• Autonomic dysfunction
• Behavioral assays
• Cognitive impairment
• Hyposmia
• Non-motor symptoms
• Parkinson's disease
• Psychiatric disorders
• Sleep disorders

• Animals
• Parkinson Disease/physiopathology
• Parkinson Disease/complications
• Disease Models, Animal
• Humans
• Sleep Wake Disorders/etiology
• Sleep Wake Disorders/physiopathology
• Cognitive Dysfunction/etiology
• Cognitive Dysfunction/physiopathology
• Mental Disorders/etiology
• Mental Disorders/physiopathology

• A53T
• Constipation
• Enteric nervous system
• Gastrointestinal dysfunction
• Parkinson’s disease

• Animals
• Enteric Nervous System/pathology
• Enteric Nervous System/physiopathology
• Enteric Nervous System/metabolism
• Mice
• alpha-Synuclein/metabolism
• alpha-Synuclein/genetics
• Parkinson Disease/pathology
• Parkinson Disease/physiopathology
• Parkinson Disease/metabolism
• Parkinson Disease/genetics
• Disease Models, Animal
• Mice, Transgenic
• Gastrointestinal Motility/physiology
• Male
• Mice, Inbred C57BL
• Gastrointestinal Tract/pathology
• Gastrointestinal Tract/physiopathology
• Gastrointestinal Tract/innervation

• GNT1183420 National Health and Medical Research Council
• Melbourne Research Scholarship, The University of Melbourne
• Jack Brockhoff Foundation

• Dementia with Lewy bodies
• Gastrointestinal tract
• Immunity
• Inflammation
• Microbiome
• Parkinson’s disease
• Parkinson’s disease dementia

• Humans
• Lewy Body Disease/pathology
• Lewy Body Disease/metabolism
• Gastrointestinal Microbiome/physiology
• Animals
• Gastrointestinal Tract
• alpha-Synuclein/metabolism
• Gastrointestinal Diseases

• ASAP-020527 Aligning Science Across Parkinson's
• RF1NS128800 NIH HHS
• R01 NS064934 NINDS NIH HHS
• PF-JFA-830658 Parkinson's Disease Foundation
• I01 BX002230 BLRD VA
• R01 NS064934 NIH HHS
• R01 ES032440 NIH HHS
• U01NS113851 NIH HHS
• National Institutes of Health
• U.S. Department of Veterans Affairs

• 3-O-Methyldopa
• Apomorphine
• Gastroparesis
• Inhaled levodopa
• Levodopa-carbidopa intestinal gel
• deep brain stimulation
• dysmotility

• Humans
• Parkinson Disease/therapy
• Antiparkinson Agents/administration & dosage

• enteric nervous system
• gastric motility
• prodromal Parkinson's disease
• rapid-eye-movement sleep behavior disorder
• real-time magnetic resonance imaging

• Humans
• Parkinson Disease/complications
• Parkinson Disease/pathology
• Synucleinopathies
• REM Sleep Behavior Disorder/pathology
• Stomach/pathology
• Sleep

• ParkinsonFonds Deutschland

• Alzheimer’s disease
• Gut-brain
• Parkinson’s disease
• fecal transplantation
• microbiota
• mood disorders
• probiotics.

• Humans
• Neurodegenerative Diseases
• Depression/therapy
• Gastrointestinal Diseases/therapy
• Anxiety
• Gastrointestinal Microbiome/physiology
• Brain-Gut Axis/physiology
• Gastrointestinal Tract

• Parkinson’s disease
• clinical study
• drug absorption
• duodenal fluid composition
• gastrointestinal fluid aspiration

• C24/17/076 KU Leuven
• 1830517N Research Foundation - Flanders
• NA UCB Biopharma SPRL

• Parkinson's disease
• gastrointestinal dysmotility
• gastrointestinal transit time
• levodopa response
• small intestinal bacterial overgrowth

