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18 Articles in Volume 11, Issue #9
Pain and Sleep: A Delicate Balance
Management of Insomnia: Considerations For Patients With Chronic Pain
PPM Editorial Board Outlines Management Strategies for Chronic Pain Patients With Insomnia
Attention Deficit Hyperactivity Disorder And Patients With Pain
Dry Needling Offers Relief From Chronic Low Back Pain
Etiology of Chronic Pain and Mental Illness: How To Assess Both
Temporomandibular Disorder: Examining the Cause And Treatments
Highlights From PAINWeek 2011
Is Your Patient Using Heroin?
Medications For Low Back Pain
Nonpharmacologic Treatments for Patients With Sleep Disorders and Pain
Man With Constant, Daily Headache Pain, Photophobia, Phonophobia, and Nausea
Successful Nonoperative Treatment of Persistently Painful Knees Following Total Knee Arthroplasty—A Case Series
Insomnia in Chronic Pain Patients
What Is Going Wrong With Research? Finding the Right Answer
Testing Positive for Marijuana in Urine
Hydrocodone, Carisoprodol, and Alprazolam—A Most Lethal Combination
Pro-inflammatory Diet

Man With Constant, Daily Headache Pain, Photophobia, Phonophobia, and Nausea

Technical description of occipital blockade in the treatment of occipital neuralgia

History: A 66-year-old man with long-standing history of chronic neuralgia of the right occipital nerve presents with constant, daily pain of variable intensity associated with photophobia, phonophobia, and frequent nausea. When the patient was 60 years old, he was in a motor vehicle collision (MVC). Acute medical workup performed immediately after the accident, which included a neurology consult, was negative for neurologic abnormality or injury to the cervical spine or cranium. Shortly after the MVC, the patient began to complain of persistent neck “stiffness” without neck or headache pain.

Twenty-eight months after the MVC, the patient developed severe right occipital pain that referred into the right parietal, frontal, and supraorbital regions, which persisted as constant pain for 90 days before spontaneously resolving without medical intervention. Three months later, 2 years and 10 months after the MVC, when the patient was 63 years old, his headache returned. As noted, the headache was associated with photophobia, phonophobia, and frequent nausea. The patient noted that the pain is constant and present all day, every day. It has never resolved without treatment.

At baseline, the patient has no pain-free days. The patient is taking Fioricet (a combination of butalbital 50 mg, acetaminophen 325 mg, and caffeine 40 mg), two tablets every 4 hours while awake, and Lortab (hydrocodone 10 mg/acetaminophen 650 mg) every 6 hours around the clock to manage his headache pain. This represents a total of 6,500 mg of acetaminophen per day, which exceeds the recommended maximum daily dose of 4,000 mg per day for a patient with normal liver function and previously raised serious concerns about the patient’s long-term health when these medications were his only treatment for his headache pain.

The patient’s medical history is positive for tension-type headache in adolescence, which is not similar to current complaints and resolved in young adulthood. The patient’s history is negative for migraine, vertigo, and blurred vision.

The patient’s family history is positive for Parkinson’s disease, bipolar disorder, depression, hypertension, and type 2 diabetes. His family history is negative for migraine. Physical examination is positive for tinel’s sign over the right occipital nerve, just inferior to the occipital protuberance and lateral to midline. Physical examination is negative for rhinorrhea, abnormal lacrimation, hyperhidrosis, facial flushing, and conjunctival erythema. Neurologic exam, including cranial nerves, is negative for deficits.

The patient has been enrolled in the author’s pain clinic, receiving repeated neural blockade of the greater occipital nerve (GON) and lesser occipital nerve (LON) for more than 3 years. After each procedure, the patient reports complete relief of his headache pain and associated symptoms for 5½ months, followed by a sudden return to pre-procedure baseline headache pain.

During the period of post-procedure analgesia, the patient reports that he is pain free and able to completely eliminate the need for all headache pain medication. In addition to pain relief, the patient also reports complete cessation of photophobia, phonophobia, and nausea during the post-procedure analgesia period.

Neuralgia of the GON or LON is a benign, extracranial cause of headache pain that has been described in the literature for more than 60 years. In the classic “neuralgia” presentation, GON typically presents as sudden, recurring hemicranial pain, often associated with tearing of the eye, flushing of the face, alteration of sweating pattern, and occlusion of the ipsilateral nasal passage.1,2 However, neuralgia of the GON and/or LON is an often-overlooked cause of chronic headache, especially when presenting in the context of occipital neuralgia with migraine headache.

The key to diagnosis is the presence of neuralgia-type pain, which is described as brief, sharp, lancinating pain in the distribution of the involved nerve.1 Blurred vision, rhinorrhea, and vertigo may be present, but are less common.2 In patients with chronic pain, there is usually a continuous, aching pain in the distribution of the occipital nerve, and sometimes the ophthalmic division of the trigeminal nerve.1,3,4 This pain may present episodically for intermittent, recurring periods of hours to days, or constantly for months or years at a time. The cardinal feature and diagnostic criteria are complete relief of pain following local anesthetic blockade of either the C2 nerve root or the greater and/or lesser occipital nerves.1,2,5,6

Case Diagnosis
With minimal response from the patient’s medications, neuralgia of the GON was suspected. As noted, complete relief of symptoms following neural blockade of the GON and/or LON with local anesthesia and steroid will confirm the diagnosis. This technical report describes a novel technique for simultaneously blocking the GON and LON (see sidebar).

