PMC4993811_01
(A) Scatter plot and linear fit between the Ccma fibers and interhemispheric transfer timer, (B) same plot after removing four outliers, (C) corpus callosum of the circled outlier of plot (A).
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However, the correlation matrix and scatter plots brought to attention that, by excluding the four outliers, a strongly red-colored (significant) link appeared between the increasing interhemispheric transfer time and the longer length of the maCC fibers: Figure 7B shows this strong correlation for the preterm group (orange circles) when the outliers are removed (as a contrast to Figure 7A), the longer the maCC fibers and the longer the interhemispheric transfer time. The real time access to clinical characteristics by right clicking the dots in BRAVIZs scatter plots eased to understand that outliers in Figure 7B were participants with either cerebral palsy or Xfragile pathology. The parallel access DTI data and scatter plots in the same workspace favored the immediate detection that the circled outlier in Figure 7A was a participant with a dramatic thinning of the maCC (Figure 7C). Infanib at 6 months of age and our neurophysiological measures known as different in the preterm group (Schneider et al.,) such as the lower excitability of the motor brain and higher occurrence of ipsilateral muscle responses to TMS of the motor brain (which is abnormal given the typical crossed organization of motor systems for hand function). In that vein, BRAVIZs applications contributed to highlight that the four participants above 20 ms thus who significantly drove the correlation in Figure 7A had a dysfunctional organization of the motor brain. One another ancillary hypothesis could be that Infanib testing at 6 months of age may be predictive of long-term impairment of the motor brain function, including a poor efficiency of the interhemispheric connections (time over 20 ms at 15 years of age, see Figure 7A).
Parallel coordinates display configured for searching possible PVL cases, lines that don't match the filters on each axis are shown in gray.
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Figure 8 shows for example that the dataset included motor and visual testing, intelligence assessment, a classical neurological evaluation to discriminate between normal and abnormal neurological status and some risk factors, such as weight and gestational age (Ballard) at birth. The line highlighted in Figure 8 showed ventricules dilatation, low white matter volume, low scores for motor and visual components of visuomotor integration testing (VMI) and low birthweight (pesnacer). The 15-year subject data associated with the top line in Figure 8 (highest ventricles volume) showed in Subject Overview a very premature birth at 31 weeks of gestational age and given by C-section in emergency because of profuse bleeding (placenta previae), signs of leucoencephalopathy and an increased volume of the left lateral ventricle in CT scan, epilepsy not yet controlled, severe bilateral hearing loss, and abnormal bilateral vision, but a normal psychomotor development.
VMI vs. M1 excitability excluding outliers (empty circles).
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The Correlation Viewer (color codes highlighting the significant links and excluding the outliers determined above) used together with the parallel coordinates application (see all studied variables in real time in the same workspace) detected that the lower (lesser) VMI StS scores of the preterm group could be explained by a lower excitability of the motor brain (higher motor threshold, i.e., higher intensity of TMS to generate a response in the muscle, RMTd in Figure 10, the excluded outliers are represented by empty circles) and higher occurence of abnormal ipsilateral responses (Ipsifreqnd in Figure 11).
VMI vs. ipsilateral corticospinal responses excluding outliers (empty circles).
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The Correlation Viewer (color codes highlighting the significant links and excluding the outliers determined above) used together with the parallel coordinates application (see all studied variables in real time in the same workspace) detected that the lower (lesser) VMI StS scores of the preterm group could be explained by a lower excitability of the motor brain (higher motor threshold, i.e., higher intensity of TMS to generate a response in the muscle, RMTd in Figure 10, the excluded outliers are represented by empty circles) and higher occurence of abnormal ipsilateral responses (Ipsifreqnd in Figure 11).
Details of a subject with possible PVL, the left panel shows values for several variables as well as the full clinical history.
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Altogether, the clinical profile and the symptoms together with the T1 image of ventricles dilatation (Figure 12) could be associated with PVL.