Assessment and management of cervicogenic headaches post traumatic injury

Definition description[edit | edit source]

Figure 1 - Areas effected by cervogenic headache [1]

A cervicogenic headache (CGH) is a chronic headache that presents as unilateral pain starting at the neck and is perceived in one or more regions of the head/face [2] (see more about cervicogenic headaches here).

A common cause of CGH is trauma that has led to dysfunction of the neck. Types of trauma that can cause CGH most commonly include: whiplash caused by car accident, contact sport injuries causing neck injury, and falls leading to upper cervical structural damage. [3]  

Mechanisms of injury caused by these types of trauma may include structural damage, development of myofascial pain and interaction of the trigeminal nociceptive system with the occipital nerves. There are also emotional and psychological factors to consider post-trauma which can impact rehabilitation and healing outcomes. [4]                                                                                                                                       

Epidemiology [2][edit | edit source]

Studies focused solely on CGH post trauma is limited. Current research states:

  • Prevalent in 30 to 44 year-olds
  • Accounts for 1-4% of headaches
  • Equally prevalent between males and females
  • Onset is said to be early 30s and diagnosis is 49.4 years-old (due to seeking medical attention late)
  • Compared to other headache patients, CGH have pericranial muscle tenderness on the painful side

Relevant anatomy[edit | edit source]

The cervical spine is made up of 7 vertebrae (C1 to C7), cranial nerves (C1 to C8), muscles and ligaments (see cervical anatomy). Trauma to any of these structures may cause an CGH. [3]

Joints [5][edit | edit source]
Figure 2 - Upper cervical spine [6]
  • C1 (atlas) supports the skull and articulates superiorly with the occiput to form the atlanto-occipital joint. This allows for 33% of flexion and extension at the C-spine
  • C2 (axis) articulates with the atlas to form the atlantoaxial joint. Its main function is to provide 60% of cervical rotation
  • C3-C7 are similar to one another and make up the rest of the movement in the C-spine                                                                                                                                                                                             
Muscles innervated by C1-C3 [5][edit | edit source]
Figure 3 - Muscles innervated by cervical spine [7]
  • Rectus capitis and lateralis
  • Longus capitis
  • Prevertebral muscle
  • Sternocleidomastoid
  • Levator scapulae
  • Upper trapezius
  • Scalenus Medius
Ligaments (C1-C3) [5][edit | edit source]
Figure 4 - Ligaments of the Cervical spine [8]
  • Apical
  • Alar
  • Cruciform
  • Anterior/posterior longitudinal
  • Ligamentum flavum
  • Interspinous
  • Nuchal
  • Transverse
Trigeminocervical nucleus [9][edit | edit source]
Figure 5 - Trigeminocervical nucleus [10]
  • Located at the lower brainstem near the upper cervical spine
  • Vertical cluster of cell bodies in the medullary region  
  • Within this area a convergence of the trigeminal sensory nerves and the C1 - C3 spinal nerves occurs
  • Sensory nerve fibers in the descending tract of the trigeminal nerve are believed to interact with sensory fibres from the upper cervical roots
  • Converged information then passed on to the somatosensory cortex

 

Aetiology [11][edit | edit source]

A CGH is believed to be pain referring from dysfunction of cervical structures innervated by cervical nerves C1, C2 and C3. Meaning, trauma causing damage to joints, intervertebral discs, ligaments and muscles can all be a source of a CGH. There is limited evidence to suggest that the lower cervical spine plays a role in referred pain causing a CGH.

The most common cause of CGH have been attributed to whiplash injury. It is believed that this type of injury accounts for up to 53% of all CGH, with 15.2% of patients having a headache lasting longer 42 days and 4.6% developing chronic daily headaches. Research also suggests that around 50% of CGH originate from the C2-C3 zygapophysial joint. [12]

Pathophysiology [13][edit | edit source]

Activation of the trigeminal nerve and its connections are well established in regards to headaches. In terms of post-traumatic CGH, activation occurs from disruption of structures innervated by spinal nerves C1-C3.

