10 tips for hitting the slopes with back pain

George Rappard, MD

 

Just because you have a bad back doesn’t mean you can’t enjoy the slopes.  Follow these tips to get yourself ready and avoid a re-injury:

1.       Don’t forget to warm up before any exercise.  Warming up improves your circulation and will help you get a good stretch.

2.       Having tight muscles and ligaments before any exercise can cause a back injury.  After a warm up make sure to stretch your ski muscles: Quads, hamstrings, calves, low back and shoulders.  Add neck stretches to improve mobility while looking around you.

3.       Get yourself conditioned.  Start with brisk walks.  The stair master is a great low impact exercise that will also work your legs.  Jumping rope is an oldie but a goodie, and you can do it anywhere.

4.       Get your Quads in shape with squats.  No need to add weights.  Use repetition.  Try wall squats.  Lean back on the wall and squat down, hold, relax, repeat.

5.       Core muscles are essential for stabilizing your back, don’t ignore them.  Consult with your therapist or chiropractor for some core exercises that can help you but be careful, overdoing it can hurt you.  Exercise should make you tired, and maybe a little sore, but it shouldn’t hurt.

6.       Modern ski boots and parabolic skis make maneuvering on the slopes easier.  If your equipment is outdated consider a demo.

7.       Snowboarders should exercise extra caution.  Snowboarding requires a lot of twisting that can strain your back.  Make sure to stretch and exercise that core.

8.       If your back starts to hurt or you experience sciatica, take it easy.  You should even think about calling it a day.  It’s better to ski or snowboard a half day and come back the next day than to ruin a vacation over a back injury.

9.       Don’t exceed your capabilities.  If you’re middle aged and have an injury, don’t expect to ski the way you did when you were 20.  The fact that you’re still on the slopes is impressive enough.

10.   This maybe about back pain, but let’s not forget one easy way to avoid a catastrophic injury:  Wear a helmet.  Modern designs are comfortable, ventilated and will protect you.  Helmets with ear buds for your music are a bad idea.  You want to hear verbal warnings from other riders and skiers. 

 

George Rappard, MD is a neurointerventional surgeon specializing in endoscopic spine surgery and spinal pain management.  Dr. Rappard is the director of the Los Angeles Minimally Invasive Spine Institute

Cervicogenic Vertigo Following Whiplash Injury

George Rappard, MD

      Cervicogenic vertigo is a common but under diagnosed manifestation of a whiplash mechanism of injury to the neck.  Understanding the temporal relationship to the injury, mechanism, differential diagnosis and potential therapies are key to the effective diagnosis and treatment of this entity.  As many cases of whiplash involve automobile accidents, it's important to document the presence of cervicogenic vertigo as an objective manifestation of a cervical acceleration-deceleration injury.

     Vertigo is defined as a sensation of disequilibrium, often characterized as dizziness.  Vertigo is different from dizziness in that the hallmark of vertigo is a sensation of motion where no motion exists, whereas dizziness is a sensation of unsteadiness.  For example, a patient with true vertigo will experience a sensation that the room is spinning, or that the floor is tilting.  Often, symptoms can be brought about by rapid head turning.

     Cervicogenic vertigo is felt to be brought on by injury to proprioceptive afferents, or specialized nerve receptors,  in the paraspinal musculature or upper cervical facet joints¹.  30% of these receptors lie in the facet joints².  The job of these receptors is to relay information to the brain as to the head’s position on the neck.  When there is a substantial enough of an injury discharges from these receptors are disturbed.  Spatial disorientation and vertigo results from this abnormal discharge³.  In order to injure these receptors, one can see that there has to be a substantial enough of an injury to the facet joints and paraspinal soft tissues that they lie in.  As a result of an injury to these structures, there is an alteration of normal sensation and relay of positional inputs from these specialized receptors.  Therefore, a substantial enough of an injury mechanism to result in pain from paraspinal soft tissue injury or facet capsular injury must be present; In other words, there is usually substantial neck pain.  The diagnosis of cervicogenic vertigo should be suspected when there has been a substantial mechanism, such as whiplash, and there is neck pain.  Keep in mind, substantial injury mechanism does not mean a high speed rear end collision.  Studies have shown that even a low speed collision can result in substantial G-forces to the neck.  White and Punjabe showed how an 8mph rear end collision can result in a 5 G force acceleration to a vehicle occupant’s head⁴.

