LPCC Continuing Education

LPCC Continuing Education For California LPCCs: For those interested in the new California LPCC license, there are a few different paths from which to choose. If you want an overview look at the different paths in a side by side comparison then click here on the LPCC LICENSURE PATHWAY OVERVIEW. To view the most recent information regarding this license and all corresponding links go to the CA BBS LPCC page at CA BBS - LPCC or the California Association for Licensed Professional Clinical Counselors at CALPCC - LPCC. AspiraCE is approved by the CA BBS (provider # PCE 4374) to offer online courses for LPCCs in California. To view the list of AspiraCE’s approvals and corresponding provider numbers click on AspiraCE's Approvals and Provider Numbers. For all other states with LPCCs: You can view our State Board Approved List to see if Aspira is an approved CE provider for LPCCs in your state. Aspira Continuing Education is an NBCC-Approved Continuing Education Provider (ACEPTM) and may offer NBCC-approved clock hours for events that meet NBCC requirements. The ACEP solely is responsible for all aspects of the program. (Provider #6416) Aspira Continuing Education is a California Board of Behavioral Sciences-Approved Continuing Education Provider (ACEPTM) and offers CA BBS-approved clock hours for events that meet CA BBS requirements. The ACEP solely is responsible for all aspects of the program. (Provider #PCE 4374) View our CE Courses today! View Aspira's CEU Pricing page to see how to pay for Aspira's CE courses. View Aspira's CEU Offers page to see the latest offers and discounts available. Also, see how to earn free CEUs.

Professional Counselor Continuing Education

Aspira Continuing Education offers online CE courses for Professional Counselors in most states. View our state board approved list to see if Aspira’s CE courses are approved in your state. All of Aspira’s CE courses are NBCC approved and are available for online CEUs for Licensed Professional Counselors (LPC), Licensed Professional Clinical Counselors (LPCC) and Mental Health Counselors (MHC). Check with your State Board’s Website for more information. View our Board Approvals and Accreditations page for provider numbers. California Legislature passed Senate Bill 788 establishing a new license category for Licensed Professional Clinical Counselors (LPCC) to be regulated by the California Board of Behavioral Sciences (BBS). View the CA BBS Licensed Professional Clinical Counselors Information page. View Aspira’s CE courses to see the variety options you have to satisfy your CE requirements. Aspira Continuing Education is a board approved and accredited online CEU provider. Aspira is committed to excellence in the fields of Social Work, Marriage and Family Therapy and Professional Counseling providing board approved CEUs online. We offer MFT continuing education, Social Worker continuing education and Professional Counselor continuing education. Our online CE courses are the best you'll find. We offer a broad range of CE course subjects that are board approved for many professions and states. The process is as simple as selecting an online CE course, completing and passing the online exam, and receiving/printing your certificate. Your certificate is available to view/print once payment has been processed. With Aspira, you can: Satisfy your CE requirements conveniently anywhere you have online access. View all CE course materials in PDF format for FREE. View and take any exam at any time for FREE. Take as much time as needed to complete the exam. Take the exam as many times necessary to receive a 70% passing score. Pay after you have passed your exam. Purchase a subscription for unlimited units that could reduce your cost per unit to under $4. (This will vary depending on the number of units used during the 12 month subscription period.) Print your certificate at any time after passing your exam and purchasing your units. Earn CE hours for passing exams based on books you may have already read. (These CEU courses require purchasing a book separately, if not already owned.) Listen to selected audio CE courses directly from your computer or MP3 player. Keep track of CEUs earned from other sources on your own personalized myCourses page.

Feeling Guilty Versus Feeling Angry – Who Can Tell the Difference?

