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PubMed2000

Multifidus spasms elicited by prolonged lumbar flexion.

STUDY DESIGN: The electromyogram of the L1-L7 multifidus muscles of the in vivo cat were recorded while applying a prolonged steady displacement to the lumbar spine through the L4-L5 supraspinous ligament, simulating a moderate anterior flexion. OBJECTIVE: To demonstrate that tension-relaxation and laxity of the viscoelastic structures (ligaments, discs, and capsules) induced by prolonged static flexion of the spine results in loss of reflexive muscular stabilizing activity and in muscular disorders that may lead to or are associated with low back pain. SUMMARY OF BACKGROUND: Epidemiologic data show that prolonged loading of the spine, such as in some occupational activities, can cause low back pain and muscle spasms. Direct experimental evidence linking prolonged loading to a decrease in spinal stability, low back pain, and muscle spasms was not found. It was hypothesized, however, that mechanoreceptors in the viscoelastic structures, when strained, reflexively activate the multifidus muscles to maintain intervertebral stability; that the reflexive muscular activity decreases with stress-relaxation and laxity in the viscoelastic structures; and that when severe strain and possible damage of the viscoelastic structures occurs with time, nociceptive receptors elicit spasms in the musculature and possible pain. METHODS: The lumbar spine of seven in vivo cat preparations was displaced through the L4-L5 supraspinous ligament into moderate flexion that was steadily maintained for 50 minutes while intramuscular electromyograms were recorded from each of the multifidus muscles of L1-L2 through L6-L7. Load and electromyogram were continuously monitored and recorded. Five additional preparations were used as controls, in which dissection and recordings were identical, but the lumbar flexion was excluded. RESULTS: Prolonged flexion of the lumbar spine resulted in initial reflexive electromyogram from the multifidus muscles that decreased to approximately 5% of its initial value as tension-relaxation began in the viscoelastic structures within the first 3 minutes, after which, random and unpredictable electromyogram discharges (i.e., spasms) of high amplitude were recorded from different levels. In some preparations the spasms were present in L1-L4, and in others in all the levels. In other preparations the spasms were recorded only at L5 and L6. The onset of the spasms was also unpredictable, because they were initiated in some cases within 2-3 minutes after the spine was loaded. In other cases, the spasms were observed anytime during the test period and up to 20 minutes after the load was removed. Spasms were also observed in the spinalis and longissimus muscles. CONCLUSIONS: Prolonged flexion of the lumbar spine results in tension-relaxation and laxity of its viscoelastic structures, loss of reflexive muscular activity within 3 minutes and electromyogram spasms in the multifidus and other posterior muscles.

Animals↗
PubMedDate not supplied

The axial spasm--the predominant type of drop seizure in patients with secondary generalized epilepsy.

In 45 patients suffering from secondary generalized epilepsy, we have recorded 239 drop seizures both by radio-telemetered EEG/split-screen video taping and polygraphically. Twenty of these patients had pure tonic drop seizures. Nine patients each had myoclonic-atonic or pure atonic seizures, whereas seven had slow falls that occurred during gradually developing tonic or akinetic seizures. We term the pure tonic drop seizure "axial spasm." It consists of a uniform pattern of movement lasting from 0.5 to 0.8 s and leading to a specific bearing characterized by a moderate flexion of the hips, the upper trunk, and the head. The arms are almost always involved being abducted, elevated and in a semiflexed position. A fall is provoked by the rapidity and violence of the flexion in the hips. The spasms can occur independently (pure axial spasm) or in connection with other seizure manifestations (combined axial spasm). In pure spasms, no disturbance of consciousness and no significant EEG changes--apart from a slight attentuation--are seen. In the combined axial spasms, distinct epileptic phenomena, in close connection with the axial spasms, can be observed, appearing either in the postspasm phase or in both the pre- and the afterphases. The prephase consists always of an absence and spike-and-wave activity. The onset of the spasm coincides with the last generalized spike, which is followed by a biphasic high-voltage slow wave. In the afterphases, various seizure patterns can be seen; quite characteristic are arrest states during which the patients are completely immobile and take up a postural-like or athetoid position. Almost as frequent are absences or absence-like states and tonic seizures. The afterphase can be compounded by two or three of these seizure patterns, the most common sequence of events in these cases being tonic--arrest state--absence. From the clinical and neurophysiological points of view, axial spasms can be regarded as a more mature form of infantile spasms. Clinical and experimental findings suppose a brainstem origin.

