Imaging diagnosis and clinical presentation of a Chiari malformation ...
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Imaging diagnosis and clinical presentation of a Chiari malformation ...

EQUINE VETERINARY EDUCATION 1Equine vet. Educ. (2012) •• (••) ••-••doi: 10.1111/j.2042-3292.2011.00359.xCase ReportImaging diagnosis and clinical presentation of a Chiarimalformation in a Thoroughbred foalA. Lempe*, M. Heine † , B. Bosch ‡ , K. Mueller § and W. BrehmLarge Animal Clinic for Surgery; † Large Animal Clinic for Theriogenology and Ambulatory Services;‡ Department of Small Animal Medicine; and § Institute of Pathology, University of Leipzig, Leipzig,Germany.Keywords: horse; Chiari malformation; spina bifida; congenital; MRISummaryA newborn Thoroughbred foal was presented to the clinicwith ambiguous neurological deficits, spinal anomalies anda soft tissue swelling dorsal to the lumbar vertebral column.The foal was alert but unable to rise and stand. Withradiography, ultrasonography, computed tomography(CT) and magnetic resonance imaging (MRI) a lumbardysraphic anomaly, cerebellar herniation and coincidentalskeletal abnormalities were documented. Finally, ameningomyelocele was defined and, in context with thecerebellar herniation through the foramen magnum, thefoal was diagnosed to have a Chiari malformation. The MRIexamination corresponded best with the post mortemfindings. Although 3-dimensional imaging methods havebeen considered superior regarding full and detailedassessment of the congenital malformation, radiographyand ultrasonography also provide essential information todiagnose dysraphic lesions at reduced costs and efforts. AChiari malformation should be considered as a differentialdiagnosis in foals with neurological deficits.IntroductionCleft anomalies and dysraphism are rare congenitalconditions in the equine species caused by an embryonicfailure of vertebral fusion (Copp and Greene 2010). Spinabifida is the most commonly used term describing suchmalformations. A more accurate definition refers to theextent of spinal cord protrusion through the cleft. In horsesmeningomyelocele and meningeal cysts of the cervicaland thoracic segment combined with dorsal or lessobvious ventral protrusion have already been described(Leathers et al. 1979; Harmelin et al. 1993; Doige 1996; Rivaset al. 1996; Jacobsen et al. 2007; Rendle et al. 2008;Gerhauser et al. 2010). Due to the variation of cleft*Corresponding author email: lempe@vetmed.uni-leipzig.deanomalies and other spinal deformities (Lerner and Riley1978; Kirberger and Gottschalk 1989; Ryan et al. 1992;Johnson et al. 1997; Wong et al. 2005) clinical signs areinconsistent including general paresis, ataxia, ‘dog-sitting’position and delayed or nonexistent response to reflextests. The majority of affected foals were diagnosed bynecropsy at only a few weeks or even months whenneurological signs had increased.A number of species, including calves (McFarland1959; Gruys 1973; Ohfuji 1999) sheep (Potter et al. 2010),dogs (Chesney 1973; Wilson et al. 1979; Ruberte et al.1995; Shamir et al. 2001) and cats (Plummer et al. 1993)can demonstrably develop spina bifida. However,the uncommon condition of a meningomyelocele inassociation with cerebellar herniation through the foramenmagnum has only been described in calves (Frauchigerand Fankhauser 1952; Gruys 1973; Cho and Leipold 1977;Madarame et al. 1993; LeClerc et al. 1997; Testoni et al.2010; Zani et al. 2010) and one dog (Schmidt et al. 2008).This complex congenital disorder has similarities withhuman Chiari malformation type II and, to date, nodescriptions exist referring to this condition in the equinespecies.The following report describes the first case of afoal with Chiari malformation using radiography,ultrasonography, MRI and CT in order to identify andto characterise the involved structures noninvasively.The imaging diagnosis which can be derived from suchtechniques was assessed and compared with the findingsof the post mortem examination.Case detailsHistoryA few hours old female Thoroughbred foal was referred tothe clinic for evaluation of a distinct swelling dorsal over thelumbar column and to clarify its inability to rise or stand. The© 2012 EVJ Ltd

