The effect of age on human striatal dopamine D2 receptors was investigated with positron emission tomography (PET) using [11C]raclopride as a radioligand. Twenty-one healthy volunteers aged from 20 to 81 years were studied. An equilibrium method was applied and two separate PET scans with different specific activities of [11C]raclopride were performed. The maximal number of receptors (Bmax) and their dissociation constant (Kd) were calculated using Scatchard analysis. There was an age-dependent decline in the Bmax (r = -0.49; p = 0.02) of striatal D2 receptors while the Kd remained unchanged. The results show that there is an age-related loss of striatal D2 receptors, which, together with other changes in the brain nigrostriatal dopaminergic system, may contribute to extrapyramidal symptoms associated with aging.

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Striatal dopamine D2 receptor binding was studied in vivo with positron emission tomography in seven patients with early Parkinson's disease using [11C]-raclopride. The patients had unilateral symptoms and none of them had received levodopa treatment. The accumulation of [11C]-raclopride in the striatum was rapid and reached a steady state at approximately 40 min after injection. The binding of [11C]-raclopride was measured in the striatum and cerebellum: The total striatal radioactivity in both hemispheres was counted and the respective striatum/cerebellum ratios were calculated. The striatum/cerebellum ratio of [11C]-raclopride binding was significantly (p less than 0.01) increased in the hemisphere contralateral to the parkinsonian symptoms as compared with the opposite hemisphere. Thus, this study demonstrates that there is denervation supersensitivity in dopamine D2 receptor binding in early Parkinson's disease.

Abstract& Recent findings point to a perceptive impairment of emotional facial expressions in patients diagnosed with Parkinson disease (PD). In these patients, administration of dopamine can modulate emotional facial recognition. We used fMRI to investigate differences in the functional activation in response to emotional and nonemotional gestures between PD patients and age-matched healthy controls (HC). In addition, we used PET to evaluate the striatal dopamine transporter availability (DAT) with [11 C]D-threo-methylphenidate in the patient group. Patients showed an average decrease to 26% in DAT when compared to age-corrected healthy references.Reduction in the DAT of the left putamen correlated not only with motor impairment but also with errors in emotional gesture recognition. In comparison to HC, PD patients showed a specific decrease in activation related to emotional gesture observation in the left ventrolateral prefrontal cortex (VLPFC) and the right superior temporal sulcus. Moreover, the less DAT present in the left putamen, the lower the activation in the left VLPFC. We conclude that a loss of dopaminergic neurotransmission in the putamen results in a reduction of ventrolateral prefrontal access involved in the recognition of emotional gestures. &

[11C]Raclopride uptake to dopamine D2 receptors was investigated with positron emission tomography (PET) in patients with early Parkinson's disease at the time of the diagnosis and after a half-year interval. During this progressive period of the disease, the patients received no antiparkinsonian medication. The upregulation of striatal D2 receptors, which was seen in all patients already at the time of the diagnosis, persisted. Although the patients initially showed unilateral disease, they had developed bilateral symptoms by the time of the second PET scan, but the disease was still asymmetric. The present results show that the relative increase in [11C]raclopride uptake in the striatum contralateral to the symptoms as compared with the opposite striatum will be preserved even during the progression of the disease, provided that the symptoms show clear-cut asymmetry.

The monoamine transporter was studied in 4 healthy controls and 5 patients with early Parkinson's disease (PD), who had not received any antiparkinsonian medication, by means of positron emission tomography (PET) using two novel ligands, [11C]beta-CIT and [11C]beta-CFT. Both ligands showed highest uptake in the striatum. There was intermediate accumulation of activity in the thalamus and midbrain, which was more marked for [11C]beta-CIT than for [11C]beta-CFT. In the cortical areas, uptake of both ligands was not different from that seen in the cerebellum. In the controls, the putamen-to-cerebellum and caudate-to-cerebellum ratios for [11C]beta-CFT were higher than those for [11C]beta-CIT (putamen: 3.15 +/- 0.39 for [11C]beta-CFT, and 1.84 +/- 0.10 for [11C]beta-CIT; caudate: 3.15 +/- 0.31 for [11C]beta-CFT, and 1.95 +/- 0.17 for [11C]beta-CIT). Reduction from mean control value in PD patients was greater for [11C]beta-CFT (45% in the putamen contralateral to the predominant symptoms, P < 0.001) than for [11C]beta-CIT (20%, P > 0.05). [11C]beta-CFT uptake in the caudate nucleus was also diminished in PD patients (to 80% of the control mean, P < 0.05), whereas [11C]beta-CIT was within normal range (reduced to 90% of the control mean). These results indicate that both [11C]beta-CIT and [11C]beta-CFT are useful PET ligands to study brain monoamine transporter in healthy controls and in patients with PD. However, [11C]beta-CFT seems superior to [11C]beta-CIT in this respect.

Nine parkinsonian patients were studied during one night using the static charge sensitive bed (SCSB) method for the monitoring of respiration, ballistocardiogram (BCG) and body movements. The parkinsonian sleep was more restless than that of the controls. As the SCSB-defined levels of autonomic nervous activity were concerned, the amount of motor active wakefulness (MAW) was significantly (P less than 0.05) increased in parkinsonian patients, who also had less quiet sleep (P less than 0.05) than the controls. Parkinsonian tremor was present during 29.8 +/- 15.8% of the time in bed. Usually it was observed during wakefulness; it disappeared when the patient fell asleep. The frequency of turning-over events in bed was smaller in the parkinsonian patients than in the controls (P less than 0.05). When the heart rate changes associated with sleep movements were studied it was found that the parasympathetic deceleration component in the parkinsonian patients was absent. The motor dysfunction associated with Parkinson's disease is reflected in many ways in the sleep movement activity. Sleep disturbances in PD seem to be secondary in character; i.e. they can be due to impaired motor functions like turning around in the bed, or due to impaired arousal mechanisms during sleep.