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PubMed1987

[CP angle meningioma presenting as hemifacial spasm].

An interesting case of CP angle meningioma presenting with hemifacial spasm is reported. The patient was a 64-year-old woman with left hemifacial spasm of 18 years' duration which was the initial and the only symptom she had had for ten years until other signs and symptoms including tinnitus and hearing decrease on the left side, vertigo and left cerebellar disturbance occurred. Preoperative CT films showed an enhancing mass at the left CP angle. Operation was performed and the diagnosis of meningioma originating at the rostral edge of the jugular foramen was made. The tumor was extending from the lower cranial nerves up to the Vth nerve burring the VIIth, VIIIth, IXth, Xth, XIIth cranial nerves and vertebral artery within it and compressing the root exit zone of the VIIth nerve. It was totally removed by microsurgical techniques. Postoperative follow-up during eight months disclosed complete disappearance of hemifacial spasm. Residual neurological deficits were left hearing loss, mild facial weakness due to previous nerve blocks on the left side and slight hoarseness. But she was doing well as a housewife. So far, the authors have experienced with 1310 cases of microvascular decompression for hemifacial spasm and 730 cases for tic douloureux. There were only 4 cases (0.3%) in which a CP angle tumor was found in hemifacial spasm series, while in tic douloureux series as many as 79 tumor cases (10.8%) were found. A review of the literature revealed that hemifacial spasm due to CP angle meningioma was very rare, particularly as an initial symptom as in our case.(ABSTRACT TRUNCATED AT 250 WORDS)

Facial Muscles↗

PubMed1985

[Synchronized hemifacial spasm induced by sound stimulation].

A 42-year-old woman whose hemifacial spasm develops not only involuntarily but also synchronously to the sound stimulation to the left ear is presented. She had about 10 years history of left hemifacial spasm which occurred only involuntarily, and she was treated successfully by microvascular decompression method on June 1982. She had been uneventful and free from facial spasm until around January 1983, about 7 months after the first surgery, when her hemifacial spasm recurred and interestingly enough, this spasm started to occur not only involuntary but also synchronously to stimulation of the sound. On her electromyography (EMG) of the face, high amplitude discharge were noted sporadically during her facial muscle twitching, but more constant and regular high amplitude discharge on EMG were also evoked invariably and synchronously with the sound stimulation which was induced by 90 dB click sound and once this sound stimulation discontinued her facial muscle twitching ceased and abnormal discharge of EMG which appeared with sound stimulation disappeared instantly. On March 18, 1983, her left posterior fossa was explored and another angled artery was found compressing the facial nerve just at the root entry zone, more proximally than the previous site where the nerve was found compressed and decompressed at the first surgery. After complete replacement of this offending artery from the nerve, her facial spasm disappeared completely and was never evoked by the sound stimulation. Her postoperative EMG revealed no abnormal discharges at all after the sound stimulation by click sound in the ear.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗

PubMed1983

[Surgical management of trigeminal neuralgia, hemifacial spasm, paroxysmal tinnitus and nystagmus by neurovascular decompression].

Trigeminal neuralgia, facial spasm, tinnitus, vertigo, and glossopharyngeal neuralgia are believed to be the symptoms complex of hyperactive dysfunction of the cranial nerve caused by vascular cross compression at the root entry (exit) zone of the appropriate nerve. Posterior cranial fossa approach for the neurovascular decompression was enhanced by Jannetta et al (1975). From their experiences of surgery, they emphasized that these symptoms were relieved by surgery. In this report, we will discuss the etiology of the disease, the neurotological examination, the angiographic findings, the operative findings and results in a series of 10 patients who have undergone neurovascular decompression. The series consisted of 4 cases with trigeminal neuralgia, 5 cases with facial spasm, and 1 case with paroxysmal tinnitus accompanied by facial spasm. The postoperative progress in these all patients was excellent and relieved of the symptoms. There was neither mortality nor any significant complication. We stress that the neurovascular decompression surgery is now well justified as the definite treatment for the trigeminal neuralgia and facial spasm, because the surgery can be performed easily and safely by the neurosurgeons. The indication of the neurovascular decompression for the acoustic nerve and glossopharyngeal nerve is still controversial. In our own case, tinnitus was paroxysmal and complicated with facial spasm, not synchronous with facial spasm, but with nystagmus. This selective synchronism between tinnitus and nystagmus is a particular feature of our clinical instance. This particular clinical experience may provide some highly significant suggestions in considering the applicability of neurovascular decompression to the acoustic nerve.

