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Introduction
Neural tube defects (NTDs) are rarely reported in
companion animals and refer to a collection of con-
genital malformations that are the result of abnormal
development during embryogenesis.1 Limited dorsal
myeloschisis (LDM) is a distinctive form of NTD,
described in humans, characterised by a focal ‘closed’
midline skin defect and a fibroneural stalk linking the
skin lesion to the underlying cord.2 It is a result of fail-
ure of the neural tube to close, with skin ectoderm
remaining attached to the borders of the neural plate.3
This prevents the vertebral arches forming, meaning
this condition is always seen concurrently with a bifid
Limited dorsal myeloschisis
in three cats: a distinctive form
of neural tube defect
Sarah Buttereld1, Beatriz Garcia-Gonzalez2,
Colin J Driver1* and Clare Rusbridge1,3
Abstract
Case series summary The aim of this case series was to describe the clinical presentation, imaging findings and
histopathology of three cats with limited dorsal myeloschisis (LDM). The history, examination and MRI sequences
were reviewed in three cases presented to a single referral hospital. The surgery report and histopathology were
described in two cases. All cats were young (10 weeks old, 5 months old, 4 years old), presenting with varying
degrees of progressive paraparesis. All had a midline skin defect overlying the spinal column that was either sunken
or saccular, containing fluid thought to be cerebrospinal fluid. MRI sequences demonstrated tissue extending
from the dura through an overlying bifid spinous process and attached to the dermis, with associated spinal cord
tethering, atrophy and syringomyelia. Lesions were located at L2–L3, T8–T9 and L4. Histopathology described a
fibroneural stalk with a glio-ependymal lining, surrounded by glial nests and nerve fibres. The youngest and most
severely affected was euthanased, while the other two underwent surgery. Both regained independent ambulation
with persistent paraparesis; however, one required ongoing management of urinary incontinence.
Relevance and novel information LDM is a primary neural tube defect that may result in neurological deficits,
including bladder dysfunction, and is characterised by a fibroneural stalk between the dermis and the spinal cord.
Distinct MRI features, such as a visible intrathecal tract, dorsally tethered cord and syringomyelia, help distinguish
this condition from the clinically similar dermoid sinus. The presence of progressive neurological signs, with a
palpable midline defect overlying the affected spinal cord segment, may raise suspicion for this clinical entity in
veterinary patients.
Keywords: Limited dorsal myeloschisis; neural tube defect; spinal dysraphism; dermoid sinus; spinal
malformation; midline defect; tethered cord
Accepted: 20 February 2020
1Fitzpatrick Referrals Orthopaedics and Neurology, Eashing, UK
2Veterinary Pathology Group (VPG) Histology, Bristol, UK
3School of Veterinary Medicine, Faculty of Health & Medical
Sciences, Vet School Main Building (VSM), University of Surrey,
Guildford, UK
*Current address: Lumbry Park Veterinary Specialists, Alton, UK
Corresponding author:
Sarah Butterfield BSc(Hons), BVSc, PGDip(VCP), MRCVS,
Fitzpatrick Referrals Orthopaedics and Neurology, Halfway Lane,
Eashing, Surrey GU7 2QQ, UK
Email: sbutterfield@fitzpatrickreferrals.co.uk; sarahbutterfield1@
hotmail.com
924307JOR0010.1177/2055116920924307Journal of Feline Medicine and Surgery Open ReportsButtereld et al
research-article2020
Case Series
2 Journal of Feline Medicine and Surgery Open Reports
vertebra. Histopathology provides a definitive diag-
nosis, describing glial tissue within the fibroneural
stalk either with scattered neurons within mesenchy-
mal tissue or arrangement in glial nests.2
A dermoid sinus, another form of NTD, forms as
a result of the failed separation of the neural tube from
the skin ectoderm.1 It appears clinically similar to LDM
and is most commonly documented in the Rhodesian
Ridgeback,4,5 where an autosomal dominant gene muta-
tion that creates the dorsal hair ridge predisposes them
to the condition.6,7 A visible midline skin defect is con-
tinuous with a ventral tubular sac that may be classed as
type I–V, depending on tissue depth penetrated.4,8 In
comparison with LDM, histologically the lumen consists
of sebum, keratin debris and hair follicles. Hair may be
seen to protrude from the sinus orifice, which, if pulled,
may lead to acute development of neurological signs in
previously normal animals.9 Neurological signs may
occur if the dermoid sinus connects to the dura mater, as
in type IV, and can be critical if infection tracks to these
structures. For this reason, dermoid sinuses that dis-
charge, become infected or cause neurological deficits,
are often treated surgically.
