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Journal articles on the topic 'Spasm'

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Published: 4 June 2021
Last updated: 25 February 2023

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1

Hendriati, Hendriati. "EFEKTIFITAS TOXIN BOTULLINUM UNTUK MANAJEMEN BLEFAROSPASME ESSENSIAL DAN SPASME HEMIFASIAL." Majalah Kedokteran Andalas 34, no. 2 (May 2, 2015): 202. http://dx.doi.org/10.22338/mka.v34.i2.p202-210.2010.

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AbstrakUntuk mengukur efektifikas toxin Botullinum pada kasus-kasus okuloplastik (blefarospasme essensial dan spasme hemifasial.Laporan kasus 16 pasien yang terdiri dari 14 kasus spasme hemifasial dan 2 kasus blefarospasme essensial. Digunakan 6 vial toxin Botullinum. Vial pertama digunakan untuk pasien spasme hemifasial dan 1 pasien blefasrospasme di minggu berikutnya. vial kedua dan ketiga masing-masing digunakan untuk 2 pasien spasme hemifasial. Vial keempat digunakan untuk pasien blefarospasme yang menggunakan vial pertama (setelah 6 bulan), dan 1 pasien spasme hemifasial yang menggunakan vial kedua ( setelah 4 bulan) dan 1 pasien spasme hemifasial baru. Setelah 1 minggu, toxin Botullinum vial keempat digunakan untuk 6 pasien spasme hemifasial dan 1 pasien blefarospasme essensial yang menggunakan vial pertama 8 hari berikutnya (setelah 7 bulan).Terdapat 16 pasien pada studi ini ; 14 spasme hemifasial dan 2 blefarospasme essensial. Pada 5 pasien dilakukan injeksi ulangan dengan jangka waktu yang berbeda. Tidak ditemukan efek samping pada pasien-pasien ini.Toxin Botulinum efektif untuk manajemen spasme hemifasial dan blefarospasme essensial tetapi efeknya temporer. Pada studi ini, jangka waktu injeksi ulangan bervariasi sekitar 4 – 7 bulan pada 5 pasien.Kata Kunci : Toxin Botulinum toxin, spasme hemifasial, blefarospasmeAbstractTo asses Botulinum Toxin efficacy in oculoplastic cases (blepharospasm and hemifacial spasm).A case report on 16 patients consisted of 14 hemifacial spasms and 2 essential blepharospasm. Six vials of botulinum toxin were used. First vial was used for two patients of hemifacial spasm and one blepharospasm patient one week later. Second and third vials were used each for two patients of hemifacial spasms. Fourth vial was used for one blepharospasm patient from first vial user (after six month), one hemifacial spasm from second vial user (after four months) and one new hemifacial spasm. After one week, Botulinum toxin from fourth vial was used for one new patient of hemifacial spasm. Fifth and sixth vial was used for sixLAPORAN KASUS203hemifacial spasms and eight days later for one blepharospasm from first vial user (after seven months).There were 16 patients in this serial study; 14 hemifacial spasms and 2 blepharospasms. Five patients had reinjections with different duration. There is no side effect in those patients.Botulinum toxin is effective in treatment of hemifacial spasm and blepharospasm, but the effects are temporary. In this study, reinjections durations about four to seven months in five patients.Key word : Botulinum toxin, hemifacial spasm, blepharospasm
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2

Manfrini, Olivia, Gabriele Bazzocchi, Alessandra Luati, Alberigo Borghi, Paola Monari, and Raffaele Bugiardini. "Coronary spasm reflects inputs from adjacent esophageal system." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 5 (May 2006): H2085—H2091. http://dx.doi.org/10.1152/ajpheart.00925.2005.

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Mechanisms underlying coronary spasm are still poorly understood. The aim of the study was to assess the hypothesis that fluctuations in the development of coronary spasm might reflect inputs from the adjacent esophageal system. We enrolled patients admitted to the coronary care unit for episodes of nocturnal angina. Seven patients with variant angina and five with coronary artery disease (CAD) had concurrent ECG and esophageal manometric monitoring. ECG monitoring documented 28 episodes of ST elevation in variant angina patients and 16 episodes of ST depression in CAD patients. Manometric analysis showed that esophageal spasms resulted remarkably more frequently in variant angina patients (143 total spasms; individual range 9–31) than in CAD patients (20 total spasms; individual range 0–9; P < 0.01). Time series analysis was used to assess fluctuations in the occurrence of abnormal esophageal waves and its relationship with spontaneous episodes of ST shift. Episodes of esophageal spasm in CAD were sporadic (<1 in 30 min) and not related to ECG-recorded ischemia. In the variant angina group, esophageal spasms were time related to ischemia (>1 into 5 min before ECG-recorded ischemia) ( P < 0.05). A bidirectional analysis of causal effects showed that the influence processes between esophageal and coronary spasms were mutual and reciprocal (transfer function model, P < 0.05) in variant angina. We concluded that in variant angina patients, episodes of esophageal spasms and myocardial ischemia influenced each other. Mechanisms that cause esophageal spasm can feed back to produce coronary spasm. Coronary spasm may feed forward to produce additional episodes of esophageal spasm.
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3

Mitchell, Joseph. "A Spism and a Spasm." Chesterton Review 34, no. 1 (2008): 189–202. http://dx.doi.org/10.5840/chesterton2008341/295.

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4

Yamashita, K., S. Okamoto, K. Hosotani, S. Nakatsu, M. Hojo, K. Miyamoto, and R. Matsumoto. "Interventional Neuroradiology in Hemifacial Spasm." Interventional Neuroradiology 3, no. 2_suppl (November 1997): 32–36. http://dx.doi.org/10.1177/15910199970030s204.

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There have never been functional studies in the diagnosis of hemifacial spasm caused by neurovascular compression. We used neurointerventional techniques to conduct a functional investigation of the artery responsible for hemifacial spasm in seven patients. A microcatheter was inserted into the various arteries of the posterior circulation under systemic heparinization, and its effect on the spasm was evaluated clinically and electromyographically. In six patients who underwent microvascular decompression surgery, the vessels compressing the root exit zone of the facial nerve were surgically determined, and compared with the result of the procedure. The catheter was inserted into twelve arteries. The spasms were stopped immediately and completely by the insertion of the catheter into seven arteries. Six of them were surgically proven to compress the root exit zone of the facial nerve. The spasm was changed in frequency or in type by the insertion into two arteries. These arteries were also compressing the root exit zone. One artery was located at a more peripheral part of it and the other was running over another artery compressing the root exit zone. The spasms were not affected at all by the insertion into three arteries. These arteries were not observed in the operative field and had no contact with the nerve. Superselective ‘angiograms showedpositional qnd configurational changes of the arteries. There was no arterial spasm and tight catheterization leading to stasis of contrast material within the arteries. There were no complications related to the procedures. Functional relationship between the artery and the spasms was established in all the patients, and one patient refused surgery because the frequency of the spasm was reduced by the procedure. The result of this study may suggest that a functional investigation of hemifacial spasm is feasible and seems useful for selecting good candidates for microvascular decompression surgery.
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5

Srinivas, Sujithra. "Infantile spasm: A review on the severity of epileptic encephalopathy." IP Indian Journal of Neurosciences 8, no. 1 (March 15, 2022): 16–20. http://dx.doi.org/10.18231/j.ijn.2022.004.

