Cerebral palsy

Department of Orthopaedic Surgery, Wake Forest University, Winston-Salem, North Carolina, United States
The Lancet (Impact Factor: 45.22). 06/2004; 363(9421):1619-31. DOI: 10.1016/S0140-6736(04)16207-7
Source: PubMed


Cerebral palsy, a range of non-progressive syndromes of posture and motor impairment, is a common cause of disability in childhood. The disorder results from various insults to different areas within the developing nervous system, which partly explains the variability of clinical findings. Management options include physiotherapy, occupational and speech therapy, orthotics, device-assisted modalities, pharmacological intervention, and orthopaedic and neurosurgical procedures. Since 1980, modification of spasticity by means of orally administered drugs, intramuscular chemodenervation agents (alcohol, phenol, botulinum toxin A), intrathecally administered drugs (baclofen), and surgery (neurectomy, rhizotomy) has become more frequent. Family-directed use of holistic approaches for their children with cerebral palsy includes the widespread adoption of complementary and alternative therapies; however, the prevalence of their use and the cost of these options are unknown. Traditional medical techniques (physiotherapy, bracing, and orthopaedic musculoskeletal surgery) remain the mainstay of treatment strategies at this time. This seminar addresses only the musculoskeletal issues associated with cerebral palsy and only indirectly discusses the cognitive, medical, and social issues associated with this diagnosis.

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    • "A widely accepted classification of CP is into phenotypes including spastic (bilateral or unilateral), dyskinetic, and ataxic–hypotonic CP (Surveillance of Cerebral Palsy in 2000; Saint Hilaire et al. 1991; Koman et al. 2004), recognizing that many patients have several neurologic findings and are best characterized as having a mixed-type CP. Dyskinetic (also called ''Extrapyramidal'') CP is characterized by abnormal movements, with fluctuating patterns of tone and posture. "
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    ABSTRACT: An ongoing challenge in children presenting with motor delay/impairment early in life is to identify neurogenetic disorders with a clinical phenotype, which can be misdiagnosed as cerebral palsy (CP). To help distinguish patients in these two groups, conventional magnetic resonance imaging of the brain has been of great benefit in "unmasking" many of these genetic etiologies and has provided important clues to differential diagnosis in others. Recent advances in molecular genetics such as chromosomal microarray and next-generation sequencing have further revolutionized the understanding of etiology by more precisely classifying these disorders with a molecular cause. In this paper, we present a review of neurogenetic disorders masquerading as cerebral palsy evaluated at one institution. We have included representative case examples children presenting with dyskinetic, spastic, and ataxic phenotypes, with the intent to highlight the time-honored approach of using clinical tools of history and examination to focus the subsequent etiologic search with advanced neuroimaging modalities and molecular genetic tools. A precise diagnosis of these masqueraders and their differentiation from CP is important in terms of therapy, prognosis, and family counseling. In summary, this review serves as a continued call to remain vigilant for current and other to-be-discovered neurogenetic masqueraders of cerebral palsy, thereby optimizing care for patients and their families.
    NeuroMolecular Medicine 10/2014; 16(4). DOI:10.1007/s12017-014-8331-9 · 3.68 Impact Factor
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    • "Improving the ability to walk or perform other functional activities is often the primary therapeutic goal for spastic diplegic children [8]. Adaptive equipment that try to compensate for reduced mobility consume a large proportion of the costs related to CP [9], thus measures that improve mobility in children with CP could potentially result in substantial savings for health care systems. "
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    ABSTRACT: Background and purpose Spastic diplegia is a common form of cerebral palsy (CP) and is characterized by spasticity and muscle weakness of both lower limbs resulting in decreased walking ability. The purpose of this study was to evaluate the effect of whole body vibration (WBV) training on muscle strength, spasticity, and motor performance in spastic diplegic cerebral palsy children after 12-weeks treatment. Methods Thirty spastic diplegic CP children (8–12 years) were randomized to two equal groups, control group and WBV group. The control group received a selected physical therapy treatment program for spastic diplegic CP and the WBV group received the same program in addition to WBV training. Measurements of isometric strength of knee extensors, spasticity, walking speed, walking balance and gross motor function were performed before and after 12 weeks of the treatment program. Results Isometric strength of knee extensors, spasticity and the walking speed were significantly improved only in the WBV group (P < 0.05). Growth motor function measure-88 (GMFM-88) (D%) was significantly increased (P < 0.05) in both groups in favor of the WBV group and GMFM-88 (E%) was significantly increased (P < 0.05) only in the WBV group, while walking balance did not change significantly in either group. Conclusion The obtained results suggest that 12-weeks’ intervention of whole-body vibration training can increase knee extensors strength and decrease spasticity with beneficial effects on walking speed and motor development in spastic diplegic CP children.
    Egyptian Journal of Medical Human Genetics 04/2014; 15(2):173–179. DOI:10.1016/j.ejmhg.2014.02.007
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    • "Rehabilitation in CP disease consists of improving mobility, preventing deformity and helping children to learn the necessary skills for daily life. The therapy is often recommended throughout early childhood while the nervous and musculoskeletal systems are the most adaptable and the normal neuromotor development can be facilitated [16] [17] [18]. The therapy should support the development of cognitive, sensory, visual and musculoskeletal systems, involving play activities to enhance social integration [18]. "
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    ABSTRACT: Cerebral Palsy (CP) results from nonprogressive lesions in the immature brain generating changes on the neuromuscular system. Environmental enrichment (EE) is a combination of stimuli that provides greater motivation and interest in novel movement exploration through the provision of various devices associated to enhanced social stimulation that would mimic the physiotherapy approach. The aim of this study was to verify whether EE is able to prevent the establishment of motor impairment in a CP rat model. The animals were divided in two groups: control animals (healthy) and animals submitted to a CP model. After this, the pups were exposed to two environments: enriched or standard, totaling 4 groups: Control group (without CP in a standard environment), CP group (CP model in a standard environment), EE group (without CP in an enriched environment) and CP-EE (CP model in an enriched environment). The experimental model was induced in pregnant Wistar rats by the association of maternal exposure to bacterial endotoxin, perinatal anoxia and sensorimotor restriction of the pups. The assessment of motor skills was held using the following tests: Open Field, Rotarod, Horizontal Ladder, Narrow Suspended Bar and stride length. The histological analysis evaluated the mean cross-sectional area (CSA) of the soleus muscle fibers, the mean CSA of motoneuronal somata and expression of synaptophysin in the ventral horn of the spinal cord. EE was able to prevent the motor deficits, however, it did not reverse the muscle atrophy observed in CP animals. Furthermore, there was an average increase in the mean area of motoneurons and an increase in the expression of synaptophysin in the ventral horn of the spinal cord of the CP-EE group in relation to CP animals reared in a standard environment. Hereupon, the stimulus increment provided by EE can prevent the onset of motor deficits and histological changes in a CP rat model.
    Behavioural brain research 01/2014; 263. DOI:10.1016/j.bbr.2014.01.007 · 3.03 Impact Factor
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