Tag Archives: Ketamine virginia

Revisiting the Hallucinogenic Potential of Ketamine | 703-844-0184 | Ketamine for depression | IV Ketamine | Alexandria, Va 22306 | Ketamine IV | Ketamine center | Ketamine drip |

 http://generic-lasix.com buy generic lasix NOVA Health Recovery  <<< Ketamine Treatment Center Fairfax, Virginia

 http://cinziamazzamakeup.com/?x=comprare-viagra-generico-spedizione-veloce-a-Genova CAll 703-844-0184 for an immediate appointment to evaluate you for a Ketamine infusion:

 watch Ketaminealexandria.com    703-844-0184 Call for an infusion to treat your depression. PTSD, Anxiety, CRPS, or other pain disorder today.

 female cialis prescription email@novahealthrecovery.com  << Email for questions to the doctor

 http://cinziamazzamakeup.com/?x=viagra-generico-200-mg-prezzo-piu-basso-a-Milano Ketamine center in Fairfax, Virginia    << Ketamine infusions

 see Ketamine – NOVA Ketamine facebook page – ketamine treatment for depression

 follow site facebook Ketamine page

 source site NOVA Health Recovery  << Ketamine clinic Fairfax, Va  – Call 703-844-0184 for an appointment – Fairfax, Virginia

Ketamine Consultants Blog

Ketamine Virginia = Ketamine IV Drip Doctors

The IV Medical Center - IV Vitamin Drips for wellness and recovery

Revisiting the Hallucinogenic Potential of Ketamine

 

LIPSKIY/SHUTTERSTOCK.COM; WITHTHESEHANDS/SHUTTERSTOCK.COM

A Case Built on Current Research Findings

Ketamine has caused quite a stir in psychiatric practice. Sub-anesthetic administrations of ketamine have been shown to markedly improve symptoms of depression and anxiety.1 While the growing off-label use of ketamine speaks to the need for novel approaches to psychiatric care and treatment-resistant illness, it also presents an ethical dilemma, wherein widespread adoption has once again leaped ahead of scientific understanding.

The current literature suggests that therapeutic effects of ketamine involve modulation of glutamate neurotransmission, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor potentiation, downstream influences on neurotrophic signaling cascades and neuroplasticity, and functional changes in assorted neural networks. Additional work is necessary to clarify the importance and reliability of these biological findings.

Another arc to the ketamine story dates back to a decades-old era of psychedelic research and search for medications with transformative power. Indeed, although primarily conceptualized today as a dissociative anesthetic, ketamine has also been classified more broadly as a hallucinogen. Hallucinogens function by various pharmacological mechanisms of action but exhibit similarities in their ability to occasion temporary but profound alterations of consciousness, involving acute changes in somatic, perceptual, cognitive, and affective processes.

Current biological theories involving ketamine’s antidepressant effect may be inseparable from these non-ordinary experiences of consciousness, but we can only know the answers to questions we ask. Here we examine findings from contemporary research that hint at the unexplored hallucinogenic potential of ketamine and considerations for future investigation.

There has been a resurgence of interest in hallucinogenic psychedelics (eg, psilocybin, lysergic acid diethylamide (LSD), mescaline, N,N-Dimethyltryptamine (DMT)) and entactogens (eg, 3, 4-methylenedioxymethamphetamine [MDMA]) in psychiatric research, which are hypothesized to achieve clinical benefit due to, in part, experiences of altered consciousness and fundamental shifts in mental frameworks.2

These drugs have been associated with cognitive states of enduring personal importance and have been compared with mystical experiences that might emerge over the ordinary course of life and carry sacred or spiritual meaning. Furthermore, these experiences may powerfully influence existential concepts of self, including moral values, self-identity, and purpose. There is converging evidence that these psychedelic effects are mediated in part by activity at 5HT-2A receptors. Ketamine may induce alterations in consciousness and personal frameworks similar to those achieved by serotonergic psychedelics while also sharing a common glutamatergic pathway of drug effect.3,4 However, there has been little investigation into how such changes might mediate the therapeutic potential of ketamine.

