Complex Regional Pain Syndrome: Pathophysiology, Diagnosis, and Treatment

Complex Regional Pain Syndrome: Pathophysiology, Diagnosis, and Treatment

Complex Regional Pain Syndrome: Pathophysiology, Diagnosis, and Treatment

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Complex regional pain syndrome (CRPS) is a chronic, predominantly neuropathic and partly musculoskeletal pain disorder often associated with autonomic disturbances. It is divided into 2 types, reflecting the absence or presence of a nerve injury.

Patients with either type may exhibit symptoms such as burning pain, hyperalgesia, and/or allodynia with an element of musculoskeletal pain. CRPS can be distinguished from other types of neuropathic pain by the presence of regional spread as opposed to a pattern more consistent with neuralgia or peripheral neuropathy. Autonomic dysfunction (such as altered sweating, changes in skin color, or changes in skin temperature); trophic changes to the skin, hair, and nails; and altered motor function (such as weakness, muscle atrophy, decreased range of motion, paralysis, tremor, or spasticity) also can be present.1,2

At least 50,000 new cases of CRPS are diagnosed in the United States annually.1 Although the incidence rate is subject to debate, a large epidemiologic study from The Netherlands involving 600,000 patients suggests an incidence of 26.2 per 100,000 individuals. The study also found that women are 3 times more likely to be affected, with postmenopausal women having the greatest risk.3

Presentation

Type 1 CRPS, formerly known as reflex sympathetic dystrophy, often is triggered by a minor or major trauma—fractures account for about 60% of cases.2 Surgery is the next most common precipitating event at 20%. Other etiologies include injections, venipuncture, infections, burns, cerebrovascular accidents, or myocardial infarctions.2,4 There are no identifiable precipitating events in about 10% of patients.2

Type 2, formerly known as causalgia, often is related to high-velocity, blunt injuries, which make up more than 75% of cases. But any process that results in nerve injury, such as surgery, fractures, or injections, also can cause type 2 CRPS.4,5 More than 50% of type 2 cases involving the upper extremities often are related to injuries of the median nerve alone or in combination with another nerve of the upper extremity.5 About 60% of cases in the lower extremities are related to injury of the sciatic nerve.5 Almost all cases involve only partial nerve transection, with upper extremity involvement more prevalent than lower extremity.

Pathophysiology

Historically, CRPS has been poorly understood, and a lack of consistent diagnostic criteria often has been cited in literature. But research in recent years has provided substantial insight into the pathophysiology of the disorder.

As with many other complex conditions, the mechanisms involved in CRPS are multifactorial (Table 1) and include the peripheral and central nervous systems (Figure 1).1 Factors such as altered sympathetic and catecholaminergic function, peripheral and central sensitization, peripheral and central neurogenic inflammation, altered somatosensory representation in the brain, genetics, and psychology all affect patients to varying degrees.

Table 1. Summary of Pathophysiologic Mechanisms That May Contribute to CRPS1
Mechanism Supporting Pattern of Findings
Altered cutaneous innervation
  • Density of C- and Aδ-fibers in CRPS-affected region
  • Altered innervation of hair follicle and sweat glands in CRPS-affected limb
Central sensitization
  • Increased windup in CRPS patients
Peripheral sensitization
  • Local hyperalgesia in CRPS-affected vs unaffected extremity
  • Increased mediators of peripheral sensitization
Altered SNS function
  • Bilateral reductions in SNS vasoconstrictive function predict CRPS occurrence prospectively
  • Vasoconstriction to cold challenge is absent in acute CRPS but exaggerated in chronic CRPS
  • Sympatho-afferent coupling
Circulating catecholamines
  • Lower norepinephrine levels in CRPS-affected vs unaffected limb
  • Exaggerated catecholamine responsiveness because of receptor up-regulation related to reduced SNS outflow
Inflammatory factors
  • Increased local, systematic, and cerebrospinal fluid levels of proinflammatory cytokines, including TNF-α, IL-1β, -2, and -6
  • Decreased systemic levels of anti-inflammatory cytokines (IL-10)
  • Increased systemic levels of proinflammatory neuropeptides, including CGRP, bradykinin, and substance
  • Animal postfracture model of CRPS-1 indicates that substance P and TNF-α contribute to key CRPS features
Brain plasticity
  • Reduced representation of the CRPS-affected limb in somatosensory cortex
  • These alterations are associated with greater pain intensity and hyperalgesia, impaired tactile discrimination, and perception of sensations outside of the nerve distribution
Genetic factors
  • In the largest CRPS genetic study to date (150 CRPS patients), previously reported associations were confirmed between CRPS and HLA-related alleles
  • A TNF-α promoter gene polymorphism is associated with “warm CRPS”
Psychological factors
  • Greater preoperative anxiety prospectively predicts CRPS symptomatology after total knee arthroplasty
  • Emotional arousal has a greater effect on pain intensity in CRPS than in non-CRPS chronic pain, possibly via associations with catecholamine release
CGRP, calcitonin gene-related peptide; CRPS, complex regional pain syndrome; IL, interleukin; SNS, sympathetic nervous system; TNF, tumor necrosis factor

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Figure 1. Speculative model of interacting CRPS mechanisms.

CGRP, calcitonin gene-related peptide; CRPS, complex regional pain syndrome; IL, interleukin; TNF, tumor necrosis factor

Central Sensitization

Central sensitization is an increased firing of nociceptive fibers in response to intense or persistent noxious stimuli. It is mediated by the nociception-induced release of neuropeptides such as bradykinin, glutamate, and substance P. This phenomenon is part of the reason patients experience allodynia and hyperalgesia. It is not known whether central sensitization precedes, occurs with, or follows development of other CRPS signs and symptoms.1,4,6

Peripheral Sensitization

Peripheral sensitization occurs when an initial tissue trauma causes proinflammatory neuropeptides to be released from primary afferent fibers. These neuropeptides increase background firing of nociceptors, decrease the firing threshold for thermal and mechanical stimuli, and increase firing in response to nociceptive stimuli. This decrease in firing threshold contributes to patients experiencing allodynia and hyperalgesia.1,4,6

Sympathetic Nervous System

Several human studies demonstrated expression of adrenergic receptors on nociceptive fibers after nerve injury. Given that there is likely some sort of nerve damage in type 1 CRPS, this explains why sympathetic outflow has an important effect on pain in patients with this condition. Manipulations with whole-body cooling and heating have supported the theory of sympatho-afferent coupling, although it would not be correct to imply that altered sympathetic function is solely responsible for the development of CRPS. Vascular abnormalities seen in CRPS also are mediated by altered levels of endothelin-1, nitric oxide synthase, nitric oxide, and impaired endothelial-related vasodilatory function. During the progression from acute to chronic CRPS, patients have intense vasoconstriction response in the setting of lowered levels of norepinephrine, implying altered local sympathetic outflow. This is believed to occur due to up-regulation of noradrenergic receptors as a response to low levels of catecholamines. When patients experience pain or regular life stress, these sensitive receptors respond intensely to the release of catecholamines, resulting in a cold, blue, and sweaty appearance.1


Inflammation

The inflammatory process is involved in at least the acute phase of CRPS. There are 2 potential sources of inflammation:

  1. Classic mechanisms through actions of immune cells, which, after tissue trauma, secrete proinflammatory cytokines, including interleukin-1, -2, and -6, and tumor necrosis factor-α.
  2. Neurogenic inflammation, which occurs through the release of proinflammatory mediators directly from injured nociceptive fibers in response to various stimuli. These neuropeptides include substance P, calcitonin gene-related peptide, and bradykinin, which promotes plasma extravasation and local tissue edema.1

A subset of patients with CRPS has been found to have low levels of anti-inflammatory and high levels of proinflammatory cytokines.4

Autoimmunity

It has been suggested that autoantibodies may play a role in CRPS. Autoantibodies found in the plasma of patients with CRPS are active at the muscarinic cholinergic and β2 adrenoceptors. Transfer of serum immunoglobulin G to mice from patients with CRPS elicited symptoms of CRPS in recipient mice.7

Genetics

Although there is no clear evidence of genetic predisposition to developing CRPS, it would be prudent to further investigate genetic factors that influence inflammatory and other mechanisms contributing to the syndrome. The largest study of 150 CRPS patients has found a link between CRPS and HLA-related alleles.1,4

Psychological Factors

To date, no evidence has suggested a purely psychological form of CRPS. However, poor coping and emotional stress can certainly raise levels of circulating catecholamines, which could exacerbate vasomotor signs of CRPS, cause pain, and maintain central sensitization.1,4

Brain Plasticity

Functional magnetic resonance imaging scans have shown that there is significant cortical reorganization of somatosensory cortex, which may underlie various manifestations of CRPS. Functional disturbances in posterior parietal cortex responsible for integrating various external stimuli and constructing real-time body schema in space, also may contribute to chronification of pain.1,4,7

Diagnosis

The diagnosis of CRPS is clinical and depends on patient history, physical examination, and findings of musculoskeletal degeneration and secondary pain that develops as a result of persistence of the disease state. CRPS is a diagnosis of exclusion and cannot be made in the presence of other diagnoses that can be responsible for the presentation. Chronic CRPS needs to have symptoms and signs consistent with time-dependent effect of CRPS (ie, atrophy, dystrophy, contractions, and secondary pain).

