In their extensive literature research , the authors came across one of my earliest case reports published in the—if we adhere to the dopa/Parkinson terminology—precursor journal of Addiction in 1992 in which we reported the case of an l-dopa-abusing Parkinson patient with an alcohol history . I treated this patient for many years afterwards and he abstained from further l-dopa overdose. Although I have seen thousands of patients with substance use disorders since then, no other patient with l-dopa abuse or dependence came across my way. This personal experience makes me a little sceptical about whether it is time and justified to define a new diagnostic entity.
There are other reasons for scepticism. First, the overall epidemiological evidence to define a new diagnostic category overall is not convincing. The abuse risk of prescription drugs in general is a hot topic at present. The issue was discussed at a recent international expert meeting at the United Nations Office on Drugs and Crime (UNODC) in Vienna, but no one raised concerns about Parkinson medication. Every neurologist knows how difficult it is to find adequate dosage of Parkinson patients switching between on- and off-periods. This therapeutic dilemma is also reflected by the number of medications currently available in this area, and some form of misuse may very well be attributed to the desperate search of patients for symptom relief and a reasonable quality of life.
The second, more important, concern is the neurobiology underlying this new defined diagnosis. Dopamine is not dopamine. Dopaminergic neurones are located in different areas in the brain, and a dopaminergic dysfunction is linked to many psychiatric and neurological disorders, including schizophrenia  and attention deficit disorder, among others .
The pathophysiology of Parkinson is linked to deficits in the basal ganglia and the nigrostriatal dopaminergic system, while for addictive disorders the mesolimbic system plays the essential role [5,6]. Only in this area (nucleus accumbens, ventral tegmental) can dopamine release be linked clearly to rewarding effects. In the nigrostriatal system, dopamine is essential for motor function. If medication was available directly and targeting only the nigrostriatal dopamine system, the abuse potential would probably be minimal. In addition, a primary ‘dopamine deficit’ as the biological basis for any kind of addiction has not been established clearly.
A (hypothetical) dopa deficit today can be measured easily by modern neuroimaging techniques, using (beta-Cit or other) SPECT techniques, as stated by Ambermoon et al.  at the end of their paper. I agree that more research is needed in this probably neglected area, but do not believe that a progressive neurodegenerative disorder could be an ideal ‘iatrogenic model of addiction’. It would be wise to first conduct some basic neurobiological research on dopamine deficits in the addiction reward system of Parkinson patients before speculating about new models or diagnostic entities. Future addicts may start taking substances for multiple reasons; Parkinson and other motor symptoms are usually not among them.