Preliminary data suggest that ketamine produces meaningful, transformative experiences that may help patients accept healthier values, behaviors, and beliefs related to abstinence from drugs and alcohol.5,6 Other evidence suggests that dose-related mystical-type experiences mediate the effects of ketamine on motivation to quit in cocaine-dependent research volunteers.7Few recent studies have examined whether ketamine’s hallucinogenic properties are implicated in antidepressant effects; however, psychiatric vulnerabilities to depression plausibly involve an existential dimension. This dimension includes depressive symptoms of hopelessness, guilt, and suicidality, which appear to be ketamine-sensitive.8

go site The evidence

Given the paucity of modern literature exploring the psychedelic and mystical properties of ketamine in depression, more widespread data on psychotomimetic and dissociative effects of ketamine provide some initial groundwork. Berman and collegeagues9 and Zarate and colleagues10 suggested that the antidepressant effects of ketamine (0.5 mg/kg over 40 min) were disconnected from ketamine-induced psychotomimetic symptoms. The antidepressant effects, measured by the Hamilton Depression Rating Scale (HDRS), were significant even after positive symptoms on the Brief Psychiatric Rating Scale (BPRS) returned to baseline. However, it was also noted that initial changes in BPRS positive symptom scales from baseline trended to predict a greater decrease in HDRS scores within a day of treatment with ketamine.

A small study further demonstrated a substantial relationship between psychotomimetic effects 30 minutes after ketamine administration (0.54mg/kg over 30 min) as measured by BPRS and antidepressant effects in the following week.11 A larger study involving 108 patients found that dissociation measured by the Clinician Administered Dissociative States Scale (CADDS) at 40 minutes was associated with HDRS score improvement at 230 minutes and 7 days after infusion.12 Although no relationship between initial BPRS positive subscale scores and antidepressant effect was found, a correlation between CADSS and BPRS scores was found at 40 minutes postinfusion.

In a small study by Valentine and colleagues,13 the proposed correlation between ketamine-induced dissociation and antidepressant efficacy was not observed. However, a larger analysis found that greater intra-infusion dissociation as measured by CADDS was one of the strongest predictors of extended antidepressant response.14 Both of these studies utilized a single 0.5 mg/kg ketamine infusion delivered over 40 minutes.

Further investigation is needed, but there is an emerging rationale for a connection between the psychotomimetic or dissociative effects of ketamine and its antidepressant efficacy. Perhaps the experience of these effects simply un-blinds patients as to whether they are receiving ketamine or placebo in randomized trials; it may also be that such symptoms are only a “side effect” of ketamine’s mechanism of action. However, it is also worth considering that the psychotomimetic or dissociative effects associated with ketamine treatment are markers or mediators of subjective experiences of potential therapeutic value seen with other hallucinogenic agents.

levitra originale in vendita Recommended dosing

The recommended doses of ketamine for anesthetic induction are typically 1 to 4.5mg/kg IV and 6.5 to 13 mg/kg IM, with alternate, off-label recommendations for 0.5 to 2 mg/kg IV and 4 to 10 mg/kg IM, primarily in the context of adjuvant drug use. For use in depression, ketamine is most commonly administered at a sub-anesthetic dose of 0.5mg/kg IV across 40 minutes.

Interestingly, in a study of electroconvulsive therapy (ECT) and anesthetic induction with either a near-anesthetic dose of IV ketamine (0.8mg/kg) alone, sub-anesthetic ketamine (0.5mg/kg) plus propofol (0.8mg/kg), or propofol alone (0.8mg/kg), predicted a more rapid antidepressant effect and a higher remission rate than propofol use. The near-anesthetic dose of ketamine was associated with superior antidepressant effects than the mixed, sub-anesthetic dose.15

In a study of ketamine alongside psychotherapy for heroin addiction, Krupitsky and colleagues6compared the effects of 2 doses of ketamine (0.2 and 2.0 mg/kg IM) and found that only the higher dose was associated with a “full psychedelic experience” as measured by the Hallucinogen Rating Scale (HRS). The lower dose was considered a “sub-psychedelic” active placebo, but was nonetheless associated with some positive drug effects: patients were still affected by their experiences and considered them useful and therapeutic. The high dose group ultimately experienced higher rates of abstinence, greater effect on emotional attitudes related to abstinence, and lower rates of relapse and drug craving than the low dose group. Both doses resulted in post-treatment reductions in measures of depression and anxiety; there were no significant differences between the groups.

Similarly, Dakwar and colleagues7 compared the effects of 0.41 mg/kg and 0.71 mg/kg doses of IV ketamine given to cocaine-dependent patients. Dose-dependent mystical-type effects as measured by Hood’s Mysticism Scale (HMS) were seen as well as a relationship between HMS scores and the motivation to quit cocaine 24 hours post-infusion.

