How Would You Know if Your Neck Causes Dizziness
Arch Physiother. 2017; seven: 12.
How to diagnose cervicogenic dizziness
Alexander S. Reiley
Md of Physical Therapy Division, Duke University, 2200 W Main St., Durham, NC 27705 USA
Frank M. Vickory
Doctor of Concrete Therapy Sectionalization, Duke University, 2200 W Chief St., Durham, NC 27705 USA
Sarah Eastward. Funderburg
Doctor of Physical Therapy Partitioning, Duke University, 2200 W Master St., Durham, NC 27705 Usa
Rachel A. Cesario
Md of Physical Therapy Division, Duke University, 2200 W Main St., Durham, NC 27705 Us
Richard A. Clendaniel
Doctor of Physical Therapy Sectionalization, Duke University, 2200 W Main St., Durham, NC 27705 USA
Received 2017 Feb ten; Accustomed 2017 Sep iv.
Abstract
Cervicogenic dizziness (CGD) is a clinical syndrome characterized past the presence of dizziness and associated cervix pain. There are no definitive clinical or laboratory tests for CGD and therefore CGD is a diagnosis of exclusion. It can exist difficult for healthcare professionals to differentiate CGD from other vestibular, medical and vascular disorders that cause dizziness, requiring a loftier level of skill and a thorough understanding of the proper tests and measures to accurately rule in or dominion out competing diagnoses. Consequently, the purpose of this paper is to provide a systematic diagnostic approach to enable healthcare providers to accurately diagnose CGD. This narrative volition outline a stepwise procedure for evaluating patients who may have CGD and provide steps to exclude diagnoses that can present with symptoms similar to those seen in CGD, including primal and peripheral vestibular disorders, vestibular migraine, labyrinthine concussion, cervical arterial dysfunction, and whiplash associated disorder.
Keywords: Cervicogenic dizziness, Cervical dizziness, Disequilibrium, Vertigo, Cervical spine, Cervical proprioception, Whiplash, Diagnosis
Background
CGD was first described equally 'cervical vertigo' by Ryan and Cope in 1955, and has at times been considered a controversial diagnosis [1]. The condition has as well been named proprioceptive vertigo, cervicogenic vertigo, and cervical dizziness; however, since truthful vertigo is rarely a symptom seen in people with CGD, information technology is at present generally termed cervicogenic dizziness [2].
Cervicogenic dizziness is characterized past the presence of imbalance, unsteadiness, disorientation, neck hurting, limited cervical range of motion (ROM), and may be accompanied by a headache [ii, 3]. The cervical spine may be considered the cause of the dizziness when all other potential causes of dizziness are excluded. To exist considered CGD, dizziness should be closely related to changes in cervical spine position or cervical joint movement [4]. Although the etiology remains unknown, many cases of CGD have been diagnosed post whiplash injury, or have been associated with inflammatory, degenerative, or mechanical dysfunctions of the cervical spine [5, 6].
What causes the symptoms of imbalance, unsteadiness, and disorientation is not fully understood. Some have suggested the presence of faulty cervical proprioceptive inputs equally a contributing factor [7]. It has been proposed that a disruption of the normal afferent signals from the upper cervical proprioceptors to the vestibular nucleus results in an inaccurate delineation of head and cervix orientation in space [8]. Another possible cause of these abnormal afferent signals is pain [6].
At present, CGD is a diagnosis of exclusion. A diagnosis of exclusion exists in situations where no unmarried test is able to diagnose the status, and the diagnosis cannot be verified by outcomes, imaging, laboratory values, or unique signs and/or symptoms [9]. Diagnoses of exclusion are challenging for health practitioners because they require high levels of clinical skill and a stiff understanding of the sequencing of proper tests and measures needed to rule out or dominion in competing diagnoses. There are many causes of dizziness, including numerous medications and a diverse assortment of vestibular, cardiovascular, metabolic, neurological, psychological, and vision problems. Therefore, a thorough, stepwise process for excluding diagnoses with symptom presentation similar to CGD would be a clinically useful tool for the differential diagnosis of CGD.
Reneker and colleagues [10] conducted a Delphi study to assess the perceived utility of different clinical tests for differentiating between cervicogenic and other causes of dizziness after a sports-related concussion. The authors institute no consensus amongst health practitioners regarding the appropriate tests to identify CGD. The lack of consensus regarding the tests for CGD was cross-professional person. Because the enigmatic nature of CGD, a systematic procedure is a pragmatic tool for differential diagnosis of CGD. The aim of this narrative is to provide a stepwise process toward the diagnosis of CGD, with utilization of a rule out, rule in epitome. The determination of which assessment tools to utilize and the order in which the examination is performed is at the discretion of the clinician.
Chief text
Our proposed clinical reasoning stepwise procedure for diagnosing CGD is depicted in Fig.i. To rule out competing diagnoses, one needs tests that accept low negative likelihood ratios (LR-) and subsequent loftier sensitivity in order to subtract the post-test probability of the condition when the finding is negative. In contrast, tests that have high positive likelihood ratios (LR+) and subsequent high specificity are used to rule in a condition. The sensitivities, specificities, and likelihood ratios of relevant tests are listed in Tablei. Descriptions and explanations of the tests are listed in Tabular array2. The background information and details of each step are presented in the following sections.
