Brain Mechanisms of Oral Sensory Functions

2021 ◽  
pp. 128-160
2008 ◽  
Vol 3 (S 1) ◽  
Author(s):  
HK Berthold ◽  
S Unverdorben ◽  
R Degenhardt ◽  
B Geypens ◽  
I Gouni-Berthold

2019 ◽  
Vol 1 (2) ◽  
pp. 11-14
Author(s):  
O. S. Levin ◽  
O. V. Matvievskaya

The article contains a comprehensive analysis of the summary epidemiological data obtained during the observational study to assess the effect of therapy with Ipigrix® on the dynamics of motor and sensory functions, as well as the severity of pain in outpatient patients with various diseases of the peripheral nervous system: mononeuropathy, polyneuropathy and polyradiculopathy of various origins.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tao Tang ◽  
Christopher R. Donnelly ◽  
Amol A. Shah ◽  
Robert M. Bradley ◽  
Charlotte M. Mistretta ◽  
...  

AbstractDuring development of the peripheral taste system, oral sensory neurons of the geniculate ganglion project via the chorda tympani nerve to innervate taste buds in fungiform papillae. Germline deletion of the p75 neurotrophin receptor causes dramatic axon guidance and branching deficits, leading to a loss of geniculate neurons. To determine whether the developmental functions of p75 in geniculate neurons are cell autonomous, we deleted p75 specifically in Phox2b + oral sensory neurons (Phox2b-Cre; p75fx/fx) or in neural crest-derived cells (P0-Cre; p75fx/fx) and examined geniculate neuron development. In germline p75−/− mice half of all geniculate neurons were lost. The proportion of Phox2b + neurons, as compared to Phox2b-pinna-projecting neurons, was not altered, indicating that both populations were affected similarly. Chorda tympani nerve recordings demonstrated that p75−/− mice exhibit profound deficits in responses to taste and tactile stimuli. In contrast to p75−/− mice, there was no loss of geniculate neurons in either Phox2b-Cre; p75fx/fx or P0-Cre; p75fx/fx mice. Electrophysiological analyses demonstrated that Phox2b-Cre; p75fx/fx mice had normal taste and oral tactile responses. There was a modest but significant loss of fungiform taste buds in Phox2b-Cre; p75fx/fx mice, although there was not a loss of chemosensory innervation of the remaining fungiform taste buds. Overall, these data suggest that the developmental functions of p75 are largely cell non-autonomous and require p75 expression in other cell types of the chorda tympani circuit.


2005 ◽  
Vol 288 (6) ◽  
pp. G1195-G1198 ◽  
Author(s):  
Shi Liu ◽  
Lijie Wang ◽  
J. D. Z. Chen

Gastric electrical stimulation (GES) has been shown to alter motor and sensory functions of the stomach. However, its effects on other organs of the gut have rarely been investigated. The study was performed in 12 dogs implanted with two pairs of electrodes, one on the serosa of the stomach and the other on the colon. The study was composed of two experiments. Experiment 1 was designed to study the effects of GES on rectal tone and compliance in nine dogs compared with colonic electrical stimulation (CES). Rectal tone and compliance were assessed before and after GES or CES. Experiment 2 was performed to study the involvement of sympathetic pathway in 8 of the 12 dogs. The rectal tone was recorded for 30–40 min at baseline and 20 min after intravenous guanethidine. GES or CES was given for 20 min 20 min after the initiation of the infusion. It was found that both GES and CES reduced rectal tone with comparable potency. Rectal compliance was altered neither with GES, nor with CES. The inhibitory effect of GES but not CES on rectal tone was abolished by an adrenergic blockade, guanethidine. GES inhibited rectal tone with a comparable potency with CES but did not alter rectal compliance. The inhibitory effect of GES on rectal tone is mediated by the sympathetic pathway. It should be noted that electrical stimulation of one organ of the gut may have a beneficial or adverse effect on another organ of the gut.


2018 ◽  
Vol 127 (12) ◽  
pp. 978-985
Author(s):  
Lotta Sjögreen ◽  
Margareta Gonzalez Lindh ◽  
Madeleine Brodén ◽  
Corinna Krüssenberg ◽  
Irvina Ristic ◽  
...  

