Cerebral Palsy: Medical Aspects

Dodge, Nancy N.

doi:10.1016/j.pcl.2008.07.003

Cited by 38 publications

(20 citation statements)

References 87 publications

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“…[4] These difficulties may include difficulty falling asleep, frequent night awakening, and sleep schedule that does not fit the needs of school or family. [12] Sleep problems in children with CP are under-reported, under recognized, and under-treated. [6] Studies regarding sleep in children with CP are rare due to absence of more simplified methods of assessment rather than polysomnography.…”

Section: Discussionmentioning

confidence: 99%

Sleep assessment of children with cerebral palsy: Using validated sleep questionnaire

Elsayed

Hasanein

Sayyah

et al. 2013

Ann Indian Acad Neurol

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Background:On the basis of clinical experience, it seems that sleep disturbances are common in children with cerebral palsy (CP); however, there is a lack of research and objective data to support this observation.Aim of Work:Our aim was to assess sleep of children with cerebral palsy, using validated sleep questionnaire.Subjects and Methods:one hundred children with diagnosis of CP were investigated via sleep questionnaires, with their ages from 2-12 years. The 100 children with CP were divided into two groups, pre-school group (52 children had a mean age 2.35 ± 1.04 years) and school ages group (48 children had a mean age 10.21 ± 3.75 years).Results:We found high incidence of sleep problem in both pre-school and school age groups. We found that pre-school children have more prevalence of early insomnia (46.2%, P value 0.028) and sleep bruxism (50%, P value 0.000), while school group suffer more sleep disordered breathing (SDB) (50%, P value 0.001), more nightmares (50%, P value 0.001), more sleep talking (12.5% P value 0.049), and more excessive daytime sleepiness (EDS) (62.5%, P value 0.001).Conclusion:Results of our study indicate that CP children have high incidence of sleep problem in both pre-school and school age groups.

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Section: Discussionmentioning

confidence: 99%

Sleep assessment of children with cerebral palsy: Using validated sleep questionnaire

Elsayed

Hasanein

Sayyah

et al. 2013

Ann Indian Acad Neurol

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“…The pathophysiology of CP is not fully understood, but might be related to events that occur during neural development triggered by pre‐, peri‐ or postnatal factors . The main prenatal factor in the aetiology of CP is infections . Preterm birth and intrapartum asphyxia increase the risk of developing CP during the perinatal period .…”

Section: Introductionmentioning

confidence: 99%

“…Preterm birth and intrapartum asphyxia increase the risk of developing CP during the perinatal period . Postnatal causes include infections, trauma and anoxic injury . Considering these risk factors, experimental models have been proposed to establish a protocol of CP using insults of prenatal exposure to lipopolysaccharide (LPS; the structural component of most Gram‐negative bacteria), perinatal anoxia and sensorimotor restriction .…”

Section: Introductionmentioning

confidence: 99%

Morphofunctional characteristics of skeletal muscle in rats with cerebral palsy

Buratti

Covatti

Centenaro

et al. 2019

Int J Experimental Path

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Summary Knowledge of skeletal muscle adaptations is important to understand the functional deficits in cerebral palsy (CP). This study aimed to investigate the morphofunctional characteristics of skeletal muscle in a CP animal model. Initially, pregnant Wistar rats were injected intraperitoneally with saline or lipopolysaccharide over the last five days of pregnancy. The control group (n = 8) consisted of male pups born to females injected with saline. The CP group (n = 8) consisted of male pups born to females injected with lipopolysaccharide, which were submitted to perinatal anoxia [day of birth, postnatal day 0 (P0)] and sensorimotor restriction (P1‐P30). The open‐field test was undertaken on P29 and P45. On P48, the animals were weighed, and the plantaris muscle was collected and its weight and length were measured. Transverse sections were stained with haematoxylin‐eosin, NADH‐TR, Masson's trichrome and non‐specific esterase reaction for analysis. and transmission electron microscopy was performed. In the CP group, reductions were observed in mobility time, number of crossings and rearing frequency, body weight, muscle weight and length, and nucleus‐to‐fibre and capillary‐to‐fibre ratios. There was a statistically significant increase in the percentage area of the muscle section occupied by collagen; reduction in the area and increase in the number of type I muscle fibres; increase in myofibrillar disorganization and Z‐line disorganization and dissolution; and reduction in the area and largest and smallest diameters of neuromuscular junctions. Thus this animal model of CP produced morphofunctional alterations in skeletal muscle, that were associated with evidence of motor deficits as demonstrated by the open‐field test.