Aged↗

PubMed1994

[A case of hemifacial spasm associated with a cerebellar hematoma].

This is a report of a hemifacial spasm associated with a cerebellar hematoma. A 60 year-old female was admitted to our hospital due to severe vertigo and nausea. On admission, the neurological examination showed drowsy conscious level, cerebellar sign dominant on the left side, and left hemifacial spasm. CT scans disclosed a large hematoma in the left cerebellar hemisphere. An angiography revealed a dominant left PICA, but showed neither vascular malformation nor aneurysm. An emergency removal of the hematoma was carried out by using suboccipital craniectomy. Three days after the surgery, the patient's left hemifacial spasm disappeared completely. She had never suffered from left hemifacial spasm prior to this cerebellar bleeding. The hemifacial spasm was thought to be due to either the compression of the left facial nerve by the PICA which had been displaced by the cerebellar hematoma, or to the fact that the nucleus of the left facial nerve might have been stimulated by the hematoma, and the hemifacial spasm might have been caused as a result of the stimulation. The total removal of the hematoma and the postoperative CSF leakage might have decompressed the facial nerve. It was considered that this might be similar to microvascular decompression.

Cerebellar Diseases↗

PubMed1994

Chemomyectomy of the orbicularis oculi muscles for the treatment of localized hemifacial spasm.

OBJECTIVE: To report our experience with doxorubicin chemomyectomy as an alternative to other treatments for hemifacial spasm (HFS). DESIGN: A prospective, open study Phase I clinical trial of chemomyectomy. SETTING: A hospital-based, referral neuro-ophthalmology and oculoplastic service. PATIENTS AND METHODS: Repeated (1-6, median: 4) local injections of doxorubicin were given in the eyelids of 8 patients (5 men, 3 women, average age: 71). MAIN OUTCOME MEASURES: Eyelid strength, self-reported spasm, and duration of improvement without seeking additional or alternative treatments. RESULTS: Chemomyectomy resulted in permanent (> or = 2.5 years) orbicularis oculi weakness and relief from spasms in the treated areas in 5 patients, although 2 patients requested occasional supplementary botulinum toxin (BT) injections in the facial muscles over the cheek. One patient had a successful result for 3 years, after which spasm recurred. One patient maintains a successful result in the eyelid but had a failed microvascular decompression in the lower face. One incompletely treated patient required microvascular decompression following spread of spasms to the lower branches of the facial nerve and increased severity of the HFS. One patient required eyelid surgery because of concurrent spastic entropion. One patient treated with a higher concentration than currently used required closure of a skin ulcer. CONCLUSIONS: Doxorubicin chemomyectomy is an effective alternative to conventional therapy for properly selected patients affected by HFS, particularly older patients with relatively localized eyelid muscle spasms. The modified technique of doxorubicin chemomyectomy has developed to the point where its safety is demonstrated and its risks are known.

Aged↗

PubMedDate not supplied

[The prognosis of the ischemic complications due to a cerebral arterial spasm after subarachnoid hemorrhages (clinico-dopplerographic comparisons)].

The clinical status, angiographic and Doppler ultrasound transcranial findings were compared in 50 patients with acute subarachnoidal hemorrhage (40 with aneurysmal hemorrhage and 10 with unknown hemorrhage). There was a correlation between the change in the linear velocity of blood flow in the cerebral arteries and the clinical manifestations of arterial spasm-induced brain ischemia. With this, Doppler signs of arterial spasm appeared as clinical manifestations 3-4 days earlier. The linear velocity of middle cerebral arterial blood flow, which is critical for the development of ischemic complications of arterial spasm was 295 +/- 6 cm/sec. The magnitude and duration of the excess critical level of the linear velocity of blood flow and the presence of arterial spasm in the contralateral hemisphere may determine whether the progressive ischemic symptoms are reversible or irreversible. A further course of arterial spasm, development of ischemic complications and their outcomes may be predicted by the increasing gradient of the linear velocity in the cerebral arteries at days 4-6 of subarachnoidal hemorrhage and the extent of spasm.