Adolescent↗
PubMed1992

Treatment of infantile spasms: medical or surgical?

Although infantile spasms were initially described in 1841, remarkably little progress has been made in understanding the pathophysiology of this "peculiar form of infantile convulsions." Consequently, our ability to treat infantile spasms is limited. Infantile spasms are classified as a "generalized" seizure disorder in the international classification system, which suggests that the underlying brain abnormality causing the seizures also must be diffuse or generalized. As the classification suggests, there are many diffuse, or multifocal, brain disorders related to infantile spasms, e.g., inborn errors of metabolism, hypoxic-ischemic brain injury, and developmental brain defects such as tuberous sclerosis or Aicardi's syndrome. On the other hand, infantile spasms have been reported in which a localized brain abnormality was present, e.g., tumor, stroke, and trauma. On rare occasions, removal of a tumor has resulted in cessation of the generalized infantile spasms. This finding suggests that focal cortical abnormalities can cause infantile spasms and that removing the abnormality can stop the seizures. At University of California, Los Angeles, the Pediatric Epilepsy Surgery Program has developed new approaches to the treatment of infantile spasms. The principal underlying concepts are (a) children with medically refractory infantile spasms may have an area of cortical defect (called the zone of cortical abnormality) that causes the seizures and (b) infantile spasms are usually generalized seizures. Thus, the goal of the surgical assessment is not the identification of the focus of seizure onset but rather the identification of the zone of cortical abnormality.

Adrenocorticotropic Hormone↗
PubMed1995

Asymmetric and asynchronous infantile spasms.

Infantile spasms most commonly show symmetric behavioral and electroencephalogram (EEG) manifestations. Asymmetric and asynchronous behavioral spasms occur occasionally, but their relationship to ictal EEG and to other localizing studies has not received much attention. We reviewed 75 consecutive video-EEG recordings, done at UCLA from 1982 to 1992, that contained infantile spasms; 8,680 spasms were scored for behavioral and EEG asymmetry and asynchrony. Of the recorded spasms, 25% were asymmetric and 7% were asynchronous. Most asymmetric of asynchronous spasms were associated with an ictal EEG discharge that was contralateral to the behaviorally more involved side. In 12 of the 60 patients (20%), more than half of the recorded spasms were asymmetric of asynchronous. Baseline EEG, magnetic resonance imaging, positron emission tomography, and neurological examination revealed structural and functional brain abnormalities that involved the contralateral central region significantly more often in the children with > 50% spasm asymmetry or asynchrony than in the other children. Partial seizures with lateralized motor behavior also occurred frequently in these children. The findings suggest that asymmetric and asynchronous spasms are generated by a cortical epileptogenic region that involves the primary sensorimotor area. The combination of asymmetric and asynchronous infantile spasms, partial motor seizures involving the same side of the body, and pathology in the contralateral central region may represent a unique subset of symptomatic localization-related infantile epilepsy.

Cerebral Cortex↗
PubMed1987

Monitoring facial EMG responses during microvascular decompression operations for hemifacial spasm.

