Artykuły w czasopismach: „Muscle rigidity”

1

Matsuki, Yuka. "Muscle Rigidity Associated with Pregabalin". Pain Physician 3;15, nr 3;5 (14.05.2012): E350. http://dx.doi.org/10.36076/ppj.2012/15/e350.

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Jenkins, J. G. "Masseter muscle rigidity after vecuronium". European Journal of Anaesthesiology 16, nr 2 (luty 1999): 137–39. http://dx.doi.org/10.1097/00003643-199902000-00011.

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Smith, H. L., i G. R. Park. "Muscle rigidity in meningococcal meningitis". Anaesthesia 48, nr 12 (22.02.2007): 1103–4. http://dx.doi.org/10.1111/j.1365-2044.1993.tb07544.x.

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Manners, J. M. "Muscle rigidity in miningococcal meningitis". Anaesthesia 49, nr 6 (czerwiec 1994): 544. http://dx.doi.org/10.1111/j.1365-2044.1994.tb03537.x.

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Jenkins, J. G. "Masseter muscle rigidity after vecuronium". European Journal of Anaesthesiology 16, nr 2 (luty 1999): 137–39. http://dx.doi.org/10.1046/j.1365-2346.1999.00448.x.

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Markelov, Grigory I. "To the symptomatology of trembling paralysis". Neurology Bulletin XVI, nr 2 (14.03.2022): 237–48. http://dx.doi.org/10.17816/nb101118.

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The main feature in the clinical picture of trembling paralysis must be recognized as increased rigidity of the muscles, muscle stiffness. This latter imposes on the patient that peculiar imprint, which often makes it possible to recognize this disease by appearance alone. Giving in various cases one or another fluctuation in distribution and intensity, this increased rigidity of the muscles is the most characteristic symptom of Parkinson's disease.

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Vankova, Miriana E., Matthew B. Weinger, Dong-Yi Chen, J. Brian Bronson, Valerie Motis i George F. Koob. "Role Central Mu, Delta-1, and Kappa-1 Opioid Receptors in Opioid-induced Muscle Rigidity in the Rat". Anesthesiology 85, nr 3 (1.09.1996): 574–83. http://dx.doi.org/10.1097/00000542-199609000-00017.

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Background Opioids appear to produce their physiologic effects by binding to at least three types of opioid receptors, the mu (mu), delta (delta), and kappa (kappa) receptors. Muscle rigidity occurs after administration of supra-analgesic doses of potent mu-preferring agonists like alfentanil. The role of different supraspinal opioid receptors in this rigidity has been addressed only recently. To elucidate the contribution of central mu, delta, and kappa receptors to muscle rigidity, the effects of intracerebroventricularly administered opioid receptor-selective agonists and antagonists on alfentanil-induced muscle rigidity were examined in rats. Methods Rats in which chronic intracerebroventricular cannulae had been implanted received an intracerebroventricular infusion of either saline or a mu (D-Ala2,N-Me-Phe4-Gly5-olenkephalin; DAMGO), delta(1) (D-Pen2,D-Pen5-enkephalin; DPDPE), or kappa(1) (trans-(+/-)-3,4-dichloro-N-methyl-N-(2-(1-pyrrolidinyl)- cyclohexyl)-benzene-acetamide methane sulfonate; U50,488H) opioid agonist. Ten minutes later, they received either saline or the mu-agonist alfentanil subcutaneously. Muscle rigidity was assessed using hindlimb electromyographic activity. Different groups of animals were pretreated with an intracerebroventricular infusion of either saline or a mu (D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2; CTAP), delta (naltrindole), or kappa(1) (norbinaltorphimine) opioid antagonist before administration of either saline or a selective intracerebroventricular agonist. Results The mu agonist DAMGO alone dose-dependently induced muscle rigidity. This effect was antagonized by pretreatment with the mu-selective antagonist CTAP. Neither DPDPE nor U50,488H, when administered alone, affected muscle tone. However, both the delta(1) and kappa(1) agonists dose-dependently attenuated alfentanil-induced rigidity. This antagonism of alfentanil rigidity was abolished after pretreatment with the delta (naltrindole) and kappa(1) (nor-binaltorphimine) antagonists, respectively. Conclusions The present data demonstrate that whereas systemic opiate-induced muscle rigidity is primarily due to the activation of central mu receptors, supraspinal delta(1) and kappa(1) receptors may attenuate this effect. This finding is consistent with previous demonstrations of functional interactions between different central opioid receptor populations in other opiate effects, and could have important pharmacotherapeutic implications.

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Khan, Bashir A., Mazhar U. Khan, Md Umar Majid i Md Mohib Hussain. "Masseter Muscle Rigidity Following Succinylcholine Administration". Journal of Contemporary Medicine and Dentistry 2, nr 2 (20.08.2014): 64–68. http://dx.doi.org/10.18049/jcmad/229a14.

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&NA;. "Benzodiazepines attenuate alfentanil-induced muscle rigidity". Inpharma Weekly &NA;, nr 972 (luty 1995): 13. http://dx.doi.org/10.2165/00128413-199509720-00028.

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Mayumi, Takahisa, Naoki Matsumiya, Satoshi Fujita i Shuji Dohi. "Diazepam prevents fentanyl-induced muscle rigidity". Journal of Anesthesia 4, nr 1 (styczeń 1990): 82–84. http://dx.doi.org/10.1007/s0054000040082.

