Degenerated Neuron Density Research Articles

Overlooked evidence for transmission deficit of pupillary light reflex can be secondary to trigeminal nerve ganglion degeneration following subarachnoid hemorrhage; preliminary experimental study

ABSTRACT Objective Although the effect of oculomotor and cervical sympathetic networks on pupil diameter is well known; the effect of the trigeminal nerve on pupil diameter has not been investigated yet. This subject was investigated. Materials and methods Five of 23 rabbits were used as a control group (GI; n = 5); 0.5 ccs saline solution into cisterna magna injected animals used as SHAM (GII; n = 5); autologous blood injected to produce SAH used as the study group (GIII; n = 13) and followed up three weeks. Light-stimulated pupil diameters were measured with an ocular tomography device before, middle, and at the end of the experiment. Considering the sclera area/pupil area ratio index (PRI) as the pupillary reaction area, we used this equation for the pupil’s rush to light. Degenerated neuron densities of trigeminal ganglia and pupil diameters compared with the Mann-Whitney U test. Results The PRI, degenerated neuron density of trigeminal ganglia (n/mm3) were: (2.034 ± 0.301)/(13 ± 3) in GI; (1.678 ± 0.211)/(46 ± 9) in GII; and (0.941 ± 0.136)/(112 ± 21) in GIII. P-values between groups as: p < 0.005 in GI/GII; p < 0.0001 in GII/GIII and p < 0.00001 in GI/GIII. Conclusion Light stimulates the cornea which is innervated by the trigeminal nerves. This experimental study indicates that the pupil remains mydriatic as the cornea is damaged by trigeminal ischemia following SAH and blocks the light flow.

From Nose to Lumbar Spinal Cord – Reduced Sperm Numbers Occur by Olfactory Bulbectomy-Related Onuf’s Nucleus Degeneration: New Experimental Evidence for Kallmann Syndrome

Introduction: Olfaction and its relation to human health is an area of growing interest. Although olfaction disorders have been considered a part of Kallmann syndrome, the role of olfactory dysfunction on spermatogenesis has not been studied yet. We studied if olfactory bulbectomy (OBX) causes dysfunction in spermatogenesis as a result of Onuf’s nucleus damage. Methods: Twenty-eight male rats were divided into three groups: six as the control (G-1; n = 6), six as the only frontal burr hole applied animals SHAM (G-2; n = 6), and 16 as the study group (G-3; n = 16) in which OBX was performed. The animals were followed for 2 months. After the decapitation of the animals, olfactory bulb (OB) volumes (mm3), the neuron density of the Onuf’s nucleus (n/mm3), and sperm density (n/mm3) were estimated stereologically and analyzed. Results: OB volumes (mm3), degenerated neuron density of Onuf’s nucleus (n/mm3), and sperm numbers of control, SHAM, and study groups were estimated as: 4 ± 0.5; 6 ± 2 and 103.245 ± 10.841 in G-1; 3.5 ± 0.7; 14 ± 4 and 96.891 ± 9.569 in G-2; and 1.3 ± 0.3; 91 ± 17 and 73.561 ± 6.324 in G-3. The statistical results of degenerated neuron density of Onuf’s nucleus and sperm numbers between groups are p < 0.005 for G-1/G-2; p < 0.0005 for G-2/G-3; and p < 0.00001 for G-1/G-3. Discussion: This study first time indicates that Onuf’s nucleus degeneration secondary to OBX seems to be responsible for reduced sperm numbers.

New determinants for causal neural mechanism of dry mouth in Parkinson’s disease induced by destruction of superior salivatory nucleus, facial nerve, and submandibular gland circuitry: an experimental study

Aim: Dry mouth has been considered a clinical finding of Parkinson’s disease (PD), but we think otherwise. We studied if the olfactory bulbectomy (OBX) might rely on the superior salivatory nucleus (SSN), submandibular ganglia (SMGn), and submandibular glands (SLGl) circuity disruption induced submandibular gland degeneration related dry mouth in rats.&#x0D; Material and Method: This study was carried out on twenty-six male rats. Five (GI-n=5), six (GII, n=6), and sixteen (GIII, n=15) of them were used as control, SHAM, and OBX groups, respectively, and followed eight weeks. PD-related clinical examinations were done before and after the experiment (1/day), and animals were decapitated. The olfactory bulb volumes (mm3), degenerated neuron densities of SSN/SMG (n/mm3 and SMGl follicles volumes were detected serologically. Olfactory bulb volume values and degenerated neuron density values of SSN/SMGn/SMGl follicles volumes were compared statistically.&#x0D; Results: OBX-applied animals showed anosmia, tremors, rigidity, and memory loss. The mean olfactory bulb volumes (mm3), degenerated neuron density of SSN (n/mm3), SMGn (n/mm3), and follicles volumes of SMGl (cubic micrometer/mm3) were measured in the order written as; (4.27±0.21), (4±1), (5±2), (81.23±13.34).106 in GI; (3.67±0.33), (14±3), (17±4), (72.45±11.78).106 in GII and (2.91±0.14), (23±5), (29±8), (57.19±11.93).106 in Group III. The mean P values between olfactory bulb volumes, degenerated neuron densities of SSN and SMGn, and salivary follicles volumes were: p

