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.