2 Chiari malformation in a foalowner reported no noticeable problems during the mare’spregnancy and, after a gestation period of 319 days,parturition had been uneventful. The foal presented wasthe third foal of the mare without repeat breeding; earlierfoals were born healthy on time. A soft swelling at the foal’sdorsal lumbar region had been present since birth. At nopoint in time had the foal been able either to rise or tostand but showed temporary movement of the front limbs.Clinical examinationOn admission, the foal was in lateral recumbency butalert and showed paroxysmal flailing movement of boththoracic limbs. The head could only be lifted for shortperiods. Turning to a sternal position to stand up wasimpossible for the foal due to the inability of anyspontaneous coordinated movement of the hindlimbs.Absence of the withdrawal reflex with nociceptivedeficiency of the pelvic limbs was noticed. Generally, thefoal had a good body condition, and temperature, pulseand respiratory rates were within the normal limits. Theowner could not provide information on whether the foalhad defaecated or urinated normally.A soft, fluctuant swelling approximately 4 ¥ 5 cm risingapproximately 3 cm above the skin was present atthe dorsal lumbar region. The skin over the swelling wascovered with focal ulcerations at the dome (Fig S1).Palpation seemed painful to the foal. The swelling hada fluid-filled consistency but the bulging dimensionsimpeded palpation of the vertebrae beneath.Additionally, a severe lateral displacement along thethoracic vertebral column was noted suggesting a scoliosismalformation.Diagnostic imagingRadiographyRadiographs (FCR 5000) 1 were obtained in laterolateral anddorsoventral projections. The images showed a severeC-shaped scoliosis (concave side left) of the thoracolumbarsegment and distinct homogenous soft tissue opacity dorsalto the 3rd to 6th lumbar vertebrae. Evaluation of theintegrity of the particular vertebrae was hindered by the2-dimensional superimposition and oblique projection.However, the spinous processes appeared abnormallythickened and misshapen in this region (Fig 1). Due tothe severe scoliosis and suspected dysraphic lesion theowner requested euthanasia. Imaging examination wascontinued immediately after death.UltrasonographySubsequently, the swelling was clipped and prepared forfurther ultrasonographical examination in transverse andlongitudinal orientation using a 10 MHz linear transducer 2 .Transverse ultrasonograms demonstrated a symmetricalsplit formation of the underlying spinous processes andthe dorsal arch of L3 to L6 allowing ultrasonographicalaccess to the soft tissue content. The depth of the cavitymeasured 5 cm from the skin to the layer of well definedhyperechoic, homogenous tissue ventrally. In transverseorientation the width measured 2 cm ventrally, divergingto 5 cm dorsally. The bone cavity and swelling containedan irregularly arranged tissue accumulation of moderateechogenicity and varying amounts of fluid-like anechoicareas, bordered by a narrow hyperechoic tissue layer(Fig 2). Considering the defect as a cleft formation ofthe vertebral column, the hyperechoic tissue layer wascharacterised as meningeal protrusion surroundingascending parts of the spinal cord, nerve filaments andcerebrospinal fluid.Computed tomography (CT)Computed tomography (Brilliance CT 6, Philips Wholebody-CT Mx8000 IDT) 3 was performed in noncontrastimages and 3D-reconstruction to visualise the thoracicand lumbar vertebral column with the foal in ventralrecumbency. On CT images the lateral deviation of thethoracic vertebral column was clearly visible, involving T14Fig 1: Radiograph in laterolateral projection. Cranial is to the left. Homogenous soft tissue opacity is visible dorsal to the lumbar vertebralcolumn (arrow), spinous processes beneath are abnormally shaped. In addition a severe scoliosis of the thoracolumbar column is visible.© 2012 EVJ Ltd

A. Lempe et al. 3Fig 2: Transverse ultrasonogram of the lumbar swelling. Left is to theleft. The arch and spinous process of the vertebra are not fusedallowing examination of the cavity, which is formed by the innersurface of the vertebra (a), thin hyperechoic bulging meninges (b)and skin (c). Within the cavity irregular arranged spinal cord tissue(d) and anechoic cerebrospinal fluid (e) are visible.and extending to L1. Additionally, there was a clockwiserotation of the vertebral bodies of T15 to L1 from 10–50°around the central spinal axis. The dorsal arches, includingthe spinous processes from L3–L6 were not fused; theyappeared almost symmetrically divided, leaving a cleftof approximately 3 cm maximum. The dorsal arches ofthe sacral vertebrae were complete but their spinousprocesses were also nonfused. Additional findings were afracture of the 18th rib on the left side and a fusion of 3 ribstructures on the right side articulating with T17. The right18th rib was not visible (Fig 3).Magnetic resonance imaging (MRI)Magnetic resonance imaging was performed tocharacterise the soft tissue using a 0.5 Tesla scanner(Gyroscan T5-NT) 3 . The foal was placed in dorsalrecumbency on the table and scanned in T1- andT2-weighted spin and gradient sequences. Images wereobtained in sagittal, transverse and dorsal planes. Tissuecharacterisation in T1-weighted sequences was made inrelation to the longissimus dorsi muscle. Tissue of isointensesignal intensity extended through the dorsal opening ofaffected vertebrae, representing grey and white matter.The isointense, inhomogenous tissue originating fromthe epidural space was enlarged in its dorsoventralFig 3: Three-dimensional computed tomography reconstruction ofthe caudal thoracic and lumbar vertebral column. Cranial is to theleft. The images show a severe scoliosis and rotation of thoracicand lumbar vertebral column. The dorsal arches of the lumbarvertebrae (a) and the spinous processes of the sacral vertebrae (b)are not fused. The 18th left rib is fractured (c) and the contralateralrib is not entirely developed (e). The 17th thoracic vertebraarticulates with 3 fused ribs (d).dimensions. The cavity contained hypointensecerebrospinal fluid and was bordered by isointensemeninges and skin which could not be visualisedseparately. In T2-weighted sequences the cerebrospinalfluid and the tissue of the spatium epidurale showedincreased signal intensities compared to T1-weightedsequences. The demarcation of the epidural spacebeneath the nonfused vertebrae was clear as there wassignal difference to the hypointense, ventral part of themeninges (Fig 4a). Due to the cross-sectional sectionsalong the arching protrusion, assessment of the originand definition of the spinal cord in transverse planes waslimited. Differentiation of grey and white matter within thespinal cord was not possible in the affected region (Fig 4b).Magnetic resonance imaging examination of the craniumrevealed a herniation of the cerebellum through theforamen magnum into the spinal canal. Diagnosis of amalformation resembling a Chiari type II malformation wasmade, founded on the previously described protrusionof the spinal cord and meninges at the lumbar region.In addition, a dilatation of the cranial spinal canal wasapparent on sagittal images indicating a hydromyelia(Fig 4c).Post mortem examinationOn post mortem examination a severe scoliosis about20 cm in length was diagnosed involving both the thoracicand lumbar segment (T13–L3) of the vertebral column.© 2012 EVJ Ltd

