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    3589 results match your criteria Advances in Neurology [Journal]

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    Behavior therapy: other interventions for tic disorders.
    Adv Neurol 2006 ;99:234-40
    Department of Psychology, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin, USA.
    This chapter reviewed other behavioral interventions for TS and discussed their efficacy. Clearly, the majority of behavioral interventions (habit/reversal excluded) have not been systematically evaluated enough to be deemed empirically supported monotherapies for TS. In addition to reviewing these interventions, recent advances in behavioral research on TS and a function-based model of treatment development and implementation were presented. Read More

    Treatment of aggression in Tourette syndrome.
    Adv Neurol 2006 ;99:222-6
    Department of Neurology, North Shore Hospital-Long Island Jewish Health System, Manhasset, New York, USA.
    The largely non-specific and/or multiply-determined etiologies of aggressive symptoms in TS pose significant impediments to effective clinical management. At this time, treatment requires comprehensive neuropsychiatric assessment with a systematic prioritization of the different psychiatric co-morbidities that require intervention. Medication side effects, psychosocial stressors and environmental triggers must also be identified and addressed. Read More

    Treatment of co-morbid obsessive compulsive disorder, mood, and anxiety disorders.
    Adv Neurol 2006 ;99:208-21
    Department of Psychiatry, New York University School of Medicine, New York, New York, USA.
    In Sumary, OCD, non-OCD anxiety disorders and mood disorders are common co-morbid psychiatric disorders are common co-morbid psychiatric disorders in clinically referred youth with TS. Emotional disorders such as anxiety and depression may be more problematic to the patient than the tics, with regard to overall illness severity and the potential for adverse outcomes, such as school and social failure. The emotional symptoms and co-morbid mood and anxiety disorders must be comprehensively identified because they will require specific intervention and treatment. Read More

    Neurobiology of basal ganglia and Tourette syndrome: basal ganglia circuits and thalamocortical outputs.
    Adv Neurol 2006 ;99:89-98
    Department of Neurology, Neurobiology and Anatomy, Pediatrics, University of Rochester, New York, USA.
    In summary, the scheme of basal ganglia function presented here, in conjunction with known features of anatomical organization and dopamine neurotransmission provides a hypothesis for the pathophysiology of tics. According to the hypothesis, clusters of striatal neurons (matrisomes) become abnormally active in inappropriate contexts leading to inhibition of GPi or SNpr neurons that would normally be active to supress unwanted movements. The inhibition of htese GPi or SNpr neurons would then disinhibit thalamocortical circuits. Read More

    Preclinical models relevant to Tourette syndrome.
    Adv Neurol 2006 ;99:69-88
    Department of Psychiatry, UCSD School of Medicine, La Jolla, California, USA.
    Preclinical models, if used appropriately, can greatly accelerate the understanding of neuropsychiatric disorders. A number of animal models have predictive validity for antidopaminergic compounds that have traditionally been used to suppress motor and vocal tics in TS. Other models have been proposed that may have construct validity for specific hypotheses of infectious/immune and neural circuit etiologies of TS. Read More

    Attention deficit hyperactivity disorder: the childhood co-morbidity that most influences the disability burden in Tourette syndrome.
    Adv Neurol 2006 ;99:17-21
    Developmental Cognitive Neurology, Kenneldy Krieger Institute, Baltinore, Mnryland, USA.
    ADHD is a complex co-morbidity, as it is heteregeneous in terms of the clinical subtypes, but also in terms of the circuits involved and the level of involvement within those circuits. Specially focusing on the relationship of ADHD to TS, this author's studies have added some neurobehavioral and some anatomical magnetic resonance imaging evidence suggesting the ADHD occurring with TS, appears like "garden-variety" ADHD, at least in the matched research sample. The similarities of neuroanatomical findings in the TS plus ADHD and ADHD groups and their distinctness from neuroanatomical findings in childdren with "pure TS provide some parallels to the observed similarity of functional deficit in TS plus ADHD and ADHD alone groups and the relative lack of functional deficits in children with TS only. Read More

    The use of glatiramer acetate in the treatment of multiple sclerosis.
    Adv Neurol 2006 ;98:273-92
    University of Texas Health Science Center at Houston, USA.
    Glatiramer acetate is a collection of synthetic polypeptides indicated as therapy for relapsing a remitting multiple sclerosis (MS). Current understanding of the immunological and neuroprotective mechanisms of action of GA makes it unique among current MS therapies. The clinical efficacy of GA appears similar to that of the recombinant beta interferons. Read More

