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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5526_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Contents
- •1.1 Introduction
- •1.2 Pathophysiology
- •1.3 Case Presentation
- •1.4 Case Discussion
- •1.5 Clinical Characteristics
- •1.6 Diagnostic Algorithm
- •1.8 Management
- •1.9 Conclusion
- •References
- •2.1 Introduction
- •2.2 Pathophysiology
- •2.3 Case Presentation
- •2.4 Case Discussion
- •2.5 Clinical Characteristics
- •1.7 Differential Diagnosis
- •2.6 Diagnostic Algorithm
- •2.7 Management
- •2.8 Conclusion
- •References
- •3.1 Introduction
- •3.2 Pathophysiology
- •3.3 Case Presentation
- •3.4 Case Discussion
- •3.5 Clinical Characteristics
- •3.6 Diagnostic Algorithm
- •3.7 Management
- •3.8 Conclusion
- •References
- •4.1 Introduction
- •4.2 Pathophysiology
- •4.3 Case Presentation
- •4.4 Case Discussion
- •4.6 Diagnostic Algorithm
- •4.7 Management
- •4.8 Conclusion
- •References
- •5.1 Introduction
- •5.2 Pathophysiology
- •5.3 Case Presentation
- •5.4 Case Discussion
- •5.5 Diagnostic Algorithm
- •5.6 Management
- •5.7 Conclusion
- •References
- •6.1 Introduction
- •6.2 Pathogenesis
- •6.3 Case Presentation
- •6.4 Case Discussion
- •6.5 Diagnostic Algorithm
- •6.6 Management
- •6.7 Conclusion
- •References
- •7.1 Introduction
- •7.2 Pathophysiology
- •7.3 Case Presentation
- •7.5 Differential Diagnosis
- •7.7 The Following Strategies Are Essential
- •7.7.1 Acute Symptom Relief
- •7.7.1.1 Pharmacological Treatment
- •7.7.2.1 Pharmacologic Prophylaxis
- •7.8 Conclusion
- •References
- •8.1 Introduction
- •8.3 Case Study
- •8.4 Case Discussion
- •8.5 Clinical Management
- •8.7 Diagnosis
- •8.8 Treatment
- •8.9 Conclusion
- •References
- •9.1 Introduction
- •9.2 Case Presentation
- •9.4 Diagnosis Algorithm
- •9.5 Secondary SUNCT
- •9.6 Management
- •9.8 Conclusion
- •References
- •10.1 Introduction
- •10.2 Pathophysiology
- •10.3 Case Presentation
- •10.4 Case Discussion
- •10.5 Clinical Characteristics
- •10.6 Diagnostic Algorithm
- •10.7 Management
- •10.8 Conclusion
- •References
- •11.1 Introduction
- •11.2 Pathophysiology
- •11.3 Case Presentation
- •11.4 Case Discussion
- •11.5 Clinical Characteristics
- •11.6 Diagnostic Algorithm
- •11.6.1 Step 1: Detailed Patient History
- •11.8 Management
- •11.9 Conclusions
- •12.2 Pathophysiology
- •12.3 Case Presentation
- •12.4 Case Discussion
- •12.6 Treatment
- •12.7 Conclusion
- •References
- •References
- •12.1 Introduction
- •13.1 Introduction
- •13.2 Pathophysiology
- •13.3 Case Presentation
- •13.4 Case Discussion
- •13.5 Clinical Characteristics
- •13.6 Diagnostic Algorithm
- •13.7 Management
- •13.8 Conclusion
- •References
- •14.1 Introduction
- •14.2 Pathophysiology
- •14.3 Case Presentation
- •14.3.1 Clinical Case 1
- •14.3.2 Clinical Case 2
- •14.4 Case Discussion
- •14.5 Clinical Characteristics
- •14.7 Treatment/Management
- •14.8 Conclusion
