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(ii) Cervical myelopathy and its management
Current Orthopaedics (1998) 12, 7 12 © 1998 Harcourt Brace & Co. Ltd
Mini-symposium: Cervical spine
(ii) Cervical myelopathy and its management
S. Kokubun, T. Sato
INTRODUCTION
EPIDEMIOLOGY
Cervical myelopathy results from compression of the spinal cord by various degenerative processes of the spine. Its symptoms such as paraesthesiae of hands and feet, clumsiness of hands and gait disturbance progress without treatment in most patients, thereby leading to severe disability. In Western countries, although neurological localization of the symptomatic disc level, radiological diagnosis and surgical treatment of cervical radiculopathy have been remarkably developed in the 1940s and 1950s,14 until recently, little attention has been paid to cervical myelopathy. On the other hand, in Japan, cervical myelopathy has been studied vigorously as one of the main subjects within spinal surgery. Its pathophysiology has been clarified to a great extent and many operative techniques have been developed. At the same time, efforts have been made to inform physicians and the general public about its symptoms and of the effectiveness of operative treatment. As a result, the number of operations for cervical myelopathy has increased to as much as that for lumbar canal stenosis. Even elderly patients in their 70s or 80s do not need to endure the disabilities but can benefit from modern cervical spinal surgery. Cervical myelopathy may be under-recognized in Western countries?.6 This paper provides the knowledge which is needed for its management and the comments made are based on our experience.
Although no epidemiological studies have been reported concerning the incidence of cervical myelopathy, the annual rate of operation for this condition was 5.7 per 100 000 people in our prefecture from 1989 to 1993.7 Approximately half the patients were in their 6th or 7th decade. However, the annual operation rate among individuals of each decade increased with age and reached the highest level in the 8th decade. The male to female ratio was approximately 2:1. No teenages were encountered unless there was flexion myelopathy?
Shoichi Kokubun MD, Professor, Tetsuro Sato MD. Associate Professor, Department of Orthopaedic Surgery, Tohoku University School of Medicine, 1-1 Seiryo-Machi, Aoba-Ku, Sendal 980-77, Japan.
Correspondence to: Professor S. Kokubun.
CLINICAL FEATURES
Symptoms and signs Patients first notice tingling, that is, paraesthesiae in the fingers. Thereafter, they sense clumsiness of the hands, tightness, cold or hot sensations in the trunk, tingling in the lower extremities, gait disturbance due to spasticity and urinary disturbance as the condition deteriorates. This indicates that the grey matter is more vulnerable to compression than the white matter. About 10-20% of patients first notice symptoms in the lower extremities. One-third of the patients have electric shock-like sensations in the extremities or trunk when extending their neck. This symptom indicates an early stage of the disease and a greater possibility of improvement through operative treatment. When the symptom disappears, howevel, patients are apt to mistakenly believe that they are improving, thereby delaying their visit to a specialist. Clinical signs can be caused by damage to the grey matter or the white matter of the spinal cord (Fig. 1). Diminished tendon reflexes, muscle weakness and sensory disturbance in the upper extremities are signs
8 Current Orthopaedics
cord
hyporeflexia muscle weakl Hoffmann
spinal factor
--~
signs referable to ~ grey matter
I-
hyperreflexla signs referableto ~ J white matter
pedicl remo~
Fig. 1 Neurological signs in cervical myelopathy.
of grey matter lesions. Exaggerated knee and ankle jerks, negative cremasteric reflex, positive Babinski sign and sensory disturbance found within the lower extremities or trunk are signs of white matter damage. Exaggerated tendon reflexes including a positive Hoffmann sign can also be found in the upper extremities. Approximately 90% of patients have a positive Hoffmann sign. An easily elicited Hoffmann sign, clonus, positive Babinski sign or the presence of pes equinus due to spasticity indicates advanced myelopathy.
Classification of symptomatology Crandall9 classified the symptomatology of cervical myelopathy into five syndromes: (i) central cord syndrome consisting of symptoms and signs in the upper extremities; (ii) transverse lesion syndrome consisting of symptoms and signs in the upper and lower extremities; (iii) Brown-Sequard syndrome; (iv) motor system syndrome without sensory disturbance; and (v) brachialgia and cord syndrome in which upper limb pain predominates with some associated long tract involvement. Central cord syndrome and BrownSequard syndrome generally develop into transverse syndrome shortly after onset, and represented about 5% of the patients in our series. Motor system syndrome, and brachialgia and cord syndrome are extremely rare and account for less than 1%. Brachialgia and cord syndrome is equivalent to radiculomyelopathy, but this is not a common condition.
