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British Journal of Neurosurgery (1995) 9, 659± 666
ORIGINAL ARTICLE
Adult postrepair myelomeningocoele and tethered cord
syndrome: good surgical outcome after abrupt neurological
decline
A. G. FILLER 1,3, J. A. BRITTON 2, D. UTTLEY1 & H. T. MARSH 1
Departments of 1Neurosurgery and 2Neuroradiology, Atkinson Morley’ s Hospital, London, UK and3Department of Neurological Surgery, University of Washington, Seattle, USA
Abstract
Adults who have had repair of an open myelomeningocoele at birth are susceptible to a variant of adult onset
tethered cord syndrome (ATCS). Precipitous and profound loss of lower extremity motor function occurred in
two postrepair adult patients, but was not seen in any of our 12 cases of adult tethered cord with any other
aetiologies. Both postrepair ATCS patients made a good recovery after surgical release of the tether. For the
patients with other aetiologies, surgery yielded improvement or recovery of urinary continence in 57%, relief from
pain in 78% and improved strength in 80%. Evidence of retethering was observed in 25% of the operated patients
at intervals ranging from 1 to 9 years postoperatively. We conclude that surgical release of tether can reverse
incontinence in ATCS of any aetiology and that in the post-myelomeningocoele repair patient, both dexam-
ethasone and surgical intervention are helpful in reversing acute neurological deterioration.
Key words: Acute paraplegia, incontinence, lipomyelomeningocoele, myelomeningocoele, spina bi® da, steroids, tethered
cord syndrome.
Introduction
The mortality of open myelomeningocoele
was nearly 90% in 1950,1 but a series of tech-
nical advances has gradually reversed the odds
so that more than 85% of such children are
now expected to survive into adulthood.2
Since the incidence of open dysraphism con-
tinues at 1± 4/1000 live births,3 the late compli-
cations of myelomeningocoele repair can
therefore be expected to become an increasing
problem in the adult patient population.
Consideration of two such patients who pre-
sented with severe and precipitous lower ex-
tremity neurological deterioration has
prompted this report. The general setting for
both cases is similar to adult onset tethered
cord syndrome in patients with spina bi® da
occulta, but may need to be considered and
managed somewhat differently because of the
rather different clinical course we have ob-
served.
In addition, we report 13 cases of adult
presentation tethered cord syndrome with
varying aetiologies other than post-repair
myelomeningocoele in patients ranging from
19 to 83 years of age. The results of their
management are then compared with the
postrepair myelomeningocoele patients and to
the results of treatment of adult tethered cord
syndrome reported from other institutions.
0268-869 7/95/050659 ± 05 Ó 1995, The Neurosurgical Foundation
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Clinical materials and methods
The case notes of all adult patients admitted
to Atkinson Morley’ s Hospital (AMH) be-
tween 1967 and 1991, and diagnosed as hav-
ing spinal dysraphism or tethered cord
syndrome were reviewed. These admissions
re¯ ect referrals from the South West Thames
region for which AMH provides neurosurgical
cover, a catchment area of approximately
three million people.
All such patients who had radiological stud-
ies (myelography or MRI) con® rming a low
lying conus medularis and who had symptoms
referable to a tethered cord were included.
Those patients who had onset of their present-
ing symptom prior to age 18 years were ex-
cluded. To con ® rm the status of postrepair
myelomeningocoele in the two patients with
that diagnosis, case notes clearly describing
surgical closure of an open defect within sev-
eral days of birth were located.
The age of the patients ranged from 19 to
83 years with a mean of 34, including six
males and eight females. Twelve of the 14
patients had surgery to relieve tethering. One
patient had three operations, each one of
which treated an apparent retethering. Follow
up varied from 1 to 20 years with a mean of
4.5 years.
Description of cases and results
Post-repair myelomeningocoele
Case 1. This was a 19-year-old male who had
closure of an open draining myelomeningo-
coele at birth (at Atkinson Morley’ s Hospital),
but who did not require a ventricular shunt.
He was able to walk during his ® rst year and
ultimately was able to play football and cricket
at school. With no prodromal symptoms, he
suffered a sudden and profound loss of
strength in his right leg while playing golf
which was associated with bilateral lower ex-
tremity paraesthesiae.
