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Pathophysiology of Excessive Sweating
Sweat glands in patients with hyperhidrosis are not histopathologically
different from those in normal patients, nor is there an increase
in the number or size of glands. The condition is caused by hyperfunction
of the sweat glands rather than hypertrophy.[51]
Patients with primary hyperhidrosis have a higher-than-normal
basal level of sweat production as well as an increased response
to normal stimuli such as emotional or physical stress.[9]
There is evidence that these patients have a reduced threshold
for emotional sweating but have normal thermoregulatory and
drug-induced sweating.[57]
Other clinicians report that patients may be hyperreactive
to thermal stimuli.[2]
Although emotional stimuli are involved in primary hyperhidrosis,
Stolman observes that it is a physiologic disorder as opposed
to a psychological disease, noting the occasional onset of
hyperhidrosis in the neonatal period as further evidence.[134]
One of the underlying mechanisms for a lowered threshold
and exaggerated response in hyperhidrosis patients may be
excessive sympathetic activity. Patients with palmoplantar
hyperhidrosis showed less reflex bradycardia in response to
Valsalva maneuver or facial immersion than healthy controls
but a higher degree of vasoconstriction in response to finger
immersion in cold water.[119]
This study suggested that increased sympathetic activity through
the T2-T3 ganglia causes palmar hyperhidrosis.
There is a vicious cycle that can occur with excessive palmar
and plantar sweating—the evaporative cooling of the
skin increases sympathetic outflow through reflex action,
in turn increasing sweat output.[119]
A recent study of recovery of excitability of the sympathetic
sudomotor skin response in patients with hyperhidrosis and
in normal controls found significant differences. Patients with
hyperhidrosis had enhanced recovery of excitability, implying
a “hyperexcitable somatosympathetic polysynaptic pathway.”[93]
In another study, patients with primary palmoplantar hyperhidrosis
and controls were asked to do mental arithmetic. Those with
hyperhidrosis had markedly increased sympathetic nerve activity
on the soles of the feet compared to controls.[65]
If there is generalized sympathetic overactivity in primary
hyperhidrosis, catecholamine levels in patients could be predicted
to be elevated. However, a study of plasma catecholamine levels
in patients before and after thoracic sympathectomy found
preoperative norepinephrine and epinephrine levels to be normal.
After sympathectomy, the norepinephrine level fell but epinephrine
was unchanged. It was thus concluded that primary hyperhidrosis
is more likely due to sympathetic overactivity in the upper
dorsal ganglia.[104]
Cardiac autonomic response was studied in patients with
primary focal hyperhidrosis and healthy controls using spectral
analysis of heart rate variability.[16]
Interestingly, there were no differences between groups in
the low-frequency band that represents sympathetic cardiac
innervation, but the high-frequency band representative of
parasympathetic innervation did show differences. These results
led the investigators to suggest that primary hyperhidrosis
may involve a more complex dysfunction of the autonomic nervous
system than previously thought, involving parasympathetic
pathway differences as well.
There may be additional mechanisms involved in primary hyperhidrosis.
An EEG and PET scan study of patients with palmoplantar hyperhidrosis
showed increased sharp wave bursts during hyperventilation
and hyperperfusion of the frontal cortex.[119]
In summary, although the exact pathophysiology of primary
hyperhidrosis is yet to be determined, there is much evidence
for abnormalities in autonomic nervous system function. Since
hyperhidrosis often begins in childhood and can be familial,
the physiologic basis for this disorder may be genetically
determined.[113]
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