Rational Roots of Sympathetic Overactivity by Neurogenic Pulmonary Edema Modeling Arising from Sympathyco-Vagal Imbalance in Subarachnoid Hemorrhage: An Experimental Study

Önen, Mehmet Reşid; Yılmaz, İlhan; Ramazanoglu, Leyla; Tanrıverdi, Osman; Aydın, Mehmet Dumlu; Kanat, Ayhan; Yolaş, Coşkun; Şipal, Sare

doi:10.1016/j.wneu.2016.04.067

Cited by 23 publications

(21 citation statements)

References 28 publications

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“…Onen et al reported recently that highly degenerated neuron density of ciliary ganglion is not responsible for pupillary dilatation owing to parasympathetic pupillary constrictor palsy, but that high neuron density of pupillary dilatory superior cervical sympathetic ganglia should be considered an important factor of pupillary dilatation. 8 This study has demonstrated that the presence of DAs in OMN or dysfunction of the parasympathetic system of rabbits due to SAH may be likewise responsible for a mydriatic pupil.…”

Section: Resultsmentioning

confidence: 73%

“…It was previously reported that superior cervical ganglia or thoracal ciliospinal reflex center pathologies may alter pupil diameter. 8 In addition to pupil diameter, VSI values of PComAs were measured in all three groups (►Table 1). However, there was no significant degenerated axon density in the control group, so we did not evaluate this parameter in that group.…”

Section: Limitations Of the Studymentioning

confidence: 99%

“…[1][2][3][4] The emergence of dedicated neurologic-neurosurgical intensive care units (ICUs), advancements, and aggressive monitoring have contributed to overall improved outcomes for patients with aneurysmal subarachnoid hemorrhage (aSAH) over the past 2 decades, but spontaneous subarachnoid hemorrhage (SAH) is still life threatening 5,6 and carries significant mortality 7 because it causes brainstem and cranial nerve injuries. 8 Expeditious treatment is critical in patients with SAH due to the risk of rebleeding. 9 The management of SAH requires a comprehensive understanding of the pathophysiology, paramount for defining treatment strategies and algorithms.…”

Section: Introductionmentioning

confidence: 99%

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How Reliable Is Pupillary Evaluation Following Subarachnoid Hemorrhage? Effect of Oculomotor Nerve Degeneration Secondary to Posterior Communicating Artery Vasospasm: First Experimental Study

Öztürk¹,

Özdemir²,

Kanat

et al. 2017

J Neurol Surg A Cent Eur Neurosurg

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Section: Resultsmentioning

confidence: 73%

Section: Limitations Of the Studymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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How Reliable Is Pupillary Evaluation Following Subarachnoid Hemorrhage? Effect of Oculomotor Nerve Degeneration Secondary to Posterior Communicating Artery Vasospasm: First Experimental Study

Öztürk¹,

Özdemir²,

Kanat

et al. 2017

J Neurol Surg A Cent Eur Neurosurg

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“…21 Sympathetic overactivity means high neuron density of STG. 22 STG block reduces pulmonary arterial resistance. 23 STG block prevents lung injury.…”

Section: Sympathetic Networkmentioning

confidence: 97%

Stellate ganglion ischemia on the prevention of pulmonary vasospasm during bilateral carotid artery ligation: The first experimental study

et al. 2020

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Fatal pulmonary edema and hemorrhage are significant complications of endovascular treatment in steno-occlusive carotid artery disease; a rational mechanism has not been adequately examined in the literature so far. We investigated if cervical sympathetic ganglia ischemia prevents pulmonary vasospasm on the prognosis of bilateral common carotid artery ligation (BCCAL). Twenty-three adult New Zealand rabbits (4.2 AE 0.3 kg) were randomly divided into three groups: the control group (G1, n = 5), the sham group (G2, n = 6), and the BCCAL group (G3, n = 12). Common carotid arteries were dissected bilaterally in G2/G3, and permanent BCCAL was applied to only in G3. All animals were followed for 3 weeks and decapitated under general anesthesia. Histopathological changes in stellate ganglia and severity of pulmonary vasospasm-related lung edema and hemorrhage were investigated. Results were analyzed by the Kruskal-Wallis test. Two animals of G3 dead within three weeks and the remainder were sacrificed three weeks later. Subpleural petechial foci and an endotracheal bloody fluid collection were grossly observed in the lungs. Histopathologically, pulmonary artery vasospasm, perivascular and subintimal edema, interalveolar hemorrhage, and alveolar wall destructions were observed with less ischemic-degenerated neuron density-determined stellate ganglia animals. Neurodegeneration of stellate ganglia may have a beneficial effect on the prevention of lung injury during stenoocclusive carotid artery disease.

