Pathological alterations of the climbing fibres of the cerebellum in vascular dementia: a Golgi and electron microscope study.
The climbing fibres originating from the inferior olivary nucleus act as a powerful excitation on the Purkinje cells of the cerebellar cortex that may play a substantial role in the motor performances and the learning of new motor skills. In vascular dementia the existent vascular alterations may induce many hypoxic or ischemic phenomena, among the others, in the olivocerebellar system affecting the climbing fibres in their way to the molecular layer of the cerebellar cortex. In autopsy cases of vascular dementia, the application of silver impregnation technique and electron microscopy revealed a substantial decrease of the number of the climbing fibres in the cortex of the vermis, the flocculus and the cerebellar hemispheres. The presynaptic varicosities and the synaptic terminals of the climbing fibres on the Purkinje cell dendrites were decreased in number and moreover were characterized by a marked poverty of synaptic vesicles. The synaptic cleft was mostly abnormal and wider than 20 nm. Mitochondrial abnormalities, such as elongated mitochondria with disruption of the cristae were seen in the terminal branches of the climbing fibre arborization as well as in the presynaptic components. The blood capillaries demonstrated a considerable thickness of the basal membrane and perivascular astrocytic proliferation, whereas the tight junctions between the endothelial cells were ultrastructurally intact. We would hypothesize that the morphological and morphometric alterations of the climbing fibres of the cerebellar cortex in cases of vascular dementia might be associated with the frequently noticed difficulty in the performance of fine and skilful movements by the patients.
Baloyannis
Stavros J
SJ
Department of Neurology, Aristotelian University, Thessaloniki, 540 06, Greece. sibh844@otenet.gr
D000368:Aged; D000369:Aged, 80 and over; D001369:Axons / Q000473:pathology*; D002196:Capillaries / Q000473:pathology; D002526:Cerebellar Diseases / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D002531:Cerebellum / Q000098:blood supply / Q000473:pathology* / Q000503:physiopathology; D015140:Dementia, Vascular / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D046529:Microscopy, Electron, Transmission; D009434:Neural Pathways / Q000473:pathology / Q000503:physiopathology; D009847:Olivary Nucleus / Q000473:pathology / Q000503:physiopathology; D017729:Presynaptic Terminals / Q000473:pathology; D011689:Purkinje Cells / Q000473:pathology; D016622:Silver Staining; D013569:Synapses / Q000473:pathology; D009435:Synaptic Transmission / Q000502:physiology