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At least 19 recordsLinked to original sources
PubMed1979

Coronary spasm: Prinzmetal's variant angina vs. catheter-induced spasm; refractory spasm vs. fixed stenosis.

An analysis of 2,394 selective coronary angiograms yielded 23 examples of coronary artery spasm. Of these, nine occurred in patients with Prinzmetal's variant angina and 14 were instances of catheter-induced spasm. Angiographic criteria can distinguish between the spasm of variant angina and catheter-induced spasm. The latter is usually asymptomatic, almost invariably in the right coronary artery, at the catheter tip, smooth, concentric, and less than 2 mm long. The former can occur in any coronary artery at a distance of 1--4 cm from the catheter tip, is usually irregular and eccentric, and is associated with angina, ST segment elevation, hypotension, and dysrhythmia. Response to nitroglycerin is often, but not always, complete in both. Stenoses that seem to be fixed in patients with Prinzmetal's angina should be suspected to be spasm even if unresponsive to nitroglycerin, especially when the rest of the vessel is normal. Additional pharmacologic manipulation and even recatheterization may be necessary to prove the dynamic nature of the lesion and avoid unnecessary surgery.

Adult↗
PubMed1976

The long-term prognosis infantile spasms--the present condition of cases of infantile spasms followed in school age.

A follow-up study has been made of 25 cases with infantile spasms, all of whom were six years old or more at review. Only four (16%) out of 25 cases made a full recovery and attended normal school. Spasms ceased in 96% of all cases, but fits other than spasms (grand mal, tonic seizure, atonic seizure, myoclonic seizure, atypical absence and psychomotor seizure) occurred subsequently in 11 cases (44%). The EEG became normal in two cases (8%), but still showed modified hypsarhythmia in three cases (12%), "epileptic non-hypsarhythmic" discharges in 17 cases (68%) and non-specific abnormalities in three cases (12%). The important factors associated with good prognosis were normal development before the onset of spasms, late onset (seven months old or over) and short duration of spasms, the absence of other types of fit following spasms and lack of neurological abnormality. A bad prognosis was associated with abnormal development prior to the onset of spasms, early onset and long duration of spasms, the presence of other types of fit following spasms and evidence of any neyrological abnormality This follow-up may confirm that the therapy with ACTH-A has no significant effect on final mental state.

Adolescent↗
PubMed1979

Cerebral arterial spasm: part 10. Reversal of acute and chronic spasm in dogs with orally administered nifedipine.

In vivo experiments in dogs demonstrated angiographically that the subarachnoid injection of blood produced cerebral arterial apasm both immediately after the injection of blood and 2 days later. The sublingual adminstration of nifedipine reversed both the acute and the delayed cerebral arterial spasm. In addition, sublingual administration of nifedipine 20 minutes before the subarachnoid injection of blood prevented the acute spasm.

Acute Disease↗
PubMed2026

Late-onset epileptic spasms: presentation, aetiology and outcome.

Late-onset epileptic spasms (LOES) are epileptic spasms (ES) commencing after age 12 months, often misdiagnosed and having uncertain relationship to infantile spasms. Previous studies of mostly small LOES cohorts frequently reported 'cryptogenic' aetiologies. We studied the presentations, aetiologies, treatment responses and outcomes in a large LOES cohort, evaluated with modern neuroimaging and genomic testing. In this retrospective cohort study, 62 children with video-confirmed epileptic spasms, diagnosed between 2011 and 2021, were included. All had epileptiform activity on EEG, but none had hypsarrhythmia. Median age at epileptic spasms onset was 23 months (range 1-15 years) and median delay to diagnosis was 8 months (interquartile range: 3-15). Only 24% children were correctly diagnosed at presentation, common misdiagnoses being myoclonic epilepsies and non-epileptic phenomenon. Aetiology was identified in 95%. Structural-malformative aetiologies were present in 63% (most commonly focal cortical dysplasia and mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy). Other aetiologies were structural-acquired in 13% (mostly postnatal stroke and CNS infections), genetic in 13% (mostly intragenic variants and chromosomopathies) and oncological in 6% (history of leukaemia, two with CNS involvement). Children with structural aetiologies often had normal development prior to onset of epileptic spasms, a later median age of epileptic spasms onset and were more likely to have asymmetric or subtle epileptic spasms and additional seizures prior to epileptic spasms. Epileptic spasms ceased in 29% children treated with prednisolone, most having genetic aetiologies and in 35% treated with vigabatrin, all having structural-malformative aetiologies. Apart from clobazam, which was effective in 17% of children, all other antiseizure medications, vagus nerve stimulation and ketogenic diet therapy were ineffective. Epileptic spasms ceased in 86% (18/21) of children who underwent epilepsy surgery. At median follow-up of 10.3 years, 53% children were free of all seizures and 76% were free of epileptic spasms. More children with unilateral structural-malformative aetiologies achieved seizure freedom than other aetiologies, most commonly following surgery but occasionally following treatment with vigabatrin or clobazam. Impairment of cognitive function or adaptive behaviour (formally assessed in 90%) was significantly more common in children with genetic than structural aetiologies, and in children with ongoing seizures than seizure freedom. Among children who underwent epilepsy surgery, 62% achieved average or low-average adaptive functioning or normal intellectual capacity. This study highlights the importance of prompt recognition of epileptic spasms in older children for improved seizure and developmental outcomes. Brain malformations and insults are the predominant causes of LOES, and when unilateral, respond best to epilepsy surgery.

