Vitamin D, cognition, and dementia

Lots of interesting articles this week in Neurology. This is one of them.

Vitamin D, cognition, and dementia
A systematic review and meta-analysis
Cynthia Balion, PhD, Lauren E. Griffith, PhD, Lisa Strifler, BSc, Matthew Henderson, PhD, Christopher Patterson, MD, George Heckman, MD, David J. Llewellyn, PhD and Parminder Raina, PhD
+ Author Affiliations

From the Departments of Pathology and Molecular Medicine (C.B., M.H.), Clinical Epidemiology and Biostatistics (L.E.G., L.S., P.R.), and Medicine (C.P.), and R. Samuel McLaughlin Center on Gerontological Research and Education (P.R.), McMaster University, Hamilton; Department of Health Studies and Gerontology (G.H.), University of Waterloo, Schlegel-UW Research Institute for Aging, Kitchener, Canada; and Peninsula College of Medicine and Dentistry (D.J.L.), University of Exeter, Devon, UK.
Correspondence & reprint requests to Dr. Balion: balion@hhsc.ca
View Complete Disclosures

ABSTRACT

Objective: To examine the association between cognitive function and dementia with vitamin D concentration in adults.

Methods: Five databases were searched for English-language studies up to August 2010, and included all study designs with a comparative group. Cognitive function or impairment was defined by tests of global or domain-specific cognitive performance and dementia was diagnosed according to recognized criteria. A vitamin D measurement was required. Two authors independently extracted data and assessed study quality using predefined criteria. The Q statistic and I2 methods were used to test for heterogeneity. We conducted meta-analyses using random effects models for the weighted mean difference (WMD) and Hedge’s g.

Results: Thirty-seven studies were included; 8 contained data allowing mean Mini-Mental State Examination (MMSE) scores to be compared between participants with vitamin D <50 nmol/L to those with values ≥50 nmol/L. There was significant heterogeneity among the studies that compared the WMD for MMSE but an overall positive effect for the higher vitamin D group (1.2, 95% confidence interval [CI] 0.5 to 1.9; I2 = 0.65; p = 0.002). The small positive effect persisted despite several sensitivity analyses. Six studies presented data comparing Alzheimer disease (AD) to controls but 2 utilized a method withdrawn from commercial use. For the remaining 4 studies the AD group had a lower vitamin D concentration compared to the control group (WMD = −6.2 nmol/L, 95% CI −10.6 to −1.8) with no heterogeneity (I2 < 0.01; p = 0.53).

Conclusion: These results suggest that lower vitamin D concentrations are associated with poorer cognitive function and a higher risk of AD. Further studies are required to determine the significance and potential public health benefit of this association.

FOOTNOTES

Study funding: Ontario Research Coalition of Research Institutes/Centres on Health & Aging, Ontario Ministry of Long-Term Care. Parminder Raina holds a Canada Research Chair in GeroScience and Raymond and Margaret Labarge Chair in Research and Knowledge Application for Optimal Aging.
Supplemental data at www.neurology.org
Received August 11, 2011.
Accepted May 1, 2012.
Copyright © 2012 by AAN Enterprises, Inc.

 

Posted in Aging, dietary, epigenetics, Health, News, Psychiatry/Neurology | Tagged , , |

Annual Members Meeting Wednesday September 12, 2012 | IDNY

Annual Members Meeting Wednesday September 12, 2012 | IDNY.

 

Posted in Events, Health, News |

‘A Leg to Stand On’ by Oliver Sacks: a unique autobiographical account of functional paralysis

Always interesting if never-ending discussion. Hope to get around to putting some remarks on paper and sending them off to JNNP (or at least post them here).

Meanwhile, two favorite quotes come to mind:

When I asked the neurologist for a prognosis, he soberly declared, it could get better, it could get worse, it could stay the same.  I burst out laughing.  He did not see the joke.

Siri Hustvedt, The Shaking Woman or A History of My Nerves

 

I solve the mind-body problem by stating that there is no such problem. There are, of course, plenty of problems concerning the “mind”, and the “body”, and all intermediate levels of integration of the nervous system. What I wish to emphasize is that there is no problem of “mind” versus “body”, because biologically no such dichotomy can be made. The dichotomy is an artefact; there is no truth in it, and the discussion has no place in science in 1943… The difference between psychology and physiology is merely one of complexity. The simpler bodily processes are studied in physiological departments; the more complex ones that entail the highest levels of neural integration are studied in psychological departments.

