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Severe glucagon-resistant spasm on double-contrast barium enema (DCE) examinations may occasionally lead to a nondiagnostic examination or erroneously suggest colonic disease. In such cases, this glucagon-resistant spasm may be overcome by refilling the colon with single-contrast barium immediately after completion of the DCE examination.
We compared various electrodiagnostical tests in patients with hemifacial spasm and in patients who developed synkinesia after Bell's palsy. We examined the evoked blink reflexes in the orbicularis oculi (o. oculi) and orbicularis oris (o. oris) muscles in 23 patients with hemifacial spasm (HFS), in 10 patients with synkinesia after Bell's palsy (BPS) and in 22 control subjects. In the patient groups, we recorded synkinesia, latency and amplitude of compound muscle action potential (CMAP) in the mental muscle after stimulation of the facial nerve and we examined electromyographic activity of the o. oculi and mental muscles synchronously. Furthermore, we studied the phenomenon of lateral spreading, also known as ephaptic transmission, between the different facial nerve branches. Patients with BPS had a prolonged R1 latency on the affected side in o. oculi and smaller mental CMAP amplitude as an indication of facial nerve damage and nerve fiber loss. This was not found in patients with HFS, who showed an increased amplitude of the R1 and R2 responses in o. oris. Patients with BPS showed only an increased R1 amplitude in o. oris. All patients had signs of synkinesia. Lateral spreading with different patterns was present in all patients with HFS and in half of the patients with BPS. Latencies of early and late responses showed no differences between HFS and BPS. In addition to alterations in facial nucleus excitability in both conditions, ectopic re-excitation of facial nerve axons in HFS may explain the differences in neurophysiological findings between HFS and BPS patients. A loss of control following synaptic stripping may also be a contributing factor.
3 patients suffering from long-lasting "cryptogenetic" hemifacial spasm in association with dolichomegavertebrobasilar anomaly, are described. The angiographic examinations confirm the anomaly and put in evidence the patholphysiologic value of segment V4 of the vertebral artery at the same side of the spasm. Classical electromyographic examinations, and methods used to study the blink reflex, seem to rule out the hypothesis of a brain stem involvement as the only and sufficient pathologic mechanism. The peripheral pathogenesis is the most likely one.
A case of classical Sturge-Weber syndrome associated with infantile spasms (female infant, aged 4 months) was presented. The association of both conditions would be very rare since no similar case was found among 214 cases of Sturge-Weber syndrome and 1,180 cases of infantile spasms gathered from the literature, except for one who was reported by Millichap et al. Evolutional changes of electroencephalographic findings were followed up for about 3 years on average in 5 personal cases of Sturge-Weber syndrome. Unilateral depression of electrical activity in the cerebral hemisphere ipsilateral to the facial nevi was the constant finding. Focal spike discharges were noticed only in the contralateral hemisphere in 3 cases, only in the ipsilateral in 1, and in the bilateral in 1.
The whole night EEG were polygraphically recorded and analyzed in 9 patients with infantile spasms prior to ACTH therapy. The subjects were divided into two groups, favorable and unfavorable, depending upon the response to the ACTH therapy. (1) Among the unfavorable group, the deep sleep stage was not observed; while the light sleep stage tended to dominate. (2) REM sleep period was noted less among the unfavorable than among the favorable group. REM density also tended to be lower among the unfavorable group. (3) Of the 4 unfavorable cases, 2 did not manifest REM sleep at all. Of the remaining 2, 1 had a remarkably long REM interval period. Even among the favorable cases, REM sleep tended to be short and appear frequently. (4) The period of muscle atonia during NREM sleep was markedly prolonged in all cases. (5) Body movements of both types (gross and twitch) were less frequent comparing to those of normal younger children, more remarkably in unfavorable cases. From the above findings, a disorder of the pontine reticular formation would be suggested in cases of infantile spasms. Reduction of body movements at each sleep stage might indicate abnormalities of monoamine metabolism in the brain stem of patients with this condition.
