Research published at International Conference on Opioids, Harvard Medical School, Boston, Massachusetts

Research published at International Conference on Opioids, Harvard Medical School, Boston, Massachusetts

 
Below is a summary of our research presented June 09-11, 2013, at the Third Annual International Conference on Opioids, Harvard Medical School, Joseph P. Martin Conference Center, Boston, Massachusetts. This study was done jointly by Dr. Damiani and Dr. Campa.

Dr. Campa was on-site to present our findings. We believe our research will help other physicians treat more safely those patients who present with persistent pain, requiring high dose and/or prolonged use of narcotics.

John A. Campa III, MD
Clinical Neurosciences
June 18, 2013

_________________________________________________

Correlation Of Oxycodone Daily Use To Oral Fluid Levels And Its Potential For Detection Of Opioid Induced Hyperalgesia 
- A Pilot Study

L. Damiani, PhD, MD-Candidate, School of Medicine, University of New Mexico, Albuquerque, NM; J. A. Campa III, MD, Albuquerque, NM; Faculty, School of Medicine, University of New Mexico, Albuquerque, NM.

Background

Clinicians who treat patients suffering from persistent pain must face the issue of monitoring and regulating opioid medication consumption. Evidence suggests prolonged exposure to opioids may lead to Opioid Induced Hyperalgesia (OIH), i.e., the patient becomes paradoxically more sensitive to pain². Hence, an easily performed lab assay, i.e., oral fluids toxicology (OFT), would be an invaluable clinical tool to assist the clinician in providing safe opioid dosing, while avoiding the induction of OIH.

Aim

The aim of this study is to assess the reliability of the oxycodone OFT therapeutic range and its potential for detecting risk for OIH.

Methods

A 10 month retrospective chart review was performed to study patient oxycodone use and its measurement by OFT (Forensic Fluids Laboratories, Inc, Kalamazoo, MI).

Hypothesized OIH Thresholds

We believe the hypothesized daily opioid amount in morphine sulfate equivalents (MSEq), where OIH is likely present, is 300 mg per day. Similarly, the hypothesized daily amount where a patient is at probable risk for OIH induction is 86.5% of 300 mg or 260 mg (MSEq). The rationale for these thresholds is based on our unpublished clinical observations and experience. The only study done within the last 10 years looking at daily morphine equivalents intake and OIH has set a range at approximately 90-200 mg/day⁶. Therefore, a better understanding of the range for morphine equivalents and OIH is required. The oxycodone MSEq is calculated by multiplying the daily amount in milligrams by 1.5. Inclusion criteria: patients taking oxycodone who had OFT.

Results

A total of 19 patients were eligible for the study. Probable OIH was postulated in four patients (P6, P7, P15, P19) and two were deemed to be at risk for OIH (P8, P16). Of the remaining 13/19 (68%) patients not at risk for or having OIH, our data reveals that OFT reliably assessed oxycodone use, relative to the therapeutic range (10-500 ng/ml), in 85% (11/13) of patients (outliers, P5, P9). Of the remaining six with abnormal results > 500 ng/ml, two of the four patients with probable OIH (P6, P15) and one of the two at risk for OIH (P16) were detected, for a reliability detection rate of 50%.

Discussion

The aim of this study was to assess the reliability of the OFT lab’s oxycodone therapeutic range and its potential for detecting risk for OIH, i.e., would it correspond to what we perceive as excessive use of oxycodone, resulting in OIH. The discrepancies between our patients perceived to be overusing oxycodone and the results returned by the lab are likely a function of at least three factors: 1. how the therapeutic range was determined, 2. high metabolizers, 3. patient non-compliance.

According to Wylie et al.⁵, the ability to detect drugs in oral fluids was based upon saliva specimens collected from a drug-free, healthy population, which were then “spiked” with varying drug concentrations. No population-based study was done to determine actual therapeutic levels. The therapeutic ranges were determined from an article stating, “we have gathered the data in the table from the literature and from personal experience. These values are not considered absolute, but are to be used as a guide in evaluating a given case. The values can be affected by dose, route of administration, absorption differences, age and sex, tolerance, method of analysis, pathological or disease state, postmortem redistribution, etc.” ⁹ Therefore, although the therapeutic range set by the lab is not necessarily inaccurate, our results demonstrate that a new therapeutic range for oxycodone may be needed, as some patients with or at risk for OIH were not detected with the lab’s current reference range.

