Pain affect in the absence of pain sensation: evidence of asomaesthesia after somatosensory cortex lesions in the rat.

Posted on March 3, 2012 by Maurice Preter MD

Pain. 2012 Feb 23. [Epub ahead of print]
Pain affect in the absence of pain sensation: evidence of asomaesthesia after somatosensory cortex lesions in the rat.
Uhelski ML, Davis MA, Fuchs PN.
Source

Department of Diagnostic and Biological Sciences, University of Minnesota Twin Cities, Minneapolis, Minnesota, USA.
Abstract

Multidimensional models of pain processing distinguish the sensory, motivational, and affective components of the pain experience. Efforts to understand underlying mechanisms have focused on isolating the roles of specific brain structures, including both limbic and non-limbic cortical areas, in the processing of nociceptive stimuli. The purpose of this study was to examine the role of the somatosensory cortex in both sensory and affective aspects of pain processing. It was hypothesized that animals with lesions of the hind limb area of the somatosensory cortex would demonstrate altered sensory processing (asomaesthesia, a deficit in the ability to detect and identify somatic sensation) in the presence of an inflammatory state when compared to animals with sham lesions. The level of pain affect produced by an inflammatory pain condition was not expected to change, as this region has not demonstrated a role in processing the affective component of pain. Seventy-nine adult female Sprague-Dawley rats were randomly assigned to receive bilateral lesions or a sham procedure. The results showed that somatosensory lesions to the hindlimb region altered responses to mechanical stimulation in the presence of experimentally-induced inflammation, but did not attenuate the inflammation-induced paw volume changes or the level of pain affect, as demonstrated by escape/avoidance behavior in response to mechanical stimulation. Overall, these results support previous evidence suggesting that the somatosensory cortex is primarily involved in the processing the sensory/discriminative aspect of pain, and the current study is the first to demonstrate the presence of pain affect in the absence of somatosensory processing.

Copyright © 2012 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

PMID:
22365310
[PubMed – as supplied by publisher]

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

Inflammation during fetal and neonatal life: Implications for neurologic and neuropsychiatric disease in children and adults.

Posted on March 3, 2012 by Maurice Preter MD

Ann Neurol. 2011 Sep 2. doi: 10.1002/ana.22620. [Epub ahead of print]
Inflammation during fetal and neonatal life: Implications for neurologic and neuropsychiatric disease in children and adults.
Hagberg H, Gressens P, Mallard C.
Source

Department of Obstetrics and Gynecology, Institute of Clinical Sciences, Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden; Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, London, United Kingdom. henrik.hagberg@obgyn.gu.se.
Abstract

Inflammation is increasingly recognized as being of both physiological and pathological importance in the immature brain. The rationale of this review is to present an update on this topic with focus on long-term consequences of inflammation during childhood and in adults. The immature brain can be exposed to inflammation in connection with viral or bacterial infection during pregnancy or as a result of sterile central nervous system (CNS) insults. Through efficient anti-inflammatory and reparative processes, inflammation may resolve without any harmful effects on the brain. Alternatively, inflammation contributes to injury or enhances CNS vulnerability. Acute inflammation can also be shifted to a chronic inflammatory state and/or adversely affect brain development. Hypothetically, microglia are the main immunocompetent cells in the immature CNS, and depending on the stimulus, molecular context, and timing, these cells will acquire various phenotypes, which will be critical regarding the CNS consequences of inflammation. Inflammation has long-term consequences and could speculatively modify the risk of a variety of neurological disorders, including cerebral palsy, autism spectrum disorders, schizophrenia, multiple sclerosis, cognitive impairment, and Parkinson disease. So far, the picture is incomplete, and data mostly experimental. Further studies are required to strengthen the associations in humans and to determine whether novel therapeutic interventions during the perinatal period can influence the occurrence of neurological disease later in life. Ann Neurol 2012;

Copyright © 2012 American Neurological Association.

PMID:
22334391
[PubMed – as supplied by publisher]

Posted in development, epigenetics | Tagged |

Psychosocial stress and cardiovascular risk : current opinion.

Posted on March 3, 2012 by Maurice Preter MD

Swiss Med Wkly. 2012 Jan 20;142:0. doi: 10.4414/smw.2012.13502.
Psychosocial stress and cardiovascular risk : current opinion.
von Känel R.
Source

Division of Psychosomatic Medicine, Department of General Internal Medicine, Inselspital, Bern University Hospital, and University of Bern, Switzerland. roland.vonkaenel@insel.ch
Abstract

Cardiovascular disease (CVD) is a major cause of morbidity and mortality worldwide. Epidemiologic research of the last half-century has clearly shown that psychosocial factors related to the social environment, personality characteristics, and negative affect increase the risk of incident CVD and also impact prognosis of cardiac patients. Several mechanisms may explain this link, including a genetic predisposition, poor lifestyle choices, low adherence to health recommendations, and direct pathophysiologic perturbations. The latter include alteration of the hypothalamic-pituitary adrenal axis and autonomic dysfunction resulting in endothelial dysfunction, inflammation, and a prothrombotic state further downstream. Screening for psychosocial factors seems appropriate as part of the standard history and based on the clinician’s knowledge of the patient and the purpose of the visit. Psychological interventions generally alleviate distress in cardiac patients, but whether they reduce the risk of hard cardiovascular endpoints and all-cause mortality is less evident. Cardiac patients with more severe depression may particularly profit from antidepressant medications. Due to their pharmacologic properties, selective serotonin reuptake inhibitors were shown to improve cardiovascular outcome. The most effective psychosocial treatment is multicomponent therapy that combines elements of cognitive behaviour therapy (“stress management”) and changes in health behaviours, including the adoption of a regular exercise regimen. Gender-specific issues should probably be considered. The field of behavioural cardiology has accumulated a wealth of epidemiological, mechanistic and clinical knowledge that undoubtedly has furthered our understanding about the important role of psychosocial risk factors in patients with a heart disease.