Spina bifida, the most common form of NTD in
humans, refers to a congenital failure of one or more ver-
tebral arches to close over the spinal cord.1 Three types
have been described: occulta (asymptomatic with no
neural tissue involvement); associated with a meningo-
coele (protrusion of the meninges through the bifid verte-
bra); or associated with a meningomyelocoele (protrusion
of meninges and spinal cord tissue).10
The intention of this case series was to describe three
cats, two of which were juveniles, that presented with
varying degrees of paraparesis and neurological deficits,
as well as a visible skin lesion in the localised spinal cord
segment. MRI findings in all cases were consistent with
a diagnosis of LDM, confirmed by histopathology in
the two cases that underwent surgical management.
This has never previously been described in veterinary
patients.
Case series description
Case 1
A 4-year and 8-month-old male neutered domestic short-
hair (DSH) cat presented with a 4-month history of
acute-onset, slowly progressive paraparesis following a
minor traumatic episode. A similar episode was noted
1 year previously, which resolved with 2 weeks of con-
servative treatment. Urination was normal. On examina-
tion, the cat was strongly ambulatory, and displayed
symmetric spastic paraparesis and pelvic limb ataxia.
Proprioceptive paw positioning and hopping reactions
were slightly delayed on the pelvic limbs with normal
segmental spinal reflexes. No pain response was elicited
on direct spinal palpation. The cat’s neurological deficits
were localised to a T3–L3 myelopathy. There was a pal-
pable depression in the vertebral column in the cranial
lumbar region that had been present since birth. MRI of
the thoracolumbar vertebral column revealed an L2–L3
malformation (Figure 1a,b). There was incomplete clo-
sure of the dorsal vertebral column at L2–L3 with exten-
sion of the meninges through the defect to create a tissue
stalk attaching to the overlying skin. There was marked
atrophy of the spinal cord at this level with a tethered
cord effect and syringomyelia. There was also dilation of
the subarachnoid space with cerebrospinal fluid (CSF).
It was elected to treat the cat surgically owing to the
progressive nature of the paraparesis. The surgical
approach involved dissection of the fibroneural stalk
from the surrounding subcutaneous tissues, a dorsal
laminectomy of the L3 vertebra and removal of the
stalk by durotomy. The dura was left open and the
laminectomy defect covered by collagen sponge.
Immediate postoperative analgesia included opioid and
non-steroidal anti-inflammatory drugs (NSAIDs).
Following surgery, the cat deteriorated neurologically
to become non-ambulatory with minimal voluntary
pelvic limb movement and absent postural reactions.
Following 1 week of hospitalisation and physiotherapy
it became ambulatory, similar to the preoperative sta-
tus, with reflex urination. One month after surgery, it
had continued to improve in activity. Spastic parapare-
sis and pelvic limb ataxia remained with voluntary uri-
nation and defaecation, although occasionally in
inappropriate locations.
The cat presented 9 months after the initial surgery
with a 2-month progressive non-painful deterioration in
pelvic limb ataxia. On presentation, it was non-ambulatory
with marked spastic paraparesis, absent proprioceptive
paw positioning in the pelvic limbs and normal segmen-
tal spinal reflexes. Repeat MRI revealed suspected adhe-
sion of the dura to the overlying laminal defect with
persistent subarachnoid dilation (Figure 2). A revision
dorsal laminectomy and durotomy confirmed this and
larger surgical margins were created. A porcine intesti-
nal submucosal graft was placed over the dural defect
and bovine collagen sponge over the laminectomy site.
