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Blackwell Publishing IncMalden, USAPPRPain Practice1530-70852006 World Institute of Pain2006628995Original ArticleOccipital Nerve Blockade for Cervicogenic HeadacheNAJA ET AL.
ORIGINAL ARTICLE
Occipital Nerve Blockade for
Cervicogenic Headache: A DoubleBlind Randomized Controlled
Clinical Trial
Zoher M. Naja, MD*; Mariam El-Rajab, MD†; Mohamad A. Al-Tannir, MPH‡;
Fouad M. Ziade, PhD§; Omar M. Tawfik, MD¶
*Chairman of Anesthesia Department, Makassed General Hospital; †Department of Pediatrics,
Makassed General Hospital; ‡Research Unit at Makassed General Hospital; §Faculty of Public
Health, Lebanese University, Beirut, Lebanon; ¶Faculty of Medicine, National Cancer Institute,
Cairo University, Egypt
Abstract: Cervicogenic headache is a chronic hemicranial
pain, usually occurring daily. This randomized, double-blind,
placebo-controlled trial evaluated the effectiveness of nerve
stimulator-guided occipital nerve blockade in the treatment
of cervicogenic headache. The reduction in analgesic consumption was the primary outcome measure. Fifty adult
patients diagnosed with cervicogenic headache were randomly divided into two equal groups of 25 patients each. All
patients in both groups received greater and lesser occipital
blocks, whereas only 16 patients in each group received facial
nerve blockade in association with the occipital blocks. The
control group received injections of an equivalent volume of
preservative-free normal saline. Pain was assessed using the
visual analog scale (VAS) and the Total Pain Index (TPI). Fortyseven patients entered into the final analysis as three
patients were lost to follow-up. Anesthetic block was effective in reducing the VAS and the TPI by approximately 50%
Address correspondence and reprint requests to: Zoher M. Naja, MD,
Chairman of Anaesthesia Department, Makassed General Hospital, P.O.
Box: 11-6301 Riad El-Solh 11072210, Beirut, Lebanon. E-mail: [email protected].
The work was conducted at the Department of Anesthesia at
Makassed General Hospital. All funding sources were departmental.
Submitted: October 19, 2005; Revision received: December 9, 2005;
Final revision accepted: February 7, 2006
© 2006 World Institute of Pain, 1530-7085/06/$15.00
Pain Practice, Volume 6, Issue 2, 2006 89–95
from baseline values (P = 0.0001). Analgesic consumption,
duration of headache and its frequency, nausea, vomiting,
photophobia, phonophobia, decreased appetite, and limitations in functional activities were significantly less in block
group compared to control group (P < 0.05). The nerve stimulator-guided occipital nerve blockade significantly relieved
cervicogenic headache and associated symptoms at two
weeks following injection. Key Words: occipital blockade, cervicogenic headache,
nerve stimulation
INTRODUCTION
Cervicogenic headache (CGH) is a chronic hemicranial
pain usually beginning in the suboccipital region and
spreading anteriorly to the ipsilateral orbital, frontal,
and temporal areas. This headache, of almost daily
occurrence, is typically dominant on one side, but may
occasionally be bilateral.1,2 It has been proposed that the
mechanism responsible for this headache is related to
the convergence of upper cervical and trigeminal sensory pathways allowing pain signals to refer from the
neck to the trigeminal sensory receptive fields of the
head and face.3–5
Greater occipital nerve (GON) and lesser occipital
nerve (LON) anesthetic blocks have been reported to be
90 • naja et al.
useful in diagnosing CGH and may sometimes provide
temporary pain relief.3,4,6,7 Pain management using medication, physical therapy, manipulative treatment, anesthetic, and surgical interventions have not consistently
provided substantial pain relief and are followed by
recurrence of pain.3,8–14 At our institution, nerve stimulator-guided blocks of GON and LON have been used
for treatment of CGH since 1998 for pain management.
The aim of this study was to assess the efficacy of
occipital nerve blocks vs. placebo injection using a nerve
stimulator in the treatment of CGH.
