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For my special experience, I reached out to a woman on Twitter who was experimenting with VR therapy for her Chronic Pain resulting from cancer treatment. She advised "VR therapy does help" she suggested that more full sense immersion with 3D HD video and audio is more effective in her experience. She also advised that Pre-Covid, Chemo centers offered them for patients, but now she has resorted to purchasing her own unit.

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@mavizzle @ThanksCancer Just now saw the ?  Not on twitter as much but VR therapy does help. At least for me. we need more full sense immersion or at least HD 360 video with audio. there isn't as much out there to give good variety. Chemo centers had units pre COVID Now - I bought my own.

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@mavizzle @ThanksCancer Just now saw the ?  Not on twitter as much but VR therapy does help. At least for me. we need more full sense immersion or at least HD 360 video with audio. there isn't as much out there to give good variety. Chemo centers had units pre COVID Now - I bought my own.

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@Lex_in_CO @ThanksCancer Hey, I know this tweet is from awhile back but how did the VR Therapy go? I'm working on a college paper about its effectiveness.

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Something went wrong, but don’t fret — let’s give it another shot.

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Just now saw the ? Not on twitter as much but VR therapy does help. At least for me. we need more full sense immersion or at least HD 360 video with audio. there isn't as much out there to give good variety. Chemo centers had units pre COVID Now - I bought my own.
— Lex (@Lex_in_CO) April 17, 2021

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@mavizzle @ThanksCancer Just now saw the ?  Not on twitter as much but VR therapy does help. At least for me. we need more full sense immersion or at least HD 360 video with audio. there isn't as much out there to give good variety. Chemo centers had units pre COVID Now - I bought my own.

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@Lex_in_CO @ThanksCancer Hey, I know this tweet is from awhile back but how did the VR Therapy go? I'm working on a college paper about its effectiveness.

# data[].attributes.attachment_link.metadata.attachment_props.original_text
@mavizzle @ThanksCancer Just now saw the ?  Not on twitter as much but VR therapy does help. At least for me. we need more full sense immersion or at least HD 360 video with audio. there isn't as much out there to give good variety. Chemo centers had units pre COVID Now - I bought my own.

# data[].attributes.attachment_link.metadata.attachment_props.text
@mavizzle @ThanksCancer Just now saw the ?  Not on twitter as much but VR therapy does help. At least for me. we need more full sense immersion or at least HD 360 video with audio. there isn't as much out there to give good variety. Chemo centers had units pre COVID Now - I bought my own.

# data[].attributes.attachment_link.metadata.attachment_props.referenced_tweets[].text
@Lex_in_CO @ThanksCancer Hey, I know this tweet is from awhile back but how did the VR Therapy go? I'm working on a college paper about its effectiveness.

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In this article, a study was done to determine the difference in brain development in opioid users who suffer from CLBP. It was shown that there are many changes that occur in the brain even before addiction can be identified. I was shocked by the findings in this article because the size of the brain can be altered by opioids. In the article it says "CLBP patients medicated with opioid analgesics are at an increased risk for developing long-term misuse, dependence, or addiction." This is the reason I am searching for an alternative in VR. From what we know as of now, there is no risk for addiction or misuse with VR.

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Introduction

Chronic low-back pain (CLBP) is a leading cause of disability worldwide and its prevalence is on the rise. OA are commonly prescribed for the management of CLBP and the most frequent indication for the use of prescription opioids in primary care settings is for CLBP. Opioids pose a high risk for addiction because their analgesic effects are mediated primarily via binding to the µ-opioid receptor. Once started on these medications, CLBP patients frequently continue using opioids for years and long-term opioid use for non-cancer pain dose-dependently increases the risk of overdose, misuse, and addiction. The misuse of prescription opioids contributes significantly to the public health crisis that we now face. In fact, a majority of today's heroin abusers were introduced to opioids via medical prescriptions. Despite their widespread use and associated morbidity/mortality, an understanding of how opioids affect brain circuitry in chronic pain patients is lacking. Such knowledge is crucial for a full understanding of the neurobiology of opioid addiction and identifying predictors of the risk of opioid misuse and addiction.

