Psoriasis is a chronic autoimmune condition that primarily affects the skin, causing thick, scaly, and inflamed patches. Evidence suggests that the chronic inflammation driving psoriasis can extend beyond the skin. This article explores the complex relationship between psoriasis and the peripheral nervous system, investigating how the inflammatory process might contribute to nerve damage and related neurological symptoms.
Psoriasis as a Systemic Inflammatory Condition
Psoriasis is an immune-mediated systemic disease, meaning the underlying inflammation affects the entire body, not just the skin. The immune system mistakenly triggers accelerated skin cell growth, and the inflammatory molecules involved circulate throughout the bloodstream. This systemic nature explains why psoriasis is frequently associated with other health issues, known as comorbidities.
These associated conditions include psoriatic arthritis, which causes joint inflammation, and an increased risk of cardiovascular disease and metabolic syndrome. The nervous system is also vulnerable to this widespread inflammation. This chronic inflammatory state can impact distant tissues, creating the potential for neurological complications.
Identifying Neuropathic Symptoms Associated with Psoriasis
When psoriasis-related inflammation affects the peripheral nerves, patients may experience peripheral neuropathy. Symptoms often include altered sensations, typically beginning symmetrically in the hands and feet. People often describe numbness, prickling, or a “pins-and-needles” sensation, medically termed paresthesia.
Other common complaints include dysesthesia, a distorted sense of touch, or neuropathic pain characterized by shooting, stabbing, or burning sensations. These neuropathic symptoms represent true nerve fiber damage. They are felt in areas where no visible skin lesions may be present, distinguishing them from the intense itching (pruritus) associated with skin plaques.
Inflammatory Pathways Linking Skin and Nerve Health
The mechanism linking skin inflammation to nerve damage centers on the excessive production of pro-inflammatory signaling molecules called cytokines. Three specific cytokines—Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-17 (IL-17), and Interleukin-23 (IL-23)—are significantly elevated in patients with moderate to severe psoriasis. These molecules, which drive skin inflammation, do not remain confined to the skin.
Once circulating in the body, these cytokines can cross the protective barriers surrounding nerves, leading to neuroinflammation. High concentrations of TNF-alpha can bind to receptors on neurons and glial cells, triggering cascades that result in cell damage and apoptosis, or programmed cell death. This inflammatory assault can lead to structural damage in the nerve fibers.
Specific damage patterns observed include demyelination (stripping away the protective sheath around the nerve axon) and axonopathy (direct loss of the nerve fiber itself). The resulting structural damage sensitizes the peripheral nerves. This sensitization causes nociceptors, the nerve endings responsible for sensing pain, to become hyper-responsive, resulting in chronic neuropathic pain symptoms.
Clinical Assessment and Treatment of Nerve Involvement
Diagnosing nerve involvement typically begins with a physical examination to assess sensory and motor function in the extremities. If neuropathy is suspected, clinicians use specific diagnostic tools to confirm the presence and type of nerve damage. Nerve conduction studies (NCS) measure the speed and strength of electrical signals traveling through the nerves.
NCS helps distinguish between demyelination (damage to the myelin sheath) and axonopathy (damage to the axon itself). Electromyography (EMG) is often performed alongside NCS to evaluate the electrical activity of muscles. This provides information about how well the nerves are communicating with the muscles.
The primary treatment strategy for psoriasis-related nerve damage is to aggressively manage the systemic inflammation. Targeted therapies, particularly biologic medications that inhibit TNF-alpha, IL-17, or IL-23, suppress the high levels of circulating cytokines. Reducing this inflammatory load can mitigate ongoing nerve damage and may prevent the progression of neuropathy. For severe symptoms, specific medications for neuropathic pain may be prescribed to manage shooting or burning sensations while the underlying psoriasis is controlled.