Mother-Infant Bonding in Patients with Bipolar Disorder.

Introduction: The quality of mother-infant bonding might play a role in future psychopathologies of the infant. The present study aims to compare the mother-infant bonding in mothers with remitted bipolar disorder (BD) and healthy mothers. Methods: We included 51 mothers who have bipolar disorder in remission and 53 healthy mothers during postpartum one-year period. All participants were interviewed with Structured Clinical Interview for DSM-IV (SCID-IV). Young Mania Rating Scale and the Hamilton Depression Rating Scale were given to the patient group to evaluate depressive and manic symptoms. Mother-infant bonding in both groups were evaluated with the Postpartum Bonding Questionnaire (PBQ). Results: There was no significant difference in PBQ scores between the bipolar group and the control group. Age was negatively correlated with PBQ scores in the patient group. Conclusion: Women with bipolar disorder can develop healthy bonding patterns with their babies, during remission.

Important interaction between urethral taste bud-like structures and Onuf's nucleus following spinal subarachnoid hemorrhage: A hypothesis for the mechanism of dysorgasmia.

BACKGROUND: We previously postulated that orgasmic sensation may occur through recently discovered genital taste bud-like structures. The interaction between the pudendal nerve and Onuf's nucleus may be important for developing orgasmic information. The study aims to investigate whether ischemic damage to Onuf's nucleus-pudendal network following spinal subarachnoid hemorrhage (SAH) causes taste bud degeneration or not. METHODS: The study was conducted on 22 fertile male rabbits who were divided into three groups: control (GI; n=5), SHAM (GII; n=5) and study (GIII; n=12). Isotonic solution, .7cm3, for the SHAM, and .7cm3 homologous blood was injected into spinal subarachnoid spaces at S2 level of the study group. Two weeks later, Onuf's nucleus, pudendal ganglia and the taste bud-like structures of the penile urethra were examined histopathologically. Degenerated neuron densities of Onuf's nucleus, pudendal ganglia and atrophic taste bud-like structures were estimated per mm3 and the results analyzed statistically. RESULTS: The mean degenerated neuron densities of taste bud-like structures, Onuf's nucleus and pudendal ganglia were estimated as 2±1/mm3, 5±1/mm3, 6±2/mm3 in GI; 12±4/mm3, 35±9/mm3, 188±31/mm3, in GII and 41±8/mm3, 215±37/mm3, 1321±78/mm3, in GIII. Spinal SAH induced neurodegeneration in Onuf's nucleus, pudendal ganglia and taste bud atrophy was significantly different between GI/GII (p<.005); GII/GIII (p<.0005) and GI/GIII (p<.0001). CONCLUSION: Ischemic neuronal degenerations of Onuf's nucleus and pudendal ganglia following spinal SAH lead to genital taste bud-like structure atrophy. This mechanism may be responsible for sexual anhedonia and sterility in cases with spinal cord injury, which has not been documented so far. More studies are needed.

Comparison of Metacognitive Beliefs Between Patients with Unipolar Depression and Bipolar Depression

ABSTRACT Objective: The aim of this article is to compare differences in metacognitive beliefs between bipolar disorder type I depressed (BPD1) patients with Unipolar Depression (UPD) patients, and a control group; and to discuss the relationship between metacognitive beliefs and depression parameters. Methods: Sixty six consecutive outpatients with a diagnosis of depressed BPD1, 70 patients with UPD and 70 healthy controls were enrolled in the study. Following assessment with the Sociodemographic Data Form, Structured Clinical Interview for DSM-IV (SCID-I), Hamilton Depression Rating Scale (HAM-D), Hamilton Anxiety Rating Scales (HAM-A), Young Mania Evaluation Scale, and the Metacognition Questionnaire-30 (MCQ-30). Results: UPD and BPD1 patients included in the study had higher scores in metacognitive beliefs other than positive beliefs compared with healthy controls (p<0.05), but no significant difference was found between the BPD1 and UPD groups (p>0.05). A statistically significant positive correlation was observed between the HAM-A, HAM-D scores and MCQ-30 scores in UPD group (p<0.05) but not in BPD1 group (p>0.05). Discussion: The metacogitive structures of UPD and BPD1, may be helpful in identifying and choosing the right treatment modality. We think that our results may have implications for the metacognitive approaches in the treatment of BPD1.