Table 1
Test | Diagnosis | Sensitivity (%) | Specificity (%) | PV+ (%) | PV- (%) | LR+ | LR- | Reference |
---|---|---|---|---|---|---|---|---|
Canadian C-Spine Dominion | Cervical Spine Trauma | 99 | 45 | half-dozen.03 | 100 | 1.81 | 0.01 | Stiell et al. [36]; Duane et al. [37] |
Cervical Arterial Dysfunction (CAD) Test | CAD | 0–57 | 87–100 | 0–100 | 26–96 | 0.22–83.3 | 0.44–i.iv | Hutting et al. [22]; Petersen et al. [38] |
Sharp Purser Test | Transverse Ligament Stability | 69 | 96 | 85 | 90 | 15.6 | 0.33 | Uitvlugt & Indenbaum [39]; Hutting et al. [40] |
Alar Ligament Test | Alar Ligament Stability | Right: 69 Left: 72 | Right: 100 Left: 96 | Right: 100 Left: 93 | Right: 80 Left: 81 | – | – | Kaale et al. [41] |
Dix-Hallpike | Posterior Culvert BPPV | 79.3 | 75 | 95.8 | 33.three | iii.17 | 0.xiv | Halker et al. [42] |
Head Thrust Examination | Unilateral Vestibular Hypofunction | 71 (88 for complete loss) | 82 | 87 | 65 | 4.16 | 0.3 | Schubert et al. [43] |
Manual Spinal Examination | Cervical Facet Joint Dysfunction | 92 | 71 | – | – | 3.17 | 0.11 | Schneider et al. [xxx] |
Palpation for Segmental Tenderness | Cervical Facet Articulation Mediated Pain | 94 | 73 | – | – | 3.48 | 0.08 | Schneider et al. [30] |
Cervical Neck Torsion Test | Cervicogenic Dizziness (versus BPPV) | 72 | 92 | – | – | 9 | 0.3 | 50'Heureux-Leabeau et al. [14] |
Cervical Relocation Test (with positive test defined by any of the iv positions with JPE >iv.5°) | Cervicogenic Dizziness (versus BPPV) | 92 | 54 | – | – | 2 | 0.15 | L'Heureux-Leabeau et al. [14] |
Cervical Relocation Exam (with positive test defined by mean JPE >4.five°) | Cervicogenic Dizziness (versus BPPV) | 72 | 75 | – | – | two.9 | 0.37 | L'Heureux-Leabeau et al. [14] |
Smooth Pursuit Neck Torsion (SPNT) Test | CGD in people with WAD and dizziness | 90 27 56 | 91 55 88 | 92 -- -- | 71 -- -- | 10 0.six -- | 0.11 1.three -- | L'Heureux-Leabeau et al. [14] Tjell & Rosenhall [34] Kongsted et al. [35] |
Table 2
Diagnosis | Examination | Performance description | Caption |
---|---|---|---|
Traumatic Cervical Spine Injury | Canadian C-Spine Rule [44] | 1) Any loftier-gamble factor present: Age ≥ 65 years OR Dangerous mechanism* of injury OR Paresthesias in extremities. If YES to any, radiography should exist performed. If NO to all, keep to ii. ii) Whatsoever low chance factor that allows safe assessment of range of motility? If NO to all, radiography should be performed; if YES to whatever, continue to 3. Depression gamble factors defined as: Elementary rear-end motor vehicle standoff† OR Sitting position in emergency department OR Ambulatory at any time OR Delayed (not immediate) onset of neck hurting OR Absence of midline cervical spine tenderness. 3) Able to actively rotate neck 45° left and right? If unable, radiography should be performed. *Fall from elevation ≥0.9 m (3 ft)/five stairs, centric load to head, motor vehicle collision at high speed (>100 km/h), rollover, ejection, motorized recreational vehicles, bicycle struck, or bicycle standoff. †Excludes: pushed into oncoming traffic, hitting by double-decker or big truck, rollover, and hitting past high speed vehicle. | Canadian C-Spine Rule is a tool to assistance clinicians decide if radiography should exist utilized in patients following traumatic injury. It is only applicable to patients who are alert (Glasgow Coma Scale score ≥ 15) and in stable condition following trauma where cervical spine injury is a concern. Canadian C-Spine Rule is not applicable in non-trauma cases, for patients with age < xvi years, during pregnancy, or for patients with unstable vital signs, astute paralysis, known vertebral disease, or previous history of cervical spine surgery. |
Upper Cervical Instability | Alar Ligament Exam [45] | one) Patient assumes sitting or supine position with head slightly flexed to appoint the Alar ligament. The clinician assesses the patient'south resting symptoms. 2) The clinician firmly stabilizes the spinous process of C2 using a pincer grasp. 3) Either lateral flexion or rotation is passively performed by the clinician (both are performed independently of each other, in either order). While performing these passive movements, the examiner attempts to experience movement of C2. iv) A positive test is divers by lack of palpable motion of the C2 spinous procedure during lateral flexion or rotation. | The purpose of this test is to examine the integrity of the alar ligaments post-obit traumatic injury involving the cervical spine. If the alar ligaments are intact, lateral flexion or rotation of the head should result in palpable contralateral movement of the C2 spinous procedure. Caution is of utmost importance when administering this test. |
Upper Cervical Instability | Abrupt Purser Test [39, 45] | 1) The patient assumes a sitting position with their caput slightly flexed. The clinician assesses the patient'due south resting symptoms. 2) The clinician stands to one side of the patient and stabilizes the C2 spinous procedure using a pincer grasp. 3) The clinician uses the opposite paw to gently apply an anterior to posterior translation strength on the patient's forehead. four) A positive test is defined by symptom reproduction during forward flexion, decrease in symptoms during posterior translation, or excessive deportation (>4 mm) during posterior translation. | This exam assesses the integrity of the transverse ligament that maintains the position of the odontoid process relative to C1. If the transverse ligament is torn, C1 will interpret frontward on C2 during flexion, indicating atlantoaxial subluxation. Atlantoaxial subluxation is the most common cervical spine complication of rheumatoid arthritis. Spinal cord pinch secondary to atlantoaxial subluxation can outcome in severe neurological damage, including quadriplegia and fatality. Extreme caution should be used when administering this examination. |
Cervical Facet Articulation Dysfunction | Manual Spinal Examination [30] | Patient positioned in prone with neutral cervical spine. Clinician applies posterior to anterior directed strength to the articular pillars of the cervical spine bilaterally, one joint at a time. In a study by Schneider, et al., a positive test was defined equally patient report of ≥3/10 increase in concordant local or referred pain intensity when clinician rated resistance to motion as 'moderate' to 'marked'. | Cervical facet joint capsules contain several sensory receptors including gratis nervus endings, mechanoreceptors, A-delta and C-fibers, making the joints nociceptive and sensitive to force per unit area and mechanical changes. |
Cervical Facet Joint Mediated Pain | Palpation for Segmental Tenderness [xxx] | Patient positioned in prone. Clinician palpates deep segmental muscles overlying cervical spine facet joints bilaterally. Schneider, et al. defined a positive test as patient study of ≥3/10 increase in concordant local or referred pain intensity rating. | Segmental muscles overlying painful facet joints ofttimes react with tenderness and spasm. Cervical facet joints and the muscles overlying them are innervated by the medial co-operative of the dorsal rami. |