     Perhaps one reason why cervicogenic vertigo is under appreciated is that it may not manifest itself until the late subacute or chronic phase following a whiplash mechanism of injury.  It is estimated that vertigo with late onset is seen in up to 58% of patients after closed head injury and whiplash injury⁵.  Appearing later in a patient’s course, vertigo may be eclipsed by the early and persistent appearance of neck pain after whiplash.  In the presence of a closed head or concussive injury cervicogenic vertigo may be confused with a post-concussion syndrome.  In this case, the absence of typical post-concussive findings can exclude vertigo as a manifestation of a post-concussive injury.  When a closed head injury and neck pain co-exist, the distinction is difficult but probably more academic than anything else, from a practical perspective.  The key to diagnosis is the exclusion of other causes and the temporal relationship between vertigonous symptoms and the injury mechanism.  Exclusion of other causes will be discussed below.  When there is a subacute injury mechanism, such as a motor vehicle accident and neck pain, cervicogenic vertigo should be high on the differential diagnosis.

     There is a broad differential diagnosis for vertigo.  Spontaneous vertigo may commonly be due to an inner ear problem, such as Menier’s disease, labrynthitis, (seen after viral infections), or benign paroxysmal positional vertigo (BPPV).  Further evaluation can be carried out.  Menier’s is associated with hearing loss and audiometry may be helpful.  Take note that a similar low tone sensineurial hearing loss can be seen in a whiplash injury with associated dural sleeve tear and CSF leak⁶.  To make matters more confusing, cervicogenic vertigo may be associated with a high pitched tinnitus³.   In BPPV, the Dix-Hallpike maneuver may be positive.  Wrisley et al describe an algorithm for working up suspected cervicogenic vertigo patients⁵.  First, patients must have neck pain to be considered for the diagnosis.  The Dix-Hallpike test can then ascertain which patients suffer from BPPV.  In patients with a negative Dix-Hallpike, or a similar tilt table maneuver, (therefore negative for BPPV) vestibular testing can determine which subset of patients may be suffering from vestibular disorders.  In this algorithm of exclusion, with negative BPPV and vestibular testing, and the presence of neck pain, cervicagenic vertigo can be entertained as the diagnosis.  As an additional test, the rotating stool examination may be helpful.  A patient sits on a rotating stool, the head is immobilized in the examiner’s hands and the neck and trunk is rotated under the head.  In a positive test for cervicogenic vertigo nystagmus is produced.  Lastly, the cervicogenic vertigo patient may be unaware of maintaining their head in a non-neutral position, they may possess a head tilt³.  It’s the author’s opinion that despite a wide differential the diagnosis can still be made somewhat empirically.  In the absence of a viral infection, hearing loss, a tremendous injury mechanism and associated neurological findings cervicogenic vertigo remains the most medically reasonable diagnosis based on its high prevalence relative to the other differential diagnosis, especially with confirmatory physical examination findings.

     

     In addition to the above differential work up, I would add that with a history of a significant injury mechanism one must also evaluate for the presence of a vertebral artery injury.  The vertebral artery is relatively fixed as it travels through the foramen transversarium of the vertebra.  As such, it is susceptible to injury from shear, flexion-extension or rotational forces.  These injuries are usually associated with substantial force.   In such cases one can elicit a history of other vertebrobasilar symptoms, such as dysmetria, diplopia, disequilibrium or sensory and motor deficits.  If the index of suspicion is high a CT angiogram of the vertebral arteries can be performed to exclude the diagnosis.  MRA can be performed but may be less sensitive.       

