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PubMed2002

Mechanism and treatment principle for cerebral vessel spasm caused by concussion.

OBJECTIVE: To discuss the mechanism of cerebral vessel spasm caused by concussion and the effect of Nimodipine on concussion. METHODS: A total of 224 patients who were treated from March 1995 to October 1999 were divided into two groups randomly, ie, Nimodipine group (113 cases) and control group (111 cases). Middle cerebral artery (MCA), basilar artery (BA) and the average peak forward velocity of cerebral blood flow were observed by color three-dimensional transcranial Doppler (3D-TCD) within 24 hours after admission and at the end of 3-6 days of treatment. Cerebral blood flow changes, characteristics and treatment effect were analyzed and determined by clinical main symptom disappearance rate. RESULTS: In concussion, cerebral blood flow was divided into 3 phases: cerebral blood flow low infusion dilation phase, cerebral blood vessel spasm phase and cerebral blood flow recovery phase. In the Nimodipine group, clinical main symptom disappearance rate was higher than that in the control group in the cerebral spasm and recovery phases with a significant difference (P < 0.01). CONCLUSIONS: Cerebral vessel spasm, hypoxia and ischemia lesion are the main pathological changes. Whether cerebral dysfunction is reversible or not is mainly determined by spasm time of cerebral blood vessel. Nimodipine has a good effect on releasing spasm and diminishing the cerebral blood flow velocity. It not only improves curative effect on concussion, but also reduces and prevents concussion sequelae. Hence, concussion patients who have cerebral spasm confirmed by 3D-TCD should be given Nimodipine routinely and early.

Adolescent↗
PubMed2006

Severe, diffuse coronary artery spasm after drug-eluting stent placement.

OBJECTIVES: Three cases of severe, diffuse coronary artery spasm after drug-eluting stent placement at our institution prompted this review. BACKGROUND: Drug-eluting stents have gained widespread use due to extraordinarily low rates of restenosis. Despite these generally superior clinical outcomes, the specter of rare idiosyncratic reactions remains a concern. METHODS: We performed searches of Medline and the U.S. FDA Manufacturer And User facility Device Experience database (MAUDE) to identify and describe spasm after coronary stent placement. Searches included drug-eluting and bare-metal stents. Institutional cases are reviewed. Location, time course and outcome of cases are described. RESULTS: Thirteen cases of spasm were identified after stent placement. Seven cases occurred after Cypher drug-eluting stent placement, 2 after Taxus drug-eluting stent placement, 1 after BiodivYsio and 3 after bare-metal stents. Five patients experienced diffuse, multivessel spasm--2 after Cypher, 2 after Taxus, and 1 after a Velocity stent. Of these 5 patients, 2 died. An additional 2 required intra-aortic balloon pump placement for cardiogenic shock. Another had persistent symptomatic, diffuse coronary spasm documented by angiography at 1 year. CONCLUSIONS: We describe coronary spasm after stent placement, particularly after drug-eluting stents. Outcomes associated with diffuse severe spasm after stenting are poor, and the pathophysiology remains poorly understood.

Angioplasty, Balloon, Coronary↗
PubMed1990

[Occluding spasm of the total left coronary artery during coronary angiography].

Catheter-induced coronary artery spasms are rare during diagnostic coronary angiography, and they occur more often after PTCA because of local vessel wall injury. These spasms are rapidly reversible after administration of nitroglycerine and are normally no cause of serious complications. We report about a catheter-induced occlusive spasm of the entire left anterior descending and circumflex coronary artery in a 56-year-old patient with coronary double-vessel disease, 70% restenosis of the LAD, and a history of two coronary angiographic procedures and one PTCA without any complication. The spasm occurred immediately after the intubation of the left main stem with a 9F PTCA guiding catheter before the coronary guide wire or balloon was advanced into the LAD. Cardiac resuscitation was necessary due to acute left heart failure. The spasm was spontaneously reversible, but reproducible. Therefore, life-threatening coronary artery spasm can occur during coronary angiography or PTCA, but the tendency of spontaneous spasm relief seems to be high.

