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PubMed1992

A study on coronary hemodynamics during acetylcholine-induced coronary spasm in patients with variant angina: endothelium-dependent dilation in the resistance vessels.

The epicardial coronary artery of patients with variant angina is hyperreactive to the constrictive effect of acetylcholine, but it is not known whether the coronary microvasculature also constricts in response to acetylcholine. Incremental doses of acetylcholine were injected into the left coronary artery of 57 patients with variant angina and with spasm in this artery. By measuring coronary sinus blood flow, coronary hemodynamic status just before angiographic documentation of spasm was examined. Acetylcholine induced spasm in the left coronary artery in all patients. It also decreased the diameter of the nonspasm artery by 36 +/- 19% from baseline. For all patients, coronary sinus blood flow was 89 +/- 38 ml/min at baseline and increased to 104 +/- 61 ml/min during an acetylcholine-induced anginal attack (p less than 0.01). In 10 patients with spasm in both the left anterior descending and left circumflex arteries (that is, multivessel spasm), coronary sinus blood flow decreased from 84 +/- 21 to 52 +/- 26 ml/min (p less than 0.01). In the other 47 patients with spasm in only one of these two arteries (that is, single-vessel spasm), coronary sinus blood flow increased from 90 +/- 41 to 115 +/- 61 ml/min (p less than 0.01) without change in the rate-pressure product. It is concluded that in patients with variant angina, acetylcholine induces spasm and constriction in the epicardial coronary artery, whereas it dilates the resistance vessels presumably through the release of the endothelium-dependent relaxing factor.

Acetylcholine↗
PubMed2002

Coronary microvascular spasm causes myocardial ischemia in patients with vasospastic angina.

OBJECTIVES: We aimed to test the hypothesis that coronary microvascular spasm (MVS) alone causes myocardial ischemia in patients with angina attributable to epicardial coronary spasm, and to determine whether there is a difference in clinical characteristics between those with and without microvascular spasm. BACKGROUND: Patients with "vasospastic angina" have epicardial coronary artery spasm, but it is unknown whether coronary microvessel disease also contributes to the occurrence of angina in these patients. METHODS: We studied 55 consecutive patients with angina in whom epicardial coronary spasm was provoked by intracoronary acetylcholine (ACH). RESULTS: In 14 patients (25.5%, Group 1), submaximal dose of ACH induced myocardial ischemia (chest pain, ischemic electrocardiogram changes, lactate production) without large epicardial spasm, suggesting the occurrence of coronary microvascular spasm. By contrast, the remaining 41 patients (Group 2) had evidence of myocardial ischemia only when epicardial spasm was angiographically demonstrated. The Group 1 patients were predominantly women (p < 0.05) and had a history of prolonged (>30 min) chest pain (p < 0.05), whereas the Group 2 patients were more likely men and smokers (p < 0.01). CONCLUSIONS: Myocardial ischemia most probably due to coronary MVS was demonstrated in a sizable portion of patients with epicardial vasospasm, preferentially in women having both typical and prolonged anginal pain. The result suggests that coronary microvascular disease may also contribute to angina in patients with "vasospastic angina."

Acetylcholine↗
PubMedDate not supplied

Spasms in spinal cord injury: a study of 72 subjects.

Seventy-two patients with spinal cord injury of at least two years duration were reviewed retrospectively to determine incidence and effects of spasms. The average time between the injury and the examination was ten years. Seventy patients experienced spasms. In 50 patients (72%) the spasms appeared within six months after the injury. Historically, the spasms reached their maximal severity within 12 months. No significant difference was found in intensity and frequency of spasms between patients with clinically complete or incomplete spinal cord injury. Extensor spasms were seen more frequently than flexor spasms in the long-term patients. Patients with incomplete myelopathies had more extensor spasms than those with complete SCI.

Adult↗
PubMed1997

Cerebral arterial spasm after penetrating craniocerebral gunshot wounds: transcranial Doppler and cerebral blood flow findings.

