Abstract

Occipital neuralgia (ON) is an often-undiagnosed cause of head and neck pain. Potential etiologies of ON are wide and include head and neck trauma, such as whiplash and concussion injuries, atlantoaxial joint instability, or as a complication after radiofrequency ablation. Patients commonly complain of severe attacks of shooting or stabbing pain in the nuchal area around the greater occipital nerve (GON) distribution that is exacerbated by movement or palpation of the neck. Because of the location and characteristics of the pain and the associated symptoms, this condition can be easily mistaken for tension headaches with myofascial components, cervicogenic headaches, radiculopathies, or atypical migraines. If precipitated by head trauma, such as a concussion, ON typically presents subacutely between 1 and 3 months postinjury. Associated symptoms can include tinnitus, nausea, dizziness, and visual changes, which lends significant overlap between ON and postconcussive syndrome (1). Pearl: Consider a diagnosis of ON in patients with a recent history of concussion who have cessation of symptomatic improvement weeks after their injury, or have worsening symptoms including headache, nausea, dizziness, and/or photophobia. The physical examination of patients with ON can be extremely helpful in differentiating it from other types of headaches and other concussive sequelae. Tenderness to compression and/or a positive Tinel's sign can often be appreciated along the course of the GON, particularly at the proximal end of the GON typically located 2 cm inferior and 2 cm lateral to the occipital protuberance. Pain may radiate along the scalp as distal as the fronto orbital region, but need not be in a contiguous distribution. The lesser occipital nerve also may be affected, which may be found lateral to the GON along the superior nuchal ridge. Of note, the Buffalo Concussion Treadmill Test (BCTT) has been used to determine if symptoms during prolonged postconcussion recovery are because of the concussion (abnormal physiologic response to exercise) or because of a concomitant depression, cervical injury, vestibular/ocular dysfunction, or a posttraumatic headache syndrome (normal physiologic response to exercise) (2). In our clinical experience, the BCTT does not perform well at distinguishing between ON and concussion. This may be because of the communications between the occipital nerves and various cranial nuclei, including that of the vagus nerve, which may contribute to an abnormal physiologic response to exercise (3). Diagnostic confirmation of ON can instead be achieved via the use of a diagnostic nerve block on the affected occipital nerve. Pearl: A diagnostic nerve block may be superior to the use of the BCTT at distinguishing between concussion and ON symptom etiologies. There is no current consensus on the optimal treatment method for ON given the lack of randomized controlled studies. Treatment options include standard conservative methods (hot or cold compresses and postural readjustments), pharmacological approaches (nonsteroidal anti-inflammatory drugs and neuropathic medications), and various intervention options (botulinum toxin injections). In our clinical experience, diagnostic blocks of the occipital nerves often have significant therapeutic benefit, which is supported by the positive findings in one medium-sized prospective study (4). Pearl: Occipital nerve blocks can be efficacious in treating patients with ON. For those patients with a positive but temporary response to the block, radiofrequency ablation of the third occipital nerve commonly results in more sustained improvement.

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