Research section. Cervical spondylitic myelopathy, Clinico-radiological approach: Correlation with the Hemorheological parameters and vascular risk factors http://yassermetwally.com http://yassermetwally.net

1. THE CERVICAL SPONDYLITIC MYELOPATHY;A CLINICO-RADIOLOGICAL APPROACH:
CORRELATION WITH THE HAEMORHEOLOGICAL PARAMETERS AND THE VASCULAR RISK
FACTORS
METWALLY,MYM:AIN SHAMS MEDICAL JOURNAL ,VOL 46,No 4,5,6,1995 | www.yassermetwally.com
INDEX
SUMMARY

INTRODUCTION

MATERIAL AND METHOD

RESULTS

DISCUSSION

SUMMARY
In the present study 20 patients with the clinical diagnosis of cervical spondylitic myelopathy are included. They
were subclassified into 4 main groups according to the presence or absence of neck pain and the clinical course
of the disease. All patients were studied radiologically by CT myelography and cervical MRI. Haemorheological
parameters that included haematocrit value, serum fibrinogen, platelet aggregation were studied. Also blood
glucose levels were estimated in all patients. Serum lipid electrophoresis was also done to all patients. The
painless myelopathy patients (18 patients) had a higher incidence of vascular risk factors such as hypertension
(100%), diabetes 80%, type IV hyperlipidemia (100%). Also the haematocrit value, serum fibrinogen and the
platelet aggregation were significantly elevated in this group, thus indicating increased whole blood viscosity in
those patients. Radiologically the spinal cord pathology of the painless myelopathy group was in the form of
segmental atrophy and/or cavitations with no evidence of cord compression by disc herniation and/or
osteophytes. The possible correlation between the clinical picture, the radiological findings and the

2. haemorheological abnormalities are discussed and lines of treatment of these patients were suggested. The
painful myelopathy group (2 patients) were significantly younger than the painless group. No vascular risk
factors were present and the haemorheological parameters studied were within normal limits. Dorso-lateral soft
disc herniations were demonstrated in the painful myelopathy group by CT myelography and/or MRI.
Introduction:
Cervical spondylosis is a common disorder, its clinical presentation ranges between accidental radiological
findings with asymptomatic clinical picture to severe radiculopathy and/or myelopathy. The cause of the cervical
spondylitic myelopathy was attributed to multiple aetiologies that included cord compression by the spondylitic
changes and impairment of blood flow to the cervical enlargement (vascular aetiology). Little attention was given
in literature to the vascular aetiology, its nature and how is it correlated with the structural cord pathology that
is demonstrated either radiologically or at necropsy. The present study is an attempt to define the vascular
aetiology of the cervical spondylitic myelopathy, its possible correlation with the clinico-radiological picture, and
its impact on the prognosis and treatment.
Material and Methods:
In the present study 20 patients with the clinical diagnosis of cervical spondylitic myelopathy are included. All
patients were subjected to the following
Clinical examination

Radiological examination that included CT myelography and MRI.

Haemorheological profile.

Follow up of patients belonging to group (A) for 3 years.

Radiological examination included CT scan with intrathecal enhancement (CT myelography) for all patients.
The whole cervical spine starting from C1, to D1 was scanned. In addition to CT scan, 12 patients were also
subjected to MRI examination of the cervical spine (see table 1) plain x-rays of the cervical spine were also done
for all patient with special emphasis on the lateral views in full flexion and full extension.
TABLE [1] DIAGNOSTIC MODALITY AND HAEMORHEOLOGICAL PROFILES FOR PATIENTS IN THE
VARIOUS GROUPS
platelet
GROUP No age sex imaging Hch fibrinogen diabetes LVH
aggregation
1 56 M CT,MRI 46 600 INCREASED + +
2 66 M CT,MRI 46 500 INCREASED + -
3 35 M CT,MRI 49 450 INCREASED - -
4 56 F CT 46 500 INCREASED + -
5 58 M CT,MRI 44 300 INCREASED + +
A
6 52 M CT 51 550 INCREASED - -
7 73 M CT 49 630 INCREASED - +
8 69 M CT,MRI 49 600 INCREASED - -
9 63 M CT,MRI 46 550 INCREASED + -
10 75 M CT,MRI 47 610 INCREASED + +
1 42 M CT 52 575 INCREASED + -
2 37 M CT 48 410 INCREASED + -
B 3 52 M CT,MRI 41 550 INCREASED - -
4 48 M CT,MRI 46 650 INCREASED + -