Short-term administration of increasing doses of OA in healthy humans undergoing fMRI shows that the limbic brain (amygdala, para-hippocampal area, and anterior insula) is exquisitely sensitive to low doses of opiates, while higher doses decrease the perception of acute pain with a corresponding decrease in brain activity in the thalamus, primary and secondary somatosensory areas, insula, and anterior cingulate cortex (ACC). Collectively, these areas are consistently active in response to acute pain.

However, the effects of chronic µ-opioid agonists on brain activity, network topology, and structure in chronic pain patients are largely unknown. Younger et al. studied the brain structure in 10 CLBP patients before and one month after the administration of morphine and identified a decrease in amygdala volume and increase in the ACC, hypothalamus and prefrontal cortex volumes relative to placebo. Martucci et al. investigated the effect of OA on reward-related decision making and brain circuitry in a cohort of fibromyalgia patients taking a stable dose of OA. Interestingly, they observed that the brain response during reward anticipation in medicated patients was not different from that of healthy controls in the nucleus accumbens and medial prefrontal cortex. Only unmedicated patients showed abnormal responses to reward anticipation in the medial prefrontal cortex. These results, unexpectedly, demonstrate a "normalization" of neural responses to rewarding stimuli in chronic pain patients medicated with OA.

In this article we study the brain structure and function of CLBP patients medicated with OA with no evidence of misuse and compare them to unmedicated CLBP patients and healthy controls. Given that the limbic system is rich in opioid receptors and the recent evidence supporting the critical role of the limbic system in chronic pain, our starting hypothesis was that the limbic brain of medicated patients should be significantly altered compared to non-medicated patients and healthy controls.

Material and methods

Participants

Eleven chronic low-back pain patients treated with opioid analgesics (CLBP-op), 30 chronic low-back pain patients not medicated with opioid analgesics (CLBP-no-op), and 30 healthy controls (HC) participated in this study. All CLBP patients reported low back pain of at least 30 out of 100 on the visual analogue scale (VAS; 0-100, where 100 = maximum imaginable pain and 0 = no pain) for at least 1 year. All CLBP-op patients were prescribed OA by their physicians for at least 1 year, except one patient who had been taking them for 4 months at the time of the study. Patients' prescription were confirmed online using the Connecticut Prescription Monitoring and Reporting System ( https://connecticut.pmpaware.net/login). Participants were excluded if they reported aberrant drug taking behavior at the intake visit, pain at other locations, systemic illnesses, psychiatric diseases, history of traumatic brain injury, or if they tested positive on a urine toxicology test for drugs other than opioid analgesics. All patients reported no or less than mild depression (i.e. Beck's Depression Inventory (BDI) scores between 14 and 19) except 3 CLBP-op and 3 CLBP-no-op patients who reported moderate depression (BDI 28; see for complete demographic and clinical data). All participants signed a consent form for the study which was approved by the Yale University Institutional Review Board.

Magnetic resonance imaging

Participants underwent an anatomical T1-weighted scan and two-consecutive 6-minute long resting-state functional (fMRI) scans. All imaging data was collected on a Siemens 3 T Trio magnet equipped with a 32-channel head-coil. The T1-weighted acquisition used a 3 D MPRAGE sequence with the following parameters: TR/TE = 1900/2.52 ms, flip angle =9°, matrix = 256 x 256 with 176-1mm slices acquired in the same orientation as the functional data. During the functional scans, participants were asked to stare at a fixed cross hair. The fMRI sequence had the following parameters: TR/TE = 1000/30.0 ms, flip angle = 60°, matrix = 110 x 110 x 60 with 2-mm isotropic voxels, and an acceleration factor of 4.

Subcortical volume calculations

Structural data were analyzed with the standard automated processing stream of the Functional Magnetic Resonance Imaging of the Brain's (FMRIB) software library (FSL), version 5.0.10, which shows high reliability across laboratories. The processing sequence includes skull removal, a two-stage linear subcortical registration, and segmentation using FMRIB's Integrated Registration and Segmentation Tool (FIRST). The volumes of the right and left nucleus accumbens (NAc), amygdala, hippocampus and thalamus were calculated for each participant and normalized to standard Montreal Neurologic Institute (MNI) space. The normalization coefficient was calculated using FSL's SIENAX. Quality control included: (i) visual inspection of subcortical segmentation to identify gross mismatches between underlying anatomy and FIRST output; (ii) identification and exclusion of outliers defined using Tukey's method; and (iii) comparison of signal-to-noise ratio (SNR) within each subcortical structure across groups. SNR was calculated as the mean signal within a certain structure minus the mean signal outside the brain divided by the standard deviation of the signal outside the brain. Outliers were defined independently for each structure. One participant's data was excluded as such; importantly, removing this individual did not change our statistical results.