Objectives: Dysphagia and impaired saliva control are common in children and adolescents with congenital and developmental disabilities. The aim of the present review was to investigate the evidence base for oral sensory-motor interventions in children and adolescents with dysphagia or impaired saliva control secondary to congenital or early-acquired disabilities and to make recommendations regarding methods for intervention. Methods: A review of the literature from 2000 to 2016, including oral sensory-motor intervention studies for children and adolescents (3-18 years of age) with dysphagia or impaired saliva control secondary to congenital or early-acquired disabilities, was performed. The literature search included the PubMed, CINAHL, Medline, SpeechBITE, OVID, ERIC, Cochrane, and Google Scholar databases. Primary studies were evaluated on a 4-grade scale using the Grading of Recommendations Assessment, Development and Evaluation. Results: Twenty primary studies of oral sensory-motor interventions for dysphagia and 6 studies for the treatment of impaired saliva control fulfilled the inclusion criteria. Of these, 3 were randomized, controlled trials. Five systematic reviews and 16 narrative reviews were also included. Limited and moderately strong recommendations were made on the basis of the grading results from the primary studies. The studies reported good results, but study design was often insufficient, and the study groups were small. The systematic reviews confirmed the lack of high scientific support for oral sensory-motor interventions in children and adolescents with congenital and developmental disabilities. Conclusions: There is an urgent need for high-quality studies that could serve as the basis for strong recommendations relating to oral sensory-motor interventions for children with dysphagia and impaired saliva control.


1996 ◽  
Vol 270 (6) ◽  
pp. R1371-R1379 ◽  
Author(s):  
K. L. Teff ◽  
K. Engelman

In animals, bypassing the oropharyngeal receptors by intragastric administration of glucose results in glucose intolerance. To determine whether the absence of oral sensory stimulation alters glucose tolerance in humans, we monitored plasma levels of glucose and hormones after intragastric administration of glucose, with and without subjects tasting food. Plasma glucose area under the curve (AUC) was significantly lower after oral sensory stimulation (3,433 +/- 783 vs. 5,643 +/- 1,397 mg.dl-1. 195 min-1; P < 0.03; n = 8). Insulin and C-peptide AUCs were higher during the first one-half of the sampling period (insulin, 5,771 +/- 910 vs. 4,295 +/- 712 microU. ml-1.75 min-1; P < 0.05; C-peptide, 86 +/- 10 vs. 66 +/- 9 ng.ml-1. 75 min-1; P < 0.03) and lower during the second one-half of the sampling period compared with the control condition (1,010 +/- 233 vs. 2,106 microU.ml-1. 120 min-1; P < 0.025; 31 +/- 8 vs. 56 +/- 18 ng.ml-1. 120 min-1; P < 0.05; insulin and C-peptide, respectively). Oral sensory stimulation markedly increased plasma glucagon compared with the control condition (1,258 +/- 621 vs. -2,181 +/- 522 pg.ml-1. 195 min-1; P < 0.002). These data provide evidence in humans that oral sensory stimulation influences glucose metabolism and suggest that the mechanisms elicited by this cephalic stimulation are necessary for normal glucose homeostasis.


Diagnostics ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. 64 ◽  
Author(s):  
Frank Twisk

Myalgic encephalomyelitis (ME), identified as a new clinical entity with distinctive features in 1956, was originally considered as a neuromuscular disease. In 1988 the Centers for Disease Control and Prevention introduced the ill-defined concept of chronic fatigue syndrome (CFS). As predicted, CFS, unjustly considered to be a synonym for ME, pushed ME to the background. To develop effective therapies for of ME and CFS, it is essential to investigate patients with ME specifically. For that reason, an operational definition of ME is indispensable. This article proposes an operational definition based on the most recent formal definitions and symptoms observed in ME. ME is a multi-systemic illness, which (1) often has a sudden onset, in most cases a respiratory and/or gastro-intestinal infection, but a gradual or more dramatic onset is also possible; (2) has an epidemic and an endemic form; (3) has an unique clinical pattern deviating from other post-viral states; (4) is distinguished by muscle fatigability/prolonged muscle weakness after trivial exertion; (5) is accompanied by symptoms relating to neurological disturbance, especially of cognitive, autonomic, and sensory functions; (6) can be accompanied by symptoms associated with cardiac and other systems; (7) is characterized by fluctuation of symptoms (within and between “episodes”); (8) has a prolonged relapsing course; and (9) has a tendency to become chronic. In conclusion, a discriminative definition for ME contains four mandatory elements: (1) muscle fatigability/post-exertional muscle weakness lasting for days; (2) operational criteria for “neurological disturbance, especially of cognitive, autonomic and sensory functions”; (3) fluctuation of symptoms; and (4) a prolonged relapsing course. This tentative definition of ME justifies the qualification “neuromuscular disease”.


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