- •References
- •15.1 Introduction
- •15.2 Case Presentation
- •15.3 Case Discussion
- •15.4 Diagnostic Algorithm
- •15.5 Pathophysiology
- •15.6 Clinical Presentation
- •15.6.1 External-Compression Headache (ECH)
- •15.6.2 External-Traction Headache (ETH)
- •15.7 Management
- •15.7.1 Nonpharmacological Strategies
- •15.7.2 Pharmacological Strategies
- •15.7.3 Patient Education and Awareness
- •15.8 Conclusion
- •References
- •16.1 Introduction
- •16.2 Pathophysiology
- •16.3 Case Presentation
- •16.4 Case Discussion
- •16.6 Diagnostic Algorithm
- •16.7 Management
- •16.8 Conclusion
- •References
- •17.1 Introduction
- •17.2 Pathophysiology
- •17.3 Case Presentation
- •17.4 Case Discussion
- •17.5 Clinical Characteristics
- •17.6 Diagnosis
- •17.7 Differential Diagnosis
- •17.8 Treatment
- •17.9 Conclusion
- •References
- •18.1 Introduction
- •18.2 Pathophysiology
- •18.3 Case Presentation
- •18.4 Case Discussion
- •18.5 Clinical Presentation
- •18.6 Diagnosis
- •18.7 Differential Diagnosis
- •18.8 Treatment
- •18.9 Conclusion
- •References
- •19.1 Introduction
- •19.2 Pathophysiology
- •19.3 Case Presentation
- •19.4 Case Discussion
- •19.5 Diagnostic Approach
- •19.6 Management
- •19.7 Conclusion
- •References
- •20.1 Introduction
- •20.3 Case Report
- •20.4 Case Discussion
- •20.6 Clinical Presentation
- •20.7 Diagnostic Algorithm
- •20.8 Conclusion
- •References
- •21.1 Introduction
- •21.2 Case Presentation
- •21.3 Clinical Characteristics
- •21.4 Diagnosis
- •21.5 Treatment
- •References
- •22.1 Introduction
- •22.3 Case Presentation 1
- •22.4 Case Discussion
- •22.5 Case Presentation 2
- •22.6 Case Discussion 2
- •22.7 Clinical Characteristics
- •22.8 Diagnostic Workup
- •22.9 Treatment
- •22.10 Prognosis
- •References
- •23.1 Introduction
- •23.2 Pathophysiology
- •23.3 Case Presentation
- •23.4 Case Discussion
- •23.6 Diagnostic Algorithm
- •23.7 Management
- •23.8 Conclusion
- •References
- •24.1 Introduction
- •24.2 Case Presentation
- •24.3 Case Discussion
- •24.4 Pathophysiology
- •24.6 Clinical Characteristics
- •24.8 Treatment Approaches
- •24.10 Conclusion
- •References
- •25.1 Introduction
- •25.2 Case Presentation
- •25.3 Case Discussion
- •25.4 Conclusion
- •References
- •26.1 Introduction
- •26.2 Pathophysiology
- •26.3 Case Presentation
- •26.4 Case Discussion
- •26.5 Clinical Characteristics
- •26.6 Diagnostic Algorithm
- •26.7 Management
- •26.8 Conclusion
- •References
- •27.1 Introduction
- •27.2 Case Presentations
- •27.3 Clinical Characteristics
- •27.4 Discussion
- •27.5 Conclusion
- •References
- •28.1 Introduction
- •28.2 Case Presentation
- •28.3 Case Discussion
- •28.4 Clinical Characteristics
- •28.5 Diagnosis
- •28.6 Conclusion
- •28.7 Key Messages
- •References
- •29.1 Introduction
- •29.2 Pathophysiology
- •29.3 Case Presentation
- •29.4 Clinical Presentation
- •29.5 Diagnosis
- •29.6 Treatment
- •29.7 Conclusion
- •References
- •30.1 Introduction
