• Kishore Kislay, Devi Bhagavatula Indira BI Departments of Neurosurgery, Nation-al Institute of Mental Health and Neu-rosciences (NIMHANS), Bangalore, India., Dhananjaya Ishwar Bhat, Dhaval Prem Shukla, Arun Kumar Gupta, and Rajanikant Panda.
• Departments of Neurosurgery, Nation-al Institute of Mental Health and Neu-rosciences (NIMHANS), Bangalore, India.
• Neurosurgery. 2018 Nov 1; 83 (5): 905-914.

BackgroundThe response of the brain to obstetric brachial plexus palsy (OBPP) is not clearly understood. We propose that even a peripheral insult at the developmental stage may result in changes in the volume of white matter of the brain, which we studied using corpus callosum volumetry and resting-state functional magnetic resonance imaging (rsfMRI) of sensorimotor network.ObjectiveTo study the central neural effects in OBPP.MethodsWe performed an MRI study on a cohort of 14 children who had OBPP and 14 healthy controls. The mean age of the test subjects was 10.07 ± 1.22 yr (95% confidence interval). Corpus callosum volumetry was compared with that of age-matched healthy subjects. Hofer and Frahm segmentation was used. Resting-state fMRI data were analyzed using the FSL software (FMRIB Software Library v5.0, Oxford, United Kingdom), and group analysis of the sensorimotor network was performed.ResultsStatistical analysis of corpus callosum volume revealed significant differences between the OBPP cohort and healthy controls, especially in the motor association areas. Independent t-test revealed statistically significant volume loss in segments I (prefrontal), II (premotor), and IV (primary sensory area). rsfMRI of sensorimotor network showed decreased activation in the test hemisphere (the side contralateral to the injured brachial plexus) and also decreased activation in the ipsilateral hemisphere, when compared with healthy controls.ConclusionOBPP occurs in an immature brain and causes central cortical changes. There is secondary corpus callosum atrophy which may be due to retrograde transneuronal degeneration. This in turn may result in disruption of interhemispheric coactivation and consequent reduction in activation of sensorimotor network even in the ipsilateral hemisphere.

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