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Infantile spasm (IS) comprises of both an age dependent epileptic seizure and distinctive seizure Onset in infants. In the recent past the key observation in classification and standardization of infantile spasm has culminated many recommendations in distinguishing and recognizing the seizure type and the epileptic syndrome or the West syndrome. The Infantile spasm is an early onset epileptic encephalopathy which presents unique electrographic and clinical features, these features are found in children in the middle of the first year of their birth .However the pathophysiology and the heterogeneity of the infantile spasm remains partially or incompletely understood. In the neurobiological basis there are multiple aetiologies converge to form similar clinical interpretations. The description of the electroencephalographic features of the spasm and its hypsarrthythmia plays a pivot role in early diagnosis. The treatment options for infantile spasm are very limited and it is also called a “catastrophic” due to the poor developmental, cognitive and epileptic progress. In the recent past more detailed information about the electrographic and clinical features of the spasms and hypsarrhythmia in EEG has emerged. The advances in the neuro imaging techniques have revealed about the aetiology and the pathophysiology of infantile spasm to yield a prognosis in patients with infantile spasms. The pathophysiology of infantile spasm needs to be better clarified for any kind of novel treatments and a wide range of preclinical animal studies are essential for advancing the knowledge. Here, in this review paper we focus on the preclinical models of Infantile spasm, with information’s regarding the existing models and research findings, elaborate on some novel models and discuss on new data that can help in advancing the understanding of the cellular mechanisms underlying the specific EEG changes such as ictal electrodecrement and interictal hypsarrhythmia presented in Infantile spasm IS.
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6

Osburn, Leisha L., Aage R. Møller, Jay R. Bhatt, and Aaron A. Cohen-Gadol. "Hemilingual Spasm." Neurosurgery 67, no. 1 (July 1, 2010): 192–96. http://dx.doi.org/10.1227/01.neu.0000370596.78384.2b.

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Abstract OBJECTIVE We report on vascular compression syndrome of the 12th cranial nerve (hypoglossal), an occurrence not previously reported, and demonstrate, through corresponding objective electrophysiological evidence, that microvascular decompression of the hypoglossal nerve root can cure hemilingual spasm. CLINICAL PRESENTATION A 52-year-old man had lower face muscle twitching and tongue spasms, which worsened with talking, chewing, or emotional stress. Carbamazepine offered only temporary relief, and relief from injections of botulinum toxin was insignificant. He was referred for surgical treatment. High-resolution magnetic resonance imaging of his posterior fossa contents revealed no obvious evidence of any compressive vessel along the facial nerve, but a compressive vessel along the hypoglossal nerve was apparent. INTERVENTION The presence of preoperative tongue spasms encouraged interoperative monitoring of tongue motor responses. The facial nerve exit zone was explored, but microsurgical inspection of the seventh/eighth cranial nerve complex did not reveal any compressive vessel. However, at the anterolateral aspect of the medulla oblongata, the hypoglossal nerve was clearly compressed and distorted laterally by a large tortuous vertebral artery. When the artery was mobilized away from the nerve, the abnormal late electromyographic response to transcranial electrical stimulation disappeared; immediately after shredded Teflon was interpositioned between the artery and the nerve, the abnormal spontaneous tongue fasciculation also disappeared. The patient has remained spasm free 6 months after surgery. CONCLUSION Hemilingual spasm may be caused by vascular contact/compression along cranial nerve XII at the lower brainstem and belong to the same family of cranial nerve hyperactivity disorders as hemifacial spasm.
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7

Harini, Chellamani, Sonal Sharda, Ann Marie Bergin, Annapurna Poduri, Christopher J. Yuskaitis, Jurriaan M. Peters, Kshitiz Rakesh, Kush Kapur, Phillip L. Pearl, and Sanjay P. Prabhu. "Detailed Magnetic Resonance Imaging (MRI) Analysis in Infantile Spasms." Journal of Child Neurology 33, no. 6 (March 26, 2018): 405–12. http://dx.doi.org/10.1177/0883073818760424.

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Purpose: To evaluate initial magnetic resonance imaging (MRI) abnormalities in infantile spasms, correlate them to clinical characteristics, and describe repeat imaging findings. Methods: A retrospective review of infantile spasm patients was conducted, classifying abnormal MRI into developmental, acquired, and nonspecific subgroups. Results: MRIs were abnormal in 52 of 71 infantile spasm patients (23 developmental, 23 acquired, and 6 nonspecific) with no correlation to the clinical infantile spasm characteristics. Both developmental and acquired subgroups exhibited cortical gray and/or white matter abnormalities. Additional abnormalities of deep gray structures, brain stem, callosum, and volume loss occurred in the structural acquired subgroup. Repeat MRI showed better definition of the extent of existing malformations. Conclusion: In structural infantile spasms, developmental/acquired subgroups showed differences in pattern of MRI abnormalities but did not correlate with clinical characteristics.
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8

Sharma, Suvasini, Shaiphali Goel, Dipti Kapoor, Divyani Garg, Isha Panda, Aman Elwadhi, Bijoy Patra, Sharmila B. Mukherjee, and Harish Pemde. "Evaluation of the Modified Atkins Diet for the Treatment of Epileptic Spasms Refractory to Hormonal Therapy: A Randomized Controlled Trial." Journal of Child Neurology 36, no. 8 (April 9, 2021): 686–91. http://dx.doi.org/10.1177/08830738211004747.

