Since the time when Centers for Disease Control and Prevention (CDC) came up with the guidelines  to further responsible attitude towards opioid prescriptions in acute pain settings, we have been wondering the status of awareness among opioid prescribers in our institution as well as their responsiveness to the CDC guidelines. Recently we theoretically proved that 28-day prescription cycle may be better than 30-day prescription cycle to avoid stockpiling of opioid pills with the chronic pain patients . Henceforth, it is time to investigate whether our acute pain settings namely our outpatient surgical services are contributing to stockpiling of opioids with our opioid naive outpatient surgical patients and if it's happening counterintuitive to the CDC recommendations, then whether simple awareness program can limit this stockpiling of opioid pills with our opioid naive outpatient surgical patients. Simplistically, the CDC guidelines  recommend that when opioids are started in opioid naive patients in acute settings, the morphine milligram equivalents should be in the dosage of < 50mg/day for a total duration of less than or equal to 3days. Essentially it means hydrocodone (with 1:1 morphine equivalence [3-4]) in the dosage of < 50mg/day for a total duration of less than or equal to 3days and oxycodone (with 1:1.5 morphine equivalence [3-4]) in the dosage of < 33mg/day for a total duration of less than or equal to 3days.
Introduction: Coccydynia (coccyx pain, tailbone pain) has many etiologies. Avascular necrosis (AVN, osteonecrosis) of the coccyx is a rarely reported cause of coccyx pain.
Case report: We present a case of a 35-year-old male who presented with complaints of four years of worsening coccyx pain. He had a history of bilateral hip replacement surgeries approximately 3 years earlier due to AVN of the bilateral femoral heads after multiple exposures to oral steroids and steroid injections at his bilateral hips. This raised our concern that his coccydynia may have been due to AVN of the coccyx. However, magnetic resonance imaging (MRI) of the sacrum and coccyx fortunately revealed no evidence of AVN.
Discussion: Our medical literature search found only two prior publications documenting AVN of the coccyx. While diagnostic workup in our particular patient did not reveal sacrococcygeal AVN, it was an important step to have assessed for that possibility, given his history of pelvic AVN and his risks for AVN via both oral and injectable steroids.
Conclusion: Although AVN of the coccyx is a rare cause of coccydynia, clinicians should consider this possible diagnosis in coccydynia patients who have risk factors for AVN.
Background: There are variety of pain scales available for use by the health care providers to assess patients' pain. Numerical rating scales (11-point 0-10 NRS) are one of the most commonly used pain scales for pain assessment, although some studies have questioned the adequacy of NRS for pain assessment.
Objectives: To assess how well the standard ordinal scale (11-point NRS) correlates with a simplified nominal scale (3-point expectation score), named by us as Yes-No-Don't Know (YNDK) scale when used in chronic pain patients presenting to our University Based Pain Clinic.
Methods: During the study period, patients in our pain clinic were assessed for pain severity score per NRS, pain relief score per NRS, satisfaction with current pain medication regimen per YNDK scale, expectation of change in current pain medication regimen per YNDK scale, and whether that expectation was eventually met at our pain clinic.
Results: A total of 243 patients were included in our study. It was worth noting that included patients were primarily middle aged (67%); new patients were primarily males (82%), while follow-up patients were primarily females (62%). There was strong correlation (positive or inverse) amongst majority of correlated NRS scores and YNDK scale scoring. Despite more than 3/4th of patients reporting severe pain (NRS 7-10), only less than half of these patients wanted their pain medications changed per YNDK scale.
Conclusions: Despite simplifying the pain assessment, 3-point YNDK score may be an appropriate adjunct for pain scoring wherein it can be used independently, complementarily or supplementary to 11-point NRS score in rapid turnover pain clinics to improve fulfillment of chronic pain patients' expectations.
