The rate of posttraumatic migraine has been reported to be as high as 49% in the first year following mild TBI, and the rate of tension-type headaches has been reported as to be high as 40% (Lucas et al. 2014). Correlation between injury severity and the development of PTH has not been identified; disabling headaches may occur in even the mildest of injuries [13].

There are multiple theories regarding the etiology of PTM , including damage to meningeal blood vessels, meningeal irritation, injury-induced neuronal hyperexcitability, alterations in the trigeminal vascular system, and cortical hyperexcitability [14].

Migraine headaches are typically unilateral in location, throbbing, moderate in intensity, and aggravated by physical activity. They are often associated with nausea, phonophobia, and photophobia and may be associated with an aura. Females and those with a prior history of HA seem to be especially at risk [15]. PTM may occur alone or as part of a constellation of symptoms referred to a post-concussive or posttraumatic syndrome. Symptoms may include poor concentration, confusion, amnesia, fatigue, irritability, depressed mood, and anxiety [15, 16].

PTM can be challenging to treat and may pose significant difficulty for individuals attempting to re-enter the workforce or continue educational endeavors.

Initial

Avoidance of migraine triggers, proper sleep, and regular exercise are all beneficial for migraine prevention. Additionally, the use of a headache diary may aid in the identification of specific headache triggers and may be a beneficial part of the overall treatment plan [17, 18].

Medication

Individuals with PTH may have one or more headache types, including migraine or tension. Watanabe et al. performed a systematic review for treatment of PTH and found insufficient evidence to support a specific treatment modality. The authors suggest categorization of primary headache typology, consideration for trial of acetaminophen or nonsteroidal anti-inflammatories, and limited use of opioids. For those meeting criteria for migraine or probable migraine, a trial of triptans is recommended [18]. Treatment for migraine headaches can be summarized in Table 19.2 and can be divided by abortive, prophylactic, and other therapies.

Procedures

Botulinum toxin injections are an effective prophylactic treatment of migraine headaches.

A recent prospective analysis of 254 patients with chronic migraine found a reduced number of headache days and improvement in the quality of life with the use of Onabotulinum toxin A [19]. Although the use of botulinum toxin for the treatment of migraine headaches has grown in recent years, there is limited data regarding the use of such intervention following TBI. A cohort study of 64 military members with chronic PTH following TBI reported improvement in headache in 64% of those receiving Onabotulinum toxin injections [20]. Although promising, further research is needed in the PTM population.

Tension-type headache (TTH) is historically the dominant classification type of PTH [21].

The pathophysiology of TTH is controversial and it likely represents a spectrum of disorders with several etiologies. Depending on the location, myofascial trigger points have been linked in literature to various categories of headaches including TTH.

A typical presentation of tension-type headache is bilateral head pain of pressing or vice-like quality of mild to moderate intensity. It generally occurs later in the day, and generally, movement does not worsen the headache. TTH are generally not associated with nausea or vomiting, photophobia, or phonophobia. Pericranial tenderness also appears characteristic of TTH. Differentiating TTH from other headache types is challenging. Medication overuse headaches described below also need to be considered. Typically, TTH is diagnosed by the absence of other symptoms that are characteristic of other primary headaches.

TTH can pose significant difficulty for individuals attempting to re-enter the workforce or attempting to continue educational endeavors.

Treatment

Standard TTH treatment overlaps with migraine HA treatment [12]. See Table 19.2.

Diagnosing a PTH due to cervical musculoskeletal causes (cervicogenic headaches) can be complex given that the primary causes of these headaches can share patterns of referred pain. Derangements of cervical joint surfaces, inflammation of nervous structures, or strain of the neck musculature can often mimic each other, which thereby mandates proper diagnosis. The prevalence lies between 0.4 and 2.5% in the general population, but can be as high as 53% for patient who sustained whiplash injuries. [22]. Cervicogenic headaches include, but are not limited to, headaches from cervical facet joints. Depending on the location, myofascial trigger points also cause cervicogenic headache. See Table 19.3 for diagnostic criteria.

The mechanism with which facetogenic headaches refer pain is similar in concept to most causes of cervicogenic headaches. Cervical spinal afferent nerves (primarily A-delta and C fibers), traveling from cervical spine structures, converge on second-order neurons within the central nervous system, which also receive ascending afferents from other cervical and even trigeminal inputs, before ascending towards the thalamic pain centers [23]. In addition, sensory fibers from upper cervical roots interact with trigeminal nerve fibers near the trigeminocervical nucleus in the upper cervical spinal cord [24]. Thus, due to convergence, cervical spine pain stimuli can be referred to the occipital, auricular, frontoparietal, and orbital regions of the head. In cervical facetogenic pain, the most common joints affected are the C2/C3 and C3/C4 levels, and thus the spinal nerves involved are most commonly C2, C3, and C4. In the atlantoaxial region, the most common joint affected is the C1/2 joint.

For cervical joint-related cervicogenic pain , typically the pain is unilateral and starts in the neck, radiating cephalad to the oculo-frontal-temporal areas. Pain is usually described as a dull headache, non-throbbing in nature; however, it is often accompanied by sharp pain on cervical extension. Pain may be triggered by certain neck postures or movements and may also be elicited by external pressure and palpation to the upper neck region bilaterally over the palpable facet joints. Though there is pain on range of motion, it is questionable whether this represents actual range of motion limitations.

Cervicogenic headaches can pose significant difficulty for individuals attempting to re-enter the workforce or continue educational endeavors.

Initial

Conservatively, treatment for most types of cervicogenic headache include physical therapy, manual massage, modalities such as heat and transcutaneous electrical nerve stimulation (TENS), as well as medications such as anti-inflammatory agents. Generally, these conservative measures are initiated prior to more targeted interventional treatments.

Rehabilitation

Myofascial pain is usually a secondary diagnosis from a primary source, whether it be poor posture, repeated manual stress, or even facet joint arthritis. Typically, postural training and myofascial release can be initiated in physical therapy; however, there has not been strong evidence to support either.

Procedures

Diagnostic medial branch blocks for the corresponding zygapophyseal joint-related pain (i.e. C2–3 and C3–4 Zygapophyseal joints), which are blocked via the C2 and C4 medial branches and C3 and C4 medial branches respectively, can be conducted. Once a successful block is obtained (characterized by a significant decrease in pain relief over the course of the half life of the anesthetic used), one can continue further and perform radiofrequency ablation (RFA) of these particular medial branches.

Conservative treatments are not strongly supported in the literature, apart from manual massage therapy, which does show promise [23]. Current literature supports the use of diagnostic medial branch blocks for the corresponding zygapophyseal joint-related, as opposed to intra-articular zygapophyseal joint injections. A prospective controlled study looking at the efficacy of dry needling in 52 subjects with MPS found that the reduction in pain, which included a significant reduction found after dry needling, was positively correlated from the transition of an active trigger point to one that was latent or absent [25]. There was also a positive correlation with improvements in range of motion. Another study, this one randomized controlled, looking at 72 subjects pre- and post-dry needling also endorsed significant decreases in pain levels measured by the visual analogue scale and pain-pressure threshold [26].

Injuries to subcutaneous tissue and nerves are common following TBI, either as a direct result of traumatic injury or secondary to neurosurgical intervention. These injuries are an important cause of PTH and must be distinguished from other PTH etiologies. Neuroma formation may result following nerve trauma and can develop many years following craniotomy [27]. See Table 19.4 regarding the diagnosis of ON.