- Email: [email protected]
SPINAL-CORD DAMAGE FROM HYPEREXTENSION INJURY IN CERVICAL SPONDYLOSIS
687
minute caused loss of systolic ejection force from the left ventricle. We believe that the generator described here fulfils these criteria.
Appendix The main problems to be solved in
pacemaker
designing the implantable
were:
1. Long-term electrical reliability. 2. The best packaging for the least weight and volume. 3. A reliable plug and socket between the leads. 4. A mechanically and electrically reliable lead.
Temporary external control of pulse-rate. Electrical reliability is a function of the number of components. The Pye pacemaker contains a complementary transistor, a stable multivibrator circuit containing two transistors, four resistors, three condensers, and five batteries. The external control is accomplished through a tuned circuit and crystal rectifier producing an auxiliary bias voltage for the multivibrator circuit. By suitable packaging of the components a weight of 3-5 oz. has been placed in a volume of 2-8 c. in, The pacemaker will deliver a 5 V pulse across 1000 ohms at a rate of 60 per min. for about 5 years. Pulse width is 2 msec. The connection between the leads and pacemaker, which must be proof against body fluids is a large-area low-contact pressure screwjoint. The body fluids are excluded by coating the lead end with a thin fihn of silicone grease and also by the pressure of the silicone rubber case on the end of the lead (this is a precaution against the possibility of faulty administration of the silicone grease). The lead and electrode is a major problem in pacemaker reliability and a multi-helix stainless-steel polyethylene insulated lead, with a Sat, slightly convex platinum disc electrode (for good tissue-electrode contact pressure) was chosen. The electrode is 0-325 in. diameter and C’125 in. thick. The multi-helix design was attractive because a number of conductors in parallel gives an added safety factor. By means of a control unit and an externally applied coil, mounted in a silicone rubber pad (fig. 3), the pulse-rate may be reduced to 5.
30 pulses per min. without needing to take out leads through the skin and thereby incurring the risk of infection. The pacemaker is shown in fig. 4.
about
We acknowledge gratefully the help provided in the Western Infirmary by Sir Charles Illingworth, and in the Southern General Hospital by Mr. R. B. Wright and Dr. S. Lazarus; the constant encouragement of Dr. J. M. A. Lenihan, regional physicist, Western Regional Hospital Board; and the assistance of Mr. D. Q. Fuller of Messrs. Pye Ltd., whose cooperation enabled us to develop the pacemaker into its present form. REFERENCES
Chardack, W. M., Gage, A. A., Greatbatch, W. (1960) Surgery, 48, 643. — — — (1961) J. thorac. Surg. 42, 814. Elmquist, R., Senning, A. Proceedings 2nd International Conference of Cardiology. Paris, 1959. Furman, S., Robinson, G. (1958) Surg. Forum, 9, 245. Glenn, W. W. L., Mauro, A., Longo, E., Lavietes, P. H., Mackay, F. (1959) New Engl. J. Med. 261, 948. Kantrowitz, A., Cohen, R., Railland, H., Schunt, J. (1961) Circulation, 24, 967. Serming, A. (1959) J. thorac. Surg. 38, 639. Weirich, W. L., Paneth, M., Gott, V. L., Lillehei, C. W. (1958) Circulat. Res. 6, 410. Zoll, P. M. (1952) New Engl. J. Med. 247, 768. Frank, H. A., Zaisky, L. R. N., Linenthal, A. J., Belgard, A. H. (1961) Ann. Surg. 154, 330. Linenthal, A. J. (1960) Circulation, 22, 341. —
—
SPINAL-CORD DAMAGE FROM HYPEREXTENSION INJURY IN CERVICAL SPONDYLOSIS M.D.
J. TREVOR HUGHES Manc., M.R.C.P.E., D.C.P.,
D.Path.
NEUROPATHOLOGIST
BETTY BROWNELL M.B. Dubl. RADCLIFFE INFIRMARY, OXFORD
IN accounts of damage to the spinal cord associated with cervical spondylosis, published by neurologists (Allen 1952, Bedford et al. 1952, Brain et al. 1952, Spillane and Lloyd 1952, Mair and Druckman 1953, Symonds 1953, Pallis et al. 1954) and by orthopxdic surgeons (Barnes 1948, Taylor and Blackwood 1948) the cases fall into three groups: (1) A group in which no history of trauma was elicited.
(2) A group in which injury was followed by slow progression of symptoms (often over years) which ultimately proved to be due to cervical spondylosis. The cases in this group suggest that trauma may initiate the cartilaginous and bony changes of cervical spondylosis. (3) A group in which injury to the cervical spine was followed by immediate severe damage to the cervical spinal cord, and in which investigation revealed coincident cervical spondylosis of long standing. Fig. 3-Control
We record here the necropsy findings in 3 cases belonging to this third group. We use the term " cervical spondylosis " to denote only the bony and cartilaginous deformity, as shown in radiographs, at operation, or at
unit.
necropsy.