• 6-OHDA rat
• gastric emptying
• nNOS
• pyloric motility

Disturbances of circulating amino acids have been demonstrated in patients with Parkinson’s disease (PD). However, there have been no consistent results for branched-chain amino acids (BCAAs) and aromatic amino acids (AAAs), and related factors have not been explored. We aimed to explore plasma BCAA and AAA profiles in PD patients, and identify their correlations with clinical characteristics and the gut microbiota. Plasma BCAA (leucine, isoleucine, and valine) and AAA (tyrosine and phenylalanine) levels were measured in 106 PD patients and 114 controls. Fecal samples were collected from PD patients for microbiota sequencing and functional analysis. We found that plasma BCAAs and tyrosine were decreased in PD patients. BCAAs and AAAs were correlated with clinical characteristics and microbial taxa, and, in particular, they were negatively correlated with the Hoehn and Yahr stage. Compared with early PD patients, BCAA and AAA levels were even lower, and microbial composition was altered in advanced PD patients. Predictive functional analysis indicated that predicted genes numbers involved in BCAA biosynthesis were lower in advanced PD patients. What’s more, the fecal abundances of critical genes (ilvB, ilvC, ilvD, and ilvN) involved in BCAA biosynthesis were reduced and fecal BCAA concentrations were lower in advanced PD patients. In conclusion, the disturbances of plasma BCAAs and AAAs in PD patients may be related to the gut microbiota and exacerbated with PD severity. The microbial amino acid metabolism may serve as a potential mechanistic link.

• Parkinson's disease
• constipation
• drooling
• dysphagia
• gastrointestinal dysfunction
• gastroparesis

• Parkinson disease
• alpha-synuclein
• gastroparesis
• vagus nerve

• Disability
• Parkinson disease
• Severity
• Weight change

Parkinson's disease (PD) is a common neurodegenerative disease in the middle-aged and the elderly. Symptoms of autonomic dysfunctions are frequently seen in PD patients, severely affecting the quality of life. This review summarizes the epidemiology, clinical manifestations, and treatment options of autonomic dysfunctions. The clinical significance of autonomic dysfunctions in PD early diagnosis and differential diagnosis is also discussed.

• Dyspepsia
• Dysphagia
• Gastroparesis
• Nausea and vomiting
• Oropharyngeal dysphagia
• Parkinson’s disease

Altered gastric motility is a frequent non-motor symptom of Parkinson’s disease (PD). It has been hypothesized that disturbed gastric motility contributes to motor fluctuations in PD due to an erratic gastro-duodenal transport and an unpredictable absorption of drugs.

We investigated whether patient-reported fluctuations are associated with parameters of gastric motility visualized by real-time magnetic resonance imaging (MRI) of the stomach.

We analyzed real-time MRI-scans of the stomach after an overnight fasting period in 16 PD patients and 20 controls. MRI was performed 1) in the fasting state, 2) directly after a test meal, and 3) 4 hours postprandially. Gastric motility indices were calculated and compared between groups.

MRI showed an attenuated gastric motility in PD patients compared to controls. The difference was most obvious in the early postprandial phase. Gastric motility was not associated with patient-reported motor fluctuations. Using an iron-containing capsule we were able to retrace retention of drugs in the stomach.

The results of this study stress the importance of considering the phase of digestion when investigating gastric motility in PD. Despite theoretical considerations, we did not find robust evidence for an association between MRI parameters of gastric motility and patient-reported motor fluctuations. For future studies that aim to investigate gastric motility in PD by MRI, we suggest multiple short-time MRIs to better track the whole gastro-duodenal phase in PD. Such an approach would also allow to retrace the retention of drugs in the stomach as shown by our approach using an iron-containing capsule.

• Parkinson’s disease
• gastrointestinal motility
• real-time magnetic resonance imaging
• stomach

• Delayed gastric emptying
• Gastroparesis
• Helicobacter pylori
• Levodopa
• Motor fluctuations
• OFF periods
• Parkinson's disease

• Dementia/diagnosis
• Dementia/therapy
• Humans
• Lewy Bodies
• Lewy Body Disease/diagnosis
• Lewy Body Disease/therapy
• Neurodegenerative Diseases/diagnosis
• Neurodegenerative Diseases/therapy
• Parkinson Disease/diagnosis
• Parkinson Disease/therapy

• G1100540 Medical Research Council
• U19 AG062418 NIA NIH HHS

• Parkinson’s disease
• gray matter
• muscle atrophy
• neurodegenerative disorder
• voxel-based morphometry

• Gastrointestinal motility
• Intestinal inflammation
• Microbiome
• Non-motor symptoms
• Parkinson’s disease
• Translational research

• Constipation
• Drooling
• Dysphagia
• Gastrointestinal symptoms
• Gastroparesis
• Parkinson disease
• Weight loss

• constipation and hyposmia
• disease origin
• parkinson-s disease
• pathology spread
• α-synuclein

To observe the occurrence and influencing factors of the symptoms related to the digestive system of people at the early and middle stages of PD and of healthy controls (HCs) using a questionnaire.