New Evidence for Regulatory Role of Trigeminal Ganglion on the Intraocular Pressure Following Subarachnoid Hemorrhage.

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. 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. 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 mm3 in the control, sham, and study groups, respectively. 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.

New Histophatological Finding About Data Destroying Amyloid Black Holes in Hippocampus Following Olfactory Bulb Lesion Like as the Universe

Background: Many infinite theories have been suggested to explain memory loss in neurodegenerative diseases. However, there is no data that iron-containing neurofibrillary networks can cause neuron death and erase the memory of neurons, just like black holes in space. Objectives: Ths study aimed to investigate the electromagnetic properties of iron-loaded neurofibrillary networks formed in the hippocampus as a result of damage to the olfactory nerves, just like black holes in space, as well as whether they cause neuron death and memory loss. Methods: All rats were tested with star maze performance before, 3 weeks, and 3 months after surgery. The data used in the study were obtained from the subjects in the experimental groups who had been followed up for 3 months with control (GI; n = 5), SHAM (GII; n = 5) with only frontal burr hole, and study (GIII; n = 15) animals with olfactory bulb lesion. All rats were tested with star maze performance before, 3 weeks, and 3 months after surgery. The olfactory bulbs and hippocampus of subjects were examined by stereological methods. Olfactory bulb volumes, degenerated neuron densities of the hippocampus, and numbers of hippocampal black holes were estimated quantitatively, and results were statistically analyzed by a 1-way analysis of variance (ANOVA). The properties of black holes in the brains and the universe were compared theoretically. Results: The mean olfactory bulb volumes, degenerated neuron density, and black holes of the hippocampus were estimated as 4.43 ± 0.22 mm3, 42 ± 9 mm3, and 3 ± 1 mm3 in GI, 4.01 ± 0.19 mm3, 257 ± 78 mm3, and 11 ± 3 mm3 in GII, and 2.4 ± 0.8 mm3, 1675 ± 119 mm3, and 34 ± 7 mm3 in GIII. All animals were tested with star maze performance before, 3 weeks, and 3 months after surgery. Latency, distance, speed, and path efficiency values of all animals were detected. The more diminished olfactory bulb volume (P &lt; 0.00001) causes more apoptotic neurons and black holes in the hippocampus (P &lt; 0.0001) and more memory loss in olfactory bulb lesion (OBL)-applied animals (P &lt; 0.005). Conclusions: Hippocampal black holes, which are similar to black holes in terms of their formation processes, may be responsible for neuronal losses and memory erasures in the brain by acting like black holes in space. These amyloid plaques, which cause neuron death and memory loss, will be called data-deleting amyloid black holes (DADA-Black Holes) in the paper.

New experimental finding of dangerous autonomic ganglia changes in cardiac injury following subarachnoid hemorrhage; a reciprocal culprit-victim relationship between the brain and heart