In the initial several months of CRPS, hypoesthesia and hyperalgesia are common, whereas ongoing disease anesthesia dolorosa can be seen.2 The pain present in later cases when compared with the acute phase is more often present at rest and resistant to treatment. One of the hallmarks of persistent CRPS is the accumulation of orthopedic and neuropathic findings due to altered biomechanics of the affected area and tissue dystrophy and atrophy in superficial and deeper tissues, as well as development of secondary pain in the contralateral limb and other parts of the body as the patient attempts to compensate.

A main reason why CRPS is difficult to diagnose and treat is because the majority of patients do not have classic “warm” (acute) or “cold” (cold) affected limbs—they fall somewhere along the spectrum.1,4 Veldman et al described more patients as having the “cold” type as the duration of CRPS increases, however, some patients with CRPS for more than 10 years still have “warm” limbs.2 And despite being classified as 2 types, there is no evidence that pathophysiologic mechanisms or treatment responsiveness differ in any appreciable way except that type 2 and underlying nerve injury may need to be addressed directly, sometimes surgically (Figure 2).

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Figure 2. Schematic representation of treatment modalities based on pathophysiologic mechanisms.7

Skin biopsies of patients with type I CRPS show a significantly decreased amount of C and Aδ-fibers after tissue injury, possibly indicating nerve damage may be present in type 1.1 However, there is no clear evidence as to whether this is a cause or effect of CRPS. Animal models support an increased nociceptive firing in response to norepinephrine, providing evidence that there is sympatho-afferent coupling, which has been suggested by human studies.1 There is further suggestion in animal models that a transcription factor, nuclear factor-β, could play a role in CRPS. This may provide an upstream link between increased proinflammatory neuropeptides and increased proinflammatory cytokines in CRPS.1,4

It also has been shown that patients with CRPS and people with prolonged immobilization, from things like casts for limb fractures, show similar signs of edema, skin color changes, limited range of motion, and altered sensation. This suggests that patients with CRPS experience derangement of normal physiologic responses, making it difficult to identify when these physiologic changes becomes pathologic CRPS and not another diagnosis.4

Diagnostic Tools

During a consensus workshop in 1994, the International Association for Study of Pain (IASP) proposed diagnostic criteria based on clinical symptomatology (Table 2).8 Criticisms of the IASP criteria included a lack of specificity and misdiagnosing other types of neuropathic pain conditions as CRPS. The false diagnosis was thought to stem from the IASP criteria being met solely by self-reported symptoms uncovered by the history without physical signs and symptoms.7

Table 2. IASP CRPS Diagnostic Criteria8
CRPS I CRPS II
2-4 of the following with 2, 3, and 4 being mandatory:

  1. The presence of an initiating noxious event, or a cause of immobilization.
  2. Continuing pain, allodynia, or hyperalgesia with which the pain is disproportionate to any inciting event.
  3. Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of the pain.
  4. This diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction.
All of the following:

  • The presence of continuing pain, allodynia, or hyperalgesia after a nerve injury, not necessarily limited to the distribution of the injured nerve.
  • Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of the pain.
  • This diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction.
CRPS, complex regional pain syndrome; IASP, International Association for the Study of Pain

In an aim to improve the IASP criteria, an international consensus meeting was held in Budapest in 2003. The results were based on the previously published Harden/Bruehl criteria (Table 3).9 A 2010 study showed the IASP criteria of being 100% sensitive but only 41% specific in 113 CRPS type 1 patients and 47 non-CRPS neuropathic pain patients. The new Budapest criteria revealed 99% sensitivity with 68% specificity.10 Veldman’s criteria includes physical signs in combination with symptoms and was derived from a cross-sectional cohort study of 829 patients (Table 4).2

Table 3. Harden/Bruehl CRPS Diagnostic Criteria9
CRPS I
  1. Continuing pain, which is disproportionate to any inciting event
  2. Must report ≤1 symptom in 3 of the following 4 categories:
    • Sensory:
      Reports of hyperesthesia and/or allodynia
    • Vasomotor:
      Reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry
    • Sudomotor/Edema:
      Reports of edema and/or sweating changes and/or sweating asymmetry
    • Motor/Trophic:
      Reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nails, skin)
  3. Must display ≤1 sign at time of evaluation in ≥2 of the following categories:
    • Sensory:
      Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or temperature sensation and/or deep somatic pressure and/or joint movement)
    • Vasomotor:
      Evidence of temperature asymmetry (>1∞C) and/or skin color changes and/or asymmetry
    • Sudomotor/Edema:
      Evidence of edema and/or sweating changes and/or sweating asymmetry
    • Motor/Trophic:
      Evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nails, skin)
  4. There is no other diagnosis that better explains the signs and symptoms
CRPS II
Same as CRPS I but with the evidence of a peripheral or central nerve injury
CRPS NOS
Patients who do not fully meet the clinical criteria, but whose signs and symptoms cannot be better explained by another diagnosis
CRPS, complex regional pain syndrome; NOS, not otherwise specified
Table 4. Veldman2 CRPS Diagnostic Criteria
CRPS I
  1. Presence of 4 or 5 of the following:
    • Unexplained diffuse pain
    • Difference in skin color relative to other limb
    • Diffuse edema
    • Difference in skin temperature relative to other limb
    • Limited active range of motion
  2. Occurrence or increase of above signs and symptoms after use.
  3. Above signs and symptoms are present in an area larger than the area of primary injury or operation and include the area distal to the primary injury.
CRPS, complex regional pain syndrome

Treatment

Although the majority of CRPS symptoms resolve within an approximate 12-month period, an estimated 25% of patients still fulfill IASP diagnostic criteria at 12 months and may suffer from CRPS chronicity. CRPS following fracture has a better resolution rate; “cold” CRPS or upper-limb involvement has the worst outcome. Because CRPS is a multifactorial disease with poorly understood mechanisms, the mainstay of treatment remains physical and occupational therapy aimed at return and preservation of function, prevention of loss of range of motion, and prevention of contractures and atrophy.4

Pharmacologic Treatment

IV Ketamine has proven to be very effective in the treatment of CRPS /RSD

At the Florida Spine Institute, treatment protocols are individually planned depending on the nature of pain and the patient’s responsiveness to initial sessions. Infusion cocktails are prepared in house so that they can be tailored to each patient’s therapeutic needs.  A variety of medications are often used:

  • Lidocaine
  • Ketamine
  • Bisphophonates
  • Magenesium

These medications are typically mixed with saline in an IV bag and infused slowly over several hours, depending on the medication and/or protocol being used.  Usually, a series of treatments will be recommended daily for a period of a week or more. The duration of pain relief following one or more ketamine infusions cannot be predicted. The goal is to achieve lasting relief as measured in weeks or months following the last treatment. Most patients who enjoy prolonged pain relief will need to return on occasion for a booster infusion, or continue to take low dose intranasal ketamine at home.

There is also convincing results with regard to IV bisphosphonates—most recently neridronate in patients with disease duration of less than 6 months. At 1-year follow-up, neridronate showed improved pain control. Multiple neuropathic medications such as gabapentin, tricyclic antidepressants, and opioids have been used through their extrapolated benefit in neuropathic conditions other than CRPS. Oral steroids continue to be used in acute CRPS, although the evidence is poor and sympatholytic drugs are used by clinicians with low success rates.7,11,12 But a recent small trial using low-dose oral phenoxybenzamine showed significant functional improvement in patients with CRPS.13 Taking everything above into consideration, we can conclude that the majority of pharmacologic treatments used by clinicians are quite empirical and largely based on personal preferences and experiences.

Interventional and Surgical Techniques

The main utility of interventional pain medicine in CRPS is to enable proper physical or occupational therapy and break the cycle of peripheral and/or central pain. Moderate evidence shows that sympathetic blockade is effective. Spinal cord stimulators appear to provide significant improvement of function in type 1 CRPS, and are more cost-effective over a patient’s lifetime compared with physical therapy and medical management.4,14 Although there is great resistance to surgery for CRPS patients, significant pain resolution may be achieved through nerve decompression or denervation procedures, neuroma resection, and neurolysis once patients are properly identified by nerve blocks. In many patients, the noxious stimulus is maintained through nerve compression; osteophytes; fibrosis; neuroma; arteriovenous malformation; or anything that entraps, compresses, or distorts the nerve. Surgery may be indicated in these cases.

