Posts Tagged TMS

[Abstract] Publication trends in transcranial magnetic stimulation: A 30-year panorama

Highlights

  • This study uses a systematic, bibliometric approach to assess the TMS literature base.
  • Annual TMS research output has increased dramatically over the period 1988–2017.
  • The top disease entities studied to date have been stroke and depression.

 

Abstract

Background

Transcranial magnetic stimulation (TMS) is a non-invasive neuromodulatory technique that has broad diagnostic and therapeutic potential across a range of neurological and psychiatric diseases.

Objective

This study utilises a bibliometric approach to systematically and comprehensively evaluate the literature on TMS from the last three decades.

Methods

The Scopus citation database was used to identify all peer-reviewed journal articles concerning TMS over the period 1988–2017. Frequency-distribution, cross-tabulation and keyword analyses were performed to determine the most prolific researchers, institutions, nations, journals and the foremost studied disease entities within the TMS field. Given recent heightened awareness of gender bias across many fields of biomedicine, female representation among the most prolific authors was determined. Open-access publication rates and types of study design utilised were also quantified.

Results

17,492 TMS-related articles were published during the study period 1988–2017. The annual TMS research output has increased dramatically over this time, despite a recent levelling-off of publications per year. The most prolific institutions were based in the United Kingdom, the United States and Canada. The top disease entities studied were stroke, depression and Parkinson’s disease. Only 4/52 of the most productive researchers during the study period were female. A minority (4.81%) of publications were published as gold open-access.

Conclusion

This study implemented a systematic, bibliometric approach to quantitively assess the breadth of the TMS literature base and identify temporal publication and authorship trends. Drawing on these insights may aid understanding of historical progress in TMS over the last 30 years and help identify into unmet needs and opportunities to improve scientific and publishing practices to contribute to the future health of the field. These findings are likely to be relevant to researchers, clinicians, funders, industry collaborators and other stakeholders.

 

via Publication trends in transcranial magnetic stimulation: A 30-year panorama – Brain Stimulation: Basic, Translational, and Clinical Research in Neuromodulation

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[WEB SITE] Transcranial Magnetic Stimulation for the Recovery of Gait and Balance in Stroke Patients – BrainPost

Post by Thomas Brown

What’s the science?

The permanent brain damage which occurs following ischemic stroke makes functional recovery difficult. While physiotherapy can result in improved voluntary motor recovery, the improvement of balance and gait can be harder. Issues with balance pose a safety risk for stroke patients, who may be more likely to fall. Ultimately, problems with balance can mean reduced independence for patients. The cerebellum, a structure located at the back of the brain, is known to regulate movement, gait and balance. Deficits to the cerebellum often result in ataxia and widened gaits, making this area a prime target for functional recovery analysis. This week in JAMA Neurology Koch and colleagues demonstrate in a phase IIa clinical trial, an increase in gait and balance in hemiparetic stroke patients, up to three weeks after physiotherapy supplemented with transcranial magnetic stimulation of the cerebellum.

How did they do it?

A group of 36 hemiparetic (one side affected) stroke patients were randomly assigned to one of two age-matched groups; control or experimental. The experimental group was treated with intermittent theta-burst magnetic stimulation (TBS) of the cerebellar region ipsilateral (same side) to their motor issues. Intermittent TBS is a process by which bursts of magnetic energy are applied to the scalp over an area of interest. TBS was administered in conjunction with physiotherapy to the experimental group for three weeks. The control group still received physiotherapy, but received sham (fake) TBS. Patients were assessed using a wide range of balance and gait analysis tests to determine the degree of recovery. The authors relied primarily on the Berg Balance Scale, which is a series of 14 tests that determine the ability of an individual to balance without aid. Gait analysis was also performed, in which patients were asked to walk while a machine measured their gait (the space between each foot while walking). Neural activity was measured with electroencephalography while transcranial magnetic stimulation was applied simultaneously (EEG-TMS). This technique was used to measure neural activity changes in motor regions of the brain following activation of the motor cortex using a different TMS paradigm than the one used for treatment.

What did they find?

The authors found that after three weeks of the last treatment with either sham or cerebellar TBS, there was an average increase in the Berg Balance Scale score in those treated with TBS compared to controls. They also showed a reduction in gait width; a wide gait is often associated with the body’s attempt to compensate for problems with balance. This finding was supported by correlational analysis which found that a reduction is step width was associated with an improvement in Berg Balance Scale score. Interestingly, three weeks after treatment there was also an increase in neural activity in the motor (M1) region of the brain in the hemispheres affected by the stoke, in treated patients compared to controls. This area of the cortex is associated with the movement execution. Altogether these findings suggest that there were significant balance, gait and motor cortex activity improvements following treatment with TBS. Critically, no adverse effects were observed following treatment with TBS during the clinical trial.

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What’s the impact?

These findings suggest that theta-burst stimulation may be an effective way of supplementing physiotherapy in those suffering with balance and gait deficits following stroke. Theta-burst stimulation in conjunction with physiotherapy, was able to improve both balance and gait in stroke patients. Treatment with theta-burst stimulation could reduce the chance of falling and improve independence in stroke patients.

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Koch et al. Effect of Cerebellar Stimulation on Gait and Balance Recovery
in Patients With Hemiparetic Stroke. JAMA Neurology (2018).Access the original scientific publication here

 

via Weekly BrainPost — BrainPost

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[Abstract] Bilateral Motor Cortex Plasticity in Individuals With Chronic Stroke, Induced by Paired Associative Stimulation

Background: In the chronic phase after stroke, cortical excitability differs between the cerebral hemispheres; the magnitude of this asymmetry depends on degree of motor impairment. It is unclear whether these asymmetries also affect capacity for plasticity in corticospinal tract excitability or whether hemispheric differences in plasticity are related to chronic sensorimotor impairment.

Methods: Response to paired associative stimulation (PAS) was assessed bilaterally in 22 individuals with chronic hemiparesis. Corticospinal excitability was measured as the area under the motor-evoked potential (MEP) recruitment curve (AUC) at baseline, 5 minutes, and 30 minutes post-PAS. Percentage change in contralesional AUC was calculated and correlated with paretic motor and somatosensory impairment scores.

Results: PAS induced a significant increase in AUC in the contralesional hemisphere (P = .041); in the ipsilesional hemisphere, there was no significant effect of PAS (P = .073). Contralesional AUC showed significantly greater change in individuals without an ipsilesional MEP (P = .029). Percentage change in contralesional AUC between baseline and 5 m post-PAS correlated significantly with FM score (r = −0.443; P = .039) and monofilament thresholds (r = 0.444, P = .044).