4 Chiari malformation in a foalFig 4: Sagittal (a) and transverse (b) MR-images of the lumbar region in T2-weighted spin echo sequence. Protrusion of the spinal cord isvisible (A) deviating from the enlarged epidural space (B). Nerve filaments of intermediate signal intensity ascend from the spinal cord(C; not visible on transverse images due to the greater slice thickness). The dorsal cavity is filled with hyperintense cerebrospinal fluid(D). Sagittal view of the cranium in a T2-weighted spin echo sequence (c). Cerebellar herniation through the foramen magnum is visible(2 arrows). Dilatation of the cranial spinal canal (hydromyelia) is marked by hyperintense signal intensity (arrowhead). Accuracy of theMR-interpretation was proved by the post mortem examination (a, c).Additionally, the lumbar vertebral column had a completedysraphic malformation dorsally from the 4th to 6thvertebrae (spina bifida aperta) with bullous protrusionof meninges and parts of the spinal cord(meningomyelocele). The cavity was filled with liquorspinalis (Fig 4a). After longitudinal sectioning of thecranium herniation of the cerebellar vermis through theforamen magnum was obvious and therefore the imagingdiagnosis of a Chiari malformation type II could beconfirmed (Fig 4c).DiscussionSpina bifida is classified as spina bifida aperta (also cystica)defined by a protrusion of spinal tissue through the cleftvertebrae or as spina bifida occulta where the spinal cordtissue remains in place. Depending on the protrudingtissue, a spina bifida aperta can be divided into 3 subtypes.In case of a meningocele only the meninges bulge out toform an apparent cyst (Leathers et al. 1979; Doige 1996)whereas a meningomyelocele is characterised by thepassage of meninges and parts of the spinal tissueincluding nerve cords through the bone cleft (Harmelinet al. 1993; Rivas et al. 1996; Jacobsen et al. 2007). Inhuman medicine this type is the most common amongall spinal defects (DeMarco et al. 2011). Myeloschisisrepresents the most severe subtype by exposing spinaltissue without a covering of skin, and to date this conditionhas not been reported in horses.A previous report of a miniature colt with a cervicalmeningomyelocele and hydrocephalus has alreadysuggested a Chiari malformation, but there was no provenevidence because of the lack of diagnostic imaging ofthe head and necropsy (Rivas et al. 1996). In our case,MR examination allowed the determining depictionof cerebellar herniation to diagnose a Chiari-like© 2012 EVJ Ltd

A. Lempe et al. 5malformation noninvasively. Even though the finaldiagnosis was based on MR findings of a foal recentlysubjected to euthanasia, such an examination is alsopractical in foals under general anaesthesia.The associated meningomyelocele was protrudingdorsal from the lumbar vertebrae, easily assessable withother imaging modalities. Radiographic indication ofspina bifida in the presented case was the appearanceof nonfused spinous processes in conjunction with aradiopaque mass dorsal to the suspected cleft. If possible,a ventrodorsal or dorsoventral orientation is preferable inyoung foals as in laterolateral views both parts of thespinous process superimpose. However, additionalcomplex malformation of the spinal column can also leadto superimposition of the dysraphic segment. Contrastmyelography may have resulted in increased informativevalue but due to the oncoming diagnostic