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Syringomyelia after decompressive laminectomy for cervical spondylosis
Surg Neural 1987;28:458-62
458
Syringomyelia
after Decompressive
Laminectomy
for
M.D., Louis H. Harkey,
M.D.,
Cervical Spondylosis Troy H. Middleton, Andrew
D. Parent,
M.D., Ossama Al-Mefty,
M.D., and John L. Fox, M.D.
Neurosurgery Service, Veterans Administration and University of Mississippi of Neurosurgery, Georgetown University, Washington, District of Columbia
Medical
Center,
Jackson,
Mississippi;
Division
Middleton TH, Al-Mefty 0, Harkey LH, Parent Syringomyelia after decompress& laminectomy spondylosis. Surg Neural 198’;28:458-62.
AD, Fox JL. for cervical
We describe a case of cervical spondylotic myelopatby in which deterioration occurred a month after decompressive laminectomy. Syringomyelia was then in evidence as seen by myelography and delayed metrizamide computed tomography scanning. The etiology of this finding and its possible relation to the course and treatment of cervical spondylotic myelopathy are discussed. KEY
WORDS:
iosis; Computed
The term gers
“syringomyelia”
in 1837
etiology
Syringomyelia; tomography;
[lo].
for cavities Davison
Myelopathy; Cervical spondyLaminectomy; Myelography
was first used by Oliver within
the cord,
and Keschner
[I21
D’An-
regardless
of
in 1933 ob-
served “myelopathy due to extramedullary or intramedullary expanding lesions may lead to cavity formation-syringomyelia.” Syringomyelia has been reported in various spinal compressive conditions [7,10,17,31,32), including the possible coexistence of syringomyelia and cervical spondylosis [9,33]. Recently, by utilizing delayed computed tomographic (CT) myelography with water-soluble contrast medium, intramedullary accumulation of contrast medium indicative of cavitation has been documented in cases of cervical spondylotic myelopathy (CSM) [19,20,23,26]. The presence of an intramedullary cavitation has been postulated as an explanation of several of the apparent clinical inconsistencies and discrepancies in CSM cases. The outcome and the significance of this intramedullary cavitation in relation to the patient’s clinical progress have not been documented. In this report a definitive delayed clinical deAddreu repriar requarJ to: Ossama Al-Mefty, M.D., Department of Neurosurgery, University of Mississippi Medical School, 2500 North State Street, Jackson, Mississippi 392164505. Received December 30, 10%; accepted April 28, 1987.
terioration occurred after decompressive laminectomy in a patient with cervical spondylotic myelopathy, and it was associated with the enlargement of an intramedullary cavitation of a previously compressed spinal cord.
Case Report A 3%year-old black male was admitted on July 8, 1985 to an outside hospital. He experienced a numb sensation in the left ulnar distribution which spread across the back of his shoulder and down his right side. He then noted that his right leg became numb with a loss of sensation from the inguinal area down. He also felt that he favored his left leg because his right leg would give away. He previously had undergone a right ulnar nerve transposition for ulnar entrapment neuropathy. The general physical exam was within normal limits. The sensory exam revealed decreased pinprick sensation on the right trunk and leg compared with the left. The arms were not affected. A level could be demonstrated at the fourth thoracic level. He was able to walk without difficulty. There was a suggestion of right-sided weakness. Reflexes were 2 A symmetrical in the upper extremities and 4+ in the knees bilaterally and 2+ at the ankles. A plantar response could not be elicited. A Pantopaque myelogram demonstrated multiple level cord compression by spinal spondylosis (Figure 1). The protein concentration in his cerebrospinal fluid was 42 mg/lOO mL and protein electrophoresis was normal. A CT scan obtained immediately after intrathecal injection of metrizamide confirmed spinal cord compression at multiple levels. Unfortunately, a delayed study was not obtained. Repeat examination at that time revealed hypesthesia in the right leg with decreased strength in that extremity. On July 18, he underwent a cervical decompressive laminectomy of vertebrae C-3 through C-6 followed by subjective improvement postoperatively. The patient began physical therapy and noted that his right leg seemed stronger. On July 27, the patient had a fall while getting out of bed without sequelae and continued oo’)o-301’)/87/$3.50
