From the Society for Neuroscience Meeting: Microglial acid-sensing t-cell death associated gene-8 (tdag8) receptor in co2 evoked behavior and physiology: Relevance to panic

Posted on October 16, 2012 by Maurice Preter MD

 

Their finding supports our position that panic/anxiety and predator stress/fear are two different phenomenological&biological animals. A true translational moment indeed.
Not sure if I am allowed to post the whole abstract, but the link is here.

 

Program#/Poster#: 68.14/V18
Presentation Title: Microglial acid-sensing t-cell death associated gene-8 (tdag8) receptor in co2 evoked behavior and physiology: Relevance to panic
Location: Hall F-J
Presentation time: Saturday, Oct 13, 2012, 2:00 PM – 3:00 PM
Authors: *L. E. LARKE1, J. RUSH1, K.-Y. LI2, I. LEWKOWICH3, R. W. PUTNAM2, R. SAH1;
1Psychiatry and Behavioral Neurosci., Univ. Of Cincinnati, Cincinnati, OH; 2Wright State Univ., Dayton, OH; 3Cincinnati Children’s Hosp. Med. Ctr., Cincinnati, OH

Our review is posted here. The abstract follows:

>>This review paper presents an amplification of the suffocation false alarm theory (SFA) of spontaneous panic (Klein, 1993). SFA postulates the existence of an evolved physiologic suffocation alarm system that monitors information about potential suffocation. Panic attacks maladaptively occur when the alarm is erroneously triggered. That panic is distinct from Cannon’s emergency fear response and Selye’s General Alarm Syndrome is shown by the prominence of intense air hunger during these attacks. Further, panic sufferers have chronic sighing abnormalities outside of the acute attack. Another basic physiologic distinction between fear and panic is the counter-intuitive lack of hypothalamic-pituitary-adrenal (HPA) activation in panic. Understanding panic as provoked by indicators of potential suffocation, such as fluctuations in pCO2 and brain lactate, as well as environmental circumstances fits the observed respiratory abnormalities. However, that sudden loss, bereavement and childhood separation anxiety are also antecedents of “spontaneous” panic requires an integrative explanation. Because of the opioid system’s central regulatory role in both disordered breathing and separation distress, we detail the role of opioidergic dysfunction in decreasing the suffocation alarm threshold. We present results from our laboratory where the naloxone-lactate challenge in normals produces supportive evidence for the endorphinergic defect hypothesis in the form of a distress episode of specific tidal volume hyperventilation paralleling challenge-produced and clinical panic.
Keywords
Affective neuroscience; Endogenous opioids; Panic disorder; Respiratory physiology; Separation Anxiety
<<
Ref: Preter M, Klein DF. Panic, Suffocation False Alarms, Separation Anxiety and Endogenous Opioids. Progress in Neuropsychopharmacology and Biological Psychiatry 32/3 (2008) 603-612.

 

 

Posted in Affective Neuroscience, epigenetics, News | Tagged , , |

“Clock-watching” and insomnia are linked to posttraumatic stress symptoms – packaged with a zolpidem ad!

Posted on October 16, 2012 by Maurice Preter MD

Just got this mass email. The ad next to it is for zolpidem – just the kind of stuff that might NOT benefit post-traumatic states. What’s the message here?

OCTOBER 2012

Advertisement

Editor’s note
Approximately 50% of chronic insomnia patients have a comorbid psychiatric disorder.1 Historically, the focus has been on depression, but in this issue we focus on insomnia’s relationship with other psychiatric disorders and symptoms.
Although posttraumatic stress disorder (PTSD) has been associated with insomnia, Krakow et al suggest the mediator of the insomnia-PTSD link is time monitoring (“clock-watching”). Nadorff et al describe a relationship between insomnia and suicidal ideation in older adults and that the mediator of this association is depressive symptoms.
Most insomnia patients don’t abuse hypnotics,2 but Ruiter et al document a 3-way relationship among personality disorders, insomnia, and hypnotic dependence. Finally, Haario et al found unhealthy behaviors—smoking, binge drinking, and inactivity—are a consequence of as well as risk factor for insomnia.
Together, these studies support the clinical wisdom of treating both conditions when patients present with insomnia and a comorbid disorder.—Thomas Roth, PhD, Director of Research and Chief of Sleep Medicine, Henry Ford Hospital, Detroit, MI

References
1. Insomnia: assessment and management in primary care. Washington, DC: National Institutes of Health; 1998.
2. Mendelson WB, Roth T, Cassella J, et al. The treatment of chronic insomnia: drug indications, chronic use and abuse liability. Summary of a 2001 New Clinical Drug Evaluation Unit meeting symposium. Sleep Med Rev. 2004;8(1):7-17.

“Clock-watching” and insomnia are linked
to posttraumatic stress symptoms
Krakow B, et al. J Nerv Ment Dis. 2012;200(9):821-825.
Researchers reviewed the medical charts of 1,078 patients who had poor sleep quality (51%), sleep-disordered breathing (26%), or insomnia (24%). Almost one-third reported moderate to severe posttraumatic stress symptoms (PSSs). Insomnia and time monitoring (“clock-watching”) severity were greater in patients with PSSs (n = 350) than in patients with minimal or no PSSs.
Read more
In older adults, insomnia is related
to suicidal ideation
Nadorff MR, et al. J Gerontol B Psychol Sci Soc Sci. Epub August 28, 2012.
Researchers surveyed 81 patients age ≥65 about their sleep habits, depressive symptoms, and suicidal ideation. Insomnia symptoms were related to suicidal ideation independent of nightmares, and depression mediated the relationship between insomnia symptoms and suicidal ideation.
Read more

©2012 Frontline Medical Communications, 7 Century Drive, Suite 302, Parsippany, NJ 07054-4609 USA

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

Fresh off the press: Angst – Origins of Anxiety and Depression by Jeffrey P. Kahn, MD

Posted on October 15, 2012 by Maurice Preter MD

My friend and colleague Dr. Kahn just published his book on Anxiety. Thorough coverage of our work on panic disorder is gratefully acknowledged.

 

Angst
Origins of Anxiety and Depression
Jeffrey P. Kahn, MD
Clinical Associate Professor of Psychiatry Weill Cornell Medical College New York, NY

Posted in Psychiatry/Neurology |

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.
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