Cervicogenic Vertigo: Controversies in Classification and Diagnosis

Everyday medical practice does not usually look at a diagnosis from the perspectives of ontology ( is it really there? ), epistemology ( how do we even know it is really there? ), and nosology ( is it really a disease? ), but cervicogenic vertigo (CV) probably justifies such considerations.

Research on VC often appears to be motivated by clinical problems frequently encountered in the context of a patient with cervical symptoms and dizziness, in whom another cause of dizziness has not been identified. Since mere simultaneity does not prove causality , an understandably skeptical audience would avoid considering VC as a "diagnosis" , preferring the more neutral term, "syndrome" .

Discussions of CV often characterize it as a “controversial” idea and recognize that the lack of a diagnostic test contributes to the controversy. Most medical phenomena that eventually come to be accepted as diagnoses began as unproven ideas, as hypotheses that required testing.

Since the absence of evidence is not evidence of absence , the authors argue that we must remain receptive to the possibility of moving forward on this issue, and that the controversy around VC may ultimately be resolved.

With these points in mind, the authors review why VC is controversial , beginning with an evaluation of candidate mechanisms for its pathophysiology, and how those mechanisms might be tested; why tests have failed, and a more general discussion of why it has been so difficult to design a sensitive and specific test. The literature on CV spans almost a century but it seems, say the authors, that successive articles have only been concerned with changing the intention of the previous one.

An initial assumption has been that the VC is the only source of symptoms, but this assumption is considered by the authors to be a misconception . They maintain that the term “vertigo,” in its technical sense, refers to a kinetic illusion; to the discrepancy between perceived movement/stasis vs. real. Although the terms "imbalance" or "dizziness" are more neutral, the word "vertigo" has taken root in the literature.

Sometimes the term "vertigo" can be used to refer more closely to the sensation of rotation, but some authors highlight that the sensation is common in the VC. The term “cervicogenic” suggests that vertigo arises (or is generated) in the cervical region, that is, the definition requires a causal relationship, beyond the problem that causes the vertigo.

To arrive at the diagnosis, most investigations require (implicitly or explicitly): 

1) The presence of cervical symptoms (pain caused by movement of the head on the neck and/or of the neck on the trunk, limited, excessive, uncontrolled , involuntary, irregular, etc.). These cervical symptoms should temporarily overlap with the vertigo symptom. 

2) There is a history of neck injury prior to the development of vertigo. 

3) Both.

When attempting to apply these assumptions, definitions, and conditions in the clinic, several problems immediately become apparent.

The first refers to the relationship between cervical disease and vertigo; while the definition of VC requires that the cause of vertigo be cervical disease. Of course, there are other possible relationships. One is that the temporal overlap of symptoms is maintained, but the causal relationship is not, that is, the relationship is one of coincidence rather than causality .

This possibility deserves to be analyzed, because neck pain and vertigo are, individually, very common human experiences, and even when each of the symptoms is the result of an etiology that occurs independently. Therefore, the probability of temporal overlap (coincidence) due to random distribution is not small.

Neck pain is common, and increasingly so. For example, it is difficult to differentiate the coincidental coincidence between neck arthritis and dizziness (two very common conditions in the population) from the situation in which neck arthritis is the cause of dizziness.

Another possibility is that the temporal overlap of symptoms remains but the relationship is reversed and instead of neck pathology causing vertigo, it is vertigo that causes neck symptoms. Often, patients with vertigo of any etiology unconsciously adopt compensatory postures that cause neck symptoms.

That is, neck symptoms may be an effect of vertigo and not the cause.

The second problem concerns the relationship between VC and neck injury . Inner ear disorders have been reported to be rare after neck trauma. However, most lesions are not focal enough to affect the neck in isolation. On the other hand, in whiplash injury , the most common of the neck injuries, in the context of which CV is suspected, it is usually not just a neck injury.

In a study it has been proven that in this injury, vertigo can appear due to several combined mechanisms. At the ear level, the otolithic system is prone to suffering inertial damage, since several researchers have highlighted that benign paroxysmal positional vertigo (BPPV) can be caused by injuries derived from acceleration-deceleration.

More generally, they say, “dizziness after a neck injury may be due to pathologies of the vestibular system, brain injury, or VC, including the ear (labyrinthine contusion), brainstem, cortical and subcortical structures, and arteries. vertebral (traumatic artery dissection).

Finally, a significant proportion of VC cases involving neck injuries are comprised of whiplash injuries, and in many of these cases, patients are litigating or are about to enter litigation.

