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Focused Review article
- Pain in amyotrophic lateral sclerosis: a narrative review
- Soyoung Kwak
- J Yeungnam Med Sci. 2022;39(3):181-189. Published online June 8, 2022
- DOI: https://doi.org/10.12701/jyms.2022.00332
- 5,994 View
- 156 Download
- 8 Web of Science
- 9 Crossref
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Abstract
PDF - Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative condition characterized by loss of motor neurons, resulting in motor weakness of the limbs and/or bulbar muscles. Pain is a prevalent but neglected symptom of ALS, and it has a significant negative impact on the quality of life of patients and their caregivers. This review outlines the epidemiology, clinical characteristics, underlying mechanisms, and management strategies of pain in ALS to improve clinical practice and patient outcomes related to pain. Pain is a prevalent symptom among patients with ALS, with a variable reported prevalence. It may occur at any stage of the disease and can involve any part of the body without a specific pattern. Primary pain includes neuropathic pain and pain from spasticity or cramps, while secondary pain is mainly nociceptive, occurring with the progression of muscle weakness and atrophy, prolonged immobility causing degenerative changes in joints and connective tissue, and long-term home mechanical ventilation. Prior to treatment, the exact patterns and causes of pain must first be identified, and the treatment should be tailored to each patient. Treatment options can be classified into pharmacological treatments, including nonsteroidal anti-inflammatory drugs, antiepileptic drugs, drugs for cramps or spasticity, and opioid; and nonpharmacological treatments, including positioning, splints, joint injections, and physical therapy. The development of standardized and specific assessment tools for pain-specific to ALS is required, as are further studies on treatments to reduce pain, diminish suffering, and improve the quality of life of patients with ALS.
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- Health-related quality of life across disease stages in patients with amyotrophic lateral sclerosis: results from a real-world survey
Katie Stenson, T. E. Fecteau, L. O’Callaghan, P. Bryden, J. Mellor, J. Wright, L. Earl, O. Thomas, H. Iqbal, S. Barlow, S. Parvanta
Journal of Neurology.2024; 271(5): 2390. CrossRef - Amyotrophic Lateral Sclerosis and Pain: A Narrative Review from Pain Assessment to Therapy
Vincenzo Pota, Pasquale Sansone, Sara De Sarno, Caterina Aurilio, Francesco Coppolino, Manlio Barbarisi, Francesco Barbato, Marco Fiore, Gianluigi Cosenza, Maria Beatrice Passavanti, Maria Caterina Pace, Enzo Emanuele
Behavioural Neurology.2024; 2024: 1. CrossRef - Non-motor symptoms in patients with amyotrophic lateral sclerosis: current state and future directions
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Journal of Neurology.2024; 271(7): 3953. CrossRef - Perceived Pain in People Living with Amyotrophic Lateral Sclerosis—A Scoping Review
Debora Rosa, Laura Ingrande, Ilaria Marcomini, Andrea Poliani, Giulia Villa, Martina Sodano, Duilio Fiorenzo Manara
Nursing Reports.2024; 14(4): 3023. CrossRef - Likely Pathogenic Variants of Cav1.3 and Nav1.1 Encoding Genes in Amyotrophic Lateral Sclerosis Could Elucidate the Dysregulated Pain Pathways
Zsófia Flóra Nagy, Balázs Sonkodi, Margit Pál, Péter Klivényi, Márta Széll
Biomedicines.2023; 11(3): 933. CrossRef - Palliative Care in Amyotrophic Lateral Sclerosis
Sebastiano Mercadante, Lou'i Al-Husinat
Journal of Pain and Symptom Management.2023; 66(4): e485. CrossRef - The blind spot and challenges in pain management
Min Cheol Chang
Journal of Yeungnam Medical Science.2022; 39(3): 179. CrossRef - Synucleinopathy in Amyotrophic Lateral Sclerosis: A Potential Avenue for Antisense Therapeutics?
Bradley Roberts, Frances Theunissen, Francis L. Mastaglia, P. Anthony Akkari, Loren L. Flynn
International Journal of Molecular Sciences.2022; 23(16): 9364. CrossRef - Herbal medicine and acupuncture relieved progressive bulbar palsy for more than 3 years: A case report
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Medicine.2022; 101(45): e31446. CrossRef
- Health-related quality of life across disease stages in patients with amyotrophic lateral sclerosis: results from a real-world survey
Original Articles
- Localization of Sensory Neurons Innervating the Rat Intestine Using the Cholera Toxin B Subunit(CTB) and Wheat Germ Agglutinin-Horseradish Peroxidase(WGA-HRP).