Angioplasty, Balloon, Coronary↗
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↗
PubMed1989

[Induction of coronary arterial spasm by intracoronary administration of acetylcholine in patients with vasospastic angina].

To examine whether intracoronary injections of acetylcholine induce coronary artery spasm in patients with vasospastic angina, incremental doses (20, 30 and 50 micrograms) were injected directly into the coronary arteries in 12 patients with variant angina (Group A: rest angina with electrocardiographic ST-segment elevation during attacks), 19 with vasospastic angina (Group B: rest angina and/or effort angina with variable threshold in the treadmill exercise stress test), 11 with organic coronary artery stenosis but without angina (Group C), and 14 without coronary artery disease (Group D). A temporary cardiac pacemaker was positioned in the right ventricle. Coronary artery spasm was defined as severe vasoconstriction (greater than or equal to 90% of reduction in the 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 all 12 patients (100%) of Group A, in 18 (95%) of Group B, in two (18%) of Group C, and in two (14%) of Group D. Thus, the sensitivity of this method for inducing coronary spasm was 100% in group A, 95% in Group B, and 97% in Group A plus Group B. The specificity for inducing spasm was 86% in Group D, and 84% in Group C and Group D. When acetylcholine was injected separately into the left and right coronary arteries, spasm of both the coronary arteries was observed in two (40%) of Group A, in five (33%) of Group B, and none (0%) of Group C and Group D. Acetylcholine (20 micrograms) induced coronary spasm in 10 (83%) of Group A and only in nine (47%) of Group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
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↗
PubMed1980

[Induced coronary spasm: immediate revascularization by the opposite coronary artery. Use of myocardial scintigraphy].

The case reported analyses the instantaneous revascularisation distal to a coronary spasm by electrocardiography and thallium scintigraphy. The patient, a 48 year old man, had an 18 months history of spontaneous anginal chest pain sensitive to trinitrin. No electrocardiogrammes had been recorded during an attack. Coronary angiography was normal apart from a slight reduction in calibre of a dominant right coronary artery. Injection of 0.4 mg methylergometrine provoked an occlusive spasm of this artery after 4 minutes. At the same time the patient experienced angina and 4,5 mm depression of the ST segment, without ST changes in D3 and AVF, was observed. Opacification of the left coronary artery during spasme of the right showed retrograde revascularisation of the posterior interventricular artery which was reversed when the coronary spasm was terminated with trinitrin. Thallium scintigraphy was performed during another spasm provocation test four days later which gave identical clinical and electrical changes. A zone of hypofixation with blurred limits over the inferior myocardial wall was demonstrated. In the absence of ST elevation and of lacuna on myocardial scanning, the myocardial ischaemia induced by this occlusive spasm could not be considered to be total. Therefore the immediate revascularisation of the coronary artery in spasm seemed to have played the role of an effective collateral circulation.

Angina Pectoris↗
PubMed1998

[Characteristics of spasm-induced vessels in patients with vasospastic angina and a history of syncope].

One hundred and eighty-seven consecutive patients with vasospastic angina and coronary spasm provoked by intracoronary injection of acetylcholine and/or ergonovine were treated from January 1991 to June 1997. Fifteen of these patients, 14 men and one woman (mean age of 63 years old), had a history of syncope. There were no significant differences in the distribution of induced spasm vessels, single spasm vs multiple spasms, variant angina pectoris and organic stenosis (< 75%) between patients with and without a history of syncope. There were no significant differences concerning the distribution of the sites of induced spasm in the circumflex artery and left anterior descending artery between the two groups. However, coronary spasm in the proximal portion of the right coronary artery (segment 1 or 2 according to the functional classification of American Heart Association) occurred more frequently in patients with a history of syncope [80.0% (12/15) vs 45.3% (78/172); p < 0.05]. Twelve of the 96 patients with coronary spasm in the proximal portion of the right coronary artery had a history of syncope, so these patients require careful management.

Acetylcholine↗
PubMed2001

Randomized trial of vigabatrin in patients with infantile spasms.

