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Journal of Parkinson's Disease 2022Parkinson's disease (PD) is defined by its motor symptoms rigidity, tremor, and akinesia. However, non-motor symptoms, particularly autonomic disorders and sleep... (Review)
Review
Parkinson's disease (PD) is defined by its motor symptoms rigidity, tremor, and akinesia. However, non-motor symptoms, particularly autonomic disorders and sleep disturbances, occur frequently in PD causing equivalent or even greater discomfort than motor symptoms effectively decreasing quality of life in patients and caregivers. Most common sleep disturbances in PD are insomnia, sleep disordered breathing, excessive daytime sleepiness, REM sleep behavior disorder, and sleep-related movement disorders such as restless legs syndrome. Despite their high prevalence, therapeutic options in the in- and outpatient setting are limited, partly due to lack of scientific evidence. The importance of sleep disturbances in neurodegenerative diseases has been further emphasized by recent evidence indicating a bidirectional relationship between neurodegeneration and sleep. A more profound insight into the underlying pathophysiological mechanisms intertwining sleep and neurodegeneration might lead to unique and individually tailored disease modifying or even neuroprotective therapeutic options in the long run. Therefore, current evidence concerning the management of sleep disturbances in PD will be discussed with the aim of providing a substantiated scaffolding for clinical decisions in long-term PD therapy.
Topics: Humans; Parkinson Disease; Quality of Life; REM Sleep Behavior Disorder; Sleep; Sleep Wake Disorders
PubMed: 35938257
DOI: 10.3233/JPD-212749 -
Revue Medicale de Liege Mar 2020Psychomotor disadaptation syndrome (PDS) was first described by the Geriatrics School of Dijon (France), three decades ago, under the name «psychomotor regression...
Psychomotor disadaptation syndrome (PDS) was first described by the Geriatrics School of Dijon (France), three decades ago, under the name «psychomotor regression syndrome». Over time, the original clinical features remained unchanged. However, progress has been made in its pathophysiology understanding and care, hence the new name, PDS, appeared in the 1990s. The PDS is also called sub-cortico-frontal dysfunction syndrome since the 2000s. It corresponds to a decompensation of posture, gait and psychomotor automatisms, related to an alteration of the postural and motor programming, which is a consequence of sub-cortico-frontal lesions. The clinical features of PDS associate backward disequilibrium, nonspecific gait disorders and neurological signs (akinesia, reactional hypertonia, impaired reactive postural responses and protective reactions, etc.). Psychological disorders of PDS are a fear of standing and walking in its acute form (the post-fall syndrome), or a bradyphrenia and anhedonia in its chronic form. The PDS occurrence results from the combination of three factors implicated in the reduction in functional reserves related to the alteration of the sub-cortico-frontal structures: ageing, chronic afflictions and acute situations, which induce a decrease in cerebral blood flow. The PDS management must be multidisciplinary, including the physician, the physiotherapist, the psychologist, nurses and care assistants.
Topics: Accidental Falls; Adaptation, Physiological; France; Gait; Humans; Postural Balance; Posture; Sensation Disorders; Syndrome
PubMed: 32157844
DOI: No ID Found -
Pharmacogenomics Feb 2018General anesthesia is a state of unconsciousness, amnesia, analgesia and akinesia induced by drugs including opioids, hypnotic-sedative agents, muscle relaxants and... (Review)
Review
General anesthesia is a state of unconsciousness, amnesia, analgesia and akinesia induced by drugs including opioids, hypnotic-sedative agents, muscle relaxants and antiemetics. Clinical and genetic factors are reported to influence the efficacy and side effects of these agents. Based on the evidence, clinical action is needed to improve clinical outcomes. This review summarizes the latest knowledge with regards to the pharmacogenetics of anesthetics and general anesthesia related complications.
Topics: Anesthesia, General; Anesthetics, General; Drug-Related Side Effects and Adverse Reactions; Humans; Pharmacogenetics; Polymorphism, Single Nucleotide
PubMed: 29318929
DOI: 10.2217/pgs-2017-0168 -
European Cells & Materials Jan 2015Foetal movements commence at seven weeks of gestation, with the foetal movement repertoire including twitches, whole body movements, stretches, isolated limb movements,... (Review)
Review
Foetal movements commence at seven weeks of gestation, with the foetal movement repertoire including twitches, whole body movements, stretches, isolated limb movements, breathing movements, head and neck movements, jaw movements (including yawning, sucking and swallowing) and hiccups by ten weeks of gestational age. There are two key biomechanical aspects to gross foetal movements; the first being that the foetus moves in a dynamically changing constrained physical environment in which the freedom to move becomes increasingly restricted with increasing foetal size and decreasing amniotic fluid. Therefore, the mechanical environment experienced by the foetus affects its ability to move freely. Secondly, the mechanical forces induced by foetal movements are crucial for normal skeletal development, as evidenced by a number of conditions and syndromes for which reduced or abnormal foetal movements are implicated, such as developmental dysplasia of the hip, arthrogryposis and foetal akinesia deformation sequence. This review examines both the biomechanical effects of the physical environment on foetal movements through discussion of intrauterine factors, such as space, foetal positioning and volume of amniotic fluid, and the biomechanical role of gross foetal movements in human skeletal development through investigation of the effects of abnormal movement on the bones and joints. This review also highlights computational simulations of foetal movements that attempt to determine the mechanical forces acting on the foetus as it moves. Finally, avenues for future research into foetal movement biomechanics are highlighted, which have potential impact for a diverse range of fields including foetal medicine, musculoskeletal disorders and tissue engineering.