Toward the first definition of taste rosea in female breasts: histological analysis / La primera definición del sabor rosea en mamas femeninas: análisis histológico

Although various neuropsychochemical theories have been established about why breastfeeding mothers feel hedonic sensation, the underlying neural mechanism has not been adequately clarified. We aimed to investigate if there is hedonic sensation-initiated taste-bud like structures stimulated by sugars in the milk-secreting lactiferous ducts of mammary glands of breastfeeding female rats. In this study, twenty-two female rats were chosen which six of the virgin (n=6), six of pregnant (n=6) and ten of breastfeeding (n=10). We examined lactiferous ducts/nipples of mammary glands of all animals. They were sacrificed following intracardiac formalin injection, and their breast tissues were removed with covering tissues and fixed with 10 % of formalin solution. After current histological procedures, the tissues were examined by light microscope to assess taste-bud like structures, and their numerical densities were calculated by using stereological methods. Results were analyzed statistically. Taste-buds like structures with neuron-like appendages at the apical ends were discovered in lactiferous ducts. The taste rosea numbers were estimated as 3±1/mm3 in virgins, 167±27/mm3 in pregnant and 375±63/mm3 in breastfeeding animals. The taste rosea numbers were greater in breastfeeding rats than those of virgins and pregnant rats. They named as taste rosea resembling flower bucket which has not been mentioned in the literature so far.

Existen varias teorías neuropsicoquímicas, referente a la sensación hedónica que sienten las mujeres al amamantar, y el mecanismo neural subyacente. No obstante, estas aún no se aclaran adecuadamente. El objetivo de este estudio, fue investigar si existen estructuras hedónicas iniciadas por la sensación gustativa estimuladas por los azúcares en los conductos mamarios secretores de leche, de las glándulas mamarias de las ratas durante el período de lactancia. En este estudio, se eligieron 22 ratas hembras, seis de estas no preñadas como grupo control, seis preñadas y diez en período de lactancia. Examinamos los conductos lactíferos / pezones de las glándulas mamarias de los tres grupos. Los animales fueron sacrificados por medio de inyección intracardíaca de formalina. El tejido mamario se fijó en solución de formalina al 10 %. La muestras histólogicas fueron examinadas a través microscopía óptica con la finalidad de evaluar estructuras con características morfológicas similares a las papilas gustativas. Su densidad de número se calculó utilizando métodos estereológicos. Los resultados fueron analizados estadísticamente. En los conductos mamarios se observaron dos estructuras con con características morfológicas tipo papilas gustativas con apéndices neuronales en los extremos apicales. Los números se estimaron en 3±1/mm3 en el grupo control, 167±27/mm3 en gestantes y 375±63/mm3 en animales lactantes. El número de estructuras características morfológicas similares a las papilas gustativas fue mayor en las ratas amamantando que en el grupo control y que en las ratas preñadas. Conocido como sabor rosea debido a que se asemeja a un ramo de flores, lo que hasta ahora no se ha mencionado en la literatura.

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.

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

BACKGROUND: Cardiac 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). METHODS: Twenty-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. RESULTS: The 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). CONCLUSIONS: Normal cardiac ganglia numbers and/or cardiac ganglia neuron density may be related to cardiac survival following brain death after subarachnoid hemorrhage.

Olfactory bulbectomy and raphe nucleus relationship: a new vision for well-known depression model.

Background/aim: The olfactory bulbectomy (OBX) technic is a well-known animal model for depression. According to serotonin hypothesis of depression, one of the possible explanations to this mechanism is the destroying effect of OBX on raphe nuclei which especially include serotonergic neurons. In this study, we aimed to explore histopathological findings in raphe nuclei in OBX rats.Materials and methods: Forty-eight rats (8 control group, 10 sham group, and 30 as the study group) were used. No procedure was applied to the control group. Only frontal burr holes were performed at the level of olfactory bulbs (OBs) on the sham group. Mechanical OBX by compression was applied to 20 rats and the OBs of 10 rats were cauterized. Their OBs, olfactory cortices, raphe nuclei were extracted, tissue specimens were taken than examined by using histopathological methods including hematoxylin and eosin, S-100, and TUNEL staining. Physical dissector method was used to evaluate the number of living and apoptotic neurons in the raphe nuclei.Results: Prominent neuronal loss and morphological changes in the dorsal raphe nuclei were detected in study groups.Conclusion: Raphe nuclei degeneration, related alterations in neurotransmitter system activities and functional brain connectivity might be related to neurobiology of depression.

Neurogenic Stress Cardiomyopathy Following Subarachnoid Hemorrhage Is Associated with Vagal Complex Degeneration: First Experimental Study.

