Obsessive-Compulsive Disorder (OCD) – Neurobiology

Posted by in Obsessive-compulsive disorder (OCD) What causes OCD? Researchers have had much recent success in elucidating the neural circuitry involved in OCD.  Advances in functional neuroimaging have identified robust alterations in neural activity within particular functional circuits in individuals with the disorder (Graybiel & Rauch, 2000).  Specifically, OCD is associated with pervasive disruptions in frontal subcortical circuitry (Luxenberg et al., 1988; Robinson et al., 1995).  Before we discuss abnormalities in this circuitry related to OCD, it is worth reviewing the generalities of this neural system. Frontal subcortical circuitry. According to Tekin and Cummings (2002), frontal subcortical circuits share several commonalities.  They often “originate in prefrontal cortex, project to the striatum (caudate, putamen, ventral striatum), connect to the globus pallidus and substantia nigra and from there connect to the thalamus.  There is a final link back to the frontal cortex [such that] each circuit forms a closed loop” .  The prefrontal cortex (PFC) can be subdivided into several regions including the dorsolateral prefrontal cortex (DLPFC), the orbitofrontal cortex (OFC) and the anterior cingulate cortex (ACC); and these subregions are involved in separate circuits (the DLPF circuit, the OF circuit, and the AC circuit, respectively).  These circuits have been implicated in various functional tasks.  Individuals with dysfunction in DLPFC areas often exhibit deficits in attention, reasoning, and mental flexibility.  Damage to OFC has been associated with personality changes including behavioral disinhibition and impaired judgment (Tekin & Cummings, 2002).  Work by Damasio and colleagues (1996; 1990) indicates that insults to OFC result in deficits in reward expectancies and preferences.  The ACC is closely interconnected with the limbic system and is thought to support motivation and affective behavior.  Due to its association with motor cortex, the ACC presumably mediates emotionally-motivated movement.  Together, the ACC and OFC influence the emotional value of stimuli and the selection of behavior based on possible reward. Saxena and Rauch (2000) have suggested that excess positive feedback within frontal subcortical circuits might drive the repetitive symptoms that characterize OCD.  What evidence supports this theory?  In individuals with OCD, resting hyperactivity within frontal subcortical loops has been observed reliably, and this activity is potentiated by symptom provocation (Saxena, Brody, Schwartz, & Baxter, 1998).  Interestingly, following either successful behavioral or pharmacologic treatment for the disorder, this hyperactivity diminishes to normal levels.  Empirical evidence implicating frontal subcortical circuitry in the etiology of OCD also includes work by Kelly (1980) who showed that lesions of the cingulate gyrus...
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Social media (Twitter, Facebook, Google+) in a psychological practice

Posted by in General Lately, I’ve been experimenting with new and better ways of incorporating social media tools into my practice.  Just yesterday, I developed a list of CBT-based exposure ideas for reducing symptoms of OCD, perfectionism, and social anxiety.  What was unique about these exposure ideas was that they were all targeted specifically toward actions one might take online using social media communities like Twitter and Facebook.  Using these very same social media tools, I was able to quickly distribute this content to several different online communities.  Although this face of my practice is virtually brand new, I can already see the power in it.  Although my readership is still small, it’s growing (of course, you could always help it grow faster by following me on Twitter, Facebook, or Google+). The use of social media tools within a professional mental health practice is potentially game-changing.  It becomes simple to disseminate information rapidly, including my blog posts which represent some of the ideas that are foremost in my mind at any given time.  Twitter, Facebook, and Google+ also allow me to interact with my readership in a new and dynamic way, giving me the means by which to get direct feedback and reactions from the larger public.  These tools give me a venue to discuss the ideas that excite me, hear about breaking news on the psychology front, get exposed to new ideas I wouldn’t have considered on my own, and connect easily with others who might either share or disagree with my opinions.  This is powerful stuff, particularly for psychologists who are involved in small private practices. However, the very ease of communication that I so enjoy in one context can become problematic in another, such as when I’m communicating with mental health consumers.  Potential pitfalls include maintaining confidentiality in an online world, explaining to consumers that I can only provide therapy within the context of a therapist-client relationship, finding the time to maintain an active and reciprocal online presence, and keeping abreast of all the rapid technological changes that define (and will continue to define) this medium.  I am cognizant of these issues, and I have informally implemented policies that safeguard against any such problems that might arise. Nevertheless, with these issues in mind, I am in the process of documenting a formal social media policy that will guide my online activities.  Fortunately, I don’t have to invent the wheel; other knowledgeable mental health...
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