cognitive outcome↗
PubMed1978

[A regional cerebral blood flow in patients with acute subarachnoid hemorrhage--with special references to spasm (author's transl)].

Measurements of the regional cerebral blood flow (rCBF) were performed 44 times on patients with subarachnoid hemorrhage, using the 133-Xe clearance method with aid of the 8 channel detector unit. The patients consisted of 31 preoperative cases within 3 weeks of the last subarachnoid hemorrhage. The sites of the ruptured aneurysms included 11 anterior communicating arteries, 8 middle cerebral arteries, 7 internal carotid arteries and 3 anterior cerebral arteries. In 2 cases, the aneurysms were not identified with the cerebral angiograms. The purpose of this study was to investigate the effect of spasm on the rCBF. The subjects were divided into two groups: those with and without spasm. Furthermore, the group with spasm was divided into three subgroups according to the degree of spasm. The findings obtained were as follows; The group with spasm showed a statistically significant decrease in the mean of the rCBF. The MrCBF was not influenced by the distribution of spasm, however. In the group without spasm, the MrCBF had a good correlation with the cerebrospinal fluid pressure (CSF-P) or the level of consciousness. In the group with spasm, there was no correlation between the MrCBF and the CSF-P or the level of consciousness. For example that marked reduction of the MrCBF were seen in some cases with low CSF-P or only slight disturbance of consciousness. The rCBF was measured 2 or 3 times in 5 cases with spasm. The decrease in MrCBF occured about one week after the incidence of the subarachnoid hemorrhage but MrCBF recovered with the disappearance of spasm 2 or 3 weeks after the attack. There was a poor correlation between spasm and relative flow patterns. The good correlation, however, was found in only one case with the severe spasm at the middle cerebral artery.

Acute Disease↗
PubMed1977

Coronary artery spasm. medical management, surgical denervation, and autotransplantation.

Coronary artery spasm was induced by intravascular administration of ergonovine maleate (Ergotrate) during cardiac catheterization. In 78 patients suspected to have Prinzmetal's angina, no morbidity or death has resulted despite complete occlusive spasm in two and three coronary arteries. Typical EKG changes and akinesia of the myocardium in the distribution of the occluded vessels documented functional myocardial ischemia during spasm. The occlusive spasm is readily reversed by sublingual or intravascular nitroglycerin, and ventricular contractility returns to normal following relief of spasm. Occlusive spasm has been demonstrated in 15 patients with clinical evidence of Prinzmetal's angina. Symptoms have been effectively relieved by coronary vasodilators in 10 patients. Of the 5 patients in whom medical therapy failed, 4 were treated surgically. These 4 patients were in the intensive care unit with protracted, prolonged pain, subendocardial infarctions, and persistent failure of coronary vasodilators. Aorta-coronary bypass grafts have been combined with total cardiac denervation by autotransplantation (one patient) and total cardiac denervation by stripping of the great vessels (3 patients). Two of the patients treated by cardiac denervation died in the early postoperative period. The patient treated by autotransplantation has total relief of symptoms but persistent spasm on angiography. The angiographic demonstration of occlusive coronary spasm remains a valuable diagnostic tool to document definitively the presence of spasm. The surgical results question the value of surgical intervention in this disease.

