3,589 results match your criteria Advances in Neurology [Journal]


Future and alternative therapies in Tourette syndrome.

Authors:
Roger Kurlan

Adv Neurol 2006 ;99:248-53

Department of Neurology, University of Rochester, Rochester, New York, USA.

View Article

Download full-text PDF

Source
May 2006
15 Reads

Behavioral neurosurgery.

Adv Neurol 2006 ;99:241-7

Department of Psychiatry, Cleveland Clinic Foundation, Cleveland, Ohio, USA.

View Article

Download full-text PDF

Source
May 2006
9 Reads

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

View Article

Download full-text PDF

Source
May 2006
7 Reads

Behavioral treatments for tic suppression: habit reversal training.

Adv Neurol 2006 ;99:227-33

Department of Psychiatry and Biobehavioral Sciences, University of California-Los Angeles Los Angeles, California, USA.

View Article

Download full-text PDF

Source
May 2006
9 Reads

Treatment of aggression in Tourette syndrome.

Authors:
Cathy L Budman

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

View Article

Download full-text PDF

Source
May 2006
7 Reads

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

View Article

Download full-text PDF

Source
May 2006
7 Reads

Attention deficit hyperactivity disorder, chronic tic disorder, and methylphenidate.

Adv Neurol 2006 ;99:197-207

Department of Psychiatry and Behavioral Science, State University of New York at Stony Brook, Stony Brook, New York 11794-8790, USA.

View Article

Download full-text PDF

Source
May 2006
6 Reads

Treatment of tics.

Adv Neurol 2006 ;99:191-6

Department of Pediatrics and Neurology, The University of Alabama at Birmingham, USA.

View Article

Download full-text PDF

Source
May 2006
9 Reads

Disruptive behavior problems in a community sample of children with tic disorders.

Adv Neurol 2006 ;99:184-90

Yale Child Study Center, Yale University School of Medicine, New Haven, Connecticut, USA.

View Article

Download full-text PDF

Source
May 2006
7 Reads

PANDAS: to treat or not to treat?

Authors:
Robert A King

Adv Neurol 2006 ;99:179-83

Tourette's/OCD Clinic, Yale Child Study Center, New Haven, Connecticut, USA.

View Article

Download full-text PDF

Source
May 2006
18 Reads

Autoimmunity and pediatric movement disorders.

Adv Neurol 2006 ;99:166-78

Division of Pediatric Neurology, Johns Hopkins Hospital, Baltimore, Maryland, USA.

View Article

Download full-text PDF

Source
May 2006
7 Reads

PANDAS: overview of the hypothesis.

Authors:
Gavin Giovannoni

Adv Neurol 2006 ;99:159-65

Department of Neuroinflammnation, Institute of Neurology, University College London, London, United Kingdom.

View Article

Download full-text PDF

Source
May 2006
9 Reads

Preclinical/Clinical evidence of central nervous system infectious etiology in PANDAS.

Adv Neurol 2006 ;99:148-58

Department of Psychiatry, University of Florida, USA.

View Article

Download full-text PDF

Source
May 2006
5 Reads

Genes and Tourette syndrome: scientific, ethical, and social implications.

Authors:
Nancy M P King

Adv Neurol 2006 ;99:144-7

School of Medicine, University of North Carolina-Chapel Hill, Chapel Hill, NC, USA.

View Article

Download full-text PDF

Source
May 2006
8 Reads

Web-based consensus diagnosis for genetics studies of Gilles de la Tourette syndrome.

Adv Neurol 2006 ;99:136-43

Tourette Research Program, University of Utah, Division of Child and Adolescent Psychiatry, Salt Lake City, Utah, USA.

View Article

Download full-text PDF

Source
May 2006
6 Reads

A genome-wide scan and fine mapping in Tourette syndrome families.

Authors:
David L Pauls

Adv Neurol 2006 ;99:130-5

Psychiatric and Neurodevelopmental Genetics Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

View Article

Download full-text PDF

Source
May 2006
7 Reads

Functional neuroimaging of Tourette syndrome: advances and future directions.

Adv Neurol 2006 ;99:115-29

Division of Neuropsychiatry, New York Presbyterian Hospital, Department of Psychiatry, Weill Medical College of Cornell University, USA.

View Article

Download full-text PDF

Source
May 2006
8 Reads

Motor cortex inhibitory function in Tourette syndrome, attention deficit disorder, and obsessive compulsive disorder: studies using transcranial magnetic stimulation.

Authors:
Donald L Gilbert

Adv Neurol 2006 ;99:107-14

Department of Neurology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.

View Article

Download full-text PDF

Source
May 2006
7 Reads

Neurobiology of basal ganglia and Tourette syndrome: striatal and dopamine function.

Authors:
Roger L Albin

Adv Neurol 2006 ;99:99-106

Department of Neurology, University of Michigan School of Medicine, Ann Arbor, Michigan, USA.

View Article

Download full-text PDF

Source
May 2006
5 Reads

Neurobiology of basal ganglia and Tourette syndrome: basal ganglia circuits and thalamocortical outputs.

Authors:
Jonathan W Mink

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

View Article

Download full-text PDF

Source
May 2006
38 Reads

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

View Article

Download full-text PDF

Source
May 2006
6 Reads

Tics associated with other disorders.

Adv Neurol 2006 ;99:61-8

Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas, USA.

View Article

Download full-text PDF

Source
May 2006
9 Reads

Behavioral and affective disorders in Tourette syndrome.