Psychological Interventions

Psychological factors play a role in the treatment of CRPS. There is likely benefit in cognitive-behavioral therapy. Correcting body image also may help in CRPS affected patients.4,7

References

  1. Bruehl S. An update on the pathophysiology of complex regional pain syndrome. Anesthesiology. 2010;113(3):713-725.
  2. Veldman PH, Reynen HM, Arntz IE, et al. Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet. 1993;342(8878):1012-1016.
  3. de Mos M, de Bruijn AGJ, Huygen FJPM, et al. The incidence of complex regional pain syndrome: a population-based study. Pain. 2007;129(1-2):12–20.
  4. Borchers AT, Gershwin ME. Complex regional pain syndrome: a comprehensive and critical review. Autoimmun Rev. 2014;13(3):242-265.
  5. Hassantash SA, Afrakhteh M, Maier RV. Causalgia: a meta-analysis of the literature. Arch Surg. 2003;138(11):1226-1231.
  6. Rockett, M. Diagnosis, mechanisms and treatment of complex regional pain syndrome. Curr Opin Anaesthesiol. 2014; 27(5):494-500.
  7. Gierthmühlen J, Binder A, Baron R. Mechanism-based treatment in complex regional pain syndromes. Nat Rev Neurol. 2014;10(9):518-528.
  8. Merskey M, Bogduk N, eds. Classification of chronic pain: descriptions of chronic pain syndromes and definition of pain terms; second edition. Seattle: WA; 1994.
  9. Harden RN, Bruehl S, Stanton-Hicks M, et al. Proposed new diagnostic criteria for complex regional pain syndrome. Pain Med. 2007;8(4):326-331.
  10. Harden RN, Bruehl S, Perez RS, et al. Validation of proposed diagnostic criteria (the “Budapest Criteria”) for complex regional pain syndrome. Pain. 2010; 150(2):268-274.
  11. Rowbotham, MC. Pharmacologic management of complex regional pain syndrome. Clin J Pain. 2006:22(5):425-429.
  12. O’Connell NE, Wand BM, McAuley J, et al. Interventions for treating pain and disability in adults with complex regional pain syndrome. Cochrane Database Syst Rev. 2013;4:CD009416.
  13. Inchiosa MA Jr. Phenoxybenzamine in complex regional pain syndrome: potential role and novel mechanisms. Anesthesiol Res Pract. 2013;2013:978615.
  14. Taylor RS, Van Buyten JP, Buchser E. Spinal cord stimulation for complex regional pain syndrome: a systematic review of the clinical and cost-effectiveness literature and assessment of prognostic factors. Eur J Pain. 2006;10(2):91-101.

 

Relief for Worst RSD May Lie With Ketamine Coma

Relief for Worst RSD May Lie With Ketamine Coma

Relief for Worst RSD May Lie With Ketamine Coma

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For the most severe cases of reflex sympathetic dystrophy (RSD), inducing a five-day coma may be the only effective treatment.

The method is akin to rebooting the central nervous systems of patients whose nerve cells have gone haywire. The FDA has yet to approve coma therapy, which is induced by administering large bolus injections of ketamine and midazolam at up to 50 times the normal dose. But that has not stopped two U.S. doctors from pioneering the use of a “ketamine coma” in American patients treated at hospitals in Germany and Mexico.

For the better part of four years, Robert Schwartzman, MD, chairman of the Department of Neurology at Drexel University College of Medicine in Philadelphia, and Anthony Kirkpatrick, MD, PhD, an anesthesiologist at the University of South Florida College of Medicine in Tampa, have been studying the effects of ketamine treatment, including induced comas, in patients with RSD. Their results suggest that the coma therapy may provide long-term and perhaps permanent relief in as many as half of the most severe cases.

Ketamine first won FDA approval in 1970 as an anesthetic. It quickly became known on the street as “Special K,” a powerful hallucinogen similar to LSD and PCP. Clinicians in the United States can legally give the drug to patients with RSD—also known as complex regional pain syndrome (CRPS) type 1—who are under conscious sedation. In this group, relief typically lasts no more than six months, Dr. Schwartzman said.

Potent Agent

Ketamine is the most potent clinically available inhibitor of N-methyl-d-aspartate (NMDA) receptors. These receptors permit the transfer of electrical signals between neurons in the brain and the spinal column. Studies support the idea that RSD results from a dynamic change in the physiology and structure of central pain neurons mediated by NMDA receptors. When these receptors malfunction, enzymatic and metabolic cascades occur in pain cells, and the degree of pain is magnified out of proportion to the physical injury causing it.

In a study of infusions of low-dose ketamine (Pain Physician 2005;8:175-179), Dr. Schwartzman and colleagues found that a critical factor in central sensitization seems to be the release of magnesium on the NMDA receptor, with an influx of calcium and the initiation of intracellular cascades. As an NMDA antagonist, ketamine blocks central sensitization. Drugs such as dextromethorphan, amantadine and memantine (Namenda, Forest Pharmaceuticals) also could be used, but they appear to have a low potential for blocking the sensitization process.

Ketamine has long been known to be able to prevent RSD/CRPS following surgery, said Scott Reuben, MD, professor of anesthesiology and pain medicine at Tufts University School of Medicine in Boston and director of pain management at Baystate Medical Center in Springfield, Mass.

“If it [ketamine] can prevent CRPS, the thought was, ‘can we use it to treat it?’ ” said Dr. Reuben, who serves as an adviser to the Mexico study. “This is just the stepping stone. Unfortunately, all we have are case reports and retrospective studies. We need prospective studies.”

Only the Worst Patients

RSD affects between 200,000 and 1.2 million Americans, according to the Reflex Sympathetic Dystrophy Association. The disorder develops without any apparent explanation in 1% to 2% of patients with fractures and in 2% to 5% of patients with peripheral nerve injuries. The RSD group claims that roughly 50,000 new cases develop each year.

For the Mexican and German research, doctors chose patients with the most severe cases of RSD who had tried everything—including blocks and hyperbaric chambers—for their pain.

Of the roughly 200 to 300 new patients with RSD whom Dr. Kirkpatrick sees each year, fewer than 5% are so unresponsive to conventional therapies that they are considered for treatment with a ketamine coma. Those who are eligible can barely endure even the most innocuous sensations, Dr. Kirkpatrick said. Patients report feeling pain at the slightest touch, from a dog’s wagging tail to air flowing over the skin. One patient lived in a box because it hurt her to wear clothes. “Some of these patients,” Dr. Kirkpatrick said, “are about ready to die.”

Frustrated physicians from around the world refer patients to Drs. Kirkpatrick and Schwartzman. “I only see the worst patients,” said Dr. Schwartzman, who took on the challenge of RSD after being unable to cure one of his patients with the condition. “Some have gone through up to 100 doctors.”

Failure in More Than Half

Dr. Schwartzman has sent a total of 38 patients to Germany for treatment with the ketamine coma, which was discovered serendipitously by Ralph-Thomas Kiefer, MD, and Peter Rohr, MD, in Tübingen. The two physicians had induced a coma in a patient with RSD and severe head trauma. When the patient awoke, the pain syndrome had vanished.

The five-day coma is induced with large bolus injections of ketamine (1-1.5 mg/kg) and midazolam (2.5-7.5 mg). The coma is maintained with infusions of ketamine (3-7 mg/kg per hour) and midazolam (0.15-0.3 mg/kg per hour), which are tapered toward the end.

Every patient in whom a coma is induced does well initially, Dr. Schwartzman said, but the pain returns in 55% to 60% of cases. Still, of the 38 patients treated in Germany, at least 12 have had minimal or no pain for more than five years. Three of the 12 required occasional subanesthetic boosters of ketamine.

“We’re blocking the RSD,” Dr. Schwartzman said. “The maintaining thing is still there. If you don’t block the maintaining problem, the same molecular genetic cascade occurs.”

A study of the full ketamine coma in the patients treated in Germany will soon appear in Pain Medicine. Of the 20 patients featured in the study who underwent the therapy, 16 experienced complete remission lasting at least six months. “While the trial suggests improvements in pain reductions,” the researchers concluded, “a randomized controlled study will be necessary to prove its efficacy.”

The coma’s side effects—precipitous weight loss, sleep disruption, anxiety, weakness and the usual complications of critical care medicine—are potentially serious. The bottom line, Dr. Schwartzman said, is that “the procedure has proven to be very safe but clearly has inherent risks.”

South of the Border

Dr. Kirkpatrick has embarked on a study in Mexico with a protocol similar to that used in the German study; he sends his patients to the San José Technological Hospital, affiliated with the Tec de Monterrey School of Medicine in Monterrey, Mexico, a few hours’ drive from the Texas border. Patients pay about $20,000 for the treatment, which is not covered by insurance.

Leading the Mexican medical team is Fernando Cantœ Flores, MD, an anesthesiologist and specialist in pain management who was trained at the University of Texas.

The study was originally approved in the United States by the institutional review boards of the University of South Florida and Tampa General Hospital, but the FDA refused to grant an exemption to its international new drug application. Rather than embark on a process that would likely cost $3 million and delay treatment for their patients, Dr. Kirkpatrick and his colleagues moved the study to Mexico. A review board in Monterrey also approved the study.

So far, eight patients have been treated in Mexico. The main difference from the German study is that pain thresholds are measured with a force gauge. The German study relied on self-reporting.

Low-Dose Conscious Sedation

A less dramatic treatment option for severe cases of RSD is a subanesthetic infusion of low-dose ketamine (10-30 mg per hour titrated according to side effects such as amnesia, blurred vision and vomiting). Dr. Schwartzman has performed close to 200 of these—about one each week for the past four years—at Hahnemann University Hospital in Philadelphia. The treatment costs about $10,000, and insurance companies will not pay for it. Dr. Schwartzman estimated that he performs 95% of all such procedures in the country. He also treats about 10 outpatients per week with lower doses in his clinic.

The infusions succeed in 70% to 80% of cases. But even in the most responsive patients, pain typically returns after approximately six months. A study published in Pain Medicine (2004;5:263-275) found similar results.

A two-hour infusion of low-dose ketamine can also be used to manage RSD or as a booster after treatment with the coma. Pretreatment with 0.2 mg of I.V. glycopyrrolate (the only other drug needed) is administered along with a ketamine drip at 100 mg per hour, supplemented with 5- to 40-mg I.V. bolus injections of ketamine. An average adult will require a total of 400 to 600 mg of ketamine over a two-hour period.

For patients with the most intractable cases of RSD, the full coma treatment may still be the only hope. In a study published online in Pain Medicine in July 2007, (online early article), Dr. Schwartzman and his German colleagues found that an “awake” version of the ketamine infusion at higher doses (50-500Êmg per day) over a 10-day period in four patients with extreme RSD did not relieve pain.

