Psoriatic arthritis (PsA) is a chronic, immune-mediated inflammatory condition that principally targets the joints, tendons, and skin. Peripheral neuropathy (PN) is a condition defined by damage to the peripheral nervous system, which includes all the nerves outside of the brain and spinal cord. Given that both conditions involve inflammation and cause significant pain, patients often ask if one can lead to the other. This article explores the established association between psoriatic arthritis and peripheral neuropathy to clarify the complex relationship between systemic inflammation and nerve health.
The Link Between Psoriatic Arthritis and Neuropathy
Psoriatic arthritis does not typically cause peripheral neuropathy directly, but a clear association exists. This suggests that individuals with PsA have a significantly higher risk of developing nerve problems compared to the general population. One study indicated that patients with PsA may be 18 times more likely to develop polyneuropathy than control subjects, although this is often linked to other contributing factors.
The prevalence of peripheral neuropathy symptoms, often described as neuropathic pain, is high in PsA patients, with reported incidence rates ranging from 9% to 49%. This suggests that the chronic, systemic nature of PsA extends its influence beyond the musculoskeletal system to affect neurological health.
The link is considered indirect; PsA creates an environment conducive to nerve damage rather than triggering a direct autoimmune attack. Many PsA patients with neuropathy also have other conditions, such as diabetes or hypertension, which are known causes of nerve damage. However, a strong association remains even after excluding these contributory causes, suggesting that inflammation from PsA itself plays a role by disrupting the health and function of peripheral nerves.
How Systemic Inflammation Impacts Nerve Health
The core mechanism linking psoriatic arthritis and peripheral neuropathy involves the chronic, high levels of systemic inflammation characteristic of PsA. This inflammation generates an environment rich in pro-inflammatory substances that can directly or indirectly injure nerve fibers. The resulting nerve damage is often categorized into three main pathways: direct inflammatory attack, vascular compromise, and physical nerve compression.
Chronic systemic inflammation leads to the overproduction of neurotoxic signaling proteins, or cytokines. Pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α) and various interleukins, including IL-17A, are central to PsA pathogenesis and can directly injure small nerve fibers. This chemical assault can lead to small fiber neuropathy (SFN), involving the destruction of fibers responsible for pain and temperature sensation. Symptoms are often described as burning, prickling, or stinging sensations, sometimes starting in the feet.
Another mechanism involves vasculitis, which is damage to the small blood vessels that supply oxygen and nutrients to the nerves. Inflammation associated with PsA can cause vasculitis, leading to the occlusion of these vessels and subsequent ischemia, or reduced blood flow, in the nerve tissue. This lack of oxygen and nutrients can cause nerve damage, often resulting in a painful, asymmetric form of neuropathy known as mononeuropathy multiplex.
Finally, localized joint and tendon inflammation can cause mechanical compression, leading to entrapment neuropathies. Swelling, thickening of the synovium, or tenosynovitis near joints can physically constrict adjacent nerves. Carpal tunnel syndrome, involving compression of the median nerve in the wrist, is the most frequently detected type of neuropathy in PsA patients. This type of neuropathy is a direct physical consequence of the arthritic process, unlike systemic damage caused by circulating cytokines.
Identifying Symptoms and Confirming Diagnosis
Recognizing the symptoms of peripheral neuropathy in a PsA patient is the first step toward diagnosis, as they can sometimes be mistakenly attributed to joint pain. Patients typically report positive sensory symptoms, such as burning, tingling, or a pins-and-needles feeling, often starting in the hands and feet. In cases where large nerve fibers are involved, patients may experience negative sensory symptoms like numbness, loss of balance, or muscle weakness.
To confirm a diagnosis, clinicians usually begin with a comprehensive clinical evaluation, including a detailed patient history and physical examination. Tools like the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) pain scale can be used to screen for neuropathic pain characteristics. This initial assessment helps distinguish nerve pain from typical inflammatory or mechanical joint pain.
Electrophysiological testing, including nerve conduction studies (NCS) and electromyography (EMG), is often performed to assess the function of the larger, myelinated nerve fibers. NCS measures how quickly electrical signals travel along the nerves, helping to identify large fiber damage. However, these studies are often normal in cases of small fiber neuropathy, which necessitates specialized testing.
For suspected small fiber neuropathy, a skin biopsy is the definitive diagnostic tool. This procedure involves taking a small sample of skin to microscopically examine the density of nerve endings. Blood tests are routinely used to exclude other common causes of neuropathy, such as Vitamin B12 deficiency, thyroid dysfunction, or undiagnosed diabetes, ensuring the correct underlying cause is identified.
Treatment Approaches for Nerve Pain
Managing nerve pain associated with psoriatic arthritis requires a dual strategy that addresses both the underlying inflammatory disease and the specific neurological symptoms. The most foundational treatment for reducing the risk and progression of neuropathy is achieving tight control over the PsA itself. This involves the use of Disease-Modifying Antirheumatic Drugs (DMARDs), including conventional agents and newer biologic therapies that target inflammatory pathways.
Biologics, such as TNF-alpha inhibitors and IL-17A inhibitors, neutralize pro-inflammatory cytokines that damage nerve tissue. Suppressing systemic inflammation reduces the neurotoxic environment and may prevent nerve damage from worsening. Effective PsA management also reduces joint swelling, which alleviates mechanical compression on entrapped nerves.
For symptomatic relief of existing nerve pain, medications specifically designed to quiet overactive nerve signals are used. These typically include anti-seizure medications, such as gabapentin or pregabalin, and specific types of antidepressants, which interfere with how the central nervous system processes pain. Topical treatments, such as capsaicin creams, can also be applied locally to desensitize pain receptors in the skin.
Physical therapy is another important component, especially for entrapment neuropathies and motor symptoms. Therapists can use techniques like transcutaneous electrical nerve stimulation (TENS) and recommend exercises to strengthen muscles and improve mobility. For mechanical compressions like carpal tunnel syndrome, splinting or, in some cases, surgery may be necessary to relieve the physical pressure on the nerve.