Adult↗
PubMed1977

[Coronary artery spasms].

In a series of 2000 coronary arteriographies, spasm of the coronary artery was found in 52 cases, which were divided into three groups: 41 cases of "iatrogenic" spasm caused by stimulating the ostium of the coronary artery (usually the right) with the tip of the catheter; 8 cases of spasm on top of an organic fixed lesion; 4 cases of coronary spasm on a coronary artery which was reported as "radiologically normal". The study includes a review of the circumstances which favour or impede discovery of coronary spasm, as well as a provocation test using methyl ergometrine. This test seems to be specific in that it only produced coronary spasm in patients with Prinzmetal's syndrome, and excluded the cases of angina with normal coronary arteriography. The patients with spasm on top of a fixed organic lesion underwent a successful aorto-coronary bypass graft together with resection of the pre- and sub-aortic nerve plexus. Patients with a spasm in an artery which was "arteriographically normal" were treated medically by nitrate compounds and vaso-dilators. Three of these patients had an excellent result with medical treatment. Treatment failed in the fourth patient, who then obtained benefit from straight-forward resection of the pre- and sub-aortic nerve plexus with an excellent result which has been maintained for over six months.

Adult↗
PubMed1977

Arteriographic evidence of coronary arterial spasm in acute myocardial infarction.

Coronary arteriography was performed before and after the intracoronary injection of nitroglycerin to determine the presence or absence of spasm in patients within the first 12 hours of acute myocardial infarction. Coronary arterial spasm was demonstrated in six of fifteen (40%) acute myocardial infarctions associated with coronary artery disease. In five of the six instances the interval from the onset of symptoms to arteriography was less than 6 hours. Spasm was superimposed on a high-grade atherosclerotic obstruction and was separated from the catheter tip by a segment of normal vessel in each instance. The coronary artery remained patent (following the initial relief of spasm) in two patients maintained on sublingual nitrates and heparin. Spasm, superimposed on an atherosclerotic obstruction, may be the primary event or a secondary occurrence in the pathophysiology of acute myocardial infarction. Catecholamines could play an important role in the early pathophysiology of acute myocardial infarction by producing spasm and/or platelet aggregation at the site of an atherosclerotic obstruction. A dynamic interaction between spasm, platelet aggregates and the atherosclerotic plaque may precede coronary thrombosis.

Acute Disease↗
PubMed1978

[Surgical treatment of hemifacial spasm associated with tortuous vertebrobasilar system (author's transl)].

Surgical treatment of hemifacial spasm associated with tortuous vertebrobasilar system was reported. A patient was 63-year-old female, who first experienced mild and intermittent muscle twitching around her left eye twenty years prior to admission. Five years later, the twitching extended to all the facial muscles on the left side. She was treated with facial nerve block, which resulted in facial palsy for about one year. Because of recurrence of the hemifacial spasm, she was admitted to the Neurosurgical Department of Bokuto Municipal Hospital on October 12, 1977. Neurological examination revealed no abnormalities except for left hemifacial spasm with slight muscular weakness. Electromyogram showed severe twitching and synkinesis of all the muscles of facial expression. Vertebral angiogram on the left side disclosed pronounced elongation of the vertebral and basilar arteries, which extended into the left cerebellopontine angle. Compression of the facial nerve root exit zone at the brainstem by the vertebral artery was considered to be the cause of the hemifacial spasm. Suboccipital craniectomy was carried out on November 29, 1977. The vertebral artery extended into the cerebellopontine angle, and adhered to the facial nerve. After mobilization of the vertebral artery from the facial nerve, a small prosthesis of non-absorbable spongy material (Teflon felt) was interposed between the vertebral artery and brainstem. Postoperatively, the hemifacial spasm disappeared, but the facial palsy, which had been observed preoperatively probably due to previous facial nerve block and long-standing hemifacial spasm, remained. The function of the acoustic nerve was preserved. Recently vascular compression of the facial nerve root exit zone has been reported as a major cause of hemifacial spasm, but such abnormal vessels are rarely demonstrated angiographically.

Basilar Artery↗
PubMed1977

Esophageal spasm: clinical and manometric response to nitroglycerine and long acting nitrites.