OBJECTIVE: The goals of the study were to determine the incidence and time course of cerebral arterial spasm in patients with penetrating craniocerebral gunshot wounds, to study the relationship between vasospasm and subarachnoid hemorrhage (SAH) in these patients, and to evaluate the effects of vasospasm on outcome. METHODS: Thirty-three patients with craniocerebral gunshot wounds underwent computed tomography at admission and then underwent transcranial doppler ultrasonography (TCD). Velocities in the middle cerebral artery and the extracranial internal carotid artery were measured. Vasospasm was defined as a middle cerebral artery velocity greater than 120 cm per second and a hemispheric index (ratio of middle cerebral artery to internal carotid artery velocity) greater than 3. Intravenous xenon-133 cerebral blood flow (CBF) studies were performed for 10 patients. RESULTS: TCD was initiated, on average, 1.1 days after injury; 205 studies (mean, 6.3 studies/patient) were performed 0 to 33 days after injury. TCD showed vasospasm in 14 patients (42.4%). Xenon-133 studies performed within 24 hours of TCD measurements indicating spasm demonstrated normal or low CBF in three of five patients with spasm, ruling out hyperemia as the cause of elevated flow velocities in these three patients. Seven patients had unilateral vasospasm, and seven had bilateral spasm. Vasospasm was most prominent from Days 5 through 11. Vasospasm was distributed across all levels of injury severity, as defined by the Glasgow Coma Scale. Initial computed tomographic scans demonstrated SAH in all 14 patients with vasospasm but in only 9 of 19 without spasm (100 versus 47%, P < 0.0001, binomial distribution probability test). Outcomes for patients with vasospasm were slightly worse than for those without spasm (35.7 versus 47.4% good outcomes, respectively); however, this difference did not reach statistical significance (P = 0.12). CONCLUSION: These findings demonstrate that delayed cerebral arterial spasm is a frequent complication in patients with craniocerebral gunshot wounds and is strongly associated with SAH. The frequency, time course, and severity of spasm are comparable with those observed with aneurysmal SAH and traumatic SAH caused by closed head injury. This study offers new insights into the hemodynamic pathophysiology after gunshot wounds to the brain and suggests that increased vigilance for vasospasm may be of benefit.

Adolescent↗
PubMed2004

Usefulness of fasudil, a Rho-kinase inhibitor, to treat intractable severe coronary spasm after coronary artery bypass surgery.

We have recently demonstrated that fasudil, a Rho-kinase inhibitor, is effective in suppressing coronary artery spasm in patients with vasospastic angina. Thus, blockade of Rho-kinase may provide a novel therapeutic strategy to treat ischemic coronary syndrome caused by the spasm. Severe coronary artery spasm still remains a life-threatening serious complication of coronary artery bypass grafting (CABG). In this study, we examined the inhibitory effect of fasudil in patients with intractable severe coronary spasm after CABG. Three patients who underwent CABG showed severe myocardial ischemia resistant to intensive therapy with intravenous conventional vasodilators, including isosorbide dinitrate (ISDN), diltiazem, and nicorandil. Coronary angiography revealed severe coronary spasm in native coronary arteries and/or bypass arterial grafts in all patients. Since intracoronary and/or intragraft administration of ISDN was ineffective to resolve the spasm, we then administered fasudil (1.5 mg/min for 15 minutes) into the spastic arteries. Fasudil successfully resolved the spasm and improved myocardial ischemia in all patients without any systemic adverse effects. In conclusion, the treatment with fasudil may be useful to treat intractable and otherwise fatal coronary spasm resistant to intensive conventional vasodilator therapy after CABG.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Role of protein kinase C-mediated pathway in the pathogenesis of coronary artery spasm in a swine model.

