Perilesional myeloradiculopathy with tethered cord in post-traumatic spinal cord injury

Abstract

Study design:
A retrospective series of cases.

Objective:
To identify, among post-traumatic myelopathies, a specific entity in which clinical and radiological features are not extensive but are strictly limited to the perilesional zone.

Setting:
The data set of the Regional Spinal Cord Injury Department of Nantes, France.

Methods:
A systematic analysis of all traumatic spinal cord injury (SCI) patients who presented with a neurological aggravation delayed from initial injury, without syringomyelia or extensive myelomalacia.

Results:
Twelve patients presenting with this type of complication were identified (that is, four tetraplegics and eight paraplegics). The neurological worsening consisted in weakness of the muscles close to the motor level in five patients, and in isolated at-level neuropathic pain in seven patients. A tethered cord was evidenced by the magnetic resonance imaging (MRI) results in all of the patients. Roots were involved by the tethering on the MRI results in eight cases. Surgery, with untethering and expansile duraplasty, was performed in all cases. Surgery allowed motor recovery in patients who presented with a motor loss (motor score gain range=1-7 points; median=3) and decreased pain in all pain patients (decrease on the 10-point numerical rating scale: range=1-6 points; median=4).

Conclusions:
In traumatic SCI patients, a tethered cord could be responsible for clinical and radiological changes, which are strictly localised to the perilesional area. The term perilesional myeloradiculopathy is proposed for this complication, which requires cord release surgery.

Full text

ORIGINAL ARTICLE
Perilesional myeloradiculopathy with tethered cord
in post-traumatic spinal cord injury
R Gross1, O Hamel2, R Robert2and B Perrouin-Verbe1
Study design: A retrospective series of cases.
Objective: To identify, among post-traumatic myelopathies, a specific entity in which clinical and radiological features are not
extensive but are strictly limited to the perilesional zone.
Setting: The data set of the Regional Spinal Cord Injury Department of Nantes, France.
Methods: A systematic analysis of all traumatic spinal cord injury (SCI) patients who presented with a neurological aggravation
delayed from initial injury, without syringomyelia or extensive myelomalacia.
Results: Twelve patients presenting with this type of complication were identified (that is, four tetraplegics and eight paraplegics).
The neurological worsening consisted in weakness of the muscles close to the motor level in five patients, and in isolated at-level
neuropathic pain in seven patients. A tethered cord was evidenced by the magnetic resonance imaging (MRI) results in all of the
patients. Roots were involved by the tethering on the MRI results in eight cases. Surgery, with untethering and expansile duraplasty,
was performed in all cases. Surgery allowed motor recovery in patients who presented with a motor loss (motor score gain range ¼1–7
points; median ¼3) and decreased pain in all pain patients (decrease on the 10-point numerical rating scale: range ¼1–6 points;
median ¼4).
Conclusions: In traumatic SCI patients, a tethered cord could be responsible for clinical and radiological changes, which are strictly
localised to the perilesional area. The term perilesional myeloradiculopathy is proposed for this complication, which requires cord
release surgery.
Spinal Cord (2013) 51, 369–374; doi:10.1038/sc.2012.154; published online 4 December 2012
Keywords: spinal cord injury; post-traumatic myelopathy; tethered cord
INTRODUCTION
The development of extensive lesions in the spinal cord after a
traumatic spinal cord injury (SCI) is known as post-traumatic
myelopathy (PTM).1–7 Cord tethering, defined as attachment of the
spinal cord to the wall of the bony spinal canal,8is known to be a
major factor in the occurrence of such a complication.3–5,9,10 The
long-term SCI patient follow-up highlights that PTM is a frequent
complication among these patients.2In addition to urinary,
respiratory, vascular or cutaneous complications, PTM should be
screened for and treated. PTMs, which can be either cystic (post-
traumatic syringomyelia) or non-cystic (post-traumatic progressive
myelomalacic myelopathy), are referred to as progressive
pathologies.3,5,6,11 The possibility that cord tethering could induce
late lesions that would not be extensive but remain strictly limited
to the injured area has not been evidenced in the literature. Our
experience allowed us to identify patients who presented with such a
pathology of the spinal cord.
