[The concept of cerebral lacunae from 1838 to the present].
The term lacunae was first used by Dechambre (1838) referring to small cavities developed during the process of resorption within cerebral softenings. Some years later, lacunae was applied by Durand-Fardel (1843) to small cavities located in the basal ganglia and hypothetically attributed to old, healed cerebral softenings. Durand-Fardel (1842, 1854) described "l'état criblé" as many round small holes ("criblures") always containing a patient blood vessel and located in the hemispheric white matter. He believed that "état criblé" was caused by mechanical compression of cerebral tissue related to the dilatation of the blood cerebral vessels during repetitive cerebral congestion. Chronic dementia or delirium were considered as the clinical counterpart of "état criblé". In the second half of the XIXth century, the few reports about lacunae were confusing due to the imprecise use of the terms "lacunae" and "état criblé". Furthermore, some authors described lacunae as sequelae of haemorrhage, others as old softenings or both. In the beginning of the XXth century, the masterly work of P. Marie (1901) established a clear distinction between the "foyers lacunaires de désintégration" and "état criblé" de Durand-Fardel or single perivascular dilatation of one of the lenticulo-striate arteries at its entrance into the lenticular nucleus or post-mortem charges (cerebral porosity, "état de fromage de gruyère"). He described lacunae as small cerebral softenings caused by occlusion of the blood vessels by a "local arteriosclerotic process". However, he also stated that some lacunae containing a patent blood vessel were due to a perivascular space dilatation destroying the adjacent brain parenchyma by a process of "destructive vaginalitis". Marie observed that lacunae were frequently clinically asymptomatic, but "that the hemiplegia of the old people was more often due to cerebral lacunae than to cerebral haemorrhage or softening". During the first half of the XXth century, all the papers devoted to cerebral lacunae were in accordance with the work of P. Marie, developing his own's contradictions. Many authors emphasized the "destructive vaginalitis way" and claimed that lacunae were dilatations of the perivascular spaces. Many other authors developed the "softening way" masterfully illustrated by Fisher who considered lacunae as small deep infarcts caused by a specific pathological process of lipohyalinosis due to arteriolar wall modification by hypertensive disease.(ABSTRACT TRUNCATED AT 400 WORDS)
D001161:Arteriosclerosis / Q000150:complications; D001921:Brain / Q000473:pathology*; D002543:Cerebral Hemorrhage / Q000266:history / Q000473:pathology; D002544:Cerebral Infarction / Q000209:etiology / Q000266:history; D002561:Cerebrovascular Disorders / Q000266:history* / Q000473:pathology / Q000503:physiopathology; D004678:Encephalomalacia / Q000266:history / Q000473:pathology; D049672:History, 19th Century; D049673:History, 20th Century; D006801:Humans; D006973:Hypertension / Q000150:complications
Le concept de lacune cérébrale de 1838 à nos jours.