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Using Google Drive to Track Client Behaviors

9 May

I came across an article at Lifehacker recently that included a downloadable Google Drive form billed as a “Daily Personal Inventory.” The article, titled “Fill Out This One-Minute Form Every Day and Find Out Why Your Life Sucks (Or Doesn’t),” got me thinking about the countless ways Google Drive could be used to track client mood, eating patterns, self-care, or other behaviors related to therapeutic goals. Because spreadsheets on Google Drive can be shared and mutually edited, I could increase accountability by periodically checking client progress and leaving comments in a designated column. Client data could also be graphed for a quick visual assessment of progress, and it could ultimately be used as a rough measure of therapist effectiveness. Google Drive documents could even be shared with psychiatrists or other health professionals involved with a client to increase integration of care.

I’ve been playing around with a simple mood-tracking spreadsheet format, and I may try creating tracking documents for other behaviors. Although confidentiality could be an issue – Google’s confidentiality policy is relatively solid, but not water-tight by any means – clients could be informed of the risks and benefits and given the opportunity to sign a consent form prior to data tracking.

Have any of you ever used Google Drive as a therapeutic aid?

 

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A Good Read on Self-Doubt in Therapy

21 Mar

My friend Molly shared this article with me today, and I thought it did a nice job of illuminating the anxiety we often feel as beginning therapists and describing one individual’s process of working through it. Check it out here:

A Crash Course in Psychotherapy: Moving Through Anxiety and Self-Doubt – by Charlotte Dailey

Inclusive Art in Therapy Rooms

4 Feb

I spent a lot of time touring mental health care facilities last month, and many of these sites – especially university counseling centers – demonstrated a clear commitment to decorating their walls in a culturally inclusive way. I saw Peruvian wall hangings, portraits of African-American jazz artists, a Buddha painting, Frida Kahlo prints, and West African masks. One training director explained the rationale for her site’s decor as she shepherded me and other internship applicants through the building: “We want everyone to feel represented here.”

I also spent a lot of time sitting around in airports last month, which provided ample opportunity to sort through my own ideas about what makes “good” therapy room decor, and what I might do to make a room feel inclusive. If I get an internship this year, it’s likely that I’ll be given a space to decorate. And I really like the idea of channeling the ol’ creative juices into making a therapy room my own. I am, after all, a person who guiltily and avidly follows a bunch of craft and decor blogs, feverishly pinning projects to a Pinterest board to make “eventually.”

Prior to my trip, I had always imagined myself decorating in a soothing, blandly nature-themed way. And while I certainly still want my theoretical room to have a positive vibe, and I like things that are shaped like branches far too much to abandon the idea of nature-themed decor entirely, I think I could accomplish more with art that conveys inclusiveness.

A small (and not at all exhaustive or fully inclusive) selection of art I’d love to put in a therapy room:

Pakistani Girls Show Their Hands Painted with Henna Ahead of the Muslim Festival of Eid-Al-Fitr by Khalid Tanveer; from allposters.com

Unite with Pride; image from advocate.com

Peaceful Moment, by Monica Stewart (from allposters.com)

Disability is an Art, from the University of New Hampshire Institute on Disability

Balloons, Mexico by David J. Negrón (see the artist’s site here)

Cherry blossoms painting, identity unknown – I came across this one here and loved it, but I can’t find its name or the artist who painted it anywhere. Does anyone recognize it?

**Note: A friend informs me this is Chinese Painting by Jun Wan. Thanks, Wes!

The Path of the Shapeshifter, by Helena Nelson-Reed (artist’s website here)

Any sculpture by Shelly Tincher Buonaiuto (below: Wind)

To other future psychologists or current therapists: do you ever daydream about therapy room decor? If you already have a room of your own, how have you chosen to decorate it?

Exercise is Depressingly Awesome

20 Dec

I hate exercising for the sake of exercise. I wouldn’t be able to pass my high school’s Presidential Fitness Test today – I mean, I barely passed it back then, and I only passed because our gym teacher let us all cheat at pull-ups – and the idea of “running for fun” is mystifying and unsettling. The only forms of exercise that truly appeal to me involve large, expensive animals that I cannot currently afford (horseback riding, doing stuff with my future giant dog), swimming leisurely, dancing, or actively accomplishing things (i.e., gardening). I also like the playground game Four Square, but it’s really hard to get a group together to play now that I’ve graduated from middle school, and these days everyone wants to do the online kind of Four Squaring anyway.

