When the body fails to produce sweat, the condition is medically termed anhidrosis (or hypohidrosis if the reduction is less severe). While excessive sweating (hyperhidrosis) receives attention, a lack of sweat can signal an underlying health issue. Anhidrosis localized to the feet means the sweat glands in that area are not functioning correctly, leading to excessively dry skin. This symptom is a warning sign that the nerve pathways or the sweat glands have been compromised.
The Physiology of Foot Sweat
The soles of the feet possess one of the highest concentrations of eccrine sweat glands, with densities reaching between 250 and 550 glands per square centimeter. These glands produce clear, watery sweat that helps regulate skin moisture and temperature. Unlike most body sweat, which is triggered by rising core temperature, foot sweat often responds to emotional or psychological stress.
The activation of these glands is controlled by the autonomic nervous system’s sympathetic branch. Postganglionic sympathetic nerve fibers release acetylcholine, the primary neurotransmitter, to stimulate sweat production. Disruption to this nerve pathway, the neurotransmitter signal, or the gland structure itself can result in localized foot anhidrosis.
Specific Causes of Localized Foot Anhidrosis
Damage to the small nerve fibers that innervate the sweat glands is the most frequent medical cause of foot anhidrosis. This condition, known as small fiber neuropathy, commonly results from systemic diseases such as diabetes mellitus or chronic alcoholism. Since nerve impairment typically affects the longest nerves first, the feet and lower legs are often the initial sites where function is lost. As these nerves degrade, the signal to produce sweat is lost, leading to dry and inelastic skin.
Physical obstruction or damage to the sweat glands can prevent moisture from reaching the skin’s surface. Localized skin conditions, including severe psoriasis, eczema, or scleroderma, can block the duct or damage the secretory coil of the eccrine gland. Scarring or trauma to the foot can also destroy the gland structures, resulting in a permanent patch of non-sweating skin.
Prescription medications may interfere with the nervous system’s ability to signal the sweat glands. Medications with anticholinergic properties, such as certain antidepressants, antipsychotics, and antispasmodics, block the action of acetylcholine required for sweat gland activation. Other drug classes, including some calcium channel blockers and alpha-adrenergic blockers, have also been implicated in causing secondary anhidrosis.
In rare instances, individuals are born with a genetic predisposition to this condition. Congenital disorders, such as hypohidrotic ectodermal dysplasia, involve the absence or underdevelopment of eccrine sweat glands, leading to anhidrosis from birth. These factors represent a fundamental structural cause where the necessary machinery for sweating is not present.
Diagnosis and Health Implications
The absence of foot sweat has direct consequences for skin health and can signal broader systemic issues. Without the natural moisture provided by sweat, the skin on the feet becomes excessively dry, flaky, and inelastic. This increases the risk of developing thickened skin or deep heel fissures. These cracks serve as entry points for bacteria and fungi, raising the susceptibility to serious infections like cellulitis or athlete’s foot.
When a healthcare provider suspects localized anhidrosis, they perform tests to confirm the diagnosis and identify the cause. A visual examination for dry, cracked skin is the first step, followed by specialized tests to assess nerve function. Diagnostic procedures like the Quantitative Sudomotor Axon Reflex Test (QSART) or a skin biopsy can directly measure the function of the small nerve fibers and sweat glands.
Since anhidrosis is frequently an early symptom of peripheral neuropathy, seeking a professional evaluation is important, especially if dry skin is accompanied by numbness or pain. A podiatrist or physician can assess the condition and guide management, which often involves using urea-based emollients to compensate for the lack of moisture. Addressing the underlying cause, whether a systemic disease or a medication side effect, is the ultimate goal of treatment.