Luria on Memory

Working Brain c 11 p 280

Luria laments the lack of effective work on memory processes up to 1960 or so when RNA was linked to memory. Specifically RNA traces remain high in glia for a long time after learning. Luria asks which brain zones contribute to memory, what are the architectonics of memory, and what is the structure of mnestic activity.



Luria cites literature (p283) that learning starts with the imprinting of sensory cues (eg. phonetic). Imprinting is selective, narrow in scope, and short, may be expandable in case of visual memory. The next intermediate step is the conversion of images to a a storable code or category. They are coded with respect to different signs and form multidimensional matrices from which the subject must choose. The process for retrieval is active, not passive. The subject uses language, that helps transfer from short to long term memory (cites Miller, 1969). He then asks what causes forgetting? Mere extinction or decay of traces is countered by idea of "reminiscences" which involve the enhancement of the traces. Then the ideas of proactive and retroactive inhibition became accepted as ideas, the idea being that forgetting is largely the regulator function of irrelevant, interfering actions that inhibit normal recall of traces. Luria cites Soviets Vygotsky and Le'ontiev as noting that recall is usually indirect and accomplished throught the use of "aids." Le'ontiev described it with respect to children's development. Motives and tasks direct what is to be recalled, and coding and categorizations increase the amount that can be recalled. Memory (optimized) requires optimal cortical tone, or vigilance, and intention, and integrity of the highest secondary or tertiary zones.

Which brain zones? Bekhterev (1900, hippocampus) and Grunthal (1939, mammillary bodies) preceded Scoville and Milner. Luria states the hippocampus is a modality independent structure of the archicortex that modulates cortical tone but compare stimuli to traces of past experience, react to changed stimuli and are therefore both "attention" and "memory"
neurons. Luria repeats that patients with pituitary tumors affecting these zones have mild memory disorders. Hippocampal memory disorders are characterized by modality nonspecificity, by primary defect of trace retention (and ability sometimes to compensate by writing down), and disturbances of consciousness.

Experimentally, subjects can repeat 5-6 words and retain it for 1-2 minutes unless there is interfering activity. Luria concludes pathological increased mutual inhibition of traces is the basic physiological factor in primary disturbance of memory observed in deep brain lesions.

Tests" Haptic fixed set illusion -- a patient with a memory disorder is given a large ball to touch with his right hand, and a small ball with his left hand, then given two balls of equal size so the one on the left appears large (fixed set illusion). Interference erases the traces of the illusion. Similarly, if an object is given and then a second object given for comparison, interference will prevent identification of same or different.

Modality specific memory loss
temporal lobe leads to acoustico-mnestic aphasia. Again Luria attributes this to increased inhibition of traces, or emergence of strong and weak traces without selection. He also calls this the "levelling of excitation of the traces."
Frontal lobes again leads to disturbance of intentions, plans, programs, and regulation. The patients are unable to use "aids" to memorize.