Discussion: There are differential responses to PAS within each cerebral hemisphere. Contralesional plasticity was increased in individuals with more severe hemiparesis, indicated by both the absence of an ipsilesional MEP and a greater degree of motor and somatosensory impairment. These data support a body of research showing compensatory changes in the contralesional hemisphere after stroke; new therapies for individuals with chronic stroke could exploit contralesional plasticity to help restore function.

 

via Bilateral Motor Cortex Plasticity in Individuals With Chronic Stroke, Induced by Paired Associative Stimulation – Jennifer K. Ferris, Jason L. Neva, Beatrice A. Francisco, Lara A. Boyd, 2018

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[WEB SITE] What effect does transcranial magnetic stimulation have on the brain?

The procedure facilitates reorganization of connections between neurons which could be useful for therapies

Date: June 5, 2018
Source: Ruhr-University Bochum
Summary:
Researchers have gained new insights on the question of how transcranial magnetic stimulation (TMS) effects functional interconnectivity of neurons. For visualization, they employed fluorescent dyes which provide information on the activity of neurons by light. Using this technique, they showed in an animal model that TMS predisposes neuronal connections in the visual cortex of the brain for processes of reorganization.
 
FULL STORY

Researchers of the Ruhr-Universität Bochum have gained new insights on the question of how transcranial magnetic stimulation (TMS) effects functional interconnectivity of neurons. For visualisation, they employed fluorescent dyes which provide information on the activity of neurons by light. Using this technique, they showed in an animal model that TMS predisposes neuronal connections in the visual cortex of the brain for processes of reorganisation.

TMS is being used as a treatment for a number of brain diseases such as depression, Alzheimer’s disease and schizophrenia, but there has been little research on how exactly TMS works. The team of associate professor Dr Dirk Jancke of the Optical Imaging Lab in Bochum describes its new discoveries in the journal Proceedings of the National Academy of Science (PNAS).

Examining the effects on cortical maps in the visual cortex

The researchers have investigated how TMS affects the organisation of so-called orientation maps in the visual part of the brain. Those maps are partly genetically determined and partly shaped by the interaction with our surroundings. In the visual cortex, for example, neurons respond to contrast edges of certain orientations, which typically constitute boundaries of objects. Neurons that preferably respond to edges of a specific orientation are closely grouped while clusters of neurons with other orientation preferences are gradually located further away, altogether forming a systematic map across all orientations.

The team employed high frequency TMS and compared the behaviour of neurons to visual stimuli with a specific angular orientation before and after the procedure. The result: After the magnetic stimulation the neurons responded more variable, that is, their preference for a particular orientation was less pronounced than before the TMS. “You could say that after the TMS the neurons were somewhat undecided and hence, potentially open to new tasks,” explains Dirk Jancke. “Therefore, we reasoned that the treatment provides us with a time window for the induction of plastic processes during which neurons can change their functional preference.”

A short visual training remodels the maps

The team then looked into the impact of a passive visual training after TMS treatment. 20-minutes of exposure to images of a specific angular orientation led to enlargement of those areas of the brain representing the trained orientation. “Thus, the map in the visual cortex has incorporated the bias in information content of the preceding visual stimulation by changing its layout within a short time,” says Jancke. “Such a procedure — that is a targeted sensory or motor training after TMS to modify the brain’s connectivity pattern — might be a useful approach to therapeutic interventions as well as for specific forms of sensory-motor training,” explains Dirk Jancke.

Methodological challenges

Transcranial magnetic stimulation is a non-invasive painless procedure: A solenoid is being positioned above the head and the brain area in question can be activated or inhibited by means of magnetic waves. So far little is known about the impact of the procedure on a cellular network level, because the strong magnetic field of the TMS superimposes signals that are used by researchers in order to monitor the neuronal effects of the TMS. The magnetic pulse interferes in particular with electrical measurement techniques, such as EEG. In addition, other procedures used in human participants, e.g. functional magnetic resonance imaging, are too slow or their spatial resolution is too low.

Dirk Jancke’s team used voltage dependent fluorescent dyes, embedded in the membranes of the neurons, in order to measure the brain’s activity after the TMS with high spatiotemporal resolution. As soon as a neuron’s activity is modulated, the dye molecules change emission intensity. Light signals therefore provide information about immediate changes in activity of groups of neurons.

Story Source: Materials provided by Ruhr-University BochumNote: Content may be edited for style and length.


Journal Reference:

  1. Vladislav Kozyrev, Robert Staadt, Ulf T. Eysel, Dirk Jancke. TMS-induced neuronal plasticity enables targeted remodeling of visual cortical mapsProceedings of the National Academy of Sciences, 2018; 201802798 DOI: 10.1073/pnas.1802798115

 

via What effect does transcranial magnetic stimulation have on the brain? The procedure facilitates reorganization of connections between neurons which could be useful for therapies — ScienceDaily

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[WEB SITE] Cognitive Behavioral Therapy (CBT) and Transcranial Magnetic Stimulation (TMS): What Are These Therapies and How Are They Used?

Published 7 Feb 2018  – Reviewed 7 Feb 2018 – Author Melissa Galinato  – Source BrainFacts/SfN

When you have a cold, you might have a runny nose, a headache, and a cough. You may take different medications to treat each symptom to soothe your throat or ease your sneezing. Like treating a cold with multiple symptoms, there are different types of therapies to treat the multiple symptoms of depressive disorder, widely known as depression. Cognitive Behavioral Therapy (CBT) and Transcranial Magnetic Stimulation (TMS) are two therapy types that address specific symptoms of depression.

More than 300 million people around the world have depression, which is a common mental illness with multiple symptoms such as persistent sadness, irritability, a feeling of worthlessness, and loss of interest in activities—especially in things that previously brought joy or excitement.

With Cognitive Behavioral Therapy (CBT), a therapist helps a patient with depression to focus on understanding how three things – thoughts, feelings, and behavior – affect each other. “The goal of CBT for depression is to start targeting problematic thoughts and actions that are occurring in the present – as opposed to looking back in the past for a cause – teaching patients skills that they can use to become more aware of their negative thoughts, evaluate their validity and, when not accurate, replace them with more realistic/balanced ways of thinking,” says Simon Rego, Chief Psychologist at Montefiore Medical Center/Albert Einstein College of Medicine in New York.

“At the same time, the other goal of CBT is to help patients change maladaptive patterns of behavior, gradually increasing activities of pleasure and accomplishment, which are known to enhance mood. Taken together, changing how you think and what you do can have a powerful positive impact on your mood.”

