a 3-month - old girl child presented to us with a history of swelling on back since birth . she had a history of full term normal vaginal delivery with no significant family history . there was complete flaccid paralysis of right lower extremity with normal anal tone . on local examination , an initial diagnosis of a myelomeningocele was made and patient was referred for magnetic resonance imaging ( mri ) of neuraxis . mri spine revealed a bony spur at d11 level dividing the spinal cord into two halves suggesting pang type 1 split cord malformation ( scm ) or diastematomyelia . right hemicord , along with meninges and cerebrospinal fluid was herniating through the defect in posterior element of same vertebra forming a large hemimeningomyelocele [ figures 1 and 2 ] . t2-weighted sagittal ( a ) and coronal ( b ) magnetic resonance imaging of dorso - lumbar spine shows a hemivertebrae from d10 to d12 level along with a bony spur at d11 . continuation of left hemicord is appreciable in coronal view ( b ) t2 weighted axial image shows a bony spur dividing the cord into two halves ( a and b ) . herniation of right hemicord , meninges and cerebrospinal fluid is noted through the defect in posterior element , forming a large hemi - meningomyelocele ( c ) . two hemicords are visible below the level of herniation ( d ) which reunites at d12 level to form a single cord ( e ) based on clinical examination and mri a final diagnosis of scm type 1 with right hemimyelomeningocele ( hmm ) was made and patient was prepared for surgery . excision of bony spur along with microneurosurgical dissection and meticulous layered closure of myelomeningocele was achieved . according to pang 's unified theory of embryogenesis , the whole spectrum of split cord syndrome originates from one basic ontogenic error occurring around the time of primitive neurenteric canal closure . this basic error is the formation of  accessory neurenteric canal  between the amniotic cavity and the yolk sac . this abnormal fistulous connection bisects the notochord and the neural plate on approximately postovulatory day 18 . final appearance of matured scm depends on the ability of the embryo to heal around this abnormal fistulous connection aka endomesenchymal tract . according to pang et al . , formation of endomesenchymal tract before postovulatory day 21 gives rise to scm type 2 or diplomyelia , whereas formation of this tract after postovulatory day 30 gives rise to scm type 1 or distematomyelia . the formation of this tract between postovulatory day 21 and 30 gives rise to composite / mixed scm . each hemineural plate undergoes neurulation in which , the neural folds converge and fuse each other in relation to their respective hemi - notochords . this process of primary neurulation occurs between postovulatory days 2228 . in case of neurulation defect on one side , hmm or hemimeningocele myelomeningocele are frequently associated with chiari malformation diastematomyelia ( up to 45% in some reported series ) and other congenital vertebral defects such as spondylocostal dysostosis , jarcho - levin syndrome , klippel - feil anomaly and a wide range of syndromic malformation complexes , but true hemimeningocele , where a single hemicord fails to neurulate is rare . the neurological deficit in children with hmm is less severe than compared to myelomeningocele patients and is limited only to the side of exposed hemicord . this case report highlights the importance of detailed imaging of complete neuraxis in cases of spinal dysraphism for optimal neurosurgical management . second the rarity of this condition suggests that formation of the endomesenchymal tract and neurulation defect are two separate embryological events , and their coexistence at the same level is only by chance though more inputs are warranted in this regard .