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Oppold, Julia, Maria-Sophie Breu, Alireza Gharabaghi, Alexander Grimm, Nicholas A. Del Grosso, Mohammad Hormozi, Benedict Kleiser i in. "Ultrasound of the Biceps Muscle in Idiopathic Parkinson’s Disease with Deep Brain Stimulation: Rigidity Can Be Quantified by Shear Wave Elastography". Diagnostics 13, nr 2 (6.01.2023): 213. http://dx.doi.org/10.3390/diagnostics13020213.

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Rigidity in Parkinson’s disease (PD) is assessed by clinical scales, mostly the Unified Parkinson’s Disease Rating Scale of the Movement Disorders Society (MDS-UPDRS). While the MDS-UPDRS-III ranges on an integer from 0 to 4, we investigated whether muscle ultrasound shear wave elastography (SWE) offers a refined assessment. Ten PD patients (five treated with deep brain stimulation (DBS) and levodopa, five with levodopa only) and ten healthy controls were included. Over a period of 80 min, both the SWE value and the item 22b-c of the MDS-UPDRS-III were measured at 5 min intervals. The measurements were performed bilaterally at the biceps brachii muscle (BB) and flexor digitorum profundus muscle in flexion and passive extension. Rigidity was modified and tracked under various therapeutic conditions (with and without medication/DBS). The feasibility of SWE for objective quantification was evaluated by correlation with the UPDRS-III: considering all positions and muscles, there was already a weak correlation (r = 0.01, p < 0.001)—in a targeted analysis, the BB in passive extension showed a markedly higher correlation (r = 0.494, p < 0.001). The application of dopaminergic medication and DBS resulted in statistically significant short-term changes in both clinical rigidity and SWE measurements in the BB (p < 0.001). We conclude that rigidity is reflected in the SWE measurements, indicating that SWE is a potential non-invasive quantitative assessment tool for PD.

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Balzan, Martin V. "Paradoxical Autonomic Response to Procyclidine in the Neuroleptic Malignant Syndrome". Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 22, nr 3 (sierpień 1995): 244–46. http://dx.doi.org/10.1017/s0317167100039937.

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AbstractBackgroundNeuroleptic Malignant Syndrome (NMS) is an adverse reaction to dopamine receptor antagonists, characterised by hyperpyrexia, extrapyramidal rigidity and impaired autonomic function. It might result from central dopamine receptor blockade that causes severe muscle contraction.MethodCase Study.ResultsHigh dose intravenous therapy with the anticholinergic drug, procyclidine hydrochloride, temporarily diminished the muscle rigidity and reversed most of the autonomic features in a patient with NMS occurring after a single intramuscular dose of the dopamine antagonist metoclopramide. Paradoxically, however, the heart rate decreased and bowel movements increased with this atropine-like drug.ConclusionSince the degree of tachypnoea, tachycardia, and bowel hypotonia closely paralleled the severity of the muscle rigidity, it is suggested that these autonomic features of NMS result from sustained muscle contraction rather than a direct effect of neuroleptic drugs on the central nervous system.

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Weinger, Matthew B., Elizabeth J. Cline, N. Ty Smith i George F. Koob. "Ketanserin Pretreatment Reverses Alfentanil-induced Muscle Rigidity". Anesthesiology 67, nr 3 (wrzesień 1987): 348–54. http://dx.doi.org/10.1097/00000542-198709000-00012.

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Kaplan, Richard, Matthew Becker i Lynn Broadman. "Isolated Masseter Muscle Spasm Versus Generalized Rigidity?" Anesthesia & Analgesia 75, nr 1 (lipiec 1992): 146. http://dx.doi.org/10.1213/00000539-199207000-00035.

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Patel, Leena R., Deepak Bose i Judith A. Littleford. "Isolated Masseter Muscle Spasm Versus Generalized Rigidity?" Anesthesia & Analgesia 75, nr 1 (lipiec 1992): 146???147. http://dx.doi.org/10.1213/00000539-199207000-00036.

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Storella, R. J., i M. M. Keykhah. "A871 ACETYLCHOLINE RECEPTCHS MEDIATE MASSETER MUSCLE RIGIDITY". Anesthesiology 73, nr 3A (1.09.1990): NA. http://dx.doi.org/10.1097/00000542-199009001-00869.

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Chen, D. Y., i M. B. Weinger. "FOCAL BRAINSTEM ELECTRICAL STIMULATION INCREASES MUSCLE RIGIDITY". Anesthesiology 81, SUPPLEMENT (wrzesień 1994): A835. http://dx.doi.org/10.1097/00000542-199409001-00834.

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McKenna, S. J. "Masseter muscle rigidity and malignant hyperthermia susceptibility". Journal of Oral and Maxillofacial Surgery 44, nr 10 (październik 1986): 839–40. http://dx.doi.org/10.1016/0278-2391(86)90179-5.

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Wong, Michael M. C. "Neuroleptic Malignant Syndrome: Two Cases without Muscle Rigidity". Australian & New Zealand Journal of Psychiatry 30, nr 3 (czerwiec 1996): 415–18. http://dx.doi.org/10.3109/00048679609065008.

