View Full Version : Articles, Abstracts and News Reports on TS
Haiqun Lin, Liliya Katsovich, Musie Ghebremichael, Diane B. Findley, Heidi Grantz, Paul J. Lombroso, Robert A. King, Heping Zhang, James F. Leckman (2007)
Psychosocial stress predicts future symptom severities in children and adolescents with Tourette syndrome and/or obsessive-compulsive disorder
Journal of Child Psychology and Psychiatry 48 (2), 157–166.
doi:10.1111/j.1469-7610.2006.01687.x
http://www.blackwell-synergy.com/doi/abs/10.1111/j.1469-7610.2006.01687.x
Abstract
Background: The goals of this prospective longitudinal study were to monitor levels of psychosocial stress in children and adolescents with Tourette syndrome (TS) and/or obsessive-compulsive disorder (OCD) compared to healthy control subjects and to examine the relationship between measures of psychosocial stress and fluctuations in tic, obsessive-compulsive (OC), and depressive symptom severity.
Methods: Consecutive ratings of tic, OC and depressive symptom severity were obtained for 45 cases and 41 matched healthy control subjects over a two-year period. Measures of psychosocial stress included youth self-report, parental report, and clinician ratings of long-term contextual threat. Structural equation modeling for unbalanced repeated measures was used to assess the temporal sequence of psychosocial stress with the severity of tic, OC and depressive symptoms.
Results: Subjects with TS and OCD experienced significantly more psychosocial stress than did the controls. Estimates of psychosocial stress were predictive of future depressive symptoms. Current levels of psychosocial stress were also a significant predictor of future OC symptom severity, but not vice versa. Current OC symptom severity was a predictor of future depressive symptom severity, but not vice versa. Current levels of psychosocial stress and depression were independent predictors of future tic severity, even after controlling for the effect of advancing chronological age.
Conclusions: The impact of antecedent psychosocial adversity is greater on future depressive symptoms than for tic and/or OC symptoms. Worsening OC symptoms are also a predictor of future depressive symptoms. Advancing chronological age is robustly associated with reductions in tic severity.
Am J Hum Genet. 2007 Feb;80(2):265-72.
Genome scan for Tourette disorder in affected-sibling-pair and multigenerational families.
Tourette Syndrome Association International Consortium for Genetics.
Tourette disorder (TD) is a neuropsychiatric disorder with a complex mode of inheritance and is characterized by multiple waxing and waning motor and phonic tics. This article reports the results of the largest genetic linkage study yet undertaken for TD. The sample analyzed includes 238 nuclear families yielding 304 "independent" sibling pairs and 18 separate multigenerational families, for a total of 2,040 individuals. A whole-genome screen with the use of 390 microsatellite markers was completed. Analyses were completed using two diagnostic classifications: (1) only individuals with TD were included as affected and (2) individuals with either TD or chronic-tic (CT) disorder were included as affected. Strong evidence of linkage was observed for a region on chromosome 2p (-log P = 4.42, P = 3.8 x 10(-5) in the analyses that included individuals with TD or CT disorder as affected. Results in several other regions also provide moderate evidence (-log P >2.0) of additional susceptibility loci for TD.
PMID: 17304708 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17304708&query_hl=5&itool=pubmed_docsum
J Neurol Sci. 2007 Mar 2; [Epub ahead of print]
Frontal dopaminergic abnormality in Tourette syndrome: A postmortem analysis.
Yoon DY, Gause CD, Leckman JF, Singer HS.
Department of Neurology, Johns Hopkins University School of Medicine, Harriett Lane Outpatient Building, 200 N. Wolfe Street, Suite 2158, Baltimore, MD, USA.
Frontal-subcortical abnormalities have been implicated in the pathophysiology of Tourette syndrome (TS). The goal of this study was to more extensively evaluate a possible underlying neurochemical abnormality in frontal cortex. Postmortem brain tissue from frontal and occipital regions (Brodmann's areas 4, 6, 9, 10, 11, 12, and 17) from three TS patients and three age-and sex-matched controls were analyzed by semiquantitative immunoblotting. Relative densities were measured for a variety of neurochemical markers including dopamine (D1, D2), serotonin (5HT-1A), and alpha-adrenergic (alpha-2A) receptors, the dopamine transporter (DAT), a monoamine terminal marker (vesicular monoamine transporter type 2, VMAT-2), and vesicular docking and release proteins (VAMP-2, synaptotagmin, SNAP-25, syntaxin, synaptophysin). Data from each TS sample, corrected for actin content, was expressed as a percentage value of its control. Results identified consistent increases of DAT and D2 receptor density in five of six frontal regions in all three TS subjects. D1 and alpha-2A receptor density were increased in a few frontal regions. These results support the hypothesis of a dopaminergic dysfunction in the frontal lobe and a likely role in the pathophysiology of TS.
PMID: 17337006 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17337006&query_hl=6&itool=pubmed_docsum
Chemar
03-25-2007, 11:43 AM
although this article specifically deals with autism...it has much of interest and so I felt it worth posting here too related to ASD
http://discovermagazine.com/2007/apr/autism-it2019s-not-just-in-the-head/article_view?b_start:int=0&-C=
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WG1-48KF9H9-2&_user=2245104&_coverDate=07%2F31%2F2003&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000056718&_version=1&_urlVersion=0&_userid=2245104&md5=b97c093fb26af0ee44c57ec46e02d5e2
Genomics. 2003 Jul;82(1):1-9.
Cntnap2 is disrupted in a family with gilles de la tourette syndrome and obsessive compulsive disorder
Verkerk AJ, Mathews CA, Joosse M, Eussen BH, Heutink P, Oostra BA; Tourette Syndrome Association International Consortium for Genetics.
_________________
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17392702&query_hl=3&itool=pubmed_docsum
Eur J Hum Genet. 2007 Mar 28
Disruption of the CNTNAP2 gene in a t(7;15) translocation family without symptoms of Gilles de la Tourette syndrome.
Belloso JM, Bache I, Guitart M, Caballin MR, Halgren C, Kirchhoff M, Ropers HH, Tommerup N, Tumer Z.
In this study, we describe a familial balanced reciprocal translocation t(7;15)(q35;q26.1) in phenotypically normal individuals. The 7q35 breakpoint disrupts the CNTNAP2 gene, indicating that truncation of this gene does not necessarily lead to the symptoms of the complex Gilles de la Tourette syndrome.European Journal of Human Genetics advance online publication, 28 March 2007; doi:10.1038/sj.ejhg.5201824.
bold added by me.
