No abstract

The hypofrontality theory ofthe pathogenesof schizophrenia predicts that cortical lesions caupsychosis. To test the hypothesis that the state of psychosis in temporal lobe epilepsy is associated with the same striatal supersensitivity that may cause psychosis in schizophrenia, we measured the rate of metabolism of an exogenous analog of dopa in both disorders, using positron emission tomography (PET) ofthe tracer 6-18Flfluoro-L-dopa (18F-dopa) (5,6).We have previously shown that the rate of metabolism of externally administered 18F-dopa is an index ofthe activity of the enzyme responsible for the decarboxylation of dopa to dopamine (EC 4.1.1.28) (7,8). We determined the brain metabolism of 18F-dopa in 31 subjects, including 10 patients with psychotic disorders, of whom 5 had schizophrenia and 5 had a history of complex partial seizures (CPS) with schizophreniform psychosis, and 21 control subjects, of whom 8 had CPS without psychosis and 13 were healthy volunteers.

No abstract

L-DOPA is a large neutral amino acid subject to transport out of, as well as into, brain tissue. Competition between dopamine synthesis and L-DOPA egress from striatum must favor L-DOPA egress if decarboxylation declines relatively more than transport in Parkinson's disease. To test this hypothesis, we injected patients with Parkinson's disease with a radiolabeled analogue of L-DOPA and recorded regional brain radioactivity as a function of time by means of positron emission tomography. We simultaneously estimated the activity of the decarboxylating enzyme and the amino acid transport. In the striatum of patients, we found the L-DOPA decarboxylase activity to be reduced in the head of the caudate nucleus and the putamen. However, the rate of egress of the DOPA analogue was unaffected by the disease and thus inhibited dopamine synthesis more than predicted in the absence of L-DOPA egress.