     Once the diagnosis is established by ruling out other entities and establishing the temporal relationship between the injury mechanism and the onset of symptoms one can initiate treatment of the patient’s cervicogenic vertigo.  In most cases, treatment of cervicogenic vertigo is identical to the treatment of the patient’s underlying neck pain.  Since the injury to proprioceptive cervical inputs co-exist with cervical paraspinal soft tissue and joint capsule injury, it makes sense that therapies that might relieve these structures might also relieve cervicogenic vertigo.  Cervical manipulation and mobilization have been described in the treatment of cervicogenic vertigo².   Physical therapy⁷, with and without vestibular rehabilitative therapy has also been described⁵.  In this case vestibular rehabilitation is rendered by a qualified therapist.   Meclizine, a now over the counter anti-vertigo medication, may provide symptomatic relief. Lastly, cervical facet blocks might theoretically improve cervicogenic vertigo, by anesthetizing the afferent inputs, although this has not been proven.  

     Vertigo following a cervical acceleration-deceleration, or whiplash injury, is common.  The diagnosis is made based on symptoms, temporal relationship to the injury mechanism and exclusion.  Treatment parallels the treatment of the patient’s neck pain.  In establishing the presence of a substantial neck injury cervicogenic vertigo is an important factor.  Injury to the neural proprioceptive inputs is not seen without substantial cervical paraspinal or facet capsular injury.  Cervicogenic vertigo can thus be both disabling and a testimonial to the substantial nature of a whiplash injury.  Treatment parallels the treatment of the painful paraspinal and cervical facet joint injuries that result in cervicogenic vertigo.

Reference List

        1.    Brown JJ. Cervical contribution to balance: cervical vertigo. In: Berthoz A, Graf W, and Vidal P.  The Head-Neck Sensory Motor System. New York: Oxford University Press; 1992;

        2.    Cote P, Mior SA, Fitz-Ritson D. Cervicogenic vertigo:  a report of 3 cases. The journal of the CCA 1991;35:89-94

        3.    McKecnie B. Cervicogenic vertigo.  2013.  Online source.

        4.    White AA, Panjabe NM. Clinical biomechanics of the spine. New York: JB Lippencott; 1978; 153-158

        5.    Wrisley DM, Sparto PJ, Whitney SL, et al. Cervicogenic dizziness: a review of diagnosis and treatment. J Orthop Sports Phys Ther 2000;30:755-66

        6.    Schievink WI. Spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension. JAMA 2006;295:2286-96

        7.    Fitz-Ritson D. Phasic exercises for cervical rehabilitation after "whiplash" trauma. J Manipulative Physiol Ther 1995;18:21-24

Minimally Invasive Surgery Case of the Day

History:  A 21 year old female dancing student presents with back pain and left sided L5 radicular pain of 3 months durantion.

Findings:  Paraspinal left sided tenderness and a positive left sided straight leg raise test is seen on examination.

Imaging:  MRI reveals a foraminal left sided L5/S1 herniation (arrows)

Procedure:  Transforaminal L5/S1 endoscopic discectomy  is performed as an out-patient procedure through a 0.5cm incision

Surgeon:  George Rappard, MD

Disposition:  The patient is discharged one hour post-procedure with resolution of radiculopathy and reversal of straight leg raise sign

Procedure Images:  

Blue stained herniated disc material is seen through scope (arrow)

Upon exploring foramen, exiting L5 nerve root (arrow) and foraminal extruded disc (star) is seen

The endoscopic bipolar (left) and 2.5mm rongeur (right) are used to remove foraminal herniation.  Arrow denotes exiting and displaced L5 nerve root.

After decompression the annular tear is probed (arrow) for loose intradiscal fragments

The nerve (arrow) is decompressed and the foraminal herniation is now seen as an empty cavity (star)

For more information on endoscopic lumber discectomy contact the Los Angeles Minimally Invasive Spine Institute or go to http://www.lamisinstitute.com/percutaneous-endoscopic-lumbar-discectomy

Platelet-rich Plasma Therapy for Back Pain:  Promise or Hype?

George Rappard, MD

     Platelet-rich plasma (PRP) is a potentially promising biologic therapy that has found itself in great demand recently, fueled by success stories of celebrity recipients and physician willingness to engage in this new therapy.  Demand has also fueled, quite appropriately, scientific investigation.  As a result PRP finds itself in the position of being both highly sought after and also highly scrutinized.  It is also widely available.  As a result, it’s relatively inexpensive and easy to produce.  While PRP holds substantial promise; demand, availability and adoption should keep pace with scientific validation.