PATIENTS AND METHODS
This study was conducted within the national reference centre for SCI patients
at the university hospital of Nantes, France. Within our cohort of around 1500
patients, we selected all of the traumatic SCI patients who presented with
changes in their neurological status (worsening) that were associated with a
tethered cord on the magnetic resonance imaging (MRI), and who underwent
surgery because of this deterioration. Patients with syringomyelia or extensive
myelomalacia,8as well as those who presented with a worsening within the first
month post-SCI, were not included.
Clinical, radiological and therapeutic data were assessed retrospectively at
the following four key follow-up periods: immediately after trauma (T0);
before the worsening (T1); after the worsening (T2); and 6 months after the
surgical treatment (T3). A standardised clinical evaluation was reproduced at
T0,T
1,T
2and T3. The neurological examination was performed according
to the International Standards for Neurological Classification of Spinal Cord
Injury.12 The American Spinal Injury Association (ASIA) Impairment Scale
(AIS), motor and sensory levels, and motor and sensory scores were
established in all of the patients. When pain was present, its typology
(nociceptive and/or neuropathic) and location were reported according to
the International Spinal Cord Injury Pain Basic Data Set.13 Pain intensity was
assessed by the average pain intensity in the last week evaluated with a
Numerical Rating Scale (NRS).13 The drugs used were identified and their
efficacy was assessed on pain intensity as abovementioned. All patients had
their analgesic drugs left unchanged between T2and T3.
In addition to these clinical data, the following data were evaluated:
At T0, the type of spinal injury was specified using the AOSpine Fracture
Classification.14 The type and delay of the surgical stabilisation procedure
performed after the trauma was specified if performed.
At T1, spinal canal stenosis was measured using the method previously
described by Perrouin–Verbe et al.2The most recent MRI was examined to
1Department of Physical and Rehabilitation Medicine, University Hospital of Nantes, Nantes cedex, France and 2Department of Neurotraumatology, University Hospital of
Nantes, Nantes cedex, France
Correspondence: Dr R Gross, Department of Physical and Rehabilitation Medicine, University Hospital of Nantes, 85, rue Saint Jacques, 44093 Nantes cedex, France.
E-mail: raphael.gross@chu-nantes.fr
Received 2 July 2012; revised 12 October 2012; accepted 21 October 2012; published online 4 December 2012
Spinal Cord (2013) 51, 369– 374
&
2013 International Spinal Cord Society All rights reserved 1362-4393/13
www.nature.com/sc

identify the post-traumatic spinal cord lesions using the criteria defined by
Wan g et al.8
At T2, the MRI that was performed because of the neurological worsening
was assessed using the abovementioned criteria.
Surgical treatment of the tethered cord was performed in all of the patients.
The procedure was initiated with a laminectomy on at least three vertebral
levels. The treatment of a residual spinal canal stenosis was necessary in two
patients. Then, the dura mater was opened on its midline. A meticulous
dissection of the arachnoiditis allowed untethering the cord and roots.
The procedure concluded with an expansile duraplasty with a supersized
synthetic tissue (Neuro-Patch, B-BRAUN Medical, Melsungen, Germany). The
duraplasty was tacked up to the paraspinal muscles laterally, and to the spinous
processes at both extremities of the zone of laminectomy.
This study was performed in agreement with the Helsinki Declaration
relative to patients’ rights and in accordance with the law on data protection
(last version no 2004–801, 6 August 2004). Because the data were collected
retrospectively and patient management was not modified and according to
French law (last version no 2004–806, 9 August 2004), this study did not
require approval by a research ethics committee.
RESULTS
Twelve patients met the inclusion criteria described above and were
analysed in this study.
