Neural bases of the clinical and neurocognitive differences between earlyand late-onset obsessive–compulsive disorder

Cortical gyrification differences between early- and late-onset obsessive–compulsive disorder: neurobiological evidence for neurodevelopmentally distinct subtypes

“…In this study, early-onset OCD patients had significantly increased gyrification in the frontoparietal and cingulate cortex, which are known as major component regions in the corticostriato-thalamo-cortical (CSTC) model of OCD pathophysiology (Milad & Rauch, 2012). Although not directly comparable due to methodological differences, the regions of hypergyrification observed in our study are consistent with other neuroimaging findings, as earlier onset age in OCD was reported to be associated with larger precentral and middle frontal volumes (Kim et al, 2020) as well as medial frontal volumes (Koprivova et al, 2009). In addition, abnormal volume in the ACC was observed in an early illness state, and its lack of association with illness duration further suggested a neurodevelopmental basis for ACC abnormalities in OCD (Rosenberg & Keshavan, 1998).…”

“…Previous systematic reviews and meta-analyses have reported that patients with early-onset OCD are reliably differentiated from those with late-onset OCD in terms of multiple etiologic and phenotypic factors, with early-onset OCD patients showing a higher prevalence in males, higher levels of genetic loading and heritability, higher comorbidity rates with other neurodevelopmental diseases such as tics and Tourette's syndrome, poorer treatment responses, and a more gradual appearance of symptoms than patients with late-onset OCD, suggesting that early-onset OCD patients have more neurodevelopmental loading than late-onset OCD patients (Geller et al, 1998;Taylor, 2011). In addition to these well-known clinical comparisons, neurobiological differences have also been evidenced in subtypes of OCD based on onset age (Boedhoe et al, 2017;Jurng et al, 2021;Kim et al, 2020), suggesting that there are distinct pathophysiological mechanisms in early-and late-onset OCD groups. However, the underlying neural markers to establish neurodevelopmental differences between patients with early-and late-onset OCD have rarely been investigated, although they need to be identified to subtype OCD patients into more biological evidence-based homogeneous subgroups to appropriately understand the neurobiological underpinnings of different etiologies.…”

“…Early-onset OCD patients are known to have onset of subclinical symptoms before puberty, while late-onset OCD patients are likely to show obsessive and compulsive symptoms after puberty (Sobin, Blundell, & Karayiorgou, 2000 ). Using this criterion, 17 years has been suggested as a cutoff onset age for classifying two OCD patient subgroups approximately at puberty and has been used in many studies including our previous work (Butwicka & Gmitrowicz, 2010 ; Fontenelle, Mendlowicz, Marques, & Versiani, 2003 ; Henin et al, 2001 ; Hesse et al, 2011 ; Hwang et al, 2007 ; Kang, Kim, Kim, Hwang, & Kim, 2017 ; Kim et al, 2020 ; Wang et al, 2012 ). Previous systematic reviews and meta-analyses have reported that patients with early-onset OCD are reliably differentiated from those with late-onset OCD in terms of multiple etiologic and phenotypic factors, with early-onset OCD patients showing a higher prevalence in males, higher levels of genetic loading and heritability, higher comorbidity rates with other neurodevelopmental diseases such as tics and Tourette's syndrome, poorer treatment responses, and a more gradual appearance of symptoms than patients with late-onset OCD, suggesting that early-onset OCD patients have more neurodevelopmental loading than late-onset OCD patients (Geller et al, 1998 ; Taylor, 2011 ).…”

“…That these neuropsychological deficits are still apparent in fully recovered OCD patients and their unaffected relatives (Rao, Reddy, Kumar, Kandavel, & Chandrashekar, 2008 ; Zartaloudi, Laws, & Bramon, 2019 ) further supports the hypothesis that these impairments are trait-related markers for OCD rather than state-dependent features of the disease. In fact, neuropsychological differences in visual memory and verbal fluency have been consistently reported between the early- and late-onset OCD subtypes (Hwang et al, 2007 ; Kim et al, 2020 ; Roth, Milovan, Baribeau, & O'Connor, 2005 ), suggesting that these deficits are prominent neurocognitive features reflecting effects of neurodevelopmental abnormalities on cortical gyrification that distinguish OCD into more homogenous subgroups.…”

Executive function in obsessive compulsive disorder at Zagazig University Hospitals: a case-control study

“…Moreover, poorer visuospatial construction in earlyonset OCD was correlated with a larger left middle frontal gyrus volume. Impaired visuospatial memory in people with early-onset OCD and cognitive inflexibility in people with late-onset OCD were correlated with increased and decreased volume in the left middle frontal gyrus, respectively [7].…”