BACKGROUND: Neurogenic stunned myocardium (NSM) is a devastating complication of subarachnoid hemorrhage (SAH). The most widely accepted mechanism in the pathogenesis of NSM and takotsubo cardiomyopathy is catecholamine-mediated direct myocardial injury. The aim of this study is to examine if there is any effect of sympathetic overactivity of the stellate ganglions on myocardial tissues, secondary to vagal complex degeneration in SAH-induced NSM. MATERIALS AND METHODS: This study was conducted on 25 New Zealand female rabbits. After the examination, all animals were assigned into 3 groups randomly: a control group (n = 5), a sham group (n = 5), and a study group (n = 15) that was subjected to experimental SAH with double injection of blood into the cisterna magna. After 7 animals exhibited NSM, all animals were killed. Their brains, vagal complexes, stellate ganglions, and hearts were extracted and examined by histopathologic methods. Degenerated nodose ganglion neurons and stellate ganglion neuron densities were compared with degenerated myocardial tissue/normal myocardial tissue ratios, and the results were analyzed with the Mann-Whitney U test. RESULTS: Three rabbits in the study group died immediately after the second injection of blood. NSM developed in 7 animals after 1 to 5 days, which was diagnosed with transthoracic echocardiography. Interestingly, the animals that developed NSM had more stellate ganglia neurons and more degenerated neuron densities of nodose ganglia (P < 0.001). CONCLUSIONS: NSM and takotsubo cardiomyopathy may be induced by vagal complex degeneration and sympathetic overactivity, which originated from more neurons, including stellate ganglia and more degenerated neuron densities of nodose ganglia.

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.

Effect of monoamine oxidase B A644G variant on nicotine dependence and/or schizophrenia risk

Abstract Objectives Schizophrenia (Sch) is a severe and chronic mental illness. Smoking prevalence is higher in patients with Sch than general population. We aimed to investigate the effects of MAOB gene A644G variant on nicotine dependence (ND) and Sch+ND risk in Turkish population and to evaluate by bioinformatic analysis. Methods Present study included 161 individuals with ND, 223 patients with Sch+ND, and 96 non-smoker controls. MAOB A644G variant was analyzed using PCR-RFLP method. As the MAOB gene is located on the X chromosome, each gender was analysed separately. Results The total distributions of AA, AG and GG genotypes of MAOB gene A644G were 44.7%, 22.4% and 32.9% in the ND group, 45.3%, 25.1% and 29.6% in the Sch+ND group and, 44.8, 22.9% and 32.3% in non-smoker controls. No significant differences were observed between groups for the MAOB A644G genotype and allele frequencies when female group compared to male group (p > 0.05). Examination of disease associations of SNPs from each miRNA gene region in GWAS databases yielded results for aging, bipolar disorder, autoimmune, and neurological diseases. Discussion Our results indicate that the MAOB gene A644G variant is not associated with ND and/or Sch susceptibility in the Turkish population.

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.

Understanding of Dry Eye in Subarachnoid Hemorrhage: An Experimental Study on the Role of Facial Nerve Ischemia.

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.

Exploring of the Unpredicted Effects of Olfactory Network Injuries on Mammary Gland Degeneration: A Preliminary Experimental Study.

Purpose of the study: Hypofunctioning breasts are typically considered a dysfunction of higher brain centers that regulate hormonal feedback, and olfactory information has been proposed as a triggering factor for lactation in the maternal body. However, there are no substantive studies regarding whether olfaction disorders and/or loss of olfactory sense may result in breast gland atrophy by causing diminished olfactory stimulation. To fill this gap in the literature, we studied the histologic features of breast glands as a sample model in animals that had undergone an olfactory bulb lesion (OBL). Materials and methods: This study was conducted on 22 rats. Six, eight, and six of them were used as control, SHAM, and OBL groups, respectively. After 10 weeks, the animals were decapitated. Olfactory bulbs and breast glands were stained with Hematoxylin-eosin and tunnel dye. Specimens were analyzed stereologically to evaluate the loss in volume of the olfactory bulbs, total breast follicle volume (TBFV) and Meissner's corpuscles per cubic centimeter, and these two senior metrics were compared with each other statistically. Results: Olfactory bulb volume loss and breast gland atrophy were both detected in study group. Mean TBFV and OB volumes were measured as: (296 ± 89) × 106 µm3/cm3 and 4.43 ± 0.98 mm3 in control (Group I); (264 ± 63) × 106 µm3/cm3 and 3.86 ± 0.81 mm3 in SHAM (Group II) and (194 ± 52) × 106 µm3/cm3 and 1.52 ± 0.36 mm3 in OBL group (Group III). It was noted that the TBFV was significantly diminished, with apoptotic degradation in the olfactory bulbs and breast glands of OBL-applied animals (p < 0.001). Conclusion: It seems that diminished milk secretion is attributable to the degradation of breast glands that results from olfaction loss in OBL animals.