Localization of symptomatic disc level
Relationship of disc level to spinal cord segment damage The spinal cord ascends approximately one segment during its development. As a result, the cervical discs generally lie opposite spinal cord segments which are numbered one lower than the number of the roots passing them. For example, the C5-6 disc lies opposite to the C7 spinal cord segment (Fig. 2). l° This discrepancy between the disc levels and the spinal cord segments varies within a range of approximately one segment from case to case and from disc level to disc
la
Fig. 2 Anatomical relation between spinal cord and nerve root compression in the cervical spine. Herniated masses at the same
levelcompressesa nerveroot and a spinalcord segment approximatelyone segmentlowerthan the segmentfromwhichthe nerve root originates&
level. Accordingly, when assessment is made for surgery for myelopathy, it is the disc level at which the spinal cord is compressed, that must be localized.
Frequency for each symptomatic disc level Radiculopathy is most common at the C6-7 disc level.l~ On the other hand, cervical myelopathy is most common at the C5-6 disc level followed by the C4-5, the C3-4 and the C6-7 disc levels. The C6-7 disc level accounts for only 5% of patients with cervical myelopathy (Fig. 3). This difference in frequency can be explained by the fact that the cervical enlargement of the spinal cord is located at the C4-5 and C5-6 disc levels. Retrolisthesis of the cervical spine seen in extension, which is a principal component of dynamic stenosis, seldom occurs at the C6-7 disc because of its anterior tilt.
Diagnostic indices Neurological localization of the symptomatic disc level in cervical myelopathy has long been thought impossible because of the complicated nature of neurological findings. The .diagnostic indices for cervical radiculopathy which are well documented in textbooks cannot be applied to myelopathy. Theoretically, detection of neurological signs referable to the grey matter of a lesion which affects the upper extremities leads to localization of the symptomatic disc level. We analysed the relationship between preoperative signs and disc levels in 108 patient who had undergone
Cervical myelopathy
IL
Radiculopathy (Murphey,1973)
Myelopathy (Kokubun,1988)
C2-3
~ ~'~,,..~"~am. Seg.~~ ~,,~
20% C3-4 ~/'////,,~
9
sis stenosis r " ~ Contin. O P L L ~ ~
C4- 5 ~"/~//////~///A2 7% z7
c s-6 JJJJJJJJJJJJJJJA 4 7
5% (n=648)
8%1~7-T 11
(n=266)
Fig. 3 Frequencyof symptomaticdisc levelsin radiculopathy and myelopathy.
Disc level
C3-4
DTR
BTRT 100% Deltoid $ 83°/,
MMT
C4-5 BTR$ 63%
Biceps$ 71%
C5-6 rrR 85%
Fig. 5 Sevenspinal factors which are known to cause cervical myelopathy.Developmentalstenosis is definedas an anteroposteriordiameter of the spinal canal of 12 mm or less. Dynamic stenosis is definedas Penning'sjaw diameter of 12 mm or less, associated with 2 mm retrolisthesisin extensionof the cervical spine. CLF: calcificationof the ligamentumflavum.
Triceps $ 79°/,
Sensory Disturb,
Fig. 4 Indicesfor neurologicallocalizationof the symptomatic disc levelof cervicalmyelopathy.The percentageat each finding indicates the reliabilityof the localization.~= single-level anterior decompression and fusion for cervical myelopathy. There was more than 50% probability of reliability of the diagnostic indices for localization (Fig. 4).~2
IMAGING DIAGNOSIS Diagnostic imaging diagnosis of cervical myelopathy involves the following three aspects: (i) detection of spinal factors responsible for the symptomatology; (ii) evaluation of the compression and deformity of the spinal cord; and (iii) evaluation of the intramedullary lesion.
Pathological spinal factors The following seven spinal factors have been described as causative components of cervical myelopathy: (i) developmental stenosis; (ii) dynamic stenosis; (iii) disc herniation; (iv) segmental ossification of the posterior longitudinal ligament (OPLL) (v) continuous OPLL, (vi) posterior spur; and (vii) calcification of the ligamentum flavum (Fig. 5). 7
Fig. 6 T2-weightedimage showingcompressionof the spinal cord by dynamicstenosis at the C3-4 disc level.