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Objective: Two patients with neuroleptic malignant syndrome without muscle rigidity are described. Clinical picture: Both patients developed fever and altered consciousness while taking neuroleptic but did not develop muscle rigidity; the symptoms subsided when the neuroleptic was stopped but recurred when it was given again. Treatment: The neuroleptic was stopped; one patient received supportive treatment and the other received bromocriptine. Outcome: One patient died while the other survived. Conclusion: The pathophysiology is proposed as a combination of involvement of the central thermoregulatory, neuroregulatory and autonomic nervous systems, and the peripheral skeletal muscle. It supports the concept of a spectrum of clinical severity of neuroleptic malignant syndrome.

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Vacaras, Vitalie, Enia Eleonora Cucu, Roxana Radu i Dafin Fior Muresanu. "Paraneoplastic Stiff Person Syndrome in Early-Stage Breast Cancer with Positive Anti-Amphiphysin Antibodies". Case Reports in Neurology 12, nr 3 (2.10.2020): 339–47. http://dx.doi.org/10.1159/000508942.

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Stiff person syndrome (SPS) is a rare neurologic disorder, characterized by muscle rigidity and spasms. Anti-glutamic acid decarboxylase (anti-GAD) antibodies are associated with the classic form of SPS, while antibodies against amphiphysin are associated with the paraneoplastic form of the disease. We present the case of a patient with paraneoplastic SPS, presenting with muscle cramps of lower extremities that progressed to severe muscle rigidity and spasms, associated with a right breast tumor and positive anti-amphiphysin antibodies. Paraneoplastic SPS is a rare neurological disorder, challenging for the physicians both to diagnose and treat.

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Ganguly, Jacky, Dinkar Kulshreshtha, Mohammed Almotiri i Mandar Jog. "Muscle Tone Physiology and Abnormalities". Toxins 13, nr 4 (16.04.2021): 282. http://dx.doi.org/10.3390/toxins13040282.

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The simple definition of tone as the resistance to passive stretch is physiologically a complex interlaced network encompassing neural circuits in the brain, spinal cord, and muscle spindle. Disorders of muscle tone can arise from dysfunction in these pathways and manifest as hypertonia or hypotonia. The loss of supraspinal control mechanisms gives rise to hypertonia, resulting in spasticity or rigidity. On the other hand, dystonia and paratonia also manifest as abnormalities of muscle tone, but arise more due to the network dysfunction between the basal ganglia and the thalamo-cerebello-cortical connections. In this review, we have discussed the normal homeostatic mechanisms maintaining tone and the pathophysiology of spasticity and rigidity with its anatomical correlates. Thereafter, we have also highlighted the phenomenon of network dysfunction, cortical disinhibition, and neuroplastic alterations giving rise to dystonia and paratonia.

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Endo, Takuyuki, Toshimitsu Hamasaki, Ryuhei Okuno, Masaru Yokoe, Harutoshi Fujimura, Kenzo Akazawa i Saburo Sakoda. "Parkinsonian Rigidity Shows Variable Properties Depending on the Elbow Joint Angle". Parkinson's Disease 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/258374.

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Parkinsonian rigidity has been thought to be constant through a full range of joint angle. The aim of this study was to perform a detailed investigation of joint angle dependency of rigidity. We first measured muscle tone at the elbow joint in 20 healthy subjects and demonstrated that an angle of approximately 60° of flexion marks the division of two different angle-torque characteristics. Then, we measured muscle tone at the elbow joint in 24 Parkinson’s Disease (PD) patients and calculated elastic coefficients in flexion and extension in the ranges of 10°–60° (distal) and 60°–110° (proximal). Rigidity as represented by the elastic coefficient in the distal phase of elbow joint extension was best correlated with the UPDRS rigidity score (r=0.77). A significant difference between the UPDRS rigidity score 0 group and 1 group was observed in the elastic coefficient in the distal phase of extension (P<0.0001), whereas no significant difference was observed in the proximal phase of extension and in each phase of flexion. Parkinsonian rigidity shows variable properties depending on the elbow joint angle, and it is clearly detected at the distal phase of elbow extension.

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Ferreira-Sánchez, María del Rosario, Marcos Moreno-Verdú i Roberto Cano-de-la-Cuerda. "Quantitative Measurement of Rigidity in Parkinson’s Disease: A Systematic Review". Sensors 20, nr 3 (6.02.2020): 880. http://dx.doi.org/10.3390/s20030880.

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Rigidity is one of the cardinal symptoms of Parkinson’s disease (PD). Present in up 89% of cases, it is typically assessed with clinical scales. However, these instruments show limitations due to their subjectivity and poor intra- and inter-rater reliability. To compile all of the objective quantitative methods used to assess rigidity in PD and to study their validity and reliability, a systematic review was conducted using the Web of Science, PubMed, and Scopus databases. Studies from January 1975 to June 2019 were included, all of which were written in English. The Strengthening the Reporting of observational studies in Epidemiology Statement (STROBE) checklist for observational studies was used to assess the methodological rigor of the included studies. Thirty-six studies were included. Rigidity was quantitatively assessed in three ways, using servomotors, inertial sensors, and biomechanical and neurophysiological study of muscles. All methods showed good validity and reliability, good correlation with clinical scales, and were useful for detecting rigidity and studying its evolution. People with PD exhibit higher values in terms of objective muscle stiffness than healthy controls. Rigidity depends on the angular velocity and articular amplitude of the mobilization applied. There are objective, valid, and reliable methods that can be used to quantitatively assess rigidity in people with PD.