- •30.2 Clinical Case
- •30.3 Clinical Presentation
- •30.4 Differential Diagnosis
- •30.5 Diagnosis
- •30.6 Treatment
- •30.7 Conclusion
- •References
- •31.1 Introduction
- •31.2 Pathophysiology
- •31.3 Case Presentation
- •31.4 Case Discussion
- •31.5 Clinical Presentation
- •31.7 Conclusion
- •References
- •32.1 Introduction
- •32.2 Pathophysiology
- •32.3 Case Presentation
- •32.4 Case Discussion
- •32.6 Diagnosis
- •32.7 Additional Diagnostic Evaluations
- •32.8 Apply ICHD-3 Diagnostic Criteria [9]
- •32.10 Management
- •32.11 Conclusion
- •References
- •33.1 Introduction
- •33.2 Pathophysiology
- •33.3 Case Presentation
- •33.4 Clinical Characteristics
- •33.5 Diagnostic Algorithm
- •33.6 Treatment
- •33.7 Conclusion
- •References
- •34.1 Introduction
- •34.2 Pathophysiology
- •34.3 Case Presentation
- •34.4 Case Discussion
- •34.6 Diagnostic Algorithm
- •34.7 Treatment
- •34.8 Conclusion
- •References
- •35.1 Introduction
- •35.3 Case Presentation
- •35.4 Case Discussion
- •35.7 Treatment
- •35.7.1 Oxygen Therapy (100% Oxygen)
- •35.8 Conclusion
- •References
- •36.1 Introduction
- •36.2 Pathophysiology
- •36.3 Case Presentation
- •36.5 Diagnostic Algorithm
- •36.6 Treatment
- •36.7 Conclusion
- •References
- •37.1 Introduction
- •37.2 Pathophysiology
- •37.3 Case Presentation
- •37.4 Headache Characteristics
- •37.5 Case Discussion
- •37.6 Treatment
- •37.7 Conclusion
- •References
- •38.1 Introduction
- •38.2 Pathophysiology
- •38.3 Case Presentation
- •38.4 Clinical Presentation
- •38.5 Diagnostic Algorithm
- •38.6 Treatment
- •38.7 Conclusion
- •References
- •39.1 Introduction
- •39.3 Case Presentation
- •39.4 Case Discussion
- •39.6 ICHD-3 Diagnostic Criteria [28]
- •39.6.1 Diagnostic Criteria
- •39.7 Diagnostic Algorithm
- •39.9 Conclusion
- •References
- •40.1 Introduction
- •40.3 Case Presentation
- •40.4 Case Discussion
- •40.5.1 Diagnostic Algorithm
- •40.6 Treatment
- •40.7 Conclusion
- •References
- •41.1 Introduction
- •41.3 Case Presentation
- •41.4 Clinical Presentation
- •41.5 Differential Diagnosis
- •41.6 Conclusion
- •41.7 Key Messages
- •References
- •42.1 Introduction
- •42.2 Pathophysiology
- •42.3 Case Presentation
- •42.5 Case Discussion
- •42.6 Clinical Presentation
- •42.7 Diagnostic Algorithm [9]
- •42.8 Preeclampsia
- •42.9 Eclampsia
- •42.10 Fetal Assessment
- •42.11 Treatment
- •42.12 Antihypertensive Management [8]
- •42.14 Conclusion
- •References
- •43.1 Introduction
- •43.2 Pathophysiology
- •43.3 Case Presentation
- •43.4 Case Discussion
- •43.5 Clinical Manifestations
- •43.6 Diagnosis
- •43.7 Treatment
- •43.8 Conclusion
- •References
- •44.1 Introduction
- •44.2 Pathophysiology
- •44.3 Case Presentation
- •44.4 Case Discussion
- •44.6 Diagnostic Approach
- •44.7 Management
- •44.8 Conclusion
- •References
- •45.1 Introduction
- •45.2 Pathophysiology
- •45.3 Case Presentation
- •45.6 Treatment
- •45.7 Conclusion
- •References
- •46.1 Introduction
