Vibration white finger or hand-arm vibration syndrome is the episodic
blanching of the fingers in response to cold occurring in those who wo
rk with hand held vibrating tools. Clinically the condition differs fr
om primary Raynaud's phenomenon as persistent paraesthesiae and pain a
re common in the hands and arms and these occur independently from the
'white attacks'. Symptoms can become severe enough to warrant a chang
e of occupation. Industrial compensation may be awarded for vibration
white finger but, at present, no simple or reliable objective diagnost
ic test is available. Calcitonin gene-related peptide (CGRP) is a neur
opeptide with powerful vasodilator properties. A deficiency of immunor
eactive CGRP nerve fibres has been previously demonstrated in the digi
tal cutaneous microvasculature of patients with primary and secondary
Raynaud's phenomenon with the distribution and quantity of other types
of nerve fibres not being significantly altered. To determine if the
innervation of the cutaneous microvasculature in vibration white finge
r was also abnormal skin biopsy samples from the fingers of 15 patient
s with vibration white finger, six healthy age matched controls who wo
rked with vibrating machinery and 26 healthy age matched controls who
were heavy manual workers without exposure to vibrating machinery were
examined by immunohistochemistry. To try to correlate any histologica
l abnormalities with clinical neurological deficit sensory nerve condu
ction studies have so far been performed in six patients with vibratio
n white finger. There was a significant reduction in both the number o
f CGRP and protein gene product 9.5 (PGP) immunoreactive nerve fibres
in the digital cutaneous biopsies from the patients with vibration whi
te finger when compared to the biopsies from the heavy manual workers
and the healthy workers exposed to vibration. The pattern of the loss
of CGRP immunoreactive nerve fibres was similar to that described prev
iously in Raynaud's phenomenon and may account for the episodic vasosp
asm seen in both conditions. PGP is a constitutive protein of all nerv
es therefore the reduced PGP immunostaining indicates generalized stru
ctural. neuronal damage which could account for the persistent pain an
d paraesthesiae characteristic of vibration white finger. The nerve co
nduction studies revealed sensory nerve action potentials within the l
ow range of normal in five patients with vibration white finger and mi
ld median nerve compression in the remaining patient implying that the
neuronal damage in the patients with vibration white finger is confin
ed mainly to the small unmyelinated nerve fibres. The immunohistochemi
cal findings may provide the basis far a diagnostic test for vibration
white finger.