Low Back Pain and Headache Pain: Practice Update

SPECIAL REPORT

By far the most common forms of chronic pain and recurring pain are back pain, especially low back pain (LBP), and headaches (HA). Although both can be a symptom of underlying pathology including potentially life-threatening diseases, in the majority of patients the exact cause remains unknown and in some cases therapies applied to alleviate the pain may end up exacerbating it.

When is a work up worth it?

For both LBP and HA there are “red flag” signs and symptoms that warn of an underlying pathology as a potential cause of pain and for which further work-up is indicated. Solutions to the underlying causes are in many cases not simple, but there are treatments primary care physicians can provide that may provide some relief.

LBP: Evaluation>>

LOW BACK PAIN

Evaluation

Four main categories of severe pathology that may cause LBP and the associated red flags that call for immediate evaluation are^1,2:

 â–º Fracture

     - Recent trauma

     - Use of steroids or immunosuppressors

 â–º Malignancy

     - Past history of cancer

     - Recent unexplained weight loss

     - Pain exacerbated by lying down (in most cases of mechanical LBP the pain is reduced or at least unchanged when lying down)

 â–º Fever or other signs of infection

 â–º Cauda equina syndrome

     - Acute changes in bowel or bladder function

     - Acute sensory or motor loss in the pelvic region or lower extremities

An additional red flag that can be associated with any of these is first episode of LBP after age 50. Most people with LBP report having the pain for years.

Of all these red flags, recent unexplained weight loss and exacerbation of the pain when lying down are most often overlooked.

Unless one of the red flags is present, there is no indication for an acute work-up with diagnostic imaging. In the absence of one or more red flag, performing imaging studies within the first 6 weeks of a visit to a physician for acute LBP does not appear to improve treatment outcome.

LBP: Etiology>>

What causes LBP?

There are many structures in the back which can be associated with pain. Most commonly the pain is ascribed to changes in the spine, particularly bulging or herniated intervertebral disks that result in pressure on spinal nerve roots. There is limited evidence, however, that disk pathology is the cause of most cases of LBP.

No clear correlation between the presence or severity of pain and changes in intervertebral disks has been established. In fact, repeated studies have demonstrated that the overwhelming majority of adults without back pain have bulging disks as demonstrated by MRI.³ Research also has shown that treatments that specifically target inflammation such as oral nonsteroidal anti-inflammatory drugs (NSAIDs) and epidural corticosteroid injections have limited efficacy for many cases of LBP. Surgery that is intended to remedy abnormalities detected by imaging often provides limited, if any, long-term relief and can exacerbate the pain.

Treating LBP

Treatments for LBP are ubiquitous yet it continues to be a widespread-and expanding-health issue. Among many reasons for the enduring presence of LBP is that because our understanding of etiology remains limited, there may actually be multiple underlying causes so that treatment that is effective for one person may be completely ineffective for another.

There are many treatments that are worth trying and although there is no evidence that invasive approaches (ie, surgery) are more effective than conservative strategies, trials of the latter are too often too brief before moving on to the former.

Prevention. We do have a good idea about what can be done to reduce the incidence of LBP and those approaches are basic and simple: encourage better posture and correct body mechanics; promote regular exercise including strengthening of the abdominal muscles; and, support weight loss for the overweight and obese.⁴ Unfortunately, many people don’t practice such good habits until directed to-after pain begins. Even then, however, each is worth trying as they still appear to be the strategies most likely to result in reduction of pain. Furthermore, in the presence of poor body mechanics and obesity, benefits from other therapies are likely to be limited.  

Non-drug therapies. Non-pharmacologic, non-surgical therapies that are worth considering because they are shown to be beneficial for some patients and have typically benign adverse event profiles include cognitive behavioral therapy, acupuncture, and transcutaneous electrical nerve stimulation (TENS).

With regard to medications for chronic LBP, over-the-counter analgesics may provide limited relief but there is little evidence for the efficacy of either acetaminophen or NSAIDs.