procedures itwas not performed. Regarding the classification of thedysraphic lesion, ultrasonography was useful to evaluatesoft tissue involvement and furthermore to exclude othercauses of swellings along the column such as haematoma,seroma, neoplasia or vertebral fractures. In comparison tothe post mortem findings this method is considered to bemore sensitive than radiography. One report documentedthe cerebellar displacement in a calf ultrasonographicallyat the craniocervical junction but due to the differentequine anatomy the approach through the foramenmagnum is impractical in horses (Testoni et al. 2010). Threedimensionalimaging techniques are advantageous forvisualising complex vertebral malformations. Both, CTand MRI provided specific information and were equallyimportant to describe the multiple malformations of thiscase in detail. Computed tomography revealed thedegree of vertebral anomaly, the extension of the scoliosisin connection with vertebral rotation and the abnormalfusion of 3 ribs, findings which were incompletelydocumented during radiography. Most likely the fractureof the left 18th rib originates from parturition or a post natalevent. The conclusive diagnosis was based on MR-images.This imaging technique depicted the lumbar dysraphiclesion in close agreement with the pathological findings byshowing the exact protrusion of spinal cord tissue andmeninges, ascending nerve filaments, bulging tissue ofthe epidural space and accumulation of cerebrospinalfluid. T2-weighted sequences provided best detail. Thecombination of a spina bifida with other skeletalabnormalities is a previously described phenomenon (Choand Leipold 1977; Madarame et al. 1993; Ruberte et al.1995; Doige 1996; Denoix 2005; Jacobsen et al. 2007;Gerhauser et al. 2010). Thus it is advisable to preciselyevaluate a neonate or yearling with skeletal deformityand/or neurological signs as there is a wide range ofdifferential neurological diseases in young horses (MacKay2005; Johnson 2010); eventually the prognosis deteriorateswhen spina bifida has been diagnosed. In dogs, attemptsto correct spina bifida surgically are described (Fingerothet al. 1989; Shamir et al. 2001) but in horses no suchinterventions have been documented as being successful(Rivas et al. 1996). For the equine species an appropriatesurgical technique to treat cerebellar herniation is currentlynot available. The MR examination is regarded as essentialto distinguish foals with a fatal Chiari-like malformation fromthose only with vertebral abnormalities and to diagnoseless obvious dysraphism such as spina bifida occulta, ameningocele, ventral or cervical meningomyelocele intravitam.The occurrence of spina bifida in man is closelyassociated with folic acid deficiency but geneticdistribution, maternal age and diet also play a role (Coppand Greene 2010; DeMarco et al. 2011). The influence ofretinoic acid excess and a zinc deficiency may also leadto an increased prevalence of congenital dysraphism(Yasuda et al. 1986; Dubrulle and Pourquie 2004; Rendleet al. 2008). Oral supplementation of the B-vitaminfolic acid reduces the incidence of spina bifida in manbut a primary folate deficiency in horses is virtuallyimpossible considering their natural diet. However, itcould be demonstrated that secondary folate deficiencyappeared in horses after administrating sulphadiazineand pyrimethamine to treat equine protozoalmyeloencephalitis (Toribio et al. 1998; Piercy et al. 2002).Unfortunately we could not receive any informationregarding possible medical treatment during gestation ofthe mare in our case. In general, the mare and her foalwere in good body condition; none of the earlier foals ofthe mare had shown signs of a developmental disease. Abreed disposition can not be derived