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PubMed1983

Calcitonin treatment for neurogenic claudication.

Forty-one patients with a possible diagnosis of neurogenic claudication were treated with Calcitonin for four weeks. Eleven responded with considerable improvement in their walking distance. Ten agreed to enter a randomized double-blind cross-over trial, and eight made a correct assessment. It is concluded that Calcitonin is effective in relieving symptoms of neurogenic claudication for some patients. Five patients have received the drug for over one year with no serious side effects, and two have not relapsed after discontinuing the drug. Patients likely to respond will probably have symptoms affecting both legs equally pain extending below the upper calf, limiting walking to under a mile; an abnormal myelogram; and no more than one inappropriate sign. They are more likely to be men in late middle age who have been engaged in manual work. The beneficial effect of Calcitonin is probably the result of an arterial shunt mechanism, whereby a reduction in skeletal blood flow provides for a deprived cauda equina.

Adult↗
PubMed1989

Electrophysiological studies of intermittent claudication in lumbar stenosis.

To clarify the pathophysiology of intermittent claudication in 37 patients with lumbar spinal stenosis, neural function was evaluated by examining somatosensory evoked potentials (stress-SEPs), and nerve action potentials (stress-NAPs) before and after walking stress. It was shown preoperatively that the stress-SEPs became abnormal immediately after walking in 31 of 37 patients. In seven of nine operated patients, the assessment clearly shows that SEPs had reverted to normal after surgery. The present method is noninvasive, simple in technique, painless, and safe, a procedure therefore that is useful as the initial step in the diagnosis and treatment of patients with lumbar canal stenosis. It also may help to differentiate neurogenic from vascular intermittent claudication.

Adult↗
PubMed1990

Myeloscopic study on lumbar spinal canal stenosis with special reference to intermittent claudication.

Twenty-five cases of lumbar spinal canal stenosis were investigated by dynamic myeloscopy to explain the pathophysiologic mechanism of intermittent claudication, one of the characteristic signs of the disorder. Myeloscopic examination revealed that, in accordance with postural alteration, the diameter of blood vessels on the cauda equinae showed significant changes in many patients in the stenosis group, but showed no changes in control group. In this series, it was suggested that the microcirculatory disturbance of vessels on cauda equinae might play an important role in the development of intermittent claudication.

Adult↗
PubMed1996

Spinal stenosis and neurogenic claudication.

Neurogenic claudication is diagnosed from a classical history and complementary spinal imaging. The abnormal signs may be few. It should be distinguished from intermittent claudication (peripheral vascular disease), referred pain from the back or root pain that is aggravated by walking, and psychological distress. Pathologically, a developmentally small canal is usually affected by multiple levels of segmental degenerative change, with venous pooling in the cauda equina between two levels of low pressure stenosis. There is probably then a failure of arterial vasodilatation of the congested roots in response to exercise, with symptoms in the legs when walking. Once established, symptoms tend neither to improve nor deteriorate. Conservative management is reasonable. Otherwise decompression at the most significant stenotic level is probably adequate to obtain a good surgical result.

Diagnosis, Differential↗
PubMed1997

Dynamic effects on the lumbar spinal canal: axially loaded CT-myelography and MRI in patients with sciatica and/or neurogenic claudication.

