Local Spasm Research Articles

Abstract 4218: Usefulness of 64-Row Multi-Detector Computed Tomography for the Evaluation of Patients with Variant Angina

Invasive coronary angiography is useful in patients with suspected variant angina to document an episode of coronary artery spasm with provocative test. Previous studies have demonstrated that atherosclerosis is present at the sites of vasospasm. The aim of this study was to clarify the relation between 64-row Multi-detector Computed Tomography (MDCT) findings of coronary artery and vasospasm. A total of 58 patients with suspected variant angina (32 females and 26 males, aged 49 to 87 years, mean 65 ± 9 years) who have no evidence of luminal narrowing in major coronary artery with MDCT and underwent ergonovine test to detect the presence of coronary artery spasm were enrolled in this study. Two patients were excluded because of poor images of MDCT. The criteria of positive ergonovine test was total occlusion or localized occlusive spasm associated with chest pain and ST segment elevation after administration of ergonovine into the left coronary artery. The existence of plaques and calcifications in major coronary artery were evaluated with MDCT. 23 of 56 (41.1%) patients were positive with ergonovine test. 9 of 23 (39.1%) were total occlusion and 14 of 23 (60.9%) were localized spasm. Using MDCT, atherosclerotic lesions were observed at all coronary spasm sites. Among the 33 patients with negative ergonovine test, 7 (21.2%) had no plaques in the coronary artery. Presence of plaques was significant factor for positive ergonovine provocation test (p = 0.03). Patients with positive ergonovine test had coronary artery plaques at the site of coronary spasm sites. Absence of coronary artery plaques with MDCT could rule out variant angina. Correlation between ergonovine provocation test and MDCT findings

Nerves in bone: the silent partners

This Perspective summarises evidence of the presence of nerves within the skeleton, where they remained silent and invisible until recent technological advances in neurohistology broke the silence. An extensive sensory nerve supply is now visible. It must impact upon our concepts of skeletal physiology and pathology. Beginning at the beginning, one might ask: do bones have a sensory nerve supply? Clinically, the answer is an unequivocal yes, although objective proof has been difficult to obtain and the true picture has been slow to emerge over the past 160 years. In clinical practice, the intense pain caused by trauma, neoplasm or inflammation in bone is proof that sensory nerves exist within bones and joints. Clinical neurologists in the past were prepared to deduce the presence of nerves in bone from clinical observations. For instance, the French neurologist Leriche endorsed Bohler’s observation that a single large injection of local anaesthetic agent between the ends of a fractured bone induces both relaxation of local spasm and anaesthesia, which facilitates relatively painless reduction of the fracture. The deep injection does not alter overlying skin sensitivity. Leriche concluded that this proved the presence of pain fibres within bone [1]. But to show nerves by anatomic dissection was an insuperable task.

Botulinum toxin injection to facilitate rehabilitation of muscle imbalance syndromes in sports medicine

Intramuscular injection of Botulinum toxin to produce reduction of focal muscle overactivity, and localized muscle spasm, has been utilized therapeutically for almost two decades. Muscle overactivity in neurologically normal muscle, where an imbalance exists between a relatively overactive muscle and its less active synergist or antagonist, can inhibit control of the antagonist producing a functional muscle imbalance. This brief review provides an overview of the role of muscle imbalance in sports-related pain and dysfunction, and outlines the potential for intramuscular injection of Botulinum toxin to be used as an adjunct to specific muscle re-education and functional rehabilitation in this patient group. A comprehensive understanding of normal movement and the requirements of the sporting activity are essential to allow accurate diagnosis of abnormal motor patterns and to re-educate more appropriate movement strategies. Therapeutic management of co-impairments may include stretching of tight soft tissues, specific re-education aimed at isolation of the non-dominant weak muscles and improvement in their activation, ‘unlearning’ of faulty motor patterns, and eventual progression onto functional exercises to anticipate gradual return to sporting activity. Intramuscular injection of Botulinum toxin, in carefully selected cases, provides short term reduction of focal muscle overactivity, and may facilitate activation of relatively ‘inhibited’ muscles and assist the restoration of more appropriate motor patterns.

