Está en la página 1de 7

Clinical Neurology and Neurosurgery 124 (2014) 4450

Contents lists available at ScienceDirect

Clinical Neurology and Neurosurgery


journal homepage: www.elsevier.com/locate/clineuro

Post-traumatic syringomyelia: Outcome predictors


Youssef Karam a , Patrick W. Hitchon b, *, Nakhle E. Mhanna b , Wenzhuan He c,
Jennifer Noeller b
a

Neurochirurgien et chirurgien de la colonne, Hpital de Hull, CSSSG 116, Boulevard Lionel-mond, Gatineau (Qubec) J8Y 1W7, Canada
Department of Neurosurgery, University of Iowa Carver College of Medicine, 200 Hawkins Dr, Iowa City, IA 52242, USA
c
Department of Neurology and Neurosciences, RutgersNew Jersey Medical School, 185 S Orange Ave, Newark, NJ 07103, USA
b

A R T I C L E I N F O

A B S T R A C T

Article history:
Received 21 May 2014
Accepted 9 June 2014
Available online 17 June 2014

Objective: To identify risk factors that predispose to post-traumatic syringomyelia (PTS) and describe the
outcome of surgical management.
Methods: Retrospective cohort study of 27 patients with post-traumatic syringomyelia. Spinal cord injury
of these patients spanned the period from 1963 to 2008. All data were collected retrospectively using
available medical records and radiological images.
Results: There were 24 males and 3 females. The level of initial spine injury was thoracic in 21, cervical in
4, and lumbar in 2. The average age (SD) at diagnosis of PTS was 40  13 years. The mean follow-up SD
from injury was 18  11 years. On admission after injury, there were 14 patients with American Spinal
Injuries Association (ASIA) disability scores of A, 3 with ASIA C, and 10 with ASIA score of D. At the time of
diagnosis of PTS, local kyphosis at the site of injury measured 28  12 , and the residual canal was
67  19% compared to the average rostral and caudal anteroposterior diameter. Fourteen patients
underwent a single operation for PTS, and 13 needed two or more procedures. In the 11 patients in whom
the initial surgery included a duraplasty, 3 required reoperation for unsuccessful reduction in the size of
the syrinx and failure to improve symptoms. In the 16 patients in whom the initial procedure was that of a
shunt alone, 10 required revision (p = 0.0718 rate of revision between shunting and duraplasty). As a
result of treatment for PTS, improvement in symptoms of PTS occurred in 14, symptoms were unchanged
in 10, and progressed in 3. In the 11 patients with sequential MRI scans, a signicant correlation was
shown between the reduction in the size of the syrinx and clinical improvement (p < 0.001).
Conclusion: PTS is often the result of severe spinal cord injuries, with over half of patients having an ASIA
disability score of A. Our review corroborates other published reports showing that PTS is associated with
signicant deformity and stenosis. Irrespective of treatment, over half of the patients required
reoperation for their PTS. Duraplasty and arachnolysis are the preferred treatment for PTS over shunting
alone. Treatment was associated with cessation of symptoms or improvement in nearly 90% of the
patients.
2014 Elsevier B.V. All rights reserved.

Keywords:
Duraplasty
Posttraumatic syringomyelia
Spinal cord injury
Spinal trauma
Syrinx

1. Introduction
Syrinx is a Greek name that means cavity of tubular shape.
Ollivier introduced this term in 1827, dening it as a pure dilatation
of the central canal [1]. The rst to describe post-traumatic
syringomyelia (PTS) was Bastian [2], in 1867, followed by Strumpell
[3], in 1880, and subsequently many other others [46]. Barnett
and Jousse [7] reviewed the literature in 1973 and described 5

* Corresponding author at: University of Iowa Hospitals and Clinics, Department


of Neurosurgery, 200 Hawkins Dr, 1826 JPP Iowa City, IA 52242, USA. Tel.: +1 319 356
2775; fax: +1 319 353 6605.
E-mail address: patrick-hitchon@uiowa.edu (P.W. Hitchon).
http://dx.doi.org/10.1016/j.clineuro.2014.06.007
0303-8467/ 2014 Elsevier B.V. All rights reserved.

cases prior to 1920 and 32 after 1940, including their 17 cases.


