Role of DaTSCAN and clinical diagnosis in Parkinson disease.

Posted on October 15, 2012 by Maurice Preter MD

Important discussion, especially with an estimated cancer incidence of 1 on 7500 DaTSCANs.

Neurology. 2012 Mar 6;78(10):696-701. Epub 2012 Feb 8.

Role of DaTSCAN and clinical diagnosis in Parkinson disease.

Source

Section of Neurology, Hospital A. Marcide, Ferrol, Spain. rfuente@medynet.com

Abstract

OBJECTIVE:

To assess the role of DaTSCAN in the diagnosis of Parkinson disease (PD).

METHODS:

Using the sensitivity and specificity values obtained in the 2 studies that recently led the US Food and Drug Administration to approve the use of DaTSCAN for the diagnosis of PD, calculations were carried out to estimate the accuracy of the clinical diagnosis taking DaTSCAN findings as the standard of truth.

RESULTS:

In early PD, a clinical diagnosis of “possible” or “probable” PD has a sensitivity of 98% and a specificity of 67%. The specificity increases to 94% once the clinical diagnosis becomes established. The overall accuracy of the clinical diagnosis is 84% in early PD and 98% at later stages. The clinical diagnostic accuracy is mathematically identical to the diagnostic accuracy of DaTSCAN imaging.

CONCLUSIONS:

In the absence of neuropathologic validation, the overall accuracy of a clinical diagnosis of PD is very high and mathematically identical to the accuracy of DaTSCAN imaging, which calls into question the use of radiotracer neuroimaging as a diagnostic tool in clinical practice.

PMID:
22323748
[PubMed – indexed for MEDLINE]

LinkOut – more resources

Posted in Aging, Forensic Neuropsychiatry, Health, metabolic, Psychiatry/Neurology | Tagged , , , |

Stronger effect of amyloid load than APOE genotype on cognitive decline in healthy older adults

Posted on October 15, 2012 by Maurice Preter MD

Good news. Time to start a proper curcumin trial.

Stronger effect of amyloid load than APOE genotype on cognitive decline in healthy older adults

  1. Yen Ying Lim, MPsych,
  2. Kathryn A. Ellis, PhD,
  3. Robert H. Pietrzak, PhD, MPH,
  4. David Ames, MD,
  5. David Darby, MBBS, PhD, FRACP,
  6. Karra Harrington, BA,
  7. Ralph N. Martins, PhD,
  8. Colin L. Masters, MD,
  9. Christopher Rowe, MD,
  10. Greg Savage, PhD,
  11. Cassandra Szoeke, PhD,
  12. Victor L. Villemagne, MD,
  13. Paul Maruff, PhD and
  14. For the AIBL Research Group

+ Author Affiliations


  1. From the Mental Health Research Institute (Y.Y.L., K.A.E., D.D., K.H., C.L.M., V.L.V., P.M.), Department of Psychiatry (Y.Y.L.), and Academic Unit for Psychiatry of Old Age, Department of Psychiatry (K.A.E., D.A.), The University of Melbourne, Parkville, Australia; National Ageing Research Institute (K.A.E., D.A., C.S.), Parkville, Australia; Department of Psychiatry (R.H.P.), Yale University School of Medicine, New Haven, CT; Florey Neuroscience Institutes (D.D.), The University of Melbourne, Carlton South, Australia; Centre of Excellence for Alzheimer’s Disease Research and Care, School of Exercise, Biomedical and Health Sciences (R.N.M.), Edith Cowan University, Perth, Australia; Department of Nuclear Medicine and Centre for PET (C.R., V.L.V.) and Department of Medicine (C.R.), Austin Health, The University of Melbourne, Heidelberg, Australia; Department of Psychology and ARC Centre of Excellence in Cognition and Its Disorders (G.S.), Macquarie University, Sydney, Australia; and CogState Ltd. (P.M.), Melbourne, Australia.

