scholarly journals Magnitude of [11C]PK11195 Binding Is Related to Severity of Motor Deficits in a Rabbit Model of Cerebral Palsy Induced by Intrauterine Endotoxin Exposure

2011 ◽  
Vol 33 (3-4) ◽  
pp. 231-240 ◽  
Author(s):  
Sujatha Kannan ◽  
Fadoua Saadani-Makki ◽  
Bindu Balakrishnan ◽  
Pulak Chakraborty ◽  
James Janisse ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Rabbit Model ◽  
Motor Deficits ◽  
Endotoxin Exposure

scholarly journals Intrauterine administration of endotoxin leads to motor deficits in a rabbit model: a link between prenatal infection and cerebral palsy

2008 ◽  
Vol 199 (6) ◽  
pp. 651.e1-651.e7 ◽  
Author(s):  
Fadoua Saadani-Makki ◽  
Sujatha Kannan ◽  
Xin Lu ◽  
James Janisse ◽  
Elizabeth Dawe ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Rabbit Model ◽  
Motor Deficits ◽  
Prenatal Infection

scholarly journals Enhanced nociception in a rabbit model of cerebral palsy

2021 ◽  
Author(s):  
Emily J Reedich ◽  
Landon T Genry ◽  
Clarissa Fantin Cavarsan ◽  
Elvia Mena Avila ◽  
Meredith A. Singer ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Thermal Sensitivity ◽  
Rabbit Model ◽  
Zealand White Rabbit ◽  
Motor Deficits ◽  
Motor Circuits ◽  
Calcitonin Gene ◽  
Isolectin B4 ◽  
The Relationship ◽  
Two Populations

The most prevalent comorbidity of cerebral palsy (CP) is pain. In order to investigate the relationship between perinatal injuries that cause CP and nociception, we investigated mechanical and thermal sensitivity of New Zealand White rabbit kits after prenatal hypoxia-ischemia (HI), sham surgery without hypoxia, and after a typical, unperturbed gestation. A range of motor deficits were observed in kits born naturally after HI (40 minutes at 70-80% gestation) as previously described. We found that HI caused mechanical and thermal allodynia at postnatal day 5, which was accompanied by an expansion of peptidergic afferents (marked by expression of calcitonin gene related peptide; CGRP) in both the superficial and deep dorsal horn. Non-peptidergic afferents (marked by expression of isolectin B4; IB4) were unaltered in HI kits but overlap of the two populations (peptidergic and nonpeptidergic nociceptors) was increased by HI. Interestingly, HI-subjected rabbits exhibited allodynia, even in the absence of motor deficits. HI motor affected and unaffected kits had similar thermal sensitivity but affected kits had less mechanical sensitivity than HI unaffected kits. These findings suggest that prenatal neural injuries impact sensory and motor networks independently and that developing sensory circuits may be more vulnerable than motor circuits to perturbation by prenatal hypoxic-ischemic injury. In conclusion, pain experienced by individuals with CP could arise from developmental insults capable of causing the condition, and therapeutics that specifically target altered nociception in these individuals could be beneficial for treating and preventing chronic pain.

P284 Predicting motor deficits in children with cerebral palsy

2017 ◽  
Author(s):  
Ermolina YV ◽  
Namazova-Baranova LS ◽  
Mamedyarov AM ◽  
Anikin AV ◽  
Maslova OI
Keyword(s):  
Cerebral Palsy ◽  
Motor Deficits ◽  
Children With Cerebral Palsy

scholarly journals Maternal Inflammation Results in Altered Tryptophan Metabolism in Rabbit Placenta and Fetal Brain

2017 ◽  
Vol 39 (5) ◽  
pp. 399-412 ◽  
Author(s):  
Monica Williams ◽  
Zhi Zhang ◽  
Elizabeth Nance ◽  
Julia L. Drewes ◽  
Wojciech G. Lesniak ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Microglial Activation ◽  
Rabbit Model ◽  
Fetal Brain ◽  
Kynurenine Pathway ◽  
Tryptophan Metabolism ◽  
Maternal Inflammation ◽  
Newborn Brain ◽  
Tryptophan Pathway ◽  
Tryptophan Metabolites