Syringomyelia
after Decompression
Surg Neural
.‘tiY
198’;28:458-62
to do well without changes in his neurological status. Ten days later the patient noticed that he could not pull himself up in bed. During physical therapy on that day, the right leg weakness progressed to involve a footdrop. In the following 3 days, his neurological deficits continued to progress. On August 13, his only motor function was slight biceps and finger movement on both sides. Evaluation by Metrizamide myelography revealed a wide shadow of the spinal cord (Figure 2). Delayed CT myelography demonstrated intramedullary accumulation of contrast medium in the cervical and upper thoracic areas indicative of a large intramedullary cavity (Figure 3). On August 14, the patient’s strength began to improve gradually. The patient was transferred to Jackson Veterans Administration Hospital on August 28, 1985. His examination on admission revealed decreased pinprick distally in both hands. He had a right T4 sensory level and on the left was intact. The motor examination of the upper extremities revealed the following findings: biceps 415, wrist extension 415, triceps 215, and no grip on the right. On the left, biceps, triceps, wrist extension, and grip were 415. The lower extremity motor function showed
hip Hexion l/5, quadriceps 315, and no foot dorsiflexion on the right. On the left, hip flexion, quadriceps, and dorsiflexion of foot were 3/5. His deep tendon reflexes were 3 ’ in the upper extremities with bilateral Hoffman sign. He had Babinski signs and sustained clonus bilaterally. Although magnetic resonance imaging (MRI) was obtained, it was inconclusive due to poor technical quality. In the light of his improvement, the patient was transferred to a rehabilitation center where he continued to improve in his neurological function. On April 13, 1987, 20 months postoperatively, the patient was reevaluated at our hospital. His current complaints were numbness, more on his right side of the body than his left, impotence, and slight ataxic gait. His examination revealed mild weakness of right biceps muscle, mild spastic gait, increased deep tendon reflexes throughout, and bilateral Babinski and Hoffman’s signs. This time MRI depicted a cavitation in the upper cervical cord (Figure 4).
460
Surg Neural 1987;28:458-62
Discussion To date, CSM continues to be an enigma in its pathoclinical, and therapeutic aspects [3,5,6,8, genetic, 13,15,18,22,27,28,30,34,37]. The conventional therapeutic method of decompressive cervical laminectomy the clinical condition improve often does not [2,4,11,13,16,28). After decompression, worsening may occur or the myelopathy may continue to progress [21,28). The central area of necrosis and/or cavitation has been demonstrated on delayed CT myelography with water-soluble contrast medium in cases of CSM [19,20,23,26], corroborating such previous pathological illustration {24,29]. A local or remote intramedullary cavitation may explain several of the apparent inconsistencies in CSM such as (a) the variable clinical findings suggestive of a transverse spinal cord lesion, amyatrophic lateral sclerosis, central cord syndrome, Brown-Sequard syndrome, or syringomyelic syndrome; (b) the atrophy of the hand muscles; (c) the lack of correlation between the neurological findings and the radiological level; (6) the cord may appear not to be com-
Middleton
et al
Figure 2. (A,B) Anteroposterior and lateral myelogram 1 month after laminectomydepicting successfuldecompreuionand enlargementof the .rpinal cord shadoouj.