BACKGROUND: The intracellular mechanism of coronary artery spasm is still unknown. The pathway mediated by protein kinase C (PKC) is an important intracellular process of various cellular responses, including vascular smooth muscle contraction. Thus, we examined the role of the PKC-mediated pathway in the pathogenesis of coronary artery spasm in our in vivo swine model. METHODS AND RESULTS: Seven Göttingen miniature pigs underwent coronary balloon injury and x-ray irradiation to induce atherosclerotic lesion. After 6 to 18 months, intracoronary serotonin (3 micrograms/kg) or histamine (3 micrograms/kg) repeatedly induced coronary artery spasm at the atherosclerotic site. At the spastic site, intracoronary administration of phorbol-12,13-dibutyrate (PDBu) (10(-9) mol/kg), a PKC-activating phorbol ester, also induced coronary artery spasm, which was completely blocked by pretreatment with intracoronary staurosporine (10 micrograms/kg), a PKC inhibitor. Intracoronary administration of an inactive phorbol ester, phorbol-12,13-didecanoate (10(-9) mol/kg), did not induce coronary vasoconstriction. Coronary artery spasm induced by the autacoids was significantly augmented by pretreatment with intracoronary PDBu and partially inhibited by staurosporine. Intracoronary administration of Bay K 8644 (10 micrograms/kg), a dihydropyridine-sensitive L-type calcium channel agonist, also induced coronary artery spasm at the spastic site, which was significantly inhibited by pretreatment with intracoronary staurosporine or nifedipine (0.1 mg/kg). CONCLUSIONS: These results suggest (1) the PKC-mediated pathway is importantly involved in the pathogenesis of coronary artery spasm, (2) activation of the PKC-mediated pathway partially accounts for serotonin- and histamine-induced coronary artery spasm, and (3) at the spastic site, calcium influx through dihydropyridine-sensitive L-type calcium channel and/or calcium sensitivity of the contractile proteins may be augmented by the PKC-mediated pathway.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

Coronary artery spasm does not depend on the intracellular calcium store but is substantially mediated by the protein kinase C-mediated pathway in a swine model with interleukin-1 beta in vivo.

BACKGROUND: The intracellular mechanism for coronary artery spasm is still unknown. Since the protein kinase C (PKC)-mediated pathway and Ca2+ release from sarcoplasmic reticulum (SR) are important intracellular mechanisms of vascular smooth muscle contraction, we examined the possible role of these two mechanisms in the pathogenesis of coronary spasm in our swine model in vivo. METHODS AND RESULTS: In 25 pigs, interleukin-1 beta (IL-1 beta) was applied chronically to the coronary arteries from the adventitia to induce an inflammatory/proliferative lesion. Two weeks after the operation, either intracoronary serotonin or histamine repeatedly induced coronary spasm at the IL-1 beta-treated site. At those spastic sites, phorbol-12, 13-dibutyrate, a PKC-activating phorbol ester, also induced coronary spasm, which was blocked by pretreatment with the PKC inhibitors staurosporine and sphingosine. Serotonin- and histamine-induced coronary spasm was also significantly inhibited by pretreatment with staurosporine, sphingosine, or nifedipine (an L-type Ca2+ channel antagonist) but not by ryanodine (an inhibitor of Ca(2+)-induced Ca2+ release from SR) or thapsigargin (an inhibitor of Ca(2+)-ATPase of SR). Bay K 8644 (an L-type Ca2+ channel agonist) also induced coronary spasm at the IL-1 beta-treated site, which was significantly inhibited by pretreatment with staurosporine, sphingosine, and nifedipine. In contrast, coronary vasoconstriction induced by prostaglandin F2 alpha was not affected by pretreatment with staurosporine or sphingosine but was significantly inhibited by pretreatment with ryanodine, thapsigargin, or nifedipine. CONCLUSIONS: These results suggest that (1) PKC activation largely accounts for the serotonin- and histamine-induced coronary spasm; (2) at the spastic site, the calcium influx through L-type Ca2+ channels may be augmented via the PKC-mediated pathway; and (3) the Ca2+ release from the SR into the cytosol may not play a primary role in coronary spasm.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

Role of extracellular Ca2+ in subarachnoid hemorrhage-induced spasm of the rabbit basilar artery.