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Objectives: We aimed to evaluate the efficacy of the modified Atkins diet in children with epileptic spasms who had failed hormonal therapy. Methods: Children aged 9 months to 3 years having daily epileptic spasms despite a trial of ACTH or oral prednisolone and 1 additional anticonvulsant medication were enrolled. Children were randomly assigned to receive the modified Atkins diet either immediately or after a delay of 4 weeks. The ongoing anticonvulsant medications were continued unchanged. The primary outcome variable was the proportion of children who achieved spasm freedom as per parental reports at 4 weeks. Secondary outcomes included time to spasm cessation, proportion of children with electroclinical remission, the proportion of children with >50% reduction of spasms at 4 weeks, and adverse effects of the diet. ( ClinicalTrials.gov Identifier: NCT03807141). Results: A total of 91 children were enrolled in the study; 46 in the diet group and 45 in the control group. At the end of 4 weeks, 11 children in the diet group were spasm free compared with none in the control group ( P ≤ .001). The median time to achieve spasm cessation was 10 days (interquartile range 9-20). Nine of these had resolution of hypsarrhythmia on electroencephalography (EEG). Thirty (65.2%) in the diet group had >50% reduction in spasms, compared with none in the control group ( P < .001). The most common side effect was constipation, noted in 34.8% of the children. Conclusions: The modified Atkins diet was found to be effective and well tolerated in children with epileptic spasms refractory to hormonal therapy.
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9

Malavika Gopi, Akshaya Suresh, Anandu H, Roshni P R, Mamatha M R, and Vinayan K P. "West syndrome - epileptic encephalopathy at early infancy." International Journal of Research in Pharmaceutical Sciences 11, no. 4 (December 25, 2020): 7492–94. http://dx.doi.org/10.26452/ijrps.v11i4.3951.

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West syndrome (WS), synonymously infantile spasm or epileptic spasm, is a rare type of epileptic encephalopathy occurring at early infancy that exists with variable life expectancy. It is the most common form of epileptic encephalopathy. WS presents with spasms marked by extensor or mixed movements with distinct electroencephalogram (EEG) pattern of hypsarrhythmia, flexor and psychomotor arrest. Children with west syndrome always depict abnormal EEG, but sometimes the abnormality is seen only during sleep. The incidence of infantile spasms is found closer to 1 in 2,000 children, that typically begins between 2-12 months of age and peaks between 4-8 months of age. It is observed in otherwise healthy infants and also among infants with abnormal cognitive development. If this spasm happens in older subjects, they are preferably called "epileptic spasms" rather than infantile spasms. The goal for treatment of infantile spasms is to have complete control of spasms. Hormonal therapy with ACTH or vigabatrin is the mainstay of treatment. In spite of the development of new antiepileptic drugs (AEDs), about 35-40% of cases are drug-resistant. Children affected with the west syndrome can be cured, but a successful therapy often depends on the timely diagnosis. This case report is one evidence highlighting the treatment strategy for the west syndrome, and this could be useful for any further study regarding this topic.
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10

Malavika Gopi, Akshaya Suresh, Anandu H, Roshni P R, Mamatha M R, and Vinayan K P. "West syndrome - epileptic encephalopathy at early infancy." International Journal of Research in Pharmaceutical Sciences 11, no. 4 (December 25, 2020): 7492–94. http://dx.doi.org/10.26452/ijrps.v11i4.3951.

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West syndrome (WS), synonymously infantile spasm or epileptic spasm, is a rare type of epileptic encephalopathy occurring at early infancy that exists with variable life expectancy. It is the most common form of epileptic encephalopathy. WS presents with spasms marked by extensor or mixed movements with distinct electroencephalogram (EEG) pattern of hypsarrhythmia, flexor and psychomotor arrest. Children with west syndrome always depict abnormal EEG, but sometimes the abnormality is seen only during sleep. The incidence of infantile spasms is found closer to 1 in 2,000 children, that typically begins between 2-12 months of age and peaks between 4-8 months of age. It is observed in otherwise healthy infants and also among infants with abnormal cognitive development. If this spasm happens in older subjects, they are preferably called "epileptic spasms" rather than infantile spasms. The goal for treatment of infantile spasms is to have complete control of spasms. Hormonal therapy with ACTH or vigabatrin is the mainstay of treatment. In spite of the development of new antiepileptic drugs (AEDs), about 35-40% of cases are drug-resistant. Children affected with the west syndrome can be cured, but a successful therapy often depends on the timely diagnosis. This case report is one evidence highlighting the treatment strategy for the west syndrome, and this could be useful for any further study regarding this topic.
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11

Hayek, Salim M. "Occipital Neurostimulation-Induced Muscle Spasms: Implications for Lead Placement." September 2009 5;12, no. 5;9 (September 14, 2009): 867–76. http://dx.doi.org/10.36076/ppj.2009/12/867.

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Background: For many headache types, occipital peripheral nerve stimulation (ONS) provides significant relief of chronic, frequent, and severe headaches. Though rarely reported, ONS may cause painful muscle spasms that make stimulator use impractical. The classic description of the technique advocates placement of the leads transversely at the level of the arch of C1 or at C1-2. At that level, the greater occipital nerve (GON) infrequently pierces the superficial fascia of the neck muscles to become superficial. However, important anatomic variability exists. Objective: To report placement of leads higher at the nuchal line rather than the classically recommended C1 level to avoid ONS-induced muscle spasm. Methods: Four interventional pain physicians independently revised ONS leads due to painful muscle stimulation. Five case reports of surgical ONS lead revision for management of ONS-induced muscle spasms are described and discussed. Results: Placement of peripheral neurostimulator leads at or above the nuchal line in these 5 cases provided good paresthesiae without causing neck muscle spasm. Conclusion: Lead placement at the level of C1 or C1-2 may cause some patients to have intolerable neck/occipital spasm during neurostimulation. This is the first known published report of technical variation in the location of lead placement, at the nuchal line in a transverse fashion, for ONS. Placing ONS leads at the level of the occipital protuberance appears to eliminate ONS-induced muscle spasm while allowing good paresthesia coverage. Limitations: Stimulation parameters vary, thus posting parameters may be misleading as muscle spasms occurred despite multiple reprogramming attempts and were a function of lead position, not program settings. Key words: Occipital nerve stimulator, peripheral neurostimulation, muscle spasm, complication, interventional pain management, cephalgia, headache, migraine, occipital neuralgia, greater occipital nerve
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12

Adhikari, Sudhir, and Deepa Gautam. "Outcome of West Syndrome: A Critical Review." Journal of Pediatric Epilepsy 09, no. 01 (March 2020): 001–6. http://dx.doi.org/10.1055/s-0040-1708809.

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AbstractWest syndrome is a genetically heterogeneous electro-clinical syndrome starting in early infancy. Short-term goal of therapy is spasm control and with standard hormonal or vigabatrin treatment, spasms can be controlled in 60 to 80% of patients in 2 weeks to 3 months period. Hormonal treatment with oral steroid is an alternative therapy to injectable adrenocorticotropin hormone, especially in low resource areas. Vigabatrin is preferred in tuberous sclerosis patients. Long-term aim of treatment is sustained remission of seizures and better neurodevelopmental outcome. About 50 to 70% of children are spasm free for prolonged duration, but epilepsy with multiple seizure types including Lennox–Gastaut syndrome is evident in 20 to 40% of children in long-term follow-up. Though hypsarrhythmia is helpful for the diagnosis, prognostic role of the resolution of electroencephalographic abnormalities is still uncertain. Seizures can be controlled in 40 to 60% of the patients, but only 12 to 40% children have normal neurodevelopmental outcome and a third of children are left with severe disabilities. Children with unknown etiology and normal development at spasm onset have better clinical outcome. Young age at onset, nonstandard therapy have less favorable outcome. Surgery is helpful for spasm control in patients with structural lesions and refractory spasms even in the absence of structural lesions.
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Cirnigliaro, Frank Arthur, Nicole Gauthier, and Moira Rush. "Management of refractory pain in Stiff-Person syndrome." BMJ Case Reports 14, no. 1 (January 2021): e237814. http://dx.doi.org/10.1136/bcr-2020-237814.