Imagine setting a goal – like running a marathon for the first time. A running coach could help you reach that goal by giving you tips and developing a training to slowly build up your strength. In CBT, the therapist acts like a coach and helps people identify goals such as driving a car or giving a speech. Then the therapist helps to figure out actions to reach those goals such as practicing thinking strategies, writing in journals, and doing homework assignments between appointments. Doing these activities in CBT can help people learn coping skills, build self-confidence, and have a sense of control, and a growing number of studies show that CBT works very well for treating depression and several other mental health conditions.

“CBT is an effective treatment for depression because it targets the two main areas where people with depression struggle: negative thoughts and unhelpful behaviors,” said Rego. “The main theory in CBT is that how we feel is directly influenced by how we think and what we do (or don’t do). In the case of depression, we know that people tend to have many negative thoughts about themselves, the world, and the future (e.g., I am a failure, I’ll never get better, no one cares about me, I don’t have the energy to do anything, etc.) which only serve to perpetuate their negative mood.”

Another therapy called Transcranial Magnetic Stimulation (TMS) can be used for some patients with depression who do not get better with antidepressant medications or other treatments. “In our experience, TMS is an appropriate treatment for major depressive disorder, moderate in severity and who are still functioning in the home, community, and who have failed multiple antidepressant medications,” said Ananda Pandurangi, medical director and chair of inpatient psychiatry in the Department of Psychiatry at Virginia Commonwealth University School of Medicine. “It is not appropriate for patients with either “mild” depression or those with severe depression including those with psychosis or catatonia,” said Pandurangi, noting that psychotherapy and medications may be more appropriate for patients with mild to severe depression.

TMS aims to alter brain circuitry. Using an electromagnetic coil, called a stimulator, to affect brain activity and treat depression, TMS treatment involves a doctor placing the stimulator near the forehead against the scalp. This activates brain cells in an area of the brain that includes the prefrontal cortex and controls mood and depression.

Sessions typically use repetitive TMS (rTMS) where recurrent magnetic pulses stimulate the brain. In 2008, the FDA approved rTMS for depression treatment after several research studies showed this TMS treatment lowers signs of depression and improves mood in people with treatment-resistant depression.

REFERENCES

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-5). 5th ed. Washington, DC: American Psychiatric Publishing; 2013. 

Butler AC, Chapman JE, Forman EM, Beck AT. The empirical status of cognitive-behavioral therapy: a review of meta-analyses. Clinical Psychology Review. 26(1), 17-31 (2006).

Depression. National Alliance on Mental Illness. Accessed 2/7/2018.

Depression. World Health Organization. February 2017.

Dobson D, Dobson KS. Evidence-based practice of cognitive-behavioral therapy. Guilford Publications. 2016. 

Gaynes BN, Lloyd SW, Lux L, Gartlehner G, Hansen RA, et al. Repetitive transcranial magnetic stimulation for treatment-resistant depression: a systematic review and meta-analysis. The Journal of Clinical Psychiatry. 75(5), 477-89 (2014).

Huguet A, Rao S, McGrath PJ, Wozney L, Wheaton M, et al. A systematic review of cognitive behavioral therapy and behavioral activation apps for depression. PLoS One. 11(5), e0154248 (2016). 

Lefaucheur JP, André-Obadia N, Antal A, Ayache SS, et al. Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS). Clinical Neurophysiology. 125(11), 2150-2206 (2014). 

Levkovitz Y, Isserles M, Padberg F, Lisanby SH, Bystritsky A, et al. Efficacy and safety of deep transcranial magnetic stimulation for major depression: a prospective multicenter randomized controlled trial. World Psychiatry. 14(1), 64-73 (2015). 

Pascual-Leone A, Rubio B, Pallardó F, Catalá MD. Rapid-rate transcranial magnetic stimulation of left dorsolateral prefrontal cortex in drug-resistant depression. The Lancet. 348(9022), 233-237 (1996). 

Psychotherapy. National Alliance on Mental Illness. Accessed 2/7/2018.

Wassermann EM, Williams WA, Callahan A, Ketter TA, Basser P, et al. Daily repetitive transcranial magnetic stimulation (rTMS) improves mood in. Neuroreport. 6, 1853-1856 (1995). 

via Cognitive Behavioral Therapy Transcranial Magnetic Stimulation what are these therapies 020718

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[Abstract] Transcranial and spinal cord magnetic stimulation in treatment of spasticity: a literature review and meta-analysis

INTRODUCTION: Spasticity is associated with various diseases of the nervous system. Current treatments such as drug therapy, botulinum toxin injections, kinesitherapy, and physiotherapy are not sufficiently effective in a large number of patients. Transcranial magnetic stimulation (TMS) can be considered as an alternative method of treatment. The purpose of this article was to conduct a systematic review and meta-analysis of all available publications assessing the efficacy of repetitive TMS in treatment of spasticity.

EVIDENCE ACQUISITION: Search for articles was conducted in databases PubMed, Willey, and Google. Keywords included “TMS”, “spasticity”, “TMS and spasticity”, “non-invasive brain stimulation”, and “non-invasive spinal cord stimulation”. The difference in scores according to the Modified Ashworth Scale (MAS) for one joint before and after treatment was taken as the effect size.
EVIDENCE SYNTHESIS: We found 26 articles that examined the TMS efficacy in treatment of spasticity. Meta-analysis included 6 trials comprising 149 patients who underwent real stimulation or simulation. No statistically significant difference in the effect of real and simulated stimulation was found in stroke patients. In patients with spinal cord injury and spasticity, the mean effect size value and the 95% confidence interval were -0.80 and (-1.12, -0.49), respectively, in a group of real stimulation; in the case of simulated stimulation, these parameters were 0.15 and (-0.30, -0.00), respectively. Statistically significant differences between groups of real stimulation and simulation were demonstrated for using high-frequency repetitive TMS or iTBS mode for the M1 area of the spastic leg (P=0.0002).
CONCLUSIONS: According to the meta-analysis, the statistically significant effect of TMS in the form of reduced spasticity was demonstrated only for the developed due to lesions at the brain stem and spinal cord level. To clarify the amount of the antispasmodic effect of repetitive TMS at other lesion levels, in particular in patients with hemispheric stroke, further research is required.

via Transcranial and spinal cord magnetic stimulation in treatment of spasticity: a literature review and meta-analysis – European Journal of Physical and Rehabilitation Medicine 2018 February;54(1):75-84 – Minerva Medica – Journals

