Academic literature on the topic 'Spasm'
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Journal articles on the topic "Spasm"
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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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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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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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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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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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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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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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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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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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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.
Dissertations / Theses on the topic "Spasm"
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Литвиненко, С. С., and О. Б. Масич. "Вивчення протисудомної дії похідного 2-оксоіндолін-3-гліоксилової кислоти." Thesis, Сумський державний університет, 2015. http://essuir.sumdu.edu.ua/handle/123456789/41536.
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Ekelund, Anders. "Detection and haemodilutive treatment of cerebral arterial vasospasm and delayed ischaemia after aneurysmal subarachnoid haemorrhage." Lund : Lund University, 1999. http://catalog.hathitrust.org/api/volumes/oclc/68945106.html.
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Hamawy, Majed Mahmood. "Antigen induced modulation of autonomic nervous system responses in immunoglobulin-E - sensitized rabbit lung." Diss., The University of Arizona, 1988. http://hdl.handle.net/10150/184590.
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The major objective of this project was to examine the potential for mediators of IgE-mediated allergic reactions to alter neural activity. The project was divided into three parts. In Part I, the ability of endogenously released chemical mediators to alter neural activity in vitro was assessed by measuring isometric contractile responses to electrical field stimulation (EFS) (2-128 Hz, 20 V, 0.5 msec. duration) of sensitized rabbit bronchi before and after exposure to the antigen horseradish peroxidase (HRP). Antigen enhanced bronchial responses to EFS with low frequencies: mean log (± S.E.) frequency which produced 20% of maximum response decreased from 1.04 (± 0.05) to 0.90 (± 0.07) Hz (p < 0.05). Responses of unsensitized bronchi were not enhanced by antigen. Chlorpheniramine, an H₁ antagonist, abolished the antigen effect. Antigen did not enhance the responses to exogenous acetylcholine. Hence, the antigen is apparently modulating neural activity and not smooth muscle per se. In Part II, the capacity for histamine to modulate vagally-induced bronchoconstriction in anesthetized, vagotomized, mechanically-ventilated rabbits was examined in vivo. Changes in pulmonary resistance induced by electrically stimulating the cut ends of the vagi (2-32 Hz, 20 V, 0.5 msec. duration) were assessed before and 10 minutes after histamine aerosolization (10 breaths of 10 mg/ml). Histamine inhalation potentiated vagally-induced bronchoconstriction at low frequencies: mean log (± S.E.) frequency producing a 20% change in pulmonary resistance decreased from 0.88 (± 0.09) to 0.56 (± 0.15) (p < 0.05). Chlorpheniramine abolished this effect. In Part III, the dependence on IgE antibodies of the in vitro modulation of neurally-induced contraction of sensitized bronchi was investigated. Rabbits were passively immunized with fractions enriched with HRP-specific IgE, IgG, or IgM antibodies. After 72 hours, rabbits were sacrificed and the responses of bronchi to EFS were assessed before and after antigen challenge. Antigen enhanced the responses to EFS only of bronchi passively sensitized with IgE. Therefore, antigen enhancement of neural activity was dependent on IgE. These studies demonstrate that the interaction between antigen and IgE antibodies can induce the release of chemical mediators which can alter neural activity.
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Pyne, Gail Jean. "Vascular smooth muscle oxidative metabolism and function during vasospasm after subarachnoid haemorrhage." Thesis, University of Oxford, 1999. http://ora.ox.ac.uk/objects/uuid:a6b78de5-1f66-4225-992e-e490cf68d0e8.
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Aims: The purpose of the research presented in this thesis is to elucidate the mechanism of the stimulation of oxidative metabolism and contractile function that occurs in vascular smooth muscle during cerebral vasospasm (CV) after subarachnoid haemorrhage (SAH). The biochemical mechanisms leading to CV were investigated using an in vitro model of CV developed for this research. CSF (cerebrospinal fluid) from SAH patients at risk of vasospasm which stimulated oxygen consumption (CSF S ) was used to model vasospasm. The hypothesis is CSFS contains a substance which stimulates tension generation over that of CSFN ,(non-stimulatory cerebrospinal fluid) and also inhibits the myosin light chain phosphatase. Methods: The porcine carotid artery was used as a model for the human basilar artery. The rate of oxygen consumption (JO2) was measured in response to CSFS and tension generation was also examined. Various agents were used to treat or pretreat the tissue such as magnesium and andalpha;1-adrenergic receptor agonists. Their effects on the CSFS-induced stimulation were measured to study the mechanism of vasospasm. A myosin light chain phosphatase (MLCP) assay was developed to study the mechanisms leading to CV. Results and conclusion: Addition of CSFS to the porcine carotid artery is a reliable and reproducible in vitro model of CV. Using this model, it was found that Mg++ loading and andalpha;1-adrenergic receptor agonists attenuated the vasospasm, but a non-specific endothelin antagonist had no effect. Acute addition of 12mM Mg++ relaxed the tissue from a CSFS induced contraction significantly and rendered the contraction rinsible. Okadaic acid (InM), a phosphatase inhibitor, had very similar effects to CSFS because it stimulated JO2 and slowed relaxation after a stretch. There was also significant inhibition of phosphatase caused by the CSFS. Vasospasm appears to be caused by a combination of a contractile stimulus, and inhibition of MLCP activity.
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Reissing, Elke D. "Re-evaluating vaginismus : an empirical investigation of diagnostic reliability, vaginal spasm, pain, and associated etiological correlates." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38514.
