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At least 127 records · Page 7Linked to original sources
PubMed2006

Nitroglycerin, nitroprusside, or both, in preventing radial artery spasm during transradial artery catheterization.

OBJECTIVE: Radial artery spasm remains a major complication of transradial coronary interventions. The aim of this study was to compare the efficacy of three different intra-arterial vasodilating cocktails in reducing the incidence of radial artery spasm in patients undergoing transradial coronary angiography. The secondary goal was to assess the predictors of arterial spasm in this large group of patients. METHODS: A total of 379 patients undergoing the procedure were randomly enrolled in 1 of 3 groups. Every patient in each of the 3 groups received intra-arterial heparin, lidocaine and diltiazem. Along with that, patients in Group A received nitroglycerin; patients in Group B received nitroprusside instead of nitroglycerin; and patients in Group C received both nitroglycerin and nitroprusside. A single experienced operator, blinded to the study drug, subjectively determined the presence of spasm. RESULTS: Of 379 patients, a total of 44 patients (11.6%) experienced spasm. The occurrence of spasm was similar, independent of the vasodilator cocktail used (Group A: 12.2%, Group B: 13.4%, Group C: 9.5%; p = 0.597). After multivariate analysis, the following variables were found to be independent predictors of spasm: radial artery diameter (RD)/height index (p = 0.005), RD/BSA index (p = 0.012), and sheath outer diameter (OD)/RD index (p = 0.024). CONCLUSION: In this prospective, randomized trial, the addition of a direct nitric oxide donor to nitroglycerin in an antispastic cocktail did not reduce the risk of spasm, and the use of nitroglycerin was found to be as effective as nitroprusside. Also, morphometric and mechanical factors play a significant role in predicting the occurrence of radial spasm. The sex of the patient, presence of diabetes, body surface area and smoking history appeared to play no role in predicting the occurrence of radial spasm.

Coronary Angiography↗
PubMed1989

Coronary artery spasm complicating PTCA: role of intracoronary nitroglycerin.

During PTCA intracoronary (ic) nitroglycerin is used in our institution only in cases of suspected coronary artery spasm. In order to estimate the incidence of true spasm, records from 1400 consecutive PTCA procedures were retrospectively reviewed for use of ic nitroglycerin. For each of the 376 procedures where ic nitroglycerin was used, angiograms were reviewed to determine whether spasm had been present or whether there was some other complicating problem which had mimicked spasm. In 191 procedures (51%), spasm had apparently occurred. In 178 procedures (47%), there was evidence for dissection rather than spasm. Seven procedures (2%) had evidence for neither spasm nor dissection. These included three cases of guiding catheter injury, two procedures where unsuspected distal disease was found after opening of total occlusions, and one case each of branch vessel occlusion and no re-flow phenomenon. Spasm was more common during right coronary PTCA. It frequently occurred in areas remote from the PTCA site. In every instance spasm was reversed following administration of one or more boluses of ic nitroglycerin. On the basis of these data, coronary artery spasm occurs in 14% of PTCA procedures.

Angioplasty, Balloon↗
PubMed2006

Outcomes of children with infantile spasms after perinatal stroke.

The object of this study was to describe the outcomes of children with infantile spasms resulting from perinatal stroke. We used International Classification of Diseases, Ninth Revision (ICD-9) searches of billing records to identify 110 children with infantile spasms examined at our hospital from 1998 through 2005. Five of the 99 with symptomatic spasms (5%) had perinatal stroke. An additional five children with spasms caused by perinatal stroke were identified from pediatric stroke clinic records. Seven of the 10 children with spasms due to perinatal stroke presented with stroke as neonates. Three initially appeared healthy but were diagnosed with "presumed perinatal stroke" after radiographic imaging for their spasms evaluation. Median age at last follow-up was 6.3 years: 9 (90%) had epilepsy, 8 (80%) manifested cognitive impairment, and all (100%) had cerebral palsy. The three children who had delayed presentation of "presumed perinatal stroke" had better epilepsy and cognitive outcomes than the seven with neonatal presentation (P = 0.03). Perinatal stroke accounts for 5% of symptomatic spasms and results in high rates of chronic disability similar to those observed with other types of symptomatic spasms. However, a subgroup of children with spasms caused by delayed presentation of "presumed perinatal stroke" appears to have better epilepsy and cognitive outcomes.