Case-reports Case 1 A man, aged 79, fell down in the street and was brought into hospital in a confused state, with a laceration on his nose and flaccid paralysis of his arms. Over the next forty-eight hours the paralysis spread to his legs, and he developed a sensory level at c5. The physical signs were asymmetrical, with predominant motor loss on the right, and sensory loss on the left. He died seven weeks after his fall.
Fig, 4-Generator, electrodes,
and leads.
Necropsy Necropsy (J. T. H.) revealed bilateral bronchopneumonia, chronic pyelonephritis, and generalised atherosclerosis which had caused cerebral atrophy with multiple small infarcts. Cervical spine.-There was partial fusion of the vertebral bodies c2 and c3, and tearing of the disc between c3 and c4
688
Fig.1
Fig.2
Fig. 1-Case 1: spinal canal opened from its posterior aspect.
Fig. 3-Case 1: anterior aspect of spinal corresponding to bulge seen in fig. 1.
cord indented at C4-5
with thickening of the posterior longitudinal ligament. Gross cervical spondylosis severely narrowed the spinal canal in its anteroposterior diameter from c3 to Tl, and two transverse cartilaginous bars protruded 0-2 cm. backwards into the canal from the discs between c3 and c4, and c7 and Tl. A decalcified sagittal section through the cervical spine showed the tear extending through the c3-4 disc (the torn edges showing necrosis) and the anterior longitudinal ligament (embedded in vascular granulation tissue), but stopping at the posterior longitudinal ligament which was intact (figs. 1 and 2). Spinal cord.-The anterior aspect was severely indented at c4-5 segments, and a transverse cut here showed a softened region only 0-5 cm. in its longitudinal extent (fig. 3).
Fig.3
Fig. 2-Case 1: cervical spine cut sagittally with spinal cord in situ. Note fusion of c2 and c3 vertebral bodies, and transverse tear through c3-4 intervertebral disc which shows a spondylotic bulge into anterior aspect of spinal cord.
Histological examination.-C2, 3, and 4 segments showed early wallerian degeneration in the posterior columns and there were ischasmic changes (shrinkage and pyknotic staining) in the anterior-horn neurones of c3 and c4 (fig. 4). The damage was most severe at the level c4 and c5, but asymmetrical (greater on the left), and involved the whole of the grey matter and adjacent white matter of all three white columns. The damaged area contained no neurones-neither cell bodies nor axons-and contained lipid phagocytes amongst young capillaries. The anterior nerve-roots were atrophied but the posterior nerveroots were intact. The leptomeninges were thickened and there
of the three casd. Fig. 4-Drawings from camera-lucida tracings of transverse sections through spinal cord at various segmental levels side of cord appears from above viewed sections Cord (left area-wallerian degeneration. Shaded area-region of necrosis. Stippled on
right).
689 was
heavy hasmosiderin deposition. In the segments c5
to
T2
early wallerian degeneration could be detected in both crossedprramidal tracts. The anterior-horn neurones showed ischsmic changes. Case2 A woman of 74 fell out of bed whilst she was in hospital undergoing investigation for mental deterioration and amnesia. Immediately after the fall there was no evidence of injury, but over the next twenty-four hours paralysis developed in all four limbs, with a sensory level in the mid-cervical region. The patient was treated by immobilisation of the neck in a collar; but her condition did not improve, and she died five months
after her fall.
-vecropsy
Necropsy (Dr. W. S. Killpack, King Edward Hospital, Ealing) revealed cystitis, ascending pyelonephritis, and mild generalised cerebral atrophy. Cervical spine.-Gross cervical spondylosis narrowed the anteroposterior diameter of the- spinal canal from c4 to c7 (fig. 5), and large transverse cartilaginous bars protruded backwards into the canal from discs c4-5, c5-6, and c6-7. c5-6 disc was torn, the tear being seen in a decalcified sagittal section to extend through the disc and the anterior longitudinal ligament which was now united only by granulation tissue. Spinal cord.-There was damage and softening of the c7 segment and the lower part of c6.
Histological examination.-Segments
c2
to
c5
showed
wallerian degeneration indicative of a total cord transection below (fig. 4). There were also minor changes suggesting ischemia, seen principally in the anterior-horn neurones, but added to in segments c4 and c5 by small areas of necrosis in the lateral columns. In segment c6, besides wallerian degeneration, there was a large area of necrosis in the left grey horn and left lateral column. The whole
spinal cord was destroyed in the upper part of segment c7, with
surviving myelin and nerve-fibres found only in a narrow rim
anteriorly and posteriorly. The remainder
was
completely necrosed
and
replaced by lipid phagocytes on a framework of vascular connective tissue. Neurones were absent, and the anterior nerveroots
were
atrophied and devoid of nerve-fibres. The F8· 5--Case 2: lateral aspect of cervical spine (sawn
Soinal
sagittally). canal narrowed
anteroposteriorly by spondylosis affecting c4-5, c5-6, and
ce:",ica1 cf,7 discs.
Note transverse
tear
of c5-6 disc
nature
and extent of damage in this section sug-
gested
trauma.