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Vaginismus is a sexual dysfunction that has received insufficient empirical attention. The first chapter of this thesis consists of a critical review of the literature and demonstrates the overall paucity of research studies and their poor methodological quality. The second and third chapter are based on the results of an experimental study comparing 87 women, matched on age, relationship status, and parity and assigned to 3 groups, vaginismus, dyspareunia/vulvar vestibulitis syndrome (VVS), and no pain. A structured interview evaluating pain with intercourse and history of gynecological problems as well as psychometric measures; evaluating sexual and physical abuse, sexual knowledge and schema, sexual functioning, relationship adjustment and psychological distress were administered. The reliability of vaginal muscle spasm as the main diagnostic criterion, differential diagnosis, and the role of pain were assessed via by 2 separate gynecological and, 2 separate physical therapist examination, 2 EMG evaluations, and a review of the interview data by 2 separate psychologists. Findings suggest that the spasm-based definition and resulting diagnostic reliability of vaginismus are not adequate. Both, women in the vaginismus and VVS groups exhibited higher levels of pelvic floor hypertonicity compared to women with no pain; however, women in the vaginismus group demonstrated the highest levels. Measures of pain did not distinguish between women with vaginismus and VVS. The only dependent measure clearly differentiating women with vaginismus was defensive and avoidant reactions during the physical exams. A re-conceptualization based on a multidimensional diagnostic framework including pelvic floor hypertonicity, avoidance and defensive reactions to vaginal penetration, and genital pain was suggested. The third paper was based on the results of questionnaires investigating etiological correlates of vaginismus, sexual and physical abuse, sexual self-schema, sexual knowled
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Adlam, Timothy. "The design of compliant seating for children with severe whole body extensor spasms." Thesis, University of Bath, 2012. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.582535.
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Children with cerebral palsy and powerful whole body extensor spasms find sitting in a rigid seat uncomfortable and sometimes painful due to the large forces they apply to their constraints. They are usually unable to speak and communication is difficult. The spasms affect every aspect of their lives. This thesis describes the genesis of a new functional dynamic seat for children with severe whole body extensor spasms, and the novel method used to design it. This novel seat technology is known as ‘Whole Body Dynamic Seating’. The thesis describes the clinical need this seat addresses, and the design and technology context in which this research takes place. The user evaluation, observation, measurement, analysis and reasoning that led to a successful seat design are described in detail. Children with cerebral palsy sometimes have whole body spasms that mean they cannot be seated in conventional static seating that positions a child in a fixed posture. For this research the children were classified as functioning at Chailey Sitting Ability Level 1 and Gross Motor Functional Classification System Level V. Such children spend much of their time being held by a person, or lying on a mat, bed or pad. This results in difficulty with social engagement and physical functioning, particularly in school. This research created a seat that such children could sit in, providing a comfortable and functional seat for use in a home or school classroom environment. This seat was designed with the direct and essential involvement of disabled children, their parents, therapists, teachers and carers. The work is part of a larger programme of research into seating and support technology that will enhance a child’s ability to gain functional movement and communication skills that can be employed to enable the child’s free self expression and social participation. The research investigated means of supporting children with whole body extensor spasms through a progressive iterative method utilizing direct user evaluation of a series of prototypes incrementing in complexity and fidelity towards a fully functional physical seat. An iterative method was used to design, build and evaluate three dynamic seats. This method incorporated two new approaches to prototyping developed for the research programme in response to difficulties encountered in designing dynamic systems for children with highly complex neuromotor disability. Soft and Semi-soft prototyping and evaluation methods provided essential feedback on dynamic seating concepts that guided proposed solutions, without requiring costly and time-consuming manufacture. Video was used to create a record of the children’s movements and responses for subsequent analysis. Instrumentation was built into the seats to enable direct objective measurement of the reaction forces and seat movement caused by extensor spasms. This thesis presents several unique features created through this research programme: 1. Independent and virtually hinged anatomical dynamic thigh supports; 2. Independent anatomical dynamic foot supports; 3. A virtually hinged dynamic back support; 4. An anatomical dynamic head support concept. The final Whole Body Dynamic Seat was child-centred in its functionality and aesthetic design, and was favourably commented upon by parents, children and school staff. Use of the new dynamic seating by three children (including one from a previous work programme) showed that children with severe whole body extensor spasms can be seated comfortably. The children also demonstrated gains in physical and social function as a result of using the dynamic seats. The two fully independent dynamic seats made advances in comfort over static seating for children with whole body extensor spasms. One of the children especially liked the seat and resisted being put back into his usual seating. An adult with severe cerebral palsy and extensor spasms evaluated a dynamic foot support concept and reported very significant reductions in spasticity and pain, and gains in physical function. The Whole Body Dynamic Seats showed gains in postural symmetry and in hand and head function over the usual static seats when used by the children with spasms. These gains were reported by staff during long term evaluations and measured specifically during the final evaluation. Two children learned to control the movement of seats in which they were sat, and were able to control their posture and use that control to carry out functions such as switch pressing. Such learning through the use of dynamic seating by children with severe dystonic cerebral palsy and whole body extensor spasms has not previously been documented. The seats did not just affect the children - school staff were affected too. School staff working around the children in the dynamic seats were observed to be more inclusive towards the children, and to expect more interaction from them. The ability of the children to move altered staff expectations of their ability to participate and communicate. This new seating has improved the quality of life of the children that use it. Future implementation of this technology in commercially produced seating offers the possibility of similar gains to many more severely disabled children who are currently less comfortable and less functional than they need to be.
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Вастьянов, Р. С., Ю. С. Крепец, and А. С. Авраменко. "Пригнічення судомної активності при блокуванні цитокінових рецепторів." Thesis, Сумський державний університет, 2017. http://essuir.sumdu.edu.ua/handle/123456789/64459.
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Вступ. За даними низки експериментальних досліджень та клінічних спостережень висунуто припущення про патогенетичну роль цитокін-індукованого запалення, а також широкої групи представників цитокінів та факторів росту у формуванні судомного синдрому. Ці ствердження підсилювалися через виявлені просудомні ефекти цитокінів, які спричиняють прозапальну та просудомні дію. З цього приводу логічним постає інше припущення стосовно можливої реалізації протисудомної дії за умов блокади активності прозапальних цитокінів. Метою серії наших дослідів було визначення ефектів блокування активності рецепторів інтерлейкін-1 (ІЛ-1) при різних формах експериментального судомного синдрому.
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Silva, José Luis Costa Guedes da. "Efeitos da laqueação proximal dos vasos curtos e da fundoplicatura total sobre a microcirculação do fundo gástrico : estudo microvascular em cobaias." Doctoral thesis, Faculdade de Ciências Médicas, 2013. http://hdl.handle.net/10362/11454.
