Cervical Spinal Disorders and Headaches










9
D
isorders of the musculoskeletal structures of the cervical
spine can contribute to the development and perpetuation of
orofacial pain complaints and various headaches. Therefore,
the clinician should be able to distinguish different types of neck
pain, understand the mechanisms of concurrent cervical spinal pain
and orofacial pain, perform a screening evaluation of the cervical
spine, and initiate appropriate referral for further evaluation and com-
prehensive management when indicated.
Key Points
Structures of the cervical spine can give rise to orofacial
pain and headaches.
A screening examination of the cervical spine is recom-
mended if there is coexisting neck pain and temporoman-
dibular disorder (TMD) pain.
Specic and individualized interventions consisting of
exercises, manual techniques, postural correction, and a
home program can assist the clinician in effectively man-
aging cervical spinal disorders to reduce pain, restore
function, and prevent recurrence of complaints.
Referral is recommended when cervical spine involve-
ment is suspected in the development of orofacial pain
complaints.
Cervical Spinal
Disorders and
Headaches

209
activities.
2
One-year prevalence estimates
of neck pain range from 30% to 50% in the
general population, while 1-year incidence es-
timates of neck pain with associated disability
range from 2% to 14%.
2
The prevalence of
Box 9-1 Neck Pain Task Force
classication system for neck pain
2
Grade I Neck pain without
signs of pathology, low
disability
Likely to respond to
minimal intervention,
such as reassurance and
pain control
Does not require
intensive investigations or
ongoing treatment
Grade II Neck pain without
signs of pathology, high
disability
Requires pain relief and
early activation aimed
at preventing long-term
disability
Grade III Neck pain with neurologic
signs
Might require
investigation and,
occasionally, more
invasive treatments
Grade IV Neck pain with signs
of pathology, such
as fracture, infection,
myelopathy, neoplasm, or
systemic disease
Requires prompt
investigation and
treatment
Note: This chart provides an overview of the classication
system. For the full description, see the original report.
3
Epidemiology of CSDs
Dening Cervical Spine Disorders
Cervical spine disorders (CSDs) encompass a
wide variety of disorders involving the muscu-
loskeletal structures, discs, and nerves of the
cervical spine. The most common symptoms
of a CSD are neck pain and movement limi-
tations. Head movements or sustained head
postures usually aggravate the pain. Although
neck pain may be a feature of virtually every
disorder or disease of the upper quadrant, it is
only rarely a symptom of a serious pathology
such as tumors or infections. If there is neuro-
logic involvement, pain can radiate toward the
head, trunk, or upper limbs.
Subclassication of CSDs includes an ex-
tensive list of diagnostic terms, such as cer-
vicalgia, cervical sprain/strain, discogenic dis-
ease, and facet syndrome.
1
In the absence of
pathology or systemic disease, neck pain is
usually referred to as nonspecic. For the most
common types of neck pain, the Neck Pain
Task Force introduced a classication system
to facilitate communication among health care
professionals (Box 9-1).
2
This classication sys-
tem differs from earlier classication systems
for neck pain and lower back pain in that the
decision for further assessment and treatment
depends not only on the clinical signs but also
on the presence of disability.
4,5
This chapter presents common CSDs
that may be associated with orofacial pain
or headaches and provides questionnaires to
rate the level of disability related to neck pain.
Together, these tools will help the clinician to
assess whether the cervical spine is involved
in the patients’ orofacial pain complaints and
whether referral for additional assessments or
treatment is necessary.
Epidemiology of CSDs
Most people will experience some neck pain
in their lifetimes, but for the majority, neck
pain will not seriously interfere with daily

210
Cervical Spinal Disorders and Headaches
9
neck pain increases with age up to the fth
decade and then decreases, and it is higher
among women than men.
2,6
Between 50%
and 85% of those who experience neck pain
at one point will report neck pain again 1 to
5 years later.
7–9
Psychologic stress, prolonged
forward head posture, and repetitive cervical
movements increase the risk for develop-
ing neck pain.
10–12
The inuence of repetitive
movements and sustained head positions is
reected in the high prevalence of neck pain in
specic populations, such as dentists, profes-
sional drivers, and adolescents with prolonged
computer use.
1316
Relationship Between CSDs and
Orofacial Pain
Many studies have reported the coexistence
of TMDs and CSD symptoms.
17–21
In a large
study of the general Dutch population, com-
plaints of neck pain were twice as prevalent
in patients with TMD pain (71% to 85%) com-
pared with persons without TMD pain (39%).
22
A case-control study on adolescent TMD pa-
tients also revealed a prevalence for neck pain
over twice that in controls of the same age
and sex.