Coccyx pain (also called coccydynia, or tailbone pain) has a broad range of etiologies, including traumatic and non-traumatic causes. Iatrogenic etiologies of coccydynia are rarely reported. This is the first report of iatrogenic coccydynia due to the use of a chiropractic actuator. An actuator (also known as an activator adjusting instrument) is a spring-loaded hand-held device that delivers a sudden mechanical force to the anatomic site where it is applied. We report a patient whose neck and shoulder pain were assumed to be due to cranio-dural stress syndrome. An actuator was used to deliver forces to the coccyx region in hopes that relieving dural tension at the coccyx might improve her neck pain, which it did not. Upon receiving the actuator treatments to her coccyx, she had immediate onset of coccyx pain, which lasted for many months. The patient had no prior history of coccyx symptoms or trauma. She eventually presented for treatment at our Coccyx Pain Center, on an academic medical school campus. Actuator use at the coccyx should be added to the list of causes of tailbone pain. Patients and clinicians should be aware of this risk.
The etiology of carpal tunnel syndrome was studied by comparing the role of genetics, sleep position and sexual intercourse as possible causes of idiopathic carpal tunnel syndrome. The etiologic potential of the three theories was analyzed using a modified version of the Bradford Hill criteria of causation. All three theories scored equally well according to eight of the nine Bradford Hill criteria. When evaluated according to the ninth criterion which represented coherence, and comprised of seven non occupational risk factors for carpal tunnel syndrome, sexual intercourse emerged with the highest score. It is concluded that among the three etiologic mechanisms under consideration, repetitive motion during sexual intercourse is the most likely cause of non occupational carpal tunnel syndrome.
As an anesthesia provider, we are responsible for ensuring adequate perioperative analgesia. One of the pain management modality that is frequently used in perioperative settings is patient-controlled analgesia (PCA) for the parenteral opioids . Since the famous presidential address of James Campbell (1996) to the American Pain Society , pain has come a long way as an established fifth vital sign . With aggressive policies at diagnosing, documenting and managing pain of the patients, PCA has become an important modality that is utilized more than often beyond the realms of perioperative settings. The application of PCA is no longer limited to acute perioperative pain; but it includes management of difficult-to-intractable acute pain in chronic pain patients who are admitted for inpatient management of pain-related or pain-unrelated symptoms. The most common pain assessment tool used in adult patient population is visual analogue scale (VAS) [4-6] that is available primarily in two forms: 0-100 mm scale and 0-10 Numerical Rating Scale (NRS). Their sensitivity to assess pain are approximately equal  and NRS is apparently more popular due to patient’s ease in reporting 0-10 VASscores.
The currently available versions of PCA deliver a-predetermined intravenous dose of opioids (as appropriately adjudged by the ordering physician) on patient’s decided dosing interval: the interval can be as low as every 6 minutes (the lockout interval). The current versions of PCA are not equipped to record the actual VAS scores because each time the patient feels pain requiring medication, irrespective of the VAS scores the patient pushes the same single-button mechanism (Figure 1) to deliver the same predetermined dose as fed in the PCA’s software. In my opinion, it is time that single-button PCA should be replaced with a 1-10 numbered-remote PCA (Figure 1). The lowest score of VAS ‘0’ in NRS scale may not be needed in this remote because VAS score ‘0’ may not prompt the patient to push the number on the remote as patient is not expecting any pain medication relief for VAS score=0. The patients will get this remote and push the number on the remote corresponding to their VAS scores. Consequently, the PCA’s software will deliverVAS-specific variable doses (including zero dose for low non-zero VAS scores) as pre-determined by the ordering and the inputting physician. To avoid inadvertent pushing of the remote's numbers, the remote will have a hard transparent plastic cover that will be lifted by the patient each time he/she will need to activate PCA for VAS-specific dose. The major advantages of this improvisation will be that
(a) In comparison to single-button PCA, the patient will have to be more alert as well as oriented to push the correct number on numbered-remote PCA for VASscores(b) The PCA’s software database will have the VAS scores recorded over times as recording of VAS will be possible at all the time; however the demands (as recorded in current versions of PCA) will be attributed to those instances when VAS-specific dose per PCA software will not be delivered due to the lockout interval(c) The patient will not have to worry about reporting VAS scores as well as requesting medications separately(d) The physicians will have option to input VAS-guided doses in the PCA’s software(e) The physicians will have option to run a 'Sham PCA' wherein the patients will be counseled to use the numbered-remote PCA only for regular recording of VAS scores; and the medications (in form of IV PUSH or oral doses) will be administered by the nursing staff.