The questionnaire was given to 108 PD patients at early and middle stages. Twelve symptoms related to the digestive system, of which seven were listed on the Parkinson's Disease Non-Motor Symptom Scale (PD-NMSS) and the Scale for Outcomes in Parkinson's disease-Autonomic (SCOPA-AUT) (dysgeusia, dysphagia/choking, salivation, early satiety, constipation, loose stools, and fecal incontinence) and five symptoms used in the diagnosis and treatment of PD (loss of appetite, dry mouth, mouth pain, nausea and vomiting), were used. The questionnaire was also given to HCs.

There was no significant difference in age, sex, height, weight, or body mass index (BMI) between the PD group and HCs. Of the 108 people at the early and middle stages of PD, the most common symptoms related to the digestive system were 64 cases of dry mouth (59.26%), 53 cases of constipation (49.07%), and 40 cases of dysgeusia (37.04%). Multivariate binary logistics regression revealed that dysgeusia (P < 0.001), dysphagia (P = 0.004), early satiety (P = 0.001), and constipation (P = 0.007) were more likely to occur in males. BMI, disease duration, and motor symptoms had no significant correlation with the symptoms related to the digestive system (P > 0.05 for all).

Dry mouth, constipation, dysgeusia, loss of appetite, early satiety, and dysphagia are the most common (and possibly characteristic symptoms) related to the digestive system in people at the early and middle stages of PD. Being male is a risk factor for dysgeusia, dysphagia, early satiety, and constipation.

The enteric nervous system is involved in the pathology of Parkinson´s disease and patients frequently have symptoms related to delayed gastric emptying. However, the pathophysiology of gastric dysmotility is yet not well understood. The objective of this study was to assess interdigestive gastric motility in Parkinson´s disease. Using an electromagnetic capsule system, the dominant gastric contraction frequency (primary outcome measure) and the gastric transit time were assessed in 16 patients with Parkinson´s disease and 15 young healthy controls after a fasting period of 8 h. Motor and non-motor symptoms were assessed using the Movement Disorder Society Unified Parkinson´s Disease Rating Scale III (MDS-UPDRS III), the Non-Motor Symptoms Questionnaire (NMS-Quest), and Hoehn & Yahr staging. The Gastroparesis Cardinal Symptom Index was used to record symptoms related to delayed gastric emptying. In healthy controls and patients with Parkinson's disease, the dominant contraction frequency was 3.0 cpm indicating normal function of interstitial cells of Cajal. In patients with Parkinson's disease, the gastric transit time was longer than in younger controls (56 vs. 21 min). The dominant contraction frequency and gastric transit time did not correlate with age, disease duration, Hoehn & Yahr stage, levodopa equivalent daily dose, MDS-UPDRS III, NMS-Quest, and Gastroparesis Cardinal Symptom Index. Changes of gastric motility in Parkinson´s disease are not caused by functional deficits of the gastric pacemaker cells, the interstitial cells of Cajal. Therefore, gastroparesis in Parkinson's disease can be attributed to disturbances in neurohumoral signals via the vagus nerve and myenteric plexus.

• Parkinson's disease
• Physiology

To investigate the correlation between dyspeptic symptoms and gastric motility parameters measured by magnetic resonance imaging (MRI) using volumetry and motility indices in patients with Parkinson’s disease (PD).

In this IRB-approved study, MRI datasets obtained from August 2014 to May 2016 in 38 PD patients were retrospectively analyzed. Patients underwent a 120-minute-long MRI study using a liquid test meal and 8 sets of scans. Gastric content volume (GCV) and total volume (TGV), gastric half emptying time (T_1/2), motility index (GMI), accommodation (GA), and emptying (GE) values were acquired. These measurements were compared between patients according to the presence of gastric symptoms: early satiety (n = 25), epigastric pain (n = 13), and dyspepsia (n = 28).

