Striatal microinfusion of Tourette syndrome and PANDAS sera: Failure to induce behavioral changes

Loiselle, Christopher; Lee, Olivia; Moran, Timothy H.; Singer, Harvey S.

doi:10.1002/mds.10522

Cited by 91 publications

(58 citation statements)

References 36 publications

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“…The prediction is that infusion of sera with autoantibodies (as determined by immunocytochemical screening) may lead to the development of stereotypies, compared to infusion of sera that lack autoantibodies. The results here have been mixed as well, with several laboratories finding significant production of stereotypies [28][29], while others have not [30] [31]. Additional research is necessary to determine whether autoantibodies are produced in vulnerable individuals and whether these are etiologically related to the symptoms observed in PANDAS cases.…”

Section: Pediatric Autoimmune Neuropsychiatric Disorder Associated Wimentioning

confidence: 68%

Tourette syndrome and obsessive–compulsive disorder

Lombroso

Scahill

2008

Brain and Development

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Tourette syndrome and obsessive-compulsive disorder are neuropsychiatric disorders that have sparked considerable interest over the decades. They are the focus of research for a remarkable diversity of disciplines, ranging from neuroimagers and prenatal epidemiologists to experts in the neural circuits that connect the cortex with the basal ganglia, as well as neuroimmunologists focusing on brain-based autoimmune phenomena. Several hypotheses have been put forward to explain the onset and exacerbation of these illnesses. Here we discuss the clinical phenomenology and treatment options that are currently available. New psychopharmacological agents are being used that are based on a greater understanding of the neurobiology and are being used in combination with behavioral interventions. Longitudinal clinical investigations into clinical symptoms and the natural course are providing additional clues on the underlying pathophysiology. Recent advances in research models are also reviewed in an attempt to clarify some of the molecular etiologies that lead to these disorders. KeywordsTorrette syndrome; obsessive-compulsive disorder; basal ganglia; autoimmune disorders; streptococcal infections; neuroleptic treatment Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) are model neuropsychiatric disorders that have been the subject of medical interest for centuries [1]. Many explanations have been suggested for the etiology of tics and OCD symptoms and have included genetic factors, the influence of toxins, psychological, and infectious processes. There have been significant advances of our understanding of the neurobiological mechanisms at work in these disorders, as well as improvements in the treatments available. Several reviews on more specialized aspect of TS, OCD and related disorders have appeared over the last several years [2][3][4]. Here we concentrate on the clinical features of tic disorders and OCD and discuss evidence-based interventions for these disorders. Tourette syndromeTourette syndrome is one of several tic disorders that are classified either by their type (motor or phonic tic) or their duration (transient or chronic). The diagnosis of a transient tic is made if the tics are present for less than 12 months. If the tics persist for more than 12 months, they

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Section: Pediatric Autoimmune Neuropsychiatric Disorder Associated Wimentioning

confidence: 68%

Tourette syndrome and obsessive–compulsive disorder

Lombroso

Scahill

2008

Brain and Development

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“…Some investigations have shown that sera from TS subjects produced a significant increase in stereotypic behaviors (e.g., licks and forepaw shakes) as well as episodic utterances (Hallett et al, 2000;Taylor et al, 2002;Liu et al, 2008). In marked contrast, other studies infusing TS or PANDAS sera at the same coordinates showed no significant increase in stereotypic behaviors and no rat developed any audible abnormality (Loiselle et al, 2004). Negative studies were also confirmed in a blinded, collaborative three-center effort involving several of the previously reporting institutions (Singer et al, 2005a).…”

Section: Autoimmune Modelsmentioning

confidence: 95%

Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation: Table 1.

Felling¹,

Singer²

2011

J. Neurosci.

203

116

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Tourette syndrome (TS) is a common, chronic neuropsychiatric disorder characterized by the presence of fluctuating motor and phonic tics. The typical age of onset is ϳ5-7 years, and the majority of children improve by their late teens or early adulthood. Affected individuals are at increased risk for the development of various comorbid conditions, such as obsessive-compulsive disorder, attention deficit hyperactivity disorder, school problems, depression, and anxiety. There is no cure for tics, and symptomatic therapy includes behavioral and pharmacological approaches. Evidence supports TS being an inherited disorder; however, the precise genetic abnormality remains unknown. Pathologic involvement of cortico-striatal-thalamo-cortical (CSTC) pathways is supported by neurophysiological, brain imaging, and postmortem studies, but results are often confounded by small numbers, age differences, severity of symptoms, comorbidity, use of pharmacotherapy, and other factors. The primary site of abnormality remains controversial. Although numerous neurotransmitters participate in the transmission of messages through CSTC circuits, a dopaminergic dysfunction is considered a leading candidate. Several animal models have been used to study behaviors similar to tics as well as to pursue potential pathophysiological deficits. TS is a complex disorder with features overlapping a variety of scientific fields. Despite description of this syndrome in the late 19th century, there remain numerous unanswered neurobiological questions.In the 1880's, Georges Gilles de la Tourette published a two-part article in which he emphasized differences between tics and chorea. Although many of the descriptions about the disorder, which now bears his name [Tourette syndrome (TS)], have been revised, his belief that tics are a neurological movement disorder and not a psychiatric condition persists to the present (Goetz and Klawans, 1982). Nevertheless, despite multiple advances and widespread acceptance of TS being a biological disorder, the precise etiology and underlying pathophysiological mechanisms remain unknown. The goals of the present review are to briefly describe the clinical phenomenology of TS and related tic disorders, to review current information on genetic and neurobiological mechanisms, and to identify areas in need of further investigation.

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“…Several labs have induced tic-like movements in laboratory animals after brain infusion of sera from TS patients with high levels of autoantibodies, 28 -32 but this finding was not replicated in another study. 33 In addition, a placebocontrolled study failed to show the effectiveness of prophylactic penicillin in preventing exacerbations of tic and obsessive-compulsive symptoms. 34 Plasma exchange, in which offending autoantibodies are presumably removed, was effective in one study in children with TS and OCD, but it has not been replicated.…”

Section: Diagnosis Of Ts and Assessment Of Ticsmentioning

confidence: 99%

Contemporary assessment and pharmacotherapy of Tourette syndrome

Scahill

Erenberg

Berlin

et al. 2006

NeuroRX

271

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Summary:To develop a guide to clinical assessment and pharmacotherapy for children and adults with Tourette syndrome (TS), we reviewed published literature over the past 25 years to identify original articles and reviews on the assessment and pharmacological treatment of Tourette syndrome, attention-deficit/hyperactivity disorder (ADHD) and obsessivecompulsive disorder (OCD). The literature search also included a survey of reviews published in book chapters. The assessment section was compiled from several reviews. Pharmacological treatments were classified into those with strong empirical support (as evidenced by two positive placebo-controlled studies for tics, OCD, or ADHD in TS samples); modest empirical support (one positive placebo-controlled study), or minimal support (open-label data only). We conclude that accurate diagnosis, including identification of comorbid conditions, is an essential step toward appropriate treatment for patients with TS. In many patients with TS, symptom management requires pharmacotherapy for tics or coexisting conditions. The evidence supporting efficacy and safety for medications used in patients with TS varies. But this evidence offers the best guide to clinical practice.

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Striatal microinfusion of Tourette syndrome and PANDAS sera: Failure to induce behavioral changes

Cited by 91 publications

References 36 publications

Tourette syndrome and obsessive–compulsive disorder

Tourette syndrome and obsessive–compulsive disorder

Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation: Table 1.

Contemporary assessment and pharmacotherapy of Tourette syndrome

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