BACKGROUND AND PURPOSE: The role of extracellular Ca2+ in the maintenance of chronic vasospasm after subarachnoid hemorrhage (SAH) is largely unknown. Indeed, studies thus far have been limited to demonstrations that L-type Ca(2+)-channel antagonists were unable to reverse the spasm. This study tested whether SAH-induced vasospasm is maintained, at least in part. through the influx of extracellular Ca2+ and whether the influx of extracellular Ca2+ occurs through L-type Ca2+ channels and possibly, in addition, through store operated channels (SOCs). Furthermore, as there is considerable evidence in the literature to suggest that the spasm is mediated through endothelin-1 (ET-1) release, we tested whether the Ca2+ dependency of the spasm was consistent with the mediation of the spasm by ET-1. METHODS: Chronic spasm of the basilar artery was induced in a double SAH rabbit model. Relaxation of SAH-, ET-1-, serotonin-, and KC1-constricted basilar artery in response to Ca(2+)-free solution, verapamil, and Ni2+ was measured in situ with the use of a cranial window. RESULTS: SAH induced 23% constriction of the basilar artery. Ca(2+)-free solution and 1 mumol/L verapamil reversed the constriction of SAH vessels by 60% and 17%, respectively. In contrast, control vessels challenged with 40 to 50 mmol/L KCl, which induced 34% constriction, relaxed in response to Ca(2+)-free solution and verapamil by 98% and 89%, respectively. In SAH vessels, verapamil followed by 0.1 mmol/L Ni2+, which is known to block SOCs, induced a combined relaxation of 67%. Control vessels challenged with 3 nmol/L ET-1, which induced a magnitude of constriction similar to that of SAH (29%), relaxed in response to Ca(2+)-free solution, verapamil, and verapamil plus Ni2+ by 69%, 20%, and 50%, respectively (P > .05) versus respective values in SAH vessels). In contrast, control vessels challenged with 2 to 8 mumol/L serotonin, which induced a magnitude of constriction similar to those of SAH and ET-1 (22%), completely relaxed in response to Ca(2+)-free solution and verapamil. CONCLUSIONS: These results demonstrate that the maintenance of chronic spasm in the two-hemorrhage rabbit model after SAH is due to smooth muscle cell contractile mechanisms partly dependent on the influx of extracellular Ca2+. The influx of extracellular Ca2+ results from the opening of L-type Ca2+ channels and an additional channel or channels. We speculate that the L-type Ca2+ channel-independent influx of extracellular Ca2+ results from the opening of SOCs. The Ca(2+)-dependent characteristics of the spasm likely reflect the mediation of the spasm by ET-1.

Animals↗
PubMed2000

Cellular and molecular mechanisms of coronary artery spasm: lessons from animal models.

Coronary artery spasm plays an important role in the pathogenesis of a wide variety of ischemic heart diseases, especially in the Japanese population. Because coronary artery spasm can be induced by a variety of stimuli with different mechanisms of action, the occurrence of the spasm appears to be due to the local hyperreactivity of the coronary artery rather than to an enhanced stimulation with a single mechanism of action. Several lines of evidence indicate that coronary artery spasm is caused primarily by smooth muscle hypercontraction whereas the contribution of endothelial dysfunction may be minimal. In order to elucidate the cellular and molecular mechanisms of the spasm, porcine models of the spasm were developed. In the first model with balloon injury and high-cholesterol feeding, a close topological correlation between the early atherosclerotic lesions and the spastic sites was noted, whereas in the second model with an inflammatory cytokine the potential importance of coronary inflammatory changes, especially at the adventitia, was noted. Subsequent studies in vivo and in vitro demonstrated that protein kinase C (PKC) and Rho-kinase are substantially involved in the intracellular mechanism of the spasm, resulting in increases in the mono- and diphosphorylations of myosin light chain (MLC). Furthermore, molecular biological analyses demonstrated that Rho-kinase is upregulated at the spastic site (at all levels, including mRNA, protein, and activity), resulting in the inhibition of MLC phosphatase through the phosphorylation of its myosin binding subunit and thereby causing the increase in MLC phosphorylations. Preliminary results also suggest that the long-term inhibition of Rho-kinase is effective in inhibiting the development of arteriosclerotic vascular lesions in several porcine models. Thus, Rho-kinase could be regarded as a novel therapeutic target for coronary arteriosclerosis in general and coronary artery spasm in particular.

Animals↗
PubMed2001

Magnesium deficiency in patients with recent myocardial infarction and provoked coronary artery spasm.