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[WEB SITE] Insights from TMS into recovery after stroke

Posted in Clinical Review Article on 11th Dec 2017

Transcranial Magnetic Stimulation (TMS) is a non-invasive technique whereby an electro-magnetic coil held over the scalp is used to induce a brief electrical current in the cortex of the underlying brain. TMS may be used in a number of ways to gain in vivo insights into brain physiology and has provided a window into the cascade of physiological changes that occur following stroke. When stimulating the primary motor cortex in a healthy subject stimuli of an intensity above the motor threshold will give rise to a detectable evoked potential in a peripheral muscle. As the stimulus intensity is gradually increased the evoked potentials increase in amplitude up to a maximum, giving rise to a measurable recruitment curve. The motor threshold and the recruitment curve both provide measures of the excitability of the corticospinal tract. This incorporates the excitability of axons within the motor cortex, synaptic inputs onto pyramidal cells and the spinal alpha motor neuron pool. In paired pulse TMS a sub-threshold pulse is delivered a few milliseconds before a second suprathreshold pulse, both through the same coil. The first pulse conditions the response to the second, resulting in inhibition or facilitation depending upon the inter-stimulus interval and reflecting the activity in intracortical regulatory circuits. If two separate TMS coils are used then one may use a similar test-conditioning approach to explore inter-regional interactions, such as interhemispheric inhibition between the two primary motor cortices (Figure 1). Alternatively pulses may be delivered during a motor task, and the resulting effect on behaviour used to infer the stimulated region’s role in task performance, for example during a simple reaction time or movement selection task. See Reis et al1 for a summary of these techniques and their physiological basis.

Figure 1. TMS measures of motor cortical physiology. a) Eliciting a Motor Evoked Potential (MEP) from the primary motor cortex, b) Measures of corticospinal tract excitability, c) Using paired pulse stimulation to measure Intracortical inhibition, d) Using two TMS coils to measure Interhemispheric Inhibition.

Strokes that cause hemiparesis usually disrupt the corticospinal tract, and when testing the stroke hemisphere this may manifest as increased motor thresholds, flattened recruitment curves, or alternatively as the inability to elicit an evoked potential at all. An absent evoked potential in the acute post-stroke period is a poor prognostic indicator for motor recovery2,3 and at that stage these markers of corticospinal excitability, when obtainable, correlate strongly with clinical measures of motor performance.4 If these corticospinal excitability measures improve then they usually do so over the early weeks post-stroke, presumably reflecting spontaneous biological recovery around the infarct, and the physiological change is reflected in clinical improvement in this group. It has been a fairly consistent finding that the correlation between corticospinal excitability and clinical status declines with time, which may reflect reduced reliance on the original corticospinal projection once the network generating the motor output has reorganised. Some studies have shown hyper-excitability of the corticospinal tract from the non-stroke hemisphere during the acute phase in more severely affected patients, which is interpreted by some as a form of diaschisis.

Paired pulse measures have fairly reliably shown reduced inhibitory activity in the intracortical circuits after stroke. Such apparent disinhibition is hard to interpret in the stroke hemisphere, as these measures depend upon an unconditioned evoked potential of reasonable amplitude which may not be available or may require high stimulus intensities. However no such technical issue affects the intact hemisphere, and the absence or reduction of inhibition when tested in the contralesional primary motor cortex suggests a reduction in the tonic level of GABA-ergic inhibitory activity in intracortical circuits that extends far beyond the site of the stroke. In one study such intracortical disinhibition of the non-stroke hemisphere was seen in patients with cortical but not subcortical infarction,5 suggesting that this phenomenon may relate to interruption of the transcallosal projection between the motor cortices. Few longitudinal studies of intra-cortical excitability have been performed but on the basis of the data available it seems that in the acute period disinhibition is seen regardless of clinical status, but that by three months it has resolved in those patients with a better clinical outcome, such that a clinical–physiological correlation emerges at around that time.6 A recent meta-analysis of TMS studies has shown no overall abnormality of excitability in the intact hemisphere:7however if disinhibition were seen only in more severely affected patients then one may see clinical correlation without a group effect.

It is recognised that in healthy humans there is tonic inhibition of each hemisphere by its opposite, a situation that is likely to be important in the generation of unimanual versus bimanual movements. When this inter-hemispheric interaction is measured at rest with two TMS coils using a paired pulse conditioning approach there is robust inhibition. When tested in healthy subjects during a reaction time paradigm the baseline inhibition disappears or reverses as the onset of movement approaches. Murase and colleagues8found that such switching-off of interhemispheric inhibition was impaired in stroke patients, and that the extent of residual interhemispheric inhibition was greater in more severely affected patients. This result has been interpreted as suggesting that after stroke there is an imbalance of such interhemispheric interactions, with pathological inhibition of the recovering stroke hemisphere by the non-stroke hemisphere.

Interpretation of the physiological changes observed after stroke remains a matter of debate. TMS as a technique operates at the level of the whole system, drawing inferences from the effect of manipulations on the overall corticospinal output, but the pathological changes observed may be the result of dysfunction at one or more of several levels. These may include the effects of cytotoxic changes on local neurochemistry, altered inhibitory vs excitatory synaptic activity, or diaschisis due to disruption of inter-regional tracts. The TMS finding of wide- spread intracortical disinhibition is in keeping with MR Spectroscopy studies that show reduced cortical GABA content during this period after stroke.9 A rapid reduction in GABA is also seen in healthy humans as a response to motor training or to experimental deafferentation of one arm by ischaemic nerve block, which likewise causes intracortical disinhibition as assessed by TMS. In those contexts it is felt that such disinhibition creates a more favourable environment for synaptic plasticity to occur, and it is tempting to conclude that the same is occurring in the post-stroke period as a way of driving reorganisation of the motor output. It is also conceivable that disinhibition allows cortical regions that are disconnected from their usual corticospinal output projection to access instead the horizontal cortico-cortical connections that are prevalent in cortical layers 2 and 3, thereby reaching an alternative output projection. Such a phenomenon would allow for the shifts in cortical motor output maps that are well documented after stroke.10 In one longitudinal study the correlation between disinhibition and clinical status was strong at three months but then became weaker in the chronic phase.6 We interpreted this as suggesting that ongoing disinhibition becomes less important for motor function as the reorganised motor network becomes better established with time. Direct evidence for such a process is lacking however, and some would argue that disinhibition is an epiphenomenon rather than an adaptive response to injury. This alternative conclusion would be supported by the observation that reduced intracortical inhibition as measured by paired pulse TMS may be observed in other pathological states, including dystonia and Attention Deficit Hyperactivity Disorder.