Cervical Arterial Dysfunction | CAD Testing [22, 46] | CAD testing should include the following sequential tests: 1) While seated, the patient performs end range agile cervical rotation in both directions. two) While seated, the patient performs active end range combined cervical extension and rotation in both directions 3) With patient supine, the clinician brings the patient into passive end range cervical rotation in both directions. iv) With patient supine, the clinician brings the patient into passive end range combined cervical extension and rotation in both directions. 5) Any position that the patient reports as provocative. All positions should be held for a minimum of ten due south, unless symptoms are provoked sooner. Subsequently each sustained position, the patient should return to neutral cervical spine position for at to the lowest degree 10 due south to allow for any latent response to emerge. Throughout CAD testing, the clinician should observe the patient's eyes for nystagmus, and the patient should report any provocation of symptoms. Positive signs and symptoms include dizziness, nystagmus, diplopia, loss of consciousness, diaphoresis, dysphagia, dysarthria, nausea, numbness around the lips, or other neurological symptoms. | CAD testing involves neck rotation and extension with a stationary body, causing decreased blood flow in the vertebrobasilar arteries with rotation lonely and internal carotid arteries with combined extension and rotation. CAD testing requires cervical extension and rotation passive range of motility that is within normal limits. |
Vestibular Hypofunction | Head Thrust Exam [43] | Grasp the patient's head firmly with both hands and pitch their head frontward 30° to align the horizontal semicircular canals. Instruct the patient to expect at your nose. Gently move the patient'due south caput dorsum and forth with intermittent high velocity, randomly timed thrusts. | While performing head thrusts, find the patient's eyes to decide whether they are able to maintain ocular fixation on your olfactory organ or non. A failure to maintain fixation on the visual target (nose) indicates hypofunction on the side that the thrust was directed toward. A refixation saccade will be visible for patients who are unable to maintain visual fixation. This exam is most valid if the thrusts are performed with random timing that does non allow anticipatory compensation. |
Peripheral Vestibular Dysfunction | Head Shaking Induced Nystagmus [47] | Grasp the patient's caput firmly with both easily and pitch their head forward 30° to align the horizontal semicircular canals. Instruct the patient to close their optics. Passively oscillate the patient'due south caput side to side 20 times at 1–2 Hz. Instruct them to open their eyes just prior to completing the 20 side to side movements. Detect for post-headshake nystagmus. | The direction of the fast stage of nystagmus denotes the side of higher vestibular performance. Therefore, the side of vestibular hypofunction is on the side contralateral to the direction of the fast phase. |
Benign Paroxysmal Positional Vertigo | Dix-Hallpike Test [42] | The patient is initially sitting upright with legs extended. The clinician passively rotates the patient's head 45° toward the side being tested. The clinician helps the patient to chop-chop lie down on the table while keeping the head slightly extended. The clinician observes the patient's optics for nystagmus for at least 60 s; there tin be a latency period of upwards to 15 s earlier the onset of nystagmus. | The direction of the nystagmus beats will be on the same side as the involved canal. With correct sided BPPV, for example, the fast phase of nystagmus will beat to the correct with a slow saccade back to the left. Patients with posterior canal BPPV volition have a positive Dix-Hallpike test and concomitant vertigo. |
Horizontal Canalilithiasis or Cupulolithiasis | Caput Roll Examination [48] | The patient is initially positioned in supine with their neck flexed xx°. The clinician quickly rotates the patient'southward head 90° to either side and observes for nystagmus for at least 60 s. The clinician slowly returns the patient's head to midline, maintaining neck flexion, then repeats the procedure on other side. | Like the Dix- Hallpike, the nystagmus volition beat towards the affected ear with a slow saccade moving in the opposite direction post-obit the fast shell of nystagmus. When the head is rolled toward the afflicted ear, the nystagmus beats will exist in a geotropic (toward the footing) manner. If the head is maintained in this position, a burst of fast chirapsia nystagmus volition occur in an ageotropic (abroad from the ground) mode. When the head is rolled away from the afflicted ear, the nystagmus beats will exist less intense and in the geotropic fashion. |
Vestibular Dysfunction, Cervicogenic Dizziness | Caput-Cervix Differentiation Test [26–28] | The patient begins seated on a swivel chair. The clinician rotates the chair both while the stabilizing patient's head and the patient reports any provocation of dizziness. The clinician and then rotates the chair without stabilizing the patient's head and the patient over again reports any provocation of dizziness. | Provocation of dizziness with torso rotation under a stabilized head implicates the cervical spine, whereas dizziness with head and trunk rotation together (en bloc rotation) indicates a vestibular component to the patient'due south symptoms. If symptoms are provoked in both scenarios, it is likely that CGD and vestibular dysfunction are comorbid. Dizziness of vertebral origin should be ruled out prior to administration of the Head-Neck Differentiation Test. |
Cervicogenic Dizziness | Cervical Neck Torsion Test [fourteen] | The patient begins seated on a hinge chair and turns their body ninety° to the either the correct or left, holding for 30 s, then returns their body to center. The patient then repeats the aforementioned process in the reverse management. Each position, including the center positions, is maintained for thirty s. Throughout the exam, the caput is stabilized past the clinician and therefore motionless. The clinician likewise must continuously observe for nystagmus. | Considered positive if nystagmus (excluding spontaneous nystagmus) of more than 2° per second is observed in any of the four positions (left torso rotation, neutral rotation, right torso rotation, neutral rotation). |
