Clinical characteristics and prognosis of paroxysmal sympathetic hyperactivity in patients with severe nontraumatic brain injury

He, Miao; Huang, Huijin; Chen, Weibi; Su, Yingying; Zhang, Yan

doi:10.1080/02699052.2023.2165151

Cited by 3 publications

(12 citation statements)

References 31 publications

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“…Following screening and appraisal, 13 pieces of literature were included in this systematic review, comprising 5 cohort analyses and 8 case reports of 178 patients diagnosed with PSH (Table 3). [11][12][13][14][15][16][17][18][19][20][21][22][23] Etiologies included TBIs, ICHs, autoimmune encephalitis, anoxic/ischemic brain injury, and hypoglycemia. Dexmedetomidine was administered to 48 (27%) patients for the acute treatment of PSH and 50 (28%) patients for prophylaxis.…”

Section: Resultsmentioning

confidence: 99%

“…The efficacy of dexmedetomidine in PSH treatment was evaluated in 12 studies, with 4 cohort analyses and 8 case reports. 11,[13][14][15][16][17][18][19][20][21][22][23] Reductions in paroxysm severity and frequency were observed in 44 of 48 patients after therapy. 11,[13][14][15][16][17]19,20,21 Etiologies of TBIs, ICHs, anoxic/ischemic brain injury, and autoimmune encephalitis were documented within this group.…”

Section: Resultsmentioning

confidence: 99%

“…11,[13][14][15][16][17][18][19][20][21][22][23] Reductions in paroxysm severity and frequency were observed in 44 of 48 patients after therapy. 11,[13][14][15][16][17]19,20,21 Etiologies of TBIs, ICHs, anoxic/ischemic brain injury, and autoimmune encephalitis were documented within this group. Dexmedetomidine was infused at 0.1-1.0 mcg/kg/h for durations of 3-7 days with or without 1-mcg/kg loading doses.…”

Section: Resultsmentioning

confidence: 99%

“…Dexmedetomidine was infused at 0.1-1.0 mcg/kg/h for durations of 3-7 days with or without 1-mcg/kg loading doses. 11,[14][15][16][17]19,23 PSH etiologies of the 4 patients who failed dexmedetomidine therapy include anoxic/ischemic brain injury, TBIs, and hypoglycemia. 15,16,21,22 Infusions of 200 mcg/day and 0.1-0.3 mcg/ kg/h were utilized in this group.…”

Section: Resultsmentioning

confidence: 99%

“…11,[14][15][16][17]19,23 PSH etiologies of the 4 patients who failed dexmedetomidine therapy include anoxic/ischemic brain injury, TBIs, and hypoglycemia. 15,16,21,22 Infusions of 200 mcg/day and 0.1-0.3 mcg/ kg/h were utilized in this group. 15,21 Prophylactic use of dexmedetomidine was compared with other sedatives (midazolam, propofol, and diazepam) in 1 study of 90 postsurgical patients with TBIs.…”

Section: Resultsmentioning

confidence: 99%

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The Role of Dexmedetomidine in Paroxysmal Sympathetic Hyperactivity: A Systematic Review

Jerousek,

Reinert

2023

Ann Pharmacother

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Objective: The objective was to evaluate the efficacy and safety of dexmedetomidine in the treatment and prophylaxis of paroxysmal sympathetic hyperactivity (PSH). Data Sources: A review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria and queried Embase, MEDLINE (PubMed), Cochrane CENTRAL, Web of Science, SciELO, Korean Journal Index (Clarivate), Global Index Medicus, and CINAHL Plus for results through June 2023. Study Selection and Data Extraction: Studies providing efficacy or safety data associated with dexmedetomidine with a reported diagnosis of PSH were included. Exclusion of studies in pediatric populations, without quantitative and qualitative outcome data, and not readily translatable to English was adhered to. Data Synthesis: Thirteen observational studies of 178 patients were included in the qualitative analysis. Reductions in PSH frequency or symptom severity were reported in 44 of 48 patients who received dexmedetomidine for acute treatment. Prophylactic use of dexmedetomidine was associated with reductions in PSH-Assessment Measure (PSH-AM) scores in postsurgical patients with traumatic brain injuries (TBIs). Adverse events associated with dexmedetomidine were either absent or reported as none. Relevance to Patient Care and Clinical Practice: This review supports the safe and effective use of dexmedetomidine in the treatment and prophylaxis of PSH. Further investigation is required to determine optimal dosing strategies and the extent to which PSH etiology correlated to the efficacy of dexmedetomidine. Conclusions: The use of dexmedetomidine appears to be both efficacious and safe for the treatment and prevention of PSH in patients experiencing a TBI. Additional research is needed to elucidate dosing strategies, titration parameters, and duration of therapy.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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The Role of Dexmedetomidine in Paroxysmal Sympathetic Hyperactivity: A Systematic Review

