LAUSR

Certain drugs are known to be associated with increased risk of cerebrovascular disease by having a prothrombotic effect, causing vasculopathy, altering blood pressure or the coagulation cascade [1]; these phenomena are a direct manifestation of their pharmacodynamics or an unexpected adverse reaction. Users of these drugs may have ischaemic or haemorrhagic stroke, but it is even less frequent for them to have transient ischaemic attacks (TIAs). An 82-year-old man with controlled rheumatoid arthritis (RA) presented acute motor aphasia that lasted 4 h, resolved without sequelae and recurred with a frequency of 2–3 events per week for 1 month. There was no association with other symptoms such as amnesia, motor automatism, hemiparesis, orolingual apraxia or behaviour arrest. One month before admission, RA treatment was changed to leflunomide and prednisolone was discontinued. He had no arterial hypertension or other relevant data in his past medical history. The physical examination on admission was normal. Recurrent TIA was diagnosed, brain magnetic resonance image ruled out lesions (Fig. 1) and the other studies did not detect heart or great vessel disease, or a state of hypercoagulability or other systemic autoimmunity. During electroencephalographic monitoring (suspecting aphasia to be an ictal manifestation), symptoms recurred but have no electrographic correlation. Because of the temporal relationship between the onset of leflunomide and TIAs, it was considered that an adverse reaction could be treated and the drug was discontinued. The patient was followed and so far has not had a recurrence of aphasia and the RA is controlled with methotrexate. It has been considered that the same drugs that can generate a cerebral infarction could cause a TIA, but until now, there was no data about leflunomide. Hepatotoxicity [2], interstitial pneumonitis [3], pancytopenia [4], arterial hypertension [5] and peripheral neuropathy (2–3% of patients) have been documented [6]. It is considered that this sensory-motor axonal neuropathy is mediated by a vasculopathic process which resolves in approximately 1 month after stopping the drug [7]; the reason for the vasculopathy is still unknown. The combined cardiovascular risk in patients with RA has been evaluated in different studies taking into account that RA per se generates endothelial and vascular dysfunction [7]. The results for leflunomide are contradictory: Solomon et al. [8]