Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease

Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality....
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	McDonell, Katherine E. [verfasserIn] Shibao, Cyndya A. [verfasserIn] Claassen, Daniel O. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	Neurogenic orthostatic hypotension Autonomic failure Neurodegeneration Pathophysiology Pharmacology

Übergeordnetes Werk:	Enthalten in: Current neurology and neuroscience reports - Philadelphia, Pa. : Current Science Inc., 2001, 15(2015), 12 vom: 20. Okt.
Übergeordnetes Werk:	volume:15 ; year:2015 ; number:12 ; day:20 ; month:10

Links:	Volltext

DOI / URN:	10.1007/s11910-015-0599-0

Katalog-ID:	SPR022977104

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520			\|a Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality. nOH results from pathology affecting either the central autonomic pathways or peripheral autonomic nerve fibers. Determining the localization and pathophysiology of nOH is critical in effectively managing this disorder and selecting appropriate treatment options. In this review, we discuss the pathophysiology of nOH with respect to the various α-synuclein-related neurodegenerative conditions. We highlight the associated clinical features, including gait instability, rapid eye movement behavior disorder, and hyposmia. We also review the current pharmacologic treatment options for nOH. Overall, the goals of therapy are to improve symptoms and prevent syncope and falls. Non-pharmacologic interventions should be introduced first, followed by carefully selected pharmacologic therapies. Treatment decisions should be directed by an understanding of the underlying pathophysiology, as well as the comorbidities and potential contributing factors present in each individual patient.
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author_variant	k e m ke kem c a s ca cas d o c do doc
matchkey_str	article:15346293:2015----::lncleeacootottcyoesoinuo
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allfields	10.1007/s11910-015-0599-0 doi (DE-627)SPR022977104 (SPR)s11910-015-0599-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl McDonell, Katherine E. verfasserin aut Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality. nOH results from pathology affecting either the central autonomic pathways or peripheral autonomic nerve fibers. Determining the localization and pathophysiology of nOH is critical in effectively managing this disorder and selecting appropriate treatment options. In this review, we discuss the pathophysiology of nOH with respect to the various α-synuclein-related neurodegenerative conditions. We highlight the associated clinical features, including gait instability, rapid eye movement behavior disorder, and hyposmia. We also review the current pharmacologic treatment options for nOH. Overall, the goals of therapy are to improve symptoms and prevent syncope and falls. Non-pharmacologic interventions should be introduced first, followed by carefully selected pharmacologic therapies. Treatment decisions should be directed by an understanding of the underlying pathophysiology, as well as the comorbidities and potential contributing factors present in each individual patient. Neurogenic orthostatic hypotension (dpeaa)DE-He213 Autonomic failure (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Pathophysiology (dpeaa)DE-He213 Pharmacology (dpeaa)DE-He213 Shibao, Cyndya A. verfasserin aut Claassen, Daniel O. verfasserin aut Enthalten in Current neurology and neuroscience reports Philadelphia, Pa. : Current Science Inc., 2001 15(2015), 12 vom: 20. Okt. (DE-627)35716833X (DE-600)2094171-7 1534-6293 nnns volume:15 year:2015 number:12 day:20 month:10 https://dx.doi.org/10.1007/s11910-015-0599-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 15 2015 12 20 10
spelling	10.1007/s11910-015-0599-0 doi (DE-627)SPR022977104 (SPR)s11910-015-0599-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl McDonell, Katherine E. verfasserin aut Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality. nOH results from pathology affecting either the central autonomic pathways or peripheral autonomic nerve fibers. Determining the localization and pathophysiology of nOH is critical in effectively managing this disorder and selecting appropriate treatment options. In this review, we discuss the pathophysiology of nOH with respect to the various α-synuclein-related neurodegenerative conditions. We highlight the associated clinical features, including gait instability, rapid eye movement behavior disorder, and hyposmia. We also review the current pharmacologic treatment options for nOH. Overall, the goals of therapy are to improve symptoms and prevent syncope and falls. Non-pharmacologic interventions should be introduced first, followed by carefully selected pharmacologic therapies. Treatment decisions should be directed by an understanding of the underlying pathophysiology, as well as the comorbidities and potential contributing factors present in each individual patient. Neurogenic orthostatic hypotension (dpeaa)DE-He213 Autonomic failure (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Pathophysiology (dpeaa)DE-He213 Pharmacology (dpeaa)DE-He213 Shibao, Cyndya A. verfasserin aut Claassen, Daniel O. verfasserin aut Enthalten in Current neurology and neuroscience reports Philadelphia, Pa. : Current Science Inc., 2001 15(2015), 12 vom: 20. Okt. (DE-627)35716833X (DE-600)2094171-7 1534-6293 nnns volume:15 year:2015 number:12 day:20 month:10 https://dx.doi.org/10.1007/s11910-015-0599-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 15 2015 12 20 10