So when I finally caught up with my backlog of APA Monitors this week, I was pleased to read this month’s Questionnaire section, in which Dr. Howard Friedman was interviewed about his longevity research. As a person who is always searching for justification to avoid the gym, I especially liked the following quote:

“…our studies suggest that it is a society with more conscientious and goal-oriented citizens, well-integrated into their communities, that is likely to be important to health and long life. These changes involve slow, step-by-step alterations that unfold across many years. But so does health. For example, connecting with and helping others is more important than obsessing over a rigorous exercise program.”

Excellent, I thought, chortling to myself. The Presidential Fitness Test can suck it. But a few pages later, I ran into Kirsten Weir’s “The Exercise Effect,” which briefly and convincingly summarizes some recent research supporting the effectiveness of exercise as an intervention for major depression and anxiety disorders. Weir’s article is the latest in a stream of exercise-related literature that has made its way into my hands in the last couple months, and while the notion that exercise can be helpful for depression and anxiety isn’t new, it seems that interest in the focused use of exercise as a behavioral intervention has been on the rise lately. So much for my plans to connect with and help others solely from a sitting position.

This isn’t to say that I neglect discussion of exercise’s benefits when working with clients who are depressed or anxious. It always shows up somewhere in the  “Here-are-some-things-that-we-know-can-be-effective” speech, and sometimes I help clients develop brief behavioral plans to get them moving. But if clients express little interest in exercising, I focus on other interventions and don’t push the issue – because after all, who am I to push someone else to exercise? Yet the research I’ve been exposed to lately suggests that maybe I should be pushing… and not just pushing clients. Weir quotes Dr. Michael Otto, who claims that “failing to exercise when you feel bad is like explicitly not taking an aspirin when your head hurts.” A physician who refuses to use aspirin because it’s “too hard” or “not interesting” would be ridiculed. Should the same level of ridicule be directed at a psychologist who explicitly refuses to exercise?

I’m admittedly biased, but I don’t think Otto’s analogy is a fair comparison. A physical workout is usually a  sweaty, gaspy, time-consuming set of behaviors that requires organizing on the part of the individual and produces effects that aren’t always immediately apparent. (I have never, ever experienced a runner’s high, and there have been times when I have tried to make exercise a serious part of my life.) Taking an aspirin is a three-second endeavor… maybe six seconds, if you have a hard time with the child-proof cap. We’re not talking about similar behavioral investments. There’s also still a lot we don’t know. Should we all be running six miles a day, or will a brisk 20-minute walk a few times a week do the trick? Does it matter if we exercise alone or with others? Weir notes that “researchers don’t yet have a handle on which types of exercise are most effective, how much is necessary, or even whether exercise works best in conjunction with other therapies.”

Despite the questions that remain, the research I’ve been reading lately has encouraged me to make more of an effort to engage my clients in exercise, and to get myself more engaged too. But if my own hate-hate relationship with exercise has taught me anything, it’s that for most of us, exercise must be rewarding in the moment for it to be truly sustainable. If you legitimately enjoy going to the gym or training for 10Ks, then that’s awesome, and I really wish I had a share of your crazy exercise-loving genes. But I don’t think there’s anything wrong with making exercise a secondary component to some other goal, whether that goal is doing something fun with your dog or doing yardwork or getting to the grocery. For me and the clients who despise the gym as much as I do, it may be worthwhile to create behavioral plans that focus on adding exercise to already-enjoyed or necessary activities rather than instituting a “traditional” exercise plan from scratch. Some examples of what I mean:

  • Primary goal: hang out with friends, family, or your partner. Exercise addition: hang out while swimming, walking, window-shopping, dancing or hiking. Or take a movement-based class with friends through a university or community center.
  • Primary goal: have a phone conversation with a family member. Exercise addition: stretch or walk around building during conversation.
  • Primary goal: make a difference in the community. Exercise addition: choose a volunteer activity that requires movement (e.g., cleaning cages at the humane society, participating in fun runs/walks for charity, helping with a Habitat build, etc.)
  • Primary goal: have a romantic evening with your partner. Exercise addition: sex, duh.
  • Primary goal: make apartment/house more attractive. Exercise addition: incorporate active DIY projects, like painting, landscaping, thorough cleaning, etc.
  • Primary goal: cook dinner. Exercise addition: turn on music that makes you want to dance and bust a move while cooking. Ke$ha and LMFAO, though not exactly highbrow, produce some pretty irresistible dance music.
  • Primary goal: play video games. Exercise addition: play games on a console that requires movement (like the Wii or Playstation Move)
  • Primary goal: keep dog from getting bored and chewing up all your stuff. Exercise addition: go on interesting walks or hikes, play frisbee at the dog park, take an agility training class.
  • Primary goal: make extra money during grad school. Exercise addition: babysit an active child or children.

