Published on February 18, 2009
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
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  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 + -
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  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.
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  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,
the following were demonstrated in the various groups (spinal cord pathology). TABLE  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
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  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  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  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
Figure  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  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  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  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
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  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
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  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.
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)
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  Similarities between the spondylitic vascular myelopathy and hypertensive microvascular brain disease
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  PATHOGENESIS OF THE CERVICAL SPONDYLITIC VASCULAR MYELOPATHY
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. References : -Bartoli V, Pasquini G , Albanese B (1982) The Influence of Haematocrit Value And Plasma Viscosity On Blood Viscosity . Clinical Hemorheology 2:319 -328 -Elshazli SM (1984) : Risk Factors In Cerebral Stroke And Normal People In Rural District, MD Thesis, Elzakaz'k University -Fisher CH (1969): The arterial lesions underlying lacunes. Acta neuropathologica (Berlin) 12-1. -Fisher CH, (1972): Cerebral miliary aneurysms in hypertension. American Journal of pathology 66: 313-319. -Furguson RJ, caplan CR: (1985): Cervical spondylitic myelopathy. Neurologic clinic of north America 2: 373- 382. -Gautier JC, (1976): Cerebral ischemia in hypertension. in cerebral arterial disease, Russell RW (ed) chapter 10 181- 209 Churchill livingstone. -Grotta J , Ackerman R, Correla J (1982): Whole Blood Viscosity Parameters And Cerebral Blood Flow. Stroke 13:192-203 -Grotta J, Ostrow P, Fraifeld (1985): Fibrinogen, Blood Viscosity And Cerebral Ischaemia. Stroke 16:192-197 -Hachinski VC, potter P, Allersk,V H, (1987) : Leukoaraiosis. Acta neurol. 44: 21-23. -Isbister JP (1987): The contracted plasma Volume syndromes (relative polycythemia) and their Haemorheological significance. Baillieres Clinical Haematology, Vol 3, No 3, 665-693. -Jestico K, (1983) : Cervical myelopathy- prospective evaluation with MRI and CT metrizamide. Radiology 161:753- 759.
-Jellinger K, (1967): Spinal Cord arteriosclerosis and progressive vascular myelopathy. J neurol neurosurg Psychiat 30: 195-206. -Jinkens JR, Bashir R, Almoty, V0, (1986): Cystic necrosis of the spinal cord in compressive cervical myelopathy, Demonstration by CT myelography, AJR, 147: 767-772. -Koski K, (1987): Threatened stroke. Research reports. Dept. of neurology. University of Turku. Turku-Finland. -Leifer D, Ferdinando S, Buonannos S, (1990): Clinico-pathological correlation of cranial MRl of periventricular white matter. AJR, 170:14-46 -Leitschuh M, Chobanian A, (1987): Vascular Changes in hypertension. Medical Clinic of north America, Vol 7 1, No 5, 827: 84 1. -Lowe GD, (1987): Blood rheology in vitro and in vivo. Baillieres clinical haematology Vol. 3, 597-636. -Manen T, (1966): Vascular Lesion in the spinal cord in the elderly. geriatrics, 4: 151-160. -Ott E., Lechner H., Aranibar 0, (1979) : Impairment of rheological conditions and cerebral blood flow in patients with cerebral vascular disease in Meger JS, Lechner H, Reivich R (eds): cerebral vascular disease-2 Elsevier- Holand. -Pearson TC, (1987): Rheology of the absolute polycythaemia. Baillieres clinical haematology Vol 3, No, 3 , 637- 664. -Pearson TC, Humphy, PRD, Thomas DJ, (1981): Haematocrit, blood viscosity, cerebral blood flow and vascular occlusion, in Low GO, Barbenel JC, Forbes CD (eds). Clinical aspect of blood viscosity and red cell deformability. Springler Verlag - Berlin, Heldolberg, New-York. -Penning L, Wilmink JT, woertien H, Knol E. (1986). CT. myelography in degenerative disorders of the cervical spine. NJR , 196:793-801. -Powers WJ (1992): Hemodynamics and metabolisms in ischemic cerebro-vascular Disease. Neurologic clinic of north America volume I0, No I, 31-48. -Schneider R, Ringelstein EB, Zeumer H, (1987): The role of plasma hyperviscosity in subcortical arteriosclerotic encephalopathy (Binswanger disease). J neurol, 234: 67-73. -Stoltz JF, Gaillard, S, Rousselle D, (1981). Rheological study of blood during hyperlipoproteinemia. clinical Haematology, I: 227 - 239. -Tsuji LI, (1982): Laminoplasty for patients with myelopathy due to cervical canal stenosis. spine, 7:28-49. -Tuli SM: TB of the spine, in TB of the spine, Tuli SM, (ed) B.V.T LTd. Bomaby, New Delhi, New York, pp 3-13, 1975 -Tuszynki ML, Petito C.K, lekv DE, (1989): Risk Factors and clinical Findings in pathologically verified Lacunar infarctions. Stroke 20: 990 - 999.
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