INTRODUCTION
A 69-year old woman with a 10-year history of Parkinson's
disease presented with a 3-month history of an
asymptomatic eruption on her legs. Two months prior
to its onset, she started rasagiline as adjunctive therapy for her
Parkinson's disease. Other medications included carbidopalevodopa,
amantadine, sertraline, clonazepam, and Neurontin.
These medications had all been taken by the patient at stable
dosages for over four years. She denied other skin problems,
recent fevers, Raynaud's phenomenon, use of heating pads, or
other excessive exposure to heat. Examination revealed retiform
violaceous patches that blanched under pressure, persisted
with warming, extending from her legs bilaterally to medial
thighs. No vesicles, erosions, ulcers, or nodules were appreciated,
and mucosal surfaces were spared.
A skin biopsy from her thigh demonstrated sparse perivascular
dermatitis with endothelial intimal thickening, consistent
with livedo reticularis (LR). Neither vasculitis nor vasculopathy
was noted. An extensive work-up was performed, including
complete blood count, comprehensive metabolic panel, coagulation
studies, proteins C and S, fibrin split products, lupus
anticoagulant, antiphospholipid antibodies, cryoglobulins,
erythrocyte sedimentation rate, rheumatoid factor, antinuclear
antibodies, cytoplasmic and perinuclear antineutrophilic autoantibodies,
and serum protein electrophoresis, all of which
were unremarkable. As her eruption was asymptomatic, she
decided to continue the rasagiline for her Parkinson's disease,
which remains well controlled.
DISCUSSION
Livedo reticularis is a vasospastic phenomenon of the cutaneous
vasculature, resulting in either increased venous plexus
visibility due to venous dilatation, or localized hypoxia due to
decreased arterial blood flow. These mechanisms can produce
the lacy reddish-blue reticulate pattern seen in LR1 (Figure 1).
Primary LR is a benign phenomenon usually limited to the lower
extremities and exacerbated by exposure to cold. Secondary
LR can be due to underlying illness or medications and may be
diffusely distributed. LR secondary to illness manifests because
of either increased blood viscosity (polycythemia vera) or increased
thickness of arteriole walls (vasculitis).2 The etiology of
medication-associated LR is not entirely understood but may
result from dysregulation of the autonomic regulation of the
superficial vasculature.1
Several drugs have been associated with LR, including pramipexole,
catecholamines, gemcitabine, and quinidine, but
amantidine is the most well known.3 Amantidine was initially
marketed as an antiviral medication but also showed N-methyl-
D-aspartic acid receptor (NMDA) antagonist properties, which
led to its use in Parkinson's disease. Studies have shown a
dose-independent correlation between amantidine use and development
of LR, although the incidence is highly variable.4-6
While the exact mechanism of NMDA antagonists is unknown,
depletion of catecholamine stores in nerve terminals may be
involved. The alteration of catecholamine levels has been proposed
as a possible mechanism for amantadine-induced LR.5,7
