Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 4886  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Resource Links
  »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
  »  Article in PDF (1,937 KB)
  »  Citation Manager
  »  Access Statistics
  »  Reader Comments
  »  Email Alert *
  »  Add to My List *
* Registration required (free)  

  In this Article
 »  Abstract
 » Literature Search
 » Clinical Features
 »  Pathophysiology ...
 » Investigations
 »  Indications for ...
 » Surgical Techniques
 » Results of Surgery
 » Complications
 » Conclusion
 »  References
 »  Article Figures
 »  Article Tables

 Article Access Statistics
    PDF Downloaded62    
    Comments [Add]    

Recommend this journal


Table of Contents    
Year : 2020  |  Volume : 68  |  Issue : 5  |  Page : 994-1002

Cervical Split Cord Malformations: A Systematic Review

Department of Neurosurgery, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India

Date of Web Publication27-Oct-2020

Correspondence Address:
Dr. Sachin Anil Borkar
Department of Neurosurgery, ROOM NO.720, CN Centre, All India Institute of Medical Sciences, Ansari Nagar, New Delhi - 110 608
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.299132

Rights and Permissions

 » Abstract 

Cervical split cord malformations are extremely rare with less than 75 cases reported in the literature worldwide. The widely different terminologies used to describe the same pathoanatomy make the documentation of all reported cases a difficult task. We conducted a systematic review of 71 cases documented over 38 reports from 1889 to 2016. The controversy regarding prophylactic surgery in asymptomatic individuals remains. We advocate prophylactic surgery in all asymptomatic individuals to preclude severe neurological deficit following trivial trauma in future. The results of surgery in asymptomatic individuals are excellent while those in symptomatic individuals are good as well.

Keywords: Cervical spine, diagnosis, split cord, treatment
Key Message: Cervical SCM is an exceptionally rare condition, with less than 75 cases documented in literature. We advocate prophylactic surgery in all asymptomatic individuals to preclude severe neurological deficit following trivial trauma in the future. The results of surgery in asymptomatic individuals are excellent while those in symptomatic individuals are good as well.

How to cite this article:
Sreenivasan R, Sharma R, Borkar SA, Arumulla S, Garg K, Chandra SP, Kale SS, Mahapatra AK. Cervical Split Cord Malformations: A Systematic Review. Neurol India 2020;68:994-1002

How to cite this URL:
Sreenivasan R, Sharma R, Borkar SA, Arumulla S, Garg K, Chandra SP, Kale SS, Mahapatra AK. Cervical Split Cord Malformations: A Systematic Review. Neurol India [serial online] 2020 [cited 2021 Aug 4];68:994-1002. Available from:

Whereas there is a decreasing trend in the incidence of neural tube defects in the world, it has been increasingly reported from the Indian subcontinent due to the widespread availability of MRI and active surveillance of scoliosis patients being referred for treatment.[1] The oldest preserved bony specimen of diastematomyelia is that of a 20-year old found at a burial tomb at the Negev desert of Israel and dates back to 100 AD.[2] Perret describes that autopsy reports as early as 1684 AD have detailed this condition in stillborn fetuses and monsters.[3] Ollivier described the earliest case of sagittal splitting of the spinal cord and named the condition diastematomyelia from Greek, diastema – cleft and melos – medulla.[4],[5] Diastematomyelia is the term used to describe a congenital cleft or splitting of the spinal cord, each portion of which may be invested in a separate arachnoid sheath under a common dura or may have separate dural sheaths as well.[5] Hertwig in 1892 was the first to experimentally produce this malformation in frogs by delaying the fertilization of the ovum.[5],[6] von Recklinghausen coined the term diplomyelia to describe a completely formed spinal cord situated anteriorly or posteriorly to the original cord.[7] Herren and Edwards defined the term diplomyelia (Greek dipulo - double) to include any complete duplication of a spinal cord segment.[8] Hamby (1936) is credited as the first surgeon to have operated on a living patient with diastematomyelia.[9] Pang et al. suggested a new classification to deal with all double spinal cord malformations and used the phrase “Split Cord Malformations”(SCM) to describe the entire spectrum of anomalies associated.[10]

