FDA Announces Medtronic Pain Pump Recall - Chronic-Intractable Pain And You, Inc. (Main Site)

FDA Announces Medtronic Pain Pump Recall

On Monday, the FDA announced that Medtronic has issued a Class I recall of their SynchroMed II Implantable Infusion Pump, models 8637-20 and 8637-40, distributed between May 2004 and July 8, 2011. These are the same pumps for which an alert was issued in July of this year.

You can read the details of the July alert here: Pain Pump Alert: Potential Problem With Medtronic SynchroMed II Pump

Reason for Recall

The reason given for the recall is that “there is a potential for reduced battery performance in the SynchroMed II infusion Pump. Medtronic’s analysis of the problem indicates it is related to the formation of a film within the pump battery. This problem can lead to the sudden loss of therapy and the return of underlying symptoms and/or therapy withdrawal symptoms. For example, patients receiving intrathecal baclofen therapy for severe spasticity are at risk for baclofen withdrawal syndrome, which can lead to a life-threatening condition if not treated quickly and effectively.”

Recall or Alert?

The FDA listed this as a Class I recall. Class I recalls are the most serious type of recall and involve situations in which there is a reasonable probability that use of these products will cause serious adverse health consequences or death.

That being said, Medtronic is not retrieving any implanted SynchroMed II pumps from the field. The announcement says, “Medtronic does not recommend prophylactic replacement of SynchroMed II pumps because of the estimated low occurrence rates, the presence of pump alarms, and the risks associated with replacement surgery.”

Instead, Medtronic encourages patients to carry their patient identification cards with them at all times and to contact their physicians immediately if they experience a return of symptoms or hear a device alarm.

My Thoughts...

I find the term “recall” a bit misleading since Medtronic is not actually replacing the pumps in question. This seems to be more of a strong alert warning you that there could be problems ahead. Actually, this seems to be little more than a repeat of the July alert. I'm not really sure why it is being reiterated unless the FDA is just a couple of months behind in making the announcement.

Although I don't personally have any experience with pain pumps, I know a number of our community members have them. If you have one of the models involved in this recall, I would encourage you to talk with your physician about what you should do if you experience a sudden return of symptoms or begin to go through withdrawal . . . particularly if this should happen at night, on a weekend or over a holiday when your doctor is not in his/her office.

If you have additional questions about this recall, contact Medtronic Patient Services at 1-800-510-6735, Monday – Friday, 8 a.m. to 5 p.m. CDT.
_______________
Source:
Medtronic Model 8637 SynchroMed II Implantable Infusion Pump. U.S. Food and Drug Administration. 9/12/11.
http://www.healthcentral.com/chronic-pain/c/5949/144117/fda-medtronic