Functional MRI preprocessing

Two 6-minute long resting-state fMRI scans were acquired consecutively while participants stared at a fixed cross hair. The preprocessing of each participant's fMRI time series was performed using FSL's Expert Analysis Tool (FEAT). Preprocessing included skull removal using Brain Extraction Tool (BET), motion correction, band pass filtering (0.008-0.2 Hz), and spatial smoothing (5-mm full width at half maximum Gaussian blur). Several sources of spurious variance were removed from the data with linear regression. The 6 parameters obtained by rigid head motion correction along with their temporal derivatives and 10 components derived from noise regions of interest (ROIs) were regressed out from the data. The latter components were identified following an anatomical approach as described previously. Briefly, cerebrospinal fluid and white matter average time series were extracted from each subject's fMRI data based on masks derived from the high-resolution anatomical image using FSL's FAST. Next, principal component analysis was applied to obtain the first 5 white matter and first 5 CSF components. After preprocessing, the functional scans were registered into the MNI space. Registration to high resolution structural and/or MNI images was carried out using FLIRT. Registration from high resolution structural to MNI space was then further refined using FNIRT nonlinear registration.

Spectral analysis

Spectral analysis was performed using custom Matlab (The MathWorks, 2018) routines and is similar to previously reported methods. The frequency power of the BOLD signal was determined voxel-wise using Welch's method and normalized by dividing by total power. This normalization was necessary as the absolute power of BOLD remains unknown simply because the absolute intensity of BOLD signal in time space is also unknown and assigned an arbitrary value in all standard fMRI analyses. The average power of each frequency band, slow-5 (0.01-0.027 Hz), slow-4 (0.027-0.073 Hz), slow-3 (0.073-0.198 Hz) and slow-2 (0.198-0.5 Hz), was calculated at each voxel and converted into 4 different maps for each subject. Individual subjects ' maps were transformed into standard space as described in the preprocessing section and multiplied by a standard gray matter mask. Subject-level maps were transformed to z-score maps by subtracting the mean voxel-wise power for the entire brain and dividing by the standard deviation. Group differences were generated using permutation based inference (p< 0.05). They were tested against 10,000 random permutations, which inherently corrects for multuple comparisons. Clusters were identified using threshold-free cluster enhancement method(TFCE).

Statistical analyses

Statistical analyses of demographic and clinical variables and of extracted sub-cortical volumes were performed using Statistica Software (TIBCO, Inc.). Between-group analysis was performed using general linear model or ANOVA. We used linear regression analyses to investigate the relationships between reported pain according to VAS scores or levels of inflammatory markers and brain measures

Results

Demographic and clinical variables

CLBP-op patients were significantly older (p < 10 −3, ANOVA post-hoc comparisons) than CLBP-no-op and HC subjects. The 3 groups did not differ in terms of the distributions of genders. Clinically, CLBP-op reported significantly larger (p < 10 −3) BDI depression scores and larger (p < 0.01) BAI anxiety scores. CLBP-op patients experienced a significantly higher pain intensity than CLBP-no-op (CLBP-op VAS = 69.1 ± 5.2 (mean ± SEM); CLBP-no-op = 46.8 ± 3.2; p < 10 −3, unpaired t-test) for a longer duration of time (CLBP-op = 11.9 ± 1.6 years; CLBP-no-op = 5.4 ± 1.0, p < 0.01). CLBP-op patients also demonstrated significantly more pain catastrophizing (p < 0.05). These results are summarized in .

