Parkinson’s syndrome and Parkinson’s disease

Parkinson’s syndrome is any clinical syndrome comprising all or part of the extra-pyramidal triad (rest tremor, bradykinesia, plastic hypertonia). Parkinson’s disease includes a parkinsonian syndrome whose specificity is to be called “dopa-sensitive” that is to say that after treatment with dopaminergic treatment (whose leaders are MODOPAR and SINEMET) we obtain an improvement in symptoms including motor more than 50% (often 60 to 70%). If this is the case, we can retain the diagnostic hypothesis that it is a Parkinson’s disease especially if the patient does not have cognitive disorders (memory loss for example), and if the symptomatology is unilateral, that is to say that it affects only one side of the body (which is most often the case at the beginning of the disease). If there is no significant improvement after putting on dopaminergic treatment at the right dose and after a few weeks of hindsight, it is necessary to know how to evoke another pathology which can be more diffuse at the level of the cerebral involvement generally exceeding the involvement of the black substance or even the basic nodes (area of the brain) and which can extend to other structures of the brain including cortical (area of the brain also). We then speak of “Parkinson-plus” or atypical parkinsonian syndrome called “non-dopa-sensitive” with an improvement under treatment that is low of the order of 20-30% or even zero in some cases. This type of more diffuse cerebral pathology can be evoked in particular if cognitive disorders are early (especially visuospatial disorders), if there are falls in the first years of the disease, if there are early dysautonomic signs (orthostatic hypotension, urinary disorders, etc.) or if the symptomatology occurs following a stroke with brain lesions of the vascular type “Vascular Parkinson’s”. In case of diagnostic doubt or if the effectiveness of the treatment is intermediate, the patient may be offered during a brief hospitalization to carry out a test with L.Dopa (a drug containing dopamine used in the context of Parkinson’s disease): the patient is put on an empty stomach in the morning, a neurological examination with motor score is carried out (the best known is the UPDRS-III score) and then given a dose of L.Dopa load orally then we follow the evolution of the UPDRS motor score in the 4 hours that follow to judge a possible improvement in symptoms. If the doubt persists after this test, we can also use cerebral metabolic imaging (PetScan) using different tracers (including glucose-derived FDG) to look for diffuse cerebral hypometabolism and if it is present we are probably moving towards a “parkinson-plus” with a neurodegenerative disease more extensive in the brain than Parkinson’s disease. All this is important because making the diagnosis of a “Parkinson-plus” so classically “non-dopa-sensitive” avoids unnecessarily increasing ineffective dopaminergic drugs and most often poorly tolerated because they have many side effects.