The irrational fear
that characterizes phobias may have been conditioned in the
individuals concerned without their having any conscious
memories associated with it. One explanation offered for
this phenomenon is that the circuits of the amygdala mature
before the circuits in the hippocampus that are responsible
for conscious memory. An implicit emotional memory could
thus become established without any explicit memory's being
associated with it.
The circuits of the
amygdala receive information about the functional
status of the body's various internal organs. The amygdala
may then relate the pieces of information about the various
organs to one another by amplifying the effects of the sympathetic
nervous system through its efferent pathways. A person
might perceive this activation of his sympathetic nervous
system consciously and then have an explicit
memory that these physical symptoms represent the onset
of a panic
attack. Knowing that a panic attack was coming would
make this person even more anxious, thus setting the vicious
cycle of the panic attack in motion.
|THE TRACES OF ANXIETY
IN THE CIRCUITS OF THE AMYGDALA
Though the amygdala appears to play
a central role in all anxiety disorders, some studies seem to
indicate that conditioned fears and generalized anxiety disorder
involve different circuits in the amygdaloid nuclei.
|In the case of conditioned
fears, the circuits involved appear to be located in the lateral
nucleus and the central nucleus of
the amygdala. Consequently, these neural pathways are believed
to play an important role in those anxiety disorders, such
as phobias, that involve specific stimuli.
In contrast, non-specific anxiogenic signals appear to be handled
by a neighbouring region, the bed nucleus of the stria terminalis.
Thus this nucleus would be associated with anxiety disorders
of more diffuse origin, such as generalized anxiety disorder
or panic disorders (see sidebar).
If these observations are confirmed, they
could open up interesting possibilities for new treatments, because
if there are any biochemical differences between these two nuclei
(for instance, in their receptors or neurotransmitters), researchers
might be able to design anxiolytic medications that were more specific
to and effective for each of them.
The specific pathways emerging from the amygdala, as well as those
entering it, have already been targeted by psychoactive medications
such as the benzodiazepines (Valium,
etc). These substances reduce the symptoms of many anxiety disorders
the natural inhibiting effect of certain neurons (GABAergic
neurons, for example). The potentiated effect of these neurons
raises the threshold for triggering anxiety, so that stimuli that
would normally be anxiogenic will no longer produce the negative
emotional responses usually associated with them.
It is thought that anxiolytic
medications may also reduce anxiety by acting on the hippocampus,
where they would suppress the emergence of anxiety-producing explicit
disorder seems to be associated with a defect in a neural
circuit that runs from the frontal lobe to the central grey
nuclei, then on to the thalamus, and finally back to the
frontal lobe. This defect might be attributable to genetic
factors, or possibly to immunological ones, since obsessive-compulsive
disorder sometimes appears after a streptococcal infection.