Tuesday, September 28, 2010

Fake Neurocritic

Lady Gaga and Her Feminist Meat Dress

Some of you might have noticed a new entry in the blogroll to the right. Or perhaps you've encountered some bizarre posts at another site that uses The Neurocritic's name. What's going on here?

I thought an interview with the two blog authors1 would be informative regarding the creative process behind the fledgling enterprise and the decision to go public with the output.

TN: What is the name of your new blog?

FN: It's currently called The Neurocritic on Lady Gaga, Marc Hauser, and Antidepressants. I like to change the name to fit the current topic.2 It started out as The Neurocritic on Lady Gaga with occasional videos, photos, and commentary. The blog was kept low key because the topic isn't especially neurocentric. Except for the very first post:

Lady GaGa - The Brain

FN: Oh, and...

Neuro Gaga

TN: I see. Why Lady Gaga?

FN: She's a pop culture icon who infuses social trends, products, and even national security with her glamour and weirdness, however contrived.

TN: National security? What are you talking about?

FN: Her name came up during the Wikileaks release of the Afghanistan war logs. The alleged leaker spoke about using her music as a decoy to download secret internal records of U.S. military actions in Afghanistan.

Lady Gaga's Role in the Afghanistan War Logs

Bradass87 [22-year-old intelligence analyst Bradley Manning] suggested that "someone I know intimately" had been downloading and compressing and encrypting all this data and uploading it to someone he identified as Julian Assange. At times, he claimed he himself had leaked the material, suggesting that he had taken in blank CDs, labelled as Lady Gaga's music, slotted them into his high-security laptop and lip-synched to nonexistent music to cover his downloading: "i want people to see the truth," he said.

from Afghanistan war logs: Story behind biggest leak in intelligence history
FN: I actually blogged about this story before Gothamist, MTV, and The Boston Phoenix. However, I did miss the pre-Wikileaks story about the Gaga smuggling ruse in the July 8, 2010 New York Times.

Wow! Do you know if she's commented publicly on this revelation?

FN: I haven't found anything. But here are the direct quotes from Bradley Manning:

"I would come in with music on a CD-RW labeled with something like 'Lady Gaga,' erase the music then write a compressed split file,” he wrote. “No one suspected a thing and, odds are, they never will."

"[I] listened and lip-synced to Lady Gaga’s 'Telephone' while exfiltrating possibly the largest data spillage in American history," he added later. "Weak servers, weak logging, weak physical security, weak counter-intelligence, inattentive signal analysis… a perfect storm."

TN: Let's move on to another topic: Marc Hauser. Why did you start to blog about him?

FN: For me (and many others), it was the irony of an expert on morality -- and the author of a book called Moral Minds -- being found guilty of eight instances of research misconduct. And the timing of the breaking news in the Boston Globe (August 10, 2010) relative to his participation in the Edge conference on THE NEW SCIENCE OF MORALITY (July 20-22, 2010) was almost comical. David Dobbs of Neuron Culture has been actively covering the Marc Hauser debacle, and his post Edge corrects — no, make that ERASES — the record on Hauser alerted me to just that fact:
...Today I got a tweet that he’d “withdrawn” his contribution at the Edge conference. I went to the conference-event site to see how Edge had announced this withdrawal … and found he had all but disappeared. Hauser’s talk and photo had been removed. I scanned the page for his talk; gone. Finally I did a text search adn found a footnote to the introduction, in brackets, that said

[EDITOR'S NOTE: Marc Hauser, one of the nine participants at the conference, has withdrawn his contribution.]

TN: At this point, I thought it was important to preserve the video of his talk, so I was able to find cryptic links that led to lectures entitled, "The New Science of Morality - Marc D. Hauser" and "The New Science of Morality - Marc D. Hauser Discussion". I posted these links on the original blog, at 'The New Science of Morality' - Edge videos with Marc Hauser.

FN: What is Edge, and why did you want to make them look bad?