3. 5 41 M CT,MRI 46 370 INCREASED + -
1 36 M CT 47 650 INCREASED - -
C 2 27 F CT 45 530 INCREASED + -
3 36 M CT,MRI 49 410 INCREASED + -
1 26 F MRI 39 270 NORMAL - -
D
2 28 M CT,MRI 37 310 NORMAL - -
The haemorheological parameters studied included the haematocrit values, serum fibrinogen, lipid profile and
serum lipid electrophoresis and the ADP induced platelets aggregation. Also blood glucose level, fasting and 2
hours post-prandial were measured. All haemorheological parameters were matched against normal controls
See table (I,2).
TABLE [2] HAEMATOCRIT VALUE AND SERUM FIBRINOGEN IN THE AGE MARCHED NORMAL
CONTROLS
number age fibrinogen haematocrit value
1 55 270 39
2 46 290 40
3 41 230 37
4 38 256 38
5 35 288 39
6 43 270 38
7 40 260 40
8 51 310 39
9 46 298 38
10 56 316 37
11 38 256 39
With regard to the platelet aggregation methodology, the ADP induced platelet aggregation and the light
transmission technique was used. A platelet rich plasma suspension was obtained from each patient and a
normal control.
The transmission of light through the platelet suspension was continuously
monitored on a pen-ink recorder. The addition of ADP resulted in the
formation of an increasingly large platelet aggregates, which in turn allows
for increasing light transmission through the platelet suspension. Percentage
of light transmission is the measure of platelet aggregation. Each patient is
controlled by a normal relative. The result is either increased platelet
aggregation (light transmission) above the normal control ( when difference
in light transmission is demonstrated between the patient and the normal
control) or not (within normal platelet aggregability) when no difference in
light transmission is demonstrated between the patient and the normal
control (Koski, 1987).
PLATELET AGGREGATION FOR PATIENTS AND CONTROL
Results
Based on the clinical picture, patients were subclassified into 4 main groups according to the following clinical
parameters.

4. 1. Onset: the presence of neck pain. Painful or painless.
2. Course: sudden regressive or chronic fluctuating.
The painless myelopathy patients comprised 18 patients, they were subclassified into three groups as follows :
(see table 3, 4).
Group A patients: 10 patients are included. The clinical picture is characterized by a painless onset with a
chronic fluctuating course and with upper motor neuron manifestations in the lower limbs constituting the main
clinical features.
Group B patients: 5 patients are included. The clinical picture is characterized by a painless sudden onset and a
regressive course. Upper motor neuron manifestations in the lower limbs constituted the main clinical features.
Group C patients: 3 patients are included the clinical picture is characterized by a painless sudden onset and a
regressive course. Bilateral asymmetric C5-C6 lower motor neuron manifestations constituted the sole clinical
feature.
The painful myelopathy patients comprised 2 patients. The clinical picture was characterized by neck rigidity
with painful limitation of neck movements of sudden onset. Radicular pain radiating to the shoulders was also
very prominent. Extensor planter responses constituted the sole manifestation of myelopathy.
To sum up the painless myelopathy groups are characterized by a mainly motor clinical presentation. Sensory
manifestation were either absent (group C) are detected only by careful clinical examination (groups A, B). In
group (A) past history of similar attacks was present, while in groups B, C, The clinical presentation constituted
the initial presentation of the disease. No past history of similar attacks was present. Clinical differences between
the various groups are present in table ( 3).
TABLE [3] CLINICAL DIFFERENCES BETWEEN THE VARIOUS GROUPS
Past history of UMN manifestation LMN manifestations Nensory
Group Neck pain
similar attacks in the lower limbs in the upper limbs manifestations
A + ++++ + + -
B - ++++ + + -
C - - ++++ - -
Mild diminution of Radicular pain
Solely in the form of
D - the biceps and radial radiating to the ++++
extensor planters
reflexes shoulders
Because the clinical presentation of groups A, B, C was dominated by motor manifestations, many of those
patients was misdiagnosed as motor neuron disease. However the onset and the course of the disease are
definitely against the diagnosis of motor neuron disease. Also careful clinical examination demonstrated sensory
manifestations in groups A, B. (see table 3).
Finally it should be mentioned that all patients belonging to groups A, B, C were hypertensive when presented
clinically (mean blood pressure 190/110). Four patients belonging to group A also demonstrated evidence of left
ventricular hypertrophy (LVH) by ECG; thus indicating the existence of long standing hypertension see table (I).
Radiological evaluation of the patients.

