Etudes anatomo-cliniques de syndromes hypercinétiques complexes

Mylle, Gilbert; Bogaert, Ludo van

doi:10.1159/000148545

Cited by 24 publications

(17 citation statements)

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“…The first published postmortem examination appeared in 1903 28. Between then and 1990, there were only seven additional reports,28–34 so that up to 17 years ago, there were fewer than 10 published pathological cases. A number of these cases exhibited unusual clinical features (e.g., choreiform movements) or evidence of other neurological disorders (e.g., marked dystonia),30, 31, 34 which casts doubt upon the clinical diagnosis of ET (Table 1).…”

Section: Postmortem Studiesmentioning

confidence: 99%

Transient elastography for diagnosis of portal hypertension in liver cirrhosis: Is there still a role for hepatic venous pressure gradient measurement?

Lim

Groszmann

2007

Hepatology

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Section: Postmortem Studiesmentioning

confidence: 99%

Transient elastography for diagnosis of portal hypertension in liver cirrhosis: Is there still a role for hepatic venous pressure gradient measurement?

Lim

Groszmann

2007

Hepatology

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“…The changes found in the present case were not noticeably different from those seen in patients with hypertensive cerebrovascular disease and without tremor. It is difficult not to agree with the implication of Mylle and van Bogaert (1948) that, up to now, no definite structural lesions have been found to which the clinical disorder can indisputably be attributed. They, however, considered it important that all cases of essential tremor with pathological examination should be published.…”

Section: Discussionmentioning

confidence: 83%

“…Post mortem findings in his brain were severe advanced and diffuse arteriosclerosis, reduction of the small nerve cells in the striatum, small softenings in the dorsal two thirds of the putamen and caudate nucleus, and rarefaction of Purkinje cells, with laminar atrophy. CASE 3 (Mylle and van Bogaert, 1940) was a man with a strong family history of psychopathies and two siblings with tremor. The tremor began when the patient was in his 40s.…”

mentioning

confidence: 99%

“…There was fibrillar gliosis of the superior cerebellar peduncles; of the cerebellar white matter and pallidum; increased cellular gliosis of the dentate nuclei and the roof nuclei; loss of Purkinje cells; loss of large nerve cells from striatum and pallidum with increased lipidic uptake. CASE 4 (Mylle and van Bogaert, 1948) was a case of non-familial tremor in a woman. When she was 16 years old, tremor commenced in head and hands.…”

mentioning

confidence: 99%

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Essential (familial, hereditary) tremor: a case report.

Herskovits¹,

Blackwood²

1969

Journal of Neurology, Neurosurgery & Psychiatry

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“…38 Third, therapeutically, cerebellar outflow (dentato-rubro-thalamic) pathways are the target of highfrequency thalamic stimulators which are highly effective in treating ET. 39 Finally, postmortem pathological study of ET cases has been scanty (14 published examinations), 18,[40][41][42][43][44][45][46] and the majority of these reports are more than 50 years old, although in several of these, 18,40,45,46 there was evidence of cerebellar Purkinje cell pathology. This ranged from occasional (one case) 18 to diffuse Purkinje cell loss (three cases), 40,45,46 and one case demonstrated laminar cerebellar cortical atrophy.…”

Section: Introduction To the Pathogenesis Of Etmentioning

confidence: 99%

Etiology of essential tremor: Should we be searching for environmental causes?

Louis

2001

Movement Disorders

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Essential tremor (ET) is an extremely common and widespread disorder.1 Its prevalence among individuals Ն65 years of age 2 is similar to that of osteoarthritis, 3 diabetes mellitus, 4 and Alzheimer's disease. 5 Also, it is a longstanding condition; humans have provided written commentary about their tremors for several thousand years. [6][7][8][9] Despite this, knowledge about the biology of this disorder remains limited. For example, the location of the primary pathology in ET is not known. It is not clear whether the problem originates in a central pacemaker in the brainstem and then secondarily involves the cerebellum, or whether the cerebellum or other central structure is the site of the primary pathology. 10 One problem is that a specific degenerative neuronal population has not been identified. In terms of etiology, while most investigators would agree that a genetic predisposition contributes to the etiology in a sizeable proportion of ET cases,11,12 whether this represents 10%, 50%, or 90% of cases is not known. 13Nature vs. Nurture How much do genetic vs. non-genetic factors contribute to the etiology of ET? There are published examples of families in which multiple relatives have ET [14][15][16][17] and in which the pattern of inheritance is most consistent with an autosomal dominant model. In a small number of these, [15][16][17] linkage has been demonstrated to regions on chromosomes 2p or 3q. It is commonly stated in the literature that 50% of ET cases occur on a genetic basis, although the studies examining this issue have methodological flaws, and some estimates are as low as 17%. 13Most important is that these studies have not enrolled control subjects, so it is not known to what extent familial occurrence of ET is explained by chance co-occurrence of a highly prevalent disorder rather than a genetic predisposition for tremor. 13ET is not completely genetic. The entity of nonfamilial ET or "sporadic" ET is well recognized by most clinicians, who distinguish this form of ET from "hereditary" ET. 11,16,18 In fact, in most series, the majority (>50%) of ET cases have not reported affected relatives, 3,[19][20][21][22] and despite the high prevalence of the disease, families that are informative for genetic linkage studies have been difficult to locate. The existence of intrafamilial differences in age of onset and severity of tremor 23,24 also suggests that environmental (or perhaps other genetic) factors may serve as modifiers of an underlying susceptibility genotype.The existence of geographic clusters of ET cases could provide further support for the notion that environmental factors contribute to the etiology of ET in these geographic regions. A large cluster of ET cases has been reported 20,25 to occur in a region of the Eastern Highlands of Papua New Guinea. In the population defined by possession of one or other of the following languages, Kamano, Ayuna, Gadsup, Tairo, or Agarabe, the prevalance of ET is 22.6 times higher than that of other areas of the Highlands (e.g., Fore, Keiagana-Kanite...

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Etudes anatomo-cliniques de syndromes hypercinétiques complexes

Cited by 24 publications

References 0 publications

Transient elastography for diagnosis of portal hypertension in liver cirrhosis: Is there still a role for hepatic venous pressure gradient measurement?

Transient elastography for diagnosis of portal hypertension in liver cirrhosis: Is there still a role for hepatic venous pressure gradient measurement?

Essential (familial, hereditary) tremor: a case report.

Etiology of essential tremor: Should we be searching for environmental causes?

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