23
Both studies also found strong as-
sociations with headache, back pain, and more
widespread pain. In addition, a strong relation-
ship was found between neck disability and
jaw disability.
24
Several mechanisms have
been suggested to explain this coexistence of
TMD pain and neck pain, including sensitiza-
tion, biomechanics, and genetics. This com-
mon co-occurrence requires health care pro-
fessionals who manage orofacial pain to also
have knowledge of neck pain.
24
Peripheral and central sensitization
Sensitization of the nervous system occurs
when persistent nociceptive facilitation ex-
ceeds its inhibitory capacity. In this situation,
a spectrum of neuroplastic changes occurs,
such as lowered nerve thresholds, enlarged re-
ceptive elds, and changed gene expression.
Peripheral sensitization refers to the situation
of increased responsiveness and reduced
threshold of peripheral neurons.
25
Central sen-
sitization refers to the increased responsive-
ness of nociceptive neurons in the central ner-
vous system to their afferent input.
26
Patients
may have allodynia (experience of pain by
stimuli that normally would not be perceived
as painful) and hyperalgesia (exaggerated pain
responses to painful stimuli). For more details
on sensitization, see chapter 1.
Craniofacial pain is mediated by the upper
cervical nerves, the sinuvertebral nerves of
C1 to C3, and cranial nerves V, VII, IX, X, XI,
and XII. Additional innervation is provided by
sympathetic afferents that course with the
rst two thoracic nerves synapsing in the tri-
geminal nucleus, as well as parasympathetic
afferents traveling with cranial nerves VII and
IX.
27
Further reading is recommended on the
innervation of the head and neck region, and
anatomy books will also be helpful on this sub-
ject.
28,29
Convergence of afferents of the cer-
vical spinal nerves and the trigeminal nerve,
together with increased responsiveness of
the central nervous system, may explain the
frequent coexistence of neck pain and oro-
facial pain. These nerves carry afferent input
from various tissues of the head and neck
and meet in the trigeminal spinal nuclei.
27
Consequently, nociceptive input from cervi-
cal structures can be referred to the orofacial
region, and vice versa. Several experimental
studies have demonstrated this mechanism.
For example, Piovesan et al
30
showed that
after painful stimulation of the greater occipi-
tal nerve, the participants experienced pain not
only in the innervation area of that nerve but
also into the projection area of the trigeminal
nerve (ophthalmic division, V1 distribution). In
another study,
31
glutamate-evoked pain in the
splenius capitis muscle (innervated by C3 and

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9Disorders of the musculoskeletal structures of the cervical spine can contribute to the development and perpetuation of orofacial pain complaints and various headaches. Therefore, the clinician should be able to distinguish different types of neck pain, understand the mechanisms of concurrent cervical spinal pain and orofacial pain, perform a screening evaluation of the cervical spine, and initiate appropriate referral for further evaluation and com-prehensive management when indicated. Key Points◊ Structures of the cervical spine can give rise to orofacial pain and headaches. ◊ A screening examination of the cervical spine is recom-mended if there is coexisting neck pain and temporoman-dibular disorder (TMD) pain. ◊ Specic and individualized interventions consisting of exercises, manual techniques, postural correction, and a home program can assist the clinician in effectively man-aging cervical spinal disorders to reduce pain, restore function, and prevent recurrence of complaints. ◊ Referral is recommended when cervical spine involve-ment is suspected in the development of orofacial pain complaints.Cervical Spinal Disorders and Headaches 209activities.2 One-year prevalence estimates of neck pain range from 30% to 50% in the general population, while 1-year incidence es-timates of neck pain with associated disability range from 2% to 14%.2 The prevalence of Box 9-1 Neck Pain Task Force classication system for neck pain2Grade I • Neck pain without signs of pathology, low disability• Likely to respond to minimal intervention, such as reassurance and pain control• Does not require intensive investigations or ongoing treatmentGrade II • Neck pain without signs of pathology, high disability • Requires pain relief and early activation aimed at preventing long-term disabilityGrade III • Neck pain with neurologic signs• Might require investigation and, occasionally, more invasive treatmentsGrade IV • Neck pain with signs of pathology, such as fracture, infection, myelopathy, neoplasm, or systemic disease• Requires prompt investigation and treatmentNote: This chart provides an overview of the classication system. For the full description, see the original report.3Epidemiology of CSDsDening Cervical Spine DisordersCervical spine disorders (CSDs) encompass a wide variety of disorders involving the muscu-loskeletal structures, discs, and nerves of the cervical spine. The most common symptoms of a CSD are neck pain and movement limi-tations. Head movements or sustained head postures usually aggravate the pain. Although neck pain may be a feature of virtually every disorder or disease of the upper quadrant, it is only rarely a symptom of a serious pathology such as tumors or infections. If there is neuro-logic involvement, pain can radiate toward the