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Background:  Increased intraocular pressure (IOP) likely secondary to an activated oculo-trigeminal reflex network is an important issue following subarachnoid hemorrhage (SAH). The relationship between the IOP and trigeminal ganglion (TGG) following experimental SAH was investigated in this study., Methods:  Twenty-three rabbits were used in this study. Five rabbits ( n  = 5) were used as the control group, another 5 as the sham group ( n  = 5), and the remaining 13 ( n  = 13) as the study group. The study group was further divided into two groups of animals with mild ( n  = 6) and severe ( n  = 7) TGG degeneration. The IOP values were recorded. After 2 weeks, the animals were decapitated. The mean degenerated neuron density of TGGs was estimated by stereological methods and analyzed statistically., Results:  The average IOP values were 11.85, 14.12, and 21.45 mm Hg in the control ( n  = 5), sham ( n  = 5), and study ( n  = 13) groups, respectively. The mean degenerated neuron density was 34, 237, and 3,165 mm 3 in the control, sham, and study groups, respectively., Conclusion:  According to the findings of this study, the experimental SAH leads to changes in IOP by affecting the TGG. By predicting and preventing IOP elevation in the setting of SAH, our findings will shed light on secondary sequelae such as glaucoma and irreversible blindness., Competing Interests: None declared., (Thieme. All rights reserved.)

Blood and cerebrospinal fluid (CSF) acidosis is the most troubling complication in subarachnoid hemorrhage (SAH) if carotid body (CB) networks are disrupted. However, histopathological examination of the choroid plexus (CP) in acidic CSF has not been evaluated so far. In this study, we aimed to investigate the CP in acidic CSF following SAH. Twenty-eight rabbits were used. Five rabbits were used to analyze CB network (control group; n = 5); seven rabbits were injected 1 mL of saline (Sham group; n = 7); and the rest 16 rabbits were given 1 mL of autologous arterial blood inject into the cisterna magna to create SAH (SAH group; n = 16). Blood and CSF pH values were recorded before/during/after the experimental procedures. Nuclear darkening, cellular shrinkage and pyknosis suggested the presence of apoptosis of epithelial cells of CP. The densities of normal and degenerated epithelial cells of CPs were estimated using stereological methods. The relationship between the pH values and degenerated epithelial cell densities of CPs were statistically compared by Mann-Whitney U-test. The pH values of blood were estimated as 7.359 ± 0.039 in the control group, 7.318 ± 0.062 in the Sham group, 7.23 ± 0.013 in the SAH group. CSF pH values were 7.313 ± 0.028 in the control group, 7.296 ± 0.045 in the Sham group, and 7.224 ± 0.012 in the SAH group. Degenerated epithelial cell density of CP was 25 ± 7 in the control group, 226 ± 64 in the Sham group, and 2115 ± 635 in the SAH group. There was a considerable link between CSF pH values and degenerated epithelial cells of CP (P < 0.0001). This study shows that CB insult causes acidosis of CSF as well as cellular degeneration of CP during SAH. This is the first description of this in the literature., (© 2020 Japanese Society of Neuropathology.)