Results of CT and MRI study of the patients are included in tables 4. Apart from the spondylitic bony changes,

5. the following were demonstrated in the various groups (spinal cord pathology).
TABLE [4] RADIOLOGICAL FINDINGS IN THE VARIOUS GROUPS
GROUP MEAN MALE - SPINAL CORD PATHOLOGY
AGE FEMALE
A 62 9-1 The spinal cord is atrophic. Atrophy is exclusively limited to the cervical
enlargement between C 4-C8 (segmental spinal cord atrophy) atrophy occurred
more frequently at C5-C6 segments. The atrophic spinal cord segments
appeared irregular, flattened collapsed and surrounded by wide subarachnoid
spaces. See Fig. 1A,1B. No evidence of soft disc herniation or osteophytes
compressing the spinal cord. No significant vertebral subluxation.
B 44 ALL Pencil - shaped, multi segmental cavitation that extended cephalocaudally
MALES between C 4-C7 Maximum cavitation occurred at C5-C6 Cavitation resulted in
widening of the spinal cord at the involved segments. See Fig. 2 . No evidence of
soft disc herniation or vertebral subluxation.
C 33 2-1 Central gray matter cavitations. They appeared radiologically as bilateral,
symmetrical, well-defined rounded intramedullary accumulation of the contrast
material. The cavitations are localized at the Topographic sites of the bilateral
anterior horns see Fig. 3 . No evidence of soft disc herniation or vertebral
subluxation.
D 27 1-1 Soft disc herniation compressing or indenting the spinal cord
Group A: spinal cord atrophy was demonstrated. Spinal atrophy was very segmental. i.e
The atrophy was exclusively limited to the cervical enlargement (between C4 - C7) and
the spinal cord above C4 and below C7 was completely normal. The frequency of
occurrence of atrophy at the various spinal segments is present in figure (5). Atrophy
occurred more frequently at C5 and C6 spinal segments, see fig 1A,1B, 4,5.
FIGURE [1A] THE SPINAL CORD ATROPHY, IN VASCULAR MYELOPATHY, IS
VERY SEGMENTAL [MRI IMAGE, T1]
FIGURE [1B] CT MYELOGRAPHY showing normal spinal cord at the level of cervical enlargement [left
image] and spinal cord atrophy in cervical spondylitic myelopathy [middle and right images], notice that the
atrophic segments are flattened,collapsed,with irregular contour and wide subarachnoid spaces
Group B: Longitudinally oriented multi-segmental cavitations were demonstrated in all patients. Cavitation

6. occurred more frequently at C5-C6 spinal segments and extended up to C4 and down to C7 in some patients (See
Figures. 2, 4,5) .
FIGURE [2] MRI T1,T2 IMAGES SHOWING PENCIL-SHAPED NECROSIS
Group C: Central gray matter cavitations were demonstrated in all patients . Cavitations were exclusively
limited to C5 - C6 segments. See fig 3.
Figure [3] CT MYELOGRAPHY showing
central gray matter cavitations as bilateral
symmetrical,well defined rounded zones of
intramedullary contrast accumulations in the
presumed anatomical areas of anterior horns
[right image is a schematic representation]
CAVITATIONS 1- pencil shaped necrosis: the cavitation is maximum at the level of c5,c6 spinal segments and
extends one ore two segments above and/or below
CAVITATIONS
2-Central gray matter cavitation: bilateral ,symmetrical,rounded cavitations,localized in the
CAVITATIONS
bilateral anterior horns of spinal segments c5,c6
Figure [4] in cervical spondylitic myelopathy, both cystic and atrophic changes are exclusively localized to the
level of cervical enlargement with maximum changes at C5,C6 spinal segments

