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Old 08-16-2007, 05:04 PM #1
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I am going to digest this one slowly Lara! thank you for posting that...lots to chew on huh
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Old 08-16-2007, 05:14 PM #2
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Originally Posted by Chemar View Post
I am going to digest this one slowly Lara! thank you for posting that...lots to chew on huh

Hi! I'm thinking you mean the "time trends" one from Denmark? I'm running out of time right now, but was looking for the full text articles from that one and also the genetic population differences one. Will post them here shortly. The one from Denmark is very interesting. Look forward to reading more about that.
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Old 08-16-2007, 05:35 PM #3
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Hi Lara...yes LOl I didnt realise you were posting more so should have quoted it....

it is this one

very interesting
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Old 08-16-2007, 06:29 PM #4
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Thanks! More awake now. Breakfast helps. I'd browsed some of these I've posted months ago, but never got around to actually reading them or posting them.

I didn't see the link to free Full Text earlier.

Full Text at http://archpedi.ama-assn.org/cgi/content/full/161/2/193

Time Trends in Reported Diagnoses of Childhood Neuropsychiatric Disorders

A Danish Cohort Study

Hjördís Ósk Atladóttir, MB; Erik T. Parner, MSc(Stat), PhD; Diana Schendel, PhD; Sřren Dalsgaard, MD, PhD; Per Hove Thomsen, DMSc; Poul Thorsen, MD, PhD

Arch Pediatr Adolesc Med. 2007;161:193-198
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Old 08-27-2007, 10:38 PM #5
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Default "Breakthrough" Dopamine Supersensitivity & Antipsychotic Treatment Failure over Time

http://www.jneurosci.org/cgi/content...act/27/11/2979

The Journal of Neuroscience, March 14, 2007, 27(11):2979-2986; doi:10.1523/JNEUROSCI.5416-06.2007

"Breakthrough" Dopamine Supersensitivity during Ongoing Antipsychotic Treatment Leads to Treatment Failure over Time

Anne-Noël Samaha, Philip Seeman, Jane Stewart, Heshmat Rajabi, and Shitij Kapur

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Antipsychotics often lose efficacy in patients despite chronic continuous treatment. Why this occurs is not known. It is known, however, that withdrawal from chronic antipsychotic treatment induces behavioral dopaminergic supersensitivity in animals. How this emerging supersensitivity might interact with ongoing treatment has never been assessed. Therefore, we asked whether dopamine supersensitivity could overcome the behavioral and neurochemical effects of antipsychotics while they are still in use. Using two models of antipsychotic-like effects in rats, we show that during ongoing treatment with clinically relevant doses, haloperidol and olanzapine progressively lose their efficacy in suppressing amphetamine-induced locomotion and conditioned avoidance responding. Treatment failure occurred despite high levels of dopamine D2 receptor occupancy by the antipsychotic and was at least temporarily reversible by an additional increase in antipsychotic dose. To explore potential mechanisms, we studied presynaptic and postsynaptic elements of the dopamine system and observed that antipsychotic failure was accompanied by opposing changes across the synapse: tolerance to the ability of haloperidol to increase basal dopamine and dopamine turnover on one side, and 20–40% increases in D2 receptor number and 100–160% increases in the proportion of D2 receptors in the high-affinity state for dopamine (D2High) on the other. Thus, the loss of antipsychotic efficacy is linked to an increase in D2 receptor number and sensitivity. These results are the first to demonstrate that "breakthrough" supersensitivity during ongoing antipsychotic treatment undermines treatment efficacy. These findings provide a model and a mechanism for antipsychotic treatment failure and suggest new directions for the development of more effective antipsychotics.
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Old 09-01-2007, 04:15 PM #6
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Default Frontal-subcortical circuitry and behavior.

PubMed Abstract

Dialogues Clin Neurosci. 2007;9(2):141-51.
Frontal-subcortical circuitry and behavior.
Bonelli RM, Cummings JL.