TN: Sigh. [I didn't necessarily want to make them look bad.] Edge is an exclusive intellectual club run by literary agent John Brockman, who gives off the impression of being (1) pompous; and (2) sexist. This is based on (1) his online presence -- photos, hobnobbing with the überwealthy, name dropping, quotes, and profiles; and (2) the number of women he includes in his conferences (e.g., only one of "THE MORAL NINE" in 2010), books (e.g., only 1 out of 23 "original thinkers" on The Third Culture in 1991), and as members of his club.
The mandate of Edge Foundation is to promote inquiry into and discussion of intellectual, philosophical, artistic, and literary issues, as well as to work for the intellectual and social achievement of society.
FN: Wow, you sound bitter.

TN: No, not really. His inclusion of women has improved from 4.3% in 1991 to 11.1% in 2010.
Now that's progress!

FN: Perhaps Patricia Churchland and Martha Farah declined invitations to attend the recent morality conference because they had better things to do.

TN: Now you're sounding pretty snarky yourself...

TN: OK. OK, back to Marc Hauser. Ten days after I posted links to the videos, a commenter noticed they had been removed from their hiding place at blip.tv.

FN: That's
when I sprang into action. Prior to their removal, I was able to download both videos and post the smaller of the two, thanks to the 50 MB limit of Posterous:

The New Science of Morality - Marc D. Hauser Discussion

Edge video with Marc Hauser

Missed seeing a key discussion with one of the "THE MORAL NINE" (now "THE MORAL EIGHT") before the video was purged from Edge's website? You can still watch it!

TN: Wow, that's fantastic!

TN: We certainly have covered a lot of ground in this interview. That's all we have time for today. Thank you very much, Fake Neurocritic.

FN: Hey! We haven't covered antidepressants yet! And Marc Hauser and antidepressants together in one post!!

FN: !!! .......... OK then. Thanks for the opportunity. See you soon.


1 The Neurocritic (TN) and Fake Neurocritic (FN) are ACTUALLY THE SAME PERSON!

2 However, The Neurocritic on Lady Gaga portion of the name will remain constant. We've also seen the name The Neurocritic on Lady Gaga and Marc Hauser and The Neurocritic on Lady Gaga and Antidepressants.

Morality Lesson with Marc Hauser + Errol Morris

"How does the human mind know that something is wrong and once it does, what does it do about it?" -Marc D. Hauser

"Morality is the combination of two things: 'I'm sorry, and I'm sorry I got caught'." -Errol Morris

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Wednesday, September 22, 2010

JFK Neurotoxin Conspiracy Theory Published in Medical Hypotheses

With fabulous hand drawn color figures!

Fig. 1 (Salerian, 2010). Drawing.


“President John F. Kennedy’s death was a neurotoxin-assisted homicide” is the hypothesis of this study.

A review of medical evidence demonstrates evidence of a neurotoxin-assisted homicide. The convergence of three independent actions, or the signature traits of a neurotoxin-assisted homicide- the emergence of neurological signs consistent with a neurotoxin-induced paralysis, the induction of a small neck wound consistent with a flechette-transported neurotoxin entry wound, and the execution of a coverup to eliminate neurotoxin evidence, supports this hypothesis.

This review suggests, JFK’s death had all the signature traits of a neurotoxin-assisted homicide.

The paper was covered by NCBI ROFL two months ago but I missed it at the time. The author is psychiatrist Dr. Alen J. Salerian of the International Center for Evidence Based History, a site that exists primarily to promote and sell his JFK artwork.

Dr. Salerian also holds some rather colorful views of neurotransmitters, or Viagra for Your Brain...
GABA is an elegant force of your calm and inner peace. For example, a brain with sickly GABA has recurrent seizures and is almost always irritable, edgy, and combative. In less traumatic cases, sickly GABA may make you fearful, easily reactive, and may cause insomnia.

Dopamine gives you energy, concentration, alertness, initiative, and perhaps most importantly the ability to enjoy life. When your dopamine is out of sorts, so is your joy.