Thereafter, PTS was more widely appreciated, but the lack of
awareness of this condition still leads to delayed diagnosis and
treatment. Before the magnetic resonance imaging (MRI) era, it
was reported to be between 1% and 8% [714]. With the advent of
MRI, in the 1980s, the diagnosis of PTS was facilitated, and
subsequently the incidence of this entity increased up to 50% [15
19].
Several treatment modalities have been used through time,
including shunting, myelotomy, lysis of adhesions, duraplasty, and
combinations of the above. With better and improved understanding of the pathophysiology of syringomyelia and PTS, treatment
now focuses on the restoration of CSF circulation at the site of
injury. In an attempt to follow the development and management

Y. Karam et al. / Clinical Neurology and Neurosurgery 124 (2014) 4450

of PTS, we reviewed the records of 27 patients in our hospital. The


objective of our study was to identify clinical and radiographic
outcomes after surgery in PTS.
2. Materials and methods
Since 1978, 27 patients with post-traumatic syringomyelia were
identied. Spinal cord injury of these patients spanned the period
from 1963 to 2008. All data were collected retrospectively using
available medical records and radiological images.
Demographic data collected included: age at time of accident,
type of accident, type of injury, level of injury, severity of injury,
clinical presentation, initial management of the injury, delay
before syrinx formation, level of syrinx, and management of the
syrinx.
The ASIA score [20] was used to score the severity of patients'
injuries as a result of the trauma and thereafter, with A = complete:
no motor or sensory function is preserved in the sacral segments
S4S5; B = incomplete: sensory but no motor function below the
injury, including sacral segments; C = incomplete: motor function
below injury present but more than half score less than antigravity
strength, or 3; D = incomplete, and at least half of the muscles
below the injury score 3 or more; and E = motor and sensory
functions are normal. The clinical symptoms that led to the
diagnosis of PTS and diagnostic tests consisted of one or more of
the following: pain, ascent of motor, or sensory decit. Where the
syrinx extended to include the cervicomedullary junction, patients
also experienced dysphagia. Patients with recent onset of
symptoms described exacerbations of pain with coughing,
sneezing, and exertion. Treatment of PTS consisted of laminectomy
for decompression, lysis of adhesions, duraplasty, and syringosubarachnoid shunting. Lysis of adhesions was performed under
the microscope until a clear subarachnoid space was identied for
placement of the shunt tube caudally. Intraoperative ultrasonography was used to identify the syrinx cavity for the placement of
the shunt rostrally. Dural graft (Durepair1, Medtronic, Memphis,
TN) was used to expand the caliber of the canal and was secured
with continuous 60 polypropylene suture. The suture line was
secured further with thrombin glue or brin sealant (TISSEEL,
Baxter, Deereld, IL). Patients were kept at bed rest for 48 h prior to
mobilization.
Clinical outcomes were assessed using the Odom score [21]. For
the purpose of analysis, a numerical score of 4 was assigned when
the outcome was deemed excellent if all preoperative symptoms
were relieved; score of 3, or good, for minimal persistence of
preoperative symptoms; score of 2, or fair, with denite relief of
some preoperative symptoms but other symptoms unchanged;
and a score of 1, or poor, when symptoms and signs remained
unchanged or exacerbated.
3. Results
3.1. Demographics and clinical presentation
The spinal fracture and spinal cord injury resulting in PTS were
the result of car accidents in 16, falls and all-terrain vehicles in 3
each, motorcycle accidents in 2, and bicycle, tractor, and airplane
accidents in 1 each. There was a male predominance of patients,
with 24 males to 3 females. The average age (SD) at diagnosis of
PTS was 40  13 years. The mean follow-up SD from injury was
18  11 years. The level of initial spine injury was thoracic in 21,
cervical in 4, and lumbar in 2. On admission after injury, there were
14 patients with ASIA disability scores of A, 3 with ASIA C, and 10
with ASIA score of D. Treatment for the spinal fracture was
instrumentation in 8, non-operative with immobilization and
bracing in 8, laminectomy for decompression in 5, traction in 3, and