7. Figure [5] in cervical spondylitic myelopathy, both cystic [left image] and atrophic [right image] changes are
exclusively localized to the level of cervical enlargement with maximum changes at C5,C6 spinal segments
Group D: Evidence of soft disc herniation was demonstrated by CT scan and MRI
See (Fig. 6) and table 4.
Figure [6] CT myelography showing a dorsolateral disc herniation compressing the
cervical spinal cord.
Results of haemorheological study

The haematocrit value, serum fibrinogen and platelet aggregation were significantly increased, compared with
normal controls, (See Tables1,2 , 5, 6) in groups A, B, C and were within normal in group D.
TABLE [5] HAEMATOCRIT VALUES OF GROUPS A,B,C AND OF CONTROLS
PARAMETER GROUP A,B,C CONTROL
Number 18 11
Mean 47.11 38.54
ST 2.64 1.034
T VALUE=10.20, DF=26, P>0.001
TABLE [6] FIBRINOGEN VALUES OF GROUPS A,B,C AND OF CONTROLS
PARAMETER GROUP A,B,C CONTROL
Number 18 11
Mean 528.6 276
ST 106 26.1
T VALUE=7.68, DF=27, P>0.001

8. Serum lipid electrophoresis demonstrated type IV hyperlipidaemia in a group A, B, C patients (reduction of
HDL and increased triglyceride levels) and was within normal in group D patients.
Eight patients in group A, 4 patients in group B and 2 patients in group C were found diabetic (See table I). Non
of the group D patients were diabetic. Diabetic was of the non insulin dependent type in all patients (NIDDM).
Non of the patients were known to be diabetic when presented clinically.
It should be mentioned that blood viscosity is mainly determined by the haematocrit value and the plasma
viscosity is mainly determined by the fibrinogen level. The significant increase of the haematocrit values and the
serum fibrinogen, especially when coupled with increased platelets aggregation and hyperlipidaemia, is an
indicator of increased whole blood viscosity in groups A, B, C patients. Ott et al, 1979, Pearson et al, 1981, Stoltz
et al, 1981, Bartoli et al, 1982, Grotta et al, 1982, 1985.
Results of follow up of cases n. 1,3,6,7 & group A patients

Longitudinal follow up of those cases over a period of 3 years (1990, 1991, 1992) showed that these patients
experienced a total of 6 episodes of recurrent exacerbation of myelopathy. All episodes occurred in July, August,
and September. Partial recovery occurred in all patients with additional residual deficits (See table 7).
TABLE [7] HAEMORHEOLOGICAL VALUES DURING THE ATTACKS AND ONE MONTH LATER IN
PATIENTS NUMBERS 1,3,6,7
During the acute attack One month later
PARAMETER
No episodes DATE Hch value fibrinogen platelet Hch value fibrinogen platelet
number mg/DL aggregation mg/DL aggregation
1 2/1990 49 630 increased 41 230 normal
1
48 530 increased 39 200 normal
2 7/1992
3 1 8/1991 47 430 increased 37 190 normal
39 210 normal
1 9/1990 46 575 increased
6 41 270 normal
49 450 increased
2 7/1992
7 1 8/1991 46 430 increased 42 240 normal
All patients were followed up radiologically and haemorheologically during the acute exacerbations and one
month later. Radiological follow up was done by CT myelography and plain films.
Radiological follow up did not demonstrate the existence of any additional structural pathology (like vertebral
subluxation and/or soft disc herniation) that would explain the exacerbation of the myelopathic state.While
haemorheological follow up demonstrated significant increase of the haematocrit value, serum fibrinogen and
platelets aggregation during the acute exacerbation (See table 7 ). Those parameter dropped down to the normal
levels one month later following the partial clinical improvement. These findings mean that the clinical
fluctuation of the myelopathic state was intimately coupled, temporally, with fluctuation of the whole blood
viscosity. Episodes of clinical deterioration were associated with increased blood viscosity, while reduction of
blood viscosity was associated with remission of the myelopathic state and partial clinical improvement.
It looks like that the painless cervical spondylitic myelopathy occurs mainly in a group of patients where the
incidence of vascular risk factor is high, and the onset of the clinical myelopathic state is ultimately triggered by

