Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, August 23, 2023

Retinal Changes Emerge Years Before Parkinson's Disease

With your risk of Parkinsons post stroke, does your doctor have enough functioning brain cells to get this into a testing protocol for all stroke patients? 

Parkinson’s Disease May Have Link to Stroke March 2017 

Do you prefer your doctor incompetence in this NOT KNOWING? OR NOT DOING?

Retinal Changes Emerge Years Before Parkinson's Disease

OCT data may one day contribute to Parkinson's screening

A photo of a female ophthalmologist performing optical coherence tomography on her senior female patient.

People with Parkinson's disease had retinal changes that could be seen with optical coherence tomography (OCT) years before diagnosis, cross-sectional data suggested.

Both incident and prevalent Parkinson's disease were associated with reduced ganglion cell-inner plexiform layer (GCIPL) and inner nuclear layer (INL) thicknesses, reported Siegfried Karl Wagner, MSc, MD, of University College London in England, and co-authors.

People with prevalent Parkinson's disease had thinner GCIPL (-2.12 μm, P=8.2 × 10-5) and INL (-0.99 μm, P=2.1 × 10-4) after adjusting for age, sex, ethnicity, hypertension, and diabetes, the researchers wrote in Neurologyopens in a new tab or window.

Incident Parkinson's also was associated with thinner GCIPL (HR 0.62 per standard deviation increase, P=0.002) and thinner INL (HR 0.70, P=0.026).

The study "sets new standards for the role of retinal morphology as potential biomarker in neurodegenerative disease," observed Valeria Koska and Philipp Albrecht, MD, both of Heinrich Heine University Düsseldorf in Germany, in an accompanying editorialopens in a new tab or window.

"It not only corroborates previous studies but also provides new evidence, e.g., a reduced thickness of the inner nuclear layer," Koska and Albrecht wrote. "It fosters our understanding that [Parkinson's] is a systemic disease, which extends beyond dopaminergic neurons and also involves the retina as peripheral part of the central nervous system already at a very early and apparently even presymptomatic stage."

The effect sizes in the study were small and the practical value of using retinal OCT images to identify early Parkinson's with the current protocols and technology in clinical care is limited, the editorialists noted.

"However, with the advent of artificial intelligence, they might prove useful for the development of new multivariable prognostic factors based on combinations of several biomarkers," they pointed out.

In previous studies, retinal OCT has shown promise as a diagnostic aid for mild cognitive impairmentopens in a new tab or window and has been studied as a potential biomarker of presymptomatic Alzheimer'sopens in a new tab or window disease.

Wagner and co-authors evaluated prevalent Parkinson's disease among people in the retrospective AlzEye cohortopens in a new tab or window in England and incident disease in the prospective U.K. Biobankopens in a new tab or window cohort.

In the AlzEye cohort, 700 individuals had prevalent Parkinson's disease and 105,770 people were controls. Mean age was about 66 and 51.7% were women. The U.K. Biobank study included 50,405 participants with a mean age of 56 and 54.7% were women. In this cohort, 53 people developed Parkinson's disease over an average of 7.3 years.

All participants had non-mydriatic macula-centered OCT imaging. In the U.K. Biobank cohort, researchers included only participants who had retinal imaging at their initial assessment visit (baseline). U.K. Biobank participants who self-reported Parkinson's disease at baseline were excluded from the study.

Parkinson's disease was defined by diagnostic codes. People with diagnostic codes for all-cause dementia were excluded.

In the AlzEye group, people with Parkinson's were older and more likely to be male, hypertensive, and have diabetes. In the U.K. Biobank cohort, adjusted survival analysis showed that age and male sex were associated with incident Parkinson's disease.

In the U.K. Biobank group, the association between thinner GCIPL or INL and incident Parkinson's disease persisted even when participants diagnosed with Parkinson's in the first 24 months after retinal imaging were excluded.

The study had several limitations, Wagner and colleagues acknowledged. The AlzEye cohort did not have detailed clinical information about Parkinson's status, and retinal changes could not be related to disease duration or severity. Because Parkinson's disease was identified by diagnostic codes, some cases may have been missed.

Future studies are needed to determine whether the progression of GCIPL atrophy is driven by Parkinson's brain changes or whether INL thinning precedes GCIPL atrophy, the researchers added.

"I continue to be amazed by what we can discover through eye scans," Wagner said in a statement. "While we are not yet ready to predict whether an individual will develop Parkinson's, we hope that this method could soon become a pre-screening tool for people at risk of disease."

  • Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

This study was funded by Fight for Sight UK, Medical Research Council, U.K. Research & Innovation, the Basque Health Department, and the Wellcome Trust.

Wagner is funded by the Medical Research Council and the Rank Prize. Co-authors reported numerous grants, awards, and fellowships.

Primary Source

Neurology

Source Reference: opens in a new tab or windowWagner SK, et al "Retinal optical coherence tomography features associated with incident and prevalent Parkinson disease" Neurology 2023; DOI: 10.1212/WNL.0000000000207727.

Secondary Source

Neurology

Source Reference: opens in a new tab or windowKoska V, Albrecht P "Inner retinal thickness changes in prevalent and incident Parkinson disease: A potential biomarker with prognostic value?" Neurology 2023; DOI: 10.1212/WNL.0000000000207780.

 

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