27 January 2013

Chronic pain in children



ScienceDirect - Pain : The impact of chronic pain in children and adolescents: Development and initial validation of a child and parent version of the Pain Experience Questionnaire
doi:10.1016/j.pain.2007.06.002 How to Cite or Link Using DOI (Opens New Window)
Copyright © 2007 International Association for the Study of Pain Published by Elsevier B.V.

The impact of chronic pain in children and adolescents: Development and initial validation of a child and parent version of the Pain Experience Questionnaire

Abstract

Psychosocial factors are crucial for understanding and treating chronic pain in adults, but also in children. For children, very few questionnaires for a multidimensional pain assessment exist. In adults, the Multidimensional Pain Inventory (MPI; [Kerns RD, Turk DC, Rudy TE. The West Haven-Yale Multidimensional Pain Inventory (WHYMPI). Pain 1985;23:345–56]) has been widely used to determine patients’ adjustment to chronic pain. Using one section of the MPI as a model, we developed and evaluated the Pain Experience Questionnaire (PEQ) – child and parent version – that assesses the psychosocial impact of chronic pain in children and adolescents. As substantiated by confirmatory factor analysis in a sample of 111 children and adolescents (7–18 years) with chronic pain, the child PEQ entails the subscales pain severity, pain-related interference, affective distress and perceived social support. The parent version contains the subscales severity of the child’s pain, interference and parental affective distress. Child and parent PEQ subscales were internally consistent. Age was unrelated to PEQ subscale scores. Girls and their mothers endorsed significantly greater pain severity, interference and affective distress. Validity analyses yielded a pattern of correlations with measures of depression, trait anxiety, pain activity, child behaviors, pain-related cognitions, and parenting behavior that is consistent with psychometric data of the adult MPI and previous findings on psychosocial aspects of chronic pediatric pain. Significant differences between children depending on patient status (participants in experimental or treatment studies, outpatients, inpatients) suggest external validity of the PEQ. Despite the preliminary nature of the psychometric evaluation, the child and parent PEQ seem promising for a comprehensive assessment of pediatric pain.

Keywords: Pediatric pain; Psychosocial impact; Assessment; Questionnaire; Child report; Parental report

22 January 2013

ScienceDirect - Pain : Catastrophizing and perceived partner responses to pain

Pain : Catastrophizing and perceived partner responses to pain:
"Catastrophizing and perceived partner responses to pain
Jennifer L. Boothby, , a, Beverly E. Thornb, Lorraine Y. Overduina and L. Charles Wardc

Received 31 July 2003; Revised 12 February 2004; accepted 23 February 2004 AIB-16214

Abstract

This study examined the relationship between catastrophizing and patient-perceived partner responses to pain behaviors. The Catastrophizing subscale of the Cognitive Coping Strategy Inventory and the West Haven–Yale Multidimensional Pain Inventory were completed by 62 adult chronic pain patients. Consistent with past research, catastrophizing and patient-perceived solicitous partner behaviors were positively correlated with negative pain outcomes. The communal coping theory of catastrophizing suggests that catastrophizing might be undertaken to solicit support and empathy from others. However, catastrophizing was not related to perceived solicitous partner behavior in this study. Rather, catastrophizing was associated with perceived punishing partner responses. Implications are that catastrophizing and perceived solicitous partner behaviors are independently associated with pain and that catastrophizing may not be reinforced by empathy from significant others."

06 December 2012

Quench the Fire Run

Quench the fire flyer

Dear SoCal friends,

Causalgia (aka CRPS II or RSD) should be very high on your list of things that you do not want. If you're the sort who runs without being chased, come out this Sunday and support the USC Pain Center.


Quench the Fire Run



Also, MacGyver will be there!



Love,

Adam



02 November 2012

Malingering in people with pain



Blackwell Synergy - Pain Medicine, Volume 1 Issue 3 Page 280-282, September 2000 (Article Abstract
Volume 1 Issue 3 Page 280-282, September 2000
(2000) A Case of Malingering: Feigning a Painful Disorder in the Presence of True Medical Illness
Pain Medicine 1 (3) , 280–282 doi:10.1046/j.1526-4637.2000.00028.x
The potential for malingering must always be considered among patients presenting with pain. When malingering is identified, care may be discontinued. This case report describes a patient who feigned sickle cell crisis, a painful condition, in the presence of other identifiable and potentially painful medical illnesses.

26 August 2012

Tierney on drugs

Tierney on drugs

http://tierneylab.blogs.nytimes.com/tag/pain/

24 July 2012

Nocebo effects

Here's a nice post on some of the latest research on nocebo effects --the placebo's evil twin.



Are Warnings About the Side Effects of Drugs Making Us Sick? | NeuroTribes

I haven't looked into the nocebo effects for pain in too much detail. But I've profited immensely from carefully working through the placebo effect literature. I expect this could be similarly useful, especially in the differences between placebos and nocebos


I'd love to hear about any good philosophical work on nocebos.

05 July 2012

Addiction in pain patients estimation

David A. Fishbain, MD, FAPA, Brandly Cole, PsyD, John Lewis, PhD, Hubert L.
Rosomoff, MD, DMedSc, FAAPM, and R. Steele Rosomoff, BSN, MBA
Pain Medicine, 
doi: 10.1111/j.1526-4637.2007.00370.x

27 June 2012

More Sphenopalatine Ganglioneuralgia

I'm not yet over losing my ranking as the internet's number one source for all things sphenopalatine ganglioneuralgia. So, in a futile attempt to reclaim my crown, I share this little bit about ice cream headaches:

01 June 2012

ScienceDirect - Pain : Nicotine differentially activates inhibitory and excitatory neurons in the dorsal spinal cord

ScienceDirect - Pain : Nicotine differentially activates inhibitory and excitatory neurons in the dorsal spinal cord:

Matilde Cordero-Erausquin, Stéphanie Pons, Philippe Faure and Jean-Pierre Changeux,

Récepteurs et Cognition, CNRS URA2182, Institut Pasteur, 25 rue du Dr Roux, 75724, Paris Cedex 15, France


Abstract

Nicotinic agonists have well-documented antinociceptive properties when administered subcutaneously or intrathecally in mice. However, secondary mild to toxic effects are observed at analgesic doses, as a consequence of the activation of the large family of differentially expressed nicotinic receptors (nAChRs). In order to elucidate the action of nicotinic agonists on spinal local circuits, we have investigated the expression and function of nAChRs in functionally identified neurons of neonate mice spinal cord. Molecular markers, amplified at the single-cell level by RT-PCR, distinguished two neuronal populations in the dorsal horn of the spinal cord: GABAergic/glycinergic inhibitory interneurons, and calbindin (CA) or NK1 receptor (NK1-R) expressing, excitatory interneurons and projection neurons. The nicotinic response to acetylcholine of single cells was examined, as well as the pattern of expression of nAChR subunit transcripts in the same neuron. Beside the most expressed subunits 4, 2 and 7, the 2 subunit transcript was found in 19% of neurons, suggesting that agonists targeting 2* nAChRs may have specific actions at a spinal level without major supra-spinal effects. Both inhibitory and excitatory neurons responded to nicotinic stimulation, however, the nAChRs involved were markedly different. Whereas GABA/glycine interneurons preferentially expressed 462* nAChRs, 327* nAChRs were preferentially expressed by CA or NK1-R expressing neurons. Recorded neurons were also classified by firing pattern, for comparison to results from single-cell RT-PCR studies. Altogether, our results identify distinct sites of action of nicotinic agonists in circuits of the dorsal horn, and lead us closer to an understanding of mechanisms of nicotinic spinal analgesia."

10 February 2012

Labor pain

ScienceDaily (Jun. 4, 1997) — For almost 20 years, researchers have been examining a centuries-old phenomenon -- women helping women through childbirth. Continuous support from an experienced female companion, called a "doula" from the Greek word for servant, has been demonstrated to have impressive benefits, including shorter labors, less need for analgesia, and reduced likelihood of cesarean delivery. These findings about a time-proven, risk-free method come at a time when the focus in childbirth is on increased use of technology and medical intervention.

In a recent study, researchers John Kennell, M.D., and Susan K. McGrath, Ph.D., from the Department of Pediatrics at the Case Western Reserve University (CWRU) School of Medicine, looked at the childbirth experience of women at a Houston maternity hospital. Thirty-nine women were randomly chosen to be supported by a doula. Another 45 first-time mothers were randomly chosen to receive epidural analgesia to help control the pain of labor and delivery but were not supported by a doula. The day after delivery, both groups of women were asked to evaluate their pain levels and ability to cope with pain at three different times during childbirth. They rated their pain as ranging from "no pain" to "maximum pain" at the following times: 1) before receiving pain intervention (epidural analgesia or doula support), 2) after pain relief intervention, and 3) 24 hours after delivery. (Women who delivered by cesarean section were not included in the pain evaluation analysis.)

For women in both groups, pain was rated highest before the pain relief intervention, significantly less after the intervention, and much less again 24 hours after delivery. More importantly, when the pain evaluations from women in the doula group were compared to those from women in the epidural group, the two groups experienced equivalent levels of pain at all three measurement points.

Laboring women supported by a doula (with no pain relief medication) experienced the same levels of pain as women who received epidural analgesia, both during and after labor. Additionally, there were no differences in a laboring woman's ability to cope with pain whether she had an epidural or the continuous emotional support of an experienced doula.