Developmental stenosis is defined as an anteroposterior diameter of the spinal canal of 12 mm or less on a plain lateral radiograph made with a tube-tofilm distance of 1.8 m. In general, patients with cervical myelopathy have a narrower canal. The average anteroposterior diameter of the spinal canals was 12.8 mm in our patients. Dynamic stenosis is defined as Penning's jaw diameter, I3 a distance from the posteroinferior corner of the vertebral body to the anterior margin of the subjacent lamina of 12 mm or less, associated with 2 mm retrolisthesis in extension of the cervical spine. Developmental or dynamic stenosis or both were found in approximately two-thirds of our patients (Fig. 6).
10
Current Orthopaedics
Fig. 8 Ossificationof the posterior longitudinal ligament. (A) Radiograph showinga continuous ossificationbehind the C2 to C4 bodies and a segmental ossificationbehind the C5 body. (B) T2-weightedimage showingseverecompressionof the spinal cord from the C2-3 to C4-5 disc levelsand a high-signal intensityarea (arrow) at the C4-5 disc levelwhere ossificationis discontinuous.
Evaluation of compression and deformity of the spinal cord
Fig. 7 Discherniation. (A) Tl-weightedMR image showing a large herniated mass at the C5-6 disc level.(B) T2-weightedMR image showing a high-signal intensityarea (arrow)in the spinal cord at the vicinityof the compression.(C) Tl-weightedMR image showing a large mass of paramedian herniation (asterisk).
Cervical disc herniation is divided into three types with respect to the intraspinal location of the herniated mass: median, paramedian and lateral herniation. Median and paramedian herniations induce myelopathy while lateral herniation induces radiculopathy. The herniated mass is clearly depicted by MRI, which is taking the place of discography (Fig. 7). O P L L is common among patients with myelopathy in Japan ~4and has been found in approximately 30% of our patients. Segmental and continuous O P L L are clearly depicted by tomography or CT scanning although the former tends to be overlooked on plain lateral radiographs (Fig. 8). Myelopathy due to posterior spur formation has received much attention in the literature under the name of spondylotic myelopathy. A posterior spur, however, is rarely a causative factor of myelopathy and has been found at the symptomatic level in less than 10% of our patients (Fig. 9). Calcification of the ligamentum flavum is a rare condition that occurs mainly among elderly women. 15 It was found in 2-3% of our patients.
Myelography was an essential means for evaluation of compression of the spinal cord before the advent of MRI. It demonstrates only the degree of the obliteration of the subarachnoid space, depicting a complete or incomplete block. In contrast, MRI directly demonstrates deformities of the compressed spinal cord on both sagittal and axial views. Its disadvantage, however, is that there is difficulty in imaging any spondylolisthesis which becomes apparent on extension of the neck; the narrow gantry of the machine prevents this manouvre.
Evaluation of an intramedullary lesion High-signal intensity is found in the spinal cord on Tz-weighted images in more than half of patients who undergo operation (Fig. 7B, 8B). This intramedullary high intensity is generally located at the disc level, which corresponds to the symptomatic disc level localized neurologically. It is believed to be caused by cavity formation or necrosis in the grey matter. However, it does not seem to correlate with the severity of myelopathy or the surgical outcome? 6
CONSERVATIVE T R E A T M E N T While the natural history of cervical myelopathy is not well understood, most patients become worse if untreated. Conservative treatment can be helpful in the early period of the disease. Immobilization with a cervical collar and medications such as NSAIDs and muscle relaxants can be used.
Cervical myelopathy
A
B
11
C
Fig. 10 Operativetechnique of anterior decompressionand fusion. (A) A i5-17 mm wide trough is made, spanning the midlevels of the bodies. The posterior longitudinal ligamentis incised and anything, such as a herniated disc, spur or ossifiedligament, compressing the spinal cord is excised.(B), (C) Split halves of a tricortical iliac strut are forcedback to back into the trough so that their cancelloussurfacescan be brought into contact with the cancellous bone of the bodies and their cortical surfacesadjoin the cortical surfaces of the bodies.
Fig. 9 Posterior spur. (A) Tomogramshowinglarge posterior spurs at the C5-6 disc level.(B) Tl-weightedMR image showing severecompressionof the spinal cord at the C5-6 disc level.
