The word dizziness is used by patients and sometimes clinicians to describe many different symptoms ranging from room spinning and light-headedness to disorientation, complex partial seizures, and anxiety. As a result, the differential diagnosis for self-reported “dizziness” is very broad. As with all of medicine, obtaining a clear history of what “dizziness” really means to the patient, followed by a careful neurologic examination, is vital to establish the diagnosis and avoid unwarranted testing. The following sections detail different types of dizziness, including the key features and underlying etiologies.

VERTIGO

Vertigo is a type of dizziness in which a patient perceives motion when there is no actual motion. This is most commonly a sensation of the room spinning in a clockwise or counterclockwise direction. Vertigo can also be a sensation of motion, as if on a boat. Some patients also experience a sensation of propulsion, as if they are being pulled or pushed in a direction. Vertigo is a descriptive term, not a diagnosis. Stating that a patient has vertigo is no more specific than saying that a patient has fever or chest pain. The specific cause of the vertigo must be established in order to establish a diagnosis.

Vertigo is caused by an asymmetric impairment in the vestibular system. This can occur at any point along the vestibular pathway from the vestibular nerve or labyrinth to the central vestibular structures. Vestibular disorders can therefore be divided into peripheral and central categories, based on the cause.

The specific details of the onset, quality, duration, triggers, and associated symptoms, as well as the patient’s medical history, aid in guiding the differential diagnosis.

Vertigo is often associated with nausea. Patients may describe a staggering gait or that they must hold on to nearby objects to avoid falling. Depending on the etiology, patients may also have symptoms of diplopia (double vision). Vertigo may be constant or intermittent, depending on the cause. The duration of symptoms and associated features aid in narrowing the diagnostic possibilities. The examination is used to evaluate further and establish the diagnosis. These are critical steps that allow a clinician to triage or distinguish an emergency cause of vertigo such as a brainstem stroke from a benign etiology, for example, benign paroxysmal positional vertigo (BPPV).

PERIPHERAL VERTIGO

There are many causes of peripheral vertigo, each with key features that allow the clinician to determine it.

BPPV is a common form of vertigo. It is caused by an otolith (also called a canalith) of calcium carbonate debris in the semicircular canal. The semicircular canals are within each inner ear and are lined with cilia and endolymph. Each time the head moves, the endolymph moves, which in turn causes the cilia to move and send signals to the central vestibular structures. When an otolith is in the semicircular canal, it disrupts the movement of the endolymph and creates a sensation of spinning. The vertigo occurs only when the person moves the head. The spinning sensation resolves, usually in under a minute, if the patient is perfectly still. Bending over, looking up, or rolling over in bed are common triggers. The vertigo may be accompanied by nausea and sometimes emesis. Importantly, BPPV is not associated with diplopia, weakness, sensory symptoms, or hearing loss.

Otoliths can form in the horizontal and anterior (superior) semicircular canals but are most common in the posterior canal. The orientation and position with which the nystagmus is elicited are slightly different depending on the location of the otolith. Episodes of BPPV often occur in bouts; patients may have recurrent episodes for several days in a row which then resolve, but BPPV may recur frequently if untreated.

BPPV patients have normal neurologic examinations, without evidence of ataxia or sustained nystagmus. The gait remains normal. The diagnosis may be corroborated by doing the Dix–Hallpike maneuver (Fig. 7-1). The maneuver is 50% to 80% sensitive, but some patients are unable to cooperate. During the test, the patient should be observed in each position for 30 to 45 seconds. Nystagmus usually appears within a few seconds and extinguishes after less than 1 minute. The nystagmus is typically upbeating and torsional. When the patient is repositioned in the upright position, the nystagmus recurs with the same cadence. The maneuver is performed with each side of the head turned downward; the side tested which provokes the nystagmus is the one with the otolith. With each repetition of the maneuver, the clinical response becomes less intense. During the maneuver, nystagmus is not always visible to the examiner, but the patient may still experience vertigo. This is referred to as “subjective BPPV” and still responds to treatment.

BPPV is treated with vestibular therapy aimed at repositioning the otolith, usually by doing the Epley maneuver (Fig. 7-2). Of note, patients with otoliths in the horizontal and anterior canals may require different repositioning maneuvers.

FIGURE 7-1. Dix–Hallpike maneuver. This bedside maneuver helps to diagnose BPPV. From Furman JM, Cass SP. Benign paroxysmal positional vertigo. N Engl J Med. 1999;341(21):1590–1596. Copyright © 1999 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.

FIGURE 7-2. The Epley maneuver. Reprinted with permission from Krebs C, Weinberg J, Akesson E. Lippincott’s Illustrated Review of Neurscience. 1st ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.

Vestibular Neuritis and Labyrinthitis

Vestibular neuritis (aka vestibular