Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spasm”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMed2001

Infantile spasms in Down syndrome: good response to a short course of vigabatrin.

PURPOSE: To evaluate the efficacy of vigabatrin (VGB) in the treatment of infantile spasms (ISs) associated with Down syndrome (DS) and to assess the feasibility of early discontinuation to reduce the possible retinal toxicity. METHODS: Five children with ISs with DS were treated with vigabatrin as first-line monotherapy in an open prospective study. The short-term response was evaluated, and VGB was continued in responders. The treatment was stopped after 6 months in children who were still spasm free. RESULTS: Four children of five became spasm free with VGB, three of them responding within 1 week. This response was maintained during the 6 months of VGB treatment. After VGB discontinuation, and with a follow-up ranging from 2 to 4 years, none of the responders experienced spasm recurrence or other types of seizures. CONCLUSIONS: This study confirms the efficacy of VGB in ISs associated with DS. Moreover, it shows that the duration of VGB treatment can be reduced to 6 months without relapse of ISs. This short treatment might reduce the risk of developing visual field constriction.

Adolescent↗
PubMed2000

Fogarty balloon dilatation for intraoperative arterial spasm.

OBJECTIVE: to describe an intraoperative technique using a Fogarty balloon to treat arterial spasm following vascular bypass and endarterectomy. DESIGN: prospective case control study. SUBJECTS AND TREATMENT: twenty-two patients following femorodistal bypass surgery and one patient following carotid endarterectomy, with arterial spasm in the distal run-off on completion angiography, were treated with Fogarty balloon dilatation. MATERIALS: Fogarty balloon catheter (Baxtertrade mark). RESULTS: twenty-three patients (100%) with arterial spasm were successfully treated by Fogarty balloon as demonstrated on completion angiography. No complications were seen. CONCLUSION: this simple technique removes vascular spasm rapidly and produces an excellent angiographic result.

Angiography↗
PubMed2001

Remission of hemifacial spasm after proximal occlusion of vertebrobasilar dissecting aneurysm with coils: case report.

Intracranial aneurysm is a rare cause of hemifacial spasm and most of the previously reported cases are treated with surgical microvascular decompression. Authors report a case of hemifacial spasm caused by a dissecting aneurysm located at the vertebrobasilar junction which improved after endovascular obliteration of the affected vertebral artery with coils. The patient was a 69-year-old man with 20 months' history of left hemifacial spasm. A vertebral angiogram showed an irregular dilatation of the right vertebral artery associated with aneurysmal dilatation at the vertebrobasilar junction. Endovascular obliteration of the abnormally dilated right vertebral artery proximal to the vertebrobasilar junction was performed. The hemifacial spasm gradually improved after the embolisation and disappeared 6 months later. Endovascular proximal obliteration of the vertebral artery may have changed the hemodynamic force inside the aneurysm and eliminated the vascular compression at the root exit zone of the facial nerve.

Aged↗
PubMed1985

Morphological aspects of aetiology and the course of infantile spasms (West-syndrome).

The present study using the results of the postmortem examination of twenty-four children, who had infantile spasms (West-Syndrome), gives a view of the aetiology and course of the West-Syndrome. According to the time of occurrence of the lesions three groups could be established: one group of six cases with only embryofetal lesions, one group of ten cases with combined embryofetal and peri/postnatal lesions and one group of eight cases with only peri/postnatal lesions. It is significant, that the time of onset of infantile spasms depends on time of manifestation of lesions. In the groups with combined embryofetal and peri/postnatal lesions the seizures were manifested at the same time as in the cases with isolated embryofetal lesions. Even in the group with combined lesions, microdysgenesis was interpreted as being embryofetal. These embryofetal lesions, as opposed to the peri/postnatal lesions thus appear to dominate and thereby to be pathoplastic. From this correlation two thirds of the cases of infantile spasms can be regarded as fetal epilepsies. The question is open if the infantile spasms which are manifested later on and develop mostly a Lennox-Syndrome indeed should be classified as a separate group together with the isolated peri/postnatal lesions.