The effect of nitroglycerine and long acting nitrites was studied in a group of 8 normal control subjects and 12 patients with esophageal spasm. The objective response of the esophagus to these drugs was recorded by obtaining esophageal manometric studies and was correlated with response in clinical symptoms. In 7 patients who had significant gastroesophageal reflux associated with spasm, the response to nitroglycerine was unpredictable. But in the group of 5 patients with diffuse esophageal spasm without gastroesophageal reflux, the response was uniformly good. All of the patients who responded to nitroglycerine also responded to long acting nitrites. These 5 patients, who were placed on long term management with long acting nitrites, remained symptom-free from 6 months to 4 years. None of them had recurrence of symptoms while they were on long acting nitrite therapy. The study suggests that if esophageal spasm is associated with reflux, the use of nitrites is less effective in controlling spasm than it is in those who do not show this association, and that diffuse esophageal spasm can be effectively managed with long acting nitrites on a long term basis in the absence of reflux. If there is esophageal spasm associated with reflux esophagitis, nitrites may be beneficial as an adjunct to antireflux therapy.

Adult↗
PubMed1979

Altered adrenergic activity in coronary arterial spasm: insight into mechanism based on study of coronary hemodynamics and the electrocardiogram.

To elucidate the pathophysiologic mechanism of coronary arterial spasm, the hypothesis was examined that underlying alterations in sympathetic activity may account for this syndrome in some patients. Observations were directed to alterations in coronary arterial hemodynamics and the electrocardiogram. Spasm of the left anterior descending coronary artery produced a mean increase in coronary vascular resistance of 107 percent (P less than 0.05) in four patients in whom coronary sinus blood flow was measured with the thermodilution technique. The alpha adrenergic blocking agent phentolamine, given intravenously, acutely reversed coronary spasm and its clinical manifestations in eight patients and reduced coronary resistance. In four patients, administration of the long-acting oral alpha blocking agent phenoxybenzamine (20 to 80 mg/day) caused disappearance of symptoms during a follow-up period of 3 to 12 months. Transient prolongation of the corrected Q-T interval preceded spontaneous or ergonovine maleate-provoked coronary spasm in 11 patients with variant angina pectoris, whereas no significant change in the Q-T interval followed ergonovine administration in 27 control patients with atypical chest pain who did not have coronary spasm. T wave inversions in the resting electrocardiogram were normalized by isoproterenol infusion in one patient and by long-term phenoxybenzamine treatment in four patients with variant angina pectoris. These Q-T and T wave changes are analogous to those described with unilateral or asymmetric stellate ganglion stimulation in animals. These observations suggest that alterations in the sympathetic nervous system that are consistent with asymmetric stellate ganglion activity and transient alpha adrenergic receptor stimulation can presage the development of coronary arterial spasm in some patients with variant angina pectoris.

Adult↗
PubMed1977

Critical evaluation of the role of immunization as an etiological factor of infantile spasms.

One hundred and ten cases of infantile spasms with detailed information about immunization available were selected as the masterial to evaluate the significance of immunization as an etiological factor of infantile spasms. In 80% of the cases, immunization could not be considered to have any relation with causation of infantile spasms, because 44 cases (40%) never had innoculations as yet, and other 44 cases (40%) had been immunized by some vaccines over one month before or after the onset of the disease. The remaining 22 cases, in whom immunization had been performed within one month before the onset of the disease, constituted the candidates for further study. The age of onset of the disease of the candidate group ranged from 3 to 9 months of age with peak incidence at 4 to 5 months old, exactly identical with that of patients with infantile spasms in general. The kind of vaccines concerned included DPT triple vaccines in 15 cases, smallpox vaccine in 4, antipolio live vaccine in 1, anti-Japanese encephalitis vaccine in 2. Causal relationship of immunization with infantile spasms in each patient was evaluated on the basis of the following three apsects: 1. Any other causal factors except immunization should be absent. 2. Psychomotor development before onset of the disease should be normal. 3. Interval from immunization to onset of the disease should be lied: a) Within 48 hours, in the case of pertussis vaccine, b) within 18 days, in the case of smallpox vaccine or anti-Japanese encephalitis vaccine or antipolio vaccine. Only five cases (4.8% of the total) were able to classify into the compatible group which should fulfill all the above three criteria. The small figure may easily be explicable on the assumption that the natural onset of spasm is chronologically superposed by chance over immunizations which have to be done within the first year of life.

Age Factors↗
PubMed1978

An investigation with serial angiography into the evolution of cerebral arterial spasm following aneurysm surgery.