Norepinephrine is a good friend of dopamine and offers you energy, alertness, and concentration.
...plus this hefty dose of 5-HT misinformation:
So what do you say to a woman who is irritable, easily frustrated, and highly moody for a week before her menstrual cycle? Your serotonin is low! {NOTE: Oh no you don't...!}

Back to our conspiracy theory (Salerian, 2010):
The evidence of a death from a flechette-transported neurotoxin injury has seven components and is summarized in Table 1.

Table 1. Evidence of flechette-transported neurotoxin injury.

IA small entry wound
IIAn instant long startled response
IIISeveral minutes long no fight or flight response
IVSeveral minutes long vocal paralysis
VSeveral minutes long muscle paralysis
VIEvidence of neurotoxin-contaminated tissue
VIIThe availability of a weapon armed with a flechette-transported neurotoxin

A poison arrow – (a flechette-transported neurotoxin) blocks voltage-gated sodium channels through the nervous system and causes conduction failure and death due to suffocation. Broadly speaking, there are two major phases with characteristic symptoms. The initial symptoms are those due to the deleterious consequences of a flechette-induced injury, i.e., a small laceration of less than 1 cm in diameter and 1 cm in depth.

The second phase consists of symptoms associated with a neurotoxin’s effect with total vocal and motor paralysis.

. . . [etc.]

OK..... Then what?

The suspense is killing me.....

Fig. 5 (Salerian, 2010). Flechette-transported neurotoxin with Popup Fins.

The paper concludes like all good conspiracy theories:
Further studies are necessary to validate this conclusion. Of importance is the necessity for the US government to fully disclose the facts about the President’s death.


Salerian AJ. (2010). President Kennedy's death: a poison arrow-assisted homicide. Med Hypotheses 75:372-7.

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Sunday, September 19, 2010

Mania and Artistic 'Surprise' Induced by Deep Brain Stimulation

Fig. 2 (Haq et al., 2010). A painting made following initial ALIC-NA [anterior limb of the internal capsule/nucleus accumbens] DBS activation. It was produced after a night-long effort and was described as a ‘surprise’ for the staff. The religious tone is typical of the patient.

Deep brain stimulation (DBS) is being tested as an experimental treatment for intractable obsessive-compulsive disorder (OCD), as well as for major depression.1 A recent review by Mian et al. (2010) discusses the three main brain regions that are targeted by DBS for OCD:
  • Target 2: the subthalamic nucleus (STN) within the basal ganglia, a major DBS target for Parkinson's disease as well
Haq et al. (2010) reported on the adverse events experienced by a patient receiving DBS in ALIC and the nucleus accumbens (part of the ventral striatum) for severe OCD. A 29 year old woman started experiencing OCD symptoms in early childhood:
...obsessions that centered on a need to be clean and a need to please. At the time of enrollment, her compulsions included counting, bra-snapping, pant-pulling and leg scratching. She completed the 12th grade but subsequently had difficulty remaining employed because of her illness. In addition to her history of OCD, she was also diagnosed as having major depressive disorder. Twice, in the remote past, she had attempted suicide via drug overdose.
Since she had failed to respond to three different classes of drugs, as well as to cognitive behavioral therapy, she was eligible to enroll in the DBS trial. The implantation surgery was uneventful, and the patient was randomized to have activation of the stimulator begin at 30 days post surgery.

In the Introduction, the authors were remarkably honest about how the choice of stimulation parameters can be hit and miss:
The published experience with DBS programming for OCD is limited. Parameters (voltage, pulse width and frequency) are commonly adjusted by trial and error with the aim of deriving the greatest possible clinical efficacy while avoiding uncomfortable side effects. As physicians’ experience with DBS programming in OCD has broadened, the potential for stimulation-induced side effects has become increasingly apparent. Novel targets, such as the anterior limb of the internal capsule/nucleus accumbens (ALIC-NA), have introduced novel stimulation-induced effects.
And Haq et al. (2010) did see some novel stimulation-induced effects that included mania ("hugging" and pressured speech), insomnia, and worsening of OCD symptoms on the first two days of stimulation (as shown below). Oops. The patient was admitted to inpatient psychiatry the next day.

