Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 1.736
5-Year Impact Factor – 2.135
Index Copernicus  – 168.52
MEiN – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

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Advances in Clinical and Experimental Medicine

2014, vol. 23, nr 5, September-October, p. 699–704

Publication type: original article

Language: English

Parallel Development of Choroid Plexus Degeneration and Meningeal Inflammation in Subarachnoid Hemorrhage – Experimental Study

Dilcan Kotan1,A,B,D,E,F, Mehmet D. Aydin2,A,E,F, Cemal Gundogdu3,C,F, Recep Aygul4,B,F, Nazan Aydin5,E,F, Hızır Ulvi5,E,F

1 Department of Neurology, Faculty of Medicine, Sakarya University, Turkey

2 Department of Neurosurgery, Faculty of Medicine, Ataturk University, Erzurum, Turkey

3 Department of Pathology, Faculty of Medicine, Ataturk University, Erzurum, Turkey

4 Department of Neurology, Ataturk University, Faculty of Medicine, Erzurum, Turkey

5 Department of Psychiatry, Ataturk University, Faculty of Medicine, Erzurum, Turkey

Abstract

Background. The choroid plexuses (CPs) are brain structures located in the brain ventricles, involved in the production and reabsorption of cerebrospinal fluid (CSF) components, cerebral immune surveillance, and various endocrine-enzymatic activities and acts as a CSF-blood barrier. This study investigated to determine if there is a link between ischemic CP injury and meningo-cerebral inflammation processes.
Material and Methods. This study was conducted on 18 rabbits. Four rabbits were used as the baseline group to examine the normal structures. Fourteen of the rabbits were used as the study group by injecting 1.00cc of homologous blood into their cisterna magna. The animals were followed by daily monitoring for ten days and then slaughtered. Apoptotic degeneration of the CP cells was determined and statistical analyses were carried out using normal and apoptotic CP cell numbers. Data analyses were comprised of Mann-Whitney U tests. Differences were considered to be significant if p < 0.005.
Results. Five animals belonging to the study group died between the 5th and 8th days. Unconsciousness, neck stiffness, convulsion, fever, apnea, cardiac arrhythmia, and breathing disturbances were observed in all of the animals who subsequently died. Intraventricular blood leakage was detected in all the dead and three surviving animals. Choroidal artery spasm, choroidal ependymal cell injury, choroidal cell apoptosis, pia-arachnoid thickening, meningocortical adhesions and blood cell density in the subarachnoid spaces were more severe in the more CP degenerated animals than those of the others. There were significant differences between the apoptotic CP cell density and blood cell density in the subarachnoid spaces (p < 0.005).
Conclusion. Subarachnoid hemorrhage (SAH) extending to brain ventricles causes ischemic degeneration of the CP by way of triggered choroidal artery vasospasm. It should be emphasized that the prevention of CP function may be an important part of the protection of the brain in SAH.

Key words

choroid plexuses, subarachnoid hemorrhage, vasospasm.

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