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 1,243 records · Page 69Linked to original sources
PubMed1994

Infantile spasms with predominantly unilateral cerebral abnormalities.

To investigate the pathogenesis of infantile spasms, 12 children underwent a combination of neurophysiologic and neuroimaging studies including brainstem evoked potentials and single photon emission computed tomography with 99mTcHMPAO. Three of the children had localized cerebral abnormalities on neuroimaging, i.e. right frontotemporal cortical microdysgenesis, left frontotemporal polymicrogyria, and right parietooccipitotemporal porencephalic cyst. Neurophysiologic studies also indicated that a single cerebral hemisphere was predominantly involved, while the other hemisphere and the brainstem were relatively spared, a result compatible with the clinical findings of hemiparesis and hemiconvulsion. In these three patients, administration of carbamazepine was followed by marked improvement of the clinical and electroencephalographic findings. Our results suggest that a combination of noninvasive examinations can distinguish a particular subtype of infantile spasms associated with a localized cerebral abnormality and responsive to carbamazepine.

Carbamazepine↗
PubMed1980

Nifedipine therapy for coronary-artery spasm. Experience in 127 patients.

We report clinical experience with the coronary vasodilator nifedipine in 127 patients with symptoms of myocardial ischemia associated with electrocardiographic or angiographic evidence, or both, of coronary-artery spasm. In the majority of patients conventional antianginal therapy including nitrates and beta-adrenergic blockers failed, and in one third of the patients at least one episode of ventricular tachycardia developed during an attack of angina. Nifedipine (40 to 160 mg every 24 hours) significantly reduced the mean weekly rate of anginal attacks from 16 to two (P less than 0.001). Similar marked reductions in the nitroglycerin requirement were noted. In 63 per cent of the patients complete control of anginal attacks was achieved, and in 87 per cent the frequency of angina was reduced by at least 50 per cent. Nifedipine was generally well tolerated, with only 5 per cent of the patients requiring termination of the drug because of intolerable side effects. This experience with nifedipine suggests that it is a highly effective drug for the treatment of coronary-artery spasm and variant angina.

Adult↗
PubMed2001

An easy method for the intraluminal administration of peppermint oil before colonoscopy and its effectiveness in reducing colonic spasm.

BACKGROUND: Systemic administration of a cholinergic blocking agent or glucagon is used to reduce spasms, but it is inconvenient and sometimes causes side effects. This study is an evaluation of the intracolonic administration of peppermint oil during colonoscopy for the control of colonic spasm. METHODS: Each patient in the treated group (n = 409) was given approximately 200 mL of the solution (a mixture of 8 mL of peppermint oil and 0.2 mL of Tween 80 per 1 L of water with 0.04% indigo carmine) by using a hand pump attached to the accessory channel of the colonoscope. Changes in patient posture were made to distribute the solution. The patients in the control group (n = 36) were given the solution without peppermint oil. RESULTS: A satisfactory spasmolytic effect was seen in 88.5% of the treated patients and in 33.3% of those in the control group (p<0.0001). No adverse effect was observed. The mean time to onset was 21.6 +/- 15.0 seconds, and the effect continued for at least 20 minutes. In patients with irritable bowel syndrome, efficacy was significantly lower (p < 0.0001). CONCLUSIONS: The intraluminal administration of peppermint oil by using a hand pump is a simple, safe, and convenient alternative to the systemic injection of a cholinergic blocking agent or glucagon during colonoscopy.

Adult↗
PubMed1976

Myocardial ischemia from coronary arterial spasm.

Spasm of coronary arteries can cause chest pain indistinguishable from classic angina pectoris in patients without atherosclerosis of these vessels or recognizable heart disease. Associated electrocardiographic changes usually correspond to the coronary artery affected and disappear when the attack of pain ends. Sublingual nitrates are excellent agents for the control of the episodic anginal symptoms. There have been scattered reports of myocardial infarction occurring in patients with normal coronary arteries; a role of arterial spasm in these cases in speculative.

Adrenergic beta-Antagonists↗
PubMed1994

Chronic vascular irritation of the facial nerve causes facial spasm in rats.

The abnormal muscle response, elicited by electrical stimulation of one branch of the facial nerve and recorded from muscles innervated by another branch, has been used previously as an objective sign of hemifacial spasm in the development of animal models of this disorder. In the present study we recorded spontaneous electromyographic activity from the orbicularis oculi muscle from both sides in rats in which a demyelination of the peripheral portion of the facial nerve and vascular contact had been made previously. The root mean square value of the electromyographic activity on the affected side was significantly larger than that on the unaffected side in all rats in which the vascular irritation had caused the abnormal muscle response to appear. The results support our earlier finding that vascular contact together with demyelination of the peripheral facial nerve can cause the development of signs of hemifacial spasm, including involuntary muscle contractions.

Animals↗
PubMed1994

Hemifacial spasm and cerebellopontine angle epidermoid: case report and review.