Adolescent↗
PubMed2001

Neurophysiology of spasms.

Spasms are a form of epileptic seizure typical of infancy. From a clinical point of view, the child presents a flexor-extensor movement involving the trunk and limbs and lasting about 1s. Although asymmetry can be present, the seizure involves both sides of the body. The ictal discharge most frequently associated with spasms in West syndrome (WS) is a diffuse triphasic slow high-amplitude wave and less frequently a low-amplitude brief rapid rhythm. The origin of the spasm in WS and classification as either partial or generalized seizure are the subject of much discussion. Factors supporting partial origin include: interictal electroencephalography (EEG) characterized by multifocal anomalies; high incidence of focal cortical lesions and remission of spasms following surgical removal of focal lesions. Factors supporting generalized origin are: clinical involvement of the entire body; mostly generalized ictal EEG pattern; existence of idiopathic cases and possibility of spasms immediately following a partial seizure like a particular form of secondary generalization. In our opinion, the categories of 'partial' and 'generalized' seizures are not applicable to spasms in WS. Sometimes the spasms in WS can be observed together with other types of partial or generalized seizures. Polygraphic recordings have demonstrated that despite being clinically similar, each spasm is different from the other because of a variable sequence in muscular contraction. These data support the peculiar nature of the spasm in WS that could be a subcortical phenomenon that requires a cortical trigger.

Brain↗
PubMed1989

The clinical features of spasms in patients with a cervical cord injury.

A study concerning subjective symptoms of spasms which occur during 24 hours was carried out in 13 quadriplegic patients. All had spasms. Tonic and clonic spasms occurred involving their limbs and trunk. Extensor spasms occurred more often in the lower limbs than in the upper limbs. The duration of spasms was 8 seconds on average and the frequency was 15 times on average per day. The spasms which were severe tended to last longer in duration and were more frequent in occurrence. No spasms occurred without a trigger. The activities in daily living were interfered with by spasms in most patients. Most of these activities also triggered spasms.

Activities of Daily Living↗
PubMed1982

A long-term follow-up study of 214 children with the syndrome of infantile spasms.

The long-term prognosis of 192 surviving children with the syndrome of infantile spasms was evaluated. The children had been admitted to three paediatric hospitals in Helsinki at the time of initial diagnosis. The aetiological factors of the syndrome were carefully studied in each case. ACTH therapy was employed in 162, usually for about six weeks. The follow-up study 3-19 (mean 10.4) years later was made at the Children's Hospital, University of Helsinki. The rate of mortality was 19.6 per cent. Normal development was seen in 12 per cent and slightly subnormal in 10.4 per cent of the surviving children. Psychiatric disorders were seen in 27.6 per cent of the survivors. Sensory defects were also common. Severe cerebral palsy was seen in 4 per cent. Other seizures after cessation of the infantile spasms were seen in 60 per cent. Serial EEG studies showed that the temporal lobe was the most common site of abnormality. Abnormalities in the temporal lobes were seen frequently in children with symptomatic neonatal hypoglycaemia as a probable cause of the spasms. Prognostically favourable factors were "idiopathic" aetiology, normal development and not other fits prior to the spasms, short treatment lag, good response to ACTH and short duration of the spasms. In this study early treatment seemed to be of great importance even with regard to mental development. The factors connected with a bad outcome were: symptomatic aetiology (especially brain malformations, early infections and tuberous sclerosis), slow development before spasms, other seizures before infantile spasms, early onset of the spasms, long treatment lag, long duration of the spasms and other later occurrence of myoclonic-astatic seizures (Lennox-Gastaut). Large doses of ACTH (120-160 units) were not associated with a better prognosis than the smaller doses (20-40 units). The benefit of long versus short treatment schedules could not be evaluated in this study. The relapse rate here was 32 per cent.