Regarding high metabolizers, the one patient who was at risk for developing OIH (P8), that remained undetected by OFT, was a smoker. Alternatively, those that remained undetected by OFT, may have simply been non-compliant, i.e., taking less medication than admitted to. Hence, the clinician must consider the potential for nicotine related (and other agents) induction of the hepatic microsomal enzyme system and non-compliance when assessing patients undergoing OFT.

Opioid Induced Pseudoneuropathy - OIP?

An unexpected finding at six weeks after patient P6 was completely withdrawn from all opioids, was his regained ability to play the saxophone after 15-20 years. He had previously been told his inability to feel the key pads on the instrument was due to his underlying and progressive neuropathy. His improved touch sensation and ability to now actually play the instrument may be explained by an additional peripheral nerve impairment induced by the high dose of opioid and/or extended exposure period for which he had been on opioids. This certainly requires more in depth study, as an underlying new iatrogenic entity may have been responsible, i.e., opioid induced pseudoneuropathy.

One way to study this problem would be to perform serial electromyography and nerve conduction velocity studies every six months, as the opioid dose is increased and OIH symptoms begin to appear. Of course, a baseline study would be crucial to quantify the degree of any opioid induced delay in nerve conduction, whether it be in the peripheral nerve itself or at the receptor level.

Screening Questionnaire

Development of a questionnaire would be a very helpful tool to screen for patients with or at risk for OIH – as it is likely that we do not completely know what the best lab and clinical therapeutic ranges are for patients taking oxycodone. One patient in this study, P15, who we thought would meet our OIH criteria, as this person did exhibit symptoms of OIH, remained outside the detection threshold (225 mg morphine equivalents per day). Hence, given the purported neurophysiopathology leading to OIH, one clinical value that should be considered is the pain score.

For this discussion, drug tolerance or tolerance to a narcotic analgesic is said to exist when greater and greater doses and/or strengths of the medication are needed to achieve the same desired effect (i.e., pain relief).¹⁰ This typically occurs within 3-6 weeks of a dose change, and there will always be a period of time after the dose is increased where pain control is deemed adequate by the patient. This is in stark contradistinction to OIH, where an increase in dose is not accompanied by any period of adequate pain relief and there is a concomitant and definite increase in pain. Suggested survey questions are outlined below, however, it is assumed that a progression of the patient's underlying pathology has been ruled-out before considering OIH or drug tolerance.

Model Questionnaire

1) On a scale of 0-10, where zero is no pain, and 10 is the worst pain imaginable, what is your average pain score over a week’s time?

- Establishes baseline score for future comparisons.

2) Is this pain score better or worse than on your last visit?

- If better, OIH not likely.

- Underlying pathology improving?

- If worse, then OIH a possibility, but drug Tolerance must also be considered.

3) Is your pain getting worse before you take your medication?

- OIH and Tolerance possible, but also End of Dose failure must be considered, due to inadequate dose or dosing interval.

4) If your pain is getting worse, does the same dose of pain medication still work?

- If no, then OIH and/or Tolerance must be considered.

- Pathology progressing?

5) Is the pain better or worse since your last dose increase?

- If worse, then OIH may be present. See #6 below.

6) If pain worse, when was your last dose increase?

- If less than 1-4 weeks à OIH likely present.

- Otherwise, then Tolerance may have developed.

Conclusions

We conclude that OFT and its current therapeutic range reliably detects when an excessive amount of oxycodone is taken in most patients (85%). However, for patients at risk for or likely having OIH, this detection rate drops to 50%.

Hence, further study is needed to refine the current oxycodone therapeutic range and OIH thresholds to improve detection efficiency. Additionally, these data suggest patients consuming ≥ 260 mg. MSEq of oxycodone per day are at risk for having or developing OIH.

References

1. Clark JD. Chronic pain prevalence and analgesic prescribing in a general medical population. J Pain Symptom Manage. 2002;23(2):131-137.

2. Angst MS, Clark JD. Oxycodone-induced hyperalgesia: A qualitative systematic review. Anesthesiology. 2006;104(3):570-587.

3. Celerier E, Laulin JP, Corcuff JB, Le Moal M, Simonnet G. Progressive enhancement of delayed hyperalgesia induced by repeated heroin administration: A sensitization process. J Neurosci. 2001;21(11):4074-4080.

4. Carroll IR, Angst MS, Clark JD. Management of perioperative pain in patients chronically consuming Oxycodone. Reg Anesth Pain Med. 2004;29(6):576-591.

5. Wylie FM, Torrance H, Anderson RA, Oliver JS. Drugs in oral fluid part I. validation of an analytical procedure for licit and illicit drugs in oral fluid. Forensic Sci Int. 2005;150(2-3):191-198.