- Dong Hyup Lee, Chang Hyun Lee, Moo Sam Lee
- Yeungnam Univ J Med. 1998;15(1):75-96. Published online June 30, 1998
- DOI: https://doi.org/10.12701/yujm.1998.15.1.75
- 1,819 View
- 8 Download
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Abstract
PDF
- The local arrangement of sensory nerve cell bodies and nerve fibers in the brain stem, spinal ganglia and nodose ganglia were observed following injection of cholera toxin B subunit(CTB) and wheat germ agglutinin-horseradish peroxidase(WGA-HRP) into the rat intestine. The tracers were injected in the stomach(anterior and posterior portion), duodenum, jejunum, ileum, cecum, ascending colon or descending colon. After survival times of 48-96 hours, the rats were perfused and their brain, spinal and nodose ganglia were frozen sectioned(40microM). These sectiones were stained by CTB immunohistochemical and HRP histochemical staining methods and observed by dark and light microscopy. The results were as follows: 1. WGA-HRP labeled afferent terminal fields in the brain stem were seen in the stomach and cecum, and CTB labeled afferent terminal fields in the brain stem were seen in all parts of the intestine. 2. Afferent terminal fields innervating the intestine were heavily labeled bilaterally gelalinous part of nucleus of tractus solitarius(gelNTS), dorsomedial part of gelNTS, commissural part of NTS(comNTS), medial part of NTS(medNTS), wall of the fourth ventricle, ventral border of area postrema and comNTS in midline dorsal to the central canal. 3. WGA-HRP labeled sensory neurons were observed bilaterally within the spinal ganglia, and labeled sensory neurons innervating the stomach were observed in spinal ganglia T2-L1 and the most numerous in spinal ganglia T8-9. 4. Labeled sensory neurons innervating the duodenum were observed in spinal ganglia T6-L2 and labeled cell number were fewer than the other parts of the intestines. 5. Labeled sensory neurons innervating the jejunum were observed in spinal ganglia T6-L2 and the most numerous area in the spinal ganglia were T12 in left and T13 in right. 6. Labeled sensory neurons innervating the ileum were observed in spinal ganglia T6-L2 and the most numerous area in the spinal ganglia were T11 in left and L1 in right. 7. Labeled sensory neurons innervating the cecum were observed in spinal ganglia T7-L2 and the most numerous area in the spinal ganglia were T11 in left and T11-12 in right. 8. Labeled sensory neurons innervating the ascending colon were observed in spinal ganglia T7-L2 in left, and T9-L4 in right. The most numerous area in the spinal ganglia were T9 in left and T11 in right. 9. Labeled sensory neurons innervating the descending colon were observed in spinal ganglia T9-L2 in left, and T6-L2 in right. The most numerous area in the spinal ganglia were T13 in left and L1 in right. 10. WGA-HRP labeled sensory neurons were observed bilaterally within the nodose ganglia, and the most numerous labeled sensory neurons innervating the abdominal organs were observed in the stomach. 11. The number of labeled sensory neurons within the nodose ganglia innervating small and large intestines were fewer than that of labeled sensory neurons innervating stomach These results indicated that area of sensory neurons innervated all parts of intestines were bilaterally gelatinous part of nucleus tractus solitarius(gelNTS), dorsomedial part of gelNTS, commissural part of NTS(comNTS), medial part of NTS, wall of the fourth ventricle, ventral border of area postrema and com NTS in midline dorsal to the central canal within brain stem, spinal ganglia T2-L4, and nodose ganglia. Labeled sensory neurons innervating the intestines except the stomach were observed in spinal ganglia T6-L4. The most labeled sensory neurons from the small intestine to large intestine came from middle thoracic spinal ganglia to upper lumbar spinal ganglia.
- Inhibitory of γ-aminobutyric acid on the contractility of isolated rat vas deferens.
- Ki Young Ahn, Oh Cheol Kwon, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim
- Yeungnam Univ J Med. 1992;9(2):382-395. Published online December 31, 1992
- DOI: https://doi.org/10.12701/yujm.1992.9.2.382
- 1,746 View
- 5 Download
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Abstract
PDF
- 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.
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