The Pathology of Sydenham's Chorea.

Greenfield, J. G.; Wolfsohn, Julian Mast

doi:10.1016/s0140-6736(01)01044-3

Cited by 75 publications

(32 citation statements)

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“…Magnetic resonance imaging showed inflammatory changes in the basal ganglia and midbrain tegmentum in 40% of patients, which resolved during convalescence. Histopathology in one case revealed perivascular cuffing of B and T lymphocytes, predominantly in the basal ganglia, reactive astrocytes and macrophages, showing remarkable similarity to the pathology of SC [46]. Two-thirds of the patients had elevated antistreptolysin-O titres during the acute phase.…”

Section: Encephalitis Lethargica and Poststreptococcal Neuropsychiatrmentioning

confidence: 81%

Antibasal ganglia antibodies and their relevance to movement disorders

Martino

Giovannoni

2004

Current Opinion in Neurology

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Antibasal ganglia antibodies are relatively specific in identifying post-streptococcal neuropsychiatric disorders, which constitute a wider spectrum of movement disorders than previously recognized. Although their sensitivity in diagnosing Sydenham's chorea seems excellent, it is not yet possible to extrapolate this sensitivity to all the recently identified post-streptococcal neuropsychiatric disorders. The antigens targeted by these autoantibodies and their pathogenic importance are currently under investigation. Preliminary evidence suggests that antibasal ganglia antibodies may be pathogenic.

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Section: Encephalitis Lethargica and Poststreptococcal Neuropsychiatrmentioning

confidence: 81%

Antibasal ganglia antibodies and their relevance to movement disorders

Martino

Giovannoni

2004

Current Opinion in Neurology

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“…Pathology reports have also shown specific changes to the basal ganglia, including cellular infiltration and neuronal loss with relative sparing of other brain areas. 9,10 Previous studies have shown that patients with SC produce antibodies that cross-react between the rheumatogenic strains of streptococci and human basal ganglia proteins. 7 The antibody is thought to derive from an immune response to streptococcal M protein, which cross-reacts with shared epitope(s) in the basal ganglia.…”

Section: Neurology 2002;59:227-231mentioning

confidence: 99%

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

Church

Cardoso²,

Dale³

et al. 2002

Neurology

253

172

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“…14,15 The evidence for basal ganglia dysfunction in SC has been derived from volumetric MRI studies that demonstrated striatal enlargement, 16 post-mortem studies that found focal cellular infiltration and neuronal loss within the basal ganglia, 17,18 as well as clinical response to dopaminergic agents. Systematic research over the past two decades has demonstrated that OCD is associated with dysfunction in the basal ganglia and orbitofrontal cortex 19 ( Figure 1).…”

Section: Sc and Pandasmentioning

confidence: 99%

PANDAS: current status and directions for research

2004

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The recognition of the five criteria for PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) by Swedo et al established a homogenous subgroup of children with childhood onset obsessive-compulsive disorder (OCD) and/or tic disorders. The five clinical characteristics that define the PANDAS subgroup are the presence of OCD and/or tic disorder, prepubertal age of onset, abrupt onset and relapsing-remitting symptom course, association with neurological abnormalities during exacerbations (adventitious movements or motoric hyperactivity), and a temporal association between symptom exacerbations and a Group-A beta-hemolytic streptococcal (GAS) infection. These five criteria have been used for the purpose of systematic research on the phenomenology and unique therapies for the PANDAS subgroup as well as studies of the pathophysiology of poststreptococcal OCD and tic disorders. The etiology of OCD and tics in the PANDAS subgroup is unknown, but is theorized to occur as a result of post-streptococcal autoimmunity in a manner similar to that of Sydenham's chorea. The working hypothesis for the pathophysiology begins with a GAS infection in a susceptible host that incites the production of antibodies to GAS that crossreact with the cellular components of the basal ganglia, particularly in the caudate nucleus and putamen. The obsessions, compulsions, tics, and other neuropsychiatric symptoms seen in these children are postulated to arise from an interaction of these antibodies with neurons of the basal ganglia.

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The Pathology of Sydenham's Chorea.

Cited by 75 publications

References 0 publications

Antibasal ganglia antibodies and their relevance to movement disorders

Antibasal ganglia antibodies and their relevance to movement disorders

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

PANDAS: current status and directions for research

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