XRCC4 rs6869366 polymorphism is associated with susceptibility to both nicotine dependence and/or schizophrenia

Abstract Background: Oxidative stress induced DNA damage has been assumed to contribute to the etiopathogenesis of schizophrenia (Sch). Smoking prevalence was more common in patients with Sch. The X-ray repair cross-complementation group 4 (XRCC4) gene plays an important role in the repair of DNA double-strand breaks. Objective: The purpose of this study was to investigate whether XRCC4 rs6869366 polymorphism has a relationship both in nicotine dependence (ND) and Sch+ND risk. Methods: One hundred and four patients with Sch+ND, 133 subjects with ND only and 70 healthy controls were enrolled in the study. XRCC4 rs6869366 polymorphism was analyzed using PCR-RFLP assay. Results: The frequency of XRCC4 rs6869366 GG genotype was more common in the ND and Sch+ND group than controls (p = 0.001 and p = 0.001, respectively). XRCC4 rs6869366 TT genotype was lower in both ND and Sch+ND group compared to controls (p = 0.001 and p = 0.001, respectively). Also, XRCC4 rs6869366 G allele was higher in Sch+ND group than controls (p = 0.001) while XRCC4 rs6869366 T allele was lower in ND group than healthy controls (p=0.001). XRCC4 rs6869366 GT genotype was lower in ND group than control group (p = 0.003). Discussion: These results suggested that the XRCC4 rs6869366 polymorphism G related genotype/allele was associated with susceptibility to both ND and Sch+ND in a Turkish population.

Uncovering the Forgotten Effect of Superior Cervical Ganglia on Pupil Diameter in Subarachnoid Hemorrhage: An Experimental Study.

AIM: To investigate the relationship between neuron density of the superior cervical sympathetic ganglia and pupil diameter in subarachnoid hemorrhage. MATERIAL AND METHODS: This study was conducted on 22 rabbits; 5 for the baseline control group, 5 for the SHAM group and 12 for the study group. Pupil diameters were measured via sunlight and ocular tomography on day 1 as the control values. Pupil diameters were re-measured after injecting 0.5 cc saline to the SHAM group, and autologous arterial blood into the cisterna magna of the study group. After 3 weeks, the brain, superior cervical sympathetic ganglia and ciliary ganglia were extracted with peripheral tissues bilaterally and examined histopathologically. Pupil diameters were compared with neuron densities of the sympathetic ganglia and ciliary ganglia which were examined using stereological methods. RESULTS: Baseline values were; normal pupil diameter 7.180±620 ?m and mean neuron density of the superior cervical sympathetic ganglia 6.321±510/mm3, degenerated neuron density of ciliary ganglia was 5±2/mm3 after histopathological examination in the control group. These values were measured as 6.850±578 ?m, 5.950±340/mm3 and 123±39/mm3 in the SHAM group and 9.910±840 ?m, 7.950±764/mm3 and 650±98/mm3 in the study group. A linear relationship was determined between neuron density of the superior cervical sympathetic ganglia and pupil diameters (p < 0.005). Degenerated ciliary ganglia neuron density had an inverse effect on pupil diameters in all groups (p < 0.0001). CONCLUSION: Highly degenerated neuron density of the ciliary ganglion is not responsible for pupil dilatation owing to parasympathetic pupilloconstrictor palsy, but high neuron density of the pupillodilatatory superior cervical sympathetic ganglia should be considered an important factor for pupil dilatation.

How Reliable Is Pupillary Evaluation Following Subarachnoid Hemorrhage? Effect of Oculomotor Nerve Degeneration Secondary to Posterior Communicating Artery Vasospasm: First Experimental Study.