Neuropsychologia. 2007 Apr 5;
Speeded processing of grammar and tool knowledge in Tourette's syndrome.
Walenski M, Mostofsky SH, Ullman MT.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17493643&query_hl=1&itool=pubmed_docsum
Tourette's syndrome (TS) is a developmental disorder characterized by motor and verbal tics. The tics, which are fast and involuntary, result from frontal/basal-ganglia abnormalities that lead to unsuppressed behaviors. Language has not been carefully examined in TS. We tested the processing of two basic aspects of language: idiosyncratic and rule-governed linguistic knowledge. Evidence suggests that idiosyncratic knowledge (e.g., in irregular past tense formation; bring-brought) is stored in a mental lexicon that depends on the temporal-lobe-based declarative memory system that also underlies conceptual knowledge. In contrast, evidence suggests that rule-governed combination (e.g., in regular past tenses; walk+-ed) takes place in a mental grammar that relies on the frontal/basal-ganglia-based procedural memory system, which also underlies motor skills such as how to use a hammer. We found that TS children were significantly faster than typically developing control children in producing rule-governed past tenses (slip-slipped, plim-plimmed, bring-bringed) but not irregular and other unpredictable past tenses (bring-brought, splim-splam). They were also faster than controls in naming pictures of manipulated (hammer) but not non-manipulated (elephant) items. These data were not explained by a wide range of potentially confounding subject- and item-level factors. The results suggest that the processing of procedurally based knowledge, both of grammar and of manipulated objects, is particularly speeded in TS. The frontal/basal-ganglia abnormalities may thus lead not only to tics, but also to a wider range of rapid behaviors, including the cognitive processing of rule-governed forms in language and other types of procedural knowledge.
PMID: 17493643
Interesting...
J Clin Child Adolesc Psychol. 2007 Jun;36(2):217-27.
Quality of Life in Youth With Tourette's Syndrome and Chronic Tic Disorder.
Storch EA, Merlo LJ, Lack C, Geffken GR, Goodman WK, Murphy TK.
Department of Psychiatry and Pediatrics, University of Florida.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17484694&query_hl=1&itool=pubmed_docsum
This study sought to examine quality of life (QoL) in clinic-referred children and adolescents (n = 59, M age = 11.4+/-2.6 years) with a chronic tic disorder. The QoL scores for tic patients were lower than for healthy controls but higher than for the psychiatric sample on the majority of domains. Children's self-reported QoL scores and a measure of tic severity were moderately and inversely correlated. Parent reports of their child's QoL were weakly related to tic severity. Correlations between parent and child ratings of QoL for children ages 8 to 11 years were generally higher than those for youth ages 12 to 17 years. Finally, externalizing behavior moderated the relations between tic severity and parent-rated QoL, such that tic severity was significantly associated with parent-rated QoL for children with below average externalizing symptoms but not for children 3with above average externalizing symptoms.
PMID: 17484694
These two are not specifically about Tourette's Syndrome but they are of interest.
The 2nd one regarding RLS is also of interest as quite a lot of people have Restless Leg Syndrome as well as their Tics or have members in their families who have RLS as well. [It fits in with the posts regarding OC behaviours or even Secondary causes of Tics or Tourettism.]
So, just some things in the news of interest...
http://www.sciencedaily.com/releases/2007/06/070615110252.htm
from Science Daily
Source: Mayo Clinic
Date: June 15, 2007
Researchers Use 'Genomic Pathway' To Predict Parkinson's
<snipped article>
The researchers speculate that common genetic variations within the same biological pathway might also contribute to a person's risk of developing other brain diseases; disorders such as Alzheimer's disease, Tourette's syndrome, dyslexia, epilepsy and schizophrenia, need to be studied.
______________
Dopaminergic Agonists Linked to Compulsions in RLS
Medscape Medical News 2007
www.medscape.com/viewarticle/558519
Registration required
Caroline Cassels
June 19, 2007 (Istanbul) — Like their counterparts with Parkinson's disease (PD), patients with restless legs syndrome (RLS) taking dopaminergic agonists (DA) are at increased risk for compulsive behaviors, new research suggests.
Presented here at the 11th International Congress of Parkinson's Disease and Movement Disorders, researchers from the Quebec Memory Motor Skills Disorders Clinic, in Quebec City, Quebec, found up to 10% of RLS patients had compulsive behaviors, including trichotillomania, a Tourette-like syndrome, and other impulse-control disorders, including shopping, overeating, and gambling.
bold added by me
Comparative Effectiveness of Off-Label Use of Atypical Antipsychotics: AHRQ Executive Summary
http://effectivehealthcare.ahrq.gov/repFiles/Atypical_Antipsychotics_Final_Report.pdf
Full Text pdf
This is very long, but worth reading if you're interested. Just use the search feature to highlight keywords in the file e.g. Tourette's syndrome or Autism or PTSD etc..
from
Medscape Medical News
07/06/2007
Comparative Effectiveness of Off-Label Use of Atypical Antipsychotics: AHRQ Executive Summary
http://www.medscape.com/viewarticle/559169_1
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17620884&ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
Curr Opin Neurol. 2007 Aug;20(4):470-6.
Surgery for other movement disorders: dystonia, tics.
Hamani C, Moro E.
PURPOSE OF REVIEW: Various movement disorders are now treated with stereotactic procedures, particularly deep brain stimulation. We review the neurosurgical treatment of dystonias and tics, focusing mainly on the surgical aspects and outcome of deep brain stimulation.
RECENT FINDINGS: Pallidal stimulation is nowadays the mainstay surgical treatment for patients with dystonia, particularly generalized dystonia. Various well designed recent clinical trials support the efficacy of the procedure. Improvements of 40-80% have been reported in primary generalized, segmental and cervical dystonia. For secondary dystonia, a similar outcome has been described in patients with tardive dystonia and pantothenate kinase-associated neurodegeneration. In patients with Tourette's syndrome, the results of the first trials with thalamic and pallidal deep brain stimulation have been very promising. Improvements of 70-90% in the frequency of tics have been reported with surgery in both targets.
SUMMARY: Deep brain stimulation has become an established therapy for dystonia and is currently being used to treat Tourette's syndrome. With accumulation of experience, clinical features that are more responsive to surgery and the best surgical candidates will be revealed. This will likely improve even further the outcome of surgery for the treatment of these disorders.
PMID: 17620884 [PubMed - in process]
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17618533&ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
Curr Neurol Neurosci Rep. 2007 Jul;7(4):278-89.
Limbic, associative, and motor territories within the targets for deep brain stimulation: potential clinical implications.