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RESUMO: A operação de Nissen, por laparoscopia, é considerada a cirurgia antirefluxo mais adequada por ser a que melhor replica a fisiologia normal da válvula gastresofágica na maioria dos doentes com sintomas típicos de doença do refluxo gastresofágico (DRGE). São critérios técnicos o encerramento seguro dos pilares do diafragma e a criação de fundoplicatura completa (360 graus), curta (inferior a dois centímetros), lassa e sem tensão – desiderando para o qual a laqueação proximal dos vasos curtos gástricos é crucial.
Realizei a operação de Nissen, por laparoscopia, em sessenta mulheres e quarenta
homens com DRGE, sem mortalidade operatória, no Serviço de Cirurgia 6 do Hospital dos Capuchos, CHLC, EPE. Os cem doentes apresentavam média etária de 46 anos e
queixas, com tempo de evolução entre 1 e 43 anos, de pirose (90%), regurgitação
(80%), azia (73%), epigastralgias (54%). A endoscopia alta revelou esofagite de grau
Savary-Miller 0-I (62%), II (23%), III (8%), IV (7%); hérnia de deslizamento (71%),
hérnia paraesofágica (8%), sem hérnia (21%); a pHmetria de 24h diagnosticou padrão
misto (38%), levantado (20%), deitado (20%), inconclusiva (22%) e a manometria
diagnosticou EEI hipotónico (35%), peristálise esofágica normal (88%), hipomotilidade ligeira (5%) e foi omissa (7%). Hérnia hiatal, esofagite grave, ineficácia do controlo sintomático com inibidor da bomba de protões e desejo de descontinuidade terapêutica constituíram as indicações para tratamento cirúrgico. Por celioscopia, efetuei laqueação dos vasos curtos gástricos (70%), cruroplastia e fundoplicatura total (seda 2/0), curta
(dimensão média 1,5-2 cm), lassa, sem tensão e sem calibração intraoperatória do
esófago. A fundoplicatura de Nissen laparoscópica mostrou-se segura e eficaz no tratamento da DRGE. A sua idoneidade foi ainda comprovada pela normalização da pHmetria de 24 horas e da manometria pós-operatórias, com significado estatístico, num grupo de catorze voluntários assintomáticos. Em catamnese com recuo médio 30,7 meses 94% dos indivíduos persistem assintomáticos. Interrogando-me acerca das repercussões desta operação sobre a microcirculação do fundo gástrico coloquei, como premissa, a possibilidade de na operação de Nissen a laqueação dos vasos curtos poder induzir modificação no diâmetro arteriolar da parede do fundo gástrico. Para pesquisar a influência da laqueação dos vasos curtos gástricos e da fundoplicatura total sobre o calibre arteriolar da parede do estômago no cárdia, no fundo e na região dos vasos curtos gástricos, idealizei um Projeto de investigação experimental em cobaias. O Projeto foi desenvolvido no Centro de Investigação do Departamento de Anatomia da FCM-UNL. Para a sua realização obtive autorização da Comissão Científica e
Pedagógica da FCM-UNL, requeri a acreditação como investigador à Direção Geral de
Veterinária e, por recorrer à utilização de animais, submeti-o à Comissão de Ética da
FCM-UNL, que o aprovou por unanimidade.
Para limitar o número de animais utilizados ao mínimo necessário, calculei, por método
estatístico, a quantidade de cobaias necessárias. Subdividindo-as num grupo de ensaio (GE), onde realizei a operação de Nissen, e num grupo de controlo (GC), onde apenas procedi a tração gástrica, defini e apliquei protocolos de anestesia, de cirurgia e de eutanásia, segundo os princípios dos 3R – Replacement, Reduction, Refinement da técnica de experimentação humana de Russell e Burch (1959) – uma estrutura ética amplamente aceite para a realização de experimentação científica humanizada com animais.
A utilização das técnicas de estudo angiomorfológico permitiu-me analisar e descrever a anatomia normal, a vascularização arterial macroscópica, a microangioarquitetura, por microscopia eletrónica de varrimento de moldes de corrosão vascular, e a histologia da
parede do estômago da cobaia. Procedi, também, à definição dos critérios morfológicos que considerei suscetíveis de validação deste modelo animal para o estudo proposto. Por razões académicas, foi necessário abreviar o Projeto encurtando, em cerca de dois anos, o prazo disponível para conclusão do estudo. Apreciando-o com o Gabinete de Análise Epidemiológica e Estatística do Centro de Investigação do CHLC, EPE, optou-se, perante a escassez de elementos após já terem sido recrutados 46 animais, por uma amostra, suplementar, de dimensão de conveniência de oito cobaias (quatro em cada grupo), condicionada pelo limite temporal universitário e pelo respeito pela dignidade dos animais. Neste subgrupo procedi, por microscopia eletrónica de varrimento, à medição dos calibres arteriolares nos moldes vasculares do cárdia, do fundo e da zona dos vasos curtos gástricos tanto no GC como no GE efetuando 469 medições no primeiro e 461 no último.
Os dados foram enviados ao Centro de Investigação do CHLC, EPE que procedeu à sua
análise estatística (ANOVA). A referida análise revelou que as arteríolas do plexo
mucoso e as do plexo submucoso do cárdia, do fundo e da região dos vasos curtos
gástricos, mostraram aumento de calibre no GE. O aumento foi, estatisticamente,
significativo por ser superior a 50% do calibre do GC. Nos vasos curtos, a diferença foi mais pequena, mas persistiu sendo, estatisticamente, significativa. Os vasos retos dilataram na base, na sua emergência do plexo seroso, apenas no fundo gástrico.