Steroid Injection, Carpal Tunnel

Overview
Carpal tunnel syndrome (CTS) is a compressive focal mononeuropathy that is brought on by compression of the median nerve as it travels through the carpal tunnel. Patients commonly experience pain, paresthesias, and weakness in the median nerve distribution. Carpal tunnel steroid injection at the wrist is used to treat the symptoms of carpal tunnel syndrome by injecting a steroid solution into the ulnar bursa surrounding the median nerve.
For mild to moderate carpal tunnel syndrome, carpal tunnel steroid injection can be used in conjunction with other conservative measures such as splinting, physical therapy, ergonomic modifications, rest, and regular exercise.^{[1, 2, 3, 4, 5]} Conservative modalities, including median nerve steroid injections, should generally be attempted prior to pursuing surgical options.^[6] Historically, carpal tunnel steroid injections were typically used for only mild median nerve entrapment (as documented by electroneurography) as well as for temporary pain relief in anticipation of definitive flexor retinaculum surgical release. In general, injected corticosteroids appear effective in reducing subjective symptoms for 1-3 months when compared to placebo.^[7] While short-term relief of symptoms after injection appears superior to relief after carpal tunnel release surgery, the advantage is lost over the course of a year.^[8]
Electrodiagnostic studies such as nerve conduction studies and electromyography are typically obtained to determine the severity of nerve damage prior to performing the procedure.^{[9, 10]} Steroid injections should be avoided prior to planned electrodiagnostic testing, as the presence of steroids may alter test results. Several clinical tests can be used to diagnose carpal tunnel syndrome. One is Tinel's sign, which is done by over the median nerve at the volar crease at the wrist to reproduce the paresthesia. The Phalen test involves holding the flexed wrists against each other for several minutes to provoke the symptoms in the median nerve distribution. Manual carpal compression testing is done by applying pressure over the transverse carpal ligament and evaluating for paresthesia within 30 seconds of applying pressure.^[11]
Carpal tunnel anatomy
The carpal tunnel of the wrist is defined anatomically by the transverse carpal ligament on the volar surface and the carpal bones on the dorsal surface. The transverse carpal ligament, also known as the flexor retinaculum, attaches radially to the trapezium and scaphoid tuberosity and ulnarly to the hamate and pisiform. The contents of the carpal tunnel include the 4 flexor digitorum profundus tendons, the 4 flexor digitorum superficialis tendons, the flexor pollicis longus tendon, and the median nerve. See images below.
Carpal tunnel anatomy. Carpel tunnel anatomy, cross-section.
There are 2 bursae in the wrist. The radial bursa contains the flexor pollicis longus tendon. The ulnar bursa, also known as the common flexor sheath, holds the flexor digitorum superficialis and profundus tendons. When the hand is supinated, the 4 superficialis tendons lay on top of the 4 profundus tendons, forming a U-shaped structure referred to as the ulnar bursa. On top of the ulnar bursa, and below the transverse carpal ligament, lies the median nerve. Although the median nerve itself has 2 sensory branches and 1 motor branch, only 1 sensory branch and the motor branch traverse through the carpal tunnel and are affected by carpal tunnel syndrome. This sensory branch is responsible for sensory innervation of the thumb, index finger, middle finger, and radial half of the ring finger. 
Indications

• Carpal tunnel syndrome not relieved by conservative measures
• Electrodiagnostic changes consistent with mild-to-moderate median nerve entrapment

Contraindications

• Adverse reaction to injectable steroid or anesthetic
• Uncontrolled diabetes mellitus
• Active systemic or local infection
• Compromised skin integrity over the area
• Immunosuppression
• Planned electrodiagnostic study

Anesthesia

• Lidocaine (Xylocaine) 1% without epinephrine, 2-3 mL
• Bupivacaine (Marcaine) 0.25%, 2-3 mL
• For more information, see Local Anesthetic Agents, Infiltrative Administration.

Equipment

• Needle, 1 in, 27 or 30 gauge (ga)
• Syringe, 5 mL
• Antiseptic solution with skin swabs
• Small rolled towel
• Triamcinolone acetonide (Kenalog), 10-20 mg; or methylprednisolone acetate (Depo-Medrol), 10-20 mg
• Lidocaine 1% or bupivacaine 0.25%

Positioning

• Patient should be positioned comfortably in a seated or supine position.
• The affected arm should be supinated with the dorsal aspect of the wrist resting over a small rolled towel.

Technique

• First, locate the flexor carpi radialis (FCR) and palmaris longus (PL) tendons. The palmaris longus tendon is medial to the flexor carpi radialis and is best located by opposing the thumb and fifth digit while the wrist is flexed. The image below depicts relevant anatomy and landmarks. For more information, see Flexor Tendon Anatomy. Solid blue line - palmaris longus tendon; solid red line - flexor carpi radialis tendon; dotted blue line - proximal palmar crease.
• Carefully disinfect the skin.
• Draw up 1 mL of 1% lidocaine and make a skin wheal ulnar to the palmaris longus and proximal to the proximal wrist crease.
• In another syringe, draw up the steroid with or without lidocaine or bupivacaine.
• Insert the needle 1 cm proximal to the proximal wrist crease and directly ulnar to the palmaris longus tendon at the skin wheal. Direct the needle distally toward the ring finger at an angle of 30 degrees. See image below. Needle placement - Medial of palmaris longus tendon.
• Advance the needle approximately 1.5-2 cm or until the tendon is touched.
• Aspirate to verify that no vasculature is affected, and inject the steroid solution with little or no resistance.
• Lastly, remove the needle and place the wrist in a gravity-dependent position.
• Advise the patient to actively move the fingers for several minutes to distribute the solution evenly.