Patients with early satiety showed significantly decreased GE of GCV and TGV (p < 0.001 and p = 0.017). Dyspeptic patients had significantly decreased GE of GCV and GMI (p = 0.001 and p = 0.029). GE of GCV at 90 and 120 minutes were significantly lower in patients with early satiety (p = 0.001 and p = 0.002). GE of GCV and GMI at 90 minutes were significantly decreased in patients with dyspepsia (p = 0.004 and p = 0.002). T_1/2 of GCV was prolonged in patients with early satiety, epigastric pain, and dyspepsia (p = 0.004, p = 0.041, and p = 0.023). T_1/2 of TGV also delayed in patients with early satiety (p = 0.023). GMI at 90 minutes was significantly correlated with dyspepsia on multivariable analysis (p = 0.028).

Gastric motility can be quantitatively assessed by MRI, showing decreased GMI, delayed GE, and prolonged T_1/2 in PD patients with early satiety or dyspepsia.

Most Parkinson’s Disease (PD) patients experience gastrointestinal (GI) dysfunction especially the gastroparesis, but its underlying mechanism is not clear. We have previously demonstrated that the neurons in the substantia nigra (SN) project to the lateral hypothalamic nucleus (LH) and the dorsal motor nucleus of vagus (DMV) receives the neural projection from LH by the means of anterograde and retrograde neural tracing technology. Orexin A (OXA) is predominately expressed in the LH. It has been reported that OXA can alter the gastric motility through the orexin receptor 1 (OX1R) in DMV. We speculated that this SN-LH-DMV pathway could modulate the motility of stomach because of the important role of LH and DMV in the regulation of gastric motility. However, the distribution and expression of dopamine receptors (DR) in the LH is unknown. In the present study, using a double-labeling immunofluorescence technique combined with confocal microscopy, we significantly extend our understanding of the SN-LH-DMV pathway by showing that (1) a considerable quantity of dopamine receptor 1 and 2 (D1 and D2) was expressed in the LH as well as the OX1R was expressed in the DMV; (2) Nearly all of the D1-immuoreactve (IR) neurons were also OXA-positive while only a few neurons express both D2 and OXA in the LH, and the DR-positive neurons were surrounded by the dopaminergic neural fibers; In the DMV, OX1R were colocalized with choline acetyltransferase (ChAT)-labeled motor neurons; (3) When the gastroparesis was induced by the destruction of dopaminergic neurons in the SN, the decreased expression of D1 and OXA was observed in the LH as well as the reduced OX1R and ChAT expression in the DMV. These findings suggest that SN might regulate the function of OXA-positive neurons via D1 receptor, which then affect the motor neurons in the DMV through OX1R. If the SN is damaged the vagal pathway would be affected, which may lead to gastric dysfunction. The present study raises the possibility that the SN-LH-DMV pathway can regulate the movement of stomach.

• Parkinson’s disease
• dopamine receptor
• gastroparesis
• lateral hypothalamic nucleus
• orexin receptor 1

• Colonic transit time
• Constipation
• Dementia with Lewy bodies
• Gastric emptying
• Parkinson disease

• Aged
• Cross-Sectional Studies
• Female
• Gastric Emptying/physiology
• Gastrointestinal Transit/physiology
• Humans
• Lewy Body Disease/physiopathology
• Male
• Parkinson Disease/physiopathology

• Epidemiology
• Functional dyspepsia
• Gastroparesis
• Incidence
• Prevalence
• Quality of life
• Risk factors

• Breath test
• Gastric emptying
• Non-motor symptom
• Parkinson
• Scintigraphy

• Gastric Emptying/physiology
• Gastrointestinal Diseases/etiology
• Humans
• Parkinson Disease/complications

• Clinical trial
• DA-9701
• Domperidone
• Gastric emptying
• Parkinson's disease

Parkinson's Disease (PD) is currently considered a systemic neurodegenerative disease manifested with not only motor but also non-motor symptoms. In particular, weight loss and malnutrition, a set of frequently neglected non-motor symptoms, are indeed negatively associated with the life quality of PD patients. Moreover, comorbidity of weight loss and malnutrition may impact disease progression, giving rise to dyskinesia, cognitive decline and orthostatic hypotension, and even resulting in disability and mortality. Nevertheless, the underlying mechanism of weight loss and malnutrition in PD remains obscure and possibly involving multitudinous, exogenous or endogenous, factors. What is more, there still does not exist any weight loss and malnutrition appraision standards and management strategies. Given this, here in this review, we elaborate the weight loss and malnutrition study status in PD and summarize potential determinants and mechanisms as well. In conclusion, we present current knowledge and future prospects of weight loss and malnutrition in the context of PD, aiming to appeal clinicians and researchers to pay a closer attention to this phenomena and enable better management and therapeutic strategies in future clinical practice.