MATERIALS AND METHODS
Study Design and Population
Following institutional Research and Ethics Committee
approval, informed consent was obtained from 50
adult patients diagnosed with CGH for participation
in this randomized, double-blind, placebo-controlled
study. The diagnosis of CGH was based on all of the
following inclusion criteria: unilateral, without sideshift, headache; precipitation of headache by neck
movement or by external pressure over the GON;
reduced range of motion in the neck; circumscribed
tenderness over the GON; and sensory changes in the
distribution of the GON. Patients with whiplash injury,
post-traumatic headache receiving concurrent psychiatric therapy, organic disease of the brain or spinal cord,
malignancy, or coagulopathy were excluded from the
study.15
All patients entered a two-week baseline evaluation
period where all patients received the same pain treatments. Patients were then randomly divided into two
equal groups of 25 patients each, based on computerized generated tables using the sealed-envelope technique. Data collected for each patient at the initial visit
included demographics and history of headache including its duration in years. For baseline assessment, each
patient received 14 time charts to record the use of
rescue medications, daily pain scores, and accompanying symptoms. The incidence of associated nausea, vomiting, photophobia, phonophobia, decreased appetite,
and limited normal activity was reported as present or
absent (yes/no).
Patients in the anesthetic block group received either
both GON and LON blocks, or GON and LON with
facial nerve blockade, depending on the extension of the
headache. Each 10 mL of the injected mixture contained: 3 mL lidocaine 2% (B/Braun, Melsugen, Germany); 3 mL lidocaine 2% with epinephrine 1:200,000;
2.5 mL bupivacaine 0.5% (Laboratoire Aguettant,
Lyon, France); 0.5 mL fentanyl 50 µg/mL (Panpharma,
Fougères, France); and 1 mL clonidine 150 µg/mL (Bouhring, Paris, France). And the control group received
injections of an equivalent volume of preservative-free
normal saline. The institutional drug service performed
randomization and preparation of the anesthetic mixture. The study was double-blinded as the operator
(responsible for the blocks) and both the patient and the
nurse responsible for data collection were blinded to the
assigned group and to the contents of the syringe. All
patients were informed prior to block performance that
slight pain and temporary numbness may occur following the performance of the blocks. Following block
performance (anesthetic mixture or normal saline),
patients received another 14 daily charts to record the
use of rescue medications, the daily pain scores, and the
accompanying symptoms.
Pain Assessment
Pain was assessed using a visual analog scale (VAS)
(0 cm––no pain; 10 cm—worst possible pain imagined).
Pain was also assessed by using the Total Pain Index
(TPI).11 The TPI is an integrated expression of the
weighted intensity and duration of the headache attacks
during a period of two weeks and defined by the
formula:
(D1·1) + (D2·2) + (D3·3)
where D1 = number of hours with headache during the
two-week period with slight pain (not limiting normal
activity); D2 = number of hours with headache during
the two weeks with moderate pain (limiting normal
activity, but not causing the subject to go to bed); and
D3 = number of hours of headache during the two
weeks where strong pain was reported (limiting all
activities and causing the subject to be bedridden).
Analgesic Consumption
Patients were asked to record the quantity of analgesics
needed per day during this trial. Patients with a VAS <4
were given either oral paracetamol 500 mg (Defalgan,
UPSA, Paris, France) with a maximum of 6 tablets per
24 h, or ketoprofen 100 mg tablet (Profenid, Aventis,
Paris, France) without exceeding 3 tablets per day.
Patients with a VAS >4 were given either an oral combination of dextropropoxyphene (30 mg) and paracetamol (400 mg) (Diantalvic, Hoechst-Marion-Roussel,
France) with a maximum of 6 capsules/day, or tramadol
hydrochloride 100 mg tablet (Tramal, Grünenthal,
Occipital Nerve Blockade for Cervicogenic Headache • 91
Aachen, Germany) without exceeding 3 tablets per day.
Patients were re-evaluated in the clinic at two weeks.
