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Improvement in clinical outcomes after dry needling in a patient with occipital neuralgia.

Introduction

Occipital neuralgia is defined according to guidelines provided by the International Headache Society (IHS). Briefly, the IHS diagnostic criteria include sharp, paroxysmal, severe pain in the occipital region along with associated tenderness and sensory disturbances. (1) Occipital neuralgia may be the result of pathology in the greater, lesser or third occipital nerves (Figure 1). (2) Previous evidence indicates that occipital neuralgia affects the greater occipital nerve in 90% of cases, lesser occipital nerve in 10% of cases, and both occipital nerves in 9% of cases. (3) However, the specific incidence and prevalence rates for occipital neuralgia remain unknown along with an elusive pathophysiology including the precise etiology. (2,4) Differential diagnoses for occipital neuralgia include cervicogenic, migraine, cluster and tension-type headaches. Treatment for occipital neuralgia may comprise interventions such as pharmacology, conservative care, interventional therapies and/or surgery. (2,5-8)

Dry needling (DN) or intramuscular stimulation is defined as a therapeutic procedure that involves inserting a dry needle, without medication, into a myofascial trigger point with the goal of inactivating a trigger point and mitigating pain. (9,10) In 1979, Karel Lewit became one of the first persons to distinguish between the effects of inserting a dry needle into a myofascial trigger point and injection of a medicinal substance into a myofascial trigger point. (11) Since that publication, there has been accumulating evidence supporting the use of DN in the management of myofascial pain along with basic science research attempting to establish therapeutic mechanisms. (12-14)

The primary purpose of this case report is to outline the diagnosis, intervention and clinical outcome of a 26-year-old female with occipital neuralgia. As part of this discussion, our article includes information outlining the anatomy, pathophysiology, clinical presentation, differential diagnosis and management of occipital neuralgia. In addition, this paper briefly reviews evidence supporting the use of DN in managing myofascial pain.

Case Report

Upon arrival, a 26-year-old female described a four-year history of neck pain and headaches. The patient related the onset of these symptoms secondary to a traumatic event four years prior to presentation. While walking a dog in damp conditions, she reported falling backwards and striking her head on the ground with a transient loss of consciousness. The day after striking her head, she proceeded to the hospital complaining of right-sided neck pain and headache in the occipital region. After an examination including x-rays, the patient described a diagnosis of "concussion" from the hospital physician. Also, she described "swelling" in her anterior neck region for approximately four weeks post-trauma, but the swelling abated with time and use of over-the-counter medications. However, her neck pain and headache continued beyond dissipation of the edema, transitioning to a persistent condition.

During the initial consultation, the patient described her right-sided neck pain and occipital headache as "knifelike" and stabbing. When asked to point to the painful region, she touched the right occipital region between the midline and the sternocleidomastoid muscle. Also, she recounted that the pain occasionally radiates into her right fronto-orbital region. She described a paroxysmal pattern to the stabbing pain, without ever experiencing complete resolution of symptoms. She indicated experiencing a severe headache in her right occipital region approximately one to two times a month with each occurrence lasting for about one week, including two to three days of high intensity pain with each episode. She denied vomiting, aura, prodrome or neurological indicators such nystagmus, numbness, nausea, dizziness, dysarthria, dysphagia, diplopia, drop attacks and ataxia. The patient rated the average daily pain as 2/10 on a verbal pain rating scale, with exacerbations or paroxysms rated as 9/10. She denied any triggers or aggravating factors related to the paroxysms, but these changes in pain seem random or unpredictable. However, the patient described several factors that afford pain relief, albeit temporary.