Sociodemographic data, type of initial vertebral lesions and post-
traumatic neurological status (T0)
Clinical and radiological data concerning the initial traumatic SCI are
detailed in Table 1. Four patients had lesions at the subaxial cervical
spine (from C3 to C7) that caused tetraplegia. Eight patients had
lesions at the thoracolumbar junction that caused paraplegia. All
patients benefited from spinal surgery in the acute phase, which
aimed to decompress the spinal cord and to realign and stabilise the
spinal lesions. Two patients had a delayed surgical treatment because
of their initially unstable haemodynamics (see Table 2).
Clinical and radiological evolution of the patients before worsening
(T1)
All of the tetraplegic patients presented with changes in their motor
level and motor score, which indicated spontaneous motor recovery.
The initial median progression of the motor score in these patients
was 7 points (min ¼6; max ¼10, see Table 3).
A major residual stenosis caused by intracanalar bony fragments
was observed on the postoperative computed tomography scan in two
patients.
A MRI of the spinal cord was performed at T1in 8 out of the 12
patients. A focal cyst was noted in six cases and a focal myelomalacia
in two cases (see Table 4).
Clinical and radiological changes after worsening (T2)
Clinical changes. Five patients complained about the onset of motor
weakness (two cases were associated with pain), and seven patients
complained about isolated pain. Therefore, these two groups of
patients are discussed separately. Detailed data concerning the changes
in the neurological status of patients between T1and T2are presented
in Figure 1.
Patients with motor loss: Five patients (that is, four tetraplegics and
one paraplegic) underwent motor loss in their most caudally
preserved muscles. The affected muscles were located at the motor
level, just above, or just below (that is, the zone of partial preservation
in AIS A patients). In all of these patients, the motor loss was
confirmed by two assessments made by at least two examiners. Four
of these patients benefited from an electromyographic study, indicat-
ing intense acute denervation in the weakened muscles (Table 5). The
delay between the initial trauma and the onset of motor loss ranged
from 6 to 40 months (median ¼16.5 months) in four patients. The
median loss on the motor score was 4 points (range: 1–8). Two
patients also exhibited neuropathic pain with the same dermatomal
distribution as motor loss.
Pain patients: Seven paraplegic patients presented with isolated
pain, which had the features of at-level neuropathic pain13 in all cases.
The onset of pain ranged from 1 to 4 months (median ¼2 months).
The pain intensity was high with a median evaluation of 8 on a 10-
point NRS (see Figure 1).
MRI scan data at T2. All of the patients benefited from a spinal MRI
at T2(see Table 4). A tethered cord was found in all cases. The data
were compared with those obtained at T1in the eight patients who
Table 1 Patient population, type of vertebral injury and initial neurological status (T0)
Patient
number
Patient
gender
Spinal injury Motor
level
(R/L)
Motor
score
(R/L)
Sensory
level
(R/L)
Sensory score
(light touch/
pinprick)
AIS
1 M Teardrop,C4(C2.3) C3/C3 3/1 C4/C4 19/19 B
2 M Teardrop,C5(C2.3) C5/C5 4/5 C5/C5 16/14 A
3 F Luxation fracture, C4-C5 (C2.2) C4/C4 3/1 C4/C4 66/22 A
4 F Luxation, C6-C7 (C3.3) C6/C7 10/10 C6/C6 76/76 B
5 F L1 complete axial burst fracture (A3.3.3) T12/T12 2/2 T12/T12 102/104 A
6 M L1 Burst-split fracture (A3.2.1) T12/T12 25/25 T12/T12 68/72 D
7 M L1 burst-split fracture (A3.2.3) L1/- 7/24 T12/- 101/102 D
8 M T10-T11 oblique fracture (C3.2) T9/T9 0/0 T9/T9 68/72 A
9 M L1-L2 anterior subluxation associated with a
complete burst fracture (B1.2.3 þA3.3)
T10/T10 0/0 T10/T10 74/70 A
10 M T12-L1 complete rotational burst fracture (C1.3.3) T10/T11 0/1 T10/T11 74/75 C
11 M T12 complete flexion burst fracture (A3.3.2) T11/T11 2/10 T11/T11 88/86 A
12 M T12 flexion spondylolysis associated with an inferior
incomplete burst fracture (B2.3.2 þA3.1.3)
T11/T10 0/0 T11/T10 74/72 A
Abbreviation: AIS: American Spinal Injury Association impairment scale.