A 58-year-old woman with long-standing hemifacial spasm experienced dramatic relief of symptomatology while receiving baclofen (Lioresal) in a daily dosage of 37.5 mg. Clinical response was noted within 48 h and she remained asymptomatic during 12 months of treatment. No toxic or side-effects were observed. Controlled studies are needed to establish the role of baclofen in hemifacial spasm.
Fifty-two patients affected by focal dystonia or hemifacial spasm were treated with repeated injections of botulinum toxin. A clinical improvement was observed in all patients with blepharospasm; clinical benefit had a mean duration of 10 weeks. Clinical results were less impressive, but also favorable in patients affected by spasmodic torticollis and by hemifacial spasm. In the latter, the incidence of drug-induced paresis was much higher than that observed in patients with blepharospasm, even though the doses of toxin injected were significantly lower.
This paper retrospectively analyses the clinical data of 65 consecutive cases of hemifacial spasm. A benign etiology was clinically evident in the majority of cases. Neuroradiologic investigation ruled out serious intracranial pathology in atypical cases. Trials of oral medication in 26 patients were consistently unsuccessful. Fifty-one patients had repeated lid and facial muscle injections of botulinum toxin during a period of 8 years. The mean duration of effective relief from spasm following an initial treatment was 18.9 weeks. This effect did not diminish with repeated injections.
Hemifacial spasm (HFS), generally a disease of the elderly, is caused by vascular compression of the seventh nerve. Vascular compression is thought to result from atherosclerotic changes within the vessels of the posterior fossa, and therefore rarely presents in childhood. Here we describe our experience with 12 patients with onset of HFS during childhood (age 18 or less) and who had surgical exploration of the cerebellopontine angle. These patients represent less than 1.2% of the patient population with HFS operated upon at this institution during the study period. Nine patients had follow-up data extending over 83 months. All 12 patients were found to have microvascular compression of the seventh nerve at the time of surgery. The most common operative finding was compression of the seventh nerve by a vein, alone or in combination with a branch of the anterior inferior cerebellar artery. At the time of discharge and after a mean follow-up period of 125 months, microvascular decompression resulted in complete relief of spasm in 67% of the patients.
We have used a placebo controlled trial to investigate the effect of long-term administration of nifedipine in the prevention of symptomatic episodes of oesophageal spasm. Diary card scoring was used to assess symptoms in 8 patients with oesophageal spasm who were each given nifedipine and placebo for at least 6 weeks. No significant differences in symptoms between the nifedipine and placebo treatment periods were seen.
A 24-year-old male student had three myocardial infarctions, one prior to and two following the angiographic documentation of normal coronary arteries. A spontaneous episode of variant angina prompted repeat coronary angiography, during which intravenous ergonovine caused spasm of the left anterior descending coronary artery, transient ST-segment elevation, and ischemic chest pain; the previously normal right coronary artery was found to be occluded proximally. This constellation of clinical and angiographic findings suggests that coronary spasm can cause acute myocardial infarction as well as variant angina.
Vigorous hyperventilation was induced for five minutes immediately after a five-minute infusion of 100 ml of Tris-buffer (pH 10) in nine patients with Prinzmetal's variant angina. In eight of the patients, chest pain with ischemic changes in the electrocardiogram occurred during this procedure or within five minutes after it ended. Coronary arterial spasm appeared after the procedure and disappeared after the administration of nitroglycerin in all four patients in whom coronary cinearteriography was performed. This was evident both before and after the procedure and after sublingual administration of nitroglycerin (0.6 mg). The oral administration of 90 mg of diltiazem, a calcium antagonistic drug, two hours before, completely suppressed the attack induced by the procedure in all of the five patients who received this drug. We conclude that hyperventilation plus Tris-buffer infusion induces coronary arterial spasm and anginal attack in patients with Prinzmetal's variant angina and that diltiazem suppresses these reactions.
