The Dynamic Factor in Spinal Cord Compression

A Study on Dogs with Special Reference to Cervical Disc Protrusions

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It is a well established fact that certain chondrodystrophic breeds of dogs have a greater tendency towards degeneration and protrusion of intervertebral discs than other breeds.3

Degeneration of discs in the chondrodystrophics is characterized by a dystrophic calcification of the nucleus pulposus. Very often there is a complete rupture of the annulus fibrosus, with a varying degree of displacement of the nucleus pulposus into the vertebral canal. Because of the calcification the displacement can, in many cases, easily be demonstrated and the allied spatial changes followed on routine roentgenograms. Almost all disc protrusions in the dog, except

It is a well established fact that certain chondrodystrophic breeds of dogs have a greater tendency towards degeneration and protrusion of intervertebral discs than other breeds.3

Degeneration of discs in the chondrodystrophics is characterized by a dystrophic calcification of the nucleus pulposus. Very often there is a complete rupture of the annulus fibrosus, with a varying degree of displacement of the nucleus pulposus into the vertebral canal. Because of the calcification the displacement can, in many cases, easily be demonstrated and the allied spatial changes followed on routine roentgenograms. Almost all disc protrusions in the dog, except a few lateral ones, compress the spinal cord. (The spinal cord extends to the last lumbar vertebrae. There are 7 lumbar vertebrae.) This combination of circumstances provides ideal material for the study of the varying factors influencing the symptoms of compression of the spinal cord.

Olsson6 and Hansen,3 on the basis of clinical, roentgenological and patho-anatomical material, discussed thoracolumbar protrusions in the dog. Observations pertinent to this paper may be summarized as follow:

In cases of complete rupture of the annulus fibrosus the protrusion may cause symptoms of varying severity: from complete paraplegia to only slight pain. The onset of pain or paresis may be sudden or insidious and the duration of symptoms variable. Some dogs with paraplegia never recover while others recover within 3 weeks or up to 6 months. In many cases pain will cease in a few days, while in other cases pain may persist for months. Olsson explains the variability in degree and duration of symptoms as follows. A complete irreversible paraplegia is more the result of how the disc protrusion occurs than the size of the protrusion. A slow-growing, large protrusion may give rise to only slight symptoms, while a sudden protrusion will act as a severe trauma to the cord sometimes with severe hemorrhage, spinal shock and even death. This is in accordance with the results obtained later by Tarlov et al.8–10 in their experimental study on compression of the spinal cord in the dog.

Healing results from the disappearance of the inflammatory reactions, bleedings and edema rather than from the disappearance or diminishing of the protrusion itself. If now and then a small amount of disc tissue is pressed out through a rupture in the annulus fibrosus by active or passive movements of the spine, the inflammatory reaction and subsequent irritation of the cord will persist together with clinical symptoms. Even very large protrusions may not cause symptoms if they are firm and do not continue to enlarge. Considering the natural mode of healing through stabilization of the protrusion, Olsson6 introduced a surgical method to prevent further protrusion of a ruptured disc. This fenestration operation consists of the removal of the remaining part of the nucleus pulposus through an incision in the annulus fibrosus outside the vertebral canal.

Laminectomy and removal of the protrusion proved to be of little value in these cases largely because of the damaged cord's low tolerance to the surgical trauma.

The above concepts were based upon studies of thoracolumbar disc protrusions. However, great muscular forces affect the thoracolumbar area. This may be the explanation why sudden and powerful protrusions followed by paraplegia are very common in this area. These cases thus are less suitable for continuous study of delicate changes in symptoms and the effects of therapeutic measures.

Cervical disc protrusions in the dog, reported for the first time by Olsson6 in 1951 and described more completely by Olsson and Hansen7 in 1952, are, in this respect, of greater interest. Pain in the neck and forelegs is the predominant symptom. Paraplegia or quadriplegia is seen only exceptionally. These differences in symptoms in the cervical and thoracolumbar regions may be explained by the different muscular forces exerted on the cervical and lumbar spine during locomotion, as well as by the somewhat wider cervical part of the vertebral canal which provides more room for the spinal cord.

