Omega fatty acid ratios and neurodegeneration in a healthy environment.

Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Multiple Sclerosis pose substantial public health challenges. While genetics play a primary role, recent research emphasizes the impact of environmental factors, particularly diet and lifestyle. This study investigates the initiating effects of Omega (ω)- 3 and Omega (ω)- 6 fatty acids on neuroinflammation, potentially contributing to these diseases. Using BV-2 microglial cells, we explored the influence of different fatty acid compositions and ratios on cell viability, cytokine production, morphological changes, and lipid peroxidation. Notably, a 2/1 ω-6:ω-3 ratio led to decreased cell viability. Fatty acid compositions influenced cytokine secretion, with reduced TNF-α suggesting anti-inflammatory effects. IL-17 increased, while IL-4 and IL-10 decreased in the 15/1 ω-6:ω-3 ratio, indicating complex cytokine interactions. This study found that polyunsaturated fatty acids interventions induced microglial activation, altering cell morphology even without immunostimulants. These findings demonstrate the intricate nature of fatty acid interactions with microglial cells and their potential implications for neuroinflammation. Further research is needed to clarify mechanisms and their relevance to neurodegenerative diseases, informing possible therapeutic strategies.

Exploring the role of polyunsaturated fatty acid ratios in modulating neuroinflammation in LPS-induced microglia: A comprehensive in vitro analysis.

The study investigated the effect of different omega (ω)- 3 and omega (ω)- 6 polyunsaturated fatty acid (PUFA) ratios on cytokine secretion, cell viability, and microglial cell shape in lipopolysaccharide (LPS)-induced microglia. The addition of PUFAs at different ratios, especially ω-3 and ratios of 7/1 and 2/1 ω-6/ω-3, resulted in a significant increase in the ameboid form of microglial cells, as well as more branching of their distal branches. Microglial cells were treated with varying ratios of PUFAs, and their cytokine secretion was measured. The results showed that all PUFA ratios had lower tumor necrosis factor (TNF)-α secretion than the control group, higher interleukin (IL)- 4 secretion in the ω-6 group, and less IL-10 secretion most down IL-6 secretion in the 7/1 ratio group. The study suggests that determining the appropriate ω-6/ω-3 consumption ratio, especially the 7/1 and 2/1 ratios, may help manage neuroinflammation, develop dietary models in immune-mediated neurodegenerative diseases, and open up new treatment possibilities.

Prevalence, comorbidities and mediators of childhood anxiety disorders in urban Turkey: a national representative epidemiological study.

PURPOSE: The aim of this study is to evaluate the prevalence of anxiety disorders, its correlation with sociodemographic characteristics, its comorbidities with other psychiatric disorders and its predictors in school-aged children. METHODS: This study is part of a representative, multi-centered national study that is planned by the Turkish Association of Child and Adolescent Mental Health to evaluate the prevalence of psychopathology among elementary school students in Turkey between the years 2014-2015. Children are screened via Kiddie Schedule for Affective Disorders and Schizophrenia for School Age Children Present and Lifetime Version. Impairment is assessed by a 3-point Likert type scale independently by the parent and the teacher. The final sample included 5842 children with the mean age of 8.7 years. RESULTS: The prevalence of any anxiety disorder without considering impairment is 16.7% and considering impairment is 5.2% in children according to our study. We found significant differences for comorbid Attention Deficit Hyperactivity Disorder, Disruptive Behavior Disorder, Mood Disorders, Tic Disorders, Obsessive Compulsive Disorder, Enuresis Nocturna, Encopresis, and Intellectual Disability. Having a history of paternal physical disorder, living in the regions of Marmara, Mediterranean and Black Sea were found to be the main predictors of having childhood anxiety disorders according to the logistic regression analysis. CONCLUSION: Better understanding of childhood anxiety disorders, comorbid conditions and predictors will result in earlier diagnosis and more appropriate treatment.

Susac Syndrome: Clinical characteristics, diagnostic findings and treatment in 19 cases.

Susac's Syndrome (SS), which was first described in 1979, is a rare and presumably autoimmune disorder characterized by encephalopathy, hearing loss, and visual disturbance resulting from branch retinal artery occlusion (BRAO). This study reports 19 SS patients' clinical characteristics, MRI features, CSF analysis, treatment strategies and outcomes. At initial presentation, only three of 19 patients demonstrated the complete clinical triad. Clinic presentation varied from isolated hemiparesis to the full triad (encephalopathy, hearing loss and visual disturbances). Corpus callosum (CC) involvement was noted in the MRI of 18 patients (97%) and BRAO was detected in 17 (95%) patients. All patients were treated with intravenous methylprednisolone after the initial assessment. This case series is presented to emphasize the differences in clinical presentation of SS and the importance of MRI and FFA in diagnosis.