Relationship of rebleeding and external ventricular drainage in patients with subarachnoid hemorrhage of aneurysmal origin

It is one of the unsolved mysteries in neurosurgery: why and when intracranial aneurysms rupture. Several causes have been adduced, like the size of the aneurysm, its location, tissue properties of the aneurysm wall and changes in transmural pressure gradients, just to name a few. Similarly, nobody knows definitely why an aneurysm stops bleeding once it has ruptured. In some instances it may be a temporary breakdown of cerebral circulation due to a massively increased intracranial pressure, while others believe that a local vasospasm and thrombus formation are functional in stopping the haemorrhage. Some more substantial ideas are available for the causes of re-haemorrhage, like thrombolysis and fibrinolysis in the vessel and around the rupture location, as well as relaxation of the local spasm. In this context, it is of utmost importance to know which factors could increase the risk of re-bleeding once the patient reached clinical service, and is suitable for treatment of the aneurysm. The paper of Fountas et al. has to be considered in this context. It reviews the literature regarding the relation of rebleeding and external ventricular drainage after aneurysmal subarachnoid haemorrhage (SAH). It is a well known fact that acute hydrocephalus after SAH can deteriorate the patient’s initial condition severely. In other words, a low—and thus favourable—Hunt Hess Grade can be masked by an acute hydrocephalus. Therefore, a timely drainage of a hydrocephalus can have a significantly positive influence on the patient’s clinical status. Thus, this therapeutic option is an essential part of the treatment of aneurysmal SAH and may be quite often necessary even before a definitive occlusion of the aneurysm is possible. In their study, the authors scanned the published patient series of the last 50 years. Unfortunately the results are ambiguous. A number of studies report an increased incidence of haemorrhages after external ventriculostomy in patients with unclipped aneurysms. The incidence ranges from 17% to 43% and is higher than in the control groups used in these studies. Some of the authors see a direct relation of the incidence of rebleeding to the level of intracranial pressure. Therefore, they recommend a special management of the ICP levels to reduce the risk of rebleeding. On the contrary to these results, Fountas et al. found several studies that could not see any influence of ventricular drainage on the incidence of re-haemorrhage at all. The rate of rebleeding ranges from 4.4% to 16% in these ‘negative’ studies. As Fountas et al. emphasise, the studies are very heterogeneous in their design. One major problem is the controls. Some studies use real controls; others compare their data with historical data. In addition, the comparison of the percentage of the re-haemorrhages reported in the ‘positive’ and ‘negative’ studies shows that there seems to be some overlap, as 16–17% does not show so much difference. In addition, the patient groups included in the studies are not homogenous, as patients with haemorrhage of unknown aetiology were included, as well. Another relevant parameter seems to be the duration of drainage, as well as the timing of aneurysm occlusion. As one could predict, the earlier the definitive occlusion of the aneurysm the less was the rebleeding rate, even in the patients with ventricular drainage. In the interpretation of the data some overlap of the natural rebleeding rate and the influence of ventriculostomy have also to be taken into account. Finally, it is well known that poor grade patients have higher incidences of hydrocephalus and rebleeding. These additional influences have been addressed clearly only in one paper. This commentary refers to the article http://dx.doi.org/10.1007/ s10143-005-0423-4

Unstable Angina in 1998

Unstable angina (UA) and non-Q-wave myocardial infarction (NQWMI) are acute coronary syndromes with repeated, severe ischemic events of short duration. These events are mainly due to a rapid decrease in coronary blood flow, and to a rapid, reversible reduction of the arterial lumen in localized areas. Episodes often are a mixture of thrombus formation due to platelet aggregation and localized spasm, leading to vasoconstriction. Due to the short interval (minutes) of ischemic events, usually no or minimal irreversible myocardial damage takes place. The main goal of treatment is to prevent progression of this unstable situation into a myocardial infarction. In the majority of cases, this is possible with adequate treatment of vasodilatory substances like nitrates, long-acting dihydropyridines like amlodipine and betablockers. In addition heparin and particular antiaggregatory drugs inhibiting platelet activation by blocking the GPIIb/IIIa receptor, the common pathway for platelet aggregation, are applied to prevent thrombus formation. This, in the majority of cases allows a passivation of the acute situation, leaving time to undertake possible further steps as coronary angiography, eventually followed by PTCA of the culprit lesion or, in advanced cases of CAD, by CABG with complete revascularization.