STUDY DESIGN: In patients with sciatica or neurogenic claudication, the structures in and adjacent to the lumbar spinal canal were observed by computed tomographic myelography or magnetic resonance imaging in psoas-relaxed position and during axial compression in slight extension of the lumbar spine. OBJECTIVES: To determine the mechanical effects on the lumbar spinal canal in a simulated upright position. SUMMARY OF BACKGROUND DATA: For years, functional myelographic investigation techniques were shown to be of value in the evaluation of suspected encroachment of the spinal canal. Since the advent of computed tomography and magnetic resonance imaging, there have been few clinical and experimental attempts that have imitated these techniques. The data indicate that the space within the canal is posture dependent. METHODS: Portable devices for axial loading of the lumbar spine in computed tomographic and magnetic resonance examinations were developed. Fifty patients (94 sites) were studied with computed tomographic myelography, and 34 patients (80 sites) with magnetic resonance in psoas-relaxed position followed by axial compression in slight extension. The dural sac cross-sectional area at L2 to S1, the deformation of the dural sac and the nerve roots, and the changes of the tissues surrounding the canal were observed. RESULTS: In 66 of the investigated 84 patients, there was a statistically significant reduction of the dural sac cross-sectional area in at least one site during axial compression in slight extension. Of the investigated patients, 29 passed the borderlines for relative (100 mm2) or absolute stenosis (75 mm2) in 40 sites. In 30 patients, there was deformation of the dural sac in 46 sites. In 11 of the patients investigated with magnetic resonance imaging, there was a narrowing of the lateral recess in 13 sites, during axial compression in slight extension. CONCLUSIONS: Axial loading of the lumbar spine in computed tomographic scanning and magnetic resonance imaging is recommended in patients with sciatica or neurogenic claudication when the dural sac cross-sectional area at any disc location is below 130 mm2 in conventional psoas-relaxed position and when there is a suspected narrowing of the dural sac or the nerve roots, especially in the ventrolateral part of the spinal canal in psoas-relaxed position. The diagnostic specificity of the spinal stenosis will increase considerably when the patient is subjected to an axial load.

Adult↗
PubMed2006

Red blood cell deformability in patients with claudication after pain-free treadmill training.

OBJECTIVES: To assess the effect of pain-free treadmill training on red blood cell deformability and walking distance in patients with claudication. DESIGN: Randomized-controlled trial of exercise training. SETTING: Patients were recruited from the primary care, vascular outpatient clinic. PATIENTS: A total of 60 patients with peripheral arterial occlusive disease (stage II according to Leriche-Fontaine) were randomized into the treadmill program or a control group. Fifty-five patients completed the study (27 in the exercising group and 28 in the control group). INTERVENTIONS: Patients in the exercising group were walking on the treadmill 3 times a week for 3 months. Each session consisted of 1 hour repetitive walking [performed to 85% of the pain-free walking time (PFWT)] was supervised by a qualified physiotherapist. MAIN OUTCOME MEASUREMENTS: Changes in erythrocyte deformability and treadmill walking performance (PFWT, maximal walking time) were assessed in both groups before the study and after 3 months. RESULTS: After 3 months of treadmill training, red blood cell deformability in the exercising group significantly increased (P<0.01). No significant changes were seen in the erythrocyte deformability in the control group. PFWT was prolonged by 102% from 191+/-34 to 386+/-60 seconds (P<0.01), and maximal walking time increased by 49% from 438+/-62 to 656+/-79 seconds (P<0.01) in the exercising group, whereas these changes were insignificant in the control group. CONCLUSIONS: A significant improvement of walking ability over 3 months of pain-free treadmill training is associated with a significant increase in red cell deformability in patients with claudication.

Aged↗
PubMed2006

F wave studies of neurogenic intermittent claudication in lumbar spinal stenosis.

OBJECTIVE: Lumbar spinal stenosis (LSS) may result in neurogenic claudication (NC), which is thought to be a result of transient ischemia during exercise. In this study we evaluated the changes in F wave studies before and immediately after walking stress in patients with NC. DESIGN: Twenty-six patients with LSS who had signs and symptoms of NC and 20 healthy volunteers were included in this study. Routine motor and sensory nerve conduction studies and tibial F wave studies were performed in both groups. Immediately after walking stress test, tibial F wave studies were repeated. Exercise treadmill protocol was used for ambulation. Time to first symptoms and total ambulation time were recorded. RESULTS: After completion of the baseline electrophysiological examination, a walking stress test was performed using a treadmill, and 16 patients (61.5%) experienced neurogenic claudication during the trial. The mean time to first symptoms was 2.0 +/- 3.5 mins (minimum = 0, maximum = 14). In the control group 18 subjects (90%) completed the trial without any symptoms, and 2 (10%) subjects had to stop at an average of 10 mins because of generalized fatigue. Within 5 mins after the walking stress test, tibial F wave studies were repeated in both groups. There were significant increases in F latency values bilaterally in the patient group (P = 0.001 for both sides) but not in control subjects (P = 0.435 for right side and P = 0.122 for left side). CONCLUSION: Our data suggest that F wave studies after walking stress test provide more information for the diagnosis of NC.