The medicolegal dimension of whiplash injuries introduces considerations beyond anatomy and physiology, whose influence on symptoms (which are subjective reports) is difficult to evaluate, as there is the potential to complicate the analysis with the involvement of components psychological, and the possibility of a secondary benefit.

The results of several studies suggest that the control of posture, the perception of body orientation and the location of objects in space requires an integration of visual and vestibular proprioceptive signals, as well as internally generated signals, related to movements of the body. the head and body, sometimes called efferent copies .

Efferent copies refer to cortical constructs that serve to anticipate head-body position under a variety of conditions, and predict the appropriate motor response. These constructs are modified throughout life based on the sensory feedback experienced.

For an individual to correctly perceive their orientation and movement through space, the brain must solve the problem of the transformation of coordinates (mapping the coordinate system, from one reference frame to another). This coordinate transformation is presumably important for controlling postural reflexes and building a central perception of body orientation and movement in space.

A failure of multisensory integration (the process of reweighting and combining multiple input streams to produce a coherent percept) is the most commonly postulated mechanism for VC, being attributed to presumed erroneous proprioceptive cervical signals.

Several pathophysiological mechanisms underlying VC have been proposed.

>  Hypoperfusion

Hypoperfusion, secondary to vascular compromise, is often considered a VC mechanism.

Rotational vertebral artery syndrome ( VRSA), also called bowhunter syndrome , is a condition in which one of the vertebral arteries is transiently extrinsically compressed during neck rotation. This will most likely cause symptoms if the contralateral vertebral artery is already narrowed, as in atherosclerotic disease.

In some cases, this compression, perhaps combined with torque of the artery, results in damage to the artery itself, such as a dissection . Some have observed nystagmus , predominantly downward, although such a pattern of nystagmus is not specific to the condition. If the vascular compromise is prolonged, it can culminate in a heart attack.

Despite the apparent enthusiasm in the literature, this condition probably comprises only a small proportion of VC cases. There is no consensus on the range of effects that neck rotation may have on the vertebral arteries, and while dynamic vascular imaging may provide corroborating evidence, other authors maintain that “vertebral artery blood flow is compromised during rotation.” complete contralateral rotation in healthy individuals.” Therefore, vascular imaging is not specific for this condition.

Furthermore, evidence from the cadaveric animal model suggests that typical physiological movements in the neck produce arterial tensions substantially lower than the point of failure (dissection), and an even less common mechanism of vascular compromise occurs in Chiari malformations. in which rotation of the neck squeezes the structures into an already compressed foramen magnum.

Hypoperfusion secondary to an autonomic abnormality triggered by neck rotation has been discussed in several ways. Barré-Lieou syndrome was thought to result from mechanical stimulation of the paravertebral sympathetic ganglia during neck rotation. However, other authors maintain that "No sympathetic or vascular pathways have been identified that could explain these symptoms, so this theory was discarded."

>  Anatomical

Another postulated mechanism is the distortion of the anatomy at the craniocervical junction , as seen in patients with craniocervical instability, in whom neck movements can cause compression of the brainstem. This anatomical disorder should be detected on the images. Given the neuroanatomical territory involved, brainstem compression must manifest with other symptoms in addition to vertigo.

>  Oculomotor abnormalities

Various oculomotor abnormalities associated with neck rotation or neck pain have been documented; In general, oculomotor abnormalities appear to be abnormalities of the cervico-ocular reflex , but other deficiencies in oculomotor control have also been reported.

>  Proprioception

Perhaps the most popular theory about VC concerns cervical proprioception. Some authors maintain that proprioception is not a function of the superficial muscles of the neck but of the short, deep intervertebral muscles of the neck, which are amply provided with muscle spindles that, of all the muscles in the body, are the deepest in the neck and those with the highest concentration of muscle spindles. As a result, the proprioceptive system of the cervical spine is extremely well developed, as reflected by the abundance of mechanoreceptors.

The dense network of mechanoreceptors in the soft tissues of the area in this region provides information to the central nervous system about the orientation of the position of the head with respect to the rest of the body, through direct neurophysiological connections to the vestibular and visual systems. Specifically, strong connections have been demonstrated between the cervical dorsal roots and vestibular nuclei with receptors in the neck (proprioceptors and joint receptors) that play a role in hand-eye coordination, balance perception, and postural adjustments.

Studies of various types of neck stimulation have shown that they can alter perception. In particular, unilateral electrical stimulation of the neck causes a subjective vertical deviation and vibration of the neck muscles, which stimulates the primary endings of the muscle spindles, as if the muscle were being stretched, causing an illusion of neck tilt. the head and the apparent movement of a visual target.