Factors that yielded provisional and limited relief of pain included spinal manipulation, transcutaneous electrical nerve stimulation (TENS), physical therapy, needling, and an orthodontic appliance. Previous physical therapy interventions included neck strengthening and relaxation exercises, while the orthodontist provided an oral appliance to reduce nocturnal "clenching" of the jaw. In addition, her family physician prescribed Maxalt (sublingual and oral) for treatment of headaches with a variable clinical response including limited relief or no effect. Finally, she recounted that "rubbing" or pressing the right temporal region above her eye reduces the severe pain associated with headaches, but this stimulation creates lacrimation and nausea. However, none of the remedies or interventions described above brought complete or lasting resolution of her pain.

She conveyed no previous specific diagnoses for her neck pain and headache. However, her past medical history included diagnoses related to low back pain, anxiety/ depression, attention deficit disorder (ADD), acne, and pre-diabetic. She reported ongoing use of medications for managing her anxiety/depression (Cymbalta), ADD (Adderall), acne (Spironolactone), and pre-diabetes (Metformin). Her past medical history also included knee reconstruction approximately ten years prior. Her social and occupational history included limited alcohol (one unit per week) and caffeine (two drinks per day) consumption along with moderate exercise (three to four days per week for 30-45 minutes per session). The patient denied tobacco use or any other diagnoses.

Examination procedures included neurological screening/testing, range of motion/mobility, palpation, and orthopedic testing. Neurological testing included cranial nerve function along with muscle/strength testing, deep tendon reflexes, and sensation. Based upon examination, cranial nerve and upper quarter neurological function appeared within normal limits. Cervical spine active range of motion (AROM) consisted of three trials of motion in each direction measured with a single inclinometer. Based upon normative comparison values (15), the patient's AROM emerged WNL, except for limited extension (Table 1). Also, the patient denied painful sensations during performance of cervical AROM.

Palpation of the cervical spine revealed elevated muscle tone in bilateral upper trapezii muscles. Using a soft tissue tenderness grading scheme (16), palpation uncovered grade I tenderness in bilateral levator scapula muscles along the superomedial border of the scapula, bilateral interscapular muscles (rhomboids, middle trapezii, lower trapezii), and right posterior cuff muscles (teres minor, teres major). In addition, palpation elicited grade II tenderness in the right upper trapezius and occipital regions. For an additional description of this soft tissue tenderness grading scheme, please see Hubbard and Berkoff. (16) Palpation revealed myofascial trigger points in bilateral upper trapezii muscles along with the right suboccipital muscles.

Orthopedic testing consisted of regional examination related to the complaint of cervical spine pain. The upper limb tension test A (ULTTA) and shoulder depression tests revealed negative results bilaterally. (17,18) However, the cervical compression test elicited localized right-sided neck pain in the upper cervical region; left cervical compression produced negative results. (17,18) Also, Spurling's tests yielded localized right-sided pain in the upper cervical region and localized left-sided pain in the mid-cervical region. (17,18) Cervical distraction test reduced the right-sided pain in the upper cervical region. (17,18)

Other outcomes measures for this case report included the neck disability index (NDI), and headache disability index (HDI). The patient completed each of these questionnaires on two occasions: pre-intervention at baseline and post-intervention at three week follow-up. Table 2 lists the NDI, and HDI scores pre and post-intervention.

The patient presentation and examination findings suggested a probable diagnosis of occipital neuralgia. Differential diagnoses included cervicogenic headache, migraine headache, and tension-type headache. After the patient read and signed the appropriate informed consent forms, the clinician initiated an intervention consisting of dry needling (DN). The patient underwent a total of four DN sessions over a two-week duration.