Exercise doesn’t have to involve weights or running shorts to count as exercise, and even small “doses” of exercise seem to produce measurable mental health benefits (see Weir’s article). And if we conceptualize exercise in a simple, essence-based way – as sustained, purposeful movement, separate from the very specific types of movement promoted by Fitness Magazine spreads and Nike commercials  – then maybe I don’t hate exercise at all. It’s the word itself that’s the problem for me, and its connotations of in-the-moment pointlessness and endless striving toward weight- or muscle-based goals that my genes never meant for me to achieve. But dancing while cooking dinner? I can do that. I can like that. And I think some of my clients could too.

Does anyone else have ideas for making exercise a natural addition to primary goals?

The Freaky and Wonderful Hippocampus

8 Dec

OK, I’m about to dork out on you big time.

I’ve been writing a paper this week about neurogenesis in the hippocampus and how it relates to depression. It’s possible that I lost you right about at the point where I said “neurogenesis in the hippocampus.” Stick with me – this is cool stuff.

Image from Wikipedia

The hippocampus, a small temporal-limbic structure generally associated with memory consolidation and retrieval , is unusual in its ability to continually support neurogenesis (the production of new neurons) in the adult brain. Very briefly, here’s how the process goes down: precursor cells form in the subgranular zone of the dentate gyrus, a flexed, layered region that is located near the center of the hippocampus. The precursor cells then migrate into another layer of the dentate gyrus known as the granule cell layer to mature. It’s assumed that the hippocampus must continually generate these new neurons in order to form distinctive episodic memories without interference from older neurons.

Neurogenesis in the hippocampus seems to be highly sensitive to a lot of factors. For example, neurogenesis declines in response to advancing age and stress, and it increases in response to estrogen levels, learning, and physical activity. Major depression appears to be related to reductions in hippocampal neurogenesis, while sustained use of antidepressants is associated with increased neurogenesis – correlations that have been highly interesting  to depression researchers, clinicians, and even tired graduate students.

We know that severe or chronic stress often precedes major depression in people who are genetically prone to the disorder. Given the particularly potent effects of stress on hippocampal neurogenesis, which have been demonstrated in a lot of animal studies, it seems likely that stress plays a key role in initiating the neurogenesis inhibition associated with depression. More disturbingly, chronic or severe stress – and the depressed behavior associated with it – has also been linked to problems with neuron survival in animal hippocampi. While current technology doesn’t allow us to safely study neurogenesis in living people , human studies do show that hippocampal volumes (and presumably hippocampal neurogenesis and neuron survival) are negatively affected by prolonged major depression. Atrophy in the hippocampus can persist for decades after remission, and the magnitude of volume loss may be as high as 20%.

If the hippocampus is implicated in depression, we’re faced with a chicken-or-the-egg question: do problems with hippocampal neurogenesis and neuron survival make people vulnerable to depression? Or does depression inhibit neurogenesis and neuron survival in the hippocampus? Most evidence seems to support the latter. A study by MacQueen and colleagues (2003) found that patients who had experienced only one major depressive episode didn’t differ from matched controls in hippocampal volume, while patients who had experienced multiple episodes demonstrated significantly smaller hippocampal volumes than controls. These changes weren’t accounted for by increasing age, providing support for the idea that reductions in hippocampal volume don’t precede depression. In a study by Santarelli and colleagues (2003), focused radiation was applied to the hippocampi of mice to end neurogenesis, a procedure that should have resulted in observably depressed behavior if inhibited hippocampal neurogenesis initiated depression. However, the behavior of mice that had undergone the procedure didn’t differ from the behavior of mice in the control condition. Interestingly, the procedure did appear to block the ability of the antidepressant fluoxetine (Prozac) to produce its usual behavioral effects. If the functional aspects of recovery from depression depended solely on changes in the neurotransmitter mechanisms that antidepressants target, halting hippocampal neurogenesis shouldn’t have impacted the effectiveness of the Prozac. This finding suggests that while hippocampal neurogenesis may not contribute significantly to the development of depression, it may be crucial to recovery from depression. Almost all antidepressants have been shown to stimulate hippocampal neurogenesis and/or improve neuron survival, and it’s probably not a coincidence that the typical delay in antidepressant effectiveness (about 6 weeks) is about the same length of time as the maturation time of new neurons in the hippocampus. Frodl and colleagues (2008) found that people who took antidepressants regularly over the course of a three-year period demonstrated increased hippocampal volume, while subjects who did not take antidepressants consistently didn’t demonstrate these gains, regardless of whether or not their depression was in remission.