     PRP has been in the news and the internet quite a bit.  A virtual who’s who of well-known athletes such as Tiger Woods, Peyton Manning, Cliff Lee, Kobe Bryant and Rafael Nudal have all had PRP treatments.  PRP has been endorsed by the NBA, NFL and MLB.  This sports celebrity A-list has naturally fueled demand by prospective patients willing to pay cash for the high end treatments that professional athletes have access to. 

     PRP is very simple in composition and collection.  PRP is a reversal of the normal 93%: 6% ratio of platelets: red blood cells (RBC).  PRP is also concentrated.  While the normal platelet concentration in plasma is 200,000/ul, to be efficacious PRP is concentrated by at least a factor of 4 (1).  The PRP is produced by collecting a patient’s own blood through a large bore needle so as not to denature the platelets.  The blood is placed in an FDA approved device and centrifuged.  The blood is then separated into platelet poor plasma, RBC and PRP.  Roughly 30cc’s of blood will yield 3cc’s of PRP.  Because PRP isnot heavily processed, it’s not a drug.  While the devices that concentrate it are FDA regulated, its human use is not.

     PRP’s contents and potential mechanisms of action are far more complex than its production and composition.  Platelets contain alpha granules that can release a host of biologically active substances, including IGF-1, TGF, VGEF, PDGF, EGF and Vitranectin.  These factors are involved in cell aggregation, cellular proliferation, angiogenesis and proteoglycan and glycosamine synthesis.  Platelets also contain dense granules rich in Adenosisne, Seratonin, Histamine and Calcium.  These molecules are felt to be cytoprotective, increase vascular permeability and vasodilation and effect cellular migration and remodeling.  In order for platelets to release the biologically complex contents of their granules they have to be activated.  Naturally occurring in-vivo activation is mimicked by activating platelets with thrombin, +/- Calcium chloride.  At least one author has investigated the activation of platelets in PRP with autologous serum (2). 

     PRP has been a focus of scientific study.   Currently, clinicaltrials.gov lists 94 ongoing research studies.  A search of PRP therapy on PubMed lists 2,385 citations.  This suggests that science may be catching up to demand and availability in some new and emerging applications of PRP.   PRP has been studied in the areas of wound healing, epichondylitis, plantar fasciitis, Achilles tendinopathy, total knee arthroplasty, rotator cuff injury and non-healing long bone fractures, with mixed results.  PRP has been found to be efficacious for the treatment of non-healing skin wounds (3; 4).  In a small, non-randomized study, PRP was shown to be effective in treating epicondylitis, a painful condition of the elbow (5).  More recently, a large randomized trial presented at the 2013 American Academy of Orthopedic Surgery Annual Meeting validated the effectiveness of PRP in treating epicondylitis, or tennis elbow.  The randomized trial enrolled 230 patients and is the largest study to date on PRP.  84% of patients treated with PRP met with success (6).  A small pilot study showed potential effectiveness in treating plantar fasciitis, a painful condition of the foot (7). The American Academy of Orthopedic Surgeons has tackled the interest in PRP by publishing a series of reviews in the Academy bulletin, AAOS Now.  PRP was reported to not be effective in the treatment of rotator cuff injuries in the shoulder or anterior cruciate ligament injuries of the knee (8; 9).  PRP was found to be a promising therapy for non-healing long bone fractures and the treatment of Achilles tendinopathy of the ankle (10; 11). 

         The use of PRP for the treatment of back pain has not been well studied clinically.  A  PubMed search reveals no cited studies for the use of PRP as an injection for painful lumbar facet joints or sacroiliac joints, yet a quick Google search reveals that there is no paucity of practitioners willing to perform these injections.  Similar results were noted for PRP injection of spinal or sacroiliac ligaments. 