This VAS-specific PCA model is not a new innovation but an improvisation of old school of pain medicine and imbibing into the PCA-based analgesia regimens wherein the patient controls his/her pain reporting and consequently appropriate analgesic administration. The physicians ordering pain medication as a range of dose as well as a range of dosing interval (e.g. morphine 1-2mg IV every 2-4 hours) was a common place till recently when patient safety regulatory entities recently curtailed this practice to avoid medication error and overdosing [8-9]. However, the regulatory entities allow the medication dose range orders  if the corresponding pain assessment tool range is also included with clear cut instructions about withholding medications depending on patient’s status and other vital signs (e.g. morphine 1-2 mg IV every 2-4 hours; 1mg for VAS scores 4-6, 2mg for VAS scores 7-10, decide dosing interval keeping Modified Ramsay Sedation Score ≥3) . These range orders have not been limited for use of intravenous medications but pain physicians have used these range orders for oral opioids with similarly clear cut directions of administration by the nursing staff.
The few cautions that will be needed for this numbered-remote PCA to succeed are that instead of wireless remotes, cables with predetermined lengths will be required so that remote-PCA by proxy can be avoided. Additionally, the wireless remotes will potentially increase the electromagnetic pollution/interference in the patient’s room. Moreover, the cables will ensure the continued safety against lost/misplaced/far-placed remotes in case the patient emergently needs to press for VAS-specific number to self-administer medication. The major incentive for patients will be that they will crowd and vouch for the hospitals that have more comprehensive pain scores databases as extracted from these VAS-specific PCA’s software. The aims of the catering hospitals will be to keep these pain scores graphs (areas under line-curve) under a minimum efficacious numbers as determined by their site-specific and general population validation studies. These target areas under curves will be different for acute pain patients, and acute on chronic pain patients. These areas under line-curve will be determined as following : the ‘area’ above the average values minus the ‘area’ below the average values wherein the "area" above the average values is the sum of (valuen - average) where valuen are the values that are greater than average value and the "area" below the average values is the sum of (average - valuen) where valuen are the values that are lower than average value.
Let us consider this example based on 10 random numbered VAS score generated from http://www.random.org/ . Random VAS numbers: 10, 9, 4, 7, 6, 1, 2,1,1,1. ‘Area’ above average (Average VAS for these ten numbers=4): Sum (2, 3, 5, 6)=16. ‘Area’ below average: Sum (3, 3, 3, 3, 2)=14. Thus the final ‘area’ under the line-curve is 2. Even though this example calculated average VAS based on the random ten numbers, the hospitals can decide to universally consider average and acceptable VAS=5 that can then used as a cut off to decide about the ‘area’ aboveVAS=5 and ‘area’ below VAS=5. The other method of ‘area under line-curve’ called ‘TRAPEZOID RULE’  cannot be used as the time difference between the two recorded VAS in the numbered-remote PCA will not be uniformly spaced and often times VAS scores will be zero that the patient will not be inputting in the software. These discontinuities and sporadic reporting ofVAS in the PCA database will interfere with the ‘TRAPEZOID RULE’ based assessment of ‘area under line-curve’.
In summary, it is high time to have this innovation in pre-existing PCA models so that clinical trials can be initiated for the validity of this scenario because in my opinion, it is worth a transition for correct VAS scores database and corresponding medication use with patient-controlled analgesia regimens.