Sudhyadhom A, Bova FJ, Foote KD, Rosado CA, Kirsch-Darrow L, Okun MS.
The use of deep brain stimulation (DBS) has recently been expanding for the treatment of many neurologic disorders such as Parkinson disease, dystonia, essential tremor, Tourette's syndrome, cluster headache, epilepsy, depression, and obsessive compulsive disorder. The target structures for DBS include specific segregated territories within limbic, associative, or motor regions of very small subnuclei. In this review, we summarize current clinical techniques for DBS, the cognitive/mood/motor outcomes, and the relevant neuroanatomy with respect to functional territories within specific brain targets. Future development of new techniques and technology that may include a more direct visualization of "motor" territories within target structures may prove useful for avoiding side effects that may result from stimulation of associative and limbic regions. Alternatively, newer procedures may choose and specifically target non-motor territories for chronic electrical stimulation.
PMID: 17618533 [PubMed - in process]
http://www.neurology.org/cgi/content/full/68/2/85
NEUROLOGY 2007;68:85
© 2007 American Academy of Neurology
January 9 Highlight and Commentary
Deep brain stimulation for a teen with tics?
Donald L. Gilbert, MD, MS
This report describes short-term changes after deep brain stimulation (DBS) in a 16-year-old boy with unusually severe Tourette syndrome (TS) symptoms.1 The report illustrates important factors in considering DBS as an experimental treatment for TS.
http://jnnp.bmj.com/cgi/content/abstract/76/7/992?ijkey=f50900d4e25873747c51639adaa5e86394bdc102&keytype2=tf_ipsecsha
Tourette’s syndrome and deep brain stimulation
J L Houeto, C Karachi, L Mallet, B Pillon, J Yelnik, V Mesnage, M L Welter, S Navarro, A Pelissolo, P Damier, B Pidoux, D Dormont, P Cornu and Y Agid
http://www.neurology.org/cgi/content/full/66/3/E12?ijkey=f88d12243710bd2e60faeed539df7b7b676cfe57&keytype2=tf_ipsecsha
NEUROLOGY 2006;66:E12
NeuroImages
Hemi tics and deep brain stimulation
Catherine L. Gallagher, MD, P. Charles Garell, MD and Erwin B. Montgomery, Jr, MD
http://www.touchbriefings.com/pdf/2785/tipuaziz.pdf
Deep Brain Stimulation—Which Patients and When?
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17598875&ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
J Intellect Disabil Res. 2007 Aug;51(Pt 8):620-4.
An individual with Gilles de la Tourette syndrome and Smith-Magenis microdeletion syndrome: is chromosome 17p11.2 a candidate region for Tourette syndrome putative susceptibility genes?
Shelley BP, Robertson MM, Turk J.
This is the first published case description in the current literature of the association of definite Gilles de la Tourette syndrome (GTS) and the Smith-Magenis syndrome (SMS), both confirmed by DSM-IV-TR criteria and molecular cytogenetic analysis, respectively. The co-occurrence of GTS, SMS and their common behavioural/neuropsychiatric abnormalities should warrant further genetic investigation of chromosome 17p11.2 deletion site as it may be a promising region for containing a gene(s) of aetiological importance in the development of the GTS phenotype. Alternatively, the co-occurrence may be due to the common endophenotypic mechanisms shared by these disorders, rather than being specific for GTS that could be explored using strategies of quantitative trait loci - endophenotype-based approach. Research into this genomic region may also benefit psychiatric genetic research in enhancing understanding of the biological and molecular underpinnings of common behavioural problems that are seen in both GTS and SMS. This would lead to advancement in neurobehavioural/neuropsychiatric genetics which will help in further explaining the broader perspective of gene-brain-behaviour interrelationships.
PMID: 17598875 [PubMed - in process]
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17594392&ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
Clin Genet. 2007 Jul;72(1):1-8.
Development of cortical GABAergic circuits and its implications for neurodevelopmental disorders.
Di Cristo G.
GABAergic interneurons powerfully control the function of cortical networks. In addition, they strongly regulate cortical development by modulating several cellular processes such as neuronal proliferation, migration, differentiation and connectivity. Not surprisingly, aberrant development of GABAergic circuits has been implicated in many neurodevelopmental disorders including schizophrenia, autism and Tourette's syndrome. Unfortunately, efforts directed towards the comprehension of the mechanisms regulating GABAergic circuits formation and function have been impaired by the strikingly heterogeneity, both at the morphological and functional level, of GABAergic interneurons. Recent technical advances, including the improvement of interneurons-specific labelling techniques, have started to reveal the basic principles underlying this process. This review summarizes recent findings on the mechanisms underlying the construction of GABAergic circuits in the cortex, with a particular focus on potential implications for brain diseases with neurodevelopmental origin.
PMID: 17594392 [PubMed - in process]
Full text article is available at cost from here. I just posted this one because I thought some people might be interested.
Full Text available (http://www.blackwell-synergy.com/doi/abs/10.1111/j.1399-0004.2007.00822.x)
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17679691&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
Proc Natl Acad Sci U S A. 2007 Aug 6; [Epub ahead of print]
Development of distinct control networks through segregation and integration.
Fair DA, Dosenbach NU, Church JA, Cohen AL, Brahmbhatt S, Miezin FM, Barch DM, Raichle ME, Petersen SE, Schlaggar BL.
Human attentional control is unrivaled. We recently proposed that adults depend on distinct frontoparietal and cinguloopercular networks for adaptive online task control versus more stable set control, respectively. During development, both experience-dependent evoked activity and spontaneous waves of synchronized cortical activity are thought to support the formation and maintenance of neural networks. Such mechanisms may encourage tighter "integration" of some regions into networks over time while "segregating" other sets of regions into separate networks. Here we use resting state functional connectivity MRI, which measures correlations in spontaneous blood oxygenation level-dependent signal fluctuations between brain regions to compare previously identified control networks between children and adults. We find that development of the proposed adult control networks involves both segregation (i.e., decreased short-range connections) and integration (i.e., increased long-range connections) of the brain regions that comprise them. Delay/disruption in the developmental processes of segregation and integration may play a role in disorders of control, such as autism, attention deficit hyperactivity disorder, and Tourette's syndrome.
PMID: 17679691 [PubMed - as supplied by publisher]
Full Text article should be available here and also at PubMed Central, although I can't get it working at present myself.
http://www.pnas.org/cgi/reprint/0705843104v1
Olanzapine (Zyprexa)
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17597439&ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
Psychiatr Prax. 2007 Jul;34(5):253-4.
