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Eight years earlier, he had reported sudden onset of right hemiparesis and hemihypoesthesia that improved over a few days. Two years before the present report, he had presented sudden onset of vertigo and "bilateral visual blurring"; computed tomography CT showed a right occipital infarct that, at that time, was not investigated.
He had been on aspirin for the past six years and had a history of arterial hypertension, diabetes mellitus, ischemic heart disease, peripheral artery disease and dyslipidemia. Magnetic resonance imaging MRI showed old infarcts in the right pons and bilateral occipital lobes Figure 1.
The right pontine and the right occipital infarcts were asymptomatic. There were no lesions in the ICA region.
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Warfarin was prescribed and the patient did not have any further symptoms. A year-old woman presented sudden onset of left hemiparesis lasting for more than 24 hours. One year earlier, she had reported vertigo that, at that time, was attributed to peripheral vestibulopathy. The neurological examination showed left hemiparesis and left hypoesthesia.
Fluid-attenuation inversion-recovery and diffusion-weighted images revealed an acute right pontine infarct and an old infarct in the right cerebellar hemisphere Figure 2. There were no abnormalities in other cervicocerebral arteries and a transthoracic echocardiogram was normal.
Both patients participated in this study on the natural history of BAOD. The protocol was approved by the local Ethics Committee and the patients provided informed consent for their participation.
In Case 1, Doppler findings raised the possibility of performing endarterectomy to treat an ICA stenosis presenting with transient right hemiparesis. After anticoagulation, the symptoms disappeared. In Case 2, replacement of antiplatelet therapy with anticoagulation also led to symptom resolution.
Cases of capsular lacunae and large hemispheric lesions in the ICA region may also present with sensory-motor stroke,4 and the clinical findings may not reliably distinguish between them. The ostia of branching arteries can become stenosed or occluded due to microatheromas or large atheroma plaque in BAOD cases. Hemodynamic insufficiency and embolism caused by BAOD or other sources may also cause pontine infarcts.
In the cases presented here, the TIAs stopped after anticoagulation. Even though there are no clear evidence-based guidelines favoring treatment with warfarin for patients with BAOD, anticoagulants may be potentially more effective than antiplatelet agents under these conditions.
However, milder clinical presentations also occur and, in some patients, they precede neurological deficits of greater severity. These tests can therefore reliably exclude the presence of intracranial stenosis. Abnormal results from these tests require a confirmatory test such as angiography.
Pontine infarcts may not be diagnosed on CT scans, even in patients presenting with hemiparesis lasting longer than one day. In addition, previous TIAs or infarcts presenting with vertigo, ataxia or other symptoms are often present in patients with hemiparesis caused by vertebrobasilar disease,2 as in our patients. These symptoms may be subtle and go unnoticed.
Such symptoms should be considered red flags and be actively investigated in patients presenting with hemiparesis.