Citations 17

Weight Loss in Parkinson’s Disease: No Evidence for Role of Small Intestinal Bacterial Overgrowth

Journal of Parkinson’s Disease | November 26, 2024 | Volume: 8 | Issue: 4 | Pages: 571-581

10.3233/jpd-181386 | PMID 30149465

Background and Objective: Weight loss and small intestinal bacterial overgrowth (SIBO) are common in Parkinson’s disease (PD). We aimed to study the relationship between weight loss and SIBO in PD. Methods: This was a cross-sectional study with a prospective, interventional component. Consecutive patients seen in the PD clinic who agreed to participate underwent extensive history, movement exam, SIBO breath testing and answered questionnaires. A subset of those in the weight loss group were treated with rifaximin for 14 days and returned 3 months later for an assessment of their weight, GI symptoms, quality of life and SIBO status. All analyses were adjusted for age and disease duration. Results: Fifty-one patients participated in the study; 37 without weight loss and 14 with weight loss. Total energy intake including the distribution of macronutrient intake was similar between groups while physical activity was less in those with weight loss. PD severity scores did not differ between groups; however, PD-specific quality of life scores were significantly worse for the summary index and the subscales of emotional well-being, social support and communication. The prevalence of constipation, dyspepsia and abdominal pain/discomfort was higher in those with weight loss. The prevalence of SIBO was 14% in the weight loss group and was not different between groups. Eight PD patients with weight loss were treated with rifaximin; no significant change in GI symptoms, quality of life or weight was seen 3 months later. Conclusion: Although a number of differences were identified in quality of life and gastrointestinal symptoms between groups with and without weight loss, SIBO was not associated with weight loss in patients with PD. Given the exploratory nature and small number of patients with weight loss, however, further study is suggested.
Migraine in Postural Orthostatic Tachycardia Syndrome (POTS) (P3.126)

Neurology | December 7, 2023 | Volume: 90 | Issue: 15_supplement | Pages: No page available

10.1212/wnl.90.15_supplement.p3.126

Elevated Paraneoplastic Markers: An Uncommon Finding in Orthostatic Intolerance and Postural Orthostatic Tachycardia (P2.134)

Neurology | December 7, 2023 | Volume: 90 | Issue: 15_supplement | Pages: No page available

10.1212/wnl.90.15_supplement.p2.134

Characterizing the spectrum of autonomic impairment in neurologic disorders with calcium channel antibodies (P2.114)

Neurology | December 7, 2023 | Volume: 90 | Issue: 15_supplement | Pages: No page available

10.1212/wnl.90.15_supplement.p2.114

Joint Hypermobility Syndrome in a Postural Orthostatic Tachycardia Syndrome (POTS) Cohort (P5.116)

Neurology | December 7, 2023 | Volume: 86 | Issue: 16_supplement | Pages: No page available

10.1212/wnl.86.16_supplement.p5.116

A Longitudinal Study Capturing the Transition in Personality (NEO-PI-R) from Preclinical AD to Incident MCI (P3.093)

Neurology | December 7, 2023 | Volume: 88 | Issue: 16_supplement | Pages: No page available

10.1212/wnl.88.16_supplement.p3.093

Psychological Stress and Age-Related Memory decline (P2.172)

Neurology | December 6, 2023 | Volume: 84 | Issue: 14_supplement | Pages: No page available

10.1212/wnl.84.14_supplement.p2.172

Vestibular Symptoms are Common in Postural Tachycardia Syndrome (PoTS) (P1.281)

Neurology | December 6, 2023 | Volume: 84 | Issue: 14_supplement | Pages: No page available

10.1212/wnl.84.14_supplement.p1.281

Evidence of Mast Cell Activation Disorder in Postural Tachycardia Syndrome (P1.277)

Neurology | December 6, 2023 | Volume: 84 | Issue: 14_supplement | Pages: No page available

10.1212/wnl.84.14_supplement.p1.277

Personality Changes During the Transition from Cognitive Health to Mild Cognitive Impairment

Journal of the American Geriatrics Society | January 17, 2018 | Volume: 66 | Issue: 4 | Pages: 671-678

10.1111/jgs.15182 | PMID 29341070

Background/Objectives Behavioral problems in individuals with Alzheimer's disease ( AD ) impose major management challenges. Current prevention strategies are anchored to cognitive outcomes, but behavioral outcomes may provide another, clinically relevant opportunity for preemptive therapy. We sought to determine whether personality changes that predispose to behavioral disorders arise during the transition from preclinical AD to mild cognitive impairment ( MCI ). Design Longitudinal observational cohort study. Setting Academic medical center. Participants Members of an apolipoprotein E ( APOE ) ɛ4 genetically enriched cohort of Maricopa County residents who were neuropsychiatrically healthy at entry (N = 277). Over a mean interval of 7 years, 25 who developed MCI and had the Neuroticism, Extraversion, and Openness Personality Inventory—Revised ( NEO ‐ PI ‐R) before and during the MCI transition epoch were compared with 252 nontransitioners also with serial NEO ‐ PI ‐R administrations. Intervention Longitudinal administration of the NEO ‐ PI ‐R and neuropsychological test battery. Measurements Change in NEO ‐ PI ‐R factor scores (neuroticism, extraversion, openness, agreeableness, conscientiousness) from entry to the epoch of MCI diagnosis or an equivalent follow‐up duration in nontransitioners. Results NEO ‐ PI ‐R neuroticism T‐scores increased significantly more in MCI transitioners than in nontransitioners (mean 2.9, 95% confidence interval ( CI ) = 0.9–4.9 vs 0, 95% CI = −0.7–0.7, P = .02), and openness decreased more in MCI transitioners than in nontransitioners (−4.8, 95% CI = −7.3 to −2.4 vs −1.0, 95% CI = −1.6 to −0.4, P < .001). Concurrent subclinical but statistically significant changes in behavioral scores worsened more in MCI transitioners than nontransitioners for measures of depression, somatization, irritability, anxiety, and aggressive attitude. Conclusion Personality and subclinical behavioral changes begin during the transition from preclinical AD to incident MCI and qualitatively resemble the clinically manifest behavioral disorders that subsequently arise in individuals with frank dementia.