Cervicogenic Dizziness, Whiplash Associated Disorder | Shine Pursuit Cervix Torsion Examination (SPNT) [34, 49] | Surface electrodes are placed on the subject'southward peel just lateral to the eyes bilaterally to record the corneo-retinal potential. The subject begins seated with their cervical spine in neutral position. The subject watches a visual target (LED or laser light) that moves through a 40° arc at a frequency of 0.2 Hz with a peak velocity of twenty° per 2d. The subject is instructed to keep their head withal and try not to blink while following the light closely with their eyes. The examiner gently holds the subject'south head in place. This process is then repeated with the subject's body rotated 45° to one side with the caput remaining in the same position to create cervical torsion. If 45° of body rotation causes discomfort, the bending can be decreased to symptom free range (minimum of thirty°). The examiner gently holds the subject'south head and trunk in the position. The test is performed to the left and right sides. The hateful gain (i.e. the ratio between eye velocity and target velocity) is calculated in all three positions. | There is a lack of consensus in the description of proper performance methodology of the SPNT. The methods described are based on the initial report of the SPNT performed by Tjell and Rosenhall in 1998. The SPNT is a examination of smooth pursuit center movement with cervical cervix torsion. The SPNT is the boilerplate value of the polish pursuit in both the right and left trunk-rotation positions. The divergence between the smooth pursuit and the smooth pursuit with neck torsion values is called the smooth pursuit cervix torsion difference. The larger the divergence betwixt smoothen pursuit with neck torsion and smooth pursuit in neutral, the more likely the patient is suffering from a whiplash associated disorder. The utility of the SPNT every bit a diagnostic tool for differentiating CGD from WAD has been studied in controlled laboratory trials, with mixed results, but has non yet been studied in a clinical setting. |
Cervicocephalic Proprioception and Neck Reposition Sense | Cervical Relocation Test [32] | The patient begins seated, facing a wall 90 cm away, and wearing a head-mounted laser pointer that is centered on a target on the wall. The patient keeps their eyes closed while moving their neck in a specified direction, then back to what they believe to be centered starting position. The patient verbally indicates when they believe they are back to center. The patient repeats this procedure for right rotation, left rotation, flexion, and extension (in no particular order). | The hateful altitude from the bodily eye to the subjective centre is used to summate the joint position error (JPE) for each motion. An error of 4.v° is the cutoff point suggesting a failure of head and neck relocalization precision. |
Stepwise process for diagnosing cervicogenic dizziness
Pace 1: Patient history
In order to make up one's mind whether a patient potentially has CGD, it is essential to analyze the symptoms and nature of onset. For CGD to be considered, the patient should have a history of neck pathology and also experience dizziness that has a close temporal relationship with the onset of cervical spine symptoms. Cervicogenic dizziness should not be considered if the patient does not take neck pain. The neck pain tin can occur at rest, with motion, or with palpation. Symptoms acquired by CGD should be exacerbated past movements that arm-twist neck hurting and should subside with interventions that alleviate neck pain.
Information technology is imperative to obtain a thorough patient history as the first step in the diagnostic process in lodge to identify ruby flags, to begin ruling out competing pathologies, and to prioritize pathologies that best fit the description of the onset, signs, and symptoms. Tablethree details the typical clinical presentations of CGD and the pathologies that can present with similar symptoms. Important information to seek for patients with both dizziness and neck pain includes presence of cardiovascular take a chance factors, history of migraines, symptoms of tinnitus or aural fullness, oscillopsia, and symptoms exacerbated by exertion, positional changes, decorated environments, or specific activities.
Table three
Diagnosis | Duration | Signs and symptoms |
---|---|---|
Acute Vestibular Loss | Single attack, several attacks, or persistent for several weeks. | Sudden vertigo or dizziness possibly accompanied by tinnitus, diplopia, nausea, vomiting [15]. |
Benign Paroxysmal Positional Vertigo | A few seconds to several minutes. | Vertigo. Occurs with changes in position relative to gravity [50]. |
Fundamental Vestibular Disorders | Several days to weeks. | Abiding vertigo, facial asymmetry, swallowing or spoken language problems, ptosis, ataxia, sensation changes, upper motor neuron signs, aberrant head thrust test, direction changing nystagmus, pure vertical nystagmus, pure torsional nystagmus, a skew deviation, and other neurological symptoms [23, 51]. |
Cervical Arterial Dysfunction | Several minutes. | Dizziness that is typically accompanied by diplopia, numbness around the lips, nystagmus, ataxia, bilateral neurological symptoms, dysphagia, dysarthria and headaches. Associated with nausea and vomiting [19]. |
Cervicogenic Dizziness | Several minutes to hours [iii]. | Dizziness and disequilibrium due to changes in cervical spine position [3]. |
Labyrinthine Concussion | Episodically over hours to days [26]. | Cervical neck pain is common. Hearing loss, tinnitus, and dizziness [eighteen]. |
Ménière's Disease | Minutes to hours, rarely longer than 24 h [12]. | Presents with episodic, intense vertigo, accompanied by aural fullness, tinnitusand fluctuating hearing loss. Attacks are typically preceded by aura and followed by a period of exhaustion and generalized dizziness. As Ménière's disease progresses, the hearing loss and tinnitus intensify and become more persistent, and the acute attacks of vertigo may be replaced by more than chronic issues with dizziness and imbalance [12, 13]. |
Vestibular Migraine | four–72 h. | Vestibular Migraine Diagnostic Criteria (International Headache Lodge) [17]. A. At least 5 episodes involving criteria C and D. B. A electric current or past history of Migraine without aureola or Migraine with aura. C. Vestibular symptoms* of moderate or severe intensity, lasting betwixt 5 min and 72 h. D. At least 50% of episodes are associated with at least one of the following three migrainous features: i) headache with at least 2 of the post-obit 4 characteristics: unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activeness; 2) photophobia and phonophobia; three) visual aura. Eastward. Not better deemed for by another ICHD-3 diagnosis or by another vestibular disorder. *Barany Society's Classification of Vestibular Symptoms: a. spontaneous vertigo: i. internal vertigo (a false awareness of self-movement) 2. external vertigo (a fake sensation of visual environs spinning or flowing) b. positional vertigo, triggered by a complex or big moving stimulus c. visually induced vertigo, triggered by a complex or large moving visual stimulus d. head motion-induced vertigo, occurring during head motion due east. caput motion-induced dizziness with nausea |
Whiplash Associated Disorder | Variable. Days to weeks and in some cases months. | Cervical neck hurting and hypersensitivity, decreased cervical range of motility, dizziness, tinnitus, and headache. Associated with psychological factors, such as low hurting tolerance and fear abstention [21]. |
The nature of the patient's symptoms can aide in determining the cause of dizziness. It is important to clarify the quality of the reported "vertigo" or "dizziness," as there is significant inconsistency in the use of these terms. Dorland'southward Illustrated Medical Dictionary [xi] defines vertigo equally an illusion of move; a sensation as if the external world were revolving effectually the private (objective vertigo), or as if the individual were revolving in space (subjective vertigo). Vertigo is not a symptom arising from the cervical spine, but rather is acquired by peripheral vestibular disorders or lesions within the vestibular pathways of the fundamental nervous system.
