A sample history from the neuro-otology clinic...

  • Definition: vertigo, impulsion, rocking, tilt, imbalance, walking on uneven surface, steps, sudden stops and starts lurching, impending faint, falls, lightheaded, disorientation, illusion of movement, any directional sensation
  • What is vertigo? Describe a typical episode of vertigo.
    • Duration of vertigo (mins, seconds, hours, days weeks, etc)
    • Provoking/positional triggers**
    • Otologic symptoms
    • Neurologic symptoms*
    • *Associations: Aura, tinnitus (pulsatile) or decreased hearing, ear pain or fullness, nausea, vomiting, oscillopsia, blurred vision, diplopia, headaches, facial numbness, twitching, weakness, tremor, incoordination, palpitations, diaphoresis, paresthesias, speech, swallowing, cough
    • **Provoking: change in position, standing up, rapid head motion, elevators, cars, darkness, altitude, loud noises, valsalva, temperature change
  • Alleviation factors: medications used
  • PMH:Surgery in ear, eye, strabismus
  • Medications: antibiotics, ASA, chemotherapy, lithium
  • Toxins: occupational, military service
  • Head/ear/neck trauma
  • Ear infection, inner ear problems, sinusitis, labyrinthitis
  • Cardiac, hypoglycemia, DM, vascular risks
  • Psychiatric illness
  • Syphilis, AIDS, dental, TMJ
  • FH: Meniere's, migraine, vertigo, hearing loss
  • Current Medications
Derived from a handout Dr Suresh Subramanian gave to me

A sample examination from the neuro-otology clinic...

  • Visual acuity was 20/__ OD and 20/__ OS with (or without) glasses.
  • Afferent pupillary function, confrontation fields and ophthalmoscopic findings were normal.
  • Ocular ductions, saccades and smooth pursuit were normal.
  • There was no spontaneous or gaze-evoked nystagmus, including when fixation was removed with Frenzel goggles.
    • first nystagmus example (video)
    • second nystagmus example (video)
  • Ophthalmoscopy also showed no nystagmus.
  • Visual acuity did not drop during head shaking. Head impulse (video) and Dix-Hallpike testing (video) was negative. No nystagmus was provoked by sustained head shaking, hyperventilation or mastoid vibration.
  • Facial sensation and movement were normal. Hearing and Weber's test were normal. Otoscopy was negative. Testing finger-nose, heel-shin, Romberg and tandem gait showed no abnormalities.
Derived from a handout Dr Suresh Subramanian gave to me

Define the dizziness syndrome

  • Acute constant dizziness (acute vestibular syndrome)
  • Recurrent spontaneous attacks of dizziness
  • Recurrent positionally trigerred dizziness
  • Chronic persistent dizziness

Acute prolonged severe dizziness (acute vestibular syndrome)

  • severe, sudden dizziness, imbalance, nausea, and vomitting...
  • is it a stroke?
  • who needs an MRI?
  • There is no definite answer... but: unilateral spontaneous horizontal nystagmus plus corresponding positive horizontal head impulse testing (h-HIT) without other neurologic findings... is suggestive of a peripheral lesion.
  • Things that suggest a central lesion:
    • direction-changing nystagmus
    • negative h-HIT test
    • other neurological findings
    • vascular risk factors.

HINTS for Acute Vestibular Syndrome

  • The HINTS test is a validated, 3-step series of bedside oculomotor examination maneuvers for the differentation of stroke from acute peripheral vertigo.
    • stands for Head Impulse, Nystagmus, Test-of-Skew.
      • benign (peripheral) pattern: abnormal h-HIT plus direction-fixed horizontal nystagmus plus absent skew
      • dangerous (central) pattern: normal/untestable h-HIT or direction-changing horizontal nystagmus present/untestable or skew deviation present/untestable
    • it outperformed initial MRI in the detection of stroke as a cause of acute vestibular syndrome (see table)
    • caveat: it takes a skilled examiner to confidently performs the HINTS assessment
    • Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y. H., & Newman-Toker, D. E. (2009). HINTS to Diagnose Stroke in the Acute Vestibular Syndrome: Three-Step Bedside Oculomotor Examination More Sensitive Than Early MRI Diffusion-Weighted Imaging. Stroke; a journal of cerebral circulation, 40(11), 3504–3510.
  • HINTS videos:
    • head impulse testing (video)
    • testing for nystagmus (video)
    • testing for skew deviation (video)
    • complete HINTS exam on normal subject (video)