Facial electromyographic (EMG) responses were monitored intraoperatively in 67 patients with hemifacial spasm who were operated on consecutively by microvascular decompression of the facial nerve near its exit from the brain stem. At the beginning of the operation, electrical stimulation of the temporal or the zygomatic branch of the facial nerve gave rise to a burst of EMG activity (autoexcitation) and spontaneous EMG activity (spasm) that could be recorded from the mentalis muscle in all patients. In some patients, the spontaneous activity and the autoexcitation disappeared after the dura was incised or when the arachnoid was opened, but stimulation of the temporal branch of the facial nerve caused electrically recordable activity in the mentalis muscle (lateral spread) with a latency of about 10 msec that lasted until the facial nerve was decompressed in all but one patient, in whom it disappeared when the arachnoidal membrane was opened. When the facial nerve was decompressed, this lateral spread of antidromic activity disappeared totally in 44 cases, in 16 it was much reduced, and in seven it was present at the end of the operation at about the same strength as before craniectomy. In four of these last seven patients there was still very little improvement of the spasm 2 to 6 months after the operation; these four patients underwent reoperation. In two of the remaining three patients, the spasm was absent at the 3- and 7-month follow-up examination, respectively, and one had mild spasm. Of the 16 patients in whom the lateral spread response was decreased as a result of the decompression but was still present at the end of the operation, 14 had no spasm and two underwent reoperation and had mild spasm at the last examination. Of the 44 patients in whom the lateral spread response disappeared totally, 42 were free from spasm and two had occasional mild spasm at 6 and 13 months, respectively, after the operation. Monitoring of facial EMG responses is now used routinely by the authors during operations to relieve hemifacial spasm, and is performed simultaneously with monitoring of auditory function for the purpose of preserving hearing. The usefulness of monitoring both brain-stem auditory evoked potentials recorded from electrodes placed on the scalp and compound action potentials recorded directly from the eighth cranial nerve is evaluated.

Electromyography↗
PubMed1989

[A case of unilateral masticatory spasm without hemifacial atrophy].

Masticatory spasm is a rare clinical feature and mostly associated with disorders of general movement. Usually it occurs bilaterally. Unilateral masticatory spasm is mostly associated with facial hemiatrophy. So, unilateral masticatory spasm without facial hemiatrophy is extremely rare. As far as we have investigated, only one case has been reported in the literature. We will report one more case herein, with some discussion on its pathogenesis. Case report A 44-year-old man presented with a 8 month history of slowly progressive recurrent spasm of the left masseter muscle. The spasm was exaggerated by tension and lasted for up to 10 seconds. Several drugs could not reduce the frequency of spasm, but only clonazepam could decrease it slightly. On admission, the spasm lasted usually for 1 or 2 seconds. Except for masticatory spasm, neurological examination comprising trigeminal nerve function, was normal and facial atrophy was not observed. On the contrary, hypertrophy of the left masseter muscle was noted. Needle electromyography (EMG) study revealed synchronized spasm discharges of the ipsilateral masseter, lateral and medial pterygoid muscles. All of other investigations, including CSF analysis, electroencephalography, somatosensory evoked potential, visual evoked potential, CT scan and vertebral angiography, showed normal findings. After all, we could not find any apparent organic lesions which cause masticatory spasm, so surgical treatments were not carried out. He was discharged and now, continues to take clonazepam daily.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Botulinum toxin-A for the treatment of hemifacial spasm.

Management of hemifacial spasm can actually be done medically, surgically and with Botulinum-A Toxin. The Botulinum-A Toxin treatment locally injected into the involved facial muscles offers a useful alternative to medical and surgical therapy. The objective of this study was to evaluate the efficacy of Botulinum-A Toxin for the treatment of hemifacial spasm in those subjects for whom the presently available medical therapy is inadequate. A total of 28 individuals were enrolled in the clinical study. Patients were evaluated using the Fahn's blepharospasm rating and disability scales. Efficacy was assessed by evaluating changes from the baseline in eyelid spasm intensity, brow spasm intensity, eyelid force and facial spasm intensity. All 28 subjects with hemifacial spasm showed clinical improvement in relation to this baseline, which was statistically significant. The mean decrease from baseline at their follow-up examination was statistically significant for all subjects and for all measurements: eyelid spasm changed from 2.3 to 0.3 (p = 0.0001); brow spasm from 1.9 to 0.1 (p = 0.0001); facial spasm from 2.3 to 0.1 (p = 0.0001) and eyelid force from 0.9 to -0.1 (p = 0.0020). We concluded that Botulinum-A Toxin provides a significant therapeutic benefit to patients with hemifacial spasm, without the risk of disabling side effects.

