Research in children and adolescents with obsessive-compulsive disorder (OCD) is increasing in both quantity and quality. This session will focus on new and exciting research findings regarding family genetic studies, infectious and immune etiologies, pediatric psychopharmacology, and cognitive behavioral treatment.

Parkinson's disease (PD) is one of the most common neurodegenerative diseases. The last 5 years have been marked by rapid developments in understanding the pathophysiology of PD as well as by the introduction of a number of new drugs for symptomatic treatment of the disease. On the other hand, the diagnosis of PD is still made purely on clinical grounds. Due to continuing advances in therapy, it is increasingly important to recognize PD in its earliest stages and to distinguish it from other causes of parkinsonism, for which prognosis and response to treatment differ. This article reviews the epidemiology of PD and then elaborates on the diagnosis and differential diagnosis.

Autism is heterogeneous with respect to clinical symptoms and etiology. A significant limitation in research of the neurobiology and treatment of autism has been the lack of attention to this heterogeneity. A dimensional approach to the study of autism is valuable in linking key symptoms to the neurobiology and treatment of the disorder in a clinically meaningful way. In this article, we outline a dimensional approach to the autism spectrum, discuss the three core dimensions of autism and their neurobiology, and review the possible links of serotonin, anterior cingulate gyrus activity, and the immune marker D8/17 to the repetitive behavior/compulsivity dimensions.

Neurobiological studies continue to generate new clues to the pathophysiology of obsessive-compulsive disorder (OCD). Currently, the weight of evidence implicates serotonin (5-hydroxytryptamine, 5-HT) receptor dysfunctions, but there is also evidence for abnormalities in other neurotransmitters, such as dopamine and noradrenaline, in neuropeptides, and for infective and immunological mechanisms. Such findings foster further questions, in particular the identification of the 5-HT receptor subtype involved, the meaning of the serotonergic abnormalities described thus far, and their relationships with the evidence of dysfunctions of other systems.

Certainly, new horizons can now be prospected for biological research in OCD with the ultimate goal of identifying the substrates of the clinical heterogeneity and of offering patients more targeted treatments.

Myriad difficulties exist in analyzing the pharmacology of the serotonin 1A (5-HT1A) receptor. The receptor may demonstrate a different activity depending on the tissue or species used for analysis, the agent used, laboratory conditions, and differences between in vitro and in vivo effects of compounds. Affinity for 5-HT receptors also varies widely, presenting difficulties in drawing definitive conclusions on affinity values for various compounds. At least two possibilities exist to explain the diversity of pharmacology of 5-HT receptors. First, it is possible that different 5-HT1A receptor subtypes exist. Second, the 5-HT1A receptors may play a far more complex role than previously believed.

Contemporary neuroimaging methods have been used to gather initial data regarding the neural substrates of posttraumatic stress disorder (PTSD). Morphometric magnetic resonance imaging (MRI) studies have reliably shown reduced hippocampal volume in subjects with PTSD vs control cohorts. Functional imaging studies have implicated a network of brain regions in PTSD, comprising the amygdala, hippocampus, and anterior paralimbic territories (including anterior cingulate cortex), as well as Broca's area and visual cortex. Extant relevant neuroimaging data are reviewed, and a tentative heuristic neuroanatomical model of PTSD is provided. In conclusion, emerging strategies for advancement in this field are outlined.