Cervical split cord malformations are extremely rare pathology with only few cases reported till date. Till 1972, most of the 11 cases described were diagnoses made at autopsy with the earliest report by Fischer et al. in 1889.[11] James et al. (1972) were the first to document the clinical picture in a 56-year-old woman with quadriplegia.[11] Whittle et al. (1983) were one of the first to document the successful surgical outcome of spur excision and repair in a 2-year-old girl with Klippel Feil Syndrome (KF) who presented with posttraumatic paraparesis.[12] There have been sporadic reports every year or two since then with the largest series reported by Mahapatra et al.[1],[13] (9 cases, 2011). Previously David et al.[14] (7 cases, 1996) and Ulmer et al.[15] (5 cases, 1993) had reported the presence of cervical SCM in patients of Klippel Feil syndrome. In this systematic review, we attempt to perform the qualitative analysis of the cervical split cord malformations reported in the literature.

 » Literature Search Top

The initial literature search was done using keywords “(split cord malformation OR SCM OR diastematomyelia OR diplomyelia) AND (cervical)” yielded 111 articles. On screening these articles, 46 relevant abstracts were retrieved, out of which only 38 accessible full articles in English language included cervical split cord malformation cases as shown in PRISMA flow diagram [Figure 1]. The qualitative analysis of these 38 reports has been summarized in [Table 1].
Figure 1: PRISMA chart outlining the search study used in this review

Click here to view
Table 1: Qualitative analysis of 71 Documented cases of cervical SCM reported in literature from 1889-2016

Click here to view

 » Clinical Features Top

Age of presentation and sex prevalence

The clinical presentation of cervical spinal cord malformations has ranged from the newborn to as late as 56 years of age with approximately 50% cases (30 cases) presenting before the age of 10.[1],[11],[12],[13],[18],[27],[28],[32],[33],[34],[35] As many as 23 cases have been reported in the adults over the age of 18.[11],[14],[15],[19],[20],[21],[23],[24],[25],[26],[29],[30],[37],[41] A female preponderance is evident (M:F l 2:5). There is no explanation in literature for this predominance and as to why the female embryo is susceptible to defects in secondary neurulation.

Symptoms and signs

Neurological deficits are reported in at least 19 out of the 38 reports (individual cases are not described in large series). A near normal neurology has been seen in six out of the 38 reports.[22],[38],[34],[35],[39],[41] Neural deficits range from a mild sensory disturbance[22] to prolonged quadriplegia with bladder and bowel involvement.[24] Neck pain and radiculopathy may be associated with underlying vertebral fusions and restricted motion.[14],[15] Gait disturbances, asymmetrical weakness, atrophy of lower limbs, neurotrophic ulcers, and incontinence are frequently seen. Neurotrophic ulcers and self-mutilation of fingers due to sucking and biting the anesthetic limb has been reported in cases of cervical SCM.[43] Ohwada et al. reported the case of a 19-year-old male with C6-C7 SCM who presented with the signs of thoracic myelopathy.[26]

Cutaneous stigmata are reported in as many as 60% cases in large series reported by Mahapatra et al.[1] Hypertrichosis, naevi, dimples, dermal sinus, and lipomatous swellings are seen in many patients with SCM.[1],[13],[40]

Associated features include torticollis, meningoceles, myelomeningoceles, KF syndrome (low-lying hair line with limitation of cervical movements, Sprengel shoulder, pterygium colli, and mirror movements of the upper limbs), and spinal deformities (kyphosis and scoliosis). Often, the routine workup for a spinal deformity correction surgery reveals a cord anomaly in a relatively asymptomatic patient.[34] Cervical SCM that are not associated with other congenital anomalies typically become symptomatic in adult life following a trivial trauma to the extent that the discovery of a cervical SCM in the absence of a traumatic history is rather rare.[29] Hemiplegia following trivial trauma is reported.[20]

Geographical distribution

Although reported from all over the world, few reports have come from Japan[23],[26] and the African nations, whereas large series have emanated from India[1],[13],[40] and Turkey.[37],[39] Underdiagnosis and underreporting could be a reason or there could be unknown ethnic or environmental factors that are still to be unearthed.