The aim of this paper, based mainly on a study of cervical disc protrusions, is to throw new light upon the problems concerned in compression of the spinal cord.

CLINICAL STUDIES

MATERIAL AND METHODS

During the eight-year period from 1949–1956 about 1300 clinical cases of disc protrusions in the dog have been studied. In 40 of these cases there were symptoms associated with protrusions of the cervical discs. The cases of protrusion of the thoracolumbar discs have been discussed in previous papers and are not included in this study except a few cases of special interest. Treatment in the latter cases has been routine in the clinic, according to the regime given by Hansen and Olsson4 in 1953.

All dogs with cervical disc protrusions were subjected to detailed neurological and roentgenological examinations during the period of clinical observation. They were reexamined several times after recovery. In all 40 cases the site of the protrusion was demonstrated on routine roentgenograms. In 10 cases, however, myelography was performed (Fig. 1) in order to establish definitely the presence of spinal cord compression. In 34 cases surgery was performed. The remnants of the nucleus pulposus of the ruptured disc were scooped out through an incision in the ventral portion of the annulus fibrosus. In the remaining 6 cases treatment was conservative, with only rest and careful nursing.

Fig. 1.
Fig. 1.

Lateral roentgenogram of part of cervical spine of a dog showing the following changes: calcification of discs C2–C3, C3–C4, and C4–C5. The latter disc shows a narrowed space. The dog had typical symptoms of spinal cord compression and, though there was little doubt that disc C4–C5 had protruded, myelography was performed to demonstrate the lesion. After cisternal puncture through the suboccipital foramen, 0.7 cc. of Thorotrast was injected. After a few minutes in a tilted position with the head high, the dog was X-rayed. The spinal cord is nicely outlined and there is a complete block (A) at the level of disc C4–C5.

RESULTS

Of the 34 dogs operated upon, 29 had been treated conservatively prior to surgery for 2 weeks or more with little or no result. Eleven of these had been treated for more than a month with the same negative results.

In 30 surgical cases recovery was complete within the period of time after operation indicated in Table 1.

TABLE 1

Time of complete recovery after operation for cervical disc protrusion

Within 1 Week1–2: Weeks2–3 Weeks
1386

One animal was killed 3 weeks after operation with nearly unchanged symptoms. Two died from intercurrent disease shortly after operation. One died in postoperative quadriplegia (no necropsy).

Of the 6 animals treated conservatively, 2 recovered after 2 months and 1 after 3 months. The 3 remaining dogs were all killed, 2 after 1 week and 1 after 4 weeks. The owners refused surgery but could not stand seeing their dogs in severe pain.

PATHO-ANATOMICAL STUDIES

As early as 1896 Dexler,1 one of the pioneers in the field of canine neuropathology, gave a thorough description of the histopathological changes in compression myelitis caused by the so-called enchondrosis intervertebralis—identical to the disc syndrome. In all of his 11 cases there were severe motor disturbances. Dexler found the symptoms closely related to the degree of changes in the spinal cord. In some cases, however, there was no correlation between changes in the cord and amount of compression of the cord. In 1 case of complete cross sectional malacia there was only a small very flat protrusion. Dexler interpreted the malacia in this case as a result of an irritation caused by the increased mobility of the spine at the site of the diseased disc. He could, however, only demonstrate this on the specimen at necropsy.

All recent studies on protrusions of the canine disc have paid more attention to the pathology of the disc than to that of the spinal cord. In the present study most animals were treated and recovered. Autopsies were performed in only 3 cases of cervical disc and 14 of lumbar disc. The vertebral columns from 13 of these dogs were deep-frozen and sawn sagittally in order to make possible the demonstration in situ of the protrusion and the degree of cord compression (Fig. 12). This procedure, however, destroyed the minute structures of the cord and in only the 4 remaining cases could the cord be properly examined histologically. This material included 5 disc protrusions. Four were acute, having caused severe symptoms with a duration of 10 to 15 days, and 1 was chronic, probably without any symptoms, at the time of death.