Objective The vagal, stellate, and cardiac ganglia cells changes following subarachnoid hemorrhage (SAH) may occur. This study aimed to investigate if there is any relation between vagal network/stellate ganglion and intrinsic cardiac ganglia insult following SAH. Materials and methods Twenty-six rabbits were used in this study. Animals were randomly divided as control (GI, n = 5); SHAM 0.75 cc of saline-injected (n = 5) and study with autologous 1.5 cc blood injection into their cisterna magna(GIII, n = 15). All animals were followed for three weeks and then decapitated. Their motor vagal nucleus, nodose, stellate, and intracardiac ganglion cells were estimated by stereological methods and compared statistically. Results Numerical documents of heart-respiratory rates, vagal nerve- ICG, and stellate neuron densities as follows: 276 ± 32/min-22 ± 3/min-10.643 ± 1.129/mm3-4 ± 1/mm3-12 ± 3/mm3 and 2 ± 1/cm3 in the control group; 221 ± 22/min-16 ± 4/min-8.699 ± 976/mm3-24 ± 9/mm3-103 ± 32/mm3 and 11 ± 3/cm3 in the SHAM group; and 191 ± 23/min-17 ± 4/min-9.719 ± 932/mm3-124 ± 31/mm3-1.542 ± 162/mm3 and 32 ± 9/cm3 in the SAH (study) group. The animals with burned neuro-cardiac web had more neurons of stellate ganglia and a less normal neuron density of nodose ganglia (p < 0.005). Conclusion Sypathico-parasympathetic imbalance induced vagal nerve-ICG disruption following SAH could be named as Burned Neurocardiac Web syndrome in contrast to broken heart because ICG/parasympathetic network degeneration could not be detected in classic broken heart syndrome. It was noted that cardiac ganglion degeneration is more prominent in animals’ severe degenerated neuron density of nodose ganglia. We concluded that the cardiac ganglia network knitted with vagal-sympathetic-somatosensitive fibers has an important in heart function following SAH. The neurodegeneration of the cardiac may occur in SAH, and cause sudden death.

Protective Felix Culpa Effect of Superior Sympathetic Cervical Ganglion Degenerations on Prevention of Basilar Artery Spasm After Subarachnoid Hemorrhage: A Preliminary Experimental Study

Posterior cerebral blood flow is regulated by the basilar arteries (BAs). Vasospasm of BAs can occur after subarachnoid hemorrhage (SAH). Superior cervical sympathetic ganglia (SCG) fibers have a vasoconstrictor effect on the BA. We aimed to investigate the relationship between the degenerated neuron density of the SCG and the severity of BA vasospasm after experimental SAH. Twenty-four rabbits were used. Five were used as the control group, and 5 were used as the sham group. Experimental SAHs were performed in the remaining 14 animals (study group) by injecting homologous blood into the cisterna magna. After 3 weeks of injection, neuron densities of SCG and the severity of BA vasospasm index values (VSI) were examined histopathologically and compared statistically. The mean VSI was 0.669 ± 0.1129 in the control group, 0.981 ± 0.159 in the sham group, and 1.512 ± 0.298 in the study group. The mean degenerated neuronal density of SCG was 436 ± 79/mm3 in severe vasospasm (n= 3), 841 ± 101/mm3 in moderate vasospasm (n= 4), and 1.921 ± 849/mm3 in the less vasospasm detected animals (n= 6). This study shows an inverse relationship between the degenerated neuronal density in the SCG and VSI values. This finding indicates a diminished sympathetic input from the SCG, resulting in a beneficial effect (the felix culpa) by dilating the lumen diameter of the BA, so SCG degeneration after SAH protects the BA spasm.

Predictive role of trigeminal ganglion ischemia on scalp survival affected by temporal artery diameters: The first experimental study

Scalp arteries are mainly innervated by trigeminal, facial, and vagal nerves. The ischemic neurodegeneration of the trigeminal ganglion can impede scalp circulation via vasospasm-creating effects. This study was designed to investigate whether there is any link between the vasospasm index of deep temporal arteries and ischemic neuron densities of the trigeminal ganglion after subarachnoid hemorrhage. The study subjects included five normal control rabbits, six sham rabbits, and nine rabbits chosen from a formerly established experimental subarachnoid hemorrhage group created by cisternal homologous blood injection (0.75mL). These rabbits, all male, were followed up for 3 weeks. The trigeminal ganglion and deep temporal artery vasospasm indexes were examined by stereological methods. Ischemic neuron densities of the trigeminal ganglion and vasospasm index values of deep temporal arteries were compared statistically. Postmortem examinations showed important vasospasms of deep temporal arteries, foramen magnum herniations, and neurodegeneration of the trigeminal ganglion. The mean vasospasm index values and degenerated neuron densities of the trigeminal ganglion were determined as 1.03±0.13 and 10±3/mm3 (p > 0.5) in the control group, 1.21±0.18 and 35±9/mm3 in the sham group (p < 0.005 for sham vs. control), and 2.54±0.84 and 698±134/mm3 in the experimental group (p < 0.0005 for sham vs. control and p < 0.00001 for study vs. control). There was an inverse relationship between the vasospasm index values and the degenerated neuronal density of the trigeminal ganglion. The high degenerated neuron density in the trigeminal ganglion had a facilitative effect on temporal artery vasospasm. Trigeminal ganglion neurodegeneration may promote temporal artery vasospasms after subarachnoid hemorrhage, which has not been previously mentioned in the literature.

