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Motor neurone disease
Published in Ibrahim Natalwala, Ammar Natalwala, E Glucksman, MCQs in Neurology and Neurosurgery for Medical Students, 2022
Ibrahim Natalwala, Ammar Natalwala, E Glucksman
Regarding the treatment of MND, which of the following statements are true and which are false? Drug therapy targeting the release of the GABA neurotransmitter is the mainstay of treatment of MND.Non-invasive ventilation (NIV) is recommended in MND patients with a forced vital capacity (FVC) of <50%.Suxamethonium is an excellent drug that can be used to help reduce spasticity of the affected muscles.Pain experienced by patients with MND is most responsive to non-opioid analgesics.
Critical care, neurology and analgesia
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
This agent produces rapid, profound and short-lived neuromuscular blockade. Its use is restricted to emergency endotracheal intubation because of the many complications associated with its use. The structural similarity between suxamethonium and acetylcholine is responsible for many of the more serious of these adverse effects, including bradycardias, tachycardias and arrhythmias. The depolarisation of muscles following administration can result in painful muscle fasciculation, myalgia and myoglobinuria. Hyperkalaemia can be a clinically important problem associated with the administration of suxamethonium. In normal circumstances, an increase in serum potassium of 0.5 mmol/1 can be expected following the administration of suxamethonium. In certain circumstances, however, this increase can be much greater. A large population of extra-synaptic, immature-type acetylcholine receptors develops after denervation of mammalian muscle, after prolonged immobility and following the administration of neuromuscular blocking agents. In these circumstances, a standard dose of suxamethonium can result in large increases in the serum potassium concentration, which may result in cardiac arrhythmias or cardiac arrest.
Major advances in ECT practice
Published in Alan Weiss, The Electroconvulsive Therapy Workbook, 2018
Suxamethonium chloride, also known as suxa-methonium (preferred term used in this book) or succinylcholine, was first trialled unsuccessfully as a cardiovascular agent in 1905, with the neuro-muscular properties being discovered much later in 1949 (Lee, 2009). It was introduced into clinical anaesthesia in Europe in 1951 and in the United States in 1952. Suxamethonium has been associated with life-threatening adverse events like malignant hyperthermia and hyperkalemia (Folk et al., 2000). This has lead to the development of at least 11 different non-depolarising agents, with most having a slow onset and offset of action. However, even to this day, of the non-depolarising agents suxamethonium continues to be the primary muscle relaxant used in ECT owing to its rapid onset and quick time to recovery (Lee, 2009).
Intercorrelation of physiological seizure parameters and hormonal changes in electroconvulsive therapy
Published in Nordic Journal of Psychiatry, 2023
Elin Thörnblom, Malin Gingnell, Janet L. Cunningham, Mikael Landén, Robert Bodén
ECT was performed with a Thymatron® System IV (Somatics LLC, Lake Bluff, IL, USA). Initial stimulus dose was decided by the local ECT practitioner based on age and sex in accordance with the manufacturer’s instruction manual [29]. Only right unilateral (RUL) electrode placement was used. Pulse width was almost exclusively 0.5 ms. Median (Q1, Q3) stimulus charge was 252 (152, 350) milliCoulomb. Information on anesthetic agent and dose was available in 106 of 131 participants. In these, thiopental was used in all treatments except one, where propofol (2.46 mg/kg) was used instead. Median (Q1, Q3) thiopental dose was 4.43 (3.91, 4.90) mg/kg. Suxamethonium was routinely used for muscle relaxation. No adjunctive medications apart from anesthetics and muscle relaxants were used as part of the routine anesthetic procedure for the first ECT treatment.
The impact of the number of electroconvulsive therapy sessions on relapse in major depressive disorder
Published in International Journal of Psychiatry in Clinical Practice, 2022
Yuta Inagawa, Katsutoshi Shioda, Rika Kato, Tsuyoshi Okada, Toshiyuki Kobayashi, Shiro Suda
The patients were anaesthetised using intravenous propofol or thiopental. Muscle relaxation was induced through intravenous rocuronium or suxamethonium. Bilateral ECT was administered two or three times a week using a Thymatron stimulation device (Somatics, Lake Bluff, IL, USA). The initial electrical dose was calculated based on the half-age method (Petrides and Fink 1996). The stimulation conditions were 0.5 ms pulses and 0.9 A. The maximum electrical dose of the Thymatron was set at 504 mC. The patients’ medications were continued during their courses of ECT. However, benzodiazepines were discontinued a day prior to initiating ECT sessions. Psychiatric clinicians stopped an acute course of ECT sessions when the patients were determined to achieve remission or showed no response based on the DSM-IV-TR or DSM-5. If the patients exhibited adverse effects, psychiatric clinicians also decided whether or not to discontinue ECT sessions balancing benefits and risks caused by continuation of ECT.
Cochlear implantation in children with congenital long QT syndrome: Introduction of an evidence-based pathway of care
Published in Cochlear Implants International, 2018
Victoria Scott-Warren, Anju Bendon, Iain A. Bruce, Lise Henderson, Jacques Diacono
If a muscle relaxant is used it is prudent to avoid suxamethonium because of its autonomic effects and its propensity to cause rapid potassium shifts. Pancuronium similarly should be avoided due to its vagolytic properties (Kies et al., 2005). Anticholinergic agents such as atropine and glycopyrrolate have been shown to prolong the QT interval in healthy subjects, as have combined anticholinergics with anticholinesterases (Kies et al., 2005). Furthermore, triggering of torsade de pointe in LQTS patients following administration of anticholinergics has been reported (Staikou et al., 2012). Our guidelines therefore recommend avoidance of these drugs. It is important that the anaesthetist takes account of the requirement to use a facial nerve stimulator as part of the surgical technique when deciding on the use of a muscle relaxant. It is imperative that any muscle relaxant has been demonstrated to have worn off before surgery in the facial nerve territory is begun.