To our knowledge, this is the first report to examine the relationship between neuromotor dysfunction and psychosocial functioning in individuals at clinical high-risk for psychosis. Previous studies using a different high-risk sample have observed that at-risk adolescents show elevated dyskinetic movements when compared to healthy and psychiatric controls (Mittal et al., 2008
; Mittal et al., 2007b
). The present investigation builds upon these results, finding that dyskinesias are associated with impairment in psychosocial functioning and also predictive of a domain specific changes one-year later. Taken together, these findings suggest that pathological processes underlying motor dysfunction may also contribute to the pervasive declines in role and social functioning characteristic of this population.
Both prospective high-risk studies (Dworkin et al., 1994
; Hans et al., 2000
) and larger birth cohort investigations (Done et al., 1994
; Jones et al., 1994
) have indicated that early social difficulties are evident in preschizophrenic individuals as early as age seven. Further, it is of interest that the progression of functioning deficits appears to follow what would predict in a two-hit model (Mednick et al., 1998
). Specifically, although the deficits are present in childhood, they become progressively worse prior to the onset of schizophrenia, potentially reflecting an underlying vulnerability interacting with maturational processes and environmental stressors. During adolescence, a time characterized by tumultuous environmental stressors and marked neuroendocrine development, these deficits become more severe in those who go on to develop psychosis (Cannon et al., 2008
; Yung et al., 2004
). In line with these findings, it is also clear that functional decline in clinically at-risk youth is intimately tied with the progression of illness (Yung et al., 2004
). Finally, it is noteworthy that functioning appears to be more tied to negative symptoms and other core features such as cognition (Niendam et al., 2007
), but not to fluctuations in acute symptoms or medication status (Green et al., 2004
). Taken together, these results suggest that psychosocial functioning is reflective of a core underlying pathology.
Results of the present study indicate that elevated dyskinetic movements are associated with deficits in psychosocial functioning, and replicate findings that the presence of baseline movement abnormalities significantly distinguishes those high-risk patients who will eventually convert to psychosis (Mittal and Walker, 2007
). Because the striatum serves as a connection point for pathways leading from the basal ganglia to the cortex (Alexander et al., 1990
; Nieoullon, 2002
), dysfunction in this region may contribute to irregularities in movement behaviors (subsumed by the motor circuit) (Mittal et al., 2010a
), as well as disruption in a host of processes integral to psychosocial functioning, ranging from those primarily regulated by the striatum (e.g., processing novel stimuli, initiation of behavioral responses), to those governed by the prefrontal cortex (e.g., decision making, planning complex cognitive behaviors, moderating correct social behavior) (Clatworthy et al., 2009
; Muller et al., 2000
). In support of this notion, Lichter and Cummings (2001)
have noted that fronto-striatal systems are involved in the integration of sensory and limbic phenomena, and play key roles in both neuromotor processes and psychosocial functioning, (e.g., motivation and goal selection).
The idea of a basal ganglia impairment underlying both movement and role/social functioning is also supported by a birth cohort study which found that delays in infant motor development were associated with poorer adult cognition in the domains of executive function, verbal learning, and spatial memory in patients who developed schizophrenia in adulthood (Murray et al., 2006
). In another important study, Schiffman and colleagues (2004)
observed a sample of school-age children interacting at lunchtime, many of whom had a parent with schizophrenia. When the authors analyzed the adult psychiatric outcomes for the children, it was found that those who developed schizophrenia as adults evidenced greater social and neuromotor deficits in childhood than those who did not go on to develop a psychotic disorder (Schiffman et al., 2004
The present findings also suggest that among a group of adolescents at high-risk for developing psychotic disorders, current abnormalities in movement are a prognostic indicator of later course of social functioning and show a strong trend in the same direction for role functioning. Support for this finding comes from a study conducted by Nuechterlein and colleagues (2008)
, who observed motor deficits in a dual interference task predicted poor occupational outcome in a population of patients with first-onset schizophrenia. It is also interesting that we found evidence to suggest predictive relationships between movement and both longitudinal social and role functioning (albeit at the trend level for role functioning), but that there was not a significant correlation between movement and social functioning at baseline. One possibility to consider is that early basal ganglia dysfunction may impact core aspects underlying more basic role functioning, but also herald more widespread behavioral dysfunction, affecting global social functioning as time progresses. Future research aimed at examining underlying components of social and role functioning, and the relationship of these constructs with neuromotor dysfunction is necessary to untie this complex question.
A limitation of this study involves the use of videotaped interviews as the sole venue for measuring movement abnormalities. While the method has yielded consistent and important results in past studies (Schiffman et al., 2004
), the inability to measure lower-body movement is a limitation. However, it should be noted that previous examinations following movement abnormalities in schizophrenia-spectrum disorders have found that lower-body movements do not significantly distinguish high-risk youth (Mittal et al., 2007b
). Another limitation relates to the modest sized sample; replication with larger samples from multisite collaboration efforts will help to elucidate subtle brain-behavior patterns among at-risk youth. A final limitation relates to the unavoidable use of psychotropic medication in naturalistic designs. Although medication was statistically controlled in the present analyses, and not found to affect the relationship between movement and psychosocial function, this does not entirely eliminate the potential confound of medication effects. Prescription of psychotropics is expected to be targeted to those with more severe behavioral dysfunction and, perhaps, concomitant movement abnormalities. Thus controlling for medication can affect the variance in ratings of disease progression and movements, thereby attenuating covariance between these two factors. Because of these constraints, the present results should be interpreted as preliminary, until larger studies can provide a supplemental analysis on high-risk youth who are medication-free in larger proportions of the sample. Taken together, these findings highlight the need to further understand etiologically factors underlying psychosocial functioning, which may be an important target for intervention, particularly during a developmental period when social and role functioning behaviors are becoming increasingly central to ones’ identity.