head, trunk, or upper limbs. Subclassication of CSDs includes an ex-tensive list of diagnostic terms, such as cer-vicalgia, cervical sprain/strain, discogenic dis-ease, and facet syndrome.1 In the absence of pathology or systemic disease, neck pain is usually referred to as nonspecic. For the most common types of neck pain, the Neck Pain Task Force introduced a classication system to facilitate communication among health care professionals (Box 9-1).2 This classication sys-tem differs from earlier classication systems for neck pain and lower back pain in that the decision for further assessment and treatment depends not only on the clinical signs but also on the presence of disability.4,5This chapter presents common CSDs that may be associated with orofacial pain or headaches and provides questionnaires to rate the level of disability related to neck pain. Together, these tools will help the clinician to assess whether the cervical spine is involved in the patients’ orofacial pain complaints and whether referral for additional assessments or treatment is necessary.Epidemiology of CSDsMost people will experience some neck pain in their lifetimes, but for the majority, neck pain will not seriously interfere with daily 210Cervical Spinal Disorders and Headaches9neck pain increases with age up to the fth decade and then decreases, and it is higher among women than men.2,6 Between 50% and 85% of those who experience neck pain at one point will report neck pain again 1 to 5 years later.7–9 Psychologic stress, prolonged forward head posture, and repetitive cervical movements increase the risk for develop-ing neck pain.10–12 The inuence of repetitive movements and sustained head positions is reected in the high prevalence of neck pain in specic populations, such as dentists, profes-sional drivers, and adolescents with prolonged computer use.13–16Relationship Between CSDs and Orofacial Pain Many studies have reported the coexistence of TMDs and CSD symptoms.17–21 In a large study of the general Dutch population, com-plaints of neck pain were twice as prevalent in patients with TMD pain (71% to 85%) com-pared with persons without TMD pain (39%).22 A case-control study on adolescent TMD pa-tients also revealed a prevalence for neck pain over twice that in controls of the same age and sex.23 Both studies also found strong as-sociations with headache, back pain, and more widespread pain. In addition, a strong relation-ship was found between neck disability and jaw disability.24 Several mechanisms have been suggested to explain this coexistence of TMD pain and neck pain, including sensitiza-tion, biomechanics, and genetics. This com-mon co-occurrence requires health care pro-fessionals who manage orofacial pain to also have knowledge of neck pain.24Peripheral and central sensitization Sensitization of the nervous system occurs when persistent nociceptive facilitation ex-ceeds its inhibitory capacity. In this situation, a spectrum of neuroplastic changes occurs, such as lowered nerve thresholds, enlarged re-ceptive elds, and changed gene expression. Peripheral sensitization refers to the situation of increased responsiveness and reduced threshold of peripheral neurons.25 Central sen-sitization refers to the increased responsive-ness of nociceptive neurons in the central ner-vous system to their afferent input.26 Patients may have allodynia (experience of pain by stimuli that normally would not be perceived as painful) and hyperalgesia (exaggerated pain responses to painful stimuli). For more details on sensitization, see chapter 1.Craniofacial pain is mediated by the upper cervical nerves, the sinuvertebral nerves of C1 to C3, and cranial nerves V, VII, IX, X, XI, and XII. Additional innervation is provided by sympathetic afferents that course with the rst two thoracic nerves synapsing in the tri-geminal nucleus, as well as parasympathetic afferents traveling with cranial nerves VII and IX.27 Further reading is recommended on the innervation of the head and neck region, and anatomy books will also be helpful on this sub-ject.28,29 Convergence of afferents of the cer-vical spinal nerves and the trigeminal nerve, together with increased responsiveness of the central nervous system, may explain the frequent coexistence of neck pain and oro-facial pain. These nerves carry afferent input from various tissues of the head and neck and meet in the trigeminal spinal nuclei.27 Consequently, nociceptive input from cervi-cal structures can be referred to the orofacial region, and vice versa. Several experimental studies have demonstrated this mechanism. For example, Piovesan et al30 showed that after painful stimulation of the greater occipi-tal nerve, the participants experienced pain not only in the innervation area of that nerve but also into the projection area of the trigeminal nerve (ophthalmic division, V1 distribution). In another study,31 glutamate-evoked pain in the splenius capitis muscle (innervated by C3 and 211Relationship Between CSDs and Orofacial PainC4) caused referral of pain to the temporal region. Even though glutamate injections into the masseter muscle (innervated by the man-dibular division of the trigeminal nerve, V3) did not result in referral of pain to the neck region in that particular study, other studies have pro-vided evidence for a bidirectional relationship in convergence of afferents from the trigemi-nal and upper cervical neural systems.32–35GeneticsFor both experimental pain and clinical pain, evidence for the contribution