Fig. 12.
Fig. 12.

A part of the left half of a frozen spine with the spinal cord in situ. Disc C3–C4 has protruded. The protrusion as well as the compression of the cord is of considerable size. The disc is narrowed in comparison with the surrounding discs. The nuclei pulposi of the discs in the picture are all calcified. The protrusion is of the type that, despite its size, gives rise to only slight symptoms.

The pathological changes caused by these protrusions were similar to those reported by Dexler. They varied from circumscribed areas of malacia, proliferation of the neuroglia, perivascular infiltrate of lymphoid cells and meningitis up to complete malacia of the compressed part of the cord (Figs. 13, 14 and 15). The chronic protrusion shown in Fig. 10, according to the clinical history, had been the cause of a posterior paresis more than half a year prior to death. Despite an obvious compression of the cord, there were no significant histopathological changes to be found.

Fig. 13.
Fig. 13.

Microphotograph of dorsocentral part of spinal cord at site of compression caused by an acute disc protrusion. The gross appearance of the protrusion is shown in Fig. 10. In the right dorsal column there is a circumscribed area of malacia and in the left a less pronounced diffuse malacia. Mahon's stain for myelin sheaths, ×154.

Fig. 14.
Fig. 14.

Microphotograph of parts of a 10-day-old disc protrusion and of the compressed cord (upper right). (The cord was compressed to more than two-thirds of its normal area of transection and the dog suffered from a complete posterior paralysis.) The light-stained portion of the protrusion consists of chondroid nucleus pulposus tissue, showing the typical cell pattern. The dark-stained areas are mainly calcified tissue. The cord shows a compact structure because of the compression. See further Fig. 15. Hemalum-eosin, ×148.

Fig. 15.
Fig. 15.

Greater magnification of the cord shown in Fig. 14. Ventral part of right dorsal column to the left and grey commissure to the right. The tissue is more compact than normal because of compression. Malacia and increase in number of glia cells is well demonstrated. In the lower left corner is a part of the dorsal septum with a vessel showing perivascular reaction. Moreover there is a great number of minute vessels scattered in the cord tissue and marked neuronophagia. Hemalum-eosin, ×506.

Fig. 10.
Fig. 10.

Part of the dorsal spine of a dog, seen from the dorsal side; the neural arches and spinal cord have been removed. There are two disc protrusions: one chronic on L2–L3 (to the left) and one acute on L3–L4. The chronic protrusion caused an attack of paresis nearly 1 year prior to death, which was caused by the acute protrusion. The difference between the two protrusions is obvious. To the left side of the chronic protrusion is shown the dorsal surface of a normal disc.

DISCUSSION

The above figures indicate that fenestration of the disc has therapeutic value in cases of cervical disc protrusion. The rapid recovery after surgery of the animals first treated conservatively particularly points in this direction.

The present material supports the statement of Olsson and Hansen7 that there seems to be less tendency to spontaneous healing in cervical disc protrusions than in thoracolumbar protrusions. This point may seem controversial in view of the fact that severe cord lesions, and subsequent motor disturbances, are less common with cervical protrusions.

A possible explanation for the decreased healing ability of cervical protrusions may be the greater mobility of the cervical spine with decreased ability to prevent further increase in size of the protrusion.

Affected dogs in acute attacks of pain keep the head in a low and fixed position, absolutely refusing to raise it. On the other hand, during a period of less pain the animal may suddenly turn the head and, thereby, initiate a severe attack. The animals that respond best to fenestration are those with a small protrusion. Most of the nucleus tissue is then still in the disc and the disc space is nearly normal. Such an animal will recover within a week (Figs. 2 and 3). This emphasizes the importance of operating before too much nucleus tissue has been pressed out.