BACKGROUND AND STUDY AIM: Basic neurophysiologic principles of the light reflex are well known. However, the effects of degenerated axon densities of oculomotor nerves (OMNs) secondary to posterior communicating artery (PComA) vasospasm following subarachnoid hemorrhage (SAH) have not been investigated. Our aim was to study this subject. METHODS: This study was conducted on 19 rabbits. There was a control group of five animals, a sham group of five animals in which saline was injected into the cisterna magna and a study group of nine animals in which homologous blood was injected into the cisterna magna. Pupillary diameters were measured for 1 week, then the animals were decapitated. The normal and degenerated axon densities of the OMNs were examined by stereological methods. Vasospasm indexes (VSIs) of posterior communicating arteries (PComAs) supplying OMNs were estimated and analyzed statistically. RESULTS: The pupillary diameter was 5.439 ± 368 µm, and the mean axon density of the OMNs was 0.924 ± 324/mm3 in the control group. The pupillary diameter and degenerated axon density of the OMNs in animals of the sham group were 6.980 ± 0.370 µm and 36 ± 8/mm3, respectively. The pupillary diameter was 9.942 ± 653 µm, and degenerated axon density of the OMNs was 265 ± 57/mm3 in animals with SAH. The mean VSI values of PComAs were 0.927 ± 0.224 in the control group, 1.542 ± 0.257 in the sham group, and 2.321 ± 0.324 in the SAH group. CONCLUSION: We found a linear relationship between the axon density of the OMNs and pupillary diameters. High degenerated neuron density in the OMNs may be responsible for an unresponsive pupillary that has not been mentioned in the literature.

The sooth beneath the taste roseas in the urethra and first description of neuro-morpho-chemical mechanism of penile erectile posture in males: an experimental study.

AIM: The morphologic mechanism of orgasmic sensation has not yet been understood. Taste roseas may be stimulated by fructose via pudendal nerves, which has not been studied yet. METHODS: In this study, 27 male adult rabbits were used, which were divided into three groups: 5 as control; 5 as SHAM and 17 used as study group. We injected 0.2 cc of distilled water to SHAM and 0.2 cc of fructose solution to the study group of their urethral orifices, and examined the occurrence of penile erection. The relationship between erection and pudendal nerve ganglia and penile tissues was statistically compared. RESULTS: In animals with high neuron density of pudendal ganglia, more erection phenomenon was observed than those animals with low neuron density. Interestingly, neuron density of pudendal ganglia was 9.243 ± 542 /mm3 in hypoactive and was 5.980 ± 463 /mm3 in non-active animals (p < 0.05). CONCLUSIONS: The seminal fructose may stimulate taste roseas of the urethra and glans penis via pudendal nerves. The present study describes a new neuro-morpho-chemical mechanism of orgasmic sensation with its neurosurgical aspect.

Rationalization of the Irrational Neuropathologic Basis of Hypothyroidism-Olfaction Disorders Paradox: Experimental Study.

OBJECTIVE: Hypothyroidism is defined as an underactive thyroid gland and one of the reasons for inadequate stimulation of thyroid is dysfunction of the hormone regulating brain centers. Olfaction disorders have been considered as a problem in hypothyroidism. It has been hypothesized that olfaction disorders reduce olfactory stimulation and diminished olfactory stimulus may trigger hypothyroidism. In this study, an examination was made of the thyroid hormone levels, histologic features of thyroid glands, and vagal nerve network degradation in an experimental animal model of olfactory bulbectomy (OBX). METHODS: A total of 25 rats were divided into control (n = 5), SHAM (n = 5), and OBX (n = 15) groups and were followed up for 8 weeks. Thyroid hormone levels were measured before (1 time), during the experiment (1 time/month) and the animals were decapitated. The olfactory bulbs, dorsal motor nucleus of the vagal nerves, and thyroid gland sections were stained with hematoxylin-eosin and tunnel dye to determine OBX-related damage. Specimens were analyzed stereologically to evaluate neuron density of the vagal nucleus and hormone-filled total follicle volume (TFV) per cubic centimeter, and these were statistically compared with thyroid hormone levels. RESULTS: The mean degenerated neuron density of the vagal nucleus was 21 ± 8/mm3. TFV and triiodothyronine (T3)-thyroxine (T4) levels were measured as TFV, (312 ± 91) × 106µm3/cm3; T3, 105 µg/dl; T4, 1.89 µg/dl in control (group I). Mean degenerated neuron density, 56 ± 12/mm3; TFV, (284 ± 69) × 106µm3/cm3; T3, 103 µg/dl; T4, 1.85 µg/dl in SHAM (group II). Mean degenerated neuron density, 235 ± 64/mm3; TFV, (193 ± 34) × 106µm3/cm3; T3, 86 µg/dl; T4, 1.37 µg/dl in the OBX group (group III). The TFV were significantly diminished because of apoptotic degradation in olfactory bulbs and thyroid gland with decreased T3- T4 levels with increased thyroid-stimulating hormone levels in OBX-applied animals of subarachnoid hemorrhage (P < 0.005). CONCLUSIONS: The results suggested that diminished hormone secretion as a result of thyroid gland degradation results in both olfaction loss and vagal complex degeneration in OBX animals, contrary to the common belief that anosmia results from hypothyroidism.

