Negative myoclonus (NM) is a jerky, shock-like involuntary movement caused by a sudden, brief interruption of muscle contraction. An 80-year-old man presented with multifocal NM and confusion. Two days before the onset of NM, he commenced the intake of pregabalin at a dose of 150 mg/day for neuropathic pain. His NM resolved completely and mental status improved gradually after the administration of lorazepam intravenously and the discontinuation of pregabalin. Our study suggests that pregabalin can cause NM even in patients without a history of seizures.
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Background Pregabalin has been studied as a single or multimodal analgesic drug for postoperative pain management in different types of surgeries. We evaluated the analgesic effect of 150 mg of pregabalin in resolving post-gastrectomy pain.
Methods Forty-four patients were randomized into two groups: a pregabalin group that received oral pregabalin (150 mg) 2 h before anesthetic induction, and a control group that received placebo tablets at the same time. Data on postoperative pain intensity (visual analog scale [VAS], at 30 min, 2 h, 4 h, and 24 h), consumption of fentanyl in patient-controlled analgesia (PCA), and the proportion of patients requiring rescue analgesics at different time intervals (0-2 h, 2-4 h, and 4-24 h) were collected during the 24 h postoperative period.
Results The VAS scores did not show significant differences at any time point and consumption of fentanyl in PCA and the proportion of patients requiring rescue analgesics did not differ between the two groups. The groups did not differ in the occurrence of dizziness, sedation, and dry mouth.
Conclusion A preoperative 150 mg dose of pregabalin exerts no effect on acute pain after gastrectomy.
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Treatment of acute postoperative pain in patients undergoing open abdominal aortic repair (current state of the problem) Anzhelika V. Kozhanova, Georgy P. Plotnikov Regional Anesthesia and Acute Pain Management.2022; 16(1): 45. CrossRef
Comparison of premedication with 75 mg and 150 mg pregabalin for postoperative analgesia in total hysterectomy patients - A randomised control trial Ajish Varghese Cheruvathur, Dilshad Thondi Parambil, Saurabh Vig, Salman Mohammed Kutty Chenath, Priyadharshini Nagaraj, Krupa Mulgaonkar, S Jeevithan Indian Journal of Clinical Anaesthesia.2022; 9(4): 467. CrossRef
BACKGROUND Gabapentin is widely used for the relief of neuropathic pain. But, there is no study of gabapentin in relation to traumatic neuropathic pain. The aim of this study is to assess the efficacy and effectiveness of gabapentin for the various clinical symptoms of traumatic neuropathic pain MATERIALS AND METHODS: 50 patients with traumatic nerve injury were assigned to receive gabapentin, titrated to 900 mg/day over 9 days, followed by further increases to a maximum of 2400 mg/day. Continuous pain, paroxysmal pain, allodynia and thermal evoked pain were measured in mean daily pain scores, based on the 11-point Likert scale. The primary efficacy parameter was compared from the baseline to the final study week. RESULTS: Over the 4.5 week study, this pain score decreased by 2.6 points in the continuous pain, 3.6 points in the paroxysmal pain, 3.1 points in the allodynia, and 2.5 points in the thermal evoked pain. The percentage of patients with over 50% improvement in pain scores was 33% in the continuous pain, 67% in the paroxysmal pain, 53% in the allodynia and 36% in the thermal evoked pain. There was no significant correlation between the effect of gabapentin and the time difference of the onset of symptoms and start of medication. CONCLUSIONS: This study shows that gabapentin reduced neuropathic pain in patients with traumatic peripheral nerve injury. Among the various characteristics of neuropathic pain, the reduction of paroxysmal pain and allodynia was greatest.