from literature.In conclusion, a Chiari malformation is a congenitaldisease also occurring in the equine species, the prognosisof which deteriorates when diagnosed. MRI is an importantdiagnostic modality to distinguish foals with this fataldisease from those with neurological disorders for otherreasons. Although 3-dimensional imaging methods weresuperior to assess the dysraphic anomaly in detail,conventional radiography and ultrasonography wereinexpensive alternatives that have proven to be sufficientlyconclusive in practice.Authors’ declaration of interestsNo conflicts of interest have been declared.Manufacturers’ addresses1 Fuji Photo Film GmbH, Düsseldorf, Germany.2 GE Healthcare Technologies, Solingen, Germany.3 Philips Healthcare, Hamburg, Germany.ReferencesChesney, C.J. (1973) A case of spina bifida in a Chihuahua. Vet. Rec. 93,120-121.Cho, D.Y. and Leipold, H.W. (1977) Arnold-Chiari malformation andassociated anomalies in calves. Acta Neuropathol. (Berl.) 39,129-133.© 2012 EVJ Ltd

6 Chiari malformation in a foalCopp, A.J. and Greene, N.D. (2010) Genetics and development ofneural tube defects. J. Pathol. 220, 217-230.DeMarco, P., Merello, E., Calevo, M.G., Mascelli, S., Pastorino, D.,Crocetti, L., DeBiasio, P., Piatelli, G., Cama, A. and Capra, A. (2011)Maternal periconceptional factors affect the risk of spina bifidaaffectedpregnancies: an Italian case-control study. Childs Nerv.Syst. 27, 1073-1081.Denoix, J.M. (2005) Thoracolumbal malformations or injuries andneurological manifestations. Equine Vet. Educ. 17, 191-194.Doige, C.E. (1996) Congenital cleft vertebral centrum and intra- andextraspinal cyst in a foal. Vet. Pathol. 33, 87-89.Dubrulle, J. and Pourquie, O. (2004) Coupling segmentation to axisformation. Development 131, 5783-5793.Fingeroth, J.M., Johnson, G.C., Burt, J.K., Fenner, W.R. and Cain, L.S.(1989) Neuroradiographic diagnosis and surgical repair of tetheredcord syndrome in an English bulldog with spina bifida andmyeloschisis. J. Am. Vet. Med. Ass. 9, 1300-1302.Frauchiger, E. and Fankhauser, R. (1952) Arnold-Chiari Hirnmissbildungmit spina bifida und Hydrocephlus beim Kalb. Schweiz. Arch. Tierhk.94, 145-149.Gerhauser, I., Geburek, F. and Wohlsein, P. (2010) Perosmus elumbis,cerebral aplasia and spina bifida in an aborted thoroughbred foal.Res. Vet. Sci. (in press).Gruys, E. (1973) Dicephalus, spina bifida, Arnold-Chiari malformationand duplication of thoracic organs in a calf. Zentralbl. vet. Med. A20, 789-800.Harmelin, A., Egozi, O., Nyska, A., Perel, S.A., Yakobson, B., Orgag, U.and Waner, T. (1993) Ventral meningomyelocele in a filly. J. Comp.Pathol. 109, 93-97.Jacobsen, B., Venner, M., Gerdwilker, A. and Wohlsein, P. (2007) Ventralmeningomyelocele in a german warmblood foal. Dtsch. Tierärztl.Wschr. 114, 470-472.Johnson, A.L. (2010) Congenital malformations – uncommon butimportant causes of neurological signs in neonates. Equine Vet.Educ. 22, 599-601.Johnson, P.J., Hohnson, C. and Pace, L.W. (1997) Thoracic vertebralmalformation in two horses. Equine Vet. J. 29, 493-496.Kirberger, R.M. and Gottschalk, R.D. (1989) Developmentalkyphoscoliosis in a foal. J. S. Afr. Vet. Ass. 60, 146-148.Leathers, C.W., Wagner, P.C. and Millesson, B. (1979) Cervical spinabifida with meningocele in an Appaloosa foal. J. Vet. Orthop. 1,55-58.LeClerc, S., Lopez, A. and Illanes, O. (1997) Central nervous system andvertebral malformation resembling the Arnold-Chiari syndrome in aSimmental calf. Can. Vet. J. 38, 300-301.Lerner, D.J. and Riley, G. (1978) Congenital kyphoscoliosis in a foal.J. Am. Vet. Med. Ass. 172, 274-276.MacKay, R.J. (2005) Neurologic disorders of neonatal foals. Vet. Clin. N.Am.: Equine Pract. 