Psychopathology and friendship in children and adolescents: disentangling the role of co-occurring symptom domains with serial mediation models.

The consolidation of social friendship groups is a vital part of human development. The objective of this study is to understand the direct and indirect influences of three major symptomatic domains-emotional, hyperkinetic, and conduct-on friendship. Specifically, we aim to study if the associations of one domain with friendship may be mediated by co-occurring symptoms from another domain. A total of 2512 subjects aged 6-14 years participated in this study. Friendship was evaluated by the Development and Well-Being Assessment's friendship section. We evaluated two main constructs as outcomes: (1) social isolation and (2) friendship latent construct. Emotional, hyperkinetic, and conduct symptomatic domains were evaluated with the Strengths and Difficulties Questionnaire (SDQ). All SDQ domains were positively associated with social isolation and negatively associated with friendship latent construct in univariate analysis. However, serial mediation models showed that the association between conduct domains with social isolation was mediated by emotion and hyperkinetic domains. Moreover, the associations between emotional and hyperkinetic domains with friendship latent construct in non-isolated children were mediated by the conduct domain. Emotion and hyperkinetic domains were directly and indirectly associated with social isolation, whereas conduct was directly and indirectly associated with overall friendship in non-isolated children. Results suggest that interventions aimed to improve social life in childhood and adolescence may have stronger effects if directed towards the treatment of emotion and hyperkinetic symptoms in socially isolated children and directed towards the treatment of conduct symptoms in children with fragile social connections.

Case 241: Hemiparkinsonism- Hemiatrophy-SPECT with 99mTc TRODAT-1 and Muscle MR Imaging Abnormalities.

History A 43-year-old right-handed man presented with a history of progressive mild left-sided weakness and slowness of movements. Symptoms began 4 years earlier, and the patient noticed a progressive decline in his daily routine due to gait difficulties in the past year. There was no history of head trauma, surgery, drug therapy, smoking, or alcohol abuse, nor was there any relevant family history. Examination revealed normal cognition (29 of 30 points on the Mini-Mental State Examination and 27 of 30 points on the Montreal Cognitive Assessment) and normal cerebellar, sensory, cranial nerve, and autonomic function. There was mild left-sided weakness involving the upper and lower limbs (medical research council graded muscle strength as 4+ out of 5) that was associated with facial hypomimia and a rigid akinetic syndrome only in the patient's left hemibody (Unified Parkinson's Disease Rating Scale [UPDRS] part III [motor examination], 23 out of 52 points). Mild atrophy in the left upper and lower limbs without pain, swelling, or skin lesions was noted at physical examination. Routine blood chemistry was normal, as were serum creatine kinase and aldolase levels and thyroid, hepatic, and renal function. T1- and T2-weighted, fluid-attenuated inversion recovery, diffusion- and perfusion-weighted, and contrast material-enhanced brain magnetic resonance (MR) imaging results were normal, without basal ganglia hyperintensity, lacunae, calcification, or heavy metal deposits. Muscle MR imaging and single photon emission computed tomography (SPECT) with technetium 99m (99mTc) tropane dopamine transporter (TRODAT)-1 were performed for further evaluation. This patient received levodopa and benserazide (200 and 50 mg, respectively) four times a day and amantadine (100 mg) three times a day without adequate improvement (UPDRS score decreased from 23 to 20 points).