Monday, June 17, 2013

Cervicogenic Vertigo Following Whiplash Injury

George Rappard, MD

      Cervicogenic vertigo is a common but under diagnosed manifestation of a whiplash mechanism of injury to the neck.  Understanding the temporal relationship to the injury, mechanism, differential diagnosis and potential therapies are key to the effective diagnosis and treatment of this entity.  As many cases of whiplash involve automobile accidents, it's important to document the presence of cervicogenic vertigo as an objective manifestation of a cervical acceleration-deceleration injury.

     Vertigo is defined as a sensation of disequilibrium, often characterized as dizziness.  Vertigo is different from dizziness in that the hallmark of vertigo is a sensation of motion where no motion exists, whereas dizziness is a sensation of unsteadiness.  For example, a patient with true vertigo will experience a sensation that the room is spinning, or that the floor is tilting.  Often, symptoms can be brought about by rapid head turning.

     Cervicogenic vertigo is felt to be brought on by injury to proprioceptive afferents, or specialized nerve receptors,  in the paraspinal musculature or upper cervical facet joints1.  30% of these receptors lie in the facet joints2.  The job of these receptors is to relay information to the brain as to the head’s position on the neck.  When there is a substantial enough of an injury discharges from these receptors are disturbed.  Spatial disorientation and vertigo results from this abnormal discharge3.  In order to injure these receptors, one can see that there has to be a substantial enough of an injury to the facet joints and paraspinal soft tissues that they lie in.  As a result of an injury to these structures, there is an alteration of normal sensation and relay of positional inputs from these specialized receptors.  Therefore, a substantial enough of an injury mechanism to result in pain from paraspinal soft tissue injury or facet capsular injury must be present; In other words, there is usually substantial neck pain.  The diagnosis of cervicogenic vertigo should be suspected when there has been a substantial mechanism, such as whiplash, and there is neck pain.  Keep in mind, substantial injury mechanism does not mean a high speed rear end collision.  Studies have shown that even a low speed collision can result in substantial G-forces to the neck.  White and Punjabe showed how an 8mph rear end collision can result in a 5 G force acceleration to a vehicle occupant’s head4.

     Perhaps one reason why cervicogenic vertigo is under appreciated is that it may not manifest itself until the late subacute or chronic phase following a whiplash mechanism of injury.  It is estimated that vertigo with late onset is seen in up to 58% of patients after closed head injury and whiplash injury5.  Appearing later in a patient’s course, vertigo may be eclipsed by the early and persistent appearance of neck pain after whiplash.  In the presence of a closed head or concussive injury cervicogenic vertigo may be confused with a post-concussion syndrome.  In this case, the absence of typical post-concussive findings can exclude vertigo as a manifestation of a post-concussive injury.  When a closed head injury and neck pain co-exist, the distinction is difficult but probably more academic than anything else, from a practical perspective.  The key to diagnosis is the exclusion of other causes and the temporal relationship between vertigonous symptoms and the injury mechanism.  Exclusion of other causes will be discussed below.  When there is a subacute injury mechanism, such as a motor vehicle accident and neck pain, cervicogenic vertigo should be high on the differential diagnosis.

     There is a broad differential diagnosis for vertigo.  Spontaneous vertigo may commonly be due to an inner ear problem, such as Menier’s disease, labrynthitis, (seen after viral infections), or benign paroxysmal positional vertigo (BPPV).  Further evaluation can be carried out.  Menier’s is associated with hearing loss and audiometry may be helpful.  Take note that a similar low tone sensineurial hearing loss can be seen in a whiplash injury with associated dural sleeve tear and CSF leak6.  To make matters more confusing, cervicogenic vertigo may be associated with a high pitched tinnitus3.   In BPPV, the Dix-Hallpike maneuver may be positive.  Wrisley et al describe an algorithm for working up suspected cervicogenic vertigo patients5.  First, patients must have neck pain to be considered for the diagnosis.  The Dix-Hallpike test can then ascertain which patients suffer from BPPV.  In patients with a negative Dix-Hallpike, or a similar tilt table maneuver, (therefore negative for BPPV) vestibular testing can determine which subset of patients may be suffering from vestibular disorders.  In this algorithm of exclusion, with negative BPPV and vestibular testing, and the presence of neck pain, cervicagenic vertigo can be entertained as the diagnosis.  As an additional test, the rotating stool examination may be helpful.  A patient sits on a rotating stool, the head is immobilized in the examiner’s hands and the neck and trunk is rotated under the head.  In a positive test for cervicogenic vertigo nystagmus is produced.  Lastly, the cervicogenic vertigo patient may be unaware of maintaining their head in a non-neutral position, they may possess a head tilt3.  It’s the author’s opinion that despite a wide differential the diagnosis can still be made somewhat empirically.  In the absence of a viral infection, hearing loss, a tremendous injury mechanism and associated neurological findings cervicogenic vertigo remains the most medically reasonable diagnosis based on its high prevalence relative to the other differential diagnosis, especially with confirmatory physical examination findings.
     