First emerging evidence of the relationship between Onuf's nucleus degeneration and reduced sperm number following spinal subarachnoid haemorrhage: Experimental study.

Lumbosacral pathologies can lead to infertility. Onuf's nucleus changes in these pathologies may have a role in low sperm number. This study aims to investigate the relationship between Onuf's nucleus degeneration and sperm number following spinal subarachnoid haemorrhage. 22 rabbits were used. They were divided into three groups; five of them were used as the control (GI), five as the SHAM (GII) and twelve as the study groups (GIII). The study group received 0.7ccs autologous blood into the spinal subarachnoid space at the T12-L1 level. After two weeks, all animals were decapitated, and S1-S3 laminectomy was done. Neurodegenerative changes of Onuf's nucleus, pudendal ganglia (S3) following two weeks after spinal SAH, were examined; sperm numbers were calculated. Degenerated neuron density of the Onuf's nucleus (n/mm3 ), the pudendal ganglia (S3) (n/mm3 ) and mean sperm numbers were calculated as 5±2, 8±3/mm3 and 98.345±12.776/mm3 in the control (GI), 20±5/mm3 , 243±66/mm3 and 91.841±9.654/mm3 in the SHAM (GII), 143±39/mm3 , 2,350±320/mm3 and 68.549±5.540/mm3 in the study group (GIII). In conclusion, there were statistically significant differences between groups. Onuf's nucleus may be responsible for decreased sperm number following spinal SAH.

Cranial hyperthermia resulting from decreased parotid gland salivation induced by ischemic degeneration of glossopharyngeal network in subarachnoid hemorrhage

Objective: We speculated that subarachnoid hemorrhage (SAH) induces ischemic lesions in the cranial parasympathetic nerves, which may decrease saliva secretion and lead to hyperthermia. We tested this hypothesis by examining histologic features of parotid glands and glossopharyngeal nerves (GPNs) in a rabbit model of SAH.&#x0D; Material and Methods: Rabbits (n = 25) were divided into control (n = 5), sham (n = 5), and SAH (n = 15) groups. Animals in the sham and SAH groups were examined over a 3-week period before sacrifice. Salivation score (SC) was determined by measuring the mean wetted area of an orally inserted cotton ball. Sections of parotid glands and intracranial and intraparotideal branches of the GPNs were stained with hematoxylin and eosin and SAH-induced damage was analyzed by terminal deoxynucleotidyl transferase dUTP nick end labeling of apoptotic cells. Specimens were stereologically examined to determine saliva-filled total vesicle volume (TVV) per cubic meter; vasospasm index (VSI) based on wall/lumen ratio of parotid glands arteries, and degenerated neuron density (DND) of glossopharyngeal ganglia.&#x0D; Results: The mean oral temperature was 36.9°C. In the control group, mean values were as follows: SC, 46±8 mm2; DND, 19±4/mm3; VSI, 1.065±0.049; and TVV, (780±1187) × 106/µm3. In the sham group, mean values were as follows: SC, 31±6 mm2; DND, 98±23/mm3; VSI, 1.67±0.32; and TVV, (617±110) × 106/µm3. In the low hyperthermia SAH group, mean values were as follows: SC, 16±5 mm2; DND, 1520±261/mm3; VSI, 2.12±0.21, and TVV, (314±98) × 106/µm3. In the high hypothermia SAH group, mean values were as follows: SC, 9±2 mm2; DND, 3210±912/mm3; VSI, 3.18±0.30; and TVV, (432±99) × 106/µm3.&#x0D; Conclusions: Decreased salivary secretion due to secretory gland atrophy originated from ischemia-induced GPN network degeneration at the brainstem, which may be responsible for cranial hyperthermia following SAH.

First histopathological bridging of the distance between Onuf's nucleus and substantia nigra after olfactory bulbectomy-new ideas about the urinary dysfunction in cerebral neurodegenerative disease: an experimental study.