Topics: Biomechanical Phenomena; Computer Simulation; Fetal Movement; Gestational Age; Humans; Models, Biological; Musculoskeletal Abnormalities
PubMed: 25552425
DOI: 10.22203/ecm.v029a01 -
Parkinsonism & Related Disorders Apr 2017Akinesia, hypokinesia, and bradykinesia are extensively used to describe motor execution disturbances, but are applied inconsistently and cover more conditions than... (Review)
Review
Akinesia, hypokinesia, and bradykinesia are extensively used to describe motor execution disturbances, but are applied inconsistently and cover more conditions than their Greek translations would suggest. We investigated the origins and changes in meaning of these terms over time, particularly in relation to Parkinson's disease (PD). We searched the literature from 1817 to 2015 for use and interpretation of the words akinesia, bradykinesia, hypokinesia, and PD. We found that akinesia and hypokinesia appeared as terms in the 19th century, opposite to hyperkinesia, but were used in the context of PD since 1920, while at the same time the 'bradykinetic syndrome' was introduced. Use of all terms increased in this period due to the encephalitis-lethargica-epidemic, and increased again with the discovery of levodopa from 1961. With the extensive use of criteria sets from the 1980s, bradykinesia replaced akinesia as the most commonly used term. The advent of the internet led to an increase in publications and an associated increase in heterogeneity in the use of the terms. This review shows the variation over time and the lack of unity in the terminology used to describe the range of movement execution disturbances. The current terminology fails to capture the nuances of the challenges we face in documenting these disturbances. We therefore recommend that the current situation may benefit from an objective and computationally solid approach using insights from network and circuitry technology and new developments in assessment technology. It is expected that this will contribute to a new framework for terminology in movement disorders.
Topics: Antiparkinson Agents; Forecasting; History, 19th Century; History, 20th Century; History, 21st Century; Humans; Hypokinesia; Levodopa; Parkinson Disease; Terminology as Topic
PubMed: 28153525
DOI: 10.1016/j.parkreldis.2017.01.010 -
Movement Disorders : Official Journal... Oct 2023Long-term use of levodopa for Parkinson's disease (PD) treatment is often hindered by development of motor complications, including levodopa-induced dyskinesia (LID)....
BACKGROUND
Long-term use of levodopa for Parkinson's disease (PD) treatment is often hindered by development of motor complications, including levodopa-induced dyskinesia (LID). The substantia nigra pars reticulata (SNr) and globus pallidus internal segment (GPi) are the output nuclei of the basal ganglia. Dysregulation of SNr and GPi activity contributes to PD pathophysiology and LID.
OBJECTIVE
The objective of this study was to determine whether direct modulation of SNr GABAergic neurons and SNr projections to the pedunculopontine nucleus (PPN) regulates PD symptoms and LID in a mouse model.
METHODS
We expressed Cre-recombinase activated channelrhodopsin-2 (ChR2) or halorhodopsin adeno-associated virus-2 (AAV2) vectors selectively in SNr GABAergic neurons of Vgat-IRES-Cre mice in a 6-hydroxydopamine model of PD to investigate whether direct optogenetic modulation of SNr neurons or their projections to the PPN regulates PD symptoms and LID expression. The forepaw stepping task, mouse LID rating scale, and open-field locomotion were used to assess akinesia and LID to test the effect of SNr modulation.
RESULTS
Akinesia was improved by suppressing SNr neuron activity with halorhodopsin. LID was significantly reduced by increasing SNr neuronal activity with ChR2, which did not interfere with the antiakinetic effect of levodopa. Optical stimulation of ChR2 in SNr projections to the PPN recapitulated direct SNr stimulation.