The first treatment session involved placing needles into myofascial trigger points located in bilateral upper trapezii muscles (see video demonstration) and bilateral cervical multifidi muscles between the C5-T1 regions. Following the first DN session, the patient reported "stiffness" in the right upper trapezius muscle that lasted approximately one hour. Also, she rated her right-sided neck pain and headache as 1/10 using the verbal pain rating scale. Orthopedic testing reproduced her neck pain and palpation elicited grade I tenderness in bilateral upper trapezii muscles and interscapular muscles, along with the right posterior cuff and suboccipital muscles. The second treatment session consisted of DN myofascial trigger points in the same anatomical regions as the first visit. A week later during the third visit, the patient reported sleeping on a "different pillow" which seemed to aggravate her condition. The patient stated that she seemed "on the verge" of an exacerbation in symptoms. During this third treatment session, needles were inserted into one additional anatomical region. On this occasion, needles were placed into bilateral upper trapezii muscles, bilateral cervical multifidi muscles, and the proximal attachment of bilateral suboccipital muscles along the nuchal line. Two days later, upon presentation for the fourth visit, the patient reported complete resolution of her neck pain and headache. Also, she felt that the last DN session had "aborted" her imminent exacerbation. Orthopedic testing demonstrated negative tests bilaterally for cervical compression and Spurling's. Again, needles were placed into myofascial trigger points in bilateral upper trapezii, cervical multifidi and suboccipital muscles. During each of the four treatment sessions, insertion of needles into the described muscles elicited palpable and/or visible local twitch responses (LTRs). Three weeks following the final treatment session, the patient completed the post-intervention neck disability index, and headache disability index questionnaires. Finally, as a result of her favorable clinical outcome, the patient was discharged from care (Figure 2).

Discussion

A. Occipital Neuralgia

Anatomy

As previously discussed, occipital neuralgia may involve the greater occipital nerve, lesser occipital nerve, third occipital nerve or a combination of these neural structures (Figure 1). (1-3) The greater occipital nerve derives from the medial branch of dorsal ramus of C2 while the lesser occipital nerve arises from branches of C2 and C3 in the cervical plexus. (19) Lastly, the third occipital nerve originates from the medial branch of C3. (19) Sensory innervation of greater occipital nerve consists of the cutaneous region on the posterior scalp between the external occipital protuberance and the vertex. (19) The lesser occipital nerve provides cutaneous innervation to the lateral region of the scalp posterior to the ear whereas the third occipital nerve innervates the upper cervical spine and inferior occipital regions. (19)

Pathophysiology

Presently, the precise etiology of occipital neuralgia remains unclear with most cases presenting as idiopathic. However, proposed mechanisms of onset for occipital neuralgia include trauma, muscular entrapment, structural lesions or secondary diseases such as multiple sclerosis and myelitis. (20-24) Based upon the potential presence of structural or organic etiologies associated with occipital neuralgia, neuroimaging modalities such as magnetic resonance imaging (MRI) may be indicated to rule out serious pathology. (2)

Clinical Presentation

The clinical presentation for occipital neuralgia has been described by the International Headache Society (IHS) including specific diagnostic criteria (Table 3). Also, according to the IHS, the pain associated with occipital neuralgia may extend to the fronto-orbital area via trigeminocervical interneuronal networks in the trigeminal spinal nuclei. (1) In addition to the IHS criteria, patients may demonstrate a positive Tinel's sign with repeated tapping over the occipital condyle producing numbness and/or tingling. (2)

Differential Diagnosis

As previously stated, differential diagnoses for occipital neuralgia include cervicogenic, migraine, cluster and tension-type headaches. These headache disorders closely resemble the clinical presentation associated with occipital neuralgia, particularly cervicogenic headache. For example, both occipital neuralgia and cervicogenic headache may present with pain the upper cervical and occipital regions. However, the pain associated with cervicogenic headache is often described as dull, while the pain description for occipital neuralgia is usually expressed as sharp, stabbing or shooting. (2) In light of the IHS diagnostic criteria for cervicogenic headache (Table 4), it becomes apparent that the clinical presentations for cervicogenic headache and occipital neuralgia overlap, thus creating a diagnostic challenge. (1) The diagnostic hallmarks of migraine headache (with or without aura) include unilateral location with pulsating quality of moderate or severe pain intensity and aggravated by or causing avoidance of routine physical activity, while cluster headaches present as brief, severe, unilateral headaches with associated lacrimation, rhinorrhea, facial sweating along with myosis and/ or ptosis. (1) The clinical presentation for tension-type headache includes bilateral location with a pressing or tightening (non-pulsating) quality of mild or moderate intensity. (1) Thus, mindful clinical evaluation is needed to ensure the correct diagnosis for a particular headache presentation.