Adult↗
PubMed1982

Perioperative coronary arterial spasm: long-term follow-up.

Six patients who survived episodes of coronary arterial spasm occurring immediately after coronary bypass grafting were followed up for 15 to 30 (mean 20) months after operation. In all patients coronary spasm occurred in an unobstructed dominant right coronary artery and caused inferior transmural ischemia. Sudden circulatory collapse occurred in five of the six patients as a consequence of acute coronary spasm. All patients were treated with nitroglycerin followed by nifedipine. No patient has had recurrent angina or other evidence of spontaneous coronary spasm since surgery. Cardiac catheterization studies, including ergonovine maleate testing, were repeated 3 to 12 months after surgery in five of the six patients. The right coronary artery and all bypass grafts were patent in all five. Four patients had new inferior wall motion abnormalities. Ergonovine provoked focal right coronary arterial spasm in one patient. It is concluded that manifestations of coronary spasm after myocardial revascularization range from asymptomatic S-T segment elevation to severe hypotension. These episodes of perioperative spasm may cause myocardial necrosis. Coronary spasm has not recurred in patients who survived perioperative spasm, but some patients may have a continued predisposition to development of coronary spasm late after surgery.

Adult↗
PubMed1997

Hyperventilation as a specific test for diagnosis of coronary artery spasm.

The hyperventilation test has been used as a clinical tool to induce coronary spasm. However, its diagnostic and prognostic values have not been fully elucidated. This study was designed to establish the sensitivity and specificity of the hyperventilation test and to clarify the characteristics of hyperventilation test-positive patients. We examined 206 patients in whom coronary spasm was documented by angiography (spasm group), and 183 patients without angina at rest in whom acetylcholine failed to induce spasm (nonspasm group). All patients performed vigorous hyperventilation for 6 minutes in the early morning. Of the spasm group patients, 127 showed positive responses to the test, including ST elevation (n = 111), ST depression (n = 15) and negative U wave (n = 1). None in the nonspasm group showed any ischemic electrocardiographic change. Thus, the sensitivity and specificity of this test for diagnosis of coronary spasm were 62% and 100%, respectively. In the spasm group, there were no significant differences between hyperventilation test-positive and test-negative patients in age, sex, the prevalence of hypertension, diabetes mellitus, obesity, smoking, and the number of diseased vessels. When clinical characteristics were compared, the proportions of the patients with high disease activity (> or =5 attacks a week), with severe arrhythmias (second- or third-degree atrioventricular block and/or ventricular tachycardia) during attacks, and with multivessel spasm were significantly higher in the hyperventilation test-positive patients than in the negative patients (69% vs 20%, p <0.0001; 31% vs 11%, p <0.005; and 58% vs 34%, p <0.01, respectively). These findings imply that hyperventilation is a highly specific test for the diagnosis of coronary artery spasm, and that hyperventilation test-positive patients are likely to have life-threatening arrhythmias during attacks and multivessel spasm.

Adult↗
PubMed1998

Angina pectoris caused by coronary microvascular spasm.