These symptoms resolved substantially over
several days, but subsequently recurred in a
series of episodes each of which left him with
a progressively severe ® xed de® cit and increas-
ing spasticity. Nine months after the ® rst epi-
sode, he developed a ® xed bilateral foot drop
and was then referred by his neurologist for a
neurosurgical evaluation. At that time, he had
0± 1/5 strength in both ankles and 3/5 strength
at his hips. He had marked bilateral hy-
perre¯ exia and was unable to walk indepen-
dently.
Myelography demonstrated a bow-stringed
tethered spinal cord with marked L2/L3
spondylolisthesis and stenosis. He had
laminectomy with release of the tether. There
was an immediate improvement of strength
although the spasticity resolved only gradually
over an 18-month period. By 2 years after the
operation, he as able to walk and drive, al-
though he still had some mild residual spastic-
ity and ankle weakness.
Case 2. This 22-year-old woman, had closure
of an open myelomeningocoele and placement
of a ventricular shunt as a neonate. She was
able to walk at 1 year of age, but remained
incontinent and so had an ileal conduit placed
at age 5 years. She tolerated a pregnancy well
(Caesarean delivery), but began experiencing
back pain about 1 year postpartum. The pain
recurred episodically for several months and
she commenced intermittently wearing a
polystyrene jacket which an orthopaedic sur-
geon had prescribed 4 weeks prior to this
admission.
On the day prior to her admission, she had
progressively severe burning pains in her legs.
On the day of admission, while sitting, she
suffered the abrupt loss of all voluntary move-
ment in both legs. Upon urgent transfer to our
neurosurgical centre, she had 1± 2/5 strength
in all muscle groups of both legs with dimin-
ished knee jerks but absent ankle jerks. She
also had some progression of her usual patchy
lower extremity sensory de® cit.
Dexamethasone, 10 mg IV initially and then
4 mg IV 6-hourly, was commenced immedi-
ately and, because she regained some move-
ment (2± 3/5) in some muscle groups, steroids
were continued for several days. Plain radio-
graphs demonstrated spondylolisthesis (Fig. 1)
and CT-m yelography demonstrated a tautly
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Adult postrepair myelomeningocoele 661
FIG. 1. Lateral radiograph demonstrating spondylolis-
thesis at L5/S1 in a postrepair myelomeningocoele
patient with acute neurological deterioration from adult
onset tethered cord syndrome.
years postoperatively. MRI performed at the
time of the transient recurrence demonstrated
the neural placode to be untethered although
possibly adherent to the posterior wall of the
thecal sac (Fig. 4).
FIG. 2. (A) Axial myelogram CT scan at the time of
acute onset of paraplegia in post-repair myelomeningo-
coele patient. The cord is attached posteriorly in the
thecal sac and the tautly stretched nerve roots can be seen
as thin black lines extending towards the foramina. (B)
1Ð articulation; 2Ð thecal sac; 3Ð portion of bi® d spinal
lamina; 4Ð nerve root under tension; 5Ð portion of
neural placode under tension; 6Ð area of adhesion
between neural placode and dura.
tethered spinal cord with stretched nerve roots
under apparent tension (Fig. 2) and with the
cord apparently drawn under bow string
tension against the laminae (Fig. 3). She did
not complain of headache, and did not have
hydrocephalus, nor hydromyelia (by delayed
postmyelogram CT).
Her improvement on steroids plateaued, so
a laminectomy and untethering of the spinal
cord were carried out. During the following
3± 5 days she had complete recovery of lower
extremity strength and was able to walk out of
the hospital unassisted upon discharge to
home. She had an episode of bilateral lower
extremity weakness nine months later, but this
resolved with steroids alone and she has since
continued with no additional symptoms to two
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FIG. 3. (A) Sagittal reconstruction of myelogram CT of
postrepair myelomeningocoele patient, demonstrating
`bow stringing’ of the spinal cord which pulls it into
contact with the laminae. (B) 1Ð thecal sac; 2Ð spinal
cord; 3Ð spinal lamina in contact with spinal cord.