Nucleus accumbens and thalamic volumes are compromised in CLBP patients on opioids

We compared subcortical volumes between the groups extracted using FIRST after correcting for age, gender, and intracranial volume. Group effects were significant for the NAc (p = 0.014, effect size partial-η = 0.12) (adding left and right) and close to significant for the thalamus (p = 0.06, partial-η = 0.07) (). Post-hoc comparisons showed that both CLBP-op (p = 0.004, Cohen's d = 0.83) and CLBP-no-op (p = 0.018, Cohen's d = 0.67) had a significantly smaller NAc compared to healthy controls, while only CLBP-op patients exhibited a significantly smaller thalamus relative to both CLBP-no-op patients (p = 0.01; Cohen's d = 0.56) and healthy control subjects (p = 0.0014;Cohen's d  = 0.83) . Amygdala and hippocampus volumes did not show any group effects. We repeated the volumetric comparisons after including potential confounders in our model like measures of depression, or anxiety which can be independently associated with cortical and sub-cortical changes. shows that results remain practically the same. Importantly, SNR group comparisons revealed a significant drop in SNR in all structures examined in the CLBP-op group (). This observation prompted us to repeat our volumetric comparisons after correcting for SNR in our GLM model, but group differences presented in Figure 1 persisted, if not, slightly increased (). We also examined the relationship between clinical variables and volumetric measures in medicated and unmedicated patients separately using correlation analyses to check whether observed group differences scale with pain intensity or duration or measures of depression or anxiety. shows that none of the clinical measures showed significant correlation to the volumetric measures .

CLBP-op have a different pattern of power spectral density changes

We also wanted to examine whether structural changes observed in CLBP-op patients is accompanied by altered brain activity dynamics collected during resting state scans. Therefore, we calculated the voxel wise power amplitude of spectral density (PSD) normalized by the sum across the whole frequency range. The amplitude of PSD of BOLD signal exhibits consistent regional distribution across studies, and moderate-to-high intra-subject reliability. In addition, it has been repeatedly shown to identify specific changes in clinical populations, including chronic pain patients. Germane to the current study, we recently identified that loss of PSD within the slow-5 (0.01-0.027 Hz) frequency band of the NAc is a reproducible signature of CLBP. Therefore, we wanted to test whether long-term exposure to opioid analgesics changes this signature. This is an important question given that the NAc is rich in opioid receptors, which are directly involved in rewarding and aversive learning, and both acute and chronic pain in humans. Slow-5 frequency maps from the 3 groups were entered into an ANCOVA (corrected for age, gender) within the bilateral NAc ROI and the differences between the groups (i.e. F-test) were significant (p < 0.05, ROI corrected). Figure 5A-C shows loss of slow-5 PSD within the NAc of CLBP-no-op and CLBP-op patients compared to healthy controls, but no significant difference was observed between CLBP-no-op and CLBP-op patients. In addition, we examined group differences in PSD of the slow-4 and slow-3 frequency bands using a similar approach. While the ANCOVA analysis did not reveal any significant differences, Figure5D-E shows loss of PSD within the slow-4 frequency band (0.027-0.073 Hz) specific to CLBP-op patients compared to healthy controls when the groups were compared post-hoc.

Discussion

CLBP patients medicated with opioid analgesics are at an increased risk for developing long-term misuse, dependence, or addiction. The neurobiological determinants of this risk are still unknown. Our data suggests that chronic treatment with opioid analgesics is associated with significant alterations in the structure and function of the limbic brain and thalamus before the appearance of any aberrant medication taking behavior. As such, both CLBP-no-op and CLBP-op patients exhibit decreased NAc volumes compared to healthy controls. In addition, only CLBP-op group exhibited a significant drop in thalamic volume compared to CLBP-no-op and healthy controls. Altered subcortical volume was accompanied with a loss of NAc PSD in the slow-5 (0.01-0.027 Hz) frequency band of all CLBP patients and a loss of PSD in the slow-4 (0.027-0.073 Hz) frequency band only in CLBP-op cohort.