Cause for Optimism

Shannon Stocker, MD, an Orlando, Fla., RSD patient, underwent coma therapy in Mexico. Dr. Stocker said the concern she felt about going into the treatment was “overwhelmed by a desire to get better because the pain was so bad it was worth all the risk. The burning pain was constant. But when there was anything like raindrops, it felt like ice picks stabbing me.”

The ketamine coma may be the key to curing other conditions directly related to either RSD or similar nerve dysfunction. As a result of her RSD, Dr. Stocker had skin ulcers all over her arms, which began to clear up while she was still in the coma.

Jim Broatch, executive director of the RSD Syndrome Association, called ketamine therapy “promising” but added that more data are needed. “We’re saying the jury is still out.”

Dr. Kirkpatrick agreed. “We’re just trying to do hard science,” he said. “We can’t make progress in this research if we ignore the bad things.”

In January 2008, Dr. Kirkpatrick plans to open The RSD/CRPS Treatment Center and Research Institute in Tampa. An entire city block has already been purchased by the International Research Foundation for RSD/CRPS, which Dr. Kirkpatrick cofounded with a patient.

Dr. Schwartzman has now written more than 60 articles on RSD and spoken about the disorder at more than 100 conferences, including the 2007 annual meeting of the American Academy of Pain Management, at which he delivered the keynote address.

The success of the various ketamine protocols has made him optimistic about the prospects for patients with previously intractable RSD. “It’s wonderful to be able to successfully treat someone in severe pain,” he said. “That’s why you go to medical school.”

by David Rosenfeld

 

The 6 Best Supplements for Fibromyalgia

The 6 Best Supplements for Fibromyalgia

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If you’re looking for natural ways to fight the aches, stiffness and inflammation of fibromyalgia, supplements can be a powerful weapon against symptoms. From vitamin D to brown seaweed extract, an arsenal of tools can help reduce pain. Here, experts reveal what works and why…

If you’re not including fibromyalgia-fighting supplements as part of your pain-management regimen, you could be missing out.

“The right supplements can help muscles relax, which leads to pain reduction, or even prevent pain altogether,” says fibromyalgia expert Jacob Teitelbaum, M.D., director of the Fatigue & Fibromyalgia Practitioners Network and author The Fatigue and Fibromyalgia Solution (Avery).

But when you’re standing in the supplement aisle, it’s hard to figure out which live up to their hype.

Read on for expert advice on the top 6 supplements for relieving fibro pain and other symptoms.

1. Vitamin D
The “sunshine vitamin” isn’t only good for building bones.

It can help fight fibro pain and fatigue, too, according to a 2014 study published in the journal Pain.

For the study, 30 women with fibromyalgia – who were also deficient in vitamin D – were divided into two groups. The treatment group received oral vitamin D supplements for 20 weeks. The control group received a placebo.

Starting after just one week, the treatment group showed improved physical functioning, had less morning fatigue than the placebo group and reported a marked reduction in pain.

The body produces vitamin D when skin is directly exposed to the sun – our best source. But some people don’t produce enough of the nutrient, according to the National Institutes of Health. These include women who are older, dark-skinned or obese.

People with certain disorders, including celiac or Crohn’s disease – as well as those who aren’t exposed to ample sunlight (or who wear sunscreen) – are also likely to be deficient. (Read about 11 natural remedies for Crohn’s management.)

Because few foods contain vitamin D, swallowing supplements is the easiest way to ensure you get enough.

The government’s daily recommendation of vitamin D is 600 international units (IU) for anyone 1 to 70 years old, and 800 IU for people 71 and up – to a maximum of 4,000 IU per day, according to the National Institutes of Health.

But ask your doctor how much you should take to combat your fibro symptoms.

2. Fish Oil
Thanks to its omega-3 fatty acids, fish oil has terrific anti-inflammatory properties, which can help reduce fibro pain.

It reduces the body’s production of inflammatory hormones (prostaglandins), says Nehad Soloman, M.D., a board-certified rheumatologist for Valley Arthritis Care in Arizona. And that may mean less stiffness or fewer tender joints.

Dr. Soloman suggests choosing a mercury-free brand (check the label), although fish oil supplements are considered safe.

Take 1 or 2 capsules (or 1 or 2 tablespoons) daily to reduce inflammation and boost your immunity, recommends the University of Maryland Medical Center. But check with your doctor first – especially if you take blood-thinning medications, such as aspirin or warfarin (Coumadin).

3. SAMe
S-Adenosyl methionine, more commonly known as SAMe, is a synthetic form of a compound the body naturally produces.

We need it for proper immune function, and it plays a role in forming cartilage and our DNA, Dr. Soloman says.

As we age, our bodies produce less of it, which may explain the increased aches after your 40th birthday. Taking a SAMe supplement not only lessens chronic pain, it also can boost your spirits. These 5 other natural mood-lifters help too.

“SAMe assists in the production and breakdown of neurotransmitters, such as serotonin, norepinephrine and dopamine – brain hormones that influence and regulate moods,” Dr. Soloman says.

In fibro studies, the recommended dosing is 400 mg twice a day for six weeks, starting with a lower dose (about 200 mg daily) and increasing gradually to avoid stomach upset, according to the University of Maryland Medical Center. But dosing varies by patient, so ask your doctor.

4. Ribose
Tight muscles are a common cause of fibro pain. To relax and release, muscles need energy, Dr. Teitelbaum says. And that’s where ribose supplements come in.

Ribose, a simple sugar, can increase energy by an average of 61% – and cut the pain experienced by fibromyalgia sufferers by an average of 15.6%, according to a 2012 study Dr. Teitelbaum led, published in The Open Pain Journal.

“The energy-building benefit of ribose directly improved the debilitating symptoms of this condition,” Dr. Teitelbaum says.

Dr. Teitelbaum recommends a 5 g dose three times a day.

5. Magnesium
This mineral is a major player in every body part.

Not only is it credited with keeping the heart, kidneys and bones strong, it also helps us avoid muscle spasms, weakness and back pain, Dr. Teitelbaum says.

Women with fibromyalgia may be deficient in magnesium, studies suggest. And magnesium may help relieve fibro pain and other symptoms.

For example, researchers from Ajou University School of Medicine in Korea analyzed hair samples from 166 women – including 44 with fibromyalgia. The hair from the fibromyalgia group contained significantly lower amounts of magnesium than that of the healthy women, according to the 2011 study.

Researchers at Acıbadem University Medical School in Istanbul, Turkey, also found that women diagnosed with fibromyalgia were likely to have “significantly lower” magnesium levels than women who didn’t have the disorder. But those who then took 300 mg/day of magnesium citrate for 8 weeks reported a reduction of “tender points” and other fibromyalgia symptoms, according to their 2013 study.

Magnesium is found in green leafy vegetables, pumpkin and sunflower seeds, 100% wheat bran cereal and raw spinach.

But these foods are a good source only if you eat them raw. Half of the minerals’ benefits are lost when cooked.

Normal daily recommended dosage for adult women is 280 to 300 mg per day, taken with meals, says the Mayo Clinic.

But if you have kidney disease or are taking medication, talk to your doctor before taking magnesium. Magnesium can interact with certain medications, including high blood pressure medicines and antibiotics, the University of Maryland Medical Center says.

6. Brown Seaweed Extract
You may not be familiar with these capsules, but this supplement is one to look for.

“It’s showing great promise in the fight against chronic pain,” Dr. Soloman says.

In fact, taking 1,000 mg of brown seaweed extract daily can reduce joint pain and stiffness by 52%, according to a 2011 study from Australia’s Centre of Health and Wellbeing, published in the journal Biologics.

Even better: These benefits kicked in after just one week, so you don’t have to wait long to find out if it’s working for you.

Supplement Smarts
Check with your doctor before taking these or other supplements.

“Like prescription drugs, it’s possible to take too much. And many supplements have side effects,” says David Pisetsky M.D., Ph.D., a professor of immunology at Duke University Medical Center in Durham, N.C.

Questions to ask your doctor include:

1. What’s the right dosage for me?

2. Should I take it with food?

3. What time of day should I take it?

4. Will this supplement interact badly with my prescriptions?

5. Does it have side effects that might mimic or aggravate my fibro symptoms (such as depression or sleep difficulties)?

For more expert advice and information, visit Lifescript’s Fibromyalgia Health Center.

Also, visit these other resources for more support:

The National Institutes of Health: Information and resources from the U.S. government’s medical research agency.

The American Fibromyalgia Syndrome Association: This group’s mission is to fund scientific studies on fibromyalgia.

Fibromyalgia Network: A nonprofit that offers information about the disease from top fibromyalgia clinicians and researchers.

Week of  July 7, 2015 Breaking Research Updates

Week of July 7, 2015 Breaking Research Updates

Weekly Breaking Research Updates

 

Scientific breakthroughs happen every day!  In an effort to help our patients stay up to speed on the most cutting edge treatment options available for them, our scientists monitor current research and publish weekly research updates.  The title of each article below is a link to the full study report.  If you’d like to make an appointment with Dr. Hanna to discuss your treatment options, please contact us.

 

Ketamine

 

Withdrawal from Acute Amphetamine Induces an Amygdala-Driven Attenuation of Dopamine Neuron Activity: Reversal by Ketamine.