-- click on table for larger image --

Table 1 (modified from Haq et al., 2010). Programming settings and patient behavior. PW=pulse width. Contacts were implanted bilaterally, and the parameters were identical for each.

The initially stimulated contacts were located in the nucleus accumbens (NAcc), considered to be one of the brain's pleasure centres. Not surprisingly, the NAcc is a rational DBS target for depression too, given the common symptom of anhedonia, i.e. the inability to experience pleasure from normally pleasurable life events (see Good News/Bad News Update on Nucleus Accumbens DBS for Treatment-Resistant Depression).

Upon transfer to the psych ward, the patient's medication regimen was extensive: one antidepressant (fluoxetine), three mood stabilizers/anticonvulsants (lamotrigine, pregabalin, topiramate), one benzodiazapine (clonazepam), and one non-benzo sedative/hypnotic (eszopiclone). Nonetheless,
Following this initial adjustment [of DBS stimulation parameters], the patient spent most of the night awake, alternating between cleaning the adjoining room and painting (see Fig. 2 above). Her painting and speech were notable for their hyperreligious content. She also reported that her OCD symptoms were more troublesome than in her preoperative state. She developed bruises on her shins and thighs from obsessively rubbing her legs and reported an increase in her counting behaviors. Her fluoxetine dose was decreased to be sure that it was not exacerbating the mania and her topiramate was discontinued.
Also, her clonazepam dose was doubled and an atypical antipsychotic (quetiapine) was initiated. Not surprisingly, "The patient showed signs of mild sedation after these changes in medication." Fortunately, her condition stabilized after a week. Her symptoms had improved (from extreme to severe) at the one month follow-up, reaching remission after six months of stimulation at the more conservative intensity.

The side effects of mania and hypomania are not uncommon after DBS in NAcc and the ventral capsule (Tsai et al., 2010). As noted by Haq and colleagues (2010):
Stimulation-induced mania may result from spread of the stimulation field from the motor regions of gray matter structures into limbic or frontal territories... The ALIC-NA is more richly connected to limbic and frontal regions than the STN or other basal ganglion targets and (based on limited experience) has a correspondingly higher incidence of postoperative psychiatric side effects. The occurrence of transient hypomania with ALIC-NA DBS has been estimated to be as high as 50–67%...
The abnormal circuitry implicated in OCD is quite complex, and is thought to include fronto-striatal- thalamic-cortical loops (Maia et al., 2008). A clearer understanding of the connectivity of these regions through the use of tractography may improve the choice of target for DBS in a number of psychiatric disorders.


1 David Dobbs has also written extensively about this topic, most recently in his post on Depression’s wiring diagram.

2 In More on Deep Brain Stimulation for OCD, Neuroskeptic explains the ventral capsule/ventral striatum procedure.


Haq, I., Foote, K., Goodman, W., Ricciuti, N., Ward, H., Sudhyadhom, A., Jacobson, C., Siddiqui, M., & Okun, M. (2010). A Case of Mania following Deep Brain Stimulation for Obsessive Compulsive Disorder. Stereotactic and Functional Neurosurgery, 88 (5), 322-328 DOI: 10.1159/000319960

Maia TV, Cooney RE, Peterson BS. (2008). The neural bases of obsessive-compulsive disorder in children and adults. Dev Psychopathol. 20:1251-83.

Mian MK, Campos M, Sheth SA, Eskandar EN. (2010). Deep brain stimulation for obsessive-compulsive disorder: past, present, and future. Neurosurg Focus 29(2):E10.
Tsai HC, Chen SY, Tsai ST, Hung HY, Chang CH. (2010). Hypomania following bilateral ventral capsule stimulation in a patient with refractory obsessive-compulsive disorder. Biol Psychiatry 68:e7-8.