According to the researchers, doula support is an effective, risk-free, non-pharmacologic, and inexpensive pain relief method that may be a viable alternative to epidural analgesia for many women in labor. Without the negative side effects and expense of an epidural, doula support offers the laboring woman a significant reduction in the pain of childbirth while also decreasing the chance for a cesarean delivery. Physicians, midwives, and consumers should consider these results when choosing obstetric pain relief.

The research team also included Vijay S. Varadarajulu, a premedical student at CWRU.

Adapted from materials provided by Johns Hopkins Children's Center.
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Johns Hopkins Children's Center (1997, June 4). Doula Support Found To Be A Risk-Free Alternative For Pain Relief During Childbirth. ScienceDaily. Retrieved March 19, 2008, from http://www.sciencedaily.com­ /releases/1997/06/970604100308.htm


Epidural Leads To Less Pain, More Assisted Deliveries

ScienceDaily (Nov. 22, 2005) — Women who receive epidurals during labor report less pain than those who choose opiates or natural childbirth, according to a systematic review of evidence.

Yet epidurals bring an increased risk of delivery assisted by forceps or vacuum. The pluses and minuses mean that a woman’s decision about pain relief is not clear-cut.

“Each woman will have to weigh how much it means to her to have a spontaneous vaginal delivery versus having more pain in labor,” said lead author Dr. Millicent Anim-Somuah of the Liverpool Women’s Hospital in England.

On a more positive note, mothers who receive the spinal injections are no more likely than others to require Caesarian sections or to suffer chronic backaches. Their infants are equally healthy soon after birth.

Epidural analgesia involves injecting a local anesthetic into the lower back to block pain impulses from the uterus and birth canal. Obstetricians introduced the technique in 1946, and 58 percent of American women now choose this form of pain relief during childbirth, according to the authors.

The review appears in the most recent issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic.

The reviewers analyzed 21 studies involving more than 6,000 women. Most of the participants were in the United States, England and Australia.

“It’s always been suspected that epidurals slow down your labor,” said Anim-Somuah. The study confirmed that the nerve block lengthens the stage during which the mother must push the baby through the birth canal. This leads to greater use of medication to stimulate contractions and a 38 percent increase in risk of instrumental delivery.

The precise timing of the epidural injection may be an important factor, says Todd Liu, M.D., a fellow of the American College of Obstetricians and Gynecologists who practices in New Jersey.

“Should you get your epidural when you first feel a contraction or when you are in a strong labor pattern?” Liu asked. “I would guess that there would be a higher [Caesarian section] rate if epidurals are given too early.”


Finally, there are certain “rare but potentially severe adverse effects” associated with epidurals, says the review. These include spinal cord injuries and permanent paralysis in the mother. These are so rare that incidence rates are currently unknown.

Randomized controlled trials like those included in Cochrane reviews are not well-suited to studying such uncommon events, said Anim-Somuah. “There should be some ongoing data collection as to whether these are occurring with epidurals.”

For now, Liu said, “My usual recommendation is that if labor is going to be long (usually with the first baby) and labor pains are very intense … then it is worth getting an epidural and accepting the potential risk.”

A potential weakness of the review is that only one trial studied childbirth without any painkillers at all.

Adapted from materials provided by Center for the Advancement of Health.
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Center for the Advancement of Health (2005, November 22). Epidural Leads To Less Pain, More Assisted Deliveries. ScienceDaily. Retrieved March 19, 2008, from http://www.sciencedaily.com­ /releases/2005/11/051122210414.htm


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From Chloroform To Epidurals: New Book By UF Physician Examines History Of Labor Pain Relief

ScienceDaily (Mar. 1, 2000) — GAINESVILLE, Fla.---Is the pain of childbirth an ancient curse, a meaningful passage to the beginning of a new life or simply a bout of agony to be endured with a generous helping of anesthesia?

Views of labor pain have shifted with the times, shaped by culture, but also by advances in medicine. Physicians have found reasonably effective ways of diminishing the most excruciating sensations, yet the 150-year history of anesthesia reveals what a complicated journey it has been, according to a University of Florida anesthesiologist.

"On the surface, it seems to be such a simple issue-there is pain and we can relieve it. Yet there are many philosophical and social ramifications, which have been viewed in very different ways through the years," said Dr. Donald Caton whose recently published book, "What A Blessing She Had Chloroform," delves into the medical and social history of relieving labor pain.

"Childbirth is such a very personal thing, so you see a range of reactions," Caton said. "Today, some women refuse anesthesia outright because they feel pain is part of the birth experience. Some refuse it for biblical reasons, citing the Book of Genesis story and its linking of punishment with childbirth."

And under the banner of feminism, women have alternated between demanding that anesthesia be given or insisting that it not.

The diversity of attitudes has at times caught the medical field off-guard. Caton, a professor of anesthesiology at UF's College of Medicine, says that early in his career he was surprised when some women would refuse his assistance. Now he sees obstetric pain relief as a fascinating case study of how science and culture evolve, influencing each other along the way.

Soon after the first modern anesthetic was introduced in 1846, some women began to push for its use in labor. Physicians, however, had to grapple with issues of safety -- and at a time when they were only beginning to learn how to investigate such questions scientifically.

"In 1820, they still had been learning that the body is composed of earth, air, fire and water and that disease is caused by an imbalance of those elements," Caton said. "So when anesthesia became available, physicians had a lot to sort through. It was first used for surgery, which makes sense because without pain relief, some operations simply couldn't be performed.

"But childbirth was seen as a natural process, and physicians had a very difficult time trying to figure out if the pain of it was a necessary part of that process. They needed to determine whether eliminating or at least diminishing pain would in itself cause labor to stop."

Though it would take into well into the next century to answer those questions, that didn't keep physicians from experimenting. In 1847, Scottish obstetrician James Young Simpson administered ether to a woman in delivery, just a few weeks after a Massachusetts dentist had publicly demonstrated its use for surgery. That same year, Fanny Wadsworth Longfellow, wife of the poet, became the first woman in the United States to give birth with the aid of pain relief.

In England, Queen Victoria was an early recipient. Then in 1859, when her oldest daughter gave birth, the queen offered the phrase that would become the title of Caton's book: "What a blessing she had chloroform."

But while physicians continued to study the effects of labor medications, obstetric anesthesia was far from routine. By the early 20th century, American feminists had become more and more impatient that labor pain relief was not widely available.

They campaigned for a new European technique called Twilight Sleep. Unfortunately, the combination of morphine and a disorienting drug called scopolamine was far from the perfect solution. Pain was still significant, and too high a dose could prove toxic. What little Twilight Sleep had to offer was of dubious value: the possibility that women would forget the birthing experience.

As the 20th century wore on, though, anesthesiologists became adept at relieving pain in a manner they believed to be safe for both mother and child. However, their confidence in its safety led to higher and higher doses, which sparked a backlash. English obstetrician Grantly Dick Read advocated a return to natural childbirth, and later French obstetrician Fernand Lamaze did as well. A new wave of feminism in 1960s and 1970s took up the cause against medicalized childbirth, arguing that physicians were taking away women's right to experience labor and delivery.

Today, Caton believes, the vehemence of the natural childbirth movement has passed. Women appear to have less pressure on them to choose or reject anesthesia. Currently, about 60 percent of women in the United States receive some form of pain relief for vaginal delivery, usually an epidural, a type of regional anesthesia.

"At the same time," Caton points out, "there is this residual idea in the culture as seen through literature, religion and politics that maybe pain has meaning and has important social benefits," such as establishing family bonds, inspiring people to try harder or as a method of controlling criminals.

"In childbirth, you continue to see that for some women, experiencing childbirth pain is extremely important to their personal and social development," Caton said. "But then there are a lot of people who think, 'I have local anesthesia when I go to the dentist's office, I'm certainly going to have it when I have my child.' So most of them do."

Adapted from materials provided by University Of Florida Health Science Center.
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University Of Florida Health Science Center (2000, March 1). From Chloroform To Epidurals: New Book By UF Physician Examines History Of Labor Pain Relief. ScienceDaily. Retrieved March 19, 2008, from http://www.sciencedaily.com­ /releases/2000/02/000228103624.htm

21 December 2011

Arthritis National Research Foundation

Arthritis sucks. Rheumatoid Arthritis is especially sucky.

Here's a gentle description of what happened to my grandmother from the Arthritis National Research Foundation.
She once swam competitively, but no longer could. She had difficulty doing the shopping for her family. Everyday pleasures were dulled by pain. The simplest movements required tremendous effort and concentration.

Joyce Sontag was a victim of rheumatoid arthritis (RA), a debilitating, progressive autoimmune disease. She was diagnosed with the disease at the age of 35 and lived 37 long years fighting the disease's progress in her body and in her life. Sadly, her family watched this decline without being given much hope for relief or remission, other than the treatment of symptoms.

Mrs. Sontag was hospitalized at the Long Beach Memorial Medical Center when she died from complications of rheumatoid arthritis in 1993. The treatments she received for RA from the late 1950s to the 1990s often had more negative side effects than positive effects for pain relief. The disease spread beyond the joints to other organs. Gradually, Mrs. Sontag became more and more debilitated, suffering acute weight loss and spinal column degeneration.