Stanley Cobb, Borderlands of Psychiatry (1943)

 

J Neurol Neurosurg Psychiatry 2012;83:864-867 doi:10.1136/jnnp-2012-302800
  • Neuropsychiatry
  • Review

‘A Leg to Stand On’ by Oliver Sacks: a unique autobiographical account of functional paralysis

Editor's ChoicePatient's Choice

  1. Jon Stone1,
  2. Jo Perthen2,
  3. Alan J Carson3,4

+ Author Affiliations


  1. 1Department Clinical Neurosciences, University of Edinburgh, Edinburgh, UK

  2. 2Newcastle University School of Medicine, Newcastle Upon Tyne, UK

  3. 3Department of Psychiatry, University of Edinburgh, Edinburgh, UK

  4. 4Neurorehabilitation, Astley Ainslie Hospital, Edinburgh, UK
  1. Correspondence to Dr Jon Stone, Department Clinical Neurosciences, Western General Hospital, Edinburgh EH4 2XU, UK; jon.stone@ed.ac.uk
  1. Contributors JS conceived the article, all authors contributed to writing.

  • Received 19 March 2012
  • Revised 20 April 2012
  • Accepted 24 April 2012

Abstract

Oliver Sacks, the well known neurologist and writer, published his fourth book, ‘A Leg to Stand On’, in 1984 following an earlier essay ‘The Leg’ in 1982. The book described his recovery after a fall in a remote region of Norway in which he injured his leg. Following surgery to reattach his quadriceps muscle, he experienced an emotional period in which his leg no longer felt a part of his body, and he struggled to regain his ability to walk. Sacks attributed the experience to a neurologically determined disorder of body-image and body ego induced by peripheral injury. In the first edition of his book Sacks explicitly rejected the diagnosis of ‘hysterical paralysis’ as it was then understood, although he approached this diagnosis more closely in subsequent revisions. In this article we propose that, in the light of better understanding of functional neurological symptoms, Sacks’ experiences deserve to be reappraised as a unique insight in to a genuinely experienced functional/psychogenic leg paralysis following injury.

Posted in Psychiatry/Neurology |

Tropical & Travel Medicine Seminar Series

Fabulous slide shows from the Tropical & Travel Medicine Seminar Series of the University of Minnesota (sic!)

via Tropical & Travel Medicine Seminar Series.

Posted in dietary, Health, Psychiatry/Neurology | Tagged , |

Endogenous opioids may protect against minor TBI symptoms

This is an interesting finding. We have shown that people (even “normal” people) with early separation events (early parental divorce, parental loss) have a totally different endogenous opioid reactivity in a challenge test. It would make sense if they therefore were predisposed to more severe TBI and mTBI symptomatology.

Morphine protects for head trauma induced cogn… [Neurosci Lett. 2006] – PubMed – NCBI.

Abstract:

Victims of minor traumatic brain injury (mTBI) can show long lasting cognitive, emotional and concentration difficulties, amnesia, depression, apathy and anxiety. The symptoms are generally known as a post-concussive syndrome without clear morphological brain defects. Endogenous opiates are released after impact to the brain, suggesting they may play a role in TBI pathophysiology. Furthermore, the administration of opiates to the brain of injured animals has been shown to affect the injury, induce cellular changes and also have protective qualities for neurological impairments. Here, we examined the protective properties of the opiate morphine on cognitive performances following minimal brain injury in mice. For this purpose, we have used our non-invasive closed-head weight drop model in mice, which closely mimics real life mTBI and examined mice performance in the Morris water maze. Our procedure did not cause visible structural or neurological damage to the mice. A single morphine injection administrated immediately after the induction of minimal TBI protected the injured mice from cognitive impairment, checked 30, 60 and 90 days post injury. However, mice injected with morphine that were examined 7 days after the injury did not show better performance than the saline injected mice. Our results indicate that morphine has long but not short-term effects on the cognitive ability of brain-injured mice. Although the exact nature of opioid neuroprotection is still unknown, its elucidation may lead to the much-needed treatment for traumatic brain injury.

 

 

Posted in Affective Neuroscience, Forensic Neuropsychiatry, Psychiatry/Neurology | Tagged , , , , , |