The type of injury is given in accordance with the AOSpine Fracture Classification.14 Motor and sensory scores and levels, as well as the AIS grade are given according to the International
Standards for Neurological Classification of Spinal Cord Injury.12 Motor scores are indicated for the upper limbs in tetraplegic patients (upper extremity motor score), and for the lower limbs in
paraplegic patients (lower extremity motor score).
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had previously undergone MRIs. Only one patient exhibited changes
of his spinal cord lesions (slight extension of a cyst).
Evolution after treatment of the aggravation (T3)
All patients who presented with motor loss benefited from surgery as
a first-line treatment, with a median delay time of 2 months (min¼1;
max ¼4). In contrast, all of the patients who presented with isolated
neuropathic pain were first treated with oral anticonvulsants. Because
of failed medical treatment, surgery was later proposed and performed
in all of these patients. The median time between the onset of pain and
the surgery was 50 months (min ¼6; max ¼103) in these patients.
The results of the surgical treatment are presented in Figure 2 for
those patients who presented with a motor loss. All of the patients
were improved by surgery. The improvement on the motor score
ranged from 1 to 7 points (median¼3 points). In three patients, this
improvement allowed the patient to gain one motor level.
The results of the surgical treatment for the pain patients are
presented in Figure 3. The median improvement on the NRS for these
patients was 4 points (min¼1.5; max ¼6). Three patients described a
partial recurrence of pain within 2 weeks after surgery. In five
patients, the drugs could be reduced from T3, as pain was frankly
reduced at this time.
DISCUSSION
This series of traumatic SCI patients is characterised by the delayed
onset of perilesional neurological aggravation (motor weakness and/
or at-level neuropathic pain), in the absence of syringomyelia or
extensive myelomalacia. The MRI data indicated the presence of a
tethered cord in all of the patients. The surgical treatment of this
tethered cord allowed symptom improvement, which indicates an
association between cord tethering and neurological worsening.
The complication that patients in this series underwent can be
considered a PTM; although, remarkable differences from the classical
picture of progressive PTMs are present. The nosological framework
of PTMs has been established by Edgar and Quail,3who distinguished
between cystic and non-cystic myelopathies. Both entities have been
considered progressive. In our patients, the aggravation, in relation to
the clinical and radiological data, remained strictly confined to the
perilesional zone. With respect to clinical signs, pain patients
complained about neuropathic pain, which was strictly at-level. The
motor loss only involved the most caudally preserved muscles. In four
Table 2 Initial spinal lesions and their surgical treatment
Patient Vertebral injury Delay of initial
surgery (days)
Surgical procedure Fused
segments
Specific findings
1 Tear drop, C4 (C2.3) 0 C4 corporectomy, arthrodesis with a graft,
anterior osteosynthesis
C3-C5
2 Tear drop, C5 (C2.3) 0 C5 corporectomy, arthrodesis with a graft,
anterior osteosynthesis
C4-C6
3 Luxation fracture, C4-C5 (C2.2) 0 C4 and C5 corporectomy, arthrodesis with a
graft, anterior osteosynthesis
C3-C6
4 Luxation, C6-C7 (C3.3) 0 C7 corporectomy, arthrodesis with a graft,
anterior osteosynthesis
C6-T1
5 L1 complete axial burst fracture (A3.3.3) 0 L1-L2 laminectomy, posterior
osteosynthesis
