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1
Castronovo, Anna Margherita, Francesco Negro, Silvia Conforto, and Dario Farina. "The proportion of common synaptic input to motor neurons increases with an increase in net excitatory input." Journal of Applied Physiology 119, no. 11 (December 1, 2015): 1337–46. http://dx.doi.org/10.1152/japplphysiol.00255.2015.
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α-Motor neurons receive synaptic inputs from spinal and supraspinal centers that comprise components either common to the motor neuron pool or independent. The input shared by motor neurons—common input—determines force control. The aim of the study was to investigate the changes in the strength of common synaptic input delivered to motor neurons with changes in force and with fatigue, two conditions that underlie an increase in the net excitatory drive to the motor neurons. High-density surface electromyogram (EMG) signals were recorded from the tibialis anterior muscle during contractions at 20, 50, and 75% of the maximal voluntary contraction force (in 3 sessions separated by at least 2 days), all sustained until task failure. EMG signal decomposition identified the activity of a total of 1,245 motor units. The coherence values between cumulative motor unit spike trains increased with increasing force, especially for low frequencies. This increase in coherence was not observed when comparing two subsets of motor units having different recruitment thresholds, but detected at the same force level. Moreover, the coherence values for frequencies <5 Hz increased at task failure with respect to the beginning of the contractions for all force levels. In conclusion, the results indicated that the relative strength of common synaptic input to motor neurons increases with respect to independent input when the net excitatory drive to motor neurons increases as a consequence of a change in force and fatigue.
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Williams, U. E., E. E. Philip-Ephraim, and S. K. Oparah. "Multidisciplinary Interventions in Motor Neuron Disease." Journal of Neurodegenerative Diseases 2014 (November 18, 2014): 1–10. http://dx.doi.org/10.1155/2014/435164.
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Motor neuron disease is a neurodegenerative disease characterized by loss of upper motor neuron in the motor cortex and lower motor neurons in the brain stem and spinal cord. Death occurs 2–4 years after the onset of the disease. A complex interplay of cellular processes such as mitochondrial dysfunction, oxidative stress, excitotoxicity, and impaired axonal transport are proposed pathogenetic processes underlying neuronal cell loss. Currently evidence exists for the use of riluzole as a disease modifying drug; multidisciplinary team care approach to patient management; noninvasive ventilation for respiratory management; botulinum toxin B for sialorrhoea treatment; palliative care throughout the course of the disease; and Modafinil use for fatigue treatment. Further research is needed in management of dysphagia, bronchial secretion, pseudobulbar affect, spasticity, cramps, insomnia, cognitive impairment, and communication in motor neuron disease.
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Nair, Jayakrishnan, Kristi A. Streeter, Sara M. F. Turner, Michael D. Sunshine, Donald C. Bolser, Emily J. Fox, Paul W. Davenport, and David D. Fuller. "Anatomy and physiology of phrenic afferent neurons." Journal of Neurophysiology 118, no. 6 (December 1, 2017): 2975–90. http://dx.doi.org/10.1152/jn.00484.2017.
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Large-diameter myelinated phrenic afferents discharge in phase with diaphragm contraction, and smaller diameter fibers discharge across the respiratory cycle. In this article, we review the phrenic afferent literature and highlight areas in need of further study. We conclude that 1) activation of both myelinated and nonmyelinated phrenic sensory afferents can influence respiratory motor output on a breath-by-breath basis; 2) the relative impact of phrenic afferents substantially increases with diaphragm work and fatigue; 3) activation of phrenic afferents has a powerful impact on sympathetic motor outflow, and 4) phrenic afferents contribute to diaphragm somatosensation and the conscious perception of breathing. Much remains to be learned regarding the spinal and supraspinal distribution and synaptic contacts of myelinated and nonmyelinated phrenic afferents. Similarly, very little is known regarding the potential role of phrenic afferent neurons in triggering or modulating expression of respiratory neuroplasticity.
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Marwa Abbas Abdulrazzak Kubba. "A Review Article: Categorization, Advancement and Obstacles of Genetic factors and types of Spinal Muscular Degeneration." International Journal for Research in Applied Sciences and Biotechnology 8, no. 2 (March 6, 2021): 29–37. http://dx.doi.org/10.31033/ijrasb.8.2.4.
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SMA (Spinal muscular atrophies) are category of hereditary inflammation in the funiculars and lower brain stem, tissue fatigue, and degeneration characterized by motor neuron failure. The analytic and genetic phenotypes incorporate a diverse continuum distinguished depending on age of onset, tissue participation arrangement, and inheritance arrangement. Rapid advancements in genetic science have expedite the discovery of causative genes over the past few years, and provide significant access in awareness the biochemical and neurological basis of Spinal muscular atrophies and insights into the motor neurons' selective deficiency. Popular path physiological topics include Ribonucleic Acid metabolism and splicing abnormalities, axonal transmission, and motor neurons' advancement and communication. These also collectively revealed possible innovative prevention methods and comprehensive attempts are what benefits does the company offer? Although a range of promising therapeutic therapies for Spinal muscular atrophies is emerging, it is essential to identify therapeutic windows and establish responsive and appropriate biomarkers to promote future analytic trial success. This research offers a description of Spinal muscular atrophies' logical manifestations and genetics. It discusses recent advancements in learning—mechanisms for the pathogenesis of inflammation and new treatment methods.
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Nguyen, P. V., and H. L. Atwood. "Altered impulse activity modifies synaptic physiology and mitochondria in crayfish phasic motor neurons." Journal of Neurophysiology 72, no. 6 (December 1, 1994): 2944–55. http://dx.doi.org/10.1152/jn.1994.72.6.2944.
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1. Crayfish phasic motor synapses produce large initial excitatory postsynaptic potentials (EPSPs) that fatigue rapidly during high-frequency stimulation. Periodic in vivo stimulation of an identified phasic abdominal extensor motor neuron (axon 3) induced long-term adaptation (LTA) of neuromuscular transmission: initial EPSP amplitude became smaller and synaptic depression was significantly reduced. We tested the hypothesis that activity-induced synaptic fatigue-resistance seen during LTA was dependent upon, or correlated with, mitochondrial oxidative competence. 2. Periodic unilateral conditioning stimulation of axon 3 entering each of two adjacent homologous abdominal segments (segments 2 and 3) increased the synaptic stamina in both "conditioned" axons; mean final EPSP amplitudes, recorded after 20 min of 5-Hz test stimulation, were significantly larger than those measured with the same protocol from contralateral unstimulated axons. 3. During 5-Hz test stimulation of the conditioned axon 3 of segment 3, acute superfusion with 0.8 mM dinitrophenol or 20 mM sodium azide [inhibitors of oxidative adenosinetriphosphate (ATP) synthesis] produced increased synaptic depression. Drug-free saline superfusion of the conditioned axon 3 of segment 2 in these same animals did not affect the increased synaptic fatigue resistance seen in this segment. Thus both successful induction (in axon 3 of saline-perfused segment 2) and attenuation (in axon 3 of drug-perfused segment 3) of the increased synaptic stamina can be demonstrated with this twin-segment conditioning protocol. 4. Confocal microscopic imaging of mitochondrial rhodamine-123 (Rh123) fluorescence was used to assess relative oxidative competence of conditioned and unconditioned phasic axons. Conditioned phasic axons showed significantly higher mean mitochondrial Rh123 fluorescence than contralateral unstimulated axons. In the same preparations that showed increased postconditioning Rh123 fluorescence, the synaptic fatigue resistance measured from conditioned axon 3 was also significantly greater than that recorded from contralateral unstimulated axon 3. 5. Axotomy of the phasic extensor nerve root (containing axon 3), before in vivo conditioning stimulation of its decentralized segment, prevented induction of both the increased synaptic stamina in axon 3 and the enhanced mitochondrial fluorescence in decentralized motor axons of the nerve root. Hence, induction of both changes requires axonal transport of materials between the soma and the motor synapses of axon 3. 5. Axotomy of the phasic extensor nerve root (containing axon 3), before in vivo conditioning stimulation of its decentralized segment, Prevented induction of both the increased synaptic stamina in axon 3 and the enhanced mitochondrial fluorescence in decentralized motor axons of the nerve root Hence, induction of both changes requires axonal transport of materials between the soma and the motor synapses of axon 3 6. Because mitochondrial Rh123 fluorescence is primarily dependent upon the oxidative activity of these organelles, our findings suggest that conditioning stimulation of phasic extensor axon 3 increases its mitochondrial oxidative competence and that the enhanced synaptic stamina seen during LTA in axon 3 is correlated with, and dependent upon, oxidative activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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Zahir, Faryal, Radha Budhwar, Gabrielle Gonsalves, Lily Green, and Aliza Barua. "The physiological basis of neuromuscular fatigue during high intensity exercise." STEM Fellowship Journal 3, no. 2 (December 1, 2017): 1–3. http://dx.doi.org/10.17975/sfj-2017-011.