P Belujon, NL Jakobowski, HK Dollish, AA Grace – … : official publication of the …, 2015

Drug addiction is a chronic disorder characterized by a cycle composed of drug seeking,

intoxication with drug taking and withdrawal associated with negative affect. Numerous

studies have examined withdrawal/negative affect after chronic use; however, very few

 

Enantioselective inhibition of D‐serine transport by (S)‐ketamine

NS Singh, M Bernier, S Camandola, MA Khadeer… – British Journal of …, 2015

Background and purpose Patients with major depressive disorder receiving racemic

ketamine,(R, S)-ketamine, experience transient increases in Clinician-Administered

Dissociative States Scale (CADDS) scores and coincident drop in plasma D-serine levels.

 

Pain Management with Low-Dose Ketamine Infusions

A Katz – Emergency Medicine News, 2015

Wolters Kluwer Health may email you for journal alerts and information, but is committed to maintaining

your privacy and will not share your personal information without your express consent. For more

information, please refer to our Privacy Policy. The M 2 E Too! Blog by Larry Mellick,

 

Sedative medications outside the operating room and the pharmacology of sedatives

TG Hansen – Current Opinion in Anesthesiology, 2015

Ketamine. Ketamine is a unique phencyclidine derivate that differs from other sedatives in several

ways. Ketamine seems to induce a dissociative anesthetic state with functional and

electrophysiological separation between the limbic system and hypothalamus.

 

Pre-Emptive Analgesia with Ketamine for Relief of Postoperative Pain After Surgical Removal of Impacted Mandibular Third Molars

A Hadhimane, M Shankariah, KV Neswi – Journal of Maxillofacial and Oral Surgery, 2015

Purpose In this study we assessed the clinical efficacy of sub-mucosal injection of ketamine

at sub-anesthetic dose of 0.5 mg/kg on post-operative pain, swelling and trismus following

surgical extraction of impacted mandibular third molars. Methods Forty bilaterally

 

Fluorescence‐guided surgery of human prostate cancer experimental bone metastasis in nude mice using anti‐CEA dylight 650 for tumor illumination

S Miwa, N De Magalhães, M Toneri, Y Zhang, W Cao… – Journal of Orthopaedic …, 2015

Tumor implantation Six to eight-week-old male mice were anesthetized by a ketamine mixture

(10 µL ketamine HCL, 7.6 Before resection of the metastatic tumor, mice were anesthetized with

the ketamine mixture (described above), and their limbs were sterilized with alcohol.

 

Reassessment of the antioxidative mixture for the challenging electrochemical determination of dopamine, noradrenaline and serotonin in microdialysis samples

J Van Schoors, C Lens, K Maes, Y Michotte, I Smolders… – Journal of Chromatography …, 2015

Diazepam 10 mg/2 mL is purchased as Valium ® from Roche (Cenexi, Fontenay-sous-Bois,

France), ketamine 1000 mg/10 mL as Ketamine 1000 ® from Ceva (Libourne, France), Ketoprofen

1% as Ketofen ® from Merial (Toulouse, France) and NaCl 0.9% from Baxter (Lessines

 

Ultrasound-induced suppression of visually-evoked potentials: experience in nonhuman primates with a clinical transcranial MRI-guided focused ultrasound system

N McDannold, C Arvanitis, N Vykhodtseva… – Journal of Therapeutic …, 2015

650 kHz. Methods. The animal was deeply anesthetized using ketamine and

dexdormitor. First we targeted the LGN using MR temperature imaging, and then

we relocated the MRI table just outside the MRI. Visually-evoked

 

Severe Acquired Idiopathic Thrombocytopenia in a Female Cynomolgus Macaque (Macaca fascicularis)

CM Parrula, J Mysore, H Burr, W Freebern, N Neef – Comparative Medicine, 2015

On day 4, a follow-up complete physical exam under ketamine sedation (10 mg/kg IM; ketamine

hydrochloride, Fort Dodge Animal Health, Fort Dodge, IA), showed diffuse, pale-red discoloration

in both inguinal regions, as noted previously, and multifocal pinpoint foci of

 

Estradiol protects female rats against sepsis induced by Enterococcus faecalis improving leukocyte bactericidal activity

RS Saia, FM Garcia, EC Cárnio – Steroids, 2015

0.5–1 × 10 10 CFU/animal) (time “zero” hour). At 6 and 24 h, rats were deeply

anesthetized (ketamine and xylazine at 55 and 10 mg/kg, respectively, ip) for sample

collection. As detailed in the subsequent sections, the blood

 

Hot Off the Press: Subdissociative‐dose Ketamine for Acute Pain in the Emergency Department

AB Drake, WK Milne, CR Carpenter – Academic Emergency Medicine, 2015

Social Media. Hot Off the Press: Subdissociative-dose Ketamine for Acute Pain in the Emergency

Department. How to Cite. Drake, AB, Milne, WK, Carpenter, CR (2015), Hot Off the Press:

Subdissociative-dose Ketamine for Acute Pain in the Emergency Department.

 

Optimization and application of an extraction procedure to determine drugs of abuse in solid environmental matrices of Turia River Basin

MJ Andres, R Alvarez, V Andreu, Y Pico – EGU General Assembly Conference …, 2015

Amphetamine, methamphetamine, ethylamphetamine, ecstasy, ethylone, bk-MMBDB and MBDB

belong to phenylethylamine group; codeine and ketamine belong to opioid and phencyclidine

group, respectively, and benzoylecgonine is the major excreted metabolite of the

 

Green spaces and cognitive growth in children

C Dieme – PNAS, 2015

AG. Previous Section. Neural mechanism of ketamine. Ketamine can produce rapid and

long-lasting antidepressant effects, but the drug’s potential for side effects and abuse limits its

widespread use, and the cellular mechanisms of ketamine’s effects are not yet known.

 

Increasing use of ‘party drugs’ in people living with HIV on antiretrovirals: a concern for patient safety

M Bracchi, D Stuart, R Castles, S Khoo, D Back… – AIDS, 2015

These substances are a combination of ‘club drugs’ (methylenedioxy- methamphetamine,

gamma-hydroxybutyrate, ketamine, benzodiazepine) and drugs that are more specifically used

in a sexualized context (methamphetamine, mephe- drone, poppers and erectile Ketamine

 

Halothane Modulates the Type I Interferon Response to Influenza and Minimizes the Risk of Secondary Bacterial Pneumonia through Maintenance of Neutrophil …

BA MacDonald, KV Chakravarthy, BA Davidson… – Anesthesiology, 2015

The authors demonstrate that halothane mitigates the risk of SBP postflu through modulation

of the effects of type I interferon (IFN). METHODS: Mice (n = 6 to 15) were exposed to halothane

or ketamine and treated with influenza and Streptococcus pneumoniae.

 

[HTML]Airtraq® laryngoscope-assisted fiberoptic bronchoscope intubation in a child with Pierre-Robin sequence: a case report

S Zhang, M Yi – International Journal of Clinical and Experimental …, 2015

Sedation was achieved with IV dexmedetomidine 1 μg/kg and ketamine 1 mg/kg. We

opted to use dexmedetomidine and ketamine in this child because they provide

sedation and analgesia without compromising respiratory drive.

 

[HTML]Transcutaneous electric acupoint stimulation alleviates remifentanil-induced hyperalgesia in patients undergoing thyroidectomy: a randomized controlled trial

Y Chen, Y Yao, Y Wu, D Dai, Q Zhao, L Qiu – International Journal of Clinical and …, 2015

Some medications, including ketamine, methadone, dextromethorphan, COX-2 inhibitors and

α 2 receptor agonists can modulate remifentanil-induced hyperalgesia [7]. Due to drug-related

side effects and longer duration of PACU stay, however, we have found these

 

Impact of Obesity on Endotoxin-Induced Disseminated Intravascular Coagulation.

T Duburcq, A Tournoys, G Viviane, T Hubert, V Gmyr… – Shock, 2015

animals). For the experiment, animals were premedicated with intramuscular injection of ketamine

(Ketamine 1000, 10 mg/kg of body weight; Virbac, Carros, France) and xylazine (Sedaxylan,

2.5 mg/kg of body weight; CEVA Santé Animale, Libourne, France). Then we

 

Endocannabinoid signaling mechanisms in the substantia nigra pars reticulata modulate GABAergic nigrotectal pathways in mice threatened by urutu-cruzeiro …

RC Almada, CM Roncon, DH Elias-Filho, NC Coimbra – Neuroscience, 2015

The surgeries were performed under deep anesthesia with 100 mg/kg ketamine (Ketamine

Agener, União Química Farmacêutica Nacional, São Paulo, Brazil) and 10 mg/kg xylazine

(Calmiun, União Química Farmacêutica Nacional, São Paulo, Brazil).

 

ACUTE INHIBITION OF MONOAMINE OXIDASE AND ISCHEMIC PRECONDITIONING IN ISOLATED RAT HEARTS: INTERFERENCE WITH POSTISCHEMIC …

MD Dănilă, AI Privistirescu, SN Mirica, A Sturza… – Canadian Journal of …, 2015

Male (body weight 400-450 g) and female (body weight 250-300 g) Wistar rats were anesthetized

with ketamine (Vetased, 30 mg/kg) and xylazine (Xylazin, 10 mg/kg) Page 4 of 23 Page 5. 5

ketamine able to induce anesthesia was chosen in order to not interfere with the IPC-

 

 

Radiofrequency Ablation (RFA)

 

In vitro artefact assessment of a new MR-compatible microwave antenna and a standard MR-compatible radiofrequency ablation electrode for tumour ablation

R Hoffmann, H Rempp, F Eibofner, DE Keßler… – European Radiology, 2015

Objective To evaluate and compare artefact configuration and diameters in a magnetic

resonance (MR)-compatible prototype microwave (MW) applicator and a standard MR-

compatible radiofrequency (RF) applicator for MR-guided tumour ablation. Methods Both

 

Does Surgical Resection Provide Better Outcomes Than Radiofrequency Ablation in Patients With BCLC Very Early-stage Hepatocellular Carcinoma?.