This is one of the very few studies examining the long term effects of opioid analgesics on the brain of CLBP pain patients. Both prescription and illicit opioids (e.g. heroin) exert their analgesic and addictive effects primarily through the µ-opioid receptor. The binding of opioids in the limbic circuitry plays a critical role in analgesia, learning and value-based decision making, and hedonic processes. For example, the infusion of naloxone, a µ-opioid receptor antagonist, into the basolateral amygdala decreases lever pressing for food in deprived rodents previously trained to associate lever pressing with delivery of a sucrose reward. On the other hand, infusion of a µ-opioid receptor agonist into the ventral striatum, which encompasses the NAc, leads to analgesia and increased palatability (i.e. hedonic value) of food. In humans, µ-opioid receptor agonists enhance the pleasantness of drinks with high levels of sweetness. It is widely argued that the ventral striatum and medial prefrontal cortex encode the subjective value of all aversive and rewarding stimuli on a common scale. Specifically, ventral striatum and medial prefrontal cortex responses to rewards including food, money, and addictive substances, correlate with subjective ratings of reward value in humans such as food liking and magnitude of drug craving, and their activity tracks also back pain intensity. Importantly, one recent study showed that increased medial prefrontal cortex activity in response to alcohol cues predicts the risk of relapse in abstinent alcohol-dependent individuals. Our results suggest that, consistent with the distribution of opioid receptors in the brain and the role of these receptors in these areas in value-based decision-making and pain, treatment with opioid based medications in chronic pain might exert its long-term effects on behaviors such as aberrant drug use via action within the limbic brain.

We also determined that long-term treatment with opioid-based medications did not alter the NAc slow-5 PSD in CLBP patients. This is an important observation given that the loss of slow-5 PSD within the NAc is a robust signature of CLBP. It implies that chronic opioid agonists binding in the NAc may not be able to reverse a central nervous system functional signature of the state of being in chronic pain. Nevertheless, patients chronically treated with opioids showed loss of slow-4 PSD, suggesting that this latter frequency band is sensitive to OA treatment.

Opioid agonists can reduce water content in brain slices hence decreasing the number of protons and leading to a weaker T1 signal. The effect of opioid agonists on water movement may therefore explain the consistent drop in SNR across all studied subcortical areas observed in CLBP-op patients. Young et al. reported a drop in amygdala volume following the long-term administration of prescription opioids compared to placebo in CLBP patients using tensor based morphometry, which is different from the subcortical extraction technique we used in this manuscript. While Upadhyay et al. reported also that opioid dependent individuals exhibit decreased amygdala volumes, Seifert et al. reported only a drop in left NAc volume. Chronic morphine administration in animals have been shown to reduce the size but not the number of dopaminergic neurons in the ventral tegmental area, induce remodeling of dendritic spines in the NAc and medial prefrontal cortex, and disinhibit mesolimbic dopaminergic firing. The effect of chronic morphine administration on thalamic structure is still unclear. However, neurochemical studies show that acute morphine administration decreases glucose utilization and the BOLD signal, while chronic administration decreases the level of glutamate, an excitatory neurotransmitter, in the thalamus hence inducing a generalized decrease in activity. Whether this decrease in activity is reflected by the volumetric shrinkage we observed remains to be determined. Interestingly, a projection from the paraventricular thalamus to the NAc has been shown to be necessary and sufficient for opioid withdrawal induced physical signs and aversive memory in rodents. Taken together, this structural brain data points to an association between thalamic and limbic brain changes and opioid use or misuse. It is still however unknown whether these changes are induced by chronic intake of opioid analgesics or predate the start of treatment. Well powered longitudinal within-subject studies using different structural analysis algorithms are needed to form a complete picture of the brain of chronic pain patients prescribed opioid analgesics.

Our study had some limitations, most notably the sample size of CLBP-op patients. Despite the modest number of CLBP-op patients, we were still able to observe the loss of NAc slow-5 PSD that we previously reported. It also remains unclear whether the functional (i.e. loss of slow-4 PSD) and structural changes (i.e. loss of thalamic volume) observed in chronically medicated patients relate to chronic back pain or to the effects of long-term OA use. Future within subject OA treatment studies are needed to test the reproducibility of the results, and to incorporate a placebo (or active control) arm to corroborate or not the specificity of the results observed in this investigation.