    The use of MRI as an outcome measure in clinical trials.
    Adv Neurol 2006 ;98:203-26
    Department of Radiology, University of British Columbia Hospital, Vancouver, Canada.
    Because the changes on MRI likely reflect various aspects of the underlying pathology of multiple sclerosis, MRI outcome measures have become an important component of most MS clinical trials, providing objective, supportive evidence for the clinical endpoints. Although there is currently insufficient evidence to support any single or combination of MRI measures as a fully validated surrogate, it is now generally accepted that if the aim of a new therapy is to prevent relapses, new Gd-enhancing and T2 lesions can be considered an appropriate surrogate outcome measure of relapses, and MRI activity outcomes can be recommended as the primary measure of treatment efficacy. Read More

    The role of MRS and fMRI in multiple sclerosis.
    Adv Neurol 2006 ;98:185-202
    Department of Neurology, University of Western Ontario, London, Canada.
    Multiple sclerosis is now recognized as more than simply a disease of inflammation and demyelination in the brain and spinal cord. Conventional MRI has been established as the most important paraclinical tool in the diagnostic assessment of patients with suspected MS, and in the monitoring of treatment efficacy in clinical trials, at least in relapsing disease. Magnetization-transfer, diffusion-weighted MRI, 1H-MRS, and fMRI improve our ability to quantify the pathological changes in MS in vivo. Read More

    Multiple sclerosis mimics.
    Adv Neurol 2006 ;98:161-6
    Department of Neurology, University of Mississippi Medical School, Jackson, USA.
    Even with all the newer diagnostic tools, including MRI with multiple sequences, evoked potentials, CSF studies, and so forth, multiple sclerosis remains a clinical diagnosis. In the past it was, to a large extent, a wastebasket diagnosis. Since we really could not do much about it, if our diagnosis was wrong it really didn't matter a great deal. Read More

    The role of MRI in the diagnosis of multiple sclerosis.
    Adv Neurol 2006 ;98:125-46
    Division of Neurology, Department of Medicine, The University of British Columbia, Vancouver, Canada.
    There is no single test that is diagnostic of MS, including MRI. The lesions detected with MRI are pathologically nonspecific. The principles of MS diagnosis are based on showing dissemination of white matter lesions in space and time. Read More

    The pathology of multiple sclerosis: evidence for heterogeneity.
    Adv Neurol 2006 ;98:27-45
    Clinical Research Training Program, Mayo Clinic College of Medicine, Mayo Graduate School, Rochester, Minnesota, USA.
    The idiopathic inflammatory demyelinating diseases (IIDDs) consist of a broad spectrum of disorders that vary in their clinical course, regional distribution, and pathology. Though pathology of these demyelinating disorders demonstrates extensive interindividual heterogeneity, there is notable homogeneity within individual patients. The relation between the diverse underlying pathology of IIDDs and the various clinical, paraclinical, and radiological findings is unclear. Read More

    Treatment issues in psychogenic-neuropsychiatric movement disorders.
    Adv Neurol 2005 ;96:350-63
    Department of Psychiatry, Columbia University, New York, New York, USA.
    Patients with PNMDs pose a fascinating challenge to clinicians at the neurology-psychiatry interface. We have outlined a diagnostic and therapeutic approach to these complex disorders. Patients with PNMDs typically manifest abnormal movements and postures that do not fit expected patterns of movement disorder phenomenology. Read More

    Psychopathological and cognitive correlates of tardive dyskinesia in patients treated with neuroleptics.
    Adv Neurol 2005 ;96:336-49
    Maryland Psychiatric Research Center, Motor Disorders Clinic, University of Maryland School of Medicine, Baltimore, Maryland, USA.
    Even though new cases of TD are on the decline in North America and other western countries, TD remains a public health concern for patients with chronic schizophrenia, PAD, and for nonpsychiatric patients treated with dopamine receptor antagonists. The new generation of atypical antipsychotic medications is believed to pose less risk for TD. However, identifying the cognitive and disease-related correlates of TD should equip clinicians with the necessary tools to reduce the prevalence of this iatrogenic movement disorder. Read More

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