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Introduction Neuromuscular fatigue refers to a reduction in maximal force generation capacity, and is categorized as central and peripheral. Central fatigue is defined as a reduction in the ability of the central nervous system to voluntarily activate muscles, and peripheral fatigue indicates a decrease in the contractile strength of muscle fibers. During high intensity exercise, motor neurons are involved in the recruitment of type IIB muscle fibers as they are fast-twitch, high glycolytic, and have low aerobic capacity. Furthermore, group III and IV muscle afferents detect the physiological circumstances in the body and convey signals to the brain that influence the onset of central and peripheral fatigue. Methods A PRISMA flow diagram was created to record relevant studies found from scholarly databases. Inclusion criteria required studies from 2005 to 2017, and subject grouping headings required key terms indicating that the presence of central and peripheral fatigue was analyzed on healthy adult subjects performing exercise. To ensure that high quality studies were analyzed, each article was independently rated using the National Institute of Health Quality Assessment Tool criteria. Discussion During low intensity exercise, asynchronous motor unit recruitment is involved in delaying the onset of muscle fatigue. However, this is not apparent in high intensity exercises, as maximal motor unit firing is required in order to sustain a maximal level of force output. Persistent firing of action potentials to maintain muscle contraction results in acetylcholine depletion at the motor end plate, initiating the process of central fatigue. Furthermore, due to prolonged metabolite accumulation in skeletal muscle fibers, group III and IV afferents convey signals to the motor cortex and cause a reduction in the action potential conduction velocities along the contracting muscle. This leads to the onset of peripheral fatigue. As high intensity exercise proceeds, electromyogram (EMG) measurements display this as an increase in amplitude to reflect heightened motor unit recruitment and a compressed power density spectrum alongside a decreased centre frequency. This is determined by the innervated muscle fiber’s conduction velocity and subsequent variations in the action potential waveform shape. Conclusion A record of current studies systematically display the overview of muscle fatigue and its underlying mechanisms during exercise. However, further research is yet to be conducted for a more comprehensive understanding regarding the onset and recovery of neuromuscular fatigue in varied population demographics and physiological circumstances. Likewise, the distinctive roles of group III and IV muscle afferents in supraspinal stimulation require further investigation in order to gain a holistic understanding of their involvement in central fatigue and resistance training. Additional research in this subject matter is currently being explored through technology involving imaging studies, as they have potential to elucidate motor cortex activity alongside other regions of the brain and portray neuromuscular muscle fatigue eminently.
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Nguyen, Peter V., Leo Marin, and Harold L. Atwood. "Synaptic Physiology and Mitochondrial Function in Crayfish Tonic and Phasic Motor Neurons." Journal of Neurophysiology 78, no. 1 (July 1, 1997): 281–94. http://dx.doi.org/10.1152/jn.1997.78.1.281.
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Nguyen, Peter V., Leo Marin, and Harold L. Atwood. Synaptic physiology and mitochondrial function in crayfish tonic and phasic motor neurons. J. Neurophysiol. 78: 281–294, 1997. Phasic and tonic motor neurons of crustaceans differ strikingly in their junctional synaptic physiology. Tonic neurons generally produce small excitatory postsynaptic potentials (EPSPs) that facilitate strongly as stimulation frequency is increased, and normally show no synaptic depression. In contrast, phasic neurons produce relatively large EPSPs with weak frequency facilitation and pronounced depression. We addressed the hypothesis that mitochondrial function is an important determinant of the features of synaptic transmission in these neurons. Mitochondrial fluorescence was measured with confocal microscopy in phasic and tonic axons and terminals of abdominal and leg muscles after exposure to supravital mitochondrial fluorochromes, rhodamine-123 (Rh123) and 4-diethylaminostyryl-N-methylpyridinium iodide (4-Di-2-Asp). Mitochondria of tonic axons and neuromuscular junctions had significantly higher mean Rh123 and 4-Di-2-Asp fluorescence than in phasic neurons, indicating more accumulation of the fluorochromes. Mitochondrial membrane potential, which is responsible for Rh123 uptake and is related to mitochondrial oxidative activity (the production of ATP by oxidation of metabolic substrates), is likely higher in tonic axons. Electron microscopy showed that tonic axons contain approximately fivefold more mitochondria per μm2 cross-sectional area than phasic axons. Neuromuscular junctions of tonic axons also have a much higher mitochondrial content than those of phasic axons. We tested the hypothesis that synaptic fatigue resistance is dependent on mitochondrial function in crayfish motor axons. Impairment of mitochondrial function by uncouplers of oxidative phosphorylation, dinitrophenol or carbonyl cyanide m-chlorophenylhydrazone, or by the electron transport inhibitor sodium azide, led to marked synaptic depression of a tonic axon and accelerated depression of a phasic axon during maintained stimulation. Iodoacetate, an inhibitor of glycolysis, and chloramphenicol, a mitochondrial protein synthesis inhibitor, had no significant effects on either mitochondrial fluorescence or synaptic depression in tonic or phasic axons. Collectively, the results provide evidence that mitochondrial oxidative metabolism is important for sustaining synaptic transmission during maintained stimulation of tonic and phasic motor neurons. Tonic neurons have a higher mitochondrial content and greater oxidative activity; these features are correlated with their greater resistance to synaptic depression. Conversely, phasic neurons have a lower mitochondrial content, less oxidative activity, and greater synaptic fatigability.
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Smith, Simone G. V. S., Geoffrey A. Power, and Leah R. Bent. "Foot sole cutaneous stimulation mitigates neuromuscular fatigue during a sustained plantar flexor isometric task." Journal of Applied Physiology 129, no. 2 (August 1, 2020): 325–34. http://dx.doi.org/10.1152/japplphysiol.00157.2020.
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Cutaneous coupling with lower limb motor neurons has long been known. We set out to establish whether this pathway could serve a purpose other than muscular modulation during standing and walking. We found that during a submaximal contraction of the plantar flexor muscles, the addition of intermittent cutaneous stimulation to the skin of the foot sole resulted in an increase in time to task failure by 15%, which was over a minute longer in duration. We conclude that skin stimulation may serve as a mechanism to mitigate fatigue.
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Robert, Riener. "Model–based development of neuroprostheses for paraplegic patients." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1385 (May 29, 1999): 877–94. http://dx.doi.org/10.1098/rstb.1999.0440.
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In paraplegic patients with upper motor neuron lesions the signal path from the central nervous system to the muscles is interrupted. Functional electrical stimulation applied to the lower motor neurons can replace the lacking signals. A so–called neuroprosthesis may be used to restore motor function in paraplegic patients on the basis of functional electrical stimulation. However, the control of multiple joints is difficult due to the complexity, nonlinearity, and time–variance of the system involved. Furthermore, effects such as muscle fatigue, spasticity, and limited force in the stimulated muscle further complicate the control task. Mathematical models of the human musculoskeletal system can support the development of neuroprostheses. In this article a detailed overview of the existing work in the literature is given and two examples developed by the author are presented that give an insight into model–based development of neuroprostheses for paraplegic patients. It is shown that modelling the musculoskeletal system can provide better understanding of muscular force production and movement coordination principles. Models can also be used to design and test stimulation patterns and feedback control strategies. Additionally, model components can be implemented in a controller to improve control performance. Eventually, the use of musculoskeletal models for neuroprosthesis design may help to avoid internal disturbances such as fatigue and optimize muscular force output. Furthermore, better controller quality can be obtained than in previous empirical approaches. In addition, the number of experimental tests to be performed with human subjects can be reduced. It is concluded that mathematical models play an increasing role in the development of reliable closed–loop controlled, lower extremity neuroprostheses.
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Fogarty, Matthew J., Maria A. Gonzalez Porras, Carlos B. Mantilla, and Gary C. Sieck. "Diaphragm neuromuscular transmission failure in aged rats." Journal of Neurophysiology 122, no. 1 (July 1, 2019): 93–104. http://dx.doi.org/10.1152/jn.00061.2019.
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In aging Fischer 344 rats, phrenic motor neuron loss, neuromuscular junction abnormalities, and diaphragm muscle (DIAm) sarcopenia are present by 24 mo of age, with larger fast-twitch fatigue-intermediate (type FInt) and fast-twitch fatigable (type FF) motor units particularly vulnerable. We hypothesize that in old rats, DIAm neuromuscular transmission deficits are specific to type FInt and/or FF units. In phrenic nerve/DIAm preparations from rats at 6 and 24 mo of age, the phrenic nerve was supramaximally stimulated at 10, 40, or 75 Hz. Every 15 s, the DIAm was directly stimulated, and the difference in forces evoked by nerve and muscle stimulation was used to estimate neuromuscular transmission failure. Neuromuscular transmission failure in the DIAm was observed at each stimulation frequency. In the initial stimulus trains, the forces evoked by phrenic nerve stimulation at 40 and 75 Hz were significantly less than those evoked by direct muscle stimulation, and this difference was markedly greater in 24-mo-old rats. During repetitive nerve stimulation, neuromuscular transmission failure at 40 and 75 Hz worsened to a greater extent in 24-mo-old rats compared with younger animals. Because type IIx and/or IIb DIAm fibers (type FInt and/or FF motor units) display greater susceptibility to neuromuscular transmission failure at higher frequencies of stimulation, these data suggest that the age-related loss of larger phrenic motor neurons impacts nerve conduction to muscle at higher frequencies and may contribute to DIAm sarcopenia in old rats. NEW & NOTEWORTHY Diaphragm muscle (DIAm) sarcopenia, phrenic motor neuron loss, and perturbations of neuromuscular junctions (NMJs) are well described in aged rodents and selectively affect FInt and FF motor units. Less attention has been paid to the motor unit-specific aspects of nerve-muscle conduction. In old rats, increased neuromuscular transmission failure occurred at stimulation frequencies where FInt and FF motor units exhibit conduction failures, along with decreased apposition of pre- and postsynaptic domains of DIAm NMJs of these units.
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Moggio, Lucrezia, Annalisa Petraroli, Nicola Marotta, Andrea Demeco, Ilaria Pino, Cinzia Marinaro, Marianna Barletta, and Antonio Ammendolia. "Rehabilitation in primary lateral sclerosis mimicking parkinsonism: A case report." NeuroRehabilitation 47, no. 4 (December 22, 2020): 381–86. http://dx.doi.org/10.3233/nre-201527.
