Chapter 23. The Craniovertebral Region

The craniovertebral region is considered as a separate entity from the rest of the cervical spine because of its distinct embryology and anatomical structure. Kapandji2 notes that the occiput, atlas, and axis actually form a primary kyphotic curve and that this curve serves as a delineation between the craniovertebral region and the cervical spine proper.

Foramen Magnum

The general shape of the foramen magnum is oval, with the longer axis oriented in the sagittal plane (Fig. 23-1).3 The margin of the foramen is relatively smooth and serves as the most superior attachment for a variety of the ligaments of the vertebral column. The smaller anterior region of the foramen magnum is characterized by a pair of tubercles to which the alar ligaments attach. The posterior portion of the foramen magnum houses the brain stem–spinal cord junction.

Figure 23-1

Bony structures of the craniovertebral joints. A. The atlas (C 1). B. The axis.

On either side of the anterolateral aspect of the foramen magnum are two ovoid projections, called occipital condyles (Fig. 23-1). The long axis of these paired occipital condyles is situated in a posterolateral to anteromedial orientation. The occipital condyles articulate with the first cervical vertebra.

Atlas

The atlas is a ring-like structure that is formed by two lateral masses, which are interconnected by anterior and posterior arches (Fig. 23-1). The demarcation of the two regions is marked by a pair of tubercles to which the transverse ligament of the atlas attaches. Although the atlas has a smaller vertical dimension than any other cervical vertebrae, it is considerably wider. Because this vertebra does not have a spinous process, there is no bone posteriorly between the occipital bone and the spinous process of C2. This results in an increase in the potential for craniovertebral extension.

The superolateral aspect of each of the posterior arches has a transverse foramen to accommodate the vertebral artery (see Chap. 24). The articular surface of the inferior facet is circular and relatively flat and slopes inferiorly from medial to lateral. The upper articular facets of C1 are elongated from anterior to posterior, with the anterior ends closer together and more upwardly curved than their posterior counterparts.3 This arrangement results in much more extension than flexion being available at the articulation between the occipital condyles and the atlas—the occipitoatlantal (O-A) joint.4

O‐A Joint

The O-A joint represents the most superior zygapophyseal joint of the vertebral column and the only vertebral level that has an articulation characterized by a convex surface (occipital condyle) moving on a concave joint partner (articulating facet of the atlas).5

Axis

The axis serves as a transitional vertebra (Fig. 23-1), because it is the link between the cervical spine proper and the craniovertebral region.

The dimensions of the axis are significantly different from those of the atlas. The atlas is considerably wider than the axis, but because of the long spinous process, the axis extends much farther posteriorly and is the first palpable midline structure below the occiput.6 Like the atlas, the transverse process of the axis has a transverse foramen to allow passage of the vertebral artery (not shown).

A unique feature of the axis is the odontoid process, or dens (Fig. 23-2). The dens, which develops with age, extends superiorly from the body to just above the C1 vertebra, before tapering to a blunt point. Very dense, thick trabecular bone is present in the center of the tip of the dens, and the cortical bone at the anterior base of the body of C2 (where the anterior longitudinal ligament attaches) is uniformly thick.7 Hypodense bone, however, is present consistently beneath the odontoid process at the upper portion of the body of C2.8 This area of hypodense bone is susceptible to fracture. The anterior aspect of the dens has a hyaline cartilage-covered mid-line facet for articulation with the anterior tubercle of the atlas (the median atlantoaxial (A-A) joint). The posterior aspect of the dens usually is marked with a groove where the transverse ligament passes. The dens functions as a pivot for the upper cervical joints and as the center of rotation for the A-A joint. The most variable dimension of the axis is the dens angle in the sagittal plane, which can range from −2 degrees (leaning slightly anterior) to 42 degrees (leaning posterior).9 This extremely variable angle can make assessment of fracture reduction challenging.7

Figure 23-2

Ligamentous structures of the craniovertebral joints.

A‐A Joint

This is a relatively complex articulation, which consists of

two lateral zygapophyseal joints between the articular surfaces of the inferior articular processes of the atlas and the superior processes of the axis;
two medial joints: one between the anterior surface of the dens of the axis and the anterior surface of the atlas, and the other between the posterior surface of the dens and the anterior hyalinated surface of the transverse ligament6 (Fig. 23-2).

The relatively large superior articular facets of the axis (Fig. 23-2) lie lateral and anterior to the dens. These facets slope considerably downward from medial to lateral in line with the zygapophyseal facets of the mid-low cervical spine.10 As the lateral A-A joints function to convey the entire weight of the atlas and the head to lower structures, the lamina and pedicles of the axis are quite robust.11 The stout, moderately long spinous process serves as the uppermost attachment for muscles that are essentially lower cervical in nature and for muscles that act specifically on the craniovertebral joints.

One of the functions of the intervertebral disk (IVD) in the spine is to facilitate motion and provide stability. Thus, in the absence of an IVD in this region, the supporting soft tissues of the joints of the upper cervical spine must be lax to permit motion, while simultaneously being able to withstand great mechanical stresses.

Craniovertebral Ligaments

The craniovertebral region is noted for a variety of ligaments, some of which have been the focus of a number of clinical tests to determine their efficiency in preventing unwanted and potentially dangerous movements. The controlling structures for these segments, which must be considered together, are the

Capsule and accessory capsular ligaments. The lateral capsular ligaments (anterolateral O-A ligament) of the O-A joints are typical of synovial joint capsules. These ligaments run obliquely from the basiocciput to the transverse process of the atlas. By necessity, they are quite lax, to permit maximal motion, so they provide only moderate support to the joints during contralateral head rotation.
Apical ligament. The apical ligament of the dens extends from the apex of the dens to the anterior rim of the foramen magnum. The ligament is short and thick. It runs from the top of the dens to the basi-occiput and is thought to be a remnant of the notochord. The apical ligament appears to be only a moderate stabilizer against posterior translation of the dens relative to both the atlas and the occipital bone.11
Vertical and transverse bands of the cruciform ligament. (See Fig. 23-2 and later discussion.)
Alar and accessory alar ligaments. (See Fig. 23-2 and later discussion.)
Anterior O-A membrane. The anterior O-A membrane is thought to be the superior continuation of the anterior longitudinal ligament. It connects the anterior arch of vertebra C1 to the anterior aspect of the foramen magnum.
Posterior O-A membrane. The posterior O-A membrane is a continuation of the ligamentum flavum. This ligament interconnects the posterior arch of the atlas and the posterior aspect of the foramen magnum and forms part of the posterior boundary of the vertebral canal.11
Tectorial membrane. The tectorial membrane is the most superficial of the three membranes and interconnects the occipital bone and the axis. This ligament is the superior continuation of the posterior longitudinal ligament and connects the body of vertebra C2 to the anterior rim of the foramen magnum. This bridging ligament is an important limiter of upper cervical flexion and holds the occiput off the atlas.12

A‐A Ligaments

The anterior A-A ligament is continuous with the anterior O-A membrane above. 13 The posterior A-A ligament interconnects the posterior arch of the atlas and the laminae of the axis.

Occipitoaxial Ligaments

The O-A ligaments are very important to the stability of the upper cervical spine.

Alar Ligament5

The alar ligaments (see Fig. 23-2) connect the superior part of the dens to fossae on the medial aspect of the occipital condyles, although they can also attach to the lateral masses of the atlas.14,15 A study of 44 cadavers16 found the orientation of the ligament to be superior, posterior, and lateral. In another study, 14 19 upper cervical spine specimens were dissected to examine the macroscopic and functional anatomy of alar ligaments. The study found that the most common orientation (10/19) was cauda-cranial, followed by transverse (5/19). In two of the specimens, a previously undescribed ligamentous connection was found between the dens and the anterior arch of the atlas, the anterior atlantodental ligament. In 12 specimens, the ligament also attached via caudal fibers to the lateral mass of the atlas. The posteroanterior orientation of the ligaments in 17 of the 19 subjects was directly lateral from the dens to the occipital attachment or slightly posterior.

The function of the ligament is to resist flexion, contralateral side bending, and contralateral O-A rotation.17 In addition, the alar ligaments restrict anteroposterior translation of the occiput on C1 to some degree.18 Because of the connections of the ligament, side bending of the head produces a contralateral or ipsilateral rotation of C2, depending on the source.19

Clinical
Pearl

Insufficiency of the alar ligaments increases the potential for occipitoaxial instability. The degree of instability can be determined in conjunction with other clinical findings, such as neurologic or vascular compromise, pain, and deformity.

The Cruciform Ligament

The cruciform (cross-shaped) ligament has superior, inferior, and transverse portions (Fig. 23-2). The superior and inferior portions of this ligament attach to the posterior aspect of the body of the dens and the anterior rim of the foramen magnum. The transverse portion, which stretches between tubercles on the medial aspects of the lateral masses of the atlas, connects the atlas with the dens of the axis. The transverse portion of the ligament is so distinct and important that it is often considered a separate ligament (Fig. 23-2). The major responsibility of the transverse ligament is to counteract anterior translation of the atlas relative to the axis, thereby maintaining the position of the dens relative to the anterior arch of the atlas.12

The transverse ligament also limits the amount of flexion between the atlas and axis.20 These limiting functions are of extreme importance because excessive movement of either type could result in the dens compressing the spinal cord, epipharynx, vertebral artery, or superior cervical ganglion. The integrity of the transverse ligament is also essential to the stability of atlas fractures; degenerative, inflammatory, and congenital disorders; and other abnormalities that affect the craniovertebral region.

The importance of the ligament is reflected in its physical properties. Spontaneous or isolated traumatic tears of this ligament are extremely rare events. The ligament is comprised almost entirely of collagen, with a parallel orientation close to the atlas and the dens, but with an approximately 30-degree obliquity at other points in the ligament. Dvorak and colleagues21 found the transverse ligament to be almost twice as strong as the alar ligaments and to have a tensile strength of 330 Newtons (N) (33 kg/73 lb).

Craniovertebral Muscles

Anterior Suboccipital Muscles

Rectus Capitis Anterior

The rectus capitis anterior (RCA) runs vertically. It travels deep to the longus capitis from the anterior aspect of the lateral mass of the atlas to the inferior surface of the base of the occiput, anterior to the occipital condyle. The RCA flexes and minimally rotates the head. Thus, an adaptively shortened RCA on the right could feasibly produce a decreased left translation in extension during mobility testing of the O-A joint. The muscle is supplied by the anterior (ventral) rami of C1 and C2.

Rectus Capitis Lateralis

This muscle arises from the superior surface of the C1 transverse process and inserts into the inferior surface of the jugular process of the occiput. It is homologous to the posterior intertransverse muscle of the spine. The rectus capitis lateralis side bends the head ipsilaterally. It is supplied by the anterior (ventral) rami of C1 and C2.

Posterior Suboccipital Muscles

The posterior suboccipitals lie beneath the splenius capitis and trapezius muscles. These muscles function in the control of segmental sliding between C1 and C222 and may have an important role in proprioception, having more muscle spindles than any other muscle for their size.22 All of the posterior suboccipital muscles are innervated by the posterior ramus of C1 and also are strongly linked with the trigeminal nerve.23,24 The suboccipitals receive their blood supply from the vertebral artery.

Rectus Capitis Posterior Major

The rectus capitis posterior major is the largest of the posterior suboccipitals. It runs from the C2 spinous process, widening as it runs cranially to attach to the lateral part of inferior nuchal line (Fig. 23-3). Located inferior and lateral to the occipital protuberances, the rectus capitis posterior major muscles, when working together, extend the head. When working individually, the muscles produce ipsilateral side bending and rotation of the head.

Figure 23-3

Muscles of the craniovertebral joints.

Rectus Capitis Posterior Minor

The rectus capitis posterior minor is a small unisegmental muscle that runs from the posterior arch tubercle of the atlas to the medial part of the inferior nuchal line (see Fig. 23-3). Because of the shortness of the atlantean tubercle, the muscle is very horizontal, running almost parallel with the occiput. The muscle functions to extend the head and provides minimal support during ipsilateral side bending of the head.

Clinical
Pearl

Connective tissue attachments between the rectus capitis posterior minor and dura mater recently have been identified.25 This finding has led to the use of cervical flexion with neurodynamic mobility tests (see Chap. 11). The differentiation between adverse neural tension and adaptive shortening of the muscle can be made by performing short neck flexion, with the neural system pretensioned and then relaxed.

Obliquus Capitis Inferior

This is the larger of the two oblique muscles and runs from the spinous process and lamina of the axis superolaterally to the transverse process of the atlas (see Fig. 23-3).

The inferior oblique muscle works to produce ipsilateral rotation of the atlas and skull and to control anterior translation and rotation of C1 (atlas). An adaptively shortened right inferior oblique may exert an inferior and posterior pull on the right transverse process of the atlas, producing a right rotated A-A joint.26,27 This results in a gross limitation of left rotation of the head while in cervical flexion, but a minimal limitation of left rotation of the head in extension.

Obliquus Capitis Superior

The superior oblique arises from the transverse process of the atlas and runs superoposterior and medially to the bone between the superior and inferior nuchal lines, lateral to the attachment of rectus capitis posterior major (see Fig. 23-3). Because of its posteromedial orientation, the superior oblique functions to provide contralateral rotation and ipsilateral side bending of the O-A joint, when acting unilaterally. When working together, the two superior obliques can produce head extension. Dysfunction of this muscle has been implicated as a common cause of chronic headaches.28–32

The posterior sub-occipital muscles can work concentrically with the larger extensors and rotators of the cervical spine, or eccentrically, controlling the action of the flexors. Because two of these muscles parallel the occiput, their controlling influence may be more linear than angular, producing or guiding the arthrokinematic, rather than the osteokinematic, motion.22

Nerve Supply

The posterior (dorsal) ramus of spinal nerve C1 is larger than the anterior (ventral) ramus. It exits from the spinal canal by passing posteriorly between the posterior arch of the atlas and the rim of the foramen magnum, along with the vertebral artery. It then enters the suboccipital triangle and supplies most of the muscles that form that triangle. It usually has no cutaneous distribution.

