Friday, May 10th, 2013
Medscape: Fran Lowry(May 2, 2013)— Bilateral prefrontal repetitive transcranial magnetic stimulation (rTMS) is a promising treatment for the negative symptoms of schizophrenia, new research shows.
Preliminary results from a double-blind, randomized controlled trial showed that patients with schizophrenia or schizoaffective disorder who were treated with rTMS had a significant improvement in their negative symptoms, as assessed on the Scale for the Assessment of Negative Symptoms (SANS), that lasted for 4 weeks post treatment.
However, after 4 weeks, this beneficial effect diminished.
The findings were presented here at the 14th International Congress on Schizophrenia Research (ICOSR).
Effective Treatment Urgently Needed
Effective treatment options for the negative symptoms of schizophrenia are urgently needed, said study investigator Jozarni Dlabac-de Lange, MD, from the University of Groningen, the Netherlands.
“The outcome for patients who are suffering from negative symptoms is much worse, and there has not been a lot of research in this subgroup of patients because they are very difficult to include in studies,” she told Medscape Medical News.
In addition, the few studies that have reported on the efficacy of rTMS treatment for negative schizophrenia symptoms have shown inconsistent results, Dr. Dlabac-de Lange said.
Each treatment lasted 20 minutes and was given in the morning and again in the afternoon. Patients were stimulated at 90% of the motor threshold.In the current study, the investigators randomly assigned 32 patients with schizophrenia or schizoaffective disorder and moderate to severe negative symptoms (Positive and Negative Syndrome Scale [PANSS] negative subscale ≥ 15) to receive either real (n = 16 patients) or sham (n = 16 patients) rTMS of the bilateral dorsolateral prefrontal cortex.
The researchers found that there was a significant improvement in the SANS measure of negative symptoms in the rTMS group compared with the sham group 4 weeks after the treatment sessions stopped (P = .04); however, the effects diminished by 3 months (P = .14).
Additionally, there was no significant difference between the 2 groups on the PANSS negative symptom score at 4 weeks (P = .38) and at 3 months (P = .32).
“Results were good at first, so the next step is to try and see how we can enhance these treatment effects, perhaps by combining rTMS with psychosocial interventions, discovering the optimal treatment parameters and learning which of the negative symptoms show a better response to rTMS,” Dr. Dlabac-de Lange said.
Tags: depression, depression treatment, major depression, MDD, negative symptoms, neuropsychiatry, neurotransmitters, psychiatrist, psychiatry, schizophrenia, tms, transcranial magnetic stimulation
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Wednesday, April 24th, 2013
Overview: The standard of care for clinical depression has significant limitations: traditional drugs that focus on monoamine neurotransmitters can take several weeks to be effective, and many patients never respond to any form of treatment. Several clinical trials have demonstrated strikingly better outcomes using the anesthetic ketamine to treat depression. Notably, a single application can have rapid and lasting antidepressant effects in patients who do not respond to other treatments. Because ketamine is an antagonist of NMDA-type glutamate receptors, research is focused on the role of glutamate neurotransmission in depression and on drug development that targets the glutamatergic system. The March 25, 2013, meeting of the Academy’s Biochemical Pharmacology Discussion Group, Treatment-resistant Depression: Glutamate, Stress Hormones, and their Role in the Regeneration of Neurons, presented this new research and the avenues it is opening for the treatment of depression.
Tags: antidepressants, Anxiety, depression, depression treatment, major depression, MDD, neuropsychiatry, neurotransmitters, psychiatrist, psychiatry, tms, transcranial magnetic stimulation
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Wednesday, April 24th, 2013
WEDNESDAY, April 3 (HealthDay News) — Rats addicted to cocaine lost the craving when researchers used laser light to stimulate a specific part of their brains.
The same team of scientists also used the laser technique to trigger new cocaine addictions in rats. They say the therapy — which targets the prefrontal cortex of the rat brain — could point the way to a new method of treating the addiction in humans.
“When we turn on a laser light in the prelimbic region of the prefrontal cortex, the compulsive cocaine seeking is gone,” study co-researcher Dr. Antonello Bonci, adjunct professor of neurology at the University of California, San Francisco, said in a university news release.
As the researchers explained, the mammalian prefrontal cortex plays an important role in impulse control, decision-making and behavioral flexibility.