Surgical outcome for the entire group was
generally quite good. Strength improved by at
least one grade in 80% of those presenting
with weakness although one patient was
weaker postoperatively. The two postrepair
myelomeningocoele patients improved in
strength by more than two grades. There was
substantial improvement or relief of pain in
78% of the patients with this symptom. In
57% (4/7) of the patients presenting with new
onset incontinence, surgery succeeded in sub-
stantially improving or completely restoring
sphincter control.
Maintenance of gains over the period of
follow-up was generally good, but two patients
reported recurrence of progressive weakness
beginning 4 years (in a patient with diastem-
atomyelia) and 6 years (in a case of thoracic
FIG. 4. Sagittal plane MRI of postrepair myelomeningo-
coele patient 1 year after operation for release of tether.
The neural placode can be seen untethered, near the
posterior wall of the thecal sac.
Summary of all cases
Of the 14 con® rmed cases of adult onset teth-
ered cord syndrome, the aetiology was
lipomyelomeningocoele in four (29%),
diastematomyelia in three (21%), thickened
® lum terminale in three (21%), postrepair
myelomeningocoele in two (14%), thoracic
meningocoele in one (7%) and multiple spinal
abnormalities in one (7%) (see Table I). The
presenting symptoms were weakness (71%),
incontinence (57%) and pain (50%). Duration
of symptoms ranged from 5 h to 10 years,
although nearly all had some accelerated pro-
gression of their symptoms over several weeks
prompting their referral to the neurosurgical
centre.
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Adult postrepair myelomeningocoele 663
TABLE I. Summary of ATCS cases
Age (years)/Sex Diagnosis Operation Outcome Presentation
19/M Myelomeningocoele Lami strengthÝ R leg weakness: 9 months
Bilat foot drop: 1 week
22/F Myelomeningocoele Lami/Unteth strengthÝ, sensÝ pain: 10 months
painß paraplegia: acute
40/F Lipomyelomeningocoele Lami/Unteth strengthÝ, painß leg weakness: 6 months, pain
GUÝÝ urgency: 3 months
29/M Lipomyelomeningocoele Lami/Unteth sensationÝ, GUÝÝ incont: 1 month
27/F Lipomyelomeningocoele Lami/Unteth pain: no D arm and leg pain: 10 years
R leg paraesthesias: 4 months
22/M Lipomyelomeningocoele no surgery L leg weakness: 1 year
83/F Lipomyelomeningocoele no surgery urinary incont: 5 weeks
leg weakness: 2 weeks
29/F Thick Filum Terminale Lami/Unteth GU: no D incont: 8 weeks
30/M Lipomyelomening/Conus Lami/Drain strengthß , painß prog. weakness: 2 year
and Cauda Equina Abscess GUß43/F Diastematomyelia Lami/Unteth painß , GUÝ double incont: weeks
pain: 10 years
19/F Diastematomyelia Lami/Unteth strengthÝ, painß pain and leg weakness
21 Recurrent tether Lami/Unteth strengthÝ, rapid prog. leg weakness
29 Recurrent tether Lami/Unteth strengthÝ, pain;ß pain and leg weakness
32/M Diastematomyelia Lami/Unteth strength: no D , prog. incont: 1 year
GU: no D weakness: 10 year
40/M T4 Meningocoele Lami/Unteth strengthÝ prog. weakness: 3 years
GUÝ prog. incont: 1 year
47F Mult. Abn./stenosis C & L Lami strengthÝ, painß , pain, urinary urgency,
GU: no D leg weakness: 5 weeks
Ýincreased; ßdecreased; ÝÝmarkedly increased; no D no change.
meningocoele) postoperatively. Another of the
diastematomyelia patients suffered an acute
deterioration 16 months postoperatively, im-
proved with a second surgery, had recurrent
weakness from retethering 9 years later, im-
proved again with surgery, but then once more
developed weakness another 9 years later. The
female postrepair myelomeningocoele patient
had a transient recurrence of weakness 1 year
postoperatively, but regained full strength
without surgical intervention.