Pearls

• Some people do not have a palmaris longus (PL) tendon.^{[12, 13]} In these cases, the needle is inserted at the midline between the radial and ulnar aspects of the wrist, proximal to the wrist crease, and is directed toward the ring finger (see image below). Needle placement in absence of palmaris longus tendon.
• If contact is made with the palmaris longus tendon while advancing the needle, retract slightly and redirect.
• The use of a needle smaller in diameter may require increased effort and slower injection time but dramatically reduces pain at the site of injection.
• Sudden worsening pain or paresthesia indicates the possibility of improper needle placement. If this occurs, retract the needle and redirect more medially (ulnar).
• To avoid potential complications of vascular or nerve ischemia, tissue necrosis, and serious damage to nerve, lidocaine with epinephrine should not be used. 

Complications

• Bleeding
• Infection
• Injury to nerve^{[14, 15]}
• Tendon rupture^[16]
• Temporary paresthesia
• Alteration in blood glucose levels in patients with diabetes mellitus
• Pain^[17]  

http://emedicine.medscape.com/article/103333-overview#a01

Steroid Injection, Carpal Tunnel - Chronic-Intractable Pain And You, Inc. (Main Site)

Steroid Injection, Carpal Tunnel

Overview
Carpal tunnel syndrome (CTS) is a compressive focal mononeuropathy that is brought on by compression of the median nerve as it travels through the carpal tunnel. Patients commonly experience pain, paresthesias, and weakness in the median nerve distribution. Carpal tunnel steroid injection at the wrist is used to treat the symptoms of carpal tunnel syndrome by injecting a steroid solution into the ulnar bursa surrounding the median nerve.
For mild to moderate carpal tunnel syndrome, carpal tunnel steroid injection can be used in conjunction with other conservative measures such as splinting, physical therapy, ergonomic modifications, rest, and regular exercise.^{[1, 2, 3, 4, 5]} Conservative modalities, including median nerve steroid injections, should generally be attempted prior to pursuing surgical options.^[6] Historically, carpal tunnel steroid injections were typically used for only mild median nerve entrapment (as documented by electroneurography) as well as for temporary pain relief in anticipation of definitive flexor retinaculum surgical release. In general, injected corticosteroids appear effective in reducing subjective symptoms for 1-3 months when compared to placebo.^[7] While short-term relief of symptoms after injection appears superior to relief after carpal tunnel release surgery, the advantage is lost over the course of a year.^[8]
Electrodiagnostic studies such as nerve conduction studies and electromyography are typically obtained to determine the severity of nerve damage prior to performing the procedure.^{[9, 10]} Steroid injections should be avoided prior to planned electrodiagnostic testing, as the presence of steroids may alter test results. Several clinical tests can be used to diagnose carpal tunnel syndrome. One is Tinel's sign, which is done by over the median nerve at the volar crease at the wrist to reproduce the paresthesia. The Phalen test involves holding the flexed wrists against each other for several minutes to provoke the symptoms in the median nerve distribution. Manual carpal compression testing is done by applying pressure over the transverse carpal ligament and evaluating for paresthesia within 30 seconds of applying pressure.^[11]
Carpal tunnel anatomy
The carpal tunnel of the wrist is defined anatomically by the transverse carpal ligament on the volar surface and the carpal bones on the dorsal surface. The transverse carpal ligament, also known as the flexor retinaculum, attaches radially to the trapezium and scaphoid tuberosity and ulnarly to the hamate and pisiform. The contents of the carpal tunnel include the 4 flexor digitorum profundus tendons, the 4 flexor digitorum superficialis tendons, the flexor pollicis longus tendon, and the median nerve. See images below.
Carpal tunnel anatomy. Carpel tunnel anatomy, cross-section.
There are 2 bursae in the wrist. The radial bursa contains the flexor pollicis longus tendon. The ulnar bursa, also known as the common flexor sheath, holds the flexor digitorum superficialis and profundus tendons. When the hand is supinated, the 4 superficialis tendons lay on top of the 4 profundus tendons, forming a U-shaped structure referred to as the ulnar bursa. On top of the ulnar bursa, and below the transverse carpal ligament, lies the median nerve. Although the median nerve itself has 2 sensory branches and 1 motor branch, only 1 sensory branch and the motor branch traverse through the carpal tunnel and are affected by carpal tunnel syndrome. This sensory branch is responsible for sensory innervation of the thumb, index finger, middle finger, and radial half of the ring finger. 
Indications