The concept of an imbalance between the two hemispheres and of excessive interhemispheric inhibition of the stroke hemisphere has gained a lot of traction and has provided the rationale for therapeutic approaches that aim to redress it. Non-invasive brain stimulation, either by repetitive TMS or transcranial direct current stimulation (tDCS), can induce measurable changes in cortical excitability that outlast the period of stimulation. Depending on the stimulation paradigm used one can induce either increases or reductions lasting minutes or in some cases hours. The most common approaches are either to apply excitatory stimulation to the stroke hemisphere or alternatively inhibitory stimulation to the non-stroke hemisphere (Figure 2), the aim being to enhance the response to conventional therapy by stimulating either before or during treatment. The concept of an overactive non-stroke hemisphere resonates with the widely reproduced functional imaging finding of increased movement-related brain activation on that side in more severely affected patients, which may normalise as clinical recovery progresses.6

 

Figure 2. The interhemispheric rivalry model, whereby the intact hemisphere exerts a pathological degree of interhemispheric inhibition on the stroke hemisphere and hinders motor function in the paretic limb. This has given rise to the therapeutic strategies of either increasing excitability in the stroke hemisphere or reducing it in the intact hemisphere.

It is by no means clear however that this contralesional activity is the same phenomenon as that which generates pathological inhibition of the recovering hemisphere, or that it is necessarily maladaptive. There is evidence that at least some regions on the non-stroke side may support movement of the paretic side, such as the contralesional dorsal premotor cortex which displays increased functional connectivity to the primary motor cortex of the stroke in more affected patients and appears to support hand movement.11,12Furthermore a recent study suggested that reducing intact hemisphere excitability may in fact be detrimental to upper limb function in more impaired patients.3

As the role of contralesional brain regions in movement appears to differ depending upon factors such as clinical severity, extent of corticospinal tract disruption and possibly stroke location it would seem that reducing excitability on that side equally in all stroke patients may represent rather a blunt therapeutic approach. This is especially true of tDCS, whose effects incorporate most of the stimulated hemisphere. However, positive studies may be found in the literature for both repetitive TMS and tDCS when applied to either side of the brain (sometimes both), and although a comprehensive review of the outcomes is beyond the scope of this article the most promising approach appears to be inhibition of the non-stroke hemisphere by tDCS.13 Non-invasive brain stimulation has not as yet entered routine clinical practice however, and there are a number of reasons why this may be, such as the large number of stimulation protocols available and uncertainty regarding the optimal time to apply stimulation. However, for the reasons discussed above it is important to consider the heterogeneity of the clinical syndrome when designing further trials. Opinions differ as to whether progress will be made using a ‘one size fits all’ design, the hope being that larger sample sizes will take care of heterogeneity, or alternatively whether targeting stimulation according to clinical and physiological factors would have a greater chance of success. This is likely to be worth getting right, as a large negative study would present an obstacle to further investigation in this field. It is likely to be the case that applying brain stimulation to the right patients could significantly enhance the outcome of post-stroke rehabilitation, with a clinically meaningful reduction in resulting impairment and disability.

References

  1. Reis J, Swayne OB, Vandermeeren Y, Camus M, Dimyan MA, Harris-Love M, Perez MA, Ragert P, Rothwell JC, Cohen LG. Contribution of transcranial magnetic stimulation to the understanding of cortical mechanisms involved in motor control. J Physiol 2008; 586(2):325-51.
  2. Stinear CM, Barber PA, Smale PR, Coxon JP, Fleming MK, Byblow WD. Functional Potential in chronic stroke patients depends on corticospinal tract integrity. Brain 2007;130:170-180.
  3. Bradnam LV, Stinear CM, Barber PA, Byblow WD. Contralesional hemisphere control of the proximal paretic upper limb following stroke. Cereb Cortex. 2012 Nov;22(11):2662-71.
  4. Traversa R, Cicinelli P, Pasqualetti P, Filippi M, Rossini PM. Follow-up of interhemispheric differences of motor evoked potentials from the ‘affected’ and ‘unaffected’ hemispheres in human stroke. Brain Research 1998; 803:1-8.
  5. Manganotti P, Patuzzo S, Cortese F, Palermo A, Smania N, Fiaschi A. Motor disinhibition in affected and unaffected hemisphere in the early period of recovery after stroke. Clin Neurophysiol 2002; 113:936-943.
  6. Swayne OB, Rothwell JC, Ward NS, Greenwood RJ. Stages of Motor Output Reorganization after Hemispheric Stroke Suggested by Longitudinal Studies of Cortical Physiology. Cereb Cortex 2008; 18:1909- 1922.
  7. McDonnell MN, Stinear CM. TMS measures of motor cortex function after stroke: A meta-analysis. Brain Stimul. 2017 Jul – Aug;10(4):721-734.
  8. Murase N, Duque J, Mazzocchio R, Cohen LG. Influence of interhemispheric interactions on motor function in chronic stroke. Ann Neurol 2004; 55:400-409.
  9. Blicher JU, Near J, Næss-Schmidt E, Stagg CJ, Johansen-Berg H, Nielsen JF, Østergaard L, Ho YC. GABA levels are decreased after stroke and GABA changes during rehabilitation correlate with motor improvement. Neurorehabil Neural Repair 2015 Mar-Apr;29(3):278-86.
  10. Delvaux V, Alagona G, Gerard P, De Pasqua V, Pennisi G, de Noordhout AM. Post-stroke reorganization of hand motor area: a 1-year prospective follow-up with focal transcranial magnetic stimulation. Clin Neurophysiol 2003; 114:1217-1225
  11. Bestmann S, Swayne O, Blankenburg F, Ruff CC, Teo J, Weiskopf N, Driver J, Rothwell JC, Ward NS. The role of contralesional dorsal premotor cortex after stroke as studied with concurrent TMS-fMRI. J Neurosci 2010; 30(36):11926-37.
  12. Johansen-Berg H, Rushworth MF, Bogdanovic MD, Kischka U, Wimalaratna S, Matthews PM. The role of ipsilateral premotor cortex in hand movement after stroke. Proc Natl Acad Sci U S A 2002; 99:14518- 14523.
  13. Kang N, Summers JJ, Cauraugh JH. Transcranial direct current stimulation facilitates motor learning post- stroke: a systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2016 Apr;87(4):345-55.