The duration of symptoms is another of import attribute of the subjective history that helps differentiate CGD from other pathologies. The duration of symptoms for CGD can range from days to months to years. Each episode of dizziness typically lasts minutes to hours [3]. The typical duration of symptoms for each pathology discussed can be plant in Table iii.
At that place are numerous vestibular causes of dizziness with characteristic presentations that tin can assistance distinguish each from CGD. Ménière's disease is a chronic vestibular disorder characterized by episodic bouts of aural fullness, vertigo, and hearing loss [12, 13]. Cervicogenic dizziness however, typically does non include aural fullness, tinnitus, or hearing loss. The presence of these symptoms does not definitively rule in Ménière's disease, but does decrease the likelihood that CGD is implicated.
Benign paroxysmal positional vertigo (BPPV) is the most common vestibular pathology. BPPV occurs when calcium carbonate crystals (otoconia) become dislodged from the utricle and migrate into one of the three semicircular canals located within the inner ear. BPPV presents as vertigo associated with changes in head position relative to gravity. The vertigo associated with BPPV is accompanied by nystagmus. The nearly common pattern of nystagmus seen in BPPV is a mixed up-beating and torsional nystagmus, simply the management of the nystagmus will vary depending on which semicircular canal is affected. If a patient has symptoms of vertigo accompanied by nystagmus in response to changing caput position in infinite, then BPPV is more than likely than CGD. In a study comparison BPPV to CGD, sensations of "drunkenness" and "fainting" were found in both groups, all the same these symptoms were reported significantly more than often by the CGD grouping than the BPPV grouping, whereas rotatory awareness and symptom duration lasting simply a few seconds were significantly more common in the BPPV group [14]. Cervical cervix move, fatigue, anxiety, and stress were likewise found to be more than common precipitating factors for exacerbation of symptoms in the CGD group every bit compared to the BPPV group.
A patient with an astute, unilateral, peripheral vestibular loss due to labyrinthitis or vestibular neuronitis volition generally present with marked vertigo and imbalance, with associated nausea and perhaps vomiting. In addition, the patient will acutely present with spontaneous horizontal, direction fixed nystagmus in room light. As the acute signs and symptoms dissipate, the patient may be left with a multifariousness of symptoms, including dizziness, motion sensitivity, imbalance, difficulty with concentration, tinnitus, and hearing loss [15]. The subjective report is useful in differentiating vestibular loss from CGD because patients with CGD typically exercise not have tinnitus, hearing loss or vertigo.
Vestibular migraines take been described as the well-nigh common cause of recurrent vertigo [16]. Refer to Tabular array 3 for the specific criteria developed by The International Headache Lodge to diagnose a vestibular migraine. Key symptoms frequently present in vestibular migraine, simply non CGD, are aureola, true vertigo, throbbing headaches, sensitivity to auditory or visual sensory stimulation, and oculomotor changes [17]. Patients with vestibular migraine do non typically feel dizziness related to mechanical neck pain or dysfunction.
Labyrinthine concussion is a vestibular disorder that tin can mimic symptoms of CGD due to the presence of dizziness and cervical cervix pain [3]. Distinguishing between CGD and labyrinthine concussion is complicated by the fact that both labyrinthine concussion and CGD can be attributed to trauma. Labyrinthine concussion often includes signs and symptoms like to those of a peripheral vestibular loss (as described in a higher place), including hearing loss, tinnitus and dizziness [18].
Cervical arterial dysfunction (CAD) and whiplash associated disorder (WAD) are non-vestibular pathologies that can mimic CGD. Cervical arterial dysfunction is a term sometimes incorrectly used interchangeably with vertebrobasilar insufficiency (VBI). Still, VBI refers only to decreased claret menses in the vertebrobasilar arteries, whereas CAD refers to restricted claret menstruum in any of the cervical arteries, including the internal carotid arteries [xix]. There are many potential underlying causes of CAD, including but not limited to atherosclerosis, thrombosis, pre-existing anatomical anomalies, cervical arterial dissection, vasospasm, and external compromise. The clinician should decide if the patient has any cardiovascular adventure factors that may increase their likelihood of CAD, such equally hypertension, hypercholesterolemia, blood clotting disorders, diabetes mellitus, smoking, vessel trauma, or history of cardiac or vascular illness [19]. CAD presents equally dizziness lasting several minutes that is related to movements of the head on the trunk [xix]. If the patient reports dizziness without other CAD symptoms, it is very unlikely that CAD is the crusade, as CAD related dizziness presents with only one symptom in less than 1% of cases [xx]. Other symptoms of CAD include severe headache, diplopia, nystagmus, numbness around lips or mouth, dysphagia, dysarthria, and upper motor neuron signs [nineteen].
