ral medication that was given according to the needs of the patient. A more strategic and planned dosing of levodopa at different doses combined with and without specific enzyme inhibitors would probably have resulted in better data. However, to perform a study according to that design is difficult from ethical point of view.

In this paper, we could conclude that levodopa, both given orally and IV in PD patient, resulted in increased levels of levodopa and DA in the BG. During oral medication levodopa and DA followed each other well showing that a PD patient with severe disease and probably pronounced nigral degeneration, still can metabolize levodopa to DA. This is an evidence of that treatment with levodopa still is beneficial, even in advanced PD. This could also be one explanation to why levodopa still is the golden standard treatment in PD. The conversion to DA gives good symptom relief and few side effects in contrast to DA agonists and enzyme inhibitors that often cause psychiatric side effects in late stages of the disease. We could also see that STN DBS seems to increase DA levels with a more pronounced effect on ipsilateral structures in striatum.

To investigate the metabolism of levodopa to DA in vivo in human brain is difficult both due to ethical considerations and because of the delicate and complex structures involved. However, more studies are of importance to get better knowledge about the mechanisms of the disease and the mechanisms of the treatments, both medication and DBS.


The present study was supported by grants from the Research Foundation of the County Council of Östergötland, FORSS, Swedish Parkinson’s Foundation, Swedish Research Council (VR), Swedish Governmental Agency for Innovation Systems (VINNOVA grant 311-2006-7661), the Swedish Foundation for Strategic Research (SSF) and Futurum―the academy of Health and Care, Region Jönkö- ping County. We gratefully thank Lars Valter at Linköping University for statistical guidance.

Conflicts of Interest

The authors declare that there is no conflict of interests regarding the publication of this paper.


BBB Blood-brain-barrier

BG Basal ganglia

CDS Continuous dopaminergic stimulation

Cmax Maximal concentration

Cmin Minimum concentration

CNS Central nervous system

COMT Catechol-O-methyltransferase

DA Dopamine

DBS Deep brain stimulation

DDI Dopa decarboxylase inhibitor

Gpi Globus pallidus interna

HPLC High-performance liquid chromatography

IV Intravenous

LID Levodopa-induced dyskinesia

NMS Non-motor symptoms

PD Parkinson’s disease

SN Substantia nigra

SNc Substantia nigra pars compacta

STN Subthalamic nucleus

T1/2 Half-life

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