- •46.2 Pathophysiology
- •46.3 Case Presentation
- •46.4 Clinical Characteristics
- •46.5 Differential Diagnosis
- •46.6 Treatment
- •46.7 Conclusion
- •References
- •47.1 Introduction
- •47.2 Pathophysiology
- •47.3 Case Presentation
- •47.4 Case Discussion
- •47.5 Clinical Presentations
- •47.6 Diagnostic Algorithm
- •47.7 Differential Diagnosis
- •47.8 Treatment
- •47.9 Conclusion
- •References
- •48.1 Introduction
- •48.2 Pathophysiology
- •48.3 Case Presentation
- •48.4 Case Discussion
- •48.5 Clinical Characteristics
- •48.7 Treatment
- •48.8 Conclusion
- •References
- •49.1 Introduction
- •49.2 Pathophysiology
- •49.3 Case Presentation
- •49.4 Clinical Presentation
- •49.5 Diagnosis
- •49.6 Treatment
- •49.7 Conclusion
- •References
- •50.1 Introduction
- •50.2 Pathophysiology
- •50.3 Case Presentation
- •50.4 Case Discussion
- •50.5 Clinical Characteristics
- •50.6 Diagnosis
- •50.7 Treatment
- •50.8 Conclusion
- •References
- •51.1 Introduction
- •51.2 Case Presentation
- •51.3 Clinical Characteristics
- •51.4 Diagnosis
- •51.5 Treatment
- •51.6 Conclusion
- •References
- •52.1 Introduction
- •52.2 Pathophysiology
- •52.3 Case Presentation
- •52.4 Case Discussion
- •52.5 Clinical Characteristics
- •52.6 Diagnosis
- •52.6.1 Cervicogenic Headache
- •52.6.2 Migraine
- •52.6.3 Neck Pain
- •52.6.4 Demyelinating Lesions
- •52.6.5 Cervical Myelitis
- •52.6.6 Occipital Allodynia
- •52.6.7 Cervical Muscle Spasms
- •52.7 Treatment
- •52.7.2 Acupuncture
- •52.7.3 Transcutaneous Electrical Nerve Stimulations (TENS)
- •52.8 Minimally Invasive Treatment
- •52.8.1 Nerve Blocks
- •52.8.2 Botulinum Toxin A
- •52.8.3 Radio Frequency
- •52.8.4 Occipital Nerve Stimulation
- •52.9 Surgical Treatments
- •52.10 Conclusions
- •References
- •53.1 Introduction
- •53.2 Pathophysiology
- •53.3 Characteristics of Pain
- •53.4 Case Presentation
- •53.5 Case Discussion
- •53.6 Clinical Characteristics
- •53.8 Treatment
- •53.9 Conclusion
- •References
- •54.1 Introduction
- •54.2 Pathophysiology
- •54.3 Case Presentation
- •54.4 Case Discussion
- •54.5 Clinical Characteristics
- •54.6 Diagnostic Algorithm
- •54.7 Management
- •54.8 Conclusion
- •References
- •55.1 Introduction
- •55.2 Pathophysiology
- •55.3 Case Presentation

492
I. Fortini
52.2 Pathophysiology
Figure 52.1 illustrates the occipital nerves and highlights their complex relationship
with the occipital muscles. The greater occipital nerve (GON) originates from the
dorsal ramus of the C2 spinal nerve. It then passes medially to the lower border of
the obliquus capitis inferior muscle and crosses the suboccipital triangle. From
there, it travels along the rectus capitis posterior major muscle, innervating it, before
piercing the semispinalis capitis muscle and the tendon of the trapezius. The GON
continues to ascend, passing the superior nuchal line of the occipital bone and proceeding toward the apex of the scalp, near the occipital artery [7, 8].