BACKGROUND: Infantile spasms are a rare but devastating pediatric epilepsy that, outside the United States, is often treated with vigabatrin. The authors evaluated the efficacy and safety of vigabatrin in children with recent-onset infantile spasms. METHODS: This 2-week, randomized, single-masked, multicenter study with a 3- year, open-label, dose-ranging follow-up study included patients who were younger than 2 years of age, had a diagnosed duration of infantile spasms of no more than 3 months, and had not previously been treated with adrenocorticotropic hormone, prednisone, or valproic acid. Patients were randomly assigned to receive low-dose (18-36 mg/kg/day) or high-dose (100-148 mg/kg/day) vigabatrin. Treatment responders were those who were free of infantile spasm for 7 consecutive days beginning within the first 14 days of vigabatrin therapy. Time to response to therapy was evaluated during the first 3 months, and safety was evaluated for the entire study period. RESULTS: Overall, 32 of 142 patients who were able to be evaluated for efficacy were treatment responders (8/75 receiving low-dose vigabatrin vs 24/67 receiving high doses, p < 0.001). Response increased dramatically after approximately 2 weeks of vigabatrin therapy and continued to increase over the 3-month follow-up period. Time to response was shorter in those receiving high-dose versus low-dose vigabatrin (p = 0.04) and in those with tuberous sclerosis versus other etiologies (p < 0.001). Vigabatrin was well tolerated and safe; only nine patients discontinued therapy because of adverse events. CONCLUSIONS: These results confirm previous reports of the efficacy and safety of vigabatrin in patients with infantile spasms, particularly among those with spasms secondary to tuberous sclerosis.

Anticonvulsants↗
PubMed1988

Management of facial spasm with Clostridium botulinum toxin, type A (Oculinum)

One hundred five patients received 391 graded injections of Clostridium botulinum type A toxin (Oculinum) to treat uncontrollable facial muscle spasm. Patients had essential blepharospasm (n = 61), hemifacial spasm (n = 24), or aberrant regeneration of the seventh cranial nerve (n = 20). Muscle spasms were reduced within two days of the first injection of toxin and, in most cases, the drug effect lasted three to four months. Control of facial muscle spasm was achieved in all patients. Complications related to treatment included transient blepharoptosis (n = 7), diplopia (n = 2), and altered facial expression (n = 11). Systemic side effects were not observed. Select chemodenervation of facial muscles with graded injections of botulinum toxin is a useful adjunct to control blepharospasm, hemifacial spasm, and facial spasm due to aberrant regeneration of the facial nerve.

Blepharoptosis↗
PubMed1992

Infantile spasms: II. Lenticular nuclei and brain stem activation on positron emission tomography.

Infantile spasms are generalized seizures specific to early infancy, and are believed to result from complex cortical-subcortical interactions during a critical period of development. We used positron emission tomography (PET) to determine local cerebral metabolic rates for glucose (1CMRG1c) in 44 infants with spasms, in an attempt to define the neuroanatomical substrates that mediate these seizures. All infants were studied in the awake state during continuous electroencephalographic monitoring. The most consistent abnormality on PET, seen in 32 infants, was the symmetrical increase in 1CMRG1c in the lenticular nuclei, compared to age-matched normal infants (p less than 0.05). In 21 infants, even though the brain stem appeared to be visually more prominent compared to normal infants, statistically significant differences could not be demonstrated. Relative hypermetabolism of the lenticular nuclei (1) occurred irrespective of whether the spasms were cryptogenic or symptomatic, (2) was associated with focal cortical hypometabolism in 22 and focal cortical hypermetabolism in 5 of the 44 infants, and (3) was not characterized by any specific electroencephalographic abnormality during PET. These findings suggest that the lenticular nuclei may contribute to the pathophysiological state that predisposes to infantile spasms, and is consistent with the observation that spasms are clinically symmetrical even when focal cortical lesions are present. A scheme describing the neuronal circuitry likely to be involved in the generation of infantile spasms is proposed.

Brain Stem↗
PubMed1996

Electrophysiological investigation of hemifacial spasm: F-waves of the facial muscles.