The posterior (dorsal) ramus of spinal nerve C2 (see Fig. 23-3), also known as the greater occipital nerve, is larger than the anterior (ventral) ramus of C2. It exits from the vertebral canal by passing through the slit between the posterior arch of the atlas and the lamina of the axis. This nerve is the largest of the cervical posterior (dorsal) rami and is primarily a cutaneous nerve. It supplies most of the posterior aspect of the scalp, extending anteriorly to a line across the scalp that runs from one external auditory meatus to the other. Because this nerve has an extensive cutaneous distribution, it has a very large posterior (dorsal) root ganglion. This ganglion is commonly located in a vulnerable location, almost directly between the posterior arch of C1 and the lamina of C2 (see Fig. 23-3). The interval between these two bony structures is small, and it is reduced with extension of the upper cervical spine. Given the sensitivity of the posterior (dorsal) root ganglion to compression, the possible relationship between the forward head position and occipital headaches is apparent.28–32 The O-A joints,33 A-A joints,34 and the C2 spinal nerve35 have all been implicated as primary nociceptors in cervicogenic headaches (CHs). Among individuals with chronic neck pain, 58–88% describe associated headaches.36,37 The prevalence of C2–3 zygapophyseal joint pain has been estimated at 50–53% in those patients with a chief complaint of headaches after whiplash injury.36,37

Blood Supply

The intradural vertebral artery supplies the most superior segments of the cervical spinal cord (see Chap. 24). The cervical cord is supplied by two arterial systems, central and peripheral, which overlap but are discrete. The first is dependent entirely on the single anterior spinal artery (ASA). The second, without clear-cut boundaries, receives supplies from the ASA and both posterior spinal arteries.38 Because the ASA is medial and dominant, unilateral spinal cord infarctions are very rare. However, they may occur in the perfusion territory supplied by the ASA.39,40 This is a result of obstruction of either a duplicated ASA40 or one of the sulcal arteries, which arise from the ASA and turn alternatively left or right to supply one side of the central cord. 41 Peripheral hemicord infarction may result from ischemia, in the territory of the ASA39 or posterior spinal artery.42

Biomechanics

The upper cervical spine is responsible for approximately 50% of the motion that occurs throughout the entire cervical spine. Motions at the O-A and A-A joints occur relatively independently, while below C2, normal motion is a combination of motion at other levels.

Articular facet asymmetry of the human upper cervical spine has been recognized for more than 30 years.43,44 The implications of this anatomic observation in the human spine has been considered in relation to joint disease, specifically, facet tropism (the phenomenon observed in living tissue, of moving toward or away from a focus of stimulus), which is associated with subsequent degenerative joint disease.45,46

Clinical
Pearl

Due to the proximity of vital structures, joint disease in this region can have severe consequences. These consequences can include

vertebral artery compromise;
compression of the spinal cord;
brainstem lesions.

O‐A Joint

The deep atlantal sockets of the atlas facilitate flexion–extension but impede other movements. In living individuals the average mean motion of flexion and extension at this joint is a combined range of 15–20 degrees.47 However, the variability in range of motion in normal subject is large. Lind et al.48 reported a mean of 14 degrees with a standard deviation of 15 degrees in normal subjects. Side bending motion occurs at an average of a little over 9 degrees to both sides,49–51 with an axial rotation range of 0 degrees (8 degrees when the movement was forced).50,51

Although it is generally agreed that rotation and side bending at this joint occur to opposite sides when they are combined, particular rules for patterns of defined coupled motion are not supported by the current literature.52

Clinical
Pearl

Clinical studies suggest that hypermobility of this joint should only be considered as a diagnosis if the range of axial rotation exceeds 8 degrees, making rotational mobility and stability testing necessary at this articulation.

A‐A Joint

The design of the ligamentous and bony structures at the A-A joint allow for a large arc of rotation.

Clinical
Pearl

Within the spine, only two articulations permit pure axial rotation:

The A-A joint
The thoracolumbar junction

The major motion that occurs at all three of the A-A articulations is axial rotation. Werne49 reported 47 degrees to each side in cadavers. A more recent study using CT scanning observed 32 degrees (SD, 10) of axial rotation to either side.51 This amount of rotation has the potential to cause compression of the vertebral artery (see Chap. 24).53,54 To help prevent this compression, as the atlas rotates, the ipsilateral facet moves posteriorly while the contralateral facet moves anteriorly, so that each facet of the atlas slides inferiorly along the convex surface of the axial facet, telescoping the head downward.

The first 25 degrees of head rotation (approximately 60%) occur primarily at the A-A articulations.55 However, the axial rotation of the atlas is not a pure motion, because it is coupled with a significant degree of extension (14 degrees) and, in some cases, flexion.56

In living individuals, the reported range of flexion–extension motion at this joint is highly variable, averaging 10 degrees.57 Flexion at the A-A joint is limited by the tectorial membrane. Extension is limited by the anterior arch of C1, as it makes contact with the odontoid process. The flexion and extension motions are associated with small anteroposterior translational movements, which can create a small space between the back of the anterior arch of the atlas and the odontoid. This space is called the atlanto-odontoid interval (ADI). Because of the arthrokinematics of the joint, flexion increases the ADI, whereas extension decreases it. Excessive gapping of the ADI can have serious consequences, as it can lead to a compression of the spinal cord by the atlas.58 An ADI of more than 3 mm in adults, and 4.5 mm in children younger than 12 years of age, detected on radiographs is indicative of gross instability and is strongly suggestive of a compromise of the transverse ligament.58 An increased ADI can be associated with a history of trauma but also may be associated with severe ligamentous laxity in patients with rheumatoid arthritis (RA), neoplastic disease, Down's syndrome, and aplasia or dysplasia of the dens.19

Side bending at this joint is approximately 5 degrees. Although coupling at this joint is commonly cited as contralateral side bending during rotation, it is highly variable because of the passive nature of the kinematics of the atlas.59 Whether the atlas flexes or extends during axial rotation depends on the geometry of the A-A joint and the precise direction of any forces acting through the atlas from the head.59 The direction of the conjunct rotation appears to be dependent on the initiating movement.60,61 If the initiating movement is side bending (latexion), the conjunct rotation of the joint is to the opposite side. If the initiating movement is rotation (rotexion), the conjunct motion (side bending) is to the same side.60,61 If correct, this principle can be exploited in the assessment of the craniovertebral joints:

1. Rotexion. During rotation of the head to the right (rotexion):
- a. Left side bending and right rotation occur at the O-A joint, accompanied by a translation to the right.
- b. Right side bending and right rotation occur at the A-A joint and at C2–3.
In other words, if the head motion is initiated with rotation, ipsilateral side bending of the A-A joint and C2–3 occurs, whereas at the O-A joint, contralateral side bending occurs.
2. Latexion. Side bending of the head to the right produces
- a. left rotation of the O-A joint, accompanied by a translation of the occiput to the left;
- b. left rotation of the A-A joint;
- c. right rotation of C2–3.

In other words, if head motion is initiated with side bending, contralateral rotation of both the O-A and the A-A joints occurs, but ipsilateral rotation occurs at C2–3.

Examination

The primary objective of the examination of this region is to rule out any serious injury, especially if the patient reports any recent trauma to the head or neck. The pain distribution from cervical structures is outlined in Table 23-1 and the differential diagnoses are described in Chapter 5. The initial examination should focus on the general appearance of the patient (including skin lesions such as rashes), vital signs (pulse, blood pressure, and temperature), and the presence of any upper motor neuron signs or symptoms.62 Once serious injury has been ruled out, a biomechanical assessment of the craniovertebral joints can be performed. In addition, because of their close relationship with the craniovertebral joints, the cervical spine (see Chap. 25) and temporomandibular joint (see Chap. 26) should be assessed as part of a comprehensive examination of this region.

Table 23-1 Pain Distribution from Cervical Structures

Table 23-1 Pain Distribution from Cervical Structures

Structure

Pain Area

Occipital condyles

Frontal

Occipitocervical tissues

Frontal

C1 posterior (dorsal) ramus

Orbit, frontal, and vertex

C1—2

Temporal and suboccipital

C3 posterior (dorsal) ramus

Occiput, mastoid, and frontal

Data from Meadows J: A Rationale and Complete Approach to the Sub-Acute Post-MVA Cervical Patient. Calgary, AB: Swodeam Consulting, 1995.

The biomechanical examination of the craniovertebral joints is best performed in a sequential manner (Fig. 23-4). In general, the O-A joint is examined and treated before the A-A joint to avoid confusion between findings from the combined testing of both joints. The examination and any intervention are terminated if any serious signs and/or symptoms are produced. In these instances, an appropriate referral is made.

Figure 23-4

Craniovertebral examination algorithm.

History

The craniovertebral region, as with the rest of the neck, is a common area for myofascial pain syndromes. These syndromes are frequently associated with complaints of local muscle soreness, and muscle spasm.63 Pain may also be referred to this region from trigger points in the upper trapezius muscle, splenius capitis, sternocleidomastoid (SCM) muscle, digastric muscle, cervicis muscles, posterior cervical muscles (semispinalis capitis, semispinalis cervicis, multifidus, and rotators), and sub-occipital muscles (rectus capitis posterior major and minor and inferior and superior obliques) (refer to “Intervention” section).63

Complaints of headaches are also common in patients with craniovertebral joint dysfunction.33–35 Some of the more common types of headaches are described in Chapter 5. In all patients presenting with an unexplained or unusual headache, a full neurologic and general physical examination is required.62 This examination should focus on the patient's mental status and speech, gait, balance and coordination, a cranial nerve and long tract examination, and an examination of visual fields, and acuity (see Chap. 3).62

Patients who complain of headaches should be asked to describe the headache. The clinician must always be alert to the potential coincidental occurrence of secondary headache syndromes. These include headache associated with trauma, vascular disease, nonvascular intracranial disorders, substance abuse or withdrawal, noncephalic infections, metabolic disorders, disorders of facial or cranial structures, and cranial neuralgia.64 Several conditions may mimic episodic or chronic tension-type headache (see Chap. 5), including muscle tension. Chronic tension-type headaches are often erroneously attributed to chronic sinusitis, but clinical and radiologic evidence must be obtained before making this diagnosis. A causal relationship between tension-type headache and oromandibular dysfunction is controversial, but the two conditions often coexist.65 The most important structures that register pain within the skull are the blood vessels, particularly the proximal part of the cerebral arteries, as well as the large veins and venous sinuses.66 The chronic headache of intracranial hypotension is most often distinguished by an increase of pain on standing. Descriptions such as throbbing and pounding are suggestive of a vascular origin but can also inculpate migraine, fever, neuralgia, or hypertension. Chronic, recurrent headaches can be associated with eyestrain, excessive eating or drinking, or smoking.

Intrinsic to the understanding of the relationship of headache to the craniovertebral region are the intracranial pain pathways and their interconnections, especially the trigeminocervical pathway (see Chap. 3).

The location of the headache can provide the clinician with useful information as to the source.

Forehead pain may be caused by sinusitis or a muscle spasm of the occipital or sub-occipital region.
Occipital pain can be caused by eyestrain, herniated cervical disk, hypertension, neuralgia, or an ear or eye disorder.
Parietal pain may be indicative of meningitis or a tumor.
Facial pain can be caused by sinusitis, trigeminal neuralgia, dental problems, or a tumor.

Dizziness (vertigo) and nystagmus are nonspecific neurologic signs that require a careful diagnostic workup (see Chap. 3). A report of vertigo, although potentially problematic, is not a contraindication to the continuation of the examination.

Clinical
Pearl

Dizziness associated with disorders of motor function, such as clumsiness, weakness, or paralysis, could suggest compromise of the vertebrobasilar system.

Systems Review

The craniovertebral region houses many vital structures. These include the spinal cord, the vertebral artery, and the brain stem. It is extremely important for the clinician to approach this area with caution and to rule out the presence of serious pathology. Craniovertebral and cranial dysfunction can be responsible for a number of signs and symptoms that may be benign or may indicate the presence of serious pathology (Table 23-2).

Table 23-2 Examination Findings and the Possible Conditions Causing Them

Table 23-2 Examination Findings and the Possible Conditions Causing Them

Findings

Possible Condition

Dizziness

Upper cervical impairment, vertebrobasilar ischemia, and craniovertebral ligament tear; also may be relatively benign

Quadrilateral paresthesia

Cord compression and vertebrobasilar ischemia

Bilateral upper limb paresthesia

Cord compression and vertebrobasilar ischemia

Hyperreflexia

Cord compression and vertebrobasilar ischemia

Babinski or clonus sign

Cord compression and vertebrobasilar ischemia

Consistent swallow on transverse ligament stress tests

Instability, retropharyngeal hematoma, and rheumatoid arthritis

Nontraumatic capsular pattern

Rheumatoid arthritis, ankylosing spondylitis, and neoplasm

Arm pain lasting >6–9 mo

Neoplasm

Persistent root pain <30 y

Neoplasm

Radicular pain with coughing

Neoplasm

Pain worsening after 1 mo

Neoplasm

>1 level involved

Neoplasm

Paralysis

Neoplasm or neurologic disease

Trunk and limb paresthesia

Neoplasm

Bilateral root signs and symptoms

Neoplasm

Nontraumatic strong spasm

Neoplasm

Nontraumatic strong pain in elderly patient

Neoplasm

Signs worse than symptoms

Neoplasm

Radial deviator weakness

Neoplasm

Thumb flexor weakness

Neoplasm

Hand intrinsic weakness or atrophy

Neoplasm, thoracic outlet syndrome, and carpal tunnel syndrome

Horner's syndrome

Superior sulcus tumor, breast cancer, cervical ganglion damage, and brain stem damage

Empty end-feel

Neoplasm

Severe post-traumatic capsular pattern

Fracture

Severe post-traumatic spasm

Fracture

Loss of ROM post-trauma

Fracture

Post-traumatic painful weakness

Fracture

Data from Meadows J. Orthopaedic Differential Diagnosis in Physical Therapy. New York: McGraw-Hill; 1999.

ROM, range of motion.

Due to the proximity of the cranial structures, the clinician should develop the habit of quickly screening patients with neck and head pain for their ability to orient to time, place, and name; concentrate; reason and process information; make judgments; communicate effectively; and recall information. Obtaining this information needs to be done in a sensitive manner. Asking questions as to whether the patients know their own name and what day it is may be considered inappropriate by some patients. Most of the concerns about the patient's mental status can be addressed through general conversation, or as part of the history. Perhaps surprisingly, the incidence of neurologic involvement in upper cervical spine injury is relatively low (18–26%).67 This may be because, significant cord damage in the upper cervical spine is usually fatal secondary to respiratory arrest.7

When compression of the spinal cord is suspected, a thorough neurologic examination should be performed. If confirmed, the appropriate medical services should be contacted. The cranial nerves should be assessed, particularly if there are complaints about vision or the patient appears to have problems with speech or swallowing. Patients with referred pain in the region of the trigeminal nerve commonly have an underlying disorder of the upper cervical spine, such as A-A instability caused by RA.63,68 As described in Chapter 3, the various cranial nerve tests can be performed in approximately 5 minutes with practice.