The Sontag Foundation




So, this is me urging you to donate to the ARNF or other organization supporting scientific research into the causes and treatment of arthritis.

Donate to the ARNF

(If you're wealthy, I will love you forever if your donation puts my Uncle in his place.)

16 December 2011

SERE training and torture

http://www.salon.com/news/feature/2007/06/21/cia_sere/print.html

The CIA's torture teachers
Psychologists helped the CIA exploit a secret military program to develop brutal interrogation tactics -- likely with the approval of the Bush White House.

By Mark Benjamin

Jun. 21, 2007 | There is growing evidence of high-level coordination between the Central Intelligence Agency and the U.S. military in developing abusive interrogation techniques used on terrorist suspects. After the Sept. 11 attacks, both turned to a small cadre of psychologists linked to the military's secretive Survival, Evasion, Resistance and Escape program to "reverse-engineer" techniques originally designed to train U.S. soldiers to resist torture if captured, by exposing them to brutal treatment. The military's use of SERE training for interrogations in the war on terror was revealed in detail in a recently declassified report. But the CIA's use of such tactics -- working in close coordination with the military -- until now has remained largely unknown.

According to congressional sources and mental healthcare professionals knowledgeable about the secret program who spoke with Salon, two CIA-employed psychologists, James Mitchell and Bruce Jessen, were at the center of the program, which likely violated the Geneva Conventions on the treatment of prisoners. The two are currently under investigation: Salon has learned that Daniel Dell'Orto, the principal deputy general counsel at the Department of Defense, sent a "document preservation" order on May 15 to the chairman of the Joint Chiefs of Staff and other top Pentagon officials forbidding the destruction of any document mentioning Mitchell and Jessen or their psychological consulting firm, Mitchell, Jessen and Associates, based in Spokane, Wash. Dell'Orto's order was in response to a May 1 request from Sen. Carl Levin, the Democratic chairman of the Senate Armed Services Committee, who is investigating the abuse of prisoners in U.S. custody.

Mitchell and Jessen have worked as contractors for the CIA since 9/11. Both were previously affiliated with the military's SERE program, which at its main school at Fort Bragg puts elite special operations forces through brutal mock interrogations, from sensory deprivation to simulated drowning.

A previously classified report by the Defense Department's inspector general, made public last month, revealed in vivid detail how the military -- in flat contradiction to previous denials -- used SERE as a basis for interrogating suspected al-Qaida prisoners at Guantánamo Bay, and later in Iraq and Afghanistan. Moreover, the involvement of the CIA, which was secretly granted broad authority by President Bush days after 9/11 to target terrorists worldwide, suggests that both the military and the spy agency were following a policy approved by senior Bush administration officials.

Close coordination between the CIA and the Pentagon is referred to in military lingo as "jointness." A retired high-level military official, familiar with the detainee abuse scandals, confirmed that such "jointness" requires orchestration at the top levels of government. "This says that somebody is acting as a bridge between the CIA and the Defense Department," he said, "because you've got the [CIA] side and the military side, and they are collaborating." Human-rights expert Scott Horton, who chairs the International Law Committee at the New York City Bar Association, also says that the cross-agency coordination "reflects the fact that the decision to introduce and develop these methods was made at a very high level."

On Wednesday, dozens of psychologists made public a joint letter to American Psychological Association president Sharon Brehm fingering another CIA-employed psychologist, R. Scott Shumate. Previous news reports led the American Medical Association and the American Psychiatric Association to ban their members from participating in interrogations, but the issue has remained divisive within the American Psychological Association, which has not forbidden the practice. "We write you as psychologists concerned about the participation of our profession in abusive interrogations of national security detainees at Guantanamo, in Iraq and Afghanistan, and at the so-called CIA 'black sites,'" the psychologists wrote. In violation of APA ethics, they said, "It is now indisputable that psychologists and psychology were directly and officially responsible for the development and migration of abusive interrogation techniques, techniques which the International Committee of the Red Cross has labeled 'tantamount to torture.'" [Ed. note: The full letter detailing the allegations of APA complicity can be read here.]

The letter cites a previously public biographical statement on Shumate that listed his position from April 2001 to May 2003 as "the chief operational psychologist for the CIA's Counter Terrorism Center." The bio also noted that Shumate "has been with several of the key apprehended terrorists" who have been held and interrogated by the agency since 9/11. At CTC, Shumate reported to Cofer Black, the former head of CTC who famously told Congress in September 2002, "There was a before 9/11, and there was an after 9/11. After 9/11 the gloves come off." Shumate's bio, obtained by Salon, has been removed from the InfowarCon 2007 conference Web site. Shumate did not return a phone call seeking comment.

The SERE-based program undermines assertions made for years by Bush administration officials that interrogations conducted by U.S. personnel are safe, effective and legal. SERE training, according to the Department of Defense inspector general's report, is specifically designed "to replicate harsh conditions that the service member might encounter if they are held by forces that do not abide by the Geneva Conventions."

"The irony -- and ultimately the tragedy -- in the migration of SERE techniques is that the program was specifically designed to protect our soldiers from countries that violated the Geneva Conventions," says Brad Olson, president of the Divisions for Social Justice within the American Psychological Association. "The result of the reverse-engineering, however, was that by making foreign detainees the target, it made us the country that violated the Geneva Conventions," he says.

There are striking similarities between descriptions of SERE training and the interrogation techniques employed by the military and CIA since 9/11. Soldiers undergoing SERE training are subject to forced nudity, stress positions, lengthy isolation, sleep deprivation, sexual humiliation, exhaustion from exercise, and the use of water to create a sensation of suffocation. "If you have ever had a bag on your head and somebody pours water on it," one graduate of that training program told Salon last year "it is real hard to breathe."

Many of those techniques show up in interrogation logs, human rights reports and news articles about detainee abuse that has taken place in Guantánamo, Afghanistan and Iraq. (The military late last year unveiled a new interrogation manual designed to put a stop to prisoner abuse.) An investigation released this month by the Council of Europe, a multinational human rights agency, added extreme sensory deprivation to the list of techniques that have been used by the CIA. The report said that extended isolation contributed to "enduring psychiatric and mental problems" of prisoners.

Isolation in cramped cells is also a key tenet of SERE training, according to soldiers who have completed the training and described it in detail to Salon. The effects of isolation are a specialty of Jessen's, who taught a class on "coping with isolation in a hostage environment" at a Maui seminar in late 2003, according to a Washington Times article published then. (Defense Department documents from the late 1990s describe Jessen as the "lead psychologist" for the SERE program.) Mitchell also spoke at that conference, according to the article. It described both men as "contracted to Uncle Sam to fight terrorism."

Mitchell's name surfaced again many months later. His role in interrogations was referenced briefly in a July 2005 New Yorker article by Jane Mayer, which focused largely on the military's use of SERE-based tactics at Guantánamo. The article described Mitchell's participation in a CIA interrogation of a high-value prisoner in March 2002 at an undisclosed location elsewhere -- presumably a secret CIA prison known as a "black site" -- where Mitchell urged harsh techniques that would break down the prisoner's psychological defenses, creating a feeling of "helplessness." But the article did not confirm Mitchell was a CIA employee, and it explored no further the connection between Mitchell's background with SERE and interrogations being conducted by the CIA.

A call to Mitchell and Jessen's firm for comment was not returned. The CIA would not comment on Mitchell and Jessen's work for the agency, though the contractual relationship is not one Mitchell and Jessen entirely concealed. They advertised their CIA credentials as exhibitors at a 2004 conference of the American Psychological Association in Honolulu.

In a statement to Salon, CIA spokesman George Little wrote that the agency's interrogation program had been "implemented lawfully, with great care and close review, producing a rich volume of intelligence that has helped the United States and other countries disrupt terrorist activities and save innocent lives."

Until last month, the Army had denied any use of SERE training for prisoner interrogations. "We do not teach interrogation techniques," Carol Darby, chief spokeswoman for the U.S. Army Special Operations Command at Fort Bragg, said last June when Salon asked about a document that appeared to indicate that instructors from the SERE school taught their methods to interrogators at Guantánamo.

But the declassified DoD inspector general's report described initiatives by high-level military officials to incorporate SERE concepts into interrogations. And it said that psychologists affiliated with SERE training -- people like Mitchell and Jessen -- played a critical role. According to the inspector general, the Army Special Operations Command's Psychological Directorate at Fort Bragg first drafted a plan to have the military reverse-engineer SERE training in the summer of 2002. At the same time, the commander of Guantánamo determined that SERE tactics might be used on detainees at the military prison. Then in September 2002, the Army Special Operations Command and other SERE officials hosted a "SERE psychologist conference" at Fort Bragg to brief staff from the military's prison at Guantánamo on the use of SERE tactics.

The chief of the Army Special Operations Command's Psychological Directorate was Col. Morgan Banks, the senior SERE psychologist, who has been affiliated with the training for years and helped establish the Army's first permanent training program that simulated captivity, according to a 2003 biographical statement. Banks also spent the winter of 2001 and 2002 at Bagram Airfield in Afghanistan "supporting combat operations against Al Qaida and Taliban fighters," according to one of his bios, which also said that Banks "provides technical support and consultation to all Army psychologists providing interrogation support."