Greater Occipital Nerve Blockade Using the
Nerve Stimulator
GON blockade was selected for patients having pain in
the parietal and occipital areas. Technique: In the sitting
position, with the hair held out of the field with an
adhesive bandage, the superior nuchal line was defined
from the mastoid to the cervical spine at C1–C2. A
parallel line to the superior nuchal line located 1 cm
below it was drawn to find the optimal injection point
to block the GON. Following aseptic preparation of
the skin, a 24-G nerve stimulator needle (Stimuplex,
B.Braun, Melsungen, Germany) was moved horizontally
on the surface of the skin toward the midline in 1-mm
increments on the previously drawn line using an initial
stimulating current of 2.5 mA (1 Hz, 9 v, duration of
voltage current was 1.0 ms) (Stimuplex). The point of
injection was defined as the most sensitive point
declared by the patient along the line. Prior to insertion
of the needle, lidocaine 0.1 mL was infiltrated using a
29-G needle to facilitate the penetration of the nerve
stimulator needle, which was then progressively
advanced perpendicularly to the skin in all planes.
Patient co-operation is required as the report of a tingling sensation must be maintained while reducing current to 0.3 mA, indicating that the tip of the needle was
in close proximity to the GON. Three milliliters of local
anesthetic mixture or normal saline was then injected.
The needle was usually inserted approximately about
2.5 cm below the greater occipital protuberance at a
depth that varied from 0.5 to 2.5 cm, depending upon
the weight and height of the patient.
progressively advanced perpendicular to the skin in all
planes. The patient was asked to inform the operator
that the sensation was still present while the current was
reduced to 0.3 Ma, indicating that the tip of the needle
was in the vicinity of LON. Three milliliters of anesthetic
mixture or normal saline were then injected. The needle
was typically inserted to a depth between 0.5 and 1.5 cm.
Facial Nerve Blockade Using the Nerve Stimulator
If the patient described pain extending to the orbital
area, an injection of 3 mL of anesthetic mixture or normal saline was applied to the facial nerve. The injection
site was determined by the guidance of a nerve stimulator as described above and was located at the angle of
the mandible corresponding to the lowest edge of the
ear while observing the muscle contractions of the orbicularis oculi, in addition to the nasal (depressor septi)
and buccolabial musculature (depressor anguli oris)
(Figure 1). The depth of needle did not exceed 1 cm.
Based upon the initial pain sites recorded by the
patient during the two weeks preceding the block performance (baseline), all patients in both groups received
both greater and lesser occipital blocks, whereas only
16 patients in each group received the facial blockade
in association with the occipital blocks.
Statistical Analysis
Sample size was based on the primary endpoint of the
consumption of paracetamol where a 20% reduction
was considered significant. A sample size of 25 patients
Lesser Occipital Nerve Blockade Using the
Nerve Stimulator
The LON blockade was selected for patients having pain
extending to the frontal and temporal areas. Technique:
After sterile preparation as described above, the tip of
the nerve stimulator needle was again moved along the
skin surface with the stimulating current of 2.5 mA
toward the superior third of the posterior limit of the
sternocleidomastoid muscle,16 in order to localize the
LON. The injection point was defined as the most sensitive point declared by the patient while feeling the
current radiating to the temporal region (Figure 1). Some
patients also sensed the current passing to the ear. Skin
infiltration with lidocaine 0.1 mL using a 29-G needle
was performed. Then the nerve stimulator needle was
Injection point of facial
nerve
Injection point of lesser
occipital nerve
Sternocleidomastoid
muscle
Trapezius muscle
Figure 1. Injection points for the lesser occipital and facial
nerves.
92 • naja et al.
per group provided 90% power. The demographic characteristics of the two groups were compared using a
t-test for continuous measures and Fisher’s exact test
for categorical measures. For the primary endpoint,
repeated-measures two-way ANOVA was used to assess
differences in cumulative analgesics, accepting a P value
of <0.05 as statistically significant. The data were compared using two-sided tests for paired comparisons.