The reports of cervical SCM have been too sporadic to discern a familial inheritance pattern.


According to Pang,[10] the formation of an abnormal fistula through the midline embryonic disc is the embryological error leading to a SCM. This fistula maintains the communication between the yolk sac and amnion which makes a continued contact between the ectoderm and endoderm possible. This leads to the regional splitting of the notochord and the overlying neural plate. The surrounding pluripotent mesenchymal tissue condenses around the fistula to form an endomesenchymal tract that bisects the notochord and forces each overlying half to neurulate against its own hemicord.

The basic anomaly thus comprises two heminotochords and two hemineural plates separated by a midline fistula containing ectoderm, endoderm, and mesenchyme. Further evolution of this anomaly into final malformation depends on the ability of the hemicords and heminotochords to heal around the endomesenchymal fistula, the fate of the three germinal elements within this fistula, and the variable extent to which this fistula persists as well as the interaction between the heminotochord and the hemineural plates during neurulation [Figure 2].
Figure 2: (a-c) Pictorial representation of normal embryology and embryological basis of split cord malformation

Click here to view

Mahapatra and Gupta further state that the precursor meninges are the likely source of midline bone, apart from the formation of the dural tubes. After the formation of the dura, the precursor meninx on the side of the median dura that faces each hemicord forms a complete arachnoid tube and the precursor meninx on the side facing the midline forms the bony spur. The extent of the disappearance of the endomesenchymal fistula and the subsequent interaction of precursor meninges with the fistula determines the position of spur as this is probably genetically controlled.[13] Many cases of cervical SCM are associated with Klippel Feil syndrome and other disorders of vertebral fusion and segmentation. The influence of homeobox genes Pax-1 and Hox are being investigated but the relationship between the genes affecting spinal cord division and primary segmentation as yet remains unknown.[14] Chandra et al.[44] postulated two mechanisms for the occurrence of a dorsal spur, a rare variant: (1) passage of an abnormal cell cluster dorsally with subsequent loss of contact with the ventrally situated cell cluster and (2) migration of cells around the hemicords and formation of passage between them in a dorsoventral direction.

 » Pathophysiology of Symptoms Top

Mechanical factors

The osseous/fibrous-cartilaginous septum anchors the spinal cord and impedes its normal ascension with growth of the skeleton leading to tethering of the cord. The plasticity of the nervous system allows for small children to remain asymptomatic for long. However, with growth spurt this plasticity is also rendered ineffective and patients become symptomatic. This tethered cord that is not normally floating in CSF space is further insulted by the coexisting spinal stenosis and deformity.[24],[45],[46]

Vascular factors

An asymmetrical distribution of blood supply to the hemicords and compression of the anterior spinal artery or veins leads to ischemic disturbances leading to symptoms.[47],[48] Yamada et al. were able to demonstrate the effect of traction on the vascular supply of the spinal cord of a cat using spectroscopy.[49]

Anatomical factors

Hypoplasia of one or both of the hemicords may give rise to any of the symptoms encountered.[10]

 » Investigations Top

Antenatal diagnosis

The literature on antenatal diagnosis of SCMs is sparse. There are isolated case reports reported in literature mentioning the use of antenatal sonogram and MRI for establishing the diagnosis.[50],[51],[52],[53],[54]

Postnatal diagnosis

Ultrasonogram is the screening tool of choice for the detection of suspected SCM and is superior to a plain radiograph in newborns. MRI is the definitive investigation of choice and can delineate the exact morphology of the cord and anomalies such as hemicords, syrinx, and intradural malformations such as fatty filum, teratomas/dermoids, lipomas, and cysts. A screening MRI of the whole spine is mandatory in all suspected cases to detect occult multisite dysraphisms.[1],[13] CT scan should be performed for highlighting the bony elements of the anomaly and their relationship with the cord, especially when associated with scoliosis or kyphosis. Conversely, all patients planned for spinal deformity correction should be screened for occult or overt spinal dysraphism before proceeding for surgery.