Na cobaia a operação de Nissen – fundoplicatura total com laqueação dos vasos curtos gástricos –, provocou vasodilatação arteriolar do fundo gástrico. Considero que essa vasodilatação constituiu acomodação à modificação introduzida e infiro que o mesmo
possa acontecer no ser humano. Admito, assim, que também ocorra vasodilatação no ser
humano, na sequência da laqueação dos vasos curtos gástricos, pela analogia
microvascular entre as duas espécies e que essa vasodilatação corresponda, igualmente,
a um mecanismo de adaptação arteriolar visando, por exemplo, suprir a perda incorrida pela laqueação. A associação experimental entre laqueação dos vasos curtos gástricos e realização de
fundoplicatura total, que exerce aumento inerente de pressão sobre a JEG, não só não
provocou défice da microcirculação do esófago distal ou do estômago proximal como
desencadeou um mecanismo de vasodilatação fúndica que reforça o conceito de
segurança da operação de Nissen para tratamento da DRGE. -------------- ABSTRACT: The laparoscopic Nissen operation is considered to be the most appropriate antirefluxsurgery because it suitably replicates the standard physiology of the gastroesophageal valve in most patients with typical symptoms of gastroesophageal reflux disease (GERD). The technical criteria includes the safe shutdown of the diafragmatic crura(cruroplasty) and the creation of a complete fundoplication (360 degrees), short (lesser than two inches), floppy and without tension – a goal for which the proximal ligation of the gastric short vessels is crucial. The laparoscopic Nissen operation was performed in sixty women and forty men with GERD, without any operative mortality, at the Surgical Department of the Hospital dos Capuchos, CHLC, EPE. The one hundred patients, averaged 46 years old, complained
of heartburn (90%), regurgitation (80%) and upper abdominal pain (54 %). The endoscopy process revealed Savary-Miller esophagitis of grade 0-I (62%), II (23%), III (8%), IV (7%), sliding hernia (71%), paraesophageal hernia (8%) or no herniation (21%). The pHmetry/24h diagnosed mixed pattern (38%), raised (20%), lying (20%) or inconclusive (22%). The manometry diagnosed hypotensive LES (35%), normal esophageal peristalsis (88%), mild hypomotility (5%) and was absent (7%). Hiatal hernia, severe esophagitis, ineffective symptomatic control with proton pump inhibitor and request for treatment discontinuation were the signs for surgical action. A laparoscopic ligation of short gastric vessels (70%), cruroplasty and fundoplication (silk 2/0), short (average size 1.5–2 cm) and floppy, without tension and without intraoperative calibration of the esophagus were thus performed.
The laparoscopic Nissen fundoplication behaved safe and effective in treating GERD. In a group of 14 asymptomatic volunteers its reputation was confirmed with statistical
significance by normalization of postoperative pHmetry/24h and manometry. 94% of the individuals remained asymptomatic up to 30.7 months (average) in the follow-up.
Interrogating myself about the impact of this operation on the microcirculation of the
gastric fundus I put premised on the possibility of the ligation of the short gastric vessels in the Nissen procedure can induce changes in the arteriolar diameter in the Wall of the gastric fundus. To explore the influence of ligation of the short gastric vessels and the fundoplication at
the arteriolar caliber of the cardia, the fundus and the region of the short vessels of the gastric wall, I designed a project of experimental research in guinea pigs with two
interdependent components: one veterinary and another technical where I applied
angiomorphological studies. The project was developed at the Research Centre of the Department of Anatomy FCMUNL. For its accomplishment I got permission from the Scientific and Pedagogical Committee of the FCM-UNL, I requested for accreditation as a researcher at the General Directorate of Veterinary and, by resorting to the use of animals I submitted it to the Ethics Committee of the FCM-UNL, which approved it unanimously. The guinea pigs were divided into two experimental groups: an experimental group (EG), in which the Nissen procedure was performed and a control group (CG) in which only a gastric traction was done. Protocols of anesthesia, surgery and euthanasia were applied according to the 3Rs – Replacement, Reduction, Refinement of the technique of human experimentation of Burch and Russell (1959) – a widely accepted ethical framework for conducting scientific experiments using animals humanely. Using histological and angiomorphological techniques, I performed the analysis and the
description of the normal, macro and microvascular, anatomy of the guinea pig stomach and I defined the morphological criteria that I considered susceptible for validation of this animal model for the proposed study. By means of scanning electron microscopy I measured the arteriolar calibers of the vascular casts of the cardia, of the fundus and of the short gastric vessels in both CG and EG, making 469 measurements in the former and 461 in the latter. The data were sent to the Research Center of the CHLC which conducted the statistical analysis (ANOVA).
The data were sent to the Centre for Research of the CHLC, EPE which proceeded to
statistical analysis (ANOVA). This analysis revealed that the arterioles plexus of the
mucosal and submucosal plexus of the cardia, fundus and region of the short gastric
vessels, showed increased caliber in EG. The increase was statistically significant for
being greater than 50% CG gauge. In the short gastric vessels, the difference was
smaller, but persisted and statistically significant. Straight vessels were dilated at the base, on its emergence of the plexus serous only in the fundus. In the guinea pig, the Nissen procedure - complete fundoplication with ligation of the
short gastric vessels - caused arteriolar vasodilation on the gastric fundus. I believe that this vasodilation constituted some accommodation to the modification introduced and infer that the same might happen in humans. I admit therefore that vasodilation also occurs in humans following the ligation of the short gastric vessels by microvascular analogy between the two species and that this vasodilation corresponds also to na adaptation mechanism arteriolar, for example, to compensate the loss incurred by ligation. The association of experimental ligation of the short gastric vessels with conducting complete fundoplication, which exerts increased pressure on the EGJ, not only did not
cause a microcirculation deficit of the distal esophagus or proximal stomach as triggered a mechanism of fundic vasodilation which reinforces the security concept of the Nissen procedure for treatment of GERD.
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Gataullina, Svetlana. "Rôle de l’altération des récepteurs de NMDA dans l’épilepsie associée à la Sclérose Tubéreuse de Bourneville étudié sur un modèle animal et le tissu humain." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T009.