In this study, the researchers used genetic engineering to insert light-sensitive proteins called rhodopsins into nerve cells (neurons) in the rats’ prefrontal cortex. Activating this brain region with a laser tuned to the rhodopsins turned the neurons on and off.
Turning on the neurons eliminated cocaine addiction while turning them off triggered addiction in the rats, according to the study published online April 3 in the journal Nature.
The findings highlight the central role the prefrontal cortex plays in cocaine addiction and also suggest a new therapy that could be immediately tested in humans, said the team of researchers from UCSF and the U.S. National Institute of Drug Abuse (NIDA).
However, human therapy would not use lasers. Instead, it would most likely rely on electromagnetic stimulation outside the scalp — in particular, a technique called transcranial magnetic stimulation (TMS) — to trigger a similar activation in the prefrontal cortex. TMS has been used to treat depression.
Research in animals often does not pan out in humans, experts note. However, clinical trials are now being designed to test the use of TMS in people, said Bonci, who is also scientific director of the intramural research program at NIDA and an adjunct professor at Johns Hopkins University in Baltimore.
In the clinical trials, TMS will be used a few sessions a week to stimulate the prefrontal cortex in cocaine addicts. The researchers will see if they can restore activity to the prefrontal cortex and help reduce the addicts’ desire for cocaine.
An estimated 1.4 million Americans are addicted to cocaine, which was the reason for more than 482,000 emergency department visits in 2008 and is a leading cause of heart attack and stroke among people younger than 35.
Along with the health toll, cocaine has a major impact on crime, imprisonment, treatment and prevention programs, lost job productivity and lost earnings, the researchers pointed out.
The U.S. National Institute on Drug Abuse has more about cocaine.
Wednesday, March 27th, 2013
Tuesday, March 26, 2013-Bob Shepard
University of Alabama at Birmingham (UAB) researchers think ketamine, an anesthesia medication in use since the 1970s, might be a valuable tool in treating severe depression and reducing suicidal urges; they have launched two studies to explore the possibility. One of the studies, ketamine is administered to suicidal patients in the UAB Hospital emergency department (ED), is the only such trial actually being conducted in an ED in the nation.
“There is a growing body of evidence that indicates that lower doses of ketamine can reduce suicidal feelings and relieve symptoms of severe depression in a very short period of time, as little as a few hours, which makes it an extremely attractive candidate for treating acute depression,” said Richard Shelton, M.D., professor in the Department of Psychiatry and Behavioral Neurobiology and lead investigator on the studies.
Shelton said ketamine appears to work on depression by blocking a neurotransmitter called glutamate from binding to the NMDA receptor on neurons. Too much glutamate on an NMDA receptor leads to the opening of a calcium ion channel, releasing too much calcium downstream. This then affects a brain chemical, brain derived neurotrophic factor (BDNF), which increases connections between neurons in the brain. These connections help the brain regulate emotions better.
In the trial, patients presenting to the ED with suicidal thoughts can be enrolled in the ketamine trial. The drug is administered via infusion, which takes about five minutes.
“We have seen a decrease in depression scores and suicide scores, sometimes within 15 minutes after giving ketamine,” said Cheryl McCullumsmith, M.D., Ph.D., assistant professor and director of hospital psychiatry. “The antidepressants commonly used to treat depression and suicidal thoughts take weeks or months to begin to show positive effects. When a patient is actively suicidal, we don’t have that much time.”
McCullumsmith said patients entered in the ketamine trial at the ED are admitted to the psychiatric inpatient unit for observation.
“We are attempting to determine just how quickly the drug produces a beneficial result, as well as how long that result lasts,” McCullumsmith said.
Shelton said a second trial, sponsored by Janssen Research & Development, LLC., is a multi-site trial of patients with severe depression and possible suicidal thoughts who are seen in an outpatient setting. Patients receive two or three infusions of ketamine or placebo each week for four-to-six weeks. Patients who do not benefit from study treatment after the first two weeks are offered two weeks of treatment with ketamine without the chance of placebo.
“We’re interested in knowing how long each infusion will sustain the beneficial effect,” said Shelton. “Ketamine does not appear to be curative, and we have a lot of work to do to see if it might be a useful drug for depression and suicide prevention on a long-term, regular-use basis.”