Fig. 2.
Fig. 2.

Lateral roentgenogram showing calcification of C2–C3 and a dorsal rupture of the annulus fibrosus. Calcified nucleus tissue has found its way out through the rupture, allowing the rupture to be demonstrated. The protrusion is not dense enough to show on the picture. (The calcified disc tissue in the protrusion is responsible for an eventual density of the protrusion. The density of the disc tissue is decreased if in a protrusion this tissue is intermingled with hemorrhages and inflammatory cells.) The disc space seems to be normal. The fenestration of a disc like this and a removal of the nucleus pulposus will prevent further protrusion and relieve pain in a few days.

Fig. 3.
Fig. 3.

The same dog as in Fig. 2. The roentgenogram was taken a week after operation when the dog was free of pain. The calcified protrusion was completely removed. Part of the removed nucleus pulposus can be seen as a slight density in the soft tissue on the ventral side of the disc.

One of the dogs operated upon, without any particular improvement after 3 weeks, was sacrificed at the owner's request. At necropsy it was demonstrated that the protrusion filled more than a third of the cross sectional area of the vertebral canal. In this case, in which the symptoms were paresis in the forelegs and pain, the static compression of the cord seemed to be of sufficient size to impair the function of the cord. This situation may have been suited for hemilaminectomy and removal of the protrusion or some other form of decompression operation. On the other hand, even larger protrusions of the chronic type have been found in dogs without symptoms.

In the case of the dog that died in postoperative quadriplegia after 6 days, necropsy could not be performed because of the owner's refusal. The operative failure may have been caused by a technical error by the surgeon. With the exception of this case and another in which there developed slight paresis of the forelegs of short duration, none of the dogs operated upon showed any side effects from the operation.

Of the conservatively treated animals, 1 is of special interest (Figs. 4, 5, 6 and 7). This dog was admitted to the clinic with rather severe symptoms of compression of the cervical spinal cord. A disc protrusion at C2–C3 was demonstrated. The dog was treated conservatively and sent home somewhat improved. At home paresis developed but the dog made a slow recovery, being completely normal in about 6 weeks. Examination at that time revealed that the symptoms had disappeared in spite of a radiologically visible enlargement of the protrusion. The entire nucleus pulposus had protruded and, therefore, become stabilized.

Fig. 4.
Fig. 4.

This roentgenogram is from a dog with rather severe symptoms of compression of the cervical spinal cord. Disc C2–C3 is calcified, slightly narrowed and protruded (A). The rather big protrusion can be seen as a long, slightly dense, curved shadow above disc C2–C3. The dog was treated conservatively and sent home in a somewhat improved condition 2 weeks later. While at home it made a sudden movement of the head and was stricken with severe pain and paresis. After a slow recovery of nearly 6 weeks, the dog regained complete health. See further Figs. 5, 6 and 7.

Fig. 5.
Fig. 5.

Ventrodorsal roentgenogram of the same dog as in Fig. 4, taken the same day.

Fig. 6.
Fig. 6.

Roentgenograms taken 2 months after the ones in Figs. 4 and 5. The entire calcified nucleus pulposus of C2–C3 has been pressed out of the disc and has contributed to a considerable enlargement of the protrusion (A). This obviously happened when the dog had the relapse of pain and paresis. It must be emphasized that this dog showed no signs of spinal cord compression when this particular roentgenogram was taken.

Fig. 7.
Fig. 7.

Ventrodorsal picture of same dog as in Figs. 4, 5 and 6. The large, calcified protrusion at C2–C3 is easily demonstrated, as well as the narrowing of the disc. Compared with Fig. 5 this roentgenogram reveals what has happened during the interval between the two roentgen-ray examinations. The disc has reached a final state. There is nothing left to protrude. Although the protrusion is of a remarkable size with a marked degree of cord compression, stabilization has been attained; the compression is static, and symptoms have disappeared. This roentgenogram was taken the same day as the one in Fig. 6.

