I like the music of Neil Young, not everything but this love for his music started way back in the seventies. Heart of Gold got me hooked. A fan of Neil Young discovered a new spider and named it after Neil Young.
A sneaky spider has been named in honor of rock musician Neil Young.
Jason Bond, a biologist at East Carolina University, named a newly discovered arachnid, Myrmekiaphila neilyoungi. It is also known as a trapdoor spider.
“There are rather strict rules about how you name new species,” Bond said. “As long as these rules are followed you can give a new species just about any name you please.”
He added, “With regards to Neil Young, I really enjoy his music and have had a great appreciation of him as an activist for peace and justice.”
Dr Crippen is a blogging doctor from the United Kingdom, his posts are of interest even if you don’t have to deal with the lousy health care system of the British Empire and full of humor. In a recent post about new treatments for menopause he exposed Jennifer Harper-Deacon who proudly proclaims that she is “Health Journalist of the Year” and who advocates “Hormonal Balance”
includes the plant essences Dioscorea villosa (wild yam), which possesses oestrogen- and progesterone-like properties and acts as a hormonal regulator; Agnus castus, a progesterone-like essence considered to be a master hormone regulator that helps with night sweats, hot flushes, reduced libido, oedema (swelling) and vaginal dryness; and salvia, an essence that helps the body to adjust to hormonal changes, inhibits perspiration and calms the mind, body and spirit. It also contains pulsatilla, known as the remedy of choice for sensitive women, as it impacts on both the psyche and ever-changing hormonal symptoms. Take three drops three times daily for the first month, gradually increasing the dosage up to seven drops, three times daily. Ideally, you should take this remedy for six months.
But what really made me laugh as well as him probably was the other cure for menopause:
I was however very taken by her second recommendation for menopausal symptoms. Ladycare from Magnopulse is only £19.95
It is a small, discreet static magnet that you attach inside your underwear, which can help alleviate a number of symptoms, including mood swings and hot flushes. Do not use it if you or your partner has a heart pacemaker, defibrillator or insulin syringe driver.
This made me very happy.
Feeling menopausal ladies? Stick a magnet in your knickers. May I just add to the caveats that users of Magnopulse may have some explaining to do at airport security.
I checked with Google if this was also available in The Netherlands but Dutch women can stay at ease, not in the news here.
Please keep on posting about these frauds , make my day
Are the recent claims to fame from a SSRI and rTMS correct for treatment of vascular depression or just treatments seeking new markets? I think the latter. rTMS is of dubious efficacy in the treatment of depression and new “me too” SSRI’s are struggling for a share.
But does the diagnostic entity of Vascular Depression really exist?
The relationship between vascular disease and depression cannot solely be explained by current established risk factors or the effects of treatment for depression. Other mechanisms must apply, and there is some evidence for common genetic factors.
This is the conclusion of a recent review in the International Journal of Geriatric Psychiatry. The current evidence regarding the relationship between vascular disease such as hypertension, coronary artery disease, and depression cannot be entirely explained by current established risk factors. They think that shared genetic factors between depression and vascular diseases can play some role. This has still to be determined.
Cerebrovascular disease may predispose, precipitate, or perpetuate some geriatric depressive syndromes. The “vascular depression” hypothesis is supported by the comorbidity of depression, vascular disease, and vascular risk factors and the association of ischemic lesions to distinctive behavioral symptoms. Drugs used for the prevention and treatment of cerebrovascular disease may be shown to reduce the risk for vascular depression or improve its outcomes.
The relationship between cardiovascular disease and depression is a bidirectional relationship.
Just as vascular disease and vascular risk factors are associated with increased rates of depression, so depression has also been shown to be an independent risk factor for cardiovascular and cerebrovascular events.
The relationship between depression and cardiovascular disease is not a simple casual one. The two conditions might also be linked via other mechanisms than risk factors such as genetic factors.
So the notion that cardiovascular disease contributes to the development of depression and vice versa is to simple. The claim that some treatments are more efficacious for vascular depression still remain shaky.
Yes Dr Shock is preparing for his yearly holiday, should he keep on blogging or just go “cold turkey”? Can he cope with his blog addiction? What do you think let me know in the comments.
As some of you will know I took part in Adbusters’ Mental Detox Week last week. This meant I stopped doing screen and computer based stuff as much as possible. I was at work so there were obviously times when I had to check email and things. But I did manage to cut it right down to a bare minimum. Outside of work it was a total no computer, no TV, no iPod existence for me. Which is quite a big thing in my ordinary daily life.