A third trial underway at UAB is testing a compound called Glyx-13, produced by Naurex, Inc. Glyx-13 may produce similar results as ketamine by blocking an amino acid called glycine, which works in tandem with glutamate. Glycine regulates glutamate signaling, so it is like an added layer of fine-tuning. When glycine and glutamate bind to NMDA together, the calcium ion channel opens widely. Blocking glutamate with ketamine can reduce the release of calcium. Blocking glycine with Glyx-13 may achieve the same result, but more subtly and with fewer side effects.
“Glyx-13 may prove to be a more promising candidate than ketamine in terms of potential side effects,” said Shelton. “Glyx-13 is being evaluated with just one infusion per week.”
Ketamine, when used in anesthesia, has some side effects, including hallucinations and psychotic symptoms. It has also been a drug of abuse, known on the street as Special K. Shelton said the dose used in the depression trials is much lower, and given over a longer period. Side effects observed thus far in the ketamine trials have been minimal, he said.
UAB is enrolling patients in the outpatient trials of ketamine and Glyx-13. Male and female patients ages 19-64 with a diagnosis of depression, who have failed two drug regimens for depression, are candidates for the trials. Total time involved in the studies, with treatment and follow-up, is about 13 weeks.
Thursday, March 21st, 2013
By RICK NAUERT PHD Senior News Editor
Reviewed by John M. Grohol, Psy.D. on March 13, 2013
Those with schizophrenia are often functionally limited by mental or cognitive impairments.
Memory, attention, IQ, and verbal and motor skills are often disrupted, and these deficits tend to compromise the ability to perform normal day-to-day activities.
Scientists have been exploring a variety of strategies to reduce these impairments, including “exercising the brain” with specially designed computer games and medications that might improve the function of brain circuits.
In a new study, Mera Barr, Ph.D., and her colleagues at University of Toronto provide evidence that stimulating the brain using repetitive transcranial magnetic stimulation (rTMS) may be an effective strategy to improve cognitive function.
“In a randomized controlled trial, we evaluated whether rTMS can improve working memory in schizophrenia,” said Barr and senior author Zafiris Daskalakis, M.D.
“Our results showed that rTMS resulted in a significant improvement in working memory performance relative to baseline.”
Transcranial magnetic stimulation is a non-invasive procedure that uses magnetic fields to stimulate nerve cells. It does not require sedation or anesthesia and so patients remain awake, reclined in a chair, while treatment is administered through coils placed near the forehead.
In 2008, rTMS was FDA-approved to treat depression for individuals who don’t respond to pharmacotherapy.
The study is presented in the journal Biological Psychiatry.
“TMS can have lasting effects on brain circuit function because this approach not only changes the activity of the circuit that is being stimulated, but it also may change the plasticity of that circuit, i.e., the capacity of the circuit to remodel itself functionally and structurally to support cognitive functions,” said Dr. John Krystal, editor of the journal.
Experts say that previous studies have shown that rTMS improves working memory in healthy individuals, and a recent open-label trial showed promising findings for verbal memory in schizophrenia patients.
These findings informed the current study to determine if high frequency rTMS could improve memory in individuals with schizophrenia.
Researchers recruited medicated schizophrenia patients who completed a working memory task before and after 4 weeks of treatment.
Research methodology involved a double-blind study, where neither the patients nor the researchers knew who was receiving real rTMS or a sham treatment that was designed to entirely mimic the procedure without actually delivering brain stimulation.
Investigators discovered TMS not only improved working memory in patients after 4 weeks, but the improvement was to a level comparable to healthy subjects.
These findings suggest that rTMS may be a novel, efficacious, and safe treatment for working memory deficits in schizophrenia.
While the current findings are preliminary, researchers hope additional investigations will replicate the findings and provide an approved treatment for cognitive impairments in schizophrenia.
The authors concluded: “Working memory is an important predictor of functional outcome. Developing novel treatments aimed at improving these deficits may ultimately translate into meaningful changes in the lives of patients suffering from this debilitating disorder.”