This study sought to clarify the relationship between magnesium (Mg) deficiency and coronary artery spasm provoked by pharmacologic agents in patients with a recent acute myocardial infarction (AMI). Twenty-three consecutive patients suffering from AMI were investigated with a Mg retention test (Mg: 0.1 mmol/kg for 4 h) in both the acute phase (within I week (3+/-2 days) of onset) and the subacute phase (3-4 weeks (24+/-6 days) of the onset). Early coronary arteriography was performed in all patients. Coronary stenosis in the infarct-related artery was less than 90% in all patients in the subacute phase. The spasm provocation test was performed in the subacute phase and coronary spasm was defined as transient subtotal or total occlusion in association with angina or electrocardiographic ST-segment deviation. Coronary artery spasm was provoked in only 13 of the 23 patients. Compared with the control subjects (12 patients without coronary artery disease or coronary spasm), the 24-h Mg retention was significantly higher in patients with AMI (acute phase: 78+/-27%, subacute phase: 66+/-32%, vs control: 48+/-12%, p<0.05). In the subacute phase, the 24-h Mg retention decreased in patients without coronary spasm (43+/-26%), but a high level of Mg retention was still observed in patients with coronary spasm (84+/-25%). There was no difference in the serum concentrations of Mg, calcium and phosphorus between the 2 groups on both phases. In conclusion, both Mg deficiency and provoked coronary artery spasm were noted in more than half of the Japanese patients with a recent AMI, suggesting a close association between Mg deficiency and AMI.

Aged↗
PubMed1992

High prevalence of coronary artery spasm in survivors of cardiac arrest with no apparent heart disease.

The pathogenesis of cardiac arrest in the absence of any apparent heart disease remains unclear. Based on the hypothesis that coronary spasm may be a cause of cardiac arrest in the absence of apparent heart disease, ergonovine testing and/or electrophysiologic studies (EPS) were performed to evaluate the cause of cardiac arrest. Fourteen patients resuscitated from cardiac arrest had no apparent heart disease. A spontaneous episode of angina with ST-segment elevation occurred in 4 patients while under observation. Ergonovine testing was performed in 9 patients, and coronary spasm was induced in 5. EPS were performed in 8 patients, including 3 patients with coronary spasm. No electrophysiologic abnormalities were found in the 3 patients with coronary spasm. Ventricular fibrillation was induced by programmed ventricular stimulation in 2 patients with documented ventricular fibrillation at the time of resuscitation. All but one of the patients with coronary spasm had chest pain preceding cardiac arrest or at least a history of chest pain at rest, while 4 of 5 patients without coronary spasm had no prodromal symptoms. Patients with coronary spasm had a good prognosis when treated with a Ca-antagonist and/or long-acting nitrate. In conclusion, coronary spasm is the most frequent cause of cardiac arrest in cardiac arrest survivors with no apparent heart disease. Ergonovine testing should be performed to evaluate the cause of cardiac arrest when patients have no apparent heart disease.

Cardiac Pacing, Artificial↗
PubMed1983

[Coronary artery spasm. Apropos of 165 cases].

This study comprised 165 cases of coronary artery spasm (147 men and 18 women) with an average age of 49,2 years (range 27 to 73 years). Smoking was a particularly significant risk factor. Symptoms were usually of recent onset (80%) and dominated by attacks of angina pectoris either at rest alone or associated with angina of effort. 14% of cases of spasm were observed during acute myocardial infarction. Some cases presented with syncope due to cardiac arrhytmias. The basal electrocardiogramme was normal in 53% of cases. Exercise stress testing may be normal (30/65 cases) or positive (ST depression recorded in 26/65 cases). In 5 cases, ST elevation was observed. Left ventricular function was usually normal: 115 patients (70%) had organic atherosclerotic lesions, with 1, 2 and 3 vessel disease in 40%, 18% and 22% respectively. Spasm was spontaneous in 24,2% of cases but most commonly provoked by ergometrine. Criteria of spasm only applied to focal spasm and exclused catheter--induced spasm. The most common site of spasm was the right coronary artery (50,3% of cases), followed by the left anterior descending (31% of cases) and left circumflex (10,3% of cases). The outcome of these 165 cases depended on the therapeutic options (surgical treatment in 48 cases). The medium term results were generally good with a low mortality rate and follow up showed that the calcium antagonists provided effective prophylaxis against recurrence of spasm.

Adult↗
PubMed1996

Increased basal tone and hyperresponsiveness to acetylcholine and ergonovine in spasm-related coronary arteries in patients with variant angina.