Role of urodynamics

A total of 60–75% patients with SCM have subtle or overt urinary tract dysfunction with the most common complaint being urge incontinence.[55],[56] They usually tend to stabilize or improve after surgery. Therefore, Perez et al.[56] concluded that all patients with SCM should undergo a urodynamic evaluation prior to surgical intervention. It bears on prognosticating the postoperative outcome as well.

 » Indications for Surgery Top

There are considerable controversies regarding the need for surgery in asymptomatic patients with no neurological deficits and SCM type II patients. David et al. reserved surgery only for those with overt spinal instability and progressive neural deficit.[14] Only 1/7 cases in their series was operated. Zuccaro states that majority of the asymptomatic patients in her series were not operated and did well at 7 year followup.[57] However Matson et al.,[58] Mahapatra et al.,[1] Proctor et al.[55] have all suggested that the aim of the surgery should be prophylactic rather than curative and as such should be offered to asymptomatic patients as well. That the treatment of intraspinal anomalies prior to deformity correction results in better outcomes is a fact endorsed by most orthopedists and neurosurgeons who operate on spinal deformities.[59],[60] Surgery can lead to healing of trophic ulcers as well.[13] Surgery is definitely indicated in every patient who presents with associated anomalies like dermal sinus, dermoids, teratomas, and cysts that can by themselves lead to complications if not treated appropriately.

 » Surgical Techniques Top

Patients are operated in the prone position. Neurophysiological monitoring is desirable but depends on the availability of personnel and equipment. Intraoperative monitoring can give the surgeon greater confidence while dissecting and manipulating around the cord by urging him to stop dissection till the reduced amplitude of evoked potentials returns to baseline levels. The use of intraoperative image intensifier/X-ray is desirable to correctly localize the site of the lesion as cutaneous markers can be segments away from the actual lesion. A laminotomy or laminectomy with a high-speed drill is done and a Kerrison's punch (or a diamond drill) can be used to nibble out the spur completely before proceeding with detethering as needed.[13] A laminoplasty is indicated for a large segment disease to prevent postlaminectomy kyphosis. Alternatively, pedicle screw fixation can be combined with the procedure, especially if deformity correction is done in the same sitting. The dural sleeve of the spur must be completely removed as there have been reports of new spurs arising from re-ossification along the remnant sleeve.[61],[62],[63] Excision of the filum prevents any traction on the tethered segment or conus.[1] This is done by a small sacral laminotomy in cases of cervical SCM.

For dorsally located spurs, a laminoplasty should never be performed for the fear of causing cord damage.[64] A laminectomy one level above and one below the level of the spur is done. The spur is drilled off gradually in a dorsal to ventral direction and the dura is opened with a gentle curve encircling the spur. The durotomy is extended about two levels cephalad and caudad to the level of the lesion so that there remains sufficient dura for watertight closure. The bony spur is thinned out with a high-speed drill and the shell remaining is removed with microrongeurs. A watertight closure is done with 5-0 Vicryl or Nylon. The rest of the wound is closed in layers [Figure 3] and [Figure 4].
Figure 3: Intraoperative photograph showing split cord malformation at C1-C2 level. Also seen is the caudal extent of the cerebellum within the sac. The child, a 16-month/M presented with an occipitocervical meningocele and had deficient lower part of occiput and C1 and C2 posterior arches

Click here to view
Figure 4: (a-d): Pictorial summary of excision and repair of split cord malformation

