Dizziness and Vertigo

Course #98400 • 10 Hours/Credits


Self-Assessment Questions

    1 . The Drachman-Hart paradigm in dizziness and vertigo management
    A) aligns with the chronic disease model.
    B) was developed from neuroscience advances.
    C) is newly introduced and based on modern diagnostic imaging.
    D) was introduced in 1972 and is based on patient symptom description.

    INTRODUCTION

    The modern paradigm for the clinical management of dizziness and vertigo was introduced by Drachman and Hart in a seminal 1972 publication [1]. Based on patient response to the question "What do you mean by 'dizzy?'," dizziness was classified into one of four types that best reflected the subjective descriptions of the symptoms [2,3]:

    • Vertigo: Dizziness experienced as a definite sensation of movement or rotation in space

    • Presyncope: A sensation of impending faint or loss of consciousness

    • Disequilibrium: A sense of unsteadiness or loss of balance without head sensations

    • Lightheadedness: Cannot be classed as vertigo, syncope, or disequilibrium

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    2 . Limitations in the Drachman-Hart dizziness and vertigo paradigm include the following, EXCEPT:
    A) Make the differential diagnosis burdensome
    B) The four symptom subtypes have been validated as accurate
    C) Symptom descriptions unreliably predict the cause of dizziness
    D) Inability to distinguish benign dizziness from life-threatening stroke

    INTRODUCTION

    By current standards, the Drachman-Hart model was based on weak evidence and developed in the absence of modern diagnostic imaging. In reality, patients often have difficulty describing their symptoms and may give conflicting accounts at different times. In one study, an estimated 62% of patients presenting to the emergency department (ED) with past-week dizziness selected more than one type of dizziness on a multi-response questionnaire, and 52% chose a different type when retested six minutes later [5,6]. As such, the character and quality of symptoms alone does not reliably predict the cause of dizziness or serve as a dependable guide to management.

    Primary care providers see at least 50% of patients who seek medical attention for dizziness or vertigo. The differential diagnosis is large, and each common etiology accounts for 5% to 10% of cases [7]. The central task for providers is to distinguish benign from serious or life-threatening causes of dizziness and vertigo, such as posterior circulation stroke. Misdiagnoses are common and diagnostic testing can be costly, especially if too much reliance is placed on this outdated diagnostic paradigm [8].

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    3 . The vestibular system is comprised of all the following, EXCEPT:
    A) Cochlea
    B) Semicircular canals
    C) Nuclei in the brainstem and cerebellum
    D) The vestibular branch of the 8th cranial nerve

    ANATOMY AND PHYSIOLOGY

    The labyrinth in each inner ear houses the systems that serve the functions of hearing (auditory) and balance (vestibular). The auditory system involves the cochlea, which transmits sound signals to the brainstem via the cochlear branch of the 8th cranial nerve. The vestibular system is comprised of the vestibular end-organs in the labyrinth, the vestibular nuclei in the brainstem and cerebellum, and the vestibular branch of the 8th nerve, which relays labyrinthine input to the vestibular nuclei. The 8th cranial nerve is also called the vestibulo-cochlear nerve [10,11,12].

    Within each labyrinth are five vestibular end-organs (three semicircular canals and two otolith organs) that help maintain spatial orientation, postural control, and egocentric perception. Changes in angular and linear head acceleration, movement, and orientation to gravity are detected and signaled via the 8th nerve to brainstem and cerebellar circuits, through thalamic and spinal vestibular projections, and finally to the cerebral cortex [13,14,15].

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    4 . Vestibular signaling that conflicts with brain integration of other peripheral sensory inputs to cause vertigo, spatial disorientation, or imbalance results from
    A) adaptation.
    B) compensation.
    C) disequilibrium.
    D) sensory mismatch.

    ANATOMY AND PHYSIOLOGY

    Vertigo, dizziness, spatial disorientation, and disequilibrium can result from: asymmetrical vestibular inputs; vestibular hypofunction causing sensory mismatch in brain integration of sensory inputs; pathologies that affect any peripheral (e.g., inner ear, 8th cranial nerve) or central (e.g., vestibular nuclei and brainstem or cerebellar connections) vestibular system component; or a host of systemic, drug-effect, psychiatric, and physical trauma-related factors [14,16,17]. Around 80% of dizziness or vertigo cases are peripheral and 20% are central in origin [11,18].