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“…All patients underwent treatment at the neuropediatric's department of the Centro de Rehabilitación Integral Teleton (CRIT) in Tlalnepanltla, Estado de México. Clinical manifestations of cerebral palsy have been described previously [26,27]. All individuals were between 7-14 years old with a mean age of cerebral palsy patients and control group at 14.3 and 12.6 years, respectively.…”

Section: Subjectsmentioning

confidence: 99%

Association of a Functional Inducible Nitric Oxide Synthase Promoter Variant with Susceptibility to Infantile Cerebral Palsy

HN¹

2015

J Neurol Disord

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IntroductionThe hypoxic ischemic encephalopathy (HIE) secondary to perinatal asphyxia, affects a 1.5 to 5% of newborns; unfortunately 10% to 20% of infants with moderate HIE die and 30% to 40% develop neurological abnormalities, whilst 50% of infants with severe HIE, die and the remainder develop neurological conditions [1]. To our knowledge, the reason why some children that suffered perinatal asphysxia develop infant cerebral palsy while other children with similar clinical histories develop memory and learning difficulties but no motor disabilities remains unknown. Infantile cerebral palsy (ICP) is a neurological disease resulting from damage of the immature brain in newborn children, clinically it is a non-progressive brain insult that produces permanent and progressive secondary postural and movement disorders [2] and induces long-term complications such as muscle hypotrophy, deformities in the skull and spine [3]. In Mexico there are approximately 500,000 diagnosed cases of CP, be the leading cause of death in children from 5 to 14 years old [4] and it is the most common cause of physical disability in children throughout the world [5]. The main clinical spectrum of ICP includes quadriparesis, hemiparesis, and diparesis that affect upper and lower limbs to varying degrees. The therapeutic management of ICP is targeted at the lesions caused on the central nervous system, bone deformations and muscle hypotrophy [6]. The initial inflammatory response in the immature brain as a result of a traumatic birth can be mapped from proteins and metabolites that participate in inflammation and oxidative stress [7,8]. The main oxidative metabolite which is produced in the inflammatory response is the Nitric oxide (NO), it is a multifunctional molecule that has been Abstract Background: Recently it has been shown an increase in the interleukin 1 beta and nitrite levels in cerebrospinal fluid as a primary response of the immature brain to oxygen deprivation in newborns that suffered perinatal asphyxia, 30% to 40% of these patients later develop neurological abnormalities incluiding cerebral palsy. Formerly was shown that an increased enzyme activity of NOS2 is responsible for the increase in nitrite levels in cerebrospinal fluid. The NOS2A gene has a polymorphic microsatellite (CCTTT) n located at -2.6 Kb from the gene promoter. The expansion of this microsatellite to 13 or 14 repeats increases transcription of the NOS2A gene and triples the nitric oxide level under hypoglycemia and hypoxia conditions. The study aim was shown that the expansion of -2.6 Kb CCTTT microsatellite in the NOS2 gene promoter, constitutes a risk factor for developing cerebral palsy in newborns that suffered perinatal asphyxia

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Cerebral Palsy: Medical Aspects

Cited by 38 publications

References 87 publications

Sleep assessment of children with cerebral palsy: Using validated sleep questionnaire

Sleep assessment of children with cerebral palsy: Using validated sleep questionnaire

Morphofunctional characteristics of skeletal muscle in rats with cerebral palsy

Association of a Functional Inducible Nitric Oxide Synthase Promoter Variant with Susceptibility to Infantile Cerebral Palsy

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