Interaction between Neurogenic Pulmonary Edema and Thoracic 3 DRG Degeneration Following Spinal Subarachnoid Hemorrhage: First Experimental Study.

BACKGROUND: Neurogenic pulmonary edema (NPE) following subarachnoid hemorrhage (SAH) is still one of the most catastrophic complications with high morbidity and mortality rates. Systemic sympathetic hyperactivity has been considered in the pathogenesis, but it has not been clarified. In this study, we investigate the relationship between the degeneration of the T3 dorsal root ganglion (DRG) and the development of NPE following spinal SAH. METHODS: The study was conducted on 23 rabbits. Five rabbits were used as the control group, 5 as the sham group (n = 5), and 13 as the study group. The correlation between the degenerated neuronal densities of the T3 nerve axons and neurons in the DRG and NPE scores was analyzed statistically. RESULTS: A correlation between the neuronal degeneration of the T3 nerve, its DRG, and high NPE scores was found in the study group and the sham group. Massive NPE was detected in the study group along with neural degeneration of T3 axons and ganglia. CONCLUSION: The present study indicates that NPE and pulmonary artery vasospasm can be prevented by reducing T3 DRG degeneration.

Hemangiopericytoma of the skull base: A long-term complete response with trimodality treatment.

Hemangiopericytoma (HPC) is a rare tumor originating from Zimmerman pericytes. It constitutes less than 1% of all intracranial tumors. Because of the high recurrence rates, radiotherapy (RT) is a vital step in the treatment, but the timing and dose remain uncertain. We presented a 39-year-old patient with a high-grade hemangiopericytoma located at the skull base. The patient presented with a severe headache. Cranial magnetic resonance imaging (MRI) revealed a mass of size of 60 × 50 mm. A subtotal resection was performed that confirmed the diagnosis of HPC. The patient received 66 Gy postoperative RT. Adjuvant sunitinib treatment was initiated after RT. The complete regression was achieved in the third month after RT. The patient has a complete response for 25 months. To our knowledge, this case is one of the rare cases in the literature in which immediate RT and adjuvant chemotherapy were used in combination with surgery. Although HPC is a radio- and chemo-resistant disease, a trimodality treatment approach can provide the patients with a complete response. In particular, patients with high-grade and inoperable tumors and patients who undergo subtotal resection should be evaluated for trimodal therapy.

Pilomatricoma Growing at the SARS-CoV-2 mRNA Vaccination Site.

A healthy 21-year-old woman was presented to our outpatient clinic with an asymptomatic swelling on her left arm. She reported the administration of two doses of BNT162b2 mRNA vaccination at the lesion site earlier. The pathology report confirmed the diagnosis of pilomatricoma. Previously, needlestick trauma and various immunisations have been attributed to the development of pilomatricoma. We present this case to emphasise the possible association between BNT162b2 mRNA vaccination and pilomatricoma development. The role of persistent inflammation is also discussed.

New histopathological evidence for the relationship between hydromyelia and hydrocephalus following subarachnoid hemorrhage: An experimental study.

Objectives: Subarachnoid hemorrhage (SAH) is a serious pathology with a high death and morbidity rate. There can be a relationship between hydromyelia and hydrocephalus following SAH; however, this subject has not been well investigated. Materials and Methods: Twenty-four rabbits (3 ± 0.4 years old; 4.4 ± 0.5 kg) were used in this study. Five of them were used as the control, and five of them as the SHAM group. The remaining animals (n = 14) had been used as the study group. The central canal volume values at the C1-C2 levels, ependymal cells, numbers of central canal surfaces, and Evans index values of the lateral ventricles were assessed and compared. Results: Choroid plexus edema and increased water vesicles were observed in animals with central canal dilatation. The Evans index of the brain ventricles was 0.33 ± 0.05, the mean volume of the central canal was 1.431 ± 0.043 mm3, and ependymal cells density was 5.420 ± 879/mm2 in the control group animals (n = 5); 0.35 ± 0.17, 1.190 ± 0.114 mm3, and 4.135 ± 612/mm2 in the SHAM group animals (n = 5); and 0.44 ± 0.68, 1.814 ± 0.139 mm3, and 2.512 ± 11/mm2 in the study group (n = 14). The relationship between the Evans index values, the central canal volumes, and degenerated ependymal cell densities was statistically significant (P < 0.05). Conclusions: This study showed that hydromyelia occurs following SAH-induced experimental hydrocephalus. Desquamation of ependymal cells and increased cerebrospinal fluid secretion may be responsible factors in the development of hydromyelia.