• Parkinson's disease
• energy homeostasis
• malnutrition
• weight evaluation
• weight loss
• weight management

Background: CVT-301, an inhaled levodopa (LD) formulation, is under development for relief of OFF periods in Parkinson's disease (PD). Previously, we reported that CVT-301 improved OFF symptoms relative to placebo. In this study, we evaluate pulmonary function in patients treated with a single dose of CVT-301 or placebo for 3 hours, or received multiple doses/day for 4 weeks.

Methods: As part of two phase 2 studies, pulmonary safety and tolerability of CVT-301 were evaluated in PD patients experiencing motor fluctuations (≥2 hours OFF/day), Hoehn and Yahr stage 1–3, and forced expiratory volume in 1 second/forced vital capacity ratio ≥75% of predicted (in ON state). In study A, patients received single doses of oral carbidopa/LD and each of the following via the inhaled route: placebo and 25 and 50 mg LD fine particle dose (FPD) CVT-301. In study B, patients received up to 3 inhaled doses/day of 35 mg (weeks 1–2) and 50 mg LD FPD CVT-301 (weeks 3–4) versus placebo. Assessments included spirometry and treatment-emergent adverse events (TEAEs).

Results: In study A, (n = 24) mean age ± standard deviation was 61.3 ± 7.4 years, mean time since diagnosis was 10.5 ± 4.6 years, and mean duration of LD treatment 8.4 ± 3.7 years. Assessment of pulmonary function (predose to 3 hours postdose) showed that spirometry findings were within normal ranges, regardless of treatment groups, or motor status at screening. In study B, (n = 86) mean age was 62.4 ± 8.7 years, time since PD diagnosis was 9.4 ± 3.9 years, and duration of LD treatment 7.8 ± 3.9 years. Longitudinal assessment of pulmonary function over 4 weeks showed no significant difference in spirometry between CVT-301 versus placebo groups. In both studies, the most common CVT-301 TEAE was mild-to-moderate cough (study A: 21%; study B: 7% vs. 2% in placebo). Other common TEAEs in study B were dizziness and nausea.

Conclusion: Acute and longitudinal assessment of pulmonary function showed that CVT-301 treatment was not associated with acute airflow obstruction in this population. CVT-301 was generally safe and well tolerated.

• Parkinson's disease
• antiparkinsonian agents
• dyskinesias
• idiopathic
• inhalation
• levodopa
• motor disorders
• safety
• spirometry

• Non-dopaminergic drugs
• Parkinson’s disease
• adenosine
• glutamate
• pharmacotherapy

• Monitoring
• Nonmotor symptoms
• Objective measurement
• Parkinson's disease

Gastrointestinal (GI) dysmotility is a common problem in the critically ill population. It can be a reflection and an early sign of patient deterioration or it can be an independent cause of morbidity and mortality. GI dysmotility can be divided for clinical purposes on upper GI dysmotility and lower GI dysmotility. Upper GI dysmotility manifests by nausea, feeding intolerance and vomiting; its implications include aspiration into the airway of abdominal contents and underfeeding. Several strategies to prevent and treat this condition can be tried and they include prokinetics and post-pyloric feeds. It is important to note that upper GI dysmotility should be treated only when there are clinical signs of intolerance (nausea, vomiting) and not based on measurement of gastric residual volumes. Lower GI dysmotility manifests throughout the spectrum of ileus and diarrhea. Ileus can present in the small bowel and the large bowel as well. In both scenarios the initial treatment is correction of electrolyte abnormalities, avoiding drugs that can decrease motility and patient mobilization. When this fails, in the case of small bowel ileus, lactulose and polyethylene glycol solutions can be useful. In the case of colonic pseudo obstruction, neostigmine, endoscopic decompression and cecostomy can be tried when the situation reaches the risk of rupture. Diarrhea is also a common manifestation of GI dysmotility and the most important step is to differentiate between infectious sources and non-infectious sources.