Tests and Measures

The examination is terminated if any serious signs and symptoms are produced.

Observation

The patient is observed in the sagittal, coronal, and transverse planes.

Sagittal Plane

Observing the status of the cervical curve and the relative position of the patient's chin to the chest helps the clinician to assess postural alignment in the sagittal plane. A popular view among clinicians is that habitual adoption of extreme cervical posture may account for symptoms of pain and dysfunction arising from the head and neck area.69 The argument is that alterations in spinal alignment may lead to changes in muscle activity and loading on the surrounding soft tissue and articular structures, which then predisposes patients to such complaints.70,71 This argument has been supported in several studies, which have found a statistically significant correlation between the tendency to hold the head forward, relative to the true vertical in the so-called forward head posture, and symptoms of pain.71,72 However, in other investigations, no such correlation has been confirmed.73,74

Tucking or elevation of the chin in the presence of a normal cervical curve may indicate craniovertebral dysfunction.75

The ears are observed for the presence of asymmetry in size, shape, or color. The top of the ear is normally in line with the eyebrow.

Coronal Plane

Alignment in the coronal plane is assessed by observing the orientation of the head relative to the trunk and shoulders, the leveling of the mastoid processes, and the symmetry of the cervical soft tissues. The face is observed for any asymmetry or indications of bruising, puffiness, prominence, swelling, perspiration, or abnormal skin color. Any asymmetry in the relative size of the pupils of the eyes and the distance between the upper and lower lids is noted. Pupillary size differences can occur in normal individuals but initially should arouse concern, because an abnormal unilateral change in size may be caused by an autonomic dysfunction or a central nervous system lesion.76 The superior lid should cover a portion of the iris but not the pupil itself, unless ptosis or drooping of the eyelid is present76 (see Chap. 3).

Missing teeth should be accounted for as a loss of teeth may be a result of trauma, avulsion, or loosening.

Transverse Plane

Alignment in the transverse plane is assessed by observing the patient from behind and noting the orientation of the head. The orientation of the head is best observed by noting any asymmetry in the position of the mastoids, which can indicate whether the head is more rotated or tilted to one side, both of which may indicate a positional fault of the craniovertebral joints. Bruising around the mastoids or around the crown of the head (Battle's sign), with a history of trauma, may indicate the presence of a cranial vault injury, such as a basilar fracture. A low hairline may indicate a condition such as Klippel–Feil syndrome,77 defined as a short neck with decreased cervical movement and low posterior hairline. Radiologically, patients with Klippel–Feil syndrome show a failure of cervical segmentation. The etiology is unclear, but the syndrome is believed to be caused by faulty segmentation of the mesodermal somites.78 The syndrome appears to be heterogeneous, with environmental factors possibly contributing.79 Autosomal dominant and recessive patterns of inheritance also have been reported.80

Active Range of Motion, Passive Overpressure, and Resistance

Short Neck Flexion

The clinician instructs the patient to place his or her chin on the surface of the throat. This motion simulates flexion at the craniovertebral joints. If this maneuver produces tingling in the feet or electric shock sensations down the neck (Lhermitte's sign), it is highly indicative of serious pathology. Although Lhermitte's sign is not a specific symptom, it is commonly encountered in patients with meningitis (see Chap. 5) and cervical spinal cord demyelination caused by multiple sclerosis.81 The sign also has been found in many other conditions that cause a traumatic or compressive cervical myelopathy, such as cervical spondylosis, cervical instability, and epidural or subdural tumors.82,83

If the patient reports a pulling sensation during short neck flexion, the cervicothoracic junction may be at fault. Active short neck flexion tests cranial nerve XI and the C1 and C2 myotomes, as well as the patient's willingness to move. Placing the neck in short neck flexion places the short neck extensors (C1), which are innervated by the spinal accessory nerve, on stretch. The clinician applies overpressure and tests the short neck extensors by asking the patient to resist (Fig. 23-5). Positive findings with this test are severe pain, nausea, muscle spasm, or cord signs, the latter of which may indicate a dens fracture or a tumor and cause the examination to be terminated.82 Thus, if a patient is able to perform short neck flexion, a cervical fracture or a transverse ligament compromise can be provisionally ruled out.

Figure 23-5

Short neck flexion with overpressure and resistance.

Short Neck Extension

The clinician instructs the patient to look upward by only lifting the chin. The patient extends the head on the neck and the clinician attempts to lift the occiput in the direction of the ceiling (Fig. 23-6). An inability to perform, or pain during, this motion (in the presence of normal motion in the other planes) may indicate significant tearing of the anterior cervical structures. If this test produces tingling in the feet, it is highly suggestive of compression to the spinal cord. This compression may occur because of “buckling” or ossification of the ligamentum flavum, with resultant loss of its elasticity.84 A loss of balance or a drop attack with this maneuver would strongly suggest compromise of the vertebrobasilar system. A drop attack is defined as a loss of balance without a loss of consciousness (see Chap. 24). The short neck flexors (C1), which are innervated by the spinal accessory nerve, can be tested in this position by applying overpressure as though lifting the patient's chin toward the ceiling while the patient resists (see Fig. 23-6).

Figure 23-6

Short neck extension with overpressure and resistance.

Clinical
Pearl

If the neck is unstable secondary to a dens fracture or a transverse ligament tear, the patient will be unable or unwilling to flex or extend the neck in the traditional manner, often because of severe muscle spasm.

Side Bending

The patient is asked to side bend their head around the appropriate axis (through the patient's nose). Side bending is included here for completeness. Much more a function of the lower cervical spine, side bending of the neck is nonetheless significantly decreased in cases of craniovertebral instability or articular fixation. It could be argued that, in the presence of serious ligamentous disruption due to a subluxation of the atlas under the occiput, this motion may provoke symptoms, but it is likely that such a significant incidence of instability would be detected earlier in the examination.85 The side-bending motions that do occur in the craniovertebral joints are essentially conjunct motions, so the results from this test are unlikely to provide much in the way of additional information.

Rotation

Neck and head rotation could be considered as the functional motion of the craniovertebral joints. Thus, if the patient's symptoms and loss of motion are not reproduced with active rotation, it is doubtful that damage to tissues making up the craniovertebral joints is significant or even present. The patient is asked to perform active neck rotation. An inability to move any amount in either direction is potentially a very serious sign, as it could indicate the presence of a dens fracture or a C1–2 dislocation–fracture. Every measure must be taken to determine the cause of this inability to move. In cases of a suspected fracture or severe instability, the patient should be placed in a cervical collar and the physician immediately notified. In addition to the presence of a fracture, some of the other serious conditions that can be provoked by cervical rotation include vertebral artery compromise—cervical rotation is the most likely (single) motion to reproduce signs or symptoms of vertebral artery compromise (see Chap. 24).82,86–88

The findings from the cervical rotation tests may also afford the clinician some information with regard to a biomechanical lesion of the craniovertebral joints:

A loss of rotation associated with pain and a history of recent trauma. This could indicate the presence of an acute/subacute, posttraumatic arthritis of the craniovertebral joints. Since it may also indicate a soft tissue injury, further testing would be required.
A loss of rotation associated with pain and a history of chronic trauma. This finding could indicate a chronic painless hypomobility with an adaptive but painful ipsilateral hypermobility involving the craniovertebral joints (e.g., pain with right rotation could occur if the right O-A joint cannot flex and there is a hypermobility of the right A-A joint). It may also occur if the left O-A joint cannot extend. Again, further testing is needed to confirm this hypothesis.
A loss of rotation range of motion associated with no pain, but with a history of chronic trauma. This finding, which could indicate a chronic, posttraumatic arthritis, is likely to be an incidental finding, since most patients seek help because of pain. However, depending on the extent of the loss of rotation, the patient may have become aware of a loss of function.
Full rotation range of motion associated with pain and a history of chronic trauma. This could indicate a chronic fibrotic (painless) hypomobility with an adaptive but painful contralateral hypermobility (e.g., pain with right rotation could occur if the left O-A joint cannot flex and the right O-A joint develops a compensatory hypermobility).

Palpation

Objective palpation of this area is guided by a sound anatomic knowledge. Palpation usually proceeds layer by layer. It should be noted that asymmetric joint geometry is common in this region.89 For spine palpation to be a valid indicator for manual techniques, the clinician applying it must first be able to differentiate between asymmetric motion caused by vertebral dysfunction and that caused by asymmetric joint anatomy.89 However, examination of the skin overlying the spine has been found to be very helpful, because certain skin changes in a particular location may point in the direction of a dysfunctional spinal area.90 The skin is assessed for its thickness, moisture, and ease of displacement in all directions. Abnormal autonomic skin reactions, such as erythematous changes, increased sweat production, and pain that can be induced with minimal palpatory pressure, may indicate a segmental dysfunction.91

Palpation may be started at that area indicated by the patient as painful. These painful sites must be correctly localized. The bony landmarks of this region that should be routinely palpated include the occiput, mastoid, atlas, and axis.

Occiput

The clinician locates the external occipital protuberance, which is the most prominent bony structure at the occiput in the midline. By following the external occipital protuberance laterally, the clinician can locate the superior nuchal line. The semispinalis capitis muscle is located about 1½ fingerbreadths below the superior nuchal line.91

Mastoid

The mastoid processes are located behind each ear. Once this structure is located, the clinician moves the fingers inferiorly toward the tip of the mastoid process. Starting from the medial tip of the mastoid process, the palpating finger is moved superiorly to the upper pole of the mastoid sulcus, an important area in the examination of the irritation zones of the occiput and C1.91

Atlas

By placing the palpating fingers between the mastoid process and the descending ramus of the mandible, the clinician can locate the transverse process of the atlas. The inferior oblique and the superior oblique both have attachments to this site.

Axis

The spinous process of C2 is the first prominent bony landmark that is accessible to palpation below the external occipital protuberance of the occiput. The spinous process of C2 serves as the origin of the inferior oblique muscle and the rectus capitis posterior major muscle.

Passive Physiologic Mobility Testing of the Occiput, Atlas, and Axis

O-A Joint

When mobility testing this joint, the first point to remember is that the joint is capable of both flexion and extension, and that side bending and rotation also can occur, albeit slight. The second point to keep in mind is that the arthrokinematics of this joint are the reverse of those occurring in the other zygapophyseal joints and that they occur in a different plane (horizontal). The joint mobility of the O-A joint can be assessed in sitting or in supine.

Supine Stretch of the OA Joint

With the patient supine, the head is extended around the axis for the O-A joint. The head is then side bent left and right. As the side bending is performed, a gradual translational force is applied in the direction opposite to the side bending. The range of movement of the side bending is assessed from side to side as is the end-feel of the translation. This procedure is then repeated for flexion.

During extension of the O-A joint (Fig. 23-7), the occipital condyles glide anteriorly to the limit of their symmetric extension range. During left side bending and right translation in extension, the coupled right rotation is produced. This rotation causes the right occipital condyle to return toward a neutral position, while the left condyle advances toward the extension barrier. If left side bending in extension is limited, then the limiting factor is on the left joint of the segment (ipsilateral to the side bending), which is preventing the advance of the condyle into its normal position. Thus, extension and right translation test the anterior glide of the left O-A joint, whereas extension and left translation stress the anterior glide of the right O-A joint (Table 23-3).

Figure 23-7

Passive mobility testing of O-A in extension.

Table 23-3 Movement Restrictions of the Craniovertebral Joints and Their Probable Causes

Table 23-3 Movement Restrictions of the Craniovertebral Joints and Their Probable Causes

Movement Restriction

Probable Causes

Flexion and right side bending

Left flexion hypomobility

Extensor muscle tightness

Posterior capsular adhesions

Left subluxation (into extension)

Extension and right side bending

Right extension hypomobility

Left flexor muscle tightness

Anterior capsular adhesions

Right subluxation (into flexion)

Flexion and right side-bending motion greater than extension and left side bending

Left capsular pattern (arthritis and arthrosis)

Flexion and right side bending equal to extension and left side bending

Left arthrofibrosis (very hard capsular end-feel)

Right-side flexion in flexion and extension

Probably an anomaly

During flexion of the O-A joint, the occipital condyles glide posteriorly (Fig. 23-8). The right rotation associated with left side bending causes the left condyle to move away from the flexion barrier toward the neutral position, while the right condyle is moved posteriorly further into the flexion barrier. Thus, flexion and translation to the right tests the posterior glide of the right O-A joint, whereas flexion and left rotation tests the posterior glide of the left O-A joint (see Table 23-3).

Figure 23-8

Passive mobility testing of O-A in flexion.

It is apparent that during these tests, the arthrokinematic and osteokinematic movements are tested simultaneously; thus, the end-feel must be used to determine the cause of the restriction. The following patterns of impairment are more or less commonly seen, and the causes of the impairments can be deduced. However, it must be remembered that deductions are only of value if the resultant intervention is successful.60

A patient who has a subluxation into flexion (loss of anterior glide) on the right O-A joint should demonstrate decreased extension, decreased right side bending and left rotation, and a jammed end-feel with translation to the left.
A patient with a periarticular restriction of the left O-A joint into flexion (loss of posterior glide) should demonstrate decreased flexion, decreased right side bending and left rotation, and a capsular end-feel with translation to the left.
A patient with a fibrous adhesion of the right O-A joint (loss of anterior and posterior guide) should demonstrate decreased extension and right side bending and decreased flexion and left side bending, with a hard capsular end-feel at both extremes.
With motion testing, a decreased flexion and right side bending with a pathomechanic end-feel indicates a left O-A joint being subluxed into extension.
With motion testing, a decreased extension and right side-bending limitation indicates a capsular pattern of the right O-A joint. A decreased extension and left side-bending limitation, with a spasmodic end-feel (flexion with greater range), indicates traumatic arthritis of the left O-A joint.
A decreased right translation of the O-A in flexion may indicate a right posterior O-A joint dysfunction or an impaired or adaptively shortened right superior oblique muscle.