pressed at surgery; and (e) the failure to improve neurologically after decompression. The clinical significance of the intramedullary cavitation seen in association with CSM is undocumented. Our case demonstrates a possible clinical course with enlargement of the intramedullary cyst. In our review of the literature, we found another case reported by Mossmann and Jestico (26) where a large syrinx in the center of the spinal cord was demonstrated on delayed CT myelography scanning in a patient who previously had a decompressive laminectomy. How frequently does this cystic cavitation enlargement occur after laminectomy?-And what is the exact mechanism of its evolution?-Is this unique to decompressive laminectomy or is it seen with anterior decompression of CSM patients?-These are matters needing further study. It would appear that the development of a syrinx
Syrmgomyelia
Surg Neui-01 1987;28:458-62
after Decompression
secondary to pressure, trauma, and/or ischemia most likely begins as a degenerative phenomenon leading to necrosis and eventual cavitation. Hydrostatic and osmotic factors may cause active expansion of these noncommunicating syrinxes. The mechanism by which the intramedullary cavity enlarges has been addressed by several authors { 1,25,35,36}. Williams et al [35,36] believe that the principle cause of cavity progression is the hydrodynamic effect produced by pressure changes upon the fluids contained in the syrinx, a mechanism he called
‘161
“slosh.” The fluid can surge within the cord as the subarachnoid space becomes compressed by thoracoabdominal pressure changes, such as coughing or strenuous exercises. This pressure change is transduced through the dura by engorgement of the epidural vein. Martin [25] postulated that the major determinant of syrinx progression was the ovoid shape imposed upon the cavity by the spinal cord with the cavity tending to conform to a stable spherical shape. Decompression of a spinal cord containing a syrinx might facilitate the expansion two of this preexisting syrinx. Aboulker [ 1) emphasized additional mechanisms, spinal cord venous stasis, and cerebrospinal fluid influx into the syrinx along the perivascular space. The latter would be enforced by decreasing the pressure outside the cord as a result of decompressive procedure. Of interest in this regard is the report of Fischer et al [14] of syringomyelia developing long after lumboureteral shunting for communicating hydrocephalus in three patients. Intramedullary cavities have been found adjacent to and extending from both metastatic tumor compressing the spine [ 171 and benign extradural tumors of the spine [7,32]. Intramedullary necrosis and cavitation are common sequelae after prolonged pressure, a phenomenon that explains the lack of neurological improvement after decompressive surgery. The CT scanning or MRI demonstration of such secondary intramedullary lesion may be difficult if the cavity is compressed by a large tumor or severe canal narrowing. However, after decompression this cavity may be become distended or even progressively dilate. In cervical spondylosis, postoperative exacerbation of the myelopathy is known to occur in the early postoperative course as well as in long-term follow-up {4,11,16,2 I]. Hypotension or abnormal positioning of the neck has been hypothesized to explain the deterioration after decompressive laminectomy 12 l] while postoperative spinal deformity or a high degree of mobility of the cervical spine has been implicated in longterm neurologic deterioration [4]. We believe that enlargement of a preexisting intramedullary cavity may also occur, thus explaining both the early and late myelopathic deterioration.
The authors wish to thank Lucia Griffin for her assistance this manuscript.
in preparing
References 1. Aboulker J. La syringomyelie et les liquides rochirurgle 19’9;25(suppl i):i-144.
intra-richidiens.
Neu-
2. Aboulkcr J, Metzger J, David M, Engel P, Ballivet J. Les mpelopathies cervicalcs d’origine rachiciienne. Neurochirurgle 1065; I 1: 8’-19X.
462
Middleton
Sure Neurol 198?;28:458-62
CBT, Logue V. Studies in cervical spondylotic myelopathy. IL The movement and contour of the spine in relation to the neural complications of cervical spondylosis. Brain 197 1;94: 569-86.
necrosis of the spinal cord in compressive AJNR 1986;7:693-701.
3. Adams
4. Adams
CBT, Logue V. Studies in cervical spondylotic myelopathy. III. Some functional effects of operations for cervical spondylotic myelopathy. Brain 1971;94:587-94.
5. Arnold JG Jr. The clinical manifestations (spondylosis)
of the cervical
of spondylochondrosis Ann Surg 1955;141:872-89.
spine.
6. Ashby JG, Ayre WB. Pathogenesis spondylosis
(Letter).
