Intimal Hemorrhage of Basilar Artery Induced by Severe Vasospasm Following Subarachnoid Hemorrhage: The Experimental Analysis.

BACKGROUND: Cerebral vasospasm, a serious complication of subarachnoid hemorrhage (SAH), has been extensively studied for its neurochemical and pathophysiologic mechanisms. However, the contribution of inner elastic membrane dissection and subintimal hemorrhage to basilar artery occlusion remains underexplored. This study investigates inner elastic membrane-related changes in the basilar artery after SAH. METHODS: Twenty-four hybrid rabbits were divided into control, sham, and SAH groups, with SAH induced by autologous blood injection. After 2 weeks, basilar artery changes, vasospasm indexes (VSIs), and dissections were evaluated. RESULTS: The SAH group showed significantly higher VSI, with vascular wall thickening, luminal narrowing, convoluted smooth muscle cells, intimal elastic membrane disruption, endothelial cell desquamation, and apoptosis. Some SAH animals exhibited subintimal hemorrhage, inner elastic membrane dissection, and ruptures. Basilar arteries with subintimal hemorrhage had notably higher VSI. CONCLUSIONS: These findings highlight the role of subintimal hemorrhage and inner elastic membrane dissection in basilar artery occlusion post-SAH, offering valuable insights into vasospasm pathophysiology.

Predestinative role acidic cerebrospinal fluid on the destiny of central channel in spinal cord following subarachnoid hemorrhage: an experimental study.

OBJECTIVE: Acidosis is the most dangerous complication in subarachnoid hemorrhage (SAH). This study aimed to investigate the effect of acidic cerebrospinal fluid on central canal structures after SAH. MATERIALS AND METHODS: Twenty-eight hybrid rabbits were studied. Blood and cerebrospinal fluid pH values were recorded before/during/after the experimental procedures. The structures related to the central canals at the level of C5 of the cervical spinal cord were then examined histopathologically. The relationship between pH values of ependymal cells and degenerated epithelial cell densities was statistically analyzed. RESULTS: Mean blood pH values and degenerated ependymal cell density (n/mm2) were as follows: 7.351 ± 0.033/23 ± 7 in control, 7.322 ± 0.059/78 ± 13 in SHAM, and 7.261 ± 0.048/254 ± 62 in study animals. Gross examinations revealed swelling, edema, pia-arachnoid adhesions, ventral canal dilatation, arachnoiditis, central canal hemorrhage, occlusions, and dilatation in the spinal cord. CONCLUSION: Cerebrospinal fluid acidosis-induced central channel pathologies should be considered an important complication of SAH following SAH.

OBJETIVO: La acidosis es la complicación más peligrosa en la hemorragia subaracnoidea (HSA). El objetivo de este estudio fue investigar el efecto del líquido cefalorraquídeo ácido en las estructuras del canal central tras la HSA. MATERIALES Y MÉTODOS: Se estudiaron 28 conejos híbridos. Se registraron los valores de pH de la sangre y del líquido cefalorraquídeo antes, durante y después de los procedimientos experimentales. A continuación se examinaron histopatológicamente las estructuras relacionadas con los canales centrales a nivel de C5 de la médula espinal cervical. Se analizó estadísticamente la relación entre los valores de pH de las células ependimarias y las densidades de células epiteliales degeneradas. RESULTADOS: Los valores medios de pH en sangre y la densidad de células ependimarias degeneradas (n/mm2) fueron los siguientes: 7.351 ± 0.033/23 ± 7 en el control, 7.322 ± 0.059/78 ± 13 en el SHAM, 7.261 ± 0.048/254 ± 62 en los animales del estudio. Los exámenes macroscópicos revelaron hinchazón, edema, adherencias pia-aracnoideas, dilatación del canal ventral, aracnoiditis, hemorragia del canal central, oclusiones y dilatación en la médula espinal. CONCLUSIONES: Las patologías del canal central inducidas por la acidosis del líquido cefalorraquídeo deben considerarse como una complicación importante de la HSA tras una hemorragia subaracnoidea.

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.

The Enigma of Basilar Artery Dissections Secondary to Vasospasm following Subarachnoid Hemorrhage; Exploration of the Unknown Effect of Superior Cervical Ganglia: A Preliminary Experimental Study.