T11-L3
6 L1 burst-split fracture (A3.2.1) 0 Posterior osteosynthesis T11-L3 No laminectomy performed
7 L1 burst-split fracture (A3.2.3) 7 T12-L1 laminectomy, duraplasty, posterior
osteosynthesis
T11-L3 Posterior dura rip
8 T10-T11 oblique fracture (C3.2) 0 posterior osteosynthesis T9-L2 No laminectomy performed
9 L1-L2 anterior subluxation
associated with a complete burst fracture
(B1.2.3þA3.3)
16 L1-L2 laminectomy , expansile duraplasty,
posterior osteosynthesis
T11-L4 Posterior dura rip with conus
and roots display
10 T12-L1 complete rotational burst fracture
(C1.3.3)
0 T12-L1 laminectomy, posterior
osteosynthesis
T10-L3 Posterior dura rip
11 T12 complete flexion burst fracture (A3.3.2) 0 T11-T12 laminectomy, posterior
osteosynthesis
T10-L2 Posterior dura rip
12 T12 flexion spondylolysis associated with an
inferior incomplete burst fracture
(B2.3.2þA3.1.3)
0 L1 laminectomy, posterior osteosynthesis T10-L2 Posterior dura rip
Table3 Initialmotorlevel(T
0) and evolution of the motor score for
the patients from T0to T3
Patient
number
T0motor
level (R/L)
T0motor
score (R/L)
T1motor
score (R/L)
T2motor
score (R/L)
T3motor
score (R/L)
1C3/C33/16/54/35/5
2C5/C54/58/86/67/7
3C4/C43/16/45/48/5
4 C6/C7 10/10 13/14 12/14 13/14
5 T12/T12 2/2 7/7 5/1 8/5
6 T12/T12 25/25 2 5/25 25/25 25/25
7 T12/L2 7/24 22/25 22/25 22/25
8 T9/T9 0/0 0/0 0/0 0/0
9 T10/T10 0/0 0/0 0/0 0/0
10 T10/T11 0/1 3/9 3/9 3/9
11 T11/T11 2/10 18/19 18/19 18/19
12 T11/T10 0/0 0/0 0/0 0/0
Motor levels and scores are given according to the International Standards for Neurological
Classification of Spinal Cord Injury.12 Motor scores are given for the upper limbs in tetraplegic
patients (upper extremity motor score), and for the lower limbs in paraplegic patients (lower
extremity motor score). Scores are given separately for the right and left limbs (R/L).
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out of five patients, aggravation led to the loss of one function level
(3/5 muscle strength or greater), level which had recovered functional
strength between T0and T1. These patients, therefore, presented with
a recovery/worsening sequence. Symptoms, such as spasticity increase,
increased autonomic dysreflexia, bowel and bladder dysfunction, or
below-level neuropathic pain, which are frequent in progressive PTM,
have not been observed in our patients. In the pain patients of this
series, the fair hindsight at surgery time (median¼50 months)
suggests withdrawing the hypothesis of a progressive PTM
beginning with at-level neuropathic pain.
Radiological data confirmed that the myelopathy in our patients
was localised. The signal intensity changes in the cord, whether cysts
or malacia, were confined to the immediate surroundings of the
initial lesion. When previous MRI data were available (8 patients), the
MRIs performed at T2were unchanged compared with the former
MRI data in all of the patients but one (see Table 4 and Figure 4).
Therefore, it appears that among the PTMs, the pathological
condition that is described in this series emerges. This focal entity
consists in myelopathy and/or radiculopathy, which is strictly con-
fined to the lesional and perilesional zones. A radiculopathy can be
suspected because of an associated tethering of the roots in 9 out of
12 patients. We hypothesise that the term perilesional myeloradiculo-
pathy (PMR) could be used to describe this condition. Although the
natural evolution of a PMR to a progressive myelopathy is possible, this
does not appear to be systematic, given our data. We, thus, consider
PMR a distinct pathological entity rather than an incipient form of
progressive PTM.