A case with hemifacial spasm with tinnitus due to right cerebellopontine angle epidermoid is reported. The tumour was supposed to have caused the displacement of the part of anterior inferior cerebellar artery in the vicinity of the root exit zone of the ipsilateral facial nerve. Near total removal of the tumour along with microvascular decompression was done and the patient was completely relieved of his symptoms. The incidence of hemifacial spasm due to cerebellopontine angle epidermoid is extremely low. The cause of such an association is discussed and relevant literature is reviewed.

Brain Neoplasms↗
PubMed1994

Recordings from the facial motonucleus in rats with signs of hemifacial spasm.

We recorded evoked potentials from the facial motonucleus of rats in response to electrical stimulation of the temporal branch of the facial nerve in which chronic irritation from a blood vessel had caused the development of an abnormal muscle response. The abnormal muscle response that can be recorded from face muscles that are innervated by one branch of the facial nerve in response to electrical stimulation of a different branch is regarded to be a sign of hemifacial spasm. In the recordings from the motonucleus in rats that showed such an abnormal muscle response (model rats) there was a late component at a latency of about 5 msec, in addition to the early component with a latency of 1.5-2.5 msec that is also observed in normal rats. The latency of the electromyographic potentials recorded from the mentalis-orbicularis oris muscles in response to stimulation of the facial motonucleus was about 2 msec. The latency of the abnormal muscle response obtained from the mentalis muscle in the model rats was about 7 msec. This value is close to the sum of the conduction time from the motonucleus to the mentalis muscle (2 msec) and the latency of the late response from the motonucleus (5 msec). Similar results were obtained in rats in which the facial nerve had been chronically stimulated electrically and which had developed an abnormal muscle response. The results of this study further support the hypothesis that the hyperactivity of the facial motonucleus is the pathophysiology of hemifacial spasm.

Animals↗
PubMedDate not supplied

Surgical management of spasticity and spasms in spinal cord injury: an overview.

Spasms and spasticity constitute a significant problem in spinal cord injured individuals. Surgical intervention may be indicated when spasms and spasticity cannot be satisfactorily controlled by medications and physical therapy. Surgical procedures carried out on the nervous system include neurotomy, rhizotomy, myelotomy, cordectomy and spinal cord stimulation. The various procedures and their indications will be discussed.

Baclofen↗
PubMed1995

Posttraumatic cerebral arterial spasm.

Posttraumatic cerebral arterial spasm (vasospasm) has been demonstrated in the past by angiography, and recently by transcranial Doppler ultrasonography. Posttraumatic vasospasm is a delayed complication that involves the large basal intracranial arteries (e.g., internal carotid, middle cerebral, basilar) and occurs in 25-40% of head trauma patient. The time course of posttraumatic vasospasm resembles that of vasospasm associated with aneurysmal subarachnoid hemorrhage with onset occurring 2 or more days after injury. A study of the relationship of admission CT scan findings to the incidence of vasospasm suggests that intradural bleeding, which extends into the CSF (subarachnoid, intraventricular, and subdural hemorrhage), plays a role in the pathogenesis of posttraumatic arterial spasm. The preliminary results of a large prospective study of head trauma patients suggest that vasospasm may be an important determinant of outcome from severe head injury.

Brain Injuries↗
PubMed1983

Hemifacial spasm: a new technique of facial nerve blockade.

A new technique of facial nerve blockade using a special needle and a nerve stimulator was introduced. The results in patients suffering from hemifacial spasm are reported. This technique reduced the difficulties in identifying the facial nerve and decreased the suffering associated with the conventional way of creating these blocks. The technique described may also allow titration of neurolytic agent which may produce complete relief from spasm with much less likelihood of facial paralysis after the nerve blockade.

Adult↗
PubMed1984

Suxamethonium spasm. A differential diagnostic conundrum.

Spasm of muscle in association with suxamethonium is not uncommon. As an accepted early sign of malignant hyperpyrexia (MH), patients have been referred for MH screening who have shown only this abnormality. Case histories of 277 probands have been analysed and grouped according to final diagnosis, depending on results of muscle biopsy and in vitro screening. When muscle spasm is induced with suxamethonium, malignant hyperpyrexia must be considered a probable diagnosis.

Diagnosis, Differential↗
PubMed1986

Physiologic evaluation of esophageal function in patients with achalasia and diffuse esophageal spasm.

To evaluate function of the normal and pathologic esophageal body under more physiologic conditions than those utilized for traditional laboratory testing, manometry was performed before and during eating using a catheter assembly containing three peripheral transducers. Studies were evaluated from seven normal volunteers, 18 typical achalasia patients (eight before and 10 after esophagomyotomy), and eight patients with diffuse esophageal spasm (DES) as characterized by frequent simultaneous and repetitive contractions. In the preprandial period, all had similar frequencies of esophageal contractions, although there was a wide range. During eating, the frequency of contractions increased in all groups; however, the contraction frequency in unoperated achalasia patients, 12.7 +/- 5.0 contractions/min, significantly exceeded the frequency in normal volunteers of 4.9 +/- 1.3 contractions/min, p less than 0.01. The frequency was lower in operated achalasia patients, 9.4 +/- 6.5 contractions/min, but still exceeded that of normal volunteers, p less than 0.01. Patients with DES also had more frequent contractions, 10.5 +/- 9.7 contractions/min, than did the normal volunteers, p less than 0.01. The mean pressure of esophageal contractions for both achalasia groups was similar and was significantly lower than for the normal volunteers. Pressure in the DES patients was intermediate. It is concluded that patients with achalasia have lower pressure but more frequent contractions than normal volunteers during eating, and this spasm-like activity may be a more important pathophysiologic factor in their dysphagia than previously recognized. Esophagomyotomy does decrease the frequency of these contractions. Frequency, but not pressure, of contractions differs from normal in patients with DES.