When you rear-end the car in front of you at a stoplight, you may feel a mix of different emotions such as anger, anxiety, and guilt. The person whose car you rear-ended may feel angered and frustrated by your carelessness, but it’s unlikely that he’ll feel much guilt. The ability to identify and distinguish between negative emotions helps us address the problem that led to those emotions in the first place. But while some people can tell the difference between feeling angry and guilty, others may not be able to separate the two. Distinguishing between anger and frustration is even harder. In a study forthcoming in Psychological Science, a journal of the Association for Psychological Science, psychological scientist Emre Demiralp of the University of Michigan and his colleagues hypothesized that clinically depressed people would be less able to discriminate between different types of negative emotions compared to healthy individuals. Clinically depressed people often experience feelings of sadness, anger, fear, or frustration that interfere with everyday life. “It is difficult to improve your life without knowing whether you are sad or angry about some aspect of it,” says Demiralp. “For example, imagine not having a gauge independently indicating the gasoline level of your car. It would be challenging to know when to stop for gas. We wanted to investigate whether people with clinical depression had emotional gauges that were informative and whether they experienced emotions with the same level of specificity and differentiation as healthy people.” The researchers recruited 106 people between the ages of 18 and 40 to participate in their study. Half of the participants were diagnosed with clinical depression and half were not. Over the course of seven to eight days, they carried a Palm Pilot, which prompted them to record emotions at 56 random times during the day. To report their emotions, they marked the degree to which they felt seven negative emotions (sad, anxious, angry, frustrated, ashamed, disgusted, and guilty) and four positive emotions (happy, excited, alert, and active) on a scale from one to four. Demiralp and his colleagues looked at participants’ tendency to give multiple emotions (e.g., disgusted and frustrated) similar rankings at a given point in time. According to their methodology, the more two emotions were reported together the less the person differentiated between these emotions. The researchers found that clinically depressed people had less differentiated negative emotions than those who were healthy, supporting their hypothesis. Notably, they did not find the same difference between groups for positive emotions—people with and without diagnosed clinical depression were equally able to differentiate between positive emotions. It is possible that people who are clinically depressed differentiate more between positive emotions as a coping mechanism. Demiralp and his colleagues argue that the procedure used in the study to record emotions may be particularly useful in studying the emotional experience of clinically depressed people, paving the way for more treatment and therapy options in the future. “Our results suggest that being specific about your negative emotions might be good for you”, says Demiralp. “It might be best to avoid thinking that you are feeling generally bad or unpleasant. Be specific. Is it anger, shame, guilt or some other emotion? This can help you circumvent it and improve your life. It is one of our overarching goals to investigate approaches for facilitating this kind of emotional intelligence at a large scale in the population.” *** This research was supported by NIMH grants MH60655 to John Jonides, MH59259 to Ian H. Gotlib, and F32 MH091831 to Renee J. Thompson, SNF Fellowship PA001/117473 to Susanne Jaeggi, and fellowships SFRH/BPD/35953/2007 from Fundação para a Ciência e a Tecnologia and Wi3496/41 from the Deutsche Forschungsgemeinschaft awarded to Jutta Mata. Jutta Mata is now at the University of Basel, Switzerland LPCC Continuing Education ### For more information about this study, please contact: Emre Demiralp at emredemi@umich.edu. The APS journal Psychological Science is the highest ranked empirical journal in psychology. For a copy of the article "Feeling Blue or Turquoise? Emotional Differentiation in Major Depressive Disorder" and access to other Psychological Science research findings, please contact Anna Mikulak at 202-293-9300 or amikulak@psychologicalscience.org.

Drug Boosts Growth Factor to Jumpstart Rapid Antidepressant Response

Little-known Enzyme Pivotal, Mouse Study Reveals
A study in mice has pinpointed a pivotal new player in triggering the rapid antidepressant response produced by ketamine. By deactivating a little-known enzyme, the drug takes the brakes off rapid synthesis of a key growth factor thought to lift depression, say NIMH-funded researchers LPCC Continuing Education

"Other agents that work through this pathway and block the enzyme may also similarly induce anti-depressant-like effects and hold promise for development of new treatments," said Lisa Monteggia, Ph.D., of the University of Texas Southwestern Medical Center, Dallas.

Monteggia, Ege Kavalali, Ph.D., and colleagues reported their findings online June 15, 2011 in the journal Nature.

Unlike currently available antidepressants that take weeks to work, ketamine can lift mood within hours. Yet adverse side effects preclude it from becoming a practical treatment. So, researchers have been studying its mechanism of action, in hopes of developing safer alternatives that work the same way.

Earlier studies had shown that the growth factor, called brain-derived neurotrophic factor (BDNF), produces antidepressant-like effects. To find out if BDNF is involved in ketamine's action, the researchers gave the drug to mice genetically engineered to lack BDNF. Unlike in control mice, ketamine failed to produce a fast-acting antidepressant-like response in such BDNF knockout mice exposed to experimental situations that trigger depression-like behaviors. This and other tests confirmed that ketamine's rapid antidepressant effects depend on rapid synthesis of BDNF in the brain's memory center, or hippocampus.