One month after surgery the cat had shown slowly pro-
gressive improvement to regain independent ambula-
tion and urination.
Histology of the resected tissue was consistent with a
diagnosis of LDM (Figure 3). The stalk extended from
the superficial dermis into the subcutis and consisted of
glial tissue supported by thick bundles of collagen. The
glial tissue presented as streams, sometimes containing
few neurons, as well as multifocal nests that were embed-
ded within an abundant eosinophilic matrix. This tissue
surrounded a cavitated space lined by a glio-ependymal
lining. Also noted within the stalk were some nerve
fibres. Bands of condensed fibrous tissue, adipose tissue
Butterfield et al 3
Figure 1 MRI sequences of all three cases. All lesions were predominantly hyperintense on T2-weighted (T2W) images and isointense
on T1-weighted (T1W) images, with no clear contrast enhancement following gadolinium administration. Spinal cord dorsal tenting and
atrophy was a common feature. (a) T2W midsagittal sequence of the spinal column from T11 to S3 in case 1 showed incomplete closure
of the dorsal vertebral column. Tissue extending from the dura is seen attaching to the overlying dermis (arrow), with spinal cord tenting,
atrophy and syringomyelia. (b) T2W transverse sequence at the level of L2–L3 in case 1 demonstrating the stalk attaching to the dermis.
(c) T1W midsagittal sequence of the spinal column from C2 to L2 in case 2 showed tissue extending from the dura to the dermis at
the level of T8–T9 (arrow). (d) T2W transverse sequence at the level of T8 in case 2. (e) T2W midsagittal sequence of the T5–S1 spinal
column in case 3 displaying the midline defect at the level of L4 (arrow). (f) T2W transverse sequence at the level of L4 in case 3
Figure 2 T2-weighted midsagittal MRI from T11 to S3 in case 1 showed adhesion of the dura to the previous dorsal laminectomy
site with persistent dilation of the subarachnoid space with cerebrospinal fluid and associated cord compression (arrow)
4 Journal of Feline Medicine and Surgery Open Reports
and bundles of skeletal muscle were noted around the
stalk. Additional immunohistochemistry of case 1 docu-
mented S100 and glial fibrillary acidic protein-positive
cells within the stalk, confirming they were of neural
origin.
Case 2
A 5-month-old male neutered Bengal cat presented
with a 3-day history of acute onset paraparesis,
which was possibly secondary to an unwitnessed trau-
matic event. Urination was normal. On presentation,
the cat was ambulatory paraparetic with normal
proprioceptive paw positioning and segmental spinal
reflexes. No pain response was elicited on direct spinal
palpation. The cat localised to a T3–L3 myelopathy. It
had a distinct area of whorled hair overlying the T8
vertebra dorsally (Figure 4a).
Haematology and biochemistry revealed a mild
anaemia (haematocrit 28.8%; reference interval [RI]
30.3–52.3%) and mild elevation in phosphate
(2.45 mmol/l; RI 1.00–2.42 mmol/l). Initial investiga-
tions included electromyography and nerve conduction
velocity testing to assess for chronic polyneuropathy
previously reported in a cohort of young Bengal cats.11
Figure 3 Histopathology with haemotoxylin and eosin stain from case 1 were consistent with a diagnosis of limited dorsal
myeloschisis (LDM). Additional immunohistochemistry confirmed cells were of neural origin. (a) A cavitated space within the
centre of the fibroneural stalk is seen lined by an epithelium, consistent with glioependymal tissue from case 1 (× 20).
(b) Neuronal bodies (arrows) shown from case 1 are characteristic of LDM (× 10). (c) Immunohistochemistry. Positive staining
with S100 confirms that these cells are of neural origin (× 2.5). (d) Immunohistochemistry. Clusters of glial fibrillary acidic protein
(GFAP)-positive glial cells are seen within the fibroneural stalk. The glioependymal lining also stains positively with GFAP (× 2.5)
Butterfield et al 5
This was deemed an unlikely cause given that the clini-
cal signs of polyneuropathy would manifest as ‘lower
motor neuron’ weakness rather than upper motor neu-
ron, as in this case. These results were normal. MRI of
the thoracolumbar vertebral column (Figure 1c,d) con-
firmed the presence of a defect in the dorsal lamina at
T8–T9, with dorsal elevation of the spinal cord and dor-
solateral cord compression.