Adv Neurol 2006 ;99:39-60

Department of Mental Health Sciences, St. Georges Hospital, London, United Kingdom.

View Article

Download full-text PDF

Source
May 2006
8 Reads

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

View Article

Download full-text PDF

Source
May 2006
10 Reads

Phenomenology of tics and natural history of tic disorders.

Adv Neurol 2006 ;99:1-16

Child Study Center, Sterling Hall of Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.

View Article

Download full-text PDF

Source
May 2006
6 Reads

Other demyelinating diseases.

Adv Neurol 2006 ;98:335-49

Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan, USA.

View Article

Download full-text PDF

Source
February 2006
9 Reads

Neuromyelitis optica.

Adv Neurol 2006 ;98:319-33

Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA.

View Article

Download full-text PDF

Source
February 2006
6 Reads

Acute disseminated encephalomyelitis: distinction from multiple sclerosis and treatment issues.

Adv Neurol 2006 ;98:303-18

Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA.

View Article

Download full-text PDF

Source
February 2006
9 Reads

Mitoxantrone in multiple sclerosis.

Adv Neurol 2006 ;98:293-302

Department of Neurology, Heinrich Heine University, Düsseldorf, Germany.

View Article

Download full-text PDF

Source
February 2006
7 Reads

The use of glatiramer acetate in the treatment of multiple sclerosis.

Authors:
Jerry S Wolinsky

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

View Article

Download full-text PDF

Source
February 2006
47 Reads

Use of interferon-beta in the treatment of multiple sclerosis.

Adv Neurol 2006 ;98:257-71

Department of Neurology, Northwestern University, Chicago, Illinois, USA.

View Article

Download full-text PDF

Source
February 2006
7 Reads

Symptom management.

Authors:
Paul O'Connor

Adv Neurol 2006 ;98:227-55

Department of Medicine (Neurology), University of Toronto, Ontario, Canada.

View Article

Download full-text PDF

Source
February 2006
6 Reads

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

View Article

Download full-text PDF

Source
February 2006
21 Reads

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

View Article

Download full-text PDF

Source
February 2006
10 Reads

The use of modern magnetic resonance techniques to monitor disease evolution in multiple sclerosis.

Adv Neurol 2006 ;98:167-83

Neuroimaging Research Unit, Department of Neurology, Scientific Institute and University Ospedale San Raffaele, Milan, Italy.

View Article

Download full-text PDF

Source
February 2006
11 Reads

Multiple sclerosis mimics.

Authors:
Robert M Herndon

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

View Article

Download full-text PDF

Source
February 2006
13 Reads

Cerebrospinal fluid analysis in the diagnosis of multiple sclerosis.

Adv Neurol 2006 ;98:147-60

Department of Neuroimmunology, National Hospital for Neurology & Neurosurgery, Queen Square, London, Ontario, Canada.

View Article

Download full-text PDF

Source
February 2006
7 Reads

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

View Article

Download full-text PDF

Source
http://eradiology.bidmc.harvard.edu/LearningLab/central/Gaud
Web Search
February 2006
20 Reads

Making the diagnosis of multiple sclerosis.

Authors:
Gary Birnbaum

Adv Neurol 2006 ;98:111-24

MS Treatment and Research Center, Minneapolis Clinic of Neurology, Golden Valley, Minnesota, USA.

View Article

Download full-text PDF

Source
February 2006
8 Reads

Human immune studies in multiple sclerosis.

Authors:
Amit Bar-Or

Adv Neurol 2006 ;98:91-109

Program in Experimental Therapeutics, Clinical Research Unit, Montreal Neurological Institute and McGill University, Quebec, Canada.

View Article

Download full-text PDF

Source
February 2006
7 Reads

Animal models for multiple sclerosis.

Authors:
Trevor Owens

Adv Neurol 2006 ;98:77-89

Department of Immunology, Montreal Neurological Institute, Quebec, Canada.

View Article

Download full-text PDF

Source
February 2006
7 Reads

The myelin basic protein gene: a prototype for combinatorial mammalian transcriptional regulation.

Adv Neurol 2006 ;98:65-76

Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada.

View Article

Download full-text PDF

Source
February 2006
6 Reads

Immunobiology of oligodendrocytes in multiple sclerosis.

Adv Neurol 2006 ;98:47-63

Neuroscience-Neuroimmunology Unit, DIBIT-San Raffaele Hospital, Milan, Italy.

View Article

Download full-text PDF

Source
February 2006
7 Reads

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

View Article

Download full-text PDF

Source
February 2006
8 Reads

The genetics and genetic epidemiology of multiple sclerosis: the "hard facts".

Authors:
A D Sadovnick

Adv Neurol 2006 ;98:17-25

Department of Medical Genetics and Faculty of Medicine, Division of Neurology, University of British Columbia, Canada.

View Article

Download full-text PDF

Source
February 2006
9 Reads

The natural history of multiple sclerosis.

Adv Neurol 2006 ;98:1-15

Multiple Sclerosis Clinic, London Health Sciences Centre, Ontario, Canada.

View Article

Download full-text PDF

Source
February 2006
8 Reads

Cognitive changes in Huntington's disease.

Adv Neurol 2005 ;96:209-25

University of Iowa, Department of Psychiatry and Neurology, Iowa City, Iowa, USA.

View Article

Download full-text PDF

Source
February 2006
6 Reads

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

View Article

Download full-text PDF

Source
February 2006
5 Reads

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

View Article

Download full-text PDF

Source
February 2006
9 Reads