In 2005, Banks helped draft ethical guidelines for the APA that say a psychologist supporting an interrogation is providing "a valuable and ethical role to assist in protecting our nation, other nations, and innocent civilians from harm." But as Salon reported last summer, six of the 10 psychologists who drafted that policy, including Banks, had close ties to the military. Some psychologists worry that the APA policy has made the organization an enabler of torture. Those ethics guidelines "gave the APA imprimatur to any of these techniques," says Steven Reisner, an APA member who has been closely tracking psychologists' role in interrogations. The policy, Reisner says, was developed by "psychologists directly involved in the interrogations."

Another of the six psychologists on the panel that drafted the guidelines who had ties to the military was Shumate. His bio for that APA task force said he worked as a "director of behavioral science" for the Defense Department. It never mentioned that he also worked for the CIA.

-- By Mark Benjamin

Link

01 September 2011

Marijuana pharmacology

Marijuana And the Brain
by John Gettman
High Times, March, 1995

In 1970, marijuana was placed on Schedule 1 of the Drug Enforcement Administration's controlled-substances list, largely because scientists feared that, like opiates, it had an extremely high potential for abuse and addiction. But the discovery of THC receptor sites in the brain refutes that thinking, and may force both scientists and the DEA to re-evaluate their positions.

Introduction

The next century will view the 1988 discovery of the THC receptor site in the brain as the pivotal event which led to the legalization of marijuana. Before this discovery, no one knew for sure just how the psychoactive chemical in marijuana worked on the brain. Throughout the 1970s and 1980s, researchers made tremendous strides in understanding how the brain works, by using receptor sites as switches which respond to various chemicals by regulating brain and body functions. The dominant fear about marijuana in the 20th century has been that its effects were somehow similar to the dangerously addictive effects of opiates such as morphine and heroin. Despite widespread decriminalization of marijuana in the United States in the 1970s, this concern has remained the basis for federal law and policies regarding the use and study of marijuana. The legal manifestation of this fear is the continued classification of marijuana as a Schedule I drug, a category shared by heroin and other drugs that are banned from medical use because of their dangerous, addictive qualities. While only 11 states have formally decriminalized possession of small amounts of marijuana, 45 states distinguish between marijuana and other Schedule I drugs for law-enforcement and sentencing purposes. Until the 1980s, technological limitations obstructed scientific understanding of the neuropharmacology of THC, of how the active ingredient in marijuana actually affects brain functions. Observations and conclusions about this subject, though based on some biological studies, were largely influenced by observations of behavior. This has allowed cultural prejudice to sustain the faith that marijuana is somehow related to heroin, and that research will eventually prove this hypothesis. Actually, the discovery of the THC receptor site and the subsequent research and observations it has inspired conclusively refute the hypothesis that marijuana is dope. Many important brain functions which affect human behavior involve the neurotransmitter dopamine. Serious drugs of abuse, such as heroin and cocaine, interfere with the brain's use of dopamine in manners that can seriously alter an individual's behavior. A drug's ability to affect the neural systems related to dopamine production has now become the defining characteristic of drugs with serious abuse potential.

According to the congressional Office of Technology Assessment, research over the last 10 years has proved that marijuana has no effect on dopamine-related brain systems - unless you are an inbred Lewis rat (see below), in which case abstention is recommended. The discovery of a previously unknown system of cannabinoid neural transmitters is profound. While century-old questions, such as why marijuana is nontoxic, are finally being answered, new, fascinating questions are emerging - as in the case of all great discoveries. In the words of Israeli researcher Raphael Mechoulam, the man who first isolated the structure of THC, "Why do we have cannabinoid receptors?" Mechoulam's theory will resonate well with marijuana smokers in the United States. He observes that "Cannabis is used by man not for its actions on memory of movement or movement coordination, but for its actions on memory and emotions," and asks, "Is it possible that the main task of cannabinoid receptors . . . (is) to modify our emotions, to serve as the links which transmit or transform or translate objective or subjective events into perceptions and emotions?" At a 1990 conference on cannabinoid research in Crete, Mechoulam concluded his remarks by saying, "Let us hope, however, that through better understanding of cannabis chemistry in the brain, we may also approach the chemistry of emotions."

A BRIEF HISTORY OF THC RESEARCH

The receptor breakthrough occurred in 1988 at the St. Louis University Medical School where Allyn Howlett, William Devane and their associates identified and characterized a cannabinoid receptor in a rat brain. The breakthrough has a long history leading up to it. Major figures in American and British organic chemistry, such as Roger Adams, Alex Todd and Sigmund Loewe, did important work in determining the pharmacology of cannabis in the 1940s and 1950s, but their work ground to a halt due to the disinterest cultivated by the 1937 federal ban on marijuana. While synthetic compounds were created which were close to the actual compound, THC, they were not equivalent to it. The structure of one related chemical, cannabidiol, was determined. After repeating the isolation of cannabidiol, in 1963 Mechoulam began work with Yehiel Gaoni that led to the determination of the biosynthetic pathway by which the plant synthesizes cannabinoids. In 1964 Gaoni and Mechoulam isolated tetrahydrocannabinol (THC) and a few years later they reported the first synthesis of THC. Following the identification of the active constituent in marijuana, scientific research began to fill in the gaps and build on Mechoulam's initial breakthrough. The neutral and acidic cannabinoids in cannabis were isolated, and their structures were elucidated. The absolute configurations were determined, as was a reasonable scheme of biogenesis. Total synthesis of the chemical was obtained, and the structure-activity relationship was established. These developments laid the foundation for pharmacological research involving animals and man. This work, along with observations of marijuana's therapeutic applications, opened up investigation into the medical properties of cannabinoids in general and THC in particular. Medical research into the health effects of cannabis also matured throughout this period. In a comprehensive 1986 article in the Pharmacological Review, Leo Hollister of the Stanford University School of Medicine concluded that "compared with other licit social drugs, such as alcohol, tobacco and caffeine, marijuana does not pose greater risks." Hollister wondered if these currently licit drugs would have enjoyed their popular acceptance based on our current knowledge of them. Nonetheless, it has been widely held throughout the 1980s, as Hollister concluded, that "Marijuana may prove to have greater therapeutic potential than these other social drugs, but many questions still need to be answered." The primary question, though, was how do cannabinoids work on the brain? By 1986, scientists were already on the slippery slope that would lead to the discovery of the cannabinoid receptor. The triennial reports from the National Institute on Drug Abuse summarizing research on marijuana had begun to omit references to research on marijuana-related brain damage and instead focus on brain receptor research. A comprehensive article by Renee Wert and Michael Raoulin was published in the International Journal of the Addictions that year, detailing the flaws in all previous studies that claimed to show brain damage resulting from marijuana use. As Hollister independently concluded, "Brain damage has not been proved." The reason, obviously, is that the brain was prepared in some respects to process THC. Also in 1986, Mechoulam put together a book reviewing this research, Cannabinoids as Therapeutic Agents (CRC Press, Boca Raton, FL). One promising area of research was the use of cannabinoids as analgesics or painkillers. A synthetic cannabinoid named CP 55,940, 10-100 times more potent than THC, was also developed in 1986; this was the key to the cannabinoid receptor breakthrough. Receptors are binding sites for chemicals in the brain, chemicals that instruct brain cells to start, stop or otherwise regulate various brain and body functions. The chemicals which trigger receptors are known as neurotransmitters. The brain's resident neurotransmitters are known as endogenous ligands. In many instances, drugs mimic these natural chemicals working in the brain. Scientists are just now confirming their determinations as to which endogenous ligands work on the cannabinoid receptors; it is likely that the neurotransmitter which naturally triggers cannabinoid receptors is one known as anandamide. Research continues. To grossly oversimplify the research involved, a receptor is determined by exposing brain tissue to various chemicals and observing if any of them uniquely bind to the tissue. The search for a cannabinoid receptor depended on the use of a potent synthetic that would allow observation of the binding. CP 55,940 provided this potency, and it allowed Howlett, Devane and their associates, working with tissue from a rat brain, to fulfill precise scientific criteria for determining the existence of a pharmacologically-distinct cannabinoid in brain tissue. A year later the localization of cannabinoid receptors in human brains and other species was determined by scientists at the National Institute of Mental Health, led by Miles Herkenham and including Ross Johnson and Lawrence Melvin, who had worked with Howlett and Devane on the earlier study.