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    5 . Compared with peripheral causes of dizziness/vertigo, central causes account for what proportion of presentations?
    A) 1% to 2%
    B) 12%
    C) 20%
    D) 35%

    ANATOMY AND PHYSIOLOGY

    Vertigo, dizziness, spatial disorientation, and disequilibrium can result from: asymmetrical vestibular inputs; vestibular hypofunction causing sensory mismatch in brain integration of sensory inputs; pathologies that affect any peripheral (e.g., inner ear, 8th cranial nerve) or central (e.g., vestibular nuclei and brainstem or cerebellar connections) vestibular system component; or a host of systemic, drug-effect, psychiatric, and physical trauma-related factors [14,16,17]. Around 80% of dizziness or vertigo cases are peripheral and 20% are central in origin [11,18].

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    6 . In benign paroxysmal positional vertigo (BPPV), the afflicted semicircular canal in 85% to 95% of cases is the
    A) lateral canal.
    B) medial canal.
    C) anterior canal.
    D) posterior canal.

    PERIPHERAL CAUSES OF DIZZINESS AND VERTIGO

    BPPV is subtyped by afflicted canal and mechanism. Posterior canal BPPV (85% to 95%) is the most common. Lateral canal BPPV (5% to 15%) is less common, likely because it self-resolves sooner. Anterior canal BPPV (<1%) is uncommon due to the orientation. Rare variants include multi-canal and bilateral multi-canal BPPV [15,22].

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    7 . In vestibular neuritis, all of the following are true, EXCEPT:
    A) It is the second most common cause of vertigo.
    B) A viral inflammatory etiology is thought to underlie vestibular neuritis.
    C) Vestibular and cochlear components of the 8th cranial nerve are both affected.
    D) The sudden onset of severe symptoms can raise concerns of a central etiology.

    PERIPHERAL CAUSES OF DIZZINESS AND VERTIGO

    Vestibular neuritis, the second most common cause of vertigo (after BPPV), is a viral or post-viral inflammatory disorder affecting the vestibular portion of the 8th cranial nerve. It most commonly affects persons 30 to 50 years of age, and men and women are equally affected. New cases are more common in the spring and early summer [10,35]. Histopathologic nerve studies of these patients are consistent with a viral inflammatory etiology [15].

    Vestibular neuritis is characterized by the sudden, acute onset of severe vertigo, nausea, vomiting, and gait instability without hearing loss, typically preceded by an upper respiratory tract infection [36]. The course and treatment of vestibular neuritis and viral labyrinthitis are similar; in both, the severity of acute vestibular symptoms can raise concerns of a central etiology, and the severity of vertigo, nausea, and vomiting reflects the severity of vestibular asymmetry [7,15,35].

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    8 . All of the following are common symptoms of bacterial labyrinthitis, EXCEPT:
    A) Ataxia
    B) Severe vertigo
    C) Aural fullness
    D) Nausea and vomiting

    PERIPHERAL CAUSES OF DIZZINESS AND VERTIGO

    Profound hearing loss, severe vertigo, ataxia, and nausea and vomiting are common symptoms of bacterial labyrinthitis. Suppurative labyrinthitis almost always results in permanent, profound unilateral hearing loss (or bilateral loss with meningitis). Serous labyrinthitis results in unilateral, high-frequency hearing loss in the affected ear. Regardless of etiology, bacterial labyrinthitis accounts for 35% of all adult-onset cases of hearing loss [36].

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    9 . Which of the following clinical features best characterizes vestibular paroxysmia?
    A) Slow, progressive loss of vestibular function
    B) Experiencing one's voice, breathing, or bodily sounds as excessively audible
    C) Accumulation of excess pressure within the inner ear endolymphatic system
    D) Brief (several seconds), frequent (up to 30 per day) recurrent spontaneous vertigo attacks

    PERIPHERAL CAUSES OF DIZZINESS AND VERTIGO

    Vestibular paroxysmia is characterized by recurrent spontaneous vertigo attacks that are brief (several seconds up to one minute), and frequent (up to 30 per day) [45]. In one study, vestibular paroxysmia accounted for 3.7% of 17,718 consecutive outpatients in a multidisciplinary vertigo and balance disorders center. Men are affected twice as often as women, and the bimodal age of onset peaks in early childhood and again between 40 and 70 years of age [46].