A dorsal surgical approach to the defect was made
(Figure 5). The fibroneural stalk was dissected from
surrounding tissues (Figure 6) and a dorsal laminec-
tomy performed. The tissue was seen to attach to the
meninges and also to the spinal cord. A circular durot-
omy was performed around the lesion, and the dura
left open. Immediate postoperative analgesia included
opioid and NSAIDs. The cat remained ambulatory but
ataxic immediately after surgery and was discharged
with rehabilitative care after 7 days of hospitalisation. It
continued to improve and had mild pelvic limb ataxia
at 14 days following surgery. Despite good voluntary
movement, the cat remained unable to urinate volun-
tarily and so was managed by manual expression, diaz-
epam, prazosin and bethanecol. This resolved after 4
weeks of supportive treatment.
Histology of the resected tissue was consistent with a
diagnosis of LDM (changes seen similar to that in Figure
3). Again, the lesion showed fibroneural tissue extending
from the superficial dermis into the subcutis. The lesion
was surrounded by thick bands of fibrous tissue.
Although nervous tissue could not be demonstrated on
Figure 4 The cutaneous defects varied in appearance. (a) An area of whorled hair with no palpable skin depression was seen
at the level of T8–T9 vertebrae in case 2. (b) A saccular cutaneous lesion was evident overlying the mid-lumbar region with
fluid discharge, likely cerebrospinal fluid in origin, as a result of rupture of the membranous sac in case 3. (c) A suspected
limited dorsal myeloschisis cutaneous saccular lesion was seen in a juvenile pug not included in this study, but included here
to show the characteristic appearance
Figure 5 Intraoperative image of case 2 showing the
fibroneural stalk extending to attach to the overlying dermis Figure 6 The fibroneural stalk can be seen in its entirety
attaching to the overlying dermis after complete surgical
excision (case 2)
6 Journal of Feline Medicine and Surgery Open Reports
the slides available, immunohistochemistry showed
many spindled-to-stellate cells present within the struc-
ture that exhibited S100 positivity, indicating a neuronal
or glial tissue origin.
Case 3
A 10-week-old male entire DSH cat presented with con-
genital non-ambulatory paraparesis and pelvic limb pro-
prioceptive deficits. The cat was also noted to have a
subcutaneous mass lesion overlying the mid lumbar ver-
tebral column, which had previously shown discharge of
a clear fluid suspected to be CSF (Figure 4b). Pro-
prioceptive paw positioning and hopping reactions were
absent on the pelvic limbs, with slightly reduced with-
drawal reflex and apparently absent pelvic limb and tail
noci ception. The cat was reportedly urinary and faecally
continent with no evidence of spinal pain. Thoracic limb
function, cranial nerves and perineal reflexes were unre-
markable. The cat localised to a L4–S3 myelopathy.
Serum haematology and biochemistry showed a
slightly decreased urea (42 µmol/l; RI 53–141 µmol/l)
and mild elevation in chloride (134 mmol/l; RI: 115–
126 mmol/l). CT (Figure 7) and MRI (Figure 1e,f) of the
thoracolumbar spine were performed, revealing a bifid
abnormality of the L4 vertebra. The spinal cord appeared
tethered at this level with a communication between that
and the cutaneous mass. The images were consistent
with a diagnosis of LDM with a saccular skin lesion. The
previous fluid discharge noted from the mass was con-
sidered highly likely to be CSF in origin. Owing to the
poor prognosis for neurological improvement, this cat
was euthanased shortly after diagnosis and no histopa-
thology was available to support our imaging findings.