OPERATIVE TREATMENT Absolute indications for operative treatment are neurological deficits which are progressive or have already developed. Although time is of the essence in the treatment of cervical myelopathy, only one-third of patients came to us within 6 months from the onset of symptoms. In general, patients with the following combination of disabilities are most satisfied with improvements due to operative treatment: severe tingling in fingers and legs, poor handling of a knife and fork or difficulty in buttoning shirts; also the need to hold on to a handrail when going downstairs is often improved following operations. There have been no controlled, prospective studies to evaluate anterior and posterior decompression of the spinal cord according to these functional criteria. Neurological results through the two approaches, in our clinical impression, are almost equal. In general, younger patients and patients with disc herniation show better improvement after surgery, whilst older patients and patients with dynamic stenosis show less improvement. Anterior decompression Anterior decompression is generally recommended in patients who have spinal problems such as disc herniation and a posterior spur compressing the spinal cord at one or two levels. Kyphotic angulation of the subaxial spine is also an indication for anterior decompression followed by correction of the deformity and intercorporal fusion. The Smith-Robinson technique 3 has the disadvantage of limited visibility when removing pathology. The Cloward technique 4 provides better visualization but has a greater potential for postoperative collapse of its dowel-shaped graft.
Our operative technique ensures thorough decompression and firm grafting without the aid of an operating microscope. A 15-17 mm wide trough is made, spanning the mid-levels of the bodies. Midline subtotal corpectomy of the middle bodies is accomplished for two-level decompression. The posterior longitudinal ligament is incised and any herniated disc, spur or ossified ligament, seen to be compressing the spinal cord is excised. In bone grafting for spinal fusion, a spreader is used. A tricortical iliac strut is harvested and split. The split halves are forced back to back into the trough so that their cancellous surfaces can be brought into contact with the cancellous bone of the bodies. The cortical surfaces of the grafts adjoin the cortical surfaces of the bodies (Fig. 10). This corticalbone to cortical-bone contact prevents any sinking of the grafts into the bodies; this is especially important in osteoporotic spines in the elderly. With a collar, the patient can sit up and walk as soon as pain subsides. The collar is discarded after 12 weeks irrespective of the state of bone union. Posterior decompression Posterior decompression is generally recommended in patients who have compression of the spinal cord at three levels or more, in those who have developmental stenosis, and in those who have calcification of the ligamentum flavum. Laminectomy for posterior decompression is popular in Western countries. Kirita's bilateral open-door laminectomy using an air drill is recommended because it is atraumatic to the spinal cord. The C2 spinous process and the semispinalis muscles attached to it should be left intact in order to prevent postlaminectomy kyphosis. Recently in Japan, spinal canal-expanding laminoplasty has almost replaced laminectomy. Hirabayashi's open-door laminoplasty 17 and Kurokawa's spinous process-splitting laminoplasty have become the most popular of the many techniques. We have adopted the latter and used hydroxyapatite spacers to stabilize the split spinous processes instead of iliac
12
Current Orthopaedics Step 1
Step 2 3.
. ~ o c v . e
~
1
~
4.
,~. an~d s~is anlngc
5.
spinous process Step 3
thread:b
HA spacer
6.
Step 4
7. 8. 9. 10. Fig. 11 Operative technique of Kurokawa's spinous processplitting laminoplasty using hydroxyapatite (HA) spacers. Step 1: A longitudinal groove is made bilaterally. Each spinous process is split and its halves are spread. Step 2: A trapezoidal-shaped spacer is placed between the two halves of each split spinous process. Steps 3 and 4: The spacer is fixed by diagonally tying two silk threads which were passed through the holes? ~
11. i2. 13.
bone grafts as in the original procedure (Fig. 11). 7 The postoperative management is the same as that for the anterior procedure.
14. 15. 16.
REFERENCES
1. Spurling RG, Scoville WB. Lateral rupture of the cervical intervertebral discs. A common cause of shoulder and arm pain. Surg Gynecol Obstet 1944; 78: 350-358. 2. Yoss RF, Corbin KB, MacCarty CS, Love JG. Significance of
17. 18.
