[Memory: clinico-pathologic data]

Synaptic modifications are probably the basis of the memory processes that take place in the central nervous system. They have been studied in Aplysia or in hippocampal slices. How these minute alterations of the synaptic strength are integrated in larger neural systems is still poorly understood. In man, hippocampal lesions, when bilateral, cause a deficit in anterograde episodic memory. The loss of previously acquired memories (retrograde amnesia) is limited. Procedural memory is spared. Young patients with hippocampal lesions remain able to learn how to read or to write (abilities that belong to semantic memories). Recordings obtained with intracerebral electrodes have shown that some neurons of the hippocampus act as "place cells". They fire when the animal is in a specific place of the experimental maze, an observation that suggests that the hippocampus acts as a map that may also be viewed as a context indicator (a "cognitive map"). Computer models have been devised to test the hypothesis that the hippocampus recorded the map of the activated synapses at a particular moment in time. This pattern of activity could secondarily be transferred to the isocortex during a process known as consolidation. The frontal lobe plays a role in attention, which greatly influences the memory process. It also plays a role in the various strategies that are used to recall a memory and in the analysis of the quality of the recall (metamemory). An asymmetry has been shown by the PET-scan: the left frontal lobe is activated during acquisition, and the right one during recall. The ability to integrate one's own memories in one's own history and consciousness (self-awareness or "autonoesis") also depends on the activity of the prefrontal region. The loss of acquired memories (retrograde amnesia) is most often observed in cases of large lesions of the anterior part of the temporal lobe. Partial amnesias are difficult to separate from possibly localized deficits of a cognitive function (some types of aphasia may be considered as an amnesia of words). Subcortical amnesias are caused by diencephalic lesions; the topography of the critical structures is still discussed: mamillary bodies and mamillo-thalamic tract or dorsomedial nucleus of the thalamus. The amygdaloid nucleus, the frontal lobe and the dorsomedial nucleus of the thalamus belong to a network of connections that could be involved in emotions. It could be responsible for the emotional flavor of a memory. Basal ganglia could play a role in procedural memory, but experimental or clinicopathological confirmations are still scarce. Finally, the involvement of the cholinergic innervation in the memory processes has been discussed: it could be direct, or according to more recent data, related to its role in attention.