45

unknown in 3. The time interval between the initial spine injury


and the diagnosis of PTS varied widely, from 3 months to 19 years,
with a mean interval of 12  11 years. Symptomatology triggering
the diagnosis and workup for syringomyelia consisted of
dysesthesia and paresthesia in 75% of this cohort, hypalgesia in
62.5%, and weakness in 58.33%. Other less common features
included hypesthesia and difculty voiding in 12.5%, and increased
spasticity in 8%.
3.2. Radiographic parameters
The level of the syrinx ranged from the medulla to the conus
medullaris. The mean number of levels involved was 12  6, with a
range from 3 to 19 levels. The syrinx extended above and below the
level of injury with myelomalacia at the site of injury. The mean
sagittal kyphosis at the site of injury between adjacent intact
endplates measured 28  12 . The residual canal at the site of
injury, expressed as a percentage of the average anteroposterior
canal above and below the fracture site, measured 67  19%.
Kyphosis at the site of injury was unchanged as a result of surgery,
as the latter was geared to restoration of CSF ow and not the
correction of long-standing deformity.
3.3. Management of syrinx and outcomes
A variety of treatments were undertaken over the years,
reecting the evolution of understanding and choice of attending
physician. All cases required a laminectomy for exposure. The
initial procedure for the treatment of the PTS was a shunting
procedure in 16, 2 of which were syringo-pleural and the rest
syringo-subarachnoid. Eleven patients underwent duraplasty, with
lysis of adhesions and shunting in 7 each. Only 2 patients were
treated in addition with fusion and instrumentation. Thirteen
patients underwent a single operation for their syrinx, 9 two
operations, and 5 a total of 3 procedures. In the 11 patients in
whom the initial surgery included a duraplasty, 3 required
reoperation for unsuccessful reduction in the size of the syrinx
and failure to improve symptoms. In the 16 patients in whom the
initial procedure was that of a shunt alone, 10 required revision
(p = 0.0718 rate of revision between shunting and duraplasty).
There was no improvement in the ASIA score from admission. As a
result of surgery for the syrinx, 14 patients (52%) had an
improvement in their symptoms, 10 (37%) remained stable, and
3 (11%) had progression without improvement in spite of surgery.
In 11 patients, sequential MRIs were available for review over a
mean period of 4  3 years with a range of 6 months to 9 years. As a
result of treatment for the syrinx, a reduction in the size of the
syrinx was encountered in 8 patients (Fig. 1AD) and remained
unchanged in the remaining 3 (Fig. 2A,B). At latest follow-up, the
size of the syrinx had decreased from the initial 12  6 levels to
6  7 levels. There appeared to be a signicant correlation between
the reduction in the size of the syrinx and clinical improvement as
assessed with the Odom outcome score (correlation coefcient
r = 0.912, p < 0.001 between reduction in the size of the syrinx and
clinical response) (Fig. 3). The extent of intradural scarring and
arachnoiditis often entails signicant dissection for untethering
and the placement of a syringo-subarachnoid shunt (Fig. 4AD). It
is this amount of scarring that explains the failure of the surgery
and the need for revision.
We had 1 complication, in a 57-year-old man with paraplegia
who 10 years earlier had suffered a bicycle injury with resultant
T67 fracture dislocation treated with instrumentation. Owing to
ascending numbness and weakness involving the upper extremities, an MRI was obtained and revealed the presence of a
cervicothoracic syrinx (Fig. 5A,B). At surgery, the hardware was
removed and the patient underwent T68 laminectomy with lysis