There were no deaths; one patient had a
super® cial wound infection and one developed
a draining cyst requiring surgical exploration.
There were two with CSF leaks, one of whom
required reoperation for repair. Drainage of an
intradural abscess of the conus and cauda
equina in one patient relieved pain, but re-
sulted in severe weakness and new onset in-
continence postoperatively.
Discussion
Aetiology of adult tethered cord syndrome
Cases of adult onset of tethered cord syn-
drome have been reported sporadically from
the mid-nineteenth century,4,5 but were gener-
ally considered to be consequent upon growth
of intradural fatty tumours.6,7 The syndrome
seems to have been de® ned initially by reports
from Lassman and James,8 and by Loeser and
Lewin,9 although the series of 12 patients re-
ported by Kaplan and Quencer,10 two patients
from Gokay et al.,11 23 patients from Pang and
Wilberger12 and eight patients from Lesoin et
al.13 have extensively de® ned the range and
character of the syndrome. In a recent review,
Yamamura et al.14 summarize reports in the
literature in a total of 57 patients.
Very few of these patients, however, are
clearly postrepair myelomeningocoele patients
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In some cases, there is uncertainty because
of imprecise use of the term `myelomenin-
gocoele’ as in a report from Logan et al.15 of
an active duty Marine described as a post-
operative myelomeningocoele patient, but also
described as having `occult spina bi® da’ .
There is also a report of a 72-year-old
woman16 who was a postrepair myelomeningo-
coele patient by her own report, and who
suffered a fairly rapid onset of leg weakness
and double incontinence (the complete time
course is not fully described). Moufarrij et al.17
report two such cases, but with limited infor-
mation given on the time course or severity of
symptoms. One of the 23 cases reported by
Pang & Wilberger12 is a postrepair patient.
Thus, including the 57 patients listed by Ya-
mamura et al.,14 and additional cases from
Moufarrij et al.,17 Logan et al.,15 and Wilden
and Hadley,16 and this report, only seven of
the eighty reported cases of adult onset teth-
ered cord syndrome or 8.8% are postrepair
myelomeningocoele patients.
This situation contrasts sharply with the mix
of aetiologies among paediatric patients where
Heinz et al.18 report that as many as two-thirds
of all tethered cord explorations were for
postrepair myelomeningocoele. A comparable
® gure from Moufarrij et al.17 is that postrepair
myelomeningocoeles make up 40% of the total
number of paediatric tethered cord patients
who come to surgery, the remainder being
attributed to various forms of spina bi® da
occulta. The difference in percentage between
these two reports may re¯ ect local differences
in practice or it may re¯ ect the increasing role
of prophylactic release of tether in spina bi® da
occulta which would dilute the impact of the
spina bi® da aperta cases upon the operative
patient population.
Incidence of postrepair tethering
In Pang & Wilberger’ s series of adult cases
from 1982,12 postrepair myelomeningocoele
cases make up 4.3% of the total, while in our
series they make up 14%. It should be noted
that if the Atkinson Morley’ s Hospital results
had been reviewed in 1982, at the same time
as the data from the University of Pittsburgh,12
we would have had eight cases of adult teth-
ered cord syndrome none of which were
postrepair myelomeningocoeles.
All postrepair myelomeningocoele patients
have low lying spinal cords upon MRI.19
Thus, it can be expected that radiological evi-
dence of tether will always be found when an
adult postrepair patient presents with new
neurological symptoms whether or not the
tether is the cause of the symptoms. In the
paediatric population, the frequency of symp-
tomatic tethering among post-repair patients is
variously reported from 3% 1 to 15%.19 Hy-
dromyelia is an alternative cause of late de-
terioration in adult patients20 and must be
carefully excluded before attributing the de-
terioration to cord tethering. There are in-
suf® cient data at this point to predict whether
symptomatic tethering will occur in adult
post-repair patients at the same frequency as it
occurs in the paediatric population.
Pathophysiology
The mechanism by which the decline develops
in adult onset tethered cord appears to be
degenerative. This is in distinction to the pae-
diatric situation where a tethered cord is
gradually stretched by normal growth. In
adults, it appears that a tethered cord decom-
pensates neurologically when a routine adult
degenerative process causes impingement
upon the abnormally positioned cord. Both of
our postrepair patients had spondylolisthesis
which appeared to have caused the decompen-
sation of the already stretched spinal cord.