In the lower part of c7 the
xiated with largest spondylotic protrusion
damage
Nrresponding to region
less
of
spinal
cord
damage.
was
extensive
confined mainly to the anterior half of the cord, but in irregular manner with fibres preserved in the anterior columns. Neurones were absent on the right, and only a few remained on the left. The principal abnormality in c8 and Tl segments was loss of pyramidal-tract fibres, due to wallerian degeneration. In addition, there were minor ischaemic changes consisting chiefly in depletion of neurones in the anterior horns. Case 3 A man, aged 59, fell forwards out of a chair, striking his face on a cupboard. After the fall he was unable to move his limbs, and, on admission to hospital twenty-four hours later, he was found to be quadriplegic with a sensory level at c5. Two weeks later laminectomy from c4 to c7 was performed. The only abnormal finding was narrowing of the spinal canal, particularly at the c5-6 disc space. No further operative treatment was carried out, and the patient’s condition remained unchanged until his death three weeks after the fall.
and
was
an
Necropsy Necropsy (Dr. D. Sennefelder, Nervenklinik, Frankfurt) showed multiple pulmonary infarcts due to emboli from thrombosed leg veins. The brain was affected by mild atherosclerotic atrophy. Cervical spine.-The spinal canal from c3 to c7 was narrowed anteroposteriorly by cervical spondylosis with added bulges related to c2-3, c3-4, c4-5, and c5-6 discs. Associated with the c5-6 disc, which was torn, was the largest protrusion which was roughened by operative interference. A decalcified sagittal section of the cervical spine showed the tear extending through the c5-6 disc and both anterior and posterior longitudinal
ligaments. Spinal cord.-The cord was indented anteriorly by the spondylotic protrusions, the largest deformity being between c6-7 segments where a transverse cut showed softening. Histological examination.-There was early wallerian degeneration in the posterior and lateral columns from c2 to c5 (fig. 4). There were three distinct areas of necrosis with blood extravasation. Each posterior horn contained an area of myelin and fibre destruction, and a further area was present lateral to the intermediate grey matter on the right side. In the right anterior horn three motoneurones were affected by central chromatolysis (axon reaction). The damage was more generalised in segment c6 than in c5 with three discrete areas of necrosis, one in the posterior columns and one in each lateral column. As in c5, chromatolytic cells were seen in the right anterior horn. These findings of axon section might have been due to injury of the intraspinal part of the anterior nerve-root. An alternative explanation is that the nerve-roots could have been damaged at operation. The damage was greatest in the upper part of c7, with surviving areas of the cord confined to a little on either side of the grey commissure and’ in the adjacent anterior columns. The remainder of the spinal cord had undergone necrosis with many dilated vessels among the lipid phagocytes. Damage to the white matter was less in the lower part of c7 and in c8, but the grey matter showed changes suggestive of hsemorrhagic infarction. The surviving neurones in the anterior horns showed ischamlic changes. The spinal-cord necrosis was seen only in discrete round areas at Tl and T2. The grey matter showed ischaemic changes also present in T3. CLINICAL DETAILS
In its essential features the history was the same in all three cases. An elderly person fell forward, striking the face with considerable violence, the deduction being that a strong sudden force applied hyperextension to the cervical spine. The result was a partial cord transection, developing swiftly in case 3 and more slowly in case 1 and case 2. Subsequent X-rays showed severe cervical spondylosis, but no evidence of fracture or displacement. Myelography in case 2 and case 3 showed a hold-up of radio-opaque material in the region of the c5-6 disc space, but was normal in case 1. In each, severe cervical spondylosis was found in the
690 form of multiple transverse bars projecting backwards into the spinal canal (figs. 1, 2, and 5). In case 2 and case 3, the largest bulges were associated with the c5-6 disc, in case 1 with the c3-4 disc. The affected disc in all showed evidence of traumatic tearing. In case 1, the vertebral bodies of c2 and c3 were partially fused. The findings in the spinal cord, similar in all three cases, can be considered under three headings-namely, direct trauma, wallerian degeneration, and ischxmic changes. In the region of greatest damage the findings pointed irresistibly to a direct traumatic lesion. The cord was indented and contused in an area corresponding exactly to the largest spondylotic bulge which arose from the torn intervertebral disc, and which suggested that this was the point where the spine was abnormally hinged at the time of injury (figs. 1, 2, and 3). The transverse sections of the spinal cord showed a well-demarcated area of damage, irregular in outline, and not corresponding to any arterial territory. Above and below this traumatic lesion was wallerian degeneration. Ischsemic changes in the neurones of the anterior horn were prominent above and below the site of greatest damage, principally below in case 1 and case 3, and principally above in case 2. In all three cases the vertebral arteries were examined and found
normal. Discussion
Barnes
in