46

Y. Karam et al. / Clinical Neurology and Neurosurgery 124 (2014) 4450

of arachnoidal adhesions, syringo-subarachnoid shunt, and duraplasty. The suture line was reinforced with a dural sealant
(DuraSealTM, Covidien, Crystal Lake, IL). His condition improved
for a short period of time. However, two months later he presented
with intractable pain involving both sides of the chest cavity and
arms, worse on the left side. He occasionally experienced difculty
swallowing his pills. An MRI was obtained (Fig. 5C), showing a
large extradural mass compressing the cord and associated with a
larger-than-before syrinx. At surgery, a sterile xanthochromic
epidural uid collection was drained, and the arachnolysis,
syringo-subarachnoid shunt, and duraplasty were revised. Three

months later his pain was improved, and sensory perception on the
chest wall had returned to baseline. MRI (Fig. 5D) showed
reduction in the syrinx cavity.
4. Discussion
As a general rule, myelomalacia is the localized destruction of
the cord resulting from injury, with syringomyelia being the
progressive chronic cavitation of the cord extending rostrally and
caudally from the site of injury. Post-traumatic syringomyelia most
commonly presents with pain, ascending sensory loss, increased

Fig. 1. At 18 years of age, this 32-year-old man was involved in a car accident with a T1112 fracture dislocation and paraplegia. He was treated with Harrington rods, which
were removed one year later. He presents on 12/24/2003 with pain and numbness in the neck, shoulder, and left arm. Symptoms are worse with exertion, sneezing, and
coughing. MRI scans of the cervical (A) and thoracic (B) spine show a holocord syrinx extending from T12 to C2. On 1/16/2004 the patient underwent T11-L1 laminectomy,
duraplasty, lysis of adhesions, and syringo-subarachnoid shunt. He was last seen on 12/15/2011. His preoperative numbness and pain have long disappeared, but his ASIA score
of A is unchanged. Postoperative MRI scans (C, D) show collapse of the syrinx without need of revision.

Y. Karam et al. / Clinical Neurology and Neurosurgery 124 (2014) 4450

47

Fig. 2. Sixty-ve-year-old man presents with increasing stiffness of neck and upper extremities with pain for the past 1.5 years. Forty-three years earlier he had been involved
in a car accident with a T3 spinal fracture that left him with paraplegia. The fracture was treated with immobilization and bracing. Preoperative MRI (A) shows a holocord
syrinx extending from C1 past the fracture and constriction to the conus. The patient was treated with T23 laminectomy, duraplasty, lysis of adhesions, and with C7-T4
instrumentation. On follow-up two months later, he is back to baseline and still complains of neck stiffness. Postoperative MRI (B) shows the syrinx unchanged in spite of the
decompression and duraplasty.

muscle weakness, lower motor neuron decits in the upper


extremities, and upper motor neuron decits in the legs.
Characteristically, a dissociated sensory loss is identied, with
loss of pain and temperature sensation and preservation of light
touch and proprioception [22,23]. These symptoms and ndings
appear months to years after spinal cord injury [13,24,25]. In our
patients, PTS developed 12  11 years after injury, with a range of 3
months to 19 years. It is the most common cause of neurological
deterioration in patients who have sustained serious spinal cord

injury. The preponderance of males, thoracic injuries, with


signicant neurological decit encountered in our series is
reected in the results of others [12,26,27].
For the diagnosis of PTS, MRI is the test of choice except in
patients with implanted hardware, where interpretation could be
difcult. Estimates for the incidence of PTS vary from 15%
depending on the source, period of time covered, and the
diagnostic modality [17,18,26]. The consensus is that, with the
advent of MRI, the incidence of symptomatic PTS could be much

Fig. 3. Clinical improvement using the Odom score from 1 to 4, correlated closely and signicantly with the reduction in the size of the syrinx (correlation coefcient r = 0.912,
p < 0.001).