Recurrent Spontaneous Attacks of Dizziness

  • Ninety percent of spontaneous recurrent vertigo and dizziness can be explained by six disorders:
    1. Ménière disease
    2. Vestibular migraine
    3. Vertebrobasilar TIA
      • yes, it does exist...
    4. Vestibular paroxysmia
    5. Orthostatic hypotension
    6. Panic attacks
  • Less common causes (that I won't talk about today): perilymph fistula, superior canal dehiscence, autoimmune inner ear disease, otosclerosis, cardiac arrhythmia, and medication side effects.
  • Clinical features discriminate between causes of recurrent spontaneous vertigo (table).

Positional Dizziness

  • Many types of dizziness get worse with changes in position
  • Consider non-vestibular causes of positional dizziness
    • orthostatic hypotension
    • other causes of transient global cerebral hypoperfusion (e.g. pre-syncope) such as valvular stenosis, arrythmia, etc.
    • cerebrovascular causes... but more typically this presents as TIA
    • uncommonly, problems of CSF flow causing intracranial hypotension (e.g. overshunting), or intracranial hypertension (e.g. transient obstruction of foramen of Monro by colloid cyst - rare!)
  • Postional vertigo is a vestibular disorder caused by...
    • inappropriate asymmetry of input arising from the labyrinths - "peripheral vertigo"
    • dysfunctional integration of vestibular inputs - "central vertigo"
    • certain clinical features distinguish central from perpiheral (positional) vertigo (see table)

Benign Paroxysmal Positional Vertigo (BPPV)

  • The most common cause of episodic vertigo in adults.
  • BPPV can be caused by:
    • Head trauma
    • Ménière disease
    • Vestibular neuritis
    • Labyrinthitis
    • Idiopathic sensineuronal hearing loss
  • Caused primarily by canalithiasis (and, to lesser extent, cupulolithiasis):
    • dense calcium carbonate crystals dislodge from the utricle and fall into one of the semicircular canals (see figure)
    • each semicircular canal can produce BPPV, but posterior canal form (p-BPPV) is most common (see table)

Posterior canal BPPV (p-BPPV)

  • posterior canal BPPV (p-BPPV) is the most common form of BPPV
    • likely because the posterior canal is the most inferiorly situated of the semicircular canals, and so otoconia tend to settle there
  • Diagnosis and treatment with canalith repositioning maneuvers
    • Dix-Hallpike and Epley maneuvers (video)
  • stimulation of the posterior canal by otoconia (as in D-H maneuver) causes characteristic upbeating and torsional nystagmus, with the upper pole of the eye beating towards the affected canal/ear
    • try to determine which side is the affected side: (video)

Horizontal canal BPPV (h-BPPV)

  • h-BPPV also causes positional vertigo
    • The vertigo can be provoked by Dix-Hallpike maneuver, leading to mis-diagnosis
  • h-BPPV produces horizontal nystagmus that is provoked by horizontal head turning
    • The direction of the nystagmus changes with the direction of head rotation
  • h-BPPV exists in the more common geotropic (towards the Earth) and less common apogeotropic (away from the Earth) forms
    • Pathophysiologic basis for this is thought to depend on whether the otoconia are lodged in the long arm (geotropic) or short arm (apogeotropic) of the semicircular duct, causing opposite hydrodynamic currents in the endolymph, and thus opposite effects on the cupula
  • There are canalith repositioning maneuvers in h-BPPV, such as the Pagnini-McClure maneuver (video)
    • P-M maneuver starts with patient lying supine, examiner rotates patient's head right, then left
    • the direction of head rotation that produces more severe nystagmus corresponds to the affected vestibular apparatus (in both apogeotropic and geotropic forms)
    • in the geotropic form, nystagmus will beat towards the affected ear (down to the Earth), in the apogeotropic form it will beat away from the affected ear (away from the Earth)
    • (see flowchart for interpretation)