an analysis of 22 cases of paraplegia (1948), caused by injury to the cervical spine, found that in 7 the injury was thought to be due to hyperextension. Only 1 of these showed dislocation; the remaining 6 had no radiological evidence of displacement or bony injury, but all were remarkable in displaying severe degenerative disease of the cervical spine. In 2 of Barnes’ fatal cases there was at necropsy a tear extending horizontally through the intervertebral disc and anterior longitudinal ligament. His group of 15 flexion injuries was strikingly different: 8 had dislocation ; 4 had a crush fracture of a vertebral body; and, in 3, acute retropulsion of an intervertebral disc was thought to have occurred. The age-distribution was equally striking. All the patients with paraplegia from hyperextension injury were over 57 years, whereas the patients with flexion injuries with paraplegia were all below 50. Our three cases were in patients aged 79, 74, and 59. Brain et al. (1952) stated that their 45 cases of cervical spondylosis included 8 where the spinal-cord damage occurred suddenly as a sequel to injury of the cervical spine by hyperextension, though no details of the manner of injury were given. Of the 21 patients of Spillane and Lloyd (1952) 2 had a history of injury which might have damaged the cord. Symonds (1953) gave several instances of spinal-cord damage where cervical spondylosis was complicated by trauma due to hyperextension of the cervical spine, either from a forward fall or by manipulation under anaesthesia. Our case 1 had fusion of c2 and c3 vertebral bodies, with the site of trauma and severest spondylotic change immediately below this at the c3-4 disc. This congenital malformation of vertebral-body fusion has been encountered repeatedly in reported cases of myelopathy associated with cervical spondylosis. It was present in 3 of the 45 cases of Brain et al. (1952), in cases 1 and 2 of Mair and Druckman (1953), and in case 1 of Symonds (1953). In these last three instances where details were given, the spondylotic protrusion was, as in our case 1, greatest immediately below the fused vertebral bodies. From the necropsy findings in our own three cases,
forcible hyperextension applied to the spondylotic cervical spine of an elderly person seemed to have torn a weakened intervertebral disc, and the angulation so produced had caused crushing of the spinal cord by pressure of a spondylotic bulge into a narrowed spinal canal. There were ischxmic effects; but these were thought to be secondary, possibly to oedema and swelling of the spinal cord within a narrowed spinal canal. Clearly, even mild hyperextension of the cervical spine is dangerous in an elderly person with spondylosis, and this hazard is further increased by anaesthesia. The common practice of limiting neck movements in the myelopathy due to cervical spondylosis is justified: not only does this partial immobilisation of the cervical spine arrest the progress of the myelopathy, but it also provides an added safeguard against the hazard of a forward fall.
Summary In three fatal cases of hyperextension injury complicating cervical spondylosis the cord was transected near the largest transverse bar of the cervical- spondylosis. The associated intervertebral disc was torn, which suggested that hinging of the cervical spine took place here at the time of trauma. The effects of ischsemia were thought to be secondary to the main lesion produced by direct trauma. In one case there was fusion of c2 and c3 vertebral bodies, with most spondylosis and laceration at the c3-4 disc, immediately below. For permission to use necropsy material and reports we thank the Max-Planck Institut fiir Hirnforschung, Frankfurt, through the courtesy of its director, Prof. Dr. W. Krucke, who made case 3 available; and Dr. W. S. Killpack, pathologist, King Edward Memorial Hospital, Ealing (case 2). We are grateful also to Mr. J. C. Scott and Mr. J. M. Potter, of the Radcliffe Infirmary, for the clinical details of case 1; and to Mr. E. L. Tugwell for photographic assistance. One of us (B. B.) is in receipt cf a grant from the National Fund for research into poliomyelitis and other crippling diseases. REFERENCES
Allen, K. L. (1952) J. Neurol. Psychiat. 15, 20. Barnes, R. (1948) J. Bone Jt Surg. 30B, 234. Bedford, P. D., Bosanquet, F. D., Russell, W. R. (1952) Lancet, ii, 55. Brain, W. R., Northfield, D., Wilkinson, M. (1952) Brain, 75, 187. Mair, W. G. P., Druckman, R. (1953) ibid. 76, 70. Pallis, C., Jones, A. M., Spillane, J. D. (1954) ibid. 77, 274. Spillane, J. D., Lloyd, G. H. T. (1952) ibid. 75, 177. Symonds, C. (1953) Lancet, i, 451. Taylor, A. R., Blackwood, W. (1948) J. Bone Jt Surg. 30B, 245.
EVALUATION OF THE PYROGEN TEST IN CHRONIC PYELONEPHRITIS
J. Z. MONTGOMERIE M.B. N.Z., M.R.A.C.P. REGISTRAR
J. D. K. NORTH M.B. N.Z., D.Phil. Oxon, M.R.C.P., M.R.A.C.P. PHYSICIAN-IN-CHARGE
MEDICAL
UNIT, AUCKLAND HOSPITAL, AUCKLAND
Pears and Houghton introduced the pyrogen test in 1959. They showed that, in patients with chronic pyelonephritis, the number of white cells excreted in,the urine increases after intravenous injection of pyrogen. This test has been regarded as useful in the diagnosis of chronic pyelonephritis (Hutt et al. 1961, Pinkerton et al. 1961). To assess the value of the test, it is important to know how frequently results are negative in chronic pyelonephritis. how specific the test is for chronic pyelonephritis, and what spontaneous variation in the urinary excretion of white cells occurs independently of pyrogen injection. In this paper we report our experience of the pyrogen test
in 51
patients.
minute caused loss of systolic ejection force from the left ventricle. We believe that the generator described here fulfils these criteria.