Another example of the importance of the dynamic factor is the following case: 1 week after the onset of pain caused by a cervical disc protrusion the roentgenogram in Fig. 8 was taken. The one in Fig. 9 was taken after a 3-week period of conservative treatment. In spite of the treatment pain persisted because of further displacement of disc tissue. The enlargement of the protrusion, as well as the narrowing of the disc space, is demonstrated in the roentgenograms. In this case stabilization had not been attained. A fenestration in the first instance would have made further protrusion of the nucleus pulposus impossible, and the symptoms would probably have disappeared in a few days.

Fig. 8.
Fig. 8.

Roentgenogram showing the following changes of disc C4–C5: calcification of the entire nucleus pulposus, a rupture in the annulus fibrosus and a small calcified protrusion. The dog suffered from rather severe pain, but it was decided that conservative treatment should be tried. Pain persisted, however, and the dog was admitted to the clinic and reexamined (see Fig. 9).

Fig. 9.
Fig. 9.

Cervical spine of the same dog as in Fig. 8. There is an interval of 3 weeks between the two roentgen-ray examinations. A narrowing of disc C4–C5 and a slight increase in size of the protrusion have taken place since the roentgenogram of Fig. 8 was taken. The continuous protrusion of the disc during the interval was probably responsible for the persistence of pain.

Hansen3 reported the great difference microscopically between acute and chronic protrusions. The former type was characterized by the presence of hemorrhage, inflammatory cells and edema. Genuine disc tissue formed only a part of the protrusion. The chronic protrusion consisted of a higher percentage of cells of degenerated nucleus pulposus and some connective tissue. This difference is macroscopically demonstrated in Fig. 10. Two adjacent discs had protruded with an interval of nearly 1 year. The dog recovered from the first attack of paresis but died after 2 days of paraplegia in the second attack. The large grainy, edematous and partly hemorrhagic, acute protrusion is easily differentiated from the dry, firm, white-spotted calcified nucleus pulposus tissue of the chronic protrusion.

The cervical disc protrusion in Fig. 12 which caused only pain and the thoracolumbar one in Fig. 11 which caused severe trauma to the cord with ascending hemorrhage, spinal shock and death may serve as examples of the discrepancy between the measurable degree of compression of the cord and the symptoms. The only reasonable explanation for the difference in effect on the cord is a different rate of protrusion. The anamnesis of a large number of clinical cases provides ample evidence to support this conception. The initial trauma from a sudden and powerful protrusion may momentarily give rise to irreversible changes in the cord. Sometimes the trauma will cause edema and hemorrhage which, within a day, may be the cause of irreversible changes. This delay may allow time for surgical release of the compression. However, the vulnerability of the damaged spinal cord, together with the often poor condition of the animal, probably renders this expedient more theoretical than practical.

Fig. 11.
Fig. 11.

A part of the right half of the spine of a dog. The specimen was frozen, sawed in the sagittal plane and fixed in formalin. The cord has been severely damaged by a protrusion (B) of disc L1–L2 (C). The space of the latter disc is narrowed in comparison to that of T13–L1 (A). (The nucleus pulposus in the young animal is very hydrophilic. In the ageing dog this is less pronounced. In this dog all the discs swelled over the cut surface when fixed in formaldehyde except the protruded one.) The measurable compression of the cord in this case is not great, but, nevertheless, there is myelomalacia with subarachnoidal hemorrhage. The protrusion consists of two parts, one firm and chronic under the dorsal longitudinal ligament and one loose, and acute spread out on the body of L1. The changes extend to the upper cervical portion of the cord. Paraplegia was sudden, and the dog died in 2 days.