Full textAbstract:
La sclérose tubéreuse de Bourneville (STB) est une maladie génétique et multi-systémique à transmission autosomique dominante due à des mutations d’un gène TSC1 ou TSC2 qui codent respectivement pour hamartine et tuberine ayant une action inhibitrice sur la voie de signalisation mTOR. L’épilepsie précoce et pharmacorésistante est la manifestation neurologique la plus fréquente et la plus délétère de la STB. Elle débute souvent dans la première année de vie par des spasmes infantiles qui évoluent avec l’âge et en absence de traitement vers des crises toniques ou tonico-cloniques. Bien que les crises soient supposées être générées dans des tubers corticaux, les mécanismes de l’épilepsie ne sont pas bien élucidés et le traitement reste souvent inefficace. Des études morphologiques ont montré une altération de l’expression ARNm des récepteurs au glutamate dans les cellules géantes et les neurones dysplasiques des tubers, mais leur implication fonctionnelle restait à montrer. Les différentes sous-unités NMDA ont une expression âge-dépendante et région-spécifique, les plus grands changements survenant au début de la vie quand l’épilepsie de la STB apparaît. Ce travail avait pour but d’étudier à l’aide de méthodes électrophysiologiques in vitro et in vivo l’expression fonctionnelle des sous-unités NMDA aberrantes et de déterminer leur rôle dans l’épileptogènese chez les souris hétérozygotes Tsc1+/- et sur le tissu humain STB post-opératoire. Nous avons pu démontrer que : i) Les souris hétérozygotes pour le gène Tsc1 sont spontanément épileptiques in vivo et in vitro dans une courte fenêtre dévelopmentale de P9 à P18. ii) Elles présentent une altération d’expression des récepteurs NMDA couche-spécifique et mTOR dépendante avec une surexpression des sous-unités GluN2C/D dans la couche 4 et 2/3 et GluN2B dans les couches 2/3. Cette expression anormale est prévenue par l’administration d’un inhibiteur de la voie mTOR, la rapamycine. iii) Les mêmes altérations d’expression des récepteurs NMDA, sont montrées sur les tissus post-opératoires, non seulement de tubers de STB mais aussi des dysplasies corticales focales (DCF), ces deux malformations ayant des similarités étiologiques et physiopathologiques. iv) La RT-PCR quantitative confirme une expression excessive de GluN2C dans le cortex de souris Tsc1+/- et sur le tissu humain des tubers et DCF. v) Les décharges épileptiques chez la souris Tsc1+/- sont générées dans la couche granulaire 4 du cortex avant de se propager vers les couches superficielles et les couches profondes, empruntant ainsi les microcircuits corticaux. vi) L’expression excessive de la sous-unité GluN2C dans le cortex contribue à l’hyperexcitabilité neuronale chez la souris Tsc1+/- et sur des tissus humains de tubers et de DCF puisque les crises et les décharges sont bloquées par les antagonistes sélectifs de GluN2C/D. vii) Les crises chez la souris Tsc1+/- suivent une séquence âge-dépendante évoluant du type «spasms-like» vers «tonic-clonic like», rappelant celle de l’épilepsie humaine, avec deux pics de haute incidence de crises à P13 et P16 correspondant chez l’homme respectivement l’âge des spasmes infantiles et celui des crises toniques. L’évolution avec l’âge du délai de propagation inter-hémisphérique pourrait contribuer à ce changement de types de crises. Ces résultats montrent donc pour la première fois qu’une happloinsuffisance pour le gène Tsc1 chez les souris Tsc1+/- sans tubers suffit à produire une altération de l’expression des récepteurs NMDA de manière mTOR dépendante et contribuer ainsi à l’épileptogènese dans la STB. La souris Tsc1+/- est le premier modèle génétique sans anomalies morphologiques présentant une épilepsie spontanée qui évolue des spasmes vers des crises toniques et tonico-cloniques. Néanmoins cette épilepsie diffère de l’épilepsie humaine de la STB par l’absence de crises focales et de pharmacorésistance, ce qui pourrait être expliqué par l’absence de tubers chez la souris Tsc1+/-. (...)Tuberous sclerosis complex (TSC) is a genetic multisystemic disease with autosomal dominant transmission due to mutations in a gene TSC1 or TSC2 respectively which encode hamartin and tuberin proteins having an inhibitory action on the mTOR signaling pathway. Early refractory epilepsy is the most common and most deleterious neurological manifestation. The epilepsy often begins in the first year of life by infantile spasms that change in the lack of treatment to tonic or tonic-clonic seizures in age-dependent manner. Although seizures are thought to be generated in cortical tubers, epilepsy mechanisms are not well understood and treatment is often ineffective. Morphological studies showed the altered expression of glutamate receptor mRNA in the giant cells and dysplastic neurons of tubers, but their functional involvement remains unknown. The different NMDA subunits have an age-dependent and region-specific expression, the greatest changes occurring early in life when the TSC epilepsy appears. This work aimed to study the functional expression of aberrant NMDA subunits expression and their role in the epileptogenesis in heterozygous Tsc1+/- mice and post-surgical human tissue of TSC patients using in vitro and in vivo electrophysiological methods. The study reveal that: i) Heterozygous tuber-free Tsc1+/- mice show spontaneous epilepsy in vivo and in vitro in a short developmental window from P9 to P18. ii) These mice exhibit an altered NMDA receptor expression in mTOR dependent and layer-specific manner with GluN2C/D subunits overexpression in layers 4 and 2/3, and GluN2B ovexpression in layers 2/3. This abnormal NMDA receptors expression is prevented by the administration of an mTOR inhibitor, rapamycin. iii) The same alterations of NMDA receptors’ expression are shown in post-surgical tissues not only in tubers from TSC patients, but also in focal cortical dysplasia (FCD), these two malformations sharing etiological and pathophysiological similarities. iv) Quantitative RT-PCR confirms the excessive GluN2C subunit expression in Tsc1+/- mouse cortex and human tissue of tubers and DCF. v) Epileptic discharges in Tsc1+/- mice are generated in the granular layer 4 of the cortex before spreading to the superficial and then to deep layers, thus borrowing the cortical microcircuits. vi) Excessive expression of GluN2C subunit in the cortex contributes to neuronal hyperexcitability in Tsc1+/- mice, as well as in human tubers and DCF tissues, since epileptic discharges are blocked by selective GluN2C/D antagonists. vii) Seizures in Tsc1+/- mice follow the age-dependent sequence, evolving from "spasms-like" to "tonic-clonic like" thus reminding the human epilepsy, with two peaks of highest seizure incidence at P13 and P16 corresponding respectively to age of infantile spasms and of tonic seizures in human. The age-dependent evolution of interhemispheric propagation delay could contribute to this change in seizure type. These results show for the first time that TSC1 happloinsuffisancy in tuber-free Tsc1+/- mice is sufficient to produce an alteration in NMDA receptor expression in an mTOR dependent manner, and thus contributes to epileptogenesis in TSC. The Tsc1+/- mouse line is the first genetic model of TSC without morphological abnormalities presenting with early spontaneous seizures which evolves from “spasms-like” to “tonic-clonic like” seizures. However, the epilepsy in Tsc1+/- mice differs from human TSC epilepsy by the absence of focal seizures and of drug-resistance. Both could be explained by the lack of tubers in the Tsc1+/- mice. It remains to determine whether the expression of GluN2C subunit is also transitional in Tsc1+/- mice and whether other factors contribute to determine the age-dependent epilepsy. This study opens new therapeutic perspectives of TSC epilepsy targeting GluN2C subunit of NMDA receptors
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Стоянов, О. М., and А. О. Капталан. "Судомні прояви після ішемії мозку." Thesis, Сумський державний університет, 2017. http://essuir.sumdu.edu.ua/handle/123456789/64787.
