An event-based analysis of the coordination of early infant vocalizations and facial actions

This study used an event-based approach to provide empirical evidence regarding the nature of coordination in 3- and 6-month-old infants. Vocalizations and facial actions of 12 normally developing infants interacting with their caregivers were coded. Coded vocalizations and facial actions were considered coordinated when they temporally overlapped. Results indicate that infants coordinated their vocalizations and facial actions more than expected by chance. Coordinated events were governed by 2 sequence patterns. When 2 communicative events were temporally associated across modalities, 1 event tended to be completely embedded within the other, and vocalizations tended to end before facial actions. This study provides new information about how infant communication is structured, confirms results from other coordination studies, and describes a new method for analysis of event-based data.     

Odor identification impairments in schizophrenia: relationship with demographic measures, clinical variables, and diagnostic subtypes

Smell identification deficits are consistently found in schizophrenia (SZ), but little is known about the nature and characterization of this deficit or its relationship to the phenomenology of the illness. This study aims to further delineate smell identification errors in SZ by examining the relationship of patient demographic differences with smell-identification performance. Our results showed that a patient's gender and education were related to odor-identification scores, with better performance seen in female patients and in those with greater educational attainment. However, there was no effect related to age, ethnicity, or socioeconomic status on odor identification. A smell identification deficit was also unrelated to clinical characteristics of the patients, including age at first hospitalization, number of psychiatric hospitalizations, and duration of illness. Odor identification also did not differ by SZ subtype, nor between SZ and schizoaffective disorder patients. These findings emphasize that odor identification deficits in SZ are unrelated to clinical illness features, cannot be explained by other confounds related to olfaction in the general population, and may be core features related to the SZ disease process.     

A Characteristic Frame for Positive Intuitionistic and Relevance Logic

Studia Logica - I show that the lattice of the positive integers ordered by division is characteristic for Urquhart’s positive semilattice relevance logic; that is, a formula is valid in...     

Basic Intuitionistic Conditional Logic

Journal of Philosophical Logic - Conditional logics have traditionally been intended to formalize various intuitively correct modes of reasoning involving (counterfactual) conditional expressions...     

Driven from distraction: how infants respond to parents' attempts to elicit and re-direct their attention

This experiment examined how parents' verbal and non-verbal behavioral cues cause infants to shift and share attention within environments where many objects compete for infants' attention. Fifteen- and 21-month-old infants played with toys while their parent periodically shifted attention to a distal object within a larger array. Parents' attention-shifts were indicated by a change in direction of gaze, a pointing gesture, and/or verbalizations. Verbalizations were either attention-eliciting or attention-directing. In some trials parents covered their eyes to occlude line-of-gaze. Both ages seldom followed simple gaze shifts, but frequently followed gaze with-points or gaze-with-directing verbalizations. Attention-eliciting verbalizations increased infants' looks to the parent. Gaze occlusion reduced infants' responses to directing verbalizations. Responses to eliciting verbalizations increased with age. Infant receptive vocabulary did not predict attention-sharing, even when parents named objects (i.e., directing verbalizations). Implications for development of attention-sharing, language and understanding of visual attention are discussed.     

Low heart rate variability is not caused by typical neuroleptics in schizophrenia patients

Both elevated cardiovascular mortality and low cardio-vagal (parasympathetic) heart rate variability (HRV)--a risk factor for postmyocardial infarction--are reported in schizophrenia (SZ). Since a number of medications have strong effects of cardiac conductivity, we thought it important to examine if typical neuroleptic medications might also affect HRV. We examined cardiac vagal activity during both neuroleptic treatment and a drug-free condition in seven SZ patients who were participating in a pilot double-blind, crossover study of placebo and haloperidol treatment. Twenty-four-hour Holter electrocardiograms were analyzed for high frequency HRV, quantitated as the percent of successive normal interbeat intervals greater than 50 milliseconds (PNN50), which is a good index of parasympathetic cardiac modulation. The patients showed unchanged PNN50 (8.4+/-9.5 versus 8.3+/-10.5; t=.22, df=6, P=.5) between the haloperidol treatment and drug-free conditions. Despite the elapsed time, change in medication, and altered clinical state, the PNN50s were highly correlated (Spearman r=.98, P=.000). SAPS positive symptom scores declined with treatment from 12.8+/-6.5 to 8.5+/-3.5; paired t=3.26: df=6; P=.01. PNN50s were significantly associated with positive (r=-.86, df=6, P=.012) and negative symptom scores (r=-.87, df=6, P=.01). We found low cardiovagal modulation in medication-free SZ patients that was associated with core SZ symptoms and was unchanged by haloperidol and benztropine treatment. The reduced HRV in SZ patients at baseline may render them at greater cardiovascular risk than healthy subjects when treated with medications having strong cardiovascular effects.     

Could stress cause psychosis in individuals vulnerable to schizophrenia?

It has long been considered that psychosocial stress plays a role in the expression of symptoms in schizophrenia (SZ), as it interacts with latent neural vulnerability that stems from genetic liability and early environmental insult. Advances in the understanding of the neurobiology of the stress cascade in both animal and human studies lead to a plausible model by which this interaction may occur: through neurotoxic effects on the hippocampus that may involve synaptic remodeling. Of late, the neurodevelopmental model of SZ etiology has been favored. But an elaboration of this schema that credits the impact of postnatal events and considers a role for neurodegenerative changes may be more plausible, given the evidence for gene-environment interaction in SZ expression and progressive structural changes observed with magnetic resonance imaging. Furthermore, new insights into nongliotic neurotoxic effects such as apoptosis, failure of neurogenesis, and changes in circuitry lead to an expansion of the time frame in which environmental effects may mediate expression of SZ symptoms.