Major depressive disorder is unremitting in 15% of cases
Major depressive disorder is recurrent in 35%.
About half of those with a first-onset episode recover and have no further episodes.
53% of those with a lifetime episode of depressive disorder either do not recover at all or have at least 1 recurrence.
What is new in this research?
The focus of this analysis is the group of 92 participants who experienced an episode of depression (meeting criteria for DSM-IV) for the first time in their life during the follow-up. Seventy-one first lifetime episodes occurred between the baseline and 1993 follow-up, and 21 occurred between the 1993 and 2004 follow-ups. The comparison group for onset consists of the 1739 participants followed up through the 1993 wave who also had the opportunity for onset but for whom onset did not occur.
This way the Neyman bias and the Berkson bias (A special example of selection bias)are avoided. The first bias is also called the “clinician’s illusion. Clinicians only see a subsample of patients with depression, those with chronic or recurrent episodes.
The Berkson Bias occurs when the combination of exposure and disease under study increases the risk of hospital admission, thus leading to a higher exposure rate among the hospital cases than the hospital controls. So the natural history of depression is best studied using a population based sample, in which individuals are selected from the general population without regard to treatment.Both these biases lead to exaggeration of the chronicity of depression. This research avoids these biases.
Besides the above mentioned results, more common findings in this research were: the 92 participants with first lifetime onset of depressive disorder were:
more likely to be women
younger of age
those with 1 or 2 short 5HTT alleles. This polymorphism has also been shown to be of importance for evidence of interaction between a functional genetic variant in the serotonin transporter gene and life events
persons with a history of drug or alcohol disorders and panic attacks were at a higher risk.
These factors raised the risk of first lifetime onset of depressive disorder.
What is more important is that the data suggest little or no acceleration or amplification of the course through time.
Another important finding in this research was the intriguing result of the paradoxical effects of the 5HTT on the natural history of MDD. Individuals with 2 long alleles are protected from the occurrence of first lifetime onset of depressive disorder,consistent with other research. However, the same configuration is related to longer, not shorter, episodes of depression.
Our speculative explanation is based on the notion that depressive disorder has multiple causes which endure in varying degrees throughout the course of life.Individuals with the protective genetic configuration sometimes are exposed to other causes whose force is sufficient to break through this protective effect, and presumably these other causes are stronger than in individualswith first episodes and a less protective genetic constellation. After the occurrence of the first episode, these causal forces remain in place, producing longer episodes andmore difficult recovery.
There is evidence of interaction between a functional genetic variant in the serotonin transporter gene and life events.
Serotonin is an important neurotransmitter believed to play an important role in depression. The variant of this gene affects how much serotonin transporter protein is produced. This protein is involved in reuptake of serotonin in the synaps. Individuals with the short allelic form of this variant showed an increased risk of depression compared to those carrying the long allele but only when exposed to adverse life events or maltreatment. There have been some nonreplications, but these have been outnumbered by the number of replicated findings.
These results are not very different from the results of patient samples from clinics and studies whose samples include cases late in the course.
Eaton, W.W. (2008). Population-Based Study of First Onset and Chronicity in Major Depressive Disorder. Archives of GeneralPsychiatry, 65(5), 513-520.
1. Medical/clinical knowledge – obviously this is a sine qua non 2. Competence and clinical reasoning 3. Positive relationships with students and supportive learning environment 4. Communication skills 5. Enthusiasm
Columbia University Medical Center has used conventional transcranial magnetic stimulation (TMS) to reduce the deficits in working memory associated with sleep deprivation.
I would propose a similar approach to tackling the problem of patient satisfaction: that we develop checklists of physician etiquette for the clinical encounter. Here, for instance, is a possible checklist for the first meeting with a hospitalized patient:
1. Ask permission to enter the room; wait for an answer.
2. Introduce yourself, showing ID badge.
3. Shake hands (wear glove if needed).
4. Sit down. Smile if appropriate.
5. Briefly explain your role on the team.
6. Ask the patient how he or she is feeling about being in the hospital.
Rapid Transcranial Magnetic Stimulation (rTMS) to the left prefrontal cortex is not more effective than sham rTMS for depression. This was the result of a recent published randomized controlled trial with 4 month follow-up.
rTMS is a non-invasive method to stimulate the brain. Weak electric currents are induced in the cortex of the brain by rapidly changing magnetic fields (electromagnetic induction). This way, brain activity can be triggered with minimal discomfort, no need for anesthesia, and no cognitive side-effects. Side effects of rTMS are: discomfort or pain from the stimulation of the scalp and associated nerves and muscles on the overlying skin and hearing from the loud click made by the TMS pulses.
