Here we report an anterior thoracic meningocele case. Twoyears- old female patient was presented with kyphosis. Azygos lobe of the lung was also demonstrated during radiological studies. Posterolateral thoracotomy incision and extralpeural approach was performed for excision of the anterior meningocele to untether the cord. Although both anomalies are related to faulty embryogenesis and it is well known that faulty embryogenesis may also reveal coexisting abnormalities, we could not speculate a common mechanism for anterior thoracic meningocele and azygos lobe of the lung association.

Background - Huntington’s disease is a progressive disease in which neurodegeneration is on-going from the early presymptomatic phase. Development of sensitive biomarkers in this presymptomatic stage that are able to monitor the disease progression and test the efficacy of putative neuroprotective treatments are essential. Methods - Seven presymptomatic Huntington mutation carriers and ten age-matched healthy controls were recruited. Six of the patients participated in a 24 months longitudinal study having MRI scans 12 and 24 months after the baseline measurements. High resolution T1 weighted images were carried out and voxel based morphometry was used to analyse the data. Apart of group differences, correlation of CAG repeat number with focal cortical thickness and with global gray matter volume was calculated. Results - Focal cortical atrophy was found bilaterally in the superior temporal sulcus and in the left middle frontal gyrus in presymptomatic Huntington patients in whom no sign of cognitive or motor deterioration was detected. Global gray matter atrophy (p<0.048) and decreased total brain volume was found. The number of CAG triplets showed no correlation with the focal gray matter atrophy and total brain volume. Strong correlation between the CAG repeat number and global gray matter volume was found (p<0.016). Conclusion - Cortical atrophy is apparent in the early, presymptomatic stage of the disease. With further validation in large patient sample atrophy measure could be biomarker of disease progression and putatively of neurodegeneration.

[Meningiomas are one of the most frequent primary intracranial tumours, representing one-third of all intracranialneoplasms. The vast majority of meningiomas are histologically benign, but recurrence and progression is quite frequent. They occur usually between the 6th and 7th decade, the female/male ratio is 3:2. Although rare in pregnancy, when occurring, they can cause serious, life-threatening complications due to rapid growth and unfavourable localisation. There are two dominant hypothesis explaining rapid growth in pregnancy: the role of hormonal effects and hemodynamic changes. Several studies tested these theories but none provided unequivocal answer probably because the pathomechanism is complex and multifactorial. We provide an overview of the pathomechanism of meningiomas in pregnancy with emphasis on data obtained by advanced neuropathological, molecular biological, bioinformatic, imaging and epidemiological methods. A better understanding of the processes leading to meningioma development and growth in pregnancy will help us to design personalized therapy and reduce morbidity and mortality.]

[Data of our 254 patients who were treated with rt-PA between 1st of Jan, 2011 and 31st of Dec, 2014 were processed. We focused on angioneurotic oedema as allergic complication of thrombolysis which caused life threatening respiratory obstruction in two cases. We describe these two patients’ history. Out of 254 patients six (2.3%) suffered angioneurotic edema caused respiratory obstruction in two (0.90%) cases. This occurrence is approximately 1.3-5.1% in literature. Five, out of six patients who suffered from angioneurotic oedema, had been treated with ACE inhibitors or ARB before. The role of ACE inhibitors is known in metabolism of bradykinin cascade. Plasmin which present during thrombolysis, precipitates biochemical mechanisms of this potential life threatening complication. Therefore rt-PA alone can be the cause of angioedema, but it can be more frequent together with ACE inhibitors therapy.]

[Aim of the study - General anesthetics, arterial hypotension and hypoxia developing during anesthesia may result in impaired memory and a decline in other abilities (such as attention, concentration, linguistic and writing abilities). Our aim was to detect changes in cognitive functions due to surgery and anesthesia with controlled arterial hypotension. Materials and methods - We studied combined and intravenous anesthesia detecting pre-and postoperative cognitive functions, intraoperative haemodynamic parameters, demographic data, other data of case history and surgical data. The Montreal Cognitive Assessment test was applied in the randomized, prospective study. The preoperative data served as basis for comparison. The second test was performed following surgery when patients were fully awake. Both groups included 30 patients. Results and conclusion - After both narcosis methods (postoperative second hour) cognitive functions were significantly deteriorated (p<0.05). Median MoCA before sevoflurane anesthesia was 24 points (interquartile range: 22-25), postoperative value was 20 (19-21) (p<0.05). Median MoCA before propofol anesthesia was 24 points (23-26), postoperative value was 20 (18-22) (p<0.01). Intraoperative arterial blood pressure, pulse rate and oxygen saturation values did not correlate with worsening of cognitive function (Pearson correlation coefficient values between -0.19 and 0.42). Execution is influenced by age (negative correlation) and education (positive correlation).]