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BACKGROUND: Primary lateral sclerosis (PLS) is an upper motor neurons disease that on rare occasions may determine bradykinesia and motor fatigue. To date, no rehabilitative treatment has been described as useful for these patients. CASE PRESENTATION: A 68-year-old male developed dysarthria, spastic laugh, impairments of handwriting and fine motor, gait and dysphagia disorders for both solids and liquids over the period from 2015 to December 2018, with normal DaT scans and no clinical benefits from therapy with levodopa, pramipexole and baclofen. The patient underwent exercises for gait training and balance control with sensory treadmill and stabilometric platform and kinesiotherapy to improve fine motor skills of both hands and postural changes, five days a week for two weeks. Based on our data, the patient showed an improvement in balance and gait parameters in T2 compared to T1. CONCLUSION: Thanks to the synergistic action of a combined treatment of physical and instrumental therapy, despite the rare pathology and complex disability, the patient had important benefits in terms of performance and independence in daily activity.
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Sidhu, Simranjit K., Andrew G. Cresswell, and Timothy J. Carroll. "Motor cortex excitability does not increase during sustained cycling exercise to volitional exhaustion." Journal of Applied Physiology 113, no. 3 (August 1, 2012): 401–9. http://dx.doi.org/10.1152/japplphysiol.00486.2012.
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The excitability of the motor cortex increases as fatigue develops during sustained single-joint contractions, but there are no previous reports on how corticospinal excitability is affected by sustained locomotor exercise. Here we addressed this issue by measuring spinal and cortical excitability changes during sustained cycling exercise. Vastus lateralis (VL) and rectus femoris (RF) muscle responses to transcranial magnetic stimulation of the motor cortex (motor evoked potentials, MEPs) and electrical stimulation of the descending tracts (cervicomedullary evoked potentials, CMEPs) were recorded every 3 min from nine subjects during 30 min of cycling at 75% of maximum workload (Wmax), and every minute during subsequent exercise at 105% of Wmax until subjective task failure. Responses were also measured during nonfatiguing control bouts at 80% and 110% of Wmax prior to sustained exercise. There were no significant changes in MEPs or CMEPs ( P > 0.05) during the sustained cycling exercise. These results suggest that, in contrast to sustained single-joint contractions, sustained cycling exercise does not increase the excitability of motor cortical neurons. The contrasting corticospinal responses to the two modes of exercise may be due to differences in their associated systemic physiological consequences.
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Blicher, Jakob U., and Jørgen F. Nielsen. "Cortical and Spinal Excitability Changes After Robotic Gait Training in Healthy Participants." Neurorehabilitation and Neural Repair 23, no. 2 (November 7, 2008): 143–49. http://dx.doi.org/10.1177/1545968308317973.
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Background. Recent studies have proposed a role for robotic gait training in participants with acquired brain injury, but the effects on the excitability of cortical and spinal neurons even in healthy participants are uncertain. Objective. To investigate changes in corticospinal excitability in healthy participants after active and passive robotic gait training in a driven gait orthosis (DGO), the Lokomat. Methods. Thirteen healthy participants took part in 2 experiments. Each participant performed 20 minutes of active and passive gait training in a DGO. Motor evoked potentials (MEP), short-interval intracortical inhibition (SICI), intracortical facilitation (ICF), F-wave frequency, and Mmax were measured in the right tibialis anterior muscle before and after training. Results. Active training led to a decline in MEP amplitude and F-wave frequency. The MEP decline was associated with subjective muscle fatigue. Passive training induced a decrease in SICI lasting for 20 minutes after training. Conclusions. The decline in MEP after active training is most likely because of central fatigue, whereas the decreased F-wave frequency might represent short-term plastic changes in the spinal cord. The decrease in SICI after passive training probably reflects a decrease in intracortical GABA activity, which could benefit the acquisition of new motor skills.
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Bergeron, Michael F. "Exertional Heat Cramps: Recovery and Return to Play." Journal of Sport Rehabilitation 16, no. 3 (August 2007): 190–96. http://dx.doi.org/10.1123/jsr.16.3.190.
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In contrast to muscle cramps that are brought on by muscle overload or fatigue, exertional heat cramps seem to be prompted by extensive sweating and a significant sweat-induced whole-body sodium deficit. As a result of a consequent contracted interstitial compartment, axon terminals of selected motor neurons can become hyper-excitable and spontaneously discharge. Barely detectable muscle fasciculations or “twitches” in the affected muscles can rapidly progress to debilitating muscle cramps in just 20 to 30 minutes. To aid recovery, salt (NaCl) and water lost from sweating should be sufficiently replaced so as to restore the extracellular volume and interstitial fluid spaces. Sweat sodium, chloride, and fluid losses incurred during training and competition need to be closely matched by daily salt and fluid intake, in order to prevent an excessive sodium deficit, maintain sufficient fluid balance, and avoid exertional heat cramps.
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Ardiel, Evan L., Troy A. McDiarmid, Tiffany A. Timbers, Kirsten C. Y. Lee, Javad Safaei, Steven L. Pelech, and Catharine H. Rankin. "Insights into the roles of CMK-1 and OGT-1 in interstimulus interval-dependent habituation in Caenorhabditis elegans." Proceedings of the Royal Society B: Biological Sciences 285, no. 1891 (November 14, 2018): 20182084. http://dx.doi.org/10.1098/rspb.2018.2084.
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Habituation is a ubiquitous form of non-associative learning observed as a decrement in responding to repeated stimulation that cannot be explained by sensory adaptation or motor fatigue. One of the defining characteristics of habituation is its sensitivity to the rate at which training stimuli are presented—animals habituate faster in response to more rapid stimulation. The molecular mechanisms underlying this interstimulus interval (ISI)-dependent characteristic of habituation remain unknown. In this article, we use behavioural neurogenetic and bioinformatic analyses in the nematode Caenorhabiditis elegans to identify the first molecules that modulate habituation in an ISI-dependent manner. We show that the Caenorhabditis elegans orthologues of Ca 2+ /calmodulin-dependent kinases CaMK1/4, CMK-1 and O-linked N-acetylglucosamine (O-GlcNAc) transferase, OGT-1, both function in primary sensory neurons to inhibit habituation at short ISIs and promote it at long ISIs. In addition, both cmk-1 and ogt-1 mutants display a rare mechanosensory hyper-responsive phenotype (i.e. larger mechanosensory responses than wild-type). Overall, our work identifies two conserved genes that function in sensory neurons to modulate habituation in an ISI-dependent manner, providing the first insights into the molecular mechanisms underlying the universally observed phenomenon that habituation has different properties when stimuli are delivered at different rates.
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Delezie, Julien, Martin Weihrauch, Geraldine Maier, Rocío Tejero, Daniel J. Ham, Jonathan F. Gill, Bettina Karrer-Cardel, Markus A. Rüegg, Lucía Tabares, and Christoph Handschin. "BDNF is a mediator of glycolytic fiber-type specification in mouse skeletal muscle." Proceedings of the National Academy of Sciences 116, no. 32 (July 18, 2019): 16111–20. http://dx.doi.org/10.1073/pnas.1900544116.
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Brain-derived neurotrophic factor (BDNF) influences the differentiation, plasticity, and survival of central neurons and likewise, affects the development of the neuromuscular system. Besides its neuronal origin, BDNF is also a member of the myokine family. However, the role of skeletal muscle-derived BDNF in regulating neuromuscular physiology in vivo remains unclear. Using gain- and loss-of-function animal models, we show that muscle-specific ablation of BDNF shifts the proportion of muscle fibers from type IIB to IIX, concomitant with elevated slow muscle-type gene expression. Furthermore, BDNF deletion reduces motor end plate volume without affecting neuromuscular junction (NMJ) integrity. These morphological changes are associated with slow muscle function and a greater resistance to contraction-induced fatigue. Conversely, BDNF overexpression promotes a fast muscle-type gene program and elevates glycolytic fiber number. These findings indicate that BDNF is required for fiber-type specification and provide insights into its potential modulation as a therapeutic target in muscle diseases.
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Mordhorst, Mylena, Thomas Heidlauf, and Oliver Röhrle. "Predicting electromyographic signals under realistic conditions using a multiscale chemo–electro–mechanical finite element model." Interface Focus 5, no. 2 (April 6, 2015): 20140076. http://dx.doi.org/10.1098/rsfs.2014.0076.
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This paper presents a novel multiscale finite element-based framework for modelling electromyographic (EMG) signals. The framework combines (i) a biophysical description of the excitation–contraction coupling at the half-sarcomere level, (ii) a model of the action potential (AP) propagation along muscle fibres, (iii) a continuum-mechanical formulation of force generation and deformation of the muscle, and (iv) a model for predicting the intramuscular and surface EMG. Owing to the biophysical description of the half-sarcomere, the model inherently accounts for physiological properties of skeletal muscle. To demonstrate this, the influence of membrane fatigue on the EMG signal during sustained contractions is investigated. During a stimulation period of 500 ms at 100 Hz, the predicted EMG amplitude decreases by 40% and the AP propagation velocity decreases by 15%. Further, the model can take into account contraction-induced deformations of the muscle. This is demonstrated by simulating fixed-length contractions of an idealized geometry and a model of the human tibialis anterior muscle (TA). The model of the TA furthermore demonstrates that the proposed finite element model is capable of simulating realistic geometries, complex fibre architectures, and can include different types of heterogeneities. In addition, the TA model accounts for a distributed innervation zone, different fibre types and appeals to motor unit discharge times that are based on a biophysical description of the α motor neurons.
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Stam, Marloes, Renske I. Wadman, Camiel A. Wijngaarde, Bart Bartels, Fay-Lynn Asselman, Louise A. M. Otto, H. Stephan Goedee, et al. "Protocol for a phase II, monocentre, double-blind, placebo-controlled, cross-over trial to assess efficacy of pyridostigmine in patients with spinal muscular atrophy types 2–4 (SPACE trial)." BMJ Open 8, no. 7 (July 2018): e019932. http://dx.doi.org/10.1136/bmjopen-2017-019932.