Opioids. It is not uncommon for an opioid to be the first prescription analgesic tried for LBP. Although opioid analgesics are widely prescribed for all forms of pain, they should be prescribed for only brief periods for all of the obvious, pressing, and logical reasons including the potential for misuse and abuse. Another important reason to limit the amount of time opioids are prescribed is the possible development of hyperalgesia, where there is a reduction in pain threshold and the pain becomes worse.

Non-opioid Treatment, Surgery>>

Non-opioids. Among non-opioid analgesics to treat chronic pain, the serotonin-norepinephrine reuptake inhibitor (SNRI) duloxetine is FDA-approved for the management of LBP but it is unclear whether it is more effective than the tricyclic antidepressants or other SNRIs. Oral steroids do not appear to be efficacious for most cases of chronic LBP and therefore are not generally recommended.³

As noted above, evidence is limited for the benefits of epidural corticosteroid injections and whether they should be offered to patients with LBP is controversial and the subject of debate.

Surgery should be considered as a last resort for LBP. Even where an etiology is identified as with a herniated disk or spinal stenosis, more conservative therapeutic modalities are often as effective in the long run and at best the surgical intervention may provide more rapid relief of the pain. Of course a problem with surgery is that it can not be undone and there are patients who have the same pain or at times worse or different pain than they did before their surgeries.

HEADACHE PAIN>>

HEADACHE PAIN

Evaluation

Red flags that can indicate serious underlying pathology and are cause for acute workup⁵:

 â–º Abnormalities on motor or sensory neurological exams

 â–º Change in mental status

 â–º Onset of pain after head trauma

 â–º Presence of fever or nuchal rigidity (may indicate meningitis)

 â–º Seizures

 â–º Sudden or explosive HA (may indicate intracranial bleed, other intracranial pathology

 â–º Headache described as being far more severe or markedly different than any previously experienced

 â–º HA unlike ones previously experienced in a patient age ≥50 years

     - Increased incidence of disease process that might cause HA including tumors, stroke, subdural hematoma, temporal arteritis

 â–º Signs of increased intracranial pressure (eg, papilledema)

 â–º Acute or recent onset HA brought on by exertion (may indicate vascular abnormality); also common in migraine HA but usually migraine headaches are a chronic problem

As with LBP, in the absence of one of the red flags, there is usually little need for an acute work-up.

HA Pain: Etiology>>

What causes headaches? 

As with LBP, the etiology of most HA is unclear. The question of why HA is a near universal experience despite the fact that the brain itself is insensitive to pain is one of medicine’s most vexing.

The two general types of HA are: primary where there is no detectable underlying pathology to explain the pain and secondary where pathology is identified.

The most common types of primary headaches are:

  ► Tension-type headaches (TTH)

  ► Migraines with (MA) and without aura (MO)

  ► Cluster headaches (CH)

Although the types are often viewed as discrete entities, many patients have a mixture of symptoms of each. There is a view that holds that TTH and migraines are better viewed along a continuum, rather than as discreet entities, with TTH at one end and MA at the other with MO in between.⁶ And although MA and MO are both under the general heading of migraine, it is unclear whether they actually share the same underlying etiology.

While there are multiple serious disorders that can cause secondary headache and many poorly understood causes of primary headache, one of the most common types of secondary HA is actually a result of treatment of primary HA: medication overuse headache where continued use of analgesics to relieve primary HA instead cause further pain.

Primary Headaches: Symptoms and Treatment>>

Tension-type Headache

 â–º Bilateral; “tightening, band-like pain” around the head

 â–º Not exacerbated by exercise

 â–º Triggers: thought to be primarily psychological stress

     - “Tension” does not refer to muscle tightness, but to psychological stress, found to be the most common trigger of TTH.⁷

Treatment

 â–º Start with OTC (acetaminophen, NSAIDs); trial triptans

 â–º For frequent TTH, migraine-type prophylaxis may be tried: tricyclic antidepressant, other SNRI; anticonvulsant (eg, topiramate).

 â–º Non-drug approach: do anything that relieves HA without making things worse.

