Dermatoses precipitated or perpetuated by
candidates for inclusion in this group of diseases are psoriasis, urticaria,
atopic eczema, pom-pholyx, discoid eczema, alopecia areata, lichen sim-plex and
lichen planus. Fancy rather than fact still rules here, but a scientific basis
for these effects is gradually being established. For example, in psoriasis,
stress increases the neuropeptide content of lesions, with a concomitant drop
in the activity of enzymes that degrade neuropeptides, especially mast-cell chy-mase.
In addition, the blood concentrations of certain neuromediators, especially β-endorphin, changes during
exacerbations. Yet an aura of doubt lingers onafor a variety of reasons. The
concept of stress is not a simple one, and the terms in which it is discussed
are sometimes used rather vaguely. Each type of stress may well provoke its own
pattern of response. For this reason many investigators have preferred to
record damaging life events rather than to speculate about the presence of
stress itself. However, there are problems with this approach too, as a barrage
of minor daily annoyances may well be more important than major life events.
Every dermatologist will have seen apparent examples of associations between
external stress and exacerbations of most of these conditions, but proof that
stress causes them is hard to find. Some studies suggest that even
hyperhidrosis of the palms and soles, once thought to be an accentu-ated
response to stress, has no relationship to chronic anxiety at all. No one questions
that stress can cause sweating of the palms, but some studies suggest that
chronic hyperhidrosis of the palms and soles, once thought to be simply an
accentuated response to stress, has no relationship to chronic anxiety at all.