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Stiff-Person syndrome (SPS) is a rare autoimmune neurological disorder characterised by episodic painful muscle rigidity and violent spasms. A significant trigger for the painful spasms experienced by patients is pain itself, making optimal pain management and avoidance a necessity. While first-line and second-line therapies for spasm prevention and termination are known, there is a paucity of evidence to guide pain management. We report the case of a 26-year-old woman with SPS referred for excruciating muscle cramping and rigidity with pain lasting beyond the episodes themselves. We report the novel use of ketamine and intravenous magnesium sulfate which may provide analgesia, spasm avoidance and early termination of exacerbations in SPS.
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Conte, Antonella, Marika Falla, Maria Concetta Diana, Matteo Bologna, Antonio Suppa, Andrea Fabbrini, Carlo Colosimo, Alfredo Berardelli, and Giovanni Fabbrini. "Spread of Muscle Spasms in Hemifacial Spasm." Movement Disorders Clinical Practice 2, no. 1 (November 4, 2014): 53–55. http://dx.doi.org/10.1002/mdc3.12106.

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15

Murakami, Hiroatsu, Tadashi Kawaguchi, Masafumi Fukuda, Yasushi Ito, Hitoshi Hasegawa, and Ryuichi Tanaka. "Monitoring of the lateral spread response in the endovascular treatment of a hemifacial spasm caused by an unruptured vertebral artery aneurysm." Journal of Neurosurgery 101, no. 5 (November 2004): 861–63. http://dx.doi.org/10.3171/jns.2004.101.5.0861.

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✓ The lateral spread response (LSR) is used in the electrophysiological diagnosis of a hemifacial spasm or for monitoring during microvascular decompression. The authors used LSRs for intraoperative monitoring during endovascular surgery in a rare case of vertebral artery (VA) aneurysm that caused intractable hemifacial spasm. A 49-year-old woman presented with a right hemifacial spasm that had persisted for 9 months. No other clinical symptom was observed. Vertebral artery angiography revealed a saccular aneurysm of the right VA. Magnetic resonance (MR) imaging demonstrated that the aneurysm was compressing the root exit zone of the right facial nerve. Endovascular treatment of the VA aneurysm was performed while monitoring the patient's LSRs. During occlusion of the VA at sites distal and proximal to the aneurysm, the LSRs temporarily disappeared and then reappeared with a higher amplitude than those measured preceding their disappearance. The hemifacial spasm alleviated gradually and disappeared completely 6 months after treatment. The LSRs changed in parallel with the improvement in the patient's hemifacial spasms and eventually disappeared. No recurrence of symptoms has been noticed as of 18 months postoperatively. This is the first report of the use of LSR monitoring during endovascular surgery for an intracranial aneurysm that causes hemifacial spasm. Intraoperative and postoperative changes in the LSRs provided useful information regarding the pathophysiology of hemifacial spasm.
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Nemoto, Daiki, Kenichi Utano, Noriyuki Isohata, Shungo Endo, Kensuke Kumamoto, Taka-aki Koshimizu, Alan Lefor, and Kazutomo Togashi. "Topical lidocaine inhibits spasm during colonoscopy: a double-blind, randomized controlled trial (with video)." Endoscopy International Open 05, no. 06 (May 30, 2017): E402—E407. http://dx.doi.org/10.1055/s-0043-105489.

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Abstract Background and study aims Topical peppermint oil prevents intestinal spasm, but can cause rebound spasm. Lidocaine hydrochloride, a local anesthetic, may work as an antispasmodic by blocking Na + channels. The aim of this study was to investigate the effect of topical lidocaine on the inhibition of colonic spasm during colonoscopy, compared with peppermint oil. Patients and methods A randomized, controlled double-blind trial was conducted in an academic endoscopy unit. Patients requiring endoscopic resection were randomly allocated to colonoscopy with topical administration of lidocaine (n = 30) or peppermint oil (n = 30). Similar vials containing different solutions were randomly numbered. Allocation was made based on the vial number. The solution used and the vial number were not revealed during the study. Two endoscopists performed all procedures using midazolam, without anticholinergic agents. When a pre-selected lesion was identified, the solution in the assigned vial was dispersed and the bowel observed for 5 minutes. The primary endpoint was the duration of spasm inhibition, and a secondary endpoint was the occurrence of rebound spasm stronger than before dispersion. Results There were no significant differences in patient demographics. Spasm was inhibited in almost all patients in both groups, with a similar median duration (lidocaine 227 sec vs. peppermint 212.5 sec, P = 0.508). In contrast, rebound spasm occurred less frequently in the lidocaine group (lidocaine 7 % vs. peppermint 47 %, P = 0.001). There were no adverse events or symptoms associated with administration of the solutions. Conclusions The inhibitory effect of lidocaine is not superior to peppermint oil. However, lidocaine significantly decreases the frequency of rebound spasms.
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Webb, PM, and A. Datta. "P.077 Response to the ketogenic diet in refractory epileptic spasms at BC Children’s Hospital." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 49, s1 (June 2022): S28. http://dx.doi.org/10.1017/cjn.2022.174.

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Background: Epileptic spasms (ES) are a devastating seizure type with poor neurodevelopmental outcome; 1/3 are resistant to treatment with first line therapies. Recently attention has been drawn to the ketogenic diet (KD) as a potentially effective therapy, though data regarding optimal time of initiation, and its sustained effectiveness, are lacking. Methods: Retrospective chart review of all patients with ES treated with KD at BC Children’s Hospital between 2002 and 2020 (n=28) with comparison of spasm response based on age of initiation of KD in two groups: < 12 months (n=11) and ≥ 12 months (n=17). Results: Comparing the <12 months and ≥ 12 months groups showed: unknown etiology in 9% vs 25%; spasm freedom for 3 months on KD in 18% vs 41%; median time to spasm freedom was 2 vs 6 weeks; relapse after a period of spasm freedom occurred in 66% vs 70%. Conclusions: Although more effective in children ≥ 12 months of age in the first 3 months, spasm freedom in either group was not sustained with KD. KD is recommended as early therapy for refractory ES, but this study suggests clinicians be aware the KD has limited efficacy in long-term control of ES and must be used with other therapies.
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Webb, PM, and A. Datta. "P.107 Response to the Ketogenic Diet in refractory epileptic spasms at BC Children’s Hospital." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 48, s3 (November 2021): S49—S50. http://dx.doi.org/10.1017/cjn.2021.384.

