THIRD OCCIPITAL NEURALGIA

Article by: Chaithannya N S

Introduction:
The concept of third occipital nerve headache was introduced by Bogduk, et al. On the basis of anatomical and circumstantial clinical evidence, they argued that in some patients with chronic headaches, the pain stemmed from the C2-3 zygapophysial joint, which is innervated by the third occipital nerve. The pain was believed to be due to post-traumatic arthropathy, and the headache constituted referred pain to the head from the cervical spine.

Occipital neuralgia is defined by the International Headache Society as paroxysmal shooting or stabbing pain in the dermatomes of the greater or lesser occipital nerve.

Anatomy:

The C3 dorsal ramus is a short nerve that arises from the spinal nerve and passes backwards through the C2-3 intertransverse space where it divides into a lateral and two medial branches. The deeper of the two medial branches winds around the waist of C3 articular pillar and enters the multifidus muscle. The superficial medial branch is known as the third occipital nerve. The third occipital nerve is also known as the lesser occipital nerve. It crosses the lateral and dorsal aspects of the lower half of the C2-3 zygapophysial joint, it then passes across the lamina of C3 before turning backward and upwards to pierce semispinalis capitis and splenius capitis to become cutaneous over the suboccipital area. The articular branches to the joint arise from the deeper aspect of the nerve as it crosses the joint.

Anatomically, the C2-3 joint differ markedly from the other upper cervical synovial joints. The joints of the atlas lie ventral to the emerging spinal nerves, the C2-3 zygapophysial joints lie behind the intervertebral foramina in sequence with the other zygapophysial joints and are the highest synovial joints associated with an intervertebral disc at the same level. Functionally they represent a transition zone between the C1-C2 level, which accommodates rotation of the head, and the lower cervical spine, which accommodates flexion and extension of the neck.

Causes of third occipital neuralgia:

• Whiplash injury- causing headache
• Post-surgical neuralgia – midline nuchal incisions
• Chronic headache.

Signs and symptoms:

Headache as the predominant complaint and tenderness over the C2-3 zygapophysial joint on the side of pain is characteristic of the condition. Tenderness is the most sensitive sign.

Diagnostic methods:

According to the International Classification of Headache Dis­ order (ICHD­II), occipital neuralgias belongs to the same family as cranial neu­ralgias, central and primary facial pain, and other headaches. The diagnostic criteria are as below:

1. Paroxysmal stabbing pain, with or without persistent aching between paroxysms, in the distribution of the greater, lesser, and/or third occipital nerve.
2. Tenderness over the affected nerve (about 3 cm superomedially to the tip of the mastoid process).
3. Pain is eased temporarily by local anaesthetic block of the nerve – definitive diagnosis.

Treatment:

Conservative management:

Conservative treatment includes posture correction and reduc­ing the neuralgic and muscle pain. Pharmacological treatment may include tricyclic antidepressants, serotonin reuptake in­hibitors, anticonvulsants (e.g., carbamazepine, oxycarbamaze­pine, gabapentin, pregabalin), and opioids. NSAID’s and paracetamol tend to have transient ef­fects. The use of ergot derivatives is controversial. Infliximab has shown some benefit.

Interventional management

Local anaesthetic with or without steroid injection: Under repeated fluoroscopic screening a 25g,90mm spinal needle is inserted by a lateral approach to the third occipital nerve. Three target points are selected to ensure that the variable course of the nerve across the C2-3 joint is adequately blocked. At each target point, 0.5ml of local anaesthetic is injected slowly, at a rate of 1.2 ml per minute. End point of the block is by achieving numbness over the cutaneous supply of third occipital nerve.

Botulinum toxin infiltrations: Botulinum A’s inhibitory effects on sensory nerve mediators like substance ­P, calcitonin gene­ related peptide, and glutamate may be involved in pain relief.

Pulsed radiofrequency treatment: Pulsed radiofrequency treatment is known to reduce pain, primarily by the induction of a low­ intensity electrical field aro­und sensory nerves that result in depressed conduction and inhibition of long ­term activation in the lightly myelinated A­ delta fibers and the small unmyelinated C fibers. PRF treatment showed short ­term to intermediate ­term pain control and the parameters used were: 40­60 V voltage output; 2 Hz frequen­cy; 20­ms pulses in a 1­second cycle, 120 seconds/cycle; 150­ 500 W impedance range; and 42°C plateau temperature.

Surgery: Indicated in refractory patients. It includes neurolysis, Occipital nerve stimulation and destructive surgeries.

Complications of interventional management

Infection or bleeding may result from any percutaneous tech­nique, though these are usually minor problems. A case of sud­den unconsciousness due to inadvertent subarachnoid injection in a patient with a craniotomy defect has been reported. Temporary dizziness, injection site soreness, focal alopecia, and paraesthesia due to nerve injury should be anticipated.

Further Reading:

1. Neuralgias of the Head: Occipital Neuralgia, Il Choi and Sang Ryong Jeon, J Korean Med Sci 2016; 31: 479-488.
2. On the concept of third occipital headache, Nikolai Bogduk, Anthony Marsland, Journal of Neurology, Neurosurgery, and Psychiatry 1986;49:775-780
3. Third occipital nerve headache: a prevalence study, Susan M Lord, Les Barmsley, Barbara J Wallis, Nikolai Bogduk, Journal of Neurology, Neurosurgery and Psychiatry 1994;57:1187-1190.