Experimental cervical myelopathy Effects of ischemia and compression of the canine cervical spinal cord

MICHAEL R. GOODING, F.R.C.S., CHARLES B. WILSON, M.D., AND JULIAN T. HOFF, M.D.

Department of Neurological Surgery, the H. C. Naffziger Laboratories for Neurosurgical Research, University of California School of Medicine, San Francisco, California ~" The authors report experiments designed to test the effect of regional ischemia induced by selective vascular ligations and anterior compression of the cervical cord at two adjacent segments (C-4, C-5) in the same dog. They conclude that local ischemia of the cervical cord, caused by local deformation, when superimposed on a regional reduction in spinal cord blood flow, accounts for the myelopathy of cervical spondylosis whether produced experimentally in animals or occurring naturally in man. KEY WORDS cervical myelopathy spinal cord compression "

T

HE role of ischemia in the pathogenesis of human cervical spondylotic myelopathy is unclear,6,s,9,21,23,2s,333e,~s and the importance of anterior compression of the spinal cord in the development of this disease remains c o n t r o v e r s i a l , l'2`l~ The study that is the subject of this report represents an effort to clarify some of these uncertainties. Materials and Methods

Twenty healthy female dogs, weighing 14 to 26 kg, were used in these studies. Dogs with chondrodystrophoid features likely to develop spontaneous disc disease le,2~ were excluded. Surgical procedures were performed under sterile conditions. The dogs were anesthetized with intravenous pentobarbital (25 mg/kg),

J. Neurosurg. / Volume 43 / July, 1975

9 ischemia

9

intubated, and allowed to breathe spontaneously. Anesthesia was supplemented with pentobarbital as needed. Blood loss was replaced with saline or whole blood during operation. Hematocrits were determined before and after each surgical procedure.

Surgical Procedures Determination o f Maximum Tolerable Compression ( M T C ) at C-4 and C-5.15'2~ In 10 dogs specially designed screws with detachable stems were placed in 5/16" holes drilled anteriorly through the midline of the C-4 and C-5 bodies. On the next day the screws were alternately tightened in 1 mm increments over a 2-hour period until the dog showed early signs of weakness in the limbs. The screw stems were then removed. Lateral 9

M. R. G o o d i n g , C. B. W i l s o n a n d J. T. H o t t

Fro. 1. Lateral x-ray film showing screws in position in C-4 and C-5.

later date, ligation of the anterior spinal artery at C-I and of both vertebral arteries proximal to C-6 were carried out (Fig. 2). Combination o f M T C and CVI Procedures. After complete neurological recovery (average 9 days, range 3 to 13 days), all 10 dogs with established MTC underwent arterial ligation procedures. Four other animals underwent the three operations described above, but without the insertion of screws or interruption of arteries. These dogs served as controls for neurological evaluation, acute bleeding tests, and pathological studies. Combination o f CVI Followed by M T C Operations. In three of the six dogs with established CVI, the MTC operation was performed later to determine if reversal of the sequence of procedures influenced the outcome.

Acute Bleeding Tests An acute bleeding test was performed in nine dogs following MTC with CVI procedures, in six dogs with CVI alone, in three dogs with CVI and later MTC, and in four control animals. This test indicated a threshold for hypovolemic reversible paraparesis in animals with ischemia after vascular ligations and in animals with compression from anterior screws. 2~ A lethal dose of pentobarbital sodium and 5000 units of heparin were injected intravenously at the conclusion of each experiment. The chest was opened immediately and the proximal aorta cannulated. The vascular system was perfused with normal saline and then with red neoprene latex (50% solution) at 120 mm Hg. ls,~~ The medulla, cervical column with the cervical cord in situ, and the remaining spinal cord were removed and fixed in 10% formalin. Following fixation, the cerFro. 2. Diagram of anterior canine spinal vical laminae were removed and the cervical circulation. Black lines indicate arterial interrupcord examined to confirm the position of tion in CVI procedure. arterial ligations. x-ray films showed the extent of canal narrowing; this was expressed as a percentage of the normal sagittal diameter of the spinal canal (Fig. 1). Selective Vascular Ligations to Achieve Moderate Cervical Vascular Insufficiency (CVI). ~4,19 In six dogs, both lateral spinal arteries at C-3 were ligated initially. At a 10