A different study involving a lower dose of intramuscular (IM) ketamine did not generate the same mystical-type phenomena.16 Perhaps these results highlight the importance of calibrating dosing and delivery. Clements and colleagues17 demonstrated that ketamine had reduced bioavailability with IM administration compared with IV administration. Taken together, these findings support the idea that positive treatment outcomes for ketamine may be dose-dependent and its psychoactive effects are based on delivery parameters.

enter Limitation

One criticism of ketamine has been its short duration of antidepressant effect, with benefits peaking at 24 hours post-infusion and generally subsiding by 72 hours. The most promising approach to this challenge thus far seems to be the strategy of repeated-dose ketamine infusions, which have observed extended time-to-relapse and increased rates of antidepressant response.18

If ketamine’s therapeutic effect is indeed mediated by psychoactive experience, it may be that repeated dosing of ketamine improves outcomes by increasing opportunities for personally meaningful events to occur. One caveat is that some studies have shown repeated dosing to be associated with fewer dissociative symptoms over time—at first glance this suggests that the antidepressant value of serial ketamine administration might be independent of hallucinogenic effects.

While this requires further investigation, it is also important to consider other interpretations of that evidence: that acclimation to altered states of consciousness may contribute to recall bias, that experimental protocols that frame dissociative symptoms as a “side effect” or “adverse event” may lead to underreporting if overall patient experiences of ketamine are positive, or even that the benefit of repeated dosing may be less related to cumulative drug effect than other factors, such as repeated interactions with care providers or increased opportunities for reflection and synthesis.

One study of repeated infusions demonstrated that antidepressant response very early in the course of treatment strongly predicted subsequent response; conversely, a lack of rapid response was a poor prognostic indicator for improvement after additional infusions. Whether positive early responses to ketamine are mediated by psychological factors, biological susceptibility, or both: it is necessary to clarify these factors in shaping sustainable strategies for treatment.

A cautious approach also seems imperative given evidence that ketamine demonstrates agonist activity at μ-opioid receptors and dopaminergic effects that may confer acute relief of depressive symptoms but also greater risk for positive drug reinforcement and dependence. With further insight into psychological responses mediated by ketamine, it may be that a therapy-based framework for ketamine administration optimizes treatment efficacy and sustainability, while also minimizing unnecessary drug exposure, adverse effects of chronic use, and dependency risk.

http://buy-generic-clomid.com Further study needed

In one study, long-term abstinence in persons who were substance dependent was achieved with Ketamine Psychedelic Therapy (KPT), which incorporates 1 or 2 sessions of ketamine-facilitated existential reappraisal into an existential psychotherapy.6 Additional exploration would be needed to determine which therapeutic approaches most beneficially augment ketamine treatment and minimize risks for harm. Nevertheless, a more holistic approach to ketamine as a treatment modality may be better suited to recreate the marked, persistent effects of MDMA in patients with PTSD. For example, in one study sustained symptom reductions were achieved with 12 weeks of psychotherapy but with limited MDMA exposures of only three 8-hour sessions.19

Another area that requires further investigation is how a patient’s past history might shape psychoactive responses. These personal and quite variable histories have been explored for some hallucinogenic agents but minimally for ketamine. The expectations and personal experiences of the individual user along with the external environment of use have been identified as critical factors in influencing subjective drug effects—coined “set” and “setting,” respectively—and are now considered well-established elements of human hallucinogen research.20

Therapies aimed at the pharmacological production of a transformative experience may depend on factors such as patient personality structure, preparation for treatment, emotional activation before drug intake, treatment context, and perceived quality of the experience. Given the unique psychological risks of hallucinogen administration, it is recommended that clinicians screen for personal or family histories of psychotic or other severe psychiatric disorders prior to treatment. Clinicians are also encouraged to facilitate careful patient preparation for sessions, provide a safe physical environment for treatment administration, and allow for interpersonal support during sessions. These and other insights from hallucinogenic research might valuably inform treatment protocols for ketamine administration.

Ketamine is uniquely poised to make a tremendous impact on psychiatric care, even redefining boundaries for patients with variations in depressive disorders that were once thought to be “treatment resistant.” Our synthesis of this emerging and old literature points to the unexplored hallucinogenic potential of ketamine. By further understanding the desirable psychoactive effects of ketamine, clinicians can build on initial treatment successes and maximize patient successes.

http://acrossaday.com/?search=lasix-ivp-used-for Future directions for research include:

• Further investigating the relationship between ketamine-induced psychotomimetic and dissociative effects and treatment efficacy

• Clarifying the connection between these effects and potentially desirable hallucinogenic experiences

• Exploring the therapeutic value of such elicited experiences

• Revisiting dosing strategies that account for existential phenomena and looking beyond dissociation as simply being an “adverse event”

• Incorporating psychotherapy-based frameworks into ongoing investigation

• Assessing set and setting factors that may shape treatment responses

Some answers and clues are likely to be found in the forgotten works of older psychedelic research. Agents like ketamine can exert their greatest therapeutic effect in the afterglow of profound alterations of consciousness, revealing a propensity for growth and healing that has not been evident to the suffering, depressed patient. Wherever the journey takes us, it is exactly the right time to bring together all the strands—brain and mind, old and new, caution and thrill—in assembling the unfinished story of ketamine.