It’s important to note that the role that the hippocampus plays in depression is still a matter of some debate, and it’s widely acknowledged that there are undoubtedly other factors that play a crucial role in the regulation of neurogenesis in the adult hippocampus that have yet to be identified or understood. We also have to remember that most studies of hippocampal neurogenesis during depression are animal studies, and depression among animals – usually measured via tests involving response to food – may not be a perfect counterpart to the complex condition that is human depression. The conclusions drawn from animal studies must be applied to humans with caution.

Limitations aside, the research literature does offer an interesting perspective on depression and has potentially exciting implications for treatment. Given the convincing body of evidence suggesting that hippocampal neurogenesis must be present for antidepressants to produce at least some of their desired effects, new types of medication may be worth exploring. Most existing antidepressants target reuptake of the neurotransmitters serotonin or norepinephrine; hippocampal neurogenesis is just a nice side effect. There are, however, several promising new compounds that have been shown to stimulate hippocampal neurogenesis and that may eventually be capable of producing antidepressant effects without the negative side effects (drowsiness, decreased libido, etc.) that so often accompany traditional antidepressants. At any rate, the superior effects of long-term antidepressant treatment suggest that clinicians should continue to strongly encourage clients who have begun antidepressant regimens to stay on their meds for at least the requisite six weeks. It’s possible that clients might be more willing to persist in taking meds despite crappy initial side effects if they’re aware of the (theoretical) role of the hippocampus in the efficacy of antidepressants and the amount of time required for successful neurogenesis to take place.

The research on this subject also offers possible new directions for our understandings of other treatments that have been shown to be effective for depression, including exercise, stress reduction and mindfulness techniques, and even electroconvulsive therapy, all of which have been associated with improvements in neurogenesis. Could hippocampal neurogenesis stimulation be the common thread underlying all of these treatments? Of course, this line of thought raises many more questions. If hippocampal neurogenesis is the mechanism underlying successful treatment, could treatments have additive effects on the hippocampus? For example, do clients who take Prozac and exercise regularly experience faster neurogenesis or better neuron survival than clients who use only one treatment? What are the limits of hippocampal neurogenesis, and what implications do these limits have for long-term use of antidepressants? Can a hippocampus generate too many new neurons? What happens if it does? And if reductions in hippocampal volume are associated with memory problems common to depression, could long-term use of antidepressants result in improvements in memory?

Ted says that he thinks science is like throwing rocks at a thing in the dark and trying to guess the shape of it by listening to the sounds the rocks make. While we still don’t know the exact shape of the relationship between the hippocampus and depression, “rocks” are being thrown with great enthusiasm – a search for “hippocampal neurogenesis” on a handful of research databases brings up a list of 1128 research articles published after 2000, many of which directly address mood and motivation – and the field has already produced findings that promise to have important ramifications for the way depression is understood and treated in the future.

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If you’re as interested in this stuff as I am and have loads of free time to read research articles (lol!), here are some articles that I found especially interesting:

Balu, D. T., & Lucki, I. (2009). Adult hippocampal neurogenesis: Regulation, functional implications, and contribution to pathology. Neuroscience and Behavioral Reviews, 33, 232-252.

Becker, S., & Wojtowicz, J. M. (2007). A model of hippocampal neurogenesis in memory and mood disorders. Trends in Cognitive Sciences, 11(2), 70-76.

Frodl, T., Jager, M., Smajstrlova, I., Born, C., Bottlender, R., Palladino, T., Reiser, M., Moller, H., Meisenzahl, E. M. (2008). Effect of hippocampal and amygdala volumes on clinical outcomes in major depression: a 3-year prospective magnetic resonance imaging study. Journal of Psychiatry and Neuroscience, 33(5), 423-430.

Hanson, N., Owens, M., & Nemeroff, C. (2011). Depression, antidepressants, and neurogenesis: A critical reappraisal. Neuropsychopharmacology, 36(13), 2589-2602.

MacQueen, G. M., Campbell, S. , McEwen, B. S., Macdonald, K., Amano, S., Joffe, R. T., Nahmias, C., & Young, L. T. (2003). PNAS, 100(3), 1387-1392.

Marcussen, A. B., Flagstad, P. P., Kristiansen, P. G., Johansen, F. F., & Englund, U. U. (2008). Increase in neurogenesis and behavioural benefit after chronic fluoxetine treatment in Wistar rats. Acta Neurologica Scandiniavica, 117(2), 94-100.