A‐A Joint

There are a number of methods to assess the passive physiologic mobility of the A-A joint. The most common method described in many texts involves the patient lying supine and the clinician passively applying full cervical flexion, and then introducing cervical rotation. The problem with this technique is that it relies on the fact that the mid-to-lower cervical spine will be locked with the flexion. Because the neck is often prevented from further flexion when the chin meets the sternum, the clinician has no way of knowing whether full cervical flexion has occurred. Thus, some of the subsequent rotation may be attributed to a combination of cervical spine and A-A motion. This assumption may not be important with asymmetric lesions but can result in false-negative findings with symmetric lesions.

Seated Mobility Testing

A better method of assessment involves the use of cervical side bending. With the patient positioned in supine, the clinician side bends the head and neck around the craniovertebral axis and then rotates the head in the direction opposite to the side bending (Fig. 23-9). The clinician assesses the amount of range available and then assesses the other side.

Figure 23-9

Passive mobility testing of A-A rotation in supine.

Clinical
Pearl

In a study by Smedmark and colleagues,92 passive intervertebral motion of the cervical spine was assessed independently by two physical therapists. The therapists had equal backgrounds concerning education and clinical experience. Sixty-one patients seeking care for cervical problems at a private clinic were included in the study where three segments of the cervical spine and the mobility of the first rib were graded as stiff or not stiff. Data were analyzed by percentage agreement and kappa coefficient. Results demonstrated interexaminer reliability of between 70 and 87% and kappa coefficients ranging between 0.28 and 0.43 considered to be only “fair to moderate.”

In a similar study by Pool and colleagues,93 which assessed the interexaminer reproducibility of physical examination of the cervical spine, two physical therapists independently judged the general mobility and intersegmental mobility (segments C0–T2) of the neck and the pain that was provoked. Agreement for general mobility showed kappa between 0.05 and 0.61, and for the intersegmental mobility, it showed kappa values between −0.09 and 0.63. Agreement for provoked neck pain within one point of an 11-point numerical rating scale varied between 46.9 and 65.7% for general mobility and between 40.7 and 75.0% for intersegmental mobility. The ICCs varied between 0.36 and 0.71 for general mobility and between 0.22 and 0.80 for intersegmental mobility. The study concluded that despite the use of a standardized protocol to assess general mobility and intersegmental mobility of the cervical spine, it is difficult to achieve reasonable agreement and reliability between two examiners. Likewise, the patients were not able to score the same level of provoked pain in two assessments with an interval of 15 minutes.

Combined Motion Testing

Flexion and extension at the O-A joints involve a posterior and anterior gliding of the occipital condyles, respectively. The same gliding (although reciprocal in opposing facets) is utilized in rotation. At the A-A joint, flexion and extension primarily involve a “rolling” action of the condyles, with an insignificant amount of gliding. Therefore, craniovertebral flexion and extension will have a minimal effect on A-A rotation.94 Thus, if a symptom or range of motion is drastically altered by craniovertebral flexion or extension, an assumption could be made that the dysfunction is at the O-A joint.94 For example, if the right occipital condyle cannot glide posteriorly, the right joint will be unable to flex or to permit rotation to the right, as both of these motions involve a posterior glide at the right O-A joint. In the combined motion tests, the right rotation restriction will be more evident when combined with craniovertebral flexion but will be less evident when combined with craniovertebral extension.

The findings from the combined motion tests can be used to determine which joint glide is to be assessed. For example, if it was determined in the combined motion testing that the right O-A joint is restricted or painful with flexion (implicating the posterior glide), the O-A joint is positioned and assessed in its extreme of flexion and right rotation (the two motions associated with a posterior glide of the right O-A joint).

Linear Segmental Stress Testing

The craniovertebral region demonstrates a high degree of mobility, but little stability, with the ligaments affording little protection during a high-velocity injury. Instability of this region can result from a number of causes:

Trauma (especially a hyperflexion injury to the neck).
RA, psoriatic arthritis, or ankylosing spondylitis. Nontraumatic hypermobility or frank instability of the O-A joint has been reported in association with RA.95
Corticosteroid use. Prolonged exposure to this class of drug can produce a softening of the dens and transverse ligament by deteriorating the Sharpey fibers, which attach the ligament to the bone. Steroid use also promotes osteoporosis, predisposing bones to fracture.
Recurrent upper respiratory tract infections or chronic sore throats in children. Grisel's syndrome96 is a spontaneous A-A dislocation, affecting children between the ages of 6 and 12 years. The outstanding symptom is a spontaneously arising torticollis. The most likely etiology seems to be an inflammation of the retropharyngeal space caused by upper respiratory tract infections or by adenotonsillectomy and producing pharyngeal hyperemia and bone absorption.
Congenital malformation. Nontraumatic hypermobility or frank instability of the O-A joint has been reported in association with congenital bony malformations.97
Down's syndrome. Nontraumatic hypermobility or frank instability of the O-A joint has been reported in children and adolescents with Down's syndrome.98,99
Immature development. Patients younger than 12 years of age often have an immature or absent dens (see later).
Osteoporosis.

It must be remembered that the A-A joint complex consists of three joints. The median joint, although it has no weight-bearing function, is extremely important in maintaining stability, while at the same time facilitating motion within this joint complex. Fielding and colleagues100 found that the stability of the A-A joint depends greatly on the ligamentous structures and on a normal and intact dens. Occasionally, the integrity of the dens can be compromised because of:

1. Anomalies of the dens, including:
- a. Os odontoideum. This is a condition in which the IVD between the developing bodies of axis and atlas does not ossify.
- b. Congenital absence of the dens.
- c. An underdeveloped dens whose lack of height renders it unchecked by the transverse ligament. The body of the dens is not of sufficient size to be retained in the osseoligamentous ring of the atlas until a child is approximately 12 years old. Great care and justification are needed with any craniovertebral mobilization or manipulative technique with this age group.
2. Pathologies affecting the dens, including:
- a. Demineralization or resorption of the dens, such as occurs with Grisel's syndrome96 or RA.
- b. An old, undisplaced fracture (especially of the dens), which originally escaped diagnosis and subsequently formed a pseudoarthrosis.

Indications for Stability Testing

The following findings are considered to be indications to perform stability or stress tests of the craniovertebral region82:

History of neck trauma or any of the causes of instability listed previously.
Patient report of neck instability usually described as the head feeling heavy.
Presence of the following signs and symptoms:
- A lump in the throat
- Lip paresthesia
- Nausea or vomiting
- Severe headache and muscle spasm
- Dizziness

The patient is positioned in supine to remove any muscular influences. If the patient is unable to lie down, the clinician may need to reconsider the appropriateness of performing these tests.

Longitudinal Stability

General traction is applied to the entire cervical region. If this maneuver does not reproduce the signs or symptoms, C2 is stabilized so that the traction force may be directed at the craniovertebral region (Fig. 23-10). The diagnostic value of this test is as yet unknown.

Figure 23-10

Longitudinal stability testing.

Anterior Shear: Transverse Ligament

The patient is positioned in supine, with his or her head cradled in the clinician's hands. The clinician locates the anterior arches of C2 by moving around the vertebra from the back to the front using the thumbs. Once the arches are located, the clinician pushes down on the anterior arches of C2 with the thumbs toward the table, while the patient's occiput and C1, cupped in the clinician's hands, is lifted, keeping the head parallel to the ceiling but in slight flexion82 (Fig. 23-11). The patient is instructed to count backward aloud. The position is held for approximately 15 seconds or until an end-feel is perceived. The diagnostic value of this test is as yet unknown.

Transverse Ligament Test

Figure 23-11

Transverse ligament test.

Sharp–Purser Test

This test was designed originally to test the sagittal stability of the A-A segment in patients with RA, because a number of pathologic conditions can affect the stability of the osseoligamentous ring of the median joints of this segment in this patient population. These changes result in degeneration and thinning of the articular cartilage between the odontoid process and the anterior arch of the atlas, or, occasionally, in a softening of the dens.

The aim of the test was to determine whether the instability was significant enough to provoke central nervous system's signs or symptoms. Uitvlugt and Indenbaum101 assessed the validity of the Sharp–Purser test in 123 outpatients with RA. The study findings indicated a predictive value of 85% and a high specificity of 96%. The sensitivity was 88% when subluxation was greater than 4 mm.101 The authors concluded that the Sharp–Purser test is a useful clinical examination to diagnose A-A instability in the RA population.101

However, the original test was poorly defined and only involved upper cervical flexion. Hence, a modified version was introduced which is described.

The patient is positioned in sitting. The patient is asked to segmentally flex the head around a craniovertebral axis (short neck flexion) and relate any signs or symptoms that this might evoke to the clinician. In addition, a positive test may be indicated by the patient hearing or feeling a clunk. Local symptoms, such as soreness, are ignored for the purposes of evaluating the test. If no serious signs or symptoms are provoked, the clinician stabilizes C2 posteriorly with one hand and applies a posteriorly oriented force to the forehead of the patient (Fig. 23-12).

The Sharp-Purser Test

Figure 23-12

Modified Sharp–Purser test.

In the presence of a positive test, a provisional assumption is made that the symptoms are caused by excessive translation of the atlas, compromising one or more of the sensitive structures listed previously, and the physical examination is terminated. No intervention should be attempted other than the issuing of a cervical collar to prevent craniovertebral flexion and an immediate referral to the patient's physician.

Coronal Stability: Alar Ligament

Rotation and side bending tighten the contralateral alar (e.g., rotation or side bending to the right tightens the left alar), whereas flexion typically tightens both alar ligaments.

The posterior aspect of the transverse process of C2 is palpated with one hand, while the patient's head is side bent or rotated (Fig. 23-13).. This is a test of immediacy. If the C2 transverse process does not move as soon as the head begins to rotate, laxity of the alar ligament should be suspected. To confirm the findings in this test, the point of rotation is maintained, as the patient's head is cradled by the clinician (Fig. 23-14), and while monitoring the motion at the C2 segment, the clinician introduces side bending through the craniovertebral joints to slacken the alar ligament. Further rotation should now be possible. The diagnostic value of this test is as yet unknown.

The Kinetic Alar Ligament Test

Supine Alar Ligament Test

Figure 23-13

Alar ligament test in sitting.

Figure 23-14

Confirmatory test for alar ligament in sitting.

Transverse Shear82

Transverse shearing of the craniovertebral joints is performed with the patient supine. The clinician stabilizes the mastoid, and C1 is moved in a transverse direction, using the soft part of the metacarpophalangeal joint of the index finger (Fig. 23-15). The test is repeated by stabilizing C1 and translating the mastoid.

Figure 23-15

Transverse shear of O-A joint.

C1 and C2 can be tested similarly. The soft aspect of each second metacarpal head is placed on the opposite transverse processes and laminae of C1 and C2, with the palms facing each other. The clinician stabilizes C1 and then attempts to move C2 transversely using the soft part of metacarpals (Fig. 23-16). No movement should be felt. The diagnostic value of this test is as yet unknown.

Figure 23-16

Transverse shear of A-A joint.

Neurologic Examination

The neurologic examination is performed to assess the normal conduction of the central and peripheral nervous systems. The presence of neurologic symptoms deserves special attention. Many of the symptoms that occur in the upper limb have their origins in the neck. The patient with neck trauma can report seemingly bizarre symptoms, but these need to be heeded until the clinician can rule out serious pathology. Cervical myelopathy, involving an injury to the spinal cord itself, is associated with multisegmental paresthesias, upper motor neuron (UMN) signs and symptoms such as spasticity, hyperreflexia, visual and balance disturbances, ataxia, and sudden changes in bowel and bladder function. The presence of any UMN sign or symptom requires an immediate medical referral.

In addition to the muscle stretch (deep tendon) reflexes and sensory tests outlined in Chapter 25, the clinician should perform the spinal cord reflexes of Babinski and Hoffman (see Chap. 3). Studies by Boden and colleagues102 and Sung and Wang have demonstrated that the Hoffman test is the most sensitive reflex test in the detection of cervical myelopathy.103

Imaging Studies

The standard, initial cervical spine radiographic series in trauma patients includes a cross-table lateral view, an anteroposterior view, and an open-mouth view, the latter of which is used to help rule out a fracture of the dens (see Chap. 7).7 The usefulness of the anteroposterior view has been questioned because it provides little additional information.104 Although this three-view screening series can detect 65–95% of axis injuries,105,106 the C2 vertebra often is obscured by overlying bony maxillary, mandibular, and dental structures; therefore, C2 fractures may be missed.7 The clinician needs to be aware of the limitations of plain radiographs, as problems exist with both specificity and sensitivity. However, radiographs can provide a gross assessment of the severity of the degenerative changes of the spine.

Thin-section CT is the best study for evaluating C2 bony fractures.107 Sagittal reconstruction of CT images is important because axial images may not detect a transverse odontoid fracture.7 Although CT is excellent in evaluating bony injuries, it can miss soft tissue and significant ligamentous injuries.7 Recently, therefore, dynamic flexion/extension lateral fluoroscopic evaluation has been advocated in polytrauma patients to identify occult ligamentous instabilities and confirm that the cervical spine is uninjured.108 As with any diagnostic study, the findings must be correlated with the history and physical examination.

Intervention Strategies

The gamut of musculoskeletal injury to the craniovertebral region of the spine ranges from a simple strain (muscle) or sprain (ligament) to injuries of the bone and neurovascular injuries. The most common injuries seen clinically are muscle strains and postural dysfunctions.

Muscle strains are common in the cervical spine because most of the cervical muscles attach via myofascial tissue inserting into the periosteum rather than by the more resilient tendon.109 The severity of the strain is dependent on the magnitude of forces involved. If the force is sufficient, both the muscle and the associated joint become involved. In an abnormal spine, the forces needed to cause injury are reduced. Repetitive microtrauma is a common cause of craniovertebral dysfunction.

Postural dysfunctions of this region, particularly the forward head posture (see Chap. 25), usually manifest themselves at the O-A joint, resulting in fixed capital extension and a loss of O-A flexion. Patients with postural dysfunctions may develop secondary myofascial trigger points (MTrPs) and myofascial pain syndromes. In postural dysfunctions and trauma-related injuries, other joints and regions may be involved and require further investigation.

Pain, tenderness, active range of motion restrictions, muscle imbalances, and segmental motion restrictions are common findings with craniovertebral dysfunction.

The structure at fault should determine the intervention110:

If ligamentous tissue damage or an intra-articular lesion is suspected, the safest initial approach would be to help in unloading the joint and controlling the extremes of motion with a soft collar for a 7–10-day period.
Within the patient's pain tolerance, contractile lesions should be treated aggressively once the acute phase has subsided, with the emphasis on regaining maximal muscle length.110

The techniques to increase joint mobility and soft tissue extensibility are described later, under “Therapeutic Techniques” section.