Alpha-interferon and isoprinosine in adult-onset subacute sclerosing panencephalitis.

We report eight patients with adult-onset subacute sclerosing panencephalitis (SSPE), of which, four were treated with oral isoprinosine and four with intraventricular alpha-interferon plus oral isoprinosine. One of the four patients treated with oral isoprinosine died within two months, and the disease progressed in three patients. Of the four patients treated with oral isoprinosine plus intraventricular alpha-interferon, one showed mild progression, one remission, and the remaining two showed stabilization. The group of patients is relatively small, but our results suggest that treatment with oral isoprinosine plus alpha-interferon is effective for SSPE.

Median nerve somatosensory evoked potentials recorded with cephalic and noncephalic references in central and peripheral nervous system lesions.

Somatosensory evoked potentials (SSEP) to electrical stimulation of the median nerve by using cephalic and noncephalic references were studied to detect the generator sources of short latency evoked potentials in 29 patients with cerebral, brainstem, spinal and peripheral nerve lesions. Patients were divided into six groups according to the localization of their lesions: group 1: cortical and subcortical lesions, group 2: basal ganglion lesions, group 3: pons and mesencephalon lesions, group 4: diffuse cerebral lesions, group 5: cervical cord lesions, group 6: brachial plexus lesions. Potentials were recorded using cephalic and noncephalic references after median nerve stimulation. Evidence obtained from patients suggested the following origins for these short latency SSEPs: P9 may arise in brachial plexus, P11 in dorsal basal ganglions or dorsal column, P13 and P14 in the nucleus cuneatus and lemniscal pathways, N16 in subthalamic structures and most likely mid and lower pons, N18 from the thalamus and thalamocortical tract, and N20 from primary somatosensory cortex.

SPECT and MRI findings in a case of extensive neuronal migration disorder.

We report a 20-year-old male with epilepsy, mild mental retardation, growth asymmetry, and MRI and SPECT features of unilateral subcortical ectopic cortex. The neurological examination showed mild growth asymmetry, hemiparesis and hemihypoesthesia and pyramidal signs on the left side. EEG showed focal abnormality in the right frontotemporal region. MRI revealed pachygyria and severe heterotopia associated with some abnormalities of ventricles and cerebellum on the right. Cortical responses were absent on stimulation of the left median and tibial nerves. Central motor conduction time from cortex to left upper extremity was prolonged in magnetic stimulation test. SPECT using 99 mTc-HMPAO revealed increased perfusion of the right subcortical region as compared with those of overlying cortical mantle and opposite hemisphere. To our knowledge, there has been no report documenting such a large and extensive subcortical ectopic cortex which appears as a mass distorting and shifting the middle structure in an adult, such as in our case.

Cytochrome P4501A1 genotypes and smoking- and hypertension-related ischemic stroke risk.

This study aimed to determine whether the coding (A4889G) and noncoding region (T6235C) polymorphisms of the gene coding for cytochrome P4501A1 (CYP1A1), a xenobiotic-metabolizing enzyme responsible for the metabolism of carcinogenic polycyclic aromatic hydrocarbons, are involved in the pathogenesis of ischemic stroke in Turkish population. Study group consisted of 226 ischemic stroke patients and 113 controls. Genotypes were attained by allele-specific polymerase chain reaction (PCR) for A4889G and PCR/restriction fragment length polymorphism analysis for T6235C. Frequency of 6235C allele was significantly lower in patients (0.151) compared with controls (0.226, P = 0.015). Prevalence of hypertension and hypertension-associated ischemic stroke risk was lower for 6235C allele carriers. This allele decreased ischemic stroke risk twofold (adjusted odds ratio = 0.48, P = 0.005). There was almost no difference in 4889G allele frequencies in patients (0.445) and controls (0.425). However, prevalence of hypertension was lower in 4889G allele carriers when compared with the wild-type genotypes. In addition, risk of ischemic stroke for smoker and hypertensive individuals was lower when they have at least one 4889G allele. The present study demonstrated that CYP1A1 genetic variants contribute to interindividual variability in smoking- and hypertension-induced ischemic stroke risk.

Efficacy of intravenous magnesium sulfate in the treatment of acute migraine attacks.