Nowadays, one cannot but recognize a key role of the peripheral and central glial cells for generation of clinical neuropathic pain. Many cytokines are released from glial cells, immune cells and nociceptive primary afferent central or peripheral terminals by injury, bacterial or viral infection, and envenomation by bee venom or scorpion. Released cytokines mutually affect by paracrine or autocrine manner among glias, immune cells and neurons, thereby produce and transmit the exaggerating pain information to the brain. Indeed, suppression of activated glia and immune cells by chemical agents or antibodies can relief abnormal pain caused by various experimental neuropathies. Thus, abnormal exaggerated pain cannot be explained without the role of glia and immune cells. Many investigators emphasized that therapeutic use of inactivating agents to glial and immune cells but not to neurons is available for alleviation of clinical pain. Thermo-TRP channels, TRPV1, TRPA1 and TRPM8 could not sense neuropathic pain by themselves without close interactions between glias, immune cells and TRP channels. The removal of persistent clinical pain will be rescued by treatment with inactivating chemicals to glias and immune cells. In addition, physiological noxious heat could be sensed by unknown sensor other than thermo-TRP channels, TRPV1, TRPA1 and TRPM8
BACKGROUND: Contrary to some beliefs, all children do experience pain, with its adverse emotional and social consequences. Pain may be of diagnostic and therapeutic origin such as lumbar puncture, bone marrow aspiration, or venipuncture. The aim of this review is to sensitise all health care providers to appreciate, prevent and control pain in children. Relevant literature from selected references on the current concepts of paediatric pain management was reviewed. Various pain assessment modalities indicate that pain is a common accompaniment and complication of paediatric surgery. Pain in children is under diagnosed and under treated in our environment. The popular dogma that âchildren do not feel painâ and âpowerful analgesics may lead to drug addictionâ is erroneous and misleading. CONCLUSION: Concerted efforts are required to enhance our understanding of the mechanisms of pain in children and its diagnosis and treatment. Fears of the side effects of analgesics and anaesthetics such as addiction in children are often exaggerated. Clinicians should be familiar with current pain management modalities in children.
Cystatin C (CC) is a cysteine protease inhibitor present in cerebrospinal fluid (CSF) at high concentration. The abnormal CSF CC levels have been associated with numerous neurological diseases. It has been proposed as a pain biomarker and as a neuroprotector factor. We had analyzed its effect on sleep and on the recovery from a traumatic brain injury (TBI) in rats. We found that high doses of CC increased rapid eye movement sleep and worsened the TBI recuperation as they increased mortality and bleeding. Because the body temperature has an impact on sleep regulation and on recuperation after a cerebral trauma, we decided to determine if the administration of CC had an effect on body temperature and if it produced a modification in the perception of pain. The intracerebroventricular injection of CC caused a significant decrease in body temperature at higher doses (90, 175, 350, 700 fmoles) and the highest doses also increased the latency of the response to a hot plate, a central pain-perception test.
A new concept was put forward by Ducic et al (1) when based on their anecdotal experience and retrospective review, they documented that macromastia was contributing to the headaches in the patients and reduction mammoplasty was shown to relieve the headaches significantly in these patients. Per Ducic et al, the underlying mechanisms for coexistent macromastia and headaches are complex and may be related to the body mass index, metabolic syndromes of obesity, increasing age of the patients and chronic occipital neuralgia secondary to the weight of the breasts. However, I want to elicit a different perspective to the mechanism of the chronic headaches secondary to the marcomastia. When Einer-Jensen and Hunter (2) brought forward the simile to the counter-current heat exchange mechanism that keeps the brains, testes and ovaries cooler, it has become my understanding that the reason for keeping these organs cooler as compared to other organs may be related to their higher cellular metabolic activities with constant vulnerability to the fragility of the nerve cells as well as the reproductive cells wherein each fragile vulnerable cell lost may interfere with either the intact higher nerve center functioning or the intact transfer of the genetic code through the generations. Herein, the importance of brain temperature was recently re-hypothesized by me (3) to possibly re-explore the multitude of patho-physiological phenomena that were un-investigated in humans because of the lack of the non-invasive brain temperature monitoring until now when Marc Abreu researched and presented the Brain Temperature Tunnelâ¢ (4) to non-invasively and continuously monitor the brain temperature. Based on this background discussion, it is my understanding that the brain temperature changes elicited by the insulating cushion of the large size breasts over the chest wall may be interfering with the adequate initiation of cooler blood flow in the arch of aorta and the origins of the carotid arteries before these arteries travel through the exposed areas of the non-hairy necks. The physiological concerns may be even worse for the deeper seated vertebral arteries and the subsequently supplied posterior intracranial structures. The cushioning insulation by the dense breast tissue at the origin of the cerebral blood flow may be worsening in amounts secondary to the essential supporting undergarments for maintaining good natural posture by the patients with macromastia. This concept may be worth exploring to better understand the headaches in the females with or without macromastia as the brain temperature fluctuations may be the underlying concern for the differential maintenance of the breast cleavage across the gender with their differential density of the breast tissues; and the breast cleavage may have been mistaken as a sexual phenomenon until now when it actually may have overriding physiological in-situ mechanisms to overcome the heat insulation of the originating cerebral blood flow as accrued by the dense breasts.