Neuronal Theory
Neuronal elements were originally thought to have a role in vitiligo
through catecholamine released from epidermal nerve endings which might
be cytotoxic to melanocytes or by autonomic dysfunction producing
pigment cell destruction [203, 204]. Clinical pointers towards
neural involvement included the distribution along blaschkoid lines in
segmental vitligo, and the occasional observation of a true dermatomal
appearance, e.g. in the trigeminal areas [167, 204].
Ultrastructurally vitiligo skin shows degeneration of fine cutaneous
nerves in 42% of cases, with Schwann cells showing thickened basement
membrane in 75% of instances and axonal damage in a half [203,
205]. Changes in neuropeptides, notably neuropeptide Y, are evident at
the margins of vitiligo patches [205]. This led to the postulation
that neuropeptides, potentially neuropeptide Y, which has effects on the
immune system through receptors located on several immunologically
active cells including T cells, NK cells, dendritic cells, granulocytes,
and macrophages, released from nerve ending release next to melanocytes,
could provoke a local immune reaction and melanocyte destruction [206,
207]. Treg cells, seen as central to melanocyte destruction in
vitiligo, can be induced by vasoactive intestinal polypeptide, and can
alter the Th1/cytotoxic T cell (Tc)1 balance that is skewed in vitiligo
[208]. Hence, the neural and neuro-endocrine systems, neuropeptides
and neurotransmitters, interacting with the immune systems, need to be
taken into account in the
causation of vitiligo [209].