of genetic factors to individual differences in pain is evolving.36 For TMD pain, there is cumulating evidence for a genetic predisposition.37 In 2011, Maixner et al38 presented a model for the development of TMD pain that proposed that TMD pain is inuenced by psychologic distress and pain amplication (eg, allodynia, hyperalgesia, and central sensitization), which in turn are subject to genetic regulation and environmental input. The mechanisms contributing to pain ampli-cation are thought to relate to a decreased function in pain inhibition as well as increased function of pain-facilitating pathways. An ex-ample of such a pain inhibitory system is the serotonergic system. A newer study has been able to replicate earlier ndings that a polymorphic variant (ie, the CC genotype) of the 5-hydroxytryptamine receptor 2A (5-HTR2A) gene is more prevalent in TMD-pain patients than in controls.39 The serotonin re-ceptor is suggested to have antinociceptive effects. Lower serotoninergic activity (eg, by less active postsynaptic receptors) may there-fore lead to a decreased ability to stimulate the central descending analgesic system and result in higher levels of pain.40 Another can-didate gene for involvement in musculoskel-etal pain is the catechol-O-methyltransferase (COMT) gene. Variants of this gene are re-ported to be associated with bromyalgia, neck pain, and TMD pain.36,41–43Biomechanical relationshipThe cranium and the mandible both have mus-cular and ligament attachments to the cervical area, forming a functional system called the craniocervical mandibular system or stoma-tognathic system. Because of this close func-tional coupling, changes in the activity of the neck muscles and head position inuence the activity of the masticatory muscles and jaw function, and vice versa.44–47 When the man-dible is at rest, its position is determined by the viscoelasticity of the muscles and the pos-tural muscle tone acting on the mandible.44 With an upright head position, the relaxed mandible maintains a fairly constant distance from the maxilla of approximately 2 to 5 mm.48 When the head is held in a forward position, the condyles are pulled slightly downward dur-ing open-close movements.49 Jaw opening and closing movements, as during eating, are ac-companied by respective extension and exion of the head, and several neck muscles are co-activated during jaw clenching.46,47,50,51As a result of these synergistic relationships between the structures of the masticatory sys-tem and the neck and the coexistence of TMDs and CSDs, poor head posture (mostly a forward head posture) and overload of the cervical spinal musculature have been suggested as etiologic factors for TMDs.52,53 Clinical studies regarding such relationships, however, show contradictory results.54 Even though some au-thors have reported small differences in head posture between TMD patients and healthy controls, the clinical relevance of these differ-ences has been disputed, and other studies did not even nd differences in head posture between TMD patients and controls.24,55–57 So although there is vast evidence showing the functional coupling between the musculoskele-tal structures of the cervical spine and the mas-ticatory system, there is only weak evidence for a direct biomechanical mechanism (eg, the effect of poor head posture on the masticatory system) as a cause for TMDs.54,58 212Cervical Spinal Disorders and Headaches9ConclusionThe examples of sensitization, genetics, and biomechanical interplay between the struc-tures of the head and neck illustrate that CSDs may inuence pain in the orofacial region. Therefore, the cervical spine needs to be con-sidered in the assessment of patients with orofacial pain complaints.59 It is quite common for physical therapists to evaluate patients who present with cervical pain as well as craniofacial pain because of the comorbidity between the disorders.17–21,33,60 A clinical evalu-ation of the cervical spine and temporoman-dibular complex helps to determine whether the complaints originate from the neck, the masticatory region, or a combination of both. Screening of the Cervical SpineAs described in Box 9-1, the Task Force on Neck Pain introduced a four-grade classi-Box 9-2 Red ags for serious pathology in neck pain patients with no exposure to blunt trauma2• Pathologic fractures (eg, resulting from decreased bone density caused by osteoporosis or corticosteroid treatment)• Neoplasms (eg, previous history of cancer, unexplained weight loss)• Failure to improve after a month of evidence-based therapy• Cervical myelopathy• Systemic diseases (eg, inflammatory arthritis)• Infections• Intractable pain or tenderness over the vertebral body• Prior neck surgerycation system of neck pain severity. Be-cause few major differences were found be-tween trauma-related neck pain and neck pain with a nontraumatic etiology, the classication is recommended for all individuals who seek clinical care.2 To use the classication system, information is needed on serious pathology, disability, and signs of nerve compression. Serious pathologyFor patients without exposure to blunt trauma, the Task Force on Neck Pain suggests ruling out serious pathology based on existing recom-mendations for the lumbar spine (Box 9-2).2,61 The presence of such red ags should prompt the clinician to seek additional evaluation and care for such patients. Though a full discussion is beyond the scope of this chapter, the Cana-dian C-Spine and NEXUS protocols provide an overview of screening