Seven patients with typical variant angina without coronary stenoses greater than 50% developed angina and ST-segment elevation during treadmill exercise testing. In all cases the ST-segment elevation occurred in the same leads during exercise testing as during spontaneous attacks at rest. Five of the patients had developed spontaneous coronary spasm during coronary arteriography, in each case in the artery corresponding to the site of ST-segment elevation. In five patients, thallium was injected during the exercise test during which angina and ST-segment elevation occurred. In each case, a large perfusion defect not present at rest was found in the zone corresponding to the site of ST-segment elevation. These findings suggest that coronary artery spasm may occur during exercise in patients with variant angina.
Thirteen patients with Prinzmetal's variant angina performed treadmill exercise tests in the early morning and in the afternoon of the same day. The attacks with ST elevation were induced repeatedly in all 13 patients in the early morning, but in only two patients in the afternoon. Propranolol did not suppress the exercise-induced attacks in all 13 patients. Diltiazem suppressed the attacks in all 13 patients and phentolamine in eight of the nine patients. Coronary arteriograms demonstrated that spasm occluding completely or almost completely the large coronary artery supplying the area of myocardium showing ST elevation appeared during the attacks and disappeared along with the attacks after nitroglycerin administration in all four patients in whom the attacks were induced by arm exercise in the catheterization laboratory. We conclude that there is circadian variation of exercise capacity in patients with Prinzmetal's variant angina caused by coronary arterial spasm induced by exercise in the early morning but not in the afternoon.
Four patients with variant angina pectoris exhibited reproducible exercise-induced chest pain and ST-segment elevation. Coronary arterial spasm was documented with arteriography during exercise-induced ST-segment elevation (three patients) or after intravenous administration of ergonovine maleate (one patient). Our observations show that in patients with variant angina exercise can trigger coronary arterial spasm, thus inducing anginal pain and ST-segment elevation.
A case is presented, believed to be the first reported, describing recurrent myocardial infarction in an athletic 25-year-old man due to coronary arterial spasm, which was demonstrated at autopsy. A previous angiogram performed during life, after the first myocardial infarction, showed normal coronary arteries. The findings in this case are discussed with a review of the current knowledge pertaining to coronary arterial spasm.
In a patient with variant angina, we have shown that the calcium-channel blocker nifedipine inhibits both spontaneous and ergonivine-induced coronary artery spasm. It had no effect, however, on the dose-related diffuse vasoconstriction caused by ergonovine, suggesting two distinct responses of coronary arteries to ergonovine provocation. Nifedipine did not cause epicardial coronary artery dilatation, as did nitroglycerin, supporting the rationale of using both therapies together to treat coronary artery spasm.
The cardiomyopathic Syrian hamster develops focal myocardial necrosis beginning at 1 month of age, which leads to eventual ventricular failure within 1 year. The pathogenesis of this myocytolytic necrosis is unknown. Based on the nature of the cell necrosis, cytochemical evidence of vascular alterations, and the sensitivity of the hamsters to catecholamines and other vasoactive substances, we believe that the cardiomyopathy may be mediated by abnormalities of the microcirculation. Nonetheless, until the present study, no significant changes have been observed in these vessels. To elucidate the pathogenesis of this disease, we perfused living cardiomyopathic hamsters with silicone rubber solutions, which revealed numerous areas of microvascular constriction, diffuse vessel narrowing and luminal irregularity. Fixed structural lesions in these vessels could not be demonstrated. Pretreatment of young hamsters with verapamil during the period when they normally develop myocardial necrosis prevented myocytolytic lesions and abolished microvascular hyperreactivity. We believe that focal, transient spasm of small blood vessels, probably secondary to vasoactive substances, may cause myocytolytic necrosis (a form of reperfusion injury) in this model. This may also be a multifactorial disease with myocellular as well as vascular abnormalities leading to myocardial degeneration. The similarity of this disease to human and experimental cardiomyopathy suggests that microvascular spasm may be a common denominator of many different cardiomyopathic syndromes.