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- BookAlexandra Armitage, editor.Contents:
The neurobiology of Parkinson's disease
The patient exam
Defining idiopathic Parkinson's disease
Imaging and advanced studies
Neuropsychological analysis
Additional evaluations
Parkinson-plus syndromes
Other Parkinsonisms
Treatment of motor symptoms
Treatment of non-motor symptoms : autonomic dysfunction
Treatment of non-motor symptoms : sleep disturbances
Treatment of non-motor symptoms : disturbances of thought
Treatment of non-motor symptoms : neuropsychiatric symptoms
Exercise
Complementary and alternative therapies
Nutrition
Caregiver burden and legal considerations.Digital Access R2Library 2018Limited to 1 simultaneous user - ArticleDavis CA, McEnery PT, Maby S, McAdams AJ, West CD.Clin Nephrol. 1978 Mar;9(3):91-101.Distinctive deposits of C3, C5 and properdin were identified in the minimally proliferative glomerular lesions of a patient with idiopathic rapidly progressive glomerulonephritis. Biopsies of her renal allograft at times of recurrences of her disease and of five other patients with progressive renal failure but less severe crescent formation showed deposits identical composition and position, giving evidence of a common pathogenesis. The deposits were subepithelial and located in that part of the basement membrane in apposition to the mesangium (capillary waist). Breaks in the basement membrane were often exclusively in this area suggesting the deposits were causative. Ancillary observations suggest that the subepithelial deposits become unidentifiable after the scarring of severe extracapillary proliferation develops. Three of the patients had, in addition, intramembranous dense deposits but in other ways their disease was not characteristic of membranoproliferative glomerulonephritis Type II. Instead, the evidence indicated that all six patients were in early or lage stages of idiopathic (non-streptococcal) rapidly progressive glomerulonephritis.