48

Y. Karam et al. / Clinical Neurology and Neurosurgery 124 (2014) 4450

Fig. 4. This 58-year-old paraparetic gentleman presented with burning sensation of the lower back and left leg for the past year. While driving, he experiences numbness in
his legs. He has experienced recent onset of urinary incontinence as noted by dribbling of urine and occasional episodes where he cannot make it to the bathroom in time. He
complains of erectile dysfunction for the past ve years. At the age of 19 he was involved in a snowmobile accident with an L1 fracture and ASIA of D. MRI (A) reveals kyphosis
at L1 with myelomalacia and a syrinx from T11 to L1. He underwent laminectomy, an attempt at lysis of adhesions, syringo-subarachnoid shunt, and duraplasty. Four months
postoperatively, he has noted improvement in his bowel and bladder control as well as pain. His gait is stable, and he still experiences erectile dysfunction. Postoperative MRI
(B) shows reduction in the size of the syrinx, but not total disappearance. Intraoperative ndings (C, D) show the severe intradural scarring and adhesions and the expected
difculty of arachnolysis and shunting.

higher, and possibly 20% [17,26,28]. Wang [29] identied the MRI
characteristics of syrinx as follows: hypo-signal on T1, hyper-signal
on T2, extending above or below the traumatic injury site (more
than two levels), tapered at one or both ends, and may appear with
loculations with well-dened borders. In the presence of pacemakers or stimulators, where MRI cannot be obtained, myelography and post-myelographic CT scan are indicated. In our study,
MRI images available for review allowed not only diagnosis but an
assessment of deformity and stenosis. In our patients, kyphosis and
the residual canal at the site of injury measured 28  12 and
67  19%, respectively. This degree of kyphosis in the thoracic spine
is signicantly greater than the normal estimate of 5 and 0
kyphosis in the thoracic and thoracolumbar spine [30,31]. These
data support the relationship between deformity and the
development of PTS. Signicant correlation of PTS with spinal
canal stenosis and spine deformity has been demonstrated in the
literature [12,17,28,29,32,33]. As in our own series, many patients
who ultimately developed PTS had been treated nonoperatively
[28], or had undergone procedures for their initial injuries without
correcting deformity. These results favor the correction of
deformity and the management of stenosis in the avoidance of
PTS [34].

Several theories have been proposed to explain the pathophysiology of PTS. A syrinx may develop after spinal cord trauma, either
soon after resorption of an intramedullary hematoma or as a delayed
phenomenon after cord contusion or compression with microcystic
cavitations [35]. Deformity and scarring from trauma results in
obstruction of CSF circulation. This can result in an increase in
intramedullary uid pressure with cyst formation [36]. Another
mechanism is the Venturi effect occurring at the site of constriction,
with a differential of pressure between the subarachnoid and
intraspinal space [36]. This difference in pressure results in the
expansion of intraparenchymal CSF accumulation and the formation
of PTS. Hence, restoring normal ow of CSF at the site of injury or
obliterating the pressure differential contributes to syrinx collapse.
With the extent of post-traumatic subdural and subarachnoid
scarring, and syrinx septation, shunting procedures have frequently not achieved the desired outcomes [37,38]. Thus, treatment
described herein, and by others [26,27], is directed more to the
release of adhesions and attempted normalization of CSF circulation and the elimination of differences in pressure in and around
the cord at the site of injury. The rate of revision surgery for
syringomyelia was 10/16 patients treated with shunt alone,
compared to 3/11 of those treated with duraplasty and lysis of

Y. Karam et al. / Clinical Neurology and Neurosurgery 124 (2014) 4450

49

Fig. 5. Ten years earlier, this 57-year-old man had suffered a T67 fracture dislocation with paraplegia. He now presents with pain and dysesthesia involving the left shoulder.
MRI shows stenosis at the site of injury with a cervicothoracic syrinx (A, B). At surgery, he underwent lysis of adhesions and duraplasty, and the suture line was secured with
the tissue adhesive (DuraSealTM, Covidien, Manseld, MA). Post-operatively, he experienced short-lived improvement. Two months later he presented with intractable pain
involving the chest and arms. An MRI was obtained, showing an extradural mass compressing the cord associated with a larger cervicothoracic syrinx (C). At surgery, a sterile
xanthochromic uid collection was drained, and the arachnolysis, syringo-subarachnoid shunt, and duraplasty were revised. Three months later his pain was improved, and
the MRI (D) shows reduction of the syrinx.