Quantitative Coronary Angiographic Analysis of Spasm and Elastic Recoil After High Speed Rotational Atherectomy

This study evaluates the short‐term changes in coronary artery segments treated with high speed rotational atherectomy (HSRA). Quantitative coronary angiographic (QCA) analysis indices, such as degree of expected ablation, elastic recoil, and segmental spasm, were examined in 133 patients and restudied 24 hours after HSRA. The study was also designed to compare the early results of three different HSRA strategies: stand‐alone (SA) HSRA; HSRA with adjunctive high (≥ 4 atm) pressure (HP BA) and low (≥ 2 atm) pressure balloon angioplasty (LP BA). Previous studies have suggested negligible elastic recoil after HSRA as well as demonstrated the possibility of further continuous improvement in vessel patency up to 24 hours postprocedure. From a total of 656 patients treated with HSRA, a cohort of 133 patients with successful HSRA of 167 lesions were restudied angiographically at 24 hours. Serial QCA evaluation of the treatment site was performed. Analysis of the relative gain in minimal luminal diameter (MLD) assessed at 24 hours postprocedure showed that the highest gain group (> 40%) had narrower initial lesions compared to moderate gain (1%–40%), or MLD loss groups (MLD 0.5 ± 0.4 mm vs 1.0 ± 0.3 and 1.5 ± 0.4, respectively, P < 0.01). The initial percent diameter stenosis was also higher in the high gain group (77.1 ± 16.0 vs 61.9 ± 11.8 and 53.0 ± 11.9, P < 0.01). Immediately postprocedure there was a significant increase in MLD and a decrease in percent diameter stenosis. There was no difference in residual lesion characteristics postprocedure. While progressive MLD decrease was observed in the loss group (MLD postprocedure 1.6 ± 0.5 and 1.2 ± 0.6 at 24 hours, P < 0.01), a continuous increase in MLD was noted in the high gain group (MLD postprocedure 1.7 ± 0.5 mm vs at 24 hours 2.0 ± 0.5 mm, P < 0.01). The high gain group was characterized by the most lesion debulking, the most pronounced segmental spasm, and the least elastic recoil. Adjunctive HP BA was associated with the largest size vessels (D ref. in SA HSRA group was 2.6 ± 0.8 mm vs 2.9 ± 0.6 mm in LP BA and 3.0 ± 0.7 mm in HP BA groups, P < 0.01), the lowest elastic recoil (SA HSRA 23.8%± 20.9% vs LP BA 15%± 16.8% and HP BA 5.7%± 14.4%, P < 0.05), and the highest incidence of vessel dissection (SA HSRA 8.1% vs LP BA 14.7% and HP BA 34.0%, P < 0.05). However, these larger vessels underwent the least amount of lesion debulking (SA HSRA 46.4%± 27.2% vs LP BA 38.6%± 24.0% and HP BA 30.5%± 19.5%, P SA HSRA vs. HP BA < 0.001). There are measurable degrees of elastic recoil and local spasm observed after HSRA. HSRA of the most severe lesions yields the highest procedural gain, the lowest elastic recoil and the highest index of lesion ablation. In addition, some late increase in the MLD due to the resolution of spasm is observed at 24 hours postprocedure. SA HSRA is associated with higher degrees of expected lesion ablation. This is comparable to the degree of improvement in MLD, where adjunctive percutaneous transluminal coronary angioplasty is utilized as assessed at 24 hours postprocedure. HSRA with adjunctive HP BA yields immediate results showing the least elastic recoil and spasm at the expense of the highest incidence of dissection and side branch loss.

Selective intra-arterial chemotherapy with a combination of etoposide and cisplatin for malignant gliomas: Preliminary report

