No abstract

Background Maturation of pharyngeal swallowing during neonatal oral feeding is unknown. Our objective was to evaluate pharyngeal functioning using high‐resolution manometry (HRM) during nutritive oral stimulus and test the hypothesis that pharyngeal contractility and regulation are distinct in preterm‐born infants. Methods High‐resolution manometry data during oral milk feeding were analyzed for pharyngeal contractile (PhCI, mm Hg cm s) and regulatory (number and frequency of pharyngeal contractions and bursts, pharyngeal activity‐to‐quiescence ratio, upper esophageal sphincter nadir pressure) characteristics in 23 preterm (<38 weeks’ gestation) and 18 full‐term‐born infants at term maturation. Mixed linear models and stepwise regression methods were used. Results Despite more oral feeding experiences (P < 0.05), preterm infants (vs full‐term), consumed less milk volume (P < 0.001), had lesser pharyngeal contractions within bursts (P = 0.04), lower pharyngeal contraction frequency (P < 0.01), and lower pharyngeal activity (P = 0.03), but higher PhCI per individual contraction (P = 0.01). PhCI is higher for longer PMA (P < 0.05), higher UES nadir pressures (P < 0.05), and lower pharyngeal contraction frequency (P < 0.05). Conclusions Nutritive oral milk stimulus provoked pharyngeal contractility characteristics is distinct in preterm‐born. Despite more oral nutritive experiences, preterm infants had underdeveloped excitatory and inhibitory rhythmic activity. Cranial nerve IX and X effects on sensory‐motor responses and feedback (excitation‐inhibitory rhythm regulation) remain immature among preterm‐born even at full‐term maturational status. We speculate the relationship between PhCI and UES regulatory activity contributes to the observed differences in preterm and full‐term infants.

PhCI is a novel reliable metric capable of distinguishing (1) proximal and distal pharyngeal activity, (2) effects of oral and pharyngeal stimulation, and (3) effects of prolonged stimulation. Changes in pharyngeal contractility with maturation, disease, and therapies can be examined with PhCI.

Objective Eating difficulties coupled with cardiorespiratory spells delay acquisition of feeding milestones in convalescing neonates, and the mechanisms are unclear. Aims were to examine and compare the pharyngoesophageal–cardiorespiratory (PECR) response characteristics: (a) in control neonates and those with recurrent bradycardia spells; and (b) during pharyngeal stimulation when bradycardia occurs versus when no bradycardia occurs. Methods Preterm infants ( N = 40, 27 ± 3 weeks gestation), underwent concurrent pharyngoesophageal manometry, electrocardiography, respiratory inductance plethysmography, and nasal airflow thermistor to evaluate pharyngoesophageal motility, heart rate (HR), and respiration during graded abrupt pharyngeal sterile water stimuli. Infants with recurrent bradycardia ( N = 28) and controls ( N = 12) were evaluated at 38 (38–40) and 39 (38–40) weeks postmenstrual age, respectively. Comparisons were performed (a) between study and control groups; and (b) among HR responses of <80 BPM, 80–100 BPM, and >100 BPM. Results Overall, characteristics of PECR responses in infants with a history of recurrent bradycardia (vs. controls) did not differ ( p > .05). However, when pharyngeal stimulus induced severe bradycardia (<80 BPM): prolonged respiratory rhythm change, increased pharyngeal activity, increased esophageal dysmotility (as evidenced by prolonged esophageal inhibition and motor activity), and prolonged lower esophageal sphincter relaxation were noted (all p < .05). Conclusions In control infants and those with recurrent bradycardia, pharyngeal stimulation results in similar PECR response characteristics. However, when severe bradycardia occurs, PECR response characteristics are distinct. The mechanisms of severe bradycardia spells are related to abnormal prolongation of vagal inhibitory effects on cardiorespiratory rhythms in conjunction with prolonged esophageal inhibition and delays with terminal swallow.

