Mechanisms of oral sensation

Sensory nerves that supply mechanoreceptors in the mucosal lining of the oral cavity, pharynx, and larynx provide the substrate for a variety of sensations. They are essential for the perception of complex or composite sensory experiences including oral kinesthesia and oral stereognosis. Relevant to the concerns of the oral health care delivery specialist they also contribute to initiation of reflexes and coordination and timing of patterned motor behaviors. The response of oral mechanoreceptors to natural stimuli is determined to a large degree by morphological factors such as the nature of the relationship between nerve ending and certain cellular specializations, their distribution in the mucosa, the diameter of their primary afferent nerve fibers, and the central distribution of these fibers in the brainstem. Because of morphological similarities to certain cutaneous mechanoreceptors, the mucosal lining may be considered as an internal continuation of the large receptor sheet for localization and detection of mechanical stimuli. In some regions of the oral, pharyngeal, and laryngeal mucosa, this analogy is appropriate whereas in others, existing data suggest a different role consistent with regionally specific demands (i.e., initiation of protective reflexes).     

Apoptotic cascade of neurons in the subcortical sensory relay nuclei following the neonatal infraorbital nerve transection

A terminal transferase-mediated dUTP nick end labeling (TUNEL) method was utilized for detection of neuronal death in the subcortical relay nuclei of the trigeminosensory system following the infraorbital nerve transection in newborn rats. At 18-24 h after injury, numerous TUNEL-positive profiles were found within the ventroposteromedial thalamic nucleus (VPM) contralateral to the injury, whereas the VPM on the ipsilateral side and of the age-matched normal control contained only a few profiles per section. Electron microscopy revealed that the TUNEL-positive profiles were apoptotic neurons. The ventral part of the ipsilateral brainstem sensory trigeminal nuclear complex (the nucleus principalis, and the subnuclei oralis and interpolaris) exhibited statistically significant 65-70% increase in number of apoptotic neurons compared to the contralateral side. Taken together with our previous study [T. Sugimoto, C. Xiao, H. Ichikawa, Neonatal primary neuronal death induced by capsaicin and axotomy involves an apoptotic mechanism, Brain Res. 807 (1998) 147-154], the present results demonstrated a cascade of apoptosis in the primary, secondary and tertiary order sensory neurons along the neuroaxis.     

Development of weakness in patients with chronic inflammatory demyelinating polyneuropathy and only sensory symptoms at presentation: A long-term follow-up study

This long-term follow-up study examined patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and only sensory symptoms at first presentation, with emphasis on the development of motor symptoms and long-term disability. From all CIDP patients referred to our Department between 1987 and 1995, seven had only sensory symptoms at first clinical presentation. These were investigated according to a standard protocol, including a quantified clinical neurological examination and nerve conduction studies. The mean duration of the disease before weakness developed was 3.1 years, but varied considerably (0.8–6.3 years). At follow-up, weakness developed in five patients and persisted in three of them. Five patients were not seriously incapacitated by their disease (Rankin 1 or 2), four of them being in remission now and one showing a very slow progression of disease. Two patients were moderately disabled (Rankin 3); one had severe persistent sensory ataxia and only weakness during relapses and one had stepwise progression and moderate weakness. Motor nerve conduction studies revealed that the most notable worsening in the entire group of patients was a decrease in distal compound muscle action potential amplitudes, indicating the development of distal conduction block or axonal degeneration. These findings show that CIDP with only sensory symptoms is a transient clinical stage that precedes the appearance of weakness in about 70% of patients. The long-term prognosis does not differ from that of patients with CIDP who have weakness at the beginning of the disease. Received: 3 December 1998 Received in revised form: 17 May 1999 Accepted: 2 July 1999     