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Albrecht, Alison, Denise J. Wedel i Gerald A. Gronert. "Masseter Muscle Rigidity and Nondepolarizing Neuromuscular Blocking Agents". Mayo Clinic Proceedings 72, nr 4 (kwiecień 1997): 329–32. http://dx.doi.org/10.4065/72.4.329.

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Lee, Robin van der, Ilse Ceelie i Saskia N. de Wildt. "Morphine-Induced Muscle Rigidity in a Term Neonate". Annals of Pharmacotherapy 43, nr 10 (15.09.2009): 1724–26. http://dx.doi.org/10.1345/aph.1m268.

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Silbert, Brendan S., i Charles A. Vacanti. "Amantidine in Prevention of Fentanyl-Induced Muscle Rigidity". Anesthesia & Analgesia 66, nr 12 (grudzień 1987): 1338. http://dx.doi.org/10.1213/00000539-198712000-00029.

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Vacanti, C. A., i F. X. Vacanti. "Sodium Thiopental To Treat Fentanyl Induced Muscle Rigidity". Anesthesia & Analgesia 67, Supplement (luty 1988): 241. http://dx.doi.org/10.1213/00000539-198802001-00241.

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Spitz, Mariana, Henrique Ballalai Ferraz, Orlando G. P. Barsottini i Alberto Alain Gabbai. "Progressive encephalomyelitis with rigidity: a paraneoplastic presentation of oat cell carcinoma of the lung. Case report". Arquivos de Neuro-Psiquiatria 62, nr 2b (czerwiec 2004): 547–49. http://dx.doi.org/10.1590/s0004-282x2004000300033.

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Progressive encephalomyelitis with rigidity and myoclonus (PEWR) is a rare neurological disorder, characterised by muscular rigidity, painful spasms, myoclonus, and evidence of brain stem and spinal cord involvement. A 73-year-old white man was admitted with a 10-day history of painful muscle spasms and continuous muscle rigidity on his left lower limb. He had involuntary spasms on his legs and developed encephalopathy with cranial nerves signs and long tract spinal cord symptomatology. Brain CT scan and spinal MRI were normal. The CSF showed lymphocytic pleocytosis and no other abnormalities. EMG showed involuntary muscle activity with 2-6 seconds of duration, interval of 30-50 ms and a frequency of 2/second in the left lower limb. Anti-GAD antibodies were detected in the blood. We detected radiological signs of lung cancer during the follow-up, which proved to be an oat cell carcinoma. The patient died two weeks after the diagnosis of the cancer.

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Sidow, Nor Osman, Faruk Odabaş, Abdiladhif Mohamed, Mohamed Sheikh Hassan i Erkan Tuner. "Drug Induced Neuroleptic Malignant Syndrome: A Case Report". Somalia Turkiye Medical Journal (STMJ) 1, nr 01 (17.10.2022): 1–3. http://dx.doi.org/10.58322/stmj.v1i01.1.

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Neuroleptic malignant syndrome (NMS) causes fever, muscle rigidity, and impaired mental status. Drugs that influence central dopaminergic neurotransmission and almost all neuroleptics, including newer atypical antipsychotics, are also associated with it. While uncommon, NMS remains a critical differential diagnosis for patients with fever and mental status changes due to the requirement for prompt resuscitation to prevent morbidity and mortality. We present a case of a 21-year-old man with schizophrenia who attended the emergency room with generalized muscle rigidity, high-grade fever, and disturbed mental status for 12 days. His serum creatine phosphokinase was elevated (CPK). The computed tomography (CT) of the brain was normal, and the CSF was clear and cell-free. The patient was given muscle relaxants, dopamine agonists, and biperiden. After three days, rigidity, fever, and consciousness improved. A few cases of antipsychotic-induced NMS have been reported. Healthcare professionals should be aware of this fatal side effect.

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Muthukrishnan, Subbaratnam, Seulgi Mun, Mi Y. Noh, Erika R. Geisbrecht i Yasuyuki Arakane. "Insect Cuticular Chitin Contributes to Form and Function". Current Pharmaceutical Design 26, nr 29 (4.09.2020): 3530–45. http://dx.doi.org/10.2174/1381612826666200523175409.

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: Chitin contributes to the rigidity of the insect cuticle and serves as an attachment matrix for other cuticular proteins. Deficiency of chitin results in abnormal embryos, cuticular structural defects and growth arrest. When chitin is not turned over during molting, the developing insect is trapped inside the old cuticle. Partial deacetylation of cuticular chitin is also required for proper laminar organization of the cuticle and vertical pore canals, molting, and locomotion. Thus, chitin and its modifications strongly influence the structure of the exoskeleton as well as the physiological functions of the insect. : Internal tendons and specialized epithelial cells called “tendon cells” that arise from the outer layer of epidermal cells provide attachment sites at both ends of adult limb muscles. Membrane processes emanating from both tendon and muscle cells interdigitate extensively to strengthen the attachment of muscles to the extracellular matrix (ECM). Protein ligands that bind to membrane-bound integrin complexes further enhance the adhesion between muscles and tendons. Tendon cells contain F-actin fiber arrays that contribute to their rigidity. In the cytoplasm of muscle cells, proteins such as talin and other proteins provide attachment sites for cytoskeletal actin, thereby increasing integrin binding and activation to mechanically couple the ECM with actin in muscle cells. Mutations in integrins and their ligands, as well as depletion of chitin deacetylases, result in defective locomotion and muscle detachment from the ECM. Thus, chitin in the cuticle and chitin deacetylases strongly influence the shape and functions of the exoskeleton as well as locomotion of insects.

