Anti–basal ganglia antibodies in acute and persistent Sydenham’s chorea

Church, Andrew J.; Cardoso, Francisco; Dale, Russell C.; Lees, Andrew J.; Thompson, E. J.; Giovannoni, Gavin

doi:10.1212/wnl.59.2.227

Cited by 253 publications

(193 citation statements)

References 14 publications

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“…TS patient sera have previously been shown to detect several protein species including a 60 kDa protein in immunoblots of human postmortem brain tissue lysates (Church et al, 2003;Singer et al, 1998;Wendlandt et al, 2001). A 60 kDa protein was similarly recognized by Sydenham's chorea patients' sera (Church et al, 2002) and recently identified as PK (Dale et al, 2006). Antibodies to PK were the most predominant of three glycolytic proteins identified as antigenic targets in the sera of patients with Sydenham's chorea.…”

Section: Discussionmentioning

confidence: 92%

Identification of pyruvate kinase as an antigen associated with Tourette syndrome

Kansy

Katsovich

McIver

et al. 2006

Journal of Neuroimmunology

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Immune responses to β-hemolytic streptococcal infections are hypothesized to trigger tic disorders and early-onset obsessive-compulsive disorder (OCD) in some pediatric populations. Here we identify the M1 isoform of the glycolytic enzyme, pyruvate kinase (PK) as an autoimmune target in Tourette syndrome and associated disorders. Antibodies to PK reacted strongly with surface antigens of infectious strains of streptococcus, and antibodies to streptococcal M proteins reacted with PK. Moreover, immunoreactivity to PK in patients with exacerbated symptoms who had recently acquired a streptococcal infection was 7-fold higher compared to patients with exacerbated symptoms and no evidence of a streptococcal infection. These data suggest that PK can function as an autoimmune target and that this immunoreactivity may be associated with Tourette syndrome, OCD, and associated disorders.

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Section: Discussionmentioning

confidence: 92%

Identification of pyruvate kinase as an antigen associated with Tourette syndrome

Kansy

Katsovich

McIver

et al. 2006

Journal of Neuroimmunology

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“…Further studies using immunofluorescence demonstrated antineuronal antibodies in 100% of acute SC although only 63% in persistent/chronic SC. 79,80 A further separate study also supported antibody reactivity in acute SC. 81 Church expanded on these findings using a different antibody technique (Western blotting) and proposed a restricted group of brain autoantigens of molecular mass 40, 45, and 60 kilodaltons (kDa) were involved in antibody binding.…”

Section: Anti-neuronal Antibodiesmentioning

confidence: 78%

Post‐streptococcal autoimmune disorders of the central nervous system

Dale

2005

Develop Med Child Neuro

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Group A Streptococcus can induce autoimmune disease in humans with particular involvement of the heart, joints, and brain. The spectrum of post‐streptococcal disease of the central nervous system (CNS) has been widened recently and includes movement disorders (chorea, tics, dystonia, and Parkinsonism), psychiatric disorders (particularly emotional disorders), and associated sleep disorders. Neuroimaging and pathological studies indicate that the most vulnerable brain region is the basal ganglia. The immunopathogenesis of the disease is incompletely defined, and although there is some support for autoantibody‐mediated disease, several conflicting studies cast doubt on the autoantibody hypothesis. It has been speculated that post‐streptococcal autoimmunity has a role in common neuropsychiatric disease but the evidence is conflicting and routine screening of patients with Tourette syndrome and obsessive‐compulsive disorder for post‐streptococcal autoimmune abnormalities is not be recommended at present. However, post‐streptococcal disorders of the CNS remain a useful model of neuropsychiatric disease, which may improve our understanding of abnormal movements and behaviours in children.

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“…1 We describe a boy who presented a mild parkinsonism and who after stopping corticoids had a dramatic evolution to an akinetic-mutism state associated with an inflammatory CSF and widespread brain lesions. Although ds-DNA was mildly positive, the diagnosis of systemic lupus erythematosus was considered less probable inasmuch as the antinuclear and anti-ENA antibodies were negative, complement levels were normal and no other clinical or laboratorial criteria was present.…”

Section: Introductionmentioning

confidence: 96%

From juvenile parkinsonism to encephalitis lethargica, a new phenotype of post-streptococcal disorders: Case report

Beleza

Soares-Fernandes

Jordão

et al. 2008

European Journal of Paediatric Neurology

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a b s t r a c tWe report the case of a 16-year-old boy presented with a mild akinetic-rigid parkinsonism shortly after a post-streptococcal infection. After stopping corticoids, he had a rapid neurological deterioration to a fatal encephalitis lethargica-like syndrome. Serum analysis demonstrated consistently elevated anti-streptolysin-O. This case illustrates a new severe phenotype in the spectrum of the post-streptococcal disorders. This etiology should be considered in the differential diagnosis of a movement disorder with a rapid detrimental evolution.

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Anti–basal ganglia antibodies in acute and persistent Sydenham’s chorea

Cited by 253 publications

References 14 publications

Identification of pyruvate kinase as an antigen associated with Tourette syndrome

Identification of pyruvate kinase as an antigen associated with Tourette syndrome

Post‐streptococcal autoimmune disorders of the central nervous system

From juvenile parkinsonism to encephalitis lethargica, a new phenotype of post-streptococcal disorders: Case report

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