CONCLUSIONS
Modulation of SNr GABAergic neurons alters akinesia and LID expression in a manner consistent with the rate model of basal ganglia circuitry. Moreover, the projections from SNr to PPN likely mediate the antidyskinetic effect of increasing SNr neuronal activity, identifying a potential novel role for the PPN in LID. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
Topics: Mice; Animals; Pars Reticulata; Levodopa; Halorhodopsins; Parkinson Disease; GABAergic Neurons; Dyskinesia, Drug-Induced; Substantia Nigra
PubMed: 37461292
DOI: 10.1002/mds.29558 -
Psychiatria Danubina Dec 2015Parkinson's disease is the second most frequent neurodegenerative disorder. There is significantly elevated risk of cognitive decline and associated neuropsychiatric... (Review)
Review
Parkinson's disease is the second most frequent neurodegenerative disorder. There is significantly elevated risk of cognitive decline and associated neuropsychiatric symptoms. Dementia may develop insidiously several years after manifestation of Parkinson motor symptoms (dementia associated with Parkinson's disease; Parkinson's disease dementia) or in close temporal relationship (within one year) after onset of motor symptoms (Dementia with Lewy bodies). There are clinical, pathophysiological and therapeutic similarities between these two conditions. Men are more frequently affected than women. Risk factor or indicators are advanced age at disease onset, disease duration, rigidity, akinesia and posture and gait impairment and falls as opposed to tremor dominance, and associated neuropsychiatric symptoms (depression, apathy, hallucinosis, delirium). Dementia is treatable with cholinesterase inhibitors (rivastigmine, donepezil), memantine, and adjustment of the pharmacological regimen of parkinsonian motor symptoms. Concomitant autonomic nervous system symptoms and neuropsychiatric complications warrant early clinical awareness and are accessible to pharmacological therapy.
Topics: Cholinesterase Inhibitors; Cognitive Dysfunction; Donepezil; Humans; Memantine; Muscle Rigidity; Parkinson Disease; Risk Factors; Rivastigmine
PubMed: 26609664
DOI: No ID Found -
Medizinische Monatsschrift Fur... Jul 2016Pharmacotherapy in Parkinson’s disease is complex and requires expertise in all health-care professions. Besides idiopathic Parkinson’s disease (IPD) secondary... (Review)
Review
Pharmacotherapy in Parkinson’s disease is complex and requires expertise in all health-care professions. Besides idiopathic Parkinson’s disease (IPD) secondary parkinsonism, monogenetic Parkinson’s disease and atypical syndromes need to be differentiated. The prevalence in the European population is estimated to be approximately 1 %. Lifestyle and age are closely linked to IPD. Neurodegeneration with formation of Lewy-bodies and increased oxidative stress in the pars compacta of the substantia nigra are closely linked to IPD. Lewy-bodies show misfolded α-Synuclein. The balance of glutamate, GABA and dopamine is essential for motor complications. Bradykinesia/akinesia, rigidity, rest tremor and postural instability are typical symptoms along with dissymmetry, shuffling gait and camptocormia, micrographia, aphasia, hypophonia, dysphagia, and hypomimia. Early symptoms are akathisia/restlessness, insomnia, somnolence, hyposmia and neck pain. With further progression of IPD, neurons of the ventral tegmental area are affected and lead to non-motor symptoms, which hence are directly related to the underlying disease. Gastric dysmotility, depression, urinary incontinence, excessive sweating, hallucinations, spasticity, muscle pain and Parkinson’s disease dementia are part of IPD.
Topics: Antiparkinson Agents; Humans; Neurologic Examination; Parkinson Disease; Pars Compacta; Risk Factors; Substantia Nigra; Ventral Tegmental Area
PubMed: 29953178
DOI: No ID Found -
International Journal of Molecular... Oct 2022Takotsubo syndrome (TTS) is a severe but reversible acute heart failure syndrome that occurs following high catecholaminergic stress. TTS patients are similar to those... (Review)
Review
Takotsubo syndrome (TTS) is a severe but reversible acute heart failure syndrome that occurs following high catecholaminergic stress. TTS patients are similar to those with acute coronary syndrome, with chest pain, dyspnoea and ST segment changes on electrocardiogram, but are characterised by apical akinesia of the left ventricle, with basal hyperkinesia in the absence of culprit coronary artery stenosis. The pathophysiology of TTS is not completely understood and there is a paucity of evidence to guide treatment. The mechanisms of TTS are thought to involve catecholaminergic myocardial stunning, microvascular dysfunction, increased inflammation and changes in cardiomyocyte metabolism. Here, we summarise the available literature to focus on the molecular basis for the pathophysiology of TTS to advance the understanding of the condition.
Topics: Humans; Takotsubo Cardiomyopathy; Electrocardiography; Arrhythmias, Cardiac; Heart Ventricles; Acute Coronary Syndrome
PubMed: 36293121
DOI: 10.3390/ijms232012262