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Background: Epileptic spasms (ES) are a devastating seizure type with poor neurodevelopmental outcome; 1/3 are resistant to treatment with first line therapies. Recently attention has been drawn to the ketogenic diet (KD) as a potentially effective therapy, though data regarding optimal time of initiation, and its sustained effectiveness, are lacking. Methods: Retrospective chart review of all patients with ES treated with KD at BC Children’s Hospital between 2002 and 2020 (n=28) with comparison of spasm response based on age of initiation of KD in two groups: < 12 months (n=11) and ≥ 12 months (n=17). Results: Comparing the <12 months and ≥ 12 months groups showed: unknown etiology in 9% vs 25%; spasm freedom for 3 months on KD in 18% vs 41%; median time to spasm freedom was 2 vs 6 weeks; relapse after a period of spasm freedom occurred in 66% vs 70%. Conclusions: Although more effective in children ≥ 12 months of age in the first 3 months, spasm freedom in either group was not sustained with KD. KD is recommended as early therapy for refractory ES, but this study suggests clinicians be aware the KD has limited efficacy in long-term control of ES and must be used with other therapies.
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19

Teragawa, Hiroki, Chikage Oshita, Yuko Uchimura, Ryota Akazawa, and Yuichi Orita. "Coronary Microvascular Vasodilatory Function: Related Clinical Features and Differences According to the Different Coronary Arteries and Types of Coronary Spasm." Journal of Clinical Medicine 11, no. 1 (December 27, 2021): 130. http://dx.doi.org/10.3390/jcm11010130.

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Background: In the clinical setting; the microvascular vasodilatory function test (MVFT) with a pressure wire has been used in ischaemia patients with non-obstructive coronary arteries (INOCA), including vasospastic angina (VSA) and microvascular angina (MVA). The exact factors that affect the microvascular vasodilatory function (MVF) in such patients are still unknown. We aimed to identify the factors, including clinical parameters and lesion characteristics, affecting the MVF in such patients. Methods: A total of 53 patients who underwent coronary angiography, spasm provocation tests (SPTs) and MVFTs were enrolled. In the MVFT, the coronary flow reserve (CFR) and index of microcirculatory resistance (IMR) were measured. Of the 53 patients, MVFT data in the left anterior descending coronary artery (LAD) were obtained from 49 patients, and the clinical parameters were checked in all of them. Based on the results of the SPT, coronary spasms were divided into focal spasm, diffuse spasm, and microvascular spasm (MVS). To assess the lesion characteristics influencing MVF, MVFT data were compared according to the types of coronary spasm and coronary vessels in 73 vessels of the 53 patients. Results: In 49 patients who underwent the MVFT in the LAD, the IMR was higher in active smokers (n = 7) than in former smokers (n = 15) and never smokers (n = 27, p < 0.01). In the 73 coronary arteries in this study, the type of coronary spasm did not correlate with the CFR or IMR, whereas a higher IMR were more frequently observed in cases of focal spasm than in cases of diffuse spasm (p = 0.03). In addition, the IMR was higher in the right coronary artery (RCA) than in the LAD (p = 0.02). Conclusion: These results indicate that the smoking status affected the MVF in patients with INOCA, suggesting the possibility of improvement in the MVF by smoking cessation in such patients. In addition, in the assessment of MVF, it may be important to take into account which coronary artery or types of coronary spasm are being evaluated.
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Subedi, Kiran, Rydam Basnet, Bikash Bhandari, Sonsy Gongal, and Ashik Rajak. "West syndrome - Diagnostic dilemma in a month old infant without typical electroencephalographic features: A case report." Journal of Kathmandu Medical College 8, no. 2 (June 30, 2019): 116–17. http://dx.doi.org/10.3126/jkmc.v8i2.28175.

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Infantile spasm constitutes 2% of childhood epilepsies but 25% of epilepsy with onset in the first year of life. The rate of infantile spasm is estimated to be 2.5-6.0 cases per 10,000 live births. Its prevalence rate is 1.5-2.0 cases per 10,000 children aged 10 years or younger. Ninety percent of infantile spasms begin in infants younger than 12 months with a peak onset at age 4-6 months. We report a case of 45 days old male child who had onset of flexor spasms since one month of age which is an unusual age of onset of West syndrome. The symptoms were initially thought as a simple startle response by the mother. This is a rare case because of its age of onset and lack of typical electroencephalographic features. Although the electroencephalography showed abnormal pattern suggesting seizure disorder, the frequently encountered pattern of hypsarrhythmia seen in children with infantile spasm was not seen in this case. It was difficult to assess developmental regression in a month old child who in subsequent visits had some degree of developmental delay. Hence fulfilling two of the three criterias for the diagnosis.
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Nahar Sumi, Most Samsun, Razia Sultana, Sufia Khatun, Mohammad Shah Jahan Chowdhury, Mohammad Enayet Hussain, Rajib Nayan Chowdhury, and Narayan Saha. "Clinical and Electroencephalographic Pattern and Short-Term Outcome to Treatment in Infantile Spasm: A Randomized Controlled Trial." Journal of National Institute of Neurosciences Bangladesh 8, no. 2 (January 15, 2023): 130–35. http://dx.doi.org/10.3329/jninb.v8i2.63747.

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Background: Infantile spasms (epileptic spasm) is an epileptic encephalopathy with unique clinical and electrographic features, which affects children mostly in the middle of the first year of life. Objective: The aim of this study was to evaluate the clinical and electroencephalographic profile and short-term outcome in infantile spasm. Methodology: This was a randomized controlled trial study done in Department of Pediatric Neurology, National Institute of Neuroscience & Hospital, Dhaka, Bangladesh. The patient of infantile spasm aged 2 months to 2 years were enrolled in the study from June 2017 to May 2018. With parent’s written informed consent, they were randomized into two groups, 25 in each. One group got ACTH only and another group got both ACTH and vigabatrin. Detailed history including seizure pattern was taken. EEG was done before and after2 -3 weeks of starting treatment. They were followed up at 8, 15, 43 days. Results: The mean age of onset of seizure (mean ±SD) was 7.24±4.13 (2 to 19) month on hormonal therapy and 6.84±5.89 (2 to 22) month on combination therapy. Most patient had history of perinatal birth asphyxia, developmental delay, seizure pattern was flexor spasm and EEG pattern were predominantly classical hypsarrhythmia in both groups. After treatment cessation of spasms occurred between 14 to 42 days in 72.0% in combination therapy and 44% in hormonal therapy (P value=0.045). EEG became normal in 60.0% and 32.0% patients in combination and hormonal therapy respectively (P value =0.047). Conclusion: In conclusion combination therapy of ACTH hormone plus vigabatrin has better than ACTH therapy alone in cessation of clinical spasms and electroencephalographic remission. Journal of National Institute of Neurosciences Bangladesh, July 2022;8(2):130-135
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22

Johnson, Donald S. "The Spasm-Pain-Spasm Cycle." Pain Medicine 13, no. 4 (April 2012): 615. http://dx.doi.org/10.1111/j.1526-4637.2012.01355.x.