Adolescent↗
PubMed1980

Transient brain shrinkage in infantile spasms after ACTH treatment. Report of two cases.

This is the report of two cases of infantile spasms, manifesting transient brain shrinkage in computerized tomography (CT) after ACTH treatment. ACTH was given for 8 weeks to a 8-months-old Japanese girl with infantile spasms. First CT performed at 2 weeks after the final ACTH injection, displayed moderate brain shrinkage. Second CT at 4 months showed marked diminution of the shrinkage. ACTH was also given for 8 weeks to a 14 months old Japanese boy with infantile spasms. First CT, just before ACTH treatment, showed mild cortical atrophy, the second at 7 days after the final ACTH injection revealed marked brain shrinkage and moderate ventricular dilatation, and the third at 2 months, disclosed mild improvement of the shrinkage. ACTH or corticoateroid has widespread effects on the developing nervous system. In animal experiments, ACTH or steroids interfere with brain growth of young rats. CT findings of transient brain shrinkage in a child with infantile spasms might suggest that intensive treatment with ACTH or steroids in infancy interferes with brain growth as seen in the results of animal experiments.

Adrenocorticotropic Hormone↗
PubMed1993

Brainstem involvement in infantile spasms: a study employing brainstem evoked potentials and magnetic resonance imaging.

Ten patients with infantile spasms underwent brainstem evoked potentials and magnetic resonance imaging (MRI) examination to evaluate brainstem involvement. Short latency somatosensory evoked potentials and auditory brainstem responses were abnormal in seven and five of the 10 patients, respectively. MRI findings were abnormal in nine of the 10 patients. Six patients demonstrated various degrees of atrophy of the brainstem. In all of these cases brainstem evoked potentials were abnormal. This study demonstrates that infantile spasms are frequently associated with brainstem dysfunction and raises the hypothesis that brain atrophy involving the brainstem might be a cause of infantile spasms. In addition, this study also documents the combination of brainstem evoked potentials and MRI examination is valuable tool in the evaluation of brainstem involvement in infantile spasms.

Adrenocorticotropic Hormone↗
PubMed1996

Occipital falcine meningioma presenting with ipsilateral hemifacial spasm: a case report.

We report a large right occipital falcine meningioma, the main presenting feature of which was ipsilateral hemifacial spasm. The patient was relieved of the hemifacial spasm after the supratentorial tumour was resected. The pathogenesis of hemifacial spasm is reviewed in light of this unusual case and the treatment of hemifacial spasm secondary to a tumour is discussed.

Brain Neoplasms↗
PubMed1986

Treatment of hemifacial spasm with botulinum A toxin. Results and rationale.

Hemifacial spasm is characterized by unilateral, periodic, tonic contractions of facial muscles, thought to be caused by mechanical compression at the root-exit zone of the facial nerve. Electrophysiologic abnormalities such as ectopic excitation and synkinesis are typical. Although posterior fossa microsurgical nerve decompression is successful in bringing about relief of the spasm in most cases, it carries a risk to hearing. As an alternative treatment, 15 patients with hemifacial spasm were given a total of 41 sets of injections with botulinum A toxin, with a mean follow-up of 14.3 +/- 1.1 months. Relief of symptoms lasted a mean of 108.3 +/- 4.2 days. Mild transient lagophthalmos and ptosis were the only complications. Although the exact mechanism of its action and beneficial effect is speculative at this time, botulinum A toxin appears to offer an effective, safe alternative to more radical intracranial surgery for patients with hemifacial spasm.

Aged↗
PubMed1983

Monitoring hepatic artery spasm for chemotherapeutic infusion by using Tc-99m labeled macroaggregated albumin.

During angiographic placement of an intra-arterial hepatic catheter, a spasm was encountered in the proper hepatic artery. Subsequent angiography, however, revealed normal arteries. Tc-99m MAA intra-arterial infusion was then performed which showed a hepatic artery spasm. Twenty-four hours after the initial hepatic arterial spasm, a repeat injection of Tc-99m MAA revealed that the spasm was no longer present and, therefore, that intra-arterial chemotherapy could be administered.

