Does vagotomy reduce the risk of Parkinson's disease?

Tysnes, Ole‐Bjørn; Kenborg, Line; Herlofson, Karen; Steding-Jessen, Marianne; Horn, Arild; Ølsen, Jørgen H.; Reichmann, Heinz

doi:10.1002/ana.24531

Cited by 87 publications

(52 citation statements)

References 3 publications

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“…When using the entire follow‐up period (0‐30 years) a smaller protective trend was observed (HR = 0.78; 95% CI 0.55‐1.09), but when restricting the follow‐up period to >5 years a larger effect was seen (HR = 0.59; 95% CI 0.37‐0.93). In summary, the analysis of Tysnes and colleagues differed from ours in a number of important ways, and the findings in the 2 studies cannot be directly compared.…”

Section: Protective Effect Of Vagotomymentioning

confidence: 65%

How does parkinson's disease begin? Perspectives on neuroanatomical pathways, prions, and histology

Borghammer

2017

Movement Disorders

120

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Parkinson's disease (PD) is a multisystem disorder with involvement of the peripheral nervous system. Misfolding and aggregation of α-synuclein is central to the pathogenesis of PD, and it has been postulated that the disease may originate in olfactory and gastrointestinal nerve terminals. The prion-like behavior of α-synuclein has been convincingly demonstrated in vitro and in animal models of PD. Lewy-type pathology have been detected in peripheral organs many years prior to PD diagnosis, and 2 independent studies have now suggested that truncal vagotomy may be protective against the disorder. Other lines of evidence are difficult to reconcile with a peripheral onset of PD, most importantly the relative scarcity of post mortem cases with isolated gastrointestinal α-synuclein pathology without concomitant CNS pathology. This Scientific Perspectives article revisits some important topics with implications for the dual-hit hypothesis. An account of the neuroanatomical pathways necessary for stereotypical α-synuclein spreading is presented. Parallels to the existing knowledge on true prion disorders, including Creutzfeld-Jakob disease, are examined. Finally, the vagotomy studies and the somewhat inconsistent findings in the growing literature on peripheral α-synuclein pathology are discussed. It is concluded that the dual-hit hypothesis remains a potential explanation for PD pathogenesis, but several issues need to be resolved before more firm conclusions can be drawn. © 2017 International Parkinson and Movement Disorder Society.

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Section: Protective Effect Of Vagotomymentioning

confidence: 65%

How does parkinson's disease begin? Perspectives on neuroanatomical pathways, prions, and histology

Borghammer

2017

Movement Disorders

120

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“…14,15 Using Danish national registers from 1977 to 1995, Svensson et al 14 reported a 15% lower PD risk >5 years after truncal vagotomy compared to the general population; the effect appeared to be stronger when restricted to >20 years after the surgery (HR 0.53, 95% CI 0.53–0.99). This Danish study, however, did not differentiate truncal from selective vagotomy and thus might have underestimated the association of truncal vagotomy with PD.…”

Section: Discussionmentioning

confidence: 99%

“…This Danish study, however, did not differentiate truncal from selective vagotomy and thus might have underestimated the association of truncal vagotomy with PD. 14 Tysnes et al, 15 who analyzed the same Danish population with extended follow-up (1977–2011), reported a nonsignificantly lower PD risk for truncal vagotomy overall (HR 0.88, 95% CI 0.55–1.21) and a nonsignificantly elevated PD risk >20 years after the surgery (HR 1.14, 95% CI 0.23–2.05). Therefore, although data on temporal relationship are inconsistent, available evidence, including that from our study, offers preliminary support that truncal vagotomy may decrease the risk of PD.…”

Section: Discussionmentioning

confidence: 99%

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Vagotomy and Parkinson disease

et al. 2017

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Objective:To examine whether vagotomy decreases the risk of Parkinson disease (PD).Methods:Using data from nationwide Swedish registers, we conducted a matched-cohort study of 9,430 vagotomized patients (3,445 truncal and 5,978 selective) identified between 1970 and 2010 and 377,200 reference individuals from the general population individually matched to vagotomized patients by sex and year of birth with a 40:1 ratio. Participants were followed up from the date of vagotomy until PD diagnosis, death, emigration out of Sweden, or December 31, 2010, whichever occurred first. Vagotomy and PD were identified from the Swedish Patient Register. We estimated hazard ratios (HRs) with 95% confidence intervals (CIs) using Cox models stratified by matching variables, adjusting for country of birth, chronic obstructive pulmonary disease, diabetes mellitus, vascular diseases, rheumatologic disease, osteoarthritis, and comorbidity index.Results:A total of 4,930 cases of incident PD were identified during 7.3 million person-years of follow-up. PD incidence (per 100,000 person-years) was 61.8 among vagotomized patients (80.4 for truncal and 55.1 for selective) and 67.5 among reference individuals. Overall, vagotomy was not associated with PD risk (HR 0.96, 95% CI 0.78–1.17). However, there was a suggestion of lower risk among patients with truncal vagotomy (HR 0.78, 95% CI 0.55–1.09), which may be driven by truncal vagotomy at least 5 years before PD diagnosis (HR 0.59, 95% CI 0.37–0.93). Selective vagotomy was not related to PD risk in any analyses.Conclusions:Although overall vagotomy was not associated the risk of PD, we found suggestive evidence for a potential protective effect of truncal, but not selective, vagotomy against PD development.

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“…This protective effect was not observed with superselective vagotomy 107 , supporting the idea that vagal innervation to the gastrointestinal tract is important for PD pathogenesis but that the area of vulnerability includes more than the stomach. Subsequent analysis by another group of this same data set expanded to include a larger time frame and using a different type of statistical analysis, however, has questioned the strength of these findings 108 ; therefore, further study is needed.…”

Section: Primary Disorders Of the Cnsmentioning

confidence: 99%

The bowel and beyond: the enteric nervous system in neurological disorders

Rao

Gershon

2016

Nat Rev Gastroenterol Hepatol

489

362

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The enteric nervous system (ENS) is large, complex and uniquely able to orchestrate gastrointestinal behaviour independently of the central nervous system (CNS). An intact ENS is essential for life and ENS dysfunction is often linked to digestive disorders. The part the ENS plays in neurological disorders, as a portal or participant, has also become increasingly evident. ENS structure and neurochemistry resemble that of the CNS, therefore pathogenic mechanisms that give rise to CNS disorders might also lead to ENS dysfunction, and nerves that interconnect the ENS and CNS can be conduits for disease spread. We review evidence for ENS dysfunction in the aetiopathogenesis of autism spectrum disorder, amyotrophic lateral sclerosis, transmissible spongiform encephalopathies, Parkinson disease and Alzheimer disease. Animal models suggest that common pathophysiological mechanisms account for the frequency of gastrointestinal comorbidity in these conditions. Moreover, the neurotropic pathogen, varicella zoster virus (VZV), unexpectedly establishes latency in enteric and other autonomic neurons that do not innervate skin. VZV reactivation in these neurons produces no rash and is therefore a clandestine cause of gastrointestinal disease, meningitis and strokes. The gut–brain alliance has raised consciousness as a contributor to health, but a gut–brain axis that contributes to disease merits equal attention.

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Does vagotomy reduce the risk of Parkinson's disease?

Cited by 87 publications

References 3 publications

How does parkinson's disease begin? Perspectives on neuroanatomical pathways, prions, and histology

How does parkinson's disease begin? Perspectives on neuroanatomical pathways, prions, and histology

Vagotomy and Parkinson disease

The bowel and beyond: the enteric nervous system in neurological disorders

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