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[PMID]: 29519947
[Au] Autor:Raucci U; Parisi P; Vanacore N; Garone G; Bondone C; Palmieri A; Calistri L; Suppiej A; Falsaperla R; Capuano A; Ferro V; Urbino AF; Tallone R; Montemaggi A; Sartori S; Pavone P; Mancardi M; Melani F; Ilvento L; Pelizza MF; Reale A
[Ad] Address:Pediatric Emergency Department, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
[Ti] Title:Acute hyperkinetic movement disorders in Italian paediatric emergency departments.
[So] Source:Arch Dis Child;, 2018 Mar 08.
[Is] ISSN:1468-2044
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Limited data exist on epidemiology, clinical presentation and management of acute hyperkinetic movement disorders (AHMD) in paediatric emergency departments (pED). METHODS: We retrospectively analysed a case series of 256 children (aged 2 months to 17 years) presenting with AHMD to the pEDs of six Italian tertiary care hospitals over a 2-year period (January 2012 to December 2013). RESULTS: The most common type of AHMD was tics (44.5%), followed by tremors (21.1%), chorea (13.7%), dystonia (10.2%), myoclonus (6.3%) and stereotypies (4.3%).Neuropsychiatric disorders (including tic disorders, psychogenic movement disorders and idiopathic stereotypies) were the most represented cause (51.2%). Inflammatory conditions (infectious and immune-mediated neurological disorders) accounted for 17.6% of the cases whereas non-inflammatory disorders (including drug-induced AHMDs, genetic/metabolic diseases, paroxysmal non-epileptic movements and idiopathic AHMDs) accounted for 31.2%. Neuropsychiatric disorders prevailed among preschoolers and schoolers (51.9% and 25.2%, respectively), non-inflammatory disorders were more frequent in infants and toddlers (63.8%), whereas inflammatory conditions were more often encountered among schoolers (73.3%). In 5 out of 36 Sydenham's chorea (SC) cases, tics were the presentation symptom on admission to emergency department (ED), highlighting the difficulties in early diagnosis of SC. Inflammatory disorders were associated with a longer hospital stay and a greater need of neuroimaging test compared with other disorders. CONCLUSIONS: This study provides the first large sample of paediatric patients presenting to the ED for AHMDs, helping to elucidate the epidemiology, aetiology and clinical presentation of these disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  2 / 3811 MEDLINE  
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[PMID]: 29518821
[Au] Autor:Chiou LC; Lee HJ; Ernst M; Huang WJ; Chou JF; Chen HL; Mouri A; Chen LC; Treven M; Mamiya T; Fan PC; Knutson DE; Witzigmann C; Cook J; Sieghart W; Nabeshima T
[Ad] Address:Graduate Institute of Pharmacology, National Taiwan University, Taipei, Taiwan.
[Ti] Title:Cerebellar α6 subunit-containing GABA receptors: A novel therapeutic target for disrupted prepulse inhibition in neuropsychiatric disorders.
[So] Source:Br J Pharmacol;, 2018 Mar 08.
[Is] ISSN:1476-5381
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND AND PURPOSE: The pathophysiological role of α6 subunit-containing GABAA receptors (α6GABA Rs), which are mainly expressed in cerebellar granule cells, remains unclear. Recently, we demonstrated that hispidulin, a flavonoid isolated from a local herb that remitted a patient's intractable motor tics, attenuated methamphetamine-induced hyperlocomotion in mice as a positive allosteric modulator (PAM) of cerebellar α6GABA Rs. Here, using hispidulin and a selective α6GABA R PAM, the pyrazoloquinolinone Compound 6, we revealed an unprecedented role of cerebellar α6GABA Rs in disrupted prepulse inhibition (PPI), which reflects sensorimotor gating deficits manifested in several neuropsychiatric disorders. EXPERIMENTAL APPROACH: PPI disruptions were induced by methamphetamine and NMDA receptor blockers in mice. GABA R modulatory effects of tested compounds were measured in Xenopus oocytes expressing recombinant α6ß3γ2sGABA Rs. KEY RESULTS: Hispidulin given by i.p. or bilateral intra-cerebellar (i.cb.) injection significantly rescued PPI disruptions induced by methamphetamine, ketamine, MK-801 and phencyclidine. Intra-cerebellar effects of hispidulin were mimicked by Ro15-4513 and loreclezole (two α6GABA R PAMs), but not by diazepam (an α6GABA R-insensitive benzodiazepine), and were antagonized by furosemide (i.cb.), an α6GABA R antagonist. Importantly, Compound 6 (i.p.) also significantly rescued methamphetamine-induced PPI disruption in a manner prevented by furosemide (i.cb.). Both hispidulin and Compound 6 significantly potentiated α6ß3γ2sGABA R-mediated GABA currents. CONCLUSIONS AND IMPLICATIONS: These results suggest that positively modulating cerebellar α6GABAARs can rescue disrupted PPI via attenuating granule cell activity, and α6GABAAR-selective PAMs are potential medicines for treating sensorimotor gating deficits in neuropsychiatric disorders. A mechanistic hypothesis is provided based on increasing evidence for a cerebellar contribution in cognitive functioning including sensorimotor gating.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1111/bph.14198

