Small fiber neuropathy (SFN) is a specific type of damage affecting the peripheral nervous system, the network of nerves connecting the brain and spinal cord to the rest of the body. SFN focuses exclusively on the smallest nerve fibers extending throughout the skin and internal organs. This condition is increasingly recognized as a source of chronic pain and complex health issues often overlooked by standard nerve tests. The damage affects tiny nerve endings responsible for transmitting sensations and regulating automatic body functions.
What Small Fiber Neuropathy Is
Small fiber neuropathy is defined by the selective damage or degeneration of the body’s smallest nerve fibers: the thinly myelinated A-delta fibers and the unmyelinated C-fibers. These fibers are present throughout the skin and organs. SFN often spares the large, heavily myelinated nerve fibers that transmit signals for motor function and deep touch. Because standard nerve conduction studies only assess these large nerves, diagnosing SFN requires specialized testing to investigate the function and density of the minute fibers.
The primary function of the small A-delta and C fibers is to convey signals related to pain, temperature, and itch. A-delta fibers are lightly insulated, transmitting faster signals for sharp, acute pain. Unmyelinated C-fibers transmit slower signals for dull, diffuse pain and thermal sensations. C-fibers also regulate involuntary body processes, known as autonomic functions, including heart rate, digestion, and sweating. Damage to these fibers explains the dual nature of SFN symptoms, involving both sensory disturbances and autonomic dysfunction.
Recognizing the Symptoms
The symptoms of small fiber neuropathy are divided into two main categories: sensory and autonomic. Sensory symptoms are the most common presentation and frequently involve neuropathic pain. This pain is often described as a burning, stinging, electric shock, or pins-and-needles sensation.
A characteristic pattern of sensory involvement is the “stocking-glove” distribution, where symptoms begin in the feet and gradually progress up the legs, eventually reaching the hands. Patients may experience allodynia (pain caused by a non-painful stimulus like light touch) or hyperalgesia (increased sensitivity to painful stimuli). In some individuals, the pain can be more generalized or patchy, particularly when related to an immune condition.
Autonomic involvement occurs when the small nerve fibers regulating involuntary processes are affected. Common issues include orthostatic intolerance, a sharp drop in blood pressure upon standing that can cause dizziness or fainting. Other manifestations include abnormal sweating, digestive problems like constipation, dry eyes or mouth, and bladder control issues. Sudomotor dysfunction, or abnormal sweating, is often one of the earliest neurophysiological signs of SFN.
Identifying Potential Causes
The origin of small fiber neuropathy is highly varied, and the cause often remains elusive even after a thorough medical workup. In over half of cases, SFN is classified as “idiopathic,” meaning the underlying cause cannot be identified. When an etiology is found, causes typically fall into metabolic, autoimmune, infectious, or genetic categories.
Metabolic disorders are the most frequently identified cause, with diabetes mellitus and impaired glucose tolerance (pre-diabetes) being the most common culprits. The strong link between blood sugar control and nerve health means a significant percentage of people with diabetes or pre-diabetes may develop SFN. Autoimmune or inflammatory conditions, such as Sjögren’s syndrome, sarcoidosis, and lupus, can trigger SFN by causing the immune system to mistakenly attack the small nerve fibers.
Infectious diseases (including HIV or hepatitis C) and exposure to certain toxins or chemotherapy drugs can also lead to nerve damage. A small percentage of cases are linked to genetic factors, specifically mutations in genes like SCN9A and SCN10A. These genes provide instructions for making sodium channels, and mutations can make the channels overly active, leading to increased pain signaling.
How Doctors Diagnose SFN
The diagnostic process begins with a detailed patient history and physical examination, looking for characteristic sensory and autonomic symptoms. Standard nerve tests, such as electromyography (EMG) and nerve conduction studies (NCS), are usually performed first to rule out damage to larger nerve fibers. A diagnosis of pure SFN is suspected when a patient has clinical symptoms but normal results on these large fiber tests.
The most definitive method for confirming SFN is the epidermal nerve fiber density (ENFD) test, considered the gold standard. This test involves a minimally invasive 3-millimeter punch skin biopsy, usually taken from the lower leg. The tissue sample is analyzed to count the number of small nerve endings present in the outer layer of the skin. A reduced density below the established normal range confirms the diagnosis.
Other specialized tests provide supporting evidence, especially when autonomic symptoms are present. The Quantitative Sudomotor Axon Reflex Test (QSART) assesses the function of small nerve fibers controlling sweating by measuring sweat volume produced in response to a chemical stimulus. Tilt table testing may also evaluate blood pressure and heart rate responses to positional changes, helping to identify autonomic dysfunction.
Treatment and Management Strategies
Management of small fiber neuropathy focuses on two main areas: addressing any identifiable underlying cause and alleviating neuropathic pain. Treating the root cause is the most effective approach for slowing the progression of nerve damage. For example, if SFN is linked to pre-diabetes, strict blood sugar control, weight loss, and lifestyle modifications are recommended to improve symptoms and nerve fiber density.
Since many cases are idiopathic or the underlying condition is not curable, symptom management becomes a primary focus. Medications used to treat neuropathic pain include:
- Anti-seizure drugs (e.g., gabapentin or pregabalin).
- Specific classes of antidepressants (e.g., tricyclics or serotonin-norepinephrine reuptake inhibitors).
These medications work by altering the chemical signals involved in pain transmission.
Topical treatments, such as lidocaine patches or capsaicin cream, can provide localized relief for specific painful areas. Non-pharmacological strategies are also important components of a comprehensive treatment plan. These include physical therapy, massage, and pain management programs. Early diagnosis allows for timely intervention, offering the best chance to manage symptoms effectively and improve quality of life.