FACTS ON BPPV:

  1. Benign Paroxysmal Positional Vertigo (BPPV) is the #1 form of vertigo.
  2. On average, BPPV requires 4.5 physician visits before it is correctly diagnosed.
  3. BPPV can be indicative of a more serious underlying inner ear problem or disease process.
  4. BPPV can lead to falls or drop-like attacks.
  5. BPPV has a 95% or greater successful treatment rate.

This is the first in a series of three articles discussing the leading form of vertigo, Benign Paroxysmal Positional Vertigo, which is more commonly referred to as BPPV. This first article will discuss the prevalence, pathophysiology and diagnosis of the condition. The second article will review treatment methodologies and outcomes using Canalith Repositioning and Liberatory Maneuvers for the various forms of the condition. The third and final article will present preliminary data of a joint research project between the author and Carl Crandall, PhD, of the Univ. of Florida on the impact on subjective health status reported via the SF-36 Health Survey with patients pre- and post-treatment of BPPV.

Pathophysiology
Barany1 was the first to describe BPPV in detail, and Dix & Hallpike2 were the first to clearly describe the provocative positioning technique and the clinical indicators of BPPV. However, it was not until the mid-1960s and the work of Dr. Harold Schuknecht3 that we had a better understanding of what was occurring during this strange collection of symptoms. Schuknecht’s work with temporal bones indicated that there was residue of the otoconia imbedded within, or adhering to, the cupula of the posterior canal. It was thought that this heavily weighted cupula was the cause of the transient vertigo and it was termed cupulolithiasis. Although this described the basic phenomenon, it did not describe it in its entirety. The later work of Parnes4 revealed that the debris may not adhere to the cupula but may rather float freely within the long process of the posterior canal. This led to the development of the canalalithiasis theory.

It was previously believed that the symptoms of BPPV were caused by a dysfunction within the otolith mechanism and, in particular, the utricle. What we have learned is that, while the otolith debris degenerates within the utricle, it is the migration of the debris into the semicircular canals—predominately the posterior canal—that causes the manifestation of symptoms. In such conditions as Lindsay-Hemenway Syndrome, there is an obstruction (ischemia) of the anterior vestibular artery. This causes both degeneration of the otolith within the utricle, as well as loss of sensitivity within the horizontal canal. The debris, however, migrates into the posterior canal which actually is an “innocent bystander” or an unwitting recipient of the debris. Note that there is no pathology within the posterior canal itself; however, the gravity-dependent material which either adheres to the cupula (cupulolithiasis) or lies within the long process of the canal (canalalithiasis) causes a deflection of the cupula with changes in head position.

The literature and clinical experience also suggests a variety of other pathologies that show a higher incidence of BPPV. In the younger population, vestibular neuritis, labyrinthitis or Meniere’s disease may be existing (antecedent) inner ear dysfunctions that later manifest with BPPV once the patient is out of the acute or chronic aspect of the disease.5

Diagnostic Considerations
The literature suggests that 30-50% of the patients with BPPV will also have a concomitant vestibulopathy in the involved ear.6 This vestibulopathy is typically indicated by reduced labyrinthine reactivity to caloric irrigations. However, there may be no other spontaneous or provocable peripheral-type nystagmus in any of the ENG subtests. This vestibulopathy is not unexpected in view of the prior discussion of the pathophysiology of the condition.

This author in previous Hearing Review articles7 has discussed the benefit of vestibular screening protocols, which can be performed by all audiologists regardless of instrumentation. Although audiologists may not be performing comprehensive vestibular assessment, it is certainly within their scope of practice to screen patients for this common cause of vertigo. (Author’s Note: As with many areas of hearing care, the author strongly advocates a multi-disciplinary approach to the evaluation and treatment of vestibular disorders, with the involvement of audiologists, physicians, physical/occupational therapists, psychologists and rehabilitation/physical medicine. It should also be understood that the diagnostic and treatment procedures described in this series are intended as an overview only. More detailed instruction on the various maneuvers, etc., is referenced in the article, and excellent training programs exist for gaining the prerequisite knowledge for implementing the procedures in a clinical practice.)

