12/02/2019    Allen Jacobs, DPM

ANS and Sudomotor Testing (Carol Moore, DPM)

The question of evaluating the diabetic patient
for manifestations of autonomic neuropathy is an
important one, whether by ANS testing, other
technologies, or by history or clinical
examination. In my opinion, investigation of the
diabetic patient for the presence of autonomic
neuropathy is largely not performed.

In the lower extremity, manifestations of
autonomic neuropathy include neuropathic edema,
sudomotor deficits ( xerosis, dry skin),
vasomotor instability, vascular calcification,
or an increased predisposition to Charcot’s
joint disease.

Importantly, peripheral autonomic neuropathy has
been demonstrated to be associated with cardiac
autonomic neuropathy ( exercise intolerance,
left ventricular disease, silent myocardial
infarction ), and orthostatic hypotension. More
generalized manifestations include a vast array
of clinical syndromes, such as erectile
dysfunction, neurogenic bladder,
gastrointestinal motility problems, post-
gustatory upper body hyperhidrosis.

Small fiber neuropathy is frequently the first
manifestation of diabetic neuropathy. This is
the argument advanced for performing epidermal
nerve fiber density testing or cutaneous sweat
gland testing in preference to nerve conduction
studies, which demonstrate large fiber
neuropathy and may be normal in patients with
small fiber neuropathy. The smallest least
myelinated nerve fibers are those of the
peripheral autonomic nerves.

We have all heard the phrase “ save a limb, save
of life “. The association of peripheral
manifestations of autonomic neuropathy with more
global disease may result in a more generalized
search for other manifestations of autonomic
neuropathy, such as previously unsuspected
cardiac disorders. It can indeed be life saving.
It is analogous to the association of PAD with
cardiac, cerebral, or renal vascular disease.

There are many publications in legitimate peer-
reviewed journals which demonstrate that a
variety of supplemental therapies, such as alpha
lipoic acid, vitamin B complexes, or L-
carnitine, can improve autonomic neuropathy.
Sudomotor problems may also be treated with
appropriate emollient or other topical therapies
to prevent secondary complicating problems such
as fissuring, tinea pedis, cutaneous infection.

While the diagnosis and treatment of sensory
neuropathy is important, so too is the
evaluation of the diabetic patient for
manifestations of autonomic ( and motor )
neuropathy. I fear this has been largely ignored
by many in daily clinical practice.

Allen Jacobs, DPM, St. Louis, MO

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