Multiple studies demonstrate decreases in striatal D2-like (D2, D3) radioligand binding in primary focal dystonias. Although most investigations have focused on D2 specific receptors (D2R), a recent study suggests that the decreased D2-like binding may be due to a D3 specific (D3R) abnormality. However, only limited data exist on the role of D1 specific receptors (D1R) and the D1R-mediated pathways within basal ganglia in dystonia. Metabolic PET data in primary generalized dystonia suggest resting state overactivity in the D1R-mediated "direct" pathway leading to excessive disinhibition of motor cortical areas. This work investigated whether striatal D1-like receptors are affected in primary focal dystonias.

We measured striatal (caudate and putamen) specific binding of the D1-like radioligand [¹¹C] NNC 112 using PET in 19 patients with primary focal dystonia (cranial, cervical or arm) and 18 controls.

We did not detect a statistically significant difference in striatal D1-like binding between the two groups. This study had 91% power to detect a 20% difference, making a false negative study unlikely.

Since [¹¹C] NNC112 has a high affinity for D1-like receptors, very low affinity for D2-like receptors and minimal sensitivity to endogenous dopamine levels, we conclude that D1-like receptor binding is not impaired in these primary focal dystonias.