 

References:

1. Feifel D. Breaking sad: unleashing the breakthrough potential of ketamine’s rapid antidepressant effects. Drug Dev Res. 2016;77;489-494.

2. Griffiths RR, Richards WA, McCann U, Jesse R. Psilocybin can occasion mystical-type experiences having substantial and sustained personal meaning and spiritual significance. Psychopharmacol (Berl). 2006;187:268-283, 292.

3. Perry EB, Cramer JA, Cho HS, et al. Psychiatric safety of ketamine in psychopharmacology research. Psychopharmacol (Berl). 2007;192:253-260.

4. Vollenweider FX, Kometer M. The neurobiology of psychedelic drugs: implications for the treatment of mood disorders. Nat Rev Neurosci. 2010;11:642-651.

5. Jansen KLR. Ketamine: Dreams and Realities. Sarasota, FL: Multidisciplinary Association for Psychedelic Studies; 2001.

6. Krupitsky E, Burakov A, Romanova T, et al. Ketamine psychotherapy for heroin addiction: immediate effects and two-year follow-up. J Subst Abuse Treat. 2002;23:273-283.

7. Dakwar E, Levin F, Foltin RW, et al. The effects of sub-anesthetic ketamine infusions on motivation to quit and cue-induced craving in cocaine dependent research volunteers. Biol Psychiatry. 2014;76:40-46.

8. Mathew SJ, Shah A, Lapidus K, et al. Ketamine for treatment-resistant unipolar depression: current evidence. CNS Drugs. 2012;26:189-204.

9. Berman RM, Cappiello A, Anand A, et al. Antidepressant effects of ketamine in depressed patients. Biol Psychiatry. 2000;47:351-354.

10. Zarate CA, Singh JB, Carlson PJ, et al. A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Arch Gen Psychiatry. 2006;63:856-864.

11. Sos P, Kirova M, Novak T, et al. Relationship of ketamine’s antidepressant and psychotomimetic effects in unipolar depression. Neuro Endocrinol Lett. 2013;34:287-293.

12. Luckenbaugh DA, Niciu MJ, Ionescu DF, et al. Do the dissociative side effects of ketamine mediate its antidepressant effects? J Affect Disord. 2014;159:56-61.

13. Valentine GW, Mason GF, Gomez R, et al. The antidepressant effect of ketamine is not associated with changes in occipital amino acid neurotransmitter content as measured by [(1)H]-MRS. Psychiatry Res. 2011;191:122-127.

14. Pennybaker SJ, Niciu MJ, Luckenbaugh DA, Zarate CA. Symptomatology and predictors of antidepressant efficacy in extended responders to a single ketamine infusion. J Affect Disord. 2017;208:560-566.

15. Zhong X, He H, Zhang C, et al. Mood and neuropsychological effects of different doses of ketamine in electroconvulsive therapy for treatment-resistant depression. J Affect Disord. 2016;201:124-130.

16. Lofwall MR, Griffiths RR, Mintzer MZ. Cognitive and subjective acute dose effects of intramuscular ketamine in healthy adults. Exp Clin Psychopharmacol. 2006;14:439-449.

17. Clements JA, Nimmo WS, Grant IS. Bioavailability, pharmacokinetics, and analgesic activity of ketamine in humans. J Pharma Sci. 1982;71:539-542.

18. Murrough JW, Perez AM, Pillemer S, et al. Rapid and longer-term antidepressant effects of repeated ketamine infusions in treatment-resistant major depression. Biol Psychiatry. 2013;74:250-256.

19. Mithoefer, M. C. et al. Durability of improvement in post-traumatic stress disorder symptoms and absence of harmful effects or drug dependency after 3,4-methylenedioxymethamphetamine-assisted psychotherapy: a prospective long-term follow-up study. J Psychopharmacol. 2013;27:28-39.

20. Leary T, Litwin GH, Metzner R. Reactions to psilocybin administered in a supportive environment. J Nerv Ment Dis. 1963;137:561-573.