     PRP has been studied in the lumbar disc, though this area remains highly investigational.  A search of clinicaltrials.gov reveals 1 human study-not enrolling patients however.  Animal studies have shown promise.  Gullung at al studied the effects of PRP on degenerative discs by studying its effects on the L4/5 discs of Sprague-Dawley rats using a 21 gage needle disc injury model (12). The investigators found that the PRP treated discs had a significantly improved disc height over controls.  Histological analysis showed that there was preservation of disc architecture compared to controls.  Additionally, on MRI analysis there was inproved disc fluid content.  The authors concluded that PRP may confer protective and even regenerative effects in this animal injury model.  Obata et al used a disc puncture model to study the effects of PRP on rabbits (2).  The authors found that the PRP treated animals had significantly increased disc height over controls and significantly increased chondrocytes seen in the injured discs on histological analysis.  No difference was seen in T2 MR analysis of the discs between treated and sham groups.  Lastly, Chen et al studied the use of PRP in a chymopapain disc injury porcine model (13).  In the PRP group an increase in mRNA involved in chondrogenesis and matrix accumulation was noted.  Increased disc height was also noted over controls.

     The only area in spine where PRP has been extensively studied in humans is in its use as an adjunct to promote fusion in surgery.  Here the anticipated results, based on the bioactivity of PRP, were not always reproducible.  2 studies of patients undergoing lumbar fusion surgery have found an increased non-union (poor bone healing) rate in patients treated with PRP and bone graft vs. bone graft alone (14; 15).  Other studies have found similar or improved rates of fusion (bone healing) in patients treated with PRP (16; 17).  This represents a very illustratable example of excitement overrunning scientific caution.  Prior to these studies physicians performing fusions were rapidly adopting PRP to augment fusion rates based solely on its potential biological mechanism.

     There are several variables that should be considered and investigated prior to moving on to human PRP studies for spine pain.  PRP, as studied and reported, is very heterogenous. Many papers do not quantify the platelet concentration used.  As a result, there is little or no experience with dose related effects.  Also, studies use different activators, whether Calcium Chloride, thrombin or plasma, potentially confounding results.  Furthermore, some formulations contain white blood cells, while others do not.  The contribution of white blood cells to PRP’s potentially therapeutic effects are not well understood.  Lastly, caution should be taken when studying any substance that requires a disc puncture.  Human and animal studies alike have already validated the potential for needle based disc punctures to result in accelerated disc degeneration (2; 12; 18).

     Despite the lack of validated human data to promote the use of PRP in treating spine pain, it’s availability and ease of production, lack of regulation, public demand and willingness of practitioners to administer it have created an extensive cash based cottage industry.  Like most drugs and devices, experience and investigation will show that there is no PRP related “Holy Grail” for the treatment of spinal pain or musculoskeletal injury.  Rather, there are and will be some applications that are better than others and probably some applications that should be avoided all together.  The use of PRP injected intramuscularly (where it can cause muscle fibrosis) and the use of PRP in fusion surgery (where it can actually result in lower fusion rates) are examples of potentially good applications based on biological mechanism that were not borne out scientifically.  While the study of PRP and other biologics for the treatment of spinal pain is reasonable and in fact supported by animal data, widespread use without scientific validity is not and restraint should be exercised.

1. Marx, R and Garg A. Dental and craniofacial applications of platelet rich plasma. Quintessence publishing company Inc, 2005.

2. Obata S et al. Effect of autologous platelet-rich plasma-releasate on intervertebral disc degeneration in the rabbit annular puncture model: A preclinical study. Arthritis research & Therapy, Nov 2012, Vol. 14, p. R241.

3. Crovetti G et al. Platelet gel for healing cutaneous chronic wounds.  Transfus Apher Sci, 2004. Vol. 30, pp. 145-51.

4. McAleer JP, Kaplan E, Persich G. Efficacy of concentrated autologous platelet-derived growth factors in chronic lower extremity wounds. J Am Podiatr Med Assoc, Vol. 96, pp. 482-8.

5. Edwards SG, Calandruccio JH. Autologous blood injections for refractory lateral epicondylitis. 2003, Am J Hand Surg, Vol. 28, pp. 272-8.

6. Platelet Rich Plasma Significantly Improves Clinical Outcomes in Patients with Chronic Tennis Elbow (abstract). Mishra AK, Skrepnik NV, Edwards, SG et al. Chicago. Proceedings of the 2013 annual meeting of the American Academy of Orthopedic Surgery.