Case-Control Studies↗
PubMed1981

Natural history of angina pectoris, possible previous myocardial infarction and intermittent claudication during the eighth decade. A longitudinal epidemiologic study.

A ten-year longitudinal cardiovascular survey of an unselected population of 70- and 80-year-old men and women was carried out as part of the Glostrup Population Studies in Denmark. With small reservations, the population at entry was representative of the Danish people of that age group, and representative in terms of mortality during the following decade. The prevalences of three major cardiovascular symptoms are given together with their courses, incidences and relationship to some common cardiovascular risk factors. At 70, the prevalence of angina pectoris was 10% in men and 5% in women, the corresponding values for possible previous myocardial infarction being 5% and 3%, and for intermittent claudication 9% and 3%, with statistically significant differences between the sexes for any of the three symptoms. At 80, the prevalences of all three symptoms in women had risen to equal that of men, which had not changed. Total ten-year mortality was significantly increased among men who had confirmed angina pectoris or possible previous myocardial infarction at 70 and among women who had confirmed intermittent claudication. Ten-year mortality from all cardiovascular diseases, and also from acute myocardial infarction alone, showed exactly the same pattern. In those examined at both 70 and 80, the ten-year incidences of the three symptoms were 3-11%. Few participants who had confirmed a symptom at 70 denied it at 80.

Aged↗
PubMed1982

Reconstructive vascular surgery for intermittent claudication.

Over an 8-year period, 140 patients underwent 172 vascular reconstructions (187 reconstructed limbs) to relieve disabling intermittent claudication: bilateral aortoiliac or aortoileofemoral thrombendarterectomy (30 limbs), unilateral iliac or ileofemoral thrombendarterectomy (41 limbs), simultaneous unilateral ileofemoral thrombendarterectomy and femoropopliteal saphenous vein bypass graft (23 limbs), femoropopliteal saphenous vein bypass graft alone (93 limbs). The cumulative 5-year limb patency rates varied between 100 and 85.6% in the four groups. Age and diabetes did not influence patency rates. Only 2 limbs required amputation. These results indicate that reconstruction can be undertaken with a high rate of long-term patency and symptomatic relief In patients with restricting claudication due to aortoiliac, ileofemoral and/or femoropopliteal occlusion.

Adult↗
PubMed1985

Factors of prognostic importance for subsequent rest pain in patients with intermittent claudication.

The risk of developing rest pain during a six-year period was studied in 224 non-diabetic patients with intermittent claudication. Both smoking and multiple arterial stenoses in the leg were significantly correlated with an increased risk of developing rest pain. In non-smokers and in those who had stopped smoking within one year after the initial examination, the cumulative percentage of patients without rest pain after six years was 92, and in smokers and those who stopped smoking after more than one year it was 79 (p less than 0.03 after adjustment for differences in the presence of multiple stenoses). In patients with single stenosis the cumulative percentage of patients without rest pain was 86, and in those with multiple stenoses 70 (p less than 0.05 after adjustment for differences in smoking habits). The results emphasize how important it is that patients with intermittent claudication do not smoke. The increased risk of rest pain associated with the presence of multiple arterial stenoses in the leg should be considered when making decisions concerning vascular surgery.

Aged↗
PubMed1984

Chronic effects of metoprolol and methyldopa on calf blood flow in intermittent claudication.

In a placebo-controlled double-blind study 14 hypertensive patients with intermittent claudication were treated with metoprolol (100-200 mg daily) and methyldopa (500-1000 mg daily) for 3 weeks and their effects on heart rate, blood pressure as well as on resting and hyperaemic calf blood flow and vascular resistance were compared. In their antihypertensive effect metoprolol and methyldopa did not differ significantly. In 23 diseased limbs the calf blood flow and vascular resistance remained unchanged at rest during the trial. The active drugs reduced hyperaemic flow (P less than 0.05). The peak flow was reduced by 20% (P greater than 0.01) with metoprolol and by 15% with methyldopa below the initial level and by 17% and by 12% below the level recorded on placebo, respectively. Neither of the drugs influenced vascular resistance during reactive hyperaemia. Thus, in patients with intermittent claudication antihypertensives should be used with care.