  1. Melbourne, biomarkers analysis

  1. Melbourne, neuropsychology

  1. Melbourne, member of management group

  1. Melbourne, member of biomarkers leadership group

  1. Perth, research assistant involved in physical activity assessments

  1. Sydney, biomarkers analysis

  1. Melbourne, blood processing and analysis

  1. Melbourne, neuropsychological assessment

  1. Perth, clinician involved in cognitive testing of AIBL participants

  1. Melbourne, neuropsychological assessment

  1. Melbourne, neuroimaging analysis

  1. Melbourne, neuroimaging analysis

  1. Melbourne, neuroimaging data acquisition

  1. Perth, research fellow involved in handling the AIBL plasma samples

  1. Melbourne, neuropsychological assessment

  1. Brisbane, neuroimaging analysis

  1. Melbourne, blood processing and analysis

  1. Melbourne, consumer representation

  1. Melbourne, clinician involved in recruitment and review of cohort

  1. Perth, research associate involved in brain imaging of AIBL participants

  1. Melbourne, neuroimaging analysis

  1. Melbourne, clinician involved in recruitment and review of cohort

  1. Melbourne, biomarkers analysis

  1. Melbourne, administration

  1. Brisbane, neuroimaging analysis

  1. Brisbane, neuroimaging analysis

  1. Melbourne, neuroimaging analysis

  1. Brisbane, neuroimaging analysis

  1. Melbourne, biomarkers analysis

  1. Perth, research assistant involved in neuropsychiatric testing

  1. Melbourne, blood processing and analysis

  1. Perth, clinician involved in AIBL participants recruitment

  1. Perth, research fellow involved in analysing and revising the manuscript

  1. Brisbane, data management

  1. Perth, research assistant involved in neuropsychiatric testing

  1. Melbourne, genetics analysis

  1. Perth, research assistant involved in dietary assessments of AIBL participants

  1. Brisbane, neuroimaging analysis.
  1. Correspondence & reprintrequests to Dr: Lim: y.lim@mhri.edu.au

View Complete Disclosures

Abstract

Objective: Although the APOE ϵ4 allele is associated with more rapid decline in memory in healthy older adults, the significance of elevated cerebral β-amyloid (Aβ) load for longitudinal changes in cognition is unclear.

Methods: Healthy and cognitively normal older adults (n = 141; mean age 76 years) underwent PET neuroimaging for cerebral Aβ, APOE genotyping, and cognitive assessment as part of their baseline assessment in the Australian Imaging Biomarkers and Lifestyle study. Cognitive function was reassessed 18 months later.

Results: Linear mixed-model analyses adjusted for baseline cognitive function indicated that, relative to individuals with low cerebral Aβ, individuals with high cerebral Aβ showed significantly greater decline in working memory and verbal and visual episodic memory at 18 months. Compared with noncarriers, APOE ϵ4 carriers showed a greater decline in visual memory at the 18-month assessment. No interaction between APOE ϵ4 and cerebral Aβ load was observed for any measure of cognitive function.

Conclusions: In this prospective study of healthy older adults, high cerebral Aβ load was associated with greater decline in episodic and working memory over 18 months. The APOE ϵ4 genotype was also associated with a decline in visual memory, although the effect was less than that observed for cerebral Aβ load.

Footnotes

  • Received February 22, 2012.
  • Accepted May 29, 2012.
Posted in Aging, dietary, epigenetics, Health, new treatments, News, Psychiatry/Neurology | Tagged , , |

An interesting blogpost on the Vitamin D controversy

Posted on October 14, 2012 by Maurice Preter MD

An excellent blogpost on the Vitamin D topic by Michael Eades MD.

http://www.proteinpower.com/drmike/supplements/sunshine-superman/

 

 

Posted in Psychiatry/Neurology |

Vitamin D overdose?

Posted on October 14, 2012 by Maurice Preter MD
This is relevant to Vitamin D self-medicators. The original was posted here: http://www.newswise.com/articles/calcium-supplements-too-much-of-a-good-thing

Calcium Supplements: Too Much of a Good Thing?

Released: 6/1/2010 3:35 PM EDT
Source: American Society of Nephrology (ASN)

Newswise — Negative health effects linked to taking too much supplemental calcium are on the rise, according to a commentary appearing in an upcoming issue of the Journal of the American Society Nephrology (JASN). The incidence of the so-called milk-alkali or calcium-alkali syndrome is growing in large part because of widespread use of over-the-counter calcium and vitamin D supplements.

