Does sacral posterior rhizotomy suppress autonomic hyper-reflexia in patients with spinal cord injury?

Summary

Objective

To study the occurrence of autonomic hyper-reflexia (AHR) after intradural sacral posterior rhizotomy combined with intradural sacral anterior root stimulation, performed to manage the neurogenic hyper-reflexic bladder, and to determine the pathophysiological basis of the uncontrolled hypertensive crisis after sacral de-afferentation.

Patients and methods

Ten patients with spinal cord injury operated using Brindley’s method between September 1990 and February 1994 were reviewed. Systematic continuous non-invasive recordings of cardiovascular variables (using a photoplethysmograph) were made during urodynamic recordings and the pre- and post-operative vesico-urethral and cardiovascular data compared.

Results

Nine of the 10 patients were examined using a new prototype measurement system; one woman refused the last urodynamic assessment. Eight of the nine patients who presented with AHR before operation still had the condition afterward. There was a marked elevation in systolic and diastolic blood pressure during the urodynamic examination in all eight patients, despite complete intra-operative de-afferentation of the bladder in five. The elevation of blood pressure started during the stimulation-induced bladder contractions and increased during voiding in all cases. Five patients showed a decrease in heart rate during the increase in blood pressure. However, in three patients the heart rate did not change or even sometimes slightly increased as the arterial blood pressure exceeded 160 mmHg, when the blood pressure and heart rate then increased together.

Conclusions

These results confirm that even after complete sacral de-afferentation, AHR persisted in patients with spinal cord injury and always occurred during the stimulation-induced voiding phase. In cases of incomplete de-afferentation, small uninhibited bladder contractions without voiding occurred during the filling phase. The blood pressure then increased but never reached the value recorded during stimulation-induced micturition. Stimulation of afferents that enter the spinal cord by the thoracic and lumbar roots and that are not influenced by sacral rhizotomy could explain why AHR increases during urine flow. The distinct threshold of decreased heart rate by increasing blood pressure to >160 mmHg focuses attention on the chronotropic influences of the sympathetic nerves in the heart by an exhausted baroreceptor reflex.

Introduction

Patients with tetraplegia and high paraplegia (above T5-T6) often have autonomic hyper-reflexia (AHR), a term describing several events which are generally manifested by cardiovascular symptoms [1]; AHR has been well documented since Head and Riddoch first described the symptoms in tetraplegic patients [2]. The work of Guttmann and Whitteridge [1] remains the main reference for knowledge of this syndrome. A spontaneous hypertensive crisis usually arises from the lower urinary
tract or from the rectum because of rectal impaction. Because tetraplegic patients are usually hypotensive, the high blood pressures that develop during AHR may be sufficient to cause cerebrovascular accidents and death. The relationship between the lower urinary tract and the sympathetic nerve responses during AHR remains poorly understood.
Intradural sacral rhizotomy combined with anterior sacral root stimulation at the cauda equina level (Brindley’s method [3]) aims to suppress all afferents of the bladder. Increased bladder capacity and compliance, release of detrusor-sphincter dyssynergia (DSD) and the disappearance of AHR are the main goals of such an
operative approach in neurogenic bladders [3]. From our experience, sacral rhizotomy does not suppress AHR during the stimulation-induced voiding phase [4]. Sacral de-afferentation provides an interesting model to study the cardiovascular responses to the filling and voiding phase of the bladder in patients with spinal cord injury (SCI). From knowledge of the neurophysiology, three hypotheses can be proposed to explain why AHR occurs after sacral differentation: (i) afferents of the bladder viscero-vascular reflex have been shown to involve both the pelvic and hypogastric nerves, the latter being unaffected by posterior sacral rhizotomy [5][6][7]; (ii) because of the known occurrence of bundle-fibres that cross between anterior and posterior roots in the cauda equina, and the likelihood that there are such crossing fibres in the short segment between their exit from the dura and the posterior root ganglion, complete de-afferentation of the bladder is impossible [8][9][10]; (iii) stimulation of the sympathetic afferents by stretching the posterior urethral structures induces a sympathetic discharge during voiding.
The aims of the present study were to assess the occurrence of AHR after sacral posterior root de-afferentation and to examine in detail the cardiovascular responses induced.

