A Systematic Review of Neuroimaging for Cerebral Palsy

Department of Epidemiology, College of Human Medicine, Michigan State University, East Lansing, MI 48824, USA.
Journal of Child Neurology (Impact Factor: 1.72). 03/2008; 23(2):216-27. DOI: 10.1177/0883073807307983
Source: PubMed


The American Academy of Neurology now recommends that all cases of cerebral palsy of unknown origin undergo neuroimaging. Controversy surrounds this recommendation because of concerns about the adequacy of the supporting evidence. This article reviews the evidence provided by magnetic resonance imaging (MRI) and computed tomography (CT) imaging studies in cerebral palsy and discusses the potential benefits of imaging, techniques in current use, and future directions, with a focus on improving etiologic understanding. Most (83%) children with cerebral palsy have abnormal neuroradiological findings, with white matter damage the most common abnormality. Combined gray and white matter abnormalities are more common among children with hemiplegia; isolated white matter abnormalities are more common with bilateral spasticity or athetosis, and with ataxia; isolated gray matter damage is the least common finding. About 10% of cerebral palsy is attributable to brain malformations, and 17% of cerebral palsy cases have no abnormality detectable by conventional MR or CT imaging. Although neuroimaging studies have increased our understanding of the abnormalities in brain development in cerebral palsy, they are less informative than they might be because of 4 common problems: (1) inappropriate assignment of etiology to morphologic findings, (2) inconsistent descriptions of radiologic findings, (3) uncertain relationship of pathologic findings to brain insult timing estimates, and (4) study designs that are not based on generalizable samples. Neuroimaging is not necessarily required for diagnosis of cerebral palsy because the disorder is based on clinical findings. The principal contribution of imaging is to the understanding of etiology and pathogenesis, including ruling in or out conditions that may have implications for genetic counseling, such as malformations. In the future, as more sophisticated imaging procedures are applied to cerebral palsy, specific morphologic findings may be linked to etiologic events or exposures, thus leading to potential pathways for prevention.