Jerousek,

Reinert

2023

Ann Pharmacother

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Clinical case report of intractable paroxysmal sympathetic hyperactivity in TANGO2 deficiency disorder

Morrison,

Koshiya,

Safier

et al. 2024

American J of Med Genetics Pt A

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TANGO2 deficiency disorder (TDD) is a neurodegenerative disease characterized by a broad and variable spectrum of clinical manifestations, even among individuals sharing the same pathogenic variants. Here, we report a severely affected individual with TDD presenting with intractable paroxysmal sympathetic hyperactivity (PSH). While progressive brain atrophy has been observed in TDD, PSH has not been reported. Despite comprehensive workup for an acute trigger, no definite cause was identified, and pharmacological interventions were ineffective to treat PSH. Ultimately care was redirected to comfort measures. This article expands the clinical phenotype of patients with TDD, highlights the possibility of PSH in these patients, and the need for continued research for better treatments of TDD.

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Paroxysmal Sympathetic Hyperactivity in Childhood Tuberculous Meningitis: A New Association

Jauhari,

Singh,

Jain

et al. 2024

J Child Neurol

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Background We sought to estimate the prevalence and clinical characteristics of paroxysmal sympathetic hyperactivity (PSH) in childhood tuberculous meningitis. Methods Hospital records of children (6 months to 14 years) with tuberculous meningitis were retrospectively analyzed from September 2019 through January 2022. In September 2019, the first case of paroxysmal sympathetic hyperactivity in tuberculous meningitis was identified in our division. Since then, all admitted children with tuberculous meningitis have been screened for paroxysmal sympathetic hyperactivity using the Paroxysmal Sympathetic Hyperactivity Assessment Measure (PSH-AM). Paroxysmal sympathetic hyperactivity is suspected when any of the following are present: recurrence of fever after initial defervescence, episodic posturing, dystonia, or unexplained tachycardia. Outcome at 3 months was prospectively scored according to the Pediatric Cerebral Performance Category score. Results Forty-one hospital records of children with tuberculous meningitis were analyzed, and 6 of them had paroxysmal sympathetic hyperactivity (probable paroxysmal sympathetic hyperactivity, 5/6; possible paroxysmal sympathetic hyperactivity, 1/6). Paroxysmal sympathetic hyperactivity appeared after a mean duration of 17 weeks (range: 12-25 weeks) from the diagnosis of tuberculous meningitis in 4 of 6 children and at 4 weeks in 2 of 6 children. Children with tuberculous meningitis who developed paroxysmal sympathetic hyperactivity were younger (median age: 5 years) compared with the nonparoxysmal sympathetic hyperactivity tuberculous meningitis cohort (median age: 10 years). A high proportion of children who developed paroxysmal sympathetic hyperactivity had hydrocephalus at presentation (5 of 6 [83.3%] vs 12 of 35 [34.3%], P = .035). Hospital stay was significantly prolonged in children with probable paroxysmal sympathetic hyperactivity (mean: 71.2 ± 26.8 days) compared with tuberculous meningitis without paroxysmal sympathetic hyperactivity (mean: 20.8 ± 11.6 days; P < .0001). Conclusion Paroxysmal sympathetic hyperactivity is a late complication of tuberculous meningitis observed in 14.6% cases and should be anticipated in children with reappearance of fever or neurologic worsening without any apparent cause.

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Clinical characteristics and prognosis of paroxysmal sympathetic hyperactivity in patients with severe nontraumatic brain injury

Cited by 3 publications

References 31 publications

The Role of Dexmedetomidine in Paroxysmal Sympathetic Hyperactivity: A Systematic Review

The Role of Dexmedetomidine in Paroxysmal Sympathetic Hyperactivity: A Systematic Review

Clinical case report of intractable paroxysmal sympathetic hyperactivity in TANGO2 deficiency disorder

Paroxysmal Sympathetic Hyperactivity in Childhood Tuberculous Meningitis: A New Association

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