  3 / 3811 MEDLINE  
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[PMID]: 29481900
[Au] Autor:O'Brien KB; Sharrief AZ; Nordstrom EJ; Travanty AJ; Huynh M; Romero MP; Bittner KC; Bowser MT; Burton FH
[Ad] Address:Department of Chemistry, University of Minnesota, 139 Smith Hall, 207 Pleasant St SE, Minneapolis, MN 55455 USA.
[Ti] Title:Biochemical markers of striatal desensitization in cortical-limbic hyperglutamatergic TS- & OCD-like transgenic mice.
[So] Source:J Chem Neuroanat;89:11-20, 2018 Feb 24.
[Is] ISSN:1873-6300
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Tics and compulsions in comorbid Tourette's syndrome (TS) and obsessive-compulsive disorder (OCD) are associated with chronic hyperactivity of parallel cortico/amygdalo-striato-thalamo-cortical (CSTC) loop circuits. Comorbid TS- & OCD-like behaviors have likewise been observed in D1CT-7 mice, in which an artificial neuropotentiating transgene encoding the cAMP-elevating intracellular subunit of cholera toxin (CT) is chronically expressed selectively in somatosensory cortical & amygdalar dopamine (DA) D1 receptor-expressing neurons that activate cortico/amygdalo-striatal glutamate (GLU) output. We've now examined in D1CT-7 mice whether the chronic GLU output from their potentiated cortical/limbic CSTC subcircuit afferents associated with TS- & OCD-like behaviors elicits desensitizing neurochemical changes in the striatum (STR). Microdialysis-capillary electrophoresis and in situ hybridization reveal that the mice's chronic GLU-excited STR exhibits pharmacodynamic changes in three independently GLU-regulated measures of output neuron activation, co-excitation, and desensitization, signifying hyperactive striatal CSTC output and compensatory striatal glial and neuronal desensitization: 1) Striatal GABA, an output neurotransmitter induced by afferent GLU, is increased. 2) Striatal d-serine, a glial excitatory co-transmitter inhibited by afferent GLU, is decreased. 3) Striatal Period1 (Per1), which plays a non-circadian role in the STR as a GLU + DA D1- (cAMP-) dependent repressor thought to feedback-inhibit GLU + DA- triggered ultradian urges and motions, is transcriptionally abolished. These data imply that chronic cortical/limbic GLU excitation of the STR desensitizes its co-excitatory d-serine & DA inputs while freezing its GABA output in an active state to mediate chronic tics and compulsions - possibly in part by abolishing striatal Per1-dependent ultradian extinction of urges and motions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