Important Finding for COVID-19 Pandemic: Hydrocephalus-producing effect of Vaporized Alcohol Disinfectant.

BACKGROUND: Alcohol exposure may cause hydrocephalus, but the effect of vaporized nasal alcohol exposure on the choroid plexus, and ependymal cells, and the relationship between alcohol exposure and developing hydrocephalus are not well known. This subject was investigated. METHODS: Twenty-four male (∼380 g) Wistar rats were used in this study. The animals were divided into three groups, as the control, sham and study groups. The study group was further divided into two groups as the group exposed to low or high dose of alcohol. The choroid plexuses and intraventricular ependymal cells and ventricle volumes were assessed and compared statistically. RESULTS: Degenerated epithelial cell density of 22 ± 5, 56 ± 11, 175 ± 37, and 356 ± 85/mm3 was found in the control, sham, low alcohol exposure, and high alcohol exposure groups, respectively. The Evans index was <34% in the control group, >36% in the sham group, >40% in the group exposed to low alcohol dose (low-dose alcohol group), and >50% in the group exposed to high dose of alcohol (high-dose alcohol group). CONCLUSIONS: It was found that alcohol exposure caused choroid plexus and ependymal cell degeneration with ciliopathy and enlarged lateral ventricles or hydrocephalus. In the COVID-19 pandemic era, our findings are functionally important, because alcohol has often been used for hygiene and prevention of transmission of the Sars-Cov-2-virus.

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.

BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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 (0.75 mL). 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.

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.

New description of vagal nerve commanted intrapancreatic taste buds and blood glucose level: An experimental analysis.

Introduction: There have been thousands of neurochemical mechanism about blood glucose level regulation, but intrapancreatic taste buds and their roles in blood glucose level has not been described. We aimed to investigate if there are taste buds cored neural networks in the pancreas, and there is any relationship between blood glucose levels. Methods: This examination was done on 32 chosen rats with their glucose levels. Animals are divided into owned blood glucose levels. If mean glucose levels were equal to 105 ± 10 mg/dL accepted as euglycemic (G-I; n = 14), 142 ± 18 mg/dL values accepted as hyperglycemic (G-II; n = 9) and 89 ± 9 mg/dL accepted as hypoglycemic (G-III; n = 9). After the experiment, animals were sacrificed under general anesthesia. Their pancreatic tissues were examined histological methods and numbers of newly described taste bud networks analyzed by Stereological methods. Results compared with Mann-Whitney U test P < 0.005 considered as significant. Results: The mean normal blood glucose level (mg/dL) and taste bud network densities of per cm3 were: 105 ± 10 mg/dL; 156±21 in G-I; 142 ± 18 mg/dL and 95 ± 14 in G-II and 89 ± 9 mg/dL and 232 ± 34 in G-III. P values as follows: P < 0.001 of G-II/G-I; P < 0.005 of G-III/G-I and P < 0.0001 of G-III/G-II. We detected periarterial located taste buds like cell clusters and peripherally located ganglia connected with Langerhans cells via thin nerve fibers. There was an inverse relationship between the number of taste buds networks and blood glucose level. Conclusion: Newly described intrapancreatic taste buds may have an important role in the regulation of blood glucose level.