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Gulati, Amitabh. "The Use of Lumbar Sympathetic Blockade at L4 for Management of Malignancy-Related Bladder Spasms." Pain Physician 3;14, no. 3;5 (May 14, 2011): 305–10. http://dx.doi.org/10.36076/ppj.2011/14/305.

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Background: Cancer-related bladder spasms may be a rare but severe symptom of bladder or metastatic cancer or its related treatments. Various treatments described in the literature include systemic medications, intravesical or epidural medications, or even sacral neurolectomies. Objective: We present 3 patients who have suffered from bladder spasm either from invasion of the bladder wall by tumor (2 patients) or from intravesical chemotherapeutic treatment. Design: Case Report. Setting: Cancer pain management hospital. Methods: For each patient, we describe the use of lumbar sympathetic block to successfully treat the bladder spasms. Sympathetic blockade was performed at the left anterolateral border of lumbar vertebra L4. We used 10 mL of local anesthetic (0.25% bupivacaine) delivered in 2 mL aliquots, each given after negative aspiration for heme. Each procedure was performed with fluoroscopic guidance (both AP and lateral views) with the use of iodine contrast (Omnipaque-180) to confirm the location of the medication and its resulting spread. Results: All 3 patients had a reduction in the frequency and intensity of spasms, with 2 out of 3 patients not having a recurrence of the spasms for up to 2 months post procedure and follow up. Limitations: Case Report. Conclusion: Lumbar sympathetic blockade could be a useful treatment for recurrent bladder spasm in the oncologic population. Based on these findings, we feel that the branches of the sympathetic nerve set at L4 may be a good target for neurolytic procedures, such as radiofrequency ablation, for long term treatment of bladder spasms. Further research is necessary to determine the efficacy of this technique for the treatment of bladder spasms in the oncologic population. Key words: Bladder spasm, cancer pain, splanchnic nerve, lumbar sympathetic block
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Pohl, Daniel, Jody Ciolino, Jason Roberts, Edoardo Savarino, Janice Freeman, Paul Nietert, Radu Tutuian, and Donald O. Castell. "M1153 Distal Esophageal Spasm Revisited - Which Spasm is a Spasm?" Gastroenterology 138, no. 5 (May 2010): S—343. http://dx.doi.org/10.1016/s0016-5085(10)61579-x.

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Barajas, Ramon F., John Chi, Lanjun Guo, and Nicholas Barbaro. "MICROVASCULAR DECOMPRESSION IN HEMIFACIAL SPASM RESULTING FROM A CEREBELLOPONTINE ANGLE LIPOMA." Neurosurgery 63, no. 4 (October 1, 2008): E815—E816. http://dx.doi.org/10.1227/01.neu.0000325734.30302.97.

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ABSTRACT OBJECTIVE Hemifacial spasm caused by a cerebellopontine angle lipoma is extremely rare. We describe a patient with left-sided hemifacial spasm caused by vascular compression of the facial and vestibulocochlear cranial nerves by the anteroinferior cerebellar artery embedded within a cerebellopontine angle lipoma. CLINICAL PRESENTATION A 77-year-old man presented with a 10-year history of left-sided facial spasms that progressively worsened over time and significantly interfered with his ability to read, drive, and interact in social situations. Neurological examination showed obvious left hemifacial spasm, including orbicularis oculi and levator labii muscles. Magnetic resonance imaging revealed characteristic abnormal signal within the cerebellopontine angle cistern that was consistent with lipoma abutting the anteroinferior cerebellar artery. INTERVENTION Surgical exploration with standard retrosigmoid craniectomy and subarachnoid dissection of the cerebellopontine angle was performed. The offending anteroinferior cerebellar artery branch was dissected away from the VIIth and VIIIth cranial nerves. Teflon felt was interposed between the artery and nerves after the artery was dissected off the surface of the lipoma. Electrophysiological monitoring showed resolution of the abnormal hemifacial spasm response during the procedure. No attempt was made to resect the lipoma, given the risk to injury of the brainstem and perforating blood vessels. Postoperatively, the patient's symptoms were completely resolved. CONCLUSION This case demonstrates that relief of the vascular compression, when present, of the VIIth cranial nerve is sufficient for resolution of hemifacial spasm symptoms, even when associated with nearby, benign lesions.
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Hu, Amanda, Murray Morrison, and Christopher R. Honey. "Hemi-laryngopharyngeal Spasm (HeLPS): Defining a New Clinical Entity." Annals of Otology, Rhinology & Laryngology 129, no. 9 (April 21, 2020): 849–55. http://dx.doi.org/10.1177/0003489420916207.

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Objective: Hemi-laryngopharyngeal spasm (HeLPS) has recently been described in the neurosurgical literature as a cause of intermittent laryngopharyngeal spasm and cough due to vascular compression of the vagus nerve at the cerebellopontine angle. We present the diagnostic criteria for this syndrome. Methods: A retrospective chart review of six patients with HeLPS and three patients misdiagnosed with this condition are presented. All patients were diagnosed and treated at a tertiary care academic centre from July 2013 to July 2017. Results: Patients with HeLPS had five defining characteristics: 1) All patients had symptoms of episodic laryngopharyngeal spasm and coughing. Patients were asymptomatic between episodes and were refractory to speech therapy and reflux management. 2) Laryngoscopy showed hyperactive twitching of the ipsilateral vocal fold in two of the six patients. No other inter-episodic abnormalities were seen. 3) Botulinum toxin A injections into the thyroarytenoid muscle on the affected ipsilateral side reduced laryngopharyngeal spasms. Botulinum toxin injection in the contralateral thyroarytenoid muscle did not improve laryngopharyngeal spasm. 4) Magnetic resonance imaging revealed ipsilateral neurovascular compression of the vagus nerve rootlets by the posterior inferior cerebellar artery. 5) Microvascular decompression (MVD) surgery of the ipsilateral vagus nerve resolved all symptoms (follow-up 2-4 years). Conclusion: The diagnostic criteria for hemi-laryngopharyngeal spasm (HeLPS) are proposed. Otolaryngology recognition of this new clinical entity may lead to a surgical cure and avoid the unnecessary therapies associated with misdiagnosis. Level of Evidence: 4
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Panda, Akhila Kumar, Godhavarma Gopinath, and Shaily Singh. "Parry-Romberg syndrome with hemimasticatory spasm in pregnancy; A dystonia mimic." Journal of Neurosciences in Rural Practice 5, no. 02 (April 2014): 184–86. http://dx.doi.org/10.4103/0976-3147.131675.