Adolescent↗
PubMedDate not supplied

Medical treatment of patients with infantile spasms.

Infantile spasms are the main feature in West syndrome, an age-related epilepsy syndrome that affects 1 in every 2,000-4,000 infants. The authors provide a comprehensive review of the literature about infantile spasms and their therapy. In the United States, the drug of choice for infantile spasms, at least the cryptogenic cases, has been adrenocorticotropic hormone (ACTH). It is generally considered to be more effective than corticosteroids. Adrenocorticotropic hormone appears to alter long-term prognosis of cryptogenic infantile spasms, and helps in some cases of symptomatic infantile spasm. Vigabatrin has been considered the drug of choice for infantile spasms secondary to tuberous sclerosis, and possibly, according to many neurologists, for all cases of infantile spasm. Recent concerns regarding retinopathy associated with vigabatrin therapy are, however, limiting the use of this drug. Valproic acid benefits 40%-70% of patients who failed a trial of ACTH. Nitrazepam is as effective as ACTH in acutely controlling infantile spasms; however, its long-term effects on prognosis have not been studied. Pyridoxine, lamotrigine, topiramate, zonisamide, ketogenic diet, immunoglobulin therapy, felbamate, and thyrotropin-releasing hormone have all been used for the treatment of infantile spasms, but are usually reserved for cases refractory to vigabatrin and/or ACTH.

Adrenocorticotropic Hormone↗
PubMed2005

Chiari type I malformation presenting as hemifacial spasm: case report.

OBJECTIVE AND IMPORTANCE: We report on a patient with a Chiari I malformation presenting with right hemifacial spasm. Clinicians should consider the downward displacement of the hindbrain as a rare cause of hemifacial spasm in Chiari I malformation. CLINICAL PRESENTATION: An 18-year-old man was admitted with right hemifacial spasm. The results of the neurological examination were normal except for the facial spasm. Magnetic resonance imaging demonstrated a Chiari I malformation without syringomyelia. After surgery, the hemifacial spasm completely resolved. INTERVENTION: Posterior fossa decompression, C1 laminectomy, and duraplasty were performed. CONCLUSION: The hemifacial spasm could be attributed to compression and/or traction of the facial nerve because of downward displacement of the hindbrain in Chiari I malformation. Compression and/or traction might create irritation of the facial nerve that causes hemifacial spasm. Resolution of the hemifacial spasm after posterior fossa decompression could explain the facial nerve irritation in Chiari I malformation. Clinicians should consider Chiari malformation as a cause of hemifacial spasm and posterior fossa decompression as a potential treatment.

Adolescent↗
PubMed2002

Newer GABAergic agents for pharmacotherapy of infantile spasms.

Infantile spasms is an age-specific epileptic syndrome in infants and young children. Although the exact mechanism is unknown, adrenocorticotrophic hormone (ACTH) has been the mainstay for the therapeutic management of infantile spasms and other developmental epilepsies. Clinical benefits of ACTH in infantile spasms could partially relate to its stimulatory effects on the release of adrenocorticosteroids and neurosteroids. Glucocorticoids, pyridoxine and ketogenic diet therapy have all been used for the treatment of refractory infantile spasms. Recent studies indicate that several newer anticonvulsant agents, which are positive allosteric modulators of GABA(A) receptors, are as effective as ACTH in acutely controlling infantile spasms. The efficacy of agents that enhance GABA-mediated inhibition (such as vigabatrin and benzodiazepines) for rapid and complete abolition of infantile spasms has been demonstrated in several clinical studies. Ganaxolone, a novel neuroactive steroid has, however, demonstrated outstanding efficacy and better tolerability in children with intractable infantile spasms. Zonisamide, topiramate, deoxycorticosterone and neurosteroids are emerging as effective treatment approaches. These new antiepileptic drugs represent a potential nonhormonal approach for infantile spasms, but additional studies are needed to verify their efficacy and tolerability. Future studies will hopefully identify rational antiseizure drugs that not only control infantile spasms but also abrogate its risk on the development of the brain.