Click here to view

 » Results of Surgery Top

The results of surgery are generally gratifying with dramatic improvement in neurology to complete recovery of symptoms reported by many workers.[1],[11],[12],[19],[21],[26],[29],[34],[35],[39] Persistent neural deficits or incomplete recovery are also reported in some cases with severe preoperative deficits.[24],[36],[43],[40] A total of 7–10% patients may develop retethering over a period of 5 years due to reossification of the spur along any remnant dural sleeve.[61],[62],[63] Mahapatra reported that none of the patients undergoing prophylactic surgery had postoperative neurological deterioration.[1]

 » Complications Top

Overall, the complications of SCM surgery are low. Preoperative complications are related to distorted anatomy and difficulties with hemostasis and watertight dura closure. Mahapatra and Gupta subclassified Type I SCM [Figure 5] into 4 types based on the position of the bony spur causing the split [Figure 6]a, [Figure 6]b, [Figure 6]c, [Figure 6]d.[13]
Figure 5: Illustrative diagram showing axial section of a cervical vertebra showing a split cord malformation type 1. Note the distinct bony spur and the individual dural sac of each hemicord

Click here to view
Figure 6: (a-d): Mahapatra and Gupta subclassification of Type 1 SCM

Click here to view

  1. Type Ia, wherein the bone spur lays in the center of the split with an equally duplicated cord above and below the spur;
  2. Type Ib, wherein the bone spur is situated at the superior pole with no space above it and a large duplicated cord lower down;
  3. Type Ic, wherein the bone spur is situated on the lower pole with a large duplicated cord above;
  4. Type Id, wherein a bone spur is straddling the bifurcation of the spinal cord with no space above or below the spur.

They found that the risk of inflicting trauma to the hemicords is highest in Type 1d, 4/6 patients in their series had post-operative deterioration.[13] Urinary retention postsurgery, arachnoiditis, and infections are the reported complications which are managed conservatively.[13],[65]

 » Conclusion Top

Cervical SCM is fortunately an exceptionally rare condition, with less than 75 cases documented in literature. MRI remains the investigation of choice. The controversy regarding prophylactic surgery in asymptomatic individuals remains. We advocate prophylactic surgery in all asymptomatic individuals to preclude severe neurological deficit following trivial trauma in the future. The results of surgery in asymptomatic individuals are excellent while those in symptomatic individuals are good as well. All cases undergoing orthopedic deformity correction surgeries should be routinely screened for cord anomalies to prevent inadvertent perioperative catastrophes.


The authors wish to thank Dr. S. Siva Chidambaram, Chief Librarian, Dr. B.B. Dikshit, Librarian, All India Institute of Medical Sciences for their help in procuring some of the lesser accessible references used in this review.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