Fig. 3 (Saxena & Rauch, 2000). Model of the pathophysiology of obsessive-compulsive disorder. Obsessive-compulsive disorder symptomatology may be the result of a captured signal in the direct orbitofrontal-subcortical pathway, a positive-feedback loop. This signal could be caused by excess tone in the direct (large arrows) relative to the indirect (small arrows) orbitofrontal-subcortical pathway, resulting in increased activity in the orbitofrontal cortex, ventromedial caudate, and medial dorsal thalamus. This orbitofrontal-subcortical hyperactivity allows for concerns about danger, violence, hygiene, order, and sex to rivet attention to themselves, compel patients to respond with ritualistic behavior, and result in an inability to switch to other behaviors.

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Wednesday, September 15, 2010

Modern Tract-Tracing for Historical Psychosurgery

Figure 3 (Schoene-Bake et al., 2010). Intersection of connectivity maps of Anterior Capsulotomy (red), Anterior Cingulotomy (blue), and Subcaudate Tractotomy (green) tracking results. Overlap of AC and ACT shown with magenta, AC and SCT in yellow, and ACT and SCT in cyan. The white area shows overlapping of AC, ACT, and SCT mean probability-tracking maps in axial (a), coronal (b), and sagittal (c) slices. Acg, anterior cingulate gyrus; ATR, anterior thalamic radiation; CST, corticospinal tract; FM, forceps minor; FP, frontal pole; Nacc, accumbens nucleus; PAG, periaqueductal grey matter; slMFB, superolateral branch of medial forebrain bundle; Thal, thalamus.

When I first saw a journal article titled Tractographic Analysis of Historical Lesion Surgery for Depression, I assumed the authors (Schoene-Bake et al., 2010) located some elderly patients who had received psychosurgery in the 1960s, then scanned them using diffusion tensor imaging to trace the white matter tracts affected by the surgeries. This was not the case, however. Instead, the paper is a lesion simulation study that used MRIs from a large sample of control participants.

Although this revelation was initially disappointing, the results included the pretty colorized DTI figure shown above.1 And it reviewed the four historical surgical approaches and their anatomical targets, shown in the table below.

Jumping ahead to the punchline, what were the conclusions?
Shared connectivities between the four surgical approaches mapped onto the most mediobasal aspects of bilateral frontal lobe fibers, including the forceps minor and the anterior thalamic radiations that contacted subgenual cingulate regions [Brodmann area 25]. Anatomically, convergence of these shared connectivities may derive from the superolateral branch of the medial forebrain bundle (MFB), a structure that connects these frontal areas to the origin of the mesolimbic dopaminergic ‘reward’ system in the midbrain ventral tegmental area [VTA]. Thus, all four surgical anti-depressant approaches may be promoting positive affect by converging influences onto the MFB.
Putting aside for a moment the actual efficacy of these surgeries, the claim is that disconnection of the "sad cingulate" from the VTA was at least partly responsible for improved mood. In modern times, the subgenual cingulate has been a target for deep brain stimulation (DBS) trials for intractable major depression (Mayberg et al., 2005; Lozano et al., 2008). In contrast to creating a permanent lesion, in DBS a stimulating electrode is stereotaxically implanted in the targeted region. Dr. Helen Mayberg and her colleagues at Emory University are still recruiting patients with treatment resistant depression to participate in a clinical trial using chronic, high frequency stimulation of the subgenual cingulate white matter.

To determine the anatomical connectivity of the subgenual cingulate region, these researchers performed tractography (using diffusion-weighted MRI) to trace the pathways mediating treatment response with DBS (Johansen-Berg et al., 2007). The authors compared the connections of the subgenual ACC (sACC, blue/cyan) and the perigenual ACC (pACC, red/yellow).

