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Posttraumatic Headache
Introduction
Post-traumatic headaches (PTHA) are a common sequela of traumatic brain injury (TBI) and may progress to chronic and possibly debilitating conditions.[1] PTHA can be further subdivided into 2 general categories. Acute PTHA is attributed to TBI that resolves within 3 months, and persistent PTHA has not resolved within 3 months.[2] There are several potentially overlapping phenotypes of PTHA.
Etiology
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Etiology
According to the latest International Classification of Headache Disorders (ICHD-3), PTHAs are defined as a secondary headache with onset within 7 days following trauma or injury, within 7 days after recovering consciousness, or within 7 days after recovering the ability to sense and report pain.[2] However, this definition has been challenged recently, as some patients may report several months to 1 year after trauma or injury.[3] The temporal definitions provided by the ICHD-3 lack specific phenotypic diagnoses that would enable practitioners to treat and manage the various forms of PTHA.
Military
PTHA is a significant cause of debility in military personnel. Due to the immense physical and psychological toll compared to civilian trauma/injury, combat TBI and the subsequent sequelae warrant separate mention. There is a considerable increase in the overlap between PTHA and post-traumatic stress disorder (PTSD). Combat-related explosions are the most common causes of U.S. military personnel injury.[3]
Epidemiology
Headache is the most common physical complaint following TBI, with a prevalence ranging from 30% to 90%. Of those patients, 18% to 22% reported PTHAs after 1 year. The wide range of prevalence may be because the majority of TBI cases are defined as mild TBI (mTBI), ie, concussions, in which patients may not seek immediate medical attention. PTHA appears to be more frequent in patients recovering from mTBI than in those who experienced moderate to severe TBI.[3] However, patients with moderate to severe TBI may be more likely to report persistent chronic PTHA. PTHA is more frequent in females than males, with a ratio of 2 to 1. Evans et al reported that 45% of patients with a past medical history of headaches are more likely to report PTHA. Of the several subtypes of headaches classified by the ICHD, migraine-like and tension-type headaches were the most commonly reported.[4] An Australian study found that m TBI patients were 7 times more likely to report headaches after trauma than non-TBI trauma patients.[5]
Pathophysiology
The pathophysiology of PTHA is still unknown; however, several theories have been proposed to explain its underlying cause. These include impaired descending modulation, neurometabolic changes, and activation of the trigeminal sensory system.[2] PTHA likely involves overlapping, multifaceted processes.
Impaired Descending Modulation
This theory derives from the similarity between migraine and PTHA. A study by Schwedt et al showed structural differences in cortical thickness and cerebral volumes in PTHA patients and healthy controls.[6] TBI may result in diffuse axonal injury that may result in structural remodeling of cortical and subcortical regions in the somatosensory and the insular cortex, leading to impaired neuromodulation of descending pain-modulating pathways.[2]
Neurometabolic Changes
Research suggests that TBI produces changes in brain metabolic activity. Physical trauma leads to cellular injury, resulting in an unregulated ion-exchange neurotransmitter release. The increased neuronal activity results in metabolic stress (lactate and free radicals), leading to axonal damage (secondary axotomy).[2] Cortical spreading depression (CSD) is an electrophysiological process that occurs during migraine auras.[7] Recent studies have shown CSD contributes to secondary injury after TBI and, therefore, may play a role in PTHA.[8] Cellular depolarization in CSD causes excessive glutamate and potassium release, increasing neuronal excitability and activation of the trigeminal sensory system. Studies have shown that TBI patients release adenosine triphosphate (ATP), similar to CSD.[2]
Trigeminal Sensory System Activation
The trigeminal sensory system may also be affected by neuroinflammation—inflammatory processes in the brain increase after TBI. Neuroinflammation may also increase the central nervous system (CNS) excitability, resulting in CSD and subsequent activation of the trigeminal sensory system.[2] The trigeminal system can also undergo stimulation by nociceptive signals from upper cervical afferents due to overlap in their respective signaling tracts.[9][10] The convergence between cervical afferents and trigeminal nerve pathways supports the observation that treatments for cervical neck pain generators can help alleviate PTHA.
