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Journal of Craniovertebral Junction and Spine
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Year : 2017  |  Volume : 8  |  Issue : 1  |  Page : 33-38

Sudden death and cervical spine: A new contribution to pathogenesis for sudden death in critical care unit from subarachnoid hemorrhage; first report – An experimental study

1 Department of Anesthesiology and Reanimation, Medical Faculty, Recep Tayyip Erdogan University, Rize, Turkey
2 Department of Neurosurgery, Medical Faculty, Recep Tayyip Erdogan University, Rize, Turkey
3 Department of Neurosurgery, Medical Faculty, Ataturk University, Erzurum, Turkey
4 Department of Neurosurgery, Medical Faculty, Karadeniz Technical University, Trabzon, Turkey
5 Department of Pathology, Medical Faculty, Ataturk University, Erzurum, Turkey

Correspondence Address:
Ayhan Kanat
Department of Neurosurgery, Medical Faculty, Recep Tayyip Erdogan University, Rize 53100
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0974-8237.199870

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Context: Sudden death from subarachnoid hemorrhage (SAH) is not uncommon. Aims: The goal of this study is to elucidate the effect of the cervical spinal roots and the related dorsal root ganglions (DRGs) on cardiorespiratory arrest following SAH. Settings and Design: This was an experimental study conducted on rabbits. Materials and Methods: This study was conducted on 22 rabbits which were randomly divided into three groups: control (n = 5), physiologic serum saline (SS; n = 6), SAH groups (n = 11). Experimental SAH was performed. Seven of 11 rabbits with SAH died within the first 2 weeks. After 20 days, other animals were sacrificed. The anterior spinal arteries, arteriae nervorum of cervical nerve roots (C6–C8), DRGs, and lungs were histopathologically examined and estimated stereologically. Statistical Analysis Used: Statistical analysis was performed using the PASW Statistics 18.0 for Windows (SPSS Inc., Chicago, Illinois, USA). Intergroup differences were assessed using a one-way ANOVA. The statistical significance was set at P < 0.05. Results: In the SAH group, histopathologically, severe anterior spinal artery (ASA) and arteriae nervorum vasospasm, axonal and neuronal degeneration, and neuronal apoptosis were observed. Vasospasm of ASA did not occur in the SS and control groups. There was a statistically significant increase in the degenerated neuron density in the SAH group as compared to the control and SS groups (P < 0.05). Cardiorespiratory disturbances, arrest, and lung edema more commonly developed in animals in the SAH group. Conclusion: We noticed interestingly that C6–C8 DRG degenerations were secondary to the vasospasm of ASA, following SAH. Cardiorespiratory disturbances or arrest can be explained with these mechanisms.

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