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ABSTRACTParry-Romberg syndrome (PRS) with hemimasticatory spasm (HMS) is quite an uncommon overlapping phenomenon which very often mimics jaw closing dystonia. A previously healthy 35-year-old female, during her 5 th month of pregnancy started developing intermittent unilateral painful spasms of jaw while conversation, clinching of teeth, or eating, which led to frequent tongue bites. The spasms were worsened during pregnancy. She used to do certain manoeuvre like sensory tricks in form of touching involved side of the face to relieve the symptoms. Apart from this, she developed progressive hemifacial and hemitongue atrophy. Other medical and neurological examinations were normal. Laboratory investigations as well as neuroimaging were noncontributory. The spasm responded to carbamazepine but hemifacial atrophy persists. To our best knowledge, onset and worsening of this syndrome in pregnancy has not been described earlier which might be correlated either with some hormonal imbalance or some unknown mechanisms.
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Bastola, P., M. Chaudhary, J. P. Agrawal, and D. N. Shah. "The role of the injection Botulinum Toxin A in cases of Essential Blepharospasm Syndrome, Hemifacial Spasm and Meige’s Syndrome." Kathmandu University Medical Journal 8, no. 3 (June 3, 2012): 305–10. http://dx.doi.org/10.3126/kumj.v8i3.6217.

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Background Benign Essential Blepharospasm Symdrome is a neuropathologic disorder. The cause of blepharospasm is multifactorial. It is unlikely that a single defect in this elusive control centre is the primary cause of this disease. Objectives To evaluate the role of botulinum toxin A in treating cases of Essential Blepharospasm Symdrome, Hemifacial Spasm and Meige’s Syndrome, and to assess orbicularis oculi muscle post treatment, in the patients who attended neuro-ophthalmology clinic and the general outpatient department of BP Koirala Lions Centre for Ophthalmic studies. Methods A prospective, interventional study was carried out on all the patients of Essential Blepharospasm Symdrome, Hemifacial Spasm and Meige’s syndrome who underwent treatment with botulinum toxin A in BP Koirala Lions Centre for Ophthalmic studies during a study period of one and half years. Pre- treatment grading of the spasm was done with Jankovic spasm grading and post treatment response was seen with assessment of orbicularis oculi muscle and improvement in functional impairment scale. Relevant findings were noted. Results A total of 40 cases were enrolled in the study. The mean Jankovic spasm grading in cases of essential blepharospasm, hemifacial spasm and Meige’s syndrome was 3.61 (±Standard deviation 0.50, range 3-4), 3.21 (±Standard deviation 0.63, range 2-4) and 3.67 (+- Standard deviation 0.57, range 3-4) respectively. The mean value for reappearance of significant spasms (in months) in cases of essential blepharospasm, hemifacial spasm and Meige’s syndrome was 4.3 (± Standard deviation 1.6, range 2.0-6.5), 5.8 (±Standard deviation 1.4, range 3-8) and 4.5 (± Std.deviation 2.8, range 2.5-6.5) respectively. Blepharoptosis was the commonest complication accounting for 66.6% of the complications.Conclusions The movement disorders like Essential Blepharospasm, Hemifacial Hpasm and Meige’s syndrome are treated by different modalities. An acceptable and effective treatment modality has been a long felt need in these cases. Our study has shown that injection of botulinum toxin A has been a safe and effective method of treating these cases in Nepal.DOI: http://dx.doi.org/10.3126/kumj.v8i3.6217 Kathmandu Univ Med J 2010;8(3):305-10
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Chandra, Mahua, Narayan Saha, SK Azimul Hoque, Provat Kumar Sarkar, Shameem Ara Begum, and Banita Mistry. "Clinical and Laboratory Profiles of Children with West Syndrome: Experience of 50 Cases in a Tertiary Hospital in Bangladesh." Bangladesh Journal of Child Health 44, no. 3 (March 29, 2021): 139–42. http://dx.doi.org/10.3329/bjch.v44i3.52704.

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Background: West Syndrome (WS) consists of epileptic spasms, hypsarrhythmia on EEG and psychomotor delay or regression in children. Objective: To observe the clinical and laboratory profiles of children with west syndrome. Materials & Methods: This was a cross sectional study and done from July 2017 to June 2018 in Pediatric Neurology OPD, NINS among total 50 cases of WS (age of > 2 month to 2 years). WS was diagnosed by direct observation or video recording of spasm, along with history of developmental delay or regression and EEG change. Collected data regarding demography, detailed of spasm, clinical examination, radiological and EEG findings were analyzed. Results: Mean age of the patients was 12.61 ± 7.11 months. Males (58.0%) were predominant than females (42.0%). Mean age of onset of spasm was 5.88 ± 3.73 months. Type of spasm: Flexor in 88.0% cases, extensor in 6.0% cases, mixed in 4.0% and asymmetric in 2.0%. Microcephaly was present in 90.0% cases and in 64% cases H/o perinatal asphyxia (PNA) was present. In EEG, Hypsarrhythmia was found in 62.0% cases and modified hypsarrhythmia in 38.0% cases. In CT scan of brain, cerebral atrophy was found in 62.5.0% cases, stroke in 6.0% cases. Out of all WS patients 82% were symptomatic and 18% were either cryptogenic or idiopathic. Conclusion: Flexor type spasm was found more commonly in West syndrome. History of perinatal asphyxia (PNA) was present in majority of cases. In EEG findings, hypsarrhythmia was found more than modified hypsarrhythmia. Bangladesh J Child Health 2020; VOL 44 (3) :139-142
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30

Barahona-Hernando, R., ML Cuadrado, S. García-Ptacek, A. Marcos-de-Vega, M. Jorquera, A. Guerrero, CM Ordás, S. Muñiz, and J. Porta-Etessam. "Migraine-triggered hemifacial spasm: three new cases." Cephalalgia 32, no. 4 (March 2012): 346–49. http://dx.doi.org/10.1177/0333102412438976.

