Neurobiologia da síndrome de Tourette: a hipótese auto-imune pós-estreptocócica: [revisão] / Neurobiology of Tourette's syndrome: the autoimmune post-streptococcal hypothesis: [review]

CONTEXTO: A síndrome de Tourette (ST) caracteriza-se pela presença de tiques motores e pelo menos um tique fônico. Algumas semelhanças clínicas com a coréia reumática ou de Sydenham (CS) incentivaram a formulação da hipótese da existência de um grupo de transtornos neuropsiquiátricos associados a processo auto-imune decorrente de infecção estreptocócica (PANDAS). OBJETIVO: Revisar a literatura quanto às evidências em relação à hipótese de que mecanismos auto-imunes pós-estreptocócicos estão envolvidos na etiopatogênese da ST. MÉTODOS: Revisão sistemática na base de dados MedLine com os termos "Tourette", "tic", "PANDAS", "antibodies", "streptococcal" e "rheumatic". RESULTADOS: Retornaram 238 artigos da busca. Selecionaram-se 53 trabalhos, os quais tiveram suas referências bibliográficas também revisadas. São apresentados os resultados de estudos que avaliaram aspectos imunes na ST, incluindo anticorpos antiestreptocócicos e antinúcleos da base, e sua terapêutica imunebaseada, discutindo a validade do conceito de PANDAS. CONCLUSÕES: As evidências ainda não são satisfatórias no que tange a uma base auto-imune pós-estreptocócica para a ST. Um aprimoramento dos métodos investigativos e na seleção das amostras pode trazer maiores contribuições à questão.

BACKGROUND: Tourette's syndrome (TS) is characterized by the presence of motor tics and at least one phonic tic. Some clinical similarities with Sydenham's chorea (SC) lead to the hypothesis of a new group of disorders associated with an autoimmune process due to a streptococcal infection (PANDAS). Objective: To review the literature in search of evidence on the existence of post-streptococcal autoimmune mechanisms involved with the etiopathogenesis of TS. METHODS: A systematic review with the terms "Tourette", "tic", "PANDAS", "antibodies", "streptococcal" and "rheumatic" was carried on using the MedLine. RESULTS: The search found 238 articles. Fifty and three articles were selected which also had their references reviewed. The results of studies that investigated autoimmune aspects of TS, including anti-streptococcal and anti-basal ganglia anti-bodies, and immune-based therapy, were presented and discussed. DISCUSSION: The evidences to date are not satisfactory regarding a post-streptococcal auto-immune process in ST. The improvement on investigative methods and sample selection might contribute to this question.

Chorea: non-genetic causes.

PURPOSE OF REVIEW: The aim of this article is to review the literature on the non-genetic causes of chorea. The differential diagnosis of the large number of causes of sporadic chorea is often a challenging task. Interest has also been growing in the possibility that the mechanism responsible for Sydenham's chorea plays a role in the pathogeneis of other neuropsychiatric disorders. RECENT FINDINGS: Stroke is the main cause of sporadic chorea. Sydenham's chorea shares clinical features with tic disorders, such as obsessive-compulsive disorder and attention deficit hyperactivity disorder. However, there are unequivocal differences between Sydenham's chorea and Tourette's syndrome. There is initial evidence suggesting the beneficial effect of immunosuppression in Sydenham's chorea. Other autoimmune causes of chorea include systemic lupus erythematosus as well as paraneoplastic syndromes. The growing list of drugs associated with chorea include lamotrigine, methadone and lithium. Among infectious agents, HIV is the leading reported cause of chorea. SUMMARY: Patients with sporadic chorea require a thorough work up because numerous causes can lead to this condition. It remains unconfirmed whether the pathogenic mechanisms of Sydenham's chorea are responsible for other conditions such as isolated obsessive-compulsive disorder or Tourette's syndrome. Drugs and infectious agents, especially HIV, are often implicated in the causes of chorea.

[D8/17 marker: implication to neuropsychiatry]. / Marcador D8-17: implicações para a neuropsiquiatria.

Recent studies suggest that there is a relationship between rheumatic fever (RF) and some neuropsychiatric disorders. Thus, it has been thought that autoimmune mechanisms might be related to the etiology of these neuropsychiatric disorders. It has also been demonstrated that a B cell alloantigen associated to RF is also abnormally overexpressed in patients with such neuropsychiatric disorders. This alloantigen is recognised by a monoclonal antibody known as D8/17. The aim of this article is to introduce the recent work done about D8/17 and its possible implications to the study of neuropsychiatric disorders related or not to RF.

Marcador D8-17: implicações para a neuropsiquiatria / D8/17 marker: implication to neuropsychiatry

Estudos recentes sugerem uma associação entre febre reumática (FR) e transtornos do espectro obsessivo-compulsivo, o que levou à hipótese de que alterações na resposta imune pudessem ter um papel na etiologia destes últimos. Um marcador biológico que talvez identifique maior susceptibilidade para o desenvolvimento de FR e desses transtornos neuropsiquiátricos tem causado grande interesse na literatura. Trata-se do D8/17, um anticorpo monoclonal contra um antígeno de membrana de linfócitos B. Neste artigo introduzimos conhecimentos sobre o D8/17 e discutimos suas implicações como um possível marcador biológico de transtornos neuropsiquiátricos associados ou não à FR.