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    10 . The most common cause of recurrent spontaneous vertigo attacks is
    A) BPPV.
    B) vestibular migraine.
    C) vestibular paroxysmia.
    D) persistent postural perceptual dizziness.

    CENTRAL CAUSES OF DIZZINESS AND VERTIGO

    Vestibular migraine is the most common central cause of recurrent spontaneous attacks of vertigo. "Vestibular migraine" is the preferred name for this disorder, because patients may experience a range of vestibular symptoms not limited to vertigo (e.g., dizziness, nausea, vomiting) [19,49].

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    11 . Which of the following statements regarding anxiety, balance, and vestibular interactions is TRUE?
    A) Anxiety can impair ocular motor reflexes.
    B) Anxiety reduces gaze stability, which may underlie dizziness.
    C) Anxious states can amplify a normative gaze bias toward potentially threatening stimuli.
    D) All of the above

    VESTIBULAR IMPAIRMENT, ANXIETY, AND PERCEPTION

    Anxiety can impair ocular motor reflexes and gaze control, which may contribute to visual and visual-vestibular syndromes. Anxious states can amplify a normative gaze bias toward potentially threatening stimuli in the visual field, which, in patients with social anxiety disorder, may drive hypervigilance-avoidance gaze patterns. The impairing effect of anxiety on gaze control reduces gaze stability on visual targets, which may underlie dizziness and visual symptoms in PPPD [73,74].

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    12 . Post-concussion syndrome persists beyond three months in up to what percentage of patients following concussion?
    A) 1%
    B) 20%
    C) 50%
    D) 90%

    POST-TRAUMA OR TOXIC EXPOSURE

    In the United States, there are approximately 3.8 million sports-related concussions annually in adolescents and adults. Concussion, the mildest form of traumatic brain injury (TBI), is a transient functional disorder caused by direct trauma, rapid acceleration-deceleration of the head, or blast forces. Post-concussion syndrome persists beyond three months in up to 20% of affected individuals [90].

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    13 . Which of the following is the most vestibulotoxic of all medications?
    A) Vancomycin
    B) Loop diuretics
    C) Aminoglycoside
    D) Antiepileptic drugs

    ADVERSE DRUG EFFECTS

    Aminoglycosides are the most vestibulotoxic of all ototoxic drugs. The introduction of streptomycin in 1944 for treatment of tuberculosis brought ototoxicity to clinical attention, as a substantial number of treated patients developed irreversible cochleo-vestibular dysfunction [97,98].

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    14 . Which of the following contributes to misdiagnosis of posterior circulation TIA or stroke as benign dizziness?
    A) Failing to consider stroke in younger patients
    B) Over-reliance on the symptom quality approach
    C) Overweighting traditional stroke risk factors for patient screening
    D) All of the above

    DIAGNOSIS: THE "TIMING AND TRIGGERS" WORKUP

    Publications have brought into focus the misdiagnosis of patients with stroke who present with isolated dizziness. The "timing and triggers" approach is shown to reduce this highly concerning problem largely resulting from [8]:

    • Over-reliance on the symptom quality approach

    • Lack of familiarity with key physical exam findings

    • Overweighting traditional stroke risk factors for patient screening (e.g., age, vascular risk factors) and not considering stroke in younger patients

    • Over-reliance on CT

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    15 . In the "timing and triggers" diagnostic workup, major medical and other obvious non-vestibular dizziness etiologies are identified or ruled out during
    A) triage.
    B) timing.
    C) testing.
    D) triggers.

    DIAGNOSIS: THE "TIMING AND TRIGGERS" WORKUP

    Accurate diagnosis is an essential precondition for effective treatment of dizziness and vertigo, best ensured by defining the rapidity of onset, the context, associated symptoms, intermittent or persistent nature of dizziness, and triggers of intermittent symptoms during patient history-taking. This is called the "timing and triggers" diagnostic workup. The workup is structured using the algorithm Triage-TiTrATE-Test [8,37,101]:

    • Triage: Identify dangerous causes by noting the presence of prominent associated symptoms, abnormal vital signs, altered mental status, or ancillary test results.