The lesser occipital nerve (LON) originates from the ventral ramus of C2 and
loops inferiorly to the spinal accessory nerve. It ascends along the posterior border
of the sternocleidomastoid muscle, piercing the deep cervical fascia. The nerve then
passes across the posterior edge of the sternocleidomastoid insertion and enters the
supercial fascia of the scalp. It divides into three branches: the auricular, mastoid,
and occipital branches [7, 8].
The third occipital nerve (TON) originates from the dorsal ramus of C3, which
divides into lateral and medial branches. The medial branch gives rise to both supercial and deep branches, with the supercial branch becoming the TON.The TON
Fig. 52.1 Occipital nerves

52 Occipital Neuralgia
493
curves around the dorsolateral surfaces of C2 and C3, travelling along the semispinalis capitis muscle. It then turns dorsally at the C2 spinous process, piercing the
semispinalis capitis, splenius capitis, and trapezius muscles. After exiting these
muscles, the TON innervates a small cutaneous area just below the nuchal line.
Additionally, the TON sends branches to the greater occipital nerve (GON) and
lesser occipital nerve (LON) [7, 8].
Both structural and non-structural causes can lead to ON.Still, almost always it
results from the compression or irritation of one of the nerves at one of several anatomic points, the great occipital nerve (GON) being responsible for the great majority of the cases. Anatomical variations, such as the course of the greater occipital
nerve through the obliquus inferior capitis muscle, may lead to nerve compression.
Other causes of compression of the occipital nerves include hypertrophic ligaments,
brosis, and bone spurs [9].
Multiple possible compression points of the GON exist that may result in
ON [10].
These points include the C2 nerve root, the obliquus capitis inferior muscle, the
semispinalis capitis muscle, points where the GON penetrates the trapezius muscle,
and points of intersection between the GON and the occipital artery [8, 10].
Muscle hypertrophy or spasms can also contribute to nerve compression. Men,
due to increased exposure to physical activities or occupations that heighten the risk
of neck injuries, may be more prone to developing ON. Additionally, postural
issues, particularly those related to prolonged use of computers or mobile devices,
can cause tension in the neck muscles and contribute to nerve compression [11].
Trauma to the occipital region, such as whiplash injuries, may lead to ON either
through direct nerve damage or secondary changes like brosis that result in nerve
compression [12].
A less common cause of ON is vascular compression of the nerves by arteries,
such as the posterior inferior cerebellar artery or the occipital artery [8, 13].
Degenerative diseases of the cervical spine, such as cervical spondylosis, may be
more prevalent in middle-aged and older men, increasing the risk of occipital neuralgia. Arthritic changes, such as C1–C2 arthrosis syndrome and atlantoaxial lateral
mass osteoarthritis, can cause nerve compression [12].
Other pathologies can also be associated with ON, such as cervical cord tumors,
Chiari malformation, arteriovenous malformation, and neurosyphilis, which may
cause secondary nerve compression or irritation [10, 14]. Systemic diseases such as
diabetes can affect nerve health, increasing susceptibility to neuropathic conditions,
including ON [11].
Familial cases of ON are extremely rare but have been reported, with an autosomal dominant or X-linked inheritance pattern. These cases often involve neuralgia
of multiple cranial nerves, suggesting potential peripheral sensory anastomoses or
central convergence of afferent pathways [15, 16].

494
I. Fortini
52.3 Case Presentation
A 65-year-old female with a medical history of well-controlled arterial hypertension and hypothyroidism presented to the headache clinic with complaints of severe,
acute, stabbing pain in the right occipital region. The pain, which started approximately 10months ago, initially occurred four times a week. However, over the last
ve months, the frequency of the episodes increased to daily occurrences, often
with multiple attacks per day, occasionally extending into the nighttime. The patient
denied any positional inuence on the pain and reported no associated symptoms,
though tenderness over the affected region was present most of the time. The patient
had been treated with a combination of non-steroidal anti-inammatory drugs
(NSAIDs), venlafaxine, pregabalin, and carbamazepine, but none provided signicant relief. Occipital nerve blocks with lidocaine offered temporary pain relief.