It has been suggested that relative to the
paediatric situation, the adult tethered cord
syndrome is typi® ed by a more gradual and
insidious onset of symptoms, and that pain is
a characteristic feature.12 In our two postrepair
myelomeningocoele patients, however, the
presentation was sudden, severe, and painless.
In both cases it was the motor rather than the
sensory change that was more striking.
As can be seen in Fig. 3, the mechanical
impact upon the spinal cord is by laminae
impinging upon its posterior aspect and this
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Adult postrepair myelomeningocoele 665
might be expected to cause sensory symptoms
to predominate. However, if the symptoms
were based on compromise of tissue in the
repaired neural placode itself, then the ventral
gray matter would be closer to the posterior
aspect of the cord. Alternatively, it may be the
extreme lordosis which causes stretching of
the anterior aspect of the cord, involving either
the ventral gray matter or the corticospinal
tracts.
Steroids and tethered cord syndrome
There has been little use of steroid medication
in the treatment of tethered cord syndrome as
it occurs in adults or in children. The presen-
tation of most tethered cord syndrome pa-
tients is with gradual progression over months
and years. Once the diagnosis is made, surgi-
cal treatment can usually be carried out before
signi® cant further deterioration can occur.
However, the sudden onset of symptoms in
our second post-myelomeningocoele repair
patient led us to a trial of steroids and, at least
in that case, they yielded a clear response.
Response to surgery
The surgical outcomes for our entire group of
14 patients is generally similar to the results
reported by Pang and Wilberger12 (see Table
I). Long-term follow-up reveals that while
most patients maintain their gains well, there
is nonetheless a de® nite risk of retethering
after successful operation in adults. Although
these patients have no further growth in height
after the release, they do continue to be sub-
ject to progressive degenerative spinal disease
which may cause the neurological symptoms
to recur. Retethering was con ® rmed in two
patients both of whom had diastematomyelia
and probably occurred in a third whose tether
was due to a thoracic meningocoele.
It is possible that such a development did
occur in the postrepair myelomeningocoele
patient who had transient recurrence after 1
year, but her improvement on steroids alone
suggests the episode was due to direct trauma
on the exposed neural placode associated with
her untreated spondylolisthesis. Two years af-
ter her surgery she retained excellent lower
extremity strength.
Surgery failed to relieve pain in one patient
who had been experiencing pain for 10 years
prior to the development of the numbness
which brought her to surgery. There was a
poor outcome in a patient whose presentation
was precipitated by the development of an
abscess in the area of the lipoma. In all the
more routine cases where mechanical factors
alone had caused symptoms of one year or less
in duration we achieved satisfactory results.
There was no regular pattern for predicting
which patients would regain urinary conti-
nence, but our 57% success rate with this
symptom does suggest that it is at least a
reasonable expectation that release of tether
can improve incontinence. Thus, new onset
incontinence in an adult with tether is not a
hopeless fait accompli but rather should be
considered an indication for prompt surgical
release of the tether.
Acknowledgements
The Neurosciences Research Foundation of
Atkinson Morley’ s Hospital and the Wellcome
Trust are thanked for their support to AGF.
Address for correspondence: A. G. Filler, Depart-
ment of Neurosurgery, Atkinson Morley’ s
Hospital, 31 Copse Hill, Wimbledon SW20
0NE, UK.
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British Journal of Neurosurgery (1995) 9, 667± 670
TECHNICAL NOTE
Long vascular pedicle cranial ¯ ap
ATUL GOEL
Department of Neurosurgery, K.E.M. Hospital, Parel, Bombay, India
Abstract
Two case reports illustrate a long vascular pedicle cranial bone ¯ ap. A split or full thickness skull bone ¯ ap is
based on the pericranium layer. The temporalis muscle with its overlying fascial layers and vascular pedicles form
the base of this ¯ ap and assure its adequate vascularization. The technique and its uses in the reconstruction of
calvarial defects is discussed.