    • Timing: In the history of presenting illness, classify the pattern of dizziness attacks as episodic, acute, or chronic in duration.

    • Triggers: In the history and review of systems, seek an underlying pathophysiologic mechanism by searching for obvious triggers or exposures.

    • Targeted exam: Differentiate benign from dangerous causes within a timing-trigger category by using specific exam findings, emphasizing a targeted eye movement exam.

    • Test: Choose the best laboratory or imaging test when clinically relevant uncertainty remains about a dangerous cause that has not been ruled out.

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    16 . To detect and localize the underlying dizziness/vertigo pathology, targeted examinations emphasize
    A) brain imaging.
    B) blood workups.
    C) neurologic exams.
    D) eye movement assessments.

    DIAGNOSIS: THE "TIMING AND TRIGGERS" WORKUP

    Accurate diagnosis is an essential precondition for effective treatment of dizziness and vertigo, best ensured by defining the rapidity of onset, the context, associated symptoms, intermittent or persistent nature of dizziness, and triggers of intermittent symptoms during patient history-taking. This is called the "timing and triggers" diagnostic workup. The workup is structured using the algorithm Triage-TiTrATE-Test [8,37,101]:

    • Triage: Identify dangerous causes by noting the presence of prominent associated symptoms, abnormal vital signs, altered mental status, or ancillary test results.

    • Timing: In the history of presenting illness, classify the pattern of dizziness attacks as episodic, acute, or chronic in duration.

    • Triggers: In the history and review of systems, seek an underlying pathophysiologic mechanism by searching for obvious triggers or exposures.

    • Targeted exam: Differentiate benign from dangerous causes within a timing-trigger category by using specific exam findings, emphasizing a targeted eye movement exam.

    • Test: Choose the best laboratory or imaging test when clinically relevant uncertainty remains about a dangerous cause that has not been ruled out.

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    17 . Almost all patients with vertigo feel worse with
    A) exertion.
    B) head movements.
    C) exposure to visual stimuli.
    D) extended time in a supine position.

    DIAGNOSIS: THE "TIMING AND TRIGGERS" WORKUP

    Almost all patients with vertigo feel worse with head movements. The critical distinction is whether head movements trigger (symptoms appear only when provoked by movements) or exacerbate (movements worsen pre-movement vertigo) symptoms [8,20].

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    18 . HINTS is an acronym for three ocular motor tests. Which of the following is NOT one of these tests?
    A) Head impulse tests
    B) Gaze testing for nystagmus
    C) MRI with diffusion-weighted imaging
    D) Alternative cover test for skew deviation

    DIAGNOSIS: THE "TIMING AND TRIGGERS" WORKUP

    HINTS is an acronym for three ocular motor tests—the head impulse test (HIT), gaze testing for nystagmus, and alternate cover test for skew deviation—that are combined to differentiate central from peripheral causes of dizziness. Nystagmus is a key observed response. Normal visual fixation can suppress mild nystagmus, but Frenzel lenses worn by the patient block visual fixation and magnify examiner view of eye movements [8,10,20]. When conducting the HIT, have the patient fixate his/her gaze on a midline target (e.g., the examiner's nose), then rapidly rotate his/her head 20 degrees to the right or left, bring head back to midline, then rotate to the other side. The presence of a corrective saccade is ''positive'' for abnormal vestibulo-ocular reflex, which generally indicates a peripheral vestibular process. Gaze that remains locked on the midline target is normal. A normal HIT in patients with AVS is highly suspicious for stroke, but HIT is only useful in patients with AVS and nystagmus. In patients with dizziness (with urosepsis or dehydration) without nystagmus, a normal HIT is a misleading false-positive for stroke.

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    19 . Within the first 48 hours of onset, posterior circulation stroke is most accurately differentiated from a peripheral dizziness cause by
    A) HINTS exam.
    B) computed tomography.
    C) magnetic resonance imaging.
    D) MRI with diffusion-weighted imaging.