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IntroductionHereditary proximal spinal muscular atrophy (SMA) is caused by homozygous loss of function of the survival motor neuron 1 gene. The main characteristic of SMA is degeneration of alpha motor neurons in the anterior horn of the spinal cord, but recent studies in animal models and patients have shown additional anatomical abnormalities and dysfunction of the neuromuscular junction (NMJ). NMJ dysfunction could contribute to symptoms of weakness and fatigability in patients with SMA. We hypothesise that pyridostigmine, an acetylcholinesterase inhibitor that improves neuromuscular transmission, could improve NMJ function and thereby muscle strength and fatigability in patients with SMA.Methods and analysisWe designed a monocentre, placebo-controlled, double-blind cross-over trial with pyridostigmine and placebo to investigate the effect and efficacy of pyridostigmine on muscle strength and fatigability in patients with genetically confirmed SMA. We aim to include 45 patients with SMA types 2–4, aged 12 years and older in the Netherlands. Participants receive 8 weeks of treatment with pyridostigmine and 8 weeks of treatment with placebo in a random order separated by a washout period of 1 week. Treatment allocation is double blinded. Treatment dose will gradually be increased from 2 mg/kg/day to the maximum dose of 6 mg/kg/day in four daily doses, in the first week of each treatment period. The primary outcome measures are a change in the Motor Function Measure and repeated nine-hole peg test before and after treatment. Secondary outcome measures are changes in recently developed endurance tests, that is, the endurance shuttle nine-hole peg test, the endurance shuttle box and block test and the endurance shuttle walk test, muscle strength, level of daily functioning, quality of and activity in life, perceived fatigue and fatigability, presence of decrement on repetitive nerve stimulation and adverse events.Ethics and disseminationThe protocol is approved by the local medical ethical review committee at the University Medical Center Utrecht and by the national Central Committee on Research Involving Human Subjects. Findings will be shared with the academic and medical community, funding and patient organisations in order to contribute to optimisation of medical care and quality of life for patients with SMA.Trial registration numberNCT02941328.
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Silva, Tatiana Mesquita e., Gustavo Antonio Moreira, Abrahão Augusto Juviniano Quadros, Márcia Pradella-Hallinan, Sergio Tufik, and Acary Souza Bulle Oliveira. "Analysis of sleep characteristics in post-polio syndrome patients." Arquivos de Neuro-Psiquiatria 68, no. 4 (August 2010): 535–40. http://dx.doi.org/10.1590/s0004-282x2010000400011.
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The main post-polio syndrome (PPS) symptoms are new weakness, new atrophy, fatigue, pain and sleep disturbances. Polysomnography is the gold standard for sleep analysis. OBJECTIVE: To analyze sleep patterns in PPS patients. METHOD: Sixty patients (mean age 46.8±11.3 years) at the Federal University of São Paulo (UNIFESP/EPM) complaining of sleep disturbances were evaluated by means of polysomnography, performed at the Sleep Institute. RESULTS: Sleep efficiency was lower due to high sleep latency and arousal index. The apnea and hypopnea index (AHI) and the periodic limb movements (PLM) index were higher. Sleep architecture was also impaired. There were no abnormalities of oxygen saturation, carbon dioxide levels, respiratory rate or heart rate. CONCLUSION: New post-polio sleep disturbances were isolated symptoms. It appears that these symptoms were not due to post-polio features, but rather, that they were due to dysfunction of the surviving motor neurons in the brainstem. Abnormal dopamine production, which is responsible for many sleep-related breathing disorders and abnormal movements, may also have been implicated in the present findings.
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Dean, J. C., L. M. Yates, and D. F. Collins. "Turning on the central contribution to contractions evoked by neuromuscular electrical stimulation." Journal of Applied Physiology 103, no. 1 (July 2007): 170–76. http://dx.doi.org/10.1152/japplphysiol.01361.2006.
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Neuromuscular electrical stimulation can generate contractions through peripheral and central mechanisms. Direct activation of motor axons (peripheral mechanism) recruits motor units in an unnatural order, with fatigable muscle fibers often activated early in contractions. The activation of sensory axons can produce contractions through a central mechanism, providing excitatory synaptic input to spinal neurons that recruit motor units in the natural order. Presently, we quantified the effect of stimulation frequency (10–100 Hz), duration (0.25–2 s of high-frequency bursts, or 20 s of constant-frequency stimulation), and intensity [1–5% maximal voluntary contraction (MVC) torque generated by a brief 100-Hz train] on the torque generated centrally. Electrical stimulation (1-ms pulses) was delivered over the triceps surae in eight subjects, and plantar flexion torque was recorded. Stimulation frequency, duration, and intensity all influenced the magnitude of the central contribution to torque. Central torque did not develop at frequencies ≤20 Hz, and it was maximal at frequencies ≥80 Hz. Increasing the duration of high-frequency stimulation increased the central contribution to torque, as central torque developed over 11 s. Central torque was greatest at a relatively low contraction intensity. The largest amount of central torque was produced by a 20-s, 100-Hz train (10.7 ± 5.5 %MVC) and by repeated 2-s bursts of 80- or 100-Hz stimulation (9.2 ± 4.8 and 10.2 ± 8.1% MVC, respectively). Therefore, central torque was maximized by applying high-frequency, long-duration stimulation while avoiding antidromic block by stimulating at a relatively low intensity. If, as hypothesized, the central mechanism primarily activates fatigue-resistant muscle fibers, generating muscle contractions through this pathway may improve rehabilitation applications.
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Glenn, William W. L., and Mildred L. Phelps. "Diaphragm Pacing by Electrical Stimulation of the Phrenic Nerve." Neurosurgery 17, no. 6 (December 1, 1985): 974–84. http://dx.doi.org/10.1227/00006123-198512000-00021.
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Abstract Sophisticated techniques for electrical stimulation of excitable tissue to treat neuromuscular disorders rationally have been developed over the past 3 decades. A historical review shows that electricity has been applied to the phrenic nerves to activate the diaphragm for some 200 years. Of the contemporary methods for stimulating the phrenic nerve in cases of ventilatory insufficiency, the authors prefer stimulation of the phrenic nerve in the thorax using a platinum ribbon electrode placed behind the nerve and an attached subcutancously implanted radiofrequency (RF) receiver inductively coupled to an external RF transmitter. Instructions are given for implanting the electrode-receiver assembly, emphasizing atraumatic handling of the phrenic nerve and strict aseptic techniques. Diaphragm pacing is conducted with low frequency electrical stimulation at a slow repetition (respiratory) rate to condition the diaphragm muscle against fatigue and maintain it fatigue-free. Candidates for diaphragm pacing are those with ventilatory insufficiency due to malfunction of the respiratory control center or interruption of the upper motor neurons of the phrenic nerve. In the Yale series, there were 77 patients treated by diaphragm pacing; 63 (82%) started before 1981 and thus were available for follow-up for at least 5 years; 33 (52%) were paced for 5 to 10 years, and 15 (24%) were paced for 10 to 16. Long term stimulation of the phrenic nerves to pace the diaphragm is an effective method of ventilatory support in selected cases
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Aryal, Sunisha, Taylor Skinner, Bronwyn Bridges, and John T. Weber. "The Pathology of Parkinson’s Disease and Potential Benefit of Dietary Polyphenols." Molecules 25, no. 19 (September 24, 2020): 4382. http://dx.doi.org/10.3390/molecules25194382.
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Parkinson’s disease (PD) is a progressive neurodegenerative disorder that is characterized by a loss of dopaminergic neurons, leading to bradykinesia, rigidity, tremor at rest, and postural instability, as well as non-motor symptoms such as olfactory impairment, pain, autonomic dysfunction, impaired sleep, fatigue, and behavioral changes. The pathogenesis of PD is believed to involve oxidative stress, disruption to mitochondria, alterations to the protein α-synuclein, and neuroinflammatory processes. There is currently no cure for the disease. Polyphenols are secondary metabolites of plants, which have shown benefit in several experimental models of PD. Intake of polyphenols through diet is also associated with lower PD risk in humans. In this review, we provide an overview of the pathology of PD and the data supporting the potential neuroprotective capacity of increased polyphenols in the diet. Evidence suggests that the intake of dietary polyphenols may inhibit neurodegeneration and the progression of PD. Polyphenols appear to have a positive effect on the gut microbiome, which may decrease inflammation that contributes to the disease. Therefore, a diet rich in polyphenols may decrease the symptoms and increase quality of life in PD patients.
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Nanou, Evanthia, Jin Yan, Nicholas P. Whitehead, Min Jeong Kim, Stanley C. Froehner, Todd Scheuer, and William A. Catterall. "Altered short-term synaptic plasticity and reduced muscle strength in mice with impaired regulation of presynaptic CaV2.1 Ca2+ channels." Proceedings of the National Academy of Sciences 113, no. 4 (January 11, 2016): 1068–73. http://dx.doi.org/10.1073/pnas.1524650113.
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Facilitation and inactivation of P/Q-type calcium (Ca2+) currents through the regulation of voltage-gated Ca2+ (CaV) 2.1 channels by Ca2+ sensor (CaS) proteins contributes to the facilitation and rapid depression of synaptic transmission in cultured neurons that transiently express CaV2.1 channels. To examine the modulation of endogenous CaV2.1 channels by CaS proteins in native synapses, we introduced a mutation (IM-AA) into the CaS protein-binding site in the C-terminal domain of CaV2.1 channels in mice, and tested synaptic facilitation and depression in neuromuscular junction synapses that use exclusively CaV2.1 channels for Ca2+ entry that triggers synaptic transmission. Even though basal synaptic transmission was unaltered in the neuromuscular synapses in IM-AA mice, we found reduced short-term facilitation in response to paired stimuli at short interstimulus intervals in IM-AA synapses. In response to trains of action potentials, we found increased facilitation at lower frequencies (10–30 Hz) in IM-AA synapses accompanied by slowed synaptic depression, whereas synaptic facilitation was reduced at high stimulus frequencies (50–100 Hz) that would induce strong muscle contraction. As a consequence of altered regulation of CaV2.1 channels, the hindlimb tibialis anterior muscle in IM-AA mice exhibited reduced peak force in response to 50 Hz stimulation and increased muscle fatigue. The IM-AA mice also had impaired motor control, exercise capacity, and grip strength. Taken together, our results indicate that regulation of CaV2.1 channels by CaS proteins is essential for normal synaptic plasticity at the neuromuscular junction and for muscle strength, endurance, and motor coordination in mice in vivo.