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“…Gangguan persarafan autonom, yang dapat diakibatkan oleh aktifitas berlebihan pada persarafan simpatis atau gangguan saraf vagal yang diakibatkan oleh vagotomi atau kerusakan nukleus vagal di medula oblongata dapat menyebabkan edem paru neurogenik yang merupakan komplikasi dari berbagai mekanisme cedera/trauma susunan saraf pusat. 13 Peningkatan Tekanan Hidrostatik Kapiler Pulmonal (Teori Blast) Edem paru neurogenik sering berkaitan dengan kejadian hipertensi pulmonal dan sistemik yang dapat diakibatkan secara sekunder oleh peningkatan tekanan intrakranial ataupun adanya pelepasan katekolamin dalam jumlah besar. Hipertensi pulmonal dan sistemik akan menyebabkan peningkatan volume darah pulmonal akibat perpindahan aliran darah sistemik menuju aliran darah arteri dan vena pulmonal.…”

Section: Etiologiunclassified

Tata Kelola Edem Paru Neurogenik

Firdaus

Gaus

Oetoro

et al. 2018

JNI

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Edem paru neurogenik merupakan salah satu komplikasi pernafasan yang dapat muncul setelah cedera/trauma susunan saraf pusat. Bervariasinya laporan epidemiologi dan patofisiologi edem paru neurogenik dapat menyebabkan misdiagnosis yang dapat memperburuk prognosis pada pasien yang mengalami edem paru neurogenik. Patofisiologi edem paru neurogenik diduga dimulai dari kerusakan pada persarafan autonom pembuluh darah pulmonal dan stimulasi berlebihan dari pusat vasomotor susunan saraf pusat, yang kemudian menyebabkan berbagai perubahan yang terjadi pada pembuluh darah pulmonal hingga disfungsi jantung. Investigasi klinis harus dilakukan hatihati karena manifestasi klinis yang dapat menyerupai edem paru kardiogenik dan non-kardiogenik lainnya, hasil pemeriksaan yang tidak spesifik, dan tidak adanya kriteria diagnosis. Saat ini belum ada pedoman tata kelola edem paru neurogenik yang dapat diterima secara luas, namun berbagai studi dan literatur menyebutkan tata kelola edem paru neurogenik berupa tata kelola suportif airway, breathing, circulation, di samping tata kelola penyebab cedera/ trauma susunan saraf pusat memiliki prognosis yang baik, oleh karena itu identifikasi, investigasi, dan tata kelola edem paru neurogenik harus dilakukan secepatnya. Edem paru neurogenik dapat beresolusi dengan baik dalam 48-72 jam setelah mendapatkan tata kelola yang adekuat.

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Rational Roots of Sympathetic Overactivity by Neurogenic Pulmonary Edema Modeling Arising from Sympathyco-Vagal Imbalance in Subarachnoid Hemorrhage: An Experimental Study

Cited by 23 publications

References 28 publications

How Reliable Is Pupillary Evaluation Following Subarachnoid Hemorrhage? Effect of Oculomotor Nerve Degeneration Secondary to Posterior Communicating Artery Vasospasm: First Experimental Study

How Reliable Is Pupillary Evaluation Following Subarachnoid Hemorrhage? Effect of Oculomotor Nerve Degeneration Secondary to Posterior Communicating Artery Vasospasm: First Experimental Study

Stellate ganglion ischemia on the prevention of pulmonary vasospasm during bilateral carotid artery ligation: The first experimental study

Tata Kelola Edem Paru Neurogenik

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