Inflammatory-mediated model of cerebral palsy with developmental sequelae

Toso, Laura; Poggi, Sarah; Park, Jane; Einat, Haim; Roberson, Robin; Dunlap, Veronica; Woodard, Jade; Abebe, Daniel; Spong, Catherine Y.

doi:10.1016/j.ajog.2005.05.072

Cited by 26 publications

(21 citation statements)

References 28 publications

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“…At 4 months, there is no more locomotor dysfunction observable. These results suggest that motor disorders observed in the first weeks improve and confirm the results of two previous studies showing that initially observed motor disorders disappear with time [13,21]. The functional deficiency observed at different tasks is not permanent.…”

Section: Discussionsupporting

confidence: 81%

“…In a schizophrenia model, maternal administration of LPS at 18 and 19 days of gestation increases motor disorders and reactivity induced by amphetamine injections in adulthood [19]. Two studies from the same group demonstrate opposite results depending on whether they induced acute (showing no behavioral phenotype) [20] or chronic (leading to developmental sequelae) [21] inflammation in the dam. Finally, maternal intrauterine endotoxin administration leads to early motor deficits in the newborn rabbit, resulting in a phenotype that resembles those found in cystic periventricular leukomalacia (PVL) and CP [22,23].…”

Section: Introductionmentioning

confidence: 99%

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Maternal Exposure to Lipopolysaccharide Leads to Transient Motor Dysfunction in Neonatal Rats

Rousset

Kassem²,

Aubert³

et al. 2013

Dev Neurosci

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Epidemiological and experimental data implicate maternal infection and inflammation in the etiology of brain white matter injury, which may lead to cerebral palsy in preterm newborns. Our aim was to investigate motor development of the offspring after maternal administration of lipopolysaccharide (LPS). Wistar rats were intraperitoneally injected with Escherichia coli LPS or saline on gestational days 19 and 20. From birth to 3 weeks, pups were tested for neurobehavioral development, neurological signs and reflexes. From 3 to 6 weeks, motor coordination was investigated. At 4 months, animals were tested for locomotion. Brain myelination was assessed by myelin basic protein immunohistochemistry. Days of appearance of several neurological reflexes were significantly delayed, and neonate LPS pups displayed retarded performance in righting, gait and negative geotaxis. At the juvenile stage, LPS animals showed important impairment in coordination. However, although the LPS group performed worse in most tests, they reached vehicle levels by 5 weeks. At 4 months, LPS animals did not show variations in locomotion performances compared to vehicle. No myelination differences have been observed in the brains at adulthood. Maternal LPS administration results in delayed motor development even though these alterations fade to reach control level by 5 weeks. Motor impairments observed at the early stage in this study could be linked to previously reported hypomyelination of the white matter induced by maternal LPS challenge in the neonates. Finally, the normal myelination shown here at adulthood may explain the functional recovery of the animals and suggest either a potential remyelination of the brain or a delayed myelination in LPS pups.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Maternal Exposure to Lipopolysaccharide Leads to Transient Motor Dysfunction in Neonatal Rats

Rousset

Kassem²,

Aubert³

et al. 2013

Dev Neurosci

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“…Studies of the effect of infective agents on brain function, however, are not entirely consistent, and there are recent reports of either no neonatal cerebral palsy phenotype associated with low-dose lipopolysaccharide administration [44 •• ], or an early abnormal phenotype, which then becomes compensated in adult rats [45]. These recent data highlight a lack of precise phenotypic characterization in some previous work, which may be important in determining the relevance of documentable [46] brain lesions.…”

Section: Experimental Studiesmentioning

confidence: 93%

Perinatal infections, prematurity and brain injury

Edwards

Tan

2006

Current Opinion in Pediatrics

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“…Toso et al [19] used the rat model to explore the potential for inflammatory mediated CP. Using serial intracervical injections of lipopolysaccharide at the equivalents of 28-36 weeks in human pregnancy they showed biochemical evidence of oligodendrocyte damage and delay in some motor milestones.…”

Section: Infection Inflammation and Hypoxiamentioning

confidence: 99%

The origins of cerebral palsy

Keogh

Badawi²

2006

Current Opinion in Neurology

102

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Papers this year have helped clarify risk groups and identify some areas (e.g. the management of thrombophilias and the potential of induced hypothermia) with the potential to be rapidly introduced into clinical practice. In this enigmatic and multifactorial condition, however, progress remains slow. New tools such as magnetic resonance imaging are providing valuable insights into the lesions that result in cerebral palsy but the pathways to injury remain unclear. The future of cerebral palsy research lies in understanding the complex interactions of multiple factors on the road to cerebral palsy or in looking for final common pathways such as inflammation which may be amenable to manipulation.

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Inflammatory-mediated model of cerebral palsy with developmental sequelae

Cited by 26 publications

References 28 publications

Maternal Exposure to Lipopolysaccharide Leads to Transient Motor Dysfunction in Neonatal Rats

Maternal Exposure to Lipopolysaccharide Leads to Transient Motor Dysfunction in Neonatal Rats

Perinatal infections, prematurity and brain injury

The origins of cerebral palsy

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