Compensatory Hyperhidrosis

Hyperhidrosis or excessive sweating may occur from abnormalities anywhere along the pathway involved with sweat control, namely brain, spinal cord, peripheral nerves or the glands themselves.  Furthermore, any process which raises body temperature, increases body metabolism, or acts on the hypothalamus thermoregulatory sensor may lead to increase in sweating.  The commonest such condition is hyperthyroidism/thyrotoxicosis, with another important condition to exclude being a phaeochromocytoma.  Nocturnal sweats are also a classic symptom of lymphomas and PUOs (pyrexia of unknown origin) being a much loved detective hunt of infectious diseases specialists, although chronic inflammatory conditions and other cancers are also responsible for a significant number of PUOs, as well as the exotic infections. Classic infections as a cause of excessive sweating include tuberculosis, characteristically causing night sweats.

When nerves become more sensitive, such as through changes in the extracellular milieu (for example, raised potassium levels), mechanostimulation, or other nerve damage, one may experience increased sweating.

Quite often during a peripheral neuropathy, particularly if the cause is an underlying toxin such as thallium, arsenic, or acrylamide poisoning, as well as certain metabolic conditions, in particular diabetes, the condition may manifest with increased sweating in the extremities along with dysesthesias (most typically burning pains) and the feeling of coldness.  Similarly, a nerve root or plexus irritative lesion may lead to hyperhidrosis in the area supplied by the nerve, with progression of the lesion then leading to decreased sweating in this area with surrounding compensatory excessive sweating.

Hyperhidrosis can be divided into generalized and focal hyperhidrosis depending on whether the entire body or just one particular region is affected.  Generalized hyperhidrosis may be caused by:

  1. Infections.
  2. Endocrine abnormalities - hyperthyroidism, diabetes, pheochromocytoma, menopause and pregnancy, carcinoid syndrome, acromegaly.
  3. Neurological disorders, particularly those involving the autonomic system such as Parkinson's.
  4. Malignancies.
  5. Medications.
  6. Intoxication.
  7. Drug withdrawal.

The commonest age for focal hyperhidrosis to develop is in puberty, typically in otherwise healthy people.  Approximately 50% have a positive family history.  The axillae are the most commonly affected site, followed by feet, hands and the face.  The sweat glands themselves are normal in hyperhidrosis, but the autonomic nervous system is overactive.

Focal hyperhidrosis characteristically does not occur during sleep, in contrast to generalized hyperhidrosis which is usually present during both wake and sleep.

Step one with palmar and plantar hyperhidrosis is prescription strength antiperspirant.  If botulinum toxin is used, euhidrosis may last as long as a year.

Secondary focal hyperhidrosis may result from either peripheral or central nervous system dysfunction.  For example, during the early stages of acquired polyneuropathy affecting small fibers, sweating may be increased, later becoming decreased as nerve damage progresses.  In complex regional pain syndrome (CRPS) hyperhidrosis may be found in the affected area.

With destructive central nervous system lesions, such as infarcts (strokes) or haemorrhages, decreased cortical inhibition results in contralateral increased sweating.  In contrast, with spinal lesions sweating is decreased ipsilaterally.  Compensatory hyperhidrosis may then develop in other body parts.

Venlafaxine, an SNRI, whilst actually utilized at a low dose for menopausal flushing (37.5mg od or bd), has also been reported as causing excessive sweating in some.