We compared the basal coronary artery tone and the constrictive responses to acetylcholine (Ach) and ergonovine (Erg) among three groups of patients: 31 patients (group 1) with variant angina in whom spasm was provoked by low doses of acetylcholine (intracoronary 20 micrograms) or ergonovine (intravenous 50 micrograms); 35 patients (group 2) in whom spasm was provoked by higher doses of acetylcholine (intracoronary 100 micrograms) or ergonovine (intravenous cumulative dose of 350 micrograms); and 26 control subjects. Patients with variant angina in whom spasm was provoked by low doses of acetylcholine or ergonovine, had a higher incidence of coexisting angiographic evidence of coronary artery disease, multi-vessel spasm and more frequent episodes of angina. The basal coronary artery tone at the spastic and non-spastic sites of the spasm-related artery was significantly elevated in group 1 compared to group 2 (44 +/- 17 vs. 14 +/- 11% and 26 +/- 14 vs. 16 +/- 10%, respectively, P < 0.05), but not in the non-spasm related artery. The magnitude of vasoconstrictive responses to acetylcholine and ergonovine at the non-spastic sites was also greater in group 1 than in group 2 and the control groups (acetylcholine: 40 +/- 20 vs. 26 +/- 11, 27 +/- 12%; ergonovine: 37 +/- 18 vs. 12 +/- 8, 13 +/- 10%, respectively, P < 0.05). However, the basal coronary artery tone was not elevated at the spastic and non-spastic sites in group 2 compared to that in the control subjects. These findings suggest that the basal coronary artery tone is increased in patients with variant angina, with increased frequency of angina suggestive of higher disease activity at the spastic and non-spastic sites of the spasm-related artery, and this may be related to pathogenesis of coronary artery spasm.

Acetylcholine↗
PubMed2005

The United Kingdom Infantile Spasms Study (UKISS) comparing hormone treatment with vigabatrin on developmental and epilepsy outcomes to age 14 months: a multicentre randomised trial.

BACKGROUND: Infantile spasms is a severe infantile seizure disorder that is difficult to treat and has a high morbidity. Absence of spasms on days 13 and 14 after randomisation is more common in infants allocated hormone treatments than in those allocated vigabatrin. We sought to assess whether early control of spasms is associated with improved developmental or epilepsy outcomes. METHODS: Infants enrolled in the United Kingdom Infantile Spasms Study (UKISS) were randomly assigned hormone treatment (n=55) or vigabatrin (n=52) and were followed up until clinical assessment at 12-14 months of age. We assessed neurodevelopment with the Vineland adaptive behaviour scales (VABS) at 14 months of age on an intention to treat basis. FINDINGS: Of 107 infants enrolled, five died and 101 survivors reached both follow-up assessments. Absence of spasms at final clinical assessment (hormone 41/55 [75%] vs vigabatrin 39/51 [76%]) was similar in each treatment group (difference 1.9%, 95% CI -18.3% to 14.4%; chi(2)=0.05; p=0.82). Mean VABS score did not differ significantly (hormone 78.6 [SD 16.8] vs vigabatrin 77.5 [SD 12.7]; difference 1.0, 95% CI -4.9 to 7.0; t(99)=0.35, p=0.73). In infants with no identified underlying aetiology, the mean VABS score was higher in those allocated hormone treatment than in those allocated vigabatrin (88.2 [17.3] vs 78.9 [14.3]; difference 9.3, 95% CI 1.2 to 17.3; t(95)=2.28, p=0.025). INTERPRETATION: Hormone treatment controls spasms better than does vigabatrin initially, but not at 12-14 months of age. Better initial control of spasms by hormone treatment in those with no identified underlying aetiology may lead to improved developmental outcome.

Adaptation, Psychological↗
PubMed1977

Recurrent catheter-induced coronary artery spasm.

Catheter-induced spasm has generally been considered to represent an iatrogenic phenomenon without important clinical significance. This report describes two patients who developed catheter-induced spasm in the proximal segment of the right coronary artery in separate studies performed in different laboratories by means of different catheter techniques. One of these patients developed right coronary spasm on three occasions and, in addition, developed catheter-induced spasm of the left main trunk during two different studies. These observations would add support to the hypothesis that a predisposition to coronary artery spasm may exist in certain individiuals. Catheter-induced spasm deserves attention, since it may provide a means of identifying spasm-prone individuals.

Arteries↗
PubMed1989

Botulinum toxin therapy in hemifacial spasm: clinical and electrophysiologic studies.