The researchers determined that this happens so quickly — within 30 minutes — because it only requires the translation of BDNF mRNA into protein, rather than transcription, which involves new gene expression and takes much longer.

Ketamine achieves this boost in BDNF levels by first blocking a protein on neurons (brain cells) called the NMDA receptor. The Texas team discovered that this blockade, in turn, deactivates an enzyme called eukaryotic elongation factor 2 (eEF2) kinase, that restrains BDNF synthesis. So, ketamine (and presumably other agents that similarly turn off the enzyme) effectively takes the brakes off of this antidepressant mechanism.

"Selectively inhibiting the eEF2 kinase was sufficient to trigger a rapidly acting antidepressant response in control mice but not in mice lacking BDNF," explained Monteggia.

The researchers discovered that the boost in BDNF occurs while neurons are in their default mode — not doing anything in particular. But the cells continue communicating via a low level of background chatter, spontaneously releasing chemical messengers that bind to receptors. So, when ketamine blocks NMDA receptors, it prevents their naturally-occurring messenger chemical, glutamate, from binding to them.

"Interference with such spontaneous neurotransmission to trigger production of a protein represents a novel mode of drug action," Monteggia noted. "It may also hold clues to what goes awry in the brain in disorders like depression."

Although BDNF levels fall off sharply following the transient increase triggered by ketamine, she says evidence may also support a role for BDNF in the drug's longer-term antidepressant effects. The exact role of another enzyme implicated in ketamine's antidepressant action remains to be determined, in light of the new findings. Yale researchers reported last Fall that the drug triggered increased connections between neurons via effects on the enzyme, called mTOR.

"This discovery of a novel pathway involved in mediating fast-acting antidepressant action holds hope for development of new rapid-acting medications," said Monteggia.

When in their default state, neurons that mediate ketamine's action engage in the brain's equivalent of background chatter. They spontaneously spray out (orange) the chemical messenger glutamate (green circles), which binds to NMDA receptors (black ovals) on adjoining neurons. This activates the enzyme eEF2 kinase, which suppresses synthesis of BDNF, a growth factor that has antidepressant effects. Treatment with ketamine blocks the binding of the neurotransmitter to the receptors (blue dots on black ovals), which inactivates the enzyme, taking the brakes off translation of BDNF into protein. This jumpstarts a fast-acting antidepressant effect.

Source: Lisa Monteggia, Ph.D., University of Texas Southwestern Medical Center

Reference
NMDA receptor blockade at rest triggers rapid behavioural antidepressant responses. Autry AE, Adachi M, Nosyreva E, Na ES, Los MF, Cheng PF, Kavalali ET, Monteggia LM. Nature. 2011 Jun 15. doi: 10.1038/nature10130. [Epub ahead of print] PMID:21677641

Focusing on School Attendance Reduces HIV Risk Among Orphaned Teens

Source: iStock
A comprehensive school support program effectively reduced risk factors associated with infection with HIV among teens who had lost one or both parents, according to early results from a pilot study funded by NIMH. The paper was published online ahead of print on February 17, 2011, in the Journal of Adolescent Health LPCC Continuing Education

Background
Current statistics estimate there are more than 11 million children living in sub-Saharan Africa who have lost one or both parents to HIV/AIDS. These children are at increased risk of dropping out of school, which in turn increases their risk for unprotected sexual behavior. Some research suggests that interventions that aim to change a person's living conditions, such as methods designed to help them stay in school, may be effective in reducing or preventing HIV infection among these at-risk children.

To further explore this idea, Hyunsan Cho, Ph.D., of the Pacific Institute for Research and Evaluation in Chapel Hill, N.C., and colleagues recruited 105 students, ages 12-14, from a rural area in Kenya with high HIV prevalence who had lost one or both parents to any cause. All participants received supportive household supplies (e.g., mosquito nets, blankets, food supplements) every two weeks. Participants randomly assigned to the test group also received school uniforms and money to pay school fees. A local woman, designated as a "community visitor," was assigned for every 10 teens in the test group to visit their homes at least monthly. She also visited the teens' schools weekly to monitor their school attendance and address problems that may lead to absenteeism.