• Carpal tunnel syndrome not relieved by conservative measures
• Electrodiagnostic changes consistent with mild-to-moderate median nerve entrapment

Contraindications

• Adverse reaction to injectable steroid or anesthetic
• Uncontrolled diabetes mellitus
• Active systemic or local infection
• Compromised skin integrity over the area
• Immunosuppression
• Planned electrodiagnostic study

Anesthesia

• Lidocaine (Xylocaine) 1% without epinephrine, 2-3 mL
• Bupivacaine (Marcaine) 0.25%, 2-3 mL
• For more information, see Local Anesthetic Agents, Infiltrative Administration.

Equipment

• Needle, 1 in, 27 or 30 gauge (ga)
• Syringe, 5 mL
• Antiseptic solution with skin swabs
• Small rolled towel
• Triamcinolone acetonide (Kenalog), 10-20 mg; or methylprednisolone acetate (Depo-Medrol), 10-20 mg
• Lidocaine 1% or bupivacaine 0.25%

Positioning

• Patient should be positioned comfortably in a seated or supine position.
• The affected arm should be supinated with the dorsal aspect of the wrist resting over a small rolled towel.

Technique

• First, locate the flexor carpi radialis (FCR) and palmaris longus (PL) tendons. The palmaris longus tendon is medial to the flexor carpi radialis and is best located by opposing the thumb and fifth digit while the wrist is flexed. The image below depicts relevant anatomy and landmarks. For more information, see Flexor Tendon Anatomy. Solid blue line - palmaris longus tendon; solid red line - flexor carpi radialis tendon; dotted blue line - proximal palmar crease.
• Carefully disinfect the skin.
• Draw up 1 mL of 1% lidocaine and make a skin wheal ulnar to the palmaris longus and proximal to the proximal wrist crease.
• In another syringe, draw up the steroid with or without lidocaine or bupivacaine.
• Insert the needle 1 cm proximal to the proximal wrist crease and directly ulnar to the palmaris longus tendon at the skin wheal. Direct the needle distally toward the ring finger at an angle of 30 degrees. See image below. Needle placement - Medial of palmaris longus tendon.
• Advance the needle approximately 1.5-2 cm or until the tendon is touched.
• Aspirate to verify that no vasculature is affected, and inject the steroid solution with little or no resistance.
• Lastly, remove the needle and place the wrist in a gravity-dependent position.
• Advise the patient to actively move the fingers for several minutes to distribute the solution evenly.

Pearls

• Some people do not have a palmaris longus (PL) tendon.^{[12, 13]} In these cases, the needle is inserted at the midline between the radial and ulnar aspects of the wrist, proximal to the wrist crease, and is directed toward the ring finger (see image below). Needle placement in absence of palmaris longus tendon.
• If contact is made with the palmaris longus tendon while advancing the needle, retract slightly and redirect.
• The use of a needle smaller in diameter may require increased effort and slower injection time but dramatically reduces pain at the site of injection.
• Sudden worsening pain or paresthesia indicates the possibility of improper needle placement. If this occurs, retract the needle and redirect more medially (ulnar).
• To avoid potential complications of vascular or nerve ischemia, tissue necrosis, and serious damage to nerve, lidocaine with epinephrine should not be used. 