Whiplash associated disorder develops after a trauma involving rapid acceleration and/or deceleration, most commonly a motor vehicle accident. Patients with WAD typically have low pain tolerance and score high on fear avoidance measures such every bit the Fearfulness Avoidance Belief Questionnaire (FABQ). Common symptoms of WAD are cervical neck pain and hypersensitivity, decreased cervical ROM, dizziness, tinnitus, and headache [21]. In some cases, the dizziness that accompanies WAD may be CGD. WAD can also be associated with a concussion that occurs during a traumatic injury. Therefore, WAD, concussion, and CGD are not mutually sectional diagnoses. When a person experiences dizziness as a symptom of concussion and/or WAD, the dizziness can exist of cervical origin.
Step 2: Triage
If the subjective written report includes blunt trauma, triage of the cervical spine should outset utilize the Canadian C-Spine (cervical spine) Rule to make up one's mind if radiography is indicated. The criteria for the Canadian C-Spine Rule are detailed in Tabular array 2. The Canadian C-Spine Rule has high sensitivity, and therefore it is very unlikely to incorrectly determine that a patient with a severe cervical spine injury does not require radiography. If the patient reports significant blood-red flag symptoms consistent with CAD, they should be referred for diagnostic imaging to rule out the cervical arteries as a potential cause of dizziness. Clinical tests for cervical instability and CAD are provocative in nature and therefore should be used sparingly and with utmost caution. Positive results on cervical instability testing or CAD testing indicate a need for firsthand medical attention and imaging [22].
If no imaging is warranted based on the Canadian C-Spine Rule or significant scarlet flag symptoms of CAD, the clinician should go on with cess of cervical range of motion. Cervical ROM is appropriate at this juncture in the triage phase because several tests that the clinician may employ after in the test, including vestibular tests discussed in Footstep three, accept minimum cervical ROM requirements. Furthermore, identifying limitations or symptom provocation with active or passive cervical ROM is an efficient way for the clinician to gain useful data prior to embarking on more complex vestibular and cervical spine testing. For case, the cervical neck torsion test simply discriminates using rotation, so if a patient'due south dizziness is provoked by extension ROM rather than rotation, the clinician may prioritize other clinical tests over the cervical neck torsion exam.
Given that patients being evaluated for CGD nowadays with an unknown crusade of dizziness and were frequently involved in a traumatic event, a neurological screen will likely be indicated. A neurological screen should include an assessment of radicular symptoms, myotomes, dermatomes, deep-tendon reflexes, upper motor neuron signs, and cranial nerve function. Abnormal neurological findings may warrant referral to either a neurologist or emergency intendance for further evaluation, depending on the severity. Primal vestibular disorders can present with a variety of symptoms, ranging from abiding vertigo to generalized symptoms of dizziness, and will typically present with red flag signs and symptoms that warrant referral to a physician [23].
If cervical instability, CAD, and neurological dysfunction are ruled out, the clinician should proceed with clinical tests to rule out vestibular pathologies.
Step iii: Vestibular assessment
If a patient has a history consequent with CGD and has been properly screened in the triage stage, the vestibular arrangement should be assessed adjacent. All patients should take a rudimentary cervical spine test prior to vestibular testing, including subjective report of cervical spine pain established in Step 1, too as assessment of cervical spine ROM and radicular symptoms in Step 2. The vestibular exam can be modified to limit the head movements to the available cervical ROM. A thorough evaluation of the cervical spine is all-time performed in Step 4 because first ruling out vestibular dysfunction increases the probability that the cervical spine is the cause of dizziness. With that being said, in that location is likely to be some overlap between Step three and Step 4; the nature of the presenting history, symptoms and signs will dictate the order of evaluation and treatment. In the case of obvious vestibular causes of dizziness (e.g. BPPV, vestibular hypofunction) without astute cervical spine involvement, handling of the vestibular pathology would be initiated prior to moving on to Stride 4. If there is markedly restricted cervical spine ROM that precludes treatment of the vestibular pathology, then cervical spine assessment and treatment would take to precede (or occur concurrently with) the treatment of the vestibular pathology.
Within the vestibular functioning stride, oculomotor evaluation should include evaluation of nystagmus, skew, smooth pursuit, saccades, Dix-Hallpike exam, static and dynamic visual acuity, and the vestibulo-ocular reflex (VOR) including VOR cancellation and the caput thrust test. The observation of nystagmus is clinically useful to determine if the vestibular arrangement is involved, and the presence of nystagmus during testing tin can help to rule out CGD.
A horizontal, direction fixed nystagmus is consequent with unilateral peripheral vestibular hypofunction. Patients with unilateral vestibular hypofunction typically have oculomotor signs such equally a positive head thrust test or head shaking induced nystagmus, and may accept abnormal dynamic visual acuity—these findings would not typically be seen in an individual with CGD. The absenteeism of spontaneous or gaze-evoked nystagmus in room light does not rule out a peripheral vestibular deficit because patients with peripheral vestibular hypofunction can apply visual fixation to suppress nystagmus. Therefore, utilization of Frenzel lenses allows for more reliable detection of unilateral peripheral vestibular hypofunction as the Frenzel lenses will remove visual fixation. Individuals who take compensated for a unilateral loss will often have no nystagmus in room low-cal, whereas individuals with bilateral vestibular loss generally take no nystagmus in either room calorie-free or with visual fixation removed. Nystagmus originating from a fundamental pathology demonstrates a different pattern; the nystagmus will be present in room low-cal and will either persist or diminish when visual fixation is removed. Direction changing nystagmus, pure vertical nystagmus, or torsional nystagmus is consistent with a central vestibular arrears.