symptoms and signs in localization of involved root in cervical disk protrusion. Neurology 1957; 7: 673-683. Smith GW, Robinson RA. The treatment of certain cervical spine disorders by anterior removal of the intervertebral disc and interbody fusion. J Bone Joint Surg 1958; 40-A: 607-624. Cloward RB. The anterior approach for removal of ruptured cervical disks. J Neurosurg 1958; 25: 491-502. Bernhardt M, Hynes RA, Blume HW, White AA III. Current concepts review. Cervical spondylotic myelopathy. J Bone Joint Surg 1993; 75A: 119-128. Law MD, Bernhardt M, White AA III. Evaluation and management of cervical spondylotic myelopathy. J Bone Joint Surg 1994; 76A: 1420 1433. Kokubun S, Sato T, Ishii Y, Tanaka Y. Cervical myelopathy in the Japanese. Clin Orthop 1996; 323: 129-138. Okumura H, Homma TT. Juvenile compression myelopathy in the cervical spine. Spine 1994; 19: 72-76. Crandall PH, Batzdorf U. Cervical spondylotic myelopathy. J Neurosurg 1966; 25: 57-66. Payne EE, Spillane JD. The cervical spine. An anatomicopathological study of 70 specimens (using a special technique) with particular reference to the problem of cervical spondylosis. Brain 1957; 80: 571-596. Murphey F, Simmons JCH, Brunson B. Surgical treatment of laterally ruptured cervical disc. Review of 648 cases, 1939 to 1972. J Neurosurg 1973; 38: 674-683. Kokubun S, Tanaka Y Types of cervical disc herniation and relation to myelopathy and radiculopathy. J Back Musculoskelet Rehab 1995; 5: 145-154. Penning L. Some aspects of plain radiography of the cervical spine in chronic myelopathy. Neurology, 1962; 12:513-519. Tsuyama N. Ossification of the posterior longitudinal ligament of the spine. Clin Orthop 1984; 18471-18484. Baba H, Maezawa Y, Kawahara N, Tomita K, Furusawa N, Imura S. Calcium crystal deposition in the ligamentum flavum of the cervical spine. Spine 1993; 18: 2174-2181. Wada E, Ohmura M, Yonenobu K. Intramedullary changes of the spinal cord in cervical spondylotic myelopathy. Spine 1995; 20: 2226-2232. Hirabayashi K, Watanabe K, Wakano K, Suzuki N, Satomi K, Ishii Y. Expansive open-door laminoplasty for cervical spinal stenotic myelopathy. Spine 1983; 8: 693-699. Kokubun Set al. Tohoku J Exp Med 1994; 173: 337-344.
Mini-symposium: Cervical spine
(ii) Cervical myelopathy and its management
S. Kokubun, T. Sato
INTRODUCTION
EPIDEMIOLOGY
Cervical myelopathy results from compression of the spinal cord by various degenerative processes of the spine. Its symptoms such as paraesthesiae of hands and feet, clumsiness of hands and gait disturbance progress without treatment in most patients, thereby leading to severe disability. In Western countries, although neurological localization of the symptomatic disc level, radiological diagnosis and surgical treatment of cervical radiculopathy have been remarkably developed in the 1940s and 1950s,14 until recently, little attention has been paid to cervical myelopathy. On the other hand, in Japan, cervical myelopathy has been studied vigorously as one of the main subjects within spinal surgery. Its pathophysiology has been clarified to a great extent and many operative techniques have been developed. At the same time, efforts have been made to inform physicians and the general public about its symptoms and of the effectiveness of operative treatment. As a result, the number of operations for cervical myelopathy has increased to as much as that for lumbar canal stenosis. Even elderly patients in their 70s or 80s do not need to endure the disabilities but can benefit from modern cervical spinal surgery. Cervical myelopathy may be under-recognized in Western countries?.6 This paper provides the knowledge which is needed for its management and the comments made are based on our experience.
Although no epidemiological studies have been reported concerning the incidence of cervical myelopathy, the annual rate of operation for this condition was 5.7 per 100 000 people in our prefecture from 1989 to 1993.7 Approximately half the patients were in their 6th or 7th decade. However, the annual operation rate among individuals of each decade increased with age and reached the highest level in the 8th decade. The male to female ratio was approximately 2:1. No teenages were encountered unless there was flexion myelopathy?
Shoichi Kokubun MD, Professor, Tetsuro Sato MD. Associate Professor, Department of Orthopaedic Surgery, Tohoku University School of Medicine, 1-1 Seiryo-Machi, Aoba-Ku, Sendal 980-77, Japan.
Correspondence to: Professor S. Kokubun.
CLINICAL FEATURES
Symptoms and signs Patients first notice tingling, that is, paraesthesiae in the fingers. Thereafter, they sense clumsiness of the hands, tightness, cold or hot sensations in the trunk, tingling in the lower extremities, gait disturbance due to spasticity and urinary disturbance as the condition deteriorates. This indicates that the grey matter is more vulnerable to compression than the white matter. About 10-20% of patients first notice symptoms in the lower extremities. One-third of the patients have electric shock-like sensations in the extremities or trunk when extending their neck. This symptom indicates an early stage of the disease and a greater possibility of improvement through operative treatment. When the symptom disappears, howevel, patients are apt to mistakenly believe that they are improving, thereby delaying their visit to a specialist. Clinical signs can be caused by damage to the grey matter or the white matter of the spinal cord (Fig. 1). Diminished tendon reflexes, muscle weakness and sensory disturbance in the upper extremities are signs
8 Current Orthopaedics
cord
hyporeflexia muscle weakl Hoffmann
spinal factor
--~
signs referable to ~ grey matter
I-
hyperreflexla signs referableto ~ J white matter
pedicl remo~
Fig. 1 Neurological signs in cervical myelopathy.