  4 / 3811 MEDLINE  
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[PMID]: 29335879
[Au] Autor:Quezada J; Coffman KA
[Ad] Address:Child Neurology Resident, Children's Mercy Hospital, Kansas City, MO, USA.
[Ti] Title:Current Approaches and New Developments in the Pharmacological Management of Tourette Syndrome.
[So] Source:CNS Drugs;32(1):33-45, 2018 Jan.
[Is] ISSN:1179-1934
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:Tourette syndrome (TS) is a neurodevelopmental disorder of unknown etiology characterized by spontaneous, involuntary movements and vocalizations called tics. Once thought to be rare, TS affects 0.3-1% of the population. Tics can cause physical discomfort, emotional distress, social difficulties, and can interfere with education and desired activities. The pharmacologic treatment of TS is particularly challenging, as currently the genetics, neurophysiology, and neuropathology of this disorder are still largely unknown. However, clinical experience gained from treating TS has helped us better understand its pathogenesis and, as a result, derive treatment options. The strongest data exist for the antipsychotic agents, both typical and atypical, although their use is often limited in children and adolescents due to their side-effect profiles. There are agents in a variety of other pharmacologic categories that have evidence for the treatment of TS and whose side-effect profiles are more tolerable than the antipsychotics; these include clonidine, guanfacine, baclofen, topiramate, botulinum toxin A, tetrabenazine, and deutetrabenazine. A number of new agents are being developed and tested as potential treatments for TS. These include valbenazine, delta-9-tetrahydrocannabidiol, and ecopipam. Additionally, there are agents with insufficient data for efficacy, as well as agents that have been shown to be ineffective. Those without sufficient data for efficacy include clonazepam, ningdong granule, 5-ling granule, omega-3 fatty acids, and n-acetylcysteine. The agents that have been shown to be ineffective include pramipexole and metoclopramide. We will review all of the established pharmacologic treatments, and discuss those presently in development.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1007/s40263-017-0486-0

  5 / 3811 MEDLINE  
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[PMID]: 29255247
[Au] Autor:Rasheed SAK; Leong HS; Lakshmanan M; Raju A; Dadlani D; Chong FT; Shannon NB; Rajarethinam R; Skanthakumar T; Tan EY; Hwang JSG; Lim KH; Tan DS; Ceppi P; Wang M; Tergaonkar V; Casey PJ; Iyer NG
[Ad] Address:Programme in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore, Singapore.
[Ti] Title:GNA13 expression promotes drug resistance and tumor-initiating phenotypes in squamous cell cancers.
[So] Source:Oncogene;37(10):1340-1353, 2018 Mar.
[Is] ISSN:1476-5594
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Treatment failure in solid tumors occurs due to the survival of specific subpopulations of cells that possess tumor-initiating (TIC) phenotypes. Studies have implicated G protein-coupled-receptors (GPCRs) in cancer progression and the acquisition of TIC phenotypes. Many of the implicated GPCRs signal through the G protein GNA13. In this study, we demonstrate that GNA13 is upregulated in many solid tumors and impacts survival and metastases in patients. GNA13 levels modulate drug resistance and TIC-like phenotypes in patient-derived head and neck squamous cell carcinoma (HNSCC) cells in vitro and in vivo. Blockade of GNA13 expression, or of select downstream pathways, using small-molecule inhibitors abrogates GNA13-induced TIC phenotypes, rendering cells vulnerable to standard-of-care cytotoxic therapies. Taken together, these data indicate that GNA13 expression is a potential prognostic biomarker for tumor progression, and that interfering with GNA13-induced signaling provides a novel strategy to block TICs and drug resistance in HNSCCs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1038/s41388-017-0038-6