BACKGROUND: Life-threatening basilar artery dissection (BAD) can be seen following subarachnoid hemorrhage (SAH), but it is not clear whether subarachnoid hemorrhage causes dissection, or not. This study aims to investigate the relationship between, degenerative changes in the superior cervical ganglia and the dissection rate of the basilar artery. MATERIAL AND METHOD: In this article, after three weeks of experimental SAH, animals were decapitated. 18 rabbits were divided into three groups, according to their vasospasm indexes. The basilar arteries were examined by anatomical and histopathological methods. RESULTS: Basilar dissection with high vasospasm index value (VSI>3) was detected in six animals (G-I, n=6); severe basilar edema and moderate vasospasm index value (VSI>2.4) in seven rabbits (G-II, n=7) and slight vasospasm (VSI<1.5) index value in five subjects (G-III, n=5) was detected. The degenerated neuron densities (n/mm3) of the superior cervical ganglia were detected as 12±4 in G-I, 41±8 in G-II; and 276±78 in G-III. The dissected surface values/lumen values were calculated as (42±1)/(64±11) in G-I; (21±6)/(89±17) in G-II; and (3±1)/(102±24) in G-III. If we look at these ratios as a percentage: 62%in G-I, 23% in G-II, and 5% in G-III. CONCLUSION: Inverse relationship between the degenerated neuron densities (n/mm3) of the superior cervical ganglia and the dissected surface values basilar artery was observed. The common knowledge is that basilar artery dissection may lead to SAH, however, this study indicates that SAH is the cause of basilar artery dissection.

Burned spinal cord in acidotic cerebrospinal fluid during subarachnoid hemorrhage: Experimental study.

OBJECTIVE: We investigated the effect of carotid body ischemia-induced cerebrospinal fluid acidosis on spinal cord during subarachnoid hemorrhage (SAH). METHODS: Twenty-three hybrid rabbits were divided into three groups: control (n = 5), Sham (injected with 0.5 ml isotonic) (n = 6), and the SAH (n = 12) (injected with 0.5 ml autologous blood into the 4th ventricle) and then monitored for 3 weeks. Cerebrospinal fluid pH and degenerated ependymal cell density and volume of cervical central canal were analyzed. RESULTS: The mean cervical central canal volumes, degenerated ependymal cells densities, and cerebrospinal pH values were 1.056 ± 0.053 mm3-6 ± 2 per mm2-7.342 ± 0.034, 1.321 ± 0.12 mm3-35 ± 9 per mm2-7.314 ± 0.056, and 1.743 ± 0.245 mm3-159 ± 24 per mm2-7.257 ± 0.049 in the Control, Sham, and SAH groups, respectively. The more degenerated carotid body neuron density induced decreased cerebrospinal fluid pH values (p < 0.0001) could result in the more ependymal cells desquamation (p < 0.0005) and central canal dilatation (p < 0.00001). CONCLUSION: Increased neurodegeneration of carotid bodies can reduce cause cerebrospinal fluid pH-induced ependymal cell degeneration and central canal dilatation following SAH.

OBJETIVO: El objetivo de este estudio fue investigar el efecto de la isquemia inducida del cuerpo carotideo por la acídosis de líquido cefalorraquídeo en la médula espinal durante una hemorragia subaracnoidea (SAH). METODO: Conejos híbridos (n = 23) fueron divididos en Control (n = 5), Sham (inyectados con 0.5 mil de solución isotónica) (n = 6), y SAH (n = 12) (inyectados en el 4º ventrículo con 0.5 ml de sangre autológa) y monitoreados por tres semanas. Se analizaron: El pH del líquido cerebro espinal, la densidad de las células ependimarias y el volúmen del canal cervical central. RESULTADOS: La media del volumen del canal cervical central, la densidad de las células ependimarias degeneradas y los valores de pH fueron 1.056 + 0.053 mm3-6 + 2 per mm2-7.342 + 0.034, 1.321 + 0.12 mm3-35 + 9 per mm2-7.314 + 0.056 y 1.743 + 0.245 mm3-159 + 24 per mm2-7.257 + 0.049 en los grupos Control, Sham y SHA, respectivamente. La mayor densidad inducida de la neurona del cuerpo carotideo degenerado, disminuyó los valores de pH del líquido cefalorraquideo lo que podría dar como resultado un aumento en la descamación de las células ependimarias asi como la dilatación del canal central. CONCLUSIÓN: Un aumento en la neurodegeneración del cuerpo carotideo puede reducir la degeneración de los ependimocitos y la dilatacióm del canal central siguiendo SAH.