• Gut motility
• Gut dysmotility
• Intensive care unit
• Gastrointestinal issues in intensive care unit
• Ileus

• Constipation
• Enteric nervous system
• Gastrointestinal symptom
• Gut
• Gut–brain axis
• Microbiome
• Nonmotor symptom
• Parkinson's disease

Research and clinical experience with vagotomy have confirmed that damage to the central nervous system severely affects physiological movement in the gastrointestinal system. The aim of this study was to investigate the effects of synchronized dual-pulse gastric electrical stimulation (SGES) on the apoptosis of enteric neurons and the possible pathways involved in these effects in vagotomized rats. For this purpose, Male Sprague-Dawley (SD) rats were randomized into a control group, an early subdiaphragmatic vagotomized group (ESDV group), an early subdiaphragmatic vagotomized group with short-term SGES (ESDV + SSGES group), a terminal subdiaphragmatic vagotomized group (TSDV group) and a terminal subdiaphragmatic vagotomized group with long-term SGES (TSDV + LSGES group). The expression levels of connexin 43 (Cx43), glial cell line-derived neurotrophic factor (GDNF), p-Akt, pan-Akt and PGP9.5 were assessed by RT-qPCR, western blot analysis and immunofluorescence staining. Apoptosis was determined by terminal-deoxynucleoitidyl transferase-mediated nick-end labeling (TUNEL) assay. We found that Cx43 expression was decreased in the ESDV and TSDV groups, but was significantly upregulated in the SSGES and LSGES groups. In addition, the GDNF and PGP9.5 expression levels were significantly decreased in the ESDV group compared with the control and TSDV groups and were upregulated in both the SSGES and LSGES groups. The LSGES group exhibited a clear increase in p-Akt expression compared with the TSDV group. Fewer TUNEL-positive cells were observed in the SSGES and LSGES groups than in the ESDV and TSDV groups. More TUNEL-positive cells were found in the stomach of rats subjected to subdiaphragmatic vagotomy. On the whole, our data indicate that SGES improved enteric neuronal survival, possibly through GDNF and the phosphatidylinositol 3-kinase (PI3K)/Akt pathways.

A diagnosis of Parkinson's disease is classically established after the manifestation of motor symptoms such as rigidity, bradykinesia, and tremor. However, a growing body of evidence supports the hypothesis that nonmotor symptoms, especially gastrointestinal dysfunctions, could be considered as early biomarkers since they are ubiquitously found among confirmed patients and occur much earlier than their motor manifestations. According to Braak's hypothesis, the disease is postulated to originate in the intestine and then spread to the brain via the vagus nerve, a phenomenon that would involve other neuronal types than the well-established dopaminergic population. It has therefore been proposed that peripheral nondopaminergic impairments might precede the alteration of dopaminergic neurons in the central nervous system and, ultimately, the emergence of motor symptoms. Considering the growing interest in the gut-brain axis in Parkinson's disease, this review aims at providing a comprehensive picture of the multiple gastrointestinal features of the disease, along with the therapeutic approaches used to reduce their burden. Moreover, we highlight the importance of gastrointestinal symptoms with respect to the patients' responses towards medical treatments and discuss the various possible adverse interactions that can potentially occur, which are still poorly understood.

Early involvement of gut is observed in Parkinson’s disease (PD) and symptoms such as constipation may precede motor symptoms. α-Synuclein pathology is extensively evident in the gut and appears to follow a rostrocaudal gradient. The gut may act as the starting point of PD pathology with spread toward the central nervous system. This spread of the synuclein pathology raises the possibility of prion-like propagation in PD pathogenesis. Recently, the role of gut microbiota in PD pathogenesis has received attention and some phenotypic correlation has also been shown. The extensive involvement of the gut in PD even in its early stages has led to the evaluation of enteric α-synuclein as a possible biomarker of early PD. The clinical manifestations of gastrointestinal dysfunction in PD include malnutrition, oral and dental disorders, sialorrhea, dysphagia, gastroparesis, constipation, and defecatory dysfunction. These conditions are quite distressing for the patients and require relevant investigations and adequate management. Treatment usually involves both pharmacological and non-pharmacological measures. One important aspect of gut dysfunction is its contribution to the clinical fluctuations in PD. Dysphagia and gastroparesis lead to inadequate absorption of oral anti-PD medications. These lead to response fluctuations, particularly delayed-on and no-on, and there is significant relationship between levodopa pharmacokinetics and gastric emptying in patients with PD. Therefore, in such cases, alternative routes of administration or drug delivery systems may be required.