protocols for neck pain patients seeking emergency medical care, mostly following a trauma.62DisabilitySeveral reliable and valid self-assessment questionnaires are available to determine the level of disability in neck pain patients, includ-ing the Neck Disability Index63 and the Neck Bournemouth Questionnaire.64 Within this framework, the Graded Chronic Pain Scale (GCPS)65 is of special interest because it is a universal system that can be used for any pain condition (eg, neck pain, headache, or temporomandibular pain), it is easy to use, and it is the most commonly used system to rate disability in scientic publications on TMD patients. In this system, GCPS grades 3 and 4 represent patients with high disability. Ac-cording to the Task Force on Neck Pain, pa-tients experiencing such pain-related disability require further assessment and treatment to prevent long-term disability (see Box 9-1). 213Screening of the Cervical SpineSigns of nerve compressionNerve compression should be suspected in patients with neck pain that radiates to the arm (for a detailed description of this condi-tion, see Radiculopathy below). Neck pain from this origin is caused by an irritation of the cervical nerve root, mostly due to prolonged compression. In typical cases, the irradiating pain closely follows the area innervated by the affected nerve root. When nerve compression is suspected, a cluster of clinical provocation tests is recommended, such as the Spurling test, traction/neck distraction, Valsalva ma-neuver, and upper limb tension test.66 A sum-mary of the testing procedures is presented in Table 9-1. These diagnostic procedures have high predictive value when compared with gold standards of nerve conduction/mag-netic resonance imaging and myelography.2 The Spurling test, traction/neck distraction, and Valsalva maneuver have high specicity, so positive test results might be suggestive of nerve compression when they are consis-tent with the history and other physical nd-ings. The upper limb tension test, on the other hand, has high sensitivity, so a negative result is highly suggestive of the absence of nerve compression. In the absence of acute trauma and symp-toms of serious pathology, the use of diagnos-tic procedures such as routine imaging, anes-thetic facet or medial branch blocks, or surface electromyography for the diagnosis of nerve compression is not supported by the literature.2Additional diagnostic procedures for neck painThe clinical physical examination of the neck, like that for back pain, is generally better at ruling out a radiculopathy than at diagnosing other specic etiologic conditions for neck pain.2 Still, a screening clinical examination often includes a chronologic history (includ-ing past and current treatments, functional limitations, and successful pain modiers), assessment of the active and passive range of motion, palpation of the cervical spine and associated muscles, and dynamic and static resistance tests of the neck.68–70 Additional studies are needed for the validity of these Table 9-1 Testing procedures of manual provocation tests for cervical radiculopathy67Name DescriptionPositive test outcomeSpurling test The patient is seated. The neck is passively bent sideways toward the symptomatic side, and overpressure (approximately 7 kg) is applied to the patient’s head.* Symptom reproductionNeck distraction testThe patient is supine. The neck is passively exed to a position of comfort, and a gradual force of distraction (up to 14 kg) is applied to the patient’s head.*Symptom reduction or eliminationValsalva maneuverThe patient is seated and instructed to take a deep breath and hold it while attempting to exhale for 2 to 3 seconds. Symptom reproductionUpper limb tension test*The patient is supine. A sequence of movements is passively performed to elongate the median nerve: depression of the scapula, abduction and external rotation of the shoulder, extension of the elbow, supination of the forearm, and dorsiexion/extension of the wrist.Symptom reproduction*Note: Passive evaluation of the neck should not be attempted unless the clinician has had specic training in this technique. 214Cervical Spinal Disorders and Headaches9diagnostic procedures, but evidence is grow-ing, and they are widely used and considered to provide useful information for prognosis and management (eg, options for treatment or evaluation of outcome).69,71–73 It is recom-mended to cluster ndings of multiple tests because this increases the diagnostic value.74 It is beyond the scope of this chapter to describe a thorough examination of the cer-vical spine, but a short overview of the most common clinical tests for neck pain is provided in Table 9-2. If further evaluation of the cervi-cal region is indicated, patients should be re-ferred to an appropriately trained clinician (eg, a physical therapist with special training in the craniocervical region). Similar to other muscu-loskeletal disorders, such as TMDs and back pain, the nding of degenerative changes on imaging has not been shown to always be as-sociated with neck pain.2Common CSDsWhile it is important for the clinician to be aware of cervical etiologic factors that can contribute to the presence or perpetuation of orofacial pain, cervical disorders should not be managed in the dental setting. Orofacial pain patients with a CSD should be referred to a physical therapist with special training in the craniocervical region (eg, a physical therapist registered by the Physical Therapy Board of Craniofacial