The canine spinal cord is considered to have more autonomy than the human cord.2 This autonomy may be one of the reasons why canine spinal cord can endure slowly increasing or large stable compression without losing its functional ability. This tolerance seems, however, to be reduced when inflammatory reaction is present in the epidural tissues.

The histopathologic background of the different symptoms in compression of the canine spinal cord can not be discussed on the basis of the cases examined. Further studies of these changes are necessary, especially of those causing only slight clinical symptoms. Because of the fairly good prognosis in many of these cases, difficulties will, however, arise in obtaining postmortem examinations, but studies are in progress and will be continued.

CONCLUSIONS

  1. A sudden, powerful compression of the canine spinal cord, even of short duration, may cause irreversible changes.

  2. Through its inflammatory effect, a dynamic factor seems to be more responsible for the maintenance of symptoms than the actual compression.

  3. Static compression of the spinal cord seems to be of little significance in maintaining the symptoms.

  4. Any method of treatment that will eliminate the dynamic factor and thus reduce the inflammatory reaction seems to be of greater therapeutic value than the direct surgical removal of the protrusion.

  5. Fenestration of the disc appears to fulfill the requirements necessary for elimination of the dynamic factor.

SUMMARY

A study on protrusion of intervertebral discs in the dog is reported. Special reference is made to 40 cases of cervical disc protrusions. The author emphasizes the importance of the dynamic and inflammatory factors for the maintenance of symptoms. A static compression, even of quite remarkable extent, is tolerated relatively well in most cases.

REFERENCES

  • 1.

    DexlerH. Beiträge zur Pathologie und pathologischen Anatomie der Compressionsmyelitis des Hundes. Öst. Z. wiss. Veterinärk.18967: 1124.DexlerÖst. Z. wiss. Veterinärk.7: 1–124.

  • 2.

    FrauchigerE.FankhauserR. Die Nervenkrankheiten unserer Hunde. Bern: H. Huber1949184 pp.FrauchigerFankhauserBern: H. Huber

  • 3.

    HansenH. J. A pathologic-anatomical study on disc degeneration in dog, with special reference to the so-called enchondrosis intervertebralis. Acta orthopaed. scand.1952suppl. 11117 pp.HansenActa orthopaed. scand.

  • 4.

    HansenH. J.OlssonS.-E. The indications for disc fenestration in dog. Proc. XV Internat. Vet. Congr. (Stockholm)1953part 12: 938943.HansenOlssonProc. XV Internat. Vet. Congr. (Stockholm)2: 938–943.

  • 5.

    OlssonS.-E. Observations concerning disc fenestration in dogs. Acta orthopaed. scand.195120: 349356.OlssonActa orthopaed. scand.20: 349–356.

  • 6.

    OlssonS.-E. On disc protrusion in dog (enchondrosis intervertebralis). A study with special reference to roentgen diagnosis and to the value of disc fenestration. Acta orthopaed. scand.1951suppl. 895 pp.OlssonActa orthopaed. scand.

  • 7.

    OlssonS.-E.HansenH.-J. Cervical disc protrusions in the dog. J. Amer. vet. med. Ass.1952121: 361370.OlssonHansenJ. Amer. vet. med. Ass.121: 361–370.

  • 8.

    TarlovI. M. Spinal cord compression studies. III. Time limits for recovery after gradual compression in dogs. 195471: 588597.Tarlov71: 588–597.

  • 9.

    TarlovI. M.KlingerH. Spinal cord compression studies. II. Time limits for recovery after acute compression in dogs. 195471: 271290.TarlovKlinger71: 271–290.

  • 10.

    TarlovI. M.KlingerH.VitaleS. Spinal cord compression studies. I. Experimental. 195370: 813819.TarlovKlingerVitale70: 813–819.