Progressive PTMs and PMR share the same pathophysiological
mechanism, which is the cord tethering. Williams considered the
presence of scars of the dura and arachnoid at the site of injury to be
a critical factor in the genesis of a syrinx.4Edgar and Quail
emphasised the role of the tethered cord in both forms of PTMs.3
Many works have confirmed the causal link between arachnoiditis and
syrinx15,16 or myelomalacic myelopathies.17 In our study, all of the
patients had spinal lesions that were located at the subaxial cervical
spine or at the thoracolumbar junction. The anterior cervical spinal
fusion allows significant motion of the spinal cord. In thoracolumbar
lesions, a short posterior fusion allows residual motion of the lumbar
spine in relation to the above fused segments. The tethering in these
mobile zones could have induced secondary lesions of the cord and/or
roots due to traction forces during spinal movements.18 These slight
lesions were not visible on MRI scans but responsible for clinical and
electromyographic changes.
We hypothesise that PMR treatment must follow the same
principles and techniques as treatment of progressive PTMs. The
aim is to release the tethered cord and prevent relapse by creating an
enlarged subarachnoid space (expansile duraplasty). If there is an
associated compression of the cord due to spinal canal stenosis, for
example, by bony fragments, this issue must also be treated. Surgical
treatment led to partial motor recovery in two patients and complete
recovery in three patients. In five out of the seven pain patients,
surgery was followed by an improvement of at least three points on
the 10-point NRS. These encouraging results and the lack of efficacy
of the previous medical treatment in these pain patients provide
arguments for performing surgery for pain patients with a PMR.
Cord release surgery is delicate. The arachnoidolysis must be
performed carefully to prevent additional lesions of the cord or roots.
No patient of our series exhibited postoperative worsening. However,
three patients experienced partial recurrence of pain within the first
two weeks after surgery, possibly caused by re-tethering of the cord
Table 4 Data of the MRI of the spinal cord performed at T1and T2
Patient number Injured
vertebra(s)
Cord lesions on MRI (T1)Cord changes on MRI (T2)Tethering of the cord
1 C4 Focal cyst at vertebral level C4
Thin myelomalacia upwards
Unchanged Ventral
2 C5 Myelomalacia at vertebral level C4 and C5 Unchanged Circumferential þC6 roots, bilateral
3C4þC5 NA Focal cyst at vertebral levels C4 and C5 VentralþC6 root, right-sided
4C6þC7 Focal cyst at vertebral level C6-C7 Focal cyst, slightly bigger Ventralþdorsal
5 T11 þT12 NA Focal cyst at vertebral level T12 Circumferential: cord þcauda equina
6 L1 Focal cyst in the conus medullaris Unchanged Dorso-lateral, left-sided
7 L1 Focal cyst in the conus medullaris Unchanged Circumferential: cord þcauda equina
8 L1 NA Myelomalacia at vertebral level T10,
T11 and T12
Conus medullaris-cauda equina junction,
right-sided
9 T12 þL1 Myelomalacia from T10 to conus medullaris Unchanged Dorsal: cord þcauda equina
10 L1 þL2 Focal cyst in the conus medullaris Unchanged Dorsal: cord þcauda equina
11 T12 NA Focal cyst at vertebral level T12 Dorso-lateral, left sided: cord þcauda equina
12 T10 þT11 Focal cyst at vertebral level T11-T12 Unchanged Circumferential
Abbreviations: MRI, magnetic resonance imaging; NA: not available.
Spinal cord signal abnormalities are given according to Wang et al.11
0
1
2
3
4
5
6
7
8
9
123456789101112
Motor loss (score) Sensory loss (score) Pain (NRS)
Figure 1 Motor and sensory score changes and pain evaluation, observed
between T1(before worsening) and T2(after worsening) in the 12 patients
of our series. Motor and sensory losses are expressed as points on the motor
or sensory ASIA score.12 Pain is evaluated using a 10-point NRS score.