and Cervical Therapeu-tics [PTBCCT] or a cervical spine specialist) for thorough evaluation and treatment.75 The remainder of this chapter highlights some of the more common CSDs that can contribute to the experience of orofacial pain and headaches and includes their codes according to the In-ternational Classication of Headache Disor-ders, third edition (beta version) (ICHD) and The International Classication of Diseases, Tenth Edition (ICD-10). This overview should be considered a description of possible causes of neck pain, allowing pattern recognition but not claiming criteria for objective diagnoses. In most cases, the below-mentioned CSDs fulll the criteria for grade I or II of the Neck Pain Task Force classication system.2 Cervicalgia (ICD-10 M54.2)Cervicalgia is a broad term meaning pain in the neck and represents the most common neck pain complaints. Although the pain may origi-Table 9-2 Diagnostic procedures for the management of neck painName Description Positive test outcomeRange of motionActive and passive* range of motion is observed during exion, extension, rotation, and side bending head movements.Limited or irregular movements and/or reproduction of neck painPalpation Important cervical muscles or muscle groups to evaluate are the sternocleidomastoid, suboccipital, paravertebral (scalenes), posterior deep cervical, and upper trapezius muscles.Symptom reproductionResistance testsDynamic (head movements against a slight manual resistance) and static (strong manual resistance while no movement occurs) resistance tests are performed in the same directions as described by range of motion.Symptom reproduction (more dynamic than static pain is indicative of arthrogenous pain; more static than dynamic pain is indicative of myogenous pain)*Note: Passive evaluation of the neck should not be attempted unless the clinician has had specic training in this technique. 215Common CSDsnate from any cervical structure, discomfort is primarily felt in the suboccipital area and ster-nocleidomastoid (SCM) and upper trapezius muscles, with possible referral to the frontal, temporoparietal, occipital, vertex, and orbital regions. The Task Force on Neck Pain dened neck pain as symptoms “located in the ana-tomical region of the neck with or without ra-diation to the head, trunk, and upper limbs.”76 Treatment of cervicalgia includes conservative techniques such as cervical physical therapy. This consists of advice, mobilizations, and exercise, which are often combined. The evi-dence for the effectiveness of this multimodal approach in the short, intermediate, and long term is growing and has been translated into clinical practice guidelines.77–79Sprain and strain of cervical spine (ICD-10 S13.4)The most frequent traumatic spinal injury en-countered in medical practice is a sprain or strain of the cervical spine following a motor vehicle accident, also known as a exion/extension injury, acceleration-deceleration injury, and whiplash-associated disorder (WAD).80 Similar to cervicalgia, or common neck pain, WADs are usually graded as grade I and II. Neck symptoms without or with only minor interference with activities in daily life (ADL) would be considered grade I, and neck symptoms with substantial interference with ADL are grade II. Grade III is reserved for those patients with neurologic signs (radicu-lopathy), and grade IV for those with major structural pathology in the anterior, posterior, or lateral structures of the cervical spine, as well as parts of the shoulder girdle.80–85 The incidence of resultant neck pain and postural changes is signicant.80,82,84,85 Patients with a WAD have signicantly more signs and symp-toms of TMDs when compared with healthy controls, as well as compared with neck-pain patients without a traumatic onset of their complaints.86–90 However, when other physical pain complaints are accounted for, the higher prevalence of TMD pain is found to be merely part of a more general widespread pain disor-der in WAD patients.90 The onset of neck pain following acute trauma may occur immediately or with a delay of up to 2 days. It may occur as an ache or stiffness in the neck. Pain referral to sites dis-tant from the original injury is common, as is the presence of headache, dizziness, tinnitus, dysphagia, and visual disturbances.82,84,91,92 Most patients show recovery after a whiplash trauma in the rst 3 months. Thereafter, little improvement is seen. Because a large pro-portion of patients (even up to 50%) will not recover completely, WAD is a therapeutic chal-lenge.80,93,94 Prognostic indicators to assess the risk of poor recovery are high scores on the Neck Disability Index, age of 40 years or older, and signs of hyperarousal.93,95For grades I and II, treatment primarily con-sists of rest, relative immobilization (ie, act as usual but temporarily prevent extreme move-ments and exercises), and, when necessary, anti-inammatory drugs or muscle relaxants until the patient is pain free and has regained full mobility of the cervical spine. When re-covery is delayed (ie, complaints are still pres-ent after 3 to 6 weeks), referral for further therapy should be considered. Conservative treatments including active exercise, manual techniques, and physical therapy can be useful to reduce pain and increase cervical range of motion.96 If the complaints are still unresolved 6 to 12 weeks after onset, referral to a multi-disciplinary team is recommended.81In the past, cervical collars were frequently prescribed to immobilize the neck in