C Li, TF Wen – Annals of Surgery, 2015

Wolters Kluwer Health may email you for journal alerts and information, but is committed to maintaining

your privacy and will not share your personal information without your express consent. For more

information, please refer to our Privacy Policy. Skip Navigation Links Home >

 

Comparing outcome of radiofrequency ablation in Barrett’s with high grade dysplasia and intramucosal carcinoma: a prospective multicenter UK registry.

RJ Haidry, G Lipman, MR Banks, MA Butt, V Sehgal… – Endoscopy, 2015

Background and study aim: Mucosal neoplasia arising in Barrett’s esophagus can be

successfully treated with endoscopic mucosal resection (EMR) followed by radiofrequency

ablation (RFA). The aim of the study was to compare clinical outcomes of patients with

 

Effectiveness of focal vs. balloon radiofrequency ablation devices in the treatment of Barrett’s esophagus

J Brown, B Alsop, N Gupta, DC Buckles, MS Olyaee… – United European …, 2015

Abstract Background and aims The safety and efficacy of radiofrequency ablation (RFA) in

treatment of Barrett’s esophagus (BE)-associated dysplasia has been well established. The

effectiveness of focal and balloon RFA devices has not been compared. Therefore, the

 

Microwave Ablation: Comparison of Simultaneous and Sequential Activation of Multiple Antennas in Liver Model Systems

CM Harari, M Magagna, M Bedoya, FT Lee Jr… – Radiology, 2015

Although both methods have been used in clinical studies of radiofrequency (RF) and microwave

ablation, an optimal delivery method has not yet been determined (6–9). Comparison studies

of sequential and simultaneous RF ablation techniques have concluded that

 

Heparin Kinetics: The “Holy Grail” of Periprocedural Anticoagulation for ablation of atrial fibrillation

DF Briceno, A Natale, LD Biase – Pacing and Clinical Electrophysiology, 2015

anticoagulation in patients undergoing radiofrequency ablation for atrial fibrillation: results from

a multicenter prospective registry. anticoagulation in patients undergoing radiofrequency ablation

for atrial fibrillation: results from a multicenter prospective registry.

 

Catheter Ablation of Atrial Fibrillation Should Be Offered as Primary Therapy: What’s Your Hurry?

EF Wedam, MCP Haigney – Cardiac Electrophysiology Clinics, 2015

medications. Radiofrequency ablation/cryoballoon ablation: a cure for atrial fibrillation?

Merriam-Webster’s unknown. Does early radiofrequency ablation/cryoballoon ablation

prevent progression to permanent atrial fibrillation? A major

 

OC-037 6 year disease durability outcomes on patients treated with endoscopic therapy for barrett’s related neoplasia from the uk registry

R Haidry, G Lipman, A Gupta, J Dunn, H Smart… – Gut, 2015

Introduction Endoscopic therapy with combined Endoscopic mucosal resection (EMR) followed

by Radiofrequency ablation (RFA) is now the recommended first line Thereafter patients underwent

RFA 3 monthly until all visible BE was ablated or cancer developed (endpoints).

 

[HTML]Hybrid atrial fibrillation ablations and the increasing importance of the hybrid cardiovascular laboratory operating room

WJ Schleifer, JF Beshai, H Ramakrishna – Annals of Cardiac Anaesthesia, 2015

the epicardium. [4] Moreover, endocardial catheters can check for the completeness

of the epicardial lesions and potentially identify gaps, which can then be addressed

with endocardial radiofrequency ablation. A similar approach

 

[PDF]Effects of Hepatitis B Virus Load on Hepatectomy

M Wang, W Peng, TF Wen, LH He, C Li – Clin Microbiol, 2015

MC: Milan Criteria; HR: Hepatic Resection; AFP: Alpha-Fetoprotein; OS: Overall Survival; RFS:

Recurrence-Free Survival; DNA: Deoxyribonucleic Acid; CT: Computed Tomography; MRI:

Magnetic Resonance Imaging; RFA: Radiofrequency Ablation; PEI: Percutaneous Ethanol

 

HEALTH-RELATED QUALITY OF LIFE AFTER PERCUTANEOUS RADIOFREQUENCY ABLATION OF COLD SOLID BENIGN THYROID NODULES: A 2-YEAR …

R Valcavi, P Tsamatropoulos – Endocrine practice: official journal of the American …, 2015

OBJECTIVE: We studied the impact of Radiofrequency ablation (RFA) on health-related

quality of life (HRQL) in patients with benign thyroid nodules (TN) in a 2-year follow-up.

METHODS: Forty patients (35 female and 5 men; age 54.9±14.3 years) with cold thyroid

 

Comparison of laparoscopic radiofrequency ablation versus open resection in the treatment of symptomatic-enlarging hepatic hemangiomas: a prospective study

X Zhang, L Yan, B Li, T Wen, W Wang, M Xu, Y Wei… – Surgical Endoscopy, 2015

Background Radiofrequency ablation (RFA) has been demonstrated to be a promising

therapy for symptomatic large hepatic hemangioma. However, there is a lack of studies to

demonstrate the benefits and disadvantages of RFA as compared with surgical resection

 

… mucosal resection on the efficacy and safety of radiofrequency ablation for treatment of Barrett’s esophagus: results from the United States Radiofrequency Ablation

N Li, S Pasricha, WJ Bulsiewicz, RE Pruitt… – Diseases of the Esophagus, 2015

Summary The effects of preceding endoscopic mucosal resection (EMR) on the efficacy and

safety of radiofrequency ablation (RFA) for treatment of nodular Barrett’s esophagus (BE) is

poorly understood. Prior studies have been limited to case series from individual tertiary

 

… MicroRNA-122 Expression is a Poor Prognostic Marker in Patients with Hepatitis B Virus-related Hepatocellular Carcinoma who undergo Radiofrequency Ablation

HJ Cho, JK Kim, JS Nam, HJ Wang, J hee Lee, SS Kim… – Clinical Biochemistry, 2015

Objectives: Aim of this study was to investigate the prognostic potential of plasma microRNA-

122 levels in patients with hepatitis B virus (HBV)-related hepatocellular carcinoma after

hepatic resection or radiofrequency ablation (RFA).

 

[HTML]… efficacy enough to prevent stroke in atrial fibrillation patient with high CHADS2 score during peri-procedural catheter radiofrequency ablation? A case report with …

XM Shi, FK Chen, Z Liang, J Li, K Lin, JP Guo, ZL Shan – International Journal of …, 2015

Abstract Atrial fibrillation (AF) is a major cause of thromboembolic (TE) events including

stroke and transient ischemic attacks, catheter radiofrequency ablation (CA) has been

demonstrated to effectively eliminate AF in majority of patients. During the peri-procedural

 

Right upper lobe lung cancer: Resection through left anterior mediastinotomy

M Sirois, WA Arab, E Turcotte, Y Poulin – Asian Cardiovascular and Thoracic Annals, 2015

evaluation revealed a forced expiratory volume in 1 s of 1.8 L with carbon dioxide diffusion

capacity of 48% and maximal uptake of oxygen 14 mL min −1 kg −1 . Treatment including

stereotactic body radiation therapy, radiofrequency ablation, and surgery were discussed.

 

Magnetic guidance versus manual control: comparison of radiofrequency lesion dimensions and evaluation of the effect of heart wall motion in a myocardial phantom

A Bhaskaran, MAT Barry, SI Al Raisi, W Chik… – Journal of Interventional …, 2015

Abbreviations MNS Magnetic navigation system MC Manual control 1 Introduction Magnetic

navigation system (MNS) allows remote guidance of ablation catheters during radiofrequency

ablation for cardi- ac arrhythmias. Page 3. 2.2 MNS versus MC radiofrequency ablation

 

Thermal necrosis induced by electrocauterization as a local adjuvant therapy in local aggressive bone tumors, what is the safe limit for surgical margins? An …

M Aydin, K Basarir, M Armangil, HY Yildiz, Y Saglik… – Archives of Orthopaedic and …, 2015

Majno PE, Mentha G, Mazzaferro V (2010) Partial hepatectomy versus radiofrequency ablation

for hepatocellular carcinoma: confirming the trial that will never be, and some comments on the

indications for liver resection. Hepatology 51(4):1116–1118PubMedView Article; 23.

 

Functional Characterization of Rare Variants Implicated in Susceptibility to Lone Atrial Fibrillation

K Hayashi, T Konno, H Tada, S Tani, L Liu, N Fujino… – Circulation: Arrhythmia and …, 2015

 

Endoscopic Management of Early Esophageal Cancer.

JA Barnes, FF Willingham – Journal of Clinical Gastroenterology, 2015

proportionately. In the past decade, radiofrequency ablation has become the standard

first-line therapy for high-grade dysplasia when found in the precursor lesion to

esophageal adenocarcinoma, Barrett’s esophagus. Success

 

Chronic Regional Pain Syndrome (CRPS/RSD)

 

V33. Functional imaging of somatosensory finger representation and intracortical inhibition modulation in complex regional pain syndrome

S Strauss, M Grothe, T Usichenko, W Byblow, M Lotze – Clinical Neurophysiology, 2015

Neurophysiological pathology in CRPS type I is characterized by somatosensory and motor deficits.

