Paroxysmal sympathetic hyperactivity: the storm after acute brain injury
A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to ext...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Meyfroidt, Geert [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Umfang: |
9 |
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| Übergeordnetes Werk: |
Enthalten in: Rejection and modeling of arsenate by nanofiltration: Contributions of convection, diffusion and electromigration to arsenic transport - Fang, Jun ELSEVIER, 2014transfer abstract, London |
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| Übergeordnetes Werk: |
volume:16 ; year:2017 ; number:9 ; pages:721-729 ; extent:9 |
| Links: |
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| DOI / URN: |
10.1016/S1474-4422(17)30259-4 |
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| 520 | |a A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. | ||
| 520 | |a A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. | ||
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10.1016/S1474-4422(17)30259-4 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000823.pica (DE-627)ELV030302765 (ELSEVIER)S1474-4422(17)30259-4 DE-627 ger DE-627 rakwb eng 570 VZ 540 VZ 35.17 bkl 58.50 bkl 43.12 bkl Meyfroidt, Geert verfasserin aut Paroxysmal sympathetic hyperactivity: the storm after acute brain injury 2017transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. Baguley, Ian J oth Menon, David K oth Enthalten in Lancet Publ. Group Fang, Jun ELSEVIER Rejection and modeling of arsenate by nanofiltration: Contributions of convection, diffusion and electromigration to arsenic transport 2014transfer abstract London (DE-627)ELV017537959 volume:16 year:2017 number:9 pages:721-729 extent:9 https://doi.org/10.1016/S1474-4422(17)30259-4 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 35.17 Katalyse VZ 58.50 Umwelttechnik: Allgemeines VZ 43.12 Umweltchemie VZ AR 16 2017 9 721-729 9 |
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10.1016/S1474-4422(17)30259-4 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000823.pica (DE-627)ELV030302765 (ELSEVIER)S1474-4422(17)30259-4 DE-627 ger DE-627 rakwb eng 570 VZ 540 VZ 35.17 bkl 58.50 bkl 43.12 bkl Meyfroidt, Geert verfasserin aut Paroxysmal sympathetic hyperactivity: the storm after acute brain injury 2017transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. Baguley, Ian J oth Menon, David K oth Enthalten in Lancet Publ. Group Fang, Jun ELSEVIER Rejection and modeling of arsenate by nanofiltration: Contributions of convection, diffusion and electromigration to arsenic transport 2014transfer abstract London (DE-627)ELV017537959 volume:16 year:2017 number:9 pages:721-729 extent:9 https://doi.org/10.1016/S1474-4422(17)30259-4 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 35.17 Katalyse VZ 58.50 Umwelttechnik: Allgemeines VZ 43.12 Umweltchemie VZ AR 16 2017 9 721-729 9 |
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10.1016/S1474-4422(17)30259-4 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000823.pica (DE-627)ELV030302765 (ELSEVIER)S1474-4422(17)30259-4 DE-627 ger DE-627 rakwb eng 570 VZ 540 VZ 35.17 bkl 58.50 bkl 43.12 bkl Meyfroidt, Geert verfasserin aut Paroxysmal sympathetic hyperactivity: the storm after acute brain injury 2017transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. Baguley, Ian J oth Menon, David K oth Enthalten in Lancet Publ. Group Fang, Jun ELSEVIER Rejection and modeling of arsenate by nanofiltration: Contributions of convection, diffusion and electromigration to arsenic transport 2014transfer abstract London (DE-627)ELV017537959 volume:16 year:2017 number:9 pages:721-729 extent:9 https://doi.org/10.1016/S1474-4422(17)30259-4 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 35.17 Katalyse VZ 58.50 Umwelttechnik: Allgemeines VZ 43.12 Umweltchemie VZ AR 16 2017 9 721-729 9 |
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10.1016/S1474-4422(17)30259-4 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000823.pica (DE-627)ELV030302765 (ELSEVIER)S1474-4422(17)30259-4 DE-627 ger DE-627 rakwb eng 570 VZ 540 VZ 35.17 bkl 58.50 bkl 43.12 bkl Meyfroidt, Geert verfasserin aut Paroxysmal sympathetic hyperactivity: the storm after acute brain injury 2017transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. Baguley, Ian J oth Menon, David K oth Enthalten in Lancet Publ. Group Fang, Jun ELSEVIER Rejection and modeling of arsenate by nanofiltration: Contributions of convection, diffusion and electromigration to arsenic transport 2014transfer abstract London (DE-627)ELV017537959 volume:16 year:2017 number:9 pages:721-729 extent:9 https://doi.org/10.1016/S1474-4422(17)30259-4 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 35.17 Katalyse VZ 58.50 Umwelttechnik: Allgemeines VZ 43.12 Umweltchemie VZ AR 16 2017 9 721-729 9 |
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10.1016/S1474-4422(17)30259-4 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000823.pica (DE-627)ELV030302765 (ELSEVIER)S1474-4422(17)30259-4 DE-627 ger DE-627 rakwb eng 570 VZ 540 VZ 35.17 bkl 58.50 bkl 43.12 bkl Meyfroidt, Geert verfasserin aut Paroxysmal sympathetic hyperactivity: the storm after acute brain injury 2017transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. Baguley, Ian J oth Menon, David K oth Enthalten in Lancet Publ. Group Fang, Jun ELSEVIER Rejection and modeling of arsenate by nanofiltration: Contributions of convection, diffusion and electromigration to arsenic transport 2014transfer abstract London (DE-627)ELV017537959 volume:16 year:2017 number:9 pages:721-729 extent:9 https://doi.org/10.1016/S1474-4422(17)30259-4 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 35.17 Katalyse VZ 58.50 Umwelttechnik: Allgemeines VZ 43.12 Umweltchemie VZ AR 16 2017 9 721-729 9 |
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Enthalten in Rejection and modeling of arsenate by nanofiltration: Contributions of convection, diffusion and electromigration to arsenic transport London volume:16 year:2017 number:9 pages:721-729 extent:9 |
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Paroxysmal sympathetic hyperactivity: the storm after acute brain injury |
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A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. |
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A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. |
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A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials. |
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