Adult↗
PubMed1980

Amyloid vascular disease: cord-like thickening of mucocutaneous arteries, intermittent claudication and angina in a case with underlying myelomatosis.

A patient with established myelomatosis and an IgG paraproteinaemia presented with intermittent claudication. Indurated cord-like structures were noted on the dorsum of the right hand and the buccal surface of the lower lip, and biopsy of the hand lesion revealed massive amyloid deposition within the wall of an artery. Cord-like thickening of mucocutaneous arteries as a presenting sign of systemic amyloidosis in the absence of glossomegaly or other cutaneous lesions has not been reported previously. The presence of intermittent claudication and angina suggested that amyloid involvement of large arteries was extensively distributed.

Amyloidosis↗
PubMed1990

Prevention of myocardial infarction and stroke in patients with intermittent claudication; effects of ticlopidine. Results from STIMS, the Swedish Ticlopidine Multicentre Study.

The Swedish Ticlopidine Multicentre Study (STIMS) was a double-blind placebo-controlled trial designed to determine whether ticlopidine, a platelet antiaggregatory agent, reduces the incidence of myocardial infarction, stroke and transitory ischaemic attacks in patients with intermittent claudication. A total of 687 patients was monitored for a minimum of 5 years or until an end-point was reached. The number of end points (99 vs. 89), analysed according to the intention-to-treat principle, was 11.4% lower in the ticlopidine group (P = 0.24). The mortality rate was 29.1% lower in the ticlopidine group (64 vs. 89, P = 0.015); this observation could be accounted for by a reduced mortality from ischaemic heart disease. On-treatment analysis showed there to be significantly fewer end points in the ticlopidine group (47 vs. 76, P = 0.017). Diarrhoea was the most common side-effect. Reversible leucopenia or thrombocytopenia was reported in seven patients on ticlopidine. It is concluded that the high morbidity and mortality from cardio- and cerebrovascular disease in patients with intermittent claudication can be reduced by long-term treatment with ticlopidine.

Aged↗
PubMed1992

EDTA treatment of intermittent claudication--a double-blind, placebo-controlled study.

A double-blind, randomized multicentre study was undertaken to evaluate the possible effect of chelation treatment with ethylenediamine-tetraacetic acid (EDTA) in patients with severe intermittent claudication. A total of 153 patients received 20 intravenous infusions of either 3 g Na2EDTA or placebo during a period of 5-9 weeks. Vitamin, mineral and trace element supplements were administered orally. The changes observed in the pain-free and maximal walking distances, measured on a treadmill, were similar in the two groups. During the 3-month (n = 149) and 6-month (n = 123) follow-up period, no long-term therapeutic effect of EDTA could be demonstrated. The ankle-brachial blood pressure index remained unchanged throughout the study period. This study failed to demonstrate any effect of EDTA chelation treatment in intermittent claudication.

Aged↗
PubMed1992

Neurogenic claudication secondary to vascular disease.

Neurogenic claudication is characterized by sensory symptoms which appear during exercise or while maintaining a fixed posture. They are paraesthetic in quality, may be associated with 'march' phenomena, and patients may have bowel and bladder disturbance. The problem is most commonly secondary to lumbar canal stenosis (LCS) but rarely due to aortic disease, as shown in this case report. This report concerns a 66 year old woman who presented with symptoms of paraesthesia radiating from the buttocks to the thigh and, intermittent loss of bladder and bowel function, all associated with walking. There were no associated symptoms of vascular claudication. Clinically, there was evidence of aorto-iliac obstruction with absence of femoral pulses and a vascular index of 0.4 at both ankles. Neurological examination was normal at rest but the left ankle jerk was absent immediately after exercise. Myelogram and computerized tomographic (CT) scan were normal. An aortogram revealed a very tight irregular stenosis of the aorta at the level of the renal and mesenteric arteries. Very few lumbar vessels were seen. An aortic endarterectomy via a thoraco-abdominal approach was performed and an aortobifemoral graft inserted. The patient's symptoms resolved following this procedure. We postulate that her symptoms were caused by a 'steal' from the blood supply to the cauda equinda due to the severe athromatous disease of her upper abdominal aorta.