Full textAbstract:
Вступ. Епілепся є одним із найскладніших захворювань нервової системи. Неефективність лікування хворих з епілепсією є наслідком різнобічності її патогенетичних механізмів. В неврологічній практиці показані епізоди виникнення судомних проявів внаслідок судинних мальформацій головного мозку. Показано, що напади епілепсії у пацієнтів із судинними захворюваннями мозку погіршують перебіг основного захворювання, погіршують їх якість життя, уповільнюють процес відновлення після інсульту та обтяжують морфо-функціональні порушення, які виникли після обмеження кровопостачання до головного мозку. Проблемою в клініці є своєчасна діагностики ризику та/або можливості виникнення епілептиформних нападів у вказаного контингенту хворих, що є неможливим без ретельного дослідження патогенезу судомного синдрому. Показано, що епізоди ішемії мозку підвищують чутливість головного мозку щодо конвульсивних впливів. Мета роботи – вивчення патогенетичних механізмів хронічного судомного синдрому, який виник після ішемії мозку.
Books on the topic "Spasm"
1
Park, Kwan, and Jae Sung Park, eds. Hemifacial Spasm. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9.
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2
Sindou, Marc, Yves Keravel, and Aage R. Møller, eds. Hemifacial Spasm. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6829-5.
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Hewett, Geoffrey. Electro spasm: Poem video. [St. John's, Nfld: Geohew Motio Co., 1999.
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Park, Sang-Ku, Byung-Euk Joo, and Kwan Park. Intraoperative Neurophysiological Monitoring in Hemifacial Spasm. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1327-2.
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Shuba, M. F. Mekhanizmy vozbuzhdenii͡a︡ i sokrashchenii͡a︡ gladkikh mysht͡s︡ mozgovykh sosudov. Kiev: Nauk. dumka, 1991.
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1929-, Nadel Jay A., Pauwels Romain, and Snashall P. D, eds. Bronchial hyperresponsiveness: Normal and abnormal control, assessment, and therapy. Oxford: Blackwell Scientific Publications, 1987.
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1934-, Conti C. Richard, ed. Coronary artery spasm: Pathophysiology, diagnosis, and treatment. New York: Dekker, 1986.
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Kroker, Arthur. SPASM: Virtual reality, android music, and electric flesh. New York: St. Martin's Press, 1993.
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Sachs, Greg A. Exercise induced bronchospasm and the effect of ascorbic acid: A study of the possible role of prostaglandins. [New Haven: s.n.], 1985.
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International Conference on Cerebral Vasospasm (5th 1993 Edmonton, Alta. and Jasper, Alta.). Cerebral vasospasm: Proceedings of the Vth International Conference on Cerebral Vasospasm, Edmonton and Jasper, Alberta, Canada, May 17-21, 1993. Amsterdam: Elsevier, 1993.
Find full textBook chapters on the topic "Spasm"
1
Park, Jae Sung. "Overview of Hemifacial Spasm." In Hemifacial Spasm, 1–5. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_1.
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Lee, Min Ho, and Jae Sung Park. "Various Applications of Microvascular Decompression Other than for Hemifacial Spasm." In Hemifacial Spasm, 75–82. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_10.
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Park, Sang-Ku. "Intraoperative Neurophysiological Monitoring in Microvascular Decompression for Hemifacial Spasm." In Hemifacial Spasm, 83–109. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_11.
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Lee, Jeong Jin. "Anesthetic Management of MVD." In Hemifacial Spasm, 111–18. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_12.
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Youn, Jinyoung, Wooyoung Jang, and Jong Kyu Park. "Botulinum Toxin Injection in Hemifacial Spasm." In Hemifacial Spasm, 119–26. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_13.
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Jang, Wooyoung, and Jinyoung Youn. "Medical Treatment of Hemifacial Spasm and Other Involuntary Facial Movement Disorders." In Hemifacial Spasm, 127–34. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_14.
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Kong, Doo-Sik. "Possible Complications of Microvascular Decompression." In Hemifacial Spasm, 135–39. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_15.
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Lee, Jeong-A., and Kwan Park. "Prognosis of Symptoms After Microvascular Decompression for Hemifacial Spasm." In Hemifacial Spasm, 141–50. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_16.
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Lee, Seunghoon, and Kwan Park. "Redo Surgery for Failed Microvascular Decompression for Hemifacial Spasm." In Hemifacial Spasm, 151–54. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_17.
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Lee, Jeong-A., and Kwan Park. "Natural History of Hemifacial Spasm." In Hemifacial Spasm, 7–12. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5417-9_2.
Full textConference papers on the topic "Spasm"
1
Emerson, Sam, Jake Ruzevick, Rajeev Sen, Kate Carroll, and Manuel Ferreira Jr. "Hemifacial Spasm: Surgical Strategies and Complications." In 30th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1702601.
