Lateralized Cerebral Amyloid Angiopathy presenting with recurrent Lacunar Ischemic Stroke

Abstract

An 84-year-old woman with history of diabetes, hypothyroidism, and hyperlipidemia presented with acute onset of paresis of left arm and paresthesia of left face and arm. She had a similar prior episode two weeks ago with only left arm paresthesia. She had a similar prior episode two weeks ago with only left arm paresthesia. On the initial encounter, the patient exam revealed BP of 150/46 and normal sinus rhythm. Neurological exam showed reduced pinprick and light touch sensations over the left side of the face, arm and leg, and mild weakness on the scale of 4/5 of the left upper extremity. The above symptoms resolved within two hours. Her workup including glucose level, vasculitis panel, ECHO and EKG, which were all normal. Carotid duplex revealed mild stenosis of the ICA bilaterally. CT angiogram of head and neck showed no hemodynamically signi icant stenosis, aneurysm, dissection or vascular malformation of the head and neck. No focal or multifocal segmental narrowing of vessels were seen. EEG did now show any abnormalities. Telemetry did not reveal an evidence of atrial ibrillation. Lumbar puncture was not performed.The MRI revealed different stages of lacunar ischemic lesions. Interestingly, the SWAN sequences showed lateralized rather than global multiple microhemorrhages over the right MCA and PCA territory, and the sulcal hyperintensity on FLAIR was also seen with no associated susceptibility effect and minimal enhancement (Figure 1 AbstractHere we reported an interesting case of an 84-year-old woman with acute onset of paresis of left arm and paresthesia of left face and arm. The symptoms resolved within two hours. She also had a similar prior episode two weeks ago with only left arm paresthesia. Her MRI revealed different stages of lacunar ischemic lesions. Interestingly, the SWAN sequences showed lateralized rather than global multiple microhemorrhages over the right MCA and PCA territory, and the sulcal hyperintensity on FLAIR was also seen with no associated susceptibility effect and minimal enhancement, indicating probable cerebral amyloid angiopathy (CAA) based on Boston Criteria.It has been acknowledged that the CAA could manifest with certain localization preference. Cerebral microinfarct and white matter disease in CAA have been more often observed in the posterior circulation territory, however the restricted lateralization reported in our case has not been seen. Since CAA is often diagnosed when the characteristic MRI fi ndings are picked up incidentally, recognizing this as a potential "TIA mimic" will be important for guiding treatment due to its higher risk of bleeding. In summary, this case highlights that the CAA could present as restricted lateralized lesions and occur as transient neurologic defi cits, which to our knowledge has not be reported before. Recognition of it as a potential manifestation of CAA will be valuable in the clinical diagnosis process.

Hemispheric Asymmetry of White Matter Hyperintensity in Association With Lacunar Infarction

“…Asymmetric growth of WMH likely occurs because lacunar infarction tends to recur in the same hemisphere where previous infarction occurred (Data S1), as previously suggested. 22 Lacunar infarcts have been linked with small-vessel disease, which is caused by lipohyalinosis or fibrinoid necrosis of small arteries or arterioles supplying the deep subcortical brain structures. 23 However, accumulating evidence indicates that atherosclerosis in the parent artery potentially contributes to the development of lacunar infarction.…”