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.
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.