Maternal inflammation has been linked to neurodevelopmental and neuropsychiatric disorders such as cerebral palsy, schizophrenia, and autism. We had previously shown that intrauterine inflammation resulted in a decrease in serotonin, one of the tryptophan metabolites, and a decrease in serotonin fibers in the sensory cortex of newborns in a rabbit model of cerebral palsy. In this study, we hypothesized that maternal inflammation results in alterations in tryptophan pathway enzymes and metabolites in the placenta and fetal brain. We found that intrauterine endotoxin administration at gestational day 28 (G28) resulted in a significant upregulation of indoleamine 2,3-dioxygenase (IDO) in both the placenta and fetal brain at G29 (24 h after treatment). This endotoxin-mediated IDO induction was also associated with intense microglial activation, an increase in interferon gamma expression, and increases in kynurenine and the kynurenine pathway metabolites kynurenine acid and quinolinic acid, as well as a significant decrease in 5-hydroxyindole acetic acid (a precursor of serotonin) levels in the periventricular region of the fetal brain. These results indicate that maternal inflammation shunts tryptophan metabolism away from the serotonin to the kynurenine pathway, which may lead to excitotoxic injury along with impaired development of serotonin-mediated thalamocortical fibers in the newborn brain. These findings provide new targets for prevention and treatment of maternal inflammation-induced fetal and neonatal brain injury leading to neurodevelopmental disorders such as cerebral palsy and autism.

Cerebral Palsy for the Pediatric Eye Care Team—Part II: Diagnosis and Treatment of Ocular Motor Deficits

2006 ◽  
Vol 56 (1) ◽  
pp. 86-96 ◽  
Author(s):  
Jorie Jackson ◽  
Claire Castleberry ◽  
Mario Galli ◽  
Kyle A. Arnoldi
Keyword(s):  
Cerebral Palsy ◽  
Care Team ◽  
Diagnosis And Treatment ◽  
Motor Deficits ◽  
Ocular Motor ◽  
Eye Care

Does Co-occurred Cerebral Palsy Change the Prognosis of West Syndrome?

2019 ◽  
Vol 51 (01) ◽  
pp. 030-036
Author(s):  
Eszter Nagy ◽  
Nelli Farkas ◽  
Katalin Hollódy
Keyword(s):  
Cerebral Palsy ◽  
West Syndrome ◽  
Motor Deficits ◽  
Brain Malformation ◽  
Motor Disability ◽  
Brain Malformations ◽  
Causative Factors ◽  
Severe Motor ◽  
Magnetic Resonance Imaging Mri ◽  
Cerebrovascular Insult

Abstract Aim We aimed to examine the occurrence of cerebral palsy (CP) in children with West syndrome (WS), to estimate the possible causative factors by analyzing the neuroimaging examinations of patients, to evaluate their cognitive/motor function and epileptic status and to compare the prognosis of children with double pathology of WS and CP and of those without CP. Methods The clinical and magnetic resonance imaging (MRI) data of 62 patients with West syndrome were evaluated. A total of 39 of 62 patients (63%) suffered from CP (CP group). The non-CP group included 23 patients. Results Abnormal MRI was found in 55/62 (89%) patients. Main anomalies were: brain malformation (21), hypoxic-ischemic encephalopathy (13), cerebrovascular insult (8), infection (7), and other anomalies (6). In the CP group, the most common MRI abnormalities included pre/perinatal hypoxia/ischemia, brain malformation, cerebrovascular insult, and infection. In the non-CP group, brain malformations were the most frequent. Significantly more negative MRIs were found in the non-CP group. More than 60% of the patients were severely cognitively impaired, almost 90% of them had CP. Not only the occurrence of intellectual disability was lower in the non-CP group, but its severity was milder as well. A total of 78% of the children with CP had a very severe motor disability. Fifty-four percent in the CP and 67% in the non-CP group had therapy-resistant epilepsy. Conclusion WS has an especially unfavorable prognosis: cerebral anomaly was confirmed in 89% of our patients. CP was present in almost two-thirds of the children with WS, most of them had severe cognitive and motor deficits.

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