RECEPTORS IN THE BRAIN

The locations of the cannabinoid receptors are most revealing of the way THC acts on the brain, but the importance of this determination is best understood in comparison with the effects of other drugs on the brain. Neurons are brain cells which process information. Neurotransmitter chemicals enable them to communicate with each other by their release into the gap between the neurons. This gap is called the synapse. Receptors are actually proteins in neurons which are specific to neurotransmitters, and which turn various cellular mechanisms on or off. Neurons can have thousands of receptors for different neurotransmitters, causing any neurotransmitter to have diverse effects in the brain. Drugs affect the production, release or re-uptake (a regulating mechanism) of various neurotransmitters. They also mimic or block actions of neurotransmitters, and can interfere with or enhance the mechanisms associated with the receptor. Dopamine is a neurotransmitter which is associated with extremely pleasurable sensations, so that the neural systems which trigger dopamine release are known as the "brain reward system." The key part of this system is identified as the mesocorticolimbic pathway, which links the dopamine-production area with the nucleus of accumbens in the limbic system, an area of the brain which is associated with the control of emotion and behavior. Cocaine, for example, blocks the re-uptake of dopamine so that the brain, lacking biofeedback, keeps on producing it. Amphetamines also block the re-uptake of dopamine, and stimulate additional production and release of it. Opiates activate neural pathways that increase dopamine production by mimicking opioid-peptide neurotransmitters which increase dopamine activity in the ventral tegmental area of the brain where the neurotransmitter originates. Opiates work on three receptor sites, and in effect restrain an inhibitory amino acid, gamma-aminobutyric acid, that otherwise would slow down or halt dopamine production. All of these substances can produce strong reinforcing properties that can seriously influence behavior. The rewarding properties of dopamine are what accounts for animal studies in which animals will forgo food and drink or willingly experience electric shocks in order to stimulate the brain reward system. It is now widely held that drugs of abuse directly or indirectly affect the brain reward system. The key clinical test of whether a substance is a drug of abuse potential or not is whether administration of the drug reduces the amount of electrical stimulation needed to produce self-stimulation response, or dopamine production. This is an indication that a drug has reinforcing properties, and that an individual's use of the drug can lead to addictive and other harmful behavior. To be precise, according to the Office of Technological Assessment (OTA): "The capacity to produce reinforcing effects is essential to any drug with significant abuse potential." Marijuana should no longer be considered a serious drug abuse because, as summarized by the OTA: "Animals will not self-administer THC in controlled studies . . . . Cannabinoids generally do not lower the threshold needed to get animals to self-stimulate the brain regard system, as do other drugs of abuse." Marijuana does not produce reinforcing effects. The definitive experiment which measures drug-induced dopamine production utilizes microdialysis is live, freely-moving rats. Brain microdialysis has proven that opiates, cocaine, amphetamines, nicotine and alcohol all affect dopamine production, whereas marijuana does not. This latest research confirms and explains Hollister's 1986 conclusion about cannabis and addiction: "Physical dependence is rarely encountered in the usual patterns, despite some degree of tolerance that may develop." Most important, the discoveries of Howlett and Devane, Herkenham and their associates demonstrate that the cannabinoid receptors do not influence the dopamine reward system.

CANNABINOID RECEPTORS Research has enabled scientists to know which portions of the brain control various body functions, and this knowledge has been used to explain the pharmacological properties of drugs that activate receptor sites in the brain. There is a dense concentration of cannabinoid binding sites in the basal ganglia and the cerebellum of the base-brain, both of which affect movement and coordination. This discovery will aid in determining the actual physical mechanism by which THC affects spasticity and provides therapeutic benefits to patients with multiple sclerosis and other spastic disorders. While there are cannabinoid receptors in the ventromedial striatum and basal ganglia which are areas associated with dopamine production, no cannabinoid receptors have been found in dopamine-producing neurons, and as mentioned above, no reinforcing properties have been demonstrated in animal studies. There is one study by Gardner and Lowinson, involving inbred Lewis rats, in which doses of THC lowered the amount of electrical stimulation required to trigger the brain reward system. However, no one has been able to replicate the results with any other species of rat, or any other animal. The finding is believed to be the result of some inbred genetic variation in the inbred species, and is both widely mentioned in the literature and disregarded. According to Herkenham and his associates, "There are virtually no reports of fatal cannabis overdose in humans. The safety reflects the paucity of receptors in medullary nuclei that mediate respiratory and cardiovascular functions." This is also why cannabinoids have great promise as analgesics or painkillers, in that they do not depress the function of the heart or the lungs. In this respect, they are far superior to opiates, which decrease the entire physiological system because the receptors are all over the medulla as well as the brain. Marijuana is distinguished from most other illicit drugs by the locations of its brain-receptor sites for two predominant reasons: (1) The lack of receptors in the medulla significantly reduces the possibility of accidental, or even deliberate, death from THC, and (2) the lack of receptors in the mesocorticolimbic pathway significantly reduces the risks of addiction and serious physical dependence. As a therapeutic drug, these features are God's greatest gifts.

THE CHEMISTRY OF EMOTIONS

Mechoulam regrets that more has not been done in the therapeutic application of THC. In a 1986 interview with the International Journal of the Addictions, he said that, "Knowing what I know today, I would have worked more on the therapeutic aspects of cannabis. This area apparently needs a major push that is has not had up till now, particularly given that it has a therapeutic potential. One of the reasons that it has not been pushed was than most pharmaceutical companies years ago were afraid to get into that field. Companies were 'burnt' working on amphetamines and LSD. . . . They are afraid of notoriety." Clearly, cannabis acts on coordination of movement by way of the receptors in the cerebellum and basal ganglia, and on memory by way of the receptors in the limbic system's hippocampus, which "gates" information during memory consolidation. Mechoulam believes that in humans these actions "are rather marginal." "Cannabis," he states, "is used . . . for its actions on mood and emotion." The key to understanding the reason for the presence of cannabinoid receptors in the human brain lies in understanding the role of the receptors in the limbic system, which has a central role in the mechanisms which govern behavior and emotions. The limbic system coordinates activities between the visceral base-brain and the rest of the nervous system. "We know next to nothing on the chemistry of emotions," Mechoulam instructs. It is his hope that future research on the role of cannabinoid receptors in the brain will shed light on this new area of investigation and reflection.

THE FUTURE OF MARIJUANA LAWS

Advances in neurobiology are redefining the scientific basis for addiction. These advances have important ramifications for addiction treatment, and for the treatment of numerous organic diseases and conditions. More importantly for marijuana users, these advances in neurobiology will ultimately force changes in the law. The law is constantly being modified in response to technological changes. The passage of the Controlled Substances Act in 1972 was in part due to a greater understanding of drug abuse brought about by the medical research of the time. The law instituted a policy by which regulation and criminal penalties regarding controlled substances were to be correlated with the harmfulness of the substance. Specifically, the law lists the "actual or relative potential for abuse" as the first matter to be considered in determining the appropriate scheduling of a drug. Schedule I is for drugs which have a "high potential for abuse." While the scheduling of marijuana and its subsequent availability for research and medical use was the subject of a 22-year unsuccessful court battle spearheaded by the National Organization for the Reform of Marijuana Laws, the question of marijuana's abuse potential was never addressed during the litigation and related proceedings. The suit over medical marijuana sought to reschedule marijuana as a Schedule II drug, which also implies a "high potential for abuse." This made the abuse question irrelevant to the court proceedings. However, the abuse question is the pre-eminent issue in attempts to reform marijuana laws, and it is the weak link upon which the entirety of marijuana prohibition rests. The most recent research indicates that marijuana does not have a high potential for abuse, especially relative to other scheduled drugs such as heroin, cocaine, sedatives and amphetamines. The medical-marijuana petition was rejected by the administrator of the DEA because of the lack of scientific studies detailing marijuana's medical value. The court appeal essentially concerned whether or not this was a reasonable standard in light of the government's historic disinterest in funding such studies. While courts have ruled that DEA can rely on research studies, or the lack thereof, in its decision-making about the scheduling of marijuana, they have not ruled on the actual issues which determine the proper legal scheduling of marijuana. The discovery of cannabinoid receptor sites, and their relevance to the understanding of the pharmacology of THC in the brain, provides the basis for a new challenge to the legitimacy of marijuana's Schedule I status, a pivotal event in marijuana's eventual legalization.
Link

29 July 2011

What cancer survival really means

I was really taken aback by this explanation of what cancer survival really means. I know that some of you are fighting cancer* or have someone in your lives who is. This may be useful.

xkcd: Lanes

(Click to make bigger)

comic explaining what cancer survival stats really mean.

Check out the rollover --the text which displays when your mouse hovers over the picture-- on the original post for how the picture reflects the stages of breast cancer.

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*Reflecting on this, I think I see a bit better why some say that 'fighting cancer' is the wrong language/metaphor. Though I'm not sure what to use instead. Help me out.

19 July 2011

Foolproof method for succeeding in modern neurochemistry

Neurochemistry Post-Docs! Looking to publish interesting and important papers on the neurochemistry of reward but don't know what to study? Then Dr. Swenson's Revolutionary Topic Selection Method is for you!

For centuries, western philosophers have thought carefully about the nature and kinds of pleasure.* You too can benefit from their efforts!

Here's the key to Dr. Swenson's Revolutionary Topic Selection Method: These philosophers have been studying mental phenomena. You study neural phenomena. And mental phenomena are ultimately neural phenomena!

Other inferior neuropsychological research programs have tried using philosophical claims to select topics. But they would have you try to prove or disprove philosophical claims with neuroscience. That may win you friends amongst philosophers. But you don't want philosopher friends!** You want prestigious publications and lucrative grants!

That's where Dr. Swenson's Revolutionary Topic Selection Method can help! You needn't worry about proving or disproving philosophical claims. With Dr. Swenson's Revolutionary Topic Selection Method, you will use writers ranging from the ancient Greeks to the modern utilitarians to help you design experimental paradigms that are the key to scientific fame.

Here's just one taste of what the system has to offer. Philosophers have, in various guises, debated whether some pleasures are better than others by virtue of being more refined and intellectually infused.

Now a lesser program might have you consider whether opera or pop music produces greater activity in dopaminergic pathways in subjects with past exposure to both. But that will impress only philosophers.