Tags: Anxiety, dementia, depression, major depression, memories, memory, neuropsychiatry, neurotransmitters, psychiatrist, psychiatry, therapy, tms, transcranial magnetic stimulation
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Thursday, March 21st, 2013
Working memory represents a core cognitive domain that is impaired in schizophrenia for which there are currently no satisfactory treatments. Repetitive transcranial magnetic stimulation (rTMS) targeted over the dorsolateral prefrontal cortex has been shown to modulate neurophysiological mechanisms linked to working memory in schizophrenia and improves working memory performance in healthy subjects and might therefore represent a treatment modality for schizophrenia patients. The objectives were to evaluate the effects of rTMS on working memory performance in schizophrenia patients and evaluate whether rTMS normalizes performance to healthy subject levels.
In a 4-week randomized double-blind sham-controlled pilot study design, 27 medicated schizophrenia patients were tested at the Centre for Addiction and Mental Health (a university teaching hospital that provides psychiatric care to a large urban catchment area and serves as a tertiary referral center for the province of Ontario). Patients performed the verbal working memory n-back task before and after rTMS magnetic resonance image targeted bilaterally sequentially to left and right dorsolateral prefrontal cortex 750 pulses/side at 20 Hz for 20 treatments. The main outcome measure was mean magnitude of change in the n-back accuracy for target responses with active (n=13) or sham (n=12) rTMS treatment course.
The rTMS significantly improved 3-back accuracy for targets compared with placebo sham (Cohen’s d=.92). The improvement in 3-back accuracy was also found to be at a level comparable to healthy subjects.
These pilot data suggest that bilateral rTMS might be a novel, efficacious, and safe treatment for working memory deficits in patients with schizophrenia.
Tags: major depression, memories, memory, neuropsychiatric, neuropsychiatry, neurotransmitters, psychiatrist, psychiatry, schizophrenia, tms, transcranial magnetic stimulation
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Tuesday, February 5th, 2013
Will Parker- Researchers are reporting a successful phase IIa clinical trial of GLYX-13, a first-of-its-kind ketamine-like antidepressant that takes effect within 24 hours and delivers double the antidepressant effect of traditional selective serotonin re-uptake inhibitor (SSRI) treatments. Details of the clinical development of GLYX-13 appear in the current issue of the journal Neuropsychopharmacology and the trial results were presented last Thursday at the 51st Annual Meeting of the American College of Neuropsychopharmacology.
GLYX-13 was developed by a team led by Joseph Moskal, research professor of biomedical engineering at Northwestern University. Moskal said the drug was novel because it targets the brain receptors responsible for learning and memory – a very different approach from SSRI antidepressants. The researchers speculate it also could be helpful in treating other neurological conditions, including schizophrenia, bipolar disorder, anxiety and Alzheimer’s disease.
GLYX-13 works by modulating the N-methyl-D-aspartate (NMDA) receptor in the brain, as do other NMDA receptor antagonists such as ketamine, but GLYX-13 does not have their serious and limiting side effects, such as hallucinations and schizophrenia-like effects. NMDA receptors play a key role in regulating synaptic plasticity – the quality of the connection between neurons – and thus are important in regulating learning and memory functions.
In trials administered at 12 sites across the country, a single dose of GLYX-13 resulted in significant reductions in depression symptoms among subjects who had shown little improvement with previous drugs. The positive effects of GLYX-13 were evident within 24 hours and lasted an average of seven days. The effect size, a measure of the magnitude of the drug’s antidepressant efficacy, at both these times after a single dose was nearly double the effect size seen with most other antidepressant drugs after four to six weeks of repeated dosing. Side effects of GLYX-13 were mild to moderate and were consistent with those observed in subjects receiving a placebo.
GLYX-13 is administered intravenously but Moskal is working on an oral version. The drug is currently undergoing a phase IIb clinical trial at 20 sites across the United States. This trial is evaluating repeated doses of the drug.
Tags: antidepressants, depression, ketamine, major depression, neuropsychiatry, neurotransmitters, psychiatrist, psychiatry, therapy, tms, transcranial magnetic stimulation
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Thursday, January 17th, 2013
Samuel Pepys was a member of parliament and a high-ranking figure in the Admiralty, where he was instrumental in strengthening the Royal Navy, but he is best remembered as a diarist. His account of the Great Fire of London, which razed the area where the city – the financial nexus of the United Kingdom – now stands, is perhaps the definitive eyewitness narrative of the tragedy. Fully six months after Pepys saw the Great Fire devour people and buildings, his sleep was broken by nightmares of the horror.