Lancet
of myelopathy 1975;i:980-1.
7. Blaylock
RL. Hydrosyringomyelia ciated with a thoracic meningioma: 54:833-5, 1981.
in cervical
of the conus medullaris assocase report. J Neurosurgery
D, Wilkinson M. The neurological 8. Brain WR, Northfield festations of cervical spondylosis. Brain 1952;75:187-225. M. Cervical arthropathy 9. Brain R, Wilkinson tabes dorsalis and diabetes. Brain 1958;81(Pt 10. Conway LW. Hydrodynamic surgery 1967;27:501-14.
studies
mani-
in syringomyelia, 3):275-89.
in syringomyelia.
11. Crandall PH, Gregorius FK. Long-term followup ment of cervical spondylotic myelopathy. Spine
J Neuro-
of surgical treat1977;2:139-46.
M. Myelitic and myelopathic lesions. VI. 12. Davison C, Keschner Cases with marked circulatory interference and a picture of syringomyelia. Arch Neurol Psychiatry 1933;30: 1074-85. from 13. Ehni G. Extradural spinal cord and nerve root compression benign lesions of the cervical area. In: Youmans JR, ed. Neurological surgery. 2nd ed. Vol 4. Philadelphia: WB Saunders, 1982:2574-612. following lum14. Fischer EG, Welch K, Shillito J Jr. Syringomyelia boureteral shunting for communicating hydrocephalus: report of three cases. J Neurosurg 1977;47:96-100.
21. Levy WJ, Dohn DF, Hardy RW. delayed postoperative complication tomy. Neurosurgery 1982;11:491-5. 22. Liversedge simulating
cervical
LA, Hutchinson EC, Lyons JB. Cervical spondylosis motor-neurone disease. Lancet 1953;ii:652-5.
and syringomielic 23. Lucci B, Reverberi S, Greco G. Syringomyelia syndrome by cervical spondylosis: report on three cases presenting with neurogenic osteoarthropathies. J Neurosurg Sci 1981;25:169-72. 24. Mair WGP, Druckman R. The pathology of spinal cord lesions and their relation to the clinical features in protrusion of cervical intervertebral discs: a report of four cases. Brain 1953;76:70-91. an hypothesis and proposed method 25. Martin G. Syringomyelia, treatment [lett]. J Neurol Neurosurg Psychiatry 1983;46:365. 26.
Mossman SS, Jestico JV. Central cord lesions dylotic myelopathy. J Neurol 1983;230:227-30.
27. Nugent GR. Clinicopathologic losis. Neurology 1959;9:273-81.
correlations
in cervical
in cervical
with 19. Iwasaki Y, Abe H, Isu T, Miyasaka K. CT Myelography intramedullary enhancement in cervical spondylosis. J Neurosurg 1985;63:363-6. 20. Jinkins
JR, Bashir
R, Al-Mefty
0, Al-Kawi
MZ, Fox JL. Cystic
spondy-
30. Payne EE, Spillane JD. The cervical spine an anatomico-pathological study of 70 specimens (using a special technique) with particular reference to the problem of cervical spondylosis. Brain 1957;80:571-96. between syringomyelia 31. Poser CM. The relationship plasms. Springfield, III: Charles C Thomas, 1956.
and its neurological 33. Smith BH. Cervical spondylosis tions. Springfield, III: Charles C Thomas, 1968.
M, Pitts L, Vilnis V, Tuerk K, Lagger R. The 18. Hoff J, Nishimura role of ischemia in the pathogenesis of cervical spondylotic myelopathy: a review and new microangiographic evidence. Spine 1977;2:100-8.
spon-
sec29. Ono K, Ota H, Tada K, Yamamoto T. Cervical myelopathy ondary to multiple spondylotic protrusions: a clinicopathologic study. Spine 1977;2:109-25.
on the course 16. Gorter K. Influence of laminectomy myelopathy. Acta Neurochir 1976;33:265-81.
