PMC10368954_01
Time course of symptoms and investigations. MRI, magnetic resonance imaging; CSF, cerebrospinal fluid; FDGPET, fluorodesoxyglucose positron emission computed tomography; M, month; MRI, magnetic resonance imaging; NP, neuropsychological testing; VGlut2 abs, vesicular glutamate transporter 2 autoantibodies.
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F1
For about half a year, she had been suffering from a depressed mood, pronounced restlessness, a concentration disorder, diffuse anxiety, and sleep disturbances (Figure 1). After careful questioning of her daughter, we learned that her retention and memory disorders had already existed for a year (Figure 1). The detailed neuropsychological examination revealed significant impairments in several cognitive domains such as orientation, semantic word fluency, confrontation naming, cognitive processing speed, visuomotor coordination, the clock test, action planning, working and figural memory, encoding and consolidation of verbal non-associated information, encoding and delayed recall of complex verbal content, visuoconstructive skills, and visual-spatial perception objectified (Figure 2, Table 1).
Neuropsychological profile.
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F2
The detailed neuropsychological examination revealed significant impairments in several cognitive domains such as orientation, semantic word fluency, confrontation naming, cognitive processing speed, visuomotor coordination, the clock test, action planning, working and figural memory, encoding and consolidation of verbal non-associated information, encoding and delayed recall of complex verbal content, visuoconstructive skills, and visual-spatial perception objectified (Figure 2, Table 1).
Magnetic resonance imaging. Magnetic resonance imaging (MRI) of the brain shows minor cerebral microangiopathy with periventricular vascular lesions in the white matter.
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F3
Cranial MRI showed isolated cerebral lesions in the periventricular white matter (Figure 3).
18F-FDG-PET. 18F-FDG-PET in coronal (A, B) and sagittal (C) view with distinct hypometabolism in the left temporal (A), left parietal, and right cerebellar cortex (B). Furthermore, hypometabolism in the left primary visual cortex was detected (C). White arrows show brain areas with lower tracer uptake.
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F4
In addition, after incubating the patient's serum with rat and monkey brain tissues, immunohistochemistry revealed relevant spotty fluorescence of the granular layer in the hippocampus and streaky fluorescence in the thalamus and molecular layer in the cerebellum caused by the antibody against VGlut2. 18F-fluorodesoxyglucose positron emission tomography (18F-FDG-PET) of the brain showed left parietal and left temporal hypometabolism (Figure 4). Furthermore, the lower 18F-FDG uptake was detected in the left primary visual cortex (Figure 4).