Figure 6 - Overview of sensory route that causes CGH [14]

Efferent innervation converges onto the second order neuron at the dorsal horn of C1/C2. At the same time, the trigeminal nerve will send sensory information from the face. The trigeminal nerve converges in the second order neuron in the at the same spinal segment as C1/C2. This sensory information will be sent to the trigeminocervical nucleus within the brain stem. When afferent nociception stimulus from the upper cervical structures travel to the trigeminocervical nucleus, the information sent to the somatosensory cortex becomes corrupt. This is due to the higher number of nociceptive efferent nerves in the face compared to the upper cervical spine. The convergence within the trigeminocervical nucleus means the brain will process this as an error, as it will assume the pain originates from the area with the higher area of nociceptive innervation. As a result, pain originating from the upper C-spine will be referred to the head and present as a CGH. Lower pain thresholds caused by emotional changes and aseptic inflammation can increase CGH pain levels further. [2]

The Biopsychosocial model[edit | edit source]

The biopsychosocial model, developed by George Engel in 1977 displays the complex relationship between biological, psychological, and social factors and the impact which it has on a patient's pain experience. It guides clinicians to develop a holistic approach to patient care, recognising that factors beyond biological changes alone may cause patients to feel pain, and highlights the importance of a detailed biopsychosocial assessment before treating this condition. [15]

Biological factors[edit | edit source]

Post traumatic head injury may cause cervicogenic headaches (CGH) and they are often a common complication [16]. As mentioned above, structural damage, development of myofascial pain, and interaction of the trigeminal nociceptive system with the occipital nerves fall under the biological factors relating to this condition. It is vital when assessing and managing patients with CGH that we investigate the biological causes through thorough subjective and objective testing.

Psychological factors[edit | edit source]

Traumatic brain injuries can be particularly emotionally traumatic. Post-traumatic stress disorder is described as re-experiencing symptoms, avoidance behaviour, and alterations in cognition and mood resulting from traumatic events. Although the mechanism of the association remains unclear, it is thought that TBI damages neural circuits which regulate fear responses, potentially explaining the heightened paranoia or stress [17]. Patients who have mild TBI are more likely to suffer from psychological symptoms and headaches compared with severe TBI (involving a loss of consciousness), suggesting a link between memory of trauma and headaches.

Some patients who have had a mild TBI misinterpret the clinical advice about their injury which often leads to catastrophising and fear avoidance [18]. Catastrophising, fear-avoidance, and depressive symptoms positively correlate with post-TBI symptoms, therefore during the treatment of patients that display these psychological symptoms – more emphasis on advice and education around pain is necessary. [19]

Patients with cervicogenic headaches often show lower spinal postural variability. When intrinsic variables such as stress and anxiety are higher, evidence suggests that this decreases the postural variability of the upper cervical spine, therefore putting emphasis on the effect that psychological symptoms have on cervicogenic headache symptom severity. [20]

Social factors[edit | edit source]

The social impacts of CGH are problematic, below are the possible social impacts of CGH: [21]

  • Work absenteeism
  • Decreased productivity
  • Decreased ability to complete activities of daily living
  • Reduced leisure time
  • Personal relationships

Social commitments are the fundamental elements of a patient's quality of life; with the inability to contribute to what a patient values, comes detrimental effects psychologically, and as mentioned, this can alter the patient's pain experience. Person-centered assessment and management of CGH is vital to aid return to what they value and care for.

Clinical Presentation[edit | edit source]

  • Restricted ROM in the cervical spine [2]
  • Head pain with neck movement or awkward head positioning [22]
  • Tenderness of the upper cervical or occipital region[23]
  • Varying duration of episodes [22]
  • Fluctuating, continuous pain [22]
  • Pain is unilateral without sideshift [2]
  • Moderate to severe pain, not excruciating [2]
  • Weakness in the deep neck flexors[3]
  • Potential neck, shoulder or arm pain ipsilaterally [22]
  • Confirmatory evidence by diagnostic anaesthetic blockades [22]
  • Less likely to present with autonomic symptoms, however still may be present E.g. vomiting, nausea, photophobia or phonophobia [2] [22]

Red Flags[edit | edit source]

Screening for red flags is crucial when assessing patients who have a cervical injury following trauma. It is important to identify and rule out serious pathology.