Olfactory bulbectomy (OBX) in experimental studies induces neurochemical, neurodegenerative changes in various parts of the body. But no information is available about how OBX affects the spinal cord in rats. Our study aims to investigate this question. Twenty-eight male rats were used. The rats were divided into three groups: six as the control, six as the SHAM, and 16 as the study group in which OBX was performed. The animals were followed for 10 weeks. After decapitation of the animals, olfactory bulb (OB) volumes, the olfactory glomerulus (OG), and the neuron density of the ON (Onuf nucleus) per cubic centimeter at the L4-S4 level were examined histopathologically and analyzed stereologically. The mean OB volume, remaining normal OG density, and degenerated neuron density (DND) of the ON was measured as 4.32 ± 0.21/mm3 , 1842 ± 114/mm3 , and 4 ± 1/mm3 in the control (group I); 3.3 ± 0.14/mm3 , 1321 ± 114/mm3 , and 43 ± 8/mm3 in the SHAM (group II); and 1.672 ± 0.12/mm3 , 852 ± 93/mm3 , and 154 ± 11/mm3 in the study group (group III). There was a statistically significant difference between the SHAM and the study group (P < .05). In this study, histopathological bridging between ON-related lower urinary tract symptoms (LUTS) and OBX was shown the first time. According to the findings, LUTS may be reversed by the protection of the affected spinal cord through the correction of olfaction impairment in neurodegenerative disease.

Letter to the Editor Regarding the Manuscript of “The Longest Angiographic and Clinical Follow-Up of Microsurgically Treated Giant Intracranial Aneurysms: Experience with 70 Cases”

Posterior cerebral blood flow is regulated by the basilar arteries (BAs). Vasospasm of BAs can occur after subarachnoid hemorrhage (SAH). Superior cervical sympathetic ganglia (SCG) fibers have a vasoconstrictor effect on the BA. We aimed to investigate the relationship between the degenerated neuron density of the SCG and the severity of BA vasospasm after experimental SAH.Twenty-four rabbits were used. Five were used as the control group, and 5 were used as the sham group. Experimental SAHs were performed in the remaining 14 animals (study group) by injecting homologous blood into the cisterna magna. After 3 weeks of injection, neuron densities of SCG and the severity of BA vasospasm index values (VSI) were examined histopathologically and compared statistically.The mean VSI was 0.669 ± 0.1129 in the control group, 0.981 ± 0.159 in the sham group, and 1.512 ± 0.298 in the study group. The mean degenerated neuronal density of SCG was 436 ± 79/mm3 in severe vasospasm (n = 3), 841 ± 101/mm3 in moderate vasospasm (n = 4), and 1.921 ± 849/mm3 in the less vasospasm detected animals (n = 6).This study shows an inverse relationship between the degenerated neuronal density in the SCG and VSI values. This finding indicates a diminished sympathetic input from the SCG, resulting in a beneficial effect (the felix culpa) by dilating the lumen diameter of the BA, so SCG degeneration after SAH protects the BA spasm.

Thoracic sympathetic nuclei ischemia: Effects on lower heart rates following experimentally induced spinal subarachnoid hemorrhage

BackgroundThe neuropathological mechanism of heart rhythm disorders, following spinal cord pathologies, to our knowledge, has not yet been adequately investigated. In this study, the effect of the ischemic neurodegeneration of the thoracic sympathetic nuclei (TSN) on the heart rate (HR) was examined following a spinal subarachnoid hemorrhage (SSAH). MethodsThis study was conducted on 22 rabbits. Five rabbits were used as a control group, five as SHAM, and twelve as a study group. The animals’ HRs were recorded via monitoring devices on the first day, and those results were accepted as baseline values. The HRs were remeasured after injecting 0.5 cc of isotonic saline for SHAM and 0.5 cc of autolog arterial blood into the thoracic spinal subarachnoid space at T4–T5 for the study group. After a three-week follow-up with continuous monitoring of their HRs, the rabbit's thoracic spinal cords and stellate ganglia were extracted. The specimens were evaluated by histopathological methods. The densities of degenerated neurons in the TSN and stellate ganglia were compared with the HRs. ResultsThe mean HRs and mean degenerated neuron density of the TSN and stellate ganglia in control group were 251±18/min, 5±2/mm3, and 3±1/mm3, respectively. The mean HRs and the mean degenerated neuron density of the TSN and stellate ganglia were detected as 242±13/min, 6±2/mm3, and 4±2/mm3 in SHAM (P>0.05 vs. control); 176±19/min, 94±12/mm3, and 28±6/mm3 in the study group (P<0.0001 vs. control and P<0.005 vs. SHAM), respectively. ConclusionsSAH induced TSN neurodegeneration may have been responsible for low HRs following SSAH. To date this has not been mentioned in the literature.

