Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression

Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to inv...
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Gespeichert in:

Autor*in:	Özyurt, Mustafa G. [verfasserIn] Topkara, Betilay [verfasserIn] İşak, Barış [verfasserIn] Türker, Kemal S. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Recurrent inhibition Renshaw cells Amyotrophic lateral sclerosis Post-activation depression Motoneuron

Übergeordnetes Werk:	Enthalten in: Clinical neurophysiology - Amsterdam [u.a.] : Elsevier Science, 1999, 131, Seite 2875-2886
Übergeordnetes Werk:	volume:131 ; pages:2875-2886

DOI / URN:	10.1016/j.clinph.2020.09.021

Katalog-ID:	ELV00507634X

Internformat


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245	1	0	\|a Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression
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520			\|a Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001).Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS.Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans.
650		4	\|a Recurrent inhibition
650		4	\|a Renshaw cells
650		4	\|a Amyotrophic lateral sclerosis
650		4	\|a Post-activation depression
650		4	\|a Motoneuron
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700	1		\|a İşak, Barış \|e verfasserin \|4 aut
700	1		\|a Türker, Kemal S. \|e verfasserin \|0 (orcid)0000-0001-9962-075X \|4 aut
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matchkey_str	article:18728952:2020----::morpiltrlceoiwaespnleurnihbtoad
hierarchy_sort_str	2020
bklnumber	44.37 44.90
publishDate	2020
allfields	10.1016/j.clinph.2020.09.021 doi (DE-627)ELV00507634X (ELSEVIER)S1388-2457(20)30496-X DE-627 ger DE-627 rda eng 610 DE-600 44.37 bkl 44.90 bkl Özyurt, Mustafa G. verfasserin aut Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001).Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS.Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans. Recurrent inhibition Renshaw cells Amyotrophic lateral sclerosis Post-activation depression Motoneuron Topkara, Betilay verfasserin aut İşak, Barış verfasserin aut Türker, Kemal S. verfasserin (orcid)0000-0001-9962-075X aut Enthalten in Clinical neurophysiology Amsterdam [u.a.] : Elsevier Science, 1999 131, Seite 2875-2886 Online-Ressource (DE-627)306654555 (DE-600)1499934-1 (DE-576)081984782 1872-8952 nnns volume:131 pages:2875-2886 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.37 Physiologie Medizin 44.90 Neurologie AR 131 2875-2886
spelling	10.1016/j.clinph.2020.09.021 doi (DE-627)ELV00507634X (ELSEVIER)S1388-2457(20)30496-X DE-627 ger DE-627 rda eng 610 DE-600 44.37 bkl 44.90 bkl Özyurt, Mustafa G. verfasserin aut Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001).Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS.Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans. Recurrent inhibition Renshaw cells Amyotrophic lateral sclerosis Post-activation depression Motoneuron Topkara, Betilay verfasserin aut İşak, Barış verfasserin aut Türker, Kemal S. verfasserin (orcid)0000-0001-9962-075X aut Enthalten in Clinical neurophysiology Amsterdam [u.a.] : Elsevier Science, 1999 131, Seite 2875-2886 Online-Ressource (DE-627)306654555 (DE-600)1499934-1 (DE-576)081984782 1872-8952 nnns volume:131 pages:2875-2886 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.37 Physiologie Medizin 44.90 Neurologie AR 131 2875-2886
allfields_unstemmed	10.1016/j.clinph.2020.09.021 doi (DE-627)ELV00507634X (ELSEVIER)S1388-2457(20)30496-X DE-627 ger DE-627 rda eng 610 DE-600 44.37 bkl 44.90 bkl Özyurt, Mustafa G. verfasserin aut Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001).Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS.Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans. Recurrent inhibition Renshaw cells Amyotrophic lateral sclerosis Post-activation depression Motoneuron Topkara, Betilay verfasserin aut İşak, Barış verfasserin aut Türker, Kemal S. verfasserin (orcid)0000-0001-9962-075X aut Enthalten in Clinical neurophysiology Amsterdam [u.a.] : Elsevier Science, 1999 131, Seite 2875-2886 Online-Ressource (DE-627)306654555 (DE-600)1499934-1 (DE-576)081984782 1872-8952 nnns volume:131 pages:2875-2886 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.37 Physiologie Medizin 44.90 Neurologie AR 131 2875-2886