Red flags for headaches post trauma that will require further investigation: [24]

  • New severe or unexpected headache
  • Progressive or persistent headache, or headache that has changed dramatically
  • Comorbidities such as current or past malignancy
  • Current or recent pregnancy

Associated features such as:

  • Fever, impaired consciousness, seizure, neck pain/stiffness, or photophobia
  • New focal neurological deficit, cognitive impairment, and/or altered consciousness, personality change
  • Atypical aura (duration >60 mins, motor weakness involvement, diplopia, one sided visual symptoms, or decreased balance)
  • Papilloedema
  • Dizziness
  • Visual disturbance
  • Vomiting

These may be indicative of CNS infection, malignancy, intercranial pathologies such as subdural haematoma, stroke or vascular pathologies such as giant cell arteritis. [25]

Differential Diagnosis[edit | edit source]

Post-traumatic headaches can present with similarities of symptoms indicative of primary and secondary type headaches so it is important to differentiate between these. See headaches and cervicogenic headaches.

Figure 7 - Types of primary headache [26]

Examination[edit | edit source]

A comprehensive assessment needs to be undertaken when a patient presents with neck pain and headache post trauma. This will include a full subjective and objective assessment of the cervical spine. See Cervical Examination.

Subjective Assessment[edit | edit source]

It is important to rule out serious pathology and red flags for patients who have had trauma to the neck. In order to do this, a thorough subjective history should be taken.

To get a detailed subjective history the patient should be asked about the trauma in more detail. For example:

  • History of trauma (onset, previous trauma etc)
  • Mechanism of the injury caused by the trauma
  • Change in symptoms since trauma occurred (i.e., new or worsening symptoms)

To rule out cervical fracture you would complete the Canadian C-Spine Rule.

Further questions should be asked regarding the headache as these will help with diagnosing the headache as cervicogenic in comparison to other headaches [25]

  • History of headaches
  • Intensity of headache
  • Headache frequency
  • Duration of headaches
  • Irritability levels

Objective Assessment[edit | edit source]

Trauma to the neck may cause damage to the cranial nerves. A neurological assessment may be completed if the patient presents with paraesthesia. A cranial nerve assessment may be completed as part of the comprehensive assessment if patients present with neurological symptoms in the face and neck and alterations in sensory and motor function. See Cranial Nerves.

Once serious pathologies have been ruled out, physical examination for cervicogenic headaches post-trauma should assess your usual objective assessment with a focus on neck ROM and strength, Passive accessory intervertebral movements (PAIVMs) tests and the cervical flexion-rotation test.

PAIVMs C1–C3 showed moderate to substantial reliability with Kappa values ranging from 0.53-0.72. The diagnostic accuracy was evaluated showing ranged sensitivity and specificity values of 59-65% and 78-87%, respectively, and positive and negative likelihood ratios from 2.9 to 4.9 and 0.43 to 0.49, respectively [27]

Cervical flexion-rotation test:

In supine position passively maximally flex the cervical spine and passively rotate left and right. Reported range of motion is determined by onset of pain or firm resistance encountered by therapist. The therapist should visually estimate the rotation range of motion. A visually estimated range reduced by 10° or more from normal range of 44° in indicative of a positive test. [28]

The cervical flexion-rotation test had excellent reliability when testing left and right movements (ICC = 0.97; 95%CI = 0.94, 0.99) and (ICC = 0.95; 95%CI = 0.90, 0.98), respectively. The diagnostic accuracy was evaluated and demonstrated a sensitivity and specificity range of 70-91.3% and 70-92%, respectively. Also, high positive likelihood ratios (2.33-10.65) and low positive likelihood ratios (0.095-0.43). [27]

Reduced range of rotation during the flexion-rotation test (mean change 17.67 [95%CI 13.69, 21.65]) and reduced neck flexion strength (mean change 23.81 [95%CI 8.78, 38.85]) in cervicogenic headache patients when compared to migraine patients. [29]

Vestibular and Oculomotor System:

A patient may present with vestibular and oculomotor dysfunction related symptoms following mild traumatic brain injury such as concussion. These symptoms may include:[30]

  • Dizziness
  • Nausea
  • Movement related blurry vision
  • Headache
  • Brain fog
  • Unsteadiness
  • Fatigue and eyestrain

This may warrant an examination using the Vestibular Ocular Motor Screening (VOMS) Tool to measure the extent of symptoms against tests including smooth pursuits, horizontal and vertical saccades, convergence, horizontal and vertical VOR and visual motion sensitivity. See VOMS Assessment for further detail.