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

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 ± 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 steno-occlusive carotid artery disease.

First definition of burned choroid plexus in acidic cerebrospinal fluid-filled brain ventricles during subarachnoid hemorrhage: Experimental study.

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.

New insights of the fever following subarachnoid hemorrhage and introducing a new thermoregulator like structure in choroid plexuses; preliminary study.

OBJECTIVE: Vagal nerves and their thermoreceptors could regulate temperature of brain. Cerebrospinal fluid (CSF) is increased in the early phases of subarachnoid hemorrhage (SAH). We hypothesised that choroid plexuses probably innervated by vagal nerves may play a role on the regulation of brain temperature and studied this subject. METHODS: This study was conducted on 32 rabbits, divided into four groups, with five rabbits in the control group (group I), five rabbits in the sham group (Group II), and 22 rabbits in the SAH group. In the SAH group, 7 of the animals were decapitated after 7 days of cisternal blood injections (Group III), and the other 15 animals were decapitated after 21 days of injections (Group IV). Brain temperature via laser thermometer 5 times a day during the experiment was measured. Normal and degenerated neuron density of nodose ganglia, water vesicles numbers of choroid plexuses were stereologicallyanalyzed. Statistical analysis was performed. RESULTS: At histopathologic analysis of present study, thermo regulator like structure was noted and the mean number of this structure was estimated.The mean number of water-filled vesicles, thermo regulator like structure, in SAH-induced animals,brain temperature and degenerated neuron density of nodose ganglia was statistically different between the early decapitated group (group III) and the late decapitated group (group IV) (P less then 0.05). CONCLUSIONS: We introduce a thermo regulator like structure, describe a new syndrome. In addition, it was noted thatwater-filled vesicles of CP are increased, brain temperature in nearly normal in the early phase of SAH due to likely irritation of vagal nerves. However in the late phase, mean number of water-filled vesicles numbers decreased in accordance with increased brain temperature with degenerative changes of the nodose ganglion.

Toward understanding the causes of blood pH irregularities and the roles of newly described binuclear neurons of carotid bodies on blood pH regulation during subarachnoid hemorrhage: Experimental study.

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/mm3 and 9 ± 3/mm3 in the control group; 15 ± 5/mm3 and 22 ± 6/mm3 in sham, 965 ± 113/mm3 and 1532 ± 176/mm3 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.

Reconsideration of Neurogenic Pulmonary Edema as Source of Metastatic Cerebral Abscess Following Subarachnoid Hemorrhages: A Preliminary Study.

BACKGROUND: Subarachnoid hemorrhage (SAH) may be a cause of neurogenic pulmonary edema (NPE). It is well known that lymphatic fluid draining by thoracic duct to lungs consists of many dangerous metabolites, degraded tissue particles, and microbiologic pathogens. However, not enough studies have investigated whether NPE causes septicemia or not. In this study, we retrospectively examined our experimental materials to determine whether there is a meaningful relationship between NPE and cerebral abscess formation. METHODS: Forty-two rabbits were divided into 3 groups: Control (n = 5), SHAM (n = 7), and SAH (n = 30) with severe neurogenic lung edema detected in rabbits. The SHAM and SAH groups received 1 mL saline and 1 mL autologous arterial blood into the Sylvian cisterna, respectively. Weight, heartbeat, respiration rate, and blood pressure were recorded by routinely using monitoring devices. All multilevel lungs and brain tissue microsections were examined by stereologic and Cavalier methods. For statistical analysis, NPE criteria and the numbers of abscess or abscess resembling cores in the brains were estimated in all groups and compared. The Mann Whitney-U test was used to analyze the results statistically. RESULTS: All rabbits were around 4 years old; body weight was between 3.94 and 4.5 kg; normal heart rhythm rate was found between 251 ± 39/minutes and 281 ± 30/minutes; and respiration rate was between 24 ± 5/minutes and 36 ± 7/minutes. Histopathologic examinations showed that abscess formations frequently spread in middle cerebral arterial territories of all animals in the NPE-detected rabbits. While average abscess numbers were estimated as 3 ± 1 in 7 animals (n = 7; P < 0.005) in severe NPE-detected rabbits, only 1 ± 1 abscess core was detected in a less severe NPE that developed in 3 (n = 3; P < 0.05) animals. The vasospasm index values of pulmonary arteries (PAs) of all animals were 1.233 ± 0.065 in the control group; 1.567 ± 0.0430 in the SHAM group, and 2.890 ± 0.0453 in the SAH group (P < 0.05). CONCLUSIONS: This experimental study showed that NPE is a relatively common pathology following experimental SAH in rabbits. The NPE is frequently complicated with brain abscess as shown in this study. The pathophysiologic mechanism was concluded, as NPE may be responsible for cerebral abscess development via bacteria/cytotoxic particles conveyed by thoracic duct to lungs and transferred from the ruptured alveoli-capillary membrane to the brain by way of systemic circulation.

