The association between idiopathic intracranial hypertension (IIH) and obstructive sleep apnea syndrome (OSAS) constitutes an interesting point of discussion regarding clinical approaches as well as the underlying pathophysiological mechanisms. Here, the case of a 42-year-old female with malignant IIH and OSAS is illustrated. Initially, the patient was treated with lumboperitoneal shunt surgery. However, OSAS surgery provided total recovery from the recurrent symptoms developing secondary to lumboperitoneal shunt malfunction. The authors point out the importance of identifying OSAS as a crucial causative agent in some IIH subtypes. Future studies are warranted to clarify this underestimated association.

Constitutive neurogenesis affects both children and adults and is known to correlate closely with neurocognitive functions such as learning and memory [1]. Infl ammation is a systemic reaction. However, the brain reacts to infl ammation differently than peripheral tissues. Under normal conditions, the Blood-Brain Barrier (BBB) is selectively permeable and allows only the passage of T-cells, macrophages, and dendritic cells [2]. However, infl ammation of the brain initiates the secretion of anti-and pro-infl ammatory cytokines by resident microglia, astrocytes, infi ltrating peripheral macrophages, and lymphocytes. This activity both stimulates the migration of leukocytes to the region and promotes astrogliosis [3]. Pathologically, Parkinson's Disease (PD) is characterized by the massive degeneration and loss of nigrostriatal dopaminergic neurons. Many studies of PD have also emphasized the

Hamilelik döneminde ve puerperium boyunca subaraknoid kanamanın en sık nedeni intrakraniyal anevrizma rüptürüdür. Gebe kadınlarda gebe olmayan kadınlara göre beş kat daha sık görülür. Primipar gebelerde ve gebeliğin 3. trimesterinde görülme oranı daha yüksektir. Ani başlayan baş ağrısı ve bilinç kaybı ile acil servise başvuran 37 yaşında, 34 haftalık gebeye orta serebral arter anevrizması rüptürüne bağlı intrakraniyal kanama tanısı konuldu. Acil sezaryen ile doğum yaptırılan hasta subaraknoid kanama nedeniyle opere edilmiştir. Hasta nadir görülen bir olgu olması nedeniyle sunulmuştur.

BACKGROUND: Alcohol exposure may cause hydrocephalus. In this study, the effect of vaporized nasal alcohol exposure on the choroid plexus, ependymal cells, and developing hydrocephalus was investigated. METHODS: 24 males (∼380g) Wistar rats were used in this study. Animals were divided into three groups, as the control, SHAM and study groups. Then, the study group was again divided into two groups as exposed to light or heavy dose alcohol. The choroid plexuses and intraventricular ependymal cells and ventricles volumes were assessed and compared. RESULTS: Degenerated epithelial cells density 22±5 /mm3 in the control group, 56±11 /mm3 in the SHAM group, 175±37 /mm3 in the light, and 356±85 /mm3 in the heavy alcohol exposure group. Evan's index was less than <34% in the control, larger than >36% in the SHAM, larger than >40% in the group which was exposed to light alcohol (light alcohol group), larger than >50% in heavy alcohol (heavy alcohol group) exposed. CONCLUSIONS: It was found that alcohol exposure causes choroid plexus and ependymal cell degeneration with ciliopathy and the enlarged lateral ventricles or hydrocephalus. In the COVID-19 Pandemic Era, our findings are functionally important; alcohol has often been used for hygiene and prevention of transmission of COVID-19 pandemic.

OBJECTIVE: Increased intracellular calcium concentration plays an important role in the secondary mechanism of spinal cord injury. In the presenting experimental study, we aimed to evaluate the healing effect of barnidipine, which has a high affinity for L-type calcium channels, on acute spinal cord injury and to compare its effects with those of methylprednisolone. METHODS: A total of 32 Spraque Dawley albino adult female rats were divided into 4 groups; group 1: sham-operated (n=8), group 2: only ischemia (n=6), group 3: barnidipine-treated (n=8), and group 4: methylprednisolone-treated (n=6). An ischemia-reperfusion model was created by clipping the abdominal aorta in the rats. Motor examination was performed 1 hour after the surgical procedure and before sacrification. Immediately following the second motor examination, rats were sacrificed and tissue samples were taken for histopathological examination and for testing of tissue malondialdehyde (MDA) levels. RESULTS: A significant correlation of motor examination was found between the sham-operated and barnidipine-treated groups and the sham-operated and only ischemia groups at the 1 st and 24 th hour (p<0.008). There was no significant difference between the only ischemia and barnidipine-treated groups and only ischemia and methylprednisolone-treated groups (p>0.008). Light microscopic examination of the sham-operated group revealed findings consistent with normal spinal cord structure. In group 2, 3, and 4, light microscopic examination revealed polymorphonuclear leukocyte infiltration and a small amount of axonal swelling. There was no significant correlation between the ischemia and barnidipine-treated groups and the barnidipine and methylprednisolone groups in terms of MDA levels (p>0.008). CONCLUSION: A single dose of barnidipine (10 mg/kg) and methylprednisolone are not effective and not sufficient to prevent spinal ischemia-reperfusion injury in rats.