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Krutli, Renata dos Santos, Géssica Soares Calixto, Mariana Midori Sime, Paulo Vinicius Braga Mendes, Alexandre Fonseca Brandão, Débora Couto De Melo Carrijo, and Daniel Marinho Cezar da Cruz. "Applicability and evaluation of the GestureChair virtual game: comparison between people with and without spinal cord injury." Journal on Interactive Systems 9, no. 1 (June 8, 2018): 1. http://dx.doi.org/10.5753/jis.2018.694.
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Introduction: Spinal cord injury rehabilitation requires updating from professionals regarding the possible interventions that can enhance recovery. Virtual reality (VR) games have become evident as a resource used in the rehabilitation process. Their effectiveness is based on the theory of neuronal reorganization, mediated by mirror neurons, responsible for motor imagery. Objectives: To test the applicability and evaluation of the virtual game Gesture Chair by people with and without spinal cord injury, to identify users' perceptions about the characteristics and demands of the VR game after its use and compare the immediate effects of the game on motor performance components in both groups. Method: We analyzed upper limb range of motion (ROM) after performing a practice using the exergame in a sample of five subjects with spinal cord injury and a comparative group with five other participants. The game was applied for 15 minutes, counting periods of activity and rest, while the subject remained seated. Results: The number of subjects in the sample does not allow statistically significant results on changes in shoulder ROM; however, factors that interfered with performance, perceptions about initial contact with the activity, presence of muscular fatigue and pain that may be present related to the increase of energy expenditure during the action were identified. Regarding the interest, there were reports of demotivation and disinterest, but there were also reports considering the activity motivating. Conclusion: The study implies the importance of the process of choosing individualized resources during the rehabilitation process and the need for adaptation among users of novel technologies. Future studies will be able to analyze the enhancement of the game with different users.
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Boisseau, Romain P., David Vogel, and Audrey Dussutour. "Habituation in non-neural organisms: evidence from slime moulds." Proceedings of the Royal Society B: Biological Sciences 283, no. 1829 (April 27, 2016): 20160446. http://dx.doi.org/10.1098/rspb.2016.0446.
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Learning, defined as a change in behaviour evoked by experience, has hitherto been investigated almost exclusively in multicellular neural organisms. Evidence for learning in non-neural multicellular organisms is scant, and only a few unequivocal reports of learning have been described in single-celled organisms. Here we demonstrate habituation, an unmistakable form of learning, in the non-neural organism Physarum polycephalum . In our experiment, using chemotaxis as the behavioural output and quinine or caffeine as the stimulus, we showed that P. polycephalum learnt to ignore quinine or caffeine when the stimuli were repeated, but responded again when the stimulus was withheld for a certain time. Our results meet the principle criteria that have been used to demonstrate habituation: responsiveness decline and spontaneous recovery. To distinguish habituation from sensory adaptation or motor fatigue, we also show stimulus specificity. Our results point to the diversity of organisms lacking neurons, which likely display a hitherto unrecognized capacity for learning, and suggest that slime moulds may be an ideal model system in which to investigate fundamental mechanisms underlying learning processes. Besides, documenting learning in non-neural organisms such as slime moulds is centrally important to a comprehensive, phylogenetic understanding of when and where in the tree of life the earliest manifestations of learning evolved.
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Abraham, Alon, and Vivian E. Drory. "Fatigue in motor neuron diseases." Neuromuscular Disorders 22 (December 2012): S198—S202. http://dx.doi.org/10.1016/j.nmd.2012.10.013.
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Drory, V. E. "Fatigue in motor neuron diseases." Clinical Neurophysiology 127, no. 3 (March 2016): e24. http://dx.doi.org/10.1016/j.clinph.2015.11.068.
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Bertazzi, Renan Nogueira, Fernanda Resernde Martins, Samir Zacarias Zica Saade, and Virgílio Ribeiro Guedes. "Esclerose lateral amiotrófica." Revista de Patologia do Tocantins 4, no. 3 (September 26, 2017): 54. http://dx.doi.org/10.20873/uft.2446-6492.2017v4n3p54.
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A Esclerose Lateral Amiotrófica (ELA) é uma desordem neurodegenerativa dos neurônios motores, invariavelmente progressiva e incapacitante. Sua complexidade e multifatorialidade são determinantes para a dificuldade de tratamentos específicos, embora este cenário tenha mudado nos últimos anos. OBJETIVOS: realizar uma revisão de literatura acerca da ELA, utilizando os agregadores de conteúdo PubMed, BVS e ScieLo. EPIDEMIOLOGIA: A ELA é rara, com predominância de 2:1 em gênero masculino e possui incidência estimada em 1 para 105 habitantes, com prevalência constante. ETIOPATOGÊNESE: Verificadas alterações genéticas em SOD1, FUS, ANG, proteínopatia em TDP-43, dentre outras, que associadas a fatores como exotocicidade, fatores quimiotáxicos de neutrófilos, estresse oxidativo, distúrbios intracelulares do metabolismo do cálcio, lesão mitocondrial, fatores ambientais, infecções e autoimunidade parecem estar implicadas na lesão neuronal. SINTOMATOLOGIA: A entidade progride para perda dos movimentos refinados de prensa, deglutição e fala, acompanhados de miastenia, fasciculações e cãimbras, alentecimento motor, e efeitos pseudobulbares com perda do controle do riso/choro, poupando as funções sensitivas, mantendo a propriocepção do doente. TRATAMENTO: somente o riluzol é aprovado para uso específico, porém outras drogas podem ser usadas: anti-inflamatórios, antiapoptose, anticititóxicos, antioxidantes e mais os inibidores da SOD1. Intervenções cirúrgicas vêm sendo experimentadas, algumas com resultados promissores. O tratamento de suporte deve permear o cuidado com a sialorréia, efeitos pseudobulbares, distúrbios do sono, insuficiência respiratória, fadiga, dor, espasticidade e o laringoespasmo. CONCLUSÃO: Nas últimas décadas, em especial, vimos avanços na determinação dos diferentes elementos da patologia, contudo a terapêutica específica continua restrita. A visibilidade midiática foi importante na implementação de novos estudos. Palavras-chave: Esclerose Amiotrófica Lateral, Doença do Neurônio Motor.
ABSTRACT
Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disorder of motor neurons, invariably progressive and incapacitating. Your complexity and multifactoriality are determinant for the difficulty of specific treatments, although this scenario has changed in recent years. OBJECTIVES: Make a literature review on ALS using the PubMed, BVS and ScieLo. EPIDEMIOLOGY: ALS is a rare condition, with a predominance of 2:1 in men and has an estimated incidence of 1 to 105 habitants, with a constant prevalence. ETHIOPATHOGENESIS: The presence of genetic alterations in SOD1, FUS, ANG, TDP-43, and others, have been verified, such as exotocicity, neutrophil quimiotaxic factors, oxidative stress, intracellular disorders of calcium metabolism, mitochondrial damage, environmental factors, infections and autoimmunity appear to be implicated in neuronal injury. SYMPTOMATOLOGY: The entity progresses to loss of refined movements of the press, swallowing and speech, accompanied by myasthenia, fasciculations and cramps, motor eningement, and pseudobulbar effects with loss of control of laughter/crying, sparing the sensory functions, preserving the proprioception of the patient. TREATMENT: Only riluzoleis approved for specific use, but other drugs may be used: anti-inflammatories, anti-apoptosis, anti-cytotoxic agents, antioxidants, and SOD1 inhibitors. Surgical interventions have been tried, some with promissory results. The supportive treatment should permeate the care with sialorrhea, pseudobulbar effects, sleep disturbers, respiratory failure, fatigue, pain, spasticity and laryngospasm. CONCLUSION: In the last decades, in particular, we have seen some advances in the determination of the different elements of the pathology, however the specific therapy remains restricted. The media visibility was important in the implementation of new studies. Keywords: Lateral Amyotrophic Sclerosis. Motor Neuron Disease.
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Rodriguez-Torres, Rafael, Julia Fabiano, Ashley Goodwin, Ashwini K. Rao, Stacy Kinirons, Darryl De Vivo, and Jacqueline Montes. "Neuroanatomical Models of Muscle Strength and Relationship to Ambulatory Function in Spinal Muscular Atrophy." Journal of Neuromuscular Diseases 7, no. 4 (September 18, 2020): 459–66. http://dx.doi.org/10.3233/jnd-200550.
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Background: Individuals with spinal muscular atrophy (SMA) III walk independently, but experience muscle weakness, gait impairments, and fatigue. Although SMA affects proximal more than distal muscles, the characteristic pattern of selective muscle weakness has not been explained. Two theories have been proposed: 1) location of spinal motor neurons; and 2) differences in segmental innervation. Objective: To identify neuroanatomical models that explain the selective muscle weakness in individuals with SMA and assess the relationship of these models to ambulatory function. Methods: Data from 23 ambulatory SMA participants (78.2% male), ages 10–56 years, enrolled in two clinical studies (NCT01166022, NCT02895789) were included. Strength was assessed using the Medical Research Council (MRC) score; ambulatory function was measured by distance walked on the 6-minute walk test (6 MWT). Three models were identified, and relationships assessed using Pearson correlation coefficients and linear regression. Results: All models demonstrated a positive association between strength and function, (p < 0.02). Linear regression revealed that Model 3B, consisting of muscles innervated by lower lumbar and sacral segments, explained 67% of the variability observed in 6 MWT performance (β= 0.670, p = 0.003). Conclusions: Muscles innervated by lower lumbar and sacral segments, i.e. hip extensors, hip abductors, knee flexors and ankle dorsiflexors, correlated with and predicted greater ambulatory function. The neuroanatomical patterns of muscle weakness may contribute to a better understanding of disease mechanisms and enable delivery of targeted therapies.