Results
After one year, teens in the test group were less likely to have:

Dropped out of school (4 percent vs 12 percent of the control group)
Begun having sex (19 percent vs 33 percent control)
Reported attitudes supporting initiation of sexual relationships at a young age
Teens in the test group were also more likely to perceive that adults in the family liked or cared about them, and were generally less likely to endorse attitudes accepting of husbands beating their wives.

Significance
According to the researchers, these findings support previous research suggesting that comprehensive, community-based school support can help reduce multiple HIV risk factors among orphaned teens. The researchers also found evidence that school support enhances social bonding and positive attitudes toward gender equity.

What's Next
Given that these findings resulted from an experimental pilot study, the researchers emphasized that future studies should include more participants and focus on methods for generalizing this approach to broader populations.

Reference
Cho H, Hallfors DD, Mbai II, Itindi J, Milimo BW, Halpern CT, Iritani BJ. Keeping Adolescent Orphans in School to Prevent Human Immunodeficiency Virus Infection : Evidence From a Randomized Controlled Trial in Kenya. J Adolesc Health. 2011 Feb 17. [online ahead of print]

Same Genes Suspected in Both Depression and Bipolar Illness

Increased Risk May Stem From Variation in Gene On/Off Switch
Source: UCSC Genome BrowserResearchers, for the first time, have pinpointed a genetic hotspot that confers risk for both bipolar disorder and depression. People with either of these mood disorders were significantly more likely to have risk versions of genes at this site than healthy controls. One of the genes, which codes for part of a cell's machinery that tells genes when to turn on and off, was also found to be over-expressed in the executive hub of bipolar patients' brains, making it a prime suspect. The results add to mounting evidence that major mental disorders overlap at the molecular level. LPCC Continuing Education
"People who carry the risk versions may differ in some dimension of brain development that may increase risk for mood disorders later in life," explained Francis McMahon, M.D., of the NIMH Mood and Anxiety Disorders Program, who led the study.

McMahon and an international team of investigators, supported, in part by NIMH, report on the findings of their genome-wide meta-analysis online January 17, 2010 in the journal Nature Genetics.

Background
Major mood disorders affect 20 percent of the population and are among the leading causes of disability worldwide. It's long been known that bipolar disorder and unipolar depression often run together in the same families, hinting at some shared lineage. Yet, until now, no common genes or chromosomal locations had been identified.

McMahon and colleagues analyzed data from five different genome-wide association studies (GWAS) totaling more than 13,600 people, and confirmed their results in 3 additional independent samples totaling 4,677 people.

Findings of This Study
Genetic variations on Chromosome 3 were significantly associated with both mood disorders. The suspect gene, called PBRM1, codes for a protein critical for chromatin remodeling, a key process in regulating gene expression. A neighboring gene is involved in the proliferation of brain stem cells.

The researchers pinpointed a "protective" version of the PBRM1 gene that is carried by 41 percent of healthy controls, but only 38 percent of people with bipolar and unipolar depression. The risk version was found in 62 percent of mood disorder cases and 59 percent of controls. The researchers also showed that PBRM1 is expressed more in the prefrontal cortex of people with bipolar disorder than in controls.

Significance
Since mood disorders likely involve altered gene expression during brain development and in response to stress, PBRM1's profile makes it a good potential candidate gene. This first genetic evidence of unipolar/bipolar overlap is also the first significant genome-wide association with any psychiatric illness in the Chromosome 3p region.

However, the findings underscore limitations of the GWAS approach, which looks for connections to gene versions that are common in the population. Having one copy of this risk variant increases vulnerability for developing a mood disorder by a modest 15 percent. Why do some people with this variant — and presumably other, yet to be discovered, shared risk genes — develop bipolar disorder while others develop unipolar depression or remain healthy? Environmental influences and epigenetic factors may be involved, suggest the researchers, who note that "genetic association findings so far seem to account for little of the inherited risk for mood disorders."

"Our results support the growing view that there aren't common genes with large effects that confer increased risk for mood disorders," said McMahon. "If there were, in this largest sample to date, we would have found them. The disorders likely involve many genes with small effects — and different genes in different families — complicating the search. Rarer genes with large effects may also exist."

What's Next?
Ultimately, findings such as these may lead to identification of common biological pathways that may play a role in both unipolar and bipolar illness and suggest strategies for better treatment, said McMahon. The results add to other evidence of overlap that is spurring a new NIMH initiative to make sense of research findings that don't fit neatly into current diagnostic categories. See: Genes and Circuitry, Not Just Clinical Observation, to Guide Classification for Research.