Appendix The main problems to be solved in
pacemaker
designing the implantable
were:
1. Long-term electrical reliability. 2. The best packaging for the least weight and volume. 3. A reliable plug and socket between the leads. 4. A mechanically and electrically reliable lead.
Temporary external control of pulse-rate. Electrical reliability is a function of the number of components. The Pye pacemaker contains a complementary transistor, a stable multivibrator circuit containing two transistors, four resistors, three condensers, and five batteries. The external control is accomplished through a tuned circuit and crystal rectifier producing an auxiliary bias voltage for the multivibrator circuit. By suitable packaging of the components a weight of 3-5 oz. has been placed in a volume of 2-8 c. in, The pacemaker will deliver a 5 V pulse across 1000 ohms at a rate of 60 per min. for about 5 years. Pulse width is 2 msec. The connection between the leads and pacemaker, which must be proof against body fluids is a large-area low-contact pressure screwjoint. The body fluids are excluded by coating the lead end with a thin fihn of silicone grease and also by the pressure of the silicone rubber case on the end of the lead (this is a precaution against the possibility of faulty administration of the silicone grease). The lead and electrode is a major problem in pacemaker reliability and a multi-helix stainless-steel polyethylene insulated lead, with a Sat, slightly convex platinum disc electrode (for good tissue-electrode contact pressure) was chosen. The electrode is 0-325 in. diameter and C’125 in. thick. The multi-helix design was attractive because a number of conductors in parallel gives an added safety factor. By means of a control unit and an externally applied coil, mounted in a silicone rubber pad (fig. 3), the pulse-rate may be reduced to 5.
30 pulses per min. without needing to take out leads through the skin and thereby incurring the risk of infection. The pacemaker is shown in fig. 4.
about
We acknowledge gratefully the help provided in the Western Infirmary by Sir Charles Illingworth, and in the Southern General Hospital by Mr. R. B. Wright and Dr. S. Lazarus; the constant encouragement of Dr. J. M. A. Lenihan, regional physicist, Western Regional Hospital Board; and the assistance of Mr. D. Q. Fuller of Messrs. Pye Ltd., whose cooperation enabled us to develop the pacemaker into its present form. REFERENCES
Chardack, W. M., Gage, A. A., Greatbatch, W. (1960) Surgery, 48, 643. — — — (1961) J. thorac. Surg. 42, 814. Elmquist, R., Senning, A. Proceedings 2nd International Conference of Cardiology. Paris, 1959. Furman, S., Robinson, G. (1958) Surg. Forum, 9, 245. Glenn, W. W. L., Mauro, A., Longo, E., Lavietes, P. H., Mackay, F. (1959) New Engl. J. Med. 261, 948. Kantrowitz, A., Cohen, R., Railland, H., Schunt, J. (1961) Circulation, 24, 967. Serming, A. (1959) J. thorac. Surg. 38, 639. Weirich, W. L., Paneth, M., Gott, V. L., Lillehei, C. W. (1958) Circulat. Res. 6, 410. Zoll, P. M. (1952) New Engl. J. Med. 247, 768. Frank, H. A., Zaisky, L. R. N., Linenthal, A. J., Belgard, A. H. (1961) Ann. Surg. 154, 330. Linenthal, A. J. (1960) Circulation, 22, 341. —
—
SPINAL-CORD DAMAGE FROM HYPEREXTENSION INJURY IN CERVICAL SPONDYLOSIS M.D.
J. TREVOR HUGHES Manc., M.R.C.P.E., D.C.P.,
D.Path.
NEUROPATHOLOGIST
BETTY BROWNELL M.B. Dubl. RADCLIFFE INFIRMARY, OXFORD
IN accounts of damage to the spinal cord associated with cervical spondylosis, published by neurologists (Allen 1952, Bedford et al. 1952, Brain et al. 1952, Spillane and Lloyd 1952, Mair and Druckman 1953, Symonds 1953, Pallis et al. 1954) and by orthopxdic surgeons (Barnes 1948, Taylor and Blackwood 1948) the cases fall into three groups: (1) A group in which no history of trauma was elicited.
(2) A group in which injury was followed by slow progression of symptoms (often over years) which ultimately proved to be due to cervical spondylosis. The cases in this group suggest that trauma may initiate the cartilaginous and bony changes of cervical spondylosis. (3) A group in which injury to the cervical spine was followed by immediate severe damage to the cervical spinal cord, and in which investigation revealed coincident cervical spondylosis of long standing. Fig. 3-Control
We record here the necropsy findings in 3 cases belonging to this third group. We use the term " cervical spondylosis " to denote only the bony and cartilaginous deformity, as shown in radiographs, at operation, or at
unit.
necropsy.
Case-reports Case 1 A man, aged 79, fell down in the street and was brought into hospital in a confused state, with a laceration on his nose and flaccid paralysis of his arms. Over the next forty-eight hours the paralysis spread to his legs, and he developed a sensory level at c5. The physical signs were asymmetrical, with predominant motor loss on the right, and sensory loss on the left. He died seven weeks after his fall.