We administered selective intra-arterial chemotherapy consisting of a combination of etoposide and cisplatin to 20 patients with malignant glioma (seven with recurrent and six with enlarged tumors after initial treatment, and seven newly diagnosed patients). Evaluation of efficacy was based on computed tomographic and magnetic resonance imaging findings. In the process of establishing a safe technique for superselective intra-arterial chemotherapy, we encountered cerebrovascular accidents in two patients (after etoposide in one and after etoposide plus cisplatin in the other). In these two cases, 100 mg/m 2 of etoposide and 100 mg/m 2 of cisplatin were delivered via the horizontal segment of the middle cerebral artery (M1) or the tip of the basilar artery, with the infusion time reduced to 20 minutes. Thereafter, the etoposide was diluted, and the doses of both drugs were reduced to 80 or 50 mg/m 2, and finally to 60 mg/m 2, and both were infused over 60 minutes. In addition, for prevention of local spasm, papaverine hydrochloride and nicardipine were given via the same catheter at 5-minute intervals during administration of etoposide and cisplatin. No complications developed in the later cases. Thereafter, selective intra-arterial infusion of etoposide and cisplatin into the anterior cerebral artery, middle cerebral artery, posterior cerebral artery, or the basilar artery for malignant gliomas in the basal ganglia, internal capsule, and brainstem-a procedure generally considered risky in terms of potential complications-was performed safely, with tolerable side effects. Computed tomography and magnetic resonance imaging indicated improvement in 13 patients, including four whose tumors completely disappeared. This method of intra-arterial chemotherapy may be useful as an adjuvant treatment for malignant glioma.

Effect of direct intracoronary administration of methylergonovine in patients with and without variant angina

The effects of intracoronary administration of methylergonovine were studied in 21 patients with variant angina and 22 patients with atypical chest pain and in others without angina pectoris (control group). Methylergonovine was administered continuously at a rate of 10 μg/min up to 50 μg. In all patients with variant angina, coronary spasm was provoked at a mean dose of 28 ± 13 μg (mean ± SD). In the control group neither ischemic ST change nor localized spasm occurred. The basal tone of the right coronary artery was significantly lower than that of the left coronary artery. The percentage of vasoconstriction of the right coronary artery was significantly higher than that of the left coronary artery. These results suggest that spasm provocation tests, which use an intracoronary injection of a relatively low dose of methylergonovine, have a high sensitivity in variant angina and the vasoreactivity of the right coronary artery may be greater than that of the other coronary arteries.

Selektive ambulante transbrachiale intraarterielle DSA der supraaortalen Arterien bei atypischen Abgängen der supraaortalen Arterien

We have already published the technique of SATISDA of supra-aortic arteries using the Tomac 1-3 catheter. In this group of 500 patients, selective demonstration of individual supra-aortic arteries was unsuccessful in 77 patients (15.4%). Demonstration was unsuccessful of three left vertebral arteries (0.6%), 45 left carotid arteries (9%), right carotid in nine (1.8%) and right vertebral artery in 20 (4%). In most cases the failure was due to an atypical origin of the vessel. To increase the success rate we used a 4-French newly developed straight Tomac 4-5 catheter. Using a combination of both catheters, selective demonstration of the left carotid was successful in 41 patients (91.1%), the right carotid in 8 (88.8%) and the right vertebral in 18 (90%). In three patients, a left-sided catheterisation had to be performed to demonstrate the left vertebral artery. Complications consisted of 17 local haematomas (3%) and reversible spasm at the puncture site in one patient (0.2%).

Mechanism of paradoxical resistance of the digastric muscle to the action of tetanus toxin

Excitability parameters of m. masseter and m. digastricus fibers (resting minute potential--MP, action potential--AP, critical level of depolarization--CLD and rheobase currents) were determined in anesthetized rats (nembutal, 40 mg/kg) on days 3-4 and 10-15 after local intramuscular tetanus toxin injection (20 and 40 mouse Dlm, respectively). The development of local tetanus in m. masseter was characterized by typical excitability changes--a decrease in MP and AP. Local spasm in m. digastricus under analogous conditions of tetanus toxin injection was absent, while excitability tests demonstrated MP, AP and CLD augmentation. As m. digastricus motoneurons are devoid of inhibitory synaptic regions, these nervous cells are not affected by tetanus toxin.

Blood-induced arterial segmental spasm.

Blood-induced arterial segmental spasm has been noticed clinically, and is thought to result from contact between a main feeding artery and extravasating blood from one of its side branches. This localized spasm can persist long enough to compromise the survival of a replantation or flap transfer. A partially amputated rat hind limb model was used to investigate this phenomenon. Bleeding from a side branch was shown to cause severe vasoconstriction and reduced limb perfusion only on direct contact with the main artery. Pretreatment with heparin and minimization of endothelial damage resulted in decreased vasospasm, but aspirin pretreatment had no effect on the degree of spasm and resulting reduced blood flow. This study demonstrates the clinical importance of careful ligation of side branches to reduce vasospasm that may compromise the survival of a replanted part or tissue flap.