Other Theories
Additional possible contributions in PTHA include hyperadrenergic activity, activation of extracranial dural afferents, and meningeal irritation due to craniotomy.[1][2] Glymphatic pathway dysfunction also carries implications in PTHA.[11]
History and Physical
Patients should be evaluated and questioned about headaches after TBI, whether mild or moderate/severe. Per ICHD-3, PTHA should occur within 7 days of acute insult. Patients with PTHA lasting more than 3 months are considered to have persistent PTHA. PTHA does not have a specific phenotype, and TBI patients report symptoms similar to different primary and secondary headaches.[1] Military personnel with a history of combat involvement may report additional symptoms. PTHA is included in the constellation of symptoms known as post-concussive syndrome (PCS), which includes dizziness, fatigue, irritability, anxiety, insomnia, and decreased cognition.[3] PTHA and PCS may be further obfuscated in this population by the greater prevalence of PTSD than in the civilian population. Patients should be questioned about headache severity and associated symptoms during the patient encounter. The physical examination should include assessing the cervical range of motion, musculoskeletal palpation of the head and cervical neck, and neurologic status.
Evaluation
PTHA, like other primary headaches, is a clinical diagnosis. Routine diagnostic imaging and laboratory tests are unnecessary and offer little clinical value.[12] Patients with PTHA after TBI show no structural abnormalities on brain imaging.[13] Patients with a diagnosis of PTHA after TBI do not require additional imaging if they have had an appropriate workup for TBI. Patients with a history of TBI and new complaints of headaches require additional imaging to rule out other causes of headaches besides PTHA. Computed tomography (CT) of the head without contrast should be completed to rule out acute cerebral hemorrhage, especially in the elderly. Cerebral magnetic resonance imaging (MRI) should be ordered to rule out ischemic infarction and masses. Also, any acute change in neurologic status or sudden change in frequency and intensity of headache may warrant additional imaging to rule out other causes.[14][15]
Treatment / Management
Management and treatment for PTHA involve a multifaceted approach that may include oral medications, musculoskeletal manipulation and treatment, interventional procedures, and behavioral therapy. A review of non-pharmacologic therapy modalities and biopsychosocial factors concluded that a multi-disciplinary approach was most effective in PTHA management. The modalities reviewed included cognitive-behavioral therapy (CBT), biofeedback, progressive muscle relaxation therapy, acupuncture, and physical therapy.[16]
The pharmacologic management should be tailored to the specific PTHA phenotype if known. Several studies have investigated the role of oral and IV medication for acute and preventative treatments. Acute treatment modalities included oral and intravenous (IV) non-steroidal anti-inflammatories (NSAIDs), triptans, and IV antiemetic medication. Preventative regimens included tricyclic antidepressants (TCAs), anticonvulsants, and gabapentin. Among TCAs, amitriptyline showed benefits in most patients; however, Cushman et al showed that patients receiving gabapentin or amitriptyline showed similar improvements compared to the non-treatment group.[17](A1)
Several interventional procedures have been trialed for PTHA; however, the research lacks controlled trials. A retrospective review of 717 patients showed reduced headache severity and frequency at 6 months.[18] Sporadic case reports have reported benefits with ultrasound-guided nerve blocks to the greater occipital nerve (GON), supraorbital nerve (SON), and lesser occipital nerve (LON).[19] Below is a summary of preferred methods to treat PTHA based on its primary headache subtype.