Acute Disease↗

PubMed1983

Continuous intracoronary nitroglycerin infusion for spasm after angioplasty.

A patient with reversible coronary artery spasm superimposed on fixed atherosclerotic coronary disease was treated with percutaneous transluminal angioplasty. The procedure successfully dilated the atherosclerotic lesion. However, 20 minutes later, the patient developed coronary artery spasm at the angioplasty site. Sublingual nitroglycerin, sublingual nifedipine, intravenous nitroglycerin, and repeated boluses of intracoronary nitroglycerin alleviated episodes of spasm, but failed to prevent recurrence. The patient was successfully treated with a continuous intracoronary infusion of nitroglycerin. Patients with coronary artery spasm in addition to fixed obstructive coronary disease may be at higher risk for spasm after percutaneous transluminal angioplasty. Continuous intracoronary infusion of nitroglycerin may be an effective therapy for recurrent coronary artery spasm occurring in the catheterization laboratory.

Aged↗

PubMed1985

Catheter-induced spasm during spontaneous attack of variant angina.

The simultaneous occurrences of spontaneous spasm and catheter-induced spasm during coronary angiography were obtained in 3 patients. Catheter-induced spasm was seen in the right coronary artery in 3 patients: 1 patient had spontaneous spasm in the distal right coronary artery and 2 patients had spontaneous spasm in the proximal left anterior descending coronary artery. These findings suggest that patients with variant angina may be susceptible to mechanical induction of spasm.

Angina Pectoris, Variant↗

PubMed1991

Usefulness of intracoronary injection of acetylcholine as a provocative test for coronary artery spasm in patients with vasospastic angina.

In order to examine both the sensitivity and specificity of coronary artery spasm induced by intracoronary injection of acetylcholine in patients with vasospastic angina, incremental doses of acetylcholine (20, 30, and 50 micrograms) were injected directly into each coronary artery in 21 patients with variant angina (group A), in 28 patients with other types of vasospastic angina (group B), and in 20 patients without any significant coronary artery disease (group C). Coronary artery spasm was defined as severe vasoconstriction (greater than or equal to 90% of reduction in luminal diameter) with chest pain and/or ischemic changes in the electrocardiogram. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in 20 patients (95%) of group A, in 27 patients (96%) of group B, and in only 2 patients (10%) of group C. The low dose of acetylcholine (20 micrograms) induced coronary spasm more frequently in group A patients (81%) than in group B patients (43%) (P less than 0.05). ST-segment elevation associated with anginal attacks was significantly (P less than 0.05) more frequent in group A (71%) than in group B (39%). When acetylcholine was injected separately into the left and right coronary arteries, spasm of both coronary arteries was observed in 7 out of 14 of group A (50%), in 8 out of 22 of group B (36%), and in none of the 20 of group C. We concluded that intracoronary injection of acetylcholine is a sensitive and reliable method for the induction of coronary spasm in patients with vasospastic angina as well as in those with variant angina.

Acetylcholine↗

PubMed1985

Coronary artery spasm induced in miniature swine: angiographic evidence and relation to coronary atherosclerosis.

