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Sensors (Basel, Switzerland) Feb 2020Rigidity 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...
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.
Topics: Electromyography; Humans; Joints; Movement; Muscle Rigidity; Muscles; Observational Studies as Topic; Parkinson Disease
PubMed: 32041374
DOI: 10.3390/s20030880 -
Journal of Addiction MedicineThis narrative review summarizes literature on pharmaceutical fentanyl's absorption, distribution, metabolism, and excretion patterns to inform research on illicitly... (Review)
Review
OBJECTIVES
This narrative review summarizes literature on pharmaceutical fentanyl's absorption, distribution, metabolism, and excretion patterns to inform research on illicitly manufactured fentanyl (IMF).
RESULTS
Fentanyl is highly lipophilic, lending itself to rapid absorption by highly perfused tissues (including the brain) before redistributing from these tissues to muscle and fat. Fentanyl is eliminated primarily by metabolism and urinary excretion of metabolites (norfentanyl and other minor metabolites). Fentanyl has a long terminal elimination, with a documented secondary peaking phenomenon that can manifest as "fentanyl rebound." Clinical implications in overdose (respiratory depression, muscle rigidity, and "wooden chest syndrome") and opioid use disorder treatment (subjective effects, withdrawal, and buprenorphine-precipitated withdrawal) are discussed. The authors highlight research gaps derived from differences in medicinal fentanyl studies and IMF use patterns, including that medicinal fentanyl studies are largely conducted with persons who were opioid-naive, anesthetized, or had severe chronic pain and that IMF use is characterized by supratherapeutic doses and frequent and sustained administration patterns, as well as adulteration with other substances and/or fentanyl analogs.
CONCLUSIONS
This review reexamines information yielded from decades of medicinal fentanyl research and applies elements of the pharmacokinetic profile to persons with IMF exposure. In persons who use drugs, peripheral accumulation of fentanyl may be leading to prolonged exposure. More focused research on the pharmacology of fentanyl in persons using IMF is warranted.
Topics: Humans; Analgesics, Opioid; Chronic Pain; Clinical Relevance; Drug Overdose; Fentanyl
PubMed: 37788600
DOI: 10.1097/ADM.0000000000001185 -
Handbook of Clinical Neurology 2018Malignant hyperthermia (MH) is a form of heat illness caused by increased heat generation exceeding the body's capacity for heat loss. It is classified separately from... (Review)
Review
Malignant hyperthermia (MH) is a form of heat illness caused by increased heat generation exceeding the body's capacity for heat loss. It is classified separately from other forms of heat illness as the latter require assessment of mental function for differential diagnosis. This is not possible with MH which occurs during general anesthesia when mental function cannot be assessed. MH occurs in genetically predisposed individuals exposed to inhalation anesthetics or succinylcholine. The genetic defects identified so far cause perturbation of skeletal muscle excitation-contraction coupling resulting in myoplasmic calcium dysregulation. The most commonly involved gene is RYR1. Increased myoplasmic calcium leads to hypermetabolism and sustained muscle contractile activity with consequent increased oxygen consumption, carbon dioxide production, sympathetic stimulation, muscle rigidity, heat production, rhabdomyolysis, and disseminated intravascular coagulation. Untreated reactions are fatal. In this chapter we summarize clinical features and management and review current understanding of the pathophysiology and molecular genetics of MH.
Topics: Animals; Humans; Malignant Hyperthermia; Muscle, Skeletal; Ryanodine Receptor Calcium Release Channel
PubMed: 30459030
DOI: 10.1016/B978-0-444-64074-1.00038-0 -
Neuropediatrics Apr 2020The aim of this paper is to provide a clinically applicable overview of different tone reducing modalities and how these can interact with or augment concurrent physical... (Review)
Review
The aim of this paper is to provide a clinically applicable overview of different tone reducing modalities and how these can interact with or augment concurrent physical therapy (PT). Botulinum toxin (BoNT), oral tone-regulating medication, intrathecal baclofen (ITB), and selective dorsal rhizotomy are discussed within a physiotherapeutic context and in view of current scientific evidence. We propose clinical reasoning strategies to identify treatment goals as well as the appropriate and corresponding treatment interventions. Instrumented measurement of spasticity, standardized clinical assessment, and 3D clinical motion analysis are scientifically sound tools to help select the appropriate treatment and, when needed, to selectively target or spare individual muscles. In addition, particular attention is given to strength training as a necessary tool to tackle muscle weakness associated with specific modalities of tone reduction. More research is needed to methodologically assess the long-term effectiveness of such individualized tone treatment, optimize parameters such as medication dosage, and gain more insight into the kind of PT techniques that are essential in conjunction with tone reduction.