A. Pencil-shaped 1983;61:219-24.
of
28. Nurick S. The natural history and the results of surgical treatment on the spinal cord disorder associated with cervical spondylosis. Brain 1972;95:101-8.
32. Schlezinger compression
Y, Iljima S, Kishimoto H, Hirano 17. Hashizume softening of the spinal cord. Acta Neuropathol
myelopathy.
Central cord syndrome as a of decompressive laminec-
15. Good DC, Couch JR, Wacaser L. “Numb, clumsy hands” and high cervical spondylosis. Surg Neurol 1984;22:285-91. of cervical
et al
NS, Ungar myelopathy.
H. Hemangioma of the vertebra AJR 1939;42:192-16.
34. Taylor AR, Aberd MB. Mechanism disorders associated with cervical 717-20. 35. Williams B. On the pathogenesis Sot Med 1980;73:798-806.
neowith
complica-
and treatment of spinal-cord spondylosis. Lancet 1953;i: of syringomyelia:
36. Williams B, Terry AF, Jones HWF, McSweeney as a sequel to traumatic paraplegia. Paraplegia 37. Wilson CB, Bertan cervical myelopathy. 1969;21:571-89.
and
a review. J R
T. Syringomyelia 1981;19:67-80.
V, Norrell HA Jr, Hukuda S. Experimental II. Acute ischemic myelopathy. Arch Neural
458
Syringomyelia
after Decompressive
Laminectomy
for
M.D., Louis H. Harkey,
M.D.,
Cervical Spondylosis Troy H. Middleton, Andrew
D. Parent,
M.D., Ossama Al-Mefty,
M.D., and John L. Fox, M.D.
Neurosurgery Service, Veterans Administration and University of Mississippi of Neurosurgery, Georgetown University, Washington, District of Columbia
Medical
Center,
Jackson,
Mississippi;
Division
Middleton TH, Al-Mefty 0, Harkey LH, Parent Syringomyelia after decompress& laminectomy spondylosis. Surg Neural 198’;28:458-62.
AD, Fox JL. for cervical
We describe a case of cervical spondylotic myelopatby in which deterioration occurred a month after decompressive laminectomy. Syringomyelia was then in evidence as seen by myelography and delayed metrizamide computed tomography scanning. The etiology of this finding and its possible relation to the course and treatment of cervical spondylotic myelopathy are discussed. KEY
WORDS:
iosis; Computed
The term gers
“syringomyelia”
in 1837
etiology
Syringomyelia; tomography;
[lo].
for cavities Davison
Myelopathy; Cervical spondyLaminectomy; Myelography
was first used by Oliver within
the cord,
and Keschner
[I21
D’An-
regardless
of
in 1933 ob-
served “myelopathy due to extramedullary or intramedullary expanding lesions may lead to cavity formation-syringomyelia.” Syringomyelia has been reported in various spinal compressive conditions [7,10,17,31,32), including the possible coexistence of syringomyelia and cervical spondylosis [9,33]. Recently, by utilizing delayed computed tomographic (CT) myelography with water-soluble contrast medium, intramedullary accumulation of contrast medium indicative of cavitation has been documented in cases of cervical spondylotic myelopathy (CSM) [19,20,23,26]. The presence of an intramedullary cavitation has been postulated as an explanation of several of the apparent clinical inconsistencies and discrepancies in CSM cases. The outcome and the significance of this intramedullary cavitation in relation to the patient’s clinical progress have not been documented. In this report a definitive delayed clinical deAddreu repriar requarJ to: Ossama Al-Mefty, M.D., Department of Neurosurgery, University of Mississippi Medical School, 2500 North State Street, Jackson, Mississippi 392164505. Received December 30, 10%; accepted April 28, 1987.
terioration occurred after decompressive laminectomy in a patient with cervical spondylotic myelopathy, and it was associated with the enlargement of an intramedullary cavitation of a previously compressed spinal cord.