In a swine model of coronary artery spasm, the pathogenetic role of coronary atherosclerosis was examined. Following endothelial balloon denudation of the left circumflex coronary artery (LCX), male miniature swine were fed a laboratory chow diet containing 2% cholesterol. Although there was no difference in the extent of coronary vasoconstrictive response to histamine, serotonin, and ergonovine between the left anterior descending coronary artery (LAD) and the LCX before the denudation, a constrictive response was significantly augmented along the denuded portion of the LCX 1 and 3 months after the denudation. Augmented vasoconstrictive responses to phenylephrine were never evidenced. Histamine was the most potent vasoactive agent, and coronary artery spasm was provoked repeatedly by intracoronary or intravenous administration of histamine in the presence or absence of cimetidine. The spasm was provoked only in the denuded portion of the LCX, the same area which was angiographically normal before the occurrence of the spasm. Histologically, atherosclerotic changes were predominant along the denuded portion of the LCX. Topologic correlation was suggested between the site of the spasm and the site of coronary atherosclerosis. It is concluded that in this swine model of coronary artery spasm, atherosclerotic changes may be an important causative factor, in terms of an activation of multiple receptor-operated calcium channels in the coronary artery.

Animals↗

PubMed1987

Left ventricular wall motion at rest in patients with organic coronary artery disease vs coronary spasm.

Left ventricular ejection fractions and regional ejection changes obtained from left ventriculograms at rest were analyzed in 15 normal subjects, in 17 patients with isolated, organic left anterior descending coronary artery disease, and in 11 patients with isolated left anterior descending coronary artery spasm. Patients with coronary artery spasm did not have significant organic lesions at the site of spasm. All patients with organic coronary artery disease and coronary artery spasm had a history of angina pectoris without myocardial infarction. No significant differences in ejection fraction were observed among the three groups. The regional ejection change of the anterolateral and apical wall supplied by the left anterior descending coronary artery was significantly decreased in patients with organic coronary artery disease compared with those in normal subjects (anterolateral 39.5 +/- 10.3% vs 48.4 +/- 7.7%, p less than 0.05; apical 48.4 +/- 8.8% vs 55.6 +/- 7.8%, p less than 0.05). However, the anterolateral and apical wall motion was not impaired in patients with coronary artery spasm. Thus, patients with organic coronary artery disease had impairment of left ventricular wall motion, while those with coronary artery spasm did not, although both groups of patients had symptoms of angina. These results suggest that patients with organic coronary artery disease may have had coronary blood flow disturbances through stenosed vessels and chronic active ischemia that produced left ventricular impairment.

Coronary Disease↗

PubMed1990

Comparative sensitivity of intracoronary injection of acetylcholine for the induction of coronary spasm in patients with various types of angina pectoris.

To elucidate the possible contribution of coronary artery spasm to the pathogenesis of angina pectoris, coronary arterial responses to intracoronary injection of acetylcholine were examined in patients with various types of angina pectoris. Coronary artery spasm with chest pain and/or electrocardiographic ischemic changes was angiographically demonstrated in 50 (85%) of 59 patients with angina pectoris. The sensitivity for coronary spasm was 92% (24 of 26) in patients with rest angina, 100% (16 of 16) in patients with both rest and effort angina, and 59% (10 of 17) in patients with effort angina, while it was only 6% (1 of 16) in patients without coronary artery disease. When patients with effort angina were subdivided according to the variability of anginal threshold for exertional angina, the sensitivity for coronary spasm was as high as 90% (9 out of 10) in patients with variable-threshold angina. In contrast, coronary spasm was less frequently (p less than 0.05) induced in patients with fixed-threshold angina (1 of 7, 14%). These results suggest that coronary arteries in patients with angina pectoris are quite susceptible to acetylcholine except in those patients with stable exercise tolerance or anginal threshold. Thus coronary artery spasm appears to play a significant role for the pathogenesis of angina pectoris in a large proportion of patients with effort angina as well as in patients with rest angina.

Acetylcholine↗

PubMed1987

Coronary artery spasm: involvement of small intramyocardial branches.