Today we would say that Pepys was probably suffering from post-traumatic stress disorder (PTSD), the mental state that we associate with the broken military dribbling back from 12 years of war in the Middle East.
PTSD denotes a psychiatric illness that follows a physical or psychological trauma, like seeing your buddy’s legs blown of by a roadside bomb. But PTSD is older even than warfare; it is probably as old as anxiety itself. However, wars have been a propitious time for studying PTSD, not least because physicians encounter so many more cases of it.
The term PTSD entered the official lexicon of psychiatric diseases in the 1980 edition of the American Psychiatric Association’s Diagnostic and Statistical Manual (DSM-III) and underwent revision in the subsequent edition of the manual; today, clinical psychiatrists, many researchers, disability evaluators, the courts and, for better or worse, anyone else who requires a standardized set of criteria, rely on DSM-IV.
Like other diseases, psychiatric illnesses are recognized by their symptoms, and the clusters of symptoms define a syndrome. PTSD has three important symptoms:
1.hyper-arousal – a state of persistent mental and physical excitation that may endure for months or years;
2.avoidance and numbing – psychological defense mechanisms to block out memories of the trauma, or even life situations that resemble the trauma;
3.re-experiencing the trauma in nightmares like Pepys’, or experiencing “flashbacks,” defined as vivid, waking remembrances of the traumatic event.
In its current incarnation, DSM classifies PTSD as an anxiety disorder, along with free-floating anxiety and panic disorder. One skeptic among many with respect to this classification is co-author James L. Knoll IV MD, associate professor of psychiatry and director of the division of forensic psychiatry at the State University of New York Upstate Medical University in Syracuse. Knoll contends there is strong overlap with other anxiety disorders, but with PTSD, there is very likely a different biological mechanism going on. As a forensic psychiatrist, Knoll is no stranger to PTSD, for he works with crime victims who may have been traumatized for protracted periods of time, if not for life.
Almost every major war in modern times has been accompanied by a different synonym for PTSD, each perhaps with a unique tweak. The first scientifically rigorous investigations of this condition were carried out by Civil War military surgeon J.M. Da Costa. Though the label “Da Costa’s Syndrome” is still used in medical histories, Da Costa himself chose the term “irritable heart” because of the severe, frightening pounding of the heart that prevented soldiers from taking to the field. And the treatment for irritable heart? The only sedative-hypnotic of the day: rum.
In the serene Victorian years that followed the Civil War, ladies of means took to their beds with symptoms of palpitations, shortness of breath, tremulousness and perspiration. Their physicians gave them the diagnosis of neurasthenia, a misleading expression which means “nervous exhaustion.” These women – and many men of the day – had most if not all of the symptoms of Da Costa’s Syndrome. By today’s diagnostic criteria, men and women previously designated as suffering from “neurasthenia” would meet the criteria for PTSD.
With the onset of World War I, British military physicians (and their counterparts in the German trenches) soon observed a cluster of symptoms that they attributed to a kind of concussion from the explosion of artillery shells. The condition was dubbed “shell shock,” but when these soldiers were examined more closely, 60-80 percent were deemed “neurasthenic” and 10 percent suffered from what was then called “a fugue state” and which we now recognize as numbing.
And so it went from war to war. Da Costa’s Syndrome became whatever psychiatric or physiological symptom seemed the most prominent: effort syndrome, neurocirculatory asthenia, combat fatigue, post-Vietnam Syndrome, and finally PTSD. As new drugs became available, physicians tried them, graduating from alcohol to laudanum (a tincture of opium) to chloral hydrate and barbiturates to benzodiazepines and Thorazine-like compounds to antidepressants.
Just as DaCosta’s Syndrome, effort syndrome, neurasthenia and PTSD have a common profile on the symptomatic level, so too do they have a common denominator on the physiological level. This was first shown by two British investigators in 1946 (M. Jones and V. Mellersh, Psychosomatics). The scientists were studying the “effort syndrome.” When these patients are exercised, it turns out that their blood lactate, a normal product of muscular exertion, is significantly higher than controls without the effort syndrome. This finding, which still has psychiatrists scratching their heads, was confirmed by several other investigators in the next few years.