[Gilles-de-la-Tourette Syndrome as a Tardive Dyskinesia.]
[Article in German]
Kozian R, Friederich M.
Asklepios-Fachklinik Stadtroda.
Following ten years of continuous olanzapine therapy a 51 years old man developed a Gilles de la Tourette syndrome which disappeared after changing to amisulprid. The Tourette-syndrome will be attributed to a tardive dyskinesia induced by olanzapine.
PMID: 17597439 [PubMed - in process]
Medical News Today article...
Neurology / Neuroscience News
Article Date: 07 Aug 2007
http://www.medicalnewstoday.com/articles/78872.php
Deep Brain Stimulation And Tourette Syndrome
Still considered experimental, the procedure used-Deep Brain Stimulation (DBS)-involves the implantation of electrodes in the brain that are stimulated by a surgically implanted pulse generator in the upper chest. Several studies have shown that this surgical intervention may aid in the amelioration of involuntary movements in patients with Parkinson's Disease and Essential Tremor. More recent studies have shown promise for other disorders including Dystonia.
Early experience with DBS for tics in TS has been mixed. While some individuals have experienced a reduction in symptoms, others have not. There is no long-term follow-up yet to indicate whether or not symptoms will return at some point. It should be understood that when undergoing this procedure, there might be serious risks involved that could include cerebral bleeding and infection.
Only rigorous, methodologically sound scientific study of DBS will provide the answers we seek.
____________________________
TSA-USA Statement: Deep Brain Stimulation and Tourette Syndrome
Following is a statement from TSA Medical and Scientific Advisors.
http://www.tsa-usa.org/news/DBSStatement.htm
(I notice this Statement has been updated 8/2007)
____________________________
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16991144&ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
Mov Disord. 2006 Nov;21(11):1831-8.
Patient selection and assessment recommendations for deep brain stimulation in Tourette syndrome.
Mink JW, Walkup J, Frey KA, Como P, Cath D, Delong MR, Erenberg G, Jankovic J, Juncos J, Leckman JF, Swerdlow N, Visser-Vandewalle V, Vitek JL; Tourette Syndrome Association, Inc.
Department of Neurology, University of Rochester, Rochester, New York, USA.
In response to recent publicity regarding the potential use of deep brain stimulation (DBS) for reducing tic severity in Tourette's syndrome (TS), the Tourette Syndrome Association convened a group of TS and DBS experts to develop recommendations to guide the early use and potential clinical trials of DBS for TS and other tic disorders. The goals of these recommendations are to ensure that all surgical candidates are (1) fully informed about the risks, benefits, and alternative treatments available; (2) receive a comprehensive evaluation before surgery to ensure that DBS is clearly the appropriate clinical treatment choice; and (3) that early clinical experience will be documented publicly to facilitate rational decision-making for both clinical care and future clinical trials.
PMID: 16991144 [PubMed - indexed for MEDLINE]
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=AbstractPlus&list_uids=17289354)
Psychiatry Res. 2007 Feb 28;154(2):181-90. Epub 2007 Feb 7.
Validity of large-deformation high dimensional brain mapping of the basal ganglia in adults with Tourette syndrome.
Wang L, Lee DY, Bailey E, Hartlein JM, Gado MH, Miller MI, Black KJ.
The basal ganglia and thalamus may play a critical role for behavioral inhibition mediated by prefrontal, parietal, temporal, and cingulate cortices. The cortico-basal ganglia-thalamo-cortical loop with projections from frontal cortex to striatum, then to globus pallidus or to substantia nigra pars reticulata, to thalamus and back to cortex, provides the anatomical substrate for this function. In-vivo neuroimaging studies have reported reduced volumes in the thalamus and basal ganglia in individuals with Tourette Syndrome (TS) when compared with healthy controls. However, patterns of neuroanatomical shape that may be associated with these volume differences have not yet been consistently characterized. Tools are being developed at a rapid pace within the emerging field of computational anatomy that allow for the precise analysis of neuroanatomical shape derived from magnetic resonance (MR) images, and give us the ability to characterize subtle abnormalities of brain structures that were previously undetectable. In this study, T1-weighted MR scans were collected in 15 neuroleptic-naïve adults with TS or chronic motor tics and 15 healthy, tic-free adult subjects matched for age, gender and handedness. We demonstrated the validity and reliability of large-deformation high dimensional brain mapping (HDBM-LD) as a tool to characterize the basal ganglia (caudate, globus pallidus and putamen) and thalamus. We found no significant volume or shape differences in any of the structures in this small sample of subjects.
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17283306&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
Arch Pediatr Adolesc Med. 2007 Feb;161(2):193-8.
Time trends in reported diagnoses of childhood neuropsychiatric disorders: a Danish cohort study.
Atladottir HO, Parner ET, Schendel D, Dalsgaard S, Thomsen PH, Thorsen P.
North Atlantic Neuro-Epidemiology Alliances at Department of Epidemiology, Institute of Public Health, University of Aarhus, Aarhus, Denmark.
OBJECTIVES: To examine trends in autism (autism spectrum disorder and childhood autism) in the context of 3 additional childhood neuropsychiatric disorders: hyperkinetic disorder, Tourette syndrome, and obsessive-compulsive disorder.
DESIGN: Population-based cohort study.
SETTING: Children were identified in the Danish Medical Birth Registry. Relevant outcomes were obtained via linkage with the Danish National Psychiatric Register, which included reported diagnoses through 2004 by psychiatrists using diagnostic criteria from the International Statistical Classification of Diseases, 10th Revision.
PARTICIPANTS: All children born in Denmark from 1990 through 1999, a total of 669 995 children.
MAIN OUTCOME MEASURES: Cumulative incidence proportion by age, stratified by year of birth, for each disorder.
RESULTS: Statistically significant increases were found in cumulative incidence across specific birth years for autism spectrum disorder, childhood autism, hyperkinetic disorder, and Tourette syndrome. No significant change in cumulative incidence was observed for obsessive-compulsive disorder.
CONCLUSIONS: Recent increases in reported autism diagnoses might not be unique among childhood neuropsychiatric disorders and might be part of a more widespread epidemiologic phenomenon. The reasons for the observed common pattern of change in reported cumulative incidence could not be determined in this study, but the data underscore the growing awareness of and demand for services for children with neurodevelopmental disorders in general.
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16581034&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
Biol Psychiatry. 2007 Feb 1;61(3):292-300. Epub 2006 Apr 11.
Tic symptom profiles in subjects with Tourette Syndrome from two genetically isolated populations.