Transcranial magnetic stimulation (TMS) and functional MRI rev. Neurophysiological pathology

in CRPS type I is characterized by somatosensory and motor deficits.

 

Exploiting resistive cross-point array for compact design of physical unclonable function

PY Chen, R Fang, R Liu, C Chakrabarti, Y Cao, S Yu – Hardware Oriented Security …, 2015

primitive that leverages the inherent randomness in the physical systems (eg the semiconductor

manufacturing process) to produce a unique response (output) for a given challenge (input)

[1]. Depending on the number of possible challenge-response pairs (CRPs), PuFs can

 

Do psychological factors influence recovery from Complex Regional Pain Syndrome Type-1? A Prospective Study.

DJ Bean, MH Johnson, W Heiss-Dunlop, AC Leed… – PAIN, 2015

Conflicts of Interest: none declared. Running Head: “Psychological factors in the recovery from

CRPS-1” Number of Pages: 19 Number of Tables: 3 Number of Figures: 1 Summary: Amongst

patients with recently-onset CRPS-1, those with higher levels of pain-related

 

A comparison of linear and non-linear data assimilation methods using the NEMO ocean model

P Kirchgessner, J Tödter, L Nerger – EGU General Assembly Conference Abstracts, 2015

pdaf.awi.de), which ensures identical experimental conditions for both filters. To

account for the nonlinearity, the assimilation skill of the two methods is assessed

by using different statistical metrics, like CRPS and Histograms.

 

The total probabilities from high-resolution ensemble forecasting of floods

J Olav Skøien, K Bogner, P Salamon, P Smith… – EGU General Assembly …, 2015

Weather Rev., 135(4), 1386-1402, doi:10.1175/MWR3341.1, 2007. Gneiting, T., Raftery,

AE, Westveld, AH and Goldman, T.: Calibrated Probabilistic Forecasting Using Ensemble

Model Output Statistics and Minimum CRPS Estimation, Mon.

 

Efficacy of combined physical and occupational therapy in patients with conservatively treated distal radius fracture: randomized controlled trial

V Filipova, D Lonzarić, BJ Papež – Wiener klinische Wochenschrift, 2015

Two participants from group A and two from group B were suspected of having complex

regional pain syndrome (CRPS) type I yet were not excluded from the trial since there

was no significant deviation regarding the observed variables.

 

Combining Graph Analysis and Recurrence Plot on fMRI data

A Lombardi, P Guccione, L Mascolo, P Taurisano… – Medical Measurements and …, 2015

Even if a visual inspection of CRPs can reveal valuable information about the relationship between

the two systems, the quantification of the structures in CRPs through CRQA has been used for

making more objective the comparison between the time series. Page 3.

 

Improving Precipitation Forecasts by Generating Ensembles through Postprocessing

DL Shrestha, DE Robertson, JC Bennett, QJ Wang – Monthly Weather Review, 2015

In this study, the forecast 3 performance is characterized by evaluating the bias, the Continuous

Ranked Probability Score 4 (CRPS), reliability and Relative Operating Characteristics (ROC)

to assess different aspects of 5 forecast quality. 6 The mean CRPS (hereafter 16

 

The Forecast Skill Horizon

R Buizza, M Leutbecher – Quarterly Journal of the Royal Meteorological Society, 2015

theoretical tools are deemed to be impractical to use. We select the continuous ranked probability

score (CRPS, Brown 1974, Hersbach 2000) as metric to decide when the closer to the observed

CDF (bottom panel). The CRPS is equal to the mean squared error

 

Functional Outcomes Following Bridge Plate Fixation for Distal Radius Fractures

A Lauder, S Agnew, K Bakri, CH Allan, DP Hanel… – The Journal of Hand …, 2015

2/134 deep infection. 2/134 extensor tendon adhesions. 1/134 EPL rupture. DASH: N/A. Hanel

et al 13, IV: retrospective chart review, 62 pts via chart review, second metacarpal, No CRPS,

1/62 ECRL rupture, 1/62 hardware failure, 0/62 postoperative digit stiffness. DASH: N/A.

 

New findings implicated in Coronary calcification in Chronic phase Kawasaki disease

T Yahata, K Ikeda, A Hamaoka, C Suzuki, A Yoshioka… – Circulation, 2015

tomography. We measured %FMD as an endothelial function marker and hs-CRPs

as an inflammatory marker, serum hydroperoxide and urinary 8-OHdG as oxidative

stress markers, and the bone mineral density (BMD). Patients

 

[PDF]Evaluation of the Red Sea State Food Security Status 2007-2009

AAA Ahmed – 2015

nutrition monitoring using MUAC Since 2006 no nutrition survey conducted. However, EWS

started collecting the nutrition information using the Community Resource Persons (CRPs)

to follow up the nutrition situation in sentinel sites in RPS and Tokar.

 

Spatio-temporal circular models with non-separable covariance structure

G Mastrantonio, GJ Lasinio, AE Gelfand – TEST, 2015

Page 1. TEST DOI 10.1007/s11749-015-0458-y ORIGINAL PAPER Spatio-temporal

circular models with non-separable covariance structure Gianluca Mastrantonio1 ·

Giovanna Jona Lasinio2 · Alan E. Gelfand3 Received: 7

 

Predictors of Spinal Cord Stimulation Success

P De La Cruz, C Fama, S Roth, J Haller, M Wilock… – … : Technology at the Neural …, 2015

Failure, Success. CRPS, Complex Regional Pain Syndrome; FBSS, Failed Back Surgery

Syndrome. Age, Mean + Range, 47.8 + 25.0, 51.2 + 53. Gender, Male : Female, 3:7, 20:27. Hybrid

(%), 0, 8.1. Indication, FBSS (%), 60, 37.8. CRPS (%), 20, 37.8. Neuritis (%), 20, 24.3.

 

Physical Therapy Examination and Assessment

JM David, C OCS, M Ariana Brutico – journal of orthopaedic & sports physical therapy, 2015

Why Are My Nerves So Sensitive? Neuroscience Education for Patients With CRPS

or RSD. Authors: Ariana Brutico, MSPT, PhD. AFFILIATION: Body Dynamic: Outpatient

Physical Therapy, Pilates, and Yoga Clarks Summit, PA.

 

Improved model output statistics of numerical weather prediction based irradiance forecasts for solar power applications

RA Verzijlbergh, PW Heijnen, SR de Roode, A Los… – Solar Energy, 2015

irradiance is zero. The evaluation of the probabilistic forecasts is carried out using

two metrics. The first is the continuous ranked probability score (CRPS): equation(9).

CRPS ( k ) = 1 T ∑ t = 1 T ∫ x F ̂ t + k | t ( x ) – H ( x – y t + k ) 2.

 

Thoracic sympathectomy: a review of current indications

M Hashmonai, AEP Cameron, PB Licht, C Hensman… – Surgical Endoscopy, 2015

However, because the role of the autonomous nervous system is obscure in the pathogenesis

of these disorders, the term “Complex regional pain syndrome” (CRPS) is preferred. There is

very little good evidence in the literature to guide treatment of CRPS.

 

NGF-induced synapse-like structures in contralateral sensory ganglia contribute to chronic mirror-image pain.

CF Cheng, JK Cheng, CY Chen, RH Rau, YC Chang… – Pain, 2015

image (contralateral) side [21]. This symptom has been observed in many clinical

pain conditions, such as complex regional pain syndrome (CRPS) [23], rheumatoid

arthritis [35], fibromyalgia [4], and neuropathic pain [27]. Mirror

 

Process Documentation Research and Impact of Community-Driven Development Grants Research in Rural India, Socioeconomics Discussion Paper Series 34

M Bhattarai, Y Mohan Rao, BL Varalakshmi, VD Duche… – 2015

Item Type: Socioeconomics Discussion Paper Series. Divisions: RP-Market Institutions

and Policies. CRPS: CGIAR Research Program on Policies, Institutions, and Markets.

Series Name: Socioeconomics Discussion Paper Series.

 

SCAMP: A new tool for an old problem

RH Rathod – Journal of Hospital Medicine, 2015

BWH, Brigham and Women’s Hospital; CRPS, complex regional pain syndrome; EPL, extensor

pollicis longus; PFL, Flexor pollicis longus; MRN, medical record number; N/A, not applicable;

OT, occupational therpay; PA, physician’s assistant. Download figure to PowerPoint.

 

Fibromyalgia

 

Results of an active neurodynamic mobilization program in patients with fibromyalgia syndrome: a randomized controlled clinical trial

JR Torres, IC Martos, IT Sánchez, AO Rubio… – Archives of Physical …, 2015

To examine the effects of an active neurodynamic mobilization program on pain, neurodynamics,

perceived health state and fatigue in patients with fibromyalgia s. Setting. A local Fibromyalgia

Association. Participants. 48 patients with fibromyalgia syndrome. Interventions.