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Fine, Michael L., Noelle M. Burns, and Thomas M. Harris. "Ontogeny and sexual dimorphism of sonic muscle in the oyster toadfish." Canadian Journal of Zoology 68, no. 7 (July 1, 1990): 1374–81. http://dx.doi.org/10.1139/z90-205.
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Previous work has shown that neurons in the sonic motor nucleus of the oyster toadfish, Opsanus tau, grow larger in males than in females and increase in size and number for 7–8 years. In order to correlate postnatal motoneuron development with growth of target muscle fibers, we examined the ontogeny of sonic muscle growth. Both the swim bladder and attached sonic muscles increased in size for life and were, respectively, 20 and 44% larger in males than in females. The muscle and swim bladder grew at an equivalent rate in males, whereas in females, muscle growth did not keep up with bladder growth. The number of muscle fibers increased about 16-fold (31 000 to 488 000), and mean minimum fiber diameter increased almost 3-fold (11.5 to 28.6 μm) as fish grew. Fibers were 15.3% larger in females than in males (adjusted means of 21.9 and 19.0 μm, respectively), but males had 47% more fibers per muscle (adjusted means of 307 000 and 209 000). Muscle fibers also exhibited morphological changes. Most of the fibers in two juveniles had yet to differentiate the core of sarcoplasm characteristic of sonic muscle, whereas the largest cells in mature males and females tended to have multiple pockets of sarcoplasm and a contractile cylinder split into fragments. Multiple pockets in large fibers and the presence of smaller fibers in males than females are interpreted as adaptations for increased speed and fatigue resistance.
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Vardarli, Emre, Nisha Bhattarai, Amina El Ayadi, Y. E. Wang, Jayson W. Jay, Anesh Prasai, Victoria G. Rontoyanni, Steven E. Wolf, and Juquan Song. "141 Mild Burns Combined with Diet Induced Demyelination Does Not Affect Skeletal Muscle Function." Journal of Burn Care & Research 42, Supplement_1 (April 1, 2021): S94. http://dx.doi.org/10.1093/jbcr/irab032.145.
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Abstract Introduction Severe burns result in decreased skeletal muscle mass and function. Recent evidence suggests that massive burns disrupt the motor-neural system including motor neurons to partially explain skeletal muscle dysfunction in response to burns. However, impact of demyelination on burn induced skeletal muscle dysfunction has not been investigated. The purpose of this study was to determine the impact of exaggerated demyelination on skeletal muscle dysfunction after burn. Methods C57BL/6 (20-25g, male, n = 26) mice were separated into 6 groups (4–5 animals per group) by diet, burn injury and timepoint (burn or sham groups with two different diets measured at two different timepoints). Mice were fed with either cuprizone diet (0.2 %) to induce severe demyelination or regular diet (18 % protein) for 5 weeks prior to injury. Burns were administered by immersing the dorsal side of the animal into ~95 °C hot water for 10 seconds (~15 % body surface area, full thickness burn). In-situ gastrocnemius function was assessed by attaching the distal tendon of the muscle to a lever arm of a force transducer and stimulating the muscle via exposed sciatic nerve while the animal was under anesthesia. In-situ gastrocnemius muscle function was evaluated 3- and 7-days after burn. Results Food intake was 30 % higher in cuprizone diet group compared to the regular diet group (p=0.002). However, there was no significant difference in body weight among groups (p=0.071). No significant difference was found in gastrocnemius wet weight, peak twitch tension, time to reach peak twitch tension, peak twitch half relaxation time, force-frequency relationship, maximum tetanic force, and fatigue index among groups (burn effect, diet effect, time effect, and their interactions; NS). Conclusions Mild burns combined with demyelination by diet had no effect on skeletal muscle function on our timepoints, and 15 % TBSA burn size was not sufficient to induce skeletal muscle dysfunction. The impact of burn induced neural damage on muscle function and performance indicates further investigation.
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Riley, Zachary, and Roger Enoka. "Motor neuron activation is conditional during muscle fatigue." Physiology News, Winter 2008 (January 1, 2009): 10–12. http://dx.doi.org/10.36866/pn.73.10.
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Ranieri, Federico, and Vincenzo Di Lazzaro. "The role of motor neuron drive in muscle fatigue." Neuromuscular Disorders 22 (December 2012): S157—S161. http://dx.doi.org/10.1016/j.nmd.2012.10.006.
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Simonds, Gary R., Cara Rogers, and Chris Busch. "309 The Effect of 24 Hour Call on Fine Motor Dexterity, Cognition, and Mood." Neurosurgery 64, CN_suppl_1 (August 24, 2017): 265–66. http://dx.doi.org/10.1093/neuros/nyx417.309.
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Abstract INTRODUCTION There continues much debate about optimal work hours for the neurosurgical resident in training. Multiple entities have asserted that cognitive and manual performance deteriorate with prolonged work shifts. We sought to study the effects of 24 hours of neurosurgical duty on manual dexterity, cognition, and mood. METHODS Subjects underwent multiple batteries of validated dexterity, cognitive, and mood evaluations before and after a 24 hour stint of neurosurgical duty. This included a night of neurosurgical call. All subjects were required to stay awake throughout their 24 hour stint. RESULTS >27 subjects underwent the full battery of testing before and after their 24 hours of neurosurgical activities. 13 were seasonedneurosurgical residents and P.A..’s- that is they had extensive experience with neurosurgical call. 14 were non-seasoned medical students who had no previous experience with 24 straight hours of medical activities. Overall performance of the group showed no significant decrement in performance in dexterity, cognition, or overall mood. When divided into a seasoned group and a non-seasoned group however, the non-seasoned group demonstrated statistically significant decrements in multiple functions in dexterity, cognitive, and mood testing. The seasoned group demonstrated no decrements in dexterity or cognition, and only limited change in isolated mood functions (no changes in overall mood). CONCLUSION We believe that this study raises interesting questions about neurosurgical training with respect to the alleged detrimental effects of prolonged work hours. The results suggest that fatigue-induced decrements in professional function can be ameliorated by experience. If this is the case, an argument can be made that we are turning the training paradigm upside down with the current ACGME restrictions. Since long and arduous hours are a fact of life in a neurosurgical career, learning how to recognize and manage fatigue during training will improve physician resilience and therefore patient care.
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Enoka, R. M., and D. G. Stuart. "Neurobiology of muscle fatigue." Journal of Applied Physiology 72, no. 5 (May 1, 1992): 1631–48. http://dx.doi.org/10.1152/jappl.1992.72.5.1631.
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Muscle fatigue encompasses a class of acute effects that impair motor performance. The mechanisms that can produce fatigue involve all elements of the motor system, from a failure of the formulation of the descending drive provided by suprasegmental centers to a reduction in the activity of the contractile proteins. We propose four themes that provide a basis for the systematic evaluation of the neural and neuromuscular fatigue mechanisms: 1) task dependency to identify the conditions that activate the various mechanisms; 2) force-fatigability relationship to explore the interaction between the mechanisms that results in a hyperbolic relationship between force and endurance time; 3) muscle wisdom to examine the association among a concurrent decline in force, relaxation rate, and motor neuron discharge that results in an optimization of force; and 4) sense of effort to determine the role of effort in the impairment of performance. On the basis of this perspective with an emphasis on neural mechanisms, we suggest a number of experiments to advance our understanding of the neurobiology of muscle fatigue.
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Gibbons, Chris J., and Carolyn A. Young. "Assessing and managing depression and fatigue in motor neuron disease." Neurodegenerative Disease Management 2, no. 4 (August 2012): 401–9. http://dx.doi.org/10.2217/nmt.12.42.
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STEPHENS, PHILIP J. "Electrical and Chemical Synapses Between Giant Interneurones and Giant Flexor Motor Neurones of the Hermit Crab (Pagurus Pollicaris)." Journal of Experimental Biology 123, no. 1 (July 1, 1986): 217–28. http://dx.doi.org/10.1242/jeb.123.1.217.
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1. An examination is made of the characteristics of the synapses between the single pair of giant interneurones (GIs) and the giant flexor motor neurones (GFMNs) in the fused thoracic-abdominal (TA) ganglion of the hermit crab Pagurus pollicaris. 2. There is an electrical synapse between each GI and its ipsilateral GFMN. Evidence for this includes (a) dye (Lucifer Yellow CH) coupling between the two neurones, (b) a short synaptic (0.2 ms) delay between spikes in the two axons, (c) the ability to pass hyperpolarizing current between the two neurones and (d) the sensitivity of the connection to bath applications of N-ethylmaleimide. This synaptic connection is rectifying, since a GFMN spike does not provoke an action potential in the GI. 3. There is a connection between the GI and the contralateral GFMN. Data indicating that this synaptic connection is chemical includes (a) a synaptic delay of between 0.6 and 0.8 ms, (b) transmission i9 easily and irreversibly fatigued, (c) the synapse is insensitive to N-ethylmaleimide and (d) there is no dye coupling between the two neurones. 4. Branches of the GFMN come in close proximity with the GI on both sides of the TA ganglion. However, it is not known whether there is a direct connection or an intervening neurone between the GI and the contralateral GFMN.