There the matter lay until 1967, when two Washington University psychiatrists conducted an ingenious experiment: they infused lactate into an arm vein of normal controls and patients suffering from chronic anxiety. The lactate had no effect on controls, but the patients with anxiety “neurosis” (to use a term that was prevalent at the time) experienced full-blown panic attacks from the lactate infusion; in some instances the reaction was so violent that the infusion had to be stopped prematurely.
So, exercise abnormally raises the level of blood lactate in patients with “effort syndrome,” while conversely, infusion of lactate into patients with a history of anxiety provokes panic attacks. Research with lactate continues; of particular interest is that several teams (i.e., Am J Psychiat 1987 Oct;1317-9) have administered lactate infusions to patients with PTSD; the infusions were found to provoke flashbacks of the traumatic event.
The word “panicogenic” was coined for a diverse group of chemicals that trigger panic attacks. Besides lactate, they include carbon dioxide and cholecystokinin. It’s not known whether these chemicals are impacting on the physiological substrate of anxiety, or whether their effects are parenthetical. Evidence from the science of pharmacology suggests that they really do mobilize the physiological mechanism of anxiety. The reasoning goes like this: it’s not known whether the diverse panicogens all act on the same underlying, natural cause or causes of anxiety. As we’ll see, drugs that block anxiety attacks (namely antidepressants) also block the action of panicogens, suggesting that panicogens hit on the underlying cause of anxiety, but this is only an educated guess.
It is well established that most antidepressants block panic attacks, but they do not work like the benzodiazepines (Klonopin, Valium, Xanax, other peer drugs). Antidepressants usually take at least two weeks to kick in, because this is thought to be the time required to boost neurotransmission of serotonin in the brain. On the other hand, benzodiazepines often calm the patient in a couple of hours by inhibiting the central nervous system through their effect on releasing the neurotransmitter GABA (gamma-amino-butyric -acid). Anti-depressants prevent the attacks from “happening.” One such antidepressant is the drug imipramine (Tofranil). It has been shown that imipramine blocks the panic attacks artificially induced by panicogens, just as it blocks “natural” panic attacks.
It is especially interesting, therefore, that antidepressants constitute front-line therapy for patients with PTSD. These days, psychiatrists generally use specific serotonin reuptake inhibitors (SSRIs) such as Zoloft, Prozac or Paxil, or a specific serotonin/noradrenaline reuptake inhibitor, notably the drug Effexor. To these, in his clinical practice, co-author Knoll may add low doses of a second generation antipsychotic, of which the most familiar are Abilify, Seroquel or Zyprexa. Antipsychotics are not curative in themselves, but they enhance the effectiveness of antidepressants. A third drug in Knoll’s armamentarium is Prazosin. Though marketed as an antihypertensive, practitioners and patients have found Prazosin effective at blocking nightmares. Of particular interest is a study by Michael H. Mithoefer, MD that MDMA (a k a ecstasy) was found to be highly effective for treating PTSD in combination with psychotherapy. And at the University of Arizona, Sue Sisley MD, a psychiatrist and internist, is awaiting delivery of a supply of marijuana from the National Institute on Drug Abuse (NIDA) to begin a trial approved by the Food and Drug Administration (FDA). There has been some interest in propranolol (Inderal) for “erasing” PTSD-type memories, but this is based on anecdotal accounts and small-scale studies. On the other hand, propranolol can cause vivid nightmares – the last thing you’d want in a patient with PTSD.
Besides drugs, psychiatrists are studying other approaches to treating PTSD. Thus, retired Lt. Gen. Stephen N. Xenakis MD is using hyperbaric oxygen therapy. In this procedure, the patient breathes in oxygen at very high pressure. This ties in neatly with what we know about lactate; high levels of oxygen would be predicted to speed up cellular metabolism, burning off lactate in the process.
A second approach for which there are a number of positive claims is transcranial magnetic stimulation (TMS). Briefly, TMS uses an oscillating magnetic field to release neurotransmitters over the course of a month of daily outpatient treatments; it bears no resemblance whatever to shock therapy. We were informed by the manufacturer of the NeuroStar TMS instrument that the military is interested in TMS and has purchased a number of instruments.