OBJECTIVE: To identify esophageal sensitivity phenotypes relative to acid (S Acid ), bolus (SBolus), acid and bolus (S Acid+Bolus ), and none (S None ) exposures in infants suspected with gastroesophageal reflux disease (GERD). METHODS: Symptomatic infants (N=279) were evaluated for GERD at 42(40–45) weeks postmenstrual age using 24-hour pH-impedance. Symptom associated probability (SAP) for acid and bolus components defined esophageal sensitivity: 1) S Acid as SAP≥95% for acid (pH<4), 2) S Bolus as SAP≥95% for bolus, 3) S Acid+Bolus as SAP≥95% for acid and bolus, or 4) S None as SAP<95% for acid and bolus. RESULTS: Esophageal sensitivity prevalence (S Acid , SBolus, SAcid+Bolus, S None ) was 28(10%), 94(34%), 65(23%), and 92(33%) respectively. Emesis occured more in SBolus and S Acid+Bolus vs S None (p<0.05). Magnitude (#/day) of cough and emesis events increased with S Bolus and S Acid+Bolu s vs S None (p<0.05). S Acid+Bolus had increased acid exposure vs S None (p<0.05). Distributions of feeding and breathing methods were distinct in infants with S Bolus vs S None (both, p<0.05). Multivariate analysis revealed that arching and irritability events/day were lesser at higher PMAs (p<0.001), greater for infants on NCPAP (p<0.01), with S Bolus and S Acid+Bolu s (p<0.05). Coughs/day was greater at higher PMAs (p<0.001), for infants with gavage and transitional feeding methods (p<0.02), with S Bolu s and S Acid+Bolus (p<0.05) but lesser with Trach (p<0.001). Number of emesis events/day were greater with SBolus and SAcid+Bolus (p<0.001). Sneezes/day decreased for infants on Trach (p=0.02). CONCLUSIONS: Feeding and breathing methods can influence the frequency and type of aerodigestive symptoms. We differentiated esophageal sensitivity phenotypes in NICU infants referred for GERD symptoms using pH-Impedance. Acid sensitivity alone was rare, which may explain poor response to acid suppressives; aerodigestive symptoms were predominantly linked with bolus spread. Magnitude of esophageal acid exposure and esophageal sensitivity to bolus spread may explain the pathophysiological basis for symptoms.

Introduction : Motor and cognitive deficits were compared in aging, chronically treated human immunodeficiency virus (HIV) people, people with mild-to-moderate stage Parkinson’s disease (PD), and healthy controls. Methods : Groups consisted of 36 people with PD, 28 with HIV infection, and 28 healthy controls. Motor function was assessed with the Unified Parkinson’s Disease Rating Scale (MDS-UPDRS-III) and a rapid alternating finger tapping (RAFT) task on an engineered keyboard known as Quantitative Digitography (QDG). Executive function, verbal memory, and visuospatial processing were assessed using standard neuropsychological tests. Results : HIV demonstrated RAFT deficits similar to PD such as reduced amplitude ( P = 0.023) and greater amplitude variability ( P = 0.019) in the index finger when compared to controls. This fine motor disturbance correlated with HIV’s immune health, measured by their CD4 + T cell count ( P < 0.01). The UPDRS did not yield motor differences between HIV and controls. Executive function and verbal memory were impaired in HIV ( P = 0.006, P = 0.016, respectively), but not in PD; visuospatial processing was similarly impaired in HIV and PD ( P < 0.05) although motor deficits predominated in PD. Conclusions : Fine motor bradykinesia measured quantitatively by QDG RAFT holds promise as a marker of motor decline related to current immune health in aging HIV patients and may be useful in longitudinal studies regarding mechanisms of immunosenescence vs. potential toxicity of combination antiretroviral therapy (cART) in this population. Additionally, motor and cognitive networks in HIV may be affected differently as the disease progresses as observed in the differential patterns of impairment between HIV and PD, providing insight into the mechanisms of brain deterioration in HIV.

No abstract

Despite the life-extending success of antiretroviral pharmacotherapy in HIV infection (HIV), the prevalence of mild cognitive impairment in HIV remains high. Near-normal life expectancy invokes an emerging role for age-infection interaction and a potential synergy between immunosenescence and HIV-related health factors, increasing risk of cognitive and motor impairment associated with degradation in corticostriatal circuits. These neural systems are also compromised in Parkinson's disease (PD), which could help model the cognitive deficit pattern in HIV. This cross-sectional study examined three groups, age 45-79 years: 42 HIV, 41 PD, and 37 control (CTRL) participants, tested at Stanford University Medical School and SRI International. Neuropsychological tests assessed executive function (EF), information processing speed (IPS), episodic memory (MEM), visuospatial processing (VSP), and upper motor (MOT) speed and dexterity. The HIV and PD deficit profiles were similar for EF, MEM, and VSP. Although only the PD group was impaired on MOT compared with CTRL, MOT scores were related to cognitive scores in HIV but not PD. Performance was not related to depressive symptoms, socioeconomic status, or CD4 + T-cell counts. The overlap of HIV-PD cognitive deficits implicates frontostriatal disruption in both conditions. The motor-cognitive score relation in HIV provides further support for the hypothesis that these processes share similar underlying mechanisms in HIV infection possibly expressed with or exacerbated by ageing.