In patients with hemifacial spasm (HFS), the spasm is due to cross-compression of the facial nerve by a blood vessel. There are currently two hypotheses for the mechanism of HFS: 1) the spasm is caused by ephaptic transmission and an increase in excitability at the site of compression; and 2) the spasm is caused by hyperexcitability in the facial nerve nucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of proximal motoneuron conduction and anterior horn cell excitability. Enhancement of the F-waves indicates increased anterior horn cell excitability. We have therefore measured F-waves in the facial muscle of HFS patients in order to investigate the excitability of the facial nerve nucleus. The authors obtained facial nerve evoked responses from 20 HFS patients before microvascular decompression (MVD), 10 HFS patients after MVD and 10 healthy controls. The F-waves, obtained with surface electrodes from the mentalis muscle, were the second response after the M-wave. On the patient's spasm side, the F-wave duration, F/M amplitude ratio and frequency of F-wave appearance significantly increased compared with those of the normal side or healthy controls; minimum latency and chronodispersion did not significantly differ between these groups. In patients whose spasm disappeared completely following MVD, the abnormal muscle response (lateral spread), which is a characteristic sign of HFS, and the enhancement of the F-wave eventually also disappeared. Because of the correlation between HFS and F-waves, the authors' study supports the hypothesis that the cause of HFS is hyperexcitability of the facial motonucleus.

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↗
PubMed1994

Kynurenic acid is decreased in cerebrospinal fluid of patients with infantile spasms.

Cerebrospinal fluid (CSF) from 8 patients with symptomatic infantile spasms was collected before specific treatment for infantile spasms. The concentration of CSF kynurenic acid (KYA) and 3-hydroxykynurenine (3-OHKY) in infantile spasms was analyzed by high-performance liquid chromatography and compared with CSF KYA from 10 age-matched controls. The levels of CSF KYA were significantly lower in infantile spasm patients compared to controls (P < .05). In contrast, the levels of CSF 3-OHKY were significantly higher in infantile spasm patients than in controls (P < .05). These findings suggest that the presence of seizures in infantile spasms is associated with altered metabolism of 3-OHKY. The possibility that seizures may be related to increased or decreased production of certain kynurenine metabolites is discussed.

Asphyxia Neonatorum↗
PubMed2004

Papaverine delivery to the internal mammary artery pedicle effectively treats spasm.

BACKGROUND: Left internal mammary artery spasm is well recognized during coronary artery bypass operations. Papaverine has been used by many surgeons to maximize mammary artery flow perioperatively, but the best delivery method is not known. We analyzed two techniques used at our institution. METHODS: Fifty-eight patients were randomized into three groups to compare papaverine's ability to prevent spasm and to treat established spasm. Group 1 was control and no treatment was employed. In group 2, papaverine was injected with a blunt needle through the endothoracic fascia parallel to the mammary artery before harvest to assess spasm prevention. In group 3, papaverine was delivered perivascular in an identical manner to group 2 but after the mammary artery was dissected from the chest wall. This group was an evaluation of spasm treatment. Drug dosage was the same for both groups and routine bypass grafting was performed. Before anastomosing the mammary artery to the left anterior descending artery, blood flow was recorded for 15 seconds and flow per minute calculated. Cardiopulmonary bypass pressures were maintained at 70 mm Hg during collection. RESULTS: Mean blood flows were: group 1 = 86.2 mL/min, group 2 = 122.5 mL/min, and group 3 = 139.7 mL/min. Left internal mammary artery flow in group 3 was statistically different from control (p = 0.0457). Group 2 flow approached but did not reach statistical significance (p = 0.0874). Mammary artery dissection times for the three groups were not different. CONCLUSIONS: Papaverine delivery to the left internal mammary artery after dissection treats spasm effectively, improves blood flow at the time of its anastamosis to the left anterior descending artery, and avoids any risk of intimal injury. Injection of papaverine before mammary artery harvest does not shorten dissection time, and flow is not statistically improved.