6. Mercadante S, Ferrera P, Villari P, Arcuri E. Hyperalgesia: An emerging iatrogenic syndrome. J Pain Symptom Manage. 2003;26(2):769-775.

7. Guignard B, Bossard AE, Coste C, et al. Acute Oxycodone tolerance: Intraoperative remifentanil increases postoperative pain and morphine requirement. Anesthesiology. 2000;93(2):409-417.

8. Fabregat-Cid G, Asensio-Samper JM, Villanueva-Perez V, Lopez-Alarcon MD, De Andres-Ibanez J. Postoperative pain management for patients who are long-term users of Oxycodone. Rev Esp Anestesiol Reanim. 2011;58(1):25-33.

9. Winek CL, Wahba WW, Winek CL, Jr, Balzer TW. Drug and chemical blood-level data 2001. Forensic Sci Int. 2001;122(2-3):107-123.

10. Campa JA. Narcotic Analgesics – A Reference For the Clinician. San Antonio, TX.: Legacy Publishing SA; 2006.

Research published at national meeting, American Academy of Pain Medicine, 28th Annual Scientific Meeting, Palm Springs, California

Below is a summary of our research presented February 24-25, 2012, at the 28th Annual Scientific Meeting of the American Academy of Pain Medicine, Palm Springs, California. This study was done jointly by Dr. Damiani and Dr. Campa.

Dr. Campa was on-site to present our findings. We believe our research will help other physicians more safely treat those patients who present with persistent pain, requiring high dose and/or prolonged use of narcotics.

Leah Damiani, PhD
John A. Campa III, MD
March 05, 2012

_________________________________________________

Correlation Of Oxycodone Daily Use To Oral Fluid Levels And Its Potential For Detection Of Opioid Induced Hyperalgesia - A Pilot Study

L. Damiani, PhD, MD-Candidate, School of Medicine, University of New Mexico, Albuquerque, NM; J. A. Campa III, MD, Albuquerque, NM; Faculty, School of Medicine, University of New Mexico, Albuquerque, NM.

Background

Clinicians who treat patients suffering from persistent pain must face the issue of monitoring and regulating opioid medication consumption. Evidence suggests prolonged exposure to opioids may lead to Opioid Induced Hyperalgesia (OIH), i.e., the patient becomes paradoxically more sensitive to pain². Hence, an easily performed lab assay, i.e., oral fluids toxicology (OFT), would be an invaluable clinical tool to assist the clinician in providing safe opioid dosing, while avoiding the induction of OIH.

Aim

The aim of this study is to assess the reliability of the oxycodone OFT therapeutic range and its potential for detecting risk for OIH.

Methods

A 10 month retrospective chart review was performed to study patient oxycodone use and its measurement by OFT (Forensic Fluids Laboratories, Inc, Kalamazoo, MI).

Hypothesized OIH Thresholds

We believe the hypothesized daily opioid amount in morphine sulfate equivalents (MSEq), where OIH is likely present, is 300 mg per day. Similarly, the hypothesized daily amount where a patient is at probable risk for OIH induction is 86.5% of 300 mg or 260 mg (MSEq). The rationale for these thresholds is based on our unpublished clinical observations and experience. The only study done within the last 10 years looking at daily morphine equivalents intake and OIH has set a range at approximately 90-200 mg/day⁶. Therefore, a better understanding of the range for morphine equivalents and OIH is required. The oxycodone MSEq is calculated by multiplying the daily amount in milligrams by 1.5. Inclusion criteria: patients taking oxycodone who had OFT.

Results

A total of 19 patients were eligible for the study. Probable OIH was postulated in four patients (P6, P7, P15, P19) and two were deemed to be at risk for OIH (P8, P16). Of the remaining 13/19 (68%) patients not at risk for or having OIH, our data reveals that OFT reliably assessed oxycodone use, relative to the therapeutic range (10-500 ng/ml), in 85% (11/13) of patients (outliers, P5, P9). Of the remaining six with abnormal results > 500 ng/ml, two of the four patients with probable OIH (P6, P15) and one of the two at risk for OIH (P16) were detected, for a reliability detection rate of 50%.

Discussion

The aim of this study was to assess the reliability of the OFT lab’s oxycodone therapeutic range and its potential for detecting risk for OIH, i.e., would it correspond to what we perceive as excessive use of oxycodone, resulting in OIH. The discrepancies between our patients perceived to be overusing oxycodone and the results returned by the lab are likely a function of at least three factors: 1. how the therapeutic range was determined, 2. high metabolizers, 3. patient non-compliance.