allfields_unstemmed	10.1007/s11910-015-0599-0 doi (DE-627)SPR022977104 (SPR)s11910-015-0599-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl McDonell, Katherine E. verfasserin aut Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality. nOH results from pathology affecting either the central autonomic pathways or peripheral autonomic nerve fibers. Determining the localization and pathophysiology of nOH is critical in effectively managing this disorder and selecting appropriate treatment options. In this review, we discuss the pathophysiology of nOH with respect to the various α-synuclein-related neurodegenerative conditions. We highlight the associated clinical features, including gait instability, rapid eye movement behavior disorder, and hyposmia. We also review the current pharmacologic treatment options for nOH. Overall, the goals of therapy are to improve symptoms and prevent syncope and falls. Non-pharmacologic interventions should be introduced first, followed by carefully selected pharmacologic therapies. Treatment decisions should be directed by an understanding of the underlying pathophysiology, as well as the comorbidities and potential contributing factors present in each individual patient. Neurogenic orthostatic hypotension (dpeaa)DE-He213 Autonomic failure (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Pathophysiology (dpeaa)DE-He213 Pharmacology (dpeaa)DE-He213 Shibao, Cyndya A. verfasserin aut Claassen, Daniel O. verfasserin aut Enthalten in Current neurology and neuroscience reports Philadelphia, Pa. : Current Science Inc., 2001 15(2015), 12 vom: 20. Okt. (DE-627)35716833X (DE-600)2094171-7 1534-6293 nnns volume:15 year:2015 number:12 day:20 month:10 https://dx.doi.org/10.1007/s11910-015-0599-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 15 2015 12 20 10
allfieldsGer	10.1007/s11910-015-0599-0 doi (DE-627)SPR022977104 (SPR)s11910-015-0599-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl McDonell, Katherine E. verfasserin aut Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality. nOH results from pathology affecting either the central autonomic pathways or peripheral autonomic nerve fibers. Determining the localization and pathophysiology of nOH is critical in effectively managing this disorder and selecting appropriate treatment options. In this review, we discuss the pathophysiology of nOH with respect to the various α-synuclein-related neurodegenerative conditions. We highlight the associated clinical features, including gait instability, rapid eye movement behavior disorder, and hyposmia. We also review the current pharmacologic treatment options for nOH. Overall, the goals of therapy are to improve symptoms and prevent syncope and falls. Non-pharmacologic interventions should be introduced first, followed by carefully selected pharmacologic therapies. Treatment decisions should be directed by an understanding of the underlying pathophysiology, as well as the comorbidities and potential contributing factors present in each individual patient. Neurogenic orthostatic hypotension (dpeaa)DE-He213 Autonomic failure (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Pathophysiology (dpeaa)DE-He213 Pharmacology (dpeaa)DE-He213 Shibao, Cyndya A. verfasserin aut Claassen, Daniel O. verfasserin aut Enthalten in Current neurology and neuroscience reports Philadelphia, Pa. : Current Science Inc., 2001 15(2015), 12 vom: 20. Okt. (DE-627)35716833X (DE-600)2094171-7 1534-6293 nnns volume:15 year:2015 number:12 day:20 month:10 https://dx.doi.org/10.1007/s11910-015-0599-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 15 2015 12 20 10
allfieldsSound	10.1007/s11910-015-0599-0 doi (DE-627)SPR022977104 (SPR)s11910-015-0599-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl McDonell, Katherine E. verfasserin aut Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality. nOH results from pathology affecting either the central autonomic pathways or peripheral autonomic nerve fibers. Determining the localization and pathophysiology of nOH is critical in effectively managing this disorder and selecting appropriate treatment options. In this review, we discuss the pathophysiology of nOH with respect to the various α-synuclein-related neurodegenerative conditions. We highlight the associated clinical features, including gait instability, rapid eye movement behavior disorder, and hyposmia. We also review the current pharmacologic treatment options for nOH. Overall, the goals of therapy are to improve symptoms and prevent syncope and falls. Non-pharmacologic interventions should be introduced first, followed by carefully selected pharmacologic therapies. Treatment decisions should be directed by an understanding of the underlying pathophysiology, as well as the comorbidities and potential contributing factors present in each individual patient. Neurogenic orthostatic hypotension (dpeaa)DE-He213 Autonomic failure (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Pathophysiology (dpeaa)DE-He213 Pharmacology (dpeaa)DE-He213 Shibao, Cyndya A. verfasserin aut Claassen, Daniel O. verfasserin aut Enthalten in Current neurology and neuroscience reports Philadelphia, Pa. : Current Science Inc., 2001 15(2015), 12 vom: 20. Okt. (DE-627)35716833X (DE-600)2094171-7 1534-6293 nnns volume:15 year:2015 number:12 day:20 month:10 https://dx.doi.org/10.1007/s11910-015-0599-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 15 2015 12 20 10
language	English
source	Enthalten in Current neurology and neuroscience reports 15(2015), 12 vom: 20. Okt. volume:15 year:2015 number:12 day:20 month:10
sourceStr	Enthalten in Current neurology and neuroscience reports 15(2015), 12 vom: 20. Okt. volume:15 year:2015 number:12 day:20 month:10