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Brain Structure and Function of Chronic Low Back Pain Patients on Long-Term Opioid Analgesic Treatment: A Preliminary Study

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Chronic low back pain (CLBP) is often treated with opioid analgesics (OA), a class of medications associated with a significant risk of misuse. However, little is known about how treatment with OA affect the brain in chronic pain patients. Gaining this ...

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In this book, David Eagleman breaks down the mystery behind the functions of the human brain, and many new questions that are still unanswered. One part that related to my central question was when Eagleman describes how the brain can be manipulated to believe false memories and "embrace and embellish them". I believe that this is similar to the application of VR, as it is used as a tool to "fool" the brain to our benefit.

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This is a very subjective question. Meaning it always depends on who you're asking. Because none of this has yet to be "proven" people will argue for This is a very subjective question. Meaning it always depends on who you're asking. Because none of this has yet to be "proven" people will argue for whoever's research and theories they agree with. I can give you some of my own personal (and I try really hard to be objective and steer clear of opinions, but that will always have a role so that's just my warning label of sorts, ha) but because this is such a big topic today it'd help if you were more specific... do you mean subconscious mind just basically like how we make decisions, fears, etc or do you want to go deeper meaning the abnormal subconscious mind and/or subconscious mind of trauma, etc. there are so many good out there. If you want recs let me know, but another good way to find is to do a bit of research online and/or going to a book store and looking at several books that deal with your specific questions... I hope this helps! ...more (less)

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This is a very subjective question. Meaning it always depends on who you're asking. Because none of this has yet to be "proven" people will argue for This is a very subjective question. Meaning it always depends on who you're asking.

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This article describes the different ways VR is being applied to relieve patients of pain. This was the article that sparked my interest in the capabilities of VR being able to manipulate the brain to not feel pain. In the article Dr. Jeffrey Gold says “It’s not just a distraction — it’s like an endogenous narcotic providing a physiological and chemical burst that causes you to feel good,” This means that VR could have the capability of being more effective or as effective as opioids

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It's more than a distraction, researchers say. It's more like a brain hack that occupies the brain so fully that it has no room to process pain sensations at the same time.

Credit... Gracia Lam

I was packing up at the end of a family vacation in Florida when my back went into an excruciating spasm unrelieved by a fistful of pain medication. As my twin sons, then 8 years old, wheeled me through the airport, one of them suggested, "Mom, if you think about something else, it won't hurt so much."

At the time, I failed to appreciate the wisdom of his advice. Now, four decades later, a sophisticated distraction technique is being used to help patients of all ages cope with pain, both acute and chronic. The method, called Virtual Reality Therapy, goes beyond simple distraction, as might result from watching television. Rather, it totally immerses the patient in an entertaining, relaxing, interactive environment that so occupies the brain, it has no room to process pain sensations at the same time.

"It's not just a distraction - it's like an endogenous narcotic providing a physiological and chemical burst that causes you to feel good," said Jeffrey I. Gold, director of the pediatric pain management clinic at Children's Hospital Los Angeles. "It's different from reading a book or playing with a toy. It's a multisensory experience that engages a person's attention on a much deeper level."

Virtual Reality Therapy is the new kid on the block for pain management, now gradually growing in use as the opioid epidemic continues to soar and the price of the needed equipment has plummeted. VR, as it is called, has been most widely and successfully used so far to help children and adults weather acute pain, as can accompany an IV insertion or debridement of burns. But it can also enhance the effectiveness of established techniques like physical therapy, hypnosis and cognitive behavioral therapy to treat debilitating chronic pain.

Hollie Davis, a 41-year-old resident of High Point, N.C., owes her current full mobility and cheerful disposition to a therapist at BreakThrough Physical Therapy in Greensboro, N.C., part of a network of outpatient physical therapy clinics run by Confluent Health. The therapist suggested she try VR as part of her treatment for persistent, life-inhibiting pain following a motorcycle accident. Months after suffering a concussion and extremely painful bruising when a car struck her motorcycle, "the prediction that I'd get better with time just wasn't happening," she told me.

"I found VR fascinating. I spent 10 or 20 minutes in a dark room while a head-mounted 3-D screen transported me to a very relaxing place, taught me about the nature of pain, how oxygen travels through the body, then how to breathe, focus on my breathing, relax my body and think of nothing else." The device engages multiple senses, essentially flooding the brain with so much input that it cannot register pain signals. When pain messages try to get through, "the brain gives a busy signal," Hunter Hoffman, director of the VR research center at the University of Washington in Seattle, said.