According to Wylie et al.⁵, the ability to detect drugs in oral fluids was based upon saliva specimens collected from a drug-free, healthy population, which were then “spiked” with varying drug concentrations. No population-based study was done to determine actual therapeutic levels. The therapeutic ranges were determined from an article stating, “we have gathered the data in the table from the literature and from personal experience. These values are not considered absolute, but are to be used as a guide in evaluating a given case. The values can be affected by dose, route of administration, absorption differences, age and sex, tolerance, method of analysis, pathological or disease state, postmortem redistribution, etc.” ⁹ Therefore, although the therapeutic range set by the lab is not necessarily inaccurate, our results demonstrate that a new therapeutic range for oxycodone may be needed, as some patients with or at risk for OIH were not detected with the lab’s current reference range.

Regarding high metabolizers, the one patient who was at risk for developing OIH (P8), that remained undetected by OFT, was a smoker. Alternatively, those that remained undetected by OFT, may have simply been non-compliant, i.e., taking less medication than admitted to. Hence, the clinician must consider the potential for nicotine related (and other agents) induction of the hepatic microsomal enzyme system and non-compliance when assessing patients undergoing OFT.

Opioid Induced Pseudoneuropathy - OIP?

An unexpected finding at six weeks after patient P6 was completely withdrawn from all opioids, was his regained ability to play the saxophone after 15-20 years. He had previously been told his inability to feel the key pads on the instrument was due to his underlying and progressive neuropathy. His improved touch sensation and ability to now actually play the instrument may be explained by an additional peripheral nerve impairment induced by the high dose of opioid and/or extended exposure period for which he had been on opioids. This certainly requires more in depth study, as an underlying new iatrogenic entity may have been responsible, i.e., opioid induced pseudoneuropathy.

One way to study this problem would be to perform serial electromyography and nerve conduction velocity studies every six months, as the opioid dose is increased and OIH symptoms begin to appear. Of course, a baseline study would be crucial to quantify the degree of any opioid induced delay in nerve conduction, whether it be in the peripheral nerve itself or at the receptor level.

Screening Questionnaire

Development of a questionnaire would be a very helpful tool to screen for patients with or at risk for OIH – as it is likely that we do not completely know what the best lab and clinical therapeutic ranges are for patients taking oxycodone. One patient in this study, P15, who we thought would meet our OIH criteria, as this person did exhibit symptoms of OIH, remained outside the detection threshold (225 mg morphine equivalents per day). Hence, given the purported neurophysiopathology leading to OIH, one clinical value that should be considered is the pain score.

For this discussion, drug tolerance or tolerance to a narcotic analgesic is said to exist when greater and greater doses and/or strengths of the medication are needed to achieve the same desired effect (i.e., pain relief).¹⁰ This typically occurs within 3-6 weeks of a dose change, and there will always be a period of time after the dose is increased where pain control is deemed adequate by the patient. This is in stark contradistinction to OIH, where an increase in dose is not accompanied by any period of adequate pain relief and there is a concomitant and definite increase in pain. Suggested survey questions are outlined below, however, it is assumed that a progression of the patient's underlying pathology has been ruled-out before considering OIH or drug tolerance.

Model Questionnaire

1) On a scale of 0-10, where zero is no pain, and 10 is the worst pain imaginable, what is your average pain score over a week’s time?

- Establishes baseline score for future comparisons.

2) Is this pain score better or worse than on your last visit?

- If better, OIH not likely.

- Underlying pathology improving?

- If worse, then OIH a possibility, but drug Tolerance must also be considered.

3) Is your pain getting worse before you take your medication?

- OIH and Tolerance possible, but also End of Dose failure must be considered, due to inadequate dose or dosing interval.

4) If your pain is getting worse, does the same dose of pain medication still work?

- If no, then OIH and/or Tolerance must be considered.

- Pathology progressing?

5) Is the pain better or worse since your last dose increase?

- If worse, then OIH may be present. See #6 below.

6) If pain worse, when was your last dose increase?

- If less than 1-4 weeks à OIH likely present.

- Otherwise, then Tolerance may have developed.

Conclusions

We conclude that OFT and its current therapeutic range reliably detects when an excessive amount of oxycodone is taken in most patients (85%). However, for patients at risk for or likely having OIH, this detection rate drops to 50%.

Hence, further study is needed to refine the current oxycodone therapeutic range and OIH thresholds to improve detection efficiency. Additionally, these data suggest patients consuming ≥ 260 mg. MSEq of oxycodone per day are at risk for having or developing OIH.