The milk-alkali syndrome arose in the early 1900s when patients ingested abundant amounts of milk and antacids to control their ulcers. This practice increased individuals’ risk of developing dangerously high levels of calcium in the blood, which could cause high blood pressure and even kidney failure. The incidence of the milk-alkali syndrome declined when newer ulcer medications became available, but it appears to be on the rise again thanks to increased use of over-the-counter calcium and vitamin D supplements used mainly as preventive and treatment measures for osteoporosis. In many cases, patients with the syndrome require hospitalization.

Stanley Goldfarb, MD and Ami Patel, MD (University of Pennsylvania School of Medicine) recommend changing the name of the milk-alkali syndrome to the calcium-alkali syndrome because the condition is now associated with a large intake of calcium, not milk. Postmenopausal women, pregnant women, transplant recipients, patients with bulimia, and individuals who are on dialysis have the highest risks of developing the calcium-alkali syndrome due to various physiological reasons.

According to the authors, the obvious preventive strategy against the calcium-alkali syndrome is to limit the intake of calcium to no more than 1.2 to 1.5 grams per day. “Calcium supplements taken in the recommended amounts are not only safe but are quite beneficial. Taken to excess is the problem,” said Dr. Goldfarb. “Even at the recommended dose, careful monitoring of any medication is wise and yearly determinations of blood calcium levels for those patients taking calcium supplements or vitamin D is a wise approach,” he added.

The authors reported no financial disclosures.

The commentary, entitled “Got Calcium? Welcome to the Calcium-Alkali Syndrome,” (doi 10.1681/ASN.2010030255) is available online at http://jasn.asnjournals.org. A detailed article on this commentary will also be included within the June issue of ASN Kidney News.

The content of this article does not reflect the views or opinions of The American Society of Nephrology (ASN). Responsibility for the information and views expressed therein lies entirely with the author(s). ASN does not offer medical advice. All content in ASN publications is for informational purposes only, and is not intended to cover all possible uses, directions, precautions, drug interactions, or adverse effects. This content should not be used during a medical emergency or for the diagnosis or treatment of any medical condition. Please consult your doctor or other qualified health care provider if you have any questions about a medical condition, or before taking any drug, changing your diet or commencing or discontinuing any course of treatment. Do not ignore or delay obtaining professional medical advice because of information accessed through ASN. Call 911 or your doctor for all medical emergencies.

Founded in 1966, the American Society of Nephrology (ASN) is the world’s largest professional society devoted to the study of kidney disease. Comprised of 11,000 physicians and scientists, ASN continues to promote expert patient care, to advance medical research, and to educate the renal community. ASN also informs policymakers about issues of importance to kidney doctors and their patients. ASN funds research, and through its world-renowned meetings and first-class publications, disseminates information and educational tools that empower physicians.

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Posted in Aging, dietary, Health, metabolic | Tagged |

False-positive breath-alcohol test after a ketogenic diet

Posted on October 14, 2012 by Maurice Preter MD

A biochemistry reminder from the International Journal of Obesity (2007) 31, 559–561.

Abstract:

A 59-year-old man undergoing weight loss with very low calorie diets (VLCD) attempted to drive a car, which was fitted with an alcohol ignition interlock device, but the vehicle failed to start. Because the man was a teetotaller, he was surprised and upset by this result. VLCD treatment leads to ketonemia with high concentrations of acetone, acetoacetate and beta-hydroxybutyrate in the blood. The interlock device determines alcohol (ethanol) in breath by electrochemical oxidation, but acetone does not undergo oxidation with this detector. However, under certain circumstances acetone is reduced in the body to isopropanol by hepatic alcohol dehydrogenase (ADH). The ignition interlock device responds to other alcohols (e.g. methanol, n-propanol and isopropanol), which therefore explains the false-positive result. This ‘side effect’ of ketogenic diets needs further discussion by authorities when people engaged in safety-sensitive work (e.g. bus drivers and airline pilots) submit to random breath-alcohol tests.

Keywords:

acetone, alcohol, breath-test, driving, ignition interlocks, VLCD

Posted in dietary, metabolic | Tagged , |