 â–º Psychological treatments for stress management, eg, relaxation techniques, biofeedback, cognitive behavioral therapy.

Migraine Headache

 â–º Unilateral, throbbing (both MO, MA); etiology of throbbing unclear; no correlation with arterial pulse

 â–º Exacerbated by movement

 â–º Accompanied by nausea, vomiting, photo-, phono-, and osmophobia

 â–º Symptoms may occur in absence of HA

 â–º MA vs MO: presence of aura, most commonly but not always visual disturbance

 â–º Research suggests MA may be associated with increased risk of stroke

 â–º Gender: before puberty, equal distribution; after puberty, twice as prevalent in women; possibly related to hormonal changes, still unclear

 â–º Triggers: Menses for women (for some, only during menses); disrupted sleep patterns (over/under sleeping); change in eating habits; specific foods (MSG, tyramine, alcohol, caffeine (excess or withdrawal)

Migraine Treatment>>

Migraine: Acute Treatment

There is a great deal of variation among patients in what relieves migraine.⁸ For many, OTC medications, including acetaminophen and NSAIDs, are sufficient.

Triptans. The triptan medications are currently the most effective prescription medications. It is important to recognize that if the first triptan tried does not provide relief, it is worth trying others in this class as response to different formulations has been shown to vary for the same patient. It is virtually impossible to predict which one will be most effective.

Ergotamines. Use of the ergotamines, once the primary drugs available to treat migraine, has been largely replaced by the triptans, owing to greater efficacy, wide availability, and better side effect profile.

Opioids. Opioid analgesics are not approved by the FDA for treatment of migraine and are not recommended as first-line therapy. Some patients may benefit from opioids (eg, those with severe pain unrelieved by triptans; those unresponsive to triptans/other medications) but their extended use is generally contraindicated.

The nausea and vomiting that often accompany migraine attacks are best treated with antiemetics such as metoclopramide, prochlorperazine, droperidol, and chlorpromazine.

Migraine Treatment: Prophylaxis>>

Migraine Treatment: Prophylaxis

Antiepileptics. For migraines of sufficient frequency to warrant prophylactic treatments the most effective preventive medications are the antiepileptic drugs topirimate, divalproex sodium, and sodium valproate; propranolol; the tricyclic antidepressants and the other SNRIs. Triptans have been shown effective for short-term prevention of menstrually-related migraine but are not indicated for daily prophylaxis.⁹ There is little evidence to support the use of opioids as prophylactic treatment of migraines. While details of the use of onabotulinumtoxinA are beyond the scope of this discussion, it is FDA-approved  for prevention of chronic migraine.⁹

Non-drug therapy. With regard to non-pharmacologic therapies for migraines, the psychological interventions, most notably biofeedback and cognitive behavioral therapy, have been found particularly effective for both prophylaxis and treatment of acute attacks. Acupuncture can be beneficial in some patients as a prophylactic treatment.

It is worth noting that although MA and MO may be quite different entities, as of yet there has been little research evaluating which medications and other therapies are beneficial for which types.

Cluster and Medication Overuse Headaches>>

Cluster Headache

  ► Cluster headaches (CH) differ from TTH and migraines

  ► Occur more frequently in men than women (unlike migraines)

  ► Very sudden onset of pain, peak occurring within 15 minutes; pain, autonomic symptoms may last up to 2 hours

     - Pain is very sharp, usually centered around the eye, often described as “stabbing”

     - Autonomic signs may be seen on affected side eg, droopy eyelid, watery, tearing eye, stuffy or runny nose, contracted pupil, facial sweating¹⁰

  ► Patients have been described as having a "leonine" look

  ► Most common trigger: Alcohol use, especially heavy use

  ► CH occur during well circumscribed periods that can last for weeks or months

     - In between headache seasons, patients usually headache free

Treatment

  ► Acute CH attacks best treated with high-flow oxygen and triptans

  ► For recurrent CH at specific times of the year, prophylactic treatment can be instituted shortly before the headaches are expected to begin

     - Most effective are verapamil and lithium

  ► Cognitive behavioral therapy and biofeedback can also be useful for managing CH

Medication overuse headache

Medication overuse headache (MOH) is the result of excessive use of medications used to treat other headaches.¹¹

It is most often the medications used for acute treatment of HA rather than prophylaxis that are the cause, including virtually all analgesics used for HA management: acetaminophen, NSAIDS, triptans, and opioids. Excessive caffeine use also appears to increase the likelihood of MOH.  