Figure 3 (Johansen-Berg et al., 2007). Connectivity-based parcellation of ACC and location of electrode contacts. (A, B) Population probability maps of connectivity-defined sACC and pACC. Color scales represent the population probability of a voxel belonging to sACC (from 50% [dark blue] to 80% [light blue] probability) or pACC (from 50% [red] to 80% [yellow] probability). Also shown are the locations of effective electrode contacts from 9 patients overlaid in black. Effective electrode locations are mainly localized within the sACC subregion.

Resting metabolic activity in subgenual cingulate was shown to be increased in the patients with treatment-resistant depression (Mayberg et al., 2005):
The baseline pattern of subgenual cingulate hyperactivity in combination with frontal hypoactivity described here in this TRD patient group is a finding that is in contrast to the hypoactivity reported in a more rostral region of subgenual medial prefrontal cortex in familial bipolar and unipolar depressed patients (Drevets et al., 1997). This distinction suggests important differences across subtypes of depression that are potentially relevant to the pathophysiology of major depressive disorders and perhaps their treatment.
Reflecting further on the historical lesion data, one might infer that a hyperactive subgenual cingulate ultimately inhibited activity in the VTA, a dopamine "reward center". The idealized lesions for all four surgical approaches are shown in the simulation below.

Figure 1 (Schoene-Bake et al., 2010). Mean probability maps of simulated lesions. (a) Anterior capsulotomy (AC); (b) anterior cingulotomy (ACT), I - sagittal, II - coronal, III - axial; (c) subcaudate tractotomy (SCT); and (d) stereotactic limbic leucotomy (SLL).

I would like to see how these simulated lesions compare to the actual surgical lesions from days of yore. Schoene-Bake et al. (2010) hope that a look back at the past will enhance the future of depression treatment:
DTI probabilistic connectivity analysis is a useful tool to explore and to simulate the structural and functional impact of past stereotactic lesion surgery approaches for treating psychiatric disorders. Our study shows overlapping fiber tracts from four classical historical lesion sites for treating depression. The most prominent shared tract revealed by the present work was the slMFB. This structure has some appeal as a new site that could be of interest for DBS in major depression, especially considering the historically established role of this brain reward-seeking network in regulating positive affective states.


1 And who isn't cheered up by pretty colorized DTI figures?


Johansen-Berg H, Gutman DA, Behrens TE, Matthews PM, Rushworth MF, Katz E, Lozano AM, Mayberg HS. (2007). Anatomical Connectivity of the Subgenual Cingulate Region Targeted with Deep Brain Stimulation for Treatment-Resistant Depression. Cereb Cortex 6:1374-1383.

Lozano AM, Mayberg HS, Giacobbe P, Hamani C, Craddock RC, Kennedy SH. (2008). Subcallosal cingulate gyrus deep brain stimulation for treatment-resistant depression. Biol Psychiatry 64:461-7.

Mayberg HS, Lozano AM, Voon V, McNeely HE, Seminowicz D, Hamani C, Schwalb JM, Kennedy SH. (2005). Deep brain stimulation for treatment-resistant depression. Neuron 45:651-60.

Schoene-Bake, J., Parpaley, Y., Weber, B., Panksepp, J., Hurwitz, T., & Coenen, V. (2010). Tractographic Analysis of Historical Lesion Surgery for Depression. Neuropsychopharmacology DOI: 10.1038/npp.2010.132

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Friday, September 10, 2010

'The New Science of Morality' - Edge videos with Marc Hauser

Missed seeing a key talk by one of the "THE MORAL NINE" (now "THE MORAL EIGHT") before the video was purged from Edge's website? You can still watch it! (for now at least)...

The New Science of Morality - Marc D. Hauser

The New Science of Morality - Marc D. Hauser Discussion

UPDATE Sept 20, 2010: The videos have been removed from the links above, but The New Science of Morality - Marc D. Hauser Discussion is available in a new location.

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Thursday, September 09, 2010

Morphine vs. Methadone for Cancer Pain

It's still too early for me to blog about aggressive measures to control severe pain in cancer patients, despite my best intentions. I don't know when/if I'll be able to write a proper post on the topic. For now, I'll just list a few references, including a study on the attitudes of pain physicians towards the use of methadone in clinical practice (Shah & Diwan, 2010).