Patients and methods

Between 1990 and 1994, 10 patients with SCI (three men and seven women) underwent operation using Brindley’s method [3]. All but one, who was operated for a thoracic ependymoma with subsequent paraplegia, had a traumatic spinal cord injury. The mean age at operation was 30.3 years (range 23-42) for men and 28 years (range 18-37) for women; the mean follow-up (to November 1996) was 45.9 months (23.1-72.4). Of the seven women with a complete neurological lesion, four were tetraplegic and three paraplegic, and two men were paraplegic (one incomplete) and one a complete tetraplegic. The mean interval between trauma (iatrogenic disorder in one case) and operation was 3.2 years (range 1.4-4.6) in the men, and 6.1 years (range 1.2-16.7) in the women.
Posterior sacral de-afferentation and electrode placement around the anterior roots were performed intrathecally at the cauda equina level. Incontinence was the indication for operation in the women, with high-pressure voiding secondary to DSD the major indication in all three men. Before operation, DSD impaired voiding in eight of the 10 patients, and severe AHR was present in eight; in all these patients the neurological deficit was above T7. In the two remaining patients (paraplegic at T10 and T6, nos 2 and 4) there was no AHR before operation. In all cases, the bladder function improved post-operatively, despite surgically incomplete de-afferentation in four, and the DSD resolved in all cases. Details of the patients’ pre-operative characteristics are given in Table 1.
Urodynamic studies were carried out regularly after surgery (at 1, 2, and 4 weeks, 3 and 6 months and thereafter annually). The last urodynamic examinations were performed with a new prototype recording system, using special hardware and software to acquire and analyse the data. The system was designed to make measurements over longer durations, permitting slow changes to be assessed, and increased time resolution (up to 1 ms) allowed precise measurements of latency. Separate devices were used to record vesico-urethral pressures, cardiovascular and respiration variables; these signals were amplified and filtered before being digitized and stored by the computer. All signals were displayed simultaneously on a monitor for immediate evaluation.
The technique of vesico-urethral and anal pressure recordings with a no.5 and a no. 3 microtransducer catheters (8 F), respectively, are described elsewhere [11][12][13]. The bladder was filled slowly (5 mL/min) with 24% contrast medium (3-acetylamino-methyl-5-acetylamino-2,4,6-triodobenzoic acid) to 500 mL. Spot films (100 mm) were taken to obtain a correlative analysis between simultaneous measurements at various anatomical locations of the vesico-urethral complex. The rectal pressure was measured to detect any pressure changes caused by abdominal artefacts.
A photoplethysmograph (Finapres Blood Pressure Monitor, Ohmeda 2300, USA) provided a non-invasive continuous pressure waveform measurement of the arterial blood pressure in the finger, and digital values of systolic, diastolic and mean pressures, as well as pulse-rate and an annotated trend display. The ambient temperature was maintained constant when the patients lay on the examination table. No patient presented with autonomic disorders or severe arteriosclerosis that may have affected the photoplethysmographic recordings. Systolic-diastolic arterial pressures and heart-rate changes were analysed during three different urodynamic phases, i.e. bladder filling, electrically induced isovolumetric contractions of the bladder (from the start of the bladder contraction to the start of the micturition) and voiding phases from the beginning to the end. Any sections of recordings which were influenced by spasm artefacts were not considered in the analyses.
Table 1 Clinical data of patients with SCI treated by posterior sacral rhizotomy and sacral anterior root stimulation

Bladder capacity (ml) Compliance PVR (mL) X-ray LUT,UUT UTI
Patient Age Sex Neurological deficit level Voiding method Incontinence Pre Post Pre Post Pre Post Pre Post Pre Post
1 24 F C5 complete T and CIC Rx 150 ≥500 N N 200 0 D, Rf, H N, No Rf, No H C No
2 29 F T6 complete T Rx 80 ≥500 na N 90 0 D N No No
3 18 F T10 complete CIC Rx 280 ≥500 N N 220 0 N N C C
4 37 F T6 complete CIC Rx 280 ≥500 low N 500 20 N N C Few
5 37 F C7 complete T Rx 70 ≥500 na N 120 40 D N No No
6 24 F C5 complete SC Rx 150 ≥500 low N 200 50 N, BRf N, LRf by stim C C
7 27 F C5 complete T Rx 75 ≥500 na low 20 0 D, LRf N, No Rf C C
8 26 M T4 complete CIC Rx 250 ≥500 low N 100 50 D, BRf N.RRf by stim c Few
9 23 M C7 complete SC Sph 1993 Rx + stress 150 ≥500 na N 60 0 D N c Few
10 42 M T6 incomplete T and CIC Sph 1989, 1990 Rx + stress 120 ≥500 na na 60 0 D, LR N, LR by stim c No
Mean 160
157 16
SD 82
138 22
CIC, Clean intermittent catheterization. LUT, Lower urinary tract. UUT, Upper urinary tract. DSD, Detrusor sphincter dyssynergia. T, Tapping. Rx, Reflex. B, Bilateral. R, Right. L, Left. PVR, Post-void residual urine volume. N, Normal. D, Diverticula. H, Hydronephrosis. Rf, Reflux. Sph, Sphincterotomy. C, Chronic, na, Not available. SC, Suprapubic catheter.

