Vitiligo is a common acquired skin disorder characterized by the loss of pigment, resulting in well-defined white patches on the skin. This depigmentation occurs because the body’s pigment-producing cells, called melanocytes, are destroyed or stop functioning. The condition is not contagious and affects people of all skin types equally, though it is more noticeable in individuals with darker skin tones. Vitiligo is categorized into two primary forms—segmental vitiligo (SV) and non-segmental vitiligo (NSV)—which differ significantly in presentation, underlying causes, disease course, and response to therapy. Understanding these distinctions is important for guiding effective management strategies.
Distinctive Patterns and Distribution
The most immediate difference between the two forms lies in the location and arrangement of the depigmented patches across the body. Non-segmental vitiligo (NSV), which accounts for approximately 85% to 95% of all cases, is defined by its bilateral and symmetrical distribution. This means that if a patch appears on one side of the body, a similar patch often appears in a mirror-image location on the opposite side, such as on both hands or both knees. NSV frequently affects the extremities, areas around body openings (periorificial areas), and sites prone to friction or trauma (the Koebner phenomenon).
Segmental vitiligo (SV) is characterized by its unilateral and localized pattern, typically affecting only one side of the body. The patches often appear to follow the path of a single spinal nerve (dermatome), and this localized arrangement means the depigmentation rarely crosses the midline of the body. SV is a less common form of vitiligo and is more frequently observed with an onset during childhood or adolescence.
Underlying Mechanisms: Autoimmune vs. Neurological
The distinct distribution patterns of the two types are rooted in fundamentally different biological mechanisms driving the loss of melanocytes. Non-segmental vitiligo is an autoimmune disorder, where the body’s immune system mistakenly targets and destroys its own melanocytes. Specifically, cytotoxic T lymphocytes infiltrate the skin and release chemicals that kill the pigment cells, indicating a systemic error in immune regulation. This theory is supported by the fact that NSV is often associated with other autoimmune conditions, such as autoimmune thyroid disease, type 1 diabetes, and pernicious anemia.
The cause of segmental vitiligo is non-autoimmune and is linked instead to the nervous system. This suggests a neurological origin, where localized dysfunction in the sympathetic nerves causes the release of neurochemicals toxic to melanocytes in that specific skin segment. These chemicals, such as neuropeptides, may cause oxidative stress and local inflammation, leading to the destruction of pigment cells along the affected nerve pathway. While genetic factors are involved in both types, the predisposition for SV appears distinct from the systemic immune genes implicated in NSV.
Progression and Long-Term Stability
The behavior of the disease over time provides a clear contrast between the two vitiligo types. Segmental vitiligo usually has a rapid onset, with patches spreading quickly over a period of six months to two years. Once this initial period of activity ends, the depigmentation generally stabilizes and rarely spreads further, offering a predictable and self-limiting course. This stability is a defining feature of SV, making recurrence of the original lesion unlikely.
Non-segmental vitiligo, in contrast, follows a more unpredictable and potentially lifelong course. It is characterized by cycles of activity, where new patches appear or existing patches enlarge, interspersed with periods of stability. This progressive nature means the condition can spread over many years, potentially covering large areas of the skin surface and remaining prone to reactivation throughout a person’s life.
Differential Treatment Approaches
The underlying mechanisms and stability profile of each form dictate different approaches to treatment. For non-segmental vitiligo, the goal is to halt the systemic autoimmune attack and encourage repigmentation across widespread areas. Medical therapies are the mainstay, including topical corticosteroids and calcineurin inhibitors, which suppress the localized immune response. For more extensive or active disease, phototherapy, such as narrowband ultraviolet B (NB-UVB) light, is commonly used to stimulate melanocyte growth over larger body surfaces.
Segmental vitiligo often shows a limited response to conventional medical treatments because its cause is not primarily autoimmune. Due to the disease’s localized nature and tendency to achieve long-term stability, surgical intervention is often the preferred route once the patches have been inactive for a period, typically six to twelve months. Surgical options, like autologous skin grafts or melanocyte-keratinocyte cellular suspension transplants, involve moving healthy pigment cells from a pigmented area of the skin to the stable white patch to restore color.