Botox helps those with depression

A study shows that depressive symptoms are improved by Botox injections.

"Study author M. Axel Wollmer, a psychiatrist at the University of Basel in Switzerland, believes the treatment “interrupts feedback from the facial musculature to the brain, which may be involved in the development and maintenance of negative emotions.” Past studies have shown that Botox impairs people's ability to identify others' feelings, and the new finding adds more evidence: the muscles of the face are instrumental for identifying and experiencing emotions, not just communicating them." JR

In the largest randomized, double-blind, placebo controlled study to date on the effect of OnabotulinumtoxinA (as known as Botox) on depression, researchers found that more than half of subjects suffering from moderate to severe depression showed a substantial improvement (greater than or equal to 50% of baseline) in their depressive symptoms as measured by the MADRS scale.

The study, conducted by Dr. Eric Finzi, MD, PhD and Dr. Norman E. Rosenthal, MD and published in the Journal of Psychiatric Research, included 74 depressed subjects injected with a single treatment of either onabotulinumtoxinA (OBA) or a placebo to the corrugator and procerus muscles between the eyebrows. Results showed that depressive symptoms (as assessed by the MADRS scale) in the OBA treatment group decreased 47 percent after six weeks, compared to 21 percent in the placebo group. This study is the first to show a significant difference in remission rate with OBA in depressed patients (27% OBA vs. 7% placebo).

Study co-author Dr. Norman E. Rosenthal, MD, Clinical Professor of Psychiatry at Georgetown Medical School, commented, "This research is groundbreaking because it offers those who suffer from depression and their doctors an entirely new approach to treating the condition -- one that doesn't conflict with any other treatments."

The study showed that Botox may help relieve depressive symptoms both as a stand-alone and an adjunctive treatment.

"This new research supports earlier facial feedback theory of Charles Darwin and William James which suggests that facial expressions influence mood," added Dr. Eric Finzi, Dermasurgeon and co-author on the paper that first reported that inhibition of frowning by facial injection of OBA could help depressed patients in a pilot study published in 2006.

Read more here

More here at scientific amaerican

How long you sleep can influence depression and anxiety development

Research shows that a person's sleep duration can influence the development and symptom severity for anxiety and depression.

Short and long sleep duration, but not insomnia, predict a chronic course of depressive and anxiety disorders independent of symptom severity, research indicates.

Patients with persistent depression or anxiety were more likely to have insomnia than those without persistent disorders. However, insomnia was not independently associated with persistence after accounting for symptom severity.

“Our results also show that it is important to differentiate between insomnia and sleep duration, since there was no interaction effect between insomnia and sleep duration,” the researchers note in the Journal of Clinical Psychiatry.

They studied 1069 individuals aged an average of 42.7 years with DSM-IV-diagnosed depression or anxiety, 59% of whom had insomnia, diagnosed as a Women’s Health Initiative Insomnia Rating Scale score of 9 or above. At 2-year follow-up, persistent depressive and/or anxiety disorder, according to the Composite International Diagnostic Interview, was seen in 61.1% of patients.

Patients who reported sleeping an average of 10 hours or more per night were a significant 2.52 times more likely to have persistent (6-month diagnosis) depression and/or anxiety over 2 years of follow-up than patients who reported sleeping for a normal 7 to 9 hours per night. This was after adjusting for sociodemographic characteristics, chronic medical disorders, psychotropic medication, and symptom severity.

Those who reported short sleep durations of 6 hours or less per night were a significant 1.64 times more likely to have persistent depression and/or anxiety, but, as with insomnia, significance was lost after adjustment for symptom severity.

Both long and short sleep duration were also independently associated with a chronic course (no remission, and at least mild symptoms for 2 years of follow-up) of depression and/or anxiety, increasing the risk a significant 2.91-fold and 1.50-fold, respectively.

When the researchers looked at the effects of sleep duration on the course of depression and anxiety separately, they found that both long and short sleep duration predicted a chronic course of anxiety symptoms, with significant odds ratios of 7.73 and 1.62, respectively. The same was true for chronic depressive symptoms, with corresponding odds of 4.34 and 2.03.

Long and short sleep duration also predicted persistent depressive disorder, at significant odds ratios of 2.52 and 1.49, respectively, but neither predicted persistent anxiety disorder.