Diagnostics
The diagnostic gold standard for BPPV for nearly 50 years has been the Hallpike Maneuver.2 This maneuver has been well published in virtually every article, chapter or book in otolaryngology and ENG texts. In recent years, however, the poor biomechanics of this maneuver, both for patients and clinicians performing it, have been reevaluated.

For many clinicians, it was thought that the maneuver must be performed in a highly aggressive manner. For patients experiencing lower back, cervical spinal problems or for the elderly, the test was often eliminated from the ENG protocols. This was unfortunate, as BPPV is the leading cause of vertigo in the older adult. It is unlikely that patients who are provoking themselves with everyday activities, such as laying back in bed and rolling over are forcing themselves into an uncomfortable body position while merely laying back in bed. There is a variety of modifications and adaptations to the Hallpike Maneuver, which have proven to be diagnostically sensitive in provoking their symptoms without requiring excessive stress or strain on the cervical spine or lower back.

Prior to placing any patient in a head hanging or modified head hanging position, this author and others8 strongly recommend that clinicians perform a Vertebral Artery Test on the patient to ensure that there is not any vertebral compression of the artery. The possibility of a patient experiencing a basilar arterial stroke should not be taken lightly. This is a simple test, which is referenced. The Modified Hallpike Positioning Maneuvers may be conducted once the Vertebral Artery Test has proved negative.

Other methods currently being investigated include the use of Stryker Circle Beds modified to move in a 360° motion, reducing the need for physical manipulation of the patient.9

  • Vertebral Artery Test: In the Vertebral Artery Test10, the patient, while in a sitting or supine position (preferably sitting), will push their head forward, turn their head comfortably to one side and pitch their head back. Positive findings for vertebral compression may include persistent dizziness, double-vision (diplopia), nausea or slurred speech. It is important to remember that the vertebral artery feeds the brainstem, inner ear, cerebellum and visual cortex. In some individuals with BPPV, they will give a minimally positive Vertebral Artery Test
    when their head is pitched back towards the offending ear. This, however, is usually transient and will clear after a few seconds. If it does not clear, then the clinician should be conservative in proceeding with a Hallpike Maneuver, particularly if the patient manifests a number of the indicators. A positive Vertebral Artery Test should be reported to the referring or attending physician.
  • Modified Hallpike Tests: The first type of modified Hallpike has the patient being moved into the supine position, their head tilted backward to a comfortable degree and then gently moved 45° to one side. In the majority of BPPV posterior-canal patients, this maneuver should be significant enough to provoke their symptoms. A second diagnostic positioning maneuver is that of a side lying position, which is identical to the initial position that the patient is moved into with a Semont Liberatory Maneuver.11

This position is particularly advantageous for those patients whose lower back discomfort or other restrictions, such as obesity, prevent them from sitting comfortably or from bending at the waist. The maneuver is very typical of patient’s normal movement as they prepare to lie in bed on their side. The side-lying maneuver, however, is contraindicated for any patient who has undergone a hip replacement within the previous 90 days.

The third type of Modified Hallpike Positioning has been found by this author to be the most comfortable and well tolerated by patients and also highly sensitive in the diagnosis. This positioning is essentially Position #1 of the Canalith Repositioning or Epley Maneuver12 where the patient, while sitting on the table, turns their head to the affective side. The clinician, while standing behind the patient, supports both their back and neck. The patient is laid back into a supine position with their head minimally hanging off the table completely supported in the hands of the clinician. As the patient is placed in the supine position, the clinician sits, thereby minimizing the poor biomechanics that occur for the clinician performing this traditional Hallpike.

