Human amnesia is a clinical syndrome exhibiting the failure to recall past events and to learn new information. Its "pure" form, characterized by a selective impairment of long-term memory without any disorder of general intelligence or other cognitive functions, has been associated with lesions localized within Papez's circuit and some connected areas. Thus, amnesia could be due to a functional disconnection between components of this or other neural structures involved in long-term learning and retention. To test this hypothesis, we measured regional cerebral metabolism with 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG) and positron emission tomography (PET) in 11 patients with "pure" amnesia. A significant bilateral reduction in metabolism in a number of interconnected cerebral regions (hippocampal formation, thalamus, cingulate gyrus, and frontal basal cortex) was found in the amnesic patients in comparison with normal controls. The metabolic impairment did not correspond to alterations in structural anatomy as assessed by magnetic resonance imaging (MRI). These results are the first in vivo evidence for the role of a functional network as a basis of human memory.

Fazio, F., Perani, D., Gilardi, M., Colombo, F., Cappa, S., Vallar, G., et al. (1992). Metabolic impairment in human amnesia: a PET study of memory networks. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 12(3), 353-358 [10.1038/jcbfm.1992.52].

Metabolic impairment in human amnesia: a PET study of memory networks

FAZIO, FERRUCCIO;GILARDI, MARIA CARLA;VALLAR, GIUSEPPE;PAULESU, ERALDO;
1992

Abstract

Human amnesia is a clinical syndrome exhibiting the failure to recall past events and to learn new information. Its "pure" form, characterized by a selective impairment of long-term memory without any disorder of general intelligence or other cognitive functions, has been associated with lesions localized within Papez's circuit and some connected areas. Thus, amnesia could be due to a functional disconnection between components of this or other neural structures involved in long-term learning and retention. To test this hypothesis, we measured regional cerebral metabolism with 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG) and positron emission tomography (PET) in 11 patients with "pure" amnesia. A significant bilateral reduction in metabolism in a number of interconnected cerebral regions (hippocampal formation, thalamus, cingulate gyrus, and frontal basal cortex) was found in the amnesic patients in comparison with normal controls. The metabolic impairment did not correspond to alterations in structural anatomy as assessed by magnetic resonance imaging (MRI). These results are the first in vivo evidence for the role of a functional network as a basis of human memory.
Articolo in rivista - Articolo scientifico
PET, PET study of memory
English
1992
12
3
353
358
none
Fazio, F., Perani, D., Gilardi, M., Colombo, F., Cappa, S., Vallar, G., et al. (1992). Metabolic impairment in human amnesia: a PET study of memory networks. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 12(3), 353-358 [10.1038/jcbfm.1992.52].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/16780
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