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We investigated safety issues and potential experimental confounds when performing functional magnetic resonance imaging (fMRI) investigations in human subjects with fully implanted, active, deep brain stimulation (DBS) systems. Measurements of temperature and induced voltage were performed in an in vitro arrangement simulating bilateral DBS during magnetic resonance imaging (MRI) using head transmit coils in both 1.5 and 3.0 T MRI systems. For MRI sequences typical of an fMRI study with coil-averaged specific absorption rates (SARs) less than 0.4 W/kg, no MRI-induced temperature change greater than the measurement sensitivity (0.1 degrees C) was detected at 1.5 T, and at 3 T temperature elevations were less than 0.5 degrees C, i.e. within safe limits. For the purposes of demonstration, MRI pulse sequences with SARs of 1.45 W/kg and 2.34 W/kg (at 1.5 T and 3 T, respectively) were prescribed and elicited temperature increases (>1 degrees C) greater than those considered safe for human subjects. Temperature increases were independent of the presence or absence of active stimulator pulsing. At both field strengths during echo planar MRI, the perturbations of DBS equipment performance were sufficiently slight, and temperature increases sufficiently low to suggest that thermal or electromagnetically mediated experimental confounds to fMRI with DBS are unlikely. We conclude that fMRI studies performed in subjects with subcutaneously implanted DBS units can be both safe and free from DBS-specific experimental confounds. Furthermore, fMRI in subjects with fully implanted rather than externalized DBS stimulator units may offer a significant safety advantage. Further studies are required to determine the safety of MRI with DBS for other MRI systems, transmit coil configurations and DBS arrangements.

Functional imaging techniques provide major insights into understanding the pathophysiology, progression, complications, and differential diagnosis of Parkinson''s disease (PD). The dopaminergic system has been particularly studied allowing now early, presymptomatic diagnoses, which is of interest for future neuroprotective strategies. The existence of a compensatory hyperactivity of dopa-decarboxylase at disease onset has been recently demonstrated in the nigrostriatal and also extrastriatal dopaminergic pathways. Modification of dopamine receptors expression is observed during PD, but the respective contribution of dopaminergic drugs and the disease process towards these changes is still debated. Abnormalities of cerebral activation are seen and are clearly task-dependent, but the coexistence of hypoactivation in some areas and hyperactivation in others is also now well established. Such hyperactivation may be compensatory but could also reflect an inability to select appropriate motor circuits and inhibit inappropriate ones by PD patients. Interestingly, dopaminergic medications or surgical therapy reverse such abnormalities of brain activation. [Copyright &y& Elsevier]