The biological origin of circumventricular organs (CVOs) evolutionally goes back to the invertebrates and even further to plants. The CVOs are classified into sensory CVOs (subfornical organ, organum vasculosum of lamina terminalis, and area postrema) and secretory CVOs (neurohypophysis, pineal gland, subcommissural organ, and median eminence). Physiological mechanisms of life-saving homeostasis arising from CVOs consist of at least the following eight axes; neuroendocrine regulation axis, circadian rhythm regulation axis, innate immune regulation axis, nociceptive response regulation axis, body fluid regulation axis, cognitive regulation axis, locomotive driving regulation axis, and inhibitory regulation axis. Summarizing the above, the CVO physiologically contributes to a wide spectrum of autonomic, endocrine, cognitive, sensory gating, and motor regulations, whose impairments potentially result in the complex symptoms being composed of sleep-related, cardiovascular, gastrointestinal, menstrual, emotional, cognitive, sensory, and motor symptoms. I propose the new clinical concept, “circumventricular organs dysregulation syndrome (CODS)” that is known to be seen in human papilloma virus vaccination-associated neuro-immunopathic syndrome (HANS), von Economo’s encephalitis lethargica, craniopharyngioma, interferon encephalopathy, metronidazole induced encephalopathy, Wernicke encephalopathy, schizohrenia with water intoxication, Alzheimer’s disease with overeating, neuromyelitis optica, stiff-person syndrome, cerebrospinal fluid hypovolemia, heat stroke, fibromyalgia, chronic fatigue syndrome / myalgic encephalomyelitis, menopausal syndrome, and frailty syndrome (sarcopenia syndrome).
This review summarized a link between respiration and olfaction, and discussed new insights into the olfactory-related respiratory function for emotion and memory. The respiratory center in the medulla generates a basic respiratory rhythm that is modulated by inputs from brain regions involved in processing sensory information and emotions. Olfaction is closely related to respiratory activity, as inspired olfactory information ascends directly to the limbic system. This direct input rapidly induces emotional changes accompanied by alternating respiratory rhythms. Autobiographical odor memory (AM-odor) accompanied by a sense of realism of a specific memory elicits strong emotions, and also increased arousal levels and the vividness of memories, and was associated with a deep and slow breathing pattern. Functional magnetic resonance imaging (fMRI) analysis indicated robust activation in the left posterior OFC (L-POFC) during AM-odor. We detected several trends in connectivity between L-POFC and bilateral precuneus, bilateral rostral dorsal anterior cingulate cortex (rdACC), and left parahippocampus. Among above areas, slow breathing observed in AM-odor was correlated with rdACC activation, meaning that subjects with slow breathing tend to increased activation in rdACC. Negative emotions such as anxiety and fear have been reported to increase respiratory frequency. Slow breathing associated with rdACC may provide insight into the potential inhibitory mechanisms of excessive activation of the amygdala observed anxiety and stress situations.
Segmental and unilateral hyperhidrosis are forms of sweating disorder. In some cases, these are accompanied by anhidrosis/hypohidrosis in other skin areas. The pathogenesis of these hyperhidrosis may be compensatory and is likely caused by underlying lesions in anhidrosis/hypohidrosis areas, but the precise mechanism remains unclear. Hyperhidrosis is often located horizontally contralateral same myelomere skin areas as the anhidrosis/hypohidrosis, whereas vertically ipsilateral adjacent to other rostral and caudal myelomere with anhidrosis/hypohidrosis. The similar efferent phase of the physiological “skin pressure-sweating reflex” might be associated with these mechanisms. This horizontal reflex is primarily due to inhibition of ipsilateral sweating by unilateral skin pressure, secondarily contralateral sweating increases. Microneurography indicates that this phenomenon occurs because unilateral skin pressure reduces the amplitude of ipsilateral sudomotor nerve activity and increases contralateral activity. Vertically, studies using the ventilated capsule method during heating, show that pressure on the bilateral skin of the back by supination decreases sweating on the upper body and increases sweating on the underbody. Central sudomotor sympathetic outflow (frequency of sweat expulsion) in response to body temperature is simultaneously hyperactivated, indicating that sweating is increased compensatorily to maintain a constant total sweating rate. In conclusion, segmental hyperhidrosis in segments other than those directly affected may be compensatory.
Segmental hyperhidrosis is a rare sweating disorder reported in various diseases. In majority of cases, however, pathophysiological mechanism of segmental hyperhidrosis remains obscure. On the other hand, in patients presenting with dysesthesia or pain, the sweat test occasionally reveals hyperhidrosis which is often segmental. Reviewing such cases suggests that pathophysiological mechanisms of segmental dysesthesia and hyperhidrosis appear multifactorial, including mechanical irritation, neural cross talk, neurogenic inflammation, sprouting of sensory fibers, altered receptor expression, and augmented spinal reflexes. With respect to segmental dysesthesia alone or in combination with hyperhidrosis, cautious investigations should be done because they are often caused by serious life-threatening diseases.