Discussion
LDM is a distinctive form of NTD characterised by an
intrathecal extraspinal fibroneural stalk extending
from the dura to the overlying dermis with a visible
external midline defect closed by a bridging layer of
squamous epithelium.2 It is thought to be a result of
incomplete disjunction between cutaneous and neural
ectoderms during embryogenesis.1–3 Development of
the surrounding myofascial tissue continues, and so
the neural tube is progressively pulled deeper into the
body, leaving a dorsal median neural tissue. This
results in incomplete dorsal midline fusion of the skin
that eventually becomes bridged by an epithelial
membrane.2
Two types of cutaneous lesion have been described in
the human literature:2 non-saccular (with a flat or sunken
squamous epithelial crater or pit); and saccular (a skin-
based CSF-filled sac covered by a squamous epithelial
dome [see Figure 4c for a suspected example in a juve-
nile Pug]). Three distinguishable internal sac types have
been proposed from imaging findings:2 a saccular mye-
locystocoele; saccular-dome stalk; or saccular-basal nod-
ule. Additionally, transitional skin lesions may occur
where there is swelling of an otherwise flat skin surface
following straining, presumably secondary to CSF being
forced through a usually collapsed dural fistula.2 LDMs
in humans have been documented in all regions of the
vertebral column cranial to the conus medullaris.2
Three characteristic features specific to an LDM have
been defined in human medicine to aid in its diagnosis.
MRI demonstrates a focal cutaneous lesion (midline
crater or saccular swelling), a well-circumscribed inter-
nal fibroneural stalk connecting the dermis to the spi-
nal cord and a dural fistula encompassing the stalk.2
The MRI characteristics of LDM and congenital dermal
sinus (CDS) have been compared in humans, in an
attempt to distinguish between these two similar enti-
ties on imaging alone.12 Clinically, a greater incidence
of potentially fatal infection is seen with CDS cases in
humans, where a cutaneous entry point and lumen
Figure 7 CT images showing the defect in case 3. (a) Midsagittal CT sequence from T1 to S3 showing the defect in the L4
vertebra (arrow). (b) Transverse CT sequence at the level of L4 vertebra
Butterfield et al 7
provides a pathway for intraspinal pathogens.13 More
immediate surgical intervention is indicated in these
cases to prevent potentially catastrophic neurological
complications,2,12 such as meningitis. Significant imag-
ing findings to diagnose LDM included greater visibil-
ity of the intrathecal tract, direct attachment to the
dorsal spinal cord and dorsal tenting of the cord at the
tract–cord union with associated tethering effect (seen
in 83% of cases).12 Additionally, only patients with
LDM showed evidence of syringo myelia near the cord–
tract union.12 The images of our three cats were consist-
ent with these imaging findings.
Neurological signs can vary, with up to 50% of patients
documented as neurologically normal in one human
study.2 All three of our cats were significantly affected,
from marked ataxia as in case 2 to non-ambulatory para-
paresis in case 3. These signs predominantly relate to
the spinal cord tethering effect by the neural stalk to the
myofascial tissue.2,14 Early surgery is recommended in
humans, often before 9 months of age.2 This tethering
effect on the cord increases the likelihood of further neu-
rological injury with longitudinal growth of the vertebral
column in humans, and so it has been suggested that, if
left untreated, it will likely worsen neurologically over
time.2 As in case 2, this may explain the young age at
onset and progression of clinical signs.
It has also been hypothesised that traumatic events
exacerbate clinical signs in humans,15 causing extra ten-
sion or injury to the fibroneural stalk. There was circum-
stantial evidence of minor trauma in cases 1 and 2.
Persistent tension, scarring or acute inflammation of the
stalk secondary to trauma may contribute to the spinal
cord injury and therefore a short-term course of cortico-
steroids could be indicated as an alternative to surgical
management. However, there is a high likelihood of pro-
gressive injury and in humans prompt surgical manage-
ment of spinal cord tethering is recommended. The main
aim of the surgery is to remove this tethering effect, with
careful resection of the stalk from the attached dura, fre-
quently requiring a durotomy in humans.