21, 387-406.Madarame, H., Ito, N. and Takai, S. (1993) Dicephalus, Arnold-chiarimalformation and spina bifida in a japanese black calf. J. Vet. Med.40, 155-160.McFarland, L.Z. (1959) Spina bifida with myelomeningocele in a calf.J. Am. Vet. Med. Ass. 134, 32-34.Ohfuji, S. (1999) Spinal dysraphism in a newborn Holstein-Frisian calf. Vet.Pathol. 36, 607-609.Piercy, R.J., Hinchcliff, K.W. and Reed, S.M. (2002) Folate deficiencyduring treatment with orally administered folic acid, sulphadiazineand pyrimethamine in a horse with suspected equine protozoalmyeloencephalitis (EPM). Equine Vet. J. 34, 311-316.Plummer, S.B., Bunch, S.E., Khoo, L.H., Spaulding, K.A. and Kornegay,J.N. (1993) Tethered spinal cord and intradural lipoma associatedwith meningocele in a Manx-type cat. J. Am. Vet. Med. Ass. 203,1159-1161.Potter, K.A., Weston, J.F., Munday, J.S. and Johnstone, A.C. (2010) Spinabifida with associated malformations of the central nervous systemin a Dorper-cross sheep. N. Z. Vet. J. 58, 315-318.Rendle, D.I., Durham, A.E., Bestbier, M., Smith, K.C. and Boswell, J.C.(2008) Neurenteric cyst with associated butterfly vertebrae in aseven-month-old colt. Vet. Rec. 162, 558-561.Rivas, L.J., Hinchcliff, K.W. and Robertson, J.T. (1996) Cervicalmeningomyelocele associated with spina bifida in a hydrocephalicminiature colt. J. Am. Vet. Med. Ass. 209, 950-953.Ruberte, J., Anor, S., Carretero, A., Vilafranca, M., Navarro, M., Mascort,J. and Pumarola, M. (1995) Malformations of vertebral bodies andthe rips associated to spinal dysraphism without spina bifida in aPekinese dog. Zentralbl. Vet. Med. A 42, 307-313.Ryan, J.A., Modransky, P.D., Welker, F.H., Moon, M.L. and Saunders, G.K.(1992) Kyphoscoliosis in two miniature horses. Equine Pract. 14,21-23.Schmidt, M., Wigger, A., Jawinski, G., Goll, T. and Kramer, M. (2008)Ultrasonographic appearance of the craniocervical junction innormal brachycephalic dogs and dogs with caudal occipital(Chiari-like) malformation. Vet. Radiol. Ultrasound 49, 472-476.Shamir, M., Rochkind, S. and Johnston, D. (2001) Surgical treatment oftethered spinal cord syndrome in a dog with myelomeningocele.Vet. Rec. 148, 755-756.Testoni, S., Pria, A.D. and Gentile, A. (2010) Imaging diagnosis –cerebellar displacement and spina bifida in a calf. Vet. Radiol.Ultrasound 51, 162-164.Toribio, R.E., Bain, F.T., Mrad, D.R., Messer, N.T., Sellers, R.S. and Hinchcliff,K.W. (1998) Congenital defects in newborn foals of mares treated forequine protozoal myeloencephalitis during pregnancy. J. Am. Vet.Med. Ass. 212, 697-701.Wilson, J.W., Kurtz, H.J. and Leipold, H.W. (1979) Spina bifida in the dog.Vet. Pathol. 16, 165-169.Wong, D.M., Scarratt, W.K. and Rohleder, J. (2005) Hindlimb paresisassociated with kyphosis, hemivertebrae and multiple vertebralmalformations in a Quarter Horse gelding. Equine Vet. Educ. 17,187-194.Yasuda, Y., Okamoto, M., Konishi, H., Matsuo, T., Kihara, T. and Tanimura,T. (1986) Developmental anomalies induced by all-trans retinoicacid in fetal mice: I. Macroscopic finding. Teratology 34, 37-49.Zani, D.D., de Zani, D., Morandi, N., Biggi, M., Belloli, A.G., Riccaboni, P.,Rodena, M., Giancamillo, M.D. and Pravettoni, D. (2010) Imagingdiagnosis – split cord malformation. Vet. Radiol. Ultrasound 51, 57-66.Supporting informationAdditional supporting information may be found in the online version ofthis article.Fig S1: Photograph of a Thoroughbred foal a few hours old showing adistinct swelling at the dorsal lumbar region. There is also a scolioticmalformation of the thoracolumbar vertebral column visible.Please note: Wiley-Blackwell are not responsible for the content orfunctionality of any supporting materials supplied by the authors. Anyqueries (other than missing material) should be directed to thecorresponding author for the article.© 2012 EVJ Ltd

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