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Ramos-Cabrera, Víctor, i Fanny Elizabeth Ramírez-Calderón. "Rigidez muscular, trastorno de sensorio y antipsicóticos: Reporte de caso". Horizonte Médico (Lima) 19, nr 3 (30.09.2019): 78–83. http://dx.doi.org/10.24265/horizmed.2019.v19n3.11.

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Nejkovic, Natasa, Snezana Protic, Nemanja Zaric, Zoran Krivokapic i Ljubomir Djurasic. "Case of leptosuccin induced malignant hyperthermia in a patient with GIST of the rectum". Acta chirurgica Iugoslavica 59, nr 2 (2012): 121–23. http://dx.doi.org/10.2298/aci1202121n.

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Malignant hyperthermia (MH) is a form of myopathy that is usually triggered by volatile anaesthetics such as halothane, sevoflurane and des flurane and depolarising muscle relaxants such as succinylcholine. Pathologic response in MH inc1ude increase in oxygen consumption, increase in endtidal C02, tachycardia, hyperthermia, hyperkalemia and muscle rigidity. Immediate recognition and treatment are crucial to avoid lethal outcome. Molecular genetic studies have confirmed that ryanodine muscle receptors are responsible for MH. We present a case of leptosuccin induced MH with masseter muscle rigidity, mild pC02 increase (6.3 kPa), elevated body temperature measured with esophageal temperature probe (39.5?C) tachycardia (115 beats/min) and respiratory and metabolic acidosis (pH was 7,23) in a patient who underwent low anterior resection of the rectum for gast rointestinal stromal tumor (GIST) of the rectum.

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Phillips, Craig. "Stability in Dance Training". Journal of Dance Medicine & Science 9, nr 1 (marzec 2005): 24–28. http://dx.doi.org/10.1177/1089313x0500900105.

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Stability training has become a recognized component of dance training in the past decade. Drawing on knowledge applied in sports and spinal rehabilitation, dancers are now able to enhance their performance by applying similar principles in their training. The main issue with stability training is one of being able to recognize the difference between muscle strength training and muscle skill acquisition. Motor control principles underlie stability training as it is the long-term, learned, skill of effective muscle recruitment that is desired rather than short-term strengthening of these muscles. We know that the musculoskeletal system is not an inherently stable structure and ultimately relies on muscle activity to maintain its integrity. This article explores both local and global stability muscle systems, the processes of skill acquisition, and highlight the differences between stability and rigidity.

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Markus, H. S., M. Cox i A. M. Tomkins. "Raised resting energy expenditure in Parkinson's disease and its relationship to muscle rigidity". Clinical Science 83, nr 2 (1.08.1992): 199–204. http://dx.doi.org/10.1042/cs0830199.

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1. Resting energy expenditure was measured, by indirect calorimetry, in 12 patients with Parkinson's disease and in eight healthy age-matched control subjects. In the patients with Parkinson's disease measurements were made in both the untreated state and after an injection of the dopamine agonist apomorphine (treated state). In each state muscle rigidity was recorded. 2. Resting energy expenditure was higher in patients with Parkinson's disease in both the treated and untreated states than in the control subjects. Of the patients with Parkinson's disease, seven showed no difference in resting energy expenditure between the two treatment states, whereas four showed markedly increased resting energy expenditure in the untreated state. The change in resting energy expenditure in the untreated state, as compared with the treated state, was significantly related to the development of muscle rigidity in the untreated state. 3. In Parkinson's disease, even in optimally treated patients, resting energy expenditure is raised and this may contribute to the weight loss seen in this disease. Severe muscle rigidity occurring during untreated periods results in a further increase in resting energy expenditure.

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Ali, Maryam Adam, Noora Adam Ali i Khurram Sarfaraz. "Neuroleptic Malignant Syndrome: Catch Me If You Can; A Case Report". International Journal of Health Sciences and Research 12, nr 3 (16.03.2022): 314–19. http://dx.doi.org/10.52403/ijhsr.20220342.

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Neuroleptic Malignant Syndrome (NMS) is a relatively rare adverse reaction to neuroleptic medications. It is characterized by a constellation of findings that usually occur concurrently. These include vital instability, fever, elevated creatinine kinase, encephalopathy, and muscle rigidity. Having a high index of suspicion can reduce mortality and long-term complications by having a broad differential diagnosis when facing a patient with these symptoms, particularly if they are on antipsychotic medications. Withdrawal of the offending medication and supportive therapy are the most important initial steps in patient management. In this case report, we discuss the case of a 95-year-old male on quetiapine and memantine with a 2-day history of fever, rigidity, cough, and reduced activity after increasing the dose of quetiapine three days prior to his presentation. Key words: Neuroleptic malignant syndrome, Antipsychotics, Neuroleptics, Muscle rigidity Creatinine Kinase.

