PMC10275489_01
PMC10275489_02
PMC10275489_03
MRI 10 days after ingestion showing bilateral symmetrical lesions in the basal ganglia. Abnormal isointensity on T1-FLAIR (A), and heterogeneous intensity on T2 propeller (B), and hyperintensity on T2-FLAIR (C), and no significant hypersignal on DWI (D). MRI: magnetic resonance imaging; FLAIR: fluid attenuated inversion recovery; DWI: diffusion-weighted imaging.
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fig1
Her brain MRI showed abnormal signals in the internal and external capsules of the basal ganglia bilaterally, confirming toxic encephalopathy (Figure 1).
MRI 2 months after ingestion showing encephalomalacia in the bilateral basal ganglia with surrounding gliosis and the lesion size was smaller than before. Symmetrical small patchy with long T1 long T2 signal on T1 Flair (A) and T2 propeller (B), and hyperintense in the edge of the lesion on T2-FLAIR (C), and no significant hypersignal on DWI (D).
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fig2
The brain MRI showed a remarkable reduction in the size of the lesions and the FLAIR hyperintensities in both basal ganglia regions, together with the observation of gliosis in the adjacent affected areas (Figures 2, 3), but NCS and EMG showed persistence of motor and sensory axonal damage in the lower limbs (Table 3).
The T1 Flair (A), T2 Propeller (B) and DWI (D) in the MRI 4 months after ingestion show similar to Figure 2. and the gliosis around the lesion is less than before which is shown in the T2 Flair (C).
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fig3
The brain MRI showed a remarkable reduction in the size of the lesions and the FLAIR hyperintensities in both basal ganglia regions, together with the observation of gliosis in the adjacent affected areas (Figures 2, 3), but NCS and EMG showed persistence of motor and sensory axonal damage in the lower limbs (Table 3).