OBJECTIVE: To study the efficacy and tolerability of 1 g of intravenous magnesium sulfate as acute treatment of moderate or severe migraine attacks. BACKGROUND: Migraine is a common disorder in which not only the pain but also the accompanying symptoms such as nausea and vomiting reduce activity and productivity of sufferers. Many drugs used for the treatment of acute migraine attacks have many side effects, are not well tolerated, are ineffective in some patients, or cannot be used during pregnancy or in patients with ischemic heart disease. Magnesium deficiency has been proposed to play a role in the pathophysiology of migraine, and recently treatment of migraine with magnesium has gained considerable interest. METHODS: This was a randomized, single-blind, placebo-controlled trial including 30 patients with moderate or severe migraine attacks. Fifteen patients received 1 g intravenous magnesium sulfate given over 15 minutes. The next 15 patients received 10 mL of 0.9% saline intravenously. Those in the placebo group with persisting complaints of pain or nausea and vomiting after 30 minutes also received 1 g magnesium sulfate intravenously over 15 minutes. The patients were assessed immediately after treatment, and then 30 minutes and 2 hours later. Intensity of pain, accompanying symptoms, and side effects were noted. RESULTS: All patients in the treatment group responded to treatment with magnesium sulfate. The pain disappeared in 13 patients (86.6%); it was diminished in 2 patients (13.4%); and in all 15 patients (100%), accompanying symptoms disappeared. In the placebo group, a decrease in pain severity but persisting nausea, irritability, and photophobia were noted in 1 patient (6.6%). Accompanying symptoms disappeared in 3 patients (20%) 30 minutes after placebo administration. All patients initially receiving placebo were subsequently given magnesium sulfate. All of these patients responded to magnesium sulfate. In 14 patients (93.3%), the attack ended; in 1 patient (6.6%), pain intensity decreased; and in all 15 patients (100%), accompanying symptoms disappeared. Both the response rate (100% for magnesium sulfate and 7% for placebo) and the pain-free rate (87% for magnesium sulfate and 0% for placebo) showed that magnesium sulfate was superior to placebo. Twenty-six patients (86.6%) had mild side effects which did not necessitate discontinuing treatment during magnesium sulfate administration. CONCLUSION: Our results show that 1 g intravenous magnesium sulfate is an efficient, safe, and well-tolerated drug in the treatment of migraine attacks. It is possible that magnesium sulfate could be used in a broader spectrum of patients than other drugs commonly used for attack treatment. In view of these results, the effect of magnesium sulfate in acute migraine should be examined in large-scale studies.

Migrainous stroke causing bilateral anterior cerebral artery territory infarction.

A 38-year-old man developed bilateral anterior cerebral artery territory infarction during the course of a migraine. Magnetic resonance imaging showed bilateral ischemic lesions involving the cortex of the paramedian region of the frontal and parietal lobes, more prominent on the right. Cerebral angiography was normal. To our knowledge, this is the first report of bilateral anterior cerebral artery territory infarction from migraine.

Malondialdehyde, glutathione peroxidase and superoxide dismutase in peripheral blood erythrocytes of patients with acute cerebral ischemia.

The levels of malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD-1) were measured in the red blood cells (RBC) of 34 patients with acute ischemic hemispheric stroke on the first and seventh day after their stroke onset, and compared with 30 control individuals matched for sex, age and stroke risk factors. Within the first 24 h after stroke, SOD and GSH-Px activities were significantly decreased and MDA levels were significantly elevated in the patients compared with control subjects. Decrease in SOD and GSH-Px activities and increase in MDA levels showed significant correlation with infarct size, initial stroke severity assessed by NIH stroke scale and poor short-term prognosis. Observed changes in the RBC oxygen scavenging process returned to values not different from those of control subjects within seven days after stroke. Our results indicated that antioxidant enzyme concentrations decreased below normal levels in the acute period following ischemic stroke. Until the recovery of antioxidant defence mechanisms, which occurred up to seven days after stroke onset according to our results, the use of neuroprotective therapy against oxyradical injury seems reliable.

Auditory brainstem responses in children with congenital heart disease.

BACKGROUND: Cyanotic congenital heart diseases usually lead to growth and developmental delay in children due to chronic hypoxemia and undernourishment that may affect the central nervous system. The auditory brainstem responses are determined to assess the maturation and function of the brainstem. Therefore, we used the auditory brainstem responses to investigate the effect of cyanotic congenital heart diseases on brainstem maturation. METHODS: The auditory brainstem responses were investigated in 45 children (23 cyanotic, 22 acyanotic) with congenital heart diseases and compared with the results of 30 healthy counterparts (all children were aged between 2 months and 15 years). RESULTS: The results of auditory brainstem responses were similar in acyanotic patients and in normal children. The cyanotic patients under 1 year of age had more prolonged I-V interpeak latencies than those of control and acyanotic patients (P < 0.05). There was no difference between all groups older than 1 year of age. In cyanotic children, I-V interpeak latencies showed significant negative correlation with arterial oxygen saturation and partial oxygen pressure (P < 0.05). CONCLUSIONS: Cyanotic congenital heart diseases may cause significant retardation on brainstem maturation due to chronic hypoxemia, especially in infants under 1 year of age, whereas acyanotic congenital heart diseases have no effect on auditory brainstem responses.