Parasomnias are a group of sleep disorders characterized by abnormal, unpleasant motor verbal or behavioral events that occur during sleep or wake to sleep transitions. Parasomnias can occur during non-rapid eye movement (NREM) and rapid eye movement (REM) stages of sleep and are more commonly seen in children than the adult population. Parasomnias can be distressful for the patient and their bed partners and most of the time, these complaints are brought up by their bed partners because of the possible disruption in their quality of sleep. As clinicians, it is crucial to understand the characteristics of various parasomnias and address them with detailed sleep history and essential diagnostic approach for proper evaluation. The review aims to highlight the epidemiology, pathophysiology and clinical features of various types of parasomnias along with the appropriate diagnostic and pharmacological approach.

Methanogenic flora was significantly lower in IBS patients from North India than in apparently healthy subjects. This may be one of the causes of flatulence in IBS patients.

Parkinson’s disease (PD) is characterized by the presence of inflammation-mediated dopaminergic neurodegeneration in the substantia nigra. Inflammatory mediators from activated microglia, astrocytes, neurons, T-cells and mast cells mediate neuroinflammation and neurodegeneration. Administration of neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induces PD like motor deficits in rodents. 1-methyl-4-phenylpyridinium (MPP+), a toxic metabolite of MPTP activates glial cells, neurons and mast cells to release neuroinflammatory mediators. Glia maturation factor (GMF), mast cells and proteinase activated receptor-2 (PAR-2) are implicated in neuroinflammation. Alpha-synuclein which induces neurodegeneration increases PAR-2 expression in the brain. However, the exact mechanisms are not yet understood. In this study, we quantified inflammatory mediators in the brains of MPTP-administered wild type (Wt), GMF-knockout (GMF-KO) and mast cell knockout (MC-KO) mice. Additionally, we analyzed the effect of MPP+, GMF and mast cell proteases on PAR-2 expression in astrocytes and neurons in vitro. Results show that the levels of interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and the chemokine (C-C motif) ligand 2 (CCL2) were lesser in the brains of GMF-KO mice and MC-KO mice when compared to Wt. mice brain after MPTP administration. Incubation of astrocytes and neurons with MPP+, GMF and mouse mast cell protease-6 (MMCP-6) and MMCP-7 increased the expression of PAR-2. Our studies show that the absence of mast cells and GMF reduce the expression of neuroinflammatory mediators in the brain. We conclude that GMF along with mast cell interactions with glial cells and neurons during neuroinflammation can be explored as a new therapeutic target for PD and other neuroinflammatory disorders.

The overlap syndrome (OS) was first coined by David C. Flenley in 1985 to describe the coexistence of obstructive sleep apnea (OSA) in patients with chronic obstructive pulmonary disease (COPD). Patients with OS experience more profound nocturnal oxygen desaturation (NOD) than patients with OSA or COPD alone. This underlying hypoxia in OS increases the risk of cardiovascular disease including atrial fibrillation, right heart failure, and pulmonary hypertension, thereby increasing the mortality associated with the disease. Keeping in mind the risk of mortality, it is crucial for clinicians to clinically evaluate the patients with OSA or COPD for the occurrence of OS and provide effective treatment options for the same. This review aims to highlight the pathophysiology and the risks associated with the OS along with early detection and appropriate management protocols to reduce the mortality associated with it.

Neurodegenerative disorders (NDs) are a diverse group of disorders characterized by selective and progressive loss of neural systems that cause dysfunction of the central nervous system (CNS). The examples of NDs include Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Huntington's disease (HD). The aggregated proteins block or disrupt the normal proteosomal turnover, autophagy, and become abnormally modified with time, generating toxicity via pathways thereby resulting in neurodegeneration and neuron death. The chapter highlights the understanding in the areas of AD, PD, HD as illustrative of major research so as to define the key factors and events in the improvement of NDs. It defines the physiological functioning of neural transmission (presynaptic, postsynaptic activity) at neural signaling pathway, then the dynamics of neuronal dysfunctioning and its molecular mechanism. Further, it also discusses the progression from synaptic dysfunction to transmission failure followed by NDs.

IntroductionZwolle risk score (ZRS) is a validated scoring system to determine the time of discharge in ST-segment elevation myocardial infarction (STEMI) patients. Left ventricular ejection fraction (LVEF) also provides prognostic information after ST-elevation myocardial infarction (STEMI). We studied that the addition of LVEF to ZRS variable can improve decision making in safe and early discharge in STEMI patients post-primary coronary intervention.MethodsOverall, 249 STEMI patients were studied retrospectively. LVEF was considered as an independent variable. The patients having LVEF <50% were under Group A and LVEF ≥50% were under Group B. Groups were analyzed by model comparison for overall hospital length of stay (LOS) and Intensive care unit (ICU) LOS post-primary percutaneous coronary intervention (PCI).ResultsThere were 123 patients in Group A and 126 patients in Group B. Comparison for primary outcomes showed significant difference with hospital length of stay (LOS) being 3.1 ± 2.3 days in Group A versus 2.1 ± 0.8 days in Group B (p < 0.001). Similarly, ICU stay was also significantly higher in Group A with 36.5 ± 31.4 hours versus 24.0 ± 11.8 hours for Group B, which led to prolonged hospitalization for patients with LVEF <50%. Model 1 that considers ZRS individually is nested within Model 2 where ZRS and LVEF are considered together. The profile log-likelihood ratio test favors model 2 over model 1 (p < 0.0001). Similarly for ICU LOS, R2 = 0.12 (Model 1) < R2 = 0.20 (Model 2). The F test favors model 2 over model 1 (p < 0.0001).ConclusionWe concluded that adding LVEF to Zwolle risk score gives a better model for risk stratification in STEMI patients to decide early and safe discharge post-primary PCI.

Lung ultrasonography has a tailored diagnostic and therapeutic approach in the critical care setting. Lung ultrasonography in critically ill (LUCI) is a helpful modality for the early detection and assessment of various lung pathologies and guides the management protocol for the same. The aim of this review was to highlight the basics of an ultrasound machine, the fundamentals of a lung ultrasound and the importance of lung artifacts in detecting the anatomy and pathology of the lung disease. In addition, we have also discussed regarding the effective approach to lung ultrasonography through the two protocols: the Bedside Lung Ultrasound in Emergency (BLUE) protocol and the Fluid Administration Limited by Lung Sonography (FALLS) protocol.

Posterior reversible encephalopathy syndrome (PRES) is a clinico-radiologic syndrome resulting in subcortical vasogenic edema appreciated on T2/fluid-attenuated inversion recovery (FLAIR) sequence of magnetic resonance imaging (MRI). PRES classically involves bilateral parieto-occipital lobes and is usually reversible. Atypical variant of PRES includes the involvement of brainstem, basal ganglia, thalami, or periventricular white matter. We report an unusual case of PRES with isolated brainstem involvement with periventricular white matter changes in a patient with renovascular hypertension from unilateral renal artery stenosis. To our knowledge, this is the first case of secondary hypertension from renal artery stenosis resulting in the atypical variant of PRES.