Results

M T C Operations Six dogs (Dogs 1, 2, 6, 7, 8, and 9) developed a mild-to-moderate tetraparesis; in all of these weakness predominated in the hind limbs. The other four dogs sustained only a mild paraparesis; the weakness was more pronounced on the right side in two

J. Neurosurg. / Volume 43 / July, 1975

Experimental cervical myelopathy dogs (Dogs 2 and 5), on the left side in one (Dog 6), and was symmetrical in the remaining dogs. Gait unsteadiness and limb weakness resolved in all dogs over an average period of 9 days (range, 3 to 13 days), a figure similar to our previous findings of 4 to 26 days (average 12). 15 Hematocrits averaged 43% (33% to 50%) (Table 1). C V I Operations Three dogs remained unaffected by the first vascular ligation operation, and the other three (Dogs 11, 12, and 15) developed a minimal tetraparesis that resolved completely in 10, 3, and 5 days respectively. Weakness was symmetrical in all three dogs; in one (Dog 11) weakness was more prominent in the forelimbs; in two, it was equal in all limbs. Hematocrits averaged 44% (39% to 50%). The second ligation operation was performed on an average of 23 days later (10 to 32 days), at which time neurological deficits had cleared. Hematocrits averaged 41% (35% to 48%). Only one dog (Dog 13) showed any adverse effects from the second operation, that being mild paraparesis lasting 2 days. Combined M T C and C V I All of these dogs, without neurological impairment despite cord compression, developed severe neurological deficits following the first CVI ligation procedure (bilateral ligation of C-3 arteries) (Table 2). Five (Dogs 1, 2, 3, 4, and 6) developed a profound tetraparesis; they were unable to stand and barely able to move their limbs, and showed a complete loss of righting and scratch reflexes, with absent or weak withdrawal reflexes. Incontinence was noted and they required hand feeding. If placed in position, two (Dogs 7 and 8) were able to stand, but could not walk without falling; these dogs also showed marked impairment of their righting, scratch, and withdrawal responses. The remaining four dogs suffered moderate disability and were able to walk with an ataxic gait; all limbs were affected equally except in one (Dog 9), which was paraparetic. N o sensory loss was detected. The weakness progressed invariably until the third or fourth postoperative day; after this time, signs improved steadily, resolving usually by the twelfth day (range, 6 to 24 days). By the time of second arterial ligations, J. Neurosurg. / Volume 43 /July, 1975

TABLE

1

Summary of clinical results in dogs undergoing MTC and CV1 procedures Dog No.

Type of Lesion

Severity of Lesion

Lateralization*

Time to Recovery (days)

Maximum tolerable compression ( MTC procedure)

equal 1 tetraparesls minimal right 2 tetrapares~s minimal minimal equal 3 paraparesls equal 4 parapares~s moderate right 5 parapares~s minimal left 6 tetrapares~s minimal equal 7 tetraparesxs minimal equal 8 tetrapares~s minimal equal 9 tetrapares~s minimal moderate equal 10 p a r a p a r e s l s Cervical vascular insufficiency (CVI procedure) 11 tetraparesis minimal equal 12 tetraparesis minimal equal 13t ---14~f ---15 tetraparesis minimal equal 16t ----

9 10 9 10 5 13 9 13 3 7 10 3 0 0 5 0

* All dogs that were affected were more severely affected in the rear limbs. t Dogs 13, 14, and 16 were not affected by the procedures. six dogs had returned to normal (Dogs 1, 5, 6, 8, 9, and 10); the remainder showed only exaggerated deep tendon jerks. The anterior spinal and vertebral arteries were ligated on an average of 14 days later (9 to 28 days) when the hematocrit averaged 37% (28% to 43%). Only two dogs (Dogs 3 and 4) were affected adversely by this procedure; one incurred mild paraparesis that resolved in 3 days, the other a tetraparesis that resolved in 5 days. C V I Combined with Later M T C The cord compression procedure was performed in three dogs I0 days after the final arterial ligations. The average hematocrit was 42% (38% to 46%), and the dogs were neurologically normal. M T C was achieved in the usual manner and all three dogs developed mild ataxia and paraparesis. Lateral x-ray films revealed the degree of compression to be less in these dogs than in the 10 with compression prior to vascular ligation. This difference disappeared when the screws were tightened under x-ray control (Table 3). The increased compression was not associated with appreciable change, and the dogs were 11

M. R. Gooding, C. B. Wilson and J. T. Hoff TABLE 2

Summary of clinical results in dogs undergoing MTC followed by CVI and C V1 followed by MTC procedures Dog No.