Other oculomotor abnormalities, such as saccadic polish pursuit or saccadic abnormalities, may be seen in patients with primal vestibular and central oculomotor deficits. While there take been some reports of abnormal eye movements in cases of WAD, the results from different studies are highly variable [24, 25]. In that location is non a single, definitive oculomotor examination that is capable of identifying CGD.
Cervicogenic dizziness and dizziness from vestibular disorders tin can be differentiated using the head-neck differentiation test, which is a variation of the cervical neck torsion exam [26–28]. The test is performed with the patient sitting on a hinge chair. Provocation of dizziness with trunk rotation under a head stabilized in space implicates the cervical spine, whereas dizziness with head and trunk rotation together (en bloc rotation) indicates a vestibular component to the patient'due south symptoms. This examination can be performed for both horizontal and pitch plane motions of the caput and cervical spine. If symptoms are provoked in both scenarios, it is likely that CGD and vestibular dysfunction are comorbid, and so both the vestibular and cervicogenic components can be addressed.
While static and dynamic balance tests are not diagnostic for vestibular dysfunction, these tests are oft abnormal in individuals with vestibular deficits [28, 29]. Studies have also shown that cervical pain can cause decreased standing residuum and postural control [8]. Patients with either vestibular dysfunction or CGD may have increased symptoms during a dynamic balance cess. While non diagnostic for either status, assessment of static and dynamic balance is of import from the perspective of a functional cess.
Positive results on vestibular tests do not rule out cervicogenic dizziness, as a patient can have two causes of dizziness simultaneously. If a patient is found to have vestibular dysfunction, the clinician may initiate treatment of the dysfunction if it is inside their capabilities, as well every bit refer to an otolaryngolist or neurologist depending on the patient's presenting signs and symptoms for further medical cess. If treatment of the vestibular impairment does not pb to consummate resolution of the patient's symptoms of dizziness, or if the head-neck differentiation examination indicates cervical and vestibular interest, the clinician should consider the possibility that the patient has both dizziness of vestibular origin and CGD, and go along with Footstep 4.
Pace 4: Detailed cervical spine evaluation
Although cervical range of motion testing and cervical instability testing are about appropriately performed as part of triage, thorough evaluation of the cervical spine should ideally be performed after vestibular testing in guild to rule out vestibular dysfunction and thereby narrow the list of potential causes of dizziness. Cervical spine evaluation includes manual spinal examination (MSE) for facet joint dysfunction, palpation for segmental tenderness (PST), assessment of postural alignment, and traction.
There is no individual test that tin can reliably diagnose the cervical facet joint every bit a source of pain. However, in i report, MSE and PST both exhibited high sensitivity (92% and 94%, respectively), demonstrating potential utility every bit screens for cervical facet joint mediated pain [30]. Manual spinal examination should include unilateral posterior to anterior mobilization of cervical facet joints with assessment of pain provocation and resistance to motion. To perform PST, the clinician palpates the muscles over the cervical facet joints and assesses for increased concordant pain. Individuals with CGD commonly present with tight posterior neck muscles and tenderness of both posterior neck muscles and cervical facet joints. In a study by L'Heureux-Leabeau et al. [14], the CGD group was significantly more likely than the BPPV group to feel hurting during physical test of the upper cervical spine and paravertebral muscles.
Postural alignment and command should be assessed considering postural impairments are normally seen in cases of CGD, specially in cases with neck pain from whiplash injury [8]. A reduction of dizziness symptoms in response to cervical traction implicates involvement of the cervical spine and is more than consistent with CGD than with vestibular dysfunction [31]. It is all-time to perform traction with the patient sitting in guild to minimize the consequence of gravity on the vestibular arrangement.
Step 5: Clinical tests for cervicogenic dizziness
While CGD is a diagnosis of exclusion and cannot be definitively ruled in with any single test, in that location are tests that have been demonstrated to exist clinically useful. Ruling out competing diagnoses in previous steps will increase the pre-exam probability of CGD, thereby increasing the post-examination probability when utilizing these clinical tests.
The test with the strongest diagnostic utility to rule in the diagnosis of cervicogenic dizziness is the cervical cervix torsion test (LR+ of ix), which measures nystagmus in response to cervical neck rotation [14]. The cervical relocation examination, a measure of joint position mistake, has good diagnostic value for ruling out the diagnosis of cervicogenic dizziness (LR- of 0.15). The diagnostic value of both the cervical neck torsion examination and cervical relocation test are limited by the fact that the likelihood ratios are based on a study comparison only CGD and BPPV. L'Heureux-Leabeau et al. [fourteen] establish that the cervical cervix torsion exam and cervical relocation test are most useful for differential diagnosis of BPPV versus CGD when the results of the 2 tests were combined. Table two describes how to perform the cervical cervix torsion test and the cervical relocation test.
Revel and colleagues [32] demonstrated that individuals with chronic neck hurting have impaired head relocation after active head rotation. Multiple studies of cervical kinesthetic sense take shown that cervical repositioning errors are greater in cases of WAD that include complaints of dizziness, equally opposed to WAD cases without dizziness, peculiarly for tests of cervical rotation [33]. While information technology is unclear whether these results are due to dizziness or pain, impaired cervical kinesthetic sense is important to consider as ane aspect of CGD.
The shine pursuit neck torsion exam (SPNT) is a laboratory exam that has been proposed for differentiating CGD from WAD. The SPNT examination is a comparing of the gain (the ratio of the heart velocity to the target velocity) of the middle response in neutral versus rotated head positions. Ane laboratory study found the proceeds difference to exist significantly greater in WAD cases that include dizziness, as compared to WAD cases without dizziness [34]. All the same, other laboratory trials using the SPNT examination take concluded that it is non useful for differentiating CGD from WAD [35]. The reliability, validity and diagnostic accurateness of a clinical version of the SPNT for differential diagnosis of CGD has not been determined. At this point, there is no clinical reward to using the SPNT test alongside cervical cervix torsion testing equally both the sensitivity and specificity are higher in cervical neck torsion testing [14]. Therefore, the SPNT test is currently not a clinically useful test for diagnosing CGD.