A correct diagnosis can usually be accomplished through detailed history and a comprehensive examination. Confirmation of the correct diagnosis can be made with an assessment of the response of the patient to the initial rehabilitation program. The intervention for the craniovertebral region may commence when the possibility of serious injury including fracture, dislocation, or injury to the spinal cord and vertebral artery have been ruled out.

Acute Phase

The goals of this phase include

reducing pain, inflammation, and muscle spasm;
reestablishing a nonpainful range of motion;
improving neuromuscular postural control;
retarding muscle atrophy;
promotion of healing.

Various electrotherapeutic modalities and physical agents may be used during the acute phase to modulate pain and to decrease inflammation and muscle spasm (see Chap. 8). Therapeutic cold and electrical stimulation may be used for 48–72 hours. The cryotherapy is continued at home. A transcutaneous electrical nerve stimulation (TENS) unit may be prescribed to help control pain and encourage range of motion. Joint protection may be appropriate. In such cases, a soft or semirigid cervical collar may be prescribed for 7–10 days to reduce muscle guarding (see Chap. 25). Nonsteroidal anti-inflammatory drugs (NSAIDs) often are prescribed for 2–3 weeks to help decrease inflammation and to control pain, thereby increasing the potential for an early return to function. Bed rest, along with analgesics and muscle relaxants for no more than 2–3 days, is prescribed for patients with a severe injury. However, in less severe cases, bed rest has not been shown to improve recovery and, compared with mobilization or patient education, rest tends to prolong symptoms.111,112

The patient also is taught how to find the neutral position for the upper cervical spine. The neutral position is defined as the least painful position that minimizes mechanical stresses.

Range of motion exercises are initiated as early as possible, based on patient tolerance, to prevent hypomobility. Neck flexion and rotation exercises usually are performed first. Extension and side-bending exercises are introduced based on the response of the patient to the flexion and rotation exercises. The rotation and side-bending exercises are performed in the supine position and then progressed to weight bearing. All of the exercises should be performed in the pain-free range.

Upper extremity range of motion and strengthening exercises should also be introduced to promote early integration of the entire upper kinetic chain. Important muscles to include are the rhomboids, middle and lower trapezius, latissimus dorsi, serratus anterior, and deltoid. In addition, the muscles of the rotator cuff should be strengthened.

Gentle manual techniques (see “Therapeutic Techniques” section later), such as sustained or rhythmic specific traction (grade I or II) mobilizations and massage, may also be used. As the patient progresses, muscle stretching may be introduced. Manual techniques can have a mechanical effect on joint mobility and soft tissue extensibility. In addition, these techniques can have beneficial neurophysiologic effects, which can help alleviate pain and muscle spasm. Self-stretching and self-mobilization techniques are taught to the patient at the earliest and appropriate opportunity (see “Therapeutic Techniques” section later).

Active joint protection techniques may be part of the acute phase. Joint protection exercises work by supporting the joint and reducing the applied stresses. Joint protection exercises include cervical stabilization exercises. These exercises initially are performed in single planes and in the neutral position, using submaximal isometric contractions. As with the range of motion exercises, it is recommended that these exercises be performed initially in the supine position, and later, in sitting, as tolerance increases. As the pain-free ranges increase, the exercises are performed throughout the newly attained pain-free ranges.

Aerobic conditioning must also be included as part of the comprehensive rehabilitation program. A stationary bike, tread-mill, or a stair-stepping machine can be used.

The patient is advanced to the functional phase when

the pain has significantly decreased so that there is minimal pain with activities of daily living;
there is significant improvement in the pain-free ranges of motion.

Functional Phase

The duration of this phase can vary tremendously and depends on several factors:

Severity of the injury.
Healing capacity of the patient.
How the condition was managed during the acute phase.
Level of patient involvement in the rehabilitation program.
The goals of this phase are to
significantly reduce or completely resolve the patient's pain;
restore full and pain-free range of motion;
fully integrate the entire upper kinetic chain;
restore full cervical and upper quadrant strength and neuromuscular control.

During this phase, the range of motion exercises are continued until maximum range of motion is attained. The strengthening program is progressed from submaximal isometrics in single planes to maximal isometrics in single planes. Then the patient is progressed to isometrics in combined motions (flexion and side bending and extension and side bending). The strength training is then progressed to concentric and eccentric exercises in single planes, using elastic tubing, pulleys, or isolation exercises. Proprioceptive neuromuscular facilitation patterns are introduced when appropriate. Elastic tubing is issued to the patient to allow training at home.

For progression to return to play, the athlete should demonstrate

normal and pain-free single-plane and multiplane range of motion;
normal cervical, cervicothoracic, glenohumeral, and scapulothoracic strength;
normal flexibility of cervical, cervicoscapular, and cervicothoracic musculature.

Return to sport activities should be designed to mimic the sport as closely as possible. The goal should be to improve the balance, power, and endurance of the cervical, cervicothoracic, glenohumeral, and scapulothoracic muscle groups and force couples.

Pattern 4D: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Connective Tissue Dysfunction

Transverse Ligament Injuries

Injuries to the transverse ligament are classified as follows49,58:

Type I injuries. Disruptions of the substance of the transverse ligament, without an osseous component.
Type II injuries. Fractures or avulsions involving the tubercle for insertion of the transverse ligament on the C1 lateral mass, without disruption of the ligament substance.

The medical literature supports the conclusion that a type I injury is incapable of healing without surgery for internal fixation but that most type II injuries heal when treated with an orthosis.113

Integration of Patterns 4B and 4D: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Secondary to Impaired Posture and Connective Tissue Dysfunction

Myofascial Pain Patterns

Myofascial pain syndromes are closely associated with tender areas that have come to be known as MTrPs (see Chap. 10). The term myofascial trigger point is a bit of a misnomer, because trigger points may also be cutaneous, ligamentous, periosteal, and fascial.114 Dysfunctional joints also are associated with trigger points and tender attachment points.115

For a more detailed description of myofascial pain patterns in the upper quadrants, including their causes, signs and symptoms, and interventions, the reader is referred to the excellent book by Travell and Simons, Myofascial Pain and Dysfunction: The Trigger Point Manual (Volume 1, The Upper Extremities).63

The interventions for MTrPs are outlined in Chapter 10. These include stretch and spray, muscle stripping, massage therapy, myofascial release, ischemic compression, stretching, postural correction and education to eliminate any causative or perpetuating factors, electrotherapeutic and thermal modalities, cryotherapy, injections, and joint mobilizations.

Integration of Patterns 4D and 4E: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Secondary to Connective Tissue Dysfunction and Localized Inflammation

Osteoarthritis

Osteoarthrosis of the A-A joints, unrelated to trauma, is a rare cause of pain in the craniovertebral region and an even more uncommon cause of A-A instability. It could be argued that if osteoarthrosis of the lateral mass articulations progresses, the synovitis may gradually involve the ligamentous structures, thereby weakening them and rendering them prone to rupture.116

Inflammatory Arthritis

The greatest risk for complications with the spondyloarthropathies in the craniovertebral region occurs at the A-A joint, where there are two different synovial articulations: the two lateral facet joints and the articulation between the odontoid process of C2 and the anterior part of C1.86 The transverse ligament is typically the weakest part of the complex in the presence of spondyloarthropathy.

Rheumatoid Arthritis

The most common inflammatory lesion found in the retro-odontoid space is RA, which induces abnormal proliferation of the synovial soft tissue (pannus) and frequently causes the destruction of the bony structure117 (see Chap. 5).

Ankylosing Spondylitis

See Chapter 5.

Gout

See Chapter 5.

Craniovertebral Instability

There has been much controversy about defining and diagnosing spinal instability. Segmental spinal instability generally is defined as a greater displacement between vertebrae than that which occurs under physiologic load. Therefore, maximum flexion and extension radiographs usually are used to determine hypermobility between vertebrae. Craniovertebral instability frequently is encountered in inflammatory, neoplastic, degenerative, and traumatic disorders, in addition to congenital and developmental abnormalities. Clinically, instability appears as a subluxation or spinal deformity accompanied by severe pain or neurologic deficits. Several types of craniovertebral instability are recognized; among them are the following:

Translational or rotary instability of C1. Translational anterior A-A instability is detected on lateral cervical radiographs as a widened, mobile atlantodental interval (ADI) of greater than 3 mm, caused by laxity or rupture of the transverse ligament or from an odontoid fracture.118 Patients with congenital abnormalities of the odontoid process may develop chronic A-A subluxation. This leads to the formation of fibrous granulation tissue or a hypertrophic scar in the peri- or retro-odontoid epidural space, which is known as a “pseudotumor.”119 Chronic mechanical irritation associated with neck movement is speculated to be one of the causes of fibrous scar formation.120 Posterior translation of C1 is also possible, but for this to occur, the dens or anterior arch of the atlas must be fractured or incompetent. Rotational A-A instability appears as asymmetric rotation of the C1 lateral masses on plain radiographs. Rotational subluxations that are irreducible, recurrent, or associated with transverse ligament disruption require surgery.118 Patients with A-A subluxations exceeding 6 mm are at high risk for neurologic injury and sudden death and are, therefore, immediately considered for fusion.121
O-A instability. O-A instability is demonstrated radiographically by movement between the dens and basion (the middle point on the anterior margin of the foramen magnum), by distraction or translation of the occipital condyles, or by vertical migration.122

Surgical stabilization is required to correct instability when conservative intervention has failed or when spontaneous healing with an orthosis, such as a halo brace, is unlikely.

Pattern 4F: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion, or Reflex Integrity, Secondary to Spinal Disorders

Peripheral Vertigo

Dizziness is the third most common complaint among outpatients, after chest pain and fatigue.123 There are several types of dizziness, some benign and some serious, and it is important that the clinician be able to make the distinction. Among the causes of dizziness that must be carefully considered by the clinician examining the cervical spine are the central and peripheral (Table 23-4) causes of vertigo or dizziness (see Chap. 3).124

Table 23-4 Peripheral Vestibular Disorders

Table 23-4 Peripheral Vestibular Disorders

Vestibular neuritis

Ramsay Hunt syndrome

Labyrinthitis

Benign proximal positional vertigo

Ménière's disease

Acute peripheral vestibulopathy

Otosclerosis

Head trauma

Cerebellopontine angle tumor

Toxic vestibulopathies

Acoustic neuropathy

Perilymphatic fistula

Autoimmune disease of the inner ear

Data from Huijbregts P, Vidal P: Dizziness in orthopaedic physical therapy practice: classification and pathophysiology. J Man Manip Ther 12:199–214, 2004.

Vestibular Neuritis

Vestibular neuritis is thought to represent a reactivated dormant herpes infection in Scarpa's ganglion, within the superior division of the vestibular nerve, which innervates the anterior and horizontal SCC.125,126

Ramsay Hunt Syndrome

Ramsay Hunt syndrome is caused by varicella zoster and is a variant of vestibular neuritis, with multiple cranial nerves involved. This involvement results in facial paresis, tinnitus, hearing loss, and a vestibular defect.127,128 It may also involve cranial nerves V, IX, and X.

Labyrinthitis

Infection of the labyrinth can be viral or bacterial. Acute labyrinthitis usually presents with severe vertigo, sudden or progressive hearing loss, nausea, vomiting, and fever. The condition lasts for 1–5 days, with subsequent resolution of complaints over a 2–3-week period.

Benign Paroxysmal Positional Vertigo

Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular disorder and the most common cause of dizziness in the elderly, with the incidence increasing with age.127 Causes of BPPV (see also Chap. 3) include head trauma, vestibular neuritis, insult to the labyrinth, surgical stapedectomy, degeneration of the inner ear, and vestibular artery compromise. Two pathophysiological theories have been proposed to explain the etiology of BPPV: cupulolithiasis, and canalithiasis129:

Cupulolithiasis. Sedimentous material, possibly macular otoconia, is released into the endolymphatic fluid in the SCC. This release of sedimentous material is hypothesized to result from trauma or degenerative changes. When the head is upright, this material will settle on the SCC cupula. Fixed deposits on the cupula increased density at the structure making the cupula, which previously had the same density as the surrounding endolymphatic fluid now sensitive to gravity and, therefore, head position.
Canalithiasis. An accumulation of utricle debris (otoconia), which can move within the posterior SCC and stimulate the vestibular sense organ (cupula), causing vertigo and nystagmus.127

The name BPPV implies that this type of vertigo is positional in nature. However, it may be more correct to call BPPV a positioning-type vertigo129 Symptom duration is brief: 30–60 seconds; hence, it is a positioning-type vertigo rather than positional-type vertigo, as occurs in vertebrobasilar insufficiency.129

The diagnosis usually is made solely on the basis of the history, although it is possible to confuse BPPV with orthostatic hypotension, another common cause of dizziness in the elderly. Whereas orthostatic hypotension causes dizziness when the patient sits up or stands, BPPV can occur in all positions, especially with changes in head position.

The side of the lesion is diagnosed with a maneuver similar to the Dix–Hallpike test (see Fig. 3-26 in Chap. 3). The intervention for posterior canal BPPV involves performing a canalith-repositioning maneuver, which is designed to return the otoconia from the SCC back to the macule of the utricle, from whence it can be reabsorbed.

Canalith-Repositioning Procedure.127 The patient is seated on the end of the bed with his or her feet dangling. The clinician stands to the side of the patient, supporting the patient's head. The patient is moved into the Dix–Hallpike position, toward the side of the involved ear and maintained there for 20 seconds. Then the head is slowly rotated through moderate extension of the cervical spine toward the uninvolved side and maintained in the new position for 20 seconds. The patient is then rolled to a side-lying position, with the head being turned 45 degrees down (toward the floor) and maintained there for 20 seconds. While keeping the head turned toward the uninvolved side and the head pitched down, the patient slowly sits up.

To maintain the otoconia in the utricle following the maneuver, the patient is fitted with a soft collar and is instructed not to bend over, lie back, move the head up or down, or tilt the head to either side for the remainder of the day.