Postoperative ‘tethered cord syndrome’ has also been
documented in humans, secondary to scar tissue forma-
tion or the use of grafts, years after the initial surgery.16
We propose this may have been the cause of clinical dete-
rioration seen in case one and its re-presentation 9 months
postoperatively.
There have been several reports of other vertebral
malformations in cats, predominantly seen in the Manx
breed. The Manx cat has been proposed as an animal
model for NTDs where the absence of the tail has been
documented in conjunction with sacrum agenesis, coccy-
geal agenesis, absence of the cauda equina and spina
bifida with a meningomyelocele, similar to that described
in humans.17,18 A meningocutaneous tract, tethered spinal
cord and intradural lumbosacral lipoma in an 8-month-
old male neutered Manx has also been reported.19
The Burmese breed has also been highlighted, with
several reports of cats presenting with progressive pelvic
limb ataxia and skin defects.20–22 A diagnosis of dermoid
sinus was made in these cases, with one kitten being
immediately euthanased,21 and one 2-year-old male
being successfully treated by a dorsal laminectomy pro-
cedure but remained persistently urinary incontinent.22
Dermoid sinus and associated spina bifida have also
been reported in dogs presenting with depressive skin
lesions, abnormal hair growth and mild pelvic limb neu-
rological deficits,4–7,20 where surgical treatment has been
successful with improvement in neurological function.20
Histopathology of these cases described a fibrous cord
with associated cystic structures containing keratinous
material, hair follicles, and apocrine and sebaceous glan-
dular tissue.20
There has been one notable case report of a 7-month-
old male neutered cat presenting with an ambulatory
T3–L3 myelopathy and a dermal lesion.23 A dorsal lami-
nectomy was performed and histopathology of the der-
mal stalk revealed the presence of neural tissue with
glial fibrillary acidic protein, as we have demonstrated
in cases 1 and 2. This may suggest this previous case
report demonstrates features consistent with a diagnosis
of LDM.
Three other dysraphic malformations have been docu-
mented in association with LDMs in humans. These are
dorsal lipomas,2 dermal sinus tracts2 and split cord mal-
formation,24,25 presumably due to similar disjunction
during primary neurulation. Other congenital abnormal-
ities have been documented in animals with other forms
of NTDs, including hydrocephalus,26 syringomyelia,26
cryptorchidism27 and cleft palate.28
Conclusions
The three cats presented showed clinical signs and MRI
findings consistent with a diagnosis of LDM; an NTD
characterised by a fibroneural stalk extending from the
dura to the overlying dermis with a visible midline skin
defect. It can be distinguished from a dermoid sinus by its
distinct intrathecal tract, dorsal tenting of the spinal cord
at the cord–tract union and the possible presence of
syringo myelia. Neurological deficits are presumed to be
related to the tethering effect on the spinal cord, which
may be exacerbated by additional trauma. Histopathology
demonstrates the presence of a fibroneural stalk directly
extending from the spinal cord to the overlying dermis.
Surgical management may provide some success in terms
of preventing disease progression. However, complica-
tions may include postoperative worsening of neurologi-
cal signs; temporary or persistent urinary incontinence;
or late recurrence of clinical signs.
8 Journal of Feline Medicine and Surgery Open Reports
Conict of interest
The authors declared no potential
conflicts of interest with respect to the research, authorship,
and/or publication of this article.
Funding The authors received no financial support for the
research, authorship, and/or publication of this article.
Ethical approval This work involved the use of non-
experimental animal(s) only (owned or unowned), and fol-
lowed established internationally recognised high standards
(‘best practice’) of individual veterinary clinical patient care.
Ethical approval from a committee was therefore not necess-
arily required.
Informed consent Informed consent (either verbal or writ-
ten) was obtained from the owner or legal custodian of all
animal(s) described in this work for the procedure(s) under-
taken. No animals or humans are identifiable within this
publication, and therefore additional informed consent for
publication was not required.
ORCID iD Sarah Butterfield https://orcid.org/0000-
0002-4064-0729
Clare Rusbridge https://orcid.org/0000-0002-3366-2110
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