The Nigrostriatal Dopaminergic System Assessed In Vivo by Positron Emission Tomography in Healthy Volunteer Subjects and Patients With Parkinson's Disease

[123I]?-CIT SPECT demonstrates decreased brain dopamine and serotonin transporter levels in untreated parkinsonian patients

“…Another recent study demonstrated a 57% reduction of 123 I‐FP‐CIT binding in the putamen and a 29% reduction in the caudate nucleus of the control mean binding in early drug‐naive PD patients 16. These findings agree with PET and pathological findings indicating relatively selective loss of dopamine in the posterior putamen,37, 38 the loss being 30–50% in the putamen and 20–25% in the caudate 39–42. In our study there was some overlap in the mean putamen DAT uptake ratios of the PD patients and the controls while the contralateral putamen DAT activity clearly distinguished the PD patients from the controls.…”

[123I]?-CIT SPECT demonstrates decreased brain dopamine and serotonin transporter levels in untreated parkinsonian patients

“…Another recent study demonstrated a 57% reduction of 123 I‐FP‐CIT binding in the putamen and a 29% reduction in the caudate nucleus of the control mean binding in early drug‐naive PD patients 16. These findings agree with PET and pathological findings indicating relatively selective loss of dopamine in the posterior putamen,37, 38 the loss being 30–50% in the putamen and 20–25% in the caudate 39–42. In our study there was some overlap in the mean putamen DAT uptake ratios of the PD patients and the controls while the contralateral putamen DAT activity clearly distinguished the PD patients from the controls.…”

Fluorodopa uptake and glucose metabolism in early stages of corticobasal degeneration

“…In patients with PD we observed a mean reduction to 47% of normal uptake into the putamen and to 25% into the caudate. These results are within the range of previous published data [3,13,18]. In our CBD patients we found a mean reduction to 33% of normal uptake into the putamen, while uptake into the caudate was relatively preserved (mean reduction to 11% of normal).…”

Anticholinergic drugs: response of parkinsonism not responsive to levodopa

“…Studies with PET showed a marked decrease in FD in the striatum, particularly in the posterior putamen, contralateral to the more affected limbs and normal binding of NMSP in the putamen. These findings are consistent with those of Parkinson's disease [4][5][6] and suggest a dysfunction of the nigrostriatal pathway that would presumably respond to treatment with levodopa or dopamine receptor agonists. Because of no response to dopaminergic medications in spite of normal D2 receptor binding in the striatum, we think that our patients had not only presynaptic dysfunction but dysfunction of striatal output pathways.…”

[123I]?-CIT SPECT demonstrates decreased brain dopamine and serotonin transporter levels in untreated parkinsonian patients

“…Another recent study demonstrated a 57% reduction of 123 I‐FP‐CIT binding in the putamen and a 29% reduction in the caudate nucleus of the control mean binding in early drug‐naive PD patients 16. These findings agree with PET and pathological findings indicating relatively selective loss of dopamine in the posterior putamen,37, 38 the loss being 30–50% in the putamen and 20–25% in the caudate 39–42. In our study there was some overlap in the mean putamen DAT uptake ratios of the PD patients and the controls while the contralateral putamen DAT activity clearly distinguished the PD patients from the controls.…”

Fluorodopa uptake and glucose metabolism in early stages of corticobasal degeneration

“…In patients with PD we observed a mean reduction to 47% of normal uptake into the putamen and to 25% into the caudate. These results are within the range of previous published data [3,13,18]. In our CBD patients we found a mean reduction to 33% of normal uptake into the putamen, while uptake into the caudate was relatively preserved (mean reduction to 11% of normal).…”

Anticholinergic drugs: response of parkinsonism not responsive to levodopa

“…Studies with PET showed a marked decrease in FD in the striatum, particularly in the posterior putamen, contralateral to the more affected limbs and normal binding of NMSP in the putamen. These findings are consistent with those of Parkinson's disease [4][5][6] and suggest a dysfunction of the nigrostriatal pathway that would presumably respond to treatment with levodopa or dopamine receptor agonists. Because of no response to dopaminergic medications in spite of normal D2 receptor binding in the striatum, we think that our patients had not only presynaptic dysfunction but dysfunction of striatal output pathways.…”

[123I]?-CIT SPECT demonstrates decreased brain dopamine and serotonin transporter levels in untreated parkinsonian patients

“…Another recent study demonstrated a 57% reduction of 123 I‐FP‐CIT binding in the putamen and a 29% reduction in the caudate nucleus of the control mean binding in early drug‐naive PD patients 16. These findings agree with PET and pathological findings indicating relatively selective loss of dopamine in the posterior putamen,37, 38 the loss being 30–50% in the putamen and 20–25% in the caudate 39–42. In our study there was some overlap in the mean putamen DAT uptake ratios of the PD patients and the controls while the contralateral putamen DAT activity clearly distinguished the PD patients from the controls.…”

Fluorodopa uptake and glucose metabolism in early stages of corticobasal degeneration

“…In patients with PD we observed a mean reduction to 47% of normal uptake into the putamen and to 25% into the caudate. These results are within the range of previous published data [3,13,18]. In our CBD patients we found a mean reduction to 33% of normal uptake into the putamen, while uptake into the caudate was relatively preserved (mean reduction to 11% of normal).…”

Anticholinergic drugs: response of parkinsonism not responsive to levodopa

“…Studies with PET showed a marked decrease in FD in the striatum, particularly in the posterior putamen, contralateral to the more affected limbs and normal binding of NMSP in the putamen. These findings are consistent with those of Parkinson's disease [4][5][6] and suggest a dysfunction of the nigrostriatal pathway that would presumably respond to treatment with levodopa or dopamine receptor agonists. Because of no response to dopaminergic medications in spite of normal D2 receptor binding in the striatum, we think that our patients had not only presynaptic dysfunction but dysfunction of striatal output pathways.…”