Diagnosis is usually made based on worsening of primary headaches despite increasing use of analgesics.

The appropriate treatment for MOH is withdrawal of the analgesics. The HA may be more severe for the first two to three days of withdrawal and may be accompanied by other symptoms (eg, nausea, vomiting) which may result in relapse. There is no professional consensus on how best to accomplish withdrawal from the agent being overused, ie, tapering, medication replacement, "cold turkey," but in some cases inpatient treatment may be required in order to control analgesic intake, and provide supportive care including nonpharmacologic and psychological strategies to help manage headache pain.

Conclusion>>

Conclusion

In the absence of red flags for LBP and HA, PCPs usually can wait for at least several weeks to see whether the pain increases, decreases, or stays the same before seeking further evaluation. Although most of the-first line medications for both forms of pain are familiar to PCPs, for LBP, assistance from physiatry and physical and occupational therapy colleagues will help to design exercise programs and to teach proper body mechanics. Psychological intervention (eg, cognitive behavioral therapy, biofeedback) usually requires referral to mental health practitioners and acupuncture referral to healthcare professionals trained in its use.

The treatment of migraines and TTH with the first line medications indicated for them is within primary care purview. However, CH and MOH can be much more difficult to diagnose and treat and may require referral to neurologists specializing in headaches or other pain specialists knowledgable about headache management.

The final message is that in treating both LBP and headaches, it is worth remembering that many of the treatments physicians provide to relieve the pain can actually end up exacerbating it and causing patients additional problems.  Therefore, in treating these painful conditions it is always important to proceed cautiously with therapies with frequent reassessments as to whether they are being beneficial.

Click here to go to Part II. 10 Opioid Myths and Facts>>

References:

1. Verhagen AP, Downie A, Popal N, et al. Red flags presented in current low back pain guidelines: a review. European Spine Jour. 2016;25:2788-2802.

2. Jarvik JG, Gold LS, Comstock BA, et al. Association of early imaging for back pain with clinical outcomes in older adults. JAMA. 2015;313:1143-1153.

3. Agency for Healthcare Quality and Research. Low back pain medical treatment guidelines. Available at www.guideline.gov/summaries/summary/49020/low-bac-pain-medical-treatment-guidelines.

4. Seffens D, Maher CG, Pereira LS, et al. Prevention of low back pain: a systematic review and meta-analysis. JAMA Intern Med. 2016;176:199-208

Delitto A, Piva SR, Moore CG, et al. Surgery versus nonsurgical treatment of lumbar spine stenosis. a randomized trial. Ann Intern Med. 2015;162:465-473.

5. American Headache Society. Choosing Wisely Headache. Available at:  http://www.american- headachesociety.org/assets/1/7/Choosing_Wisely_Headache_article.pdf

6. Turner DP, Smitherman TA, Black AK, et al. Are migraine and tension-type headache diagnostic types or points on a severity continuum? An exploration of the latent taxometric structure of headache. Pain. 2015;156:1200-1207

7. Loden E, Rizzoli P.  Tension type headache. BMJ. 2008;336:88-92.

8. Marmura MJ, Silberstein SD, Schwedt TJ. The acute treatment of migraine in adults: The American Headache Society evidence assessment of migraine pharmacotherapies. Headache. 2015:55:3-20

9. Estermalik E, Tepper S. Preventive treatment in migraine and the new US guidelines. Neuropsych Dis Treatment. 2013;9:709-720.

10. Nesbitt AD, Goadsby PJ. Cluster headache. BMJ. 2012;344:e2407.

11. Kristoffersen ES, Lundqvist C. Medication-overuse headache: a review. J Pain Res. 2014;7:367-378.