References

1. Clark JD. Chronic pain prevalence and analgesic prescribing in a general medical population. J Pain Symptom Manage. 2002;23(2):131-137.

2. Angst MS, Clark JD. Oxycodone-induced hyperalgesia: A qualitative systematic review. Anesthesiology. 2006;104(3):570-587.

3. Celerier E, Laulin JP, Corcuff JB, Le Moal M, Simonnet G. Progressive enhancement of delayed hyperalgesia induced by repeated heroin administration: A sensitization process. J Neurosci. 2001;21(11):4074-4080.

4. Carroll IR, Angst MS, Clark JD. Management of perioperative pain in patients chronically consuming Oxycodone. Reg Anesth Pain Med. 2004;29(6):576-591.

5. Wylie FM, Torrance H, Anderson RA, Oliver JS. Drugs in oral fluid part I. validation of an analytical procedure for licit and illicit drugs in oral fluid. Forensic Sci Int. 2005;150(2-3):191-198.

6. Mercadante S, Ferrera P, Villari P, Arcuri E. Hyperalgesia: An emerging iatrogenic syndrome. J Pain Symptom Manage. 2003;26(2):769-775.

7. Guignard B, Bossard AE, Coste C, et al. Acute Oxycodone tolerance: Intraoperative remifentanil increases postoperative pain and morphine requirement. Anesthesiology. 2000;93(2):409-417.

8. Fabregat-Cid G, Asensio-Samper JM, Villanueva-Perez V, Lopez-Alarcon MD, De Andres-Ibanez J. Postoperative pain management for patients who are long-term users of Oxycodone. Rev Esp Anestesiol Reanim. 2011;58(1):25-33.

9. Winek CL, Wahba WW, Winek CL, Jr, Balzer TW. Drug and chemical blood-level data 2001. Forensic Sci Int. 2001;122(2-3):107-123.

10. Campa JA. Narcotic Analgesics – A Reference For the Clinician. San Antonio, TX.: Legacy Publishing SA; 2006.

Research published at national meeting, American Pain Society, 30th Annual Scientific Meeting, Austin, Texas

Below is a summary of our research presented May 19-21, 2011, at the 30th Annual Scientific Meeting of the American Pain Society, Austin, Texas. The study was done jointly by Dr. Campa and Dr. Larison over the last three years. Both physicians were on-site to present our findings. This research should help other physicians more accurately diagnose and treat those patients who present with mid back pain, that may involve contact with the spinal cord.

John A. Campa III, MD
Tom C. Larison, DC
July 31, 2011
_________________________________________________

The Usefulness Of Somato Sensory Evoked Potentials in the Diagnosis of Persistent Thoracic Pain and Extrinsic Myelopathy

J. A. Campa III, MD, T. C. Larison, DC, Pain Diagnosis Consultants, LLC, Albuquerque, NM; Faculty, School of Medicine, University of New Mexico, Albuquerque, NM.

INTRODUCTION:
Persistent mid back pain presents a special challenge to the diagnostician, as both intrinsic- and extrinsic medullary etiologies must be considered. The upper and lower extremity Somato Sensory Evoked Potentials studies (SSEP), in their functional assessment of the relevant spinal segmental levels C4-5/N9-N13 Latency (N9-N13), T11-12/T12 Latency (T12) and L3-4/L3-P37 (L3-P37) would assist in resolving the primary pain generator, especially when correlated with EMG and neuroimaging findings.

AIM:
The goal of this study is to assess the value of SSEP in the diagnosis of patients with persistent mid back pain, particularly in the presence of potential extrinsic, medullary pain generators.

METHODS:
A 30-month retrospective chart review was performed; 13 patients underwent SSEP, excluding those with intrinsic spinal cord lesions at the site of mid back pain; Results were correlated with clinical findings, paraspinal thoracic EMG and CT, MRI lesions between T1 and T12 (cord contact or impingement, calcific nodules posterior to cord, disc bulge-degeneration-herniation-protrusion, vertebral anterior wedging). Positive study criteria were: mid back pain, prolonged L3-P37 latency, normal N9-N13 latency, normal T12 latency.

RESULTS:
Results revealed the following - Positive SSEP: 11/13 (84.6%); Positive SSEP, with correlating neuroimaging: 9/11 (81.8%); Positive SSEP, without correlating neuroimaging: 2/11 (18.2%); Positive SSEP, with correlating neuroimaging and EMG: 7/11 (63.6%); Negative SSEP: 2/13 (15.4%); EMG findings: 7/7 chronic polyphasia-reinnervation; 2/7 acute fibrillation potentials;

CONCLUSIONS:
We conclude that the SSEP is a valuable diagnostic tool in the assessment of persistent mid back pain. We recommend its routine use in the evaluation of thoracic pain, particularly in patients with known thoracic spinal segmental lesions.