Department of Psychiatry, Graz Medical University, Auenbruggerplatz 31, 8036 Graz, Austria.

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The neuropsychiatric manifestations of neurodegenerative diseases are closely linked to neurocircuitry defects. Frontal-subcortical circuits, in particular, are effector mechanisms that allow the organism to act on its environment. In this paper, we present the three main frontal-subcortical circuits: the dorsolateral prefrontal circuit allows the organization of information to facilitate a response; the anterior cingulate circuit is required for motivated behavior; and the orbitofrontal circuit allows the integration of limbic and emotional information into behavioral responses. Impaired executive functions, apathy, and impulsivity are hallmarks of frontal-subcortical circuit dysfunction. A variety of other neuropsychiatric disorders, such as Tourette's syndrome, Huntington's disease, obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, schizophrenia, and mood disorders may result from disturbances that have a direct or indirect impact on the integrity or functioning of these loops.

PMID: 17726913 [PubMed - in process]
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Old 09-01-2007, 04:19 PM #7
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Default Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome.

PubMed Abstract ahead of print

Mov Disord. 2007 Aug 20; [Epub ahead of print]
Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome.
Behen M, Chugani HT, Juhász C, Helder E, Ho A, Maqbool M, Rothermel RD, Perry J, Muzik O.

Quote:
Symptoms in Tourette syndrome (TS) are likely related to abnormalities involving multiple neurotransmitter systems in striatal-thalamo-cortical circuitry. Although prior studies have found abnormal levels of tryptophan, serotonin, and their metabolites in blood, cerebrospinal fluid and brain tissue of TS patients, understanding of focal brain disturbances and their relationship to clinical phenotype remains poor. We used alpha-[(11)C]methyl-L-tryptophan (AMT) positron emission tomography (PET) to assess global and focal brain abnormalities of tryptophan metabolism and their relationship to behavioral phenotype in 26 children with TS and nine controls. Group comparisons on regional cortical and subcortical AMT uptake revealed decreased AMT uptake in bilateral dorsolateral prefrontal cortical and bilaterally increased uptake in the thalamus (P = 0.001) in TS children. The ratio of AMT uptake in subcortical structures to dorsolateral prefrontal cortex was significantly increased bilaterally (P < 0.01) in TS patients also. Behaviorally defined subgroups within the TS sample revealed differences in the pattern of AMT uptake in the fronto-striatal-thalamic circuit. This study demonstrates cortical and subcortical abnormalities of tryptophan metabolism in TS and provides neuroimaging evidence for a role of serotonergic mechanisms in the pathophysiology of TS. (c) 2007 Movement Disorder Society.

PMID: 17708557 [PubMed - as supplied by publisher]
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Old 04-08-2013, 02:33 PM #8
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Default Immune System and Schizophrenia

Not regarding TS however these are very interesting findings regarding Schizophrenia and the Immune System. Just posting here because I think this could be relevant to a number of conditions. Just my thoughts.

UTI Far More Likely After Schizophrenia Relapse
By Traci Pedersen Associate News Editor
from PsychCentral

http://psychcentral.com/news/2013/04...pse/53514.html
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Old 05-02-2013, 03:55 PM #9
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Default Antibacteral Soap

Just FYI

Decades-old question: Is antibacterial soap safe?

Regarding Triclosan in Antibacterial soap.
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Old 05-05-2013, 03:23 PM #10
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Post Sensory Tricks - geste antagoniste

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3607913/
Tic Modulation Using Sensory Tricks
Rebecca Wolf Gilbert
Tremor Other Hyperkinet Mov (N Y). 2013; 3: tre-03-115-3129-1.
Published online 2013 March 26.
PMCID: PMC3607913

Quote:
A sensory trick, or geste antagoniste, is defined as a physical gesture (such as a touch on a particular body part) that mitigates the production of an involuntary movement. This phenomenon is most commonly described as a feature of dystonia. Here we present a case of successful modulation of tics using sensory tricks.
National Library of Medicine (NLM)
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