Parallel development of choroid plexus degeneration and meningeal inflammation in subarachnoid hemorrhage - experimental study.

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). CONCLUSIONS: 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.

Toward changing of the pathophysiologic basis of acute hydrocephalus after subarachnoid hemorrhage: a preliminary experimental study.

BACKGROUND: Acute hydrocephalus (ventricular enlargement within 72 hours) is a common complication in patients with aneurysmal subarachnoid hemorrhage (SAH). Cerebrospinal fluid (CSF) secretion may be increased in the early phases of SAH, but it has not been proved definitively. We studied the histologic features of choroid plexus (CP) in the early and late phases of SAH. METHODS: This study was conducted on 20 rabbits, with 5 rabbits in the control group, 5 rabbits in the sham group, and 10 rabbits in the SAH group. In the SAH group, five of the animals were decapitated after 2 days of cisternal blood injections, and the other five animals were decapitated after 14 days of injections. The CP of lateral ventricles were obtained from coronary sections of brains at the level of the temporal horns of the lateral ventricles. Sections were stained with hematoxylin and eosin and Masson trichrome for SAH-related damage and examined stereologically to discern water-filled vesicles, which were counted. Sections were compared statistically. RESULTS: The mean numbers of water vesicles were different after SAH between the early decapitated group (group III) and the late decapitated group (group IV). The mean numbers of water vesicles were 2.80 (± 0.05) in the control group (group I), 2.76 (± 0.02) in the sham group (group II), 14.68 (± 0.06) in the early decapitated group (group III), and 4.78 (± 0.13) in the late decapitated group (group IV). Total number of fluid-filled vesicles of CP was also assessed stereologically; the total numbers were 840 (± 16) in group I, 828 (± 7) in group II, 4404 (± 19) in group III, and 1434 (± 41) in group IV. The numbers of water-filled cisterns were significantly increased in the early phases of SAH (P < 0.05). CONCLUSIONS: In SAH with aneurysm rupture, increased CSF secretion seems to be triggered by hemorrhage in the early phase, but it is not possible in the late phase because of CP degeneration. In the early phase of hemorrhage, CSF secretion may be stimulated by the irritant receptor glossopharyngeal and vagal nerve endings, which innervate the healthy CP epithelium and arteries. Our findings may be accepted as being causative. It is likewise possible that CSF blockage per se leads to hydrocephalus, and the morphologic changes are sequelae that occur later in the course of disease. This is the first study to show the water vesicles of CP as a causative factor in the development of acute hydrocephalus after SAH.

Effects of haloperidol on striatal neurons: relation to neuronal loss (a stereological study).

In the present work, we investigated the effect of chronic haloperidol administration on the number of striatal neurons in guinea pigs. For this purpose, adult male guinea pigs were given daily injections of 1, 2 or 3 mg/kg of haloperidol for 6 weeks. After treatment, the animals were anesthetized via brief inhalation of ether, the brains were removed and the corpus striatum was dissected. Then the tissues were processed and semi-thin sections were stained with toluidine blue for stereological and histopathological evaluation. The physical disector was used for measurements of nuclear height and numerical density of striatal neurons and also to evaluate both normal and degenerated neurons within the corpus striatum of treated animals and untreated controls. In the control group, the mean numerical density of neurons was calculated as 47.92 cell/mm3 and the mean nuclear height as 3.58 µm. Mean densities of all (both viable and degenerated) neurons were calculated to be 45.46 in the low-dose (p < 0.01), 39.73 in the medium-dose (p < 0.001) and 30.31 cell/mm3 in the high-dose group (p < 0.001). Mean densities of degenerated neurons in the low, medium and high dose group were 30.72, 22.93 (p < 0.001) and 15.56 cell/mm3 (p < 0.001) respectively. Mean nuclear heights were 2.804 (p < 0.0001), 2.78 (p < 0.0001) and 2.33 µm (p < 0.00001) in the low, medium and high dose group, respectively.