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Et-Taouil, Karima, Michel Safar i Gérard E. Plante. "Mechanisms and consequences of large artery rigidity". Canadian Journal of Physiology and Pharmacology 81, nr 3 (1.03.2003): 205–11. http://dx.doi.org/10.1139/y03-022.

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In this review paper, the classical and more recently described mechanisms responsible for the structural and functional characteristics of large artery rigidity are described. Mostly important, these characteristics appear to be nonspecific to the primary disease process involved in arterial hypertension, diabetes mellitus, dyslipidemia, congestive heart failure, chronic uremia, and perhaps senescence, including vascular dementia. Nonspecific in terms of aetiology, the vasculopathy encountered in these diseases exhibits common structural and functional abnormalities. The identification of such abnormalities could well become the target of potent nonpharmacological and (or) pharmacological interventions capable of preventing or retarding morbidity and mortality. The structural characteristics responsible for large artery rigidity include smooth muscle cell hypertrophy, matrix collagen deposition, and recently described, dysfunction in proteoglycan metabolism. Functional abnormalities, such as bradykinin-dependent hyper-reactivity of smooth muscle cells and vasa vasorum microcirculation network disturbances, also appear to alter aortic wall rigidity. The physiopathology of target organ damage is then revisited, based on endothelial dysfunction, documented in large and resistance arteries, as well as in microcirculation networks, where altered permeability to macromolecules leads to interstitial matrix disorganization and cell damage. The clinical evaluation of large artery rigidity is described, and one of the noninvasive methods, evaluation of pulse-wave velocity, is validated in normal conditions and in disease processes. Finally, nonpharmacological and pharmacological therapeutic measures are presented, and includes physical exercise to reduce insulin resistance, and reninangiotensin-IIaldosterone modulators.Key words: large artery compliance, aortic structure, collagen, elastin, proteoglycans, vascular smooth muscle cells, vasa vasorum, target organ damage, pulse wave velocity, vascular pharmacology.

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Khan, Fayaz, Mohamed Faisal Chevidikunnan, Raghad Ahmad Almalki, Mawada Khaled Mirdad, Khadeeja Abdulaziz Nimatallah, Shahad Al-Zahrani i Aysha Abdulmalek Alshareef. "Stiff-Person Syndrome Outpatient Rehabilitation: Case Report". Journal of Neurosciences in Rural Practice 11, nr 04 (20.08.2020): 651–53. http://dx.doi.org/10.1055/s-0040-1715081.

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AbstractStiff-person syndrome (SPS) is a rare neurological disorder that causes muscle rigidity and stiffness of the trunk and proximal limb muscles, leading to movement difficulties and impaired function. Due to the rarity of the disease, studies on the benefit of rehabilitation for this disorder are quite limited. A 46-year-old female patient diagnosed with SPS complained of imbalance and movement difficulty. We prescribed therapeutic exercises aimed to reduce the stiffness of the trunk and proximal limbs and improve her function. Baseline measurement of the patient's range of motion, muscle power and tone, balance and functional abilities were taken pre- and post-program. Outcome measures showed a general improvement in the patient's muscle flexibility, balance, and functionality.

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Grazko, M. A., K. B. Polo i B. Jabbari. "Botulinum toxin A for spasticity, muscle spasms, and rigidity". Neurology 45, nr 4 (1.04.1995): 712–17. http://dx.doi.org/10.1212/wnl.45.4.712.

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MAROHN, MARY L., i ALI H. NAGIA. "Masseter Muscle Rigidity after Rapid-sequence Induction of Anesthesia". Anesthesiology 77, nr 1 (1.07.1992): 205–6. http://dx.doi.org/10.1097/00000542-199207000-00028.

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OʼFlynn, R., J. Shutack DO, H. Rosenberg MD i J. Fletcher PhD. "MASSETER MUSCLE RIGIDITY (MMR) AND MALIGNANT HYPERTHERMIA SUSCEPTIBILITY (MHS)". Anesthesiology 77, Supplement (wrzesień 1992): A917. http://dx.doi.org/10.1097/00000542-199209001-00917.

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Medina, Karla A., i James F. Mayhew. "Generalized Muscle Rigidity and Hypercarbia with Halothane and Isoflurane". Anesthesia & Analgesia 86, nr 2 (luty 1998): 297–98. http://dx.doi.org/10.1097/00000539-199802000-00014.

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Medina, Karla A., i James F. Mayhew. "Generalized Muscle Rigidity and Hypercarbia with Halothane and Isoflurane". Anesthesia & Analgesia 86, nr 2 (luty 1998): 297–98. http://dx.doi.org/10.1213/00000539-199802000-00014.

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Hadad, Eran, Avi A. Weinbroum i Ron Ben-Abraham. "Drug-induced hyperthermia and muscle rigidity: a practical approach". European Journal of Emergency Medicine 10, nr 2 (czerwiec 2003): 149–54. http://dx.doi.org/10.1097/00063110-200306000-00018.

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Canepa-Raggio, Carlo, i Mohammad Choudhury. "STIFF PERSON SYNDROME (SPS) THE IMPORTANCE OF EXTENSIVE PHYSICAL EXAMINATION". East European Journal of Parkinson`s Disease and Movement Disorders 6, nr 1-2 (27.05.2020): 20–23. http://dx.doi.org/10.33444/2414-0007.6.1-2.20-23.