WAD pa-tients. Several studies have evaluated the ad-ditional effect of soft collars on WAD patients and found that soft collars in combination with other interventions resulted in delayed recov-ery in terms of pain and range of motion.81 Therefore, the use of soft collars is no longer recommended to prevent inactivity of the cer-vical spine.81 216Cervical Spinal Disorders and Headaches9Cervical osteoarthritis (ICD-10 M47.8)With increasing age, degenerative changes can occur in the vertebral body, adjacent uncinate processes (joints of Luschka), posterior facet areas, and intervertebral discs.97,98 Degenera-tive changes include inammation of the joint linings with osteophyte formation, along with bony and cartilaginous exostoses. The most common regions of degenerative changes of the intervertebral disc are in the area of C5 to C6 and C6 to C7.99 Osteoarthritis (OA) of the synovial joints is more commonly found in the more mobile upper cervical segments.97OA is common in individuals over the age of 50 years. By the seventh decade of life, 75% of individuals display signs and symptoms of OA, and it is generally considered that 100% of individuals will develop signs and symptoms of OA during the course of a normal lifetime.98 As the elasticity of tissues decreases with age, there is a concomitant loss of range of motion, the neck becomes less resilient, and muscle strength declines. Early subjective complaints of OA include occasional episodes of neck pain triggered by activity. These episodes often re-solve in a couple of days with little more than rest (ie, act as usual but temporarily prevent extreme movements and exercises). More advanced symptoms include stiffness, limita-tion of movements, crepitus, and chronic neck pain. Progressive degeneration can lead to nar-rowing of the intervertebral spaces and may result in radiculopathy. However, no associa-tion between degenerative changes on imag-ing and neck pain has been found, indicating that degenerative changes without pain and vice versa are common ndings.2Mild and moderate stages of cervical OA will normally respond to comprehensive physical therapy management, including mobilization, exercise, and transcutaneous electrical nerve stimulation, with or without medication.100,101 However, once osteoarthritic changes have reached the point of neural compression and radiculopathy (grade III or IV of the Task Force on Neck Pain), remission of symptoms is more difcult and the patient should be referred to a medical specialist (eg, a neurologist or an orthopedist). Radiculopathy (ICD-10 M54.1)Radiculopathy is a pain and/or sensorimotor decit syndrome caused by compression of a nerve root. The compression can occur as a result of disc herniation, spondylosis, instabil-ity, trauma, or—rarely—tumors. Patient com-plaints related to radiculopathy in the cervical region range from pain, numbness, and/or tingling in the upper extremity to electric-type pains or even weakness.102The cervical spinal nerves are named cor-responding to the vertebral body below the nerve.26 Radicular pain from the C2 nerve roots can manifest itself as eye and/or ear pain and headache.102 In addition, involvement of the C1 to C3 nerve roots may be accompanied by sub-occipital or occipital headaches, neck pain, or pain referred to the shoulder girdle region.70,102Radiculopathies are not managed by the dentist and should be referred to the proper health professional for evaluation and manage-ment. Further reading may include guidelines such as The Clinical Guideline for the Diagno-sis and Treatment of Cervical Radiculopathy from Degenerative Disorders.103If space-occupying lesions or malignant processes have been ruled out as the source of the pain, comprehensive noninvasive treat-ment may include physical therapy. There is widespread indication that prolonged use of a cervical collar leads to deconditioning of the neck musculature and tissue damage; hence, such use should be avoided.102 Active inter-ventions with education, instructions in proper postural techniques, and therapeutic exercises are more favored in the literature.104,105 217Common CSDsCervical dystonia (ICD-10 G24.3)Cervical dystonia, or spasmodic torticollis, is a condition characterized by sustained contrac-tions of the neck muscles and sometimes the shoulder muscles.106 The head is typically tilted laterally, bending toward the affected muscle and rotated toward the opposite side. It may be spasmodic (clonic) or permanent (tonic). Bilateral SCM involvement will yield the head in an extended position (retrocollis) and is often associated with dysphagia and vocal disturbances.107 It can be a primary (idiopathic) or secondary condition. Secondary cervical dystonias can be a consequence of disease processes (eg, Wilson disease), or they may be linked to the use of medications (eg, neu-roleptics) or excessive toxin introduction into the body (eg, carbon monoxide poisoning).107 Structural lesions, primarily of the basal ganglia, such as trauma or vascular insults, can also be a cause.107 Cervical dystonia is one of the most common forms of focal dystonia, occurring in approximately 5 per 100,000 individuals in the general population.108 A recent meta-analysis revealed no signicant differences between men and women, with a prevalence of 6.5 per 100,000 in women and 5.0 per 100,000 in men.108 Cervical dystonias usually develop from age 45 years (ie, late-onset).107 Although pain is not the dominant complaint of patients with other types of dystonia, cervical