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.

Isolated abducens nerve palsy due to pituitary apoplexy after mild head trauma.

Pituitary apoplexy is a relatively rare condition. Cranial nerve palsies may develop due to compression of the surrounding structures by the rapidly expanding tumor. While the most commonly affected nerve is the oculomotor nerve, abducens nerve palsy may also occur less commonly. A 68-year-old male patient was admitted to the emergency department with complaints of severe headache, nausea, vomiting, and diplopia after head trauma due to falling. His magnetic resonance imaging evaluation demonstrated a large pituitary adenoma and bleeding into the tumor, which was acutely expanding and leading to compression of the abducens nerve laterally. Isolated abducens palsy due to posttraumatic pituitary apoplexy is a rare clinical condition, and as the symptoms and signs are nonspecific, it can commonly remain clinically undiagnosed. In this article, our aim was to draw attention to a clinical condition in which unfavorable complications may develop if the diagnosis is overlooked.

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

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.

Syringic acid protects against thioacetamide-induced hepatic encephalopathy: Behavioral, biochemical, and molecular evidence.

The objective of this study was to elucidate the effects of syringic acid on thioacetamide-induced hepatic encephalopathy which is a complex serious syndrome with neuropsychiatric abnormalities related to acute liver dysfunctions like cirrhosis. Rats were treated with syringic acid (50 and 100 mg/kg, p.o.) for 14 days in treatment groups. Hepatic encephalopathy was induced by three doses of (200 mg/kg i.p.) thioacetamide injection. Syringic acid effectively alleviated thioacetamide-induced hepatic injury via reduction in ammonia, AST, ALT, ALP, LDH and decrease in oxidative stress (decreased MDA, ROS and increased SOD and GSH). Syringic acid also attenuated inflammatory injury by suppressing TNF-α, IL-1ß, and NF-κB and increasing IL-10. The caspase-3 expression was also down-regulated in both liver and brain tissues. Immunohistochemical results confirmed the recovery with syringic acid by downregulation of iNOS, 8-OHdG and GFAP expression. Syringic acid decreased the deteriorating effects of thioacetamide as seen by reduced ammonia concentration and also preserved astrocyte and hepatocyte structure. The behavioral test results from elevated plus maze test, similar to the open-field locomotor test results, confirmed that syringic acid can reverse behavioral impairments. In conclusion, syringic acid exerted hepatoprotective and neuroprotective effects against hepatic encephalopathy by mitigating hepatotoxicity biomarkers, exerting antioxidant, anti-inflammatory effects in addition to suppressing hyperammonemia.

Effects of valproate, carbamazepine, and levetiracetam on the antioxidant and oxidant systems in epileptic patients and their clinical importance.

PURPOSE: This study was carried out to determine the effects of valproate (VPA), carbamazepine, and levetiracetam (LEV) on antioxidant and oxidant enzyme activities and the clinical importance of these effects. METHODS: We enrolled 32 patients receiving VPA, 17 receiving carbamazepine, 8 receiving LEV, 11 on multidrug therapy, and 30 sex- and age-matched healthy volunteers. We measured the serum activities of paraoxonase and arylesterase and the levels of 8-hydroxyguanine (8-OHG) and oxidized low-density lipoprotein in all the subjects. We also determined the clinical features of the patients. RESULTS: The serum paraoxonase and arylesterase activities were significantly lower (P = 0.003 and P = 0.0001, respectively), and the oxidized low-density lipoprotein and 8-OHG levels were higher (P = 0.029 and P = 0.0001, respectively) in the patients than in the controls. The serum antioxidant activity was low, and the oxidant activity was high in the monotherapy patients (P < 0.05). Comparing the monotherapy with the polytherapy, only the combination of VPA-LEV was associated with a high 8-OHG level (P = 0.04). The serum 8-OHG level was higher in the patients taking antiepileptic drugs (AEDs) for the first 2 months than in the controls (P = 0.0001) and positively correlated with the duration of epilepsy (r = 0.387, P < 0.01). CONCLUSIONS: Oxidative stress is seen in each of the AEDs after the first 2 months. There was no dominance of the monotherapy over the polytherapy, except for the VPA-LEV combination. None of the patients' characteristic features were related to oxidative damage, except for the duration of the epilepsy and the AED therapy.

Zuclopenthixol-induced neuroleptic malignant syndrome presenting as fever of unknown origin, hyperglycaemia and acute myocardial infarction in a 60-year-old man.

Neuroleptic malignant syndrome (NMS) is a rare clinical condition and potentially life-threatening complication of antipsychotic medications. We report a patient with an atypical presentation of NMS. A 60-year-old man with schizophrenia was admitted to our hospital with disturbed consciousness, fever and marked extrapyramidal rigidity both in the upper and lower extremities. He had been given i.m. zuclopenthixol 200 mg/month but had not taken the last dose. Laboratory investigations showed that creatinine phosphokinase 428 IU/l (normal up to 130), lactate dehydrogenase 772 IU/l (normal up to 450), blood glucose 256 mg/dl (65-110). Urine analyses revealed ketonuria. White blood cell (WBC) count was 6100 cells/mm(3). Therefore, the patient was diagnosed as having NMS and antipsychotic medications were stopped. Adequate hydration was provided and bromocryptine 5 mg was started three times a day. Despite treatment, the patient died due to acute myocardial infarction after 3 days of hospitalization.