Results

Nine of the 10 patients were examined using the prototype measurement system; one woman refused the last urodynamic assessment, having no problems with her bladder. In all cases, the bladder function was improved after surgery, despite surgically incomplete de-afferentation in four patients (Table 2). After implantation, all patients emptied their bladder completely with the stimulator. Stimulation of S3 and S4 was used to empty the bladder in seven of 10 patients (one with additional stimulation of S2); all voided 3-4 times per day with stimulation. In one patient, S4 and S5 were of primary importance, whereas in the remaining two, bladder contractions were induced by stimulating only S3 (Table 2). In none of the nine patients assessed did co-contraction of the trunk or lower limbs occur during stimulation-induced micturition. The DSD resolved in all cases after de-afferentation. An electrophysiologically induced bulbocavernous reflex (BCR) was recorded in six of the nine patients; BCR latencies were normal in two patients with incomplete and one with complete de-afferentation, and prolonged in three with complete de-afferentation. An electrophysiologically induced H-reflex was recorded in eight of 10 patients and was normal in all. There was a marked elevation in systolic and diastolic blood pressure during the urodynamic examination in all eight patients who presented with AHR before operation, despite complete intra-operative bladder de-afferentation in five (Table 2). The mean (SD) systolic and diastolic blood pressures, and pulse rates, at the end of the filling phase and before stimulation were 116.4 (17.6) and 60.6 (9.7) mmHg and 58.3 (10.8) b.p.m, respectively. The elevation of blood pressure started about 3-6 s after the beginning of the stimulation burst, was present during the stimulation-induced bladder contraction and increased during the voiding-phase in all patients (Fig. 1). The mean (sd) systolic and diastolic blood pressures reached 180.4 (45.8) and 98.9 (25.8) mmHg, respectively, whereas the mean pulse rate decreased to 54.8 (12.1) b.p.m. The mean arterial blood pressure was calculated as [diastolic + (systolic -diastolic)/3], and increased significantly from 79.2 (11.8) before stimulation to 126.0 (31.9) mmHg during stimulation-induced voiding (paired two-sample t-test, P<0.01); the mean decrease in the pulse rate during stimulation was not statistically significant. The blood pressure increase during voiding was not related to the increase in bladder pressure, as this always decreased when micturition started (Fig. 1).
Table 2 Post-operative clinical data of patients with SCI treated by posterior sacral rhizotomy and sacral anterior root stimulation
Patient no. 1 2 3 4 5 6 7 8 9 10
Sacral root stimulation S2-S4B S3-S4B S3-S4B S3B S3B S3-S4B S4-S5B S3-S4B S3-S4B S3-S4B
Muscle responses* S2R Bl (50) S3R Bl (60) S3R Bl (70) S3R Bl (80) S3R Bl (65) S3R Bl (40) S4R Bl (40) S3R Bl (25) S3R Bl (50) S3R Bl (100)

S2L Bl (30) S3L Bl (30) S3L (70) S3L Bl (70) S3L Bl (75) S3L Bl (50) S4L Bl (170) S3L Bl (50) S3L Bl (40) S3L Bl (60)

S2B EAS PFF S3B PFF S3B PTF S3B PTF S3B PFF S3B PTF EAS S4B EAS S3B PFT S3B PFT S3B PFT

S3R Bl (60) PTF EAS EAS EAS PFT EAS S4B Bl (40) S5B Bl(75) EAS EAS EAS

S3L Bl (40) S4R Bl (90) S4B Bl (50)

S4B EAS
S4R Bl (100) S4R Bl (40) S4R Bl (100)