Adult↗
PubMed1986

The effect of acid and bethanechol stimulation in patients with symptomatic hypertensive peristaltic (nutcracker) esophagus. Evidence that this disorder may be a precursor of diffuse esophageal spasm.

The hypertensive peristaltic (nutcracker) esophagus represents a motility disorder characterized clinically by squeezing retrosternal chest pain and manometrically by high amplitude esophageal peristaltic contractions. This study was designed to examine whether the nutcracker esophagus is: (a) a distinct entity, (b) a member of the spectrum of primary esophageal dysmotilities (e.g., diffuse esophageal spasm and achalasia), or (c) is secondary to reflux-induced acid sensitivity. Thirteen patients with a nutcracker esophagus by baseline manometry were subsequently studied after acid perfusion and bethanechol stimulation (0.08 mg/kg). Records were analyzed for symptomatic response and motility changes. Eight of 13 (62%) experienced chest pain during acid perfusion, but none had significant motility changes documented during this period. After bethanechol injection, chest pain occurred in six of 12 (50%) patients; two had burning pain and in the other four (33%) their squeezing chest pain was reproduced. Changes in the motility tracing with evidence of disordered motility suggestive of diffuse esophageal spasm were seen after bethanechol in seven of the 12 tracings analyzed (58%), including all six patients who developed chest pain. We conclude that patients with nutcracker esophagus on baseline manometry may develop motility patterns consistent with diffuse esophageal spasm after provocation with bethanechol. We take this to suggest that the nutcracker esophagus is part of the continuum of primary motility disorders and may actually be a precursor of diffuse esophageal spasm.

Adult↗
PubMed1999

Anchoring method for hemifacial spasm associated with vertebral artery: technical note.

OBJECTIVE: We describe an easy and useful method for treating hemifacial spasm related to the vertebral artery. METHODS: The technique entails the manufacture of a dural belt harvested from the cerebellar convexity dura and a dural bridge made at the petrous dura combined with the use of an aneurysm clip. The dural belt holds the vertebral artery and is anchored to the dural bridge by fixation with an aneurysm clip after the vertebral artery is transposed to an appropriate position. RESULTS: The technique proved to be safe and effective in a series of six patients with hemifacial spasm who were followed up for a period of 2 months to more than 10 years after surgery. All patients were affected on the left side. Multiple offending arteries were present in three cases. Hemifacial spasm completely disappeared in all patients. CONCLUSION: This method represents a feasible option for the treatment of hemifacial spasm caused by a tortuous, elongated, or enlarged vertebral artery.

Adult↗
PubMed2002

Spasm of accommodation associated with closed head trauma.

Spasm of accommodation, creating pseudomyopia, is generally associated with miosis and excess convergence as part of spasm of the near reflex. It may also exist as an isolated entity, usually attributed to psychogenic causes. We present six cases of accommodative spasm associated with closed head injury. All patients were male, ranging in age between 16 and 37 years. The degree of pseudomyopia, defined as the difference between manifest and cycloplegic refraction, was 1.5 to 2 diopters. A 3-year trial of pharmacologically induced cycloplegia in one patient did not lead to reversal of the spasm when the cycloplegia was stopped. All patients required the manifest refraction to see clearly at distance. The pseudomyopia endured for at least 7 years following head trauma. This phenomenon may represent traumatic activation or disinhibition of putative brain stem accommodation centers in young individuals.

Accommodation, Ocular↗
PubMed1997

Effect of glyceryl trinitrate on the sphincter of Oddi spasm evoked by prostigmine-morphine administration.