With Dr. Swenson's Revolutionary Topic Selection Method you will instead find in these disputes some promising leads for experimentation. You may, for example, design your experiments to investigate connections between the reward pathway activity, memories, and higher order processes. You don't care whether the refined music elicits more apparent reward. You care about whether pop music and opera elicit systematically different connections throughout the brain.***

Now, it is true that Dr. Swenson's Revolutionary Topic Selection Method can't promise experimental results that will woo philosophers.**** But Dr. Swenson's Revolutionary Topic Selection Method can help you select topics which will uncover processes which underlie our complex mental lives. And that's what you want.

And lucrative grants!

Act now and Dr. Swenson's Revolutionary Topic Selection Method can be yours for a pathetically small amount of money. First 10 callers get a free T-shirt and Shamwow.


*Yes, this comes dangerously close to 'since the dawn of time'. I cringe too.

**I'm serious.

***I know, music isn't the best example. But it's easy to set out. Thanks a lotOliver Sacks.

****Philosophers will nonetheless distort your results and woo themselves.


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This post was inspired by

Heterogenerity of Reward Mechanisms

SpringerLink - Neurochemical Research, Volume 35, Number 6: "The finding that many drugs that have abuse potential and other natural stimuli such as food or sexual activity cause similar chemical changes in the brain, an increase in extracellular dopamine (DA) in the shell of the nucleus accumbens (NAccS), indicated some time ago that the reward mechanism is at least very similar for all stimuli and that the mechanism is relatively simple. The presently available information shows that the mechanisms involved are more complex and have multiple elements. Multiple brain regions, multiple receptors, multiple distinct neurons, multiple transmitters, multiple transporters, circuits, peptides, proteins, metabolism of transmitters, and phosphorylation, all participate in reward mechanisms. The system is variable, is changed during development, is sex-dependent, and is influenced by genetic differences. Not all of the elements participate in the reward of all stimuli. Different set of mechanisms are involved in the reward of different drugs of abuse, yet different mechanisms in the reward of natural stimuli such as food or sexual activity; thus there are different systems that distinguish different stimuli. Separate functions of the reward system such as anticipation, evaluation, consummation and identification; all contain function-specific elements. The level of the stimulus also influences the participation of the elements of the reward system, there are possible reactions to even below threshold stimuli, and excessive stimuli can change reward to aversion involving parts of the system. Learning and memory of past reward is an important integral element of reward and addictive behavior. Many of the reward elements are altered by repeated or chronic stimuli, and chronic exposure to one drug is likely to alter the response to another stimulus. To evaluate and identify the reward stimulus thus requires heterogeneity of the reward components in the brain. "



(Via http://mindhacks.com/.)



LSD analogue and cluster headaches

Whoa. Check out this abstract an annual International Headache Congress paper.

Cluster headache attack cessation and remission extension of months or longer in six treatment-refractory patients administered only 3 doses of BOL-148

J. Halpern, M. Karst, T. Passie


Five male patients with treatment-refractory chronic cluster headache and one female patient with treatment-refractory mixed cluster/migrainous headache were administered 2-bromo-LSD (BOL-148) (20mcg/kg) at five-day intervals for a total of three treatments. Sixteen-week outcome data on the five male patients revealed a robust treatment response, with three of the five having no attacks for more than one month, thereby shifting their diagnosis back to the episodic form of cluster headache. Similarly, the female patient reported quiescence of cluster attacks for greater than one month and 'significant' improvement in migraine in the following weeks from last dose of BOL-148. This poster presents longterm outcome data on all 6 patients who received BOL-148. In follow-up with these patients, BOL-148 provided significant headache relief that lasted for several months to more than one-year. Data suggests that BOL-148 may function as an important new treatment, though, at present, there is no explanation for such long-term prophylactic effects with no later drug re-administrations. There is some evidence that BOL-148 is affecting epigenetic mechanisms and may open the possibility for a near-cure-like treatment for patients afflicted with vascular headaches."

In English: in small study, a chemical cousin of LSD pretty much cured cluster headaches in some patients. It may have done this through changes at the genetic level.
All the usual caveats apply --small study, limited time frame, et cetera. Still, whoa.

Here's a better summary.

-------

And, though there's no reason whatsoever to think there's any relationship with the long-term gene-level effects in this study, I've been looking for an excuse to post this: John's Hopkins Study Probes "Sacred Mushroom" Chemical. Amongs the results
Looking back over a year later, most of the experiment’s 18 volunteers (94 percent) rated a psilocybin session as among the top five most or as the topmost spiritually significant experience of his or her life....Most volunteers (89 percent) also reported positive changes in their behaviors, and those reports were corroborated by family members or others, the researchers say. The behavior changes most frequently cited were improved relationships with family and others, increased physical and psychological self-care, and increased devotion to spiritual practice.

22 February 2011

The Strange Powers of the Placebo Effect

Some of the interesting features of the placebo effect:

Darvocet decision a prelude a warm up for banning methadone?

Christian Sinclair over at Pallimed does some sleuthing into the FDA's rationale for pulling propoxyphene and comes away concerned:

He notes that
* Propoxyphene is a synthetic derivative of methadone.

* Methadone causes QT prolongation of questionable clinical significance in palliative care patients.

* QT prolongation is a risk factor for ventricular arrhythmias.


Combined with some FDA memo analysis (go read the post) he concludes

Well all this may be a whole lot of nothing but my real concern is that methadone may be a drug in the crosshairs of the FDA soon. It already has four strikes against it:

1) documented QT prolongation

2) stigma of heroin treatment programs

3) accelerating percent of all deaths related to opioids

4) methadone could be considered an orphan drug

This would be bad news indeed.

(Via: Pallimed: A Hospice & Palliative Medicine Blog: Are You Glad Darvocet Got Pulled by the FDA? Are You Sure?)

10 February 2011

Images from the History of Medicine (NLM)

Just discovered the National Library of Medicine's archive of images. Pretty neat (in a depressing sort of way).
Here's the main site:
http://www.nlm.nih.gov/hmd/ihm/

and here's a link to search results for pain:

Images from the History of Medicine (NLM) - Search Results: All Fields SimilarTo 'Pain'


14 January 2011

Open placebos

By now I'm sure you've all heard the exciting news: Placebos work even if the patients know that they are taking placebos!
At least in a controlled study. Where their doctors give them lots of attention. Where they, as participants in a study, may be hoping that the 'treatment' works. When they've been told that science says placebos can work. Et cetera....

No need for me to recapitulate the debates. Instead, links!
The original paper, Placebos Without Deception

Steve Silberman, author of the awesome Wired magazine article on placebos, has a nice rundown here.

I suppose you can guess Respectful Insolence's Orac's take from his introduction of the topic
The investigators, led by Dr. Ted J. Kaptchuk of Harvard's Osher Research Center. The Osher Center, for those of you not familiar with it, is Harvard's center of quackademic medicine; only this time they seem to be trying to do some real research into placebo effects.

Skepticism aplenty there.

Ed Young likes the study a bit better.

02 September 2010

From Overheard in New York: sphenopalatine ganglioneuralgia

This cautionary tale from Overheard in New York provides me an opportunity to shamelessly boost my Google rating for sphenopalatine ganglioneuralgia (ice cream headache/brain freeze).

Overheard in New York | God Has Played a Cold Joke on Us All.: "God Has Played a Cold Joke on Us All.

Guy #1: Owwww! Fuck! Owwwwwwwww!
Guy #2: You won't get an ice cream headache if you drink it slower.
Guy #1: I'm trying, but it's too delicious!

--9th St. & 3rd Ave


And just for good measure: sphenopalatine ganglioneuralgia

Menstrual cramps even suckier than previously thought

In short, this suggests that menstrual cramps not only suck, they make other pains that happen to be around worse.


Brain morphological changes associated with cyclic menstrual pain: "Volume 150, Issue 3, Pages 462-468 (September 2010)

Cheng-Hao Tuab, David M. Niddambc, Hsiang-Tai Chaod, Li-Fen Chenbce, Yong-Sheng Chenf, Yu-Te Wubeg, Tzu-Chen Yehbe, Jiing-Feng Lirngh, Jen-Chuen HsiehabceCorresponding Author Informationemail addressemail address

Primary dysmenorrhea (PDM) is the most prevalent gynecological disorder for women in the reproductive age. PDM patients suffer from lower abdominal pain that starts with the onset of the menstrual flow. Prolonged nociceptive input to the central nervous system can induce functional and structural alterations throughout the nervous system. In PDM, a chronic viscero-nociceptive drive of cyclic nature, indications of central sensitization and altered brain metabolism suggest a substantial central reorganization. Previously, we hypothesized that disinhibition of orbitofrontal networks could be responsible for increased pain and negative affect in PDM. Here, we further tested this hypothesis....Abnormal decreases were found in regions involved in pain transmission, higher level sensory processing, and affect regulation while increases were found in regions involved in pain modulation and in regulation of endocrine function. Moreover, GM changes in regions involved in top-down pain modulation and in generation of negative affect were related to the severity of the experienced PDM pain. Our results demonstrate that abnormal GM volume changes are present in PDM patients even in the absence of pain. These changes may underpin a combination of impaired pain inhibition, increased pain facilitation and increased affect. Our findings highlight that longer lasting central changes may occur not only in sustained chronic pain conditions but also in cyclic occurring pain conditions."