BACKGROUND: Microvascular angina can occur during exercise and at rest. Reduced vasodilator capacity of the coronary microvessels is implicated as a cause of angina during exercise, but the mechanism of angina at rest is not known. Our aim was to test the hypothesis that primary hyperconstriction (spasm) of coronary microvessels causes myocardial ischaemia at rest. METHODS: Acetylcholine induces coronary artery spasm in patients with variant angina. We tested the effects of intracoronary acetylcholine at graded doses in 117 consecutive patients with chest pain (at rest, during exertion, or both) and no flow-limiting (>50%) organic stenosis in the large epicardial coronary arteries. We also assessed the metabolism of myocardial lactate during acetylcholine administration in 36 of the patients by measurement of lactate in paired blood samples from the coronary artery and coronary sinus vein. FINDINGS: Of the 117 patients, 63 (54%) had large-artery spasm, 29 (25%) had microvascular spasm, and 25 (21%) had atypical chest pain. The 29 patients with microvascular spasm developed angina-like chest pain, ischaemic electrocardiogram (ECG) changes, or both spontaneously (two patients) or after administration of acetylcholine (27 patients) without spasm of the large epicardial coronary arteries. Testing of paired samples of arterial and coronary sinus venous blood showed that lactate was produced during angina attack in nine of 11 patients with microvascular spasm. There was more women (p<0.01) and fewer coronary risk factors (p<0.01) in patients with microvascular spasm than in those with large-artery spasm. INTERPRETATION: Coronary microvascular spasm and resultant myocardial ischaemia may be the cause of chest pain in a subgroup of patients with microvascular angina.

Acetylcholine↗
PubMed2000

Comparison of the risk factors for coronary artery spasm with those for organic stenosis in a Japanese population: role of cigarette smoking.

We compared the risk factors for coronary spasm with those for coronary atherosclerosis in 183 patients with coronary spasm, 132 patients with coronary organic stenosis, and 224 control subjects with chest pain syndrome. Our findings confirmed that, when compared with controls, age, gender, total cholesterol, LDL-cholesterol, hypertension, diabetes mellitus, and cigarette smoking are all significant risk factors for coronary organic stenosis. On the other hand, only cigarette smoking proved to be a significant risk factor for coronary spasm. Also, when compared between coronary spasm group and coronary organic stenosis group, the incidence of cigarette smoking in males was significantly higher in the coronary spasm group than in the coronary organic stenosis group. We conclude that cigarette smoking is a crucial risk factor for coronary spasm. On the other hand, serum lipid levels and the incidence of hypertension and diabetes mellitus were within the normal ranges in the coronary spasm patients and were thus poorly associated with coronary spasm. These results showed that the risk factors for coronary spasm differ significantly from those for atherosclerosis-based coronary stenosis in the Japanese. Among the risk factors for coronary atherosclerosis (organic stenosis) smoking alone was a significant preventable risk factor for coronary artery spasm.

Aged↗
PubMed1999

The application of air bag technology: an objective clinical measure of involuntary muscle spasm.

OBJECTIVES: To develop a technique which could objectively monitor and quantify spasms in spinal cord injured persons. METHODS: This technique used accelerometers to detect movements in the limb caused by spasms. Accelerometer signals from movements caused by spasms and a variety of movements caused by other subject activities (movement in a wheelchair, transfers etc) were recorded and linear discriminant analysis was used to distinguish between spasms and other activities. Individual spasms were quantified by their duration, magnitude and energy and were recorded over a 24-h period. RESULTS: Limb movements caused by spasms were shown to be well correlated with the EMG activity of the muscles causing the movement. Movements caused by spasms and movements caused by other subject activities could be reliably distinguished. Subjects showed a characteristic spasm pattern and it was possible to quantify the severity of the spasms and to determine precisely when they occurred. CONCLUSION: This technique for monitoring and quantifying spasms has the potential to be used as a clinical tool to aid in the evaluation and prescription of treatment.

Biomechanical Phenomena↗
PubMed2005

Severe coronary artery spasm can be associated with hyperthyroidism.