7. Barrett S, Erredge S. Growth factors for chronic plantar fascitis. 2004, Podiatry Today, Vol. 17, pp. 37-42.

8. PRP does not improve rotator cuff healing. AAOS Now. April 2011.

9. Stanton, T. PRP shows little benefit in ACL reconstruction at 6 months. AAOS Now. April 2010.

10. Stanton, T. High-concentrate PRP Promotes Healing in Long-Bone. AAOS Now. February 2010.

11. Leahy, M. PRP effective in treating chronic Achilles tendinosis. AAOS Now. March 2010.

12. Gullung G et al. Platelet-rich plasma effects on degenerative disc disease: analysis of histology and imaging in an animal model. Evidence-Based Spine-Care Journal. 2011, Vol. 21, 4, pp. 13-18.

13. Chen WH et al. Intervertebral dsic regeneration in an ex vivo culture system using mesenchymal stem cells and platelet-rich plasma. Biometerials. Oct 2009, Vol. 29, pp. 5523-33.

14. Carreon LY et al. Platelet gel (AGF) fails to increase fusion rates in instrumented posterolateral fusions. Spine. 2009, Vol. 30, 9, pp. E243-7.

15. Weiner BK, Walker M. Efficacy of autologous growth factors in autologous intertransverse fusions. Spine. 2003, Vol. 28, pp. 1968-70.

16. Jenis LG, Banco RJ, Kwon B. A prospective study of Autologous Growth Factors (AGF) in lumbar interbody fusion. Spine J. 2006, Vol. 6, 1, pp. 14-20.

17. Hee HT et al. Do autologous growth factors enhance transforaminal lumbar interbody fusion? Eur Spine J. 2003, Vol. 12, 12, pp. 400-7.

18.  Carragee EJ et al.  2009 ISSLS prize winner:  Does discography cause accelerated progression of degenerative changes in the lumbar disc.  Spine.  2009.  Vol. 34, 12 pp 2338-45

Combining Spinal Injections with Chiropractic Adjustments: A Chiropractor’s Perspective

By Brian Renner, D.C.

     B.J. Palmer, a chiropractic pioneer once said "Team work is important. Even a banana gets skinned when it leaves the bunch."  It comes particularly to mind right now in regards to a recent discussion I had with a local spine interventionist. He was discussing with me his preference to work with chiropractors in the area to help bring difficult patients out of what seems to be a “plateau” in the course of their treatment. The interventionist lamented over what he perceived to be a lack of coordination between the two specialties and how, by working together, some patients can get the most out of chiropractic care.  Over the past several decades, chiropractic medicine has gained much recognition in its effectiveness in treating spinal pain. In fact, some would say that chiropractors have evolved as the current day primary care providers for spinal pain. The field of interventional pain management has also blossomed, similarly to chiropractic care.  However, most patients come to pain management at the end of chiropractic care, when they plateau.  Perhaps, now that these two fields have matured, it’s time to consider how they might best intersect to serve patients; in other words, team work.

     Spinal injections consisting of epidural steroid and facet injections have been shown to be effective in treating back pain (1; 2). Research suggests that collaborative efforts of combining spinal injections with chiropractic adjustments may be beneficial in cases of chronic low back pain patients that have plateaued in their progress. According to Nelson et al, the use of epidural spinal injection and spinal manipulation together offers promise and “should be considered in patients who do not respond to conventional forms of care.” (3) Why might this show promise? Is it simply because the injection causes pain relief? Does it make it easier for the patient to accept the adjustment? Does it allow the patient to move with more normal movement patterns and better accept rehabilitative exercises? Actually, all of the above appear to be reasons contributing to this conclusion.

      Injectional therapy may help some chiropractic patients better receive adjustments and tolerate prescribed exercises.  I will probably always remember the drills we did in school which developed our speed at delivering the thrust for the adjustment. For a patient in pain, being controlled and quick at delivering the thrust is paramount. In fact, not only does it seem to contribute to the patient’s comfort, but it may “comprise part of the mechanism contributing to this intervention’s physiologic effects.” (4) The findings in this study suggest that the quicker the thrust, the more effective it may be. How much easier would it be to deliver a quick thrust to a spinal vertebra if the patient is not in pain? Maybe that’s actually a contributing factor to some patients’ roadblock to recovery. By utilizing injectional therapy in our plateaued patients, we could likely get through the patient’s muscle guarding and pain receptors to deliver a better adjustment.  In addition, the patient may also be more likely to perform the exercises prescribed in order to facilitate the rehabilitation process. In fact, this may actually be one of the big ways that injections help spine pain patients improve. (5)