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[WEB SITE] Doctors Successfully ‘Rewire’ The Brain Of People With Depression.(Video)

Americans spend billions of dollars each year on antidepressants, but the National Institutes of Health estimates that those medications work for only 60 percent to 70 percent of people who take them. In addition, the number of people with depression has increased 18 percent since 2005, according to the World Health Organization, which this year launched a global campaign encouraging people to seek treatment.

The Semel Institute for Neuroscience and Human Behavior at UCLA is one of a handful of hospitals and clinics nationwide that offer a treatment that works in a fundamentally different way than drugs. The technique, transcranial magnetic stimulation, beams targeted magnetic pulses deep inside patients’ brains — an approach that has been likened to rewiring a computer.

TMS has been approved by the FDA for treating depression that doesn’t respond to medications, and UCLA researchers say it has been underused. But new equipment being rolled out this summer promises to make the treatment available to more people.

“We are actually changing how the brain circuits are arranged, how they talk to each other,” said Dr. Ian Cook, director of the UCLA Depression Research and Clinic Program. “The brain is an amazingly changeable organ. In fact, every time people learn something new, there are physical changes in the brain structure that can be detected.”

Nathalie DeGravel, 48, of Los Angeles had tried multiple medications and different types of therapy, not to mention many therapists, for her depression before she heard about magnetic stimulation. She discussed it with her psychiatrist earlier this year, and he readily referred her to UCLA.

Within a few weeks, she noticed relief from the back pain she had been experiencing; shortly thereafter, her depression began to subside. DeGravel says she can now react more “wisely” to life’s daily struggles, feels more resilient and is  able to do much more around the house. She even updated her resume to start looking for a job for the first time in years.

During TMS therapy, the patient sits in a reclining chair, much like one used in a dentist’s office, and a technician places a magnetic stimulator against the patient’s head in a predetermined location, based on calibrations from brain imaging.

Dr. Andrew Leuchter talks with a patient who is about to undergo transcranial magnetic stimulation, which treats depression by sending magnetic pulses to a specific area of the brain. Credit: UCLA

The stimulator sends a series of magnetic pulses into the brain. People who have undergone the treatment commonly report the sensation is like having someone tapping their head, and because of the clicking sound it makes, patients often wear earphones or earplugs during a session.

TMS therapy normally takes 30 minutes to an hour, and people typically receive the treatment several days a week for six weeks. But the newest generation of equipment could make treatments less time-consuming.

“There are new TMS devices recently approved by the FDA that will allow patients to achieve the benefits of the treatment in a much shorter period of time,” said Dr. Andrew Leuchter, director of the Semel Institute’s TMS clinical and research service. “For some patients, we will have the ability to decrease the length of a treatment session from 37.5 minutes down to 3 minutes, and to complete a whole course of TMS in two weeks.”

Leuchter said some studies have shown that TMS is even better than medication for the treatment of chronic depression. The approach, he says, is underutilized.

“We are used to thinking of psychiatric treatments mostly in terms of either talk therapies, psychotherapy or medications,” Leuchter said. “TMS is a revolutionary kind of treatment.”

Bob Holmes of Los Angeles is one of the 16 million Americans who report having a major depressive episode each year, and he has suffered from depression his entire life. He calls the TMS treatment he received at UCLA Health a lifesaver.

“What this did was sort of reawaken everything, and it provided that kind of jolt to get my brain to start to work again normally,” he said.

Doctors are also exploring whether the treatment could also be used for a variety of other conditions including schizophrenia, epilepsy, Parkinson’s disease and chronic pain.

“We’re still just beginning to scratch the surface of what this treatment might be able to do for patients with a variety of illnesses,” Leuchter said. “It’s completely noninvasive and is usually very well tolerated.”

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[ARTICLE] Insights from TMS into recovery after stroke – Full Text

Orlando Swayne completed a PhD at UCL and a fellowship at the NINDS in the US, investigating mechanisms of post-stroke neuroplasticity. He is a Consultant Neurologist at the National Hospital for Neurology & Neurosurgery (NHNN) on the Neurorehabilitation Unit. He also works as a Neurologist at Northwick Park Hospital and is an Honorary Senior Lecturer at the UCL Institute of Neurology.

Correspondence to: Orlando Swayne,
National Hospital for Neurology & Neurosurgery, Queen Square,
London WC1N 3BG, UK.
Acknowledgments: Orlando received funding from the UCLH Biomedical Research Centre.
Conflicts of interest statement: None declared
Provenance and peer review: Submitted and externally reviewed.
Date submitted: 20/8/17
Date submitted after peer review: 27/10/17 Acceptance date: 9/11/17
To cite: Swayne O. ACNR 2017;17(2):11-13.
Published online: 11/12/17


Transcranial Magnetic Stimulation (TMS) is a non-invasive technique whereby an electro-magnetic coil held over the scalp is used to induce a brief electrical current in the cortex of the underlying brain. TMS may be used in a number of ways to gain in vivo insights into brain physiology and has provided a window into the cascade of physiological changes that occur following stroke. When stimulating the primary motor cortex in a healthy subject stimuli of an intensity above the motor threshold will give rise to a detectable evoked potential in a peripheral muscle. As the stimulus intensity is gradually increased the evoked potentials increase in amplitude up to a maximum, giving rise to a measurable recruitment curve. The motor threshold and the recruitment curve both provide measures of the excitability of the corticospinal tract. This incorporates the excitability of axons within the motor cortex, synaptic inputs onto pyramidal cells and the spinal alpha motor neuron pool. In paired pulse TMS a sub-threshold pulse is delivered a few milliseconds before a second suprathreshold pulse, both through the same coil. The first pulse conditions the response to the second, resulting in inhibition or facilitation depending upon the inter-stimulus interval and reflecting the activity in intracortical regulatory circuits. If two separate TMS coils are used then one may use a similar test-conditioning approach to explore inter-regional interactions, such as interhemispheric inhibition between the two primary motor cortices (Figure 1). Alternatively pulses may be delivered during a motor task, and the resulting effect on behaviour used to infer the stimulated region’s role in task performance, for example during a simple reaction time or movement selection task. See Reis et al1 for a summary of these techniques and their physiological basis.

Figure 1. TMS measures of motor cortical physiology. a) Eliciting a Motor Evoked Potential (MEP) from the primary motor cortex, b) Measures of corticospinal tract excitability, c) Using paired pulse stimulation to measure Intracortical inhibition, d) Using two TMS coils to measure Interhemispheric Inhibition.

