I. Cervicogenic headache
It is a group of syndromes with chronic head pain as the main clinical manifestation caused by organic or functional lesions of the cervical spine and/or soft tissues of the neck, and the nature of the pain is a kind of involvement pain. Dull or aching pain in the occipital, top, temporal, frontal, or orbital regions of the head or both of these areas. The headache is accompanied by upper neck pain, neck pressure, neck stiffness, or upper neck pain and limited movement with activity, and there is a history of head and neck injury.
In 1983, Sjaastad introduced the concept of cervicogenic headache, and in 1990, the International Headache Committee issued the classification criteria for cervicogenic headache. 1995, Bogduk pointed out cervical degeneration and muscle spasm as the direct cause. It may also be referred to as posterior cervical nerve branch origin headache. Cervicogenic headache has also been referred to as high-grade radicular cervical spondylosis. Cervicogenic headache has been widely accepted in clinical practice. Early descriptions of cervicogenic headache were of moderate to severe headache almost entirely confined to one side, beginning in the neck or occipital region and eventually spreading to the forehead and temporal region. The attacks are intermittent, of variable duration in the early stages and become more frequent later on, with pain that is sometimes mild and sometimes severe. Clinical symptoms and signs show cervical involvement.
Anatomical classification of cervicogenic headache
Classified according to the different involved parts of nerve roots.
1.Neurogenic pain: the sensory root fibers of the nerve roots are stimulated.
2. Myogenic pain: stimulation of ventral motor nerve roots.
3. Mechanisms of cervicogenic headache.
1.Inflammatory mechanism of cervicogenic headache
(1) The branches of the high cervical nerve are easily stimulated and injured by the vertebral prominence and muscles at the attachment. Hyperalgesia, hypersensitivity or sensory loss can occur on the scalp when these nerves are compressed and stimulated.
The sensory fibers of these cervical nerves may extend forward to the forehead, temporal region, and inferior orbital region, and may cause involvement head pain, tinnitus, eye swelling, and altered sense of smell and taste when stimulated by compression or inflammation, similar to the manifestations of sinus, ear, or eye disease. In addition, the 1st, 2nd, and 3rd cervical nerves leave the spinal canal and travel through soft muscle tissue, triggering cervicogenic headaches when inflammation, ischemia, injury, compression, or irritation of the nerve occurs in the soft tissue.
(2) Martelletti found in his experiment that serum IL-1β and tumor necrosis factor (TNF-α) levels were significantly higher in patients with cervicogenic headache than in patients with migraine without aura and healthy individuals.
2. Convergence theory and the development of cervicogenic headache
It is believed that the occurrence of cervicogenic headache is a kind of involvement pain caused by the disruption of injury sensory input through the central convergence between the afferent fibers of the high cervical nerve and the afferent fibers of the high cervical nerve and the trigeminal nerve caused by the lesion of the structures innervated by the high cervical nerve.
IV. Treatment of cervicogenic headache.
(I) General treatment
For patients with short duration and mild pain, rest and head and neck physiotherapy can be taken, along with oral non-steroidal anti-inflammatory drugs.
(II) Nerve block injection therapy
Injecting anti-inflammatory and analgesic drugs in the corresponding focal area plays both a diagnostic and therapeutic role. Whether in the acute attack or chronic phase, injection therapy is an effective means of pain relief. It is applicable to those with positive nerve block test.
Before injection therapy, carefully analyze the condition and confirm the specific lesion site. We should carefully analyze the condition and confirm the specific site of the lesion before the injection treatment, and formulate a targeted injection treatment plan for the patient. In addition, the treatment should be continuously evaluated and verified during the course of treatment. When the initial or the first two injections are not effective, the treatment plan should be rediagnosed and adjusted in time. In recent years, a combination treatment is recommended, i.e. local nerve block + drug + non-drug.
(C) Nerve destruction treatment
If various non-surgical treatments are ineffective, minimally invasive ablative blockade under imaging guidance can be used with the consent of the patient.