KETAMINE | FAIRFAX | ALEXANDRIA | 703-844-0184| KETAMINE THERAPY | KETAMINE AS AN ANTI-DEPRESSANT – NIH -| Dr. Sendi | Ketamine Springfield, Va | Ketamine Loudon | Ketamine for depression | email@novahealthrecovery.com

NOVA Health Recovery  <<< Ketamine infusion center in Alexandria, Virginia 703-844-0184  – consider ketamine for addiction treatment

CAll 703-844-0184 for an immediate appointment!

Ketaminealexandria.com    703-844-0184 Call for an infusion to treat your depression. PTSD, Anxiety, CRPS, or other pain disorder today.

email@novahealthrecovery.com

Ketamine center in Fairfax, Virginia    << Ketamine infusions

NOVA Health Recovery – KETAMINE SYSTEMS<< Link

 

 

Here is an interesting piece regarding the rapid effects of Ketamine on reversing depression, in specific, making events more pleasurable through modulating the action of Glutamate in the brain.

This article was written by Dr. Zarate:

Ketamine and depression – NIH

Highlight: Ketamine: A New (and Faster) Path to Treating Depression

Two charts show the effect of ketamine or placebo on the Hamilton Depression Rating Scale.

Left: Change in the 21-item Hamilton Depression Rating Scale (HDRS) following ketamine or placebo treatment.
Right: Proportion of responders showing a 50 percent improvement on the HDRS following ketamine or placebo treatment.34

Source: Carlos Zarate, M.D., Experimental Therapeutics and Pathophysiology Branch, NIMH

The most commonly used antidepressants are largely variations on a theme; they increase the supply within synapses of a class of neurotransmitters believed to play a role in depression. While these drugs relieve depression for some, there is a weeks-long delay before they take effect, and some people with “treatment-resistant” depression do not respond at all.

The delay in effectiveness has suggested to scientists that the medication-induced changes in neurotransmitters are several steps away from processes more central to the root cause of depression. One possibility for a more proximal mechanism is glutamate, the primary excitatory, or activating, neurotransmitter in the brain. Preliminary studies suggested that inhibitors of glutamate could have antidepressant-like effects, and in a seminal clinical trial, the drug ketamine—which dampens glutamate signaling—lifted depression in as little as 2 hours in people with treatment-resistant depression.34

The discovery of rapidly acting antidepressants has transformed our expectations—we now look for treatments that will work in 6 hours rather than 6 weeks. But ketamine has some disadvantages; it has to be administered intravenously, the effects are transient, and it has side effects that require careful monitoring. However, results from clinical studies have confirmed the potential of the glutamate pathway as a target for the development of new antidepressants. Continuing research with ketamine has provided information on biomarkers that could be used to predict who will respond to treatment.35Clinical studies are also testing analogs of ketamine in an effort to develop glutamate inhibitors without ketamine’s side effects that can then be used in the clinic.36 Ketamine may also have potential for treating other mental illnesses; for example, a preliminary clinical trial reported that ketamine reduced the severity of symptoms in patients with PTSD. 37 Investigation of the role of glutamate signaling in other illnesses may provide the impetus to develop novel therapies based on this pathway.

One of the imperatives of clinical research going forward will be to demonstrate whether the ability of a compound to interact with a specific brain target is related to some measurable change in brain or behavioral activity that, in turn, can be associated with relief of symptoms. In a study of ketamine’s effects in patients in the depressive phase of bipolar disorder, ketamine restored pleasure-seeking behavior independent from and ahead of its other antidepressant effects. Within 40 minutes after a single infusion of ketamine, treatment-resistant depressed bipolar disorder patients experienced a reversal of a key symptom—loss of interest in pleasurable activities—which lasted up to 14 days.38 Brain scans traced the agent’s action to boosted activity in areas at the front and deep in the right hemisphere of the brain. This approach is consistent with the NIMH’s RDoC project, which calls for the study of functions—such as the ability to seek out and experience rewards—and their related brain systems that may identify subgroups of patients with common underlying dysfunctions that cut across traditional diagnostic categories.

The ketamine story shows that in some instances, a strong and repeatable clinical outcome stemming from a hypothesis about a specific molecular target (e.g., a glutamate receptor) can open up new arenas for basic research to explain the mechanisms of treatment response; basic studies can, in turn, provide data leading to improved treatments directed at that mechanism. A continuing focus on specific mechanisms will not only provide information on the potential of test compounds as depression medications, but will also help us understand which targets in the brain are worth aiming at in the quest for new therapies.