Eating↗
PubMed2002

Advanced magnetic resonance imaging techniques for patients with hemifacial spasm.

PURPOSE: To review the underlying causes, diagnostic issues, and treatment of hemifacial spasm, with emphasis on advanced MRI techniques. METHODS: Brief technical note. RESULTS: High-resolution T1- and T2-weighted spin-echo and/or gradient echo imaging of the posterior fossa should be performed with the use of intravenous gadolinium for maximum contrast between CSF, vessel, and nerve. Magnetic resonance angiography is often useful, and new state-of-the-art sequences provide more detail. CONCLUSIONS: As MRI techniques improve, diagnosis and treatment of patients with hemifacial spasm will become easier. Ophthalmologists should be aware of these new magnetic resonance techniques.

Hemifacial Spasm↗
PubMed1996

Gabapentin for the treatment of hemifacial spasm.

Pharmacologic therapy for hemifacial spasm is often limited by the paucity of effective medications and problems with side effects. Gabapentin is a novel antiepileptic drug that is generally well tolerated. Its anticonvulsant effect is independent of gamma-aminobenzoic acid (GABA) receptor mechanisms. We report a patient with hemifacial spasm who responded well to gabapentin therapy. Gabapentin may be a useful alternative medical therapy to currently used drugs.

Acetates↗
PubMed1979

Transition from diffuse esophageal spasm to achalasia.

A 19-year-old man first presented with clinical, radiological, and manometric features of diffuse spasm. Within a year his motility disorder progressed to "vigorous" and, finally, classic achalasia. After pneumatic dilatation and subsequent long myotomy, the features of classic achalasia disappeared and he again exhibited radiological and manometric evidence of "vigorous" achalasia. The evolution of this patient's disease provides evidence that diffuse spasm and achalasia are different stages of the same disease and lie at opposite ends of a spectrum of related esophageal motility disorders.

Adult↗
PubMed1982

Diffuse esophageal spasm in patients with undiagnosed chest pain.

Many previous studies have shown diffuse esophageal spasm (DES) to be an infrequent clinical disorder. Over a 15-month period, 122 patients were evaluated by low-compliance pneumohydrolic esophageal manometry. The patients were referred for obscure undiagnosed chest pain. Diffuse esophageal spasm or its variance was found in 22 patients (18%). All patients had chest pain and 77% had associated solid and liquid food dysphagia. Medical therapy included treatment with a combination of anticholinergic medications, short- and long-acting nitrates, mild sedatives, and dietary adjustments. Follow-up clinical evaluation have been obtained in 73% of patients: medical treatment alone has been successful in impressively relieving symptoms in 10 patients, two have benefited from repeat pneumatic dilatations, and one patient has improved after pneumatic dilatation and subsequent Heller myotomy. A combination of accurate clinical history, endoscopy, barium swallow, and esophageal manometry should allow a reliable diagnosis of DES with a good chance of successful medical therapy.

Esophageal Diseases↗
PubMed1985

Ultrasound in the diagnosis of sphincter of Oddi spasm.

Biliary colic from spasm of the sphincter of Oddi has been a difficult diagnosis to prove. We describe a patient in whom the diagnosis was arrived at using a pharmacological provocative test employing codeine to reproduce pain and a change in liver and pancreatic serum enzymes, and ultrasound to demonstrate a transient increase in common bile duct diameter. Testing carried out before surgical sphincteroplasty reproduced symptoms, and brought about marked pancreatic and liver enzyme elevation and an increase in common bile duct diameter measured by ultrasound (0.4 to 1.0 cm). Such events did not occur after sphincteroplasty. This case study suggests that codeine may be a useful provocative agent and that ultrasound measurements of changes in common bile duct diameter may provide a useful method in the diagnostic approach to Sphincter of Oddi Spasm.

Acetaminophen↗
PubMed1997

Pitfalls in the diagnosis of hemifacial spasm.

Hemifacial spasm (HFS), a condition characterized by involuntary unilateral facial spasms, is a disabling disorder resulting in functional compromise, patient frustration, cosmetic deformity, and social embarrassment. Compression of the seventh nerve at the root entry zone via vascular loop is presently the most widely accepted causative theory. Although less common, there are other entities that can result in HFS. Basic evaluation, including a thorough history, physical examination, and magnetic resonance imaging (MRI) scan, is important to confirm the diagnosis and rule out other causes. The relation of vascular loop syndrome to HFS is well enough established that radiologic documentation of a vascular loop is probably not necessary in every case. Here we present 12 cases of HFS, 6 without VLS. The etiology and evaluation of HFS are reviewed.

Adult↗