning ability in animals with PBI. In conclusion, MSC exosomes represent a novel prevention strategy with substantial clinical potential as they can be administered intranasally, prevent gray and white matter alterations and improve long-term neurodevelopmental outcome after PBI.

scholarly journals Multiple Doses of Umbilical Cord Blood Cells Improve Long‐Term Perinatal Brain Injury

2020 ◽  
Vol 9 (S1) ◽  
Author(s):  
Tayla Penny ◽  
Yen Pham ◽  
Amy Sutherland ◽  
Jamie Mihelakis ◽  
Joohyung Lee ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cord Blood ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Blood Cells ◽  
Perinatal Brain Injury ◽  
Multiple Doses ◽  
Cord Blood Cells ◽  
Umbilical Cord Blood Cells

scholarly journals Hypopituitarism after traumatic brain injury

2005 ◽  
Vol 152 (5) ◽  
pp. 679-691 ◽  
Author(s):  
Marta Bondanelli ◽  
Maria Rosaria Ambrosio ◽  
Maria Chiara Zatelli ◽  
Laura De Marinis ◽  
Ettore C degli Uberti
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Acute Phase ◽  
Clinical Evidence ◽  
Hormone Secretion ◽  
Pituitary Hormone ◽  
Pituitary Dysfunction ◽  
Cognitive Behavioural ◽  
Long Term Follow Up

Traumatic brain injury (TBI) is one of the main causes of death and disability in young adults, with consequences ranging from physical disabilities to long-term cognitive, behavioural, psychological and social defects. Post-traumatic hypopituitarism (PTHP) was recognized more than 80 years ago, but it was thought to be a rare occurrence. Recently, clinical evidence has demonstrated that TBI may frequently cause hypothalamic–pituitary dysfunction, probably contributing to a delayed or hampered recovery from TBI. Changes in pituitary hormone secretion may be observed during the acute phase post-TBI, representing part of the acute adaptive response to the injury. Moreover, diminished pituitary hormone secretion, caused by damage to the pituitary and/or hypothalamus, may occur at any time after TBI. PTHP is observed in about 40% of patients with a history of TBI, presenting as an isolated deficiency in most cases, and more rarely as complete pituitary failure. The most common alterations appear to be gonadotropin and somatotropin deficiency, followed by corticotropin and thyrotropin deficiency. Hyper- or hypoprolactinemia may also be present. Diabetes insipidus may be frequent in the early, acute phase post-TBI, but it is rarely permanent. Severity of TBI seems to be an important risk factor for developing PTHP; however, PTHP can also manifest after mild TBI. Accurate evaluation and long-term follow-up of all TBI patients are necessary in order to detect the occurrence of PTHP, regardless of clinical evidence for pituitary dysfunction. In order to improve outcome and quality of life of TBI patients, an adequate replacement therapy is of paramount importance.

Traumatic Brain Injury: A Trauma Surgeon's Perspective

2012 ◽  
Vol 22 (3) ◽  
pp. 82-89
Author(s):  
Oscar D. Guillamondegui
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Multidisciplinary Approach ◽  
Trauma Team ◽  
The United States ◽  
Long Term Outcomes ◽  
Term Care ◽  
Injured Brain ◽  
The Moment

Traumatic brain injury (TBI) is a serious epidemic in the United States. It affects patients of all ages, race, and socioeconomic status (SES). The current care of these patients typically manifests after sequelae have been identified after discharge from the hospital, long after the inciting event. The purpose of this article is to introduce the concept of identification and management of the TBI patient from the moment of injury through long-term care as a multidisciplinary approach. By promoting an awareness of the issues that develop around the acutely injured brain and linking them to long-term outcomes, the trauma team can initiate care early to alter the effect on the patient, family, and community. Hopefully, by describing the care afforded at a trauma center and by a multidisciplinary team, we can bring a better understanding to the armamentarium of methods utilized to treat the difficult population of TBI patients.

Prosodic Impairment Associated With Traumatic Brain Injury

2009 ◽  
Vol 19 (3) ◽  
pp. 97-102
Author(s):  
Billy Irwin
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Detailed Analysis ◽  
Acoustic Characteristics ◽  
Individual Variations

Abstract Purpose: This article discusses impaired prosody production subsequent to traumatic brain injury (TBI). Prosody may affect naturalness and intelligibility of speech significantly, often for the long term, and TBI may result in a variety of impairments. Method: Intonation, rate, and stress production are discussed in terms of the perceptual, physiological, and acoustic characteristics associated with TBI. Results and Conclusions: All aspects of prosodic production are susceptible to the effects of damage resulting from TBI. There are commonly associated prosodic impairments; however, individual variations in specific aspects of prosody require detailed analysis.

Sign in / Sign up

Export Citation Format

Share Document