of grey matter lesions. Exaggerated knee and ankle jerks, negative cremasteric reflex, positive Babinski sign and sensory disturbance found within the lower extremities or trunk are signs of white matter damage. Exaggerated tendon reflexes including a positive Hoffmann sign can also be found in the upper extremities. Approximately 90% of patients have a positive Hoffmann sign. An easily elicited Hoffmann sign, clonus, positive Babinski sign or the presence of pes equinus due to spasticity indicates advanced myelopathy.
Classification of symptomatology Crandall9 classified the symptomatology of cervical myelopathy into five syndromes: (i) central cord syndrome consisting of symptoms and signs in the upper extremities; (ii) transverse lesion syndrome consisting of symptoms and signs in the upper and lower extremities; (iii) Brown-Sequard syndrome; (iv) motor system syndrome without sensory disturbance; and (v) brachialgia and cord syndrome in which upper limb pain predominates with some associated long tract involvement. Central cord syndrome and BrownSequard syndrome generally develop into transverse syndrome shortly after onset, and represented about 5% of the patients in our series. Motor system syndrome, and brachialgia and cord syndrome are extremely rare and account for less than 1%. Brachialgia and cord syndrome is equivalent to radiculomyelopathy, but this is not a common condition.
Localization of symptomatic disc level
Relationship of disc level to spinal cord segment damage The spinal cord ascends approximately one segment during its development. As a result, the cervical discs generally lie opposite spinal cord segments which are numbered one lower than the number of the roots passing them. For example, the C5-6 disc lies opposite to the C7 spinal cord segment (Fig. 2). l° This discrepancy between the disc levels and the spinal cord segments varies within a range of approximately one segment from case to case and from disc level to disc
la
Fig. 2 Anatomical relation between spinal cord and nerve root compression in the cervical spine. Herniated masses at the same
levelcompressesa nerveroot and a spinalcord segment approximatelyone segmentlowerthan the segmentfromwhichthe nerve root originates&
level. Accordingly, when assessment is made for surgery for myelopathy, it is the disc level at which the spinal cord is compressed, that must be localized.
Frequency for each symptomatic disc level Radiculopathy is most common at the C6-7 disc level.l~ On the other hand, cervical myelopathy is most common at the C5-6 disc level followed by the C4-5, the C3-4 and the C6-7 disc levels. The C6-7 disc level accounts for only 5% of patients with cervical myelopathy (Fig. 3). This difference in frequency can be explained by the fact that the cervical enlargement of the spinal cord is located at the C4-5 and C5-6 disc levels. Retrolisthesis of the cervical spine seen in extension, which is a principal component of dynamic stenosis, seldom occurs at the C6-7 disc because of its anterior tilt.
Diagnostic indices Neurological localization of the symptomatic disc level in cervical myelopathy has long been thought impossible because of the complicated nature of neurological findings. The .diagnostic indices for cervical radiculopathy which are well documented in textbooks cannot be applied to myelopathy. Theoretically, detection of neurological signs referable to the grey matter of a lesion which affects the upper extremities leads to localization of the symptomatic disc level. We analysed the relationship between preoperative signs and disc levels in 108 patient who had undergone
Cervical myelopathy
IL
Radiculopathy (Murphey,1973)
Myelopathy (Kokubun,1988)
C2-3
~ ~'~,,..~"~am. Seg.~~ ~,,~
20% C3-4 ~/'////,,~
9
sis stenosis r " ~ Contin. O P L L ~ ~
C4- 5 ~"/~//////~///A2 7% z7
c s-6 JJJJJJJJJJJJJJJA 4 7
5% (n=648)
8%1~7-T 11
(n=266)
Fig. 3 Frequencyof symptomaticdisc levelsin radiculopathy and myelopathy.
Disc level
C3-4
DTR
BTRT 100% Deltoid $ 83°/,
MMT
C4-5 BTR$ 63%
Biceps$ 71%
C5-6 rrR 85%
Fig. 5 Sevenspinal factors which are known to cause cervical myelopathy.Developmentalstenosis is definedas an anteroposteriordiameter of the spinal canal of 12 mm or less. Dynamic stenosis is definedas Penning'sjaw diameter of 12 mm or less, associated with 2 mm retrolisthesisin extensionof the cervical spine. CLF: calcificationof the ligamentumflavum.