PMID:
22271452
[PubMed – in process]

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Posted in epigenetics, Psychiatry/Neurology | Tagged , , |

The older people, omega-3, and cognitive health (EPOCH) trial design and methodology: a randomised, double-blind, controlled trial investigating the effect of long-chain omega-3 fatty acids on cognitive ageing and wellbeing in cognitively healthy older adults.

Posted on March 3, 2012 by Maurice Preter MD

Nutr J. 2011 Oct 20;10:117.
The older people, omega-3, and cognitive health (EPOCH) trial design and methodology: a randomised, double-blind, controlled trial investigating the effect of long-chain omega-3 fatty acids on cognitive ageing and wellbeing in cognitively healthy older adults.
Danthiir V, Burns NR, Nettelbeck T, Wilson C, Wittert G.
Source

Preventative Health Research Flagship, Commonwealth Scientific and Industrial Research Organisation – Food and Nutritional Sciences, Adelaide, South Australia, Australia. vanessa.danthiir@csiro.au
Abstract

BACKGROUND: Some studies have suggested an association between omega-3 long-chain polyunsaturated fatty acids (n-3 LC PUFAs) and better cognitive outcomes in older adults. To date, only two randomised, controlled trials have assessed the effect of n-3 LC PUFA supplementation on cognitive function in older cognitively healthy populations. Of these trials only one found a benefit, in the subgroup carrying the ApoE-ε4 allele. The benefits of n-3 LC PUFA supplementation on cognitive function in older normal populations thus still remain unclear. The main objective of the current study was to provide a comprehensive assessment of the potential of n-3 LC PUFAs to slow cognitive decline in normal elderly people, and included ApoE-ε4 allele carriage as a potential moderating factor. The detailed methodology of the trial is reported herein. METHODS: The study was a parallel, 18-month, randomised, double-blind, placebo-controlled intervention with assessment at baseline and repeated 6-monthly. Participants (N = 391, 53.7% female) aged 65-90 years, English-speaking and with normal cognitive function, were recruited from metropolitan Adelaide, South Australia. Participants in the intervention arm received capsules containing fish-oil at a daily dosage of 1720 mg of docosahexaenoic acid and 600 mg of eicosapentaenoic acid while the placebo arm received the equivalent amount of olive oil in their capsules. The primary outcome is rate of change in cognitive performance, as measured by latent variables for the cognitive constructs (encompassing Reasoning, Working Memory, Short-term Memory, Retrieval Fluency, Inhibition, Simple and Choice-Reaction Time, Perceptual Speed, Odd-man-out Reaction Time, Speed of Memory Scanning, and Psychomotor Speed) and assessed by latent growth curve modeling. Secondary outcomes are change in the Mini-mental State Examination, functional capacity and well-being (including health status, depression, mood, and self-report cognitive functioning), blood pressure, and biomarkers of n-3 LC PUFA status, glucose, lipid metabolism, inflammation, oxidative stress, and DNA damage. TRIAL REGISTRATION: Australia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12607000278437.

PMID:
22011460
[PubMed – indexed for MEDLINE]
PMCID:
PMC3210089

Free PMC Article

Posted in Aging, Health, metabolic, new treatments | Tagged , , |

Psychoneuroimmunology meets neuropsychopharmacology: translational implications of the impact of inflammation on behavior.

Posted on March 3, 2012 by Maurice Preter MD

Neuropsychopharmacology. 2012 Jan;37(1):137-62. doi: 10.1038/npp.2011.205. Epub 2011 Sep 14.
Psychoneuroimmunology meets neuropsychopharmacology: translational implications of the impact of inflammation on behavior.
Haroon E, Raison CL, Miller AH.
Source

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA.
Abstract

The potential contribution of chronic inflammation to the development of neuropsychiatric disorders such as major depression has received increasing attention. Elevated biomarkers of inflammation, including inflammatory cytokines and acute-phase proteins, have been found in depressed patients, and administration of inflammatory stimuli has been associated with the development of depressive symptoms. Data also have demonstrated that inflammatory cytokines can interact with multiple pathways known to be involved in the development of depression, including monoamine metabolism, neuroendocrine function, synaptic plasticity, and neurocircuits relevant to mood regulation. Further understanding of mechanisms by which cytokines alter behavior have revealed a host of pharmacologic targets that may be unique to the impact of inflammation on behavior and may be especially relevant to the treatment and prevention of depression in patients with evidence of increased inflammation. Such targets include the inflammatory signaling pathways cyclooxygenase, p38 mitogen-activated protein kinase, and nuclear factor-κB, as well as the metabolic enzyme, indoleamine-2,3-dioxygenase, which breaks down tryptophan into kynurenine. Other targets include the cytokines themselves in addition to chemokines, which attract inflammatory cells from the periphery to the brain. Psychosocial stress, diet, obesity, a leaky gut, and an imbalance between regulatory and pro-inflammatory T cells also contribute to inflammation and may serve as a focus for preventative strategies relevant to both the development of depression and its recurrence. Taken together, identification of mechanisms by which cytokines influence behavior may reveal a panoply of personalized treatment options that target the unique contributions of the immune system to depression.

PMID:
21918508
[PubMed – in process]
PMCID:
PMC3238082
[Available on 2013/1/1]

Posted in Psychiatry/Neurology |