Complications

• Bleeding
• Infection
• Injury to nerve^{[14, 15]}
• Tendon rupture^[16]
• Temporary paresthesia
• Alteration in blood glucose levels in patients with diabetes mellitus
• Pain^[17]  

http://emedicine.medscape.com/article/103333-overview#a01

38 Questions to Ask Your Surgeon Before Having Back Surgery

38 Questions to Ask Your Surgeon Before Having Back Surgery

By: Stephanie Burke

This subject comes up a lot in our forums - "I'm considering surgery, what questions should I ask my surgeon?" From articles on Spine-health.com and contributions from our discussion forum members, we've compiled a list that you can print up and take with you to your consultation. Good luck!

Questions before you decide to have the surgery

1.     What type of surgery are you recommending? Why?

2.     What is the source of the painthat is being addressed? How do you know this? (Exploratory back surgery is not done).

3.     Please explain the procedure - at a very high level/with some detail/in great detail. The amount of information depends on your personal preference – some want to know everything, some not so much! To actually see the surgery (animated – no gore) – view our Spine surgery animated videos.

4.     What are my non-surgical options?

5.     What is the natural course of my condition if it is not surgically addressed?

6.     What would you recommend if this were your friend/wife/sister/daughter etc…?

7.     How long will the surgery take?

8.     What are side effects, potential risks and complications?

9.     Please explain the risks and how they relate to me personally. For example, chances of having a non fusion if you are overweight, a smoker, risks if have a grade 3 spondy, etc.

10.                        What if you get in there and see something different than you expected?

11.                        Do I need to donate my own blood? If yes, why? For most types of back surgery, blood does not need to be donated ahead of time.

12.                        Do you perform the whole procedure? Will any students/other surgeons be doing any parts of the operation? If yes, who are they and what are their qualifications? Some surgeons only do a small part of the operation, others do the whole thing. If another surgeon is required, e.g. a vascular surgeon, their role is important and it would be good to know their qualifications..

13.                        Who else will assist you in the operation? What is their background and qualifications?

14.                        What are the long-term consequences of the proposed procedure? E.g. will the operation ever need to be re-done? If it is a fusion, will it lead to degeneration at other levels of the spine?)

Questions about the surgeon

15.                        How many times have you done this procedure? In general, when it comes to surgery "practice makes perfect", so more is better. (However, if the doctor is recommending something that is not often done, such as multi-level fusions, more would not necessarily be better.)

16.                        Are you board eligible or board certified? You can usually look on the wall and see a certificate.

17.                        Are you fellowship trained in spine surgery? This is more important if the surgery is a fusion, artificial disc replacement, or other more extensive procedure.

18.                        If I want to get a second opinion, who would you recommend? (Someone not in the same practice)

19.                        Statistically the success rate for this type of surgery is _%. What is your personal success rate, and how many of this type of surgery have you done?

20.                        Can I talk to other patients who have had a similar procedure?

Any defensiveness on the part of the surgeon when you ask these types of questions may be a red flag. A surgeon with good results and appropriate qualifications will not be threatened by these types of questions and will respect your attention to these matters.

Questions about what to expect after the surgery

21.                        What kind of pain should I expect after the surgery and for how long?

22.                        How long is the hospital stay?

23.                        May a family member spend the night with me in the hospital?

24.                        How do you manage the pain in the hospital?

25.                        Which pain medications will I be sent home with? What are possible side effects of these prescriptions? E.g. Constipation, drowsiness, etc.

26.                        Will you know before the surgery if I will need a backbrace afterwards? If so, will I be fitted for one before the surgery?