dysto-nia is an exception, with 75% of the patients reporting neck pain.107 The usual treatment for torticollis is botulinum toxin injection.109 Usually, these injections need to be readmin-istered every couple of months. A relatively common side effect of botulinum injections is dysphagia (problems with swallowing). Bilat-eral SCM injections are more often associated with dysphagia. It is usually mild (severe in less than 5% of cases) and disappears gradu-ally after 2 to 3 weeks.109 Studies as to the ad-ditional effects of behavioral interventions in cervical dystonia are scarce and usually of low methodologic quality. The limited data indicate, however, that behavioral therapies including cognitive behavioral and relaxation exercises could have a benecial effect for enabling indi-viduals to manage their dystonia.109Occipital neuralgia (ICHD 13.4; ICD-10 G52.8)Occipital neuralgia is a primary headache dis-order characterized by paroxysms of sharp, shooting occipital pain that last for seconds to minutes. The pain is associated with dyses-thesia and/or allodynia in the area and tender-ness over the affected nerve branches.110 The pathogenesis is unknown, and most cases are considered idiopathic. In some cases, head trauma or nerve entrapment has been sug-gested as a cause of occipital neuralgia.111 The differential diagnosis includes migraine, cluster headache, hemicrania continua, tension-type headache, and temporal arteritis involving the occipital artery.111 Occipital referral of pain from the atlantoaxial or upper zygapophyseal joints, resulting in cervicogenic headache, should also be considered in the differential diagno-sis, as should neoplasms or other destructive lesions affecting the spine or occiput.111,112 Initial conservative treatment including physical therapy directed at alleviating second-ary muscle tension and improving posture is often an effective approach.112 Low-dose an-tiepileptic drugs and tricyclic antidepressants may reduce acute pain, while refractory cases may respond to pulse radiofrequency or occipi-tal nerve stimulation.111Head or facial pain attributed to inammation of the stylohyoid ligament (ICHD 11.8)This type of head or facial pain, previously called Eagle syndrome, is a rare condition that is caused by inammation of the stylohyoid ligament.113 The pain is generally perceived in the oropharynx, neck, and/or face, but some 218Cervical Spinal Disorders and Headaches9patients experience a more diffuse headache. This type of headache is usually unilateral, with neck, pharyngeal, and/or facial pain that is pro-voked by turning the head. Examination should include palpation of the stylohyoid ligament and/or provocation tests, such as turning the head in ipsilateral as well as contralateral direc-tions. Radiographic examination will reveal an elongated or calcied stylohyoid process and/or stylohyoid ligament.114 Pain is signicantly improved by local injection of local anesthetics or by styloidectomy.113 Treatment may consist of pharmacologic management with analge-sics or anti-inammatory agents and/or surgi-cal excision via either an intraoral or extraoral approach.115–117Cervicogenic headache (ICHD 11.2.1; ICD-10 G44.841)Cervicogenic headache is described as a “headache which is caused by a disorder of the cervical spine and its component bony, disc and/or soft tissue elements, usually but not invariably accompanied by neck pain.”110 To classify this type of headache, there should be evidence of a cervical disorder or lesion with a known ability to cause headache. In ad-dition, at least three of the following criteria should be present: (1) headache has devel-oped in temporal relation to the onset of the cervical disorder or lesion, (2) headache has signicantly improved or resolved in paral-lel with improvement in or resolution of the cervical disorder or lesion, (3) cervical range of motion is reduced and headache is made signicantly worse by provocative maneu-vers, and (4) headache is abolished following diagnostic blockade of a cervical structure or its nerve supply.110 Features that tend to dis-tinguish this type of headache from migraine and tension-type headache (while not unique for cervicogenic headache) include side-locked pain, provocation of the typical headache by digital pressure on neck muscles and by head movement, and posterior-to-anterior radiation of pain.110 ,118 It should be noted that the coex-istence of headache and neck pain does not automatically imply a causal relationship. Ma-nipulative therapy and exercise can reduce the symptoms of cervicogenic headache.119In the ICHD, the condition formerly known as neck-tongue syndrome is now encom-passed by the less specic diagnosis of cervi-cogenic headache.110,120 The understanding of the neck-tongue syndrome pathology involving C2 nerve root entrapment by subluxation of the atlantoaxial joint is better accounted for by cervicogenic headache than by its previ-ous classication as a cranial neuralgia. It is a rare disorder characterized by abrupt unilat-eral pain in the neck or occiput with associ-ated abnormal sensation involving the ipsilat-eral tongue and precipitated by sudden neck movements.120 It has a duration of seconds to minutes.120 The proposed mechanism for neck-tongue syndrome involves subluxation of the atlantoaxial joint, producing neck pain and irritation of the C2 nerve.121 In the absence of pathologic ndings, the disorder appears be-nign, and it is treated conservatively. 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