Management

As outlined earlier, management considerations for occipital neuralgia may include pharmacology, conservative care, interventional therapies and/or surgery. With regards to pharmacological approaches, previous literature describes using non-steroidal anti-inflammatory drugs (NSAIDs), muscle relaxers, tricyclic antidepressants, and antiepileptics to manage occipital neuralgia. (2,7) Conservative or non-pharmacological interventions targeting abnormal muscle tone involve rest, cryotherapy or thermotherapy, soft-tissue massage, and physical therapy. (7)

Interventional therapies (ITs) for managing occipital neuralgia consist of injections, pulsed radio-frequency ablation, and occipital neurostimulation. (2,6,7,25) Briefly expanding on these ITs, injection or infiltration of the greater occipital nerve or lesser occipital nerve with anaesthetic (i.e., lidocaine) is considered diagnostic for occipital neuralgia, but also therapeutic by providing transient pain relief. (20,25) In addition, botulinum toxin type A is another infiltrate that has been reported as beneficial for managing occipital neuralgia. (26) According to Dougherty, pulsed radiofrequency (PRF) exposes afferent nerve endings to intermittent short duration, high-voltage radiofrequency signals creating a low-intensity electrical field around sensory nerves, thus modulating pain via ablation or degeneration. (2) Lastly, occipital neurostimulation involves implantation of electrodes in the occipital region that produce paresthesia with resultant pain modulation in the distribution of the occipital nerves. (27)

Previous research indicates surgical excision of the greater occipital nerve may provide pain relief for occipital neuralgia. (5) However, this surgical procedure should only be considered as a last resort in response to unsuccessful attempts to resolve pain via other interventions. (5)

B. Dry Needling

As previously mentioned, dry needling (DN) or intramuscular stimulation is defined as a therapeutic procedure that involves inserting a dry needle, without medication, into a myofascial trigger point with the goal of inactivating a trigger point and mitigating pain. (9,10) By comparison, a fundamental premise of acupuncture is controlling and regulating energy flow and balance via needling of defined points. (9) Also, acupuncture is founded on Eastern concepts, while DN is based on neurophysiological and biomechanical principles. (9,28) However, according to scientific literature, acupuncture and DN employ the same therapeutic tool, namely a solid filament needle. For a more detailed discussion of DN and acupuncture, please review an article written by Dommerholt. (9)

By definition, a myofascial trigger point is described as a hyperirritable point in a taut band of skeletal muscle fibers with resultant local ischemia and hypoxia along with peripheral and central sensitization. (12) A theoretical construct outlining the outcomes of DN proposes that needling of myofascial trigger points induces physiological effects that modulate muscle tension, local ischemia and hypoxia, along with peripheral and central sensitization. (12)

Previous literature describes that DN of myofascial trigger points elicits a local twitch response (LTR) thus changing muscle length and tension through regulation of spontaneous electrical activity. (29,30) By definition, a LTR is a localized contraction within a muscle produced by an involuntary spinal reflex as a result of being stretched, injected or dry needled. (12) Also, previous research suggests that eliciting a LTR improves the clinical outcomes associated with DN. (31) In addition to changing muscle length and tension, DN may stimulate a change in blood flow within the ischemic and hypoxic tissues of a myofascial trigger point. (32) Lastly, research indicates that DN may modulate pain through peripheral and central pathways including segmental inhibition and biochemical cascades such as endogenous opioids, and serotonergic and adrenergic mediators. (33-37)