A study was conducted to determine if the small (resistance) vessels of the coronary circulation could undergo spasm comparable to that of the major conductance (epicardial) arteries which in the rat measure 275-300 micron in diameter. This information may be relevant to the growing evidence of ischemic myocardial disease without significant coronary atherosclerosis or even spasm of the larger vessels. Vascular corrosion casts of the coronary circulation were prepared in the rat 20 min after intravenous injection of arginine vasopressin, a powerful coronary constrictor substance, under continuous electrocardiographic monitoring. Electrocardiographic changes observed consisted of S-T segment elevation and conduction disturbances, implying ischemic effects on the myocardium. Corrosion casts revealed spasm of smaller arteries only (50-150 micron diameter). Controls (vehicle-injected or untreated) showed no abnormalities of the coronary vasculature. These results suggest that myocardial vessels of this size are comparable in their potential for spasm to the large conductance arteries. Similar findings in patients involving smaller vessels could explain ischemic myocardial events in the absence of significant spasm, or organic stenosing pathology of major coronary arteries. As a corollary, it is suggested that the term "coronary artery spasm" could be enlarged in its definition to include other levels of the coronary circulation rather than that of the large conductance arteries alone.

Animals↗

PubMed1988

Incidence of spontaneous and provoked coronary spasms after percutaneous transluminal coronary angioplasty.

We studied the incidence of spontaneous and ergonovine-induced coronary arterial spasm during repeat coronary angiography in 96 consecutive patients with single-vessel disease who had undergone successful angioplasty. Follow-up angiography was performed after a mean of 6 months (1-8 months). Sixty patients demonstrated no restenosis and in 36 patients restenosis (greater than 50% restenosis) occurred. Spasms of the arteries at the site of dilatation were significantly (P less than 0.001) more frequent in patients with restenosis (18/36; 50%) than in patients without restenosis (4/60; 7%). Before angioplasty, no differences were found in the clinical characteristics between the two groups. Likewise, the morphologic results of angioplasty were identical. Despite long-term treatment with nifedipine (30-60 mg daily) and aspirin (0.5 g daily), 14 of 18 patients with restenosis and coronary spasm suffered from spontaneous angina, as compared to only 3 of 18 patients with restenosis without demonstrable spasm. Three of the 4 patients without restenosis but with detectable spasm were also symptomatic. Thus our findings suggest that spasm of the coronary arteries achieves some importance as a pathophysiological factor for recurrence following coronary angioplasty.

Angina Pectoris↗

PubMed1988

Hyperventilation-induced simultaneous multivessel coronary spasm in patients with variant angina: an echocardiographic and arteriographic study.

Left ventricular wall motion abnormalities during an attack of coronary spasm induced by hyperventilation were examined with use of two-dimensional echocardiography in 27 patients with variant angina. Transient abnormal wall motion (asynergy) confined to one coronary artery region was found in 18 of the 27 patients and transient abnormal motion extending over more than one coronary artery region in the remaining 9 patients. Spasm of more than one major coronary artery was demonstrated separately by coronary arteriography during an attack induced by injection of acetylcholine or ergonovine in seven of the nine patients who manifested asynergy in more than one coronary artery region. In one patient, spasm was demonstrated in one major coronary artery, and the other coronary arteries were severely stenosed or occluded organically. In the remaining patient, acetylcholine was not injected into both arteries; however, the attack was sometimes associated with ST segment elevation in the anterior leads and at other times in the inferior leads. Therefore, simultaneous multivessel coronary spasm seems to have occurred in eight of the nine patients who exhibited asynergy in more than one coronary artery region. The 8 patients with simultaneous multivessel coronary spasm had a higher degree and longer duration of ST segment elevation and a higher incidence of arrhythmias during the attack induced by hyperventilation than did the 19 patients with single vessel coronary spasm, and all of them had no significant organic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris, Variant↗

PubMed1996

A case of coronary artery spasm during spinal anesthesia.

We present a rare case of coronary artery spasm during spinal anesthesia in a patient who had neither complications nor prior history of coronary artery disease. Some factors are involved in the occurrence of perioperative coronary artery spasm. Many cases of coronary artery spasm during general anesthesia, or general plus epidural anesthesia, have been reported. Although spinal anesthesia by itself has not been reported to be a cause of coronary artery spasm, it is likely, in the current case, that the combination of the activated parasympathetic nerve system by the retraction of the peritoneum and spinal anesthesia might have caused the coronary artery spasm. Anesthesiologists need to be aware that coronary artery spasm may occur during spinal anesthesia, especially when the peritoneum is retracted.

