Spectrum of gustatory sweating, with especial
reference to its presence in diabetics with
autonomic neuropathy
Michael M. Bronshvag,4
Certain otherwise normal individ-
uals may have an idiosyncratic response to
one or several foods, and the mechanism of
this sensitivity is not known . It may also be
seen after parotid surgery (auriculotemporal
syndrome) (4), cervical sympathectomy
(usually bilateral) (1) and in diabetic neu-
ropathy (2). The common denominator in
these conditions seems to be damage to the
autonomic nervous system.
Less easy to understand is the syndrome
after cervical sympathectomy (usually bilat-
eral) (1). As with the auniculotemporal syn-
drome, the onset occurs weeks to months
after the surgery and apparently does not
correlate with relapse of the surgical condi-
tion. Although anesthetic block or excision
of the stellate ganglion abolishes the gusta-
tory sweating response in “normal” pa-
tients, it does not have a similar effect in
postsympathectomy gustatory sweating.
Sweating is more profuse if there is no
ipsilateral Homer’s syndrome . The distni-
bution of sweating is the face and almost
always the arm, corresponding to the distni-
bution of innervation from the cervical sym-
pathetic ganglia. Although sensitivity to cm-
culating acetylcholine has been postulated
as the mechanism of production of sweating,
injection of cholinergic substances or acetyl-
choline does not reproduce the syndrome,
and ganglionic blocking agents can interrupt
the syndrome, suggesting that the response
is neural rather than humoral. It is now felt
that sprouting of cholinergic fibers into the
area of the surgical lesion is the cause.
Whether the sprouting axons arise from the
thoracic sympathetic ganglia and meander
past the surgical site, or whether they arise
from the vagus nerve is not established.
Diabetic patients with autonomic neurop-
athy may present with a similar syndrome
(2). The similarity of the syndrome in dia-
betes to that occurring in postsurgical pa-
tients makes it most reasonable to assume
that a lesion has occurred in the autonomic
nervous system with subsequent sprouting
between healthy cholinergic axons and dis-
eased ones. A careful study of diabetic
patients manifesting this phenomenon re-
vealed widespread deficits in the sympa-
thetic and parasympathetic nervous systems .
This suggests that
abnormal sprouting and unusual relation-
ships of unmyelinated fibers to Schwann
cells may be the anatomic bases for painful
diabetic neuropathy . In view of this histo-
logical evidence , it seems reasonable to sug-
gest that the mechanism for gustatory sweat-
ing in diabetic patients with autonomic neu-
ropathy is also axonal degeneration with
abnormal sprouting from continguous ax-
ons. Since in gustatory sweating it is pre-
sumed that the stimulus to the sweat glands
originates in the dorsal motor nucleus of
the medulla, and is diverted to sympathetic
cholinergic axons destined for the face and
perhaps the arm, it is likewise plausible that
adrenergic vasomotor impulses from the
cervical sympathetic chain cause the other
less constant parts of these syndromes such
as goose flesh, vasoconstniction, paraesthes-
ias and flushing.
TheAmericanJournalClinicalNutrition31:FEBRUARY 1978, pp. 307-309. Printed in U.S.A.