17 August 2010

The most obnoxious email my hand surgeon has ever received

I managed to badly break my thumb during judo last week. I'm having surgery to repair it this Friday. After spending all this time learning about pain/pain medicine, I've learned just enough about drugs to be dangerous. Today, that danger has manifested in what I'm guessing is the most obnoxious email my hand surgeon has ever received from a patient.

For your enjoyment:

Dear [Dr's assistant],

....The pharmacy has a prescription of Darvocet for me. But, I'd actually like to avoid both the propoxyphene and APAP in Darvocet. I'd appreciate it if you could ask Dr. xxxxxx to cancel that prescription and write me one for something different. He might find the following useful:

The Vicodin prescription [which I had been written for the initial pain of the injury] worked fine. Still, I had forgotten that there is some evidence of an interaction between acetaminophen and xxxxxx. See, for example, [3]. So I'd prefer something without APAP. It's not a big deal, but I'd prefer to keep on the safe side.

I'd prefer to avoid anything containing propoxyphene for two reasons. First, it's somewhat contraindicated with xxxxxxx (propoxyphene can potentiate the xxxxxxxxxx). Second, there are some concerns about its cardiotoxic metabolites. See [1] and [2]. I know it's a tiny risk. But, again, I'd prefer to stay on the safe side wherever possible.

To make things just a bit more complicated: I don't think anything with straight codeine will be very useful. I'm fairly certain that both my mother and my sister are poor metabolizes, so I don't want to trust my CYP2D6's any more than I have to. Moreover, according to Cochrane Reviews [7], with a NNT=12, codeine just doesn't seem very trustworthy.

Finally, just in case this is relevant, I'd prefer to use the narcotics to hit the acute pain hard for 1-2 days and then get off of them as quickly as possible. There seems to be evidence that early aggressive treatment helps cut the overall duration of post surgical pain and, more important to me, reduce the risk of chronic pain (see, e.g., [4], [5], [6], [8]). Thus I'd prefer very few doses of something strong to more of something weaker.

These are just some very weak preferences based on my rudimentary understanding of pain management protocols. I trust your judgment completely.

Thanks
Adam

References
[1] http://www.citizen.org/publications/publicationredirect.cfm?ID=7420

[2]http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm170268.htm

[3] Miners JO, Attwood J, Birkett DJ. Determinants of acetaminophen metabolism: effect of inducers and inhibitors of drug metabolism on acetaminophen's metabolic pathways. Clin Pharmacol Ther. 1984; 35:480-486.

[4] Leibeskind, J. C. (1991). "Pain Can Kill." Pain 44: 3-4.

[5] Merskey, H. (1999). Pain and Psychological Medicine. Textbook of Pain. P. D. Wall and R. Melzack. Edinburgh, Churchill Livingstone: 929-949.

[6] Harman, K. (2000). "Neuroplasticitiy and the Development of Chronic Pain." Physiotherapy Canada 52(64-71).

[7] Derry, S., R. A. Moore, et al. (2010) "Single dose oral codeine, as a single agent, for acute postoperative pain in adults." Cochrane Database of Systematic Reviews DOI: 10.1002/14651858.CD008099.pub2.

[8] Kehlet, H., T. S. Jensen, et al. (2006). "Persistent postsurgical pain: risk factors and prevention." Lancet 367(9522): 1618-1625.
Acute postoperative pain is followed by persistent pain in 10-50% of individuals after common operations, such as groin hernia repair, breast and thoracic surgery, leg amputation, and coronary artery bypass surgery. Since chronic pain can be severe in about 2-10% of these patients, persistent postsurgical pain represents a major, largely unrecognised clinical problem. Iatrogenic neuropathic pain is probably the most important cause of long-term postsurgical pain. Consequently, surgical techniques that avoid nerve damage should be applied whenever possible. Also, the effect of aggressive, early therapy for postoperative pain should be investigated, since the intensity of acute postoperative pain correlates with the risk of developing a persistent pain state. Finally, the role of genetic factors should be studied, since only a proportion of patients with intraoperative nerve damage develop chronic pain. Based on information about the molecular mechanisms that affect changes to the peripheral and central nervous system in neuropathic pain, several opportunities exist for multimodal pharmacological intervention. Here, we outline strategies for identification of patients at risk and for prevention and possible treatment of this important entity of chronic pain.

29 May 2010

Meditation science

UCLA center
http://www.marc.ucla.edu/index.php?option=com_frontpage&Itemid=1

Physiological effects of meditation
http://www.noetic.org/research/medbiblio/index.htm
http://natural-meditation.org/ResearchedEffects.htm

Control over body temperature
http://www.hno.harvard.edu/gazette/2002/04.18/09-tummo.html
http://en.wikipedia.org/wiki/Tummo

28 May 2010

Aerobic exercise: More pain now for less later

A useful bit from The Well's interview with sports medicine specialist Dr. Vijay Vad
Link

Q: What else can someone do to relieve pain besides take a prescription pain reliever or undergo a procedure?

A: There are so many self-help things you can do. Something as simple as trying to do 30 minutes of aerobic exercise can help. With pain, you’re in a vicious cycle – you take more narcotics, your REM sleep decreases, and then you’re tired and you don’t want to exercise. If you can get through the first week or two of extra pain by doing the proper exercise, like 30 minutes of walking daily, long term that’s going to have an impact. Most people give up on simple walking, but it can have a huge impact long term.

Q: For people treating pain with exercise, do you have to be willing to get worse in order to get rid of pain eventually?

A: In the case of exercises, that’s true. If the pain goes up four-fold, you’re doing something wrong, but proper exercise will make you a little worse for a while before it makes you better. It’s a pain desensitization period. Think about if you have raw skin on your knuckle and you tap it. At first it hurts, but if you tap it more and more it will get desensitized. You’re doing the same to your chronic pain structure when you exercise. There is so much data on this with rehabilitation for back pain, for instance. You become pain desensitized by proper exercise with gradual increases in stress. The overall consensus for exercise therapy is that it has a positive impact. It can be something simple — it doesn’t have to be fancy machines or stretches.

19 May 2010

Torture's effect on society

http://digbysblog.blogspot.com/2005_11_20_digbysblog_archive.html#113260251820960071

http://nationaljournal.com/about/njweekly/stories/2005/1119nj1.htm#

13 May 2010

Heat therapy for abdominal pain

Hot.
ScienceDaily (Jul. 5, 2006)The old wives’ tale that heat relieves abdominal pain, such as colic or menstrual pain, has been scientifically proven by a UCL (University
College London) scientist, who will present the findings today at the
Physiological Society’s annual conference hosted by UCL.

Dr Brian King, of the UCL Department of Physiology, led the research
that found the molecular basis for the long-standing theory that heat,
such as that from a hot-water bottle applied to the skin, provides
relief from internal pains, such as stomach aches, for up to an hour.
Dr King said: “The pain of colic, cystitis and period pain is caused
by a temporary reduction in blood flow to or over-distension of hollow
organs such as the bowel or uterus, causing local tissue damage and
activating pain receptors.

“The heat doesn’t just provide comfort and have a placebo effect –
it actually deactivates the pain at a molecular level in much the same
way as pharmaceutical painkillers work. We have discovered how this
molecular process works.”
If heat over 40 degrees Celsius is applied to the skin near to where
internal pain is felt, it switches on heat receptors located at the
site of injury. These heat receptors in turn block the effect of
chemical messengers that cause pain to be detected by the body.

The team found that the heat receptor, known as TRPV1, can block
P2X3 pain receptors. These pain receptors are activated by ATP, the
body’s source of energy, when it is released from damaged and dying
cells. By blocking the pain receptors, TRPV1 is able to stop the pain
being sensed by the body.

Dr King added: “The problem with heat is that it can only provide
temporary relief. The focus of future research will continue to be the
discovery and development of pain relief drugs that will block P2X3
pain receptors. Our research adds to a body of work showing that P2X3
receptors are key to the development of drugs that will alleviate
debilitating internal pain.”

Scientists made this discovery using recombinant DNA technology to
make both heat and pain receptor proteins in the same host cell and
watching the molecular interactions between the TRPV1 protein and the
P2X3 protein, switched on by capsaicin, the active ingredient in
chilli, and ATP, respectively.

Adapted from materials provided by University College London.
University College London (2006, July 5). Heat Halts Pain Inside The Body. ScienceDaily. Retrieved March 19, 2008, from http://www.sciencedaily.com­ /releases/2006/07/060705090603.htm

11 May 2010

Carnival

As always I'm super late on this, but the April pain blog carnival is up at How to Cope With Pain:
http://www.howtocopewithpain.org/blog/2361/pain-blog-carnival-april-2010/

Definitely check it out.

Contest!

Our friends at How to Cope With Pain are having a contest. The winners get the opportunity to write a guest post at the site. This is an excellent opportunity for those of you looking to bring your voice to a wider audience.
The contest details are here:
http://www.howtocopewithpain.org/blog/2287/contest-write-a-guest-article/

The deadline is 16th May, so hurry......