 

Paired pulse measures have fairly reliably shown reduced inhibitory activity in the intracortical circuits after stroke. Such apparent disinhibition is hard to interpret in the stroke hemisphere, as these measures depend upon an unconditioned evoked potential of reasonable amplitude which may not be available or may require high stimulus intensities. However no such technical issue affects the intact hemisphere, and the absence or reduction of inhibition when tested in the contralesional primary motor cortex suggests a reduction in the tonic level of GABA-ergic inhibitory activity in intracortical circuits that extends far beyond the site of the stroke. In one study such intracortical disinhibition of the non-stroke hemisphere was seen in patients with cortical but not subcortical infarction,5 suggesting that this phenomenon may relate to interruption of the transcallosal projection between the motor cortices. Few longitudinal studies of intra-cortical excitability have been performed but on the basis of the data available it seems that in the acute period disinhibition is seen regardless of clinical status, but that by three months it has resolved in those patients with a better clinical outcome, such that a clinical–physiological correlation emerges at around that time.6 A recent meta-analysis of TMS studies has shown no overall abnormality of excitability in the intact hemisphere:7 however if disinhibition were seen only in more severely affected patients then one may see clinical correlation without a group effect.

It is recognised that in healthy humans there is tonic inhibition of each hemisphere by its opposite, a situation that is likely to be important in the generation of unimanual versus bimanual movements. When this inter-hemispheric interaction is measured at rest with two TMS coils using a paired pulse conditioning approach there is robust inhibition. When tested in healthy subjects during a reaction time paradigm the baseline inhibition disappears or reverses as the onset of movement approaches. Murase and colleagues8 found that such switching-off of interhemispheric inhibition was impaired in stroke patients, and that the extent of residual interhemispheric inhibition was greater in more severely affected patients. This result has been interpreted as suggesting that after stroke there is an imbalance of such interhemispheric interactions, with pathological inhibition of the recovering stroke hemisphere by the non-stroke hemisphere.

Interpretation of the physiological changes observed after stroke remains a matter of debate. TMS as a technique operates at the level of the whole system, drawing inferences from the effect of manipulations on the overall corticospinal output, but the pathological changes observed may be the result of dysfunction at one or more of several levels. These may include the effects of cytotoxic changes on local neurochemistry, altered inhibitory vs excitatory synaptic activity, or diaschisis due to disruption of inter-regional tracts. The TMS finding of wide- spread intracortical disinhibition is in keeping with MR Spectroscopy studies that show reduced cortical GABA content during this period after stroke.9 A rapid reduction in GABA is also seen in healthy humans as a response to motor training or to experimental deafferentation of one arm by ischaemic nerve block, which likewise causes intracortical disinhibition as assessed by TMS. In those contexts it is felt that such disinhibition creates a more favourable environment for synaptic plasticity to occur, and it is tempting to conclude that the same is occurring in the post-stroke period as a way of driving reorganisation of the motor output. It is also conceivable that disinhibition allows cortical regions that are disconnected from their usual corticospinal output projection to access instead the horizontal cortico-cortical connections that are prevalent in cortical layers 2 and 3, thereby reaching an alternative output projection. Such a phenomenon would allow for the shifts in cortical motor output maps that are well documented after stroke.10 In one longitudinal study the correlation between disinhibition and clinical status was strong at three months but then became weaker in the chronic phase.6 We interpreted this as suggesting that ongoing disinhibition becomes less important for motor function as the reorganised motor network becomes better established with time. Direct evidence for such a process is lacking however, and some would argue that disinhibition is an epiphenomenon rather than an adaptive response to injury. This alternative conclusion would be supported by the observation that reduced intracortical inhibition as measured by paired pulse TMS may be observed in other pathological states, including dystonia and Attention Deficit Hyperactivity Disorder.

The concept of an imbalance between the two hemispheres and of excessive interhemispheric inhibition of the stroke hemisphere has gained a lot of traction and has provided the rationale for therapeutic approaches that aim to redress it. Non-invasive brain stimulation, either by repetitive TMS or transcranial direct current stimulation (tDCS), can induce measurable changes in cortical excitability that outlast the period of stimulation. Depending on the stimulation paradigm used one can induce either increases or reductions lasting minutes or in some cases hours. The most common approaches are either to apply excitatory stimulation to the stroke hemisphere or alternatively inhibitory stimulation to the non-stroke hemisphere (Figure 2), the aim being to enhance the response to conventional therapy by stimulating either before or during treatment. The concept of an overactive non-stroke hemisphere resonates with the widely reproduced functional imaging finding of increased movement-related brain activation on that side in more severely affected patients, which may normalise as clinical recovery progresses.6

Figure 2. The interhemispheric rivalry model, whereby the intact hemisphere exerts a pathological degree of interhemispheric inhibition on the stroke hemisphere and hinders motor function in the paretic limb. This has given rise to the therapeutic strategies of either increasing excitability in the stroke hemisphere or reducing it in the intact hemisphere.

 

It is by no means clear however that this contralesional activity is the same phenomenon as that which generates pathological inhibition of the recovering hemisphere, or that it is necessarily maladaptive. There is evidence that at least some regions on the non-stroke side may support movement of the paretic side, such as the contralesional dorsal premotor cortex which displays increased functional connectivity to the primary motor cortex of the stroke in more affected patients and appears to support hand movement.11,12Furthermore a recent study suggested that reducing intact hemisphere excitability may in fact be detrimental to upper limb function in more impaired patients.3

As the role of contralesional brain regions in movement appears to differ depending upon factors such as clinical severity, extent of corticospinal tract disruption and possibly stroke location it would seem that reducing excitability on that side equally in all stroke patients may represent rather a blunt therapeutic approach. This is especially true of tDCS, whose effects incorporate most of the stimulated hemisphere. However, positive studies may be found in the literature for both repetitive TMS and tDCS when applied to either side of the brain (sometimes both), and although a comprehensive review of the outcomes is beyond the scope of this article the most promising approach appears to be inhibition of the non-stroke hemisphere by tDCS.13 Non-invasive brain stimulation has not as yet entered routine clinical practice however, and there are a number of reasons why this may be, such as the large number of stimulation protocols available and uncertainty regarding the optimal time to apply stimulation. However, for the reasons discussed above it is important to consider the heterogeneity of the clinical syndrome when designing further trials. Opinions differ as to whether progress will be made using a ‘one size fits all’ design, the hope being that larger sample sizes will take care of heterogeneity, or alternatively whether targeting stimulation according to clinical and physiological factors would have a greater chance of success. This is likely to be worth getting right, as a large negative study would present an obstacle to further investigation in this field. It is likely to be the case that applying brain stimulation to the right patients could significantly enhance the outcome of post-stroke rehabilitation, with a clinically meaningful reduction in resulting impairment and disability.