 » References Top

Mahapatra AK. Split cord malformation - A study of 300 cases at AIIMS 1990-2006. J Pediatr Neurosci 2011; 6(Suppl 1):S41-5.  Back to cited text no. 1
Edelson JG, Nathan H, Arensburg B. Diastematomyelia--the “double-barrelled” spine. J Bone Joint Surg Br 1987;69:188-9.  Back to cited text no. 2
Perret G. Diagnosis and treatment of diastematomyelia. Surg Gyn Obstet 1957;105:69-83.  Back to cited text no. 3
Ollivier C. Traité des Maladies de la Moelle Épinière., 3rd ed. Paris: Méquignon Marvis; 1837.  Back to cited text no. 4
Cohen J, Sledge CB. Diastematomyelia. An embryological interpretation with report of a case. Am J Dis Child 1960;100:257-63.  Back to cited text no. 5
Hertwig O. Urmund und Spina Bifida. Arch Mikr Anat 1892;39:353-503.  Back to cited text no. 6
Von Recklinghausen F. Untersuchungen über die spina bifida. Virchows Arch Path Anat 1886;105:243-330.  Back to cited text no. 7
Herren RY, Edwards JE. Diplomyelia (Duplication of the Spinal Cord). Arch Path 1940;30:1203-14.  Back to cited text no. 8
Hamby W. Pilonidal cyst, spina bifida occulta abd bifid spinal cord. Report of a case with review of the literature. Arch Pathol 1936;21:831-8.  Back to cited text no. 9
Pang D, Dias MS, Ahab-Barmada M. Split cord malformation: Part I: A unified theory of embryogenesis for double spinal cord malformations. Neurosurgery 1992;31:451-80.  Back to cited text no. 10
Simpson RK, Jr., Rose JE. Cervical diastematomyelia. Report of a case and review of a rare congenital anomaly. Arch Neurol 1987;44:331-5.  Back to cited text no. 11
Whittle IR, Besser M. Congenital neural abnormalities presenting with mirror movements in a patient with Klippel-Feil syndrome. Case report. J Neurosurg 1983;59:891-4.  Back to cited text no. 12
Mahapatra AK, Gupta DK. Split cord malformations: A clinical study of 254 patients and a proposal for a new clinical-imaging classification. J Neurosurg 2005;103(6 Suppl):531-6.  Back to cited text no. 13
David KM, Copp AJ, Stevens JM, Hayward RD, Crockard HA. Split cervical spinal cord with Klippel-Feil syndrome: Seven cases. Brain 1996;119(Pt 6):1859-72.  Back to cited text no. 14
Ulmer JL, Elster AD, Ginsberg LE, Williams DW 3rd. Klippel-Feil syndrome: CT and MR of acquired and congenital abnormalities of cervical spine and cord. J Comput Assist Tomogr 1993;17:215-24.  Back to cited text no. 15
Gunderson CH, Solitare GB. Mirror movements in patients with the Klippel-Feil syndrome. Neuropathologic observations. Arch Neurol 1968;18:675-9.  Back to cited text no. 16
Giordano GB, Davidovits P, Cerisoli M, Giulioni M. Cervical diplomyelia revealed by computed tomography (CT). Neuropediatrics 1982;13:93-4.  Back to cited text no. 17
Naidich TP, McLone DG, Fulling KH. The Chiari II malformation: Part IV. The hindbrain deformity. Neuroradiology 1983;25:179-97.  Back to cited text no. 18
Beyerl BD, Ojemann RG, Davis KR, Hedley-Whyte ET, Mayberg MR. Cervical diastematomyelia presenting in adulthood. Case report. J Neurosurg 1985;62:449-53.  Back to cited text no. 19
Anand AK, Kuchner E, James R. Cervical diastematomyelia: Uncommon presentation of a rare congenital disorder. Comput Radiol 1985;9:45-9.  Back to cited text no. 20
Kuchner EF, Anand AK, Kaufman BM. Cervical diastematomyelia: A case report with operative management. Neurosurgery 1985;16:538-42.  Back to cited text no. 21
Levine RS, Geremia GK, McNeill TW. CT demonstration of cervical diastematomyelia. J Comput Assist Tomogr 1985;9:592-4.  Back to cited text no. 22
Okada K, Fuji T, Yonenobu K, Ono K. Cervical diastematomyelia with a stable neurological deficit. Report of a case. J Bone Joint Surg Am 1986;68:934-7.  Back to cited text no. 23