Three patients with idiopathic hemifacial spasm were studied clinically and electrophysiologically before and after injections of botulinum toxin into the involved periocular and facial muscles. The spasms were improved for approximately 3 months, and the effect was repeatable on reinjection. The spasms diminished only as long as the muscles were clinically weak, and spasms were observed electromyographically even though therapy eliminated the clinical spasms. Uninjected muscles continued to have spasms. Transmission of excitation from the zygomatic branch to the marginal mandibular branch of the facial nerve and vice versa in all patients was unaltered after therapy, but the amplitude of the response was decreased. The efficacy of botulinum toxin in hemifacial spasm appears to be related to the production of muscle weakness; there is no demonstrable effect on phenomena believed to be ectopic excitation or ephaptic transmission in the facial nerve.

Adult↗
PubMed1996

Intra-operative monitoring by facial electromyographic responses during microvascular decompressive surgery for hemifacial spasm.

The facial electromyographic response was monitored intraoperatively in 40 patients with hemifacial spasm who were operated on by microvascular decompression of the facial nerve. All 40 patients showed an abnormal facial electromyographic response (lateral spread response) with a latency of about 10 msec after stimulation. The abnormal response resolved before decompression in 22, resolved immediately with decompression in 16, and failed to resolve in two. Of the 38 patients in whom the abnormal response disappeared during surgery, 36 were postoperatively free from hemifacial spasm and two had mild hemifacial spasm. The two patients in whom the lateral spread response did not disappear during surgery showed persistent hemifacial spasm. In conclusion. Disappearance of the lateral spread response during surgery correlated with the absence of hemifacial spasm in the early postoperative period. The prognosis of hemifacial spasm was good in cases in whom the lateral spread response disappeared. Therefore, the authors think that intra-operative facial electromyography is very useful in assessing the efficacy of microvascular decompression and in predicting the prognosis of hemifacial spasm.

Adult↗
PubMed2000

Microvascular decompression of the facial nerve for the treatment of hemifacial spasm: preoperative magnetic resonance imaging related to clinical outcomes.

BACKGROUND: The objective of this study was to investigate the role of preoperative three dimensional short-range magnetic resonance angiography (3D-TOF MRA) in predicting the clinical outcomes following microvascular decompression for the treatment of hemifacial spasm. METHOD: Preoperative magnetic resonance (MR) imaging was performed on all patients with hemifacial spasm (564 cases) between January 1992 and September 1998. Of the 564 patients, 440 patients were included in this retrospective study. The presence of vascular contact, offenders, and anomalies in the vertebro-basilar system, were determined by 3D-TOF MRA prior to microvascular decompression of the facial nerve. The preoperative findings were compared with the surgical findings and clinical outcomes. Findings. A correlation was found between the clinical outcome (p < 0.01) and the presence of a vascular indentation at the root entry zone (REZ) of the facial nerve. A shift of the vertebrobasilar system to the symptomatic side was found in 214 (48.6%) patients with hemifacial spasm, compared to only 10 (13.5%) patients in the control group (p < 0.01). The unilateral vertebral artery was observed in 43 (9.8%) patients with hemifacial spasm and in 8 (10.8%) of the control patients. A hypoplasia of the artery was found in 8 (1.8%) patients with hemifacial spasm and in 1 (1.4%) control patient. The compressing offenders in the patients, discovered by MRI in conjunction with MRA, were as follows: 45.9% (202 patients) in the anterior inferior cerebellar artery (AICA), 34.8% (153 patients) in the posterior inferior cerebellar artery (PICA), 12.5% (55 patients) in the vertebral artery (VA) and 6.8% (30 patients) in multiple vessels. In contrast to the compressing offenders seen on the MRA, the offenders confirmed during surgery were as follows: 43% (189 patients) in the AICA, 36.4% (160 patients) in the PICA, 1.4% (6 patients) in the VA, 19% (84 patients) in multiple vessels, and 0.2% (1 patient) in the vein. In our long-term follow-up series of the 440 patients with hemifacial spasm, an excellent surgical outcome was obtained in 86.3% of cases and a good outcome was achieved in 6.4% (mean follow-up duration, 45.5 months). INTERPRETATION: Preoperative 3D-TOF MRA can identify the relationship between the facial nerve and adjacent vessels in patients with a hemifacial spasm and assist in preoperative planning. This study suggests that 3D-TOF MRA is useful for selecting appropriate patients for surgical treatment and, to some extent, as an additional role for predicting the clinical outcome.

Adult↗