The most recent Cochrane review concluded that there is no strong evidence for benefit from using transcranial magnetic stimulation to treat depression, although the small sample sizes do not exclude the possibility of benefit. Since then (2002) 8 randomized controlled trials were published about rTMS and depression, you can read about these trials here.
Considering the outcome on the time point at week 4, Dr Shock is not very impressed by the results. For significant difference with the primary outcome 6 patients had to be excluded from the analysis. The mean difference between active and sham on the severity scales is in the range of 2-3 points, significant but hardly clinical relevant. Absolute figures on response and remission at week 4 are not given in this article. Remission rate at 6 weeks on the HAMD-17 was 15.5% increasing to 22.6% at week 9 with open labeled therapy. Not very impressive.
Since some previous studies used relatively non-intense stimulation parameters in the absence of a true placebo condition this trial used an intensive form of rTMS treatment:
Research physicians administered TMS at 110% resting MT (motor threshold) at frequency 10 Hz, in 5-second trains. Twenty trains were given each session with inter-train intervals of 55 seconds. Thus a total of 1000 TMS pulses were given per session and 10 000 per course.
In addition, very few reported meaningful follow-up data, in this study subjects were followed up for 4 months. To prevent unblinding placebo rTMS was delivered in the same way as real rTMS but using a purpose-built sham coil (Magstim Co.,Whitland, UK) that was visually identical to the real coil and made the same clicking sound but did not deliver a magnetic field to scalp or cortex.
And these are the results:
Overall, Hamilton Depression Rating Scale (HAMD) scores were modestly reduced in both groups but with no significant grouprtime interaction (p=0.09) or group main effect (p=0.85) ; the mean difference in HAMD change scores wasx0.3 (95% CIx3.4 to 2.8). At end-of-treatment time-point, 32% of the real group were responders compared with 10% of the sham group (p=0.06) ; 25% of the real group met the remission criterion compared with 10% of the sham group (p=0.2) ; the mean difference in HAMD change scores was 2.9 (95% CI x0.7 to 6.5). There were no significant differences between the two groups on any secondary outcome measures. Blinding was difficult to maintain for both patients and raters.
In a comment they still want us to believe that rTMS can be promising. In the comment comparison is mad with antidepressants and ECT but these treatments have been studied far more often resulting in not very great advantages but much more evidence and meta analysis with greater power. Moreover, as with other failing treatments in the past rTMS is studied in all kinds of diagnoses. rTMS for Stroke?
A study by a group out of the University of Cologne in Germany has demonstrated that rTMS over the unaffected motor cortex of patients that have had a stroke will make their use of the affected hand more efficient and quicker.
Most studies to date have shown beneficial effects of rTMS or tDCS on clinical symptoms in Parkinson’s disease (PD) and support the notion of spatial specificity to the effects on motor and nonmotor symptoms. Stimulation parameters have varied widely, however, and some studies are poorly controlled. Studies of rTMS or tDCS in dystonia have provided abundant data on physiology, but few on clinical effects.
This specific technology can excite or inhibit more areas of the brain than conventional TMS. Regular TMS is basically limited the brain’s outer layer, the neocortex, and can only reach about 1 to 2 centimeters into the brain. So it is limited in its ability to affect many brain areas. The new deep tms can stimulate inner brain areas without inducing unbearable electromagnetic fields cortically. This device currently has almost magical properties and it is somewhat difficult to distinguish company hype from real clinical benefit. I’m not sure at this point how selective this targeting technique is. I think it will be fairly difficult to selectively turn on or off specific brain areas without having unintentional effects.
Researchers have developed a better way to manipulate a person’s brain functioning. They have created a new type of transcranial magnetic stimulation (TMS) device (called controllable pulse width TMS or cTMS for short) that will allow rectangular pulse shapes of the magnetic fields. This device will enable researchers to control the width of the magnetic pulse that passes through the subjects skull.
Will keep you posted on all this, will it help TMS?. Let me know in the comments what you think?
Mogg, A., Pluck, G., Eranti, S., Landau, S., Purvis, R., Brown, R., Curtis, V., Howard, R., Philpot, M., McLoughlin, D. (2008). A randomized controlled trial with 4-month follow-up of adjunctive repetitive transcranial magnetic stimulation of the left prefrontal cortex for depression. Psychological Medicine, 38(03) DOI: 10.1017/S0033291707001663 Ebmeier, K., Herrmann, L. (2008). TMS – the beginning of the end or the end of the beginning?. Psychological Medicine, 38(03) DOI: 10.1017/S0033291707001651
