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Memory can be defined as mental time traveling. Seen in this way, memory provides the glue which combines different time episodes and leads to a coherent view of one’s own person. The importance of time becomes apparent in a neuroscientific comparison of animals and human beings. All kinds of animals have biorhythms — times when they sleep, prefer or avoid sex, or move to warmer places. Mammalian brains have a number of time sensitive structures damage to which alters a subject’s behavior to his or her environment. For human beings, damage to certain brain regions may alter the sense of time and consciousness of time in quite different ways. Furthermore, brain damage, drugs, or psychiatric disturbances may lead to an impaired perception of time, sometimes leading to major positive or negative accelerations in time perception. An impaired time perception alters consciousness and awareness of oneself. A proper synchronized action of time perception, brain activation, memory processing, and autonoetic (self-aware) consciousness provides the bases of an integrated personality.

Despite extensive experimental investigations of human amnesia, the basic nature of this vivid syndrome remains surrounded by controversy. The dynamics of amnesia, the rapid, selective and long-lasting plasticity of hippocampal synapses, and the connections between the hippocampal formation and association neocortex. all suggest that amnesia may result from damage to the medial temporal site where the recent declarative memory trace is temporarily laid down. Alternatively, amnesics' preserved capacity for procedural learning on indirect memory tests suggests that their deficit may rather be in intentional, sustained and directed (i.e., active) encoding/retrieval processes. It has been difficult to distinguish between these possibilities because amnesics are most impaired on direct memory tasks that involve both a new integrative trace and active processes. It is possible that different amnesics may have a relatively greater defect either in the memory trace, or in active memory processes, or both, and these differences could correspond to differences in their anatomical lesions. Specifically, hippocampal formation lesions may disrupt all recent declarative memory traces, whereas brainstem lesions could produce amnesia by impairing modulatory processes essential for encoding/retrieval or for storage. In this model, the different areas of association neocortex with bidirectional hippocampal connections would contribute specificity to encoding/retrieval, with posterior areas encoding the sensory/semantic aspects of events, and prefrontal cortex the ongoing context. Active modulatory processes arising in the brainstem would then function to integrate this extensive declarative memory system. The cognitive correlates and neural substrates of the evoked potentials recorded during declarative memory tasks suggest that they may embody such modulatory processes. Finally, since the prefrontal cortex and the medial temporal lobe appear to control the onset, intensity and duration of the ascending neuromodulation, lesions of these structures may impair aspects of both the trace and of the processes supporting declarative memory. In summary, a model is proposed in which the association neocortex (encoding/retrieval) and hippocampus (trace) are integrated by the brainstem (modulation) to produce the psychological properties of declarative memory.

Memory performance following callosotomy suggests that in normal subjects the hippocampus actively integrates information across the hemispheres (Phelps et al. in press). The present interpretation of hippocampal function from studies on humans with hippocampal lesions suggests that the hippocampus is involved in explicit access to declarative information (Squire & Zola-Morgan 1991). While this description may adequately describe the behavioral outcome of hippocampal lesions in humans, the work on split brain patients implies that the underlying processing of the hippocampus does more than allow conscious access to information. In the present chapter we propose that the hippocampus is necessary for forming relations between multiple cues. We present research from rats, monkeys and humans suggesting this to be the case and point out the similarities in the current theories of “relational” (Eichenbaum et al. 1990) or “configural” (Sutherland & Rudy 1989) processing in animals and “cohering” (Hirst 1988) processing in human amnesia. Finally, we discuss how this approach to hippocampal functioning may account for the behavioral consequences of disconnecting or lesioning the hippocampus in humans and hypothesize as to what mnemonic processes may be unique to humans.

In man, the localized thalamic lesions giving rise to memory disorders have generally a vascular origin (infarcts). They very often affect several nuclei or associated tracts, which makes the pathophysiologic interpretations more difficult. Disorders are furthermore partially regressive with time, in their severity but also in their quality, which explains why some of the classical dissociations in amnesia are only observed at the late stage. Memory disorders are variable according to the lesion site and their uni or bilateral character. The “purest” and most severe amnesia are observed in bilateral injury of the anterior or antero-internal structures, which is much more rare in unilateral ones. Severe deficits in “declarative” learning tasks and in long term memory are then observed, which predominate in free recall. Short-term memory is often deficient at the initial and secondary stages, even when late evaluation may find it to be relatively unimpaired. Retrograde amnesia is frequent, but less severe than anterograde amnesia and the temporal gradient, frequently described by the patients, is difficult to assess with the classical tests (questionnaires). These patients have important and often lasting impairment in the control of time, which would contribute to the explanation of their amnesia (source amnesia). In the case of paramedian and moreover subthalamic extension of the lesions, patients frequently have at the initial stage vigilance disorders and then attention impairment and cognitive slowing. Their short-term memory and retrograde memory disorders could be more severe. One of the other factors which may contribute to the severity of amnesia is the extension of the lesions in the more external structures, dorsomedial and lateral nuclei: patients then present supplementary cognitive disorders in language (left lesions) or treatment of spatial information (right lesions). At the late stage, a memory disorder corresponding to the main initial deficit may persist. This phenomenon, related to the hemispheric specialization, is more easily observed in unilateral lesions. Amnesia could also be more severe in the case of left thalamic injury, and this could be related to the “declarative” character of most of the tests used.