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Ruggiero, Luca, Alexandra F. Yacyshyn, Jane Nettleton, and Chris J. McNeil. "Acute Hypoxia Exacerbates Central Fatigue but not the Fatigue-related Reduction in Motor Neuron Responsiveness." Medicine & Science in Sports & Exercise 49, no. 5S (May 2017): 251. http://dx.doi.org/10.1249/01.mss.0000517539.91908.77.
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Dideriksen, Jakob L., Dario Farina, and Roger M. Enoka. "Influence of fatigue on the simulated relation between the amplitude of the surface electromyogram and muscle force." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 368, no. 1920 (June 13, 2010): 2765–81. http://dx.doi.org/10.1098/rsta.2010.0094.
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A linear relation between surface electromyogram (EMG) amplitude and muscle force is often assumed and used to estimate the contributions of selected muscles to various tasks. In the presence of muscle fatigue, however, changes in the properties of muscle fibre action potentials and motor unit twitch forces can alter the relation between surface EMG amplitude and force. A novel integrative model of motor neuron control and the generation of muscle fibre action potentials was used to simulate surface EMG signals and muscle force during three fatigue protocols. The change in the simulated relation between surface EMG amplitude and force depended on both the level of fatigue and the details of the fatiguing contraction. In general, surface EMG amplitude overestimated muscle force when fatigue was present. For example, surface EMG amplitudes corresponding to 60 per cent of the amplitude obtained at maximal force without fatigue corresponded to forces in the range 10–40% of the maximal force across three representative fatigue protocols. The results indicate that the surface EMG amplitude cannot be used to predict either the level of muscle activation or the magnitude of muscle force when the muscle exhibits any fatigue.
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ATWOOD, H. L., and C. K. GOVIND. "Activity-dependent and age-dependent recruitment and regulation of synapses in identified Crustacean Neurones1." Journal of Experimental Biology 153, no. 1 (October 1, 1990): 105–27. http://dx.doi.org/10.1242/jeb.153.1.105.
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Adaptation of neural systems to altered activity and age often involves recruitment, inactivation or modification of synapses. Crustacean motor systems are amenable to experimental investigation of these processes. They possess large identifiable neurones that can be observed over long periods during development, adulthood, regeneration and degeneration. Numerous small individual synapses are present on the transmitting terminals of the motor neurones; their ultrastructural features are non—uniform, indicating different degrees of functional potency. Ultrastructural studies show many more individual synapses than required for maximal quantal output; probably some are ineffective, but can be brought into a transmitting state in a short time by neural activity. During development, progressive reorganization and relocation of synapses take place. As the size of a postsynaptic target changes, synapses are added, and functionally adaptive alterations in quantal content and quantal effectiveness occur. Sectioning an axon results in slow degeneration of distal processes, but transmission is sustained for months. Short—term adjustments in number of effective synapses occur in response to altered activity. If activity of a neurone is chronically increased or decreased, characteristic semi—permanent adaptations in physiology and ultrastructure are seen. Synaptic transmission at low frequencies is down—regulated, while resistance to synaptic depression increases. These effects require protein synthesis, and at least two different changes 舑 one related to down-regulation of synapses, the other related to fatigue resistance 舑 can be selectively demonstrated through critically timed interruption of axoplasmic transport or imposition of different patterns of neural activity. In older animals, the ability to adapt to activity is reduced in some neurones, but may be restored during regeneration of neural processes. Selective changes in activity in one of several neurones innervating a common postsynaptic target lead to adaptive changes in synaptic transmission of non-active neurones, indicating activity-mediated interaction and adjustment. Mechanisms of adaptation similar to those outlined here probably occur in nervous systems of otherspecies.
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Iyer, Shama R., Sameer B. Shah, and Richard M. Lovering. "The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease." International Journal of Molecular Sciences 22, no. 15 (July 28, 2021): 8058. http://dx.doi.org/10.3390/ijms22158058.
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The neuromuscular junction (NMJ) is a specialized synapse that bridges the motor neuron and the skeletal muscle fiber and is crucial for conversion of electrical impulses originating in the motor neuron to action potentials in the muscle fiber. The consideration of contributing factors to skeletal muscle injury, muscular dystrophy and sarcopenia cannot be restricted only to processes intrinsic to the muscle, as data show that these conditions incur denervation-like findings, such as fragmented NMJ morphology and corresponding functional changes in neuromuscular transmission. Primary defects in the NMJ also influence functional loss in motor neuron disease, congenital myasthenic syndromes and myasthenia gravis, resulting in skeletal muscle weakness and heightened fatigue. Such findings underscore the role that the NMJ plays in neuromuscular performance. Regardless of cause or effect, functional denervation is now an accepted consequence of sarcopenia and muscle disease. In this short review, we provide an overview of the pathologic etiology, symptoms, and therapeutic strategies related to the NMJ. In particular, we examine the role of the NMJ as a disease modifier and a potential therapeutic target in neuromuscular injury and disease.
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Gibbons, Chris J., Roger J. Mills, Everard W. Thornton, John Ealing, John D. Mitchell, Pamela J. Shaw, Kevin Talbot, A. Tennant, and Carolyn A. Young. "Development of a patient reported outcome measure for fatigue in motor neurone disease: the Neurological Fatigue Index (NFI-MND)." Health and Quality of Life Outcomes 9, no. 1 (2011): 101. http://dx.doi.org/10.1186/1477-7525-9-101.
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Berns, Christina, Wanja Brüchle, Sebastian Scho, Jessica Schneefeld, Udo Schneider, and Karin Rosenkranz. "Intensity dependent effect of cognitive training on motor cortical plasticity and cognitive performance in humans." Experimental Brain Research 238, no. 12 (October 6, 2020): 2805–18. http://dx.doi.org/10.1007/s00221-020-05933-5.
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Abstract Intervention-induced neuroplastic changes within the motor or cognitive system have been shown in the human brain. While cognitive and motor brain areas are densely interconnected, it is unclear whether this interconnectivity allows for a shared susceptibility to neuroplastic changes. Using the preparation for a theoretical exam as training intervention that primarily engages the cognitive system, we tested the hypothesis whether neuroplasticity acts across interconnected brain areas by investigating the effect on excitability and synaptic plasticity in the motor cortex. 39 healthy students (23 female) underwent 4 weeks of cognitive training while revision time, physical activity, concentration, fatigue, sleep quality and stress were monitored. Before and after cognitive training, cognitive performance was evaluated, as well as motor excitability using transcranial magnetic stimulation and long-term-potentiation-like (LTP-like) plasticity using paired-associative-stimulation (PAS). Cognitive training ranged individually from 1 to 7 h/day and enhanced attention and verbal working memory. While motor excitability did not change, LTP-like plasticity increased in an intensity-depending manner: the longer the daily revision time, the smaller the increase of neuroplasticity, and vice versa. This effect was not influenced by physical activity, concentration, fatigue, sleep quality or stress. Motor cortical plasticity is strengthened by a behavioural intervention that primarily engages cognitive brain areas. We suggest that this effect is due to an enhanced susceptibility to LTP-like plasticity, probably induced by heterosynaptic activity that modulates postsynaptic excitability in motorcortical neurones. The smaller increase of PAS efficiency with higher cognitive training intensity suggests a mechanism that balances and stabilises the susceptibility for synaptic potentiation.
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Walsh, Laura J., and Desmond M. Murphy. "The Benefit of Non-invasive Ventilation in Motor Neuron Disease." Open Respiratory Medicine Journal 14, no. 1 (December 15, 2020): 53–61. http://dx.doi.org/10.2174/1874306402014010053.
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Background: Motor Neuron Disease (MND) is a progressive neurodegenerative disorder leading to respiratory muscle weakness with dyspnoea, morning headaches, orthopnoea, poor concentration, unrefreshing sleep, fatigue and daytime somnolence. Respiratory failure is the primary cause of death in those with MND. Methods: Although guidelines suggest the use of non-invasive ventilation (NIV) in MND, there lacks clear guidance as to when is the optimal time to initiate NIV and which markers of respiratory muscle decline are the best predictors of prognosis. There have been a number of studies that have found a significant survival advantage to the use of NIV in MND. Similarly, in quality-of-life questionnaires, those treated with NIV tend to perform better and maintain a better quality of life for longer. Furthermore, studies also suggest that improved compliance and greater tolerance of NIV confer a survival advantage. Results and Discussion: Forced Vital Capacity (FVC) has traditionally been the main pulmonary function test to determine the respiratory function in those with MND; however, FVC may not be entirely reflective of early respiratory muscle dysfunction. Evidence suggests that sniff nasal inspiratory pressure and maximum mouth inspiratory pressure may be better indicators of early respiratory muscle decline. These measures have been shown to be easier to perform later in the disease, in patients with bulbar onset disease, and may indeed be better prognostic indicators. Conclusion: Despite ongoing research, there remains a paucity of randomised controlled data in this area. This review aims to summarise the evidence to date on these topics.
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Berg, Leonard H. van den. "The Long-term Treatment of Multifocal Motor Neuropathy with Intravenous Immunoglobulin." European Neurological Review 7, no. 2 (2012): 128. http://dx.doi.org/10.17925/enr.2012.07.02.128.
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Multifocal motor neuropathy (MMN) is a rare, purely motor neuropathy. It is a progressive disorder, most patients eventually developing severe fatigue and weakness in the arm muscles that severely impair daily functioning and quality of life. Unlike other motor neuropathies such as motor neurone disease, MMN is treatable with regular infusions of intravenous immunoglobulin (IVIg). Four double-blind, randomised, placebo-controlled studies have shown that in the short term, IVIg significantly improves muscle strength and disability in more than 70 % of patients. The 11 observational studies reviewed in this article confirm that long-term maintenance treatment with IVIg maintains clinical improvement compared to pre-treatment baseline in most patients. Infusions are generally well tolerated, but regular monitoring and re-evaluation of the IVIg maintenance regimen is essential, as most patients need progressive increases in dosage or reduced intervals between infusions to maintain their response to treatment. In the absence of accepted predictive markers, maintenance IVIg should be individualised, based on each patient’s initial response, disability and the interval between the first infusion and decline in muscle strength.
