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A hypertensive male in his 50s with frequent transient ischaemic attacks (TIAs) was admitted to our facility with an acute onset of right-sided sensorimotor deficit. Over the preceding 3 months, the patient experienced recurrent bi-hemispheric TIAs, occurring two to three times per week. Each episode was characterised by sudden-onset focal neurological deficits, including transient unilateral limb weakness and sensory disturbances, alternately involving either side of the body. All episodes resolved spontaneously within 30–60 min, with no residual deficits. There was no associated loss of consciousness, seizure activity or visual symptoms. The frequency of these episodes remained stable until the index event, when he presented with a persistent right-sided sensorimotor deficit. He had no other significant medical history and his family history was unremarkable. Clinical examination revealed a mild right hemiparesis and hemi-paraesthesia; multiple yellowish papules coalescing into large plaques involving the neck, giving a lax and wrinkled appearance, were noted ( figure 1A,B). Similar lesions were noted in the axilla and other flexural areas (figure 1C) and characteristic angioid streaks were noted on funduscopy. Multifocal lacunar infarcts were detected in brain imaging (figure 2A,B) and he was treated with antiplatelets, statins and antihypertensives. Echocardiography and prolonged rhythm monitoring did not detect a cardioembolic source. Detailed cardiological evaluation only revealed minor coronary artery disease. Although digital subtraction angiography was not performed as the patient did not consent, magnetic resonance angiography and carotid Doppler studies revealed no evidence of intracranial or extracranial stenosis. Laboratory investigations for hypercoagulable states, including protein C, protein S, antithrombin III, homocysteine, antiphospholipid antibodies and factor V Leiden mutation, were unremarkable.