## 2 Materials and Methods  
### Study Hypothesis  
This project aims to identify the bio-clinical signatures specific to each OCD subgroup. To this end, we will develop the study along three main objectives:  
* To test whether individuals living with a classic OCD form (including OCD\({}_{\text{EO}}\) and OCD\({}_{\text{LO}}\)) might have a distinct pattern of clinical, neurocognitive, neurophysiological (including sleep disorders, such as periodic limb movements [PLMD], anomalies in the sleep micro- or macrostructure, anomalies in EEG or in REM sleep), and biological markers that might allow distinguishing from OCD\({}_{\text{PANS}}\);
* To test whether it could be possible to differentiate such signatures between OCD\({}_{\text{EO}}\) and OCD\({}_{\text{LO}}\);
* To test whether OCD\({}_{\text{PI}}\) may be distinguished from classic OCD forms (i.e., OCD\({}_{\text{EO}}\) and OCD\({}_{\text{LO}}\)) based on such signatures. The classification of one of the study groups will be based on the following criteria:
* OCD\({}_{\text{EO}}\): defined on the basis of symptoms onset \(\leq\) 17 years of age [15];
* OCD\({}_{\text{LO}}\): defined on the basis of symptoms onset after age 17 [15] with a total BABS score < 13 [23];
* OCD\({}_{\text{PANS}}\): defined according to the National Institute of Health 2010 pediatric acute-onset neuropsychiatric syndrome (PANS) criteria [24];
* OCD\({}_{\text{PI}}\): defined according to a total BABS score \(\geq\) 13 points [23] with the age of onset > 17 years of age. More specifically, our general hypothesis is that:
* Study subjects living with a classic form of OCD (OCD\({}_{\text{EO}}\) + OCD\({}_{\text{LO}}\)) differ from OCD\({}_{\text{PANS}}\) in terms of (1) OCD symptoms severity and quality; (2) comorbidity for a sleep disorder, nonrestorative sleep, and specific sleep patterns; (3) cognitive functioning; and (4) biomarkers levels (the null hypothesis would be that OCD\({}_{\text{EO}}\) + OCD\({}_{\text{LO}}\) = OCD\({}_{\text{PANS}}\));
* OCD\({}_{\text{EO}}\) may differ from OCD\({}_{\text{LO}}\) in terms of (1) symptoms severity and quality; (2) sleep disorder comorbidity, nonrestorative sleep, and EEG patterns; (3) cognitive functioning; and (2) biomarker levels (the null hypothesis is that OCD\({}_{\text{EO}}\) = OCD\({}_{\text{LO}}\));
* OCD\({}_{\text{PI}}\) may differ from OCD\({}_{\text{EO}}\) + OCD\({}_{\text{LO}}\) and from OCD\({}_{\text{PANS}}\) in terms of (1) symptoms severity and quality; (2) comorbidity for sleep disorders, nonrestorative sleep, and EEG patterns; (3) cognitive functioning; and (4) biomarker levels (the null hypothesis is that OCD\({}_{\text{PI}}\) = OCD\({}_{\text{EO}}\) + OCD\({}_{\text{LO}}\) and OCD\({}_{\text{PI}}\) = OCD\({}_{\text{PANS}}\)). Considering the exploratory nature of the present study, it is difficult to hypothesize the direction of the observed difference in terms of either neuropsychological tests, plasmabiomarkers, or EEG/polysommographic markers or indeed, the required sample size to detect a difference between study groups. Notwithstanding these limitations, we anticipate the following:  
* Higher symptoms severity for OCDEO vs. OCDLO;
* Worse cognitive performances for OCDPANS vs. OCDEO and OCDLO;
* Greater impact on sleep architecture for OCDPANS as compared with the remaining subtypes.