“[O]ur study adds significant information on the impact of sleep disturbances on the course of psychopathology,” say lead researcher Josine van Mill (EMGO Institute for Health and Care Research, Amsterdam, the Netherlands)and colleagues.

They add: “In clinical practice, routinely asking for sleep duration might identify subjects at risk for a chronic course.”

Read more here

Study: Concussion can mean depression years later

A study done in mice shows that concussions can lead to the development of depression later in life.

A head injury can lead immune-system brain cells to go on "high alert" and overreact to later immune challenges by becoming excessively inflammatory -- a condition linked with depressive complications, a new animal study suggests.

The findings could help explain some of the midlife mental-health issues suffered by individuals who experience multiple concussions as young adults, researchers say. And these depressive symptoms are likely inflammation-related, which means they may not respond to common antidepressants.

An added complication is that aging already increases brain inflammation. So on top of normal aging concerns, people who have had a traumatic brain injury (TBI) experience added inflammation caused by magnified immune responses to so-called "secondary challenges," such as a second head injury, infections or other stressors.

In mice, these high-alert cells in the brain -- called microglia -- had an exaggerated response to an immune challenge one month after a moderate brain injury. This increased brain inflammation corresponded with the development of depressive behaviors that were not observed in uninjured mice.

"If we had waited three, six or nine months, the symptoms probably would have gotten even worse," said lead author Jonathan Godbout, associate professor of neuroscience at The Ohio State University and a researcher in the Institute for Behavioral Medicine Research.

"A lot of people with a history of head injury don't develop mental-health problems until they're in their 40s, 50s or 60s. That suggests there are other factors involved, and that's why we're looking at this two-hit idea -- the brain injury being the first and then an immune challenge. It's as if one plus one plus one equals 15. There can be a multiplier effect."

The research is published online in the journal Biological Psychiatry.

This work applies to concussive brain injuries that result in a diffuse -- or spread out -- trauma to the brain. These are also concussive injuries from which people and animals recover fairly quickly, typically showing no problems with thinking or moving about a week after the injury to the brain.

In the study, researchers compared uninjured mice with mice that had experienced a moderate TBI. Injured mice showed some initial coordination problems, but those resolved within a week.

The injured mice also showed signs of depressive symptoms that improved within one month. Godbout and colleagues attributed those symptoms to the expected neuroinflammation that occurs after a traumatic brain injury. In these mice, most of the inflammation had cleared within seven days.

Thirty days after injury, researchers examined the brains of the injured mice to determine whether immune cells had remained on high alert since the injury. As expected, the injured brains contained microglia that had stayed in a "primed" state -- meaning they were on standby to respond to a challenge to the immune system. The cells in the brains of uninjured mice did not have the same characteristics.

Under normal circumstances, microglia are the first line of defense and help protect the brain after injury or infection by making proteins and other chemicals that generate just enough inflammation to repair the problem. When they are primed, however, these cells are in a higher state of alert and when they are activated, they generate an amplified immune response that lasts longer than necessary. When these systems are activated with nothing to fight, the circulating chemicals and proteins generate excessive inflammation.

"The young adult mice that have a diffuse head injury basically recover to normal, but not everything is normal. The brain still has a more inflammatory makeup that is permissive to hyperactivation of an immune response," Godbout said.

At 30 days after TBI, the mice were injected with lipopolysaccharide (LPS) -- the dead, outer cell wall of bacteria that stimulates an immune reaction in animals. Tests showed that over the course of 24 hours after the injection, TBI mice were much less social than uninjured mice -- one type of depressive symptom in these animals. The brains of the TBI mice also had dramatically higher levels of two inflammation-related proteins than did brains from normal mice.

Seventy-two hours after the LPS challenge, injured mice showed additional depressive symptoms, including minimal interest in sugar water -- a sign that they avoided what is typically a pleasurable activity. They also showed increased resignation, or a sign of "giving up."

Uninjured mice behaved normally and the levels of inflammatory proteins in their brains had returned to baseline over the same time period.

"These results tell us the TBI mice are having an amplified and prolonged activation of microglia, and that was associated with development of depressive symptoms in the mice," Godbout said.

His lab is now investigating potential treatments that could either prevent the priming of microglia immediately after injury or later reverse the high-alert characteristics of these cells.

Read more here