Inflammation-induced changes in peripheral glutamate receptor populations

The ionotropic glutamate receptors N-methyl-d-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate (KA) have been localized on subpopulations of unmyelinated and myelinated sensory axons in normal skin. Behavioral studies indicate that activation of these receptors results in nociceptive behaviors and contributes to inflammatory pain. The goal of the present study was to determine if these glutamate receptors might contribute to the peripheral hypersensitivity observed in inflammation. The major findings were that 48 h following complete Freund's adjuvant (CFA)-induced inflammation, the proportions of unmyelinated axons labeled for NMDA, AMPA or KA receptors were 61%, 43% and 48%, respectively, in cutaneous nerves in the inflamed paw compared to 48%, 22% and 27%, respectively, in the non-inflamed paw. The proportions of myelinated axons labeled for NMDA, AMPA or KA receptors were 61%, 61% and 43%, respectively, compared to 43%, 42% and 28%, respectively, in the non-inflamed hindpaw. These increases were all significant. These data indicate that the number of sensory axons containing ionotropic glutamate receptors increases during inflammation, and this may be a contributing factor to peripheral sensitization in inflammation.     

The timing of galvanic vestibular stimulation affects responses to platform translation

We compared the effects of galvanic vestibular stimulation applied at 0, 0.5, 1.5 and 2.5 s prior to a backward platform translation on postural responses. The effect of the galvanic stimulation was largest on the final equilibrium position of the center of pressure (CoP). The largest effects occurred for the 0.5 and 0-s pre-period, when the dynamic CoP pressure changes in response to both the galvanic stimulus and the platform translation coincided. The shift in the final equilibrium position was also larger than the sum of the shifts for the galvanic stimulus and the platform translation alone for the 0.5 and 0-s pre-periods. The initial rate of change of the CoP response to the platform translation was not significantly affected in any condition. Changes in the peak CoP position could be accounted for by local interaction of CoP velocity changes induced by the galvanic and translation responses alone, but the changes in final equilibrium position could only be accounted for by a change in global body orientation. These findings suggest that the contribution of vestibulospinal information is greatest during the dynamic phase of the postural response, and that the vestibular system contributes most to the later components of the postural response, particularly to the final equilibrium position. These findings suggest that a nonlinear interaction between the vestibular signal induced by the galvanic current and the sensory stimuli produced by the platform translation occurs when the two stimuli are presented within 1 s, during the dynamic phase of the postural response to the galvanic stimulus. When presented at greater separations in time, the stimuli appear to be treated as independent events, such that no interaction occurs.     

Medial plantar nerve conduction velocities among patients with vibration syndrome due to chain-saw work

Objective: The present study examined the effect of the vibration syndrome (VS) on the peripheral nervous system in the lower extremities. Methods: Thirty-eight patients with VS due to previous exposure to vibration from chain-saw work and 55 age-matched controls were examined for sensory nerve conduction velocities in the medial plantar nerve (SCV-P). The patient group was divided into two subgroups, one with (n=19) and the other without vibration-induced white finger (VWF; n=19). Results: Analysis of variance of SCV-P for the three groups showed significant difference (F _2,89=10.65, P < 0.0001). A significant difference was found between the controls and the VWF⁺ group (P < 0.0001) but not between the controls and the VWF⁻ group (P=0.0508) by multiple comparison using Scheffe's method. Conclusion: These findings suggest that VS affects the peripheral nervous system function in the lower extremities via mediation of circulatory disturbance manifested as VWF. Received: 7 May 1998 / Accepted: 15 June 1999     

Friedreich's ataxia presenting with pure sensory ataxia: a long-term follow-up study of two patients

We describe two patients with Friedreich's ataxia whose presenting symptomatology was for years progressive tabetic ataxia. Based upon the initial clinical, electrophysiological and nerve biopsy data, a diagnosis of idiopathic sensory neuropathy was established. Subsequent examination of the kin showed that three sisters of case 1 had Friedreich's ataxia. Upon serial clinical and electrocardiographic study, both patients eventually developed a florid Friedreich's ataxia, including cardiomyopathy. Our findings indicate that at onset Friedreich's ataxia may be indistinguishable from sensory neuropathy and also that serial examination and investigation of kinship are essential steps for accurate diagnosis.     