Research published at national meeting, American Academy of Pain Medicine, 27th Annual Scientific Meeting, National Harbor, Maryland

Below is a summary of our research presented March 24-27, 2011, at the 27th Annual Scientific Meeting of the American Academy of Pain Medicine, National Harbor, Maryland. The study was done jointly by Dr. Campa and Dr. Larison over the last three years. Dr. Campa was on-site to present our findings. This research should help other physicians more accurately diagnose and treat those patients who present with head and face pain.

John A. Campa III, MD
Tom C. Larison, DC
July 31, 2011
_________________________________________________

The Value Of High Cervical EMG In Patients With Non-migrainous Persistent Head Pain

J. A. Campa III, MD, T. C. Larison, DC, Pain Diagnosis Consultants, LLC, Albuquerque, NM; Faculty, School of Medicine, University of New Mexico, Albuquerque, NM.

BACKGROUND: Non-migrainous, persistent head pain presents a special challenge to the diagnostician, as both intra- and extra-cranial etiologies must be considered. The high cervical electromyogram (HC-EMG), in its assessment of the relevant cervical musculature and paraspinal muscles [C2, C3, C4, Sternocleidomastoid (C2, C3; CN-11), Trapezius (C3, C4; CN-11)], would assist in resolving the primary pain generator.

AIM: To assess the value of HC-EMG in identifying extra-cranial potential pain generators in non-migrainous, persistent head pain.

METHODS: 30-month retrospective chart review; 24 patients underwent HC-EMG; excluding migraine/migraine-like presentations. Results correlated with clinical findings, and where available, X-ray, CT, MRI lesions at C1-2, C2-3, C3-4 (disc bulge, protrusion, extrusion, disc osteophyte complex, listhesis, foraminal/recess narrowing, root/cord impingement, thecal sac effacement, canal stenosis).

RESULTS: Abnormal HC-EMG: 14/24 (58.3%); Abnormal HC-EMG, with neuroimaging available: 11/14 (78.6%); Abnormal HC-EMG, with correlating neuroimaging: 7/11 (63.6%); Acute root findings: C2(2), 25%; C3(4) 50%; C4(2), 25%; Chronic root findings: C2(5), 25%; C3(8), 40%; C4(7), 35%; Pain location: Abnormal HC-EMG - Occipital(14), 100%;

CONCLUSIONS: We conclude that the HC-EMG, is a valuable diagnostic tool in the assessment of non-migrainous, persistent head pain of extra-cranial origin. We recommend its routine use in the evaluation of occipital head pain, particularly in patients with known high cervical spinal segmental lesions at the C2-3 level.

Personal Drug Security Recommendations For Patients And Caregivers

As many pain medications possess a high potential for abuse and a correspondingly high street value, to avoid loss, theft and injury, the following personal drug security recommendations are made:

• Patient should never discuss their medications with anyone! This includes friends, family, teenagers (or their friends) neighbors and coworkers.

• Patient should always carry their medications in a nontransparent case/container so that they are not easily visible.

• At home, work, school or in a vehicle, do not leave medications out in the open, in plain view where they may be stolen or tampered with.

• A dedicated lockbox at home is recommended to secure medications from tampering or theft.

• When away from home, always have medications in an appropriately labeled container. This is especially important and helpful should the patient be stopped by law enforcement officials who must verify that they are in lawful possession of a controlled substance.

Never tell family or friends that they are expecting a package from the pharmacy.

Research Published - August 31, 2010 at International Meeting

Below is a summary of our research presented at the 13th World Congress on Pain for presentation in Montreal, Canada, August 31, 2010. The study was done jointly by Dr. Campa and Dr. Larison over the last two years. Both physicians will be on-site to present our findings. This research is a follow-up, expanded study to our prior investigation, Median Nerve H-reflex and Pain Diagnosis, and should continue to help other physicians to more accurately and timely diagnose those individuals who present with neck and upper extremity pain.