Mathews CA, Jang KL, Herrera LD, Lowe TL, Budman CL, Erenberg G, Naarden A, Bruun RD, Schork NJ, Freimer NB, Reus VI.
Department of Psychiatry, University of California, San Diego, La Jolla, California 92093-0810, USA.
BACKGROUND: Tourette Syndrome (TS) has a complex etiology and wide variability in phenotypic expression. Identifying underlying symptom patterns may be useful for etiological and outcome studies of TS.
METHODS: Lifetime tic and related symptom data were collected between 1996 and 2001 in 121 TS subjects from the Central Valley of Costa Rica and 133 TS subjects from the Ashkenazi Jewish (AS) population in the US. Subjects were grouped by tic symptoms using an agglomerative hierarchical cluster analysis. Cluster membership was tested for association with available ancillary information (age of onset, tic severity, comorbid disorders, medication treatment and family history).
RESULTS: Cluster analysis identified two distinct groups in each sample, those with predominantly simple tics (cluster 1), and those with multiple complex tics (cluster 2). Membership in cluster 2 was correlated with increased tic severity, global impairment, medication treatment, and presence of comorbid obsessive-compulsive symptoms in both samples, and with family history of tics, lower verbal IQ, earlier age of onset, and comorbid obsessive-compulsive disorder and attention-deficit/hyperactivity disorder in the AS sample.
CONCLUSIONS: This study provides evidence for consistent and reproducible symptom profiles in two independent TS study samples. These findings have implications for etiological studies of TS.
Chemar
08-16-2007, 06:04 PM
I am going to digest this one slowly Lara! thank you for posting that...lots to chew on huh
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.
Chemar
08-16-2007, 06:35 PM
Hi Lara...yes LOl I didnt realise you were posting more so should have quoted it....
it is this one (http://neurotalk.psychcentral.com/showpost.php?p=137509&postcount=17)
very interesting
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; Søren Dalsgaard, MD, PhD; Per Hove Thomsen, DMSc; Poul Thorsen, MD, PhD
Arch Pediatr Adolesc Med. 2007;161:193-198
http://www.jneurosci.org/cgi/content/abstract/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
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.
PubMed Abstract (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17726913&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
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.
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]
PubMed Abstract ahead of print (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17708557&ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
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.
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]
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 (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17717739&ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
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.
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]
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/18184945?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
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/druginfo/medmaster/a601209.html
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.
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/18079308?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
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
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/18066728?ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum)
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]
Chemar
03-01-2008, 07:49 AM
downloadable info on Toxicology and Neurological Development
http://psr.igc.org/ihw-report.htm#ihwRptDwnld
Chemar
03-13-2008, 07:04 PM
as depression is something many people with TS deal with, I thought this might be helpful here
http://psychcentral.com/news/2008/03/13/the-role-of-heredity-in-mood-disorders/2038.html
Chemar
06-28-2008, 09:58 AM
just recently I have heard from many parents who are struggling to get needed 504 or IEP accomodations for their TS child(ren)
remember that TS is classified under IDEA under the Americans with Disabilities Act as "other health impaired" and so the accommodations are entitled by Law!!
The TSA has really helpful info
education strategies http://www.tsa-usa.org/educ_advoc/educ_ed_strat_main.htm
education advocacy http://www.tsa-usa.org/educ_advoc/education_advocacy_main.html
PubMed (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=18704019&log$=activity)
CNS Spectr. 2008 Aug;13(8):643-4.Click here to read Links
Parkinson's disease, Tourette syndrome, and the changing nature of depression: the dog days of summer.
Hollander E.
PMID: 18704019 [PubMed - indexed for MEDLINE]
Cnsspectrums (http://cnsspectrums.com/aspx/articledetail.aspx?articleid=1664)
Parkinson’s Disease, Tourette Syndrome, and the Changing Nature of Depression: The Dog Days of Summer
Eric Hollander, MD
CNS Spectr. 2008;13(8):643-644
This month’s CNS Spectrums describes medication-related side effects (compulsivity and impulsivity) that can have important implication’s for understanding symptom classification and the neurobiology of disease (behavioral addictions); assesses subtypes of illness (tic-related OCD) with distinct presentations; highlights changes in our understanding of illnesses such as depression over time (drug-nonresponsive sadness), and describes unusual cases with NMDA receptor encephalitis with highly specific treatment response (immunomodulatory treatment).
I can't actually get the PDF to load. weird.
I may delete this in the morning. Haven't finished reading it but I thought I'd post it here for the moment as it's certainly topical for some
- Blood Brain Barrier, Rheumatic Fever, Sydenham's Chorea, Anxiety, tics, ocd. It's like a timewarp.
International Journal of Neuropsychiatric Medicine (http://cnsspectrums.com/aspx/article_pf.aspx?articleid=1917)
Anxiety Disorders and Rheumatic Fever: Is There an Association?
André Augusto Anderson Seixas, MD, Ana Gabriela Hounie, MD, PhD, Victor Fossaluza, BS, Mariana Curi, MSc, Pedro Gomes Alvarenga, MD, Maria Alice De Mathis, BS, Maria Eugênia De Mathis, BS, Homero Vallada, MD, PhD, David Pauls, PhD, Carlos Alberto de Bragança Pereira, PhD, and Eurípedes Constantino Miguel, MD, P
CNS Spectr. 2008;13(12):1039-1042,1044-1046
Med Clin (Barc). 2008 Nov 22;131(18):689-92.
An open study evaluating the efficacy and security of magnesium and vitamin B(6) as a treatment of Tourette syndrome in children.
[Article in Spanish]
PubMed Article (http://www.ncbi.nlm.nih.gov/pubmed/19087826?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/19103702?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Clin Child Psychol Psychiatry. 2009 Jan;14(1):13-23.
The Diagnosis of Tourette's Syndrome: Communication and Impact.
Rivera-Navarro J, Cubo E, Almazán J.
Salamanca University, Spain.
<snipped abstract>
The most important conclusion was that the current method for communicating the diagnosis of TS to patients and relatives should be improved to facilitate better understanding and interpretation.
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/19099145?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Arq Neuropsiquiatr. 2008 Dec;66(4):918-21.)
Charcot's contribution to the study of Tourette's syndrome
We review the history of Tourette syndrome, emphasizing the contribution of Jean-Martin Charcot.
Teive HA, Chien HF, Munhoz RP, Barbosa ER.
Movement Disorders Unit, Hospital de Clínicas, Hospital de Clínicas, Federal University of Paraná, Curitiba PR, Brazil.
__________
Full text...