Ménière's Disease

This condition is characterized by paroxysmal vertigo, lasting minutes to days, accompanied by tinnitus, fluctuating low-frequency hearing loss, and a sensation of fullness in the ear.129,130 Attacks are often associated with nausea and vomiting. Age at onset is usually between the ages of 20 and 50 years, and men are more often affected than women.130 The underlying cause is thought to be an increase in the volume of the endolymphatic fluid in the membranous labyrinth, which displaces the inner ear structures with resultant signs and symptoms of horizontal or rotary nystagmus.130

Acute Peripheral Vestibulopathy

This condition is characterized by a sudden onset of vertigo, nausea, and vomiting, which last for up to 2 weeks and is not associated with hearing loss. Differential diagnosis from central disorders characterized by acute vertigo is imperative.130

Otosclerosis

The pathophysiologic mechanism behind otosclerosis is immobility of the stapes and resultant conductive hearing loss. Associated signs and symptoms include vertigo and nystagmus.

Head Trauma

Head trauma may result in labyrinth damage and subsequent vertigo.

Cerebellopontine Angle Tumor

This is a benign acoustic neuroma that can produce insidious unilateral sensorineural hearing loss, vertigo, and tinnitus.130

Toxic Vestibulopathies

Ingested alcohol differentially distributes between the cupula and the endolymphatic fluid: It initially diffuses preferentially into the cupula, decreasing its density relative to that of the endolymphatic fluid, thus rendering the peripheral vestibular apparatus unusually sensitive to gravity.129 The vertigo and nystagmus are evident in the lateral recumbent position and are accentuated when the eyes are closed.129,130 Aminoglycosides (streptomycin, gentamicin, and tobramycin), salicylates (aspirin and derivatives) quinine and quinidine, and various chemotherapeutic drugs have all been associated with producing vertigo, nausea, and vomiting, and occasionally nystagmus.

Acoustic Neuropathy

Conditions such as basilar meningitis, hypothyroidism, diabetes mellitus, and Paget's disease can lead to compression of the vestibulocochlear nerve.129,130

Perilymphatic Fistula

A rare cause of vertigo, which can result from head injury, barotrauma due to diving or flying, or a very forceful Valsalva maneuver, which results in a rapid loss of perilymphatic fluid.129,130

Autoimmune Disease of the Inner Ear

Diseases such as RA, Crohn's disease, or polyarthritis are often concurrently present with fluctuating deafness and recurrent vertigo.129,130

Vestibular Rehabilitation

The use of a custom-designed physical therapy program in the rehabilitation of patients with unilateral peripheral vestibular hypofunction is aimed at promoting vestibular compensation, promoting central habituation, and readjusting the vestibulo-ocular and vestibulospinal reflexes (see Chap. 3).131,132

Repetition of movements and positions that provoke dizziness and vertigo form the basic premise of habituation training, even though many of the exercises may initially increase the patient's symptoms. Several progressions have been devised (Table 23-5 and Box 23-1). Brown and colleagues, in a retrospective case series of 48 patients with central vestibular dysfunction noted improvement in both subjective and objective measures of balance after physical therapy intervention.134 The treatment consisted of one or more of the following: balance and gait training, general strengthening and flexibility exercises, vestibular adaptation exercises, education in the use of assistive devices and safety awareness techniques to avoid falls, and utilization of varied senses, particularly somatosensation and vision, to aid in maintaining balance.134

Table 23-5 Cawthorne–Cooksey Exercises for Patients with Vestibular Hypofunction

Table 23-5 Cawthorne–Cooksey Exercises for Patients with Vestibular Hypofunction

A. In bed
- 1. Eye movements—at first slow, then quick
  - a. Up and down
  - b. From side to side
  - c. Focusing on a finger moving from 3 to 1 ft away from face
- 2. Head movements—at first slow, then quick; later with eyes closed
  - a. Bending forward and backward
  - b. Turning from side to side
B. Sitting
- 1. Same as A1 and A2, above
- 2. Shoulder shrugging and circling
- 3. Bending forward and picking up objects from ground
C. Standing
- 1. Same as A1 and A2 and B3, above
- 2. Changing from sitting to standing position with eyes open and shut
- 3. Throwing a small ball from hand to hand (above eye level).
- 4. Throwing ball from hand to hand under knee
- 5. Changing from sitting to standing and turning round in between
D. Moving about (in class)
- 1. Circle around center person who will throw a large ball and to whom it will be returned
- 2. Walk across room with eyes open and then closed
- 3. Walk up and down slope with eyes open and then closed
- 4. Walk up and down steps with eyes open and then closed
- 5. Any game involving stooping and stretching and aiming, such as skittles, bowls, or basketball
Diligence and perseverance are required, but the earlier and more regularly the exercise regimen is carried out, the faster and more complete will be the return to normal activity.

Data from Herdman SJ, Borello-France DF, Whitney SL: Treatment of vestibular hypofunction. In: Herdman SJ, ed. Vestibular Rehabilitation. Philadelphia, PA: FA Davis, 1994:287–315.

Data from Dix MR: The rationale and technique of head exercises in the treatment of vertigo. Acta Oto-Rhino-Laryngol Belg 33:370, 1979.

Box 23-1 Exercises to Improve Postural Stability

Box 23-1 Exercises to Improve Postural Stability

These exercises are devised to incorporate head movement (vestibular stimulation) or to foster use of different sensory cues for balance.

1. The patient stands with his or her feet as close together as possible, with both or one hand helping maintain balance by touching a wall if needed. The patient then turns his or her head to the right and to the left horizontally, while looking straight ahead at the wall for 1 minute without stopping. The patient takes his or her hand or hands off the wall for longer and longer periods of the time while maintaining balance. The patient then tries moving his or her feet even closer together.
2. The patient walks, with someone for assistance if needed, as often as possible (acute disorders).
3. The patient begins to practice turning his or her head while walking. This will make the patient less stable, so the patient should stay near a wall as he or she walks.
4. The patient stands with his or her feet shoulder-width apart with eyes open, looking straight ahead at a target on the wall. He or she progressively narrows the base of support from feet apart to feet together to a semi-heel-to-toe position. The exercise is performed first with arms outstretched, then with arms close to the body, and then with arms folded across the chest. Each position is held for 15 seconds, before the patient does the next-most-difficult exercise. The patient practices for a total of 5–15 minutes.
5. The patent stands with his or her feet shoulder-width apart with eyes open, looking straight ahead at a target on the wall. The patient progressively narrows his or her base of support from feet apart to feet together to a semi-heel-to-toe position. The exercise is performed with eyes closed, at first intermittently and then for longer and longer periods of time. The exercise is performed first with arms outstretched, then with arms close to the body, and then with arms folded across the chest. Each position is held for 15 seconds, and then the patient tries the next position. The patient practices for a total of 5–15 minutes.
6. A headlamp can be attached to the patient's waist or shoulders, and the patient can practice shifting weight to place the light into targets marked on the wall. This home “biofeedback” exercise can be used, with the feet in different positions and the patient standing on surfaces of different densities.
7. The patient practices standing on a cushioned surface. Progressively more difficult tasks might be standing on hard floor (linoleum, wood), thin carpet, shag carpet, thin pillow, and sofa cushion. Graded-density foam can also be purchased.
8. The patient practices walking with a more narrow base of support. The patient can do this first, touching the wall for support or for tactile cues and then gradually touching only intermittently and then not at all.
9. The patient practices turning around while walking, at first making a large circle but gradually making smaller and smaller turns. The patient must be sure to practice turning in both directions.
10. The patient can practice standing and then walking on ramps, either with a firm surface or with more cushioned surface.
11. The patient can practice maintaining balance while sitting and bouncing on a Swiss ball or while bouncing on a trampoline. This exercise can be incorporated with attempting to maintain visual fixation of a stationary target, thus facilitating adaptation of the otolith-ocular reflexes.
12. Out in the community, the patient can practice walking in a mall before it is open and, therefore, while it is quiet; can practice walking in the mall while walking in the same direction as the flow of traffic; and can then walk against the flow of traffic.

See reference 133

Cervical Vertigo

Cervical vertigo is a diagnosis and a disorder that seems to be poorly understood, and yet dizziness is a common clinical symptom in patients with cervical and upper quadrant syndromes.124 Cervical or reflex vertigo is thought to originate from a disturbance of the tonic neck reflex input from the neck to the vestibular nucleus. This disturbance can be caused by a dysfunction in the cervical joints135 or the SCM.136 As early as 1926, Barré137 described a syndrome involving sub-occipital pain and vertigo, which was usually precipitated by turning the head. Ryan and Cope138 coined the term “cervical vertigo” in 1955 for this syndrome.

Cervical vertigo symptoms appear to result from an alteration to proprioceptive spinal afferents from the mechanoreceptors of the neck, usually, but not always, resulting from trauma.139 Macnab133 thought that the 575 patients he studied exhibited little evidence of overt neck damage, or of neurologic damage. He thought areas other than the neck itself, such as the brain, brain stem, cranial nerves, cervical nerve roots, or inner ear, might be responsible for the symptoms. Biesinger,140 on the other hand, proposed two possible neurologic origins:

A contributor from the sympathetic plexus surrounding the vertebral arteries.
Functional disorders of proprioception in segments C1–2.

It would seem likely that direct damage to the vestibular apparatus, or severe damage to the vertebral artery, will produce immediate dizziness, whereas dizziness arising from the cervical joints or a less severely injured vertebral artery may not occur until the joints themselves became abnormal, or until the ischemia has had time to make itself felt (Table 23-6).110 Because cervical pain also frequently is delayed, it is at least arguable that delayed dizziness commonly originates from injured cervical joints and less commonly from ischemia.110

Table 23-6 Differential Diagnostic Characteristics of Cervicogenic Dizziness, BPPV, and VBI

Table 23-6 Differential Diagnostic Characteristics of Cervicogenic Dizziness, BPPV, and VBI

Vertigo Type

Nystagmus Characteristics

Associated Signs and Symptoms

Cervicogenic dizziness

Positioning type

No latency period

Nystagmus

Brief duration

Neck pain

Fatigable with repeated motion

Suboccipital headaches

Cervical motion abnormality

BPPV

Positioning type

Short latency: 1–5 s

Nystagmus

Brief duration: <30 s

Fatigable with repeated motion

VBI

Positional type

Long latency: 55 ± 18 s

Dizziness

Increasing symptomatology with maintained head position

Drop attacks

Diplopia

Not fatigable with repeated motion

Dysarthria

Dysphagia

Ataxia of gait

Nausea

Numbness

Nystagmus

BPPV, benign paroxysmal positional vertigo; VBI, vertebrobasilar insufficiency.

Data from Huijbregts P, Vidal P: Dizziness in orthopaedic physical therapy practice: classification and pathophysiology. J Man Manip Ther 12:199–214, 2004; Terrett AGJ: Current Concepts in Vertebrobasilar Complications Following Spinal Manipulation, 2nd edn. Norwalk, IA: Foundation for Chiropractic Education and Research, 2001.

The intervention for cervical vertigo generally begins with conservative physical therapy and anti-inflammatory medications, once testing rules out other causes. With time and therapy, most patients with abnormal electroneurograms end up having normal results at follow-up testing.110

Cervicogenic Headache

CHs, also known as cervical headaches, are loosely defined as “any headache beginning in the neck.”30 These types of headaches are difficult to define and classify because of their variable distribution and character of symptoms. Neck pain can arise from injuries of the cervical muscles, ligaments, disks, and joints. From lower cervical segments, the pain may be referred to the shoulder and upper limb (see Table 22-1). From upper segments, neck pain may be referred to the head and manifested as headache.141 The World Cervicogenic Headache Society has defined CH as “referred pain perceived in any part of the head and caused by a primary nociceptive source in musculoskeletal tissues that are innervated by cervical nerves.” According to the International Headache Society (IHS),142 a CH is defined as one that meets the following criteria: (1) pain localized to the neck and occipital region that may project to the forehead, orbital region, temples, vertex, or ears; (2) pain precipitated or aggravated by specific neck movements or sustained neck posture; and (3) resistance to or limitation of active or passive physiologic and accessory neck movements or abnormal tenderness of neck muscles, or both. In addition, the IHS guidelines require radiographic examination to diagnose CHs. According to the IHS, radiologic examination must reveal at least one of the following: (1) movement abnormalities during flexion–extension, (2) abnormal posture, or (3) fractures, bone tumors, RA, congenital abnormalities, or other distinct pathology other than spondylosis or osteochondrosis.142 To help in the determination when examining a patient complaining of headache, the clinician is advised to follow the simple diagnostic clinical algorithm set out below:62

Exclude possible intracranial causes on history and physical examination. If intracranial pathology is suspected, then an urgent workup is required, which may include neuroimaging studies and laboratory investigations.
Exclude headaches associated with viral or other infective illness.
Exclude a drug-induced headache or headache related to alcohol or substance abuse.
Consider an exercise-related (or sex-related) headache syndrome (see Chap. 5).
Differentiate between vascular, tension, cervicogenic, or other causes of headache.

With CHs, pain is precipitated or aggravated by specific neck movements or sustained neck posture.

Clinical
Pearl

CHs tend to be unilateral and accompanied by tenderness of the C2–3 articular pillars on the affected side.143 The patient with a CH usually reports a dull aching pain of moderate intensity, which begins in the neck or occipital region and then spreads to include a greater part of the cranium.144

CHs can emerge from a number of sources, including145

irritation of the posterior (dorsal) root ganglia and nerve root components caused by compression of the C2 posterior (dorsal) root ganglia between the C1 posterior arch and the superior C2 articular process146;
compression of the C2 anterior (ventral) ramus at the articular process of C1–288;
entrapment of the C2 posterior (dorsal) root ganglia by the C1–2 epistrophic ligament.147

Neck pain and headache are also the cardinal features of a whiplash mechanism.37,148,149 According to the international classification, headache after whiplash is best classified as cervicogenic (group 11.2.1) and thus related to injured structures around the cervical spine.142 The incidence of headache after whiplash injury is said to decrease during the first 6 months after trauma.150 Headache after whiplash can be from cervical spine trauma as listed or from a possible coup–contracoup injury from the rapid acceleration–deceleration of the brain in a closed calverium. Particularly relevant is the relation between a history of headache and the development of a trauma-related headache after whiplash injury. In addition, psychological variables, which may be important in idiopathic headache,151,152 should be evaluated in relation to the development and recovery from headache after whiplash.