John A. Campa III, MD
Tom C. Larison, DC
October 10, 2010
_________________________________________________
Research Summary

The Usefulness Of The Median Nerve H-reflex, Median Nerve F-wave And Radial Nerve F-wave In Pain Diagnosis Of Multilevel Degenerative Disc Disease Of The Cervical Spine

J. A. Campa III, MD, T. C. Larison, DC, Neurology, Pain Diagnosis Consultants, LLC, Albuquerque, NM, Faculty, School of Medicine, University of New Mexico, Albuquerque, NM, Electrodiagnostic Medicine, Pain Diagnosis Consultants, LLC, Albuquerque, NM

Abstract:
BACKGROUND:
We have previously reported the value of the Flexor Carpi Radialis Median nerve H-reflex study (FCR-HR; root derivation: C6, C7) in assessing patients with neck and upper extremity pain and underlying multilevel cervical disc disease (C5-6, C6-7). These lesions present special problems in the diagnosis and management of the primary pain generator, as they are commonly diagnosed on X-ray, CT and MRI as degenerative, and not usually considered as a legitimate source for the patient's pain complaints, resulting in undertreatment and delay in improving the baseline pain control. The FCR-HR, Median nerve F-wave (MNF; root derivation: C6, C7, C8, T1) and Radial nerve F-wave (RNF; root derivation: C5, C6, C7, C8) in their assessment of the functional impact of these lesions, would help clinicians resolve the primary source of the patient’s pain, and permit a focused and directed approach to more definitive management.

AIM:
To assess the usefulness of the MNF and RNF, when correlated with an abnormal FCR-HR, in identifying cervical degenerative discs as potential pain generators.

METHODS:
A 24-month retrospective chart review was performed of patients with neck and upper extremity pain, who underwent electromyography/nerve conduction velocity studies (EMG), where Median nerve neuropathy above the wrist was excluded, and the FCR-HR was abnormal. Results were correlated with MNF, RNF, EMG paraspinal, X-ray, CT, MRI, and clinical findings.

RESULTS:
68 cases underwent EMG for neck and extremity pain; Abnormal FCR-HR: 43/68 (63%); Abnormal FCR-HR and correlating X-ray/CT/MR (C5-6/C6-7): 31/43 (72%); Abnormal FCR-HR and C6, C7 correlating EMG paraspinals: 28/43 (65%); Abnormal FCR-HR and Abnormal MFW: 9/43 (21%); Abnormal FCR-HR and Abnormal RFW: 5/43 (12%); Correlating imaging lesions: DDD, disc bulge, protrusion, extrusion, listhesis, foraminal narrowing, cord impingement, thecal sac effacement, osteophytic ridging, Modic Type I, central canal stenosis.

CONCLUSIONS:
We conclude that the MNF (21%), when combined with the FCR-HR (63%), is a useful diagnostic tool in the assessment of C5-6, C6-7 cervical disc disease as a primary pain generator. We recommend its routine use in the evaluation of patients with neck and upper extremity pain, who present with multilevel cervical disc disease. The RNF (12%) was less helpful.

End.

What is Neuropathy ?

Understanding Peripheral Neuropathy - the Basics
- courtesy of WebMD & Pain Diagnosis Consultants, LLC

The name of the condition tells you a bit about what it is:
Peripheral: Beyond (in this case, beyond the brain and the spinal cord.)
Neuro-: Related to the nerves
-pathy: Disease

Put these concepts together and this is what peripheral neuropathy means: It refers to the conditions that result when nerves that connect to the brain and spinal cord from the rest of the body are damaged or diseased.

The peripheral nerves make up an intricate network that connects the brain and spinal cord to the muscles, skin, and internal organs. Peripheral nerves come out of the spinal cord and are arranged along lines in the body called dermatomes. Typically, damage to a nerve will affect one or more dermatomes, which can be tracked to specific areas of the body. Damage to these nerves interrupts communication between the brain and other parts of the body and can impair muscle movement, prevent normal sensation in the arms and legs, and cause pain.

Click for graphic of the body's nerves.
- University of Chicago.

Types of Peripheral Neuropathy
There are many different kinds of peripheral neuropathy with many different causes. The range from carpal tunnel syndrome (an injury common after chronic repetitive use of the hands and wrists, such as computer use) to Guillain-Barre syndrome (a rare, sudden paralysis).

As a group, peripheral neuropathies are common, especially among people over the age of 55. All together, the conditions affect 3% to 4% of people in this group.

Classification:
Neuropathies are typically classified according to the problems they cause or what is at the root of the damage. There also are terms that express how extensively the nerves have been damaged.

Mononeuropathy
Damage to a single peripheral nerve is called mononeuropathy. Physical injury or trauma such as from an accident is the most common cause. Prolonged pressure on a nerve, caused by extended periods being sedentary such as in a wheelchair or bed, or continuous, repetitive motions can trigger mononeuropathy. If the fibrous, shock-absorbing discs that lie between the bones in the back are damaged, they could press on a nerve and cause this type of neuropathy.