BACKGROUND: Coronary artery spasm is not infrequently seen in Korea. Most of the patients with coronary spasm show a focal spasm in coronary angiography. However, the cause of the disease is not well known. There have been a few anecdotal case reports of coronary artery spasm associated with hyperthyroidism, but there has not been a report concerning a large series of such patients. Over a period of 5 years and 8 months, we experienced eight patients having the diffuse or severe type of coronary artery spasm in association with hyperthyroidism. METHODS: We investigated the characteristics of the patients with coronary artery spasm, which was diagnosed by coronary angiography or by provocation with an intracoronary injection of acetylcholine or ergonovine. The demographic data, coronary angiographic findings, thyroid function test results, and the follow-up clinical data of the eight patients having coronary artery spasm associated with hyperthyroidism were analyzed. RESULTS: All eight patients had Graves' disease. In six patients, the coronary arterial vasoconstriction developed during the coronary angiography without an injection of ergonovine. In three patients, the left main stem coronary artery was involved in the spasm. Among these eight patients, five were female, and all of these female patients were < or = 51 years old. All of the patients were treated with anti-thyroid medications, calcium channel blockers, and long-acting nitroglycerines; they all remained free of chest pain during the median follow-up period of 5 years. CONCLUSIONS: A severe form of coronary artery spasm could be associated with hyperthyroidism. A high level of suspicion and the thyroid function study should be mandatory for patients with coronary artery spasm, especially for the young female patients.

Angina, Unstable↗
PubMed1992

Purinoceptors mediating relaxation and spasm in the rat gastric fundus.

1. The relaxant and spasmogenic effects of purines and analogues were studied in longitudinal strips of rat gastric fundus to characterize the purinoceptors involved. Classification was studied by use of agonist potency orders and of antagonists in circumstances where the influence of confounding factors was reduced. In general tone was raised by carbachol (0.1 microM). 2. Adenosine produced relaxation and was potentiated by nitrobenzylthioinosine (NBTI, 0.3 and 30 microM), an adenosine-uptake inhibitor. 8-Sulphophenyl-theophylline (8-SPT, 30 microM), a selective P1-purinoceptor antagonist, antagonized adenosine and 5'-N-ethylcarboxamidoadenosine (NECA), a selective agonist at P1-purinoceptors. 3. At resting tone, adenosine 5'-triphosphate (ATP) induced a small, phasic relaxation followed by a maintained spasm. When tone was raised by carbachol, ATP induced a larger relaxation followed by a smaller spasm. NBTI did not potentiate ATP, nor did 8-SPT antagonize ATP, suggesting that ATP does not act directly or indirectly at P1-purinoceptors. 4. With raised tone, and in the presence of indomethacin (10 microM) and 8-SPT (30 microM), 2-methylthio ATP (2-MeSATP) and ATP produced relaxations followed by spasms while alpha,beta-methylene ATP (alpha,beta-MeATP) induced only relaxation; all responses were concentration-dependent. The compounds had similar slopes and maxima for relaxation and spasm. The rank orders of potency were 2-MeSATP much greater than alpha,beta-MeATP greater than ATP for relaxation and 2-MeSATP much greater than ATP for spasm.5. With raised tone, and in the presence of indomethacin and alpha 8-SPT, desensitization to alpha,beta-MeATP (100microM) completely and only slightly suppressed responses to ATP and 2-MeSATP, respectively, as relaxants but had no effect on relaxant responses to adenosine. The magnitude of the spasms to ATP and 2-MeSATP was considerably increased by desensitization with alpha,beta-MeATP but the spasm to KCl was not affected.6. With raised tone, and in the presence of indomethacin and 8-SPT, reactive blue 2 (10 AM) nonselectively antagonized ATP, 2-MeATP, a,P-MeATP, adenosine and isoprenaline as relaxants. Reactive blue 2 prevented the spasms to ATP and 2-MeSATP but not spasm to KC1.7. With raised tone, and in the presence of indomethacin, suramin (100 microM) antagonized ATP, but not adenosine, as relaxants and antagonized ATP, but not KC1, as spasmogens.8. It is proposed that adenosine is susceptible to nucleoside-specific uptake and acts predominantly via a P,-purinoceptor and also by a non-PI-purinoceptor mechanism. ATP- and alpha,beta-MeATP-induced relaxations probably occur via a P2x-purinoceptor. The anomalous nature of the 2-MeSATP-induced relaxation suggests it acts both via a P2x-purinoceptor and an additional mechanism. A P2y-purinoceptor is most likely to be involved in the spasms to ATP and 2-MeSATP. Therefore, the functional nature of the responses mediated by P2X- and P2y-purinoceptors, relaxation and spasm respectively, are opposite to those seen in most smooth muscles.