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Stiff Person Syndrome (SPS) is a rare condition with a prevalence of one to two cases per million and an incidence of one case per year. Characterized by progressive muscle stiffening, rigidity and spasm, mainly involve the axial muscles, resulting in severely impaired ambulation. The pathogenesis is not that clear. Classic SPS presents with extreme and persistent rigidity and stiffness of truncal and proximal limb muscles, significant lumber/cervical lordosis resulting from simultaneous actions of opposing paraspinous muscles are the hallmark. Wide and unsteady gait (Frankenstein’s gait) resulting from stiff muscles increases the risk of fall and fracture. Patient’s ADLs get severely restricted progressively. Startle reflex which is a superimposed episodic muscle spasm precipitated by sudden movement, noise, or emotional upset is a sensitive and specific feature of SPS and can be visible and palpable. Autonomic dysfunctions are common and are common cause of death in patients with SPS. In cases of partial SPS, we can find that truncal muscles are spared and limb muscles are affected, hence the term stiff-limb syndrome is used sometimes. Can involve a limb or focal part of a limb. As for treatment, symptom control and improving mobility and overall functionality is the primary target. High dose benzodiazepine is the best initial treatment. Those who are refractory can be benefit from Baclofen, IVIG, Plasma exchange, biological agent, e.g. Rituximab. Treatment of primary malignancies in paraneoplastic SPS can achieve remission. Keywords: Stiff Person Syndrome, clinical features, diagnosis and treatment.

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Lacson, A. G., S. S. Seshia, H. B. Sarnat, J. Anderson, W. R. DeGroot, A. Chudley, C. Adams i in. "Autosomal Recessive, Fatal Infantile Hypertonic Muscular Dystrophy Among Canadian Natives". Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 21, nr 3 (sierpień 1994): 203–12. http://dx.doi.org/10.1017/s0317167100041172.

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Abstract:We describe eleven mid-western Canadian aboriginal infants with a unique, progressive muscle disorder. All except one had muscle biopsy and/or autopsy. The infants were normal newborns who rapidly developed rigidity of all skeletal muscles, with early, respiratory insufficiency. Death occurred before 18 months of age. Electromyography showed increased insertion activity and profuse fibrillation potentials; motor unit potentials and interference pattern are normal until late in the course. Pathologic features include progressive, granular to powdery Z-band transformation, myofibrillar loss, and muscle regeneration. SDS-gel electrophoresis of one muscle sample revealed increased 54kDa and reduced 80kDa protein fractions. This disease differs from other conditions with Z-band alterations because of continuous muscle activity and relentless clinical progression. The clinical features, elevated serum creatine kinase, electromyographic and muscle biopsy findings suggest a dystrophic process. The recognition of this condition as an autosomal recessive disorder allows appropriate genetic counselling.

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Marcucci, Lorenzo, i Carlo Reggiani. "Increase of resting muscle stiffness, a less considered component of age-related skeletal muscle impairment". European Journal of Translational Myology 30, nr 2 (17.06.2020): 223–33. http://dx.doi.org/10.4081/ejtm.2020.8982.

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Elderly people perform more slowly movements of everyday life as rising from a chair, walking, and climbing stairs. This is in the first place due to the loss of muscle contractile force which is even more pronounced than the loss of muscle mass. In addition, a secondary, but not negligible, component is the rigidity or increased stiffness which requires greater effort to produce the same movement and limits the range of motion of the joints. In this short review, we discuss the possible determinants of the limitations of joint mobility in healthy elderly, starting with the age-dependent alterations of the articular structure and focusing on the increased stiffness of the skeletal muscles. Thereafter, the possible mechanisms of the increased stiffness of the muscle-tendon complex are considered, among them changes in the muscle fibers, alterations of the connective components (extracellular matrix or ECM, aponeurosis, fascia and tendon) and remodeling of the neural pattern of muscle activation with increased of antagonist co-activation.

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Mileykovskiy, Boris Y., Lyudmila I. Kiyashchenko i Jerome M. Siegel. "Muscle Tone Facilitation and Inhibition After Orexin-A (Hypocretin-1) Microinjections Into the Medial Medulla". Journal of Neurophysiology 87, nr 5 (1.05.2002): 2480–89. http://dx.doi.org/10.1152/jn.2002.87.5.2480.