Case Report A 3%year-old black male was admitted on July 8, 1985 to an outside hospital. He experienced a numb sensation in the left ulnar distribution which spread across the back of his shoulder and down his right side. He then noted that his right leg became numb with a loss of sensation from the inguinal area down. He also felt that he favored his left leg because his right leg would give away. He previously had undergone a right ulnar nerve transposition for ulnar entrapment neuropathy. The general physical exam was within normal limits. The sensory exam revealed decreased pinprick sensation on the right trunk and leg compared with the left. The arms were not affected. A level could be demonstrated at the fourth thoracic level. He was able to walk without difficulty. There was a suggestion of right-sided weakness. Reflexes were 2 A symmetrical in the upper extremities and 4+ in the knees bilaterally and 2+ at the ankles. A plantar response could not be elicited. A Pantopaque myelogram demonstrated multiple level cord compression by spinal spondylosis (Figure 1). The protein concentration in his cerebrospinal fluid was 42 mg/lOO mL and protein electrophoresis was normal. A CT scan obtained immediately after intrathecal injection of metrizamide confirmed spinal cord compression at multiple levels. Unfortunately, a delayed study was not obtained. Repeat examination at that time revealed hypesthesia in the right leg with decreased strength in that extremity. On July 18, he underwent a cervical decompressive laminectomy of vertebrae C-3 through C-6 followed by subjective improvement postoperatively. The patient began physical therapy and noted that his right leg seemed stronger. On July 27, the patient had a fall while getting out of bed without sequelae and continued oo’)o-301’)/87/$3.50
Syringomyelia
after Decompression
Surg Neural
.‘tiY
198’;28:458-62
to do well without changes in his neurological status. Ten days later the patient noticed that he could not pull himself up in bed. During physical therapy on that day, the right leg weakness progressed to involve a footdrop. In the following 3 days, his neurological deficits continued to progress. On August 13, his only motor function was slight biceps and finger movement on both sides. Evaluation by Metrizamide myelography revealed a wide shadow of the spinal cord (Figure 2). Delayed CT myelography demonstrated intramedullary accumulation of contrast medium in the cervical and upper thoracic areas indicative of a large intramedullary cavity (Figure 3). On August 14, the patient’s strength began to improve gradually. The patient was transferred to Jackson Veterans Administration Hospital on August 28, 1985. His examination on admission revealed decreased pinprick distally in both hands. He had a right T4 sensory level and on the left was intact. The motor examination of the upper extremities revealed the following findings: biceps 415, wrist extension 415, triceps 215, and no grip on the right. On the left, biceps, triceps, wrist extension, and grip were 415. The lower extremity motor function showed
hip Hexion l/5, quadriceps 315, and no foot dorsiflexion on the right. On the left, hip flexion, quadriceps, and dorsiflexion of foot were 3/5. His deep tendon reflexes were 3 ’ in the upper extremities with bilateral Hoffman sign. He had Babinski signs and sustained clonus bilaterally. Although magnetic resonance imaging (MRI) was obtained, it was inconclusive due to poor technical quality. In the light of his improvement, the patient was transferred to a rehabilitation center where he continued to improve in his neurological function. On April 13, 1987, 20 months postoperatively, the patient was reevaluated at our hospital. His current complaints were numbness, more on his right side of the body than his left, impotence, and slight ataxic gait. His examination revealed mild weakness of right biceps muscle, mild spastic gait, increased deep tendon reflexes throughout, and bilateral Babinski and Hoffman’s signs. This time MRI depicted a cavitation in the upper cervical cord (Figure 4).