Thursday, January 17th, 2013
By Helen Albert, Senior medwireNews Reporter-A month of daily transcranial magnetic stimulation targeting the supplemental motor area (SMA) results in lasting improvements in symptoms of Tourette syndrome, show study findings.
“Repetitive transcranial magnetic stimulation (rTMS)… involves repetitive generation of a brief, powerful magnetic field by a small coil positioned over the scalp that induces an electric current in the brain,” explain Nong Xiao (Chongqing Medical University, Yuzhong district, China) and colleagues.
The technique is designed as a noninvasive treatment for a range of neurological and psychiatric disorders including migraine, stroke, and Parkinson’s disease.
In this study, the researchers tested the capacity of low-frequency 1 Hz rTMS applied at 20 daily sessions (Monday-Friday) over 4 weeks for treatment of the motor and speech neurological tics displayed by patients with Tourette syndrome, on the basis that low-frequency rTMS (≤1 Hz) inhibits and high-frequency rTMS (>5 Hz) promotes cortical excitability.
In total, 25 children under 16 years took part in the study. After 4 weeks of treatment, the team observed no improvements in tic symptoms in six children, but significant improvements in these symptoms that lasted until 3 months in 19 children, and until 6 months in 17 children (68%).
On average, significant reductions were seen in the scores obtained on various tests by the children at 4 weeks compared with baseline. These included the Yale Global Tic Severity Scale; Clinical Global Impression Scale; Swanson, Nolan and Pelham Rating Scale, version IV for attention-deficit hyperactivity disorder (SNAP-IV); Children’s Depression Inventory; Spence Children’s Anxiety Scale; and a novel Attention Test.
Overall scores for all these tests were lower at 6 months than at baseline, but only the SNAP-IV and Attention test scores were significantly lower at 6 months than at 4 weeks.
“Low-frequency (1 Hz) rTMS to the SMA significantly improved Tourette syndrome symptoms, suggesting that it is effective on tics, hyperactivity, attention deficit, depression and anxiety in children with Tourette syndrome,” write Xiao and co-workers in the Journal of Clinical Neuroscience.
“These collective results suggest the need for further studies using rTMS as a research and clinical therapeutic tool in psychiatric and neurological diseases, with particular attention to patients with Tourette syndrome.”
Thursday, January 17th, 2013
ScienceCodex- By using noninvasive stimulation, researchers were able to temporarily improve the ability of people with spinal cord injuries to use their hands. The findings, reported on November 29th in Current Biology, a Cell Press publication, hold promise in treating thousands of people in the United States alone who are partially paralyzed due to spinal cord injury.
“This approach builds on earlier work and highlights the importance of the corticospinal tract—which conducts impulses from the brain’s motor cortex to the spinal cord and is a major pathway contributing to voluntary movement—as an important target for intervention after spinal cord injury,” said Monica Perez of the University of Pittsburgh.
The researchers tested the new method in 19 people with chronic cervical spinal cord injury and 14 uninjured people. The treatment was customized to each individual and paired transcranial magnetic stimulation delivered to a specific part of the motor cortex with electrical stimulation to peripheral nerves found in the wrist.
One hundred paired pulses were delivered every 10 seconds for a period of around 20 minutes to produce volleys of neural activity. The timing of arrival of those volleys in the spinal cord was absolutely essential to the treatment’s success, the report shows.
“This short, noninvasive stimulation protocol has the potential to be used within a clinic setting as part of a rehabilitation technique,” said study coauthor Karen Bunday, also of the University of Pittsburgh. “When pulses from the motor cortex were precisely timed to arrive at the spinal cord one or two milliseconds before pulses from the peripheral nerve, we observed an increase in spinal cord transmission and voluntary motor output for up to 80 minutes.”
After the noninvasive treatment, the majority of the participants in the study could exert more force with their hand muscles. Those effects translated into greater manual dexterity when participants were asked to grasp and manipulate small pegs with their index fingers and thumbs.
More prolonged use of the technique or its combination with other rehabilitation strategies may well improve its therapeutic benefits, the researchers say. The protocol might also be used in the treatment of other kinds of motor disorders involving damage to the corticospinal tract.
“Human electrophysiology can be a powerful tool for developing therapies,” Perez concluded. “We need to explore new targets to improve rehabilitation strategies by taking advantage of our knowledge in human physiology and their mechanisms.”