Fig, 4-Generator, electrodes,
and leads.
Necropsy Necropsy (J. T. H.) revealed bilateral bronchopneumonia, chronic pyelonephritis, and generalised atherosclerosis which had caused cerebral atrophy with multiple small infarcts. Cervical spine.-There was partial fusion of the vertebral bodies c2 and c3, and tearing of the disc between c3 and c4
688
Fig.1
Fig.2
Fig. 1-Case 1: spinal canal opened from its posterior aspect.
Fig. 3-Case 1: anterior aspect of spinal corresponding to bulge seen in fig. 1.
cord indented at C4-5
with thickening of the posterior longitudinal ligament. Gross cervical spondylosis severely narrowed the spinal canal in its anteroposterior diameter from c3 to Tl, and two transverse cartilaginous bars protruded 0-2 cm. backwards into the canal from the discs between c3 and c4, and c7 and Tl. A decalcified sagittal section through the cervical spine showed the tear extending through the c3-4 disc (the torn edges showing necrosis) and the anterior longitudinal ligament (embedded in vascular granulation tissue), but stopping at the posterior longitudinal ligament which was intact (figs. 1 and 2). Spinal cord.-The anterior aspect was severely indented at c4-5 segments, and a transverse cut here showed a softened region only 0-5 cm. in its longitudinal extent (fig. 3).
Fig.3
Fig. 2-Case 1: cervical spine cut sagittally with spinal cord in situ. Note fusion of c2 and c3 vertebral bodies, and transverse tear through c3-4 intervertebral disc which shows a spondylotic bulge into anterior aspect of spinal cord.
Histological examination.-C2, 3, and 4 segments showed early wallerian degeneration in the posterior columns and there were ischasmic changes (shrinkage and pyknotic staining) in the anterior-horn neurones of c3 and c4 (fig. 4). The damage was most severe at the level c4 and c5, but asymmetrical (greater on the left), and involved the whole of the grey matter and adjacent white matter of all three white columns. The damaged area contained no neurones-neither cell bodies nor axons-and contained lipid phagocytes amongst young capillaries. The anterior nerve-roots were atrophied but the posterior nerveroots were intact. The leptomeninges were thickened and there
of the three casd. Fig. 4-Drawings from camera-lucida tracings of transverse sections through spinal cord at various segmental levels side of cord appears from above viewed sections Cord (left area-wallerian degeneration. Shaded area-region of necrosis. Stippled on
right).
689 was
heavy hasmosiderin deposition. In the segments c5
to
T2
early wallerian degeneration could be detected in both crossedprramidal tracts. The anterior-horn neurones showed ischsmic changes. Case2 A woman of 74 fell out of bed whilst she was in hospital undergoing investigation for mental deterioration and amnesia. Immediately after the fall there was no evidence of injury, but over the next twenty-four hours paralysis developed in all four limbs, with a sensory level in the mid-cervical region. The patient was treated by immobilisation of the neck in a collar; but her condition did not improve, and she died five months
after her fall.
-vecropsy
Necropsy (Dr. W. S. Killpack, King Edward Hospital, Ealing) revealed cystitis, ascending pyelonephritis, and mild generalised cerebral atrophy. Cervical spine.-Gross cervical spondylosis narrowed the anteroposterior diameter of the- spinal canal from c4 to c7 (fig. 5), and large transverse cartilaginous bars protruded backwards into the canal from discs c4-5, c5-6, and c6-7. c5-6 disc was torn, the tear being seen in a decalcified sagittal section to extend through the disc and the anterior longitudinal ligament which was now united only by granulation tissue. Spinal cord.-There was damage and softening of the c7 segment and the lower part of c6.
Histological examination.-Segments
c2
to
c5
showed
wallerian degeneration indicative of a total cord transection below (fig. 4). There were also minor changes suggesting ischemia, seen principally in the anterior-horn neurones, but added to in segments c4 and c5 by small areas of necrosis in the lateral columns. In segment c6, besides wallerian degeneration, there was a large area of necrosis in the left grey horn and left lateral column. The whole
spinal cord was destroyed in the upper part of segment c7, with
surviving myelin and nerve-fibres found only in a narrow rim
anteriorly and posteriorly. The remainder
was
completely necrosed
and
replaced by lipid phagocytes on a framework of vascular connective tissue. Neurones were absent, and the anterior nerveroots
were
atrophied and devoid of nerve-fibres. The F8· 5--Case 2: lateral aspect of cervical spine (sawn
Soinal
sagittally). canal narrowed
anteroposteriorly by spondylosis affecting c4-5, c5-6, and
ce:",ica1 cf,7 discs.
Note transverse
tear
of c5-6 disc
nature
and extent of damage in this section sug-
gested
trauma.