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Guo, Jiayu, Shasha Zhao, Mao Shu, Zhongguang Yan, Mingzhu Sun, Xin Zhao, and Xizeng Feng. "Trajectory tracking of spasm-oriented zebrafish larvae." In 2014 33rd Chinese Control Conference (CCC). IEEE, 2014. http://dx.doi.org/10.1109/chicc.2014.6896128.
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Chauhan, Balwantray C., Rajinder S. Rathee, Dianne Mosher, Charles E. Maxner, Christine A. MacDonald, and Terry A. McCormick. "Effect of Cold Provocation on the Visual Fields of Subjects with Raynaud’s Phenomenon and Normal Controls." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1996. http://dx.doi.org/10.1364/vsia.1996.thc.3.
Full textAbstract:
Vasospasm is defined as contraction or hypertonia of the muscular coats of blood vessels. It may result in decreased blood flow to perfused tissues followed by reversible ischemia of varying severity. Vasospasm is present and believed to be a pathogenetic factor in many diseases such as Raynaud’sphenomenon, migraine, and Prinzmetal’s variant angina.1 Cold is known to provoke spasm, as are nicotine and emotional or physical stress.
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Damasceno Júnior, Eustáquio Costa, Isabella Sabião Borges, João Victor Aguiar Moreira, Pedro Otávio Rego de Aguiar, Thaciany Soares Ferreira, Leonardo Peixoto Garcia, Glauber Mota Pacheco, et al. "Successful treatment with rituximab in a refractory Stiffperson syndrome (SPS)." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.507.
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Background: SPS is a disorder consisting of rigidity of axial muscles with painful spasms. More than 80 % of SPS patients have high titer antibodies against glutamic acid decarboxylase (GAD). The use of rituximab for the treatment of SPS is a recent therapeutical approach showing promising results. We present a case of SPS treated with rituximab, showing a good and safe response. Case: A 38-year-old female patient presented with a history of rigidity of abdominal and paravertebral muscles associated with painful spasms in lower back region, increased tonus, lumbar lordosis, frequent falls and severe functional limitation. The anti-GAD antibodies were positive in high titles. Electromyography showed continuous motor activity with normal morphology especially on paravertebral muscles. She had a partial response to baclofen and diazepam, but could not tolerate it because of somnolence, and started the treatment with rituximab. After one year, the baclofen was discontinued and the diazepam reduced. The axial stiffness and spasm frequency improved, including postural instability, without new episodes of falls. Discussion: Rituximab is a monoclonal antibody targeting the CD20 antigens on the surface of mature B lymphocytes. After binding to these antigens, it initiates a cascade of biochemical events leading to apoptosis. Its use has been approved for numerous diseases with promising results. The use of rituximab in the treatment of SPS is a recent approach and good results have been reported. Conclusion: Rituximab may be a promising option in SPS treatment. However, this is a preliminary paper showing partial results requiring long-term follow-up.
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Khoshnevis, Sepideh, Natalie Craik, and Kenneth R. Diller. "Cryotherapy Modification to Overcome Uninterrupted Ischemia." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14423.
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Localized cooling is commonly used following orthopedic surgery and in sports medicine to reduce swelling, pain, inflammation, metabolism, muscle spasm, and bleeding[1,2]. The therapeutic application of cold therapy has a long history dating from the time of Hippocrates and has been widely documented in the literature[3,4]. Nonetheless, there remains to the present time considerable controversy over the appropriate protocol for application of cryotherapy and the risk factors associated with its use[5].
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Cordeiro, Júlia Coutinho, and José Gilberto de Brito Henriques. "Hemifacial spasm caused by posterior fossa arachnoid cyst: Case Report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.134.
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Context: Hemifacial spasm (HFS) is characterized by continuous or intermittent spasmodic movements at the facial nerve motor territory.1,2,3 It mainly affects middle- aged adults and usually occurs by compression of the facial nerve by anomalous vascular loops of the anteroinferior and vertebral cerebellar artery.2,3,4,5 The arachnoid cyst at the cerebellopontine angle (CPA) is an rare cause of HFS, especially in children. Case report: A six-year-old female patient started presenting at 18 months HFS on the right side. She was initially treated with anticonvulsant without improvement. The patient came to our care at the age of six presenting 2-3 HFS per day and remissions lasting 3-4 weeks. Image exams reveled a CPA arachnoid cyst compressing the VII and VIII nerves complex. Surgical drainage of the cyst was performed as the treatment of choice. In postoperative period, the patient presented remission of HFS, and cranial tomography showed a decrease in cyst volume. In three months, there was remission of the signs without use of any medications. Conclusions: There was no report of arachnoid cyst in CPA as a cause of HFS in children. HFS occurs probably by chronic irritation, since birth, because of the contact of arachnoid cyst in the emergence of the VII and VIII nerves complex in the PCA. Therefore, treatment was chosen according to the cause of HFS. Movement disorder as a clinical manifestation of the cyst is rare, especially in pediatric population, and should be considered as one of the diagnostic hypotheses.
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Khoshnevis, Sepideh, and Kenneth R. Diller. "Cryosurgery Causes Profound and Persistent Ischemia." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80635.
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Cryotherapy has been used in the treatment of soft tissue trauma and other ailments since the time of Hippocrates. Currently it is commonly applied in conjunction with surgical procedures and by athletic trainers and physical therapists to control pain, swelling, bleeding, and inflammation. Localized cooling also results in slowing of the nerve conduction velocity and reduced muscle spasm and secondary hypoxic injury1,2. Cooling is commonly used for soft tissue injuries in combination with rest, compression and elevation to minimize inflammation.
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Wang, Zhong-Gao. "A belated revelation: From Gastroesophageal Reflux related asthma to laryngotracheal spasm." In 2008 International Conference on Technology and Applications in Biomedicine (ITAB). IEEE, 2008. http://dx.doi.org/10.1109/itab.2008.4570512.
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Blendea, Dan. "EXPERIENCE OF TARGETED RADIOFREQUENCY THERAPY APPLIED IN MEDICAL RECOVERY." In eLSE 2016. Carol I National Defence University Publishing House, 2016. http://dx.doi.org/10.12753/2066-026x-16-224.