Modulation of the cutaneous responsiveness of neurones in the primary somatosensory cortex during conditioned arm movements in the monkey

Summary The present experiments were designed to investigate the neuronal mechanisms, at the level of the primary somatosensory cortex, which underlie the observation that somatosensory cortical potentials evoked by air puff stimuli directed at the forearm are decreased, in a nonspecific and widespread manner, during voluntary movements about the elbow. Unitary discharge was recorded from 131 cells receiving cutaneous input from the hairy skin of the forearm or hand (areas 3b and 1) of two monkeys trained to perform rapid movements of the contralateral arm (elbow flexion or extension). Evoked unitary responses to air puff stimuli applied to the centre of the cell's receptive field, at various delays before and after the onset of movement, were recorded. Movement produced a significant decrease in the short latency excitatory response to the air puff in 89% of the cells (117/131); the remaining 11% were not modulated by movement. This movement-related gating of cutaneous inputs occurred regardless of the response pattern of the cells to movement alone, being observed in 91% of the cells with no movement-related discharge, and 89% of those with movement-related discharge. The air puff responses of cells with inputs from the forearm and the dorsum of the hand were all similarly modulated by movement and the modulation was clearly present prior to the onset of movement (mean onset, -66 ms). Variation in the depth of modulation as a function of the direction of the movement, flexion or extension, was observed in only a very small proportion of the modulated units (16/117); most showed no relationship to direction. It is suggested that, in this experimental situation, much of the modulation appears to occur at a pre-cortical level since there was no relationship between the pattern of discharge of cells in relation to movement alone and the pattern of movement-related gating of their responses to the air puff. Effects which might be consistent with a cortical origin for the modulation were only infrequently observed. The present results are strikingly similar to those obtained using the evoked potential method, and thus support the hypothesis that, in this task of rapid elbow movements, movement modulates the transmission of cutaneous signals from the hairy skin of the distal forelimb to primary somatosensory cortex in a nonspecific and widespread fashion.     

Lateral asymmetries in the trigeminal ganglion of the male rat

We have applied stereological methods to estimate the number and perikaryal size of primary sensory neurons in celloidin-embedded trigeminal ganglia of male albino rats, specifically looking for inter-individual and side variability. The mean total number of neurons per ganglion was 35,300, with a moderate variability among ganglia. On average, 66% of the neurons were classified as A-type and 34% as B-type. Although for individual cases there could be notable side differences in the number of neurons of each type, on a population basis these differences were not significant. Mean neuronal volume was four times larger for A- than for B-cells, and both populations exhibited a moderate variability among individuals. High intra-animal side differences were found for A-cells, which were on average a significant 23.5% larger in the right ganglia. B-cells did not show significant side differences. The distribution of individual volumes around the mean value was consistently skewed to the right, particularly in the case of A-cells, which partially overlapped with the largest B-cells. In the right ganglion the distribution of A-cells, but not of B-cells, showed a rightward bias, revealing the increase in bigger neurons. The existence of larger A-type neurons in the right trigeminal ganglion may provide a structural substrate for some somesthetically based complex behaviors which are best performed by rats using their right vibrissae.     

Inflammation-induced changes in primary afferent-evoked release of substance P within trigeminal ganglia in vivo

Substance P (SP) is synthesized in a subset of nociceptive sensory neurons and is released from their peripheral and central terminals. Here we demonstrate with the use of in vivo microdialysis and radioimmunoassay techniques that SP is also released within trigeminal ganglia following intraganglionic application of KCl, veratridine or capsaicin, and after electrical stimulation of peripheral afferent fibers. Both the basal and KCl-evoked release of SP are shown to be dependent on extracellular calcium. Using the turpentine-induced model of unilateral orofacial inflammation we also show that both the basal and KCl-evoked release of SP within trigeminal ganglia are greatly increased on the inflamed side 48 h after induction of inflammation. Coupled with previous demonstrations of excitatory effects of SP on sensory neurons, these results suggest that SP fulfils the role of a non-synaptically released diffusible chemical messenger that may modulate the somatic excitability of neurons within sensory ganglia in inflammatory pain states.