A recent systematic review and meta-analysis recommended DN for patients with upper-quarter myofascial pain syndrome, compared to sham or placebo, for reducing pain immediately following treatment and at four weeks post-intervention. (38) According to Vulfsons et al, DN performed by a competent clinician may be considered a safe intervention. (13) However, mild adverse events have been reported including localized muscle soreness and hemorrhaging, or more seriously, spinal epidural hematoma. (39,40) Evidence suggests that the incidence of severe adverse events associated with needling is very rare. (41) Moreover, caution is advised while DN around potentially vulnerable anatomical structures such as those within the cervical and thorax regions. (13)

In the context of this case report, the patient presentation closely matched the International Headache Society (IHS) criteria for occipital neuralgia including unilateral, severe, stabbing, paroxysmal pain in the greater occipital nerve region with associated tenderness and myofascial trigger points. The patient presentation did not meet the IHS criteria of temporary pain relief provided by local anaesthetic block of the affected nerve. However, fol lowing the four sessions of myofascial trigger point dry needling in our case report, the patient reported a 32-point change on a 100-point scale in her neck disability index score along with a 28-point change on a 100-point scale in her headache disability index score. According to recent literature, the minimum detectable change (MDC) for the neck disability index is approximately 10/100 for uncomplicated neck pain and 20/100 for cervical radiculopathy. (42,43) Also, the described clinically important difference (CID) for the neck disability index varies amongst reports ranging from 10/100 to 38/100. (43) In order to ascribe the effects of clinical improvement to an intervention, a patient must report a 29-point change in headache disability index scores from pre to post-intervention. (44) Thus, it appears that following four sessions of DN over two weeks, our patient experienced meaningful improvement in her neck pain and headaches.

Previous literature supports the theory that the therapeutic mechanism of pain relief following anaesthetic injection of myofascial trigger points might be the associated neuromechanical stimulation of the needle itself. (9,11,14,31) For example, a recent study compared the effects of dry needling, lidocaine injections and botulinum toxin type A injections into myofascial trigger points of patients presenting with myofascial pain syndrome. (45) Using a syringe (not an acupuncture needle) for each of the three needling interventions, the researchers reported clinical outcomes such as pain pressure threshold and pain scores significantly improved in all three groups. When contrasting injection therapy with DN of myofascial trigger points, numerous investigators have proposed that "dry needling of the myofascial trigger point provides as much pain relief as injection of lidocaine but causes more post-injection soreness". (46) Thus, using DN to manage the myofascial trigger points associated with occipital neuralgia may have implicitly met the IHS criteria of pain relief following anaesthetic block of the affected nerve.

Previous case reports using acupuncture to manage occipital neuralgia have described favorable clinical outcomes. (8,47,48) However, to the best of our knowledge, this is the first case report describing dry needling to successfully improve clinical outcomes in a patient diagnosed with occipital neuralgia.

Limitations

As this paper describes a single case report involving occipital neuralgia and dry needling, there may be possible limitations. Although diagnosed with occipital neuralgia based upon the IHS criteria, the patient may have exhibited an alternative diagnosis or a more complex diagnosis with associated co-morbidities. Also, the clinical presentation might have mimicked another closely related condition such cervicogenic headache. Also, it is not plausible to establish a causal relationship between DN and occipital neuralgia based upon a single case report. However, the information from this case report may stimulate critical thinking and appraisal leading to a more sophisticated experimental design examining the effects of DN in patients presenting with occipital neuralgia.

Consent

The patient provided written informed consent acknowledging permission for publication of this case report. A copy of the written consent is accessible for review from the Editor of this journal.

Authors' Contributions

BB provided patient care along with conducting the literature review and composing the manuscript. CK also assisted with the literature review and manuscript preparation. Both author's read and approved the final manuscript.