As a tool for overcoming pain and fear of an injection or IV insertion, for example, children may strive to earn points by launching Nerf balls at teddy bears on one VR program, Dr. Gold said. "Kids may say 'When are you going to do it?' and we've done it five minutes ago."

One of the first VR programs, called SnowWorld, was designed by Dr. Hoffman for treating burn patients, who often say "getting their wounds cleaned is like being burned again," he said. The virtual snowy environment is a stark contrast with the cause of their burns.

Of course, if the treatment of persistent pain only involved virtual reality, once the headset and its computerized program are removed, the pain can and would return. Larry Benz, a physical therapist and chief executive of Confluent Health, explained, "VR is not a cure - it's an adjunct to other methods that we know work" but that often involve many months of costly treatment and still may not achieve a desired result.

"If I teach you in a virtual environment, you're more likely to retain it, engage with it and comply with what you've been taught," Dr. Benz said. "When you're fully immersed in a virtual environment, it's like a 'brain hack' - you can't be engaged in anything else."

Too often, patients with chronic pain become afraid to move, which can actually make their problem worse. Various VR programs get patients to gently exercise their injured body parts and extend their range of motion while blocking their brain's ability to register pain.

"Using VR as an adjunct, we can teach coping skills, techniques patients can use on their own that will help diminish chronic pain," Dr. Hoffman said. "Learning changes the brain and gives patients something that continues to work when they take the helmet off. When patients realize their pain isn't inevitable, they're more receptive to doing physical therapy exercises and more likely to move on their own."

David R. Patterson, a University of Washington researcher who pioneered the combined use of VR and hypnosis, said the techniques can foster mindfulness, "enhancing patients' ability to come into the moment rather than pay attention to their pain. Mindfulness can train the brain not to react to thoughts or emotions associated with suffering. Pain may be inevitable, but suffering isn't."

Dr. Gold explained, "Mindfulness teaches the mind how to quiet the body and nervous system through breathing and focusing on one's breath. Thoughts may come into your head but then go out. You don't obsess about them or catastrophize."

Still, Dr. Patterson and others said, VR is not yet ready for prime time to treat chronic pain, nor should it be considered a replacement for medication.

"Pilot studies are underway using different kinds of VR content to help patients learn skills for managing their pain and be less quick to grab medication," Dr. Gold said. With VR headsets now priced around $300 or $400, patients may be able to use them at home several times a day. A number of companies are developing various software programs that create therapeutic virtual environments, with the ultimate goal of using the mind to change the brain - "like learning to play the piano or ride a bike," he said.

"VR is not a panacea or silver bullet, but a tool to teach many different things," Dr. Gold said. "Unlike opioids, you don't become dependent on VR. Rather, you learn skills that can generalize into life without VR. It's a tool for breaking the cycle of pain and stress that drives the nervous system through the roof. You can learn to think yourself well instead of thinking yourself sick."

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Virtual Reality as Therapy for Pain (Published 2019)

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It's more than a distraction, researchers say. It's more like a brain hack that occupies the brain so fully that it has no room to process pain sensations at the same time. I was packing up at the end of a family vacation in Florida when my back went into an excruciating spasm unrelieved by a fistful of pain medication.

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This article details a study where brain activity was monitored amongst subjects whom were given opioids and exposed to pain, and subjects whom were placed in VR an exposed to pain. It found that the VR group had the greatest reduction in pain. I was thoroughly impressed by the outcome of this study because it brought me to a clear answer that VR is more effective than opioids. One part I found particularly interesting was when two participants reported a paradoxical increase in subjective pain unpleasantness and worst pain intensity ratings during the opioid condition (no VR)" This shows that the use of opioids alone brought a negative result while VR did not.

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This Article talks about a study which was completed by Cedar-Sinai Hospital. They found that VR was more effective than guided meditation in managing pain. I think it is fantastic that VR is becoming used in a medical environment as it can become a very accessible form of treatment. The article says "Several patients have found VR so helpful in managing pain that they are now using it regularly at home" As the technology becomes more available. VR may be the future of pain management.