Type of Lesion

MTC followed by CVI procedure

Lesion Severity

Lateralization

Limbs Most Affected

Time to Recovery (days)

Time to Sacrifice (days)

1 2 3* 4* 5 6 7 8 9 10

tetrapar~sis tetraparesls tetrapares~s tetraparesls paraparesm tetraparesm tetrapares~s tetraparesm paraparesls tetrapareszs

severe severe severe severe moderate severe moderate moderate moderate moderate

right equal equal equal left equal left equal equal equal

equal rear rear rear rear equal equal equal rear rear

16 24 22 14 9 9 10 10 6 5

59 106 118 102 96 14 22 23 58 51

11 12 13

paraparesis paraparesis tetraparesis

minimal minimal minimal

equal left equal

rear rear rear

6 10 9

30 28 24

CVI followed by MTC procedure

* These dogs only developed minimal signs after second part of CVI procedure. TABLE 3

TABLE 4

Values for reduction of canal diameter before and after compression corrected in CVI followed by MTC procedures *

Values for reduction of canal diameter in MTC and CVI procedures*

C-4 Segment C-5 Segment Dog Canal Screw ~ Canal Screw ~ No. Diam. Depth Reduc- Diam. Depth Reduc(mm) (mm) tion (mm) (ram) tion

C-4 Segment C-5 Segment Dog Canal Screw ~o Canal Screw No. Diam. Depth Reduc- Diam. Depth Redue(mm) (mm) tion (mm) (ram) tion

Before correction 11 12 13

11.0 11.0 10.5

3.5 3.5 3.0

31.8 31.8 28.5

11.5 12.0 11.5

2.0 3.0 2.5

17.4 25.0 21.7

11 12 13

11.0 11.0 10.5

3.5 3.5 3.0

31.8 31.8 28.5

11.5 12.0 11.5

2.5 3.0 3.0

21.7 25.0 26.0

After correction

* Before correction average reduction of canal diameter at C-4 = 30.7~; at C-5 = 21.3~o. After correction, average reduction of canal diameter at C-4 = 30.77.; at C-5 = 24.2~. Overall average reduction of canal diameter before correction = 25.9%, and after correction = 27.4~.

neurologically normal days. N o d o g in this s e v e r e deficits seen in o p e r a t i o n s e q u e n c e was

Maximum

within four to nine g r o u p exhibited the those for which the reversed.

Tolerable C o m p r e s s i o n

In a n i m a l s u n d e r g o i n g c o m b i n e d M T C C V I , the a v e r a g e n a r r o w i n g o f the cervical

12

1 2 3 4 5 6 7 8 9 10

10.5 11.0 9.5 10.25 11.0 9.5 11.25 10.5 12.5 11.0

3.0 3.5 2.25 2.5 3.0 2.75 3.0 3.25 3.5 3.0

28.5 31.8 23.6 24.3 27.2 28.9 26.6 30.9 28.0 27.2

11.0 11.5 10.0 10.75 11.5 10.0 11.5 11.25 13.0 11.5

4.0 3.5 3.0 2.5 2.0 2.5 2.0 3.5 3.0 2.5

36.3 30.4 30.0 23.2 17.4 25.0 17.4 31.1 23.0 21.7

* Average reduction of sagittal diameter of canal at C-4 = 27.8 %, and at C-5 = 25.4 ~. Average reduction of canal diameter = 26.5~.

canal at C- 4 was 27.8%, and at C-5 was 25.4%, with an a v e r a g e o f 26.5% ( T a b l e 4). T h e s e results w e r e consistent with those of earlier e x p e r i m e n t s : 14 26.2% at C- 4 and 23% at C-5, with an a v e r a g e of 24.6%. This corr e l a t i o n was f u r t h e r su p p o r t ed by similar n e u r o l o g i c a l findings in the two groups. W h e n M T C was i m p o s e d following arterial ligations, the d e g r e e s o f c o m p r e s s i o n at C-4