    DIAGNOSIS: THE "TIMING AND TRIGGERS" WORKUP

    In the first 48 hours, physical examination outperforms MRI. If the initial physical examination suggests stroke, a negative MRI result should not be interpreted as excluding stroke. Delayed MRI (three to seven days post-onset) may be required to confirm the presence of a new infarct [8]. Posterior circulation stroke should be differentiated from benign peripheral vestibular disorder (Table 1) [8,10,19]. Nearly all patients with AVS due to a peripheral cause exhibit nystagmus, which may be inhibited if benzodiazepines/other vestibular suppressants are taken before the exam. When possible, assess for nystagmus before medications to manage symptoms are administered [8,10].

    TESTING TO DIFFERENTIATE POSTERIOR CIRCULATION STROKE FROM BENIGN PERIPHERAL VESTIBULAR DISORDER

    HINTS is performed in sequence. Test nystagmus first; HINTS is validated only in patients with nystagmus, and gaze testing is non-intrusive (i.e., head movement unnecessary).

    • Gaze testing: Is there a central pattern of nystagmus?

    • Alternate cover test: Is skew deviation present?

    • HIT: Is the head impulse test result negative?

    Patients with s-AVS and worrisome nystagmus, skew deviation, or bilateral normal HIT have a presumed stroke and should be admitted to a hospital. If all three tests seem reassuring, perform a targeted neurologic exam to determine if there are any CNS signs. This involves testing for:

    • 4D symptoms:

      • Diplopia (double vision)

      • Dysphagia (difficulty swallowing)

      • Dysarthria (difficulty with speech)

      • Dysmetria (lack of coordination)

    • The cranial nerves for hearing

    • Anisocoria (unequal pupil size)

    • Facial loss of pain or temperature sensation

    • Cerebellar function for limb ataxia.

    The next step is gait testing to determine if the patient can walk unassisted.
    If the answer to any of these questions is yes, the cause is presumed central and treated as stroke. If the answer to all questions is no, the cause is presumed peripheral. All answers must be no in order to exclude stroke because none is sufficiently sensitive individually.
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    20 . In central paroxysmal positional vertigo, all of the following are true, EXCEPT:
    A) It always has a dangerous etiology.
    B) Downbeat or vertical nystagmus can distinguish it from BPPV.
    C) It can have a relatively benign etiology, such as acute alcohol intoxication.
    D) It is the primary serious cause of triggered episodic vestibular syndrome and mimic of BPPV.

    DIAGNOSIS: THE "TIMING AND TRIGGERS" WORKUP

    As mentioned, clinicians should distinguish triggers from exacerbating features [37]. Prototype t-EVS causes are BPPV and orthostatic hypotension; less commonly, it is caused by superior canal dehiscence syndrome [8]. Possible dangerous causes include central paroxysmal positional vertigo and serious causes of orthostatic hypotension, such as internal bleeding. Patients with panic or anxiety disorders may also complain of episodic vertigo, lightheadedness, or dizziness during panic attacks that are triggered or spontaneous. Studies show a high prevalence of vestibular dysfunction for these patients [112].

    Episodic positional symptoms are common to all causes of t-EVS, differentiated by targeted history and exams. BPPV is identified by maneuvers that reproduce dizziness combined with an observed pattern of nystagmus. Orthostatic hypotension is diagnosed by observing a significant fall in blood pressure upon sitting and standing. Dangerous t-EVS mimics are identified by careful attention to the corresponding signs and symptoms that differentiate these benign conditions from potentially more serious disorders [37]. Positional triggers, such as rolling over in bed or reclining, are common in BPPV but should not occur in orthostatic hypotension [8]. Unlike head position changes in BPPV, the vertigo and oscillopsia attacks in superior canal dehiscence syndrome are triggered by pressure-related changes of the external auditory canals (e.g., loud sounds, Valsalva maneuver) [22].

    The nystagmus characteristics of BPPV and central paroxysmal positional vertigo are distinct. Atypical nystagmus (downbeat or horizontal) is suggestive of central paroxysmal positional vertigo, and pure vertical (up- or downbeating) nystagmus should be considered of central origin until proven otherwise [8,23]. Central mimics of BPPV less often involve strokes and more often involve posterior fossa neoplasm, hemorrhage, or demyelination recognized by association with other abnormalities [104,113].

    Central paroxysmal positional vertigo also includes common, benign causes, such as alcohol or sedative intoxication. Such patients are more apt to complain of continuous, persistent dizziness exacerbated (not triggered) by position change, often readily diagnosed based on context and other signs of intoxication [8,37].