Report limitations
It is worth noting that the diagnostic utility of many special tests used for the diagnosis of CGD take been studied by comparing two specific populations. For example, differentiating just between BPPV and CGD or between CGD and WAD. Therefore, this paper is express by the goal of portraying a comprehensive, generalized clinical thought process by combining the insights of a wide variety of studies, each offer conclusions about specific questions. Each test and technique discussed has its ain limitations. For example, the nearly well-known test for CGD is the head-neck differentiation test, which has not yet been studied for diagnostic utility. The clinical tests are each limited by their telescopic. For instance, the cervical neck torsion test only examines dizziness provocation using rotation, so these tests may not reproduce dizziness in patients with CGD that is provoked by movement into other planes. The tests with the most clinically useful likelihood ratios, the cervical neck torsion test and cervical relocation test, were established in a study comparing merely CGD and BPPV, and therefore are non sufficiently validated to exist considered independently conclusive measures for ruling CGD in or out in the general population. The value of this framework for the diagnosis of CGD has not yet been validated using a controlled clinical trial. This newspaper is an amalgamation of the electric current evidence for best-practice in the diagnosis of CGD combined with the opinions of clinical experts (RC).
Conclusions
Without robust diagnostic tests to definitively diagnose or exclude CGD, it is currently best categorized equally a diagnosis of exclusion. To diagnose CGD, masquerading pathologies must be identified and excluded. All the same, a thorough subjective history and triage screening can narrow the listing of potential pathologies. If a patient does not report both dizziness and cervical involvement, CGD is unlikely. CGD is also less probable if the patient reports tinnitus, hearing loss or migraines. Duration of symptoms can further narrow the listing of probable pathologies. After obtaining the subjective report, information technology is sometimes necessary to screen for neck instability and CAD involvement before moving on to clinical tests. Vestibular testing, such as the caput-neck differentiation test and Dix-Hallpike maneuver, tin can then be used to determine if the vestibular organisation is causing the dizziness. In one case vestibular pathologies have been ruled out, the clinician should examine the cervical spine, followed by the cervical neck torsion test and cervical relocation examination to help confirm or exclude the diagnosis of CGD. If all other pathologies have been ruled out and the examination results are generally consistent with CGD, the clinician should make the diagnosis of CGD. It is possible for patients to accept both CGD and some other cause of dizziness, such as WAD or a vestibular pathology. In this scenario, the clinician can exist most confident most diagnosing the patient with cervicogenic dizziness after they have thoroughly addressed the comorbidity with appropriate interventions, just dizziness however persists.
Acknowledgements
We would similar to thank Dr. Chad Cook PT, PhD for his assistance with this project.
Funding
There are no possible sources of financial support, funding, or grants to written report.
Availability of data and materials.
Data sharing is not applicative to this article equally no datasets were generated or analyzed.
Abbreviations
BPPV | Beneficial paroxysmal positional vertigo |
CAD | Cervical arterial dysfunction |
CGD | Cervicogenic dizziness |
CTA | Computerized tomography angiography |
ERT | Extension-rotation test |
FABQ | Fear-abstention beliefs questionnaire |
JPE | Articulation position error |
LED | Light emitting diode |
LR- | Negative likelihood ratio |
LR+ | Positive likelihood ratio |
MRA | Magnetic resonance angiography |
MRI | Magnetic resonance imaging |
MSE | Manual spinal exam |
PST | Palpation for segmental tenderness |
PV- | Negative predictive value |
PV+ | Positive predictive value |
ROM | Range of motion |
SPNT | Smooth pursuit neck torsion |
VBI | Vertebrobasilar insufficiency |
VOR | Vestibulo-ocular reflex |
WAD | Whiplash associated disorder |
Authors' contributions
The stated authors have met all four criteria for authorship as recommended past International Committee of Medical Journal Editors (ICMJE). All authors listed on the title page have contributed to the enquiry, organizations, and writing of the manuscript, read the concluding manuscript, attest to the validity and legitimacy of the information and its interpretation, and hold to the submission to Archives of Physiotherapy. All authors read and approved the final manuscript.
Notes
Authors' information
At the time this article was completed, Alexander Reiley, PT, DPT, Frank Vickory, PT, DPT, Sarah Funderburg, PT, DPT, and Rachel Cesario, PT, DPT were all recent graduates of the Doctor of Physical Therapy Plan, Class of 2017 at Duke University, Durham, NC 27705, U.s.. Richard Clendaniel, PT, PhD earned his PhD in Behavioral Neuroscience at the University of Alabama at Birmingham. He completed a two-yr post-doctoral fellowship in Neuro-Otology at The Johns Hopkins University School of Medicine, Department of Otolaryngology-Head and Cervix Surgery. He has authored numerous articles and book capacity on vestibular organisation neurophysiology, vestibular rehabilitation and cervicogenic dizziness. He is co-editor of the text: Vestibular Rehabilitation (fourth edition). He is currently a faculty fellow member in the Duke University Doc of Physical Therapy program, and he has an offshoot appointment at the Academy of N Carolina in the Department of Allied Health Sciences, Division of Speech and Hearing Sciences. He besides serves on the Medical and Scientific Advisory Board of Vestibular Disorders Clan. Dr. Clendaniel has no competing interests to written report.
Ethics approval and consent to participate
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Not applicable
Competing interests
The authors declare that they have no competing interests.
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Contributor Information
Alexander Southward. Reiley, E-mail: moc.liamg@tpyeliera.
Frank Grand. Vickory, Email: ude.usf.ym@90vmf.
Sarah E. Funderburg, Email: moc.liamg@23rednufs.
Rachel A. Cesario, E-mail: moc.liamg@31oiraseclehcar.
Richard A. Clendaniel, Email: ude.ekud@leinadnelc.drahcir.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5759906/
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