RESULTS
Forty-seven patients were entered into the final analysis;
three patients were lost to follow-up (Figure 2). The two
study groups had similar baseline characteristics
(Table 1).
There was a significant reduction in analgesic consumption in block group compared to placebo group.
Paracetamol and dextropropoxyphene consumption
were significantly less in block patients compared to
placebo patients (P = 0.0001) (Table 2). In addition, the
consumption of tramadol and ketoprofen was significantly reduced in block group compared to placebo
group (P = 0.006 and P = 0.01, respectively) (Table 2).
Two weeks after the injection of the anesthetic mixture, block patients reported nearly a 50% improvement
in the TPI and VAS scores compared to basal values and
to placebo patients (P = 0.0001) (Table 2). The frequency of headaches was reduced in block group compared to placebo group (P = 0.026) (Table 2). Block
patients had significantly reduced accompanying symptoms such as nausea, vomiting, photophobia, phonophobia, decreased appetite, and limiting normal activity
compared to control group (P values ranged from 0.045
to 0.012) (Table 2). Two weeks following the intervention, the pain site in block group changed compared to
control group, with significant reductions in occipital
and frontal symptoms (Table 2).
The duration of pain relief after block performance
was significantly longer in the block group compared to
the placebo group (P = 0.0001) (Table 2). For the block
group (n = 24), the mean number of days with pain
relief (days prior to need of analgesics after injections)
was 3.67 (±1.71 SD), whereas for the control group, the
Randomization
(n = 50 Patients)
mean was 1.52 (±1.20 SD). For those who had combined GON, LON, and facial (n = 16 in each group),
there was a significant difference among the mean durations of pain relief (3.93 ± 1.79 SD vs. 1.56 ± 1.26 SD;
P = 0.0001). Patients who had anesthetic GON and
LON alone (n = 8) had significantly longer duration of
pain relief compared to the placebo GON and LON
(n = 7), with mean duration of relief of 3.22 (±1.56 SD)
and 1.43 (±1.34 SD), respectively (P = 0.029).
DISCUSSION
CGH remains a major problem as most therapeutic
regimes are followed by the recurrence of pain. To date
arguably the most effective treatment for CGH is the
interruption of pain transmission via the occipital nerves
(GON, LON) or their component nerve roots or ganglia, either by means of an anesthetic block or through
a surgical intervention.10 Our clinical trial was conducted during a two-week period in order to assess the
effectiveness of stimulation-guided occipital blockade in
reducing the intensity of pain in CGH patients.
The findings of this study confirmed our hypothesis
that patients receiving anesthetic blockade had
decreased analgesic consumption compared to those
receiving placebo in CGH patients. Secondary findings
included reduced VAS and TPI scores by early 50% of
basal values (P = 0.0001). Moreover, accompanying
symptoms such as nausea, vomiting, loss of appetite,
and extension of pain site were significantly reduced in
block group compared to the placebo group during the
two-week period of study.
One important factor that might contribute to a prolonged pain-free period (outlasting the expected duration of the analgesics administered) is the ability to
detect and block the GON precisely rather than simply
infiltrating its general location using a field block technique. Accurate injection is also important diagnostically as false localization might lead to unnecessary
surgical transection or other neurolytic procedures.4,6
Hence, the nerve stimulator technique enables the operator to determine the exact location of the nerve,
increasing the chance for success.
Placebo blockade
(n = 25)
Loss of follow-up
(n = 2)
Anesthetic blockade
(n = 25)
Loss of follow-up
(n = 1)
47 patients completed
the two-week trial
Figure 2. CONSORT: Patients’ randomization and follow-up through the clinical trial.