 

The evaluation in terms of sarcopenia of patients with fibromyalgia syndrome

I Koca, E Savas, ZA Ozturk, A Boyaci, A Tutoglu… – Wiener klinische …, 2015

Background Fibromyalgia syndrome (FMS) is an extra-articular rheumatic illness,

characterized by widespread body pain and decreased muscle function. Generalized loss of

muscle mass and strength is named as sarcopenia. The objective of this study was to

 

Stigma, Unspeakable Dilemmas, and Somatic Symptoms–a Legacy of Suffering in CFS/ME and Fibromyalgia

J Griffith, N Ryan – Meanings of ME: Interpersonal and Social Dimensions …, 2015

Chronic fatigue syndrome (CFS) and fibromyalgia are both illnesses for which suffering is

amplified by stigmatisation. People with these illnesses often feel judged, devalued,

marginalised, or discriminated against by employers, family members, friends and, most of

 

[PDF]Quantitative analysis of nailfold capillary morphology in patients with fibromyalgia

DH Choi, HS Kim – Korean Journal of Internal Medicine, 2015

Background/Aims: Nailfold capillaroscopy (NFC) has been used to examine morphological

and functional microcirculation changes in connective tissue diseases. It has been

demonstrated that NFC patterns reflect abnormal microvascular dynamics, which may play

 

Fibromyalgia incidence among patients with hepatitis B infection

L Yazmalar, Ö Deveci, İ Batmaz, D İpek, T Çelepkolu… – International Journal of …, 2015

Aim The purpose of our investigation was to evaluate the incidence of fibromyalgia

syndrome (FMS) and identify FMS-related clinical symptoms in hepatitis B virus (HBV)

patients. Methods One hundred and eighteen HBV surface antigen (HbsAg)-positive

 

[PDF]Rheumatology: Current Research

EÖ Bulduk, B Biral – 2015

Page 1. Treatment Approaches of Juvenile Fibromyalgia Syndrome Abstract Juvenile

fibromyalgia syndrome (JFMS) is an idiopathic long-term health condition characterized

by widespread musculoskeletal pain in children and adolescents.

 

Meanings of ME: Interpersonal and Social Dimensions of Chronic Fatigue

CD Ward – 2015

10 11 12 13 14 The Challenge of CFS/ME in Primary Care Laura Saunders The Said and the

Unsaid: Ambivalence in CFS/ME Christopher D. Ward Stigma, Unspeakable Dilemmas, and

Somatic Symptoms–a Legacy of Suffering in CFS/ME and Fibromyalgia James Griffith and

 

AMPK phosphorylation modulates pain by activation of NLRP3-inflammasome

P Bullon, E Alcocer-Gómez, AM Carrión… – Antioxidants and Redox …, 2015

Deficient AMPK activation and over-activation of NLRP3-inflammasome axis was also observed

in blood cells from patients with Fibromyalgia (FM), a prevalent human some pain conditions as

neuropathic pain, fibromyalgia (FM), and complex regional pain syndrome (6,15,16).

 

Is Chronic Pain a Disease in Its Own Right? Discussions from a Pre-OMERACT 2014 Workshop on Chronic Pain

AM Taylor, K Phillips, JO Taylor, JA Singh… – The Journal of …, 2015

In a review of functional disorders36, various mechanisms were proposed to explain the cause

of conditions such as irritable bowel syndrome, fibromyalgia, temporomandibular joint disorder,

and inter- stitial cystitis, including enhanced pain perception, altered brain activation

 

Compendium for the Antenatal Care of High-Risk Pregnancies

H Narayan – 2015

AB1222-HPR Hypervigilance to Emotional Subliminal Images in Patients with Fibromyalgia

I Peláez, F Mercado, P Barjola, S Cardoso – Annals of the Rheumatic Diseases, 2015

Background Fibromyalgia (FM) is a chronic condition characterized by the presence of pain,

fatigue and cognitive dysfunction, among other symptoms. Previous research (Duschek et

al., 2014) also indicated that patients show an hypervigilance pattern to pain and negative

 

[HTML]Temporal analysis of pain responders and common adverse events: when do these first appear following treatment with pregabalin

J Fink, B Emir, B Parsons, A Clair – Journal of Pain Research, 2015

Clair Pfizer, New York, NY, USA Background: Pregabalin is an α2δ ligand indicated in the USA

for treatment of a number of chronic pain conditions, including diabetic peripheral neuropathy,

postherpetic neuralgia, pain associated with spinal cord injury, and fibromyalgia.

 

SP0133 Juvenile Idiopathic Arthritis and Other Pediatric Rheumatic Diseases

T Avcin – Annals of the Rheumatic Diseases, 2015

The clinical trials of CCX168, a small molecule antagonist of human C5aR, in human is underway.

Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2015-eular.6705 FRIDAY, 12

JUNE 2015 WIN session 5 SP0131 FIBROMYALGIA: WHAT IS NEW LJ Crofford.

 

Neuropathic pain as part of chronic widespread pain: environmental and genetic influences.

SK Momi, SM Fabiane, G Lachance, G Livshits… – Pain, 2015

frances.williams@kcl.ac.uk; +44 (0) 20 7188 6765 Keywords: chronic widespread pain;

neuropathic pain; genetic; fibromyalgia; twin ACCEPTED ABSTRACT Chronic widespread pain

(CWP) has complex aetiology and forms part of the fibromyalgia syndrome.

 

SP0130 C5A and its Receptor in Anca-Associated Vasculitis

MH Zhao – Annals of the Rheumatic Diseases, 2015

The clinical trials of CCX168, a small molecule antagonist of human C5aR, in human is underway.

Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2015-eular.6705 FRIDAY, 12

JUNE 2015 WIN session 5 SP0131 FIBROMYALGIA: WHAT IS NEW LJ Crofford.

 

The spectrum of noncoeliac gluten sensitivity

I Aziz, M Hadjivassiliou, DS Sanders – Nature Reviews Gastroenterology & …, 2015

with NCGS is described as well as the symptom manifestations commonly reported after gluten

exposure, which include intestinal symptoms consistent with IBS, and extraintestinal symptoms

such as neurological dysfunction, psychological disturbances, fibromyalgia and skin

 

Neuro-Bio-Behavioral Mechanisms of Placebo and Nocebo Responses: Implications for Clinical Trials and Clinical Practice

M Schedlowski, P Enck, W Rief, U Bingel – Pharmacological Reviews, 2015

 

Health-related quality of life improvements among women with chronic pain: comparison of two multidisciplinary interventions

SV Björnsdóttir, M Arnljótsdóttir, G Tómasson, J Triebel… – Disability & Rehabilitation, 2015

18,19]. Recently published systematic reviews on multidisciplinary programs for

people with chronic pain [19], chronic low back pain [20] or fibromyalgia syndrome

[21] agree on recommended content in such programs. This

 

NGF-induced synapse-like structures in contralateral sensory ganglia contribute to chronic mirror-image pain.

CF Cheng, JK Cheng, CY Chen, RH Rau, YC Chang… – Pain, 2015

image (contralateral) side [21]. This symptom has been observed in many clinical

pain conditions, such as complex regional pain syndrome (CRPS) [23], rheumatoid

arthritis [35], fibromyalgia [4], and neuropathic pain [27]. Mirror

 

Physical Therapy Examination and Assessment

JM David, C OCS, M Ariana Brutico – journal of orthopaedic & sports physical therapy, 2015

and nerve sensitivity. It is one of several manuals written by the primary author, all

of which discuss concurrent topics involving pain and recovery from injury, including

whiplash, headaches, and fibromyalgia. The manual begins

First Clinical Trial Shows Efficacy of IV Ketamine for Suicidal Thoughts

First Clinical Trial Shows Efficacy of IV Ketamine for Suicidal Thoughts

Ketamine is a long known anesthetic agent that is still used for induction anesthesia in medicine today.  It is also used off label for the treatment of various treatment-resistant diseases ranging from depression to various pain disorders.  For the treatment of pain, intravenous ketamine has proven successful in countless case studies and numerous placebo-controlled clinical trials.  Interestingly, ketamine has gained much attention in the media recently as a possible treatment for depression.  Since originally reported as efficacious in certain cases of depression, it has proven successful in subtypes of this disease, like post-traumatic stress disorder (PTSD).

Although suicidality (suicidal thoughts) is commonly expected to accompany depression, this is not always the case.  The two diseases are clinically different as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM).  Interestingly, a recent clinical study aimed to assess the efficacy of intravenous (IV) ketamine for the treatment of suicidal cognition in symptomatic patients with treatment-resistant unipolar major depression.  The patients that were entered into this trial had inadequate responses to more than three other antidepressant medications.  Interestingly, there is currently no FDA-approved drug for the treatment of suicidality.  A team of researchers from the University of Pittsburgh, Icahn School of Medicine at Mount Sinai, Baylor College of Medicine, and the Michael E. Debakey VA Medical Center conducted a placebo controlled clinical trial to evaluate the efficacy of intravenous ketamine for the treatment of suicidality.  Fifty seven patients completed the trial and were assessed by the researchers using a composite index of explicit suicidal ideation.  A psychoactive placebo, midazolam, was used.

The researchers published their findings in the journal of Depression and Anxiety.  They found that the intravenous ketamine group had rapid reductions in suicidal cognition “over and above” the active placebo group.  This finding could be critical for the development of an FDA-approved medication for the treatment of suicidality, a would-be first for this indication.  The researchers concluded that their findings warrant further study into ketamine’s antisuicidal effects in higher-risk patients.

Intravenous ketamine is offered at the Florida Spine Institute by Dr. Ashraf Hanna’s clinical team.  Dr. Hanna has achieved great success using IV ketamine for the treatment of many diseases that fail to respond adequately to conventional therapies.  To find out if this therapy might be right for you, please make an appointment to see Dr. Hanna.

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