Neurological examination was unremarkable, and systemic diseases other than
hypertension and hypothyroidism were ruled out. Magnetic resonance imaging
(MRI) revealed no abnormalities. The patient also underwent acupuncture and
transcutaneous electrical nerve stimulation (TENS) sessions, but there was no
improvement. Subsequently, she underwent rhizotomy of the right greater occipital
nerve. No tissue abnormalities were observed during the procedure, and immediate
pain relief was achieved, which persisted during follow-up visits.
52.4 Case Discussion
This case is characteristic of ON with a prolonged duration of symptoms. The positive response to the anesthetic block further supports the diagnosis. In some cases,
a Tinel’s sign may be present at the site of the greater occipital nerve emergence, but
it was not noted in this case.
It is crucial to rule out systemic, cranial, and cervical causes of ON during diagnosis. While non-invasive treatments such as acupuncture, TENS, and nerve blocks
are commonly attempted, they do not always provide sufcient relief. In such cases,
more invasive treatments, such as occipital nerve stimulation (ONS) or radio frequency ablation, may be necessary to achieve sustained pain relief.
52.5 Clinical Characteristics
The pain associated with this condition is typically paroxysmal, sharp, and intense,
often originating from the posterior region of the head. It lasts from seconds to minutes and may radiate toward the front of the head and face [10, 17]. Tenderness over
the affected nerve area is commonly present, along with a Tinel’s sign at the point
where the nerve emerges. The pain may be exacerbated by movement or pressure
applied to the posterior region of the head.

52 Occipital Neuralgia
495
52.6 Diagnosis
The diagnosis of occipital neuralgia (ON) is primarily clinical, based on the presence of intermittent, typically unilateral, painful episodes of stabs in the occipital
region. However, bilateral involvement can occur in some cases. The individual pain
episodes can last seconds to minutes, and physical examination often reveals tenderness over the affected occipital nerves [10, 17].
The diagnostic criteria for occipital neuralgia (ON) according to the International
Classication of Headache Disorders, 3rd edition (ICHD-3), are as follows [18]:
A. Unilateral or bilateral pain in the distribution(s) of the greater, lesser and/or third
occipital nerves and fullling criteria B–D
B. Pain has at least two of the following three characteristics:
1. Recurring in paroxysmal attacks lasting from a few seconds to minutes
2. Severe in intensity
3. Shooting, stabbing or sharp in quality
C. Pain is associated with both of the following:
1. Dysesthesia 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
distribution of C2
D. Pain is eased temporarily by local anesthetic block of the affected nerve(s)
E. Not better accounted for by another ICHD-3 diagnosis.
Pain usually begins unilaterally and may extend into a bilateral distribution over
time. Bilateral symptoms are present in one-third of cases. A positive Tinel’s sign
may be present over the nerve’s distribution, especially where the GON emerges at
the base of the skull over the greater occipital notch [7, 8].
According to ICHD-3 standards, diagnosis of occipital neuralgia requires conrmation through a local anesthetic blockade of the suspected nerve. Pain relief following the nerve block should last for at least the duration of the local anesthetic.
Since single diagnostic blocks can yield false-positive rates of up to 40%, performing a second block may help improve diagnostic accuracy [7, 8].
Occipital neuralgia (ON) can be easily confused with several other neurological
conditions due to overlapping symptoms, particularly pain in the occipital region.