The role of ischemic neurodegeneration of the nodose ganglia on cardiac arrest after subarachnoid hemorrhage: an experimental study.

BACKGROUND: The heart is innervated by several systems that contribute to the control of the heart's rhythm. The cardiac fibers of the vagus nerve have an important role in the regulation of heart rhythm under many emotional and physical conditions. Severe electrocardiographic disturbances have been reported following subarachnoid hemorrhage (SAH), but ischemic neuronal degeneration of the nodose ganglion of the vagus nerve has not been previously investigated. We examined if there is a relationship between ischemic injury of the nodose ganglion of the vagus nerve and the severity of heart rhythm disorders after subarachnoid hemorrhage. METHODS: This study was conducted on 20 rabbits. Four rabbits were used as a baseline group. Experimental subarachnoid hemorrhage was applied to half of the remaining animals (n = 8) by injecting homologous blood into the cisterna magna, and the others (SHAM group, n = 8) were injected with isotonic saline solution in the same manner. For 20 days after the injection, heart rhythm changes were observed daily. After the experiment, normal and ischemic neuron densities in the nodose ganglia of the vagus nerves were examined stereologically. The number of heart rhythm irregularities and the number of degenerated neurons in the nodose ganglia were compared statistically. RESULTS: The normal heart rhythm rate was 280 ± 45/min. At the beginning of the SAH, the average heart rate was 220 ± 30/min; about 10 hours later, it decreased to 189 ± 30/min, indicating severe bradycardia. However, after 7 days, the average heart rate had increased to 350 ± 30/min. Six animals died due to irregularities in cardiac function and respiration. Histopathological examinations showed that the average density of normal neurons in the nodose ganglion was 10,500 ± 2500 in the baseline animals and the SHAM group, but the normal neuron density was 8250 ± 1500 in survivors and 6450 ± 1330 in dead animals. The ischemic neuronal degeneration in the nodose ganglia was more severe in the dead animals than in the survivors (p < 0.0001). CONCLUSION: Afferent vagus nerves originating from the nodose ganglia have an important role in regulating heart rhythm via their afferent fibers and efferent connections. If neurons of the nodose ganglia are lesioned due to ischemic insult during subarachnoid hemorrhage, heart rhythm regulation by vagus afferent reflexes is disturbed. Vagus pathway paralysis may result in indirect sympathetic overactivity. The development of tachycardia causes depletion of the heart's reserves, and cardiac arrest may be inevitable following extensive subarachnoid hemorrhage.

Role of degenerated neuron density of dorsal root ganglion on anterior spinal artery vasospasm in subarachnoid hemorrhage: experimental study.

BACKGROUND: The spinal arteries are innervated by several systems that contribute to the control of spinal cord blood flow. The sensory fibers of upper cervical nerves have vasodilatatory effect on the anterior spinal arteries (ASA). Subarachnoid hemorrhage (SAH) causes severe vasospasm by various neurochemical mechanisms. We examined whether there is a relationship between the neuron density of the C3 dorsal root ganglion and the severity of ASA vasospasm in SAH. METHODS: This study was conducted on 20 rabbits. Four of them were used as baseline group. Experimental SAH has been applied to all of 16 animals by injecting homologous blood into cisterna magna. After 20 days of injection, ASA and C3 dorsal root ganglia (C3DRG) were examined histopathologically. ASA volume values and normal and degenerated neuron densities of C3DRG were estimated stereologically and the results were analyzed statistically. RESULTS: The mean ASA volume was 1.050±0.450 mm³, [corrected] and the mean neuronal density of C3DRG was 10,500 ± 850 in all animals. The mean volume value of ASA was 0.970±0.150 [corrected] mm³, and the normal neuron density of C3DRG fell to 8,600 ± 400/mm³ in slight vasospasm group. In severe vasospasm-developed animals, mean volume value of ASA was 0.540±0.90 [corrected]mm³ and the normal neuron density of C3DRG fell to 5,500 ± 360/mm³. An inverse relationship between the degenerated neuronal density of the C3DRG and ASA volume values may indicate the severity of ASA vasospasm. CONCLUSION: The neuron density of C3DRG may be an important factor on the regulation of ASA volume values and the continuation of spinal cord blood flow. Low neuron density of C3DRG may be considered as an important factor in the pathogenesis of severe ASA vasospasm in SAH.

