Towards defining a rigidity-associated pathogenic pathway in idiopathic parkinsonism.
Neurodegener Dis
; 10(1-4): 183-6, 2012.
Article
em En
| MEDLINE
| ID: mdl-22205039
ABSTRACT
Helicobacter pylori eradication has a differential effect on the facets of idiopathic parkinsonism (IP) brady/hypokinesia improves, but rigidity worsens. Small intestinal bacterial overgrowth is common in IP and has been described as a sequel to Helicobacter eradication. The hyperhomocysteinaemia of IP is, in part, explained by serum vitamin B(12), but the concentration is not explained by Helicobacter status. Moreover, Helicobacter-associated gastric atrophy is uncommon in IP. However, overgrowth both increases B(12) utilization and provides a source of inflammation to drive homocysteine production. It is not a bystander event in IP clouds of lysosomes are seen in duodenal enterocytes. Its candidature for causality of a rigidity-associated pathway is circumstantial there are biological gradients of rigidity on natural killer and T-helper blood counts, both being higher with hydrogen breath test positivity for overgrowth.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Doença de Parkinson
/
Infecções por Helicobacter
/
Rigidez Muscular
Tipo de estudo:
Etiology_studies
/
Risk_factors_studies
Limite:
Humans
Idioma:
En
Revista:
Neurodegener Dis
Ano de publicação:
2012
Tipo de documento:
Article