Key words: Calvarium, reconstruction, temporalis muscle, vascularized ¯ ap.
Introduction
Temporalis muscle and pericranium have
been used to nourish cranial bone ¯ aps.1 ± 5 The
¯ ap described in this report is a split or full
thickness cranial bone ¯ ap based on the peri-
cranial layer which receives its vascular
nourishment from the temporalis muscle and
its overlying fascial layers. Such ¯ aps have
been described in plastic surgery literature and
have been used in malar reconstruction in
Treacher Collins syndrome.6 The dependable
vascularity, long length, local availability and
manoeuvrability of the ¯ ap render it versatile
with great potential for reconstruction of skull
convexity and basal defects. The described
¯ ap can be used particularly to reconstruct
cranial defects where there is poor local
nourishment and potentially infective areas
which are cosmetically crucial as in the de-
scribed reports.
Technique
Subgaleal elevation of the scalp is carried out.
The temporalis muscle with its overlying fas-
cial layers and the pericranial layer is retained
with the skull. The outer table of the skull
bone is split as shown in the Fig. 1 preserving
FIG. 1. Drawing showing the splitting of the calvarial
bone. The bone ¯ ap as shown by arrows is being elevated
along the pericranium. The temporalis muscle and its
fascial envelope form the pedicle of the ¯ ap.
0268-869 7/95/050667 ± 04 Ó 1995, The Neurosurgical Foundation
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668 A. Goel
FIG. 2. Drawing shows an asterisk placed in the centre
of the frontal skull defect. The described ¯ ap will be cut
along the bold lines and rotated in the direction of the
arrows.
FIG. 3. The ¯ ap has been rotated over the frontal bone
defect. The temporalis muscle has been split vertically.
the overlying pericranial layer. A part of the
temporalis muscle (and fascial layers) along
with the pericranium is elevated and rotated as
required (Figs 2 and 3).
Case report 1
A 32-year-old man was admitted with a com-
plaint of frontal headache and a swelling on
the right side of the forehead for 5 years. He
also complained of diplopia and decreased vi-
sion in the right eye for 3 years. He had a well
circumscribed 6 3 6 cm. bony swelling over
the right supra-orbital region. Computer to-
mography (CT) and magnetic resonance
imaging (MRI) showed a right frontal extra-
cerebral enhancing lesion extending into the
ethmoid sinus. The thickening of the bone was
noted. A transnasal biopsy by the otolaryngol-
ogy unit con ® rmed that the lesion was a
meningioma. Four weeks after the ® rst pro-
cedure, the lesion was excised by the transcra-
nial route. The pericranium was thickened
and the region of the swelling was soft and
friable bone. There were large vascular chan-
nels from the scalp converging over the pro-
tuberance. The bony swelling and the
thickened pericranium were excised till normal
areas were seen. The dura underneath the
swelling was tumour ridden and was excised
with the intradural tumour. Tumour extension
into the ethmoid sinus was removed en-masse.
The dural defect was covered by a pericranial
graft. The bone defect was covered by a split
thickness posterior frontal ¯ ap with a vascular-
ized pedicle based on the pericranium and
temporalis muscle. The ethmoid sinus was
packed with fat taken from the abdominal
wall. The wounds healed well. When the pa-
tient was seen 4 months after the surgery the
¯ ap was well accepted (Fig. 4).
Case report 2
A 12-year-old boy underwent nephrectomy for
a Wilm’ s tumour. He developed a swelling on
the forehead considered to be a solitary met-
astasis from the kidney tumour. The swelling
was treated by local irradiation, but local pain
forced neurosurgical treatment. CT showed
the bony lesion in the frontal midline over the
forehead. Radiographs showed a sun-ray ap-
pearance of the lesion. The tumour was re-
sected piece meal with the help of chisel and
hammer and microdrill. After the entire tu-
mour had been resected a large bone defect
had been created. There was poor vascularity
of the area secondary to local irradiation and it
was considered that a free ¯ ap would not be
suitable for the large defect. A vascularized
pedicle temporalis musculofacial full thickness
bone ¯ ap was turned from the posterior fron-
toparietal region and placed over the bone
defect and sutured in place. Splitting of the
¯ ap was not possible due to the thin skull bone
in this child. Histological examination showed
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Calvarial ¯ ap 669
FIG. 4. Radiograph with white arrow showing the donor
site where the cranial bone was split and black arrows
showing the receptor (case 1).
as described, and results in a viable ¯ ap with
an abundance of vascular supply.