Adult↗

PubMed1998

Vitamin C attenuates abnormal vasomotor reactivity in spasm coronary arteries in patients with coronary spastic angina.

OBJECTIVES: This study sought to examine effect of vitamin C, an antioxidant, on the abnormal vasomotor reactivity in spasm coronary arteries. BACKGROUND: Oxygen free radicals generated in the arterial walls have been shown to cause endothelial vasomotor dysfunction. METHODS: Responses of the epicardial arterial diameters of the left coronary arteries to the intracoronary infusion of acetylcholine (ACh) (10 and 50 microg/min) were measured by quantitative coronary angiography before and during combined intracoronary infusion of vitamin C (10 mg/min) or saline as a placebo in 32 patients with coronary spastic angina and in 34 control subjects. RESULTS: Vitamin C infusion suppressed the constrictor response of the epicardial diameter to ACh in spasm coronary arteries but had no significant effect in the control coronary arteries (percent change in distal diameter in response to 10 microg/min of ACh [constriction (-), dilation (+), mean +/- SEM] before vitamin C: -8.2 +/- 2.9% in spasm arteries, +8.4 +/- 2.9%* in control arteries; during vitamin C: +0.2 +/- 3.8%* in spasm arteries, +7.2 +/- 1.3%* in control arteries [*p < 0.01 vs. spasm arteries before vitamin CI). The coronary sinus-arterial difference in plasma thiobarbituric acid reactive substances during ACh infusion, an indicator of lipid peroxidation in coronary circulation, was higher in patients with coronary spastic angina than in control subjects (p < 0.01) but was suppressed in patients with coronary spastic angina to comparable levels in control subjects by combined infusion of vitamin C. Saline infusion had no effect. CONCLUSIONS: The results indicate that vitamin C attenuates vasomotor dysfunction in epicardial coronary arteries in patients with coronary spastic angina. Oxygen free radicals may at least in part play a role in the abnormal coronary vasomotor reactivity in response to ACh in spasm coronary arteries.

Acetylcholine↗

PubMed1992

Life-threatening ventricular arrhythmias in patients with silent myocardial ischemia due to coronary-artery spasm.

BACKGROUND: Silent myocardial ischemia in patients with coronary atherosclerosis is associated with an increased risk of adverse cardiac events, including sudden death. The relation between silent ischemia and the initiation of potentially fatal ventricular arrhythmias has not been defined, however. METHODS: As part of a long-term study of sudden cardiac death, data on arrhythmias, coronary anatomy, and responses to ergonovine testing to provoke coronary-artery spasm were collected prospectively among survivors of out-of-hospital cardiac arrest who had no flow-limiting coronary-artery lesions, prior myocardial infarctions, or other structural causes of cardiac arrest and no angina pectoris. Associations between silent myocardial ischemia due to coronary-artery spasm and the occurrence and characteristics of life-threatening ventricular arrhythmias were studied by both invasive and noninvasive techniques. RESULTS: Silent ischemic events were associated with the initiation of life-threatening ventricular arrhythmias in five patients with induced or spontaneous focal coronary-artery spasm (or both). These patients were identified among a group of 356 survivors of out-of-hospital cardiac arrest who were evaluated between 1980 and 1991. In two of the five patients reperfusion, rather than ischemia itself, correlated with the onset of the ventricular arrhythmia. Only one of the five had an inducible arrhythmia during electrophysiologic testing. Titration of the dose of a calcium-entry-blocking agent (verapamil, diltiazem, or nifedipine) against the ability of ergonovine to provoke spasm was successful in preventing both the provocation of spasm and arrhythmias in all four patients who were tested. CONCLUSIONS: Silent myocardial ischemia due to coronary-artery spasm can initiate potentially fatal arrhythmias in patients without flow-limiting structural coronary-artery lesions. The role of silent ischemia, reperfusion, or both in the initiation of fatal arrhythmias in larger groups of patients with advanced coronary-artery lesions remains to be defined.

Adult↗