Several interventions have been recommended for CHs, including posture training, manual therapy, exercise, rest, and minor analgesics.64 Manual therapy studies have demonstrated positive effects at both the impairment (pain and muscle function) and the disability level, with most studies focusing on short-term outcomes.153,154

In a single case study, McDonnell and colleagues153 described an intervention approach for CH, consisting of a specific active exercise program and modification of postural alignment, with good results after seven visits over a 3-month period. The intervention focused on

increasing the strength and control of the abdominals;
increasing the length of the anterior thorax muscles;
increasing the length of the posterior cervical extensor muscles;
improving the strength and decreasing the length of the posterior scapulothoracic muscles;
increasing shoulder joint and cervical motion.

Schoensee et al.155 found that a treatment regimen of joint mobilization to the upper cervical spine in 10 CH patients decreased headache frequency, duration, and intensity.156 CH frequency remained lower 1 month after the study.155

McKenzie157 recommends a home program of cervical retraction exercises to decrease CH symptoms and maintain correct cervical alignment. These exercises, which are performed throughout the day, are progressed based on changes in symptom location and intensity. If an exercise fails to reduce CH pain, a new component is added and the prior exercise is discontinued.156

Active Cervical Rotation

For the prevention of chronic tension-type headaches, behavioral approaches commonly involve regular sleep and meals, stress coping, meditation, or relaxation strategies, and avoidance of initiating or trigger factors, including work-related or family stress and emotional problems.64

Hammill and colleagues158 conducted a study, in which 20 subjects with tension-type headaches were treated with posture training, massage, and stretches. The results showed a significant decrease in headache frequency and in sickness impact profile scores at the end of the 6-week treatment period and again 12 months after the treatment concluded.156

Bronfort and colleagues159 performed a systematic review of randomized controlled trials to include nine trials of 683 subjects with chronic headaches. They found that spinal mobilization treatment had a better effect than massage for CH and that it had a comparable effect to commonly used prophylactic prescription medications for tension-type and migraine headaches.156,159

Chiari Malformations

Chiari malformations are a group of disorders that manifest varying degrees of inferior displacement of the cerebellum and brain stem through the foramen magnum. Four types are recognized160:

Chiari type I malformation. This type consists of the inferior displacement of the cerebellar hemispheres (cerebellar tonsils) through the foramen magnum. This tongue-like projection of the medial inferior cerebellum envelops the medulla. The fourth ventricle is in a normal position. As the degree of descent increases, the outflow of cerebrospinal fluid decreases, and a tubular cavitation of the upper spinal cord, called syringomyelia, then occurs. Syringomyelia is distinct from hydromyelia, which is an enlargement of the central canal of the spinal cord.
Chiari type II malformation. Chiari type II malformation is associated with inferior displacement of the brainstem and fourth ventricle through the foramen magnum into the vertebral canal, often with hydrocephalus and meningomyelocele.
Chiari type III malformation. This type is associated with a herniation of the cerebellum into a high cervical meningocele.
Chiari type IV malformation. In Chiari type IV malformation, the cerebellum is generally hypoplastic.

Chiari types II–IV typically present with florid symptoms and are usually diagnosed in infancy or childhood.160 In contrast, in Chiari type I malformation, the signs of brainstem dysfunction evolve slowly over years and are, thus, more likely than the other types to be encountered in physical therapy.

The clinical manifestations of Chiari I malformation are among the most protean in clinical medicine, which can lead to a delay in diagnosis. The most common presenting symptoms are upper extremity weakness and various pain syndromes that often include neck and arm pain.161 Occipital headaches, which are exacerbated by coughing, sneezing, stooping, or lifting, are also frequent.161 Clumsiness, upper extremity sensory changes ataxia, vertigo, hearing loss, tinnitus, dysphagia, hiccups, dysarthria, and hoarseness of voice are some of the other reported symptoms.161

The diagnosis of Chiari malformation is most commonly made with MRI. If surgical intervention is necessary, it involves decompression of the Chiari malformation with or without drainage of the syringomyelia.160

Pattern 4G: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Fracture

Although the intervention for fractures is beyond the scope of practice for a physical therapist, being able to detect their presence, especially in this region, is critical. Clinical findings that could suggest the possibility of a craniovertebral fracture include162,163:

painful neck muscle splinting;
neck and occipital numbness;
pain and stiffness in the neck, with a reluctance to move the head;
presence or absence of neurological signs and symptoms.

Fractures of the Axis

There are three types of fractures of the C2 (axis) vertebra: odontoid fractures involving the dens, bilateral traumatic spondylolisthesis of the pars interarticularis (“hangman's” fracture), and nonodontoid/nonhangman's (miscellaneous) fractures.164

Odontoid Fractures

Odontoid fractures are a relatively common upper cervical spine injury, comprising nearly 60% of all fractures of the axis and 10–18% of all cervical spine fractures.67,165–168 Although odontoid fractures occur in all age groups, the mean age is approximately 47 years with a bimodal distribution.7 In younger patients, who comprise the first peak, these fractures are usually secondary to high-energy trauma; motor vehicle accidents are responsible for the majority of the odontoid injuries.169 The second peak in the incidence of odontoid fractures is in the elderly.106 In fact, odontoid fractures are the most common cervical spine fracture in patients older than age 70.7 These fractures, unlike those in the younger patients, tend to result from low-energy injuries, such as falls from a standing height.7 The mechanism of injury often is hyperextension resulting in posterior displacement of the odontoid.7

Described in 1974, the Anderson and D'Alonzo system divides fractures into three types based on anatomic location166:

Type I. Type I is an oblique avulsion fracture from the tip of the odontoid above the transverse ligament, attached to the alar ligament. This fracture is clinically rare, accounting for 1–5% of odontoid fractures, and may be associated with O-A dislocation.167
Type II. Type II fractures occur through the neck of the odontoid. They are the most common type of odontoid fracture (38–80%).
Type III. Type III fractures extend into the body of C2. They account for 15–40% of all odontoid fractures.

Current management of odontoid fractures is based on three principles: timely diagnosis, reduction of the fracture, and sufficient immobilization to permit healing.168 Numerous treatment methods have been developed to achieve anatomic alignment and optimal stability, including cervical orthoses, Minerva jackets, halo-thoracic vests, posterior cervical fusion, and direct anterior dens screw fixation.170

Jefferson Fracture

Jefferson fracture was defined as the association of a lateral mass fracture of C1 and the disruption of the C1 ring (either on the posterior or on the anterior arch).171 Jefferson fractures now represent a spectrum of injuries from bilateral ring fractures, to lateral mass fracture, to the pathognomonic four-point fracture (both anterior and posterior arches) of the C1 ring that the fracture was originally named for.172 Jefferson fracture classically results from axial loading on the atlas and is generally associated with minimal neurologic deficit and good prognosis for neurologic recovery.173 Presently, three general types of Jefferson fractures are described174:

Type I. Type I involves bilateral single-arch (anterior or posterior, but not both) fractures.
Type II. Type II is the concurrent anterior and posterior arch fractures, which include the classic four-point break Jefferson fracture.
Type III. Type III is the lateral mass fracture of C1, which may extend into the anterior or the posterior osseous arch.

No prognostic significance has been attached to the different types of Jefferson fracture.174 Isolated Jefferson fracture can be treated effectively with external immobilization. The traditional mode of cervical immobilization is the halo vest.172

Therapeutic Techniques

Techniques to Increase Soft Tissue Extensibility

Soft tissue techniques generally are applied before performing the local segmental examination and in preparation for a mobilization or manipulation intervention. Soft tissue techniques are capable of producing a strong analgesic, and relaxing, effect. With a reduction in cervical muscle tension, or spasm, it becomes much easier for the clinician to palpate and register movement.

General Kneading

General kneading techniques can be applied to the soft tissues of the craniovertebral region. These techniques are especially useful before performing a specific mobilization or manipulation.

Suboccipital Massage

Soft tissue techniques can be performed at several sites in the cervical region. In principle, every tender site can be treated, even though it usually involves areas of referred pain or tenderness.175

The patient is positioned prone or sitting, and the head is positioned in slight flexion, without rotation. The clinician stands on the uninvolved side. The SCM may need to be displaced laterally, in order to palpate the muscles attaching to the transverse process of C1. The clinician locates the most tender area and places the thumb directly lateral to the tender spot (Fig. 23-17). During the massage, the thumb moves from laterally to medially and slightly cranially, while at the same time, pressure is exerted in an anteromedial and superior direction.

Figure 23-17

Suboccipital massage.

A similar technique is used in a combination of upper cervical traction and soft tissue mobilization of the suboccipital muscles. This technique is best performed with the patient supine, because the neck is unloaded and the patient can relax more in the supine versus seated position. While one hand grasps the patient's head, the clinician uses the fingers of the other hand to press gently into the muscles between two vertebrae. While maintaining the pressure on the muscles, a slight traction force is applied and sustained for several seconds before being released. The procedure is repeated in a rhythmic manner.

The paravertebral muscles can be treated in a similar fashion. With one hand, the clinician stabilizes the patient's head at the forehead. With the index or middle finger of the left hand, or both fingers, the clinician pulls the musculature in a lateral and anterior direction. At the same time, the hand on the patient's forehead rotates the patient's head away from the side being treated. The end position is held for 2–3 seconds, before returning to the initial position. The clinician repeats this technique for several seconds or minutes in a rhythmic manner.

Muscle Stretching of the Suboccipital Muscles

Rectus Capitis Posterior Major and Minor

To stretch these muscles, the patient is positioned in supine or sitting. The clinician fixes C2 into craniovertebral flexion (see Fig. 23-18). To stretch the left muscle, a right side bending and right rotation motion is added, and the patient is instructed to not let the head drop back. Hold–relax or contract–relax techniques can be used.

Figure 23-18

Stretch for rectus capitis posterior major and minor.

Inferior Oblique

To stretch the left muscle, the patient's head and neck are positioned into flexion (see Fig. 23-19), left side bending, and right rotation. A massage to the muscle can be applied by stroking the muscle from the C1 transverse process to the C2 spinous process, applying a force in the direction of less pain.

Figure 23-19

Stretch for inferior oblique.

Superior Oblique

The patient is positioned in sitting. The clinician places the index finger over the posterior aspect of the transverse process of C1, and the other hand wraps around the patient's head. To stretch the right superior oblique, the patient's head and neck must be placed in flexion, left side bending, and right rotation (see Fig. 23-20). Hold–relax or contract–relax techniques can be used.

Figure 23-20

Stretch for superior oblique.

Self-Stretching

The following exercises should be performed at an intensity level that achieves an improvement without a regression of status.

Chin Retraction

The patient is seated in the correct posture. The patient is instructed to attempt to move the head, as a unit, in a posterior direction, while maintaining eye level. The clinician should limit the number of chin tucks the patient performs, to remove any potential for harm to the cervical structures from overuse.

Patient Exercises: CV Distraction

Patient Exercises: CV Side Flexion

C2–3 Side Bending and Rotation

The pattern of limitation for this area is usually one of a closing restriction. The patient is seated in the correct posture. The patient places both hands behind the neck, with the ulnar border of the little finger being just below the C2 spinous process and the rest of the hand covering as much of the midcervical region as possible. The patient then simultaneously side flexes and rotates the neck and head in the direction of the restriction (Fig. 23-21), by attempting to look downward and backward (for a closing restriction).

Figure 23-21

C2–3 side-bending and rotation exercise.

A‐A Rotation

The patient is seated in the correct posture. The patient places both hands behind the neck, with the ulnar border of the little finger being at the level of the C2 spinous process and the rest of the hand covering as much of the midcervical region as possible. The patient then gently turns the head in the direction of the restriction (Fig. 23-22). Coupled motions should be encouraged. For example, if the patient has a restriction with right rotation, right rotation and left side bending are emphasized.

Patient Exercises: AA Rotation

Figure 23-22

Exercise to increase right rotation at the A-A.

O‐A Flexion

The patient is seated in the correct posture. The patient performs a chin tuck. From the chin-tucked position, the patient is instructed to place the tips of the index and middle fingers of both hands over the anterior aspect of the chin (Fig. 23-23). The fingertips provide resistance for an attempted extension movement of the head on the neck. The patient then attempts to look upward, while resisting the motion with the fingertips. This is followed by relaxation and then another chin tuck. An alternative method involves asking the patient to clasp their figures behind the neck so that the little fingers are placed at the base of the skull.

Figure 23-23

Home exercise for O-A flexion.

O‐a Extension

The patient is seated in the correct posture. The patient places both hands behind the neck, with the ulnar border of the little finger being at the level of the C1 spinous process and the rest of the hand covering as much of the midcervical region as possible. The patient then gently lifts the chin around the appropriate axis (Fig. 23-24).

Figure 23-24

Home exercise for O-A extension.

Techniques to Increase Joint Mobility

A series of studies that have investigated the efficacy of manual therapy in the treatment of upper cervical dysfunction and headache are outlined in Table 23-7.