460
Surg Neural 1987;28:458-62
Discussion To date, CSM continues to be an enigma in its pathoclinical, and therapeutic aspects [3,5,6,8, genetic, 13,15,18,22,27,28,30,34,37]. The conventional therapeutic method of decompressive cervical laminectomy the clinical condition improve often does not [2,4,11,13,16,28). After decompression, worsening may occur or the myelopathy may continue to progress [21,28). The central area of necrosis and/or cavitation has been demonstrated on delayed CT myelography with water-soluble contrast medium in cases of CSM [19,20,23,26], corroborating such previous pathological illustration {24,29]. A local or remote intramedullary cavitation may explain several of the apparent inconsistencies in CSM such as (a) the variable clinical findings suggestive of a transverse spinal cord lesion, amyatrophic lateral sclerosis, central cord syndrome, Brown-Sequard syndrome, or syringomyelic syndrome; (b) the atrophy of the hand muscles; (c) the lack of correlation between the neurological findings and the radiological level; (6) the cord may appear not to be com-
Middleton
et al
Figure 2. (A,B) Anteroposterior and lateral myelogram 1 month after laminectomydepicting successfuldecompreuionand enlargementof the .rpinal cord shadoouj.
pressed at surgery; and (e) the failure to improve neurologically after decompression. The clinical significance of the intramedullary cavitation seen in association with CSM is undocumented. Our case demonstrates a possible clinical course with enlargement of the intramedullary cyst. In our review of the literature, we found another case reported by Mossmann and Jestico (26) where a large syrinx in the center of the spinal cord was demonstrated on delayed CT myelography scanning in a patient who previously had a decompressive laminectomy. How frequently does this cystic cavitation enlargement occur after laminectomy?-And what is the exact mechanism of its evolution?-Is this unique to decompressive laminectomy or is it seen with anterior decompression of CSM patients?-These are matters needing further study. It would appear that the development of a syrinx
Syrmgomyelia
Surg Neui-01 1987;28:458-62
after Decompression
secondary to pressure, trauma, and/or ischemia most likely begins as a degenerative phenomenon leading to necrosis and eventual cavitation. Hydrostatic and osmotic factors may cause active expansion of these noncommunicating syrinxes. The mechanism by which the intramedullary cavity enlarges has been addressed by several authors { 1,25,35,36}. Williams et al [35,36] believe that the principle cause of cavity progression is the hydrodynamic effect produced by pressure changes upon the fluids contained in the syrinx, a mechanism he called
‘161
“slosh.” The fluid can surge within the cord as the subarachnoid space becomes compressed by thoracoabdominal pressure changes, such as coughing or strenuous exercises. This pressure change is transduced through the dura by engorgement of the epidural vein. Martin [25] postulated that the major determinant of syrinx progression was the ovoid shape imposed upon the cavity by the spinal cord with the cavity tending to conform to a stable spherical shape. Decompression of a spinal cord containing a syrinx might facilitate the expansion two of this preexisting syrinx. Aboulker [ 1) emphasized additional mechanisms, spinal cord venous stasis, and cerebrospinal fluid influx into the syrinx along the perivascular space. The latter would be enforced by decreasing the pressure outside the cord as a result of decompressive procedure. Of interest in this regard is the report of Fischer et al [14] of syringomyelia developing long after lumboureteral shunting for communicating hydrocephalus in three patients. Intramedullary cavities have been found adjacent to and extending from both metastatic tumor compressing the spine [ 171 and benign extradural tumors of the spine [7,32]. Intramedullary necrosis and cavitation are common sequelae after prolonged pressure, a phenomenon that explains the lack of neurological improvement after decompressive surgery. The CT scanning or MRI demonstration of such secondary intramedullary lesion may be difficult if the cavity is compressed by a large tumor or severe canal narrowing. However, after decompression this cavity may be become distended or even progressively dilate. In cervical spondylosis, postoperative exacerbation of the myelopathy is known to occur in the early postoperative course as well as in long-term follow-up {4,11,16,2 I]. Hypotension or abnormal positioning of the neck has been hypothesized to explain the deterioration after decompressive laminectomy 12 l] while postoperative spinal deformity or a high degree of mobility of the cervical spine has been implicated in longterm neurologic deterioration [4]. We believe that enlargement of a preexisting intramedullary cavity may also occur, thus explaining both the early and late myelopathic deterioration.