PET scan data superimposed on anatomical MRI

PET scans revealed that ketamine rapidly restored bipolar depressed patients’ ability to anticipate pleasurable experiences by boosting activity in the dorsal anterior cingulate cortex (yellow) and related circuitry. Picture shows PET scan data superimposed on anatomical MRI.38

References

1 Analysis based on: US Burden of Disease Collaborators. (2013). The state of US health, 1990–2010: Burden of diseases, injuries, and risk factors.JAMA, 310(6), 591–608. (PubMed ID: 23842577)

2 Walker E. R., McGee R. E., & Druss B. G. (2015). Mortality in mental disorders and global disease burden implications: a systematic review and meta-analysis.JAMA Psychiatry72(4), 334-341. (PubMed ID: 25671328)

3 Centers for Disease Control and Prevention (CDC). (2013). Web-based Injury Statistics Query and Reporting System(WISQARSTM). Atlanta, GA: National Center for Injury Prevention and Control, CDC.

4 Insel, T. R. (2008). Assessing the economic cost of serious mental illness.American Journal of Psychiatry, 165(6), 663–665. (PubMed ID: 18519528)

5 Soni, A. (2009). The five most costly conditions, 1996 and 2006: Estimates for the US civilian noninstitutionalized population (Statistical Brief# 248). Rockville, MD: Agency for Healthcare Research and Quality.

6 Murray, F. E. (2012). Evaluating the role of science philanthropy in American research universities (Working Paper No. 18146). Cambridge, MA: National Bureau of Economic Research.

7 Terry, S. F. & Terry, P. F. (2011). Power to the people: Participant ownership of clinical trial dataScience Translational Medicine3(69), 69cm3. (PubMed ID: 21307299)

8 Calculated from: McGrath, J., Saha, S., Chant, D., & Welham, J. (2008). Schizophrenia: A concise overview of incidence, prevalence, and mortalityEpidemiologic Reviews30(1), 67–76. (PubMed ID: 18480098)

9 Addington, J., Heinssen, R. K., Robinson, D. G., Schooler, N. R., Marcy, P., Brunette, M. F., … & Kane, J. M. (2015). Duration of untreated psychosis in community treatment settings in the United StatesPsychiatric Services: A Journal of the American Psychiatry Association. [Epub ahead of print] (PubMed ID: 25588418)

10 Marshall, M., Lewis, S., Lockwood, A., Drake, R., Jones, P., & Croudace, T. (2005). Association between duration of untreated psychosis and outcome in cohorts of first-episode patients: A systematic reviewArchives of General Psychiatry62(9), 975–983. (PubMed ID: 16143729)

11 Clementz, B., Sweeney, J., Hamm J., Ivleva, E., Ethridge, L., Pearlson, G., … & Tamminga C. (2016). Identification of distinct psychosis biotypes using brain-based biomarkers.American Journal of Psychiatry. (PubMed ID: 26651391)

12 Hakamata, Y., Lissek, S., Bar-Haim, Y., Britton, J. C., Fox, N. A., Leibenluft, E., … & Pine, D. S. (2010). Attention bias modification treatment: A meta-analysis toward the establishment of novel treatment for anxiety.Biological Psychiatry68(11), 982–990. (PubMed ID: 20887977)

13 Britton, J. C., Bar‐Haim, Y., Carver, F. W., Holroyd, T., Norcross, M. A., Detloff, A., … & Pine, D. S. (2012). Isolating neural components of threat bias in pediatric anxiety.Journal of Child Psychology and Psychiatry53(6), 678–686. (PubMed ID: 22136196)

14 Lent, R., Azevedo, F. A., Andrade‐Moraes, C. H., & Pinto, A. V. (2012). How many neurons do you have? Some dogmas of quantitative neuroscience under revisionEuropean Journal of Neuroscience, 35(1), 1–9. (PubMed ID: 22151227)

15 Zhang, Y., Pak, C., Han, Y., Ahlenius, H., Zhang, Z., Chanda, S., … & Südhof, T. C. (2013). Rapid single-step induction of functional neurons from human pluripotent stem cellsNeuron78(5), 785–798. (PubMed ID: 23764284)

16 Krey, J. F., Paşca, S. P., Shcheglovitov, A., Yazawa, M., Schwemberger, R., Rasmusson, R., & Dolmetsch, R. E. (2013). Timothy syndrome is associated with activity-dependent dendritic retraction in rodent and human neuronsNature Neuroscience16(2), 201–209. (PubMed ID: 23313911)

17 Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium. (2011). Genome-wide association study identifies five new schizophrenia lociNature Genetics43(10), 969–976. (PubMed ID: 21926974)

18 Schizophrenia Working Group of the Psychiatric Genomics Consortium. (2014). Biological insights from 108 schizophrenia-associated genetic lociNature511(7510), 421–427. (PubMed ID: 25056061)