Carpal tunnel syndrome is a common type of mononeuropathy. It is called an overuse strain injury, which occurs when the nerve that extends through the wrist is compressed. People whose work requires repeated motions with the wrist extended (such as assembly-line workers, physical laborers, and those who use computer keyboards for prolonged periods) are at greater risk.

The damage to the nerve can result in numbness, tingling, unusual sensations, and pain in the first three fingers on the thumb side of the hand, particularly while sleeping. In time, carpal tunnel injuries can weaken the muscles in the hand. You may also feel pain, tingling, or burning in your arm and shoulder.

Here are examples of other mononeuropathies that can cause weakness in the affected parts of the body, such as hands and feet:
* Ulnar nerve palsy occurs when the nerve that passes close to the surface of the skin at the elbow is damaged.
* Radial nerve palsy is caused by injury to the nerve that runs along the underside of the arm.
* Peroneal nerve palsy results when the nerve at the top of the calf behind the knee is compressed. This leads to a condition called "foot drop".

Neuropathy can affect nerves that control muscle movement (motor nerves) and those that detect sensations such as coldness or pain (sensory nerves). In some cases, it can affect internal organs, such as the heart, blood vessels, bladder, or intestines. Neuropathy that affects internal organs is called an autonomic neuropathy.

Mononeuropathy multiplex is when several isolated nerves are involved.

Polyneuropathy
Polyneuropathy accounts for the greatest number of peripheral neuropathy cases. It occurs when many peripheral nerves throughout the body malfunction at the same time.

Polyneuropathy can have a wide variety of causes, including exposure to certain toxins, poor nutrition (particularly vitamin B deficiency), and complications from diseases such as cancer or kidney failure.

One of the most common forms of chronic polyneuropathy is diabetic neuropathy, a condition that occurs in people with diabetes. It is the result of poorly controlled blood sugar levels. Though less common, diabetes can also cause mononeuropathy, often characterized by weakness of the eye or of the thigh muscles.

These are the most common symptoms of polyneuropathy:
* Tingling
* Numbness
* Loss of sensation in the arms and legs

Because people with chronic polyneuropathy often lose their ability to sense temperature and pain, they can burn themselves and develop open sores as the result of injury or prolonged pressure. If the nerves serving the organs are involved, diarrhea or constipation may result, as well as loss of bowel or bladder control. Sexual dysfunction and abnormally low blood pressure also can occur.

Joints are particularly vulnerable to stress in people with polyneuropathy because they are often insensitive to pain.

One of the most serious polyneuropathies is Guillain-Barre syndrome, a rare disease that strikes suddenly when the body's immune system attacks nerves in the body. Symptoms tend to appear quickly and worsen rapidly, sometimes leading to paralysis. Early symptoms include weakness, tingling, and loss of sensation in the legs that eventually spreads to the arms. Blood pressure problems, heart rhythm problems, and breathing difficulty may occur in critical cases. However, despite the severity of the disease, recovery rates are good when patients receive treatment early.

What Causes Peripheral Neuropathy?
Many things can cause peripheral neuropathies so it is often difficult to know the cause.

Neuropathies occur by one of three methods:
- Acquired neuropathies are caused by environmental factors such as toxins, trauma, illness, or infection. Known causes of acquired neuropathies include:

* Diabetes - responsible for many cases of peripheral neuropathy
* Several rare inherited diseases
* Alcoholism
* Poor nutrition or vitamin deficiency
* Herniated discs in the back
* Certain kinds of cancer
* Conditions where nerves are mistakenly attacked by the body's own immune system or damaged by an overaggressive response to injury
* Certain medications
* Kidney or thyroid disease
* Infections such as Lyme disease, shingles, or AIDS

- Hereditary neuropathies are not as common. Hereditary neuropathies are diseases of the peripheral nerves that are genetically passed from parent to child.
The most common of these is Charcot-Marie-Tooth disease type 1. It is characterized by weakness in the legs and, to a lesser degree, the arms -- symptoms that usually appear between mid-childhood and age 30. This disease is caused by degeneration of the insulation that normally surrounds the nerves and helps them conduct the electrical impulses needed for them to trigger muscle movement.

- Idiopathic neuropathies are from an unknown cause.
As many as one-third of all neuropathies are classified in this way.

- courtesy of WebMD & Pain Diagnosis Consultants, LLC