Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury: What Is Important to Know?

Louraoui, Sidi Mamoun; Fliyou, Fadwa; Aasfara, Jehanne; Azhari, A. El

doi:10.7759/cureus.24693

Cited by 3 publications

(3 citation statements)

References 10 publications

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“…Accumulating studies confirmed that overwhelming sympathetic hyperactivity following brain injury impairs prognosis. [11][12][13] Moreover, β adrenergic blockers, targeting the sympathetic nervous system, reduced mortality of traumatic brain injury (TBI) by decreasing TBI-related catecholamine surge. [14,15] In short, it is reasonable to speculate that sympathetic nervous system controlled by β blockers might be an optional remedy to ameliorate survival for PBH.…”

Section: Discussionmentioning

confidence: 99%

How to predict the outcome of primary brainstem hemorrhage: Six-year results of a single-center retrospective analysis

Geng,

Wang,

Liu

et al. 2023

Medicine

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Primary brainstem hemorrhage (PBH) is one of the most fatal intracranial hemorrhages, evaluating the prognosis in the early stage is vital for appropriate therapeutic planning. Our study aimed to identify risk factors for 30-day mortality and 90-day functional recovery of PBH. Data from 63 patients with PBH admitted to Beijing Chaoyang Hospital between 2016 and 2022 were retrieved for this study. We grouped the patients according to 30-day survival or 90-day functional recovery. Independent risk factors of 30-day mortality and 90-day functional recovery were identified by univariate and multivariate logistic regression analyses. 31 patients (49.2%) died within 30 days and 22 patients (34.9%) achieved better functional recovery. By multivariate analysis, Glasgow coma scale <9 on admission and tachycardia were significantly associated with 30-day mortality, while the hematoma volume >5 mL was an independent risk factor for 90-day functional recovery. Initial level of consciousness, tachycardia, massive hematoma were risk factors for prognosis, which must be seriously evaluated for therapeutic planning.

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Section: Discussionmentioning

confidence: 99%

How to predict the outcome of primary brainstem hemorrhage: Six-year results of a single-center retrospective analysis

Geng,

Wang,

Liu

et al. 2023

Medicine

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“…These mechanisms also affect adipose tissue, leading to lipolysis and the release of cytokines and adipokines. [70][71][72] The central mechanism of sympathetic activation is still poorly understood, but is probably driven by a loss of inhibitory control over excitatory autonomic centers. 73 Figure 3 illustrates how, in these situations of sympathetic hyperactivity, serum S100B levels rise at the expense of central and peripheral secretion.…”

Section: Does the Increase In S100b In The Csf Imply An Increase In S...mentioning

confidence: 99%

How S100B crosses brain barriers and why it is considered a peripheral marker of brain injury

Gayger-Dias,

Vizuete,

Rodrigues

et al. 2023

Exp Biol Med (Maywood)

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S100B is a 21-kDa protein that is produced and secreted by astrocytes and widely used as a marker of brain injury in clinical and experimental studies. The majority of these studies are based on measurements in blood serum, assuming an associated increase in cerebrospinal fluid and a rupture of the blood–brain barrier (BBB). Moreover, extracerebral sources of S100B are often underestimated. Herein, we will review these interpretations and discuss the routes by which S100B, produced by astrocytes, reaches the circulatory system. We discuss the concept of S100B as an alarmin and its dual activity as an inflammatory and neurotrophic molecule. Furthermore, we emphasize the lack of data supporting the idea that S100B acts as a marker of BBB rupture, and the need to include the glymphatic system in the interpretations of serum changes of S100B. The review is also dedicated to valorizing extracerebral sources of S100B, particularly adipocytes. Furthermore, S100B per se may have direct and indirect modulating roles in brain barriers: on the tight junctions that regulate paracellular transport; on the expression of its receptor, RAGE, which is involved in transcellular protein transport; and on aquaporin-4, a key protein in the glymphatic system that is responsible for the clearance of extracellular proteins from the central nervous system. We hope that the data on S100B, discussed here, will be useful and that it will translate into further health benefits in medical practice.

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“…У 2010 році був затверджений термін ПСГ. Крім того, встановлено визначення та критерії діагностики: ускладнення різноманітних гострих уражень головного мозку незалежно від причини (травматичної чи іншої), що призводять до порушення центральної регуляції вегетативної функції, таким чином виключаючи клінічні синдроми з парасимпатичним компонентом [1].…”

Section: вступunclassified

Methods of Labor Analgesia by Determing the Level of Childbirth Satisfaction

CHERNIAIEV¹,

DUBROV²,

SEREDA³

et al. 2022

Pain Anaesth Int Care

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Introduction. Paroxysmal sympathetic hyperactivity (PSH) can occur as a result of brain injury, hypoxic brain damage, acute cerebrovascular accident (ACVA). The clinical picture of PSH is caused by excessive sympathetic activity and includes transient paroxysms of tachycardia, hypertension, hyperventilation, hyperthermia, and diaphoresis. PSH is a neurological emergency, which in the vast majority of cases is a diagnosis of exclusion. Lack of adequate detection and treatment of the disease leads to a high mortality rate. The diagnosis is exclusively clinical, so other pathologies must be excluded. Currently, the most widely accepted diagnostic criteria for PSH are the criteria proposed by Baguley et al. Case description. Patient D., 29 years old, was hospitalized with a diagnosis of middle cerebral artery stroke. The patient had attacks which were characterized by tachycardia, hypertension, tachypnea with asynchrony with the ventilator, diaphoresis and hypertension every day with a frequency of 2-3 times per day and were ending approximately 30-40 minutes after the onset. The diagnosis of PSH was established according to the score on the scale proposed by Baguley et al., 25 points (17 or more points – a probable diagnosis of PSH). Conclusions. It is believed that the cause of PSH is a violation of the inhibition function of the cortex on the brain structures located below, as a result of which paroxysms of sympathetic activation occur, manifested by tachycardia, hypertension, hyperventilation, diaphoresis, and hyperthermia. In this clinical case, resolution of paroxysms was observed faster with the combination of morphine and propofol. An important aspect of therapy is adequate rehydration therapy to compensate for fluid losses due to hyperthermia and diaphoresis, as well as the administration of beta-blockers on an ongoing basis

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Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury: What Is Important to Know?

Cited by 3 publications

References 10 publications

How to predict the outcome of primary brainstem hemorrhage: Six-year results of a single-center retrospective analysis

How to predict the outcome of primary brainstem hemorrhage: Six-year results of a single-center retrospective analysis

How S100B crosses brain barriers and why it is considered a peripheral marker of brain injury

Methods of Labor Analgesia by Determing the Level of Childbirth Satisfaction

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