Adrenocorticotropic Hormone↗
PubMed2003

Epileptic spasms in clusters without hypsarrhythmia in infancy.

Spasms are defined as epileptic seizures characterized by brief axial contraction, in flexion, extension or mixed, symmetric or asymmetric, lasting from a fraction of a second to 1-2s, and are associated with a slow-wave transient or sharp and slow-wave complex, followed or not by voltage attenuation. Epileptic spasms usually appear in clusters and are age-dependent. This type of epileptic spasms associated with the particular EEG pattern, hypsar rhythmia, constitutes the basis for the diagnosis of West syndrome. The question is, how to nosologically define those patients who clearly present epileptic spasms in clusters without modified or typical hypsarrhythmia and with or without focal paroxysmal discharges on the interictal EEG. In the present series, the four patients show that epileptic spasms in clusters may occur in infancy, without hypsarrhythmia. They all presented the following features: normal neuropsychological development before onset of epileptic spasms, clusters of epileptic spasms, focal clinical and/or EEG abnormalities, normal neuroradiological imaging, neurometabolic investigations and karyotypes. In three of the patients, seizures were refractory to AEDs. Epileptic spasms in clusters without hypsarrhythmia that start in the first year of life represent a subtype of infantile spasms that generally are refractory to AEDs. It is not yet clear whether it should be considered as a variant of West syndrome or not [Published with Video sequence].

Anticonvulsants↗
PubMed1991

Therapeutic trial of vigabatrin in refractory infantile spasms.

Infantile spasms usually start during the first year of life and constitute one of the most difficult types of epilepsy to treat. They carry a very poor prognosis for both epilepsy and mental development. Seventy children, including 47 infants, with intractable infantile spasms were entered into an open study with vigabatrin as add-on therapy to the usual anticonvulsant treatment. All were resistant to previous treatments, including corticosteroids (43 patients), carbamazepine, benzodiazepines, and sodium valproate. Two children withdrew from the study because of intolerance to vigabatrin (hypotonia or hypertonia) before evaluation of efficacy could be made. Of the remaining 68 children, 29 (43%) showed complete suppression of spasms. Forty-six children had a greater than 50% reduction in spasms. The best response was observed in those with tuberous sclerosis (12/14 compared with 12/18 with symptomatic infantile spasms of other origin and 22/36 with cryptogenic infantile spasms). Following the initial response to treatment of these patients (n = 68), a long-term response was confirmed in 75% of children with symptomatic infantile spasms and 36% of children with cryptogenic infantile spasms. In eight children, all other anticonvulsant medication could be definitively withdrawn. Tolerability appeared excellent, with 52 of 70 patients reporting no side effects. Somnolence, hypotonia, weight gain, excitation, and insomnia were the most common problems at the beginning of the study and were usually transient. Given the poor prognosis of this type of childhood epilepsy, vigabatrin appears to be a very interesting advance in the management of drug-resistant infantile spasms.

Adolescent↗
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↗
PubMed2003

Myocardial bridging increases the risk of coronary spasm.