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This paper presents our interest in new therapies like Targeted Radiofrequency Therapy. Targeted Radiofrequency Therapy distributes high-frequency electromagnetic energy into the desired tissue which leads to selective tissue hyperthermy. Thanks to this mechanism patients experience instant pain relief, muscle relaxation, edema reduction, tissue regeneration support and healing. The most common indications include: local muscle spasm, trigger points, myalgia, tendinitis, cervical pain, and post-traumatic edema. The immediate therapeutic effect is noticed by the patient instantly and lasts long after the therapy. The goal of the present study is to highlight the medical effect in recovery by using the Targeted Radiofrequency Therapy. The main method used to fulfill this study has been even the implementation of the mechanism of action of Targeted Radiofrequency Therapy. The findings are regarding to the muscle relaxation, tissue regeneration and healing, pain relief. So, the Targeted Radiofrequency Therapy helps relieve trigger points and muscle spasms that prevent regaining the full range of joint movement. For example use of the Targeted Radiofrequency Therapy in combination with passive stretching of the shortened structures leads to their relief and immediately broadens the range of motion in the given segment. Combining the Targeted Radiofrequency Therapy and isometric or isotonic muscle contraction focuses the hyperthermy into the contracted muscle. Delivered radiofrequency energy facilitates these fibers and leads to their incorporation in the performed muscle stereotypes. Combining the Targeted Radiofrequency Therapy and isometric or isotonic muscle contraction focuses the hyperthermy into the contracted muscle. Delivered radiofrequency energy facilitates these fibers and leads to their incorporation in the performed muscle stereotypes.
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Tomaru, Takanobu, Fumitaka Nakamura, Atsuko Miwa, Yoshiharu Fujimori, and Yasumi Uchida. "Laser irradiation reduces vasoreactivity of coronary artery: implication for prevention of coronary spasm." In OE/LASE'93: Optics, Electro-Optics, & Laser Applications in Science& Engineering, edited by George S. Abela. SPIE, 1993. http://dx.doi.org/10.1117/12.146576.
Full textReports on the topic "Spasm"
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Palmer, S. C., and J. D. Ancrile. SLCA/IP power alternative screening method (SPASM). Office of Scientific and Technical Information (OSTI), March 1995. http://dx.doi.org/10.2172/179237.
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Chen, Baoshan, Rigun A, Ruizhen Yue, and Guangrong Zhang. Qianzheng powder for the treatment of primary Hemifacial spasm. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0008.
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Bide, R. W., and D. J. Risk. Rapid Estimation of Post Exposure Incapacitation: 1. Definition of the Rotopad and Spasm Tests. Fort Belvoir, VA: Defense Technical Information Center, March 1992. http://dx.doi.org/10.21236/ada251570.
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Zhong, ZhiYing, Jun Xiong, and GenHua Tang. Efficacy of fire needle on patients of facial spasm: A protocol of meta-analysis and systemic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0036.
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Chen, Baoshan, Rigun A, Ruizhen Yue, and Guangrong Zhang. Qianzheng powder for the treatment of primary Hemifacial spasm A protocol for a systematic reviews and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0037.
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Liu, Qilin, Tao Zhang, Yi Xue, Dayong Du, Yang Liu, and Yuntian Li. A systematic review and meta-analysis of impact of statins use on the clinical outcome of patients with coronary spasm. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0066.
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Wei, Dongmei, Yang Sun, and Hankang Hen. Effects of Baduanjin exercise on cardiac rehabilitation after percutaneous coronary intervention: A protocol for systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0080.
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Review question / Objective: Can Baduanjin exercise improve the cardiac rehabilitation of patients with coronary artery disease after percutaneous coronary artery surgery? Condition being studied: Coronary heart disease (CHD), also known as coronary artery disease (CAD), is the single most common cause of death globally, with 7.4 million deaths in 2013, accounting for one-third of all deaths (WHO 2014). PCI has been shown to be effective in reducing mortality in patients with CHD. During follow-up, it has been shown that the benefits of PCI can be offset by the significant risks of coronary spasm, endothelial cell injury, recurrent ischemia, and even restenosis or thrombus. Numerous guidelines endorse the necessity for cardiac rehabilitation (CR), which is recommended for patients with chronic stable angina, acute coronary syndrome and for patients following PCI. Baduanjin have been widely practised in China for centuries, and as they are considered to be low risk interventions, their use for the prevention of cardiovascular disease is now becoming more widespread. The ability of Baduanjin to promote clinically meaningful influences in patients with CHD after PCI, however, still remains unclear.
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Ma, He, Jifu Zhao, and Zhilei Wang. Efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease：A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0114.
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Review question / Objective: This study is the protocol for a systematic review to evaluate the efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease. we conducted a systematic review and meta-analysis of published randomized clinical trials (RCTs) of such combined therapy in the treatment of AECOPD, It provides a reliable scientific basis for clinicians to use this approach to treat AECOPD. Condition being studied: Chronic obstructive pulmonary disease is the third leading cause of death worldwide. AECOPD is the most common cause of hospitalization and death in patients with COPD. As lung function deteriorates and the disease progresses, the risk of alveolar hypoxia and consequent hypoxemia increases. Inflammation plays an important role in the progression of AECOPD. Modern medicine mainly treats AECPD by anti-inflammatory, relief of airway spasm, glucocorticoids, inhalants and other methods. Long-term application can easily lead to bacterial flora imbalance and drug resistance in patients. Comparatively, traditional Chinese medicine and acupuncture therapy are safe and effective.To assess the therapeutic efficacy and safety of HuaYu TongFu Method combined with acupuncture in AECOPD, we created a protocol for a systematic review to inform future clinical applications.
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Seybold, Patricia. The Spam Conspiracy. Boston, MA: Patricia Seybold Group, September 2002. http://dx.doi.org/10.1571/psgp9-5-02cc.
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Bock, Nicolas, and William M. Challacombe. SpAMM - The Power of N. Office of Scientific and Technical Information (OSTI), June 2012. http://dx.doi.org/10.2172/1044117.
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