Mechanism of cerebral fat embolism in subarachnoid hemorrhage: an experimental study.

Subarachnoid hemorrhage (SAH) may cause neurogenic pulmonary edema (NPE), and chylomicron metabolism may be destroyed in injured lungs. We aimed to investigate the effect of neurogenic pulmonary edema (NPE), if present, on the development of cerebral fat embolism. This study has been conducted on 20 rabbits. Experimental SAH has been applied to half of the animals by injecting homologous blood into the cisterna magna, and the remaining half was applied only isotonic saline solution in the same manner under general anesthesia. After 20 days, all animals were killed. Their lungs and brains were examined histopathologically. Six animals died of SAH between 16 and 20 days, and foamy hemorrhagic parenchymal lesions and intra-alveolar hemorrhage were observed in their lungs. Fat globules were abundantly found in cerebral arteries of six of all the non-surviving animals. But, minimal histopathological changes were found in the lungs and brains of the surviving animals. Cerebral fat embolism was detected in only one animal that was given isotonic solution. SAH may cause NPE and result in lung tissue destruction. Chylomicron metabolism may be disordered in the destructed lungs and leakage of chylomicrons into systemic circulation may be facilitated via destroyed lung barrier. These pathologic processes may lead to cerebral fat embolism.

Histopathologic evaluation of neurogenic pulmonary edema after subarachnoid hemorrhage in rabbits.

OBJECTIVE: To investigate the effects of subarachnoid hemorrhage (SAH) on lung tissue. METHODS: We conducted this study on 20 rabbits in the Ataturk University Medical Faculty, Erzurum, Turkey in 2005. Experimental SAH was applied to all animals under general anesthesia. After 20 days, all animals were sacrificed. Their lungs were examined histopathologically. RESULTS: Foamy hemorrhagic parenchymal lesions, alveolar rupture, and subintimal fluid collection in the pulmonary vasculature were observed in the lungs of the non-surviving animals. However, minimal changes were found in the lungs of the surviving animals (p<0.01). CONCLUSION: Our results suggest that luminal narrowing of the lung vessels due to subintimal fluid collection plays an important role in the development of pulmonary hypertension and neurogenic pulmonary edema in SAH.

Disappearance of phantom limb pain during cauda equina compression by spinal meningioma and gradual reactivation after decompression.

UNLABELLED: We describe a 65-yr-old woman, whose right lower limb had been amputated at the mid-femoral level because of complicated femur fracture sustained at the age of 5 yr. After amputation, she experienced phantom limb pain (PLP), which gradually decreased in intensity but persisted for 60 yr. At this point the pain diminished progressively, in parallel with the evolution of cauda equina compression caused by an intraspinal tumor. The PLP gradually reappeared over 3 mo after surgical removal of the tumor. IMPLICATIONS: We present a case in which phantom limb pain (PLP) in an amputated leg disappeared during cauda equina compression by meningioma and reactivated after surgical decompression. This case suggests that complete compression or blockade of nerves, a nerve plexus, the cauda equina, or the medullary cord may result in suppression of PLP, and decompression of or recovery from the block may cause reactivation.

Malignant peripheral nerve sheath tumor of the orbit: case report and literature review.

A 68-year-old woman with progressive visual loss and exophthalmos in her right eye had been operated on for a mass in her right calf 3 years earlier. Imaging showed a huge mass invading the orbital structures and temporal pole. The presumptive diagnosis was a malignant orbital tumor. The tumor was resected totally and eroded tissues such as the lateral rectus muscle and dural compartments were repaired. The histological diagnosis was a malignant peripheral nerve sheath tumor (MPNST). The patient recovered uneventfully and was discharged 8 days after surgery. Two years later she died from a liver tumor. Few MPNSTs involving the orbit have been reported.