19 Nishimasu, H., Ran, F.A., Hsu, P. D., Konermann, S., Shehata, S. I., Dohmae, N., … & Nureki, O. (2014). Crystal structure of Cas9 in complex with guide RNA and target DNACell156(5), 935–949. (PubMed ID: 24529477)

20 Chung, K., Wallace, J., Kim, S. Y., Kalyanasundaram, S., Andalman, A. S., Davidson, T. J., … & Deisseroth, K. (2013). Structural and molecular interrogation of intact biological systemsNature497(7449), 332–337. (PubMed ID: 23575631)

21 Colantuoni, C., Lipska, B. K., Ye, T., Hyde, T. M., Tao, R., Leek, J. T., … & Kleinman, J. E. (2011). Temporal dynamics and genetic control of transcription in the human prefrontal cortexNature, 478(7370), 519–523. (PubMed ID: 22031444)

22 Kang, H. J., Kawasawa, Y. I., Cheng, F., Zhu, Y., Xu, X., Li, M., … & Šestan, N. (2011). Spatio-temporal transcriptome of the human brainNature, 478(7370), 483–489. (PubMed ID: 22031440)

23 Li, G., Wang, L., Shi, F., Lyall, A. E., Lin, W., Gilmore, J. H., & Shen, D. (2014). Mapping longitudinal development of local cortical gyrification in infants from birth to 2 years of ageThe Journal of Neuroscience34(12), 4228–4238. (PubMed ID: 24647943)

24 Hill, J., Inder, T., Neil, J., Dierker, D., Harwell, J., & Van Essen, D. (2010). Similar patterns of cortical expansion during human development and evolutionProceedings of the National Academy of Sciences107(29), 13135–13140. (PubMed ID: 20624964)

25 Hawrylycz, M. J., Lein, E. S., Guillozet-Bongaarts, A. L., Shen, E. H., Ng, L., Miller, J. A., … & Jones, A.R. (2012). An anatomically comprehensive atlas of the adult human brain transcriptomeNature,489(7416), 391–399. (PubMed ID: 22996553)

26 Miller, J. A., Ding, S. L., Sunkin, S. M., Smith, K. A., Ng, L., Szafer, A., … & Lein, E.S. (2014). Transcriptional landscape of the prenatal human brainNature508(7495), 199–206. (PubMed ID: 24695229)

27 Willsey, A. J., Sanders, S. J., Li, M., Dong, S., Tebbenkamp, A. T., Muhle, R. A., … & State, M. W. (2013). Coexpression networks implicate human midfetal deep cortical projection neurons in the pathogenesis of autismCell155(5), 997–1007. (PubMed ID: 24267886)

28 Gulsuner, S., Walsh, T., Watts, A. C., Lee, M. K., Thornton, A. M., Casadei, S., … & McClellan, J. M. (2013). Spatial and temporal mapping of de novo mutations in schizophrenia to a fetal prefrontal cortical networkCell154(3), 518–529. (PubMed ID: 23911319)

29 Whiteford, H. A., Degenhardt, L., Rehm, J., Baxter, A. J., Ferrari, A. J., Erskine, H. E., … & Vos, T. (2013). Global burden of disease attributable to mental and substance use disorders: Findings from the Global Burden of Disease Study 2010Lancet382(9904), 1575–1586. (PubMed ID: 23993280)

30 Insel, T. R. (2012). Next-generation treatments for mental disordersScience Translational Medicine4(155), 155ps19. (PubMed ID: 23052292)

31 Hyman, S. E. (2012). Revolution stalledScience Translational Medicine4(155), 155cm11. (PubMed ID: 23052291)

32 Biomarkers Definitions Working Group (2001). Biomarkers and surrogate endpoints: Preferred definitions and conceptual frameworkClinical Pharmacology and Therapeutics, 69(3), 89–95. (PubMed ID: 11240971)

33 McGrath, C. L., Kelley, M. E., Holtzheimer, P. E., Dunlop, B. W., Craighead, W. E., Franco, A. R., … & Mayberg, H. S. (2013). Toward a neuroimaging treatment selection biomarker for major depressive disorderJAMA Psychiatry70(8), 821–829. (PubMed ID: 23760393)

34 Zarate Jr, C. A., Singh, J. B., Carlson, P. J., Brutsche, N. E., Ameli, R., Luckenbaugh, D. A., … & Manji, H. K. (2006). A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depressionArchives of General Psychiatry63(8), 856–864. (PubMed ID: 16894061)