In the lower part of c7 the
xiated with largest spondylotic protrusion
damage
Nrresponding to region
less
of
spinal
cord
damage.
was
extensive
confined mainly to the anterior half of the cord, but in irregular manner with fibres preserved in the anterior columns. Neurones were absent on the right, and only a few remained on the left. The principal abnormality in c8 and Tl segments was loss of pyramidal-tract fibres, due to wallerian degeneration. In addition, there were minor ischaemic changes consisting chiefly in depletion of neurones in the anterior horns. Case 3 A man, aged 59, fell forwards out of a chair, striking his face on a cupboard. After the fall he was unable to move his limbs, and, on admission to hospital twenty-four hours later, he was found to be quadriplegic with a sensory level at c5. Two weeks later laminectomy from c4 to c7 was performed. The only abnormal finding was narrowing of the spinal canal, particularly at the c5-6 disc space. No further operative treatment was carried out, and the patient’s condition remained unchanged until his death three weeks after the fall.
and
was
an
Necropsy Necropsy (Dr. D. Sennefelder, Nervenklinik, Frankfurt) showed multiple pulmonary infarcts due to emboli from thrombosed leg veins. The brain was affected by mild atherosclerotic atrophy. Cervical spine.-The spinal canal from c3 to c7 was narrowed anteroposteriorly by cervical spondylosis with added bulges related to c2-3, c3-4, c4-5, and c5-6 discs. Associated with the c5-6 disc, which was torn, was the largest protrusion which was roughened by operative interference. A decalcified sagittal section of the cervical spine showed the tear extending through the c5-6 disc and both anterior and posterior longitudinal
ligaments. Spinal cord.-The cord was indented anteriorly by the spondylotic protrusions, the largest deformity being between c6-7 segments where a transverse cut showed softening. Histological examination.-There was early wallerian degeneration in the posterior and lateral columns from c2 to c5 (fig. 4). There were three distinct areas of necrosis with blood extravasation. Each posterior horn contained an area of myelin and fibre destruction, and a further area was present lateral to the intermediate grey matter on the right side. In the right anterior horn three motoneurones were affected by central chromatolysis (axon reaction). The damage was more generalised in segment c6 than in c5 with three discrete areas of necrosis, one in the posterior columns and one in each lateral column. As in c5, chromatolytic cells were seen in the right anterior horn. These findings of axon section might have been due to injury of the intraspinal part of the anterior nerve-root. An alternative explanation is that the nerve-roots could have been damaged at operation. The damage was greatest in the upper part of c7, with surviving areas of the cord confined to a little on either side of the grey commissure and’ in the adjacent anterior columns. The remainder of the spinal cord had undergone necrosis with many dilated vessels among the lipid phagocytes. Damage to the white matter was less in the lower part of c7 and in c8, but the grey matter showed changes suggestive of hsemorrhagic infarction. The surviving neurones in the anterior horns showed ischamlic changes. The spinal-cord necrosis was seen only in discrete round areas at Tl and T2. The grey matter showed ischaemic changes also present in T3. CLINICAL DETAILS
In its essential features the history was the same in all three cases. An elderly person fell forward, striking the face with considerable violence, the deduction being that a strong sudden force applied hyperextension to the cervical spine. The result was a partial cord transection, developing swiftly in case 3 and more slowly in case 1 and case 2. Subsequent X-rays showed severe cervical spondylosis, but no evidence of fracture or displacement. Myelography in case 2 and case 3 showed a hold-up of radio-opaque material in the region of the c5-6 disc space, but was normal in case 1. In each, severe cervical spondylosis was found in the
690 form of multiple transverse bars projecting backwards into the spinal canal (figs. 1, 2, and 5). In case 2 and case 3, the largest bulges were associated with the c5-6 disc, in case 1 with the c3-4 disc. The affected disc in all showed evidence of traumatic tearing. In case 1, the vertebral bodies of c2 and c3 were partially fused. The findings in the spinal cord, similar in all three cases, can be considered under three headings-namely, direct trauma, wallerian degeneration, and ischxmic changes. In the region of greatest damage the findings pointed irresistibly to a direct traumatic lesion. The cord was indented and contused in an area corresponding exactly to the largest spondylotic bulge which arose from the torn intervertebral disc, and which suggested that this was the point where the spine was abnormally hinged at the time of injury (figs. 1, 2, and 3). The transverse sections of the spinal cord showed a well-demarcated area of damage, irregular in outline, and not corresponding to any arterial territory. Above and below this traumatic lesion was wallerian degeneration. Ischsemic changes in the neurones of the anterior horn were prominent above and below the site of greatest damage, principally below in case 1 and case 3, and principally above in case 2. In all three cases the vertebral arteries were examined and found
normal. Discussion
Barnes
in