  • Roll Test: Patients with a horizontal canal BPPV will not provoke in a Modified Hallpike position as the head is at a 45° angle. In order for the horizontal canal BPPV to be provoked, their head must be at a 90° rotation. For many individuals, especially those older adults who may have a cervical spondylosis or osteoarthritis, a 90° rotation of the head is ulikely. Therefore, the roll test is ideal to move the patient into the affected state. Unlike posterior or anterior canal BPPV, which produces a rotary-torsional nystagmus, a horizontal canal BPPV produces a linear nystagmus. The nystagmus will be geotropic (beating towards the undermost ear) and the other cardinal indicators will be present, the transient nature with the nystagmus and vertigo subsiding usually in less than 30 seconds. If the nystagmus is ageotropic and the patient is only mildly symptomatic, this indicates that the debris is in the opposite or upper-most ear. The roll test should then be repeated to the opposite side with observation of a change to a geotropic nystagmus with a greater subjective vertigo.

Summary
The diagnosis of BPPV is based on clinical observation of the cardinal indicators and does not require electrophysiologic recording. Many clinicians persist in trying to detect rotary-torsional nystagmus via vertical or horizontal recording systems. The only technology presently available that can accomplish this is with commercially available Infrared Videooculography or sclera coils (used almost exclusively in research environments). While there is a linear component to the rotary torsional nystagmus, it may not produce a positive recording and should be based on visual observation. This author has found that the use of Infrared Videogoggles has been indispensable in the fine differentiation of the various types and forms of BPPV.

In the second article of this three-part series, the author will present the various treatment methodologies for both cupulolithiasis and canalalithiasis in all canal variations. A discussion of treatment efficacy for the American Institute of Balance’s 500-plus BPPV patients over a six-year period will also be presented.

Correspondence can be addressed to HR or Richard E. Gans, PhD, American Institute of Balance, 11290 Park Blvd., Seminole, FL 33772; email: [email protected]; website: www.dizzy.com.

References
1. Barany R: Diagnose von Krankeitserschernungenin Bereiche des Otolithenapparaten. Acta Otolaryngol (Stockh) 1921: 2: 434-7.
2. Dix MR & Hallpike CS: The pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Ann Otol Rhinol Laryngol 1952; 61: 987-1016.
3. Schuknecht HF: Cupulolithiasis, Arch Otolaryngol 1969; 90: 113-26.
4. Parnes LS & McClure JA: Free-floating endolymph particles: a new operative finding during posterior canal occlusion. Laryngoscope 1992; 102: 988-92.
5. Bath AP, Walsh RM, Ranalli P, Tyndel F, Bance ML, Mai R & Rutka JA: Experience from a multidisciplinary “Dizzy” Clinic. Amer Jour Otology 2000; 21: 92-97.
6. Pardal Refoyo JL, Perez Plasencia D & Beltran Mateos LD: Ischemia of the anterior vertebral artery (Lindsay-Hemenway syndrome) review and comments. Acta Otorhinolaryng Esp 1998; 49(8): 599-602.
7. Gans RE: Evaluating the Dizzy Patient: Establishing Clinical Pathways. Hearing Review 1999; 6 (6): 45-47.
8. Gans RE: ENG-VNG Handbook: A Clinical Guide. San Diego: Singular Publishing (In Press).
9. Brey R & Burton J: BPPV and vestibular rehabilitation. Seminar presented at the American Auditory Soc. Scientific Meeting, Scottsdale, AZ, April 2000.
10. Aspinall W: Clinical testing for the craniovertebral hypermobility syndrome. J Orthop Sports Physician Ther 1989; 12: 180-181.
11. Semont A, Fryss G & Vitte E: Curing the BPPV with a liberatory maneuver. Adv Otorhinolaryng 1988; 42: 290-293.
12. Epley JM: The Canalith Repositioning Procedure: For treatment of benign paroxysmal positional vertigo. Otolaryngol Head-Neck Surg 1992; 107: 399-404.
13. Herdman S: Comprehensive Vestibular Rehabilitation Course Workbook, 1998.