References

  1. Reis J, Swayne OB, Vandermeeren Y, Camus M, Dimyan MA, Harris-Love M, Perez MA, Ragert P, Rothwell JC, Cohen LG. Contribution of transcranial magnetic stimulation to the understanding of cortical mechanisms involved in motor control. J Physiol 2008; 586(2):325-51.
  2. Stinear CM, Barber PA, Smale PR, Coxon JP, Fleming MK, Byblow WD. Functional Potential in chronic stroke patients depends on corticospinal tract integrity. Brain 2007;130:170-180.
  3. Bradnam LV, Stinear CM, Barber PA, Byblow WD. Contralesional hemisphere control of the proximal paretic upper limb following stroke. Cereb Cortex. 2012 Nov;22(11):2662-71.
  4. Traversa R, Cicinelli P, Pasqualetti P, Filippi M, Rossini PM. Follow-up of interhemispheric differences of motor evoked potentials from the ‘affected’ and ‘unaffected’ hemispheres in human stroke. Brain Research 1998; 803:1-8.
  5. Manganotti P, Patuzzo S, Cortese F, Palermo A, Smania N, Fiaschi A. Motor disinhibition in affected and unaffected hemisphere in the early period of recovery after stroke. Clin Neurophysiol 2002; 113:936-943.
  6. Swayne OB, Rothwell JC, Ward NS, Greenwood RJ. Stages of Motor Output Reorganization after Hemispheric Stroke Suggested by Longitudinal Studies of Cortical Physiology. Cereb Cortex 2008; 18:1909- 1922.
  7. McDonnell MN, Stinear CM. TMS measures of motor cortex function after stroke: A meta-analysis. Brain Stimul. 2017 Jul – Aug;10(4):721-734.
  8. Murase N, Duque J, Mazzocchio R, Cohen LG. Influence of interhemispheric interactions on motor function in chronic stroke. Ann Neurol 2004; 55:400-409.
  9. Blicher JU, Near J, Næss-Schmidt E, Stagg CJ, Johansen-Berg H, Nielsen JF, Østergaard L, Ho YC. GABA levels are decreased after stroke and GABA changes during rehabilitation correlate with motor improvement. Neurorehabil Neural Repair 2015 Mar-Apr;29(3):278-86.
  10. Delvaux V, Alagona G, Gerard P, De Pasqua V, Pennisi G, de Noordhout AM. Post-stroke reorganization of hand motor area: a 1-year prospective follow-up with focal transcranial magnetic stimulation. Clin Neurophysiol 2003; 114:1217-1225
  11. Bestmann S, Swayne O, Blankenburg F, Ruff CC, Teo J, Weiskopf N, Driver J, Rothwell JC, Ward NS. The role of contralesional dorsal premotor cortex after stroke as studied with concurrent TMS-fMRI. J Neurosci 2010; 30(36):11926-37.
  12. Johansen-Berg H, Rushworth MF, Bogdanovic MD, Kischka U, Wimalaratna S, Matthews PM. The role of ipsilateral premotor cortex in hand movement after stroke. Proc Natl Acad Sci U S A 2002; 99:14518- 14523.
  13. Kang N, Summers JJ, Cauraugh JH. Transcranial direct current stimulation facilitates motor learning post- stroke: a systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2016 Apr;87(4):345-55.

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via Insights from TMS into recovery after stroke | ACNR | Online Neurology Journal

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[WEB SITE] Magnetic brain stimulation helps “unlearn” crippling fear of heights

 

New research suggests a little magnetic brain stimulation prior to being exposed to your greatest fear...

New research suggests a little magnetic brain stimulation prior to being exposed to your greatest fear in a VR headset could help you “unlearn” your anxiety response(Credit: DanRoss/Depositphotos)

Advances in technology over the last decade have led to a swift rise in the volume of research surrounding transcranial magnetic stimulation (TMS) and its therapeutic effects. A team from the Würzburg University Hospital in Germany has just published a new study demonstrating how TMS, in conjunction with a virtual reality experience, can help alleviate anxiety disorders and essentially help people “unlearn” fears.

Transcranial magnetic stimulation works by directing a targeted magnetic field toward specific areas in the brain. Depending on the frequencies delivered this can either stimulate or inhibit the brain activity of the targeted area. Initially conceived as a research tool allowing scientists to understand exactly what roles certain areas of the brain play, TMS has more recently been explored as a potential new tool for treating an assortment of problems.

TMS devices have already been approved to treat migraines and some major depressive disorders, but other research is looking into its uses as a learning aid and a way to help visually-impaired people navigate the world.

This new study looks at how the technology could improve a patient’s response when used in conjunction with a more traditional treatment method. Anxiety disorders are incredibly debilitating for many, from social phobias to more specific problems such as a fear of heights. Classically, the treatment for people with these disorders has been a type of cognitive behavioral therapy where one is exposed to the source of their anxiety under the supervision of a psychologist.

The team at the Würzburg University Hospital decided to examine whether this kind of classic therapy could be improved using TMS. Previous studies have shown that by targeting the frontal lobe with magnetic stimulation an anxiety response can be reduced, but the new research looks at how this could be incorporated into a specific treatment method for a targeted anxiety.

Even though the subject knows it is fake, exposure to great heights in a virtual reality...

Even though the subject knows it is fake, exposure to great heights in a virtual reality headset still triggers an anxiety response in sufferers(Credit: VTplus)

Thirty-nine subjects with an active fear of heights were split into two groups, including a control group which received fake TMS. The groups received 20 minutes of either real or fake TMS directed at the ventral medial prefrontal cortex, followed by virtual reality exposure to a dizzying height. After two sessions the group treated with the TMS prior to VR exposure exhibited reduced anxiety and avoidance symptoms compared to the control group that didn’t receive the TMS.

“The findings demonstrate that all participants benefit considerably from the therapy in virtual reality and the positive effects of the intervention are still clearly visible even after three months,” explains Professor Martin J. Herrmann, one of the researchers working on the study.

The researchers suggest that adding TMS and VR to an already well-proven treatment process increases the overall efficacy and essentially helps the brain “unlearn” its anxiety responses. The next phase for the study is to look at other forms of anxiety and see if the process is equally effective.

And the next fear that is being tackled? Arachnophobia.

The research was published in the journal Brain Stimulation.

Source: Würzburg University Hospital

Source: Magnetic brain stimulation helps “unlearn” crippling fear of heights

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