Triceps $ 79°/,
Sensory Disturb,
Fig. 4 Indicesfor neurologicallocalizationof the symptomatic disc levelof cervicalmyelopathy.The percentageat each finding indicates the reliabilityof the localization.~= single-level anterior decompression and fusion for cervical myelopathy. There was more than 50% probability of reliability of the diagnostic indices for localization (Fig. 4).~2
IMAGING DIAGNOSIS Diagnostic imaging diagnosis of cervical myelopathy involves the following three aspects: (i) detection of spinal factors responsible for the symptomatology; (ii) evaluation of the compression and deformity of the spinal cord; and (iii) evaluation of the intramedullary lesion.
Pathological spinal factors The following seven spinal factors have been described as causative components of cervical myelopathy: (i) developmental stenosis; (ii) dynamic stenosis; (iii) disc herniation; (iv) segmental ossification of the posterior longitudinal ligament (OPLL) (v) continuous OPLL, (vi) posterior spur; and (vii) calcification of the ligamentum flavum (Fig. 5). 7
Fig. 6 T2-weightedimage showingcompressionof the spinal cord by dynamicstenosis at the C3-4 disc level.
Developmental stenosis is defined as an anteroposterior diameter of the spinal canal of 12 mm or less on a plain lateral radiograph made with a tube-tofilm distance of 1.8 m. In general, patients with cervical myelopathy have a narrower canal. The average anteroposterior diameter of the spinal canals was 12.8 mm in our patients. Dynamic stenosis is defined as Penning's jaw diameter, I3 a distance from the posteroinferior corner of the vertebral body to the anterior margin of the subjacent lamina of 12 mm or less, associated with 2 mm retrolisthesis in extension of the cervical spine. Developmental or dynamic stenosis or both were found in approximately two-thirds of our patients (Fig. 6).
10
Current Orthopaedics
Fig. 8 Ossificationof the posterior longitudinal ligament. (A) Radiograph showinga continuous ossificationbehind the C2 to C4 bodies and a segmental ossificationbehind the C5 body. (B) T2-weightedimage showingseverecompressionof the spinal cord from the C2-3 to C4-5 disc levelsand a high-signal intensityarea (arrow) at the C4-5 disc levelwhere ossificationis discontinuous.
Evaluation of compression and deformity of the spinal cord
Fig. 7 Discherniation. (A) Tl-weightedMR image showing a large herniated mass at the C5-6 disc level.(B) T2-weightedMR image showing a high-signal intensityarea (arrow)in the spinal cord at the vicinityof the compression.(C) Tl-weightedMR image showing a large mass of paramedian herniation (asterisk).
Cervical disc herniation is divided into three types with respect to the intraspinal location of the herniated mass: median, paramedian and lateral herniation. Median and paramedian herniations induce myelopathy while lateral herniation induces radiculopathy. The herniated mass is clearly depicted by MRI, which is taking the place of discography (Fig. 7). O P L L is common among patients with myelopathy in Japan ~4and has been found in approximately 30% of our patients. Segmental and continuous O P L L are clearly depicted by tomography or CT scanning although the former tends to be overlooked on plain lateral radiographs (Fig. 8). Myelopathy due to posterior spur formation has received much attention in the literature under the name of spondylotic myelopathy. A posterior spur, however, is rarely a causative factor of myelopathy and has been found at the symptomatic level in less than 10% of our patients (Fig. 9). Calcification of the ligamentum flavum is a rare condition that occurs mainly among elderly women. 15 It was found in 2-3% of our patients.
Myelography was an essential means for evaluation of compression of the spinal cord before the advent of MRI. It demonstrates only the degree of the obliteration of the subarachnoid space, depicting a complete or incomplete block. In contrast, MRI directly demonstrates deformities of the compressed spinal cord on both sagittal and axial views. Its disadvantage, however, is that there is difficulty in imaging any spondylolisthesis which becomes apparent on extension of the neck; the narrow gantry of the machine prevents this manouvre.
Evaluation of an intramedullary lesion High-signal intensity is found in the spinal cord on Tz-weighted images in more than half of patients who undergo operation (Fig. 7B, 8B). This intramedullary high intensity is generally located at the disc level, which corresponds to the symptomatic disc level localized neurologically. It is believed to be caused by cavity formation or necrosis in the grey matter. However, it does not seem to correlate with the severity of myelopathy or the surgical outcome? 6
CONSERVATIVE T R E A T M E N T While the natural history of cervical myelopathy is not well understood, most patients become worse if untreated. Conservative treatment can be helpful in the early period of the disease. Immobilization with a cervical collar and medications such as NSAIDs and muscle relaxants can be used.
Cervical myelopathy
A
B
11
C
Fig. 10 Operativetechnique of anterior decompressionand fusion. (A) A i5-17 mm wide trough is made, spanning the midlevels of the bodies. The posterior longitudinal ligamentis incised and anything, such as a herniated disc, spur or ossifiedligament, compressing the spinal cord is excised.(B), (C) Split halves of a tricortical iliac strut are forcedback to back into the trough so that their cancelloussurfacescan be brought into contact with the cancellous bone of the bodies and their cortical surfacesadjoin the cortical surfaces of the bodies.
Fig. 9 Posterior spur. (A) Tomogramshowinglarge posterior spurs at the C5-6 disc level.(B) Tl-weightedMR image showing severecompressionof the spinal cord at the C5-6 disc level.
OPERATIVE TREATMENT Absolute indications for operative treatment are neurological deficits which are progressive or have already developed. Although time is of the essence in the treatment of cervical myelopathy, only one-third of patients came to us within 6 months from the onset of symptoms. In general, patients with the following combination of disabilities are most satisfied with improvements due to operative treatment: severe tingling in fingers and legs, poor handling of a knife and fork or difficulty in buttoning shirts; also the need to hold on to a handrail when going downstairs is often improved following operations. There have been no controlled, prospective studies to evaluate anterior and posterior decompression of the spinal cord according to these functional criteria. Neurological results through the two approaches, in our clinical impression, are almost equal. In general, younger patients and patients with disc herniation show better improvement after surgery, whilst older patients and patients with dynamic stenosis show less improvement. Anterior decompression Anterior decompression is generally recommended in patients who have spinal problems such as disc herniation and a posterior spur compressing the spinal cord at one or two levels. Kyphotic angulation of the subaxial spine is also an indication for anterior decompression followed by correction of the deformity and intercorporal fusion. The Smith-Robinson technique 3 has the disadvantage of limited visibility when removing pathology. The Cloward technique 4 provides better visualization but has a greater potential for postoperative collapse of its dowel-shaped graft.
Our operative technique ensures thorough decompression and firm grafting without the aid of an operating microscope. A 15-17 mm wide trough is made, spanning the mid-levels of the bodies. Midline subtotal corpectomy of the middle bodies is accomplished for two-level decompression. The posterior longitudinal ligament is incised and any herniated disc, spur or ossified ligament, seen to be compressing the spinal cord is excised. In bone grafting for spinal fusion, a spreader is used. A tricortical iliac strut is harvested and split. The split halves are forced back to back into the trough so that their cancellous surfaces can be brought into contact with the cancellous bone of the bodies. The cortical surfaces of the grafts adjoin the cortical surfaces of the bodies (Fig. 10). This corticalbone to cortical-bone contact prevents any sinking of the grafts into the bodies; this is especially important in osteoporotic spines in the elderly. With a collar, the patient can sit up and walk as soon as pain subsides. The collar is discarded after 12 weeks irrespective of the state of bone union. Posterior decompression Posterior decompression is generally recommended in patients who have compression of the spinal cord at three levels or more, in those who have developmental stenosis, and in those who have calcification of the ligamentum flavum. Laminectomy for posterior decompression is popular in Western countries. Kirita's bilateral open-door laminectomy using an air drill is recommended because it is atraumatic to the spinal cord. The C2 spinous process and the semispinalis muscles attached to it should be left intact in order to prevent postlaminectomy kyphosis. Recently in Japan, spinal canal-expanding laminoplasty has almost replaced laminectomy. Hirabayashi's open-door laminoplasty 17 and Kurokawa's spinous process-splitting laminoplasty have become the most popular of the many techniques. We have adopted the latter and used hydroxyapatite spacers to stabilize the split spinous processes instead of iliac
12
Current Orthopaedics Step 1
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1
~
4.
,~. an~d s~is anlngc
5.
spinous process Step 3
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7. 8. 9. 10. Fig. 11 Operative technique of Kurokawa's spinous processplitting laminoplasty using hydroxyapatite (HA) spacers. Step 1: A longitudinal groove is made bilaterally. Each spinous process is split and its halves are spread. Step 2: A trapezoidal-shaped spacer is placed between the two halves of each split spinous process. Steps 3 and 4: The spacer is fixed by diagonally tying two silk threads which were passed through the holes? ~
11. i2. 13.
bone grafts as in the original procedure (Fig. 11). 7 The postoperative management is the same as that for the anterior procedure.
14. 15. 16.
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17. 18.
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