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neurons in the pons (a medullar structure) become active after a period of non-
REM sleep (slow-wave, synchronized sleep).
Sleep paralysis is an evolutionarily old function to keep animals still while
they are sleeping and prevent them falling off cliffs, trees or attracting predators.
Certainly it must have emerged simultaneous with REM dream state to prevent
motor response to dream imagery. The most obvious neurotransmitter agents
to sleep paralysis would be inhibitors GABA and glycine, but it probably more
complex than that. Those that become “aware” of being paralyzed descend to Theta
of hypnogogic states without going through the normal phases that kick in the
loss of consciousness, so they are conscious while paralyzed, usually with amazing
visions to account for their journey. The lucid perception of sleep paralysis can
give one the sensation of compression on the chest and suffocation as energy is
removed from the diaphragm. It is the sympathetic side of the nervous system that
stimulates breathing activity and thereby raises blood oxygen.
Besides Robert Scaers idea of the dorsal vagus complex causing freeze paralysis
another possible cause of paralysis during extreme spiritual energy states could be
the hyperactivation of the limbic system and brainstem and its consequent effects
on incapacitating the motor-sensory cortex. Rhawn Joseph at Brain-mind.com
says that freezing is brought about by both the overload/overwhelm of the motor
and frontal lobes and the consequent burnout of dopamine and serotonin in these
areas. Freezing is a life preserving reaction in nature that is apparently mediated by
the amygdala and striatum. He writes the amygdala under conditions of extreme
fear and arousal, can induce catatonic-like frozen panic states—resulting in a
inability to initiate a voluntary movement, and the “Will” to move or vocalize
maybe completely negated. Given the extensive interconnections of the medial
frontal lobes, corpus and limbic striatum with amygdala, it appears that when
exceedingly aroused or emotionally stressed, the amygdala is able to inhibit (by
over activation) the frontal-striatal motor centers. When this occurs, the organism
may fall and cease to move, blink or even breathe, thus appear to be dead and in a
state of rigor mortis.
Rawl Joseph suggests the numbing during the fear response is caused by a
massive secretion of opiates within the amygdala and basal ganglia, while the
rigidity and loss of Will is a consequence hyper-amygdala influences on the medial
frontal lobe and corpus and limbic striatum. The amygdala is able to induce these
catatonic states, via interconnections with the basal ganglia, brainstem, as well as
the medial frontal lobes. Under extremely stressful conditions the striatal, frontal
lobe and amygdala, are simultaneously undergoing dopamine depletion, which
in turn results in hyperactivation of these areas. In the Eastern traditions there
is a catatonic deathlike state called nirodha “meaning “prior to the arising of
ignorance and volitional impulse.” Like deep Samadhi, Nirodha is a very high
non-meditative meditative state. During Nirodha there is no time sense, heartbeat
and metabolism are slow and practically cease so very little energy is burned, and
body temperature drops well below normal. In fact this spiritual catatonia is so
deathlike that there is the danger of being mistaken as dead and so buried alive. It