Santarelli, L., Saxe, M., Gross, C., Surget, A., Battagila, F., Dulawa, S., Weisstaub, N., Lee, J., Duman, R., Arancio, O., Belzung, C., Hen, R. (2003). Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants. Science, 301(5634), 805-809.

Sapolski, R. M. (2001). Depression, antidepressants, and the shrinking hippocampus.  PNAS, 98(22), 12320-12322.

Van Bokhoven, P. P., Oomen, C. A., Hoogendik, W. G., Smit, A. B., Lucassen, P. J., & Spijker, S. S. (2011). Reduction in hippocampal neurogenesis after social defeat is long-lasting and responsive to late antidepressant treatment. European Journal of Neuroscience, 33(10), 1833-1840.

Yan, H. C., Cao, X., Gao, T. M., & Zhu, X. H. (2011). Promoting adult hippocampal neurogenesis: A novel strategy for antidepressant drug screening. Current Medicinal Chemistry, 18, 4359-4567.

Skittle-Free Methods for Getting Kids to Cooperate with Testing

29 Nov

I gave the Woodcock-Johnson III Tests of Achievement to an 8-year-old yesterday. While the Woodcock Johnson (WJ-III) is widely loved by graduate students for its excellent name, it is not widely loved for the length of its administration. My clinic’s policy is to administer half of the subtests in the extended battery in addition to the standard 12-subtest battery, which can easily extend testing time to 2.5 hours or beyond – especially if you’re working with a small wiggly person who needs a lot of breaks.

My 8-year-old, like most of the children I have tortured with given the WJ-III, was not at all enthused about testing, and the situation was looking bleak: my sticker supply had been exhausted, I had no change for a bag of Skittles from the vending machine, and my kid’s parents had left the building, removing any chance of negotiating for post-assessment incentives from mom and dad.

It’s amazing what you can do with a blank piece of paper, though, and I managed to scrounge up a reinforcement strategy that kept my kiddo engaged for a full 2.5 hours. She was a self-professed horse lover, and we agreed that for every subtest she completed, I would draw a small portion of a horse – an ear, an eye, a leg – so that at the end of testing, she would have a complete picture to take home. I let her choose which part I drew after each test, where spots should go, what the horse’s legs should be doing, etc. It worked like a charm, and it got me thinking about other simple methods I might use to motivate children to cooperate during assessments… methods that did not encourage cavities or require frequent trips to the sticker aisle at Hobby Lobby. If you’ve been looking for quick, cheap reinforcers to use during testing with elementary-age kids, here are some ideas:

  • This is one that has worked well for another therapist in my program: Draw a path on a piece of paper, and draw lines across the path to divide it into sections representing subtests. Tell the child it’s a game board, and give her a small object or coin she can use as a game piece. Allow her to advance the game piece forward after completing each subtest.
  • Draw a series of circles on a piece of paper (one circle per subtest) and tell the child you’ll draw in a smiley face for each subtest he completes. Tell him that once every face is smiling, the two of you will do something fun together. Agree on what that activity will be. In the past I’ve used a game of red light/green light as a testing reinforcer, but the fun activity you choose could be anything: playing a quick board game, drawing a goofy picture together, playing trash can basketball with a wad of paper, and so on.
  • Draw a large slice of pizza with no toppings on it. Tell the child that whenever you notice that she is doing an exceptionally good job of sitting still and following directions, you’ll draw a pepperoni on the pizza. Tell her that if the pizza is covered with pepperoni by the end of the testing session, you’ll do a fun activity together (see above).
  • If you know how to do any sort of origami or paper folding – paper cranes, “fortune-tellers,” sailboats – tell the child you’re going to make him a surprise out of folded paper. Explain that you’ll make one fold for every subtest he completes. If you finish your creation before testing is done, tell him that now you’ll show him how to make the folds, and teach one fold per subtest.

A note of caution: if you use subtests as units of achievement, a child may get in the habit of asking how long each subtest will take (“Is it almost over?”). You can avoid this entirely by framing achievement as “doing a good job of sitting still and following directions” and reinforcing accordingly, as in the pizza example above. I like the structure of subtest-based achievement, and I’ve found that I can usually get kids to stop asking how long subtests will take by explaining that these questions make the subtests last longer. “Oh, man, it’s a shame you’re asking me that, because whenever you do, it takes us even longer to get done with the section.”

I’d be interested to hear from others who do assessments with children. What reinforcement strategies work for you?

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