     Injectional therapy is complementary to the anti-inflammatory effects of chiropractic manipulation. A study done in 2006 demonstrated a significant reduction in severity and duration of IVF and DRG inflammation using Activator adjustments. (6) In some patients though, injury mediated inflammation may become chronic.  What kind of outcome could we see in recoveries of these patients by combining injections, which are anti-inflammatory, as well as high-speed adjustments, which have also shown to be anti-inflammatory?  From a purely mechanistic point of view, a combined approach might well be promising.

     While little research has been done to specifically analyze the potential benefits of combining spinal injections with spinal adjustments it seems likely that some groups of patients could greatly benefit from spinal injections in combination with chiropractic care.  This would most likely benefit the patient who has reached a plateau in their chiropractic regimen and has become chronic.  Such use of injectional therapy would be in keeping with the current standard of referring patients for injections only after a lack of improvement in conservative care.  Importantly, such patients would not “fail” chiropractic care if injectional therapy returned the patient to a successful chiropractic regimen. Though the intersection of pain management and chiropractic care may not be exactly what Palmer had in mind when he discussed teamwork in the chiropractic community, the potential benefit of such team work is undeniable.

(1)    T.L. Shulte, T.A. Pietila, J. Heidenreich, M. Brock, R. Stendel. (2006). Injection therapy of lumbar facet syndrome: a prospective study. Acta Neuroshirurgica, 148(11):1165-1172

(2)    Buchner, Matthias MD; Zeifang, Felix MD; Brocai, Dario R.C. PhD; Schiltenwolf, Marcus MD. (2000). Epidural Corticosteroid Injection in the Conservative Management of Sciatica. Clinical Orthopaedics & Related Research, 375:149-156

(3)    Nelson L., Aspegren D., & Bova C. (1997). The use of epidural steroid injection and manipulation on patients with chronic low back pain. Journal of Manipulative and Physiological Therapeutics, 20(4):263-266

(4)    Sung, Paul S. PT, DHSc, PhD; Kang, Yu-Ming PhD; Pickar, Joel G. DC, PhD. (2005). Effect of Spinal Manipulation Duration on Low Threshold Mechanoreceptors in Lumbar Paraspinal Muscles: A Preliminary Report. Spine, 30(1):115-122

(5)    Robert F. McLain, MD; Leonardo Kapural, MD, Nagy A. Mekhail, MD, PhD. (2005). Epidural steroid therapy for back and leg pain: mechanisms of action and efficacy. The Spine Journal, 5(2):191-201

(6)    Xue-Jun Song, MD, PhD; Qiang Gan, MS; Jun-Li Cao, MD; Zheng-BejWang, MD; Ronald L. Rupert, DC, MS. (2006). Spinal Manipulation Reduces Pain and Hyperalgesia After Lumbar Intervertebral Foramen Inflammation in the Rat. Journal of Manipulative and Physiological Therapeutics, 29(1):5-13

 

The 4 Pillars of Chronic Spine Pain Care

By George Rappard

     Spinal back and neck pain is a big healthcare issue in the United States, accounting for the most common cause of work related disability and 15 billion dollars in yearly healthcare costs.  Additionally, there are 14 billion dollars in yearly indirect costs related to lost wages.  Despite these costs, the likelihood of chronicity and recurrence is high.  With such economic impact and mediocre prognosis, it’s clear that more effective approaches are needed.  The 4 pillars of effective chronic spine care,  tailored physical and manual therapy, appropriate medical management, effective interventional care and minimally invasive surgical solutions, may make a difference for some patients as well as helping clinicians to avoid common pitfalls.