Factors in delayed onset muscular soreness of man

In this study 11 subjects performed exercise resulting in delayed onset muscular soreness in m. gastrocnemius with one leg, the experimental leg. The other leg served as control. Pre-exercise and 24, 48 and 72 h postexercise, soreness perception, resting EMG level of m. gastrocnemius, and volume and skin temperature of both legs were measured, and a leukocyte count was performed. Perception of soreness in m. gastrocnemius reported 24, 48, and 72 h postexercise was not accompanied by an increase in resting EMG level. This result indicates that soreness perception is not related to a tonic localized spasm in sore muscles. A rise in volume of the experimental leg relative to volume of the control leg was found 24, 48, and 72 h postexercise (P less than 0.05). It is suggested that the volume rise is due to edema formation in the experimental leg and that this edema formation is responsible for soreness perception. Since granulocytosis was not found, the hypothesis that edema formation reflects muscle inflammation is not substantiated.

Functional differences in blood vessels determined from studies with calcium-channel blockers: Functional changes in forearm resistance vessels of men with primary hypertension

Vascular smooth muscle is activated through 2 major systems. One, which can be inhibited by calcium-entry blocking agents, involves the influx of calcium through potential-sensitive channels. The other, which can be inhibited by sodium nitroprus-side, involves the entry of calcium through agonist-controlled channels and probably its mobilization from within the cell as well. Human veins, muscular arteries and resistance vessels show differing patterns of response to agents that selectively inhibit the 2 activation systems. The responses indicate that physiologic contractions of cutaneous veins and muscular arteries depend on the agonist-controlled system; contractions of veins induced by high concentrations of potassium depend on the potential-sensitive system as, probably, does local spasm in arteries. The tone of resistance vessels depends on a balance between the potential-sensitive and agonist-controlled systems. The forearm resistance vessels of men with primary hypertension respond to verapamil with larger-than-normal dilatation compared with that induced by nitroprusside. This is interpreted as showing an increased contribution to resistance vessel tone from the potential-sensitive system. This functional abnormality does not depend on the inhibition of sodium pump activity that is known to occur in hypertension, because it cannot be reproduced by local infusion of ouabain. It probably results from a primary disorder of calcium handling by the cell membrane.

Vasospasm of the vertebrobasilar system in cases of ruptured intracranial aneurysm.

Abstract The reported incidence of vasospasm in cases of ruptured vertebrobasilar (VB) aneurysm varies considerably. The classification into local and diffuse spasm may partially explain the discrepancy. In the present small series, we found that local spasm is more common than diffuse spasm, which is rare in cases of ruptured VB aneurysm when compared with ruptured supratentorial aneurysm. It is hoped that further work may help to explain this apparent difference between the anterior and the posterior circulation and may contribute to the understanding of vasospasm.

Coronary Artery Spasm With Sinus Node Dysfunction and Syncope

In a 55-year-old man, attacks of spontaneous angina were associated with dizziness and syncope. Holter ECG monitoring disclosed evidence of sinus node dysfunction. Dizziness and syncope were corrected by a permanent ventricular demand pacemaker. Coronary cineangiography showed spontaneous, severe, diffuse spasm in a dominant left coronary artery and localized spasm in a nondominant right coronary artery. The patient died of pump failure shortly after cardiac catheterization. An autopsy disclosed only minimal coronary atherosclerosis. This patient's condition shows that (1) coronary spasm may cause sinus node dysfunction, dizziness, and syncope, (2) severe spasm that involves all the coronary artery branches may be fatal, and (3) severe spasm occur in minimally diseased coronary arteries confirmed by pathologic examination.

Ergonovine maleate test in various anginal syndromes.

The ergonovine maleate (EM) test has been performed in four groups of 10 patients each: (A) variant angina; (B) angina at rest with ST segment depression during pain; (C) effort angina; (D) atypical chest i pain. EM was injected i.v. (highest dose 0-4 mg) first in the Coronary Care Unit and thereafter during coronary angiography. EM caused coronary spasm with angina and ST segment elevation in every patient of group A and in one patient of group B. In five and four patients of groups B and C, respectively, EM induced angina and ST segment depression without any localized coronary spasm, the coronary angiography showing only a diffuse narrowing of the coronary vessels; these patients had the lowest effort tolerance and the most severe coronary lesions. Spontaneous or induced coronary spasm in patients with angina at rest and ST segment depression during chest pain did not occur in this study. An increase of the peripheral and/or coronary resistances due to EM could be the mechanism of the ischemic attack in patients with severe coronary lesions.