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Background: The occurrence of hemifacial spasm (HFS) during an episode of migraine has been seldom reported. Here we describe three new cases presenting with HFS in association with migraine attacks. Case results: Three patients (one woman and two men, aged 31–36 years) developed HFS in close temporal relationship with migraine headaches. All of them started having the muscle spasms after pain onset. Two of them had electromyographic evidence of facial nerve damage, and continued having HFS once the pain abated. Conclusions: Migraine attacks may be associated with HFS. The appearance of HFS could be related to migraine activity. A mechanism of central hyperexcitability in connection with nociceptive inputs on the trigeminal nucleus caudalis and/or a dilation of vessels compressing the facial nerve at the root exit zone could lead to the development of HFS in predisposed patients. ‘Migraine-triggered hemifacial spasm’ could possibly be regarded as a complication of migraine.
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31

Armstrong, Dallas, and Rana R. Said. "Outcomes of High-Dose Steroid Therapy for Infantile Spasms in Children With Trisomy 21." Journal of Child Neurology 34, no. 11 (May 22, 2019): 646–52. http://dx.doi.org/10.1177/0883073819850650.

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Objective: We performed a retrospective chart review of patients with trisomy 21 and infantile spasms in our university-based pediatric epilepsy center between 2002 and 2016 in order to describe the clinical characteristics of children with these diagnoses as well as to evaluate their response to first-line treatments. Methods: Patients with infantile spasms were identified via the neurophysiology database. Charts were reviewed with attention to infantile spasms diagnosis, presence of trisomy 21, age of reported clinical onset, treatment lag, treatments used, response to treatment, imaging findings, electroencephalography (EEG) data, and developmental outcomes. Results: Of the 310 patients with infantile spasms, 24 also had trisomy 21. Three patients did not meet inclusion criteria. Ten of the 21 patients received nonstandard therapies first line; 2 of the 10 (20%) achieved spasm control, and 4 of the 8 who failed therapy (50%) progressed to Lennox-Gastaut syndrome. Eleven of the 21 patients received standard therapies as first-line treatments (10 with prednisolone according to the protocol in the United Kingdom Infantile Spasms Study [UKISS] and 1 with adrenocorticotrophic hormone [ACTH]). Nine of the 10 patients (90%) who received prednisolone achieved spasm resolution, 6 (60%) of these without relapse. The final patient (10%) failed prednisolone as well as ACTH. One patient received ACTH first line with success. Conclusion: This is the only series to follow children with trisomy 21 and infantile spasms in which a significant proportion received UKISS-protocol prednisolone. It adds to current knowledge about safety, tolerability, and effectiveness of prednisolone in this group.
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32

Zalyalova, Z. A. "Hemifacial spasm." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 120, no. 8 (2020): 140. http://dx.doi.org/10.17116/jnevro2020120081140.

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33

Crozier, Robert E., Richard C. T. Dai, F. Henry Ellis, S. Peter Gibb, and Kathleen R. Micheli. "Esophageal spasm." Postgraduate Medicine 80, no. 6 (November 1986): 73–78. http://dx.doi.org/10.1080/00325481.1986.11699590.

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34

Geist, Michael, and Daniel Tarchitzky. "Coronary Spasm." New England Journal of Medicine 346, no. 8 (February 21, 2002): 579. http://dx.doi.org/10.1056/nejmicm010757.

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35

Perkin, G. D. "Hemifacial spasm." Journal of Neurology, Neurosurgery & Psychiatry 57, no. 3 (March 1, 1994): 284. http://dx.doi.org/10.1136/jnnp.57.3.284.

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36

Maroun, F., J. Jacob, and M. Mangan. "Hemifacial spasm." Neurosurgery 20, no. 6 (June 1987): 994???5. http://dx.doi.org/10.1097/00006123-198706000-00033.

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37

VANDERSPEK, A. F. L., and N. WILTON. "SUXAMETHONIUM SPASM." British Journal of Anaesthesia 57, no. 3 (March 1985): 353–54. http://dx.doi.org/10.1093/bja/57.3.353.

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38

ELLIS, F. RICHARD, and P. JANE HALSALL. "SUXAMETHONIUM SPASM." British Journal of Anaesthesia 57, no. 3 (March 1985): 354. http://dx.doi.org/10.1093/bja/57.3.354.

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39

Palacios, Enrique, Jack Breaux, and Jorge E. Alvernia. "Hemifacial Spasm." Ear, Nose & Throat Journal 87, no. 7 (July 2008): 368–70. http://dx.doi.org/10.1177/014556130808700704.

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40

Johnson, Ernest W. "Spasm—Revisited." American Journal of Physical Medicine & Rehabilitation 80, no. 11 (November 2001): 797. http://dx.doi.org/10.1097/00002060-200111000-00001.

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41

Tankéré, F., T. Maisonobe, I. Bernat, G. Lamas, J. Soudant, E. Vitte, P. Bouche, E. Fournier, and J. C. Willer. "Hemifacial Spasm." Otology & Neurotology 23, Sup 1 (2002): S68. http://dx.doi.org/10.1097/00129492-200200001-00173.

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Magnan, Jacques. "Hemifacial Spasm." Otology & Neurotology 23, Sup 1 (2002): S68—S69. http://dx.doi.org/10.1097/00129492-200200001-00175.

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43

Moller, Aage R. "Hemifacial Spasm." Otology & Neurotology 23, Sup 1 (2002): S70. http://dx.doi.org/10.1097/00129492-200200001-00180.

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44

DiPalma, Jack A., and Charles E. Brady. "Steakhouse Spasm." Journal of Clinical Gastroenterology 9, no. 3 (June 1987): 274–78. http://dx.doi.org/10.1097/00004836-198706000-00006.

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REIGOSA, R. P., and J. P. RIOS. "Hemifacial spasm." Journal of Neurology, Neurosurgery & Psychiatry 64, no. 5 (May 1, 1998): 687. http://dx.doi.org/10.1136/jnnp.64.5.687.

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JANNETTA, P. J., A. KASSAM;, and R. P. REIGOSA. "Hemifacial spasm." Journal of Neurology, Neurosurgery & Psychiatry 66, no. 2 (February 1, 1999): 255a—256a. http://dx.doi.org/10.1136/jnnp.66.2.255a.

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Garland, Paul E., James R. Patrinely, and Richard L. Anderson. "Hemifacial Spasm." Ophthalmology 94, no. 3 (March 1987): 288–94. http://dx.doi.org/10.1016/s0161-6420(87)33458-x.

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48

GILBERTSON, A. A. "LARYNGEAL SPASM." British Journal of Anaesthesia 71, no. 1 (July 1993): 168–69. http://dx.doi.org/10.1093/bja/71.1.168-b.

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LANGTON, J. A. "LARYNGEAL SPASM." British Journal of Anaesthesia 71, no. 1 (July 1993): 169. http://dx.doi.org/10.1093/bja/71.1.169.

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50

Wilkins, Robert H. "Hemifacial Spasm." Contemporary Neurosurgery 13, no. 6 (1991): 1. http://dx.doi.org/10.1097/00029679-199113060-00001.

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