Other tests for concussion can be found here.

Outcome Measures[edit | edit source]

  • Numerical Pain Rating Scale (NPRS)
    • In cervicogenic headache, NPRS showed moderate reliability (ICC = 0.72; [95 % CI: 0.08–0.90])[31]

Both NDI and NRS Demonstrates good construct validity at 1 week, 4 weeks and 3 months (p=0.0001) in cervicogenic headache [31]

Management: A multi-disciplinary approach  [edit | edit source]

Figure 8: Biopsychosocial Management of post-traumatic CGHs

The evidence suggests a multi- disciplinary biopsychosocial model in order to effectively treat and manage post-traumatic cervicogenic headaches [32] Post-traumatic cervicogenic headaches are multi-dimensional and often part of the larger persistent post-traumatic symptom picture.  

Mental Health[edit | edit source]

Clinical psychologists and neuro psychologically are key members of the multidisciplinary team when treating post traumatic cervicogenic headaches. Symptoms of anxiety and depression are tragically common post traumatic injuries [32] This is vital to consider when planning a treatment model for a patient post-traumatic injury to the head and/or neck. Depression and anxiety have been proven to continue to increase negative symptoms and worsened prognosis in headache disorders. Mental health challenges paired with ongoing pain are linked with poor sleep quality, deficient nutrient, decreased exercises, pain catastrophising post trauma, emotional distress and post-traumatic stress disorder are linked with persistent post-traumatic cervicogenic symptoms [33]  

Figure 9 : Consideration of Mental Health

In alignment with a holistic management approach, cognitive behavioural therapy has been suggested to aid with post-traumatic cervicogenic symptoms and the burden it carries. A journal from Brain Injury, by Gurr & Coetzer explore the effectiveness of CBT for post traumatic headaches. This study hones into the importance of psychological factors presenting as  highly influential in increasing or decreasing pain. [34] In this study, Forty-five participants attended the Brain Injury Service for initial three weekly relaxation group sessions. Following this, participants received 6 fortnightly 30 minute individual therapy sessions with one follow up. Interventions included: progressive muscle relaxation combined with imager, psycho-education, cognitive-behavioural strategies, life management, maintenance and relapse prevention. The findings present with over half participants of the brain therapy programme reporting significant decrease oh headache symptoms and disability of function, as well as intensity, frequency per month and pain levels. Although the inclusion criteria does not specify cervicogenic headaches within the population’s diagnosis, the mechanism of injury of a cervicogenic headache discussed is synonymous with post-traumatic headache: a new onset of head and neck pain following a traumatic injury (road traffic accident, sporting injury, fall). [34]

Graded Exposure to Exercise[edit | edit source]

Figure 10: Return to exercise

Sport-related conclusion is defined as a mild traumatic brain injury caused by direct force to the head causing a degree of functional impairments. Cervicogenic headaches are a secondary type of headache and can occur in response to a sporting injury to the head. Prevalence of post-concussion symptoms has been reported in previous studies with 90-92.2% of athletes experiencing headaches, 90% experiencing neck pain, and 68.9% experiencing dizziness.  [35]A 2021 journal from Sports Health clinically reviews the effect of exercise for persistent post-concussive symptoms [36]A majority of studies show that spontaneous physical activity is safe after SRC and that sub-symptom threshold aerobic exercise safely speeds up recovery after SRC and reduces symptoms in those with PPCS. [36]Exercise tolerance can safely be assessed using graded exertion test protocols within days of injury, and the degree of early exercise tolerance has diagnostic and prognostic value. It is key to note clinicians must provide patients with specific instructions regarding acceptable activity levels post head and neck injury as intense physical and cognitive activity can exacerbate symptoms. A method to monitor exercise tolerance is for concussed patients to calculate their age-appropriate maximum heart rate using the Karvonen equation (maximum heart rate HRmax = 220 – age in years) and begin exercising at 50% of their maximum using a consumer-approved heart rate monitoring device.(13) Patients should aim to exercise without symptomatic experiences (sweating, heavy breathing, panting, etc.) Graded exposure to walking, stationary cycling, swimming are recommended for the optimal graded return to aerobic exercise [37]