Diagnosis of pulmonary embolism: experimental evaluation of the accuracy of scintigraphically guided pulmonary arteriography.

Technically refined angiograms and scintigrams were extremely sensitive in demonstrating experimental canine thromboemboli, both immediately after embolization and during the entire course of embolic lysis. Technical refinements included subselective, scintigraphically guided, magnification arteriography and eight-view perfusion scintigraphy. During thromboembolic lysis, excellent angiographic-scintigraphic correlation persisted. For every postembolic perfusion defect, the embolic basis could be demonstrated angiographically. Thus, apparent disparities between angiographic and scintigraphic evidence of embolism can no longer be attributed to lysis. Studies using nonresorbable Ivalon emboli indicated that localized spasm may play an important role in the perfusion defects that develop within a half hour after embolization, and that this spasm subsides considerably within 24 hours.

Arterial spasm and recovery from subarachnoid haemorrhage.

In a series of 120 cases of subarachnoid haemorrhage due to ruptured intracranial aneurysm the occurrence of preoperative arterial spasm was found to have no effect upon the clinical outcome. After surgery, generalised arterial spasm was found to lead to an increased probability of fatality, and to an increased probability of psychological impariment among the survivors. The occurrence of spasm only in the vessels immediately adjacent to the haemorrhage did not constitute a risk to survival. However, the presence of generalised or localised spasm led to an increased risk of neurological impairment. It is suggested that the mechanisms by which postoperative arterial spasm is responsible for fatalities and for neurological impairment are distinct.

Chronic cerebral arterial spasm. The role of intracranial pressure.

The author used isolated rabbit common carotid and femoral arteries perfused at a constant pressure of 90 mm Hg to examine the variation of flow (F) with transmural pressure (TMP). When the TMP was reduced below 50 to 60 mm Hg in arteries with normal smooth muscle tone, arterial resistance increased significantly causing a reduction in flow. It is suggested that the diffuse arterial narrowing that occurs in patients with severe intracranial hypertension may be the result of a similar reduction in TMP. In the presence of active vasoconstriction, any increase in extraluminal (intracranial) pressure (ICP) resulted in a substantial increase in arterial resistance and subsequent reduction of flow. This F-TMP relationship depended only on the initial degree of constriction and was independent of the vasoconstrictor used to achieve this constriction and of the artery in which this constriction was produced. A review of the literature suggests that human cerebral arteries normally exhibit only mild constrictions in response to subarachnoid blood during the chronic phase of spasm. In the present study, a mild constriction in the absence of increased ICP or a moderate increase in ICP (45 mm Hg) in the absence of constriction produced minor reductions in arterial diameter and an average flow reduction of only 5% to 10%. However, when ICP was increased to 45 mm Hg in the presence of a mild constriction, severe arterial narrowing resulted and flow was reduced by 50%. Therefore, it is suggested that chronic arterial spasm is the result of a mild constriction which is amplified by the simultaneous occurrence of increased ICP. Phenoxybenzamine was found to be effective in reversing and preventing these contractions. The improvement in flow produced by phenoxybenzamine decreased as the TMP was reduced below 60 mm Hg. The effects of both diffuse and local spasm on cerebral blood flow are discussed.

Letter: Adynamic ileus of the colon.

To the Editor. –In his report on the management of adynamic ileus of the colon ( Arch Surg 109:503, 1974), Dr. Adams notes that, among his 20 patients, maximal distention was invariably segmental with an apparently abrupt cutoff of the more severely distended proximal part of the colon. The only possible explanation for this situation, in the absence of organic obturation or extrinsic compression, would be a kink or local spasm of the bowel. The fact that in every case the location of the cutoff was at one of the major bowel flexures, and the ease with which contrast agent administered under pressure in retrograde fashion flowed through the cutoff point, strongly suggest a kink due to overdistention. It would appear, therefore, that the basic objective of management in such cases is prompt decompression of the proximal part of the dilated segment. An ordinary rectal tube would rarely be long enough