Associação Arquivos de Neuro-Psiquiatria (http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X2008000600035&lng=en&nrm=iso&tlng=en)
Arquivos de Neuro-Psiquiatria
Print ISSN 0004-282X
Arq. Neuro-Psiquiatr. vol.66 no.4 São Paulo Dec. 2008
Charcot's contribution to the study of Tourette's syndrome
Hélio A.G. Teive; Hsin Fen Chien; Renato Puppi Munhoz; Egberto Reis Barbosa
Movement Disorders Unit, Neurology Service, Hospital de Clínicas, Federal University of Paraná, Curitiba PR, Brazil
Movement Disorders Clinic, Department of Neurology, Hospital das Clínicas, University of São Paulo, São Paulo SP, Brazil
J Am Acad Child Adolesc Psychiatry. 2008 Aug 21.
Neuropsychiatric Disorders Associated With Streptococcal Infection: A Case-Control Study Among Privately Insured Children.
Leslie DL, Kozma L, Martin A, Landeros A, Katsovich L, King RA, Leckman JF.
Dr. Leslie is with the Department of Health Administration and Policy, Medical University of South Carolina; Ms. Kozma is with the Department of Chemistry, Yale University; and Drs. Martin, Landeros, King, and Leckman and Ms. Katsovich are with the Child Study Center, Yale University School of Medicine.
OBJECTIVE:: To assess whether antecedent streptococcal infection(s) increase the risk of subsequent diagnosis of obsessive-compulsive disorder (OCD), Tourette syndrome (TS), other tic disorders, attention-deficit/hyperactivity disorder (ADHD), or major depressive disorder (MDD) in a national sample of privately insured children.
PubMed Abstract (http://www.ncbi.nlm.nih.gov/pubmed/18724258?ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
CONCLUSIONS:: These findings provide epidemiologic evidence that some pediatric-onset neuropsychiatric disorders, including OCD, tic disorders, ADHD, and MDD, may be temporally related to prior streptococcal infections. Whether this is the result of a nonspecific stress response or secondary to an activation of the immune system remains to be determined.
Journal of the American Academy of Child & Adolescent Psychiatry:
October 2008 - Volume 47 - Issue 10 - pp 1166-1172
doi: 10.1097/CHI.0b013e3181825a3d
New Research
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/17665279?ordinalpos=20&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Eur Child Adolesc Psychiatry. 2007 Jun;16 Suppl 1:15-23.
Erratum in:
Eur Child Adolesc Psychiatry. 2007 Dec;16(8):536.
Tic disorders and ADHD: answers from a world-wide clinical dataset on Tourette syndrome.
Freeman RD; Tourette Syndrome International Database Consortium.
CONCLUSION: Subjects with TS have high rates of ADHD and complex associations with other disorders. Clinically the findings confirm other research indicating the importance of ADHD in understanding the behavioural problems often associated with the diagnosis of TS. Additional ADHD comorbidity should be taken into account in diagnosis, management, and training.
PubMed Abstract (http://www.ncbi.nlm.nih.gov/pubmed/18519489?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Pediatrics. 2008 Jun;121(6):1188-97.)
Pediatrics. 2008 Jun;121(6):1188-97.
Comment in:
Pediatrics. 2008 Nov;122(5):1157; author reply 1157-8.
Streptococcal infection and exacerbations of childhood tics and obsessive-compulsive symptoms: a prospective blinded cohort study.
Kurlan R, Johnson D, Kaplan EL; and the Tourette Syndrome Study Group.
University of Rochester School of Medicine,
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/18940380?ordinalpos=19&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
J Psychosom Res. 2008 Nov;65(5):497-500. Epub 2008 Oct 1.
Air swallowing as a tic.
Weil RS, Cavanna AE, Willoughby JM, Robertson MM.
Institute of Neurology, Queen Square, London, UK.
The authors present a patient with Gilles de la Tourette syndrome who developed abdominal distension and bloating due to air swallowing. We suggest that this air swallowing may have been due to a tic.
Chemar
01-15-2009, 09:39 AM
http://content.nejm.org/cgi/content/short/360/3/225
Conclusions: Current users of typical and of atypical antipsychotic drugs had a similar, dose-related increased risk of sudden cardiac death.
From Bot's news -
Parasite may trigger schizophrenia (http://news.yahoo.com/s/nm/20090318/hl_nm/us_parasite_schizophrenia)
The team found the parasite's genetic make-up included an enzyme that aids in the production of dopamine. "At this point the research is too premature to suggest changes in treatment" of schizophrenia, McConkey continued. Nonetheless, "Toxoplasmosis screening would be warranted in psychological analysis."
He and his colleagues now plan to explore the possible role of toxoplasma in other neurological diseases associated with dopamine, including autism, Parkinson's disease, and Tourette's syndrome.
A Unique Dual Activity Amino Acid Hydroxylase in Toxoplasma gondii
Elizabeth A. Gaskell, Judith E. Smith, John W. Pinney, Dave R. Westhead, and Glenn A. McConkey
from PubMed Central (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2653193)
PLoS ONE. 2009; 4(3): e4801.
Published online 2009 March 11. doi: 10.1371/journal.pone.0004801.
http://jcn.sagepub.com/cgi/content/abstract/24/2/170
Journal of Child Neurology, Vol. 24, No. 2, 170-175 (2009)
DOI: 10.1177/0883073808322666
Tourette Syndrome and Comorbid Pervasive Developmental Disorders
Larry Burd, Qing Li, Jacob Kerbeshian, Marilyn G. Klug, Roger D. Freeman
We found 334 (4.6%; 1 of every 22 participants) with Tourette syndrome had a comorbid pervasive developmental disorder.
Variables from logistic modeling that were significant predictors of Tourette syndrome and pervasive developmental disorders were: male gender; no family history of tics/Tourette syndrome; and an increased number of comorbidities (P < .001).
We found rates of comorbid Tourette syndrome and pervasive developmental disorders to be increased by 13 times. Identification of differences between subgroups of patients with Tourette syndrome may increase understanding of syndromal susceptibility, severity, and outcome.
Note: this study involved the Tourette Syndrome International Database Consortium Registry.
PubMed Article (http://www.ncbi.nlm.nih.gov/pubmed/19359447?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
J Neuropsychiatry Clin Neurosci. 2009 Winter;21(1):13-23.Links
The behavioral spectrum of Gilles de la Tourette syndrome.
Cavanna AE, Servo S, Monaco F, Robertson MM.
This paper provides an updated review of the literature on the multifaceted phenotype of Tourette's syndrome, with special attention to the behavioral problems and the relationship between Tourette's syndrome and comorbid neuropsychiatric conditions. The issue of whether Tourette's syndrome should still be considered as a unitary nosological entity is also addressed.