Placebo blockade
(n = 23)
Anesthetic blockade
(n = 24)
Occipital Nerve Blockade for Cervicogenic Headache • 93
Table 1. Baseline Patient Characteristics
Block Group
Number of patients
Age
Sex
Female
Male
History of headache (years)
Pain site
Temporal
Occipital
Parietal
Frontal
Ocular
Frequency of headaches/2 weeks
Duration of crises (h)
Number of analgesics consumed/2 weeks
Paracetamol (tablet 500 mg)
Number of patients
Dextropropoxyphene (capsule 30 mg)
Number of patients
Tramadol hydrochloride (tablet 50 mg)
Number of patients
Ketoprofen (tablet 100 mg)
Number of patients
Visual analog scale
(Maximum score obtained in 2 weeks)
Total Pain Index
(Total Pain Index in 2 weeks)
Accompanied symptoms
Nausea
Yes
No
Vomiting
Yes
No
Phonophobia and/or photophobia
Yes
No
Decreased appetite
Yes
No
Limited normal activity
Yes
No
Placebo Group
P value
25
46.44 (9.63)
25
47.36 (10.25)
0.745
19 (76%)
6 (24%)
12.52 (9.37)
9 [1–32]
18 (72.0%)
7 (28%)
13.20 (9.75)
9 [1–34]
0.999
18 (72%)
25 (100%)
6 (24%)
16 (64%)
16 (64%)
7.36 (2.67)
8 [3–12]
37.04 (16.75)
35 [12–72]
15 (60%)
22 (88%)
8 (32%)
17 (68%)
16 (64%)
7.48 (2.58)
7 [3–12]
35.16 (17.09)
34 [6–72]
0.55
0.363
0.753
0.999
1
0.873
74.16 (12.83)
76 [40–96]
25 (100%)
40.4 (14.13)
42 [0–60]
24 (96%)
4.80 (4.44)
6 [0–13]
15 (60%)
4.20 (5.07)
0 [0–13]
11 (44%)
6.26 (1.65)
7 [3–8]
358.68 (69.98)
369.5 [198–495]
71.04 (18.79)
76 [22–96]
25 (100%)
37.92 (15.91)
40 [0–60]
23 (92%)
5.52 (4.78)
6 [0–12]
16 (64%)
4.48 (5.45)
0 [0–13]
11 (44%)
6.28 (1.79)
7 [3–9]
352.46 (96.90)
373.5 [143–480]
0.496
0.803
0.696
0.563
0.584
0.852
0.967
0.796
13 (52%)
12 (48%)
13 (52%)
12 (48%)
1
6 (24%)
19 (76%)
8 (32%)
17 (68%)
0.753
13 (52%)
12 (48%)
15 (60%)
10 (40%)
0.776
6 (24%)
19 (76%)
7 (28%)
18 (72%)
0.999
12 (48%)
13 (52%)
14 (56%)
11 (44%)
0.777
Data are reported as mean (SD), median [minimum–maximum], or number (%) as appropriate.
P < 0.05 was considered significant.
The anesthetic mixture selected has produced excellent long-lasting pain relief in a variety of surgical
settings.17–20 This multi-anesthetic mixture plays a role
in achieving a pain-free period. Others have reported
the use of clonidine for migraine.21,22 The addition of
clonidine and opioids to local anesthetic solutions has
also been found to prolong the duration of nerve
blocks.23–25 The observed period of analgesia following
the use of the current mixture of local anesthetics, fen-
tanyl, and clonidine may have resulted from a synergistic effect. Clonidine might interact with the immune
system, resulting in reduced recruitment of macrophages
and lymphocytes at the nerve site and a shift in the
proportion of macrophages from the pro-inflammatory
to the anti-inflammatory phenotype.26
Many authors consider entrapment of the GON to
be one of the major underlying causes of CGH.1,4,7 They
theorize that the pathogenesis of CGH involves a dis-
94 • naja et al.