Aged↗
PubMed1981

Reproducibility of treadmill exercise in patients with intermittent claudication.

The reproducibility of pain limited exercise time (ET) and heart rate (HR) have been evaluated in repeated treadmill exercise tests in 24 patients with arterial occlusive disease of the lower limbs and intermittent claudication. The protocol includes a walking speed of 1 m/s and load increments of 10 watt/min and the two tests were separated by 1--14 days. The total ET was systematically increased by about 30 sec (P less than 0.05) at the second exercise test. The reproducibility of ET at the onset of leg pains was 34%, whereas the corresponding value at maximal leg pain was 16%. HR at the termination of the test did not differ systematically between the two tests and the reproducibility of HR was 6.1% and 5.5% at the onset of pain and maximal pain, respectively. It is concluded that a slight improvement in walking capacity at a second exercise test must be taken into account when evaluating different types of therapy in patients with intermittent claudication and, furthermore, that ET, walking distance or work load, should preferably be evaluated at or near maximal leg pain.

Adult↗
PubMed1987

Effect of training on the post-exercise ankle blood pressure reaction in patients with intermittent claudication.

The effect of physical training on the post-exercise blood pressure reaction in the ankle was studied in 63 patients with intermittent claudication but without angina pectoris. After three months of supervised training the maximal walking distance increased by 67% and the pain-free walking distance by 73%. Compared with that after the pre-training treadmill test, the ankle blood pressure was significantly higher 2-16 min after the post-training test and more rapidly returned to the initial resting value, both with similar work loads and with a higher post-training work load. Blood pressure measurement in the ankle after exercise is useful as an objective test of the circulatory effect of training in patients with intermittent claudication.

Aged↗
PubMed1988

Excretion of thromboxane A2 and prostacyclin metabolites during treadmill exercise in patients with intermittent claudication.

Platelet activation, with subsequent formation of thromboxane A2 (TxA2), is thought to play a role in the development of arterial occlusion. In patients with severe atherosclerosis of the lower limbs, characterized by leg ulcers and rest pain, the basal formation of TxA2 and prostacyclin (PGI2) is increased. Corresponding data in patients with more moderate atherosclerosis of the lower limbs have not been reported. Since the capacity to physical exercise is not blunted in such patients proper evaluation of their TxA2-PGI2 synthesis should comprise not only assessment of the basal formation, but also TxA2/PGI2 biosynthesis during conditions of elevated cardiovascular activity. To address this, we analysed these eicosanoids in patients with a history of intermittent claudication. Urinary dinor-metabolites of TxB2 and PGI2 (Tx-M and PGI-M, respectively) were estimated by gas chromatography/negative ion-chemical ionization mass spectrometry in samples collected prior to, during and immediately after 20 min of severe treadmill exertion. The basal excretion of Tx-M was 105 +/- 26 pg/mg creatinine. It was not changed during exercise, but increased to 176 +/- 48 pg/mg creatinine (P less than 0.05) during the recovery. The basal excretion of PGI-M was 142 +/- 25 pg/mg creatinine. The PGI-M response to exercise varied from no change at all to a 30-fold increase, without any obvious correlation to experienced leg pain, walking distance or other recorded variables. During the recovery period the outflow of PGI-M was significantly higher than at rest (482 +/- 145 pg/mg creatinine; P less than 0.01). We conclude that in patients with intermittent claudication due to atherosclerosis (1) platelet activation does not occur during the course of the exercise, and (2) vascular prostacyclin formation can be dissociated from of TxA2 synthesis. The observed increase in PGI-M in some of the patients is suggested to reflect tissue ischaemia induced by the lack of adequate hyperaemia during exercise.

6-Ketoprostaglandin F1 alpha↗