29 April 2010

Aquinas on privation

Because evil is the privation of good, and not a mere negation, as was said above (A[3]), therefore not every defect of good is an evil, but the defect of the good which is naturally due. For the want of sight is not an evil in a stone, but it is an evil in an animal; since it is against the nature of a stone to see. [ST]

As was said above (A[1]), evil imports the absence of good. But not every absence of good is evil. For absence of good can be taken in a privative and in a negative sense. Absence of good, taken negatively, is not evil; otherwise, it would follow that what does not exist is evil, and also that everything would be evil, through not having the good belonging to something else; for instance, a man would be evil who had not the swiftness of the roe, or the strength of a lion. But the absence of good, taken in a privative sense, is an evil; as, for instance, the privation of sight is called blindness. Now, the subject of privation and of form is one and the same---viz. being in potentiality, whether it be being in absolute potentiality, as primary matter, which is the subject of the substantial form, and of privation of the opposite form; or whether it be being in relative potentiality, and absolute actuality, as in the case of a transparent body, which is the subject both of darkness and light. It is, however, manifest that the form which makes a thing actual is a perfection and a good; and thus every actual being is a good; and likewise every potential being, as such, is a good, as having a relation to good. For as it has being in potentiality, so has it goodness in potentiality. Therefore, the subject of evil is good.

08 April 2010

NY Times Patient Voices series

I just happened across the NY Times' Patient Voices series. Check it out.
Here're some of the pain related ones:

Patient Voices: Rheumatoid Arthritis


Patient Voices: Migraine


Patient Voices: Fibromyalgia


01 April 2010

Review of David Biro's The Language of Pain

Cover of Biro's Language of Pain

Short story: David Biro's The Language of Pain: Finding Words, Compassion and Relief is very good.
Go buy it.

Longer story: The publisher sent me an advance copy of Biro's The Language of Pain a few months ago. I've read it several times and been working on a review to share with y'all. But the review is getting too long and though I think I agree with most of his conclusions, I'm still not entirely sure what I think about about several of his arguments. Nonetheless, I've certainly profited from engaging with them.

Thus in the interest of posting something while the book is still (somewhat) fresh, I've pasted some of the early parts of the review below. I may post the rest later, or I may work it into something for a more formal venue. I'm omitting the philosophical discussion of the arguments. Though I will list a couple of the topics that concern me. I'm sure the list won't make sense until you've read the book. But perhaps they'll serve as discussion-starters


----
Those interested in learning about pain can profit from David Biro’s The Language of Pain: Finding Words, Compassion and Relief. It will probably be the most useful to people with chronic pain and those close to them. At the very least, the vast array of nuanced metaphors and literary sources he canvases can serve as raw material for their attempts to communicate and understand the experience of pain. But I expect that his lucid exploration of the structure of these metaphors will provide important conceptual tools for crafting more systematic and effective narratives. Though the applicability of some of his particular insights may be limited by culture and language.

Clinicians and scientists should be impressed by the conceptual structure that Biro uncovers in the language many sufferer's use to describe their pains. He succeeds in showing that this metaphorical talk, while necessarily imprecise and often obscure, must be taken seriously. In his wake, the same cannot be said for those who dismiss or deride these ways of talking about pain.

At a minimum, researchers interested in developing pain measurement tools and many philosophers will find in it a rich repository of examples and ideas to use in their work.

Philosophers should also find much to be intrigued by in Biro’s arguments. Here are a few of points that I think are worth engaging with:
  • Chapter 2 is occupied with a theoretical response to the charge that pain is completely resistant to language. This is unnecessary. The main thrust of the book is an empirical argument that, in several important ways, pain is in fact amenable to language.
  • The Wittgensteinian argument of chapter 2 can at best show that we must be able to communicate that we are in pain. But his project is to show that we can communicate what it is like to be in pain. He's not confusing the two in chapter 2. He wants to use the former as a wedge to open the door for the latter. But later on they sometimes seem to get run together in significant ways.
  • His discussion of the language/metaphors of agency does a lot to support and build on Elaine Scarry's articulation of the concept (I profited a great deal from this part since the pain-agency connection is important in my own work). The discussions of the x-ray and mirror metaphors/language are much weaker. Indeed, I'm not convinced that these can't be folded into the agency metaphor. [Unlike the others, this concern has significant philosophical consequences for our understanding of pain]
  • I'm probably being overly picky --but, hey, that's what analytic philosophers are for-- but his project is about language (hence the title and the claim to be constructing a 'rhetoric'). I usually think of language as propositional. His discussions using art to express pain thus seem incongruous. This is probably innocuous. At most it's a concern about whether the thesis should be framed in terms of language or more broadly in terms of our ability to meaningfully communicate. Though I sometimes think that there may be something lurking here that's related to the more substantive questions about whether the x-ray and mirror metaphors are really separate from the agency metaphors.
  • I'm betting that analytic philosophers of language who work on metaphor will find a great deal to disagree with in some of his arguments. Though I myself don't know enough about these issues to have more than hazy suspicions at various points.

Like I said, I'm not entirely sure what I think about these and other points. But I've certainly profited from thinking about them. And in any event, none of them undermine the practical import of the book or the philosophical suggestiveness of the overall picture. Indeed, his subtle discussions of pain language’s structure do not require the conceptually strong thesis that the experience of pain is necessarily expressible. By weaving together art, literature, personal experience, and patient testimony, he has demonstrated that many aspects of many pain experiences can, to a practically useful degree, be meaningfully shared.

A critique and new version of the Wong-Baker Pain Faces Scale

I'm passing along this excellent critique and suggestion from Allie at Hyperbole and a Half: Hyperbole and a Half: Boyfriend Doesn't Have Ebola. Probably. *UPDATED*

We're all familiar with the Wong-Baker Pain Faces Scale.
Wong-Baker Pain Faces Scale


But as our Hyperbolic critic notes, this is easily misunderstood. For example, she interprets it as
0: Haha! I'm not wearing any pants!

2: Awesome! Someone just offered me a free hot dog!

4: Huh. I never knew that about giraffes.

6: I'm sorry about your cat, but can we talk about something else now? I'm bored.

8: The ice cream I bought barely has any cookie dough chunks in it. This is not what I expected and I am disappointed.

10: You hurt my feelings and now I'm crying!

Thus she has come up with a better scale:
0:  Hi.  I am not experiencing any pain at all.  I don't know why I'm even here.

1:  I am completely unsure whether I am experiencing pain or itching or maybe I just have a bad taste in my mouth.

2:  I probably just need a Band Aid.

3:  This is distressing.  I don't want this to be happening to me at all.

4:  My pain is not fucking around.

5:  Why is this happening to me??

6:  Ow.  Okay, my pain is super legit now.
7:  I see Jesus coming for me and I'm scared.   

8:  I am experiencing a disturbing amount of pain.  I might actually be dying.  Please help.

9:  I am almost definitely dying.

10:  I am actively being mauled by a bear.

11: Blood is going to explode out of my face at any moment.

Too Serious For Numbers:  You probably have ebola.  It appears that you may also be suffering from Stigmata and/or pinkeye.

Which she interprets as:
0: Hi. I am not experiencing any pain at all. I don't know why I'm even here.

1: I am completely unsure whether I am experiencing pain or itching or maybe I just have a bad taste in my mouth.

2: I probably just need a Band Aid.

3: This is distressing. I don't want this to be happening to me at all.

4: My pain is not fucking around.

5: Why is this happening to me??

6: Ow. Okay, my pain is super legit now.

7: I see Jesus coming for me and I'm scared.

8: I am experiencing a disturbing amount of pain. I might actually be dying. Please help.

9: I am almost definitely dying.

10: I am actively being mauled by a bear.

11: Blood is going to explode out of my face at any moment.

Too Serious For Numbers: You probably have ebola. It appears that you may also be suffering from Stigmata and/or pinkeye.

I expect to see this written up in Pain shortly.

14 March 2010

Mutations in the SCN9A gene and pain sensitivity

The article emphasizes the genetics, but I'm more interested in the implication that the heightened sensitivity relates to the speed at which sodium channels close in nociceptive neurons.

Gene Linked To Pain Perception - Science News: "Gene linked to pain perception
Common genetic variant makes some people more sensitive
By Laura Sanders
Web edition : Monday, March 8th, 2010

[....]
The team found that people who reported higher levels of pain were more likely to carry a particular DNA base, an A instead of a G, at a certain location in the gene SCN9A. The A version is found in an estimated 10 to 30 percent of people, Woods says, though its presence varies in populations of different ancestries.

[....]
The same trend — higher pain levels reported by people who carried the A — held true in cohorts of people with other painful conditions including sciatica, phantom limb syndrome and lumbar discectomy.
[....]

The genetic variation affects the structure of a protein that sits on the outside of nerve cells and allows sodium to enter upon painful stimuli. The sodium influx then spurs the nerve cell to send a pain message to the brain.

This channel protein is a promising target for extremely specific and effective pain drugs, Waxman says: ‘Given that this channel has been indicted, it would be nice if we could develop therapeutic handles that turn it off or down.’

Researchers already knew that people with mutations in SCN9A can have extreme pain syndromes. Genetic changes that render the protein completely inactive can leave a person impervious to pain, although otherwise healthy. Other mutations can lead to conditions such as ‘man on fire’ syndrome, in which people experience relentless, searing pain.
[....]
In additional laboratory studies, the researchers found that nerve cells carrying the A variant of the gene took longer to close their sodium gates, allowing a stronger pain signal to be sent to the brain. Nerve cells carrying the more common G version of the gene snapped shut faster, stopping the pain signal sooner. "