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Neurogenic orthostatic hypotension Autonomic failure Neurodegeneration Pathophysiology Pharmacology
dewey-raw	610
isfreeaccess_bool	false
container_title	Current neurology and neuroscience reports
authorswithroles_txt_mv	McDonell, Katherine E. @@aut@@ Shibao, Cyndya A. @@aut@@ Claassen, Daniel O. @@aut@@
publishDateDaySort_date	2015-10-20T00:00:00Z
hierarchy_top_id	35716833X
dewey-sort	3610
id	SPR022977104
language_de	englisch
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author	McDonell, Katherine E.
spellingShingle	McDonell, Katherine E. ddc 610 bkl 44.90 misc Neurogenic orthostatic hypotension misc Autonomic failure misc Neurodegeneration misc Pathophysiology misc Pharmacology Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease
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topic_title	610 ASE 44.90 bkl Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease Neurogenic orthostatic hypotension (dpeaa)DE-He213 Autonomic failure (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Pathophysiology (dpeaa)DE-He213 Pharmacology (dpeaa)DE-He213
topic	ddc 610 bkl 44.90 misc Neurogenic orthostatic hypotension misc Autonomic failure misc Neurodegeneration misc Pathophysiology misc Pharmacology
topic_unstemmed	ddc 610 bkl 44.90 misc Neurogenic orthostatic hypotension misc Autonomic failure misc Neurodegeneration misc Pathophysiology misc Pharmacology
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title	Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease
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title_full	Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease
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title_sort	clinical relevance of orthostatic hypotension in neurodegenerative disease
title_auth	Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease
abstract	Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality. nOH results from pathology affecting either the central autonomic pathways or peripheral autonomic nerve fibers. Determining the localization and pathophysiology of nOH is critical in effectively managing this disorder and selecting appropriate treatment options. In this review, we discuss the pathophysiology of nOH with respect to the various α-synuclein-related neurodegenerative conditions. We highlight the associated clinical features, including gait instability, rapid eye movement behavior disorder, and hyposmia. We also review the current pharmacologic treatment options for nOH. Overall, the goals of therapy are to improve symptoms and prevent syncope and falls. Non-pharmacologic interventions should be introduced first, followed by carefully selected pharmacologic therapies. Treatment decisions should be directed by an understanding of the underlying pathophysiology, as well as the comorbidities and potential contributing factors present in each individual patient.
abstractGer	Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality. nOH results from pathology affecting either the central autonomic pathways or peripheral autonomic nerve fibers. Determining the localization and pathophysiology of nOH is critical in effectively managing this disorder and selecting appropriate treatment options. In this review, we discuss the pathophysiology of nOH with respect to the various α-synuclein-related neurodegenerative conditions. We highlight the associated clinical features, including gait instability, rapid eye movement behavior disorder, and hyposmia. We also review the current pharmacologic treatment options for nOH. Overall, the goals of therapy are to improve symptoms and prevent syncope and falls. Non-pharmacologic interventions should be introduced first, followed by carefully selected pharmacologic therapies. Treatment decisions should be directed by an understanding of the underlying pathophysiology, as well as the comorbidities and potential contributing factors present in each individual patient.
abstract_unstemmed	Abstract The autonomic nervous system appears to be uniquely susceptible to degeneration in disorders of α-synuclein pathology. Clinically, autonomic dysfunction in these disorders manifests as neurogenic orthostatic hypotension (nOH), a condition that results in substantial morbidity and mortality. nOH results from pathology affecting either the central autonomic pathways or peripheral autonomic nerve fibers. Determining the localization and pathophysiology of nOH is critical in effectively managing this disorder and selecting appropriate treatment options. In this review, we discuss the pathophysiology of nOH with respect to the various α-synuclein-related neurodegenerative conditions. We highlight the associated clinical features, including gait instability, rapid eye movement behavior disorder, and hyposmia. We also review the current pharmacologic treatment options for nOH. Overall, the goals of therapy are to improve symptoms and prevent syncope and falls. Non-pharmacologic interventions should be introduced first, followed by carefully selected pharmacologic therapies. Treatment decisions should be directed by an understanding of the underlying pathophysiology, as well as the comorbidities and potential contributing factors present in each individual patient.
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container_issue	12
title_short	Clinical Relevance of Orthostatic Hypotension in Neurodegenerative Disease
url	https://dx.doi.org/10.1007/s11910-015-0599-0
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author2	Shibao, Cyndya A. Claassen, Daniel O.
author2Str	Shibao, Cyndya A. Claassen, Daniel O.
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doi_str	10.1007/s11910-015-0599-0
up_date	2024-07-03T16:05:10.487Z
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