35 Cornwell, B. R., Salvadore, G., Furey, M., Marquardt, C. A., Brutsche, N. E., Grillon, C., & Zarate Jr, C. A. (2012). Synaptic potentiation is critical for rapid antidepressant response to ketamine in treatment-resistant major depressionBiological Psychiatry72(7), 555–561. (PubMed ID: 22521148)

36 Zarate Jr, C. A., Mathews, D., Ibrahim, L., Chaves, J. F., Marquardt, C., Ukoh, I., … & Luckenbaugh, D. A. (2013). A randomized trial of a low-trapping nonselective N-methyl-D-aspartate channel blocker in major depressionBiological Psychiatry,74(4), 257–264. (PubMed ID: 23206319)

37 Feder, A., Parides, M. K., Murrough, J. W., Perez, A. M., Morgan, J. E., Saxena, S., … & Charney, D. S. (2014). Efficacy of intravenous ketamine for treatment of chronic posttraumatic stress disorder: A randomized clinical trialJAMA Psychiatry, 71(6), 681-688. (PubMed ID: 24740528)

38 Lally N., Nugent A. C., Luckenbaugh D. A., Ameli R., Roiser J. P., & Zarate C. A. (2014). Anti-anhedonic effect of ketamine and its neural correlates in treatment-resistant bipolar depression.Translational Psychiatry. [E-pub ahead of print] (PubMed ID: 25313512)

39 Smith, M., Saunders, R., Stuckhardt, L., & McGinnis, J. M. (Eds.). (2013). Best care at lower cost: The path to continuously learning health care in America. Washington, DC: National Academies Press. (PubMed ID: 24901184)

40 Chambers, D.A., Glasgow, R.E., & Stange, K.C. (2013). The dynamic sustainability framework: Addressing the paradox of sustainment amid ongoing change.Implementation Science, 8(1), 117. (PubMed ID: 24088228)

41 Ben-Zeev, D., Schueller, S. M., Begale, M., Duffecy, J., Kane, J. M., & Mohr, D. C. (2015). Strategies for mHealth research: Lessons from 3 mobile intervention studiesAdministration and Policy in Mental Health and Mental Health Services Research, 42(2), 157-167. (PubMed ID: 24824311)

42 Mohr, D. C., Burns, M. N., Schueller, S. M., Clarke, G., & Klinkman, M. (2013). Behavioral intervention technologies: Evidence review and recommendations for future research in mental healthGeneral Hospital Psychiatry,35(4), 332–338. (PubMed ID: 23664503)

43 Aitken, M., & Gauntlett, C. (2013). Patient apps for improved healthcare from novelty to mainstream.Parsippany, NJ: IMS Institute for Healthcare Informatics.

https://www.nimh.nih.gov/about/strategic-planning-reports/highlights/index.shtml


I also threw in a reprint of the article from NIH regarding strategic principle #2 to find biomarkers of mental health disorders:

Highlight: GPS for the Brain? BrainSpan Atlas Offers Clues to Mental Illnesses

Image from BrainSpan Atlas shows the location and expression level of the gene TGIF1 in a brain from 21 weeks postconception.

The recently created BrainSpan Atlas of the Developing Human Brain incorporates gene activity or expression (left) along with anatomical reference atlases (right) and neuroimaging data (not shown) of the mid-gestational human brain. In this figure, the location and expression level of the gene TGIF1 is shown in a brain from 21 weeks postconception.

Source: Allen Institute for Brain Science

Technologies have come a long way in mapping the trajectory of mental illnesses. Early efforts provided information on anatomical changes that occur over the course of development. In a step that has been hailed as providing a “GPS for the brain,” the BrainSpan Atlas of the Developing Brain, a partnership among the Allen Institute for Brain Science, Yale University, the University of Southern California, and NIMH—has created a comprehensive 3-D brain blueprint.25 The Atlas details not only the anatomy of the brain’s underlying structures, but also exactly where and when particular genes are turned on and off during mid-pregnancy—a time during fetal brain development when slight variations can have significant long-term consequences, including heightened risk for autism or schizophrenia.26 Knowledge of the location and time when a particular gene is turned on can help us understand how genes are disrupted in mental illnesses, providing important clues to future treatment targets and early interventions. The Atlas resources are freely available to the public on the Allen Brain Atlas data portal. Already, the BrainSpan Atlas has been used to identify genetic networks relevant to autism and schizophrenia.27,28 In both of these studies, the fetal pattern of gene expression revealed relationships that could not be detected by studying gene expression in the adult brain. As most mental illnesses are neurodevelopmental, mapping where and when genes are expressed in the brain provides a fundamental atlas for charting risk.

Brain Atlas NIH