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and roots, which has been previously emphasised.5Because
arachnoiditis is a form of healing, the possibility to prevent
postoperative arachnoiditis is poor. The prevention of postoperative
re-tethering could be based upon the quality of the expansile
duraplasty, which must be tacked up to the paraspinal muscles or
spinous processes, as well as the absence of a subarachnoid
haemorrhage. Lee et al.5also advocated the frequent turning of the
patient from side-to-side into the prone position in the postoperative
period, which could prevent the deposit of sediment in the recumbent
position and the creation of a new tethering scar. Nevertheless,
Table 5 EMG data in the patients who presented with a motor loss
Patient
number
T1motor
score (R/L)
T2motor
score (R/L)
Weakened muscles EMG data (T2): location
of acute denervation
Intensity of spontaneous activity
(fibrillations and/or positive waves)
Delay between
trauma and EMG
1 6/5 4/3 Elbow flexors (R þL)
Wrist extensors (R)
Not available —
2 8/8 6/6 Wrist extensors (R þL) Wrist extensors (R þL) þþþ 40 Months
3 6/4 5/4 Wrist extensors (R) Wrist extensors (R) þþ 18 Months
4 13/14 12/14 Triceps brachii (R) Wrist extensors (R)
Triceps brachii (R þL)
þþþþ 24 Months
5 7/7 5/1 Hip flexors (R þL)
Knee extensors (R þL)
Knee extensors (R þL)
(hip flexors not explored)
þþþ 30 Years
Abbreviation: EMG, electromyographic.
(R: right side. L: left side). The intensity of the acute denervation (fibrillations and/or positive sharp waves) is semi-quantified using the gradation from þ(rare) to þþþþ(intense).
Motor score
0
5
10
15
20
25
30
T0 T1 T2 T3
Patient 1 Patient 2 Patient 3 Patient 4 Patient 5
Figure 2 Evolution of the ASIA/ISCOS (International Spinal Cord Society)
motor score for the five patients who presented with a motor weakness.
Scores are given for T0(time of initial injury), T1(before worsening), T2
(after worsening) and T3(after surgical treatment). The lower extremity
motor score is given for patient 5.
0
1
2
3
4
5
6
7
8
9
Pre-operative NRS score Post-operative NRS score (6 months)
Pain : NRS
Figure 3 Effects of cord release surgery on pain in our paraplegic patients
(mean NRS score).
Figure 4 MRI scans of patient 4 before and after the neurological
deterioration. (a) MRI scan performed at T1, before worsening. A focal cyst
is visible at level C6-C7, and the cord is tethered ventrally and dorsally.
(b) MRI scan performed at T2 (after worsening), 3 months later, showing
the cyst, possibly slightly bigger and the tethering.
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preventing re-tethering after surgery of a tethered cord remains poorly
controlled. Because the risk of pain recurrence, possibly due to re-
tethering, is well known, the pertinence of performing a DREZotomy
in association with the cord release should be discussed. DREZotomy
has been shown to be effective in relieving pain in SCI patients with
chronic at-level neuropathic pain. Some studies have demonstrated
pain improvement in 68%19 or 74%20 of patients with this technique.
Sindou et al. recently described a two-step technique for SCI patients
with at-level neuropathic pain.19 The first step was to release the cord
androots,andthesecondstepwastheDREZotomy.Ourstudy
supports the efficacy of cord release surgery alone. A prospective study
that compares the results of cord release surgery alone versus cord
release associated with a DREZotomy could help to identify the best
treatment for at-level neuropathic pain in traumatic SCI patients.
CONCLUSIONS
PMR is a potential complication after a traumatic SCI, consisting in
motor loss and/or at-level neuropathic pain. PMR can occur as soon
as in the first 6 months post injury. It is caused by damage to the
spinal cord and roots if these structures are tethered and submitted to
traction, lengthening and compression constraints. This study stresses
the necessity of performing an MRI for every SCI patient who
presents with chronic neuropathic pain. An MRI can detect a curable
cause, such as a tethered cord, for which surgical treatment is
effective. This work suggests that to relieve symptoms and prevent
further deterioration, early surgery should be proposed for patients
who present with PMR.
DATA ARCHIVING
There were no data to deposit.
CONFLICT OF INTEREST
The authors declare no conflict of interest.
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