Adenosine Triphosphate↗
PubMed1968

Atropine-resistant longitudinal muscle spasms due to excitation of non-cholinergic neurones in Auerbach's plexus.

1. In accordance with the dual histology of Auerbach's plexus (Dogiel, 1899; Hill, 1927) two types of neurone can be shown to be humorally active in plexus-containing preparations of longitudinal muscle from guinea-pig ileum, taken at measured distances up to 95 cm above the ileocaecal valve, when such preparations are stimulated electrically under different conditions.2. The rapid twitch, lasting 3-8 sec, which is elicited by single shocks of 0.1 or 0.2 msec pulse width, and the effect of 5-15 ng doses of acetylcholine which matched this twitch, were both extinguished equally effectively and completely by atropine sulphate (0.4-1 x 10(-8) g/ml.) or by hyoscine hydrobromide. This twitch-response is therefore caused by an excitation of cholinergic motor neurones of normal susceptibility to atropine. These are believed to be the Dogiel (1899) Type II cells of Auerbach's plexus, as suggested by Hill (1927).3. After extinction of the twitch by the invariably effective atropineblock, a second type of muscle response was revealed by tetanic stimulation with 1 sec trains of 50 pulses of the same voltage and of pulse width preferably 0.2 msec. The tetanic responses consisted of spasms of longer delay and duration (20-60 sec). These spasms could be matched by doses of acetylcholine of the order of 200 ng. However, if the atropine concentration was now raised to 10(-7), or even 10(-6) g/ml., the effect of 200-1000 ng of acetylcholine was abolished, but the tetanic spasms persisted without decrease in amplitude. In other experiments the height of the spasms remained constant as the concentration of atropine sulphate was raised from 10(-8) to 10(-6) g/ml. and was only slightly decreased by 10(-5) g/ml. Hence, these tetanic contractions are not due to a surmounting of the atropine-block by the increased release of acetylcholine following the 50 pulses.4. The tetanic spasms originate from excitation of non-cholinergic neurones, perhaps the associative Dogiel Type I cells of Auerbach's plexus (Hill, 1927), since the spasms were abolished reversibly by tetrodotoxin 2 x 10(-7) g/ml. and were absent from plexus-free, nicotine-insensitive preparations of the longitudinal muscle, both before and after atropinization.5. The tetanic spasms were not reduced by ganglion-block with paralysing doses of nicotine, with (+)-tubocurarine or with hexamethonium.6. The tetanic spasms are not mediated by a release of 5-hydroxytryptamine (5-HT) or of histamine, since they persisted in concentrations of methysergide and mepyramine adequate to block matching doses of histamine or 5-HT, or multiples thereof. Catecholamines were also excluded.7. The tetanic spasms are not mediated by a release of a prostaglandin, because they were not reduced by 0.5-2 x 10(-6) g/ml. of patulin (Ambache, 1957), which blocked the contractions evoked by matching doses of prostaglandins PGE(2) or PGF(2alpha); even after this block, PGE(2) still potentiated subsequent tetanic responses.8. The tetanic spasms were reduced or virtually abolished by strychnine in concentrations which did not depress the twitch.

Acetylcholine↗
PubMed1996

Nitric oxide activity is deficient in spasm arteries of patients with coronary spastic angina.