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Bryan M. Bond, BSc, BS, DC, MS [1]

Christopher Kinslow, PT, DC [2]

[1] Professor, Department of Physical Therapy, University of Saint Mary

[2] Assistant Professor, Department of Physical Therapy, University of Saint Mary

Corresponding Author:

Bryan M. Bond

Email: bryan.bond@stmary.edu

Department of Physical Therapy, University of Saint Mary, Leavenworth, Kansas, 66048, USA

Phone: (913) 758-4398

Declaration: The authors have no conflicts of interest to declare regarding this paper or the material described therein.

Consent: The patient provided written informed consent acknowledging permission for publication of this case report.

Table 1:

Pre-intervention Cervical Spine Active Range of Motion

Trial               RR ([degrees])      LR ([degrees])

1                         78                  74
2                         82                  78
3                         76                  78
Mean [+ or -] SD   78.7 [+ or -] 3.1   76.7 [+ or -] 2.3

Trial               RLF ([degrees])     LLF ([degrees])

1                         38                  42
2                         44                  42
3                         45                  51
Mean [+ or -] SD   42.3 [+ or -] 3.8   45.0 [+ or -] 5.2

Trial                F ([degrees])       E ([degrees])

1                         60                  40
2                         54                  39
3                         59                  41
Mean [+ or -] SD   57.7 [+ or -] 3.2   40.0 [+ or -] 1.0

RR = right rotation; LR = left rotation; RLF = right lateral flexion;
LLF = left lateral flexion; F = flexion; E = extension; SD = standard
deviation

Table 2:

Pre-intervention and Post-intervention
Neck Disability Index (NDI), and
Headache Disability Index (HDI) Scores

Outcome Measure   Pre-Intervention   Post-Intervention

NDI                    42/100             10/100
HDI                    62/100             34/100

Table 3:

IHS Diagnostic Criteria for Occipital Neuralgia (1)

Reproduced from: International Classification of Headache Disorders,
3rd edition. Cephalalgia: An International J Headache.
2013;33(9):629-808. With permission: SAGE Publications.

A.    Unilateral or bilateral pain fulfilling criteria
      B-E

B.    Pain is located in the distribution of the
      greater, lesser and/or third occipital nerves

C.    Pain has two of the following three
      characteristics:

      1. recurring in paroxysmal attacks lasting from a
      few seconds to minutes

      2. severe intensity

      3. shooting, stabbing or sharp in quality

D.    Pain is associated with both of the following:

      1. dysaesthesia and/or allodynia apparent during
      innocuous stimulation of the scalp and/or hair

      2. either or both of the following:

      a. tenderness over the affected nerve branches

      b. trigger points at the emergence of the greater
      occipital nerve or in the area of distribution of
      C2

E.    Pain is eased temporarily by local anaesthetic
      block of the affected nerve

F.    Not better accounted for by another ICHD-3
      diagnosis.

Table 4:

IHS Diagnostic Criteria for Cervicogenic Headache (1)

Reproduced from: International Classification of Headache Disorders,
3rd edition. Cephalalgia: An International J Headache.
2013;33(9):629-808. With permission: SAGE Publications.

A.    Any headache fulfilling criterion C

B.    Clinical, laboratory and/or imaging evidence
      of a disorder or lesion within the cervical
      spine or soft tissues of the neck, known to
      be able to cause headache

C.    Evidence of causation demonstrated by at
      least two of the following:

      1. headache has developed in temporal
      relation to the onset of the cervical
      disorder or appearance of the lesion

      2. headache has significantly improved or
      resolved in parallel with improvement in or
      resolution of the cervical disorder or lesion

      3. cervical range of motion is reduced and
      headache is made significantly worse by
      provocative maneuvers

      4. headache is abolished following diagnostic
      blockade of a cervical structure or its nerve
      supply

D.    Not better accounted for by another ICHD-3
      diagnosis.
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Author:Bond, Bryan M.; Kinslow, Christopher
Publication:Journal of the Canadian Chiropractic Association
Article Type:Report
Date:Apr 1, 2015
Words:5191
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