S3B EAS S4L Bl (20) S4B EAS



EAS S4L Bl (10) S4L Bl (40)

S4R Bl (20) S4B EAS




S4L Bl (50) S4B EAS S4B EAS
De-afferentiation I C I I C I C C C C
IJBW (post-op) No No Yes No No Yes No No No Yes
Continence Full Full Full (Ach) Full Full Full Full (Ach) Full (Ach) Stress only Stress only
BCR latency (min/max, ms) na na 32.2/42.8 44.5/84.5 32.8/44.7 na 59 na 33.1/34.8 61.1/85.7
H reflex (ms) na na 25.6 39.8 31.0 31.7 31.8 35 30 32.3
AHR
Before Yes No Yes No Yes Yes Yes Yes Yes Yes
After Yes No Yes No Yes Yes Yes Yes Yes Yes
BP systolic/diastolic (pulse rate)
Before 110/60 (60) No last 140/68 (70) 115/78 (50) 88/55 (53) 110/53 (45) 107/53 (49) 124/64 (65) 112/52 (50) 140/80 (75)
After 140/70 (50) Control 162/88 (62) 117/77 (50) 43/83 (51) 228/133 (41) 268/133 (60) 150/78 (57) 162/85 (40) 190/121 (77)
*Responses to stimulation. Bl, Bladder pressure (cmH20). B, Bilateral. L, Left. R, Right. I, Incomplete. C, Complete. Ach, Anticholinergic therapy. BP, Blood pressure. HR, Heart rate. PFT, Plantar toe flexors. PFF, Plantar feet flexors. EAS, External anal sphincter. UBW, Uninhibited bladder waves.
In one patient, the stimulation parameters were adjusted to induce a single bladder contraction first without and thereafter with a consecutive voiding (Fig. 2a,b). Bladder contractions without voiding caused a 6 s delay in the blood pressure increase, which then decreased as bladder pressure decreased. On the contrary, stimulation-induced bladder contractions with consecutive voidings were paralleled by an increase in blood pressure despite a concomitant decrease in the intravesical pressure.
Five patients showed a decrease in heart rate during the increase in blood pressure (Fig. 3, Table 2, nos 1,3, 6, 8, 9). However, in three patients the heart rate did not change or even increased slightly as the arterial blood pressure exceeded 160 mmHg (Table 2, nos 5, 7, 10). There was then a parallel increase in blood pressure and heart rate (Fig. 1). In four patients, the occurrence of uninhibited bladder contractions without micturition during the filling phase indicated incomplete de-afferentation; in all four patients, there was only a small increase in blood pressure during the uninhibited bladder contractions, which never reached the values observed during the stimulation-induced voiding phase (Fig. 4).
Recordings from a paraplegic patient
Fig. 1. Recordings from a paraplegic patient (T6, no 10). The upper part of the graph traces the bladder (BLA, green) and external urethral sphincter (EUS, red) recording, the lower part the continuous blood pressure (BP, green) and heart rate (HR, red). There is an increase in blood pressure after stimulation (ST) which persists during voiding (MI), despite a concomitant decrease in bladder pressure. HR before stimulation, 75 b.p.m.; BP before stimulation, 140/80 mmHg, not shown. There was no decrease in the HR during stimulation-induced voiding as the BP increased (170/100 mmHg); during stimulation, there were parallel changes in blood pressure and heart rate. Cal, calibration loop from the Finapres device. Missing values were interpolated.
Traces from a woman with complete tetraplegia
Fig. 2. Traces from a woman with complete tetraplegia (C5, no 1), showing recordings after sacral posterior de-afferentation and anterior sacral root stimulation. Upper graph, urodynamic recordings of the bladder pressure (BLA, green) and external urethral sphincter (EUS, red); lower graph, continuous trend display of blood pressure (BP, green) and the heart rate (HR, red) during urodynamic examination. The stimulation parameters were adjusted to induce a single bladder contraction first without a, and thereafter with b, consecutive voiding. Bladder contraction without voiding led to a 6 s delay in blood pressure increase, that then decreased as bladder pressure decreased. On the contrary, stimulation (ST)-induced bladder contraction with consecutive voiding (Mi) paralleled the blood pressure increase despite a concomitant decrease in intravesical pressure.
Traces from a man with complete tetraplegia
Fig. 3. Traces from a man with complete tetraplegia (C7, no. 9), showing recordings after sacral posterior de-afferentation and anterior sacral root stimulation. Upper graph, urodynamic recordings of the bladder pressure (BLA, green) and external urethral sphincter (EUS, red); lower graph, continuous trend display of the blood pressure (BP, green) and the heart rate (HR, red) during urodynamic examination. Stimulation induced an increase in blood pressure (maximum 162/85 mmHg, versus 120/70 mmHg before stimulation) with a parallel decrease in heart rate (40 versus 50 b.p.m. before stimulation). ST, stimulation.
Traces from a another woman with complete tetraplegia
Fig. 4. Traces from a woman with complete tetraplegia (C5, no. 6), showing recordings after sacral posterior de-afferentation and anterior sacral root stimulation; the de-afferentation was incomplete. Upper graph, urodynamic recordings of the bladder pressure (BLA, green) and external urethral sphincter (EUS, red); lower graph, continuous trend display of the blood pressure (BP, green) and the heart rate (HR, red) during urodynamic examination. There are uninhibited bladder contractions during the filling phase, resulting from incomplete de-afferentation, with a concomitant small elevation in the blood pressure (BP) and decrease in heart rate.