allfieldsGer	10.1016/j.clinph.2020.09.021 doi (DE-627)ELV00507634X (ELSEVIER)S1388-2457(20)30496-X DE-627 ger DE-627 rda eng 610 DE-600 44.37 bkl 44.90 bkl Özyurt, Mustafa G. verfasserin aut Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001).Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS.Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans. Recurrent inhibition Renshaw cells Amyotrophic lateral sclerosis Post-activation depression Motoneuron Topkara, Betilay verfasserin aut İşak, Barış verfasserin aut Türker, Kemal S. verfasserin (orcid)0000-0001-9962-075X aut Enthalten in Clinical neurophysiology Amsterdam [u.a.] : Elsevier Science, 1999 131, Seite 2875-2886 Online-Ressource (DE-627)306654555 (DE-600)1499934-1 (DE-576)081984782 1872-8952 nnns volume:131 pages:2875-2886 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.37 Physiologie Medizin 44.90 Neurologie AR 131 2875-2886
allfieldsSound	10.1016/j.clinph.2020.09.021 doi (DE-627)ELV00507634X (ELSEVIER)S1388-2457(20)30496-X DE-627 ger DE-627 rda eng 610 DE-600 44.37 bkl 44.90 bkl Özyurt, Mustafa G. verfasserin aut Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001).Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS.Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans. Recurrent inhibition Renshaw cells Amyotrophic lateral sclerosis Post-activation depression Motoneuron Topkara, Betilay verfasserin aut İşak, Barış verfasserin aut Türker, Kemal S. verfasserin (orcid)0000-0001-9962-075X aut Enthalten in Clinical neurophysiology Amsterdam [u.a.] : Elsevier Science, 1999 131, Seite 2875-2886 Online-Ressource (DE-627)306654555 (DE-600)1499934-1 (DE-576)081984782 1872-8952 nnns volume:131 pages:2875-2886 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.37 Physiologie Medizin 44.90 Neurologie AR 131 2875-2886
language	English
source	Enthalten in Clinical neurophysiology 131, Seite 2875-2886 volume:131 pages:2875-2886
sourceStr	Enthalten in Clinical neurophysiology 131, Seite 2875-2886 volume:131 pages:2875-2886
format_phy_str_mv	Article
bklname	Physiologie Neurologie
institution	findex.gbv.de
topic_facet	Recurrent inhibition Renshaw cells Amyotrophic lateral sclerosis Post-activation depression Motoneuron
dewey-raw	610
isfreeaccess_bool	false
container_title	Clinical neurophysiology
authorswithroles_txt_mv	Özyurt, Mustafa G. @@aut@@ Topkara, Betilay @@aut@@ İşak, Barış @@aut@@ Türker, Kemal S. @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	306654555
dewey-sort	3610
id	ELV00507634X
language_de	englisch
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To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. 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author	Özyurt, Mustafa G.
spellingShingle	Özyurt, Mustafa G. ddc 610 bkl 44.37 bkl 44.90 misc Recurrent inhibition misc Renshaw cells misc Amyotrophic lateral sclerosis misc Post-activation depression misc Motoneuron Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression
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topic_title	610 DE-600 44.37 bkl 44.90 bkl Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression Recurrent inhibition Renshaw cells Amyotrophic lateral sclerosis Post-activation depression Motoneuron
topic	ddc 610 bkl 44.37 bkl 44.90 misc Recurrent inhibition misc Renshaw cells misc Amyotrophic lateral sclerosis misc Post-activation depression misc Motoneuron
topic_unstemmed	ddc 610 bkl 44.37 bkl 44.90 misc Recurrent inhibition misc Renshaw cells misc Amyotrophic lateral sclerosis misc Post-activation depression misc Motoneuron
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title	Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression
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title_full	Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression
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title_sort	amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression
title_auth	Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression
abstract	Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001).Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS.Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans.
abstractGer	Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001).Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS.Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans.
abstract_unstemmed	Objectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients.Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects.Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001).Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS.Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans.
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title_short	Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression
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author2	Topkara, Betilay İşak, Barış Türker, Kemal S.
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doi_str	10.1016/j.clinph.2020.09.021
up_date	2024-07-06T16:44:23.820Z
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Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression

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