The GON and LON originate from the C2 nerve root.2 The relationship between occipital neuralgia and migraine is often poorly appreciated. However, there is a growing understanding that irritation or inflammation of the greater occipital nerve can produce referred pain in diverse cranial structures, not only within the C2 distribution but also within other nerves as well—particularly the ophthalmic division of the trigeminal nerve.4 Occipital neuralgia is also associated with migraine, either as a potential trigger or a late complication.3,5 In one study of 383 patients diagnosed with migraine headaches, 184 (48%) were found to have headaches caused by irritation of the GON that could be arrested by injecting the ipsilateral GON with local anesthetic.3

The mechanism by which irritation of the occipital nerves can be associated with migraine derives from the trigeminocervical complex. As reported by Bartsch et al, “neurons in the trigeminocervical complex are the major relay neurons for nociceptive, afferent input from the meninges and cervical structures; therefore, they are the neural substrates of head pain.”7 Stimulation of trigeminally innervated intracranial structures, such as supratentorial dura mater and large cranial vessels, evoke painful sensations, implying that afferent input from dural structures is the likely neural substrate in head pain and migraine.7 Nociceptive input from the dura mater is transmitted by small-diameter A and C fiber afferents in the ophthalmic division of the trigeminal nerve to nociceptive second-order neurons in the superficial and deep layers of the medullary dorsal horn of the trigeminocervical complex.7 Occipital and suboccipital structures, such as vessels and the dura mater of the posterior fossa, deep paraspinal neck muscles, upper cervical zygapophyseal (facet) joints, and ligaments, have nociceptive inflow that is also mediated by small-diameter afferent fibers, which synapse with nociceptive second-order neurons in the trigeminocervical complex.4,7 Thus, there is a direct coupling between meningeal afferents and cervical afferents in the spinal dorsal horn.8

The patient described in this case report complained of frequent nausea associated with his headache pain, which is completely relieved by occipital neural blockade. A recent study found that patients with chronic migraine who reported nausea associated with their headaches at least half of the time have significantly higher scores on the Migraine Disability Assessment when compared with those with no or rare nausea.9 Also, those with frequent nausea have significantly higher scores on the Headache Impact Test (HIT-6). Frequent nausea worsens all items examined by HIT-6, including more severe pain and more limited activities.9 Frequent nausea is associated with less treatment satisfaction, and those with nausea at least half of the time were more likely to report medication side effects.9 Migraine patients with nausea at least half of the time also were significantly more likely to report that their headache medication interferes with their ability to function at work or school, perform household chores, and participate in family or social activities.9

In my experience, patients who have effective pain relief following occipital neural blockade also experience relief of nausea and other associated symptoms, such as phonophobia and photophobia, during the period of post-procedure analgesia. In many cases, as with the patient described here, neural blockade of the GON and/or LON also produces a significant reduction in use of systemically absorbed oral medications. Chronic use of these medications can often pose potential risks to patients. Such risks can be both physical, such as chronic ingestion of acetaminophen and nonsteroidal anti-inflammatory drugs—which can potentially cause harm to the liver, kidneys, and gastrointestinal tract—or psychological, given the potential for the development of addiction or relapse of preexisting addiction disorders with the long-term use of controlled substances.

Neural blockade of the occipital nerves offers pain practitioners an addition to their armamentarium for the treatment of complex patients who may already have preexisting medical or psychiatric conditions that limit the use of pharmacologic treatments. This highlights its valuable role in the treatment of chronic headache with occipital neuralgia, both by offering another tool with which to offer relief to what may be otherwise intractable pain and the potential for significant long-term benefits in terms of the patient’s overall physical and mental health.

How To Perform the Block

The physiologic solution is mixed by combining 0.5 mL of 40 mg/mL triamcinolone acetonide solution with 2.5 mL of 2% lidocaine to produce 20 mg triamcinolone suspended in 3 mL of 1.66% lidocaine solution. Skin puncture site is prepped with chlorhexidine gluconate and isopropyl alcohol (ChloraPrep) or povidone-iodine (Betadine).

  • First, the external occipital protuberance is identified by palpation in the midline. Second, the skin puncture site is identified 2 to 2.5 cm lateral to the midline and 2.5 to 3 cm inferior to the external occipital protuberance. Third, a 25-gauge, 1.5-inch needle is inserted at the skin puncture site, angled 20 to 30 degrees cephalad in a posterior to anterior, parasagittal trajectory without medial or lateral deviation, until the needle tip makes gentle contact with the occipital bone (position 1) (Figures 1-4). A volume of 1 mL of physiologic solution is injected at position 1.

  • The needle is then withdrawn almost to the skin and reoriented 30 to 40 degrees medially while maintaining the 20- to 30-degree cephalad angulation. The needle is then reinserted on this trajectory until its tip makes gentle contact with the occipital bone, ideally in the anatomic midline (position 2) (Figures 5-7). A volume of 0.5 mL of physiologic solution is injected at position 2.

  • The needle is then withdrawn almost to the skin again and reoriented 40 to 50 degrees laterally while maintaining the 20- to 30-degree cephalad angulation. The needle is then reinserted on this trajectory until its tip makes gentle contact with the occipital bone, slightly medial and posterior to the mastoid process (position 3) (Figures 8-11). A volume of 0.5 mL of physiologic solution is injected at position 3.

  • The needle is then withdrawn almost to the skin again and reoriented 10 to 20 degrees caudad to the skin puncture site and inserted on a posterior to anterior, parasagittal trajectory without medial or lateral deviation to a depth of 1.5 inches (position 4) (Figures 12-14). The needle tip should not contact bone. If the needle tip contacts bone, it should be withdrawn and reoriented more caudally prior to reinsertion. A volume of 1 mL of physiologic solution is injected at position 4.
  • The needle is withdrawn, and pressure may be applied at skin puncture site as needed if there is bleeding.

Last updated on: December 16, 2011
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