Neue Beobachtungen über die Hallervorden-Spatzsche Krankheit

Eicke, Werner J.

doi:10.1007/bf01814385

Cited by 25 publications

(3 citation statements)

References 14 publications

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“…However, abandoning the eponym entirely will prevent recognition of the ethical violations to future generations unaware of the crimes involved. In addition, and ironically, 2 Hallervorden-Spatz disease patients were apparently victims of Nazi ''euthanasia,'' 23 thus entirely abandoning the eponym does not bring light to the crimes against them, and does them no honor. A better solution is likely to add ''formerly,'' ''previously,'' or ''once known as'' to eponyms of those who shouldn't be honored further (eg, ''pantothenate kinase-associated neurodegeneration, formerly known as Hallervorden-Spatz disease'').…”

Section: Discussionmentioning

confidence: 99%

Declining Use of the Hallervorden–Spatz Disease Eponym in the Last Two Decades

Zeidman

Pandey

2012

J Child Neurol

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There has been a movement to rename Hallervorden-Spatz disease to pantothenate kinase-associated neurodegeneration given Hallervorden and Spatz's complicity in murderous Nazi programs. Similar controversy surrounds Reiter syndrome, and 2 studies demonstrated decreased unqualified use of that eponym in the literature, but not in textbooks. There have been no similar studies regarding Hallervorden-Spatz disease. The authors performed a MEDLINE search (1990-2010) looking for unqualified use of Hallervorden-Spatz disease and performed statistical analysis. They defined "unqualified" as having no reference to the eponym's disfavored use. They then looked in 6 neurology textbooks. The authors identified 156 of 278 articles (56.1%) containing unqualified use of Hallervorden-Spatz disease. But there was a declining trend (P = .000), with 70/80 (87.5%) of articles from 1990 to 1999 and 86/198 (43.4%) from 2000 to 2010. There was also decreased unqualified use of the eponyms in textbooks, with all recent editions using pantothenate kinase-associated neurodegeneration instead. The significant decrease in unqualified use of Hallervorden-Spatz disease is reassuring.

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Section: Discussionmentioning

confidence: 99%

Declining Use of the Hallervorden–Spatz Disease Eponym in the Last Two Decades

Zeidman

Pandey

2012

J Child Neurol

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“…(b) Second group: The sporadic and atypical cases. Some authors have given more emphasis to clinical symptomatology (Jakob & Montanaro 1918, Meyer & Earl 1936, and Wahlstrom 1946 and others to the histopathological findings (Eicke 1940, Seitelberger 1963/4, 1966 when considering the diagnosis. It is clear to us after the analysis of this family and the reported cases that there is such a condition as Hallervorden-Spatz disease.…”

Section: Discussionmentioning

confidence: 99%

“…The sporadic cases were reported from: Germany, 5 (Helfand 1935, Eicke 1940, Seitelberger 1963; France, 2 (Vincent & Van Bogaert 1936; Giraud & Roualt de la Vigne 1959); and one from each of the following countries: Switzerland (Bischoff & Regli 1963), Belgium (Radermecker & Rizzuto 1967), Sweden (Wahlstrom 1946), Holland (Wigboldus & Bruyn 1968, England (Meyer & Earl 1936, and Israel (Bornstein et al 1966).…”

Section: Discussionmentioning

confidence: 99%

Hallervorden‐Spatz disease

Elejalde

López

1979

Clinical Genetics

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We had the opportunity to study a family, five of whose members were affected by the Hallervorden‐Spatz disease (three males and twin girls). The characteristics of the condition were analyzed and compared with those cases considered by other authors to be affected by the condition. Intrafamilial and interfamilial variations were analysed, and it was the latter that contributed most to the overall variation of the condition. It was clearly established from the reported cases and our family that this is an autosomal recessive condition (P> 0.23 ± 0.08). It is suggested that the condition probably originated in Europe and that it is caused by an inborn error of metabolism related to neuromelanin and the dopaminergic system. The condition affects the muscular tone and voluntary movements progressively, making voluntary coordinated movements, and chewing and swallowing almost impossible, and in the last part of its development mental deterioration, emaciation, severe feeding difficulties and visual impairment are common clinical manifestations. The ages of both onset and death are distributed in a unimodal curve. The mean survival time after diagnosis was 11.18 ± 7.8 years.

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Hallervorden-Spatz Syndrome

Dooling¹,

Schoene²,

Richardson³

1974

Archives of Neurology

244

125

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(Fig 1) (Fig 3). Lewy bodies were also found within neurons of the substantia innominata and of the locus ceruleus.The cerebral cortex in general showed no cytoarchitectural abnormalities or changes in the nerve fibers or glia (except for the expected scarring at the biopsy site). Adja¬ cent to many of the nerve cells, espe¬ cially in the frontal and insular cortex, there were hyaline eosinophilic bodies of rounded or irregular contour, which in their appearance and staining properties resembled the swollen axons seen else¬ where; but they differed from the Lewy bodies (Fig 4). These structures, identified as juxtaneuronal axonal swellings, could also be found in the cerebral biopsy speci¬ men. In the hippocampus, many of the pyramidal neurons showed granulovacuolar degeneration.

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Neue Beobachtungen über die Hallervorden-Spatzsche Krankheit

Cited by 25 publications

References 14 publications

Declining Use of the Hallervorden–Spatz Disease Eponym in the Last Two Decades

Declining Use of the Hallervorden–Spatz Disease Eponym in the Last Two Decades

Hallervorden‐Spatz disease

Hallervorden-Spatz Syndrome

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