  6 / 3811 MEDLINE  
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[PMID]: 29499655
[Au] Autor:Tao Y; Gross N; Fan X; Yang J; Teng M; Li X; Li G; Zhang Y; Huang Z
[Ad] Address:Department of Otolaryngology-Head and Neck Surgery, Key Laboratory of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.
[Ti] Title:Identification of novel enriched recurrent chimeric COL7A1-UCN2 in human laryngeal cancer samples using deep sequencing.
[So] Source:BMC Cancer;18(1):248, 2018 03 02.
[Is] ISSN:1471-2407
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: As hybrid RNAs, transcription-induced chimeras (TICs) may have tumor-promoting properties, and some specific chimeras have become important diagnostic markers and therapeutic targets for cancer. METHODS: We examined 23 paired laryngeal cancer (LC) tissues and adjacent normal mucous membrane tissue samples (ANMMTs). Three of these pairs were used for comparative transcriptomic analysis using high-throughput sequencing. Furthermore, we used real-time polymerase chain reaction (RT-PCR) for further validation in 20 samples. The Kaplan-Meier method and Cox regression model were used for the survival analysis. RESULTS: We identified 87 tumor-related TICs and found that COL7A1-UCN2 had the highest frequency in LC tissues (13/23; 56.5%), whereas none of the ANMMTs were positive (0/23; p < 0.0001). COL7A1-UCN2, generated via alternative splicing in LC tissue cancer cells, had disrupted coding regions, but it down-regulated the mRNA expression of COL7A1 and UCN2. Both COL7A1 and UCN2 were down-expressed in LC tissues as compared to their paired ANMMTs. The COL7A1:ß-actin ratio in COL7A1-UCN2-positive LC samples was significantly lower than that in COL7A1-UCN2-negative samples (p = 0.019). Likewise, the UCN2:ß-actin ratio was also decreased (p = 0.21). Furthermore, COL7A1-UCN2 positivity was significantly associated with the overall survival of LC patients (p = 0.032; HR, 13.2 [95%CI, 1.2-149.5]). CONCLUSION: LC cells were enriched in the recurrent chimera COL7A1-UCN2, which potentially affected cancer stem cell transition, promoted epithelial-mesenchymal transition in LC, and resulted in poorer prognoses.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process
[do] DOI:10.1186/s12885-018-4161-8

  7 / 3811 MEDLINE  
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[PMID]: 29392455
[Au] Autor:Jalenques I; Guiguet-Auclair C; Derost P; Joubert P; Foures L; Hartmann A; Muellner J; Rondepierre F; Syndrome de Gilles de La Tourette Study Group
[Ad] Address:Service de Psychiatrie de l'Adulte A et Psychologie Médicale, Centre de Compétence Gilles de la Tourette, CHU Clermont-Ferrand, Université Clermont Auvergne, 58 rue Montalembert, 63003, Clermont-Ferrand Cedex 1, France. ijalenques@chu-clermontferrand.fr.
[Ti] Title:The MOVES (Motor tic, Obsessions and compulsions, Vocal tic Evaluation Survey): cross-cultural evaluation of the French version and additional psychometric assessment.
[So] Source:J Neurol;265(3):678-687, 2018 Mar.
[Is] ISSN:1432-1459
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:INTRODUCTION: The Motor tic, Obsessions and compulsions, Vocal tic Evaluation Survey (MOVES) is a self-report scale suggested as a severity scale for tics and related sensory phenomena observed in Gilles de la Tourette syndrome (GTS) and recommended as a screening instrument by the Committee on Rating Scale Development of the International Parkinson's Disease and Movement Disorder Society. OBJECTIVES: To cross-culturally adapt a French version of the MOVES and to evaluate its psychometric properties. METHODS: After the cross-cultural adaptation of the MOVES, we assessed its psychometric properties in 53 patients aged 12-16 years and in 54 patients aged 16 years and above: reliability and construct validity (relationships between items and scales), internal consistency and concurrent validity with the Yale Global Tic Severity Scale (YGTSS) and the Children's Yale-Brown Obsessive-Compulsive Scale (CY-BOCS) or the auto-Yale-Brown scale. RESULTS: The results showed very good acceptability with response rates greater than 92%, good internal consistency (Cronbach's alpha ranging from 0.62 and 0.89) and good test-retest reliability (ICCs ranging from 0.59 to 0.91). Concurrent validity with the YGTSS, CY-BOCS and auto-Yale-Brown scales showed strong expected correlations. The cut-off points tested for diagnostic performance gave satisfactory values of sensitivity, specificity, and positive and negative predictive values. DISCUSSION: Our study provides evidence of the good psychometric properties of the French version of the MOVES. The cross-cultural adaptation of this specific instrument will allow investigators to include French-speaking persons with GTS aged 12 years and over in national and international collaboration research projects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process
[do] DOI:10.1007/s00415-018-8769-z