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    • "Although the timing of brain insults is extremely unclear and unreliable, but the findings from abnormality reported by MRI, suggest that MRI, may be a useful tool for diagnosing of the etiology and pathogenesis of abnormal growth during antenatal, perinatal and neonatal damages. Korzeniewski et al (2008) believe that methods of timing brain insult based on CT/MRI findings should be clarified and standardized to avoid further confusion (12). "
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    ABSTRACT: Cerebral Palsy is the most common chronic motor disorder of childhood, that affecting approximately 3 infants per 1000 live-births. The risk of brain injuries that potentially cause Cerebral Palsy has amplified with increasing in survival rates for preterm infants. In addition Cerebral Palsy has a huge economic impact, to immeasurable health, social, and psychological problems that affected children and their families suffer. Cerebral Palsy, among 18 common congenital disorders, has the highest lifetime costs per new case. Thus, efforts to prevent its occurrence, minimize the morbidity, and improve the patient outcomes are important at both the individual and societal levels. In each trimester, different patterns of brain damage or abnormal insults can represent times and etiology of injuries. Knowledge of the etiology and pathogenesis of abnormal brain growth during antenatal, perinatal and neonatal damages can be helping us for prevention. Also Magnetic Resonance Imaging (MRI) studies of subjects with multiple forms of cerebral palsy reported significantly more overall abnormalities, malformations, and white matter damage but in this review study we discuss in what extent MRI is useful in detecting cerebral palsy pathogenesis. Introduction Due to a defect or lesion of the immature brain, the term cerebral palsy (CP) describes a group of disorders of movement and posture (1,2), with various types and degrees of motor impairment (3) and is the commonest physical disability in childhood (4-8). In many cases the cause remains unknown (9-11). The definition is usually based on phenomenology; it only specifies that CP originates from an interference, lesion, or abnormality of the developing brain (12-14). CP may cause a range of associated problems including; hearing and visual deficits, nutritional and feeding problems, respiratory infections, epilepsy, pain, cognitive and communicative impairments in children (11). Due to prenatal or perinatal brain damage, CP is a permanent and non-progressive disorder become manifest early in life (12). Congenital hemiplegia is the most common form of cerebral palsy among children born at term, and second to diplegia among children born prematurely (8-11). The cerebral palsy that affecting approximately 3 in 1000 newborns (12), has not diminished in recent decades despite advances in obstetric and neonatal care . In fact, in the world, the risk of CP among term infants may have increased between the years 1975 and 1991, from 1.7 to 2.0 per 1000 live births. Approximately 8000 children with CP, based on these numbers, are born annually in the United States and approximately 10 to15% of very preterm children (born < 30 weeks gestational age) develop cerebral palsy, and 30 to 60% of them experience cognitive impairments (15). The decrease in perinatal mortality in very and extremely pre-term infants has led to an increasing prevalence of cerebral palsy (3-5,16). Over the past 20 years, there have been radical changes in our understanding of etiology. Most cases of cerebral palsy, for over 100 years, were thought to be caused by asphyxia during either labor or the perinatal period. However there is a plethora of accepted medical and rehabilitative interventions, there is not often a complete understanding of the
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    • "However, the decrease in resting inter-hemispheric coherence we found in individuals with secondary dystonia compared to controls has not been previously reported and may be related to decreased connectivity of the hemispheres through the corpus callosum. There are common neuroanatomical signs of white matter damage in individuals with early brain injury (Korzeniewski et al., 2008), and white matter damage has been related to thinning of the corpus callosum (Panigrahy et al., 2005). Based on a theory of the excitatory function of the corpus callosum, decreased size would reflect more laterality of brain function (Bloom and Hynd, 2005). "
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    ABSTRACT: Dystonia is a disabling motor disorder often without effective therapies. To better understand the genesis of dystonia after childhood stroke, we analyzed electroencephalographic (EEG) recordings in this population.Methods Resting spectral power of EEG signals over bilateral sensorimotor cortices (Powrest), resting inter-hemispheric sensorimotor coherence (Cohrest), and task-related changes in power (TRPow) and coherence (TRCoh) during wrist extension were analyzed in individuals with dystonia (age 20±3 years) and healthy volunteers (age 17±5 years).ResultsIpsilesional TRPow decrease was significantly lower in patients than controls during the more affected wrist task. Force deficits of the affected wrist correlated with reduced alpha TRPow decrease on the ipsilesional and not the contralesional hemisphere. Cohrest was significantly lower in patients than controls, and correlated with more severe dystonia and poorer hand function. Powrest and TRCoh were similar between groups.Conclusions The association between weakness and cortical activation during wrist extension highlights the importance of ipsilesional sensorimotor activation on function. Reduction of Cohrest in patients reflects a loss of inter-hemispheric connectivity that may result from structural changes and neuroplasticity, potentially contributing to the development of dystonia.SignificanceCortical and motor dysfunction are correlated in patients with childhood stroke and may in part explain the genesis of dystonia.
    Clinical Neurophysiology 11/2014; 126(8). DOI:10.1016/j.clinph.2014.11.002 · 3.10 Impact Factor
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    • "Our aim was to derive a representative BP response from the EEG for the participants with CP, in order to examine potential differences to healthy participants. Even within a specific CP subtype, CP inherently has significant variability, as lesions can occur at different locations or take different forms such as malformations, periventricular lesions or cortico-subcortical lesions (Wu et al., 2006; Korzeniewski et al., 2008). We therefore averaged the BP of the nine CAR channels described above to attempt to correct for inter-participant differences in spatial locations of greatest ERD/S manifestation. "
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    ABSTRACT: Cerebral palsy (CP) includes a broad range of disorders, which can result in impairment of posture and movement control. Brain-computer interfaces (BCIs) have been proposed as assistive devices for individuals with CP. Better understanding of the neural processing underlying motor control in affected individuals could lead to more targeted BCI rehabilitation and treatment options. We have explored well-known neural correlates of movement, including event-related desynchronization (ERD), phase synchrony, and a recently-introduced measure of phase dynamics, in participants with CP and healthy control participants. Although present, significantly less ERD and phase locking were found in the group with CP. Additionally, inter-group differences in phase dynamics were also significant. Taken together these findings suggest that users with CP exhibit lower levels of motor cortex activation during motor imagery, as reflected in lower levels of ongoing mu suppression and less functional connectivity. These differences indicate that development of BCIs for individuals with CP may pose additional challenges beyond those faced in providing BCIs to healthy individuals.
    Frontiers in Neuroengineering 07/2014; 7:20. DOI:10.3389/fneng.2014.00020
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