Discussion

AHR is a clinical phenomenon affecting patients with SCI above the sympathetic outflow at the T5-T6 level [1][2][14][15]. Any noxious stimulus below this level may initiate reflex sympathetic activity which results in lifethreatening hypertension; stimulation from the lower urinary tract accounts for most such episodes. Sympathetic overactivity below the level of the lesion causes vasoconstriction of both the peripheral and splanchnic vessels, pallor and piloerection. A limited parasympathetic response above this level secondary to the activation of the central feedback mechanisms is seen as bradycardia. Bradycardia caused by parasympathetic activity is frequent, but tachycardia has also been described [1].
The evaluation of rapid changes in the blood pressure and heart rate during urodynamic examination requires a continuous measurement of the arterial blood pressure. The photoplethysmograph measures reliably and noninvasively the individual changes of mean and diastolic pressure during steady-state conditions, and during manoeuvres such as Valsalva’s or orthostatic stress [16]. The finger-to-brachial differences within one subject are relatively stable; the 95% individual limits of agreement of the sd are between 0 and 4 mmHg [16][17].
Many reports on the cardiovascular responses to the bladder (detrusor muscle) activity in patients with SCI have been published but most have focused only on the effect of bladder distension on the cardiovascular system [1][15][18]. From our experience with continuous cardiovascular monitoring in patients with SCI, increased blood pressure seems to be maximal during voiding and not during the bladder contraction, suggesting that stretching of the posterior urethral receptors by the urine flow plays a major role in the maintenance of AHR. The analysis of the urodynamic recordings obtained in the present patients tends to confirm this hypothesis. Despite large posterior sacral de-afferentation in five cases, AHR present before operation in eight patients persisted afterwards in all. The increase in the arterial blood pressure mainly occurred 3-6 s after stimulation and increased during voiding, as bladder pressure decreased concomitantly. A 3-6 s delay between the AHR stimulus and the hypertensive response was reported previously [19]. In four cases, incomplete de-afferentation was suspected during the filling phase, through the occurrence of small residual uninhibited bladder contractions without voiding. In all these cases no or only a slight increase of the blood pressure was recorded during the uninhibited bladder contractions without voiding, and which never reached the values observed during the stimulation-induced voiding phase.
It is already established beyond doubt that for some segments in some people there are afferent parasympathetic fibres that enter the cord by the anterior roots [9]. It is uncertain how numerous and how physiologically important such fibres are, and it is uncertain whether they exist in all roots in all people. In six of eight patients, electrophysiological recordings were obtained of the BCR latency; it was normal in each incompletely de-afferentated patient and prolonged in all but one of those completely de-afferentated. The presence of the BCR and prolonged latency in the latter patients tends to confirm that sensitive afferents exist in the somatic nervous system. Prolonged latency reflex responses caused by antidromic stimulation of the anterior roots have been confirmed and are related to myelinated afferent fibres [11]. An electrophysiologically induced H-reflex was recorded in eight of 10 patients and was normal in all; thus, the sacral root (S1) remained intact in all cases after operation.
The present cardiovascular and urodynamic findings support the hypothesis that parasympathetic afferents in the S2-S4 anterior roots exist in all people but are only able to trigger small increases in blood pressure. On the contrary, afferents from the posterior urethra entering the spinal cord by thoracic and lumbar roots that are not influenced by sacral posterior rhizotomy could explain why AHR reaches a maximum during voiding. In principle, it might be possible to discover whether the afferent impulses that trigger the pressure rise are provoked directly (in sacral roots) by the stimulus or are secondary to the rise in the bladder or filling of the urethra, by giving atropine to block the response of the bladder to the stimulation. However, the dose would need to be so large that patients may be unwilling to take it, so this experiment is impracticable.
