Article Figures & Data
Figures
- Fig 1.
Patient 1. Initial MR examination at 2 weeks from the onset of symptoms.
A and B, Axial T2-weighted images show multiple hyperintense lesions involving the corpus callosum and cerebral white matter.
C and D, Axial FLAIR images at almost the same levels as in A and B show hyperintense lesions not only in the corpus callosum and cerebral white matter but also in the cerebral cortex (arrows).
E, Contrast-enhanced axial T1-weighted image shows diffuse leptomeningeal enhancement.
F, Axial DWI shows several hyperintense lesions in the cerebral white matter (arrows), with a cluster of lesions in the corpus callosum.
- Fig 2.
Patient 1. Second MR examination shortly after relapse of the symptoms (8 weeks from initial onset).
A and B, Axial FLAIR images show that the lesions in the corpus callosum have decreased in size and number compared with those in Figure 1. However, new punctate hyperintense lesions appeared in the cerebral cortex (arrows).
C, Axial DWI also reveals the scattered hyperintense lesions in the cerebral cortex (arrows).
- Fig 3.
Patient 1. Third MR examination at 2 weeks following relapse of the symptoms (10 weeks from initial onset).
A and B, Axial FLAIR images show multiple hyperintense lesions in the basal ganglia and thalami bilaterally, as well as in the left cerebellar peduncle and left dentate nucleus. A questionable small lesion is seen in the cortex (arrow in A).
C, Axial DWI shows a hyperintense lesion in the right caudate head (arrow), which was not depicted by either FLAIR or T2-weighted images (not shown).
- Fig 4.
Patient 1. Fourth MR examination at 8 months from the onset of symptoms. Axial FLAIR image shows diffuse, bilateral, confluent increased signal intensity in the deep white matter. Note the enlarged ventricles and mildly prominent sulci; this is consistent with cerebral atrophy.
Tables
Clinical course Symptoms MR Examination Auditory Findings Retinal Findings Treatment* Patient 1 Initial admission, 2 wk after onset Headaches, vomiting, R arm feeling loss, impaired balance, urinary incontinence, dysarthria, decreased attention span, gait ataxia 2 wk after onset Normal R branch retinal artery occlusion IV SoluMedrol 1 g/d × 5, IVIG 0.4 g/d × 5, prednisone 60 mg/d (with taper) Symptom relapse, 8 wk after initial onset Headaches, cognitive decline, clumsiness, worsened gait ataxia, upper extremity ataxia 8 and 10 wk after initial onset L high-frequency hearing loss New L branch retinal artery occlusion IVIG 0.4 g/d × 5, prednisone 50 mg/d (with taper) Stable condition, 8–9 mo after initial onset Difficult in tandem walking, mild dysmetria 8 mo after initial onset No change No new occlusion Prednisone 20 mg/d Patient 2 Initial admission, 2 wk after onset Headaches, R partial vision loss 2 wk after onset Normal R branch retinal artery occlusion Aspirin Symptom relapse, 6 wk after initial onset Headaches, R face and arm numbness 6 wk after initial onset Normal New L branch retinal artery occlusion IV methylprednisolone 1 g × 1, prednisone 80 mg/d (with taper) Symptom relapse, 4 mo after initial onset L arm parethesias, R extremity weakness, staggering walking 4 mo after initial onset R partial hearing loss New R/L branch retinal artery occlusion IVIG 0.4 g/d × 5 (monthly basis for 4 consecutive mo), prednisone 60 mg/d (with taper) Worsening symptoms, 11 mo after initial onset Worsening in vision, poor concentration, confusion, impaired balance 11 mo after initial onset No change No change IVIG 0.4 gm/d × 5 (almost every 6–8 wk for 1 y) Stable condition, 2 y later Mild ataxia, poor tandem Normal Normal Note.—IV indicates intravenous; IVIG, intravenous immunoglobulin.
Clinical Course and MR Study Cerebral White Matter Cerebral Cortex Corpus Callosum Basal Ganglia Cerebellar Hemisphere Cerebellar Peduncle 2 wk after onset T2WI 18 0 22 5 4 8 FLAIR 22 15 20 5 2 4 DWI 2 0 11 3 3 0 8 wk, relapse of symptoms T2WI 28 0 14 4 0 6 FLAIR 31 37 15 5 0 1 DWI 4 32 9 1 0 0 10 wk, relapse of symptoms T2WI* 13 0 16 20 4 1 FLAIR 32 6 17 23 11 1 DWI 0 0 5 1 0 0 8 mo, stable condition T2WI 4 0 7 3 0 1 FLAIR 2 0 3 3 0 1 DWI 0 0 0 0 0 0 Note.—T2WI indicates T2-weighted imaging.
* Some small lesions could not be identified because of motion artifact.
Clinical Course and MR Study Cerebral White Matter Cerebral Cortex Corpus Callosum Basal Ganglia Cerebellar Hemisphere Cerebellar Peduncle 2 wk after onset T2WI 2 0 0 0 0 0 FLAIR 4 0 0 0 1 0 DWI 1 7 0 0 0 0 6 wk, relapse of symptoms T2WI 7 0 5 1 0 2 FLAIR 9 0 5 1 0 2 DWI 0 3 2 1 0 0 4 mo, relapse of symptoms T2WI 13 0 5 1 0 2 FLAIR 10 1 5 1 0 2 DWI 1 1 3 0 0 0 11 mo, worsening of symptoms T2WI 43 3 4 19 4 6 FLAIR 52 15 5 17 8 6 DWI 7 2 7 5 0 2 Note.—T2WI indicates T2-weighted imaging.
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