Longitudinal evaluation of cerebral morphological changes in Parkinson's disease with and without dementia

2005 ◽  
Vol 252 (11) ◽  
pp. 1345-1352 ◽  
Author(s):  
B. Ramírez–Ruiz ◽  
M. J. Martí ◽  
E. Tolosa ◽  
D. Bartrés–Faz ◽  
Ch. Summerfield ◽  
...  
2020 ◽  
Author(s):  
Mahmut Atum ◽  
Bekir Enes Demiryurek

Abstract Background: The study aims to investigate the relationship between the progression of idiopathic Parkinson's disease (IPD) and retinal morphology. Methods: The study was carried out with 23 patients diagnosed with early-stage IPD (phases 1 and 2 of the Hoehn and Yahr scale) and 30 age-matched healthy controls. All patients were followed up at least two years, with 6-month intervals (initial, 6th month, 12th month, 18th month, and 24th month), and detailed neurological and ophthalmic examinations were performed at each follow-up. Unified Parkinson's Disease Rating Scale part III (UPDRS Part III) scores, Hoehn and Yahr (H&Y) scores, best-corrected visual acuity (BCVA), intraocular pressure (IOP) measurement, central macular thickness (CMT) and retinal nerve fiber layer (RNFL) thickness were analyzed at each visit. Results: The average age of the IPD and control groups was 43.96 ± 4.88 years, 44.53 ± 0.83 years, respectively. The mean duration of the disease in the IPD group was 7.48 ± 5.10 months at the start of the study (range 0-16). There was no statistically significant difference in BCVA and IOP values between the two groups during the two-year follow-up period (p> 0.05, p> 0.05, respectively). Average and superior quadrant RNFL thicknesses were statistically different between the two groups at 24 months and there was no significant difference between other visits (p = 0.025, p=0.034, p> 0.05, respectively). There was no statistically significant difference in CMT between the two groups during the follow-up period (p> 0.05). Conclusion: Average and superior quadrant RNFL thicknesses were significantly thinning with the progression of IPD.


Author(s):  
Peter Falkai ◽  
Bernhard Bogerts

The traditional domains of neuropathology are well-defined organic brain diseases with an obvious pathology, such as tumours, infections, vascular diseases, trauma, or toxic and hypoxemic changes, as well as degenerative brain diseases (e.g. Alzheimer's disease, Parkinson's disease, and Huntington's chorea). Neuropathological investigations of these brain disorders have been rewarding, because patients with any of these conditions can be expected to have gross morphological or more or less specific neurohistological anomalies related to the clinical symptoms of the disorders. Moreover, the type of brain pathology of these well-defined disease entities is quite homogenous. For example, it is highly unlikely that a patient with Parkinson's disease would not exhibit morphological changes and Lewy bodies in the nigrostriatal system, just as much a person with Huntington's chorea would have a normal striatum, or a patient with Pick'sor Alzheimer's disease would have no changes in the cerebralcortex. In contrast, the history of the neuropathology of psychiatric disorders outside primary degenerative diseases is much more controversial, because no such obvious and homogenous types of brain pathology (as seen in neurological disorders) have yet been detected for the major psychiatric illnesses such as schizophrenia, affective disorders, substance-related disorders, or personality disorders. The scope of this chapter is to summarize the neuropathological findings in schizophrenia, affective disorders, and alcoholism. Tables 2.3.5.1, 2.3.5.2, 2.3.5.3, and 2.3.5.4 highlight the significant findings. It goes beyond the scope of this chapter to review thelarge body of literature on the dementias, including specifically Alzheimer's disease. Concerning this matter, the reader is referred to several comprehensive reviews (e.g. Jellinger and Bancher 1998).


2020 ◽  
Author(s):  
Kenji Ohira ◽  
Hajime Yokota ◽  
Shigeki Hirano ◽  
Motoi Nishimura ◽  
Hiroki Mukai ◽  
...  

Abstract Taq1A polymorphism is a DRD2 gene variant located in an exon of the ANKK1 gene and has an important role in the brain’s dopaminergic functions. Some studies have indicated that A1 carriers have an increased risk of developing Parkinson’s disease (PD) and show poorer clinical performance than A2 homo carriers. Previous studies have suggested that A1 carriers had fewer dopamine D2 receptors in the caudate and increased cortical activity as a compensatory mechanism. However, there is little information about morphological changes associated with this polymorphism in patients with PD. The study aim was to investigate the relationship between brain volume and Taq1A polymorphism in PD using voxel-based morphometry (VBM). Based on Taq1A polymorphism, 103 patients with PD were divided into two groups: A1 carriers (A1/A1, A1/A2) and A2 homo carriers (A2/A2). The volume of the left prefrontal cortex (PFC) was significantly decreased in A2 homo carriers compared to A1 carriers. This finding supports the association between Taq1A polymorphism and brain volume in PD and may explain the compensation of cortical function in A1 carriers with PD.


2001 ◽  
Vol 8 (1) ◽  
pp. 41-50 ◽  
Author(s):  
Margaret Schenkman ◽  
Carolyn Wei Zhu ◽  
Toni M. Cutson ◽  
Kathryn Whetten-Goldstein

2021 ◽  
Vol 65 (s1) ◽  
Author(s):  
Carolina Pellegrini ◽  
Vanessa D'Antongiovanni ◽  
Chiara Ippolito ◽  
Cristina Segnani ◽  
Luca Antonioli ◽  
...  

Gastrointestinal dysfunctions represent the most common non-motor symptoms in Parkinson’s disease (PD). Of note, changes in gut microbiota, impairments of intestinal epithelial barrier (IEB), bowel inflammation and neuroplastic rearrangements of the enteric nervous system (ENS) could be involved in the pathophysiology of the intestinal disturbances in PD. In this context, although several review articles have pooled together evidence on the alterations of enteric bacteria-neuro-immune network in PD, a revision of the literature on the specific morphological changes occurring in the intestinal mucosal barrier, the ENS and enteric muscular layers in PD, is lacking. The present review provides a complete appraisal of the available knowledge on the morphological alterations of intestinal mucosal barrier, with particular focus on IEB, ENS and enteric muscular layers in PD. In particular, our intent was to critically discuss whether, based on evidence from translational studies and pre-clinical models, morphological changes in the intestinal barrier and enteric neuromuscular compartment contribute to the pathophysiology of intestinal dysfunctions occurring in PD.


Sign in / Sign up

Export Citation Format

Share Document