Moreover, further evidence supports aerobic exercise to aid with diminishing the burden of a cervicogenic headache with the proposed mechanisms of upregulation of brain-derived neurotropic factor BDNF, improved neurovascular regulation and modulation of pain [37]

Pharmacological[edit | edit source]

Table 1: Pharmacological Treatments

Figure 10: A table to demonstrate pharmacological treatment options in the management of CGHs post trauma. Pharmacological treatment can be used as an adjunct to managing patients with CGHs post trauma. Patients should be referred on to the relevant medical professional with competencies in this area. Some examples of pharmacological treatments and their role can be seen in figure 10.
Pharmacological Treatment: Purpose:
Over the counter medication (i.e. NSAIDs) Pain relief; should not be started until after first 3 days due to the risk of delayed bleeding[38]
Peripheral nerve blocks To treat persistent post traumatic CGHs; decrease in afferent feedback to trigeminal nucleus caudalis, decreasing nociceptive transmission[39]
Botox injections Induces muscle relaxant, encouraging reduced tone and decreased response to nerve stimulation[40]
Trigger point injections Alleviate head and neck pain; most commonly injected into trapezius, sternocleidomastoid, temporalis and levator scapulae [41]
Triptan medications Treat migraines

Physiotherapy Management[edit | edit source]

Conflicting evidence remains for the efficacy of physiotherapy management post traumatic CGHs. In accordance with the biopsychosocial model of post traumatic CGH (figure 8), patient education with detailed explanation of the condition; support of normal movement; avoiding immobilisation; resumption of work and targeted physiotherapy have been suggested [42].  An update on the management of post traumatic headache concluded intense physiotherapy is not superior to standard therapy with simple patient education, hence cannot be recommended when considering cost-benefit ratios[42]. The managing injuries of neck trial (MINT) [43] investigated the effects of ‘standard treatment’, including  simple treatment of symptoms and brief information about the condition was compared to an active treatment and detailed information given in a Whiplash information booklet.  Patients were able to report back after 3 weeks if showing unsatisfactory symptom improvement and randomised into a group of 6 physical therapy sessions including manual therapy, soft tissue techniques, endurance training and behavioural techniques, or one physical therapy session with a refresh of advice. The groups showed no significant difference in the primary outcome, neck disability index (NDI).  

PROMSIE study [44]compared extensive physical therapy including tailored exercise programmes over 12 weeks (cervical spine exercises; posture re-education; sensorimotor exercise; manual therapy) to advice given in booklet form, with minimally assisted exercises in a 30-minute session. No treatment effect was observed after 12 weeks.  

Contradictory evidence shows patients randomised to additional manual therapy techniques (including temporomandibular region) experienced statistically significant decrease in headache intensity at 3 and 6 months when compared to usual care of just manual therapy for cervical spine region[45]. A further study with patients experiencing CGHs and cervical trigger points underwent manual therapy techniques or simulated manual therapy. The treatment group experienced increased cervical range of motion and greater reduction in headache intensity[46].  

To summarise, more conclusive evidence with larger sample sizes is required to make better judgement about the efficacy and significance of physical therapy interventions in the management of CGHs post trauma.  

Summary[edit | edit source]

Table 2: Summary of Treatments

The overall goal to treat patients with post-cervicogenic headaches is to decrease headache frequency, severity, duration or disability, and thereby improve quality of life. If the patient is not sleeping, unable to play the sport they love, is avoidant of their teammates and friends, and overall are not able to enjoy life, their headaches are frequently refractory to treatment. Moreover, the combination of pharmacotherapy, education, cognitive restructuring, aerobic reconditioning, physical therapy, management of sleep disturbance, and when appropriate, psychotherapy, self-regulated intervention (breathing and relaxation exercises) can appropriately target physiologic causes of post-traumatic headaches with renewed efficacy.  
Pharmacological: Non-Pharmacological:
Muscle relaxants (cervical spasms) Physiotherapy (upper back and neck)
Trigger Point Injections Accupuncture
Anti-epileptics (e.g. gabapentin, topiramate) Greater occipital neurolysis/ neuroectomy
Tricyclic Antidepressents (e.g. amitriptyline) Cognitive Behavioural Therapy
Serotonin-norepinephrine reuptake inhibitor (e.g. venlafaxine) Massage
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