While these conditions share similar symptoms, they have distinct etiologies and
treatment approaches. Therefore, a thorough clinical evaluation, along with the use
of imaging tests when necessary, is essential for accurate diagnosis. Conditions that
may be mistaken for occipital neuralgia include:

496
I. Fortini
52.6.1 Cervicogenic Headache
In cervicogenic headache, the pain is referred to the occipital region and is caused
by dysfunction in the cervical spine. While it shares similarities with occipital neuralgia (ON), cervicogenic headache is a secondary headache disorder typically
linked to mechanical issues in the cervical spine. Unlike the sharp, excruciating pain
of ON, cervicogenic headache pain tends to be more constant and less paroxysmal,
lacking the intense, sudden episodes characteristic of occipital neuralgia [19].
52.6.2 Migraine
Migraine has distinct features such as photophobia, phonophobia, and nausea, but
occasionally occipital pain may be a symptom, leading to confusion with
ON. Additionally, migraine pain is usually throbbing, unlike the stabbing pain
of ON [2].
52.6.3 Neck Pain
Pain in the neck, especially when associated with muscle spasms and stiffness, can
radiate to the occipital region, mimicking ON.Neck pain generally does not present
the paroxysmal, stabbing pain typical of ON [20].
52.6.4 Demyelinating Lesions
Multiple sclerosis and the neuromyelitis optica spectrum of disorders may present
with neuralgiform pain in the occipital region due to lesions in the cervical spinal
cord, which may be confused with ON.Still, it is often associated with other neurological symptoms, such as sensory loss or weakness, which help differentiate it
from isolated ON [5].
52.6.5 Cervical Myelitis
Inammation of the cervical spinal cord may present as occipital neuralgia, especially when there are lesions at high levels of the cervical spine, such as C2, but is
often associated with additional neurological decits, such as sensory or motor
changes, that are not typical of ON [5, 21].

52 Occipital Neuralgia
A thorough differential diagnosis is essential and can be supported by anesthetic
occipital nerve blocks, which help conrm occipital neuralgia (ON) if pain relief is
achieved [2, 22]. In addition, there are less common symptoms of ON that may be
present and can be useful in distinguishing this condition from others:
497
52.6.6 Occipital Allodynia
Increased sensitivity to light touch in the occipital region, which may be indicative
of occipital neuralgia.
52.6.7 Cervical Muscle Spasms
Although pain is the predominant symptom, some patients may experience spasms
in the cervical muscles, which can contribute to pain and stiffness in the region.
52.6.8 Radiation ofPain toFrontal Areas
Pain from occipital neuralgia can radiate to areas innervated by the trigeminal nerve,
leading to migraine-like symptoms such as photophobia and nausea, especially
when the pain extends to the frontal region. These less common symptoms can
complicate the diagnosis, necessitating careful clinical evaluation to differentiate
occipital neuralgia from other neurological conditions [5, 23].
52.7 Treatment
Treatment of occipital neuralgia is multimodal and may include both conservative
interventions and more invasive procedures, depending on the severity and the
patient’s response to initial therapies. Non-steroidal anti-inammatory drugs, tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and anticonvulsants may help to alleviate symptoms.
52.7.1 Conservative andComplementary Treatments
Conservative treatments are often recommended as rst-line treatment and include
pain education, self-care, physical therapy to reduce muscle tension and improve
posture, and the use of transcutaneous electrical nerve stimulation (TENS) [24, 25].

498
Complementary therapies that have demonstrated effectiveness in treating occipital neuralgia include acupuncture and transcutaneous electrical nerve stimulation
(TENS). These alternative therapies can be integrated into a multimodal treatment
plan, especially in patients who do not respond well to conventional interventions.
However, it is important to consider that more research is needed to validate the
long-term effectiveness and safety of these approaches.
I. Fortini
52.7.2 Acupuncture
Studies indicate that acupuncture can be effective in treating occipital neuralgia,
showing a signicantly higher effectiveness rate compared to drug treatment alone.
Acupuncture has also been associated with a signicant reduction in adverse events
compared to medications. Side effects are generally mild and may include pain or
bruising at the needle insertion site, dizziness, or fatigue [26, 27].
