signals that originate largely from subcortical regions (the thalamus,
basal ganglia, and brainstem). Each functional column has a
component at the surface (layers 1–3), so that meningitis effectively
disrupts the function of each column just by damaging the surface
layers of the cortex. The anatomical distribution of inhibitory and
excitatory cells, which have a fairly balanced distribution within the
six layers, does not support this hypothesis. Diffuse meningitis over
the brain’s surface effectively disables the entire neocortex due to this
columnar architecture. Full-thickness destruction is unnecessary for
total functional disruption. Given the prolonged course of my poor
neurological function (seven days) and the severity of my infection, it
is unlikely that even deeper layers of the cortex were still functioning.
- The thalamus, basal ganglia, and brainstem are deeper brain structures
(“subcortical regions”) that some colleagues postulated might have
contributed to the processing of such hyperreal experiences. In fact,
none of those structures could play any such role without having at
least some regions of the neocortex still intact. All agreed in the end
that such subcortical structures alone could not have handled the
intense neural calculations required for such a richly interactive
experiential tapestry.
- A “reboot phenomenon”—a random dump of bizarre disjointed
memories due to old memories in the damaged neocortex, which
might occur on restarting the cortex into consciousness after a
prolonged system-wide failure, as in my diffuse meningitis.
Especially given the intricacies of my elaborate recollections, this
seems most unlikely.
- Unusual memory generation through an archaic visual pathway
through the midbrain, prominently used in birds but only rarely
identifiable in humans. It can be demonstrated in humans who are
cortically blind, due to damaged occipital cortex. It provided no clue
as to the ultra-reality I witnessed, and failed to explain the auditory-