Arterial Occlusive Diseases↗
PubMed2002

Role of subcortical structures in the pathogenesis of infantile spasms: what are possible subcortical mediators?

Infantile spasms present a constellation of symptoms and laboratory findings that suggest a role of subcortical circuits in the pathogenesis of this illness. The clinical features of spasms and the influence of subcortical circuits in the regulation of the electroencephologram, along with frequent abnormalities in subcortical structure and functional anatomy, brain stem electrophysiology, sleep regulation, and subcortical neurotransmitter levels, point to the importance of subcortical circuits in the generation of spasms. Furthermore, laboratory evidence shows that modulation of subcortical nuclei may attenuate and ameliorate seizures. We review clinical evidence indicating abnormal function in subcortical circuits and present a hypothesis that the development of infantile spasms requires dysfunction in both cortical and subcortical circuits. The confluence of evidence suggesting a role of subcortical structures in the origin of spasms and laboratory data indicating an anticonvulsant role on some subcortical nuclei raise the possibility of novel approaches to the treatment of infantile spasms.

Animals↗
PubMedDate not supplied

The United Kingdom Infantile Spasms Study comparing vigabatrin with prednisolone or tetracosactide at 14 days: a multicentre, randomised controlled trial.

BACKGROUND: Infantile spasms, which comprise a severe infantile seizure disorder, have a high morbidity and are difficult to treat. Hormonal treatments (adrenocorticotropic hormone and prednisolone) have been the main therapy for decades, although little evidence supports their use. Vigabatrin has been recorded to have a beneficial effect in this disorder. We aimed to compare the effects of vigabatrin with those of prednisolone and tetracosactide in the treatment of infantile spasms. METHODS: The United Kingdom Infantile Spasms Study assessed these treatments in a multicentre, randomised controlled trial in 150 hospitals in the UK. The primary outcome was cessation of spasms on days 13 and 14. Minimum doses were vigabatrin 100 mg/kg per day, oral prednisolone 40 mg per day, or intramuscular tetracosactide depot 0.5 mg (40 IU) on alternate days. Analysis was by intention to treat. FINDINGS: Of 208 infants screened and assessed, 107 were randomly assigned to vigabatrin (n=52) or hormonal treatments (prednisolone n=30, tetracosactide n=25). None was lost to follow-up. Proportions with no spasms on days 13 and 14 were: 40 (73%) of 55 infants assigned hormonal treatments (prednisolone 21/30 [70%], tetracosactide 19/25 [76%]) and 28 (54%) of 52 infants assigned vigabatrin (difference 19%, 95% CI 1%-36%, p=0.043). Two infants allocated tetracosactide and one allocated vigabatrin received prednisolone. Adverse events were reported in 30 (55%) of 55 infants on hormonal treatments and 28 (54%) of 52 infants on vigabatrin. No deaths were recorded. INTERPRETATION: Cessation of spasms was more likely in infants given hormonal treatments than those given vigabatrin. Adverse events were common with both treatments.

Anticonvulsants↗
PubMed1987

[Ambulatory 24-hour EEG recording in epileptic infantile spasms].

Twenty-four h cassette recording (MEDILOG 9000) where obtained in 22 untreated infants (23 records) with a West syndrome (idiopathic: n = 12, symptomatic: n = 10). All these infants had had a 3 h polygraphic recording. Tracings were visually analyzed for sleep stages. Electro-clinical seizures and infraclinical discharges were listed according to their type and the stage of vigilance. Two hundred twenty-eight critical events were recorded in 22 cassette recordings: isolated spasms, clusters of spasms, partial or generalized discharges followed or not by clusters of spasms. Sixty per cent of these fits occurred during wakefulness, 27% during non REM sleep, 13% during awakening and none during REM sleep. Partial discharges, followed or not by clusters of spasms, were only present in cases with unfavourable outcome. In benign spasms the hypsarrhythmic pattern was present between spasms in each cluster, but not in cases with unfavourable outcome. Compared with 3 h polygraphic recordings, 24 h cassette recordings gave supplementary data on the presence, type and timing of seizures in 16 of out 22 cases.

Ambulatory Care↗