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Kontos, Anthony P., R. J. Elbin, Alicia Trbovich, Melissa Womble, Azkya Said, Vanessa Fazio Sumrok, Jonathan French, et al. "Concussion Clinical Profiles Screening (CP Screen) Tool: Preliminary Evidence to Inform a Multidisciplinary Approach." Neurosurgery 87, no. 2 (January 17, 2020): 348–56. http://dx.doi.org/10.1093/neuros/nyz545.
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Abstract BACKGROUND Current concussion symptom inventories emphasize total number or symptoms and severity and overlap with other conditions, such as mental health disorders, which may limit their specificity and clinical utility. OBJECTIVE To develop and test the reliability and validity of a new Concussion Clinical Profiles Screening tool (CP Screen) in both healthy controls and concussed. METHODS CP Screen is a 29-item self-report, clinical profile-based symptom inventory that measures the following 5 concussion clinical profiles: 1) anxiety/mood, 2) cognitive/fatigue, 3) migraine, 4) ocular, and 5) vestibular; and the following 2 modifying factors: 1) sleep and 2) neck. Post-Concussion Symptom Scale (PCSS), vestibular/ocular motor screening (VOMS) tool, and Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT) were conducted. CP Screen was administered in community a concussion surveillance program and 2 sports medicine concussion clinics. Responses include 248 athletes, 121 concussed, and 127 controls, enrolled between 2018 and 2019. RESULTS Internal consistency of the CP Screen in the control (Cronbach's alpha = .87) and concussed (Cronbach's alpha = .93) samples was high. Moderate to high correlations among the CP Screen factors and PCSS factors and VOMS items, supporting concurrent validity. ROC curve analysis for identifying concussed from controls was significant (P < .001) for all CP Screen factor and modifier scores with excellent AUCs for migraine (.93), ocular (.88), vestibular (.85), and cognitive (.81) factors, demonstrating predictive validity. CONCLUSION The CP Screen demonstrated strong reliability, concurrent validity with commonly used concussion assessment (ie, PCSS, VOMS, and ImPACT), and predictive validity for identifying concussion. The CP Screen extends current symptom inventories by evaluating more specific symptoms that may reflect clinical profiles and inform better clinical care.
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Catania, Kenneth C. "Electric Eels Wield a Functional Venom Analogue." Toxins 13, no. 1 (January 10, 2021): 48. http://dx.doi.org/10.3390/toxins13010048.
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In this paper, I draw an analogy between the use of electricity by electric eels (Electrophorus electricus) to paralyze prey muscles and the use of venoms that paralyze prey by disrupting the neuromuscular junction. The eel’s strategy depends on the recently discovered ability of eels to activate prey motor neuron efferents with high-voltage pulses. Usually, eels use high voltage to cause brief, whole-body tetanus, thus preventing escape while swallowing prey whole. However, when eels struggle with large prey, or with prey held precariously, they often curl to bring their tail to the opposite side. This more than doubles the strength of the electric field within shocked prey, ensuring maximal stimulation of motor neuron efferents. Eels then deliver repeated volleys of high-voltage pulses at a rate of approximately 100 Hz. This causes muscle fatigue that attenuates prey movement, thus preventing both escape and defense while the eel manipulates and swallows the helpless animal. Presumably, the evolution of enough electrical power to remotely activate ion channels in prey efferents sets the stage for the selection of eel behaviors that functionally “poison” prey muscles.
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Catania, Kenneth C. "Electric Eels Wield a Functional Venom Analogue." Toxins 13, no. 1 (January 10, 2021): 48. http://dx.doi.org/10.3390/toxins13010048.
Full textAbstract:
In this paper, I draw an analogy between the use of electricity by electric eels (Electrophorus electricus) to paralyze prey muscles and the use of venoms that paralyze prey by disrupting the neuromuscular junction. The eel’s strategy depends on the recently discovered ability of eels to activate prey motor neuron efferents with high-voltage pulses. Usually, eels use high voltage to cause brief, whole-body tetanus, thus preventing escape while swallowing prey whole. However, when eels struggle with large prey, or with prey held precariously, they often curl to bring their tail to the opposite side. This more than doubles the strength of the electric field within shocked prey, ensuring maximal stimulation of motor neuron efferents. Eels then deliver repeated volleys of high-voltage pulses at a rate of approximately 100 Hz. This causes muscle fatigue that attenuates prey movement, thus preventing both escape and defense while the eel manipulates and swallows the helpless animal. Presumably, the evolution of enough electrical power to remotely activate ion channels in prey efferents sets the stage for the selection of eel behaviors that functionally “poison” prey muscles.
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Bunevicius, Adomas, Sarunas Tamasauskas, Vytenis Deltuva, Edward R. Laws, and Arimantas Tamasauskas. "153 Prognostic Role of the Low Tri-Iodothyronine Syndrome in Brain Tumor Patients." Neurosurgery 64, CN_suppl_1 (August 24, 2017): 237. http://dx.doi.org/10.1093/neuros/nyx417.153.
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Abstract INTRODUCTION Reduced triiodothyronine (T3) concentrations were implicated in worse prognosis of brain tumor patients. We investigated the association of thyroid hormone concentrations with health-related quality of life (HRQoL), discharge outcomes and prognosis of brain tumor patients. METHODS Two-hundred and thirty brain tumor patients (70% women) before brain tumor surgery were evaluated for HRQoL (ERTC QLQ-C30 and QLQ-BN20 questionnaires); and thyroid function profile. The Low tri-iodothyronine (T3) syndrome was defined as T3 concentration below the reference range. Unfavorable hospital discharge outcomes were determined as Glasgow outcome scale score of = 3. Follow-up continued until November, 2015. RESULTS >Seventy-four percent of patients had Low T3 syndrome. After adjusting for the brain tumor histological diagnosis, patients' age, gender and functional status, lower free T3 concentrations were associated with worse HRQOL on the QLQ-C30 Global health status (ß = 0.302, P = 0.017), Emotional functioning (ß = 0.422, p<.001) and Cognitive functioning (ß = 0.259, P = 0.042) domains, and with greater symptom severity on the QLQ-BN20 Fatigue (ß = −0.238, p = .041), Motor dysfunction (ß = −0.283, P = 0.013) and Weakness of legs (ß = −0.269. P = 0.027) domains. Preoperative Low T3 syndrome increased risk for unfavorable discharge outcomes adjusting for age, gender and histological diagnosis (OR = 2.944, 95%CI [1.314-6.597], p = .009). In all patients, lower total (p = .038) and free (p = .014) T3 concentrations were associated with greater mortality adjusting for age, gender, extent of resection, adjuvant treatment and histological diagnosis. The Low T3 syndrome was associated with greater 5-year mortality for glioma patients (HR = 2.197; 95%CI [1.160-4.163], p = .016) and with shorter survival (249 [260] vs. 352 [399] days; p = .029) of high grade glioma patients independent of age, gender, extent of resection and adjuvant treatment. CONCLUSION The Low T3 syndrome is common in brain tumor patients and is associated with worse health status, impaired emotional and physical aspects of HRQoL and worse discharge outcomes. The Low T3 syndrome is associated with shorter survival of glioma patients.
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Helleman, Jochem, Esther T. Kruitwagen-van Reenen, J. Bakers, Willeke J. Kruithof, Annerieke C. van Groenestijn, Rineke J. H. Jaspers Focks, Arthur de Grund, Leonard H. van den Berg, Johanna M. A. Visser-Meily, and Anita Beelen. "Using patient-reported symptoms of dyspnea for screening reduced respiratory function in patients with motor neuron diseases." Journal of Neurology 267, no. 11 (June 23, 2020): 3310–18. http://dx.doi.org/10.1007/s00415-020-10003-5.
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Abstract Background Poor monitoring of respiratory function may lead to late initiation of non-invasive ventilation (NIV) in patients with motor neuron diseases (MND). Monitoring could be improved by remotely assessing hypoventilation symptoms between clinic visits. We aimed to determine which patient-reported hypoventilation symptoms are best for screening reduced respiratory function in patients with MND, and compared them to the respiratory domain of the amyotrophic lateral sclerosis functional rating scale (ALSFRS-R). Methods This prospective multi-center study included 100 patients with MND, who were able to perform a supine vital capacity test. Reduced respiratory function was defined as a predicted supine vital capacity ≤ 80%. We developed a 14-item hypoventilation symptom questionnaire (HYSQ) based on guidelines, expert opinion and think-aloud interviews with patients. Symptoms of the HYSQ were related to dyspnea, sleep quality, sleepiness/fatigue and pneumonia. The diagnostic performances of these symptoms and the ALSFRS-R respiratory domain were determined from the receiver operating characteristic (ROC) curves, area under the curve (AUC), sensitivity, specificity, predictive values and accuracy. Results Dyspnea-related symptoms (dyspnea while eating/talking, while lying flat and during light activity) were combined into the MND Dyspnea Scale (MND-DS). ROC curves showed that the MND-DS had the best diagnostic performance, with the highest AUC = 0.72, sensitivity = 75% and accuracy = 71%. Sleep-quality symptoms, sleepiness/fatigue-related symptoms and the ALSFRS-R respiratory domain showed weak diagnostic performance. Conclusion The diagnostic performance of the MND-DS was better than the respiratory domain of the ALSFRS-R for screening reduced respiratory function in patients with MND, and is, therefore, the preferred method for (remotely) monitoring respiratory function.