Review
Gastrointestinal dysfunction in Parkinson’s disease☆,☆☆,☆☆☆

https://doi.org/10.1016/j.parkreldis.2010.08.003Get rights and content

Abstract

In recent years, an increasingly detailed picture of gastrointestinal dysfunction in the setting of Parkinson’s disease has emerged. Abnormalities of function may occur at virtually all levels of the gastrointestinal tract. Weight loss, dental deterioration, salivary excess, dysphagia, gastroparesis, decreased bowel movement frequency, and anorectal dysfunction all may occur. The pathophysiologic basis for this dysfunction entails both central and enteric nervous system involvement.

Introduction

While recognition that Parkinson’s disease (PD) involves far more than just motor dysfunction has blossomed in recent years, James Parkinson quite clearly describes some of the nonmotor aspects of the disorder in his 1817 treatise [1]. In particular, he indicates his awareness of gastrointestinal (GI) dysfunction with vivid descriptions of drooling, dysphagia, and bowel dysfunction in some of the individuals he examined.

A much more detailed picture of the presence and extent of GI dysfunction in PD is now emerging and abnormalities or disturbances in function at virtually all levels of the GI system have been identified. Weight loss, dental deterioration, salivary excess, dysphagia, impaired gastric emptying, decreased bowel movement frequency, and difficulty with the act of defecation itself all may occur in the setting of PD.

In addition to being the source of significant clinical symptoms and dysfunction in individuals with PD, a much more fundamental role of the GI system in the genesis of PD has also been hypothesized. It has now been suggested that the enteric nervous system (ENS) may actually be the port of entry of the pathologic process that eventually culminates in the clinical picture of PD.

Section snippets

Weight loss

Unintended weight loss is frequently reported by patients with PD. In one study, weight loss was documented in 52% of persons with PD [2]. The weight loss was rather modest in most individuals, but exceeded 28 pounds in 22% of the study participants [2]. In another study, the mean weight loss of PD patients was 7.2 pounds, compared with a weight gain of 2.1 pounds in the control group [3]. Women with PD are more likely to lose weight than men [4].

The reason for weight loss in PD is not at all

Dental deterioration

An increased incidence of oral health problems, such as loss of teeth, chewing difficulty, and denture discomfort has been described in the setting of PD [8]. Increased periodontal pathology has also been reported [9]. However, disproportionate deterioration in dental function has not been identified in all studies of PD patients [10], [11]. Even though no specific treatment recommendations regarding dental difficulties in PD patients have been formulated, increased attention to and regular

Salivary excess

The presence of excess saliva within the mouth is evident in many persons with PD [16], [17], [18]. Survey studies indicate that 70–78% of PD patients are aware of excessive amounts of saliva, compared with only 6% of controls [19], [20].

The excess saliva noted by PD patients is not the result of increased salivary production. In fact, saliva production is actually decreased in the setting of PD [21], [22], [23], [24]. Saliva accumulation is, instead, the consequence of diminished frequency and

Dysphagia

Survey studies vary broadly in their recording of the presence of difficulty swallowing in individuals with PD, with reports ranging from 30% to over 80% [19], [20], [30], [31]. Studies utilizing objective measures, such as the modified barium swallow (MBS) test, provide more consistent – and even higher – percentages of functional impairment, with abnormalities noted in 75–97% of individuals [32], [33], [34]. It is not entirely clear whether dysphagia is a reflection of disease progression.

Nausea/gastroparesis

Nausea in the setting of PD is most often due to dopaminergic antiparkinson medication. However, nausea may also develop in individuals who are receiving no antiparkinson medication. In one study, nausea was present in 16% of untreated PD patients and a sense of bloating in 43% [20]. Other investigators have subsequently documented the presence of impaired or delayed gastric emptying in PD as the probable etiology for these symptoms [52], [53], [54], [55], [56]. Most studies indicate that

Decreased bowel movement frequency

Diminished frequency of bowel movements is probably the most widely recognized aspect of GI dysfunction in PD. The actual frequency with which this problem occurs, however, is not entirely clear. Even when the currently accepted dividing line of fewer than three bowel movements per week is employed as a measure, the reported number of PD patients experiencing decreased bowel movement frequency ranges from 20–89% in various studies [20], [79], [80], [81]. Survey studies have indicated that the

Defecatory difficulty

Difficulty with the act of defecation, resulting in excessive straining, pain, and incomplete evacuation, may be present in up to two-thirds of individuals with PD [20], [97]. For effective elimination to occur, coordinated action of multiple muscles must take place. The internal and external anal sphincter muscles and puborectalis muscle must relax while adequate rectosigmoid tone must develop and the abdominal wall muscles, diaphragm and even glottic muscles must contract in order to increase

Pathophysiology of GI dysfunction in PD

While dopaminergic deficiency secondary to nigrostriatal damage may be responsible for some aspects of GI dysfunction in PD, it is also quite clear that additional sites of involvement, both within the central nervous system (CNS) and beyond it, also play important roles. The dorsal motor nucleus of the vagus (DMV), which provides parasympathetic innervation to much of the GI tract, is profoundly involved in PD [112], [113]. In fact, recent work by Braak and colleagues has demonstrated that the

Conclusion

GI dysfunction is receiving increasing attention and recognition as an important clinical component of PD. Beyond this, however, evidence is now emerging that the ENS may even be the pathophysiologic “ground zero” of the disorder. GI dysfunction in PD involves virtually all levels of the GI tract and is the source of significant functional impairment for many individuals with PD. All of this makes it important for neurologists and other clinicians to be familiar with the GI features of PD and

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    ☆

    Disclosures (2009–2010): Honoraria for lectures: Boehringer-Ingelheim, Novartis, Teva. Honoraria for consulting: Solvay, Theravance, Genactis, Schlesinger Associates. Research Grants/Contracts: Novartis, Boehringer-Ingelheim, UCB/Schwarz, Santhera, Molecular Biometrics. Royalties (for books edited): CRC Press (Taylor & Francis), Humana Press. Legal Consulting: Spriggs & Hollingsworth, Davis Graham & Stubbs, Tucker Ellis & West.

    ☆☆

    This paper was presented at the XVIII WFN World Congress on Parkinson's Disease and Related Disorders Miami December 2009.

    ☆☆☆

    The review of this paper was entirely handled by the Co-Editor-in-Chief Prof. Z.K. Wszolek.

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