Table 23-7 Summary of Published Studies Investigating Manual Therapy Treatment for Upper Cervical Dysfunction and Headache

Table 23-7 Summary of Published Studies Investigating Manual Therapy Treatment for Upper Cervical Dysfunction and Headache

Author

Sample Size

Intervention Group

Control Group

Outcome Measured

Number of Visits and Duration of Care

Boline et al.a

150

Manipulation

Medication

Headache frequency and intensity. Number of medications. SF-36 score

12 visits

6 wks

Howe et al.b

Manipulation ± Injection + Medication

Medication only

Cervical range of motion. Neck, scapular, arm, and hand pain. Neck stiffness. Headache intensity

1 visit only

Jensen et al.c

Mobilization Muscle energy

Cold packs

Frequency of medications. Pain intensity, dizziness, visual, and hearing

6 visits

12 wks

Nilssond

Manipulation

Laser Friction massage

Headache duration and intensity. The number of nonsteroidal anti-inflammatory drugs

6 visits

3 wks

Nilsson et al.e

Manipulation

Laser Friction massage

Cervical passive range of motion

6 visits

3 wks

Osterbauer et al.f

Manipulation Electrical ± stimulation ± Medication

No treatment (10 nonimpaired)

Pain intensity. Cervical range of motion. Kinesthesia

2–3 visits per wk

6 wks

Parker et al.g

Manipulation by Chiropractor Manipulation by physical therapist

Mobilization by a physical therapist

Migraine frequency, intensity, and duration. Disability

Up to 16 visits

8 wks

Rogersh

Manipulation

Stretching

Pain. Kinesthesia

6 visits

Schoensee et al.156,i

Mobilization

None

Headache frequency, duration, and intensity

3–4 wks

9–12 visits

3–4 wks

Vernonj

Manipulation

None

Headache frequency, duration, and intensity

9 visits

Unspecified

Whittingham et al.k

Manipulation at C1 and C2

None

Headache frequency, duration, and intensity

4 visits

2 wks

Yeomansl

Manipulation

None

Cervical intersegmental range of motion

3 visits per wk

2–6 wks

aData from Boline PD, Kassak K, Bronfort G, et al.: Spinal manipulation vs. amitriptyline for the treatment of chronic tension-type headaches: a randomized clinical trial. J Manip Physiol Ther 18:148–154, 1995.

bData from Howe DH, Newcombe RG, Wade MT: Manipulation of the cervical spine—a pilot study. J R Coll Gen Pract 33:574–579, 1983.

cData from Jensen OK, Nielsen FF, Vosmar L: An open study comparing manual therapy with the use of cold packs in the treatment of post-traumatic headache. Cephalalgia 10:241–250, 1990.

dData from Nilsson N: A randomized controlled trial of the effect of spinal manipulation in the treatment of cervicogenic headache. J Manip Physiol Ther 18:435–440, 1995.

eData from Nilsson N, Christensen HW, Hartvigsen J: Lasting changes in passive range motion after spinal manipulation: a randomized, blind, controlled trial. J Manip Physiol Ther 19:165–168, 1996.

fData from Osterbauer PJ, Derickson KL, Peles JD, et al.: Three-dimensional head kinematics and clinical outcome of patients with neck injury treated with spinal manipulative therapy: a pilot study. J Manip Physiol Ther 15:501–511, 1992.

gData from Parker GB, Tupling H, Pryor DS: A controlled trial of cervical manipulation of migraine. Aust N Z J Med 8:589–593, 1978.

hData from Rogers RG: The effects of spinal manipulation on cervical kinesthesia in patients with chronic neck pain: a pilot study. J Manip Physiol Ther 20:80–85, 1997.

iData from Schoensee SK, Jensen G, Nicholson G, et al.: The effect of mobilization on cervical headaches. J Orthop Sports Phys Ther 21:184–196, 1995.

jData from Vernon H: Chiropractic manipulative therapy in the treatment of headaches: a retrospective and prospective study. J Manip Physiol Ther 5:109–112, 1982.

kData from Whittingham W, Ellis WB, Molyneux TP: The effect of manipulation (toggle recoil technique) for headaches with upper cervical joint dysfunction: a pilot study. J Manip Physiol Ther 17:369–375, 1994.

lData from Yeomans SG: The assessment of cervical intersegmental mobility before and after spinal manipulative therapy. J Manip Physiol Ther 15:106–114, 1992. With permission from Molina P: Upper cervical dysfunction and cervicogenic headache. In: Wilmarth MA, ed. Evidence-Based Practice for the Upper and Lower Quarter. Orthopaedic Physical Therapy Home Study Course 13.2.1. La Crosse, WI: Orthopaedic Section, APTA, Inc, 2003:1–44.

Joint Mobilization Techniques

O‐A Joint

Specific Traction175

Patient Exercises: Auto OA Mobilization

Patient Exercises: OA Mobilization

Specific traction is used here, as elsewhere in the spine, to apply a gentle degree of distraction and mechanical stimulation. It typically is used with acute conditions.

The patient is positioned in supine. The clinician stabilizes the C1 vertebra using a wide pinch grip, and the patient's forehead is stabilized against the clinician's shoulder (see Fig. 23-25). A traction force is then applied, a graded cranial force (I to II) by the occipital hand and the chest.

Figure 23-25

Specific traction to O-A joint in supine.

Supine Technique for a Symmetrical Loss of O-A Extension

The patient is positioned in supine, head on a pillow, and knees flexed over a pillow. The clinician is positioned at the head of the table. The clinician cradles the patient's head in both hands with the finger pads under the occiput and places each thumb over the zygomatic arches of the patient. Using thumb pressure, the clinician tilts the patient's head into craniovertebral flexion, while the finger pads produce a posterior glide of the occipital condyles (see Fig. 23-26).

Figure 23-26

Supine technique for a symmetrical loss of O-A extension.

The joint slack is taken up. The patient is instructed to attempt to place the chin on their throat. After an isometric contraction of 3–5 seconds, the patient is instructed to relax, and the resultant joint slack is taken up by the clinician. When, following repeated muscle-assisted mobilizations, no further increased motion is apparent, it can be assumed that the inert barrier to motion has been reached. Passive soft tissue mobilization is then performed. This combination of muscle-assisted and passive mobilizations is continued until no further soft-tissue slack is appreciated.

Seated Technique for a Loss of Extension at the Left O-A Joint175

The following mobilization techniques can be used for a restriction of the anterior glide of the left O-A joint. The reader is expected to extrapolate the information to produce the necessary technique for a restriction of the anterior glide of the right joint.

The patient is seated with the clinician standing on the right side. C1 is stabilized anteriorly, using a wide pinch grip by the left hand and wrapping the pads of the index finger and thumbs around the front of the transverse process (Fig. 23-27). The right arm stabilizes the patient's head against the clinician's chest, and the right hand grasps the occiput. The patient's head is then extended and left side flexed around the appropriate axes, with right translation being produced by means of the side bending until the extension barrier is reached. The mobilization is then performed by applying a graded force against the translation barrier.

Figure 23-27

Seated technique for a loss of extension at the left O-A joint.

Active participation from the patient can be introduced. From the motion barrier, the patient is asked to gently meet the clinician's resistance. The direction of resistance is that which facilitates further extension, left side bending, and right rotation. The isometric contraction is held for up to 5 seconds and followed by a period of complete relaxation. The joint is then passively taken to the new motion barrier. The technique is repeated three times and followed by a reexamination.

Supine Technique for an Asymmetrical Loss of O-A Extension (e.g., Loss of Left O-A Joint Extension)94

The patient is positioned in supine, head on a pillow, and knees flexed over a pillow. The clinician is positioned at the head of the table. The clinician cradles the patient's head in both hands. The left index and middle finger pads are placed just medial to the patient's left mastoid process, with the palm supporting the occiput. The clinician's right hand is placed over the right side of the patient's head.

Using both hands, the clinician passively moves the patient's head into craniovertebral extension and right translation, until the extension motion barrier of the left O-A joint is reached. The joint slack is taken up by the clinician using their left fingers to push upward toward the patient's lips and the clinician's right hand, thereby inducing side flexion of the patient's head to the left.

The patient is instructed to resist left side flexion of the O-A joint using the command “Don't let me pull your left ear upwards.” The contraction is held for 3–5 seconds, and the patient is asked to relax. As the patient relaxes, the new joint slack is taken up by the clinician pushing further toward the patient's lips with the left finger pads and side flexing the patient's head to the left with clinician's right hand. To ensure that the extension is occurring around a craniovertebral axis, the clinician looks at the patient's face. As slack is taken up, flexion of the right O-A joint should simultaneously produce chin movement toward the ceiling, while the forehead moves toward the bed. To ensure that the left side flexion is occurring around the correct axis, the clinician should note the chin movement occurring to the right, while the forehead moves to the left. During the conjunct right rotation, the chin and forehead should both be seen to rotate to the right.

As with the technique to increase unilateral flexion, once the inert barrier is reached, the combined passive motion into the barrier is stressed with oscillatory passive stretch, and then muscle-assisted mobilizations are repeated. This is continued until there is no further “give” to the motion barrier.

Supine Technique for an Asymmetrical Loss of O-A Flexion (e.g., Loss of Left O-A Joint Flexion)94

The patient is positioned in supine, head on a pillow, and knees flexed over a pillow. The clinician is positioned at the head of the table. The clinician cradles the patient's head in both hands, so that the right hand is placed over the right side of the patient's head and the clinician's left index and middle finger pads are placed just medial to the patient's left mastoid processes, with the palm supporting the patient's occiput.

Using both hands, the clinician produces craniovertebral flexion to the barrier. At this point, the patient's head is translated to the left until a firm end-feel is encountered. This maneuver induces a right side bending and a left rotation at the O-A joints. The barrier to flexion of the left O-A joint is thus achieved.

Joint slack is taken up as the clinician uses a lumbrical action to pull on the patient's left mastoid process, in the direction toward the bed surface, with the left index and middle fingers. Simultaneously, the patient's head is side flexed to the right by the clinician's right hand. Using fingertip pressure through the right hand, the clinician instructs the patient: “Don't let me lift your right ear upwards.” The clinician then attempts to draw the patient's right mastoid process superiorly. This produces an isometric resistance of right side flexion of the O-A joint (and, therefore, left rotation).

After an isometric contraction of 3–5 seconds, the patient is instructed to relax, and as the relaxation is felt by the clinician, the resultant joint slack is taken up by the clinician by simultaneously pulling the patient's left mastoid process toward the bed (with the left hand) and side bending the head to the right (with the right hand). When, following repeated muscle-assisted mobilizations, no further increased motion is apparent, it can be assumed that the inert barrier to motion has been reached. Passive soft tissue mobilization is then achieved by pushing further into the left O-A joint flexion barrier by simultaneously pulling the left mastoid process toward the bed (left hand) and right side bending of the head (right hand). This combination of muscle-assisted and passive mobilizations is continued until no further soft tissue slack is appreciated. To ensure that the flexion is occurring around a craniovertebral axis, the clinician looks at the patient's face. As slack is taken up, flexion of the left O-A joint should simultaneously produce

a downward motion of the patient's chin and an upward motion of the patient's forehead (flexion);
a left-sided motion of the patient's chin with a left-sided motion of the forehead (right side flexion);
a rotation of chin and forehead to the left (left rotation).

If these facial movements are not seen, then the right hand is used to ensure that these motions are occurring, thus maintaining a craniovertebral axis.

A‐A Joint

Loss of the Anterior-Inferior Glide of the Left A-A Joint (e.g., Loss of Right Rotation in A-A Joint—Loss of Left Anterior/Inferior Glide)94

The patient is positioned in supine, head on a pillow, and knees flexed over a pillow. The clinician is positioned at the head of the table. The clinician cradles the patient's head in both hands. The clinician's right index and middle finger pads are placed around the left side of the patient's C2 neural arch, making firm contact with the left side of the C2 spinous process. The clinician's left hand supports the left side of the patient's head. The patient's head is side flexed by clinician's left hand. Using the fingers of the right hand, the clinician feels for the C2 spinous process to move to the right. At this point, the C2 spinous process is pulled by the index and middle fingers of the right hand until the motion barrier is detected. The patient is instructed to push their head into clinician's left hand, i.e., resisted left side flexion. The C2 spinous process should be felt to move to the right, and the clinician's right fingers move to fix it, as the patient is instructed to relax. As patient relaxes, the slack in left side bending of the head is taken up. This is repeated until no further motion of C2 spinous process is detected.

A similar technique can be performed with the patient in sitting (Fig. 23-28). Using one hand (left, in the photo), the clinician stabilizes the C2 segment and the inferior vertebral segments using a lumbrical grip. The fifth digit of the other hand wraps around the neural arch of C1 and supports the head. The patient's head is side flexed by clinician's shoulder and rotated by the clinician's right hand until the rotation barrier is reached. The mobilization is then performed by applying a graded force against the barrier. Active participation from the patient can be introduced. From the motion barrier, the patient is asked to gently meet the clinician's resistance. The direction of resistance is that which facilitates further rotation. The isometric contraction is held up to 5 seconds and followed by a period of complete relaxation. The joint is then passively taken to the new motion barrier. The technique is repeated three times and followed by a reexamination.

Figure 23-28

Seated technique for loss of right rotation in A-A joint—loss of left anterior/inferior glide.

Mobilizations with Movement176

Upper Cervical Traction

This is an excellent technique for the intervention of upper cervical headaches. The patient is positioned in sitting, with the clinician standing in front, facing the patient. The patient's head against the clinician's chest, and the fingers wrap around the patient's head to provide firm support (Fig. 23-29). The clinician's other hand is used to stabilize the inferior segment (see Fig. 23-29).

Figure 23-29

Upper cervical traction.

The clinician applies pressure on the inferior segment while preventing motion of the head and applying a longitudinal force through the head. The end-feel is obtained and is maintained for 10–20 seconds.

To Improve Right Rotation of the A‐A Joint

The patient is positioned in sitting, with the clinician sitting behind. The clinician places the thumb of one hand over the left aspect of the transverse process of C2, and the other thumb over the first thumb to help reinforce it. The remaining fingers of the hands are placed around the patient's neck and upper back, or to the side of the head (Fig. 23-30).

Figure 23-30

Mobilization to increase right rotation of the A-A.

The patient is asked to rotate the head and neck slowly to the right, while the clinician simultaneously assists the movement using pressure from both thumbs, rotating C2 to the left.

This technique can be taught as part of the patient's home exercise program, using a to wel, belt, or a strap (Fig. 23-31). The same technique can be used to improve cervical rotation to the left by altering the position of the thumbs.

Figure 23-31

Home exercise to increase right rotation of the A-A.

Case Study: Headache and Neck Pain

History

A self-employed 42-year-old man presented to the clinic complaining of posterior upper neck pain and right suboccipital and occipital headache, which began 2 months earlier after a diving accident. He denied being knocked unconscious and could remember everything about the accident except for the period a few minutes after it. The posterior neck pain was felt immediately but was much worse the next morning upon waking. The occipital headaches started a few days later and became worse with fatigue or exertion. The patient also reported difficulty concentrating and sleeping and had occasional bouts of dizziness, especially when turning his head to the left, during which he would become unsteady, but denied vertigo. When the neck and occipital pain flared up, it spread from the occipital region over the head to the right eye. Previous interventions included physical therapy in the form of ultrasound, massage, spray and stretch, myofascial release, and cranial sacral therapy, which had provided no relief.

The patient had no history of back or neck pain, apart from the occasional ache, and his medical history was unremarkable.

Questions

1. List the concerns the clinician should have following this history.

2. Using a flow diagram describe how you would proceed with this patient following the history.

3. What special tests should be considered at this point?

4. Are additional questions needed with regard to the history?

Review Questions

1. Describe the anatomy of the craniovertebral region.

2. What structures provide stability in the craniovertebral region?

3. Which of the following is not a suboccipital muscle: rectus capitis lateralis, rectus capitis posterior major, rectus capitis posterior minor, obliquus capitis inferior, and obliquus capitis superior?

4. What is the extension of the posterior longitudinal ligament called?

5. Which muscle produces side bending of the O-A joint to the same side, as well as extension and contralateral rotation of the O-A?

Answers

References