9. increase of the whole blood viscosity that results in spinal card ischaemia and/or infarction. The spinal cord
cavitations demonstrated in groups B, C, most probably represent spinal lacunar infarctions.
To end up it should be mentioned that group C patients were significantly younger than group B patients and
both were significantly younger than group A patients, Table (8). This observation had given us a general
overview on the natural history of the painless myelopathy patients. The disease starts, at a younger age group,
by acute spinal cord infarctions (groups B, C). However, later on, Repetition of spinal cord infarction and/or
ischaemia, secondary to recurrent episodes of increased whole blood viscosity, ultimately results in spinal cord
atrophy at an older age group (group A).
TABLE [8] AGES OF PATIENTS IN GROUP A COMPARED WITH PATIENTS IN GROUP B,C
PARAMETER GROUP A GROUP B,C
Number 10 18
Mean 62.81 39.61
ST 8.21 7.61
T VALUE=6.13, DF=16, P>0.001
Discussion
In the present study 20 patients with spondylitic cervical myelopathy are
included. They were subclassified into painless myelopathy group (18 patients)
and painful myelopathy group (2 patients).
In the painless myelopathy group, apparently the natural history of the disease
is determined by the interaction of 3 main pathogenic factors. Spondylitic
factor, vascular factor and haemorheological factor.
The spondylitic factor ultimately results in bony and soft tissue hypertrophy that causes cervical canal stenosis,
and encroach upon the subarachnoid space, reducing its volume. Lack of the CSF cushioning effect will cause
embarrassment of the spinal circulation at the level of cervical enlargement since optimum blood supply to the
spinal cord needs an optimum CSF cushioning effect.
The second factor is the vascular factor. Apparently the painless myelopathy groups (A, B, C) comprised a group
of patients where the incidence of vascular risk factors was found to be very high. Essential hypertension,
NIDDM, hyperlipidaemia, hyperfibrinogenemia, increased platelet aggregation. The incidence of arteriosclerosis
is known to be high among patients with vascular risk factors.
This is consistent with the necropsy finding of Manen, 1966 and Jellinger 1967. The authors reported
arteriolosclerosis, lipohyalinosis and fibrosis of the perforating intramedullary vessels and the fine vessels lying
on the surface of the spinal cord . These changes were maximum in the cervical enlargement and the overlapping
zone in the cervico-dorsal region, making the spinal cord especially vulnerable at this zone to vesico-circulatory
disorders, mainly of extra-medullary origin, which cause critical decrease in spinal cord flow. It should be
mentioned that the area of the spinal cord between C4 and D1 is a watershed area with marginal blood supply.

