Early lacunar strokes complicating polyarteritis nodosa

Abstract

Objective: To determine the patterns and mechanisms of polyarteritis nodosa (PAN)–associated strokes (PANAS).

Background: Strokes are reputed to be rare complications of PAN and to occur at a late stage (2 to 3 years). The cause of stroke is unknown but may be related either to atherosclerosis-like occlusive vasculopathy, caused possibly by hypertension or corticosteroid (CS) use, or to vasculitic arterial occlusion.

Methods: Clinical and radiologic patterns, latencies, and current therapy at onset in 15 PANAS patients (4 of the authors’ and 11 published cases) were analyzed.

Results: A lacunar stroke syndrome (11/15 cases, 73%) was the most frequent stroke pattern in PANAS (multiple, small, deep infarcts in 6, [55%], pontine lacunae in 3 [27%], and leukoaraiosis in 2 [18%]), followed by pure lobar hematoma and bilateral, possibly cardioembolic, large ischemic infarcts (2 cases each). A stroke latency shorter than that previously established (within 8 months in 73% of cases; mean latency, 6.5 months) and a close relationship between the use of CS and stroke in PAN also were found. Of the 77% of first-time or recurrent lacunar strokes that developed despite CS therapy, 80% appeared within 6 months and 50% within 3 weeks of CS initiation.

Conclusion: Early lacunar stroke syndrome, related to deep small- or pontine-penetrating artery thrombotic microangiopathy rather than vasculitis, was the most frequent PANAS pattern. This vasculopathy may be aggravated by corticosteroid (CS) therapy enhancement of either platelet thromboxane A₂ production or arterial wall fibrosis. Thus, antiplatelet drugs in association with CS may be advisable for preventing stroke occurrence or recurrence in PAN.