BACKGROUND: Myocardial bridging (MB) has been associated with cardiac events. Whether coronary spasm is one factor contributing to those events is unknown. HYPOTHESIS: This study investigated whether the likelihood of coronary spasm is increased in patients with MB. METHODS: A spasm-provocation test was performed by infusing acetylcholine into the left coronary artery in 114 Japanese patients with chest pain. The test result was defined as positive when the diameter of the coronary artery was reduced by > or = 50% and ST-segment changes were documented. Myocardial bridging was defined as a > 15% reduction in coronary arterial diameter during systole after intracoronary injection of nitroglycerin. RESULTS: Myocardial bridging was identified in 41 patients (36%) and was located in the mid-segment of the left anterior descending coronary artery (LAD) in all patients. Patients with MB experienced coronary spasm more frequently than patients without MB (MB+: 73%; MB-: 40%, p = 0.0006). Furthermore, among patients with a positive spasm-provocation test, coronary spasm occurred more frequently in the mid-segment of the LAD in patients with MB than in those without MB (MB+: 73%; MB-: 45%, p = 0.0259). Multivariate regression analysis demonstrated that MB was a predictor of coronary spasm (odds ratio: 3.478, p = 0.0088). CONCLUSIONS: These results suggest that MB increases the risk of coronary spasm and that coronary spasm may be the proximate etiology of cardiac events associated with MB.

Acetylcholine↗
PubMed2001

Paraoxonase gene Gln192Arg (Q192R) polymorphism is associated with coronary artery spasm.

We recently reported that oxidative stress is involved in the pathogenesis of coronary spasm. We hypothesized that oxidative-stress-related genetic factors and certain polymorphisms in the paraoxonase gene (PON1) and platelet-activating factor acetylhydrolase (PAF-AH) might influence the pathogenesis of coronary spasm. We therefore examined the possible association between the PON1 Q192R or PAF-AH V279F polymorphisms and coronary spasm in 214 patients with coronary spasm and 212 control subjects. Genotypes were determined by polymerase chain reaction/restriction fragment length polymorphism analysis. The incidence of the PON1-192R allele was significantly higher in the coronary spasm group than in the control group (65% vs 53%; P=0.0005). The PAF-AH-279F allele was not associated with coronary spasm (15% vs. 16%; P=0.8781). Multiple logistic regression analysis with forward stepwise selection involving the PON1-192R allele and the environmental risk factors revealed that the most predictive independent risk factor for coronary spasm was the PON1-192R allele (significance=0.0016, OR=2.52), followed by cigarette smoking (significance=0.0007, OR=2.01). We also measured plasma levels of TBARS (thiobarbituric acid-reactive substances) as a marker of oxidative stress. TBARS levels were higher in R/R types than in Q/Q types (2.115+/-0.086 nmol/ml [ n=25] vs 1.676+/-0.102 nmol/ml [ n=11], P<0.01). Thus, there is a significant association between the PON1-192R allele and coronary spasm; the PON1-192R allele may play an important role in the genesis of coronary spasm, probably by attenuating the suppression of oxidative stress.

Adult↗
PubMed1998

A missense Glu298Asp variant in the endothelial nitric oxide synthase gene is associated with coronary spasm in the Japanese.

Coronary spasm plays an important role in the pathogenesis of not only variant angina but also ischemic heart disease in general. However, the precise mechanism(s) by which coronary spasm occurs remains to be elucidated. Coronary spasm may arise from interactions between environmental and genetic factors. Endothelial-derived nitric oxide (NO) has been implicated in the control of vascular tone. We have recently shown that both basal and acetylcholine (ACh)-induced NO activities are impaired in the coronary arteries of patients with coronary spasm. The purpose of this study has been to elucidate the possible variants that occur in the coding region of the endothelial nitric oxide synthase (eNOS) gene and that may be associated with coronary spasm. After initial screening in the entire 26 coding regions of the eNOS gene, we found a missense Glu298Asp variant in exon 7 in patients with coronary spasm. We subsequently performed a larger scale study involving 113 patients with coronary spasm and 100 control subjects, who were all diagnosed by intracoronary injection of ACh. The analysis revealed a significant difference in the distribution of the variant between the coronary spasm group (21.2%) and control group (9.0%; P=0.014 for dominant effect). Thus, we have found the missense Glu298Asp variant in the eNOS gene by the analysis of its entire 26 coding regions. The variant is significantly associated with coronary spasm.