Various studies have shown that vascular-
ized membranous bone transfers retain their
osseous mass to a greater degree than non-vas-
cularized bone grafts.1,3,12 The skull bone is
thickened superior to the temporal line which
marks the attachment of the temporalis mus-
cle. Splitting of the skull bone is easier in the
paramedian frontoparietal area bone owing to
the well formed diploic channels. The split
thickness graft can be broken into pieces and
can be suitably contoured preserving the at-
tachment of the pericranium. The dependable
blood supply, long length, ease of harvesting
and the ability to alter the arc of rotation of
this ¯ ap are advantageous. The other advan-
tages of such a ¯ ap include harvesting of grafts
of adequate size, ease of access within the
same operative ® eld, and no or minimal post-
operative morbidity and discomfort for the
patient. Such vascularized ¯ aps are more re-
sistant to infection, are mechanically stronger
and survive better in poorly vascularized bed
when compared with free bone grafts.
Acknowledgements
The author acknowledges with gratitude the
support and constant guidance of Dr Sunil K.
Pandya. Dr J. Nitta drew the illustrations. Dr
Naina Goel did the proof-reading.
Address for correspondence: A. Goel, Depart-
ment of Neurosurgery, K.E.M. Hospital,
Parel, Bombay 400 012, India.
References
1 Bite U, Jackson IT, Wahner HW, Marsh RW.Vascularized skull bone grafts in craniofacialsurgery. Ann Plast Surg 1987 ; 18:3 ± 15.
2 Casanova R, Cavalcante D, Grotting JC, VasconezLO, Psillakis JM. Anatomic basis for vascularizedouter-table calvarial bone ¯ aps. Plast Reconstr Surg1986; 78:300 ± 8.
3 Cutting CB, McCarthy JG, Berenstien A. Bloodsupply of the upper craniofacial skeleton: the searchfor composite calvarial bone ¯ aps. Plast ReconstrSurg 1984 ; 74:603 ± 10.
4 Price JC, Loury M, Carson, Johns ME. The peri
that the lesion was a benign ® brous dysplasia.
The forehead contour was acceptable when
the child was seen 6 months after the oper-
ation.
Discussion
An improved understanding of the vascular
supply of the temporalis muscle and its invest-
ing fascial layers has been exploited in various
reconstructive procedures.7 ± 10 The peri-
cranium comprises of an outer layer of loose
aereolar tissue and an inner layer of os-
teoblasts and contains extensive vascular net-
work.11 The pericranium can sustain the
calvarial ¯ ap by means of multiple small, verti-
cal perforators.2 The super® cial fascial layer
over the temporalis muscle is a part of the
pericranial aponeurosis whilst the deep tempo-
ral fascial layer completely invests the su-
per® cial aspect of the temporalis muscle. The
temporalis muscle and its fascial envelope re-
ceive their blood supply from the anterior,
middle and posterior deep temporal and su-
per® cial temporal arteries. Subperiosteal elev-
ation of the temporalis muscle along with the
fascial layers preserves the integrity of all the
major vascular supply. The split or full thick-
ness cranial bone is based on the pericranial
layer and the temporalis musculofascial layer
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6 G. McCarthy JG, Zide BM. The spectrum of cal-varial bone grafting: Introduction of the vascu-larised calvarial bone ¯ ap. Plast Reconstr Surg1884; 74:10 ± 17.
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8 Habel G, Hensher R. The versatility of the tempo-ralis muscle ¯ ap in reconstructive surgery. Br J OralMaxillofac Surg 1986; 24:96 ± 101.
9 Abul Hassan HS, von Drasek Ascher G, AclandRD. Surgical anatomy and blood supply of thefascial layers of the temporal region. Plast ReconstrSurg 1986 ; 77:17 ± 28.
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