According to the model – Deja Vu/Jamais Vu

Deja Vu is the sensation that an experience is familiar despite it being novel.

Jamais Vu is the sensation that an experience is unfamiliar despite prior experience.

Both of these experiences are common around “puberty”, “psychotic episodes”, and in “dementia”.

Under the model, these are physiological artifacts of a “bad” dorsal/ventral map bind.

We should be able to induce either of these artifacts by manipulating methylation rates in the rhinal cortexes, particularly manipulations of the perirhinal cortex and parahippocampal cortex. The effect itself should be evident in entorhinal cortex astrocyte activation patterns.

Jamais Vu is an artifact of overweight dorsal/underweight ventral stream binding. It’s the experience of inadequate/”inappropriate” ventral context binding to the scene map, which is dumped leaving a “contextless” stream until enough new stimuli is acquired to correct the map/association.

Deja Vu is an artifact of the opposite mechanics, a high strength “context” bind being written on top of whatever stimuli is available.

We can expand this understanding to provide solutions for some traits of “depersonalization/derealization”, which are represented by the suppression of ventral context as a whole, and are experienced as a sense of persistent “unfamiliarity”.

The “anxiety” which accompanies these experiences is an artifact of the nervous system in a high activation state, attempting to correct the stream activation imbalance/issue.

Edit: We might even be able to lump stuff like “impostor syndrome” and “narcissism” into this mechanic.

Allocentric information represented by self-referenced spatial coding in the primate medial temporal lobe

Hippocampal spatial view cells for memory and navigation, and their underlying connectivity in humans

Spatial coordinate transforms linking the allocentric hippocampal and egocentric parietal primate brain systems for memory, action in space, and navigation

Forward Processing of Object–Location Association from the Ventral Stream to Medial Temporal Lobe in Nonhuman Primates

Integration of allocentric and egocentric visual information in a convolutional/multilayer perceptron network model of goal-directed gaze shifts – Mostly no, but some important yeses.

Normal and Abnormal Sharp Wave Ripples in the Hippocampal-Entorhinal Cortex System: Implications for Memory Consolidation, Alzheimer’s Disease, and Temporal Lobe Epilepsy

Are Grid-Like Representations a Component of All Perception and Cognition? – Yes, at the top level. Maps.

Excitatory-inhibitory recurrent dynamics produce robust visual grids and stable attractors – They still don’t love you like I love you.

Impaired cognitive performance in older adults is associated with deficits in item memory and memory for object features – Yep.

Aging and Alzheimer’s Disease Have Dissociable Effects on Medial Temporal Lobe Connectivity (Pre-Print)

Infusing zeta inhibitory peptide into the perirhinal cortex of rats abolishes long-term object recognition memory without affecting novel object location recognition

Neural distinctiveness and reinstatement of hippocampal representations support unitization for associations

Entorhinal grid-like codes and time-locked network dynamics track others navigating through space – It’s important to understand that dorsal “object” and ventral “context” are discrete networks which are integrated both at the map level and at the engram level in cortical areas.

Differences in structural MRI and diffusion tensor imaging underlie visuomotor performance declines in older adults with an increased risk for Alzheimer’s disease – As the underlying networks become less “specific” in matching dorsal and ventral activity, prediction accuracy collapses.