We made a review on the nature of physiological gustatory sweating in the 1st part of this article. The 2nd part is focussed to the pathogenesis of pathological gustatory sweating. Pathological gustatory sweating includes auriculo-temporal syndrome (Frey syndrome), post-sympathectomy gustatory sweating, diabetic gustatory sweating, etc. Auriculo-temporal syndrome is gustatory sweating and flushing in the distribution of the auriculo-temporal nerve following injury, operation, or inflammation of the parotid gland. Thermoregulatory sweating seems to be preserved in most cases. Glaister et al. (1958) reported that gustatory sweating in auriculo-temporal syndrome was abolished by blocking the otic ganglion, but unaffected by cervical sympathectomy, confirming that gustatory sweating was mediated by the parasympathetic fibers. It is widely accepted that auriculo-temporal syndrome is resulted from misdirection of the regenerating parasympathetic fibers to sweat glands. Post-sympathectomy gustatory swating is coexistent with decrease in thermoregulatory sweating in the same side, and lacking facial flushing. Although recent articles describe that the pathogenesis of post-sympathectomy gustatory sweating is uncertain, Guttmann (1931) had postulated that sweat glands received dual innervation from the sympathetic and the parasympathetic nerves, and that loss of the sympathetic innervation enhanced parasympathetic sweating. We assume that all variants of pathological gustatory sweating develop by disinhibition of gustatory-sudorific reflex, the efferent pathway of which comprises both sympathetic and parasympathetic fibers (see the 1st part). While parasympathetic sweating is suppressed by the sympathetic activity in the physiological condition, it may be manifested by loss of the sympathetic innervation.
Mastication not only assists eating and digesting, but also effects the brain eliciting awakening and attention. It is known that the cerebral cortical regional blood flow (rCBF) increases during human mastication, but the mechanism behind this has remained unknown. We found that repetitive electrical stimulation of the cortical masticatory area of anesthetized rats induces a marked increase in rCBF that is independent of blood pressure changes, and is preceded by an increase in neuronal activity in the nucleus basalis of Meynert (NBM). The inhibition of the NBM activity attenuates the rCBF increase, suggesting that NBM activation is involved in the rCBF increase during mastication. In addition, since the increase in rCBF due to stimulation of the masticatory area is unaffected by suppressing masticatory muscle activity, we hypothesize that motor imagery of mastication potentially activates the NBM neurons and increases rCBF similar to actual masticatory jaw movement.
The cholinergic neurons originating in the basal forebrain send projections to the neocortex, hippocampus, and olfactory bulb that contribute to cognition, memory, and olfactory function, respectively. These cholinergic projections to the neocortex and the hippocampus act as vasodilator nerves similar to autonomic nerves. We have recently examined the role of cholinergic projections to the olfactory bulb in blood flow regulation. The cholinergic input to the olfactory bulb releases acetylcholine, but the amount of acetylcholine is less than half of that of the neocortex, and does not influence the regional blood flow in the olfactory bulb. In contrast, the odor-induced increase response of the olfactory bulb blood flow is potentiated by activation of nicotinic acetylcholine receptors in the brain. This indicates that cholinergic transmission enhances olfactory sensitivity in the olfactory bulb. Cholinergic dysfunction may cause the olfactory dysfunction known as an early symptom of dementia.
The aim of this study was to evaluate the nausea and autonomic dysfunction induced by virtual reality (VR) using electrogastrogram (EGG) and heart rate variability (HRV) analysis that were obtained from sixteen male normal volunteers. The VR video had a cylindrical shape with alternating black and white vertical stripes inside, that have been rotated for 15 min around the clock. The total study protocol time was the 45 min divided into the 15 min before period, 15 min VR video stimulation period, and the 15 min after period, respectively. The control group had been only seen just still images of stripes. Also, it had been evaluated that the nausea, and recording of EGG and HRV were demonstrated though into the all experimental periods. VR video stimulation had induced the nausea at motion sickness in the subjects of 90%. It had been obtained that the decrease of normogastria (p<0.05), which was accompanied with an increase of dysrhythmia (p<0.05) in EGG. However, there were no changes in heart rate, HF and LF/HF. Therefore, we had established inducing the nausea at motion sickness and dysrhythmia of EGG by the VR video stimulation with easy.
We report new findings for patients suffering discomfort from the glare of LED (light emitting diodes) and periocular discomfort or ocular pain without any causes in the eyeballs and optic pathways. The total number of cases was nine (age range, 34–62 years old; male to female ratio, 3:6). Clinical characteristics were ocular photophobia, and ocular and periocular pain. The causes of photophobia and photosensitivity were interior lighting, digital devices (displays on PCs and smartphones) and car headlights. In the contrast sensitivity visual acuity test, visual acuity on glare stimulation did not reduce. Abnormalities were not detected in pupillary examinations using pupillography with red / blue light stimulation. Photophobia or ocular pain were the main complaints, despite the absence of pathology in the ocular and optic pathways, and most of the cases had disturbed daily vision. These cases possibly have disorders of higher brain dysfunction related to vision, but the detailed mechanism is not known.
We tracked the changes in the pupillary light reflex and near pupil constriction, as well as refractive values and ocular pressure, in the recovery process in patient with Fisher’s syndrome. The patient, a 61-year-old woman, became aware of double vision after awakening two days after developing upper respiratory inflammation. She was referred to our hospital for pupil dilation in both eyes and exotropia. Her visual acuity was 1.2 in the right eye and 0.9 in the left eye, indicating mild hyperopia. Ocular hypertension was noted, with ocular pressure of 22.2 mmHg in the right eye and 23.7 mmHg in the left eye. Disturbance of eye movement, blepharoptosis, and convergence paralysis were observed. In a bright room, the pupil diameter increased to 6.5 mm in both eyes, while the light reflex and near pupil constriction had disappeared. Based on the patient’s dizziness, a lack of knee reflex, and anti-GQ1b antibody positivity, a diagnosis of Fisher’s syndrome was made. As the patient had severe ocular motility disorder, immunoglobulin therapy was administered. On day 11 after onset, the light reflex had started to improve but near pupil constriction had not returned. Repeat administration of immunoglobulin therapy resulted in improvement in adduction, but the convergence insufficiency remained. The diopter value of hyperopia increased and ocular pressure exhibited marked variation. Our findings imply dissociation of the light reflex and near pupil constriction, as well as dissociation between adduction and convergence insufficiency, suggesting that Fisher’s syndrome causes not only peripheral neuropathy but also central neuropathy.