10. This last field zone is most likely to suffer from insufficiency of blood and has been shown to be a preferential
zone for vascular damage. Tuli, 1975, Jellinger, 1967.
According to the necropsy results of Jellinger, 1967 the arteriosclerotic changes in the overlapping cervico-dorsal
region were isolated findings. They did not depend on age and were negatively correlated with arteriosclerosis in
the rest of the body. A finding that probably denotes that the injurious effect of the spondylitic changes
accelerate the arteriosclerotic changes in the region of the cervical enlargement.
However it should be noted that both cervical spondylosis and arteriosclerosis are slowly progressive pathology
and they can not be held responsible for the sudden onset of the clinical symptomatology seen in groups A, B, C.
No compressing agents (like soft disc herniation, or osteophytes) were demonstrated radiologically that can
explain the clinical symptomatology in terms of compression of the spinal cord and/or an important radicular
artery. In short both cervical spondylosis and arteriosclerosis serve by furnishing the background for the
ultimate determinant of the clinical symptomatology.
Cervical spondylosis will result in canal stenosis, loss of the CSF cushioning effect and embarrassment of the
spinal circulation in the region of the cervical enlargement. Arteriosclerosis will result in reduction of the caliber
of the radicular and the perforating intramedullary arterioles with loss of the auto-regulatory physiological
process. Flow in the perforating arteries is dependent on the auto-regulatory process of the penetrating
intramedullary arterioles on one hand and the whole blood viscosity on the other hand. Loss of the auto-
regulatory process, secondary to advanced arteriosclerosis, will simply mean that the spinal cord perfusion, in
the vulnerable region of the cervical enlargement, will fluctuate with fluctuation of the whole blood viscosity.
Powers, 1992.
Whole blood viscosity is a collective terminology that reflects the influence of various factors that include mainly
the corpuscular and the plasmatic components of the blood. Grotta, et al, 1982, Schneider et al, 1987.
Blood viscosity is mainly determined by the hematocrit value and the plasma viscosity is mainly determined by
the plasma fibrinogen level. High values of serum lipid have also been found to increase whole blood viscosity.
Pearson et al, 1981, Pearson, 1987, Stoltz et al, 1981, Grotta et al, 1982, 1985.
Increased platelet aggregation also increases whole blood viscosity. The behavior of the red blood cells was also
found to affect the blood viscosity. Increased red cell aggregation and reduced red cell deformability increase
whole blood viscosity. Lowe, 1987.
Although RBCs deformability and aggregability were not selectively tested in the present study, however the
RBCs deformability is invariably reduced and their aggregability is invariably increased in the presence of high
fibrinogen level and high haematocrit values. Fibrinogen in particular is a strong RBCs aggregant agent. Inverse
correlation is present between the red cell deformability and the haematocrit value and serum fibrinogen level.
Grotta, et al, 1985, Pearson, 1987.
Increase of the whole blood viscosity is a common finding in essential hypertension and NIDDM . The vascular
resistance of the perforating blood vessels of the spinal cord and the brain is dependent upon the ratio between
the whole blood viscosity over the caliber of the blood vessel. Increase of the whole blood viscosity results in high
vascular resistance to blood flow and subsequently low perfusion pressure and neuronal tissue ischaemia.
Stenosis of the perforating blood vessel secondary to arteriosclerosis further aggravates the problem. Powers,
1992. Inverse correlation is present between the neuronal tissue blood flow and serum fibrinogen level and the
haematocrit value. Grotta et al, 1985, Schneider et al, 1987.
Hyperfibrinogenemia and increased RBCs and platelet aggregation reflect a hypercoagulable state with
increased thrombotic tendency that selectively affects the small perforating blood vessels and the
microcirculation of the brain and spinal cord. Microvascular occlusion can occur either by local aggregation of
hyperaggragable platelets, Pearson, 1987, or by red cell aggregation with impaction of rigid red cells in the
microcirculation. Lowe, 1987. This is more likely to occur with the existence of high red cell mass (Hematocrit
value) that can displace the hypersensitive platelets Towards the arteriolar wall resulting in platelet aggregation
and thrombus formation. Thrombus formation is enhanced if the arteriolar wall is abnormal (arteriolosclerosis)