The results of other studies lead to the current theory that cervicogenic dizziness is the result of abnormal input to the vestibular nuclei of stimuli from the proprioceptors of the upper cervical region.

While there may be compelling evidence for erroneous cervical proprioception , this in itself does not necessarily explain why such altered sensory input would manifest as vertigo, and two mechanisms have been proposed.

1. The first way that erroneous cervical proprioception could manifest as vertigo occurs through a "sensory mismatch ," that is, a discrepancy between the erroneous input from cervical proprioception and the correct input from vision and the inner ear.
    
2. The second way that erroneous cervical proprioception could manifest with vertigo occurs through a mismatch between the intended movement (“efference copy” or “corollary discharge”) and the actual misperceived movement.

>  Motor mechanism

While most discussions of the mechanism of VC focus on a problem in input, the possibility of impaired motor output is rarely mentioned . This hypothesis maintains that VC is due to impaired motor activity, perhaps due to incorrect modulation of the motor pathways, due to an abnormality in the neck, and that this motor alteration truly manifests itself with instability that the patient perceives as correct. .

These patients usually have normal motor semiology , so, if this hypothesis is correct, the findings may be more subtle than what is perceived in the physical examination. However, when performing triceps vestibular myogenic evoked potentials in patients with a history compatible with VC, to detect alteration of vestibulospinal reflexes, the authors were unable to identify any specific finding.

>  Migraine mechanism

Migraine has been proposed as a mechanism associated with VC (migraine-associated vertigo). This concept is beginning to gain traction but the authors report that the evidence is contradictory. Actually, there are 2 possibilities

1. One is that neck problems can trigger migraines and migraines can cause vertigo. According to this hypothesis, neck problems are the initial trigger of migraine, and migraine in turn causes vertigo.
    
2. Another possibility is that migraine can manifest itself with both neck pain and vertigo. According to this hypothesis, migraine is the common underlying etiology of both symptoms.

The idea of ​​a relationship between migraine, neck pain and vertigo is attractive, in the sense that it suggests a unifying diagnosis, but its limitation is that it exchanges one unverifiable diagnosis (VC) with another (migraine-associated vertigo). . However, a merit of this theory is that it opens a potential therapeutic avenue (migraine prophylaxis).

> Attempts to develop objective diagnostic tests and their failures

The varied pathophysiological proposal explains the wide range of studies of all types that have been developed for each proposal.

>  Images

In general, they are used to investigate whether there is dynamic vascular compromise , as in rotational vertebral artery syndrome, but, in this case, since normal subjects can exhibit similar images, the finding is not specific.

>  Posturography

Numerous studies have explored computerized dynamic posturography in patients with possible VC. However, increased postural sway is a nonspecific finding that is also evident in patients with vestibular injury. On the other hand, postural instability can be simulated.

>  Oculomotor studies

Given that the relevant multisensory inputs converge in the vestibular nuclei, from where the efferent pathways project to the oculomotor nuclei, it is logical to explore whether the VC manifests with oculomotor abnormalities. A variety of oculomotor findings have been detected in patients with a history of possible VC, including abnormalities in caloric response testing, spontaneous and positional nystagmus, latent nystagmus, and abnormalities in the rotary chair test. These tests have not been shown to be sensitive or specific for VC.

>  Smooth tracking

Some researchers report smooth tracking abnormalities in patients with dizziness after whiplash. However, fluid ocular pursuit is a complex, multi-input system that is vulnerable to cognitive variables, age, and sedation. It also seems very likely that neck pain and secondary gain, both disruptive of cognition, influence pursuit performance. For these reasons, due to an intrinsic problem of specificity, it seems unlikely that any soft pursuit test can be generally useful for the diagnosis of VC.

>  Post optokinetic nystagmus

It has been hypothesized that optokinetic post-nystagmus may be abnormal in patients with VC. However, optokinetic post-nystagmus is difficult to provoke in humans, and is generally of small speed, even in normal subjects. This makes it unlikely that this test could be sensitive enough to be useful in VC.

>  Cervicoocular reflex in the trunk rotation protocol with head still

An oculomotor testing protocol deserves special attention. In theory, fixing the head in space (thus neutralizing labyrinthine input) while swinging the trunk underneath should approximate selective manipulation of proprioceptive cervical input, and then an outcome such as eye movements could be analyzed. .

A passive version of this test has been done. An active version has also been studied, in which the subject must attempt to keep the head stationary, aiming a "gun sight" laser at a stationary target while the trunk rotates underneath. While this test seems very logical, it has not been shown to be sensitive or specific for VC.