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New Study Shows Value of Virtual Reality for Pain Management

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A new study, published today in PLOS|ONE, the Public Library of Science, demonstrates the effectiveness of using virtual reality (VR) to combat pain for hospitalized patients. The study builds on previous work led by Brennan Spiegel, MD, MSHS, director of Cedars-Sinai's Health Service Research, who brought VR to the medical center.

For the purposes of the new study, researchers conducted a randomized comparative-effectiveness trial. The 120 adults in the study were admitted to Cedars-Sinai Medical Center for a variety of ailments including orthopaedic problems, gastrointestinal diseases and cancer. All of the patients had an average pain score of at least three out of 10 during the 24 hours prior to participating in the study.

Half of the patients were given VR goggles with a variety of relaxing and meditative experiences to choose from. They were advised to use the headsets three times a day for 10 minutes per session-and as needed for breakthrough pain-over three days.

The other half of the patients were instructed to tune their in-room TVs to the health and wellness channel, which included guided-relaxation content such as yoga and meditation. They also were asked to view the channel three times a day for 10 minutes per session and as needed for breakthrough pain. Several times a day, nurses asked all the patients in the study to rate their pain using the standard zero to 10 scale.

The study's findings showed the on-demand use of VR resulted in statistically significant improvements in pain compared to the TV group, with patients in the VR group averaging 1.7 points lower on the pain scale. When researchers analyzed findings from the subgroup of patients with the most severe baseline pain of seven or above, VR patients averaged three points lower than the TV group.

"This is our largest and most ambitious VR study to date," Spiegel said. "Our results support previous research that VR can meaningfully reduce pain using a nonaddictive, drug-free treatment for people experience a range of different pain conditions."

In Spiegel's previous study of short-term VR therapy, completed in 2017, the results published in JMIR Mental Health showed patients using VR reported a 24% drop in pain scores.

The current study underscores that VR can be an effective tool to add to traditional pain-management protocols.

"Virtual reality is a mind-body treatment that is based in real science," Spiegel said. "It does more than just distract the mind from pain, but also helps to block pain signals from reaching the brain, offering a drug-free supplement to traditional pain management."

Several patients have found VR so helpful in managing pain that they are now using it regularly at home. One patient, Joseph Norris, said he has suffered from chronic pain for 30 years after undergoing radiation treatment to his hip and pelvic area. The former U.S. Air Force lieutenant colonel took pain medication for 20 years until he began searching for alternative methods.

Norris tried VR six months ago, and today he uses his VR headset once a week. Norris said, "VR is a tool I use to successfully divert attention away from my pain, and it helps me reinforce my breathing pattern."

Spiegel and his team are currently involved in a study following patients using VR in their homes for 60 days.

"I believe that one day soon VR will be part of every doctor's tool kit for pain management," Spiegel said.

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New Study Shows Value of Virtual Reality for Pain Management

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A new study, published today in PLOS|ONE, the Public Library of Science, demonstrates the effectiveness of using virtual reality (VR) to combat pain for hospitalized patients. The study builds on previous work led by Brennan Spiegel, MD, MSHS, director of Cedars-Sinai's Health Service Research, who brought VR to the medical center.For the purpos...

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This essay poses the question: Is VR a more effective form of pain management than opioids? It explains how the brain processes pain and how it can be manipulated to not recognize pain through the application of these methods. I was very satisfied with the answers I discovered on my journey. The essay became more personal as I revised it for my second draft. The new questions that I ended the essay with "Can long term VR use have negative effects, and can the human brain build a tolerance to VR pain treatment, or even become addicted?" are questions that I plan on seeking the answers to even after this class wraps up

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This Article explains how VR is capable of tricking the brain into feeling less pain, and how it can also be applied to also treat other ailments. I am impressed that VR can be used for so many different treatments. Dr.Mark Young says in the article “Virtual Reality is an excellent approach to pain management. It captures the mind’s attention and blocks pain signals from reaching the brain." This makes sense, as other evidence suggests that pain is a very complex sensation perceived by the brain. It is also subjective amongst different individuals.