The authors wish to thank Lucia Griffin for her assistance this manuscript.
in preparing
References 1. Aboulker J. La syringomyelie et les liquides rochirurgle 19’9;25(suppl i):i-144.
intra-richidiens.
Neu-
2. Aboulkcr J, Metzger J, David M, Engel P, Ballivet J. Les mpelopathies cervicalcs d’origine rachiciienne. Neurochirurgle 1065; I 1: 8’-19X.
462
Middleton
Sure Neurol 198?;28:458-62
CBT, Logue V. Studies in cervical spondylotic myelopathy. IL The movement and contour of the spine in relation to the neural complications of cervical spondylosis. Brain 197 1;94: 569-86.
necrosis of the spinal cord in compressive AJNR 1986;7:693-701.
3. Adams
4. Adams
CBT, Logue V. Studies in cervical spondylotic myelopathy. III. Some functional effects of operations for cervical spondylotic myelopathy. Brain 1971;94:587-94.
5. Arnold JG Jr. The clinical manifestations (spondylosis)
of the cervical
of spondylochondrosis Ann Surg 1955;141:872-89.
spine.
6. Ashby JG, Ayre WB. Pathogenesis spondylosis
(Letter).
Lancet
of myelopathy 1975;i:980-1.
7. Blaylock
RL. Hydrosyringomyelia ciated with a thoracic meningioma: 54:833-5, 1981.
in cervical
of the conus medullaris assocase report. J Neurosurgery
D, Wilkinson M. The neurological 8. Brain WR, Northfield festations of cervical spondylosis. Brain 1952;75:187-225. M. Cervical arthropathy 9. Brain R, Wilkinson tabes dorsalis and diabetes. Brain 1958;81(Pt 10. Conway LW. Hydrodynamic surgery 1967;27:501-14.
studies
mani-
in syringomyelia, 3):275-89.
in syringomyelia.
11. Crandall PH, Gregorius FK. Long-term followup ment of cervical spondylotic myelopathy. Spine
J Neuro-
of surgical treat1977;2:139-46.
M. Myelitic and myelopathic lesions. VI. 12. Davison C, Keschner Cases with marked circulatory interference and a picture of syringomyelia. Arch Neurol Psychiatry 1933;30: 1074-85. from 13. Ehni G. Extradural spinal cord and nerve root compression benign lesions of the cervical area. In: Youmans JR, ed. Neurological surgery. 2nd ed. Vol 4. Philadelphia: WB Saunders, 1982:2574-612. following lum14. Fischer EG, Welch K, Shillito J Jr. Syringomyelia boureteral shunting for communicating hydrocephalus: report of three cases. J Neurosurg 1977;47:96-100.
21. Levy WJ, Dohn DF, Hardy RW. delayed postoperative complication tomy. Neurosurgery 1982;11:491-5. 22. Liversedge simulating
cervical
LA, Hutchinson EC, Lyons JB. Cervical spondylosis motor-neurone disease. Lancet 1953;ii:652-5.
and syringomielic 23. Lucci B, Reverberi S, Greco G. Syringomyelia syndrome by cervical spondylosis: report on three cases presenting with neurogenic osteoarthropathies. J Neurosurg Sci 1981;25:169-72. 24. Mair WGP, Druckman R. The pathology of spinal cord lesions and their relation to the clinical features in protrusion of cervical intervertebral discs: a report of four cases. Brain 1953;76:70-91. an hypothesis and proposed method 25. Martin G. Syringomyelia, treatment [lett]. J Neurol Neurosurg Psychiatry 1983;46:365. 26.
Mossman SS, Jestico JV. Central cord lesions dylotic myelopathy. J Neurol 1983;230:227-30.
27. Nugent GR. Clinicopathologic losis. Neurology 1959;9:273-81.
correlations
in cervical
in cervical
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