     The first pillar, tailored physical or manual therapy, is important in the early course of the patient’s pain.  PT is not one size fits all.  It has been shown that some patients may benefit more from conditioning therapy, like Pilates or aerobics, than from passive exercises.  Some patients with back pain may suffer from segmental instability, meaning that a portion of their spine may not resist motion well.  In these cases core strengthening should be the focus of physical therapy.  In other patients, pain may be exacerbated and relieved by opposite motions.  Extension may relieve pain and flexion may aggravate it.    This is called a directional preference.  These patients may benefit more from mechanical diagnosis and therapy, a unique form of PT that requires patients to perform end stage range of motion exercises in a posture that relieves pain.  Additionally, patient satisfaction rates from manual therapies, usually chiropractic manipulation, run high.  Some chiropractors are also experts at posture training, a specialized form of therapy designed to combat the mechanical stress of poor posture.

     The second pillar in effective spine care is appropriate medical management of chronic pain.  While narcotics and anti-inflammatories are key in the treatment of acute exacerbations, they can have significant side effects if taken chronically.    Narcotics may lead to dependence and addiction, while anti-inflammatories can have effects to the stomach or kidneys.  Alternative medications can reduce the potential for these side effects.   Cymbalta, an antidepressant, has recently been cleared by the FDA for use in patients with chronic back pain.  Lyrica and Neurontin, both anti-convulsants, seem to be effective in treating neuropathic pain, such as radiculopathy.  The use of these drugs should be determined based on the over-riding complaints; back/neck pain or radiculopathy (usually intense leg or arm pain).  Note that these alternative medications themselves may possess side effects.  Some chronic patients have skin hypersensitivity as a result of chronic pain.  Recent data suggests that analgesic patches, such as a 5% Lidoderm® patch may be effective in relieving back pain in these patients.  Lastly, spinal cord stimulation may serve as an alternative to chronic use of narcotics in treating patients who have failed most other therapies.  

     Effective interventional pain management is the third pillar in chronic spinal care.  Patients are usually referred for interventional pain management when other therapies have not succeeded.  The most commonly performed interventional pain procedure, the epidural steroid injection, may not always be what is needed.  A careful history and physical can determine what the patient’s pain generator might be.  A neck pain patient involved in a restrained motor vehicle accident is more likely to suffer from a cervical facet injury.  A younger patient with disc herniation probably has discogenic back pain.  An older patient with similar symptoms probably has pain originating from the lumbar facet joints.  If the patient has had a lumbar fusion or has given birth several times, the sacroiliac joints may be the cause of pain.  In these cases, an epidural injection may not be the best option.  Also, there would be little basis for repeating an ineffective epidural injection.  Alternative, targeted procedures may be more effective.  These might include facet blocks, median branch blocks and discography.  Performing the appropriate procedure is important so that patients are not unnecessarily deemed treatment failures when they might not have had the right treatment to begin with. 

     As a last resort, surgery may be required to treat chronic spinal pain.  The first 3 pillars are very important prior to referring a patient to surgery because with tailored physical and manual therapy, appropriate medical therapy and effective pain management patients may never need to be referred to surgery.  If it comes down to surgery though, it’s important to perform surgery in a way that maximizes rehabilitation potential and recovery by maintaining spinal stability and motion.  That is the 4^th pillar.  A conventional spinal discectomy surgery requires the surgeon to incise fascia, dissect and incise posterior spinal muscles, remove facet joints and cut ligaments to access the disc.  These structures are critical biomechanically to the stability of the spine.  Therefore, much of the recovery associated with surgery is due to the surgery itself.  Affecting stability may also lead to biomechanical problems in the future.  The common alternative, fusion, restricts motion in the treated segment and may lead to hypermobility and accelerated degeneration in the adjacent spine.  Commonly practiced forms of minimally invasive surgery are less damaging but really are only mini versions of the original procedures.  The incisions and dissections are smaller, but the same structures are affected.  Percutaneous surgery, often with the use of an endoscope, can achieve the same surgical goals without the collateral effects on stability and motion.  Recovery and rehabilitation is quicker and the results are similar to other surgical techniques in properly selected patients.

     Chronic spinal pain is a huge economic burden and there is a high recurrence rate.  By adhering to these four pillars of effective care: tailored physical and manual therapy, appropriate medical management, effective interventional care and minimally invasive surgical solutions, providers may be able to have a greater impact on outcomes and patient satisfaction rates.