Colonic Transit Time in Nonidiopathic Parkinson’s Syndrome

Jost, Wolfgang H.; Jung, Gum Mo; Schimrigk, К.

doi:10.1159/000117072

Cited by 22 publications

(8 citation statements)

References 8 publications

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“…symptomatic cases [21]. This is in agreement with our own study [75] which revealed no significant deviation in intestinal transit time between non-IPS patients (Parkinson's syndrome due to vascular disease) and a control group [75]. The observed fact that non-IPS patients tend to have borderline transit time is more likely linked to advanced age and lack of mobility rather than to the presence of severe motility disorder.…”

Section: Discussionsupporting

confidence: 90%

Gastrointestinal dysfunction in Parkinson's Disease

Jost

2010

Journal of the Neurological Sciences

185

129

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Section: Discussionsupporting

confidence: 90%

Gastrointestinal dysfunction in Parkinson's Disease

Jost

2010

Journal of the Neurological Sciences

185

129

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“…Prevalence estimates of constipation in PD have been inconsistent because of variable definitions of constipation, but a conservative estimate would be at least 20% [65]. Colonic transit time is raised from control values of around 20 h to 44–130 h [66,67], probably worsening as the disease advances.…”

Section: Evidence For Pd‐related Autonomic Dysfunctionmentioning

confidence: 99%

Parkinson's disease: a dual‐hit hypothesis

Hawkes

Tredici

Braak

2007

Neuropathology Appl Neurobio

833

675

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Accumulating evidence suggests that sporadic Parkinson's disease has a long prodromal period during which several non-motor features develop, in particular, impairment of olfaction, vagal dysfunction and sleep disorder. Early sites of Lewy pathology are the olfactory bulb and enteric plexus of the stomach. We propose that a neurotropic pathogen, probably viral, enters the brain via two routes: (i) nasal, with anterograde progression into the temporal lobe; and (ii) gastric, secondary to swallowing of nasal secretions in saliva. These secretions might contain a neurotropic pathogen that, after penetration of the epithelial lining, could enter axons of the Meissner's plexus and, via transsynaptic transmission, reach the preganglionic parasympathetic motor neurones of the vagus nerve. This would allow retrograde transport into the medulla and, from here, into the pons and midbrain until the substantia nigra is reached and typical aspects of disease commence. Evidence for this theory from the perspective of olfactory and autonomic dysfunction is reviewed, and the possible routes of pathogenic invasion are considered. It is concluded that the most parsimonious explanation for the initial events of sporadic Parkinson's disease is pathogenic access to the brain through the stomach and nose - hence the term 'dual-hit'.

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“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] Case reviews further suggest that constipation can precede the extrapyramidal symptoms of clinical PD by many years. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] Case reviews further suggest that constipation can precede the extrapyramidal symptoms of clinical PD by many years.…”

mentioning

confidence: 99%