Some practical and theoretical issues concerning fetal brain tissue grafts as therapy for brain dysfunctions

1995 ◽  
Vol 18 (1) ◽  
pp. 36-45 ◽  
Author(s):  
Donald G. Stein ◽  
Marylou M. Glasier
Keyword(s):  
Brain Injury ◽  
Multiple Testing ◽  
Nonhuman Primates ◽  
Fetal Brain ◽  
Neural Tissue ◽  
Target Article ◽  
Tissue Grafts ◽  
Theoretical Issues ◽  
Host Brain

AbstractGrafts of embryonic neural tissue into the brains of adult patients are currently being used to treat Parkinson's disease and are under serious consideration as therapy for a variety of other degenerative and traumatic disorders. This target article evaluates the use of transplants to promote recovery from brain injury and highlights the kinds of questions and problems that must be addressed before this form of therapy is routinely applied. It has been argued that neural transplantation can promote functional recovery through the replacement of damaged nerve cells, the reestablishment of specific nerve pathways lost as a result of injury, the release of specific neurotransmitters, or the production of factors that promote neuronal growth. The latter two mechanisms, which need not rely on anatomical connections to the host brain, are open to examination for nonsurgical, less intrusive therapeutic use. Certain subjective judgments used to select patients who will receive grafts and in assessment of the outcome of graft therapy make it difficult to evaluate the procedure. In addition, little long-term assessment of transplant efficacy and effect has been done in nonhuman primates. Carefully controlled human studies, with multiple testing paradigms, are also needed to establish the efficacy of transplant therapy.

scholarly journals Transient late gestation prenatal hypoxic insult results in functional deficits but not gross neuroanatomic deficits in mice

2021 ◽  
Author(s):  
Ana G Cristancho ◽  
Elyse C Gadra ◽  
Ima M Samba ◽  
Chenying Zhao ◽  
Minhui Ouyang ◽  
...  
Keyword(s):  
Cell Death ◽  
Brain Injury ◽  
Visual Learning ◽  
Fetal Brain ◽  
Developing Brain ◽  
Late Gestation ◽  
Prenatal Hypoxia ◽  
Seizure Threshold ◽  
Intrauterine Hypoxia

Intrauterine hypoxia is a common cause of brain injury in children with a wide spectrum of long-term neurodevelopmental sequela even after milder injury that does not result in significant neuroanatomical injury. Published prenatal hypoxia models generally require many days of modest hypoxia or are invasive, difficult to replicate surgery to ligate the uterine artery. Postnatal models of neonatal hypoxic brain injury are not able to study the effects of antenatal risk factors that contribute to outcomes of hypoxia to the developing brain. In addition, the most common postnatal hypoxia models induce significant cell death and large focal neuroanatomic injury through unilateral ischemia, which is not a common pattern of injury in children. Large animal models suggest that brief transient prenatal hypoxia alone is sufficient to lead to significant functional impairment to the developing brain. Thus, to further understand the mechanisms underlying hypoxic injury to the developing brain, it is vital to develop murine models that are simple to reproduce and phenocopy the lack of neuroanatomic injury but significant functional injury seen in children affected by mild intrauterine hypoxia. Here we characterized the effect of late gestation (embryonic day 17.5) transient prenatal hypoxia on long-term anatomical and neurodevelopmental outcomes. Prenatal hypoxia induced hypoxia inducible factor 1 alpha in the fetal brain. There was no difference in gestational age at birth, litter size at birth, survival, fetal brain cell death, or long-term changes in gray or white matter between offspring after normoxia and hypoxia. However, there were several long-term functional consequences from prenatal hypoxia, including sex-dichotomous changes. Both males and females have abnormalities in repetitive behaviors, hindlimb strength, and decreased seizure threshold. Males demonstrated increased anxiety. Females have deficit in social interaction. Hypoxia did not result in motor or visual learning deficits. This work demonstrates that transient late gestation prenatal hypoxia is a simple, clinically-relevant paradigm for studying putative environmental and genetic modulators of the long-term effects of transient hypoxia on the developing brain.

Rat fetal brain tissue grafts survive and innervate host brain following five day pregraft tissue storage

1985 ◽  
Vol 60 (2) ◽  
pp. 133-137 ◽  
Author(s):  
Fred H. Gage ◽  
Patrik Brundin ◽  
Ole Isacson ◽  
Anders Björklund
Keyword(s):  
Brain Tissue ◽  
Fetal Brain ◽  
Tissue Storage ◽  
Tissue Grafts ◽  
Host Brain

scholarly journals Fetal Brain Injury in Survivors of Twin Pregnancies Complicated by Demise of One Twin: A Review

2016 ◽  
Vol 19 (3) ◽  
pp. 262-267 ◽  
Author(s):  
Fiona L. Mackie ◽  
R. Katie Morris ◽  
Mark. D. Kilby
Keyword(s):  
Brain Injury ◽  
Brain Injuries ◽  
Fetal Brain ◽  
Neurological Complications ◽  
Pathological Process ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Increased Risk ◽  
Twin Pregnancies

Perinatal mortality is increased considerably in multiple pregnancies compared to singleton pregnancies, with single intrauterine fetal demise (sIUFD) presenting a rare but unique perinatal problem. Monochorionic pregnancies are at particular risk of sIUFD due to bidirectional inter-twin placental vascular anastomoses. The resulting inter-twin blood flow can become unbalanced, causing acute and chronic inter-twin transfusion and profound anemia secondary to fetal exsanguination into the low-pressure circulation of the dead fetus. If the sIUFD occurs after 14 weeks’ gestation it is believed to have the most significant effect on the continuing pregnancy as the co-twin is at increased risk of preterm delivery, long-term neurological complications, and death. This article will focus on fetal brain injury in the surviving co-twin in the case of sIUFD, as it is the most common kind of injury in sIUFD, and one which concerns parents and may be the basis for terminating the pregnancy. We will outline how these brain injuries are thought to occur and describe potential pathophysiological mechanisms. We will discuss risk factors for brain injury in cases of sIUFD, including: chorionicity, cause of the sIUFD (spontaneous or secondary to an underlying pathological process such as twin-to-twin transfusion syndrome), gestation of delivery and how to prevent brain injury in the co-twin. We also review modes of imaging, discuss the difficulties in predicting the long-term outcome for co-twin survivors, and highlight the dearth of research in this area.

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.

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