Vagosympathetic imbalance induced thyroiditis following subarachnoid hemorrhage: a preliminary study

Introduction: This preliminary study evaluates the possible responsibility of ischemia-induced vagosympathetic imbalances following subarachnoid hemorrhage (SAH), for the onset of autoimmune thyroiditis. Methods: Twenty-two rabbits were chosen from our former experimental animals, five of which were picked from healthy rabbits as control (nG-I=5). Sham group (nG-II=5) and animals with thyroid pathologies (nG-III=12) were also included after a one-month-long experimental SAH follow-up. Thyroid hormone levels were measured weekly, and animals were decapitated. Thyroid glands, superior cervical ganglia, and intracranial parts of vagal nerve sections obtained from our tissue archives were reexamined with routine/immunohistochemical methods. Thyroid hormone levels, hormone-filled total follicle volumes (TFVs) per cubic millimeter, degenerated neuron density (DND) of vagal nuclei and neuron density of superior cervical ganglia were measured and statistically compared. Results: The mean neuron density of both superior cervical ganglia was estimated as 8230±983/ mm3 in study group animals with severe thyroiditis, 7496±787/mm3 in the sham group and 6416±510/mm3 in animals with normal thyroid glands. In control group (group I), T3 was 107±11 μg/dL, T4: 1,43±0.32 μg/dL and TSH &lt;0.5, while mean TFV was 43%/mm3 and DND of vagal nuclei was 3±1/mm3. In sham group (group II), T3 was 96±11 μg/dL, T4: 1.21±0.9 μg/ dL and TSH&gt;0.5 while TFV was 38%/mm3 and DND of vagal nuclei was 13±4. In study group, T3 was 54±8 μg/dL, T4: 1,07±0.3 μg/dL and TSH &gt;0.5, while TFV was 27%/mm3 and DND of vagal nuclei was 42±9/mm3. Conclusion: Sympathovagal imbalance characterized by relative sympathetic hyperactivity based on vagal insufficiency should be considered as a new causative agent for hypothyroidism.

New Histopathologic Evidence for the Parasympathetic Innervation of the Kidney and the Mechanism of Hypertension Following Subarachnoid Hemorrhage.

The Cushing response was first described in 1901. One of its components is elevated systemic blood pressure secondary to raised intracranial pressure. However, controversy still exists in its pathophysiologic mechanism. Hypertension is attributed to sympathetic overactivity and vagotomy increased renal-based hypertension. However, the role of the parasympathetic system in hypertension has not been investigated. This subject was investigated following subarachnoid hemorrhage (SAH). A total of 24 rabbits were used: control group (n = 5), SHAM group (n = 5), and an SAH group (n = 14; bolus injection of blood into the cisterna magna). Blood pressures were examined before, during, and after the experiment. After 3 weeks, animals were decapitated under general anesthesia. Vagal nodose ganglion, axonal degeneration, and renal artery vasospasm (RAV) indexes of all animals were determined histopathologically. Significant degenerative changes were detected in the vagal axons and nodose ganglia following SAH in animals with severe hypertension. The mean degenerated neuron density of nodose ganglions, vasospasm index (VSI) values of renal arteries of control, SHAM, and study groups were estimated as 9.0 ± 2.0 mm, 1.87 ± 0.19; 65.0 ± 12.0 mm, 1.91 ± 0.34; and 986.0 ± 112.0 mm, 2.32 ± 0.89, consecutively. Blood pressure was measured as 94.0 ± 10.0 mmHg in control group, 102.0 ± 12.0 mmHg in SHAM; 112.0 ± 14.0 mmHg in middle (n = 9); and >122.0 ± 10.0 mmHg in severe RAV-developed animals (n = 5). Differences VSI values and blood pressure between groups were statistically significant (P < 0.05). The degeneration of vagal nodose ganglion has an important role in RAV and the development of RAV and hypertension following SAH.