J. Neurosurg. / Volume 43 / July, 1975

Experimental cervical myelopathy TABLE 5 Results of acute bleeding tests*

Procedure control CVI MTC + CVI CVI + MTC

No. of Dogs

4 5 9 3

Weightof Dog

(kg)

21.75 19.1 16.9 17.3

Total Blood BloodLoss/ Loss Weight (ml) (ml/kg) 908 723 450 561

41.5 37.8 28.8 32.2

Hematocrit .o7oo

Fall in BP (mm/Hg)

Rate of Blood Loss (ml/min)

43 44 42 41

55.0 40.0 33.3 45.0

50.0 46.0 48.6 46.7

* Values given represent averages for each group of dogs. BP= blood pressure. and C-5 were 30.7% and 21.3% respectively, with an average of 25.9%. Increase in the degree of compression to 24.2% at C-5 raised the combined average to 27.4%, but produced no apparent clinical sequelae.

posterior nerve roots, ganglia, or both (Fig. 3). Demyelination was diffuse in both the anterior and lateral columns of white matter (Fig. 4). No clear-cut signs of glial proliferation or gray matter infarction as described by Hukuda and Wilson 2~ were present. M T C and CFI. Interruption of the anterior Acute Bleeding Tests spinal, both vertebral, and the lateral spinal This test was done in nine dogs from the arteries at C-3, was confirmed in all dogs. All combined MTC and CVI group, in six dogs 10 cervical cords showed evidence of from the CVI group (three of these underwent histological damage, consisting of changes further bleeding tests after MTC was imposed similar in distribution, but more pronounced following the arterial ligations), and in the in MTC-CVI animals than in those with CVI four control animals. Results are given in alone. In the remainder, however, demyelinaTable 5. The rates of blood removal averaged tion was more widespread, involving all the 46 ml/min, 48.6 ml/min, and 46.7 mg/min white matter to varying degrees. In parfor the CVI, combined MTC-CVI, and comticular, the junctional zones around the bined CVI-MTC groups respectively. Almost anterior gray matter showed disproportionate invariably, blood pressure fell during damage (Fig. 5). bleeding, averaging 40 mm Hg, 33.3 mm Hg, In four cords, demyelination of the and 45 mm Hg for the same groups of posterior corticospinal tracts was pronounced animals. In all experimental groups, the fall (Fig. 6), being marked in C-4, but detectable in blood pressure was less than in control throughout the cord as far caudally as T-5. animals in which it averaged 55 mm Hg. In No evidence of gliosis or infarction of the MTC animals, neurological deficits recurred gray matter was present, and the intramedto some degree, but resolved within a few minutes after blood volume was restored to ullary blood vessels were unaffected. CFI and MTC. Each of the three cords control levels. showed the same features described previously in the animals in which cord comPathology pression preceded the arterial ligations. The spinal cords of all dogs were examined Degeneration of the junctional zones around histologically. Sections were stained by the the anterior gray horns was evident in all Marchi method and by hematoxylin and cords, and two showed demyelination of the eosin. posterior corticospinal tract. CVI. In three spinal cords, areas of Comment. Despite the clinical and demyelination in the fasciculus cuneatus were physiological differences between the two evident in the upper three cervical segments. groups, the absence of pathological One cord, that of Dog 14, showed mild differences suggests the same overall condemyelination of the posterior spinocer- clusions: 1) the corticospinal tracts were most ebellar tract. These changes were attributed severely damaged; 2) C-4 and C-5 segments to mechanical or ischemic damage of the C-3 were the most affected; 3) damage at thejuncJ. Neurosurg. / Volume 43 / July, 1975

13

M. R. Gooding, C. B. Wilson and J. T. Hoff

FIG. 3. Microscopic section at C-3 following Fi6. 4. Microscopic section at C-4 following CVI procedure, demonstrating traumatic changes CVI procedure, demonstrating diffuse demyelination in anterior and lateral white matter. Marchi in fasciculus cuneatus. Marchi method, • method, • 9.