11. Koski, 1987, Schneider, et al, 1987.
The high blood viscosity observed in groups A, B, C patients (painless myelopathy patients) should simply mean,
especially when coupled with arteriosclerosis of the small perforating blood vessels, that the blood flow to the
spinal cord at the level of cervical enlargement is subjected to high vascular resistance that could ultimately
result in low perfusion pressure and chronic ischaemia. The increased thrombotic tendency observed in those
patients should mean that the chronic ischemia state could be interrupted by acute thrombotic microvascular
occlusion that can result, pathologically, in spinal cord lacunar infarction at the level of cervical enlargement and
clinically in lower cervical painless myelopathy of sudden onset and regressive course. The acute thrombo-
occlusive episodes are responsible for the intramedullary cavitations observed in groups B, C. Those cavitations,
most probably, represent lacunar infarctions. The segmental spinal cord atrophy observed in group A patients
could be the result of long standing chronic ischaemia interrupted by recurrent thrombo-occlusive episodes.
All the atrophic and cystic changes were exclusively limited to the spinal cord area between C4 and C7. The C5-
C6 segments were most frequently involved. The C5-C6 segments are the most vulnerable to vascular damage as
they represent a watershed area with higher incidence of segmental arteriosclerosis. Jillenger, 1987, Furguson
and Caplan, 1985. The central grey matter cavitations demonstrated in group C patients represent lacunar
infarctions involving the bilateral anterior horns. This was described before, Jillenger, 1967, Jinkens et al,1986,
it resulted clinically in a purely LMN picture.
The association between spondylitic myelopathy and spinal cord atrophy and/or cavitation was described before
Tsuji, 1982, Jestico 1983, Furguson and Caplan, 1985, Penning et al, 1986, Jinkens et al, 1986. All these reports
used only CT myelography and non used MRI. The pathology was collectively described without sufficient
specification and no correlation with the clinical picture was made. A possible vascular aetiology for the spinal
cord atrophy and/or cavitation was vaguely proposed by Furguson and Caplan, 1985, Jinkens et al, 1986, but
without defining in which way this vascular aetiology is implicated in the pathogenesis. No haemorheological
study was done in any of the previous reports.
The ischaemic aetiopathogenesis of myelopathy in group A patients is further substantiated by the observation
that relapses of myelopathy in patients 1, 3, 6, 7 were intimately coupled temporally with rise of whole blood
viscosity and thrombotic tendency. Relapses occurred more frequently in the summer time. Dehydration is more
common in summer time, it results in contraction of the plasma volume and rise of the haematocrit value and
subsequently blood viscosity. Isbister, 1987.
The ischaemic aetiology of myelopathy in groups A, B, C patients is consistent with the necropsy findings of
Jellinger, 1967. The author reported, in spondylitic myelopathy patients, white matter ischaemic demyelination,
neuronal degeneration and a diffuse lacunar state similar to those seen in the basal ganglion in the hypertensive
small vessel disease of the brain. It should also be mentioned that increased whole blood viscosity is also the
ultimate aetiopathogenic factor in hypertensive microvascular brain disease (diffuse lacunar state, leukoaraiosis,
etc.). Elshazli, 1984, Schneider, et al, 1987.
The haemorheological profile of vascular spondylitic myelopathy is similar to the haemorheological profile of
hypertensive micro-vascular brain disease (Lacunar infarction, leukoaraiosis etc.) previously reported by
Elshazli, 1984, Schneider et al, 1987. The haemorheological parameters tended to drop down to the normal levels
following the acute phase in myelopathy patients and this has also been reported in ischaemic brain disease ,
Koski, 1987.
The hypertensive micro-vascular brain disease was found to be similar in many ways to the spondylitic vascular
myelopathy regarding vascular risk factors, the vascular arteriolar pathology, parenchymatous pathology and
the haemorheological profile. Similarities are listed in table (9).
Table [9] Similarities between the spondylitic vascular myelopathy and hypertensive microvascular brain disease