OBJECTIVE: In this study the effect of glyceryl trinitrate on the prostigmine-morphine-induced sphincter of Oddi spasm was evaluated in nine female patients with sphincter of Oddi dyskinesia. METHOD: Sphincter of Oddi spasm was induced by prostigmine-morphine administration (0.5 mg prostigmine intramuscularly and 10 mg morphine subcutaneously) and visualized by quantitative hepatobiliary scintigraphy. The entire procedure was repeated during glyceryl trinitrate infusion (Nitrolingual 1 microg/kg/min for 120 min). RESULTS: Prostigmine-morphine provocation caused significant increases in the time to peak activity (Tmax) over the hepatic hilum (HH: 34.33 +/- 5.05 vs. 22.77 +/- 3.26) and the common bile duct (CBD: 60.44 +/- 5.99 vs. 40.0 +/- 2.88) and in the half-time of excretion (T1/2) over the liver parenchyma (LP: 120.04 +/- 16.01 vs. 27.37 +/- 2.19), HH (117.61 +/- 14.71 vs. 31.85 +/- 3.99) and CBD (158.11 +/- 9.18 vs. 40.1 +/- 6.24), indicating a complete spasm at the level of the sphincter of Oddi. Glyceryl trinitrate infusion completely normalized the prostigmine-morphine-induced alterations in these quantitative parameters (TmaX over the LP: 11.33 +/- 1.13; over the HH: 18.88 +/- 1.48; and over the CBD: 36.22 +/- 1.92; and T1/2 over the LP: 28.21 +/- 1.83; over the HH: 33.42 +/- 3.10; and over the CBD: 41.66 +/- 6.33), suggesting an effective sphincter-relaxing effect of glyceryl trinitrate. CONCLUSION: These results provide the first evidence of the effectiveness of glyceryl trinitrate on the morphine-induced sphincter of Oddi spasm in humans. Since glyceryl trinitrate is able to overcome even the drastic effect of morphine, it might be of relevance in the treatment of sphincter of Oddi dyskinesia.

Adult↗
PubMed2006

Botulinum toxin type A for chronic pain and pelvic floor spasm in women: a randomized controlled trial.

OBJECTIVE: To estimate whether botulinum toxin type A is more effective than placebo at reducing pain and pelvic floor pressure in women with chronic pelvic pain and pelvic floor muscle spasm. METHODS: This study was a double-blinded, randomized, placebo-controlled trial. All participants presented with chronic pelvic pain of more than 2 years duration and evidence of pelvic floor muscle spasm. Thirty women had 80 units of botulinum toxin type A injected into the pelvic floor muscles, and 30 women received saline. Dysmenorrhea, dyspareunia, dyschezia, and nonmenstrual pelvic pain were assessed by visual analog scale (VAS) at baseline and then monthly for 6 months. Pelvic floor pressures were measured by vaginal manometry. RESULTS: There was significant change from baseline in the botulinum toxin type A group for dyspareunia (VAS score 66 versus 12; chi2 = 25.78, P < .001) and nonmenstrual pelvic pain (VAS score 51 versus 22; chi2 = 16.98, P = .009). In the placebo group only dyspareunia was significantly reduced from baseline (64 versus 27; chi2 = 2.98, P = .043). There was a significant reduction in pelvic floor pressure (centimeters of H2O) in the botulinum toxin type A group from baseline (49 versus 32; chi2 = 39.53, P < .001), with the placebo group also having lower pelvic floor muscle pressures (44 versus 39; chi2 = 19.85, P = .003). CONCLUSION: Objective reduction of pelvic floor spasm reduces some types of pelvic pain. Botulinum toxin type A reduces pressure in the pelvic floor muscles more than placebo. Botulinum toxin type A may be a useful agent in women with pelvic floor muscle spasm and chronic pelvic pain who do not respond to conservative physical therapy. CLINICAL TRIAL REGISTRATION: Australian Clinical Trials Registry, http://www.actr.org.au/, ACTRN012605000515695 LEVEL OF EVIDENCE: I.

Adult↗
PubMedDate not supplied

Pathogenesis of infantile spasms: a model based on developmental desynchronization.

Infantile spasms is a severe epileptic encephalopathy of infancy. The fundamental cause is unknown, although a number of predisposing conditions are recognized. In this article, the authors critically review current knowledge concerning the pathophysiologic basis of infantile spasms and propose a new model based on developmental desynchronization. It is suggested that infantile spasms may result from a particular temporal desynchronization of two or more central nervous system developmental processes, resulting in a specific disturbance of brain function. The disturbance of function is postulated to be crucially dependent on an unbalanced maturational pattern, in which certain brain systems become dysfunctional owing to divergent developmental status. An important aspect of this model is the idea that disturbed function of a specific kind can result from multiple causative factors, and so can be associated with a variety of different anatomic and/or biochemical abnormalities. Thus, this concept is compatible with the observed diversity of pathologic findings and multiplicity of etiological associations observed in infantile spasms patients.