Tension-type (TTHA)
The preferred treatment for acute episodic tension-like PTHA is NSAIDs.[20] Trials have shown the efficacy of the non-selective COX-2 inhibitor lumiracoxib in treating acute episodic tension-type headaches (ETTHA).[21] TCAs (most notably amitriptyline and nortriptyline) have been the first-line modality of choice in the prophylactic treatment of chronic tension-type headaches (CTTHA).[22] Mirtazapine has also shown promising results in reducing the frequency of TTH.[23] Butalbital-containing medications have shown benefit in refractory TTHA.[24] Triptan medications are ineffective in TTHA management.[25] Craniomandibular headaches are considered a subtype of tension-type headaches. Intraoral devices can manage headaches related to craniomandibular dysfunction.[26] Patients with headache refractory to intraoral device implants may benefit from botulinum toxin injection into the temporomandibular joint.[27](A1)
Migraine-type
Herbal and vitamin supplements have shown some benefits in managing migraine headaches. There is evidence that magnesium, feverfew, vitamin B2, CoQ10, and Petasites can help prevent migraine headaches.[28] Triptans are the mainstay treatment of acute migraines.[29] Other abortive treatments for migraine include acetaminophen, NSAIDs, butalbital-containing medications, ergot derivatives, and antiemetics.[30] Opioids are not recommended for acute migraine therapy.[31] Monoclonal antibodies to calcitonin gene-related peptides (CGRP-mAbs) were developed to prevent migraine headaches. Other prophylactic therapies include TCAs, the anticonvulsants topiramate and valproate, and beta-blockers.[32] Botulinum toxin injection is another treatment modality for the management of chronic migraines.[33](A1)
Neuralgias and Neuromas
Patients with neuralgias (occipital and cervical) typically do not respond to oral medication or botulinum toxin injections.[34][35] Steroid injections and radiofrequency ablations targeting the GON, SON, and LON have been efficacious.[36] Neuromas can be treated conservatively or surgically. Conservative treatments include opioids, antidepressants, and antispasmodics; however, gabapentin and pregabalin are the drugs of choice for initial treatment. Alternative interventions include transcutaneous magnetic stimulation, ethanol or steroid injections, and radiofrequency ablation. Surgical management includes neuroma resection with or without nerve stimulator implantation.[37](A1)
Cervicogenic-type (CHA)
Cervicogenic-type PTHA is typically refractory to oral pharmacological treatment like the neuralgia and neuroma phenotype.[34] Physiotherapy and manual manipulation of the cervical spine have demonstrated benefits.[38][39] Interventional procedures that have shown promising results in CHA management include occipital nerve blocks (GON and LON) and continuous radiofrequency ablation to the C2 and C3 dorsal root ganglions.[36][40] Linde M et al reported that botulinum toxin injections were not effective in treating cervicogenic headaches.[35](A1)
Differential Diagnosis
The differential diagnosis for PTHA can be categorized into non-emergent and emergent conditions.
Non-emergent Differential Diagnoses
- Tension headache
- Migraine headache
- Neuralgias/neuromas
- Cervicogenic headache
- Medication overuse
- Craniomandibular headache
Emergent Differential Diagnoses
Prognosis
In a study by Hoffman et al, 71% of patients reported headaches within the first year after moderate or severe TBI. 46% of patients reported headaches at initial evaluation, and 44% reported new or persistent headaches at 1-year follow-up.[43] A similar study reported that 91% of patients experienced headaches after mTBI. Furthermore, 54% reported headaches at initial evaluation, and 58% of patients reported headaches 1 year after injury.[44]
Complications
PTHA can be a considerable psychosocial deterrent for patients returning to their baseline activity before TBI. Up to 35% of PTHA patients do not return to work after 3 months.[2] Also, due to the possible chronicity of PTHA, patients are at an increased risk of developing opioid dependence.[1]
Postoperative and Rehabilitation Care
No formal rehabilitation guidelines exist for PTHA. Physical therapy is indicated for cervicogenic headaches.
Deterrence and Patient Education
Patients who have experienced traumatic brain injury should be educated on the potential for PTHA. While these headaches may be debilitating and possibly life-long, treatment options are available and include behavioral, pharmacological, and interventional. Furthermore, providers should reassure patients that PTHA is not life-threatening. While there is no concrete clinical presentation for PTHA, patients and the care team should be aware that PTHA may take characteristics of primary and other secondary headaches.
Pearls and Other Issues
The clinician should attempt to identify the primary phenotype or nociceptive driver for the headache since not all PTHAs are the same. Future research in the treatment of PTHA should investigate the efficacy of cervical trigger point injections and sphenopalatine nerve blocks. These therapies are currently being investigated for migraine headaches.[19]
Enhancing Healthcare Team Outcomes
PTHA requires an interprofessional team involving the patient, clinicians, pharmacists, and therapists. Providers must identify, evaluate, and manage PTHA as it can be debilitating and significantly affect the patient's quality of life after injury. While the IHS has attempted to classify PTHA based on chronology (acute versus persistent) and type of injury (mild vs. moderate/severe), there is a need to subdivide the various presentations of PTHA rather than simply by which characteristic primary headache fits the clinical presentation. Medical providers should seek to determine the primary headache phenotype and manage it accordingly. Additionally, patients with chronic PTHA should be assessed for medication-induced headaches that may arise due to the overuse of abortive headache therapy. The IHS acknowledges the lack of characteristic qualities in diagnosing PTHA, and more research is needed to assist providers in its overall management.[45]
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