Idiopathic basal ganglia calcification (IBGC) is a neuropathological finding known to manifest motor disturbance, cognitive impairment and psychiatric symptoms. Pathophysiology of psychiatric symptoms, however, remains controversial. Previous biochemical study suggests that dopaminergic impairment is involved in IBGC. We therefore performed positron emission tomography (PET) to elucidate the pre- and postsynaptic dopaminergic function and glucose metabolism in two IBGC patients.

Case 1 is a 44 years old woman presented with disorganized thought, echolalia, verbigeration and parkinsonism. She was administered bitemporal electro-convulsive therapy (ECT). Case 2 is a 35 years old woman with persecutory delusion. Computed tomography showed bilateral symmetric calcification of striatum, globus pallidus and dentate nucei. Other causes of intracranial calcification were excluded. PET scans were obtained using [11C]-labeled 2β-carbomethoxy-3β-(4-flurophenyl)-tropane, [11C]-labeled raclopride and [18F] fluorodeoxyglucose.

The decreased binding potential was severe in bilateral head of caudate nuclei and anterior putamen. In case 1, the decline was also found in posterior putamen. There were widespread decreases of glucose uptake in frontal, temporal and parietal cortices bilaterally in case 1. Significant hypometabolism was observed in the right frontal, temporal and parietal cortices. After the ECT session, the previous areas of significant hypometabolism in the right hemisphere had improved. In case 2, there was no significant change of glucose metabolism in cerebral cortex.

The difference in affected region within basal ganglia might be associated with the diverse clinical pictures in IBGC. Particularly, in the psychiatric manifestation, dopaminergic dysfunction in caudate nucleus and anterior putamen could be participated.