Bengoechea I, Gutiérrez SG, Vrotsou K, Onaindia MJ, Lopez JM. (2010). Opioid Use at the End of Life and Survival in a Hospital at Home Unit. J Palliat Med. Aug 28. [Epub ahead of print].

Mercadante S. (2010). Intravenous morphine for management of cancer pain. Lancet Oncol. 11:484-9.

Pollock AB, Tegeler ML, Morgan V, Baumrucker SJ. (2010). Morphine to Methadone Conversion: An Interpretation of Published Data. Am J Hosp Palliat Care. Jun 16. [Epub ahead of print].

Shah S, Diwan S. (2010). Methadone: does stigma play a role as a barrier to treatment of chronic pain? Pain Physician 13:289-93.

NOTE: The frequency and content of future posts will be lighter for a while...

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Sunday, September 05, 2010

Limbaugh/Palin "death panels" extend the lives of terminally ill patients

What is palliative care? Until quite recently, it's something I haven't given much thought. Although there was a highly regarded article on hospice and palliative care by Atul Gawande in last month's New Yorker, I didn't read it or think it applied to my life. All that changed less than two weeks ago, when my father was hospitalized in critical condition after collapsing. First he went to the ER, then the transitional ICU, and finally he was placed in the palliative care unit by the time I arrived. You see, my father has metastatic lung cancer, for which he had refused treatment for more than a year. Instead, he decided to stay home with my mother, watch DVDs, go out to eat, and do yard work.1

A recent paper in the New England Journal of Medicine demonstrated that the introduction of palliative care shortly after the diagnosis of metastatic lung cancer not only improved the patients' quality of life, but also extended median survival from 8.9 months to 11.6 months (Temel et al., 2010). According to the American Academy of Hospice and Palliative Medicine:
The goal of palliative care is to prevent and relieve suffering and to support the best possible quality of life for patients and their families, regardless of the stage of the disease or the need for other therapies. Palliative care is both a philosophy of care and an organized, highly structured system for delivering care. Palliative care expands traditional disease-model medical treatments to include the goals of enhancing quality of life for patient and family, optimizing function, helping with decision-making and providing opportunities for personal growth. As such, it can be delivered concurrently with life-prolonging care or as the main focus of care.
This finding is critically important for providers of medical care for terminally ill cancer patients as well as for health policy, because it provides categorical, scientific proof that the notion of "death panels" is false. As stated in the New York Times:
“It shows that palliative care is the opposite of all that rhetoric about ‘death panels,’ ” said Dr. Diane E. Meier [@DianeEMeier], director of the Center to Advance Palliative Care at Mount Sinai School of Medicine and co-author of an editorial in the journal accompanying the study. “It’s not about killing Granny; it’s about keeping Granny alive as long as possible — with the best quality of life.”
A straw man in the 2009 health care debate, "death panels" invoked the specter of rationing medical procedures provided for the sick and the elderly. In the name of cost cutting, blared the phony rhetoric on talk radio and Sarah Palin's Facebook page, the Obama administration would sanction euthanasia for elders and the terminally ill under provisions of the health care bill. This would save on expensive treatments that prolong patients' lives but increase the deficit, claimed the conservative crew. However, these scare tactics were an outright lie, as we learn from the Wall Street Journal:
Palin’s “Death Panels” Charge Named “Lie of the Year”


“Of all the falsehoods and distortions in the political discourse this year, one stood out from the rest,” writes Politifact.com, the non-partisan, Pulitzer Prize-winning site run by the St. Petersburg Times. Palin’s “assertion — that the government would set up boards to determine whether seniors and the disabled were worthy of care — spread through newscasts, talk shows, blogs and town hall meetings.”

“Opponents of health-care legislation said it revealed the real goals of the Democratic proposals. Advocates for health reform said it showed the depths to which their opponents would sink,” Polifact.com says.

