Improvement Of Sensory Deficits Research Articles

Improvement of sensory deficits in fragile X mice by increasing cortical interneuron activity after the critical period

Changes in the function of inhibitory interneurons (INs) during cortical development could contribute to the pathophysiology of neurodevelopmental disorders. Using all-optical invivo approaches, we find that parvalbumin (PV) INs and their immature precursors are hypoactive and transiently decoupled from excitatory neurons in postnatal mouse somatosensory cortex (S1) of Fmr1 KO mice, a model of fragile X syndrome (FXS). This leads to a loss of parvalbumin INs (PV-INs) in both mice and humans with FXS. Increasing the activity of future PV-INs in neonatal Fmr1 KO mice restores PV-IN density and ameliorates transcriptional dysregulation in S1, but not circuit dysfunction. Critically, administering an allosteric modulator of Kv3.1 channels after the S1 critical period does rescue circuit dynamics and tactile defensiveness. Symptoms in FXS and related disorders could be mitigated by targeting PV-INs.

Chronic Pain: Management Strategies That Work

Chronic Pain: Management Strategies That Work

Laryngopharyngeal sensory deficits in patients with laryngopharyngeal reflux and dysphagia.

There are no reliable means of quantifying the edema that results from acid exposure to the posterior larynx in patients with laryngopharyngeal reflux (LPR). However, it is possible to quantify laryngopharyngeal sensitivity in these patients by endoscopic administration of air pulses to the laryngeal mucosa in order to elicit the laryngeal adductor reflex. The purpose of this study was to determine whether patients with LPR have sensory deficits in the laryngopharynx, and whether treatment of these patients with a proton pump inhibitor (PPI) results in resolution of sensory deficits. Flexible endoscopic evaluation of swallowing with sensory testing was prospectively performed in 54 patients with dysphagia without neurologic disease and in 25 healthy controls. The laryngopharyngeal sensory level, posterior laryngeal edema, and LPR were assessed. We defined LPR as passage of food material from the esophageal inlet retrograde into the hypopharynx. Patients with LPR were placed on 3 months of omeprazole or lansoprazole and then retested. Patients without LPR were placed on H2 blockers for 3 months and then retested. In the dysphagia group, 48 of 54 patients (89%) had edema of the posterior larynx, and 42 of 54 (78%) had laryngopharyngeal sensory deficits. We noted LPR in 38 of 54 (70%). In the control group, 1 of 25 subjects (4%) had edema, sensory deficits, and LPR. The differences in incidence of edema, sensory deficits, and LPR between the dysphagia group and the control group were significant (p < .001, chi2 test). Twenty-three patients with LPR placed on a PPI returned for follow-up, with improvement in laryngeal edema in 14 of the 21 (67%) who had pretreatment edema and resolution of sensory deficits in 15 of the 19 (79%) who had pretreatment deficits. In the non-LPR, non-PPI group, 11 of 16 patients returned for follow-up, with improvement in laryngeal edema in none of the 11 and improvement in sensory deficits in 1 of the 11 (9.1%). The differences in improvement in laryngeal edema and sensory deficits between the LPR, PPI group, and the non-LPR, non-PPI group were significant (p < .01, Fisher's exact test). We conclude that patients with dysphagia and edema of the posterior larynx as a result of LPR have sensory deficits in the laryngopharynx. Treatment of these patients with a PPI appears to result in resolution of laryngopharyngeal edema and improvement of sensory deficits, both subjectively and objectively.