  8 / 3811 MEDLINE  
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[PMID]: 29508917
[Au] Autor:Ganos C; Rothwell J; Haggard P
[Ad] Address:Department of Neurology, Charité, University Medicine, Berlin, Germany.
[Ti] Title:Voluntary inhibitory motor control over involuntary tic movements.
[So] Source:Mov Disord;, 2018 Mar 06.
[Is] ISSN:1531-8257
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Inhibitory control is crucial for normal adaptive motor behavior. In hyperkinesias, such as tics, disinhibition within the cortico-striato-thalamo-cortical loops is thought to underlie the presence of involuntary movements. Paradoxically, tics are also subject to voluntary inhibitory control. This puzzling clinical observation questions the traditional definition of tics as purely involuntary motor behaviors. Importantly, it suggests novel insights into tic pathophysiology. In this review, we first define voluntary inhibitory tic control and compare it with other notions of tic control from the literature. We then examine the association between voluntary inhibitory tic control with premonitory urges and review evidence linking voluntary tic inhibition to other forms of executive control of action. We discuss the somatotopic selectivity and the neural correlates of voluntary inhibitory tic control. Finally, we provide a scientific framework with regard to the clinical relevance of the study of voluntary inhibitory tic control within the context of the neurodevelopmental disorder of Tourette syndrome. We identify current knowledge gaps that deserve attention in future research. © 2018 International Parkinson and Movement Disorder Society.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher
[do] DOI:10.1002/mds.27346

  9 / 3811 MEDLINE  
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[PMID]: 29506749
[Au] Autor:Savitt D; Jankovic J
[Ad] Address:Parkinson's Disease and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, United States.
[Ti] Title:Tardive syndromes.
[So] Source:J Neurol Sci;, 2018 Feb 05.
[Is] ISSN:1878-5883
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Tardive syndromes are a group of hyperkinetic and hypokinetic movement disorders that occur after some delay following exposure to dopamine receptor blocking agents such as antipsychotic and anti-emetic drugs. The severity of these disorders ranges from mild to disabling or even life-threatening. There is a wide range of recognized tardive phenomenologies that may occur in isolation or in combination with each other. These phenomenologies include stereotypy, dystonia, chorea, akathisia, myoclonus, tremor, tics, gait disorders, parkinsonism, ocular deviations, respiratory dyskinesia, and a variety of sensory symptoms. Recognition of the various tardive phenomenologies may not only lead to early diagnosis but also to appropriate therapeutic intervention. This review focuses on the diagnosis and clinical course of tardive syndromes and how to distinguish between the various phenomenologies as well as how to differentiate them from other, similar but etiologically different, movement disorders.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher

  10 / 3811 MEDLINE  
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[PMID]: 29503330
[Au] Autor:Tater P; Pandey S
[Ad] Address:Department of Neurology, Govind Ballabh Pant Postgraduate Institute of Medical Education and Research, New Delhi, India.
[Ti] Title:Botulinum toxin in movement disorders.
[So] Source:Neurol India;66(Supplement):S79-S89, 2018 Mar-Apr.
[Is] ISSN:0028-3886
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:Botulinum toxin has gained immense popularity since its introduction for therapeutic use. It is used in a variety of movement disorders like hemi-facial spasm, focal dystonias like blepharospasm, cervical dystonia, oromandibular dystonia, limb dystonias. It is also being used in patients with tremors, tics and for a variety of indications in Parkinson's disease as well. There are eight subtypes of toxins available, but type A and B are the ones used in movement disorder clinics. The toxin mainly acts by inhibiting the release of acetylcholine at the neuromuscular junction and causing weakness. Type B toxin has more effect over the autonomic nervous system and hence is preferred for hyper-secretory disorders. The use of electromyography and ultrasound further improve the accuracy of the procedure. It is a relatively safe therapeutic option with its effect lasting for around three months. It has very few side effects. The key is to start with the lowest possible dose and then gradually increase the dose depending upon the patient's response. Selecting the right muscles for injection is of utmost importance and is guided by the knowledge of anatomy of the muscles.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:In-Data-Review
[do] DOI:10.4103/0028-3886.226441


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