an analysis of 22 cases of paraplegia (1948), caused by injury to the cervical spine, found that in 7 the injury was thought to be due to hyperextension. Only 1 of these showed dislocation; the remaining 6 had no radiological evidence of displacement or bony injury, but all were remarkable in displaying severe degenerative disease of the cervical spine. In 2 of Barnes’ fatal cases there was at necropsy a tear extending horizontally through the intervertebral disc and anterior longitudinal ligament. His group of 15 flexion injuries was strikingly different: 8 had dislocation ; 4 had a crush fracture of a vertebral body; and, in 3, acute retropulsion of an intervertebral disc was thought to have occurred. The age-distribution was equally striking. All the patients with paraplegia from hyperextension injury were over 57 years, whereas the patients with flexion injuries with paraplegia were all below 50. Our three cases were in patients aged 79, 74, and 59. Brain et al. (1952) stated that their 45 cases of cervical spondylosis included 8 where the spinal-cord damage occurred suddenly as a sequel to injury of the cervical spine by hyperextension, though no details of the manner of injury were given. Of the 21 patients of Spillane and Lloyd (1952) 2 had a history of injury which might have damaged the cord. Symonds (1953) gave several instances of spinal-cord damage where cervical spondylosis was complicated by trauma due to hyperextension of the cervical spine, either from a forward fall or by manipulation under anaesthesia. Our case 1 had fusion of c2 and c3 vertebral bodies, with the site of trauma and severest spondylotic change immediately below this at the c3-4 disc. This congenital malformation of vertebral-body fusion has been encountered repeatedly in reported cases of myelopathy associated with cervical spondylosis. It was present in 3 of the 45 cases of Brain et al. (1952), in cases 1 and 2 of Mair and Druckman (1953), and in case 1 of Symonds (1953). In these last three instances where details were given, the spondylotic protrusion was, as in our case 1, greatest immediately below the fused vertebral bodies. From the necropsy findings in our own three cases,
forcible hyperextension applied to the spondylotic cervical spine of an elderly person seemed to have torn a weakened intervertebral disc, and the angulation so produced had caused crushing of the spinal cord by pressure of a spondylotic bulge into a narrowed spinal canal. There were ischxmic effects; but these were thought to be secondary, possibly to oedema and swelling of the spinal cord within a narrowed spinal canal. Clearly, even mild hyperextension of the cervical spine is dangerous in an elderly person with spondylosis, and this hazard is further increased by anaesthesia. The common practice of limiting neck movements in the myelopathy due to cervical spondylosis is justified: not only does this partial immobilisation of the cervical spine arrest the progress of the myelopathy, but it also provides an added safeguard against the hazard of a forward fall.
Summary In three fatal cases of hyperextension injury complicating cervical spondylosis the cord was transected near the largest transverse bar of the cervical- spondylosis. The associated intervertebral disc was torn, which suggested that hinging of the cervical spine took place here at the time of trauma. The effects of ischsemia were thought to be secondary to the main lesion produced by direct trauma. In one case there was fusion of c2 and c3 vertebral bodies, with most spondylosis and laceration at the c3-4 disc, immediately below. For permission to use necropsy material and reports we thank the Max-Planck Institut fiir Hirnforschung, Frankfurt, through the courtesy of its director, Prof. Dr. W. Krucke, who made case 3 available; and Dr. W. S. Killpack, pathologist, King Edward Memorial Hospital, Ealing (case 2). We are grateful also to Mr. J. C. Scott and Mr. J. M. Potter, of the Radcliffe Infirmary, for the clinical details of case 1; and to Mr. E. L. Tugwell for photographic assistance. One of us (B. B.) is in receipt cf a grant from the National Fund for research into poliomyelitis and other crippling diseases. REFERENCES
Allen, K. L. (1952) J. Neurol. Psychiat. 15, 20. Barnes, R. (1948) J. Bone Jt Surg. 30B, 234. Bedford, P. D., Bosanquet, F. D., Russell, W. R. (1952) Lancet, ii, 55. Brain, W. R., Northfield, D., Wilkinson, M. (1952) Brain, 75, 187. Mair, W. G. P., Druckman, R. (1953) ibid. 76, 70. Pallis, C., Jones, A. M., Spillane, J. D. (1954) ibid. 77, 274. Spillane, J. D., Lloyd, G. H. T. (1952) ibid. 75, 177. Symonds, C. (1953) Lancet, i, 451. Taylor, A. R., Blackwood, W. (1948) J. Bone Jt Surg. 30B, 245.
EVALUATION OF THE PYROGEN TEST IN CHRONIC PYELONEPHRITIS
J. Z. MONTGOMERIE M.B. N.Z., M.R.A.C.P. REGISTRAR
J. D. K. NORTH M.B. N.Z., D.Phil. Oxon, M.R.C.P., M.R.A.C.P. PHYSICIAN-IN-CHARGE
MEDICAL
UNIT, AUCKLAND HOSPITAL, AUCKLAND
Pears and Houghton introduced the pyrogen test in 1959. They showed that, in patients with chronic pyelonephritis, the number of white cells excreted in,the urine increases after intravenous injection of pyrogen. This test has been regarded as useful in the diagnosis of chronic pyelonephritis (Hutt et al. 1961, Pinkerton et al. 1961). To assess the value of the test, it is important to know how frequently results are negative in chronic pyelonephritis. how specific the test is for chronic pyelonephritis, and what spontaneous variation in the urinary excretion of white cells occurs independently of pyrogen injection. In this paper we report our experience of the pyrogen test
in 51
patients.