Article Information

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Figures

  • View in gallery

    Lateral roentgenogram of part of cervical spine of a dog showing the following changes: calcification of discs C2–C3, C3–C4, and C4–C5. The latter disc shows a narrowed space. The dog had typical symptoms of spinal cord compression and, though there was little doubt that disc C4–C5 had protruded, myelography was performed to demonstrate the lesion. After cisternal puncture through the suboccipital foramen, 0.7 cc. of Thorotrast was injected. After a few minutes in a tilted position with the head high, the dog was X-rayed. The spinal cord is nicely outlined and there is a complete block (A) at the level of disc C4–C5.

  • View in gallery

    A part of the left half of a frozen spine with the spinal cord in situ. Disc C3–C4 has protruded. The protrusion as well as the compression of the cord is of considerable size. The disc is narrowed in comparison with the surrounding discs. The nuclei pulposi of the discs in the picture are all calcified. The protrusion is of the type that, despite its size, gives rise to only slight symptoms.

  • View in gallery

    Microphotograph of dorsocentral part of spinal cord at site of compression caused by an acute disc protrusion. The gross appearance of the protrusion is shown in Fig. 10. In the right dorsal column there is a circumscribed area of malacia and in the left a less pronounced diffuse malacia. Mahon's stain for myelin sheaths, ×154.

  • View in gallery

    Microphotograph of parts of a 10-day-old disc protrusion and of the compressed cord (upper right). (The cord was compressed to more than two-thirds of its normal area of transection and the dog suffered from a complete posterior paralysis.) The light-stained portion of the protrusion consists of chondroid nucleus pulposus tissue, showing the typical cell pattern. The dark-stained areas are mainly calcified tissue. The cord shows a compact structure because of the compression. See further Fig. 15. Hemalum-eosin, ×148.

  • View in gallery

    Greater magnification of the cord shown in Fig. 14. Ventral part of right dorsal column to the left and grey commissure to the right. The tissue is more compact than normal because of compression. Malacia and increase in number of glia cells is well demonstrated. In the lower left corner is a part of the dorsal septum with a vessel showing perivascular reaction. Moreover there is a great number of minute vessels scattered in the cord tissue and marked neuronophagia. Hemalum-eosin, ×506.

  • View in gallery

    Part of the dorsal spine of a dog, seen from the dorsal side; the neural arches and spinal cord have been removed. There are two disc protrusions: one chronic on L2–L3 (to the left) and one acute on L3–L4. The chronic protrusion caused an attack of paresis nearly 1 year prior to death, which was caused by the acute protrusion. The difference between the two protrusions is obvious. To the left side of the chronic protrusion is shown the dorsal surface of a normal disc.

  • View in gallery

    Lateral roentgenogram showing calcification of C2–C3 and a dorsal rupture of the annulus fibrosus. Calcified nucleus tissue has found its way out through the rupture, allowing the rupture to be demonstrated. The protrusion is not dense enough to show on the picture. (The calcified disc tissue in the protrusion is responsible for an eventual density of the protrusion. The density of the disc tissue is decreased if in a protrusion this tissue is intermingled with hemorrhages and inflammatory cells.) The disc space seems to be normal. The fenestration of a disc like this and a removal of the nucleus pulposus will prevent further protrusion and relieve pain in a few days.

  • View in gallery

    The same dog as in Fig. 2. The roentgenogram was taken a week after operation when the dog was free of pain. The calcified protrusion was completely removed. Part of the removed nucleus pulposus can be seen as a slight density in the soft tissue on the ventral side of the disc.

  • View in gallery

    This roentgenogram is from a dog with rather severe symptoms of compression of the cervical spinal cord. Disc C2–C3 is calcified, slightly narrowed and protruded (A). The rather big protrusion can be seen as a long, slightly dense, curved shadow above disc C2–C3. The dog was treated conservatively and sent home in a somewhat improved condition 2 weeks later. While at home it made a sudden movement of the head and was stricken with severe pain and paresis. After a slow recovery of nearly 6 weeks, the dog regained complete health. See further Figs. 5, 6 and 7.

  • View in gallery

    Ventrodorsal roentgenogram of the same dog as in Fig. 4, taken the same day.

