Abnormal movements are associated with poor psychosocial functioning in adolescents at high risk for psychosis

Abstract

The period immediately preceding the onset of overt psychosis is characterized by a range of symptoms and behaviors including emerging attenuated psychosis, spontaneous movement abnormalities, and a broad decline in role and social functioning. Recent evidence suggests that basal ganglia dysfunction, which is implicated in the development of psychotic symptomatology, may manifest in the form of both movement abnormalities and deficits in processes integral to psychosocial functioning. However, little is known about the relationship between abnormal movement function and the observed psychosocial deficits. In the present study, 40 clinical high-risk participants meeting criteria for a prodromal syndrome were assessed for movement abnormalities and global role and social functioning at baseline. Role and social functioning was then followed up after a one-year period. At baseline, the severity of spontaneous movement abnormalities was associated with poor role functioning. Further, when controlling for baseline functioning, movement abnormalities predicted changes in social functioning one-year later, with a trend in the same direction for role functioning. Exploratory analyses also indicated that elevated baseline movement abnormalities distinguished those at-risk participants who eventually converted to psychosis and that this was also the case for poorer baseline global role functioning (at the trend level). Taken together, the results suggest that movement abnormalities are closely associated with deficits in psychosocial functioning. Elucidating the link between these phenomena may serve to refine etiological models of frontal-subcortical circuit dysfunction and inform understanding of functioning and outcome of these affected youth.

Hyperactivity of caudate, parahippocampal, and prefrontal regions during working memory in never-medicated persons at clinical high-risk for psychosis

“…In the frontal cortex, CHR exhibit both structural alterations (e.g., gray matter, cortical surface, integrity)(Bloemen et al, 2010; Fusar-Poli et al, 2011a; Iwashiro et al, 2012; Jung et al, 2012; Kambeitz-Ilankovic et al, 2015; Mechelli et al, 2011; Nenadic et al, 2015; Pantelis et al, 2009) (reviewed in (Brent et al, 2013; Smieskova et al, 2013) and functional changes in response to WM and other cognitive tasks (Allen et al, 2011; Dutt et al, 2015; Fusar-Poli et al, 2011b; Natsubori et al, 2014). In the PHP and medial temporal lobe (MTL, including the hippocampus, amygdala and surrounding entorhinal and perirhinal cortices), CHR most reliably demonstrate structural alterations (e.g., reduced gray matter, cortical thinning)(Buehlmann et al, 2010; Jung et al, 2011; Mechelli et al, 2011; Mittal et al, 2011; Pantelis et al, 2003; Tognin et al, 2013), with one previous study demonstrating task-induced functional alterations in antipsychotic naïve CHR (Allen et al, 2011). In the striatum, altered striatal activity, as well as altered striatal dopamine (Allen et al, 2012; Fusar-Poli et al, 2011e), glutamate (de la Fuente-Sandoval et al, 2011), GABA (Kang et al, 2014) and 5HT(2A) binding (Hurlemann et al, 2008), have been reported in CHR.…”

Cross-Cutting Advancements Usher in a New Era for Motor Research in Psychosis

“…Second, evidence has been gathering over the past two decades to suggest that spontaneous motor abnormalities can occur as a function of pathophysiology in a sizeable subsample of individuals with schizophrenia. 15,16 This has been demonstrated in studies of unaffected relatives, 17 prodromal youth, 18,19 as well as medication naïve groups (for a review see Pappa and Dazzan 20 ). Although it is still difficult to study motor behaviors in patients treated with any medications that affect subcortical dopamine (DA) activity, a more widespread understanding that these behaviors reflect pathogenic processes, research approaches with low dosage inclusion criteria and medication-free or medication-naïve patients, as well as designs focusing on individuals who represent a lower vulnerability loading on the psychosis continuum (ie, populations with elevated schizotypy, schizotypal personality disorder, and nonclinical psychosis exhibit motor abnormalities but are often unmedicated), [21][22][23][24][25][26] will continue to open new avenues.…”

Social Motor Coordination in Unaffected Relatives of Schizophrenia Patients: A Potential Intermediate Phenotype

“…Unfortunately, the cross-sectional design of our study does not allow us to conclude for the fourth criterion “state independent in affected individuals,” (i.e., manifests in an individual whether or not illness is active). But, several studies suggest that adolescents who later develop schizophrenia exhibit motor behavior disorders, particularly motor dyscoordination, well before overt manifestations of the illness (Leask et al, 2002; Mittal et al, 2011). Future research should assess the presence of IMC impairment in adolescents with a high risk of schizophrenia in order to confirm the fourth criterion.…”

“…NSS are observable in first-episode patients (Bachmann et al, 2005), and even prior to antipsychotic administration (Scheffer, 2004; Chen et al, 2005). Additionally, adolescents who later develop schizophrenia exhibit signs of neurological abnormalities, particularly motor dyscoordination, well before overt manifestations of the illness (Leask et al, 2002; Mittal et al, 2011), providing further evidence for a fundamental role of motor dysfunctions as an early constitutional vulnerability of schizophrenia. Several studies showed that NSS are present in relatives of schizophrenia patients (Chan et al, 2010; Neelam et al, 2011), and are among the most promising of the candidate intermediate phenotypes (Chan and Gottesman, 2008).…”