The authors describe a 35-year-old man suffering from homonymous hemianopia after head trauma 4 years before but with negative magnetic resonance imaging (MRI) findings. Brain fluorine-18 fluorodeoxyglucose positron emission tomography (18FDG-PET) showed hypometabolism at the unilateral occipital lobe and crossed cerebellar hemisphere, and diffusion tensor imaging (DTI) revealed that the ipsilateral optic radiations were completely interrupted. The crossed cerebellar diaschisis (CCD) observed in the chronic stage of brain damage was caused by cerebellar suppression of the cerebral blood flow due to an involvement of the corticopontocerebellar tract. PET and DTI provide objective means for determining the relationship of functional deficits to head trauma, even in cases where the injury was sustained years prior to the evaluation.
Keywords: Crossed cerebellar diaschisis; diffusion tensor imaging; homonymous hemianopia; traumatic brain injury.