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).
Feeding behavior is important to maintain health and is closely associated with the gustatory and visceral senses that receive information contained in food. The caudate putamen (striatum) is involved in food, water, and fat intake, and has been reported to affect feeding motivation; however, it is unclear where the neural circuits of the gustatory and visceral senses connect with the caudate putamen. Here, a morphological relationship was identified between the gustatory/visceral neural circuits and the caudate putamen, mainly through parabrachio-thalamo-striatal pathways.
The Parabrachial nucleus complex (PB), consisting of the lateral parabrachial nucleus, medial parabrachial nucleus, and Kolliker-Fuse nucleus, is known as a respiratory modulating center. We examined how the PB participates in respiratory modulation using pons-medulla-spinal cord preparations obtained from 0-4-days old rats. First, the effects of PB electrical stimulation on C4 ventral nerve inspiratory activity were examined. The electrical stimulation induced a transient depression or termination in C4 inspiratory activity. This inhibition of C4 inspiratory activity was greatly reduced by perfusion of NMDA antagonists and the inhibition was blocked by perfusion of a GABAA-antagonist. Inspiratory-expiratory (I-E) neurons were mainly recorded in the PB. In the medulla, the inspiratory neurons received IPSPs and the expiratory neurons received EPSPs when PB was stimulated. It seems that PB is an active inspiratory-expiratory phase-switching system. In conclusion, PB is involved in the inspiratory termination in neonatal period; and PB might be an active mode switching system that switches from unconscious respiration to conscious vocalization.
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.
Harlequin syndrome and segmental anhidrosis represent segmental dyshidrosis. Harlequin syndrome is defined as paroxysmal hemifacial flushing and hyperhidrosis, and many cases accompany contralateral segment anhidrosis. This syndrome is considered as idiopathic segmental anhidrosis with compensatory hyperhidrosis in the contralateral side. Harlequin syndrome is divided into secondary and idiopathic types by its etiology. Lung cancer (pancoast tumor), neurinoma and carotid artery dissection are main causes of secondary harlequin syndrome. It is classified into three groups by anatomical focus as follows: 1) hypothalamus to spinal cord, 2) apex area and superior mediastinum, 3) cervical part or internal carotid artery area. Idiopathic segmental anhidrosiss is often associated with Adie’s syndrome (Adie’s pupil plus absence of tendon reflex), and this state is called Ross syndrome. Sjögren syndrome and herpes zoster virus infection are considered as causative diseases of Ross syndrome and/or idiopathic segmental anhidrosis. It is considered that the pathogenesis of Ross syndrome is an immunological mechanism for target antigens of the sympathetic ganglion, the ciliary ganglion, and the dorsal root ganglion.
Gentle tactile stimulation of the skin using a roller (somaplane) has an inhibitory effect on micturition contraction of the urinary bladder in anesthetized rat. The stimulation is clinically applied to self-care of overactive bladder. On the other hand, basic and clinical studies on neuromodulation in which electrical stimulation of pudendal nerve or tibial nerve regulates bladder function has been extensively studied recently. These effects are thought to be produced because the excitatory transmission of micturition reflex in the central nervous system is inhibited by segmental somatic afferent input. In order to investigate the action site of opioids mediating this inhibition and the action on descending or ascending transmission related to micturition reflex, we administered naloxone intrathecally, stimulated pontine micturition center or descending pathway therefrom, and recorded response of lumbosacral blood flow during bladder distention and evoked potential by pelvic afferent stimulation using anesthetized rats. In this article, I will introduce the recent findings on the central mechanism of somato-bladder inhibitory reflexes, mainly on our research on gentle skin stimulation.
Overactive bladder (OAB, urinary urgency and frequency) in Parkinson’s disease (PD) is a major autonomic disorder and related with dopamine transporter scan imaging. When OAB does not respond to levodopa and dopaminergic drugs, appropriate add-on therapy is recommended in order to maximize the quality of life in PD patients.