Chronic Subjective Dizziness

  • Sometimes, patients are just dizzy "all the time"
    • important to clarify whether this represents dizziness for most of the day, or frequent attacks of episodic dizziness with asymptomatic intervals
  • Differential diagnosises to consider:
    • past vestibular disorders (e.g. "chronic vestibulopathy")
    • recurrent vestibular conditions
    • panic and generalized anxiety disorders
    • depressive disorders
    • vestibular migraine
    • recent traumatic brain injuries
    • dysautonomias (e.g. POTS)
    • cardiac dysrhythmias.
    • ... CSD syndrome

Chronic Subjective Dizziness Syndrome

  • There is a recognized syndrome of chronic subjective dizziness (CSD) which has three core features of:
    1. persistent nonvertiginous dizziness lasting 3 months or more
    2. hyper-sensitivity to motion stimuli, including a patient’s own movement and motion of objects in the visual surround
    3. difficulty with precision visual tasks, such as reading or using a computer
      • older names include phobic postural vertigo (PPV) or Phobischer Attacken-Schwankschwindel, originally called agoraphobia by Westphal... until psychiatrists co-opted the term!
  • CSD often develops following an acute vertiginous disorder
    • e.g. otogenic CSD
    • Three forms of CSD have been described:
      1. otogenic CSD
      2. psychogenic CSD
      3. interactive CSD (basically, otogenic CSD with a pre-existing anxiety disorder)
  • The current concept of CSD describes it as a "failure of readaptation": (figure)
    • that is, there is maladjustment during the early period of illness (vertigo),
    • followed by persistent failure to readapt after acute injuries (vertiginous symptoms) resolve
    • the patient suffers the adverse effects of acute anxiety during the readaptation process, starting from the early phases of illness.

References

  1. Fife, T. D. (2012). Positional dizziness. CONTINUUM-MINNEAPOLIS.
  2. Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y. H., & Newman-Toker, D. E. (2009). HINTS to Diagnose Stroke in the Acute Vestibular Syndrome: Three-Step Bedside Oculomotor Examination More Sensitive Than Early MRI Diffusion-Weighted Imaging. Stroke; a journal of cerebral circulation, 40(11), 3504–3510.
  3. Kerber, K. A., & Baloh, R. W. (2011). The evaluation of a patient with dizziness. Neurology: Clinical Practice, 1(1), 24–33.
  4. Kerber, K. A. (2012). Acute constant dizziness. CONTINUUM-MINNEAPOLIS.
  5. Lempert, T. (2012). Recurrent spontaneous attacks of dizziness. CONTINUUM-MINNEAPOLIS.
  6. Staab, J. P. (2012). Chronic subjective dizziness. CONTINUUM-MINNEAPOLIS.