27.                        Who can I call if I have questions after the surgery? What is the process for communication?

28.                        How often will I see you after my surgery?

29.                        What symptoms would warrant a call to your office?

30.                        What symptoms would warrant immediate medical attention?

31.                        What limitations will I have after surgery and for how long?

32.                        How long will I be out of work? School? Whatever...

33.                        What kind of help will I need when I return home?

34.                        When can I drive again?

35.                        When can I resume normal (light) household chores?

36.                        What expectations do you have for my recovery?

37.                        When is it safe for my spouse and I to have sexual relations again?

38.                        How soon after the surgery can I start physical therapy?

Good luck with your decision and your recovery!

http://www.chronicpainconnect.com/news-articles/162-5-tips-for-dealing-with-depression-and-chronic-pain-around-the-holidays/portal

 

ASAM Redefines Addiction as a Brain Disease - Chronic-Intractable Pain And You, Inc. (Main Site)

ASAM Redefines Addiction as a Brain Disease

Friday, August 26, 2011

Addiction is a primary, chronic brain disease, not just bad behavior or bad choices, according to a new definition from the American Society of Addiction Medicine (ASAM). Pain practitioners need to understand the ramifications of addiction — especially involving Rx-opioid use — as a complicating factor in patient care. However, casual use of the term “addiction” or inaccurate diagnosis of the disorder is counterproductive for effective pain management and unjustly stigmatizing to patients.
According to ASAM in a news release [here], when people see compulsive and damaging behaviors in friends or family members — or public figures such as celebrities or politicians — they often focus only on the behaviors or substance use as the problem. However, these outward signs are actually manifestations of an underlying disease that involves various areas of the brain.
“At its core, addiction isn't just a social problem or a moral problem or a criminal problem. It's a brain problem whose behaviors manifest in all these other areas,” said Michael Miller, MD, past president of ASAM who oversaw the development of the new definition. “Many behaviors driven by addiction are real problems and sometimes criminal acts. But the disease is about brains, not drugs. It's about underlying neurology, not outward actions.”
The new definition resulted from an intensive, 4-year process with more than 80 experts actively working on it, including top addiction authorities, addiction medicine clinicians, and leading neuroscience researchers from across the country. The full Public Policy Statement on addiction [here] also includes this short version of the definition:
“Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. This is reflected in an individual pathologically pursuing reward and/or relief by substance use and other behaviors.”

“Addiction is characterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of significant problems with one’s behaviors and interpersonal relationships, and a dysfunctional emotional response. Like other chronic diseases, addiction often involves cycles of relapse and remission. Without treatment or engagement in recovery activities, addiction is progressive and can result in disability or premature death.”
By defining addiction as a primary disease, ASAM stresses that it is not the result of other causes, such as emotional or psychiatric problems. Addiction also is recognized as a chronic disease — like cardiovascular disease or diabetes — that must be treated, managed, and monitored over a life-time.
Two decades of advancements in neurosciences convinced ASAM that addiction needed to be redefined by what is going on in the brain. Research shows that the disease of addiction affects neurotransmission and interactions within neural reward circuitry, leading to addictive behaviors that supplant healthy ones, while memories of previous experiences with food, sex, alcohol, and other drugs trigger craving and renewal of addictive behaviors.
Meanwhile, brain circuitry that governs impulse control and judgment also is altered in this disease, resulting in the dysfunctional pursuit of rewards such as alcohol and other drugs. This area of the brain is still developing during teen-age years, which may be why early exposure to alcohol and drugs is related to greater likelihood of addiction later in life.
“There is longstanding controversy over whether people with addiction have choice over anti-social and dangerous behaviors,” said Raju Hajela, MD, in the news release (he is past president of the Canadian Society of Addiction Medicine and was chair of the ASAM committee on the new definition). He further states, “the disease creates distortions in thinking, feelings and perceptions, which drive people to behave in ways that are not understandable to others around them. Simply put, addiction is not a choice. Addictive behaviors are a manifestation of the disease, not a cause.”
However, Hajela continues, “Choice still plays an important role in getting help. While the neurobiology of choice may not be fully understood, a person with addiction must make choices for a healthier life in order to enter treatment and recovery. Because there is no pill which alone can cure addiction, choosing recovery over unhealthy behaviors is necessary.”
COMMENTARY: The interface of pain, opioid analgesics, and addiction has been of great concern in the pain management field. Commonly, the term “addiction” has been loosely applied by practitioners, researchers, and the public, and this has frequently resulted in faulty diagnoses, unjust accusations, and stigmatization of patients.
Furthermore, there have been many studies in the field using definitions that inaccurately assess addiction among patients with pain prescribed opioid analgesics; consequently, more often than not, the prevalence of addiction has been inflated. Good quality studies, of which there have been few, suggest that de novo iatrogenic addiction in patients appropriately prescribed opioid analgesics for chronic pain is a relatively rare occurrence [see UPDATE here].
Will this reinterpretation of addiction from ASAM help to clarify the issues or add further confusion? In many respects, the definition is comprehensive but not entirely new thinking. In 2001, a trio of organizations — the American Academy of Pain Medicine, American Pain Society, and ASAM — released a consensus document, “Definitions Related to the Use of Opioids for the Treatment of Pain,” that defined addiction as follows:
“Addiction is a primary, chronic, neurobiological disease, with genetic, psychosocial, and environmental factors influencing its development and manifestations. It is characterized by behaviors that include one or more of the following: impaired control over drug use, compulsive use, continued use despite harm, and craving.”
The new definition, from ASAM, notes that addiction is characterized by 5 features:

1. Inability to consistently Abstain;
2. Impairment in Behavioral control;
3. Craving, or increased “hunger” for drugs or rewarding experiences;
4. Diminished recognition of significant problems with one’s behaviors and interpersonal relationships; and
5. A dysfunctional Emotional response.

These are quite similar to features noted in the consensus statement of a decade ago, and ASAM emphasizes that the 5 “new” features are not diagnostic criteria for addiction. Rather, the diagnosis of addiction requires “a comprehensive biological, psychological, social and spiritual assessment by a trained and certified professional.” However, this raises some concerns about the new definition:

• Who is a “trained and certified professional” qualified to make a bona fide diagnosis of addiction in a patient? Presumably, ASAM members are qualified; pain practitioners are not. However, chronic pain and instinctual human drives for pain relief may result in expression of any or all of the 5 features of addiction noted above, which can confound the diagnosis by someone inexperienced in both pain and addiction medicine.
• Acknowledgment of addiction as a chronic brain disease, which actually occurred some time ago, was a major breakthrough from a medical science perspective; although, when used inappropriately, as often has been the case, this viewpoint has stigmatized those afflicted with the disorder as being mentally unfit. Particularly in the pain management field, even a hint of past or present addiction in a patient can radically alter the sort of treatments that will be offered to them.
• The ASAM document catalogs many of the interesting and important neurobiological structures and functions that have been discovered in research studies to play a role in addictive processes. However, this knowledge has not been translated into everyday clinical application for the diagnosis and treatment of addiction.
• ASAM further notes that “genetic factors account for about half of the likelihood that an individual will develop addiction,” and these are further influenced by environmental factors. This may be of some importance from prevention perspectives but, since a person’s genetic makeup cannot be remediated, it is unhelpful in the treatment of current addiction.
• The inclusion by ASAM of a spiritual dimension in their definition and the assessment of addiction, which is so prominent and important in 12-Step recovery groups, is controversial from a medical science standpoint. Delving into patients’ connections (or disconnects) with a “Higher Power” is generally outside the bounds of typical clinical practice.

Finally, it is curious that ASAM released this extensive definition of addiction at this time, when the American Psychiatric Association (APA) is finalizing the 5th revision of their Diagnostic & Statistical Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Is this new ASAM definition intended to complement DSM-5, to supersede the APA’s work in defining addictive disorders, or as a standalone interpretation of the disorders by ASAM? Interestingly, other than a major section heading in DSM-5 titled “Substance Use and Addictive Disorders,” the APA continues to shun use of the term “addiction” as a descriptor, as they have in the past.
In any case, the new ASAM document [here] is recommended reading for all healthcare providers who want an understanding of addiction and addictive behaviors.
Posted bySB. Leavitt, MA, PhDat9:45 AM 

http://updates.pain-topics.org/2011/08/asam-redefines-addiction-as-...