Hazardous Hyperglisemic Effect of Facial Ischemia Following Subarachnoid Hemorrhage: An Experimental Study

Background: Hyperglycemia has been tried to explain by different mechanisms, but glucose-sensing tongue taste buds-geniculate ganglia-facial nerve-vagal nerve-pancreas web relation has not been adequately investigated. Objectives: We aimed to investigate if there is any relationship between the described taste buds network degeneration and blood glucose levels following subarachnoid hemorrhage (SAH). Methods: This study was conducted on 32 rabbits. Blood glucose levels were measured at the beginning, mid-phase, and the end of the experiment. Animals were divided into the groups of control (n = 5), physiologic serum saline (SHAM; n = 5), and subarachnoid hemorrhage with 0.5 cc homolog blood injection into cisterna magna (study; n = 22) three times a week and were sacrificed under general anesthesia after two weeks. The blood glucose level of 113 ± 20 mg/dL was accepted as normal (G-I; n = 11), lower than 80 mg/dl as hypoglycemic (G-II; n = 6), and higher than 149 mg/dl as hyperglycemic (G-III; n = 5). Their neuron densities of geniculate ganglia were examined by stereological methods. The statistical analysis was done between glucose levels/degenerated taste bud/neurons using Kruskal-Wallis and Mann-Whitney U tests. We accepted P > 0.005 as non-significance. Results: The mean normal blood glucose level was 115 ± 9 mg/dl before surgery. The pre-sacrificed glucose level was 113 ± 8 mg/dL and the neuron density of the geniculate ganglia was 7.421 ± 530/mm3. The degenerated neuron density of geniculate ganglia was 13 ± 4/mm3 in controls 21 ± 7/mm3 in SHAM, 27 ± 7/mm3 in G-I, 21 ± 5/mm3 in G-II, and 112 ± 18/mm3 in G-III groups. The P values of glucose levels-degenerated neuron density of geniculate ganglia between control/G-III was: P < 0.00001; SHAM/G-III: P < 0.0005; GI/GII: P < 0.005. Conclusions: Glucose sensing tongue taste buds-geniculate ganglia-facial nerve-vagal nerve-pancreas circuitry should be an unexplained web for the regulation of blood glucose level.

Predestinating Role of Cardiac Ganglia on Heart Life Expectancy in Rabbits After Brain Death Following Subarachnoid Hemorrhage: An Experimental Study

BackgroundCardiac ganglia are rechargeable batteries of the heart. The essential role of cardiac ganglia on cardiac life expectancy has not been examined following brain death. The aim of this study was to determine cardiac ganglia numbers and neuron density following subarachnoid hemorrhage (SAH). MethodsTwenty-five hybrid rabbits were grouped as control (n = 5), sham (n = 5), and SAH (n = 15). The SAH groups’ animals were subjected to injections of lethal dose of 2.00 cc autologous blood into their cisterna magna until linear EEG was obtained. The hearts of all animals were extracted following intracardiac formalin injection and examined. Cardiac ganglia and normal/degenerated neuron densities of cardiac neurons were recorded. ResultsThe mean volume of normal neuron density of ganglia was 6.980 ± 830/mm3, and the degenerated neuron density of ganglia was 3 ± 1/mm3 in the control group, 6134 ± 712/mm3; 23 ± 9/mm3 in the sham group, 3456 ± 589; 1161 ± 72/mm3 in the surviving group; and 1734 ± 341/mm3, 4259 ± 865/mm3 in the dead animals in the SAH group. The algebraic results of heart work capacity (Wh) were estimated as 1375 ± 210 Wh in the control group, 1036 ± 225 in the sham group, 800 ± 110 Wh in the surviving group, and < 100 ± 20 in the dead animals in the SAH group. Degenerated cardiac neuron density/Wh correlation is statistically meaningful between the dead in the SAH group versus the SAH-surviving, sham, and control groups (P < .0005). ConclusionsNormal cardiac ganglia numbers and/or cardiac ganglia neuron density may be related to cardiac survival following brain death after subarachnoid hemorrhage.

Disruption of the network between Onuf’s nucleus and myenteric ganglia, and developing Hirschsprung-like disease following spinal subarachnoid haemorrhage: an experimental study