BACKGROUND: Coronary spasm can be induced by acetylcholine, serotonin, ergonovine, or histamine, all of which cause vasodilation when the endothelium is intact by releasing nitric oxide (NO). Coronary spasm is promptly relieved by nitroglycerin, which vasodilates through its conversion to NO. It is thus possible that NO release may be deficient in the spasm arteries in patients with coronary spastic angina (CSA). The aim of this study was to determine whether NO release is deficient in coronary arteries of patients with CSA. METHODS AND RESULTS: NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, was infused into coronary arteries in 21 patients with coronary spastic angina (CSA) and in 28 control patients. Coronary spasm was induced by intracoronary injection of acetylcholine and was documented angiographically in all patients with CSA. L-NMMA dose-dependently decreased basal luminal diameter of coronary arteries in control patients, whereas it had no effect on basal diameter of the spasm arteries in patients with CSA. L-NMMA abolished the dilator response to acetylcholine and enhanced the constrictor response to acetylcholine in control arteries, whereas it had no effect on the constrictor response to acetylcholine in spasm arteries. Intracoronary infusion of L-arginine did not affect the diameter of spasm or control arteries. The dilator response to nitroglycerin was increased markedly in spasm arteries compared with control arteries, whereas response to diltiazem did not differ between them. CONCLUSIONS: There is a deficiency in endothelial NO activity in spasm arteries, which leads to the supersensitivity of the artery to the vasodilator effect of nitroglycerin and to the vasoconstrictor effect of acetylcholine in patients with CSA. This deficient endothelial NO activity plays an important role in the pathogenesis of coronary spasm.

Acetylcholine↗
PubMed1994

Clinical and angiographic characteristics of patients with multivessel coronary spasm in variant angina. Significance of progressive course of angina and disease activity.

The purpose of this study was to investigate the incidence of multivessel coronary spasm and compare the clinical characteristics between patients with and without multivessel coronary spasm. In variant angina, it is controversial whether coronary hyperreactivity to vasoconstrictor stimuli is localized to a segmental lesion in only one coronary artery. Moreover, the clinical characteristics of patients with multivessel coronary spasm have never been investigated. Sixty-three patients (51 men and 12 women; mean age, 56 years; range 35-72 years) with variant angina and documented ST-segment elevation during a spontaneous attack underwent spasm provocation testing with selective intracoronary injection of ergonovine. All but 4 patients who experienced spontaneous attacks during cardiac catheterization had induced coronary spasm associated with ST-segment elevation and chest pain. Multivessel coronary spasm was found in 27 (43%) of 63 patients. By univariate analysis, a high frequency of angina (> or = 3 times/week), occurrence of a spontaneous attack within 24 hours after withdrawal of medication, a long history of angina and a progressive course of angina were significantly associated with multivessel coronary spasm. Multivariate analysis indicated a positive correlation between multivessel coronary spasm and progressive angina. Multivessel coronary spasm was found in 43% of patients with variant angina. Patients with multivessel coronary spasm have some unique clinical features. These results may increase the understanding of the pathophysiology and natural course of variant angina.

Adult↗
PubMed2005

The incidence of stent-edge spasm after stent implantation in patients with or without vasospastic angina pectoris.

Although several investigations have reported that stent implantation is an option for the treatment of vasospastic angina (VSA) that is resistant to medical treatment, we are concerned about the occurrence of new stent-edge spasms after stenting. The purpose of this study was to determine the incidence of new stent-edge spasms after stenting. Twenty-seven patients with VSA and 23 patients without VSA were enrolled. About 6 months after stent implantaion, a spasm provocation test was performed by intracoronary infusion of acetylcholine or ergonovine in 26 patients with VSA and all patients without VSA, and the induced stent-edge spasms were classified as either moderate (stent-edge spasm > 75% and < 95% reduction in coronary artery diameter) or severe (stent-edge spasm > 95% reduction in coronary artery diameter). In one patient with VSA, stent-edge spasm and acute thrombosis occurred several hours after stent implantation. The remaining 26 patients with VSA had no complications during or after stent implantation. However, during the chronic phase, severe stent-edge spasm was provoked in 5 patients with VSA (19.2%) and in 2 patients without VSA (8.7%). Moderate stent-edge spasm was provoked in 5 patients with VSA (19.2%) and 5 patients without VSA (21.7%). The results suggest new onset stent-edge spasm in patients either with or without VSA should not be neglected.

Acetylcholine↗