• Parkinson’s disease
• Gut dysfunction
• Sialorrhea
• Dysphagia
• Gastroparesis
• Constipation
• Gut microbiota

• Antiparkinson Agents/metabolism
• Constipation/etiology
• Constipation/physiopathology
• Deglutition Disorders/etiology
• Deglutition Disorders/physiopathology
• Enteric Nervous System/physiopathology
• Gastrointestinal Absorption
• Gastrointestinal Microbiome
• Gastrointestinal Tract/metabolism
• Gastroparesis/etiology
• Gastroparesis/physiopathology
• Humans
• Malnutrition/etiology
• Malnutrition/physiopathology
• Parkinson Disease/complications
• Parkinson Disease/drug therapy
• Parkinson Disease/metabolism
• Parkinson Disease/physiopathology
• Sialorrhea/etiology
• Sialorrhea/physiopathology
• alpha-Synuclein/metabolism

AIM: To determine gastric emptying, blood pressure, mesenteric artery blood flow, and blood glucose responses to oral glucose in Parkinson’s disease.

METHODS: Twenty-one subjects (13 M, 8 F; age 64.2 ± 1.6 years) with mild to moderate Parkinson’s disease (Hoehn and Yahr score 1.4 ± 0.1, duration of known disease 6.3 ± 0.9 years) consumed a 75 g glucose drink, labelled with 20 MBq ^99mTc-calcium phytate. Gastric emptying was quantified with scintigraphy, blood pressure and heart rate with an automated device, superior mesenteric artery blood flow by Doppler ultrasonography and blood glucose by glucometer for 180 min. Autonomic nerve function was evaluated with cardiovascular reflex tests and upper gastrointestinal symptoms by questionnaire.

RESULTS: The mean gastric half-emptying time was 106 ± 9.1 min, gastric emptying was abnormally delayed in 3 subjects (14%). Systolic and diastolic blood pressure fell (P < 0.001) and mesenteric blood flow and blood glucose (P < 0.001 for both) increased, following the drink. Three subjects (14%) had definite autonomic neuropathy and 8 (38%) had postprandial hypotension. There were no significant relationships between changes in blood pressure, heart rate or mesenteric artery blood flow with gastric emptying. Gastric emptying was related to the score for autonomic nerve function (R = 0.55, P < 0.01). There was an inverse relationship between the blood glucose at t = 30 min (R = -0.52, P < 0.05), while the blood glucose at t = 180 min was related directly (R = 0.49, P < 0.05), with gastric emptying.

CONCLUSION: In mild to moderate Parkinson’s disease, gastric emptying is related to autonomic dysfunction and a determinant of the glycaemic response to oral glucose.

• Gastric emptying
• Hypotension
• Parkinson’s disease
• Blood pressure
• Glucose

• Aged
• Autonomic Nervous System/physiopathology
• Biomarkers/blood
• Blood Glucose/metabolism
• Blood Pressure
• Female
• Gastric Emptying
• Gastroparesis/etiology
• Gastroparesis/physiopathology
• Heart Rate
• Humans
• Hyperglycemia/etiology
• Hyperglycemia/physiopathology
• Hypotension/etiology
• Hypotension/physiopathology
• Male
• Mesenteric Artery, Superior/diagnostic imaging
• Mesenteric Artery, Superior/physiopathology
• Middle Aged
• Parkinson Disease/blood
• Parkinson Disease/complications
• Parkinson Disease/diagnostic imaging
• Parkinson Disease/physiopathology
• Postprandial Period
• Regional Blood Flow
• Severity of Illness Index
• Splanchnic Circulation
• Surveys and Questionnaires
• Time Factors
• Ultrasonography, Doppler