In greater detail, the cervical rotation test is actually a test of the cervicoocular reflex, which consists of rotating the body about the vertical axis of the earth, keeping the head still in space, and evaluating nystagmus. This procedure has not been widely accepted.

The cervicoocular reflex also appears in other conditions, so even if it were sensitive enough, the finding of a cervicoocular reflex may not be a specific test for VC. On the other hand, it has been pointed out that cervical nystagmus also occurs in healthy subjects, and even in normal subjects, it is possible to induce asymmetry in the vestibulo-ocular reflex by passive turning, holding the head on the trunk.

>  Why do tests for cervicogenic vertigo fail?

It seems that it should be possible to isolate individual sensory inputs, especially for the VC, but this has proven to be a challenge for future research. Essentially, it has proven difficult to selectively manipulate an individual input while completely isolating the other inputs. Thus, the failure to develop a test that is specific and sensitive for VC is due, at least in part, to the complex organization of the system and, in particular, its multimodal nature.

Input (perception of movement and orientation) and output (execution of movement to maintain balance) are processes that involve multimodal sensory afferents (vestibular, vision, proprioception), the integration of those inputs, and multimodal efferents ( oculomotor, somatomotor). This system has advantages and disadvantages.

An example of an advantage to the patient is that the multiple inputs do not completely overlap, but as they overlap and provide concordant information, this redundancy makes the system more resilient. An example of a disadvantage is that, when sensory inputs are discordant, the resulting mismatch can be perceived as vertigo. A major disadvantage for the researcher is that it is difficult to selectively manipulate a single input while holding the other inputs constant.

What should a test be like to be successful?  

A general principle of sensory information is that biological sensors are better at detecting changes (dynamic stimulation) than static ones (constant stimulation). Following this general principle, VC is expected to be caused by a multisensory mismatch . Said mismatch would be greatest during active head movements (when the expected and actual reafferent input do not coincide).

Since evaluation of all these measures under static conditions are inconclusive, future research should focus on dynamic studies. Based on these considerations, if a test were ever designed that successfully identified VC (and distinguished it from other diseases), it would likely involve dynamic input, probably represented by some change in position. Until such testing is developed, it should be noted that patients with suspected VC often find their symptoms to be more pronounced during movement.

Dynamic tests may be more sensitive than static tests, but a test that involves a change in position will still run the risk of stimulating multiple inputs. Changes in position can trigger vertigo in diseases other than CV.

Other researchers noted that 4 of 5 cases classified as CV were probably benign paroxysmal positional vertigo (BPPV).

These patients with BPPV are likely to have presented in the context of head or neck trauma. Since BPPV is the most common cause of vertigo, it is statistically likely that its onset coincides with that of other diseases (such as neck pain, head trauma, etc.).

Other researchers proposed that BPPV is often misdiagnosed as VC or, more generally, as lesions of the vestibular organs, particularly the otolithic organs after whiplash injuries. In these cases, it is likely to be underestimated, attributing dizziness and vertigo to cervical damage and lesions of the central nervous system.

It is important that in the patient with vertigo, before considering the evasive diagnosis of VC, the doctor evaluates the diagnosis of BPPV.

Confusing benign paroxysmal positional vertigo (BPPV) with VC is a very apt example to explain why, when considering the diagnosis of VC, a broad differential diagnosis should be considered. Reliable, well-established signs and tests can support an alternative diagnosis in almost all patients presenting with vertigo.

Given the difficulty of designing a test that can be classified as a "positive test" for VC, and the observation that the majority of cases diagnosed with VC were eventually proven to have a different cause, most reviews reach the conclusion conclusion that VC is a diagnosis of exclusion .

Taking the “diagnosis of exclusion” criterion with the definitions, conditions and assumptions mentioned above, the authors consider that the diagnosis of cervicogenic dizziness is suggested by: 1) a close temporal relationship between neck discomfort and dizziness, including the moment of appearance and occurrence of episodes; 2) previous injury or pathology of the neck and, 3) elimination of other causes of dizziness.

The authors express that, if VC is a diagnosis of exclusion, then the question arises: what else needs to be excluded?

Beyond a complete history and physical examination, there is no consensus on what constitutes an appropriate diagnosis to exclude alternative diagnoses. In practice, since inner ear disorders are so common, it is reasonable to consider an otovestibular screening exam . At the doctor’s discretion, this could include:

• Evoked ocular vestibular myogenic potentials and videonystagmography.

• Rotary chair tests and computerized dynamic posturography.

• If the patient’s neck tolerates it, cervical vestibular myogenic evoked potentials can be measured and head impulse tests can be performed, via video.