Background:  The pterygopalatine ganglion (PPG) and ophthalmic arteries (OpAs) have important roles in ocular autoregulation and retinal and visual functions. The relationship between PPG neuron density, OpA vasospasm, and retinal detachment in subarachnoid hemorrhage (SAH) has never been studied., Methods:  This study was conducted on 25 rabbits. Five animals were in the control group (GI; n  = 5), five in the sham group (GII; n  = 5), and 15 in the study group (GIII; n  = 15). After injection of 1 cc serum saline into the cisterna magna in the sham group, and autologous blood in the SAH group, the animals were followed for 3 weeks. All animals underwent a retinal examination five times a week for 3 weeks before and after the experiment. After the experiment, the neuron density of PPGs of the facial nerves, vasospasm index (VSI) of OpAs, and total basal surface values of the detached retinal parts (DRPs) were calculated., Results:  In the funduscopic examination, intravitreous hemorrhage ( Terson's syndrome) was detected in four animals in the SAH group. In the control groups, neuron density was 12,000 ± 1,240/mm 3 , VSI = 0.345 ± 0.076, and DRP = 0 to 1.5 mm 2 . Mean neuron density was 9,450 ± 940/mm 3 , VSI = 1.645 ± 0.940, and DRP = 6.23 ± 1.61 mm 2 in the sham group ( p  < 0.05). Neuron density was 6,890 ± 932/mm 3 , VSI = 2.92 ± 0.97, and DRP = 9.43 ± 2.54 mm 2 in SAH group., Conclusion:  Mean neuron density, VSI of OpAs, and DRP values differed statistically significant between the SAH group and other groups ( p  < 0.005). There is an inverse relationship between PPG neurons and DRP. However, a direct relationship was observed between the mean VSI and DRP values., Competing Interests: None declared., (Georg Thieme Verlag KG Stuttgart · New York.)

Acidosis is the most dangerous complication of subarachnoid hemorrhage (SAH). Although the carotid bodies (CBs) network is essential for pH regulation, neither binuclear neurons (BNN) nor their functions have been mentioned so far in the literature. The aim of this study was to investigate the crucial roles of mononuclear (MNN) or BNN in CBs on acidosis following SAH. Twenty-five hybrid rabbits were used. Five rabbits were used as a control group, six for sham, and the remaining 14 rabbits were used as the study group by injection of 1 mL of autologous arterial blood into the cisterna magna to produce SAH. Normal and degenerated MNN/BNN densities of CBs were counted by stereological methods. The mean blood pH values were: 7.362 ± 0.041 in the control group; 7.324 ± 0.064 in sham, 7.272 ± 0.062 in the SAH group. The degenerated MNN and BNN values were 5 ± 1/mm 3 and 9 ± 3/mm 3 in the control group; 15 ± 5/mm 3 and 22 ± 6/mm 3 in sham, 965 ± 113/mm 3 and 1532 ± 176/mm 3 in the SAH group. Mean pH values were under 7.212 ± 0.130 in animals with prominent degenerated BNN. The differences between MNN/pH changes were significant between the SAH and control groups (P < 0.005); whereas BNN/pH values were significant between the SAH and sham groups (pH < 0.005), SAH and control (P < 0.0001). BNN degeneration could result in more severe acidosis than MNN following SAH which has not been described so far., (© 2019 Japanese Society of Neuropathology.)

Purpose: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage., Methods: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded., Results: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001)., Conclusion: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.

Aim: To understand possible mechanisms underlying lacrimal gland degeneration when facial nerve root ischemia induces pterygopalatine ganglion injury and subsequent dry eye in a rabbit model of subarachnoid hemorrhage., Material and Methods: Rabbits were divided into four groups: control, sham, moderate subarachnoid hemorrhage, and severe subarachnoid hemorrhage. Autologous blood recovered from the auricular artery was injected into the cisterna magna to induce subarachnoid hemorrhage in the two subarachnoid hemorrhage groups; animals were then monitored for dry eye development over 21 days before removal of their facial nerve roots, pterygopalatine ganglia, and lacrimal glands for immunohistochemical analyses. Neuronal viability in the pterygopalatine ganglia was measured; lacrimal gland vesicles were counted by stereological methods., Results: The mean tear-filled vesicle number and lacrimal gland volumes significantly decreased with an increase in facial nerve root injury severity and damaged neuron numbers in the pterygopalatine ganglion. Increase in injury severity most significantly decreased the tear-filled vesicle numbers in the pterygopalatine ganglion., Conclusion: Subarachnoid hemorrhage degenerates facial nerve parasympathetic branches entering the pterygopalatine ganglion, and neuronal density in this ganglion may be correlated with tear secretion. Our data suggest that pterygopalatine ganglion degeneration following subarachnoid hemorrhage induces dry eye.