The NEJM study enrolled 151 patients with newly diagnosed metastatic non–small-cell lung cancer. Seventy-four received standard care and 77 patients received palliative care, which included meetings with a member of the palliative care team (board-certified palliative care physicians and advanced-practice nurses). The first meeting was within 3 weeks of enrollment, and subsequent meetings were held on a monthly basis, with additional sessions at the discretion of the patient and the clinical treatment team. Patients assigned to standard care did not meet with the palliative care team (unless requested). All patients continued to receive standard oncology care for the duration of the study.

These meetings are the so-called "death panels" that would have been covered by Medicare, as mentioned by the NYT in Palliative Care Extends Life, Study Finds:
During the debate over President Obama’s 2009 health care bill, provisions to have Medicare and insurers pay for optional consultations with doctors on palliative and hospice care led to rumors, spread by talk-show hosts like Rush Limbaugh and Glenn Beck and by the former vice-presidential candidate Sarah Palin, that the bill empowered “death panels” that would “euthanize” elderly Americans. [emphasis mine]
The primary outcome measure of the study was quality of life at 12 weeks (compared to baseline), as assessed by the Functional Assessment of Cancer Therapy–Lung (FACT-L) scale. Mood was assessed using the Hospital Anxiety and Depression Scale (HADS) and the Patient Health Questionnaire 9 (PHQ-9).

Results indicated that patients in the palliative care group had a significantly higher quality of life at 12 weeks (see Table 2) and a lower incidence of depression (but similar levels of anxiety).

[click on Table for larger image]

Table 2 (Temel et al., 2010). Plus–minus values are means ±SD. Quality of life was assessed with the use of three scales: the FACT-L scale, on which scores range from 0 to 136, with higher scores indicating better quality of life; the lung-cancer subscale (LCS) of the FACT-L scale, on which scores range from 0 to 28, with higher scores indicating fewer symptoms; and the Trial Outcome Index (TOI), which is the sum of the scores on the LCS and the physical well-being and functional well-being subscales of the FACT-L scale (scores range from 0 to 84, with higher scores indicating better quality of life).

In addition, patients in the palliative care group lived longer:
Despite receiving less aggressive end-of-life care,2 patients in the palliative care group had significantly longer survival than those in the standard care group (median survival, 11.6 vs. 8.9 months; P=0.02).
The study has its limitations, however, as noted by Dr. Meier in Palliative Care: We Still Have a Lot to Learn:
...The patients (and doctors) were not blinded to their treatment group, that is, they knew which group they were in, which could have affected their outcomes. Also, there was no “attention-control” group—a group that got the same amount of human time and attention that the palliative care group got but without the palliative care skill and expertise.
Nonetheless, the purpose and goals of palliative care cannot be understated. As I mentioned in my previous post (Ketamine for Depression: Yay or Neigh?), reducing the pain and suffering of terminally ill patients is of utmost importance. Watching a terminally ill loved one suffer from unbearably excruciating pain is one of the most emotionally wrenching experiences you'll ever have. Anything, and I mean anything, that will relieve this sort of suffering (including heroin) should be administered without reservation or stigma. The options offered by hospice and palliative care should be made freely available to patients as part of a comprehensive health care plan. But Sarah Palin is still spewing her falsehoods a year after she started, despite all the evidence to the contrary.

UPDATE Sept 6, 2010: My father died at 12:30PM today. I'll miss him terribly.


1 In other words, he chose to live as normally as possible.

2 Aggressive care was defined as chemotherapy within 14 days before death; no hospice care; or admission to hospice 3 days or less before death.


J.S. Temel et al. (2010). Early Palliative Care for Patients with Metastatic Non–Small-Cell Lung Cancer. N Engl J Med, 363, 733-742. 10.1056/NEJMoa1000678

Additional Reading from Pallimed blog:

Game Changer: Early Palliative Care for Lung Cancer Patients Improves QOL AND Median Survival

You had me at 'improves HRQOL'...

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