Serial postoperative angiograms were performed in 28 patients with intracranial aneurysms, 26 of whom had presented with a subarachnoid hemorrhage. The clinical state and intracranial pressure (ICP) were also measured. Angiograms were performed in the ward using a cannula, which was passed into the proximal external carotid artery via the superficial temporal artery. Measurements of the vessel diameters were made, with the preoperative angiogram as a baseline. Patients could be placed into one of five groups depending on the presence or absence of significant arterial spasm, the clinical state of the patient, and the normality or otherwise of the ICP. No patient's condition deteriorated without an elevated ICP and/or significant arterial spasm. The study shows that this spasm is usually associated with a poor clinical state if it reaches a maximum 8 to 12 hours after the operation, although the clinical deterioration is not apparent for a further 6 to 12 hours. Knowledge of the natural history of postoperative arterial spasm may allow earlier treatment of the spasm, which may be more successful than delaying treatment until clinical deterioration has occurred. The worth of the varied drugs proposed for the treatment of spasm may be assessed using this type of protocol.

Adolescent↗
PubMed1978

Recognition of renal artery spasm during renal angiography.

During the performance of routine angiography in a community hospital, three different forms of renal arterial spasm were encountered. Renal artery spasm may involve either large or small arteries of the kidneys. The temporary nature of the spasms may be demonstrated by additional angiography which shows no defect. Either a sufficient waiting period for the spasm to relent or the employment of a vasodilating drug through the catheter will usually suffice for this demonstration. Differentiation of spasm from fixed, organic disease is essential to prevent diagnostic error and improper therapy.

Adolescent↗
PubMed1979

Central retinal artery spasm.

Central retinal artery spasm, a seldom witnessed ocular sign, has been recognized in one eye of a patient complaining of transient monocular blindness. Removal of an ulcerative atheromatous plaque of the carotid artery on the same side as the eye with central retinal artery spasm resulted in complete disappearance of symptoms. No other signs of ocular pathology were noted in addition to the central retinal artery spasm. Central retinal artery spasm occurring in both eyes simultaneously may be the mechanism explaining the visual loss of amaurosis fugax. Physiologic mechanisms associating brief episodes of monocular blindness and carotid artery obstructive disease with atherosclerosis are discussed. The possibility of central retinal artery spasm initiating occlusion of the same vessel is mentioned.

Arteriosclerosis↗
PubMed1979

The mechanism of coronary artery spasm: roles of oxygen, prostaglandins, sex hormones and smoking.

A reduced oxygen supply to the heart causes coronary vasodilatation in the first instance. But if the hypoxia is severe or prolonged, the dilatation passes off and coronary vasospasm develops leading to a vicious circle with a further reduction of myocardial oxygenation. The spasm is associated with increased outflow of prostaglandin (PG)-like material and can be prevented or reversed by inhibitors of PG synthesis such as indomethacin or antagonists of PG action such as chloroquine. The spasm does not appear to be caused by thromboxane (TX) A2 since selective inhibitors of TXA2 synthesis enhance the hypoxic spasm and by themselves can cause spasm even in oxygenated hearts. The mechanism may be related to loss of negative feedback control of the PG pathway by TXA2. Oxygen may enhance TXA2 production and reduce formation of vasoconstrictor PGs, while smoking, because of the formation of carboxyhaemoglobin, may have the opposite effect. Oestradiol and testosterone do not influence the hypoxic spasm but progesterone at physiological concentrations blocks it completely. Progesterone may be the protective female hormone and the increased susceptibility to myocardial infarction in women on oral contraceptives may be related to reduced formation of endogenous progesterone.

Coronary Circulation↗
PubMedDate not supplied

Cerebral arterial spasm: A discussion of present and future research.

The author presents a discussion of research on cerebral arterial spasm. Arterial smooth muscle contraction, receptor and relaxation mechanisms are presented in the context of what is known about cerebral arterial spasm and the biochemistry of vascular smooth muscle. Several new experimental approaches are suggested and a theoretical biochemical basis for the idea that damage to the artery alone could cause cerebral arterial spasm is postulated. Methods of determining cerebral arterial spasm and the need for a quantitative, in vivo method are discussed and the question of an irreversible stage of cerebral arterial spasm is considered. Finally, the problems associated with the delivery of a potentially successful treatment to the cerebral arterial smooth muscle cells are examined.

Actins↗