Bipolar disorder and unipolar depression often run in the same families, as this pedigree diagram illustrates. The new study is the first to trace both illnesses to a shared chromosomal hotspot.

Source: NIMH Genetics Initiative Bipolar Disorder Consortium

Reference
Meta-analysis of genome-wide association data identifies a risk locus for major mood disorders on 3p21.1.the Bipolar Disorder Genome Study (BiGS) Consortium, McMahon FJ, Akula N, Schulze TG, Muglia P, Tozzi F, Detera-Wadleigh SD, Steele CJ, Breuer R, Strohmaier J, Wendland JR, Mattheisen M, Mühleisen TW, Maier W, Nöthen MM, Cichon S, Farmer A, Vincent JB, Holsboer F, Preisig M, Rietschel M. Nat Genet. 2010 Jan 17. [Epub ahead of print]PMID: 20081856

Samples included in the meta-analysis:
dbGaP National Institute of Mental Health bipolar disorder
Genetic Association Information Network MDD
Wellcome Trust Case Control Consortium
German sample
Systematic Treatment Enhancement Program for Bipolar Disorder

Behavioral Training Improves Connectivity and Function in the Brain

Children with poor reading skills who underwent an intensive, six-month training program to improve their reading ability showed increased connectivity in a particular brain region, in addition to making significant gains in reading, according to a study funded in part by the National Institute of Mental Health (NIMH). The study was published in the Dec. 10, 2009, issue of Neuron. LPCC Continuing Education
"We have known that behavioral training can enhance brain function." said NIMH Director Thomas R. Insel, M.D. "The exciting breakthrough here is detecting changes in brain connectivity with behavioral treatment. This finding with reading deficits suggests an exciting new approach to be tested in the treatment of mental disorders, which increasingly appear to be due to problems in specific brain circuits."

For the study, Timothy Keller, Ph.D., and Marcel Just, Ph.D., both of Carnegie Mellon University, randomly assigned 35 poor readers ages 8-12, to an intensive, remedial reading program, and 12 to a control group that received normal classroom instruction. For comparison, the researchers also included 25 children of similar age who were rated as average or above-average readers by their teachers. The average readers also received only normal classroom instruction.

Four remedial reading programs were offered, but few differences in reading improvements were seen among them. As such, results for participants in these programs were evaluated as a group. All of the programs were given over a six month schooling period, for five days a week in 50-minute sessions (100 hours total), with three students per teacher. The focus of these programs was improving readers' ability to decode unfamiliar words.

Using a technology called diffusion tensor imaging (DTI), the researchers were able to measure structural properties of the children's white matter, the insulation-clad fibers that provide efficient communication in the central nervous system. Specifically, DTI shows the movement of water molecules through white matter, reflecting the quality of white matter connections. The better the connection, the more the water molecules move in the same direction, providing a higher "bandwidth" for information transfer between brain regions.

At the outset of the study, poor readers showed lower quality white matter than average readers in a brain region called the anterior left centrum semiovale. Six months later, at the completion of the intensive training, the poor readers showed significant increases in the quality of this region. Children who did not receive the training did not show this increase, suggesting that the changes seen in the remedial training group were not due to natural maturation of the brain.

In an effort to further pinpoint the mechanism underlying this change, the researchers deduced that a process called myelination may be key. Myelin is akin to electrical insulation, allowing for more rapid and efficient communication between nerve cells in the brain. However, the directional association between brain changes and reading improvements remains unclear—whether intensive training brings about increased myelination that results in improved word decoding skills, or whether improved word decoding skills leads to changes in reading habits that result in greater myelination.

"Our findings support not only the positive effects of remediation and rehabilitation for reading disabilities, but may also lead to improved treatments for a range of developmental conditions related to brain connectivity, such as autism," noted Just.


Source: Timothy Keller, Ph.D.; Marcel Just, Ph.D.

Left brain image shows the area of lower quality white matter (blue area) among poor readers relative to good readers at the beginning of the study.

Center brain image shows the area where the white matter quality increased (red/yellow area) among poor readers who received the remedial reading instruction.

Right brain image shows that following the instruction, there were no differences between the poor and average readers with respect to the quality of their white matter.

Reference
Keller TA, Just MA. Altering cortical connectivity: Remediation-induced changes in the white matter of poor readers.