This case describes an unusual cardioembolic cause of CWS. The exact pathophysiological mechanism of CWS remains unclear. Diabetes, hypertension, hyperlipidemia, and smoking have been correlated to CWS, and most studies suggest atherosclerosis of small penetrating vessels as the likely underlying pathology [3, 9]. When Donnan et al. first described CWS, he specified no evidence of thrombo- or cardioembolic phenomena when cerebral infarction did develop [1]. As the CTA does show mild atherosclerotic disease, one can perhaps argue this is a case of small vessel CWS, and the atrial fibrillation might merely be a pure coincidence or a result of stroke-induced sympathetic stimulation. A series of transesophageal echocardiograms performed on patients with ischaemic strokes did illustrate 20% of those with lacunar infarcts actually had a cardiac cause with major risk factors for embolization [10]. Though we are unable to definitively prove the etiology in this case, the new-onset atrial fibrillation demonstrates at least an association and possibly a causational relationship where a cardiac embolus might have travelled into a lenticulostriate artery.

As the mechanism of CWS remains unclear, there is also uncertainty as to whether proposed therapies alter the natural progression of the disease. Different treatment strategies have been considered, including thrombolysis, anti-coagulation, dual anti-platelet agents, elevating blood pressure, and aggressive intravenous hydration [11]. Existing evidence published thus far is mostly limited to observational studies and case series. Functional prognosis is depicted to be favourable in most patients with CWS, but the 7-day stroke risk can reach as high as 60% [12].

Studies have shown the mean duration of recurrent TIA episodes in CWS to vary from 6 to 24 min, and the internal capsule remains the most frequently involved location of established infarct on MRI at 50 to 70% [11]. Our patient had multiple episodes each lasting less than 10 min and fortunately did not suffer residual functional deficits despite MRI depicting a left corona radiata infarct. He was initially loaded with dual anti-platelet agents, and there was a standing order by the consulting neurologist to offer intravenous recombinant tissue plasminogen activator (rTPA) should an episode persist beyond 30 min. Current rTPA trials based their decisions on CT and clinical findings, and in many cases, MRI findings are uncertain. The definition of CWS should therefore include patients with TIA and those with transient symptoms of infarction because most of them were diagnosed clinically without the benefit of MRI before treatment [13]. A post hoc analysis of the WAKE-UP trial did show similar favourable functional outcomes between patients with lacunar infarcts and other stroke subtypes who were treated with rTPA, suggesting it could possibly be an effective treatment measure for CWS though more studies will need to be done to ascertain this [14]. Thus far, limited studies have shown no statistically significant difference in therapeutic effects or functional outcome amongst CWS patients treated with rTPA or anti-platelet agents [3, 15, 16]. There is also no strong evidence for the efficacy of anti-coagulant therapy in the acute phase of CWS. Some case studies have shown benefit of double anti-platelet therapy over single therapy as a secondary prevention strategy [17, 18].

In conclusion, this case demonstrates that CWS can be caused by cardioembolic phenomena in the setting of atrial fibrillation. The rarity of this entity has limited research on optimal management, but dual anti-platelet agents have been safely used in non-cardioembolic CWS and appear to be a viable treatment in cardioembolic CWS patients prior to transitioning to anti-coagulants. There needs to be more research or randomised controlled trials focused on treatment options that can alter the disease progression of CWS, but this would be difficult considering the paucity of cases.