adhesions (p = 0.0718). Three patients did not improve, and 14/27


needed more than 1 operation for their PTS.
Conclusion
Our review suffers from the relatively small number of patients
with available MRI imaging before and after treatment of the

syrinx. Nevertheless, this review supports the literature in that PTS


is not a rarity following spinal trauma and generally severe spinal
cord injury. PTS appears to be correlated with deformity and
stenosis of the canal subsequent to injury. In the above review of
PTS, only 8/27 patients underwent instrumentation subsequent to
initial injury. It is safe to say that correction of deformity with
surgery and instrumentation, where necessary, may reduce the

50

Y. Karam et al. / Clinical Neurology and Neurosurgery 124 (2014) 4450

development of PTS. Though our study is limited by small numbers,


the ndings support the restoration of CSF circulation by
duraplasty and arachnolysis as the treatment of choice. Shunting
procedures alone are associated with less desirable outcomes and
more revisions. Revisions were needed irrespective of the rst
index operation, and clinical improvement accompanied reduction
in syrinx size.
Acknowledgements
Patrick W. Hitchon is the recipient of research support for the
Neurosurgery Biomechanics Laboratory from DePuy Spine, Raynham, MA. No nancial support was received for this project.
The authors thank Faith Vaughn for her invaluable help in the
editing and preparation of this manuscript.
References
[1] Ollivier C. Trait de la moelle pinire et de ses maladies. Paris: Chez Crevot;
1827.
[2] Bastian HC. On a Case of Concussion-Lesion, with extensive secondary
degenerations of the Spinal Cord, followed by General Muscular Atrophy. Med
Chir Trans 1867;542:491.
[3] Strumpell A. Beitrge zur Pathologie des Rckenmarks. Archiv fr Psychiatrie
und Nervenkrankheiten 1880;10:676717.
[4] Holmes G. The goulstonian lectures on spinal injuries of warfare: delivered
before the Royal College of Physicians of London. Br Med J 1915;2:76974.
[5] Strong OS. A case of sacral cord injury and a subsequent unilateral
syringomyelia. Neurol Bull 1919;2:277.
[6] Weisenberg TH. Sensory and motor disturbances in parts above the
distribution involved by denite organic lesions of the spinal cord. J Nerv
Ment Dise 1907;34:43446.
[7] Barnett HJM, Jousse AT. Syringomyelia as a late sequel to traumatic paraplegia
and quadriplegia - clinical features. In: Barnett HJM, Foster JB, Hudgson P,
editors. Syringomyelia: major problems in neurology. London: Saunders & Co;
1973. p. 12953.
[8] Barnett HJ, Botterell EH, Jousse AT, Wynn-Jones M. Progressive myelopathy as a
sequel to traumatic paraplegia. Brain 1966;89:15974.
[9] Edgar R, Quail P. Progressive post-traumatic cystic and non-cystic myelopathy.
Br J Neurosurg 1994;8:722.
[10] Grifths ER, McCormick CC. Post-traumatic syringomyelia (cystic myelopathy). Paraplegia 1981;19:818.
[11] Rossier AB, Foo D, Shillito J, Dyro FM. Posttraumatic cervical syringomyelia.
Incidence, clinical presentation, electrophysiological studies, syrinx protein
and results of conservative and operative treatment. Brain 1985;108(Pt
2):43961.
[12] Schurch B, Wichmann W, Rossier AB. Post-traumatic syringomyelia (cystic
myelopathy): a prospective study of 449 patients with spinal cord injury. J
Neurol Neurosurg Psychiatry 1996;60:617.
[13] Vernon JD, Silver JR, Ohry A. Post-traumatic syringomyelia. Paraplegia
1982;20:33964.
[14] Watson N. Ascending cystic degeneration of the cord after spinal cord injury.
Paraplegia 1981;19:8995.