Acupuncture has been assessed in systematic reviews and meta-analyses, demonstrating signicantly higher efcacy compared to drug treatment alone. It is associated with a notable reduction in pain on the visual analogue scale and fewer
adverse events [26].
52.7.3 Transcutaneous Electrical Nerve Stimulations (TENS)
Although evidence is limited, TENS is a conservative option that can be used to
relieve muscle tension and improve posture, contributing to the management of pain
associated with ON [24, 25].
Immobilization of the neck by the cervical collar, physiotherapy, and cryotherapy have not been shown to perform better than placebo [28].
52.8 Minimally Invasive Treatment
52.8.1 Nerve Blocks
Injections of local anesthetics, such as lidocaine or bupivacaine, with or without
corticosteroids, are often used for short-term pain relief and may have diagnostic
value [11, 12, 17].
Ultrasound guidance was introduced to increase the effectiveness of the procedure. Greher etal. (2010) described the original ultrasound-guided technique for
injection of the GON.It targets the nerve as it courses supercial to the obliquus
capitis inferior muscle at the C1–C2 level [29].

52 Occipital Neuralgia
499
52.8.2 Botulinum Toxin A
Botulinum toxin A injection has emerged as a treatment with a relatively lower side
effect prole compared to many other approaches. Recent trials have shown that it
can result in a 50% or greater improvement in symptoms [10, 28].
52.8.3 Radio Frequency
Pulsed radio frequency (PRF) ablation of the occipital nerves is effective in providing long-term pain relief in refractory patients. Studies indicate that PRF may provide greater pain relief compared to steroid injections [24, 30].
52.8.4 Occipital Nerve Stimulation
Occipital nerve stimulation (ONS) is a valuable option for treating refractory cases
of occipital neuralgia and can provide signicant pain relief in some patients. This
minimally invasive procedure has shown promising results, though further studies
are needed to conrm its long-term effectiveness [24, 31].
Salmasi etal. (2020) followed three patients for an average of eight months, with
an average pain reduction of approximately 50% [31].
Occipital nerve stimulation (ONS) is both safe and effective, with response rates
ranging from 63 to 100% in patients with occipital neuralgia. Furthermore, a high
percentage of patients continue to respond positively to ONS over the long term [32].
52.9 Surgical Treatments
In very refractory cases, surgical procedures such as occipital nerve decompression
or neurectomy may be considered, but there are associated risks [11, 33, 34].
Occipital neuralgia can be difcult to manage, and treatment options should be
carefully considered based on the patient’s unique clinical presentation and their
response to previous interventions. Treatment decisions must be personalized,
weighing factors such as efcacy, potential risks, and the patient’s preferences. A
systematic review investigated 12 articles on the surgical management of occipital
neuralgia and did not nd sufcient evidence to recommend neurolysis versus neurotomy [35].

500
I. Fortini
52.10 Conclusions
Occipital neuralgia is an uncommon but signicant cause of intense, paroxysmal,
sharp headaches that typically last from seconds to minutes. These headaches are
localized in the areas innervated by the greater occipital nerve (GON), lesser occipital nerve (LON), or third occipital nerve (TON). The primary etiologies include
anatomical, traumatic, iatrogenic, and vascular causes. Diagnosis is based on a thorough patient history, clinical examination, and a positive response to an anesthetic
block of the occipital nerves. Other conditions may mimic occipital neuralgia and
can also respond to nerve blocks, so these must be ruled out through careful clinical
assessment and, if necessary, imaging studies. Conservative treatments, such as
pharmacological therapy combined with physical therapy, are often effective.
Minimally invasive interventions, such as occipital nerve blocks, can be both diagnostic and therapeutic. In cases that are refractory to these treatments, additional
options like radio frequency (RF) ablation or neuromodulation may be required for
long-term relief. Surgical decompression, neurotomy, and neurolysis are considered
last-resort options for particularly challenging cases.
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