Purpose/Aim of the study: Auerbach/Meissner network of lower abdominopelvic organs managed by parasympathetic nerve fibres of lumbosacral roots arising from Onuf’s nucleus located in conus medullaris. Aim of this study is to evaluate if there is any relationship between Onuf’s nucleus ischemia and Auerbach/Meissner network degeneration following spinal subarachnoid haemorrhage (SAH).Materials and Methods: Study was conducted on 24 male rabbits included control (Group I, n = 5), serum saline-SHAM (Group II, n = 5), and spinal SAH (Group III, n = 14) groups. Spinal SAH performed by injecting homologous blood into subarachnoid space at Th12–L4 level and followed three weeks. Live and degenerated neuron densities of Onuf’s nucleus, Auerbach and Meissner ganglia (n/mm3) were determined by Stereological methods.Results: The mean degenerated neuron density of Onuf’s nucleus was significantly higher in Group III than in Groups I–II (152 ± 26, 2 ± 1 and 5 ± 2/mm3 respectively, p < 0.005). The degenerated neuron density of Auerbach’s ganglia was significantly higher in Group III than in Groups I–II (365 ± 112, 3 ± 1 and 9 ± 3/mm3 respectively, p < 0.005). The degenerated neuron density of Meissner’s ganglia was significantly higher in Group III than in Groups I–II (413 ± 132, 2 ± 1 and 11 ± 4/mm3 respectively, p < 0.005).Conclusions: Onuf’s nucleus pathologies should be considered as Auerbach/Meissner ganglia degeneration and also related Hirschsprung-like diseases in the future.

First emerging objective experimental evidence of hearing impairment following subarachnoid haemorrhage; Felix culpa, phonophobia, and elucidation of the role of trigeminal ganglion

Objective: The exact mechanism of phonophobia induced by subarachnoid hemorrhage (SAH) has not been understood well. This subject was investigated.Material and methods: This study was conducted on 25 rabbits. They divided into three groups: Five as control, five as SHAM, 20 as SAH group. All animals objected to 85 dB impulse noise by daily periods, and their phonophobic score values were examined by daily periods for 20 days. Their brains, trigeminal ganglia were extracted bilaterally. The normal and degenerated neuron densities of trigeminal ganglia were examined by stereological methods and compared with phonophobia scores.Results: Phonophobic score was 19-17, mean live neuron density (LND) of the trigeminal ganglia was 16.321 ± 2.430/mm3, and degenerated neuron density (DND) was 1.15 ± 0.120/mm3 in animals of control groups (n = 5). The phonophobic score was 17-14, LND: 14.345 ± 1.913/mm3, DND of the trigeminal ganglia was 1.150 ± 0.110/mm3 in SHAM group (n = 5). The phonophobic score was 14-8, LND: 12.987 ± 1.966/mm3, mean DND of the trigeminal ganglia was 2.520 ± 510/mm3 in animals with high phonophobia scores (n = 6). The phonophobic score was 7-4, LND: 9.122 ± 1.006, mean DND of the trigeminal ganglia was 5.820 ± 1.610/mm3, in animals with fever phonophobia scores (n = 9).Conclusion: An inverse relationship between DND trigeminal ganglion (TGG) and phonopobic score was found. The paralysis of tensor tympani muscle owing to trigeminal ganglia ischemia may be responsible for phonophobic clinical state in animals with SAH. In addition, there seems to be an important concern for the verbal component of GCS in SAH. These two important findings have not been published previously.

A New Neuropathologic Mechanism of Blood pH Irregularities After Neck Trauma: Importance of Carotid Body−Glossopharyngeal Nerve Network Degeneration

We created a neck trauma model by injecting blood into the sheath of rabbits' carotid bodies (CBs). Then we determined the relationship between neuronal degeneration of the CB due to hemorrhage of this organ and its clinical effects such as blood pH and heart rhythm. The present study included 24 adult male New Zealand rabbits. The animals were divided into 3 groups: control (n= 5); sham (0.5 mL saline injected into CBs; n= 5); and study (CB trauma model; n= 14). pH values and heart rhythms were recorded before the experiment to determine the values under normal conditions, and measurements were repeated thrice in the days following the experiment. The number of normal and degenerated neuron density of CBs was counted. The relationship between the blood pH values, heart rhythms, and degenerated neuron densities was analyzed. Heart rhythms were 218 ± 20 in the control group, 197 ± 16 in the sham group (P= 0.09), and 167 ± 13 in the study group (P < 0.0005). pH values were 7.40 ± 0.041 in the control group, 7.321 ± 0.062 in the sham group (P=0.203), and 7.23 ± 0.02 in study group (P < 0.0005). Degenerated neuron densities were 12 ± 4/mm3 in the control group, 430 ± 74/mm3 in the sham group (P < 0.005), and 7434 ± 810/mm3 in the study group (P < 0.0001). A high degenerate neuron density in the CB can decrease blood pH and hearth rhythm after neck trauma, and there might be a close relationship between the number of degenerated neurons and clinical findings (such as heart rhythm and blood pH). This relationship suggests that injury to the glossopharyngeal nerve-CB network can cause acidosis by disturbing the breathing-circulating reflex and results in respiratory acidosis.