Topics: Cerebral Palsy; Child; Humans; Muscle Rigidity; Muscle Spasticity; Physical Therapy Modalities
PubMed: 31777043
DOI: 10.1055/s-0039-3400987 -
Brain and Nerve = Shinkei Kenkyu No... Jun 2023Stiff-person syndrome (SPS) is a rare autoimmune neurological disorder characterized by progressive axial muscle stiffness, central nervous system hyper-excitability,...
Stiff-person syndrome (SPS) is a rare autoimmune neurological disorder characterized by progressive axial muscle stiffness, central nervous system hyper-excitability, and painful stimulus-sensitive muscle spasms. SPS is classified into classic SPS and SPS variants, including stiff-limb syndrome (SLS) and progressive encephalomyelitis with rigidity and myoclonus (PERM), based on clinical presentation. SPS responds to immunotherapy, and several autoantigens have been identified. Most patients with SPS have high-titers of antibodies against glutamic acid decarboxylase (GAD), the rate-limiting enzyme for the synthesis of γ-aminobutyric acid (GABA), and up to 15% of the patients have antibodies against the glycine receptor α-subunit.
Topics: Humans; Stiff-Person Syndrome; Muscle Rigidity; Encephalomyelitis; Autoimmune Diseases of the Nervous System; Central Nervous System; Glutamate Decarboxylase
PubMed: 37287358
DOI: 10.11477/mf.1416202410 -
Brain and Nerve = Shinkei Kenkyu No... May 2021Stiff-person syndrome (SPS) is a neurological disorder characterized by fluctuating muscle rigidity and painful spasms that occur spontaneously or are triggered by...
Stiff-person syndrome (SPS) is a neurological disorder characterized by fluctuating muscle rigidity and painful spasms that occur spontaneously or are triggered by diverse stimuli. Partial or segmental forms of the disorder, such as stiff-limb syndrome (SLS) and the more severe disease called progressive encephalomyelitis with rigidity and myoclonus (PERM), are usually considered within the spectrum of SPS. SPS responds to immunotherapies, and several autoantigens have been identified. Most patients with SPS have high titers of antibodies against glutamic acid decarboxylase (GAD), the enzyme that limits the rate of the synthesis of γ-aminobutyric acid (GABA), and up to 15% have antibodies against the glycine receptor α-subunit.
Topics: Encephalomyelitis; Glutamate Decarboxylase; Humans; Muscle Rigidity; Receptors, Glycine; Stiff-Person Syndrome
PubMed: 34006698
DOI: 10.11477/mf.1416201808 -
JBR-BTR : Organe de La Societe Royale... Jun 2015A 28-year-old man was referred to the neurology department of our hospital with difficulty of social interaction, impairment in carrying out daily life activities and...
A 28-year-old man was referred to the neurology department of our hospital with difficulty of social interaction, impairment in carrying out daily life activities and muscle rigidity. He had a history of head trauma 3 years ago. Neurological examination revealed bradykinesia, hypophonic speech, resting and postural tremor, rigidity, spasticity, hyperreflexia and psychosis.
PubMed: 30394416
DOI: 10.5334/jbr-btr.791 -
Journal of Neurophysiology Jan 2022Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, mainly affecting people over 60 yr of age. Patients... (Review)
Review
Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, mainly affecting people over 60 yr of age. Patients develop both classic symptoms (tremors, muscle rigidity, bradykinesia, and postural instability) and nonclassical symptoms (orthostatic hypotension, neuropsychiatric deficiency, sleep disturbances, and respiratory disorders). Thus, patients with PD can have a significantly impaired quality of life, especially when they do not have multimodality therapeutic follow-up. The respiratory alterations associated with this syndrome are the main cause of mortality in PD. They can be classified as peripheral when caused by disorders of the upper airways or muscles involved in breathing and as central when triggered by functional deficits of important neurons located in the brainstem involved in respiratory control. Currently, there is little research describing these disorders, and therefore, there is no well-established knowledge about the subject, making the treatment of patients with respiratory symptoms difficult. In this review, the history of the pathology and data about the respiratory changes in PD obtained thus far will be addressed.
Topics: Humans; Parkinson Disease; Respiration Disorders
PubMed: 34817281
DOI: 10.1152/jn.00363.2021