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    21 . The vestibular suppressant of choice in pregnancy is
    A) diazepam.
    B) meclizine.
    C) metoclopramide.
    D) diphenhydramine.

    CLINICAL MANAGEMENT

    Drug classes and agents commonly used as vestibular suppressants include antihistamines, benzodiazepines, scopolamine, dopamine antagonists, and ondansetron (Table 2). Antihistamines (e.g., meclizine, diphenhydramine, dimenhydrinate) block the release of histamine and acetylcholine and are especially beneficial in vestibular-mediated nausea, vomiting, and motion sickness. Side effects include sedation, confusion, dry mouth, and urinary retention. Meclizine is preferred because it has minimal anticholinergic effects, causes less sedation, and is effective in the treatment of vertigo due to labyrinth dysfunction. It is also the drug of choice in pregnancy [123].

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    22 . Which of the following drugs reduces sensory mismatch and is one of the most effective agents for preventing motion sickness?
    A) Ondansetron
    B) Scopolamine
    C) Amitriptyline
    D) Promethazine

    CLINICAL MANAGEMENT

    Scopolamine is a belladonna alkaloid that blocks CNS neurotransmission of acetylcholine and is one of the most effective agents for preventing motion sickness. Scopolamine is also effective for vestibular-mediated nausea/vomiting and is better tolerated as a transdermal patch than when taken orally. Common side effects are sedation, constipation, dry mouth, and urinary retention [114,124].

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    23 . Vestibular suppressants should generally not exceed three days to avoid
    A) sedation.
    B) tardive dyskinesia.
    C) QT interval prolongation.
    D) interference with central compensation.

    CLINICAL MANAGEMENT

    In peripheral vestibular disorders, all vestibular suppressants can interfere with central compensation, and their use is recommended to not exceed three days [15,22,125]. The goal is for patients to rapidly receive specialist care, but patients may not get an immediate appointment and remain highly symptomatic. In this context, vestibular suppressants should continue for symptom control until optimized treatment is initiated by a specialist [119].

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    24 . Vestibular rehabilitation promotes vision and proprioception to substitute for loss of vestibular inputs through
    A) reconditioning.
    B) optokinetic stimuli.
    C) strategic substitution.
    D) central compensation.

    CLINICAL MANAGEMENT

    Strategic substitution exercises promote the use of sensory stimuli and spatial cues from vision and proprioception to substitute for loss of vestibular inputs. Cervico-ocular reflex input is strengthened to reduce spatial uncertainty, and alternative spatial cues can improve balance and walking [44,132].

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    25 . Vestibular rehabilitation reduces visual motion sensitivity through
    A) habituation.
    B) cervico-ocular exercises.
    C) smooth-pursuit exercises.
    D) vestibulo-ocular exercises.

    CLINICAL MANAGEMENT

    Habituation exercises reduce visual motion sensitivity (e.g., visual vertigo, space and motion discomfort) through systematic exposure to noxious stimuli evoking mild, temporary symptoms. Approaches include optokinetic stimuli and virtual reality for immersion in repetitive moving and visually challenging environments [44,132].

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    26 . BPPV is best managed by
    A) medication therapy.
    B) extensive diagnostic testing.
    C) canalith repositioning procedures.
    D) observation to allow spontaneous remission.

    CLINICAL MANAGEMENT

    Canalith repositioning procedures (CRPs) are the first-line therapy option and the most effective treatment for BPPV for patients with prolonged symptoms and/or frequent recurrences. Vestibular suppressants are generally avoided, though a brief course of an antihistamine (e.g., meclazine) may be indicated for initial symptom control. This may be all that is needed for patients with mild, self-limited symptoms and infrequent recurrences. Rarely, BPPV can be refractory to CRPs and require surgical occlusion of the affected semicircular canal [15].

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    27 . The preferred canalith repositioning procedure in posterior canal BPPV is the
    A) supine roll.
    B) Epley maneuver.
    C) Gufoni maneuver.
    D) head-shaking maneuver.