If neck rotation causes symptoms other than vertigo or reveals signs of brainstem dysfunction, different imaging is justified, as needed:

• Vascular imaging, preferably dynamic, such as computed tomography (CT), magnetic resonance imaging (MRI), or catheter angiography. There is some evidence that transcranial Doppler ultrasound may also be helpful.

• Images of the bony structures (usually by CT) and soft tissue structures (usually by MRI) of the cervical spine.

The controversy surrounding VC does not preclude therapeutic attempts, although the optimal treatment is uncertain as the disease mechanism remains unclear.

>  Physiotherapy

There are many reports on neck physiotherapy as a treatment for VC, but the treatment of proprioceptive cervical vertigo, imbalance or vertigo are limiting symptoms. Some authors suggest that a multimodal therapeutic approach would be warranted as it is likely to better address the perpetuation of a vicious cycle of events where secondary adaptive changes of the sensorimotor control system could lead to altered cervical muscle function and joint mechanics, further altering afferent inputs.

Physical therapy for pain management, chiropractic, active range of motion exercises, and exercises to improve neuromuscular control are important to reduce potential causes of altered cervical afferent input and subsequent disturbances in sensorimotor control. It may also be helpful to incorporate treatment from other disciplines, such as vision therapy. Although vertigo is one of the cardinal symptoms of VC, vestibular physical therapy does not replace neck physical therapy.

>  Why does physical therapy provide partial improvement?

If the pathophysiological mechanism of VC is not yet known, the indication for physiotherapy is to do the treatment blindly, and it is unlikely to correct the problem by chance. However, physical therapy literature generally describes encouraging results. How can this be? the authors ask. Whichever factor initiates the process that manifests with one of the symptoms (vertigo or neck pain) can in turn trigger the other, leading to the vicious cycle of a feedback loop.

Patients who become dizzy from any cause tend to develop neck stiffness, and neck problems that cause vertigo meet the definition of VC. In other words, these phenomena can exacerbate each other; Interconnections between the cervical proprioceptors and the vestibular nuclei may contribute to a cyclical pattern, such that cervical muscle spasms contribute to dizziness and dizziness contributes to muscle spasm.

Whether for one reason or another, any treatment that reduces neck pain and normalizes cervical muscle tone and joint mobility (i.e., basically any treatment that normalizes cervical mechanics) will interrupt that positive feedback loop, thus increasing the opportunity for recovery. If VC exists, appropriate management is the same as for cervical pain syndrome.

>  Medications

Most attempts at pharmacological treatment have included muscle relaxants, although there is no good data to definitively support their effectiveness. According to the migraine-associated CV theory, a trial of migraine prophylaxis may be reasonable. Other approaches have been explored, such as moxibustion and onabotulinum toxin.

>  Invasive and other surgical procedures

Various invasive interventions have been explored : medial cervical branch block, percutaneous cervical nucleoplasty, radiofrequency ablation nucleoplasty, percutaneous laser intervertebral disc decompression, disc replacement, and surgery for cervical spondylosis or herniated disc. Case series of various invasive treatments for suspected CV often report variable results. Given the uncertainty in establishing the diagnosis and the risks of invasive procedures, the authors consider these to be an approach of last resort.

> Alternative therapies

Dry needling and acupotomy have been explored, with limited data.

Specialists in vestibular pathology often see patients with neck symptoms and vertigo, in whom it may seem logical to postulate a causal relationship between the two symptoms. The most popular theory is that VC is due to an abnormality in cervical proprioception. Etiologies such as vascular compromise, although sometimes correct, probably represent only a modest proportion of cases.

There have been numerous attempts to develop a test for VC but none appear sensitive or specific enough nor have they gained widespread acceptance. This failure is likely due, at least in part, to the fact that the system in question involves multimodal sensory integration, and in practice it is difficult to selectively manipulate an individual sensory modality, leaving the other modalities unchanged.

In the absence of a confirmatory test, VC remains a diagnosis of exclusion. Depending on the clinical scenario and findings on physical examination, other alternative diagnoses may require otovestibular testing and imaging.

Neck physical therapy has been studied more than other treatment modalities, and its results are generally considered favorable. Due to the lack of understanding of the underlying mechanism of the disease, it is difficult to understand why physical therapy is useful, but one possibility is that such therapy normalizes cervical mechanics and therefore interrupts the maladaptive positive feedback loop, in which each symptom (vertigo, neck pain) exacerbates the other.

VC most often causes symptoms during position changes and other movements. These movements can also cause other forms of vertigo, so when formulating a differential diagnosis of VC, it is prudent to also consider common causes, such as BPPV.