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Old 08-16-2007, 06:35 PM   #21
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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, 07:29 PM   #22
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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, 11:38 PM   #23
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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

Quote:
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, 05:15 PM   #24
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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.

Quote:
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, 05:19 PM   #25
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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 09-01-2007, 05:26 PM   #26
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Default Durability, Negative Impact, and Neuropsychological Predictors of Tic Suppression

I find this one really strange.
Note this study contained 13 children only. I wonder if the same results would have been found if the participants had been adults.
Frankly I find it very difficult to believe that periods of tic suppression do not result in a rebound. Waiting now to read the full article when I can.

PubMed abstract ahead of print

J Abnorm Child Psychol. 2007 Aug 24; [Epub ahead of print]
Durability, Negative Impact, and Neuropsychological Predictors of Tic Suppression in Children with Chronic Tic Disorder.
Woods DW, Himle MB, Miltenberger RG, Carr JE, Osmon DC, Karsten AM, Jostad C, Bosch A.
Quote:
Chronic tic disorders are characterized by involuntary motor and vocal tics, which are influenced by contextual factors. Recent research has shown that (a) children can suppress tics for brief periods of time, (b) suppression is enhanced when programmed reinforcement is provided for tic-free intervals, and (c) short periods of suppression do not result in a paradoxical "rebound" in tic frequency when active suppression has ceased. The current study extended existing research in three important ways. First, we examined whether tic suppression ability decreased as suppression duration increased from 5 to 25 to 40 min. Second, we examined post-suppression tic frequency to test whether longer periods of suppression were more likely to be associated with a rebound effect. Finally, we explored neuropsychological predictors of tic suppression. Thirteen children with Tourette syndrome or a chronic tic disorder completed the study. Results showed that (a) tic suppression was sustained for all of the suppression durations, (b) rebound effects were not observed following any of the suppression durations, and (c) ability to suppress was correlated with omission, but not commission errors on a continuous performance task. Implications of these findings are discussed.

PMID: 17717739 [PubMed - as supplied by publisher]
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Old 01-11-2008, 05:48 PM   #27
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Default Interesting

PubMed

Quote:
J Child Neurol. 2008 Jan;23(1):108-11.

The successful use of ondansetron in a boy with both leukemia and tourette syndrome.

Rizzo R, Marino S, Gulisano M, Robertson MM.

Section of Child Neuropsychiatry, Department of Pediatrics University of Catania, Azienda Policlinico, Catania, Italy.

This article reports an 8-year-old boy with both acute lymphoblastic leukemia and Gilles de la Tourette syndrome. Initially, for his leukemia, he was treated with chemotherapy, which resulted in severe nausea and vomiting for which he was given ondansetron. This not only relieved the target symptoms, but also those of his Gilles de la Tourette syndrome. Following a reduction of the ondansetron dosage, his Gilles de la Tourette syndrome symptoms reemerged.

PMID: 18184945 [PubMed - in process
Medline info. about Ondansetron
http://www.nlm.nih.gov/medlineplus/d...r/a601209.html

Quote:
Ondansetron is used to prevent nausea and vomiting caused by cancer chemotherapy, radiation therapy and surgery. Ondansetron is in a class of medications called 5-HT3 receptor antagonists. It works by blocking the action of serotonin, a natural substance that may cause nausea and vomiting.
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Old 01-11-2008, 05:57 PM   #28
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Default Mycoplasma pneumoniae Infection and OCD: A Case Report.

PubMed

Quote:
J Child Neurol. 2007 Dec 13 [Epub ahead of print]

Mycoplasma pneumoniae Infection and Obsessive-Compulsive Disease: A Case Report.

Erener Ercan T, Ercan G, Severge B, Arpaozu M, Karasu G.

Maltepe University Medical Faculty, Department of Pediatrics, Maltepe, Istanbul, Turkey.

It has been demonstrated that obsessive-compulsive disease and/or tic syndromes in children may be triggered by an antecedent infection especially with group A beta-hemolytic streptococci, and this subgroup of children has been designated by the acronym PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections). Other infectious agents such as viruses and bacteria have also been reported to be associated with the acute onset or dramatic exacerbation of obsessive-compulsive disease or Tourette syndrome, and another acronym, PITAND (pediatric infection-triggered autoimmune neuropsychiatric disorder) has appeared in the literature. The involvement of other infectious agents such as Mycoplasma pneumoniae has been described in single case reports. We describe a case of a 5.5-year-old boy who suddenly developed obsessive-compulsive disease symptoms during a M. pneumoniae pneumonia. After treatment with oral clarithromycin, all his obsessive-compulsive disease symptoms disappeared. To our knowledge, this is the first report that shows the association between Mycoplasma pneumoniae infection and obsessive-com-pulsive disease.

PMID: 18079308 [PubMed - as supplied by publisher
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Old 01-11-2008, 06:11 PM   #29
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Default Vomiting and tics

PubMed

Quote:
Turk Psikiyatri Derg. 2007 Winter;18(4):375-8

[Gilles de la tourette syndrome mimicking an eating disorder.]
[Article in Turkish]

Eynde FV, Sentürk V, Naudts K.

Vomiting and retching are behaviours that are part of the clinical manifestation of several disorders. Rarely, vomiting is actually tic and, when not recognized, may mislead physicians and other caregivers to erroneously diagnose a medical or psychiatric disorder without considering a tic-disorder. We report on an 18 year old male patient who demonstrated vomiting as main symptom. Initially, he was diagnosed with an eating disorder, bulimia nervosa purging type (DSM-IV TR). Firstly, he was not very able to suppress his vomiting, but later the vomiting became forced by putting fingers in his throat. This self-induced vomiting had a compulsive component and was performed after almost every meal. Psychiatric assessment disclosed a specific sequence of a premonitory epigastric feeling preceding the vomiting and relief after vomiting. History taking revealed that he had a childhood onset of motor tics (copropraxia which consisted of grabbing his genitalia, bilateral facial grimacing and sudden movements of the head) and phonic tics (sniffing and gargling). Furthermore, he had been treated with methylphenidate for a childhood diagnosis of Attention Deficit and Hyperactivity Disorder and suffered from obsessive-compulsive symptoms (OCS). His vomiting was considered a tic in the course of a Tourette syndrome. His score on the Yale Global Tic Severity Scale dropped from 74 at the first assessment to a score of 50 at week 4 of treatment with risperidone 0,5 mg/day and sertralin 25 mg/day. Sedation and sexual dysfunction occurred as adverse events. Vomiting as a tic is rare clinical manifestation, but this possibility should be considered when patients have a history of tics.

PMID: 18066728 [PubMed - in process]
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Old 03-01-2008, 07:49 AM   #30
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downloadable info on Toxicology and Neurological Development

http://psr.igc.org/ihw-report.htm#ihwRptDwnld
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