  • View in gallery

    Roentgenograms taken 2 months after the ones in Figs. 4 and 5. The entire calcified nucleus pulposus of C2–C3 has been pressed out of the disc and has contributed to a considerable enlargement of the protrusion (A). This obviously happened when the dog had the relapse of pain and paresis. It must be emphasized that this dog showed no signs of spinal cord compression when this particular roentgenogram was taken.

  • View in gallery

    Ventrodorsal picture of same dog as in Figs. 4, 5 and 6. The large, calcified protrusion at C2–C3 is easily demonstrated, as well as the narrowing of the disc. Compared with Fig. 5 this roentgenogram reveals what has happened during the interval between the two roentgen-ray examinations. The disc has reached a final state. There is nothing left to protrude. Although the protrusion is of a remarkable size with a marked degree of cord compression, stabilization has been attained; the compression is static, and symptoms have disappeared. This roentgenogram was taken the same day as the one in Fig. 6.

  • View in gallery

    Roentgenogram showing the following changes of disc C4–C5: calcification of the entire nucleus pulposus, a rupture in the annulus fibrosus and a small calcified protrusion. The dog suffered from rather severe pain, but it was decided that conservative treatment should be tried. Pain persisted, however, and the dog was admitted to the clinic and reexamined (see Fig. 9).

  • View in gallery

    Cervical spine of the same dog as in Fig. 8. There is an interval of 3 weeks between the two roentgen-ray examinations. A narrowing of disc C4–C5 and a slight increase in size of the protrusion have taken place since the roentgenogram of Fig. 8 was taken. The continuous protrusion of the disc during the interval was probably responsible for the persistence of pain.

  • View in gallery

    A part of the right half of the spine of a dog. The specimen was frozen, sawed in the sagittal plane and fixed in formalin. The cord has been severely damaged by a protrusion (B) of disc L1–L2 (C). The space of the latter disc is narrowed in comparison to that of T13–L1 (A). (The nucleus pulposus in the young animal is very hydrophilic. In the ageing dog this is less pronounced. In this dog all the discs swelled over the cut surface when fixed in formaldehyde except the protruded one.) The measurable compression of the cord in this case is not great, but, nevertheless, there is myelomalacia with subarachnoidal hemorrhage. The protrusion consists of two parts, one firm and chronic under the dorsal longitudinal ligament and one loose, and acute spread out on the body of L1. The changes extend to the upper cervical portion of the cord. Paraplegia was sudden, and the dog died in 2 days.

References

1.

DexlerH. Beiträge zur Pathologie und pathologischen Anatomie der Compressionsmyelitis des Hundes. Öst. Z. wiss. Veterinärk.18967: 1124.DexlerÖst. Z. wiss. Veterinärk.7: 1–124.

2.

FrauchigerE.FankhauserR. Die Nervenkrankheiten unserer Hunde. Bern: H. Huber1949184 pp.FrauchigerFankhauserBern: H. Huber

3.

HansenH. J. A pathologic-anatomical study on disc degeneration in dog, with special reference to the so-called enchondrosis intervertebralis. Acta orthopaed. scand.1952suppl. 11117 pp.HansenActa orthopaed. scand.

4.

HansenH. J.OlssonS.-E. The indications for disc fenestration in dog. Proc. XV Internat. Vet. Congr. (Stockholm)1953part 12: 938943.HansenOlssonProc. XV Internat. Vet. Congr. (Stockholm)2: 938–943.

5.

OlssonS.-E. Observations concerning disc fenestration in dogs. Acta orthopaed. scand.195120: 349356.OlssonActa orthopaed. scand.20: 349–356.

6.

OlssonS.-E. On disc protrusion in dog (enchondrosis intervertebralis). A study with special reference to roentgen diagnosis and to the value of disc fenestration. Acta orthopaed. scand.1951suppl. 895 pp.OlssonActa orthopaed. scand.

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