[15] Backe HA, Betz RR, Mesgarzadeh M, Beck T, Clancy M. Post-traumatic spinal
cord cysts evaluated by magnetic resonance imaging. Paraplegia 1991;29:607
12.
[16] Betz RR, Gelman AJ, DeFilipp GJ, Mesgarzadeh M, Clancy M, Steel HH. Magnetic
resonance imaging (MRI) in the evaluation of spinal cord injured children and
adolescents. Paraplegia 1987;25:929.
[17] Perrouin-Verbe B, Lenne-Aurier K, Robert R, Auffray-Calvier E, Richard I,
Mauduyt de la Greve, Mathe JF. Post-traumatic syringomyelia and posttraumatic spinal canal stenosis: a direct relationship: review of 75 patients
with a spinal cord injury. Spinal Cord 1998;36:13743.
[18] Sett P, Crockard HA. The value of magnetic resonance imaging (MRI) in the
follow-up management of spinal injury. Paraplegia 1991;29:396410.
[19] Silberstein M, Hennessy O. Cystic cord lesions and neurological deterioration
in spinal cord injury: operative considerations based on magnetic resonance
imaging. Paraplegia 1992;30:6618.
[20] American Spinal Injuries Association and, International Medical Society of
Paraplegia (ASIA/IMSOP). International standards for neurological and
functional classication of spinal cord injury. Chicago: American Spinal
Injuries Association; 1992.
[21] Odom GL, Finney W, Woodhall B. Cervical disk lesions. J Am Med Assoc
1958;166:238.
[22] Biyani A, el Masry WS. Post-traumatic syringomyelia: a review of the
literature. Paraplegia 1994;32:72331.
[23] Bleasel A, Clouston P, Dorsch N. Post-traumatic syringomyelia following
uncomplicated spinal fracture. J Neurol Neurosurg Psychiatry 1991;54:5513.
[24] Umbach I, Heilporn A. Review article: post-spinal cord injury syringomyelia.
Paraplegia 1991;29:21921.
[25] Yarkony GM, Shefer LR, Smith J, Chen D, Rayner SL. Early onset posttraumatic
cystic myelopathy complicating spinal cord injury. Arch Phys Med Rehabil
1994;75:1025.
[26] Klekamp J. Treatment of posttraumatic syringomyelia. J Neurosurg Spine
2012;17:199211.
[27] Sgouros S, Williams B. Management and outcome of posttraumatic
syringomyelia. J Neurosurg 1996;85:197205.
[28] Abel R, Gerner HJ, Smit C, Meiners T. Residual deformity of the spinal canal in
patients with traumatic paraplegia and secondary changes of the spinal cord.
Spinal Cord 1999;37:149.
[29] Wang D, Bodley R, Sett P, Gardner B, Frankel H. A clinical magnetic resonance
imaging study of the traumatised spinal cord more than 20 years following
injury. Paraplegia 1996;34:6581.
[30] Bernhardt M, Bridwell KH. Segmental analysis of the sagittal plane alignment
of the normal thoracic and lumbar spines and thoracolumbar junction. Spine
(Phila Pa 1976) 1989;14:71721.
[31] Farcy JP, Weidenbaum M, Glassman SD. Sagittal index in management of
thoracolumbar burst fractures. Spine (Phila Pa 1976) 1990;15:95865.
[32] Perrouin-Verbe B, Robert R, Lefort M, Agakhani N, Tadie M, Mathe JF. [Posttraumatic syringomyelia]. Neurochirurgie 1999;45(Suppl 1):5866.
[33] Williams B, Terry AF, Jones F, McSweeney T. Syringomyelia as a sequel to
traumatic paraplegia. Paraplegia 1981;19:6780.
[34] Syringomyelia: Diagnosis and Treatment. In: Klekamp J, Samii M, editors.
Berlin: Springer-Verlag; 2002.
[35] Van den Bergh R. Pathogenesis and treatment of delayed post-traumatic
syringomyelia. Acta Neurochir (Wien) 1991;110:826.
[36] Greitz D. Unraveling the riddle of syringomyelia. Neurosurg Rev 2006;29:251
63 discussion 264.
[37] Appleby A, Bradley WG, Foster JB, Hankinson J, Hudgson P. Syringomyelia due
to chronic arachnoiditis at the foramen magnum. J Neurol Sci 1969;8:45164.
[38] Sgouros S, Williams B. A critical appraisal of drainage in syringomyelia. J
Neurosurg 1995;82:110.

También podría gustarte