    CLINICAL MANAGEMENT

    CRP is strongly recommended as initial therapy for pc-BPPV [22]. The Epley maneuver is the preferred CRP for pc-BPPV and has more than 20 years of evidential support. Meta-analyses have found that, compared with sham or control groups, the Epley led to significantly greater rates of complete vertigo resolution and conversion from a positive to a negative Dix-Hallpike. After 12 months, the Epley was superior to sham maneuver in conversion to negative Dix-Hallpike and perceived disability [22,140].

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    28 . Which of the following medications is recommended in the first tier treatment of Ménière disease?
    A) Betahistine
    B) Metoprolol
    C) Topiramate
    D) Carbamazepine

    CLINICAL MANAGEMENT

    Based on clinical experience with long-term treatment in patients with Ménière disease, long-term, high-dose betahistine is the recommended therapy, initiated at 48 mg three times per day [40,61]. If symptom alleviation is insufficient after three months, the dose can be increased up to 480 mg/day [119,152]. As noted, betahistine can be obtained at compounding pharmacies in the United States with a prescription [15].

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    29 . Which of the following drugs is a first-line treatment of vestibular paroxysmia?
    A) Diazepam
    B) Acetazolamide
    C) Carbamazepine
    D) Dimenhydrinate

    CLINICAL MANAGEMENT

    With vestibular paroxysmia, the characteristic brevity (seconds up to a few minutes, very seldom many hours) and frequently of recurring vertigo attacks makes the differential diagnosis generally straightforward [46]. The frequent vertigo attacks respond to carbamazepine (200–800 mg/day) or oxcarbazepine (300–900 mg/day), even in the lower dose range. Both drugs are recommended to start with a low dose, slowly progressing to higher doses as necessary [119].

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    30 . Vestibular dysfunction in older adults
    A) should prompt a fall-risk screening evaluation.
    B) involves age-related loss of proprioceptive and vestibular function.
    C) substantially increases the risk for falls, the leading cause of disability and premature mortality from injury.
    D) All of the above

    DIZZINESS AND FALLS PREVENTION IN OLDER PATIENTS

    During 2001–2004, an estimated 35.4% of adult Americans had vestibular dysfunction requiring medical attention. The prevalence of balance impairment and vestibular dysfunction increases with age—the rate is 75% among persons older than 70 years and 85% among persons 80 years of age or older. Persons with vestibular disorders have an eight-fold increase in risk of falling and resultant morbidity/mortality. Uncompensated vestibular hypofunction results in postural instability, visual blurring with head movement, and subjective complaints of dizziness and/or imbalance [44].

    Falls typically result when age-related and environmental (e.g., unfamiliar surroundings, unsafe walking surface) risk factors intersect. Gait and balance impairment are the most consistent risk factors, followed by medications (e.g., benzodiazepines, antidepressants) and polypharmacy [174]. Older patients may have multiple risk factors, including vestibular dysfunction, cerebrovascular disease, cervical spine disorders, physical deconditioning, and postural hypotension. Visual impairment is common and promotes multisensory deficit [173,175].

    Postural control and balance rely on sensory input from proprioceptive and vestibular systems. Age-related changes in these systems impair postural control and increase the risk of falls; they include loss of proprioceptive sensitivity in the lower extremities and loss of labyrinthine hair cells, vestibular ganglion cells, and nerve fibers in the vestibular system [174]. Compounding the loss of proprioceptive and vestibular function are age-related changes in the CNS, including neuronal loss and neurotransmitter depletion, causing further impairments in postural control [174].

    A targeted history and physical exam can identify patients at risk for falling. All older patients, especially patients with a dizziness/vertigo diagnosis, should be asked at least once yearly about falls [174]. Questions for initial screening of falls risk include [22]:

    • Have you had a fall in the past year? How many times? Were you injured?

    • Do you feel unsteady when standing or walking?

    • Do you worry about falling?

    With positive response, the clinician can perform a more detailed assessment or refer the patient to a specialist [22]. Treatment should be directed at the most readily modifiable fall risk factor(s) [173].

    Clinicians should counsel patients and their families on the risk of falls with any balance, dizziness, or vestibular disorder, especially the frail elderly, who are more susceptible to serious injury from falling. Counseling should occur during the initial diagnosis and can include assessment of home safety, activity restrictions, and the need for home supervision until symptoms resolve. Healthcare providers should also ask about dizziness while driving, which may require intervention to prevent patient and public injury or fatality [22,173,176].

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