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Antineuronal antibodies (ANAs) have been implicated in the pathophysiology of postinfectious movement disorders, such as Sydenham's chorea. However, their relevance in other movement disorders-in the absence of infectious triggers-remains much disputed. We sought to assess the frequency of ANAs in idiopathic Parkinson's disease (IPD) and to explore whether a specific phenotype is associated with the presence of ANAs. For this purpose, we recruited 76 IPD patients, 9 patients with genetic parkinsonism, and 10 with one of the parkinson-plus syndromes. They were all subjected to a comprehensive clinical review. In addition, 50 patients with non-extrapyramidal neurological disease and 30 healthy blood donors served as control populations. Blood samples were tested for the presence of ANAs with Western blotting, using recombinant proteins of the three putative antigens (aldolase C, neuron-specific enolase, and pyruvate kinase M1). We found these antibodies in 11.8% of the 76 IPD patients, which differed significantly from healthy controls (0%, P = 0.043), but nonsignificantly from patients with genetic parkinsonism (11.1%), with a parkinson-plus syndrome (10%), or from neurological disease controls (4%). With respect to relevant disease characteristics, IPD patients with or without ANAs were indistinguishable, except for atypical disease features (mainly early falls or freezing and marked Pisa syndrome), which were more frequent in the ANA-positive IPD group. We conclude that ANAs do not play a role in the majority of patients with IPD, but might be relevant in the pathogenesis of IPD with atypical features. © 2008 Movement Disorder Society [ABSTRACT FROM AUTHOR]

Examines the recent evolution of a sub-regional planning initiative in the Thames Gateway which is part of London and the South East region of England. Analysis of economic and social change affecting the characteristics of sub-areas of the Thames Gateway; Aims of redevelopment strategies in the late 1980s; Thames Gateway Planning Framework's principles.

The Gilles de la Tourette syndrome (GTS) spectrum includes psychiatric comorbidities, mainly obsessive-compulsive disorder (OCD) and attention-deficit-hyperactivity disorder (ADHD). The role of environmental factors, e.g., antineuronal antibodies (ANeA), remains unclear. We compared the clinical features of ANeA-positive and ANeA-negative patients in 53 children and 75 adults with GTS. All diagnoses were made according to DSM-IV-TR criteria. A positive ANeA Western immunoblot showed bands for at least 1 of 3 reported striatal antigens (40, 45, and 60 kDa). Twelve children (23%) and 18 adults (25%) with GTS were ANeA-positive. Disease duration, tic phenomenology and severity, frequency of echo/pali/coprophenomena, self-injurious and aggressive behavior, or frequency of OCD comorbidity did not significantly differ between ANeA-positive and negative patients. Similar findings were obtained analyzing separately the three different antibody reactivities. A comorbid diagnosis of ADHD was significantly less frequent in GTS patients positive for the anti-60 kDa antibody only. Using a multivariate logistic regression model, adjusting for age, gender, and age at disease onset, a comorbid diagnosis of ADHD remained inversely associated with anti-60 kDa antibodies (odds ratio = 0.14; P = 0.002; 95% confidence interval 0.04-0.49). ANeA status does not differentiate a specific phenotype of GTS. [ABSTRACT FROM AUTHOR]

The onset of tics in adulthood is rare and, unlike the childhood variety, there is commonly a secondary environmental cause. We present four cases (1 man, 3 women) with an adult onset tic disorder (mean age of onset, 36 years; range, 27-42 years) associated with the presence of serum antibasal ganglia antibodies (ABGA). One patient had motor tics and unusual motor stereotypies, 2 had multiple motor and vocal tics, and the remaining patient had motor tics only. Concomitant psychiatric disturbance was noted in 3 cases. In 2 cases, there was a close temporal relationship between upper respiratory tract infection and the subsequent onset of tics. Imaging was possible in three cases and was normal in two but revealed a lesion involving the right caudate and lentiform nuclei in the other. We suggest that there might be a causal relationship between ABGA and the clinical syndrome in these cases and that ABGA should be considered as a possible etiology for adult-onset tics. © 2004 Movement Disorder Society [ABSTRACT FROM AUTHOR]