Introduction: In clinical practice, post-operative cerebral dysfunction may not be accounted for by direct tissue injuries following brain surgeries. Herein, we report a case with transient severe hemispheric dysfunction after left temporal lobectomy with cerebral hypometabolism in 18F-fluorodeoxyglucose (18F-FDG) Positron Emission Tomography (PET).
Method: A 15-year-old right-handed boy underwent left temporal lobectomy for newly diagnosed meningioma. After the brain surgery, he presented with severe left-hemispheric dysfunction including apraxia of the right upper extremities, global aphasia, dysarthria, and cognitive impairment. However, there was no definite abnormality which can be associated with the neurologic impairments in the postoperative T1-, T2-, diffusion-, and perfusion-weighted MR images. No epileptiform discharge was observed except diffuse cerebral dysfunction at the left hemisphere in the EEG. Sleep tendency was improved after setting changes of the ventriculoperitoneal shunt, however, the symptoms of left-hemispheric dysfunction remained. Brain 18F-FDG PET was performed to investigate altered metabolism of the left hemisphere, and showed a prominent hypometabolism at the left cerebral hemisphere, including the dorsolateral prefrontal cortex, primary motor cortex, and language centers, and crossed cerebellar diaschisis in the right cerebellum (Fig. 1). Previously, he underwent brain tumor resection around the third ventricle, resulting in injuries of the corpus callosum 8 years ago (Fig. 2). After then, he additionally underwent several times of brain hemorrhages and surgeries with concomitant transient neurologic dysfunctions including drowsiness, weakness, apraxia, and aphasia, which were not explained by direct tissue injuries.
Result: His neurologic symptoms were remarkably improved after 1 month of rehabilitation. The functional measurements showed improvement from 54 to 83 for Modified Barthel Index, 0/38 (right/left) to 51/67 for Jebsen Hand Function Test, and 0/27 (right/left) to 30/20 for grip strength. At four months after brain surgery, the neurologic impairments were nearly recovered to the preoperative state, which was consistent with normalized left-hemispheric hypometabolism in the 18F-FDG PET (Fig. 1).
Conclusion: 18F-FDG PET is a useful method to identify the cause of hemispheric dysfunctions which may not be irrelevant to the structural changes following brain surgery. Underlying transcallosal injuries can be one of the plausible mechanisms to induce transient cerebral hypometabolism after brain surgery. |
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Figure 1. Hypometabolism at the left cerebral and right cerebellar hemispheres representing crossed cerebellar diaschisis (A-C) in the initial Brain 18F-FDG PET, which was nearly normalized 4 months after brain surgeries (D-F).
Figure 2. Postoperative brain magnetic resonance images. Previous injury at the anterior corpus callosum (A) and postoperative change at the left temporal lobe (B) were shown in the T1-weighted sagittal and the T2-weighted axial images, respectively.
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