173LLINÁS AND RIBARY: CONSCIOUSNESS AND THE BRAIN
Indeed spontaneous magnetoencephalography (MEG) activity from pa-
tients suffering from neurogenic pain, tinnitus, Parkinson’s disease or depression
showed increased low-frequency theta rhythmicity, in conjunction with a widespread
and marked increase of coherence among high- and low-frequency oscillations.
These data indicate the presence of a thalamocortical dysrhythmia which we pro-
pose is responsible for all the above-mentioned conditions. The coherent theta activ-
ity, which results from a resonant interaction between thalamus and cortex, is due to
the generation of low-threshold calcium spike bursts by thalamic cells. The presence
of these bursts is directly related to thalamic cell hyperpolarization brought about by
either excess inhibition or disfacilitation.
The emergence of positive clinical symp-
toms is viewed as resulting from ectopic gamma-band activation, which we refer to
as the “edge effect.” This effect is observable as increased coherence between low-
and high-frequency oscillations, probably resulting from inhibitory asymmetry be-
tween high- and low-frequency thalamocortical modules at the cortical level.
The basic assumption concerning the genesis of this syndrome is that thalamo-
cortical dysrhythmia is a CNS intrinsic property brought about by changes in intrin-
sic voltage-gated ionic conductances at the level of thalamic relay cells, namely the
deinactivation of T channels by cell membrane hyperpolarization.
spike bursts are thus produced and lock the related thalamocortical circuits in low-
frequency resonance. Low-frequency loops interact at the cortical level with high-
frequency ones, giving rise to the edge effect and the generation of a positive symp-
tom. In tinnitus, peripheral neurogenic pain, Parkinson’s disease, and some neuro-
psychiatric disorders with striatal origin, the dysrhythmic mechanism is triggered
“bottom up,” which means from the thalamus toward the cortex. In other situations
like epilepsy, neuropsychiatric conditions of cortical origin, and central cortical neu-
rogenic pain, we may have a “top down” mechanism, triggered by a reduction of the
cortico-thalamic input. Both “bottom up” and “top down” situations result in excess
inhibition or disfacilitation, generating thalamic cell membrane hyperpolarization
and low-frequency oscillation. And so, the same mechanism responsible for the or-
ganization of consciousness, when altered in its organization and timing, can be the
genesis of neuropsychiatric conditions.
Cognition, a property of thalamocortical cycling, appears to function on the basis
of temporal coherence. Such coherence would be embodied by the simultaneity of
neuronal firing based on passive and active dendritic conduction along the apical den-
dritic core conductors. In this fashion, the time-coherent activity of the specific and
nonspecific oscillatory inputs, obtained by summing distal and proximal activity in
given dendritic elements, would enhance de facto 40-Hz cortical coherence by their
multimodal character. And in this way it provides one mechanism for global binding.
The “specific” system would supply the content that relates to the external world, and
the nonspecific system would give rise to the temporal conjunction, or the context (on
the basis of a more interoceptive context concerned with alertness). Together they
would generate a single cognitive experience. Furthermore, when this rhythmicity is
altered in particular fashions, neurological and psychiatric conditions ensue.