PubMed Article (http://www.ncbi.nlm.nih.gov/pubmed/19353683?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Mov Disord. 2009 Apr 7
Immunopathogenic mechanisms in tourette syndrome: A critical review.
Martino D, Dale RC, Gilbert DL, Giovannoni G, Leckman JF.
Tourette syndrome (TS) has a multifactorial etiology, in which genetic, environmental, immunological and hormonal factors interact to establish vulnerability
<snipped article>
Although the pathogenic role of immune activation in TS has not been definitively proven, a pathophysiological model is proposed to explain the possible effect of immunity upon dopamine transmission regulation and the generation of tics.
PubMed Article (http://www.ncbi.nlm.nih.gov/pubmed/19288046?log$=activity)
J Neurol. 2009 Mar 14.
A preliminary study of the frequency of anti-basal ganglia antibodies and streptococcal infection in attention deficit/hyperactivity disorder.
Sanchez-Carpintero R, Albesa SA, Crespo N, Villoslada P, Narbona J.
This preliminary study indicates that frequency of ABGA in children with nc-ADHD does not differ from that in matched controls, despite the fact that our ADHD patients had had more recent GABHS infections than the controls. This suggests that ABGA do not have a role in the pathogenesis of nc-ADHD.
Note: small number involved in study
We compared 22 children with nc-ADHD (DSM-IV-TR) and 22 healthy controls matched by age, gender and season of sample collection, for the frequency of recent GABHS infection and the presence of ABGA.
http://neurotalk.psychcentral.com/post499139-46.html
I already posted this one but I'll leave it here and quote the material regarding T cells.
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/19353683?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Mov Disord. 2009 Apr 7.
Immunopathogenic mechanisms in tourette syndrome: A critical review.
Martino D, Dale RC, Gilbert DL, Giovannoni G, Leckman JF.
Department of Neurological and Psychiatric Sciences, University of Bari, Bari, Italy.
<snipped abstract>
Finally, a general predisposition to autoimmune responses in TS patients is indicated by the reduced frequency of regulatory T cells, which induce tolerance towards self-antigens. Although the pathogenic role of immune activation in TS has not been definitively proven, a pathophysiological model is proposed to explain the possible effect of immunity upon dopamine transmission regulation and the generation of tics.
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/18484991?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Eur J Neurol. 2008 Jul;15(7):749-53. Epub 2008 May 15.
Immunophenotyping in Tourette syndrome--a pilot study.
Möller JC, Tackenberg B, Heinzel-Gutenbrunner M, Burmester R, Oertel WH, Bandmann O, Müller-Vahl KR.
Department of Neurology, Philipps-University, Marburg, Germany
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/16996487?ordinalpos=&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.SmartSearch&log$=citationsensor)
Biol Psychiatry. 2007 Feb 1;61(3):273-8. Epub 2006 Sep 25.
Decreased numbers of regulatory T cells suggest impaired immune tolerance in children with tourette syndrome: a preliminary study.
Kawikova I, Leckman JF, Kronig H, Katsovich L, Bessen DE, Ghebremichael M, Bothwell AL.
Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut
<snipped article>
CONCLUSIONS: These data support our hypothesis that at least some TS patients may have a decreased capacity to inhibit autoreactive lymphocytes through a deficit in T reg cells. Interactions of host T cell immunity and microbial factors may also contribute to the pathogenesis of TS.
http://linkinghub.elsevier.com/retrieve/pii/S0006322306008043
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/16546348?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Genomics. 2006 Jun;87(6):693-703. Epub 2006 Mar 20
Genomic profiles for human peripheral blood T cells, B cells, natural killer cells, monocytes, and polymorphonuclear cells: comparisons to ischemic stroke, migraine, and Tourette syndrome.
Du X, Tang Y, Xu H, Lit L, Walker W, Ashwood P, Gregg JP, Sharp FR.
MIND Institute, University of California at Davis
old abstract - 1999
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/10494449?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Biol Psychiatry. 1999 Sep 15;46(6):810-4.
Immunological alterations in adult obsessive-compulsive disorder.
Marazziti D, Presta S, Pfanner C, Gemignani A, Rossi A, Sbrana S, Rocchi V, Ambrogi F, Cassano GB.
Dipartimento di Psichiatria, Neurobiologia, Farmacologia e Biotecnologie, University of Pisa, Italy.
CONCLUSIONS: These data indicate that patients with adult OCD showed increased CD8+, i.e., suppressor T lymphocytes, and decreased CD4+, which identify helper T lymphocytes, as compared with a similar group of healthy control subjects. The findings appear peculiar to patients with OCD and are suggestive of an immunologic imbalance, which might be related to the stress deriving from the frustrating situation determined by the disorder itself.
Then again...
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/11728611?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&logdbfrom=pubmed)
Psychiatry Res. 2001 Nov 30;104(3):221-5.
The use of antibody D8/17 to identify B cells in adults with obsessive-compulsive disorder.
Eisen JL, Leonard HL, Swedo SE, Price LH, Zabriskie JB, Chiang SY, Karitani M, Rasmussen SA.
Department of Psychiatry and Human Behavior, Butler Hospital, Brown University School of Medicine,
Compared with healthy control subjects, individuals with childhood-onset obsessive-compulsive disorder (OCD) have been reported to have a higher percentage of B cells that react with the monoclonal antibody D8/17, a marker for rheumatic fever. This study sought to replicate these findings in adults with OCD. Double-blind analyses of blood samples from 29 consecutive adults with primary OCD and 26 healthy control subjects were conducted to determine the percentage of B cells identified by D8/17. Using a standard criterion of > or =12% labeled B cells to denote positivity, rates of D8/17 positive individuals did not significantly differ between the OCD (58.6%) and control (42.3%) groups. Early age of onset was not a predictor of D8/17 positivity in the OCD group. The percentage of B cells identified by the monoclonal antibody marker D8/17 did not distinguish adults with OCD from control subjects, nor did it distinguish a sub-group of adults with OCD who described pre-pubertal onset of their OCD symptoms.
PubMed Central Full Text Article (http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17304708)
Am J Hum Genet. 2007 February; 80(2): 265–272.
Published online 2006 December 12.
PMCID: PMC1785345
Genome Scan for Tourette Disorder in Affected-Sibling-Pair and Multigenerational Families
The Tourette Syndrome Association International Consortium for Genetics
excerpt from Book...
