Does damage to somatosensory circuits underlie motor impairment in cerebral palsy?
2009-08-06

Motor dysfunction in children with cerebral palsy (CP) due to periventricular brain lesions is traditionally attributed to structural damage to the corticospinal tract.1 In this issue of DMCN, Hoon et al. employ diffusion tensor imaging to study alterations in various white matter tracts in children with CP following preterm birth.2 Based on their previous findings,3 they hypothesized that the decisive injury (determining clinical impairment) would be to ascending, somatosensory rather than to descending, motor tracts. And indeed, they found a significant correlation between measures of motor impairment and damage to the posterior thalamocortical radiation. In our opinion, this is an interesting paper, and the authors touch on important issues related to neural plasticity following periventricular white matter injury. Some points seem worth mentioning: first, this paper strongly supports the recent prediction4 that diffusion tensor imaging may turn out to be the method of choice to assess white matter injury and to correlate the extent of white matter damage with (neurological or cognitive) outcome in children born preterm. It seems that this approach, combining careful clinical assessment in well-defined groups with state-of-the-art image analyses methods, harbours great potential to advance our understanding of the underlying pathophysiology in disorders such as CP. Second, as the authors themselves acknowledge, the data is provocative with regard to challenging the traditional assumption that motor impairment in CP is a function of the impairment of descending pathways.1 In light of the increasingly recognized importance of neural networks, including the contributions of somatosensory input to motor execution especially in the developing neural system,5 the suggestion that a lack of somatosensory input due to a primarily sensory deficit is behind the prominent motor impairment in this common disorder may not be revolutionary anymore; however, it certainly puts a system into the spotlight that has not been the focus of many researchers as yet, in this disorder. However, there are also a number of critical points. For example, there is good evidence of ‘spatial plasticity’, especially of ascending fiber tracts in the developing human brain. Those tracts carry function and, especially in the presence of large white matter lesions, literally ‘go to great lengths’ to reach their final target, the primary somatosensory cortex. This capacity for ‘axonal plasticity’ especially of developing thalamocortical projections is explained by the timing of the maturation of these fibers.6 In other words, all normal anatomical rules may not apply in these children, and measuring white matter properties that usually correspond to a given tract may be misleading as this tract might be located in a completely different position in the pathological setting. This possibility is not explicitly acknowledged in the approach chosen by Hoon et al. Accordingly, a recent study7 directly comparing fiber tracking with conventionally placed regions of interest concluded that fiber tracking may be more appropriate for identifying damage to the white matter architecture (albeit in the corticospinal tract). Also, in the present study, the age range of included participants was quite large, allowing, as the authors concede, for influences of brain maturation that are difficult to account for. These points may be among the factors that may need to be taken into account when trying to reconcile the evidence implicating ascending (Hoon et al.2, 3) or descending6, 7 fiber tracts in the etiology of motor impairment in CP. In the end, both mechanisms may turn out to be relevant; for example, they might influence the clinical manifestation to different degrees in distinct subgroups. Such relations will only be found if larger and well-defined groups are investigated. To conclude, the paper in question is an interesting contribution to the ongoing discussion on what mechanisms underlie sensorimotor impairment in CP. Further research on the contributions of damage to somatosensory circuits to the clinical picture in CP therefore seems warranted.