Age Factors↗
PubMed2004

Long-term cognitive outcomes of a cohort of children with cryptogenic infantile spasms treated with high-dose adrenocorticotropic hormone.

PURPOSE: To evaluate the outcome of children with cryptogenic infantile spasms treated with high-dose synthetic adrenocorticotropic hormone (ACTH) and the relation between early treatment, within 1 month of onset, and outcome. METHODS: We assessed the long-term cognitive and seizure outcomes of 37 patients with cryptogenic infantile spasms (onset, age 3 to 9 months) receiving standardized treatment regimen of high-dose tetracosactide depot, 1 mg IM every 48 h for 2 weeks, with a subsequent 8- to 10-week slow taper and followed by oral prednisone, 10 mg/day for a month, with a subsequent slow taper for 5 months or until the infant reached the age of 1 year, whichever came later. Development was assessed before treatment. Seizure outcomes were followed up prospectively. Cognitive outcomes were determined after 6 to 21 years and analyzed in relation to treatment lag and pretreatment regression. RESULTS: Twenty-two infants were treated within 1 month of onset of infantile spasms, and 15 after 1 to 6.5 months. Normal cognitive outcome was found in all 22 (100%) patients of the early-treatment group, and in 40% of the late-treatment group. Normal cognitive outcome was found in all 25 (100%) patients who had no or only mild mental deterioration at presentation, including four in the late-treatment group but in only three of the 12 patients who had had marked or severe deterioration before treatment. CONCLUSIONS: Early treatment of cryptogenic infantile spasms with a high-dose ACTH protocol is associated with favorable long-term cognitive outcomes. Once major developmental regression lasts for a month or more, the prognosis for normal cognitive outcome is poor. Further studies are needed on the optimal treatment regimen for this disorder.

Administration, Oral↗
PubMed1990

Efficacy of diltiazem in the treatment of diffuse oesophageal spasm.

Calcium antagonist relax smooth muscle, a possible useful concept in treatment of diffuse oesophageal spasm. Therefore the effects of oral diltiazem (60 mg t.d.s.) and placebo were compared in eight patients with diffuse oesophageal spasm in a 10-week double-blind crossover study. The patients recorded the severity of chest pain and/or dysphagia in daily pain diaries using visual analogue scales. Chest pain index and dysphagia index were calculated by multiplying frequency with daily intensity of each individual symptom. When compared to placebo, diltiazem did not significantly change the overall dysphagia index and chest pain index. An individual sizeable reduction of dysphagia was attained on diltiazem in four out of six patients and in six out of eight patients suffering from chestpain. Side effects were not seen during diltiazem therapy. Diltiazem, in our study, did not yield in a significant improvement of symptoms in diffuse oesophageal spasm. Diltiazem, however, can offer relief in selected individual patients suffering from diffuse oesophageal spasm.

Adult↗
PubMed1980

Coronary artery spasm.

Variant angina with ST elevation indicates transmural myocardial ischaemia and is due to spasm of a large epicardial coronary artery. Spasm occurs in arteries with varying degrees of fixed obstruction, giving rise to different clinical profiles of variant angina. However, coronary angiography is required to differentiate between those with minor coronary disease, and those with significant (greater than 70%) obstruction. In patients with minor coronary disease or normal arteries, beta-blockers are contraindicated, and treatment with calcium antagonist vasodilators should be commenced after documentation of spontaneous or ergonovine induced spasm. Patients with significant fixed coronary obstructions require bypass grafting if technically feasible. The role of coronary spasm is not confined to variant angina, as it causes angina at rest with ST depression, and may also cause myocardial infarction and sudden death.

Angina Pectoris↗