Approach to Vertigo

August 9th, 2013

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  • Supplemental Digital Content 4-1 Video demonstrates the Dix-Hallpike maneuver to the right. This maneuver should evoke paroxysmal positional nystagmus for right-sided benign paroxysmal positional vertigo related to the posterior semicircular canal. The mirror image of this maneuver constitutes a left-sided Dix-Hallpike maneuver. links.lww.com/CONT/A7 Reproduced with permission from Fife TD, Iverson DJ, Lempert T, et al. Practice parameter: therapies for benign paroxysmal positional vertigo (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2008;70(22):2067Y2074. B 2008, American Academy of Neurology.
  • Supplemental Digital Content 3-1 Video demonstrates a head-impulse test with scaled peak head velocities of 100°/s (A), 200°/s (B), and 300°/s (C) in a patient with left vestibular loss. Note the increasing salience of the catch-up saccades with stimulus size. The picture-in picture shows the online feedback trace (500 milliseconds) of angular head velocity (°/s) for the examiner. Head velocity was measured with a search coil mounted on a dental impression plate. links.lww.com/CONT/A1 Reproduced with permission from Weber KP, Aw ST, Todd MJ, et al. Head impulse tests in unilateral vestibular loss: vestibulo-ocular reflex and catch-saccades. Neurology 2008;70(6):454Y463. B 2008, American Academy of Neurology.
  • Supplemental Digital Content 3-3 Video demonstrates head-impulse, nystagmus, test of skew (HINTS) assessment: Head-impulse test in acute vestibular syndrome. The patient's head is quickly moved to one side and then to the other. On movements to the patient's left side, the eyes stay focused on the target in front of him. With head movements to the patient's right side, however, the eyes move off the target (move with the head to the right side), and then he makes a voluntary corrective saccade to bring the eyes back to the target. This is considered a positive headimpulse test to the right side. Note that the corrective saccade is more obvious after some of the head-impulse tests than others. This is likely due to variation in the speed of the movement and the patient's ability to predict the movement. links.lww.com/CONT/A4
  • Supplemental Digital Content 3-4 Video demonstrates head-impulse, nystagmus, test of skew (HINTS) assessment: Spontaneous nystagmus and gaze testing in acute vestibular syndrome. Spontaneous nystagmus and gaze testing in a patient who presented with acute vestibular syndrome and findings that localize to the right vestibular nerve. The patient has spontaneous left-beat nystagmus. The velocity of the nystagmus increases when he looks to the left and decreases when he looks to the right. When he looks to the right, the nystagmus does not change direction. When he looks up, the nystagmus remains left-beat. Thus, the patient has a unidirectional horizontal nystagmus. links.lww.com/CONT/A5
  • Supplemental Digital Content 3-5 Video demonstrates head-impulse, nystagmus, test of skew (HINTS) assessment: Test of skew in acute vestibular syndrome. The cross-cover test is performed with the patient focusing on an object in the distance. No vertical misalignment is observed, so the test is negative for skew. links.lww.com/CONT/A6
  • 3-Component H.I.N.T.S. battery
    Accessed from http://content.lib.utah.edu/cdm/singleitem/collection/ehsl-dent/id/6
    from the David Newman-Toker Collection; Neuro-Ophthalmology Virtual Education Library: NOVEL
  • Central Lesion with Direction-Changing Nystagmus
    Accessed from http://content.lib.utah.edu/cdm/singleitem/collection/ehsl-dent/id/2
    from the David Newman-Toker Collection; Neuro-Ophthalmology Virtual Education Library: NOVEL
  • Peripheral Lesion with Direction-Fixed Nystagmus
    Accessed from http://content.lib.utah.edu/cdm/singleitem/collection/ehsl-dent/id/1
    from the David Newman-Toker Collection; Neuro-Ophthalmology Virtual Education Library: NOVEL
  • Benign Paroxysmal Positional Vertigo
    Benign paroxysmal positional vertigo is a common peripheral vestibular disorder... The most common form of the disorder affects the posterior semicircular canal and is diagnosed with the Dix–Hallpike maneuver. A positive Dix–Hallpike test is manifested as upbeating torsional nystagmus with a fast component that rotates toward the undermost ear (video). This nystagmus may be seen with the unaided eye but is often more pronounced if fixation is eliminated with the use of Frenzel lenses or video-oculography goggles.
    Heidenreich, K. Benign Paroxysmal Positional Vertigo. N Engl J Med 2010; 362:e70June 24, 2010
    Accessed from http://www.nejm.org/doi/full/10.1056/NEJMicm0907386
  • Video demonstrates the supine roll (Pagnini-McClure) test to determine the affected side in horizontal canal benign paroxysmal positional vertigo. The side that induces the most intense horizontal positional nystagmus is presumed to be the affected side.
    Accessed from http://links.lww.com/CONT/A10
    Reproduced with permission from Fife TD, Iverson DJ, Lempert T, et al. Practice parameter: therapies for benign paroxysmal positional vertigo (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2008;70(22):2067Y2074.