New Evidence for Causal Central Mechanism of Hyperglycemia in Subarachnoid Hemorrhage Secondary to Ischemic Degenerative Disruption of Circuitry Among Insular Cortex, Nodose Ganglion, and Pancreas: Experimental Study.

INTRODUCTION: Although hyperglycemia is a serious complication of subarachnoid hemorrhage, its pathophysiologic mechanism based on neural circuitry has not been known. MATERIALS AND METHODS: Twenty-five rabbits were divided into 4 groups, with 5 in the control group. The SHAM and study groups received 1 mL saline and 1 mL autologous arterial blood into the sylvian cisterna, respectively. Blood glucose values (BGVs) of all animals were recorded 3 times weekly. After 2 weeks, animals were decapitated. BGVs, the number of normal and degenerated neuron densities (DNDs) of insular cortex (IC), and nodose ganglia, degenerated islands of Reil's surfaces values, were estimated by stereologically and analyzed statistically. RESULTS: The mean blood glucose values were measured as 101 ± 10 mg/dL in the control group (n = 5), 114 ± 11 mg/dL in the SHAM group (n = 5), and 137 ± 12 mg/dL in the subarachnoid hemorrhage (SAH) group (n = 15). The DND of the nodose ganglion was 10 ± 3/mm3 in the control group, while it was 45 ± 7/mm3 in the SHAM group and 1688 ± 191/mm3 in the SAH group. The DND of the IC was 65 ± 12/mm3 in the control group, 689 ± 112/mm3 in the SHAM group, and 3709 ± 643/mm3 in the SAH group. In addition, the proportion of degenerated surface areas in the islet of Langerhans was 0.3% in the control group, 6% in the SHAM group, and 28% in the SAH group. CONCLUSION: There is an important linear relationship among the blood glucose levels, DND of the IC, and nodose ganglia and degenerated surface areas of IL following experimentally induced sylvian SAH.

A New Determinant of Poor Outcome After Spontaneous Subarachnoid Hemorrhage: Blood pH and the Disruption of Glossopharyngeal Nerve-Carotid Body Network: First Experimental Study.

OBJECTIVE: The chemoreceptor network, consisting of the glossopharyngeal nerve and carotid body (GPN-CB), is essential for the regulation of blood pH. Its ischemic insults after subarachnoid hemorrhage (SAH), which may contribute to acidosis, have not been investigated. METHODS: Twenty-three hybrid rabbits were used. They were divided into 3 groups: 5 as a control group, 5 as a sham group, and the remaining 13 as the study group. Injections included 1 cm3 serum saline and 1 cm3 autolog arterial blood into the cisterna magna in the sham and study group, respectively. Blood pH values of all animals were recorded. After 2 weeks, animals were euthanized. The number of normal and degenerated neurons of the carotid bodies (CBs) was counted by stereologic methods and analyzed statistically. RESULTS: Two of 13 rabbits died within the second week. The mean blood pH values were measured as 7.35 ± 0.07 in the control group (n = 5), 7.33 ± 0.06 in the sham group (n = 5), 7.29 ± 0.05 in rabbits with slight acidosis (n = 6), and 7.23 ± 0.02 in rabbits with prominent acidosis (n = 7). In the control group, the average normal neuronal density of the CBs was 6432 ± 790/mm3 and the degenerated neuron density was 11 ± 3/mm3, whereas the degenerated neuronal density in CBs was 35 ± 8/mm3 in the sham group and 1034 ± 112/mm3 in the slight acidosis-developed group (n = 6; P < 0.05). Conversely, degenerated neuron density of CBs was 2134 ± 251/mm3 in the prominent acidosis-developed animals (n = 7; P < 0.005). Interestingly, in the rabbits who died, the degenerated neuron density of the CB was 3160 ± 840/mm3. CONCLUSION: An inverse relationship between neurodegeneration in the CB and pH values secondary to the disruption of the GPN-CB network after SAH was found, which may contribute to developing acidosis.