Wolf AL, Tubman DE, Seljeskog EL. Diastematomyelia of the cervical spinal cord with tethering in an adult. Neurosurgery 1987;21:94-8.  Back to cited text no. 24
Nakamura Y, Soga F, Takahashi M, Tarui S, Yamashita K. [Two patients with cervical diastematomyelia]. Rinsho Shinkeigaku 1989;29:371-5.  Back to cited text no. 25
Ohwada T, Okada K, Hayashi H. Thoracic myelopathy caused by cervicothoracic diastematomyelia. A case report. J Bone Joint Surg Am 1989;71:296-9.  Back to cited text no. 26
Pfeifer JD. Basicranial diastematomyelia: A case report. Clin Neuropathol 1991;10:232-6.  Back to cited text no. 27
Herman TE, Siegel MJ. Cervical and basicranial diastematomyelia. AJR Am J Roentgenol 1990;154:806-8.  Back to cited text no. 28
Rawanduzy A, Murali R. Cervical spine diastematomyelia in adulthood. Neurosurgery 1991;28:459-61.  Back to cited text no. 29
Birch BD, McCormick PC. High cervical split cord malformation and neurenteric cyst associated with congenital mirror movements: Case report. Neurosurgery 1996;38:813-5; discussion 5-6.  Back to cited text no. 30
Jaeger HJ, Schmitz-Stolbrink A, Mathias KD. Cervical diastematomyelia and syringohydromyelia in a myelomeningocele patient. Eur Radiol 1997;7:477-9.  Back to cited text no. 31
Andronikou S, Fieggeru AG. Klippel-Feil syndrome with cervical diastematomyelia in an 8-year-old boy. Pediatr Radiol 2001;31:636.  Back to cited text no. 32
Balci S, Oguz KK, Firat MM, Boduroglu K. Cervical diastematomyelia in cervico-oculo-acoustic (Wildervanck) syndrome: MRI findings. Clin Dysmorphol 2002;11:125-8.  Back to cited text no. 33
Korinth MC, Kapser A, Nolte K, Gilsbach JM. Cervical diastematomyelia associated with an intradural epidermoid cyst between the hemicords and multiple vertebral body anomalies. Pediatr Neurosurg 2004;40:253-6.  Back to cited text no. 34
Huang SL, Shi W, Zhang LG. Characteristics and surgery of cervical myelomeningocele. Childs Nerv Syst 2010;26:87-91.  Back to cited text no. 35
Rustamzadeh E, Graupman PC, Lam CH. Basicranial diplomyelia: An extension of the split cord malformation theory. Case report. J Neurosurg 2006;104(5 Suppl):362-5.  Back to cited text no. 36
Ozturk E, Sonmez G, Mutlu H, Sildiroglu HO, Velioglu M, Basekim CC, Kizilkaya E. Split-cord malformation and accompanying anomalies. J Neuroradiol 2008;35:150-6.  Back to cited text no. 37
Andro C, Pecquery R, De Vries P, Forlodou P, Fenoll B. Split cervical spinal cord malformation and vertebral dysgenesis. Orthop Traumatol Surg Res 2009;95:547-50.  Back to cited text no. 38
Orakdogen M, Turk CC, Ersahin M, Biber N, Berkman Z. Spinal dysraphisms of the cervicothoracic region in childhood. Turk Neurosurg 2009;19:400-5.  Back to cited text no. 39
Borkar SA, Mahapatra AK. Split cord malformations: A two years experience at AIIMS. Asian J Neurosurg 2012;7:56-60.  Back to cited text no. 40
[PUBMED]  [Full text]  
Oyar O, Ismailoglu O, Albayrak B. Coexistence of occipital and infratorcular meningocele with cervical split cord anomaly. Singapore Med J 2012;53:e145-7.  Back to cited text no. 41
Maloney PR, Murphy ME, Sullan MJ, Van Abel KM, Cofer SA, Cheville JC, Wetjen NM. Clinical and surgical management of a congenital Type II split cord malformation presenting with progressive cranial neuropathies: Case report. J Neurosurg Pediatr 2017;19:349-53.  Back to cited text no. 42
Myles LM, Steers AJ, Minns R. Cervical cord tethering due to split cord malformation at the cervico-dorsal junction presenting with self-mutilation of the fingers. Dev Med Child Neurol 2002;44:844-8.  Back to cited text no. 43