GABA is an inhibitory neurotransmitter in central nervous system and produce sedative, antianxiety and muscle relaxing effects via GABA(A) receptor or GABA(B) receptor. Recently it is known that GABA is widely distributed throughout peripheral organs and may play a physiological role in certain organ. The vas deferens is innervated by species-difference. These study, therefore, was performed to investigate the mode and the mechanism of action of GABA on the norepinephrine-, ATP- and electric stimulation-induced contraction of vas deferens of rat. Sprague-Dawley rats were sacrificed by cervical dislocation. The smooth muscle strips were isolated from the prostatic portion and were mounted in the isolated muscle bath. PSS in the bath was aerated with 95/5%-O₂/CO₂ at 33℃. Muscle tensions were measured by isometric tension transducer and were recorded by biological recording system. 1. GABA, muscimol, a GABA(A) agonist, and baclofen, a GABA(B) agonist inhibited the electric field stimulation (EFS, 0.2Hz, 1mSec, 80V, monophasic square wave)-induced contraction with a rank order of potency of GABA greater than baclofen greater than muscimol. 2. The inhibitory effect of GABA was antagonized by delta aminovaleric acid (DAVA), a GABA(B) antagonist, but not by bicuculline, a GABA(A) intagonist. 3. The inhibitory effect of baclofen was antagonized by DAVA, but the effect of muscimol was not antagonized by bicuculline. 4. Exogenous norepinephrine (NE) and ATP contracted muscle strip concentration dependently, but the effect of acetylcholine was negligible and GABA did not affect the NE-and ATP-induced contractions. 5. GABA, baclofen and muscimol did not affect basal tone, and GABA did not affect the NE-and ATP-induced contractions. 6. EFS-induced contraction was inclucling 2 distinctable components. The first phasic component was inhibited by beta gamma-methylene ATP (mATP), a desensitizing agent of APT receptor and the second tonic component was reduced by pretreatment of reserpine (3 mg/Kg, IP). 7. GABA inhibited the EFS-induced contraction of reserpinized strips, but not the mATP-treated strips. These results suggest that in the prostatic portion of the rat vas deferens, adrenergic and purinergic neurotransmissions are exist, and GABA inhibits the release of ATP via presynaptic GABA(B) receptor on the excitatory neurons.
This study was designed to investigate the effect of diazepam on the spontaneous contraction and oxytocin induced contraction of the isolated rat uterus. Female rat (Sprague-Dawley) pretreated with oophorectomy and 4 days administration of estrogen. Weighing about 200 g, was sacrificed by cervical dislocation, and the uteruses were isolated. A longitudinal muscle strip was placed in temperature controlled (37℃) muscle chamber containing Locke's solution and myographied isometrically. Diazepam inhibited the spontaneous contraction and oxytocin induced contraction of the isolated rat uterus in a concentration-dependent manner. GABA, muscimol, a GABA A receptor agonist, bicuculline, a competitive GABA A receptor antagonist, picrotoxin, a non competitive GABA A receptor antagonist, baclofen, a GABA B receptor agonist, and delta-aminovaleric acid, a GABA B receptor antagonist, did not affect on the spontaneous and oxytocin induced contraction of the isolated rat uterus. The inhibitory actions of diazepam on the spontaneous and oxytocin induced contraction were not affected by all the GABA receptor agonists and antagonists, but exceptionally potentiated by bicuculline. This potentiation-effect by bicuculline was not antagonized by muscumol. In normal calcium PSS, addition of calcium restored the spontaneous contraction preinhibited by diazepam and recovered the contractile of oxtrocin preinhibited by diazepam. A23187, a calcium inophore, enhanced the restoration of both the spontaneous and oxytocin induced contraction by addition of calcium. In calcium-free PSS, diazepam suppressed the restoration of spontaneous motility by addition of calcium but allowed the recovery of spontaneous motility to a considerable extent. Diazepam could not inhibit some development of contractility by oxytocin in calcium-free PSS, but inhibited the increase in contractility by subsequent addition of calcium. These results suggest that the inhibitory action of diazepam on the rat uterine motility does not depend on or related to GABA receptors and that diazepam inhibits the extracellular calcium influx to suppress the spontaneous and oxytocin induced contractilities.
This study was designed to investigate the effect of GABA and related substances on the spontaneous contraction of rat small intestine. The rats (Sprague-Dawley), weighing 200-250g, were sacrificed by cervical dislocation, and the small intestine was isolated. Longitudinal muscle strips from duodenum, jejunum and ileum were suspended in Biancani's isolated muscle chambers and myographied isometrically. GABA and muscimol, a GABA A receptor agonist relaxed the duodenum and jejunum significantly, but baclofen-induced relaxation in those muscle strips negligible. The effectiveness of GABA and muscimol in various regions were the greatest on duodenum, and greater on jejunum than on ileum The effect of GABA and muscimol was antagonized by bicuculline, a competitive GABA A receptor antagonist and picrotoxin, a noncompetitive GABA A receptor antagonist. Duodenal relaxation induced by GABA and muscimol was unaffected by hexamethonium, but was prevented by tetrodotoxin. These results suggest that GABA inhibit the contractility of smooth muscle with distinct regional difference of efficacy, and the site of inhibitory action is the GABA A receptor existing at the presynaptic membrane of postganglionic excitatory nerves.