Thanks to recent developments in information and communications technology, we may enjoy comfortable lives by taking advantage of visual information transmitted via the internet, and may even work in virtual environments using a head-mounted display (HMD). These benefits may open a new era of human activities, but unfortunately may be accompanied by undesirable biomedical discomforts, such as visually-induced motion sickness (VIMS), photosensitive seizure, and visual display terminal (VDT) syndrome. Among them, VIMS has symptoms similar to motion sickness: nausea, vomiting, asthenopia and disorientation, accompanied by dysfunction of various parts of the autonomic nervous system. In this review, the symptoms and mechanisms of VIMS are discussed, including an advanced interpretation of the sensory conflict theory. Special attention is paid to children in the sensitive period and younger users of virtual reality (VR), who have high plasticity of the developing brain.

GI symptoms are generated when signals through luminal stimuli propagate to the brain. Pathological conditions in the route of propagation may cause uncomfortable symptoms. Deviation of central function triggers gastrointestinal dysfunction through the hypothalamus-pituitary-adrenal axis and autonomic nerve functions. Such bidirectional communication is the underlying key condition in functional gastrointestinal disorders. Recent studies have revealed the critical roles of the luminal microbiome and microinflammation of the intestinal epithelium, involving cytokines, gut hormones, and neurotransmitters. The relationships among psychosocial stress, gut wall and intraluminal microbiome could be a new paradigm, the next target for gastrointestinal functional disorder research.

Functional dyspepsia (FD) is a syndrome in which there are no organic diseases that cause symptoms and there are unpleasant chronic symptoms caused by the gastroduodenal region. Although the pathophysiology has not been elucidated yet, not only gastrointestinal dysmotility, visceral hypersensitivity, and sociopsychiatric stress, but also genetic factors, dietary factors, low-grade inflammation and mucosal hyperpermeability, gut infection and microbiota is also associated. In addition, these factors are deeply involved in the gut-brain interaction, and in Rome IV, the subtitle "Disorders of the gut-brain axis" is attached, and the importance of the brain-gut-gut bacterial axis is proposed. Rome IV has shown advances in diagnostic technology and therapeutics based on advances in pathological research over the last decade, but research in this area has continued to make progress, and they have become the basis for new discussions in 2026 as Rome V.

Functional constipation is common in general population, which is defined as at least two of any kinds of defecation difficulties or fewer than 3 spontaneous bowel movements per week (Rome IV criteria). Constipation increases significantly with age (up to 50% among octogenerians), affects significantly the quality of life, and causes morbidity. Recently it is being recognized that Lewy body diseases (LBD), including Parkinson’s disease (PD) and dementia with Lewy bodies (DLB), can become a cause of functional constipation particularly in older persons. This is because LBD leads to neuronal loss and appearance of Lewy bodies in the myenteric plexus. Arriving at a diagnosis is not always easy. Therefore, collaboration of gastroenterologists and neurologists are highly recommended in order to maximize patients’ quality of life.

A novel coronavirus named SARS-CoV-2 was identified in unexplained pneumoniae case in Wuhan, China in December 2019, and its entry into human host cells was mediated by the same receptor, the angiotensin-converting enzyme 2 (ACE2), as in severe acute respiratory syndrome coronavirus (SARS-CoV). This report provides an overview of the proposed neuro-invasive viral mechanisms of SARS-CoV-2, and the significance of ACE2 in a genome-wide association study of severe COVID-19 with respiratory failure, as well as the currently reported frequencies of dysosmia or dysgeusia, brain MRI findings, encephalopathy, and peripheral neuropathy in patients with SARS-CoV-2. We discuss the persistent COVID-19 symptoms which resemble CSF hypovolemia or myalgic encephalomyelitis, and support for this hypothesis provided by damage to the ACE2-expressing choroid plexus epithelium and immune disorder with breakdown of the blood-CSF-barrier induced by experimental SARS-CoV-2 infection.

A single taste bud comprises approximately 50–100 taste cells. Taste substances are detected by taste cells. The taste signal is transmitted to gustatory nerves via the intracellular transduction system, and then input to the central nervous system. In mammals, taste is classified into five basic taste qualities: sweet, bitter, umami, sour, and salty. Taste cells are responsible for detecting each taste by expressing taste receptors, which specifically detect each taste quality. In this manuscript, we review recent knowledge regarding taste detection and transduction mechanisms in taste cells.

For rodents, the olfaction is an important sensory function that it is a lifeline. Olfactory receptors sense the odors that enters through the nose. Linda Buck and Richard Axel discovered that there are as many as 1,000 olfactory receptor genes in 1991, and later won the Nobel Prize. Recent studies have shown that African elephants have more olfactory receptor genes than rodents, and African elephants have an acute sense of smell. Humans have only about one-fifth the number of olfactory receptors of African elephants. Studies have shown that the human olfaction declines with age. In addition to the olfaction that is impairment of olfaction with aging, there are neurodegenerative diseases in which the “smell” is no longer recognized and the “smell itself” is not input. Parkinson’s disease (PD) and Alzheimer’s disease (AD) are representative of the neurodegenerative diseases that present with olfactory dysfunction. In this article, the olfactory dysfunction in PD and AD is discussed.

Physicians might encounter patients with acute urinary retention due to benign inflammatory nervous diseases. Based on the mechanism of urinary retention, these disorders can be divided into two subgroups: disorders of the peripheral nervous system (e.g., sacral herpes with skin rash) or the central nervous system (e.g., meningitis-retention syndrome [MRS] with mild pyramidal signs). Laboratory abnormalities include positive herpes virus PCR, and increased myelin basic protein/ oligoclonal band in the cerebrospinal fluid (CSF) in MRS. Acute urodynamic abnormality in both conditions is detrusor underactivity, while in MRS detrusor overactivity might follow, indicating selective involvement of the spinal descending tract to the bladder (acute shock phase) in MRS that might affect the thoracic spinal cord. There are few cases with CSF abnormality alone, including ours. Management of the acute urinary retention is necessary to avoid bladder injury due to overdistension.

In recent years, neuromodulation therapy, which is the treatment of diseases by stimulating nerves using a device, has been attracting attention. Our previous study indicated that the low intensity electrical stimulation of intact superior laryngeal nerves (SLN) promoted calcitonin secretion from the thyroid gland in anesthetized rats. Calcitonin inhibits bone resorption by directly suppressing osteoclast functions. In order to apply this discovery to the development of a neuromodulation treatment for osteoporosis, it is necessary to confirm the safety of SLN stimulation and its effect on calcitonin secretion in conscious animals as well as the efficacy of chronic stimulation on bone mineral density in osteoporosis model rats. We introduce our recent research findings on the effects of SLN stimulation in conscious rats in this mini-review article.