Adult↗
PubMed1983

Catheter-induced coronary artery spasm: an angiographic manifestation of vasospastic angina?

During a 4-year period, 33 patients with angiographic coronary artery spasm in the absence of significant fixed occlusive disease were reviewed. Sixteen patients had typical variant angina and 17 had catheter-induced spasm. All patients had one or more episodes of rest angina. Left ventriculography demonstrated mitral valve prolapse in 14 patients (42%) and end-systolic cavity obliteration in six (18%). Spasm was demonstrated to occur in the right coronary artery in 26 patients and in the left coronary artery in seven. Two patients had multivessel spasm. Comparing patients with variant angina and catheter-induced spasm demonstrated no significant difference in clinical, ECG, or angiographic parameters. Two patients with catheter-induced spasm had healed myocardial infarctions and both developed spontaneous non catheter-induced spasm in the infarct vessel. The majority of patients responded to long-acting nitrate therapy, though those with catheter-induced spasm tended to have more recurrent chest pain. Six patients were placed on calcium antagonist drugs with marked symptomatic improvement in five. This study suggests that patients with catheter-induced spasm are similar to those with variant angina and its angiographic documentation may be a marker for the identification of patients with vasospastic angina.

Adult↗
PubMed2005

Focal cortical high-frequency oscillations trigger epileptic spasms: confirmation by digital video subdural EEG.

OBJECTIVE: To localize high-frequency oscillations (HFOs) on the cortex during epileptic spasms using video subdural EEG and Multiple Band Frequency Analysis (MBFA). METHODS: Using video subdural EEG sampled at 1 kHz, we studied a 14-year-old boy with asymmetric epileptic spasms of possible left frontal origin. We identified HFOs, then analyzed and localized their distributions by MBFA. We correlated HFO distribution to clinical spasm intensity. RESULTS: Ictal subdural EEG recorded HFOs at 60-150 Hz lasting 0.3-4 s. MBFA showed extensive but noncontiguous distribution of HFOs predominantly over the left frontal and temporal regions. HFOs began and became quasiperiodic before manifestation of clinical spasms. As clinical spasms intensified, HFOs persisted in regions where they initiated subclinically but were of higher frequency and greater power than HFOs in other regions. We performed cortical resections over the left frontal and temporal regions with predominant HFOs. Six months after surgery, the patient remained seizure free. CONCLUSIONS: HFOs were present over the ictal onset zone during epileptic spasms. Periodic spasms in this patient had the characteristics of partial seizures. SIGNIFICANCE: We show that HFOs occurred over the cerebral cortex during epileptic spasms, and we suggest that these focal cortical HFOs triggered the spasms.

Adolescent↗
PubMed2006

Generalized spasm of the right coronary artery after successful stent implantation provoked by intracoronary administration of ergonovine.

Coronary spasm may be one of the reasons for the appearance of chest pain after successful percutaneous coronary interventions, and is potentially hazardous when myocardial ischemia occurs. Coronary spasm can be diagnosed by intracoronary administration of ergonovine as a selective spasm provocative test. We report here the case of a patient who had chest pain and ST segment elevation 10 days after successful right coronary artery stent implantation. Repeat angiography was performed, with results of no in-stent stenosis and no stenosis in other segments. Since coronary artery spasm was considered as a possible reason, a spasm provocative test was attempted. Following ergonovine administration (total dose, 50 mug) into the right coronary artery, severe spasm with 99% stenosis developed over the whole artery except the stented segment. Isosorbide dinitrate was injected immediately, and the provoked spasm was soon relieved. Intravascular ultrasound revealed no neointima at the stented segment and diffuse and mild low-echogenic concentric plaque at the distal as well as proximal segment of the stent. Most reports regarding coronary artery spasm provocative tests have focused on focal lesions before interventional therapy, or during interventional procedures. Although it is quite rare, potential coronary spasm should be considered when chest symptoms recur after percutaneous coronary interventions without angiographic representation.

Coronary Angiography↗