Tourette's syndrome--tics, obsessions, compulsions
By James F. Leckman, Donald J. Cohen (1998)
from Google Books (http://books.google.com.au/books?id=rZ-qKfBhQvIC&pg=PA222&lpg=PA222&dq=T+cells+and+tics&source=bl&ots=S5TDpC1sda&sig=4WoAmIbazkBqgTnBghgOaKj4EvM&hl=en&ei=hhQXStjXIYP8swOM1ITgCA&sa=X&oi=book_result&ct=result&resnum=1)
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/19448188?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Am J Psychiatry. 2009 May 15.
Functional Disturbances Within Frontostriatal Circuits Across Multiple Childhood Psychopathologies.
Marsh R, Maia TV, Peterson BS.
<snipped abstract>
Conclusions Analogous brain mechanisms in parallel frontostriatal circuits, or even in differing portions of the same frontostriatal circuit, may underlie the differing behavioral disturbances in these multiple disorders, although further research is needed to confirm this hypothesis.
Note: small sized study.
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/19435502?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
BMC Neurosci. 2009 May 12;10(1):47.
Prefrontal and anterior cingulate cortex abnormalities in Tourette Syndrome: evidence from voxel-based morphometry and magnetization transfer imaging.
Muller-Vahl KR, Kaufmann J, Grosskreutz J, Dengler R, Emrich HM, Peschel T.
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/19395047?ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Psychiatry Res. 2009 May 30;167(3):202-20.
Electrophysiological manifestations of stimulus evaluation, response inhibition and motor processing in Tourette syndrome patients.
Thibault G, O'Connor KP, Stip E, Lavoie ME.
Centre de Recherche Fernand-Seguin and Hôpital Louis-H. Lafontaine, Montréal, Québec, Canada; Département de Psychologie, Université de Montréal, Montréal, Québec, Canada.
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/19391534?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Zhongguo Zhen Jiu. 2009 Feb;29(2):115-8.Links
Clinical study on scalp acupuncture with long needle-retained duration for treatment of Tourette syndrome
[Article in Chinese]
Zhu BC, Shi-fen X, Shan YH.
Department of Acupuncture, Shanghai Hospital of TCM, Shanghai
PubMed (http://www.ncbi.nlm.nih.gov/pubmed/19359447?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
J Neuropsychiatry Clin Neurosci. 2009 Winter;21(1):13-23.
The behavioral spectrum of Gilles de la Tourette syndrome.
Cavanna AE, Servo S, Monaco F, Robertson MM.
Sobell Department of Movement Disorders, Institute of Neurology, London, UK.
<snipped abstract>
This paper provides an updated review of the literature on the multifaceted phenotype of Tourette's syndrome, with special attention to the behavioral problems and the relationship between Tourette's syndrome and comorbid neuropsychiatric conditions. The issue of whether Tourette's syndrome should still be considered as a unitary nosological entity is also addressed.
NOTE: http://neuro.psychiatryonline.org/cgi/content/abstract/21/1/13
Full Text at a price
http://www.ncbi.nlm.nih.gov/pubmed/10907717
J Commun Disord. 2000 May-Jun;33(3):227-39;
Dysfluency and phonic tics in Tourette syndrome: a case report.
Van Borsel J, Vanryckeghem M.
http://www.mnsu.edu/comdis/isad2/papers/molt2.html
The Basal Ganglia's Possible Role in Stuttering: An Examination of Similarities between Stuttering, Tourette Syndrome, Dystonia, and other Neurological-Based Disorders of Movement
by Larry Molt
http://www.mnsu.edu/comdis/isad6/papers/donaher6.html
Disfluency Associated with Tourette's Syndrome: Two Case Studies
by John Tetnowski and Joseph Donaher
http://www.stutteringhelp.org/Default.aspx?tabid=440
Stuttering and Tourette's Syndrome
This material was compiled by Luc De Nil, Ph.D., Chair of the
Graduate Department of Speech-Language Pathology, University of
Toronto, and by Paul Sandor, M.D., Director of the Tourette’s
Syndrome Clinic, University Health Network.
http://www.cmaj.ca/cgi/content/full/162/13/1849
Stuttering: an update for physicians
Daniel Costa and Robert Kroll
http://www.ncbi.nlm.nih.gov/pubmed/15856831
Rev Laryngol Otol Rhinol (Bord). 2004;125(5):297-301. Links
Stuttering and Tourette's syndrome: a short tutorial and account of a four years experience in a stuttering clinic constriction of the vocal tract
[Article in French]
Monfrais-Pfauwadel MC.
Hopital Europeen Georges Pompidou, AP-HP, Paris, France
The author presents a short tutorial of Gilles de la Tourette's syndrome followed by a state of the art of review of the clinical links between stuttering and the different kinds of Tourette and tics disorders. The author relates her own experience of working for four consecutive years at the new stuttering diagnostic center at the "Hopital Europeen Georges Pompidou ". The article ends with a practical review of the actual therapies available when such a diagnosis is made.
http://www.mnsu.edu/comdis/isad6/papers/monfrais-pfauwadel6.html
Differential Diagnosis of Stuttering and Self-referral
by Marie-Claude Monfrais-Pfauwadel
from France
http://www.unboundmedicine.com/medline/ebm/related/17195723/Improvement_in_speech_dysfluency_in_Tourette's_dis order_after_tongue_piercing?start=10&prev=true
PubMed Abstract (http://www.ncbi.nlm.nih.gov/pubmed/19546859?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum)
Mol Psychiatry. 2009 Jun 23.
Rare structural variants found in attention-deficit hyperactivity disorder are preferentially associated with neurodevelopmental genes.
Elia J, Gai X, Xie HM, Perin JC, Geiger E, Glessner JT, D'arcy M, Deberardinis R, Frackelton E, Kim C, Lantieri F, Muganga BM, Wang L, Takeda T, Rappaport EF, Grant SF, Berrettini W, Devoto M, Shaikh TH, Hakonarson H, White PS.
Department of Child and Adolescent Psychiatry, The Children's Hospital of Philadelphia, Philadelphia, PA, USA. Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Although no excess CNVs, either deletions or duplications, were found in the ADHD cohort relative to controls, the inherited rare CNV-associated gene set was significantly enriched for genes reported as candidates in studies of autism, schizophrenia and Tourette syndrome, including A2BP1, AUTS2, CNTNAP2 and IMMP2L.
___________
from Psych Central News (http://psychcentral.com/news/2009/06/25/gene-variations-linked-to-adhd/6734.html)
Gene Variations Linked to ADHD
By Psych Central News Editor
Reviewed by John M. Grohol, Psy.D. on June 25, 2009
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