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Orexins/hypocretins are synthesized in neurons of the perifornical, dorsomedial, lateral, and posterior hypothalamus. A loss of hypocretin neurons has been found in human narcolepsy, which is characterized by sudden loss of muscle tone, called cataplexy, and sleepiness. The normal functional role of these neurons, however, is unclear. The medioventral medullary region, including gigantocellular reticular nucleus, alpha (GiA) and ventral (GiV) parts, participates in the induction of locomotion and muscle tone facilitation in decerebrate animals and receives moderate orexinergic innervation. In the present study, we have examined the role of orexin-A (OX-A) in muscle tone control using microinjections (50 μM, 0.3 μl) into the GiA and GiV sites in decerebrate rats. OX-A microinjections into GiA sites, previously identified by electrical stimulation as facilitating hindlimb muscle tone bilaterally, produced a bilateral increase of muscle tone in the same muscles. Bilateral lidocaine microinjections (4%, 0.3 μl) into the dorsolateral mesopontine reticular formation decreased muscle rigidity and blocked muscle tone facilitation produced by OX-A microinjections into the GiA sites. The activity of cells related to muscle rigidity, located in the pedunculopontine tegmental nucleus and adjacent reticular formation, was correlated positively with the extent of hindlimb muscle tone facilitation after medullary OX-A microinjections. OX-A microinjections into GiV sites were less effective in muscle tone facilitation, although these sites produced a muscle tone increase during electrical stimulation. In contrast, OX-A microinjections into the gigantocellular nucleus (Gi) sites and dorsal paragigantocellular nucleus (DPGi) sites, previously identified by electrical stimulation as inhibitory points, produced bilateral hindlimb muscle atonia. We propose that the medioventral medullary region is one of the brain stem target for OX-A modulation of muscle tone. Facilitation of muscle tone after OX-A microinjections into this region is linked to activation of intrinsic reticular cells, causing excitation of midbrain and pontine neurons participating in muscle tone facilitation through an ascending pathway. Moreover, our results suggest that OX-A may also regulate the activity of medullary neurons participating in muscle tone suppression. Loss of OX function may, therefore, disturb both muscle tone facilitatory and inhibitory processes at the medullary level.

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Vita, Gary M., Antonel Olckers, Anne E. Jedlicka, Alfred L. George, Terry Heiman-Patterson, Henry Rosenberg, Jeffrey E. Fletcher i Roy C. Levitt. "Masseter Muscle Rigidity Associated with Glycine1306-to- Alanine Mutation in the Adult Muscle Sodium Channel α-Subunit Gene". Anesthesiology 82, nr 5 (1.05.1995): 1097–103. http://dx.doi.org/10.1097/00000542-199505000-00002.

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Background Succinylcholine-induced masseter muscle rigidity (MMR) is a potentially life-threatening complication of anesthesia and is closely correlated with the heterogeneous disorder malignant hyperthermia (MH) susceptibility. MMR also is identified with a variety of neuromuscular disorders, including the myotonias, that are associated with abnormal in vitro contracture test (IVCT) results. Recently, mutations in the adult skeletal muscle sodium channel alpha-subunit gene (SCN4A) have been shown to cause generalized nondystrophic myotonias, some of which are associated with mild nonspecific symptoms. The purpose of the current investigation was to begin to evaluate the molecular genetic relationship between known mutations in the SCN4A gene, MMR, and the results of the IVCT used to diagnose MH-susceptibility. Methods A single extended pedigree of 16 individuals was ascertained through a proband who experienced MMR and whole-body rigidity after succinylcholine administration. Subsequently, four individuals were shown to have a mild form of myotonia on clinical and laboratory examination. IVCT was carried out according to standardized protocols. Mutations in the SCN4A gene were sought in exons 22 and 24 using single-strand conformational analyses. Variability in the SCN4A gene sequence was confirmed by direct DNA sequence analyses. Results Four individuals with myotonia were shown to carry a guanine-to-cytosine mutation at nucleotide position 3917 of the reported SCN4A sequence. This DNA mutation was coinherited with MMR and an abnormal IVCT result in this family. Previous studies have demonstrated that the glycine1306-to-alanine substitution is associated with a mild clinical syndrome referred to as myotonia fluctuans. Conclusions The current report provides direct evidence that succinylcholine-induced MMR, whole-body rigidity, and an abnormal IVCT result are associated with a mutation in the SCN4A gene.

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Chini, Giorgia, Tiwana Varrecchia, Mariano Serrao i Alberto Ranavolo. "Lower Limb Muscle Co-Activation Maps in Single and Team Lifting at Different Risk Levels". Applied Sciences 14, nr 11 (28.05.2024): 4635. http://dx.doi.org/10.3390/app14114635.

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The central nervous system uses muscle co-activation for body coordination, effector movement control, and joint stabilization. However, co-activation increases compression and shear stresses on the joints. Lifting activity is one of the leading causes of work-related musculoskeletal problems worldwide, and it has been shown that when the risk level rises, lifting enhances trunk muscle co-activation at the L5/S1 level. This study aims to investigate the co-activation of lower limb muscles during liftings at various risk levels and lifting types (one-person and vs. two-person team lifting), to understand how the central nervous system governs lower limb rigidity during these tasks. The surface electromyographic signal of thirteen healthy volunteers (seven males and six females, age range: 29–48 years) was obtained over the trunk and right lower limb muscles while lifting in the sagittal plane. Then co-activation was computed according to different approaches: global, full leg, flexor, extensor, and rostro-caudal. The statistical analysis revealed a significant increase in the risk level and a decrease in the two-person on the mean and/or maximum of the co-activation in almost all the approaches. Overall, our findings imply that the central nervous system streamlines the motor regulation of lifting by increasing or reducing whole-limb rigidity within a distinct global, extensor, and rostro-caudal co-activation scheme, depending on the risk level/lifting type.

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Yemen, Terrance A. "Are We Obsessed with Masseter Muscle Rigidity? Temporomandibular Joint Disease Mistakenly Diagnosed as Masseter Muscle Rigidity on Two Separate Occasions in One Patient". Anesthesia & Analgesia 77, nr 4 (październik 1993): 848???850. http://dx.doi.org/10.1213/00000539-199310000-00032.

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