Saturday, February 03, 2007

Livedo reticularis and neurologic disease

Kraemer M et al. Differential diagnosis in Neurological Patients with livedo reticularis and livedo racemosa. J Neurol 2005;252:1155-1166

review article. LRET is physiological and reversible with warming. LRAC is always pathological. LRET is induced by cold and certain drugs including amantadine, quinine and quinidine. LRAC has a slightly different morphology with irregular and broken segments, sometimes in a "starburst" pattern, whereas LRET is regular. Semantically, LRAC is identical to "symptomatic" LRET. LRAC is caused by obstructive disorders of the veins or viscosity changes in the blood. It is essentially "watershed ischemia" due to stagnation of flow in border zones between adjacent arterioles. LRAC occurs in Sneddon's syndrome and may precede ischemic strokes and be associated with apl antibodies. Diagnosis is by skin biopsy that shows proliferative non-vaculitic occlusion of the small arterioles (which is also seen in brain tissue in Sneddon's syndrome).

LRAC is most common in lupus and PAN, and following cholesterol embolization (CE) which is usually a complication of angiography, and which also can cause stroke. In CE, LRAC only occurs when the patient is standing. LRAC also is seen in essential thrombocythemia, DIC, and atrial myxoma.

1 comment:

Neurodoc said...

from NEJM 2009 Case Records 5 ddx of Livedo reticularis includes: HEM DISEASES: APL syndrome, Sneddon's s, cryoglobulinemia, cryofibrinogemia, multiple myeloma, myeloproliferative disorder ( P Vera, essential thrombocythemia) RHEUM DISEASES vasculitis of medium size vessels (PAN, ANCA associated vasculitis, mixed cryoglobulinemia) CARDIOVASCULAR DISEASES: emboli (cholesterol, septic, atrial myxoma) MALIGNANT: renal cell CA, intravascular lymphoma, mycosis fungoides) ENDO: hypothyroid, PA, pheo, carcinoid