Nitric oxide (NO) molecules have one of the most important roles in the pathogenesis of multiple sclerosis (MS). It has been stated that a continuous and high concentration of NO metabolites in CSF and in the serum of MS patients in relapse may cause toxic damage to myelin and oligodendroglia. The aim of this study was to investigate whether NO is a marker of disease activity and is correlated with other disease activity markers such as active lesions on brain magnetic resonance imaging (MRI) and increased immunoglobulin G (IgG) index. Cerebrospinal fluid (CSF) and peripheral serum (PS) samples were taken from patients with definite MS (n = 24) during relapse and remission and from control subjects (n = 18). The Griess reaction was used to measure the NO metabolites, nitrite and nitrate in CSF and PS. Cranial MRI was carried out with triple dose (0,3 mmol/kg) gadolinium and the IgG index was determined. Nitrite and nitrate concentrations (NNCs) of CSF were 11.16 +/- 8.60 micromol/ml in relapse and 6.72 +/- 3.50 micromol/ml in remission, whereas in PS they were 12.89 +/- 7.62 micromol/ml during relapse and 12.35 +/- 6.62 micromol/ml during remission. In control subjects NNCs in CSF and PS were 7.42 +/- 2.81 micromol/ml and 4.37 +/- 1.63 micromol/ml respectively. NNCs in CSF during relapse period were significantly higher than those of both remission phase and control subjects (p = 0.000). Although serum NNCs did not differ in relapse and remission, they were still higher than normal controls. Validity analysis revealed that NNC measurement in CSF was 71 % specific and 66 % sensitive to disease activity. The most important result was the significant correlation of increased NNCs with the existence of active lesion in cranial MRI and an increase in IgG index (p < 0.05).In conclusion, these results add background data to assist in further outlining the possible role of NO in the pathogenesis of MS. Together with the other markers it may be used as an activity marker in relapses of MS.

Case Presentation: A 54-year-old male patient presenting probable multiple system atrophy with predominant parkinsonism who underwent bilateral deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) is presented. The patient had dominant freezing of gait (FOG), levodopa-resistant bradykinesia, and autonomic disturbances, but with a good cognitive condition. Methods: The patient underwent bilateral DBS of the PPN, which ended with modest benefits. Results and Conclusion: Although he had a short postoperative follow-up (6 months), his neurological status remained stable and PPN DBS provided modest improvements in the gait disorder and freezing episodes. This unusual case suggests that the mesencephalic pedunculopontine region may have a role in locomotor symptoms and the potential to provide a limited improvement in FOG.

The aim of this study was to retrospectively determine if patients with medically refractory epilepsy, due to hippocampal sclerosis, who underwent selective amygdalohippocampectomy (SAH) with a transcortical approach experienced improved seizure outcome. Thirty-nine patients with mesial temporal lobe epilepsy and hippocampal sclerosis were included in the study. The mean follow-up was 25.88 ± 17.69 months. Antiepileptic medication use and seizure frequency were significantly reduced after SAH. After surgery, 32 patients (82.05%) were completely seizure free (Engel class IA), and 2 patients experienced transient memory difficulty. In conclusion, SAH with a transcortical approach can lead to favorable seizure control with a low irreversible complication risk.

AIm:The molecular mechanism of epileptogenesis in temporal lobe epilepsy is still unclear. Experimental studies have suggested that matrix metalloproteinases have important roles in this process, but human studies are limited. The aim of this study was to assess the expression of MMP-9, MMP-2 and their tissue inhibitors (TIMP-1 and TIMP-2) in patients with temporal lobe epilepsy with hippocampal sclerosis (TLE-HS). mAterIAl and methOds:The tissue samples from temporal neocortex and hippocampus were obtained from patients with temporal lobe epilepsy with hippocampal sclerosis who had undergone anterior temporal lobectomy for recurrent medically resistant seizures. Immunohistochemical methods were used to determine the expression of MMP-9, MMP-2 and their tissue inhibitors. Tissue samples were also analyzed with transmission electron microscopy. results:The immunoreactivity for MMP-9 both in hippocampal and temporal neocortical neurons was stronger than that of MMP-2. Additionally, there was a mild reaction for its tissue inhibitor TIMP-1 as with TIMP-2. The TEM analysis of the hippocampus revealed that there was apparent ultra-structural damage on the pericarya and neuropil of some neurons. There was obvious damage in the mitochondria and the nuclear membrane. COnClusIOn:The preliminary results of this study revealed that MMP-9 may have a role in patients with drug resistant TLE-HS. KeywOrds:Hippocampal sclerosis, Matrix metalloproteinase-9, Temporal lobe epilepsy ÖZ AmAÇ: Temporal lob epilepsisinde moleküler epileptogenez mekanizmalar halen tam anlaşılamamıştır. Deneysel çalışmalar matriks metaloproteinazların bu süreçte önemli rolü olduğunu ileri sürmektedir, ancak bu konuda insan çalışmaları kısıtlıdır. Çalışmanın amacı, hipokampal sklerozun eşlik ettiği temporal lob epilepsisi (TLE-HS) olan hastalarda MMP-9, MMP-2, TIMP-1 ve TIMP-2 ekspresyonunu değerlendirmektir. yÖntem ve GereÇler: İlaca dirençli epilepsi nedeniyle anterior temporal lobektomi yapılan TLE-HS hastalarından alınan hipokampus ve temporal neokorteks dokuları kullanıldı. MMP-9, MMP-2, TIMP-1 ve TIMP-2 ekspresyonunu incelemek için immünohistokimyasal yöntemler kullanıldı ve dokular transmisyon elektron mikroskopisiyle incelendi.BulGulAr: MMP-9 immünoreaktivitesi hem hipokampal hem de neokortikal nöronlarda MMP-2'ye göre daha güçlü bulundu. Doku inhibitörüü olan TIMP-1'in de ılımlı bir immünoreaktivite gösterdiği tespit edildi. TEM analizinde hipokampal nöronlarda özellikle mitokondriyal ve nükleer membranın belirgin derecede hasara uğradığı tespit edildi.sOnuÇ: Çalışma, MMP-9'un TLE-HS'da rol oynayabileceğini düşündürmektedir.AnAhtAr sÖZCÜKler: Hipokampal skleroz, Matriks metalloproteinaz-9, Temporal lob epilepsi

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