Table 2. Comparison Between Block Group and Placebo Group at Two Weeks after Treatment
Block Group
Number of patients
Pain site
Temporal
Occipital
Parietal
Frontal
Ocular
Duration of pain relief (days)
Frequency of headaches/2 weeks
Duration of crises (hours)
Number of analgesics consumed/2 weeks
Paracetamol (tablet 500 mg)
Number of patients
Dextropropoxyphene (capsule 30 mg)
Number of patients
Tramadol hydrochloride (tablet 50 mg)
Number of patients
Ketoprofen (tablet 100 mg)
Number of patients
Visual analog scale
(Maximum score obtained in 2 weeks)
Total Pain Index
(Total Pain Index in 2 weeks)
Accompanied symptoms
Nausea
Yes
No
Vomiting
Yes
No
Phonophobia and/or photophobia
Yes
No
Decreased appetite
Yes
No
Limited normal activity
Yes
No
Placebo Group
P value
24
23
7 (29.2%)
11 (45.8%)
3 (12.5%)
9 (37.5%)
9 (37.5%)
3.67 (1.71)
5.50 (1.84)
5.5 [2–8]
24.13 (9.55)
26.0 [4–40]
13 (56.5%)
20 (87%)
6 (26.1%)
17 (73.9%)
13 (56.5%)
1.52 (1.20)
7.04 (2.69)
7 [3–12]
35.17 (17.71)
34 [5–72]
0.109
0.031
0.416
0.027
0.311
0.0001
0.026
48.0 (17.57)
49 [10–70]
24 (100%)
18.33 (16.45)
15.0 [0–48]
17 (70.8%)
2.33 (2.87)
0 [0–8]
11 (45.8%)
0.50 (1.06)
0 [0–3]
5 (20.8%)
4.42 (1.39)
4.5 [2–7]
194.25 (54.08)
202 [56–340]
70.96 (17.44)
72 [20–96]
23 (100%)
40.17 (15.59)
42 [0–60]
22 (95.7%)
5.56 (4.62)
6 [0–13]
15 (65.2%)
4.30 (4.98)
0 [0–13]
11 (47.8%)
6.35 (1.86)
7 [2.5–8.5]
329.96 (99.26)
315 [110–475]
0.0001
5 (20.8%)
19 (79.2%)
12 (52.2%)
11 (47.8%)
0.025
0 (0%)
24 (100%)
7 (30.4%)
16 (69.6%)
0.012
6 (25%)
18 (75%)
14 (60.9%)
9 (39.1%)
0.028
1 (4.2%)
23 (95.8%)
7 (30.4%)
16 (69.6%)
0.045
6 (25%)
18 (75%)
14 (60.9%)
9 (39.1%)
0.028
0.10
0.0001
0.006
0.01
0.0001
0.0001
Data are reported as mean (SD), median [minimum–maximum], or number (%) as appropriate.
P < 0.05 was considered significant.
turbance of the nerve ending and the contractile mechanism at multiple dysfunctional endplates, resulting in
trigger points.27,28 Chu further illustrated that entrapment of the nerve root could be documented with electromyographic studies.29 Thus, occipital blockade may
result in local muscle relaxation and liberation of the
entrapped nerve.
There was considerable interpatient variability in the
nerve location. The use of nerve stimulator technique improved accuracy, but required the patient’s co-operation
for optimal detection of the nerve. Therefore, effective
might not always be initially achieved, making repeated
blocks necessary to increase the likelihood of success. A
major limitation of this study is the short duration of follow-up. However, as our research activity is compliant
with the principles enunciated in the Declaration of
Helsinki,30 acting only in the patients’ interest and their
well-being, we decided to limit the duration of this controlled clinical trial for a period of two weeks in order
not to deprive the patients in the control group from any
beneficence. Consequently, long-term outcome was not
evaluated in this study. Another limitation of this clinical
trial was the difficulty in blinding when numbness
resulted in patients who received anesthetic blockade.
In conclusion, the nerve stimulator-guided occipital
nerve blockade is a treatment that provides relief of
Occipital Nerve Blockade for Cervicogenic Headache • 95
CGH and accompanying symptoms for up to two
weeks. This simple technique merits further investigation for patients suffering from CGH.
ACKNOWLEDGMENTS
The authors gratefully acknowledge the financial support from Makassed General Hospital and the suggestions of the peer-reviewers in the preparation of this
article.
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