     In addition to the above differential work up, I would add that with a history of a significant injury mechanism one must also evaluate for the presence of a vertebral artery injury.  The vertebral artery is relatively fixed as it travels through the foramen transversarium of the vertebra.  As such, it is susceptible to injury from shear, flexion-extension or rotational forces.  These injuries are usually associated with substantial force.   In such cases one can elicit a history of other vertebrobasilar symptoms, such as dysmetria, diplopia, disequilibrium or sensory and motor deficits.  If the index of suspicion is high a CT angiogram of the vertebral arteries can be performed to exclude the diagnosis.  MRA can be performed but may be less sensitive.       

     Once the diagnosis is established by ruling out other entities and establishing the temporal relationship between the injury mechanism and the onset of symptoms one can initiate treatment of the patient’s cervicogenic vertigo.  In most cases, treatment of cervicogenic vertigo is identical to the treatment of the patient’s underlying neck pain.  Since the injury to proprioceptive cervical inputs co-exist with cervical paraspinal soft tissue and joint capsule injury, it makes sense that therapies that might relieve these structures might also relieve cervicogenic vertigo.  Cervical manipulation and mobilization have been described in the treatment of cervicogenic vertigo2.   Physical therapy7, with and without vestibular rehabilitative therapy has also been described5.  In this case vestibular rehabilitation is rendered by a qualified therapist.   Meclizine, a now over the counter anti-vertigo medication, may provide symptomatic relief. Lastly, cervical facet blocks might theoretically improve cervicogenic vertigo, by anesthetizing the afferent inputs, although this has not been proven.  

     Vertigo following a cervical acceleration-deceleration, or whiplash injury, is common.  The diagnosis is made based on symptoms, temporal relationship to the injury mechanism and exclusion.  Treatment parallels the treatment of the patient’s neck pain.  In establishing the presence of a substantial neck injury cervicogenic vertigo is an important factor.  Injury to the neural proprioceptive inputs is not seen without substantial cervical paraspinal or facet capsular injury.  Cervicogenic vertigo can thus be both disabling and a testimonial to the substantial nature of a whiplash injury.  Treatment parallels the treatment of the painful paraspinal and cervical facet joint injuries that result in cervicogenic vertigo.

Reference List

        1.    Brown JJ. Cervical contribution to balance: cervical vertigo. In: Berthoz A, Graf W, and Vidal P.  The Head-Neck Sensory Motor System. New York: Oxford University Press; 1992;
        2.    Cote P, Mior SA, Fitz-Ritson D. Cervicogenic vertigo:  a report of 3 cases. The journal of the CCA 1991;35:89-94
        3.    McKecnie B. Cervicogenic vertigo.  2013.  Online source.

        4.    White AA, Panjabe NM. Clinical biomechanics of the spine. New York: JB Lippencott; 1978; 153-158
        5.    Wrisley DM, Sparto PJ, Whitney SL, et al. Cervicogenic dizziness: a review of diagnosis and treatment. J Orthop Sports Phys Ther 2000;30:755-66
        6.    Schievink WI. Spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension. JAMA 2006;295:2286-96
        7.    Fitz-Ritson D. Phasic exercises for cervical rehabilitation after "whiplash" trauma. J Manipulative Physiol Ther 1995;18:21-24


Minimally Invasive Surgery Case of the Day

History:  A 21 year old female dancing student presents with back pain and left sided L5 radicular pain of 3 months durantion.

Findings:  Paraspinal left sided tenderness and a positive left sided straight leg raise test is seen on examination.

Imaging:  MRI reveals a foraminal left sided L5/S1 herniation (arrows)



Procedure:  Transforaminal L5/S1 endoscopic discectomy  is performed as an out-patient procedure through a 0.5cm incision

Surgeon:  George Rappard, MD

Disposition:  The patient is discharged one hour post-procedure with resolution of radiculopathy and reversal of straight leg raise sign

Procedure Images:  


Blue stained herniated disc material is seen through scope (arrow)


Upon exploring foramen, exiting L5 nerve root (arrow) and foraminal extruded disc (star) is seen


The endoscopic bipolar (left) and 2.5mm rongeur (right) are used to remove foraminal herniation.  Arrow denotes exiting and displaced L5 nerve root.


After decompression the annular tear is probed (arrow) for loose intradiscal fragments


The nerve (arrow) is decompressed and the foraminal herniation is now seen as an empty cavity (star)

For more information on endoscopic lumber discectomy contact the Los Angeles Minimally Invasive Spine Institute or go to http://www.lamisinstitute.com/percutaneous-endoscopic-lumbar-discectomy