12. Vascular risk Hypertension, NIDDM, type IV hyperglycaemia, old age, LVH are common in both
factors diseases.
hypertensive Lipohyalinosis and arteriolar wall fibrosis are common in vascular myelopathy (Mannen,
vascular pathology 1966, Jillengern 1967, Furguson and Caplan, 1985) and in microvascular brain disease
(Fisher 1969, 1972, Gautier, 1976, Leitschuh and Chobanian, 1987, Hachinski et al, 1987,
Tuszynki, et al, 1989, Leifer et al, 1990).
pathological Neuronal degeneration, ischaemic demyelination, diffuse lacunar state are common in
findings vascular myelopathy (Jillenger, 1967) and in hypertensive microvascular brain disease
(Hachinski, et al, 1987, Leifer, et al, 1990).
haemorheological Increased whole blood viscosity and increased thrombotic tendency are common in
profile vascular myelopathy (this study) and in ischaemic brain disease ( Koski, 1987, Schneider et
al, 1987)
Spinal cord ischaemia is far much less well studied compared with cerebral ischaemia. Although a vascular
aetiology is occasionally vaguely implicated in the pathogenesis of the spondylitic vascular myelopathy. Furguson
and Caplan, 1985, Jinkens et al, 1986. However, practically, little attention was given in literature to the exact
spinal cord pathological findings in the spondylitic vascular myelopathy and how is it correlated with any
vascular aetiology and/or haemorheological abnormalities and in which way the spondylitic process is related to
the whole problem.
In fact the present study, to the best of our knowledge, is probably the only study where the spinal cord ischemic
pathology (as demonstrated radiologically) was correlated with the haemorheological factors. This correlation
was made necessary since the incidence of hypertension and NIDDM was found to be high among patients with
the painless spondylitic myelopathy. Haemorheological abnormalities are known to be common in diabetes and
hypertension. Also failure to find, radiologically, evidence of compressing agents (like soft disc herniation etc.)
that can explain the ischaemic episodes in terms of compression of an important radicular artery has made it
necessary to search for anther aetiology of the ischaemic episodes.
Because the vascular spondylitic myelopathy has an sudden painless onset and a fluctuating course with
remission and exacerbation, it was frequently misdiagnosed as multiple sclerosis or transverse myelitis. The
demonstration of haemorheological abnormalities in those patients should suggest important lines of treatment.
Antiplatelet medications, drugs that improve RBCs deformability, reduce whole blood viscosity and fibrinogen
level (like pentoxifylline bezafibrate etc) will be of great value in those patient. Also maintenance of good body
hydration is of paramount importance especially in the older age group. Control of risk factors like hypertension
and NIDDM is essential.
Although the prognosis following a single ischaemic episode is good (Groups B, C), however repetition of the
ischaemic episodes will ultimately result in spinal cord atrophy with irreversible neurological deficits (Group A).
So patients with the spondylitic vascular myelopathy probably need prophylactic treatment like cerebrovascular
patients following the first acute myelopathic episode.
In general the vascular aetiology is the most common cause of the spondylitic myelopathy. The spondylitic
vascular myelopathy is present mainly in males and is characterized, clinically, by a painless clinical picture and
radiologically by the presence of segmental spinal cord atrophy or cavitations. Incidence of vascular risk factors
was high among patients with vascular myelopathy with frequent haemorheological abnormalities denoting
increased whole blood viscosity. Although central disc herniation can cause a painless clinical picture, but this
can easily be excluded radiologically. The roles played by the spondylitic process, the vascular pathology and the
haemorheological abnormalities in the pathogenesis of the spondylitic vascular myelopathy are summarized in
table (10).
TABLE [10] PATHOGENESIS OF THE CERVICAL SPONDYLITIC VASCULAR MYELOPATHY

13. Pathological phenomenon Detrimental effect
Cervical spondylosis & cervical 1. Loss of the CSF cushioning effect with embarrassment of spinal cord
canal stenosis circulation in the region of cervical enlargement
2. ? accelerate arteriolosclerosis in the region of cervical enlargement
Hypertensive vascular changes 1. Stenosis of the perforating intramedullary arterioles in the region of
in the region of cervical cervical enlargement.
enlargement
2. Loss of the auto-regulatory physiological phenomena of the stenosed
arterioles
Increased whole blood viscosity 1. Chronic ischaemia in the region of cervical enlargement.
and thrombotic tendency of the
blood 2. Acute microvascular thrombo-occlusive episodes in the region cervical
enlargement
In group D myelopathy patients, although spinal cord compression was demonstrated radiologically by soft disc
herniation, yet the resulting myelopathic symptoms was mild. Patients belonging to group D were younger and
non of them had evidence of vascular risk factors or haemorheological abnormalities. This probably indicates
that spinal cord compression alone does not necessarily result in significant compromise of spinal cord function
so long as adequate blood supply to the spinal cord is maintained.
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