The present findings are of interest because they are new and previously unsuspected. Candidates for posterior rhizotomy who suffer from dysreflexia should be informed that they may have less trouble from these attacks after the operation, but they should also be informed that the susceptibility to AHR triggered by the pelvic organs does not disappear entirely. They must also be informed that there is a remote possibility that they may be unable to use their implants because of autonomic dysreflexia, although other reports suggest that this risk is very small [3], and no such case occurred in the present series.
Increased cardiac output and increased stroke volume have been reported to occur during AHR [20][21]. Any decrease in heart rate during AHR is caused by an intact baroreceptor vagal reflex, and this was the case in most of the present patients with AHR. In part, the increased stroke volume may arise through improved filling of the ventricles, but this cannot account for the large increase in stroke volume or for the increase in cardiac output [20][21]; it must arise partly from the inotropic effects of the sympathetic nerves, which are activated by the spinal reflexes [22][23][24][25] There was no marked decrease, or even in some cases an increase, in the heart rate in three of the present patients when the arterial blood pressure was >160 mmHg. This tends to confirm the findings of Naftchi [19] suggesting that baroreceptors are ineffective or less effective at a mean arterial blood pressure >160 mmHg. In these cases, sympathetically induced chronotropic effects of the heart probably dominate the vagal induced bradycardia with subsequent increase of the heart rate.
AHR secondary to neurogenic voiding dysfunction has been linked to bladder distension. From experience with continuous cardiovascular monitoring, blood pressure increases in patients with high SCI seemed to be maximal during voiding and not during bladder contraction, and did not resolve after sacral posterior de-afferentation. As some afferents are abolished by de-afferentation, sacral posterior rhizotomy provides an interesting model to study the cardiovascular responses to the filling and voiding phases of the bladder in patients with SCI. The results of the present study confirm that even after complete de-afferentation, AHR persists in patients with SCI and always occurred during the stimulation-induced voiding phase. In cases of incomplete de-afferentation, small uninhibited bladder contractions occurred during the filling phase of the bladder but which never induced micturition. The blood pressure then increased, but did not reach the values observed during stimulation-induced micturition. The stimulation of afferents that enter the spinal cord by thoracic and lumbar roots and are uninfluenced by sacral rhizotomy could explain why AHR increases during urine flow. This is the first report of the consistent occurrence of AHR after sacral posterior de-afferentation, possibly because discontinuous recordings of the cardiovascular variables, as made in most urological departments, fail to detect such rapid events. It does not mean that sacral posterior rhizotomy is contraindicated in patients with autonomic dysreflexia, as in all the present patients who had dysreflexia before sacral rhizotomy had less troublesome dysreflexia afterward. However, it is important to inform candidates for posterior rhizotomy who suffer from autonomic dysreflexia that the susceptibility to AHR triggered by the bladder may not disappear completely[26]. In all the present patients, the increase in blood pressure during AHR was paralleled by a decrease in heart rate, providing the systolic pressure did not exceed 160 mmHg. Beyond this limit, a smaller decrease in heart rate, and even slight tachycardia, occurred during the hypertensive episodes. The sharp threshold in the decreasing heart rate focuses attention on the chronotropic influences of the sympathetic nerves on the heart.

Acknowledgement

We thank Dr G.S. Brindley for constructive comments. This work was partially funded by the International Institute for Research in Paraplegia (P17/94-97).

Authors

  • B. Schurch, MD.
  • P.A. Knapp, MSc.
  • D. Jeanmonod, MD.
  • B. Rodic, MD.
  • A.B. Rossier, MD.
  • Correspondence: Dr B. Schurch, Swiss Paraplegic Centre, University Hospital Balgrist, Forchstrasse 340, 8008 Zurich, Switzerland.

References

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