tional areas of the gray and white matter was disproportionate; and 4) histological abnormalities in all 13 dogs with combined compression and ischemia were more pronounced than in dogs with either compression or ischemia alone. Discussion

We reported earlier that the effects of anterior cervical cord compression at a single level and induced vascular insufficiency are additive?~ Subsequently, we observed that the effects of compression at two separate levels are additive, and that compression to the same degree at a single level had no neurological effect. 15 In the current study, bilateral ligation of the C-3 spinal arteries produced a mild deficit that rapidly resolved in only half the dogs; when the anterior spinal and both vertebral arteries were subsequently ligated, little additional clinical effect was observed. These 14

results confirm those of Shimomura, et al., 29 who ligated the vertebral artery at its origin, unilaterally or bilaterally; subsequent vertebral artery ligations at C3-4 produced no neurological deficit. In seven other dogs, both vertebral and lateral spinal arteries were occluded on one or both sides with minimal clinical and histological effect. They concluded that localized cord ischemia occurs rarely, principally because of the pial anastomoses, and that the importance of the segmental vessels has been overstressed. T M Our findings, however, indicate that prior establishment of minimal cord compression followed by otherwise innocuous vascular ligations results in a profound neurological deficit. When ischemia was superimposed on dogs with compression of the cervical cord at two adjacent levels, neurological changes were dramatic. Half the animals became mildly to moderately tetraplegic, and the other half severely tetraparetic. Nonetheless, recovery J. Neurosurg. / Volume 43 / July, 1975

Experimental cervical myelopathy

Fl~. 6. Microscopic section at C-4 following FIG. 5. Microscopic section at C-4 following CVI and MTC procedures, demonstrating CVI and MTC procedures, demonstrating marked demyelination at the junction of the anterior gray demyelination of posterior corticospinal tract. Note also the severe, diffuse demyelination and white matter. Marchi method, • 19. tttroughout all the white matter. Marchi method, )48. was complete within 3 to 4 weeks. Their rapid recovery could be explained partially by the unique vascular resiliency of the canine cervical cord, 25which rapidly restores blood flow to hypoxic tissue to reverse functional depression. This explanation is supported by results of the acute bleeding test: before collapsing, control animals had lost 41,5 ml/kg, the animals with ischemic cores had lost 37.8 ml/kg, and those with combined ischemia and compression had lost only 28.8 ml/kg. However, when compression followed ischemia, blood loss was 32.2 ml/kg, and so approximated the critical blood loss (32.6 ml/kg) observed in animals subjected to compression alone. TM The difference in blood loss between our control and CVI animals was 4 ml/kg, and 9 ml/kg between the control and MTC animals. If the sum of these differences were subtracted from the blood loss in control animals (41,5 ml/kg), the resulting 28.5 ml/kg would coincide closely with the 28.8 J. Neurosurg. / Volume 43 / J u l y , 1975

ml/kg observed in animals with combined MTC-CVI. Thus the effects of multiple-level cor.d compression and systemic ischemia were additive. The pathological changes affecting the cervical spinal cord were less severe than expected from the extent of the neurological deficits. This discrepancy may be explained in part by the recent work of Gledhill, et al., ~4 who also found a correlation between the degree of demyelination following cord compression and the observed neurological deficit. While demyelination produced a functional block, in their study only 3% of the normal myelin thickness was sufficient to restore function. Since remyelination may be delayed from 7 to 21 days following compression, 14 the rapid recovery of our animals suggests other processes contribute to restoration of function. Two additional factors may be significant in this regard; first, postoperative anemia reaches a peak on the third day and resolves within 3 weeks. Second, spinal cord 15