Chandra PS, Kamal R, Mahapatra AK. An unusual case of dorsally situated bony spur in a lumbar split cord malformation. Pediatr Neurosurg 1999;31:49-52.  Back to cited text no. 44
Pang D, Wilberger JE, Jr. Tethered cord syndrome in adults. J Neurosurg 1982;57:32-47.  Back to cited text no. 45
Pang D. Ventral tethering in split cord malformation. Neurosurg Focus 2001;10:e6.  Back to cited text no. 46
Vandresse JH, Cornelis G. Diastematomyelia: Report of eight observations. Neuroradiology 1975;10:87-93.  Back to cited text no. 47
Hulser PJ, Schroth G, Petersen D. Magnetic resonance and CT imaging of diastematomyelia. Eur Arch Psychiatry Neurol Sci 1985;235:107-9.  Back to cited text no. 48
Yamada S, Zinke DE, Sanders D. Pathophysiology of “tethered cord syndrome”. J Neurosurg 1981;54:494-503.  Back to cited text no. 49
Sonigo-Cohen P, Schmit P, Zerah M, Chat L, Simon I, Aubry MC, Gonzales M, Pierre-Kahn A, Brunelle F. Prenatal diagnosis of diastematomyelia. Childs Nerv Syst 2003;19:555-60.  Back to cited text no. 50
Biri AA, Turp AB, Kurdoglu M, Himmetoglu O, Tokgoz Ercan N, Balci S. Prenatal diagnosis of diastematomyelia in a 15-week-old fetus. Fetal Diagn Ther 2005;20:258-61.  Back to cited text no. 51
Li SL, Luo G, Norwitz ER, Wang C, Ouyang S, Wen HX, Xia X, Yao Y. Prenatal diagnosis of diastematomyelia: A case report and review of the literature. J Clin Ultrasound 2012;40:301-5.  Back to cited text no. 52
Turgal M, Ozyuncu O, Talim B, Yazicioglu A, Onderoglu L. Prenatal diagnosis and clinicopathologic examination of a case with diastematomyelia. Congenit Anom (Kyoto) 2013;53:163-5.  Back to cited text no. 53
Lituania M, Tonni G, Araujo Junior E. First trimester diagnosis of cervico-thoracic diastematomyelia and diplomyelia using three-dimensional ultrasound. Childs Nerv Syst 2015;31:2245-8.  Back to cited text no. 54
Proctor MR, Scott RM. Long-term outcome for patients with split cord malformation. Neurosurg Focus 2001;10:e5.  Back to cited text no. 55
Perez LM, Barnes N, MacDiarmid SA, Oakes WJ, Webster GD. Urological dysfunction in patients with diastematomyelia. J Urol 1993;149:1503-5.  Back to cited text no. 56
Zuccaro G. Split spinal cord malformation. Childs Nerv Syst 2003;19:104-5.  Back to cited text no. 57
Matson DD, Woods RP, Campbell JB, Ingraham FD. Diastematomyelia (congenital clefts of the spinal cord); diagnosis and surgical treatment. Pediatrics 1950;6:98-112.  Back to cited text no. 58
Frerebeau P, Dimeglio A, Gras M, Harbi H. Diastematomyelia: Report of 21 cases surgically treated by a neurosurgical and orthopedic team. Childs Brain 1983;10:328-39.  Back to cited text no. 59
McMaster MJ. Occult intraspinal anomalies and congenital scoliosis. J Bone Joint Surg Am 1984;66:588-601.  Back to cited text no. 60
Gilmor RL, Batnitzky S. Diastematomyelia--rare and unusual features. Neuroradiology 1978;16:87-8.  Back to cited text no. 61
Pang D, Parrish RG. Regrowth of diastematomyelic bone spur after extradural resection. Case report. J Neurosurg 1983;59:887-90.  Back to cited text no. 62
Gupta DK, Ahmed S, Garg K, Mahapatra AK. Regrowth of septal spur in split cord malformation. Pediatr Neurosurg 2010;46:242-4.  Back to cited text no. 63
Prasad GL, Borkar SA, Satyarthee GD, Mahapatra AK. Split cord malformation with dorsally located bony spur: Report of four cases and review of literature. J Pediatr Neurosci 2012;7:167-70.  Back to cited text no. 64
[PUBMED]  [Full text]  
Pang D. Split cord malformation: Part II: Clinical syndrome. Neurosurgery 1992;31:481-500.  Back to cited text no. 65


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]

  [Table 1]


Print this article  Email this article
Online since 20th March '04
Published by Wolters Kluwer - Medknow