M. R. Gooding, C. B. Wilson and J. T. Hoff 7. Bradshaw P: Some aspects of cervical sponedema resulting from ischemia induced by dylosis. Q J Med 26:177-208, 1957 arterial ligations m a y temporarily reduce 8. Brain R: Cervical spondylosis. Ann Intern segmental perfusion. 3,13,26 Med 41:439-446, 1954 We were able to demonstrate d a m a g e to 9. Breig A, Turnbull I, Hassler O: Effects of the border zones between the intra- and exmechanical stresses on the spinal cord in cert r a m e d u l l a r y circulation under the exvical spondylosis. J Neurosurg 25:45-56, 1966 perimental conditions reported previously by 10. Burrows EH: The sagittal diameter of the H u k u d a and Wilson 2~ and, while no areas of spinal canal in cervical spondylosis. Clin focal necrosis or glial proliferation were Radiol 14:77-86, 1963 observed, the histological appearance closely I I. Clarke E, Robinson PK: Cervical myelopathy: a complication of cervical spondylosis. Brain resembled that described in human spon79:483-510, 1956 dylotic myelopathy. 19,~2,31,37,4~ The rapid development of collateral cir- 12. Doppman JL, Ramsey R, Thies RJ: A percutaneous technique for producing intraspinal culation in the dog, 4,~,17,3~ which has large mass lesions in experimental animals. J lateral spinal arteries at each cervical segNeurosurg 38:438-447, 1973 ment, renders it particularly resistant to 13. Fried LC, Goodkin R: Microangiographic obchronic ischemia. On the other hand, the servations of the experimentally traumatized effects of compression apparently persist inspinal cord. J Neurosurg 35:709-714, 1971. definitely. We concur with Doppman, et al., 12 14. Gledhill RF, Harrison BM, McDonald WI: t h a t m o n k e y s are m o r e suitable for Demyelination and remyelination after acute evaluating the effects of chronic cervical cord spinal cord compression. Exp Neurol ischemia; they resemble man more closely 38:472-487, 1973 since they have few large lateral spinal 15. Gooding MR, Wilson CB: Experimental cervical myelopathy. J Neurosurg (In press) arteries supplying the cervical spinal cord. 16. Hansen H J: A pathologic-anatomical interpretation of disc degeneration in dogs. Acta Orthop Seand 20:280-293, 1951 17. Hill L: Cerebral ischemia and the effects which References follow ligation of the cerebral arteries. Trans R Med Soe 193:69-82, 1900 1. Adams CBT, Logue V: Studies in cervical spondylotic myelopathy. 1. Movement of the 18. Hinck VC, Sachdev NS: Developmental stenosis of the cervical spinal canal. Brain cervical roots, dura and cord, and their rela89:27-36, 1956 tion to the course of the extrathecal roots. 19. Hughes JT, Brownell B: Spinal cord ischaemia Brain 94:557-568, 1971 due to arteriosclerosis. Arch Neurol 2. Adams CBT, Logue V: Studies in cervical 15:189-202, 1966 spondylotic myelopathy. 2. The movement and contour of the spine in relation to the 20. Hukuda S, Wilson CB: Experimental cervical myelopathy: effects of compression and neural complications of cervical spondylosis. ischemia on the canine cervical cord. J Brain 94:569-586, 1971 Neurosurg 37:631-652, 1972 3. Allen AR: Remarks on the histopathological changes in the spinal cord due to impact. An 21. Logue V: Thoracic intervertebral disc prolapse with spinal cord compression. J Neuroi experimental study. J Nerv Ment Dis Neurosurg Psychiatry 15:227-241, 1952 41:141-147, 1941 4. Andreyev LA: Functional changes in the brain 22. Mair WGP, Druckman R: The pathology of spinal cord lesions and their relation to the of the dog after reduction of the cerebral blood clinical features in protrusion of cervical insupply. 1. Cerebral circulation and the tervertebral discs. A report of four cases. development of anastomosis after ligation of Brain 76:70-91, 1953 the arteries. Arch Neurol Psychiatry 23. Nugent GR: Clinicopathologic correlations in 34:481-507, 1935 cervical spondylosis. Neurology (Minneap) 5. Andreyev LA: Functional changes in the brain 9:273-281, 1959 of the dog after reduction of the cerebral blood supply. 2. Disturbances of conditioned reflexes 24. Nurick S: The pathogenesis of the spinal cord disorder associated with cervical spondylosis. after ligation of arteries. Arch Neurol Brain 95:87-100, 1972 Psychiatry 34:699-713, 1935 6. Bedford PD, Bosanquet FD, Russell WR: 25. Olssen SE: The dynamic factor in spinal cord compression: a study on dogs with special Degeneration of the spinal cord associated reference to cervical disc protrusions. J with cervical spondylosis. Lancet 2:55-59, Neurosurg 15:308-321, 1958 1952 16

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Experimental cervical myelopathy 26. Palleske H: Experimental investigations on 36. Tarlov IM, Klinger H, Vitale S: Spinal cord the regulation of the spinal cord circulation. 3. compression studies. 1. Experimental techThe regulation of the blood flow in the spinal niques to produce acute and gradual comprescord altered by edema. Acta Neurochir (Wien) sion. Arch Neurol Psychiatry 70:813-819, 21:319-327, 1969 1953 27. Pallis C, Jones A, Spillane J: Cervical spon- 37. Taylor AR: Mechanism and treatment of dylosis. Incidence and implications. Brain spinal-cord disorders associated with cervical 77:274-289, 1954 spondylosis. Lancet 1:717-720, 1953 28. Payne EE, Spillane JD: The cervical spine. An 38. Taylor AR: Vascular factors in the anatomico-pathological study of 70 specimens myelopathy associated with cervical spon(using a special technique) with particular dylosis. Neurology (Minneap) 14:62-68, 1964 reference to the problem of cervical spon- 39. Whisnant JP, Millikam CH, Wakim KG, et dylosis. Brain 80:571-596, 1957 al: Collateral circulation to the brain of the 29. Shimomura Y, Hukuda S, Mizuno S: Exdog following bilateral ligation of the carotid perimental study of ischemia damage to the and vertebral arteries. Am J Physiol cervical spinal cord. J Neurosurg 28:565-581, 186:275-277, 1956 1968 40. Wilkinson M: The morbid anatomy of cervical 30. Stewart GN, Guthrie CC, Burns RL, et al: spondylosis and myelopathy. (Abstract) The resuscitation of the central nervous Neurology Neurosurg Psychiatry 23:353, 1960 system of mammals. J Exp Med 8:289-321, 41. Wilkinson M: The morbid anatomy of cervical 1906 spondylosis and myelopathy. Brain 31. Stoltmann HF, Blackwood W: The role of the 83:589-617, 1960 ligamenta flava in the pathogenesis of 42. Wilson CB, Bertran V, Norrell HA Jr, et al: myelopathy in cervical spondylosis. Brain Experimental cervical myelopathy. 2. Acute 87:45-50, 1964 ischemic myelopathy. Arch Neurol 32. StSrtebecker TP: Disturbance of arterial 21:571-589, 1969 supply to the spinal cord and brain stem 43. Wolf BS, Khilnani M, and Malis LL: The caused by spondylosis, disc protrusions and sagittal diameter of the bony cervical spinal root-sleeve fibrosis. A concept concerning faccanal and its significance in cervical spontors eliciting amyotrophic lateral sclerosis. dylosis. J Mt Sinai Hosp 23:282-292, 1956 Acta Orthop Stand Suppl 42:1-20, 1960 44. Woollam DHM, Millen JW: The arterial 33. Tarlov IM: Spinal Cord Compression: supply of the spinal cord and its significance. J Mechanism of Paralysis and Treatment. Neurol Neurosurg Psychiatry 18:97-102, 1956 Springfield, I11, Charles C Thomas, 1957 34. Tarlov IM: Spinal cord compression studies. This work was supported in part by NINDS 3. Time limits for recovery after gradual com- Training Grant 5593, and NINDS NS 11539. pression in dogs. Arch Neurol Psychiatry Dr. Hoff is recipient of Teacher-Investigator 71:588-597, 1954 Award NS 11051 NSRB. 35. Tarlov IM, Klinger H: Spinal cord compresAddress reprint requests to: Charles B. Wilson, sion studies. 2. Time taken for recovery after M.D., Department of Neurological Surgery, acute compression in dogs. Arch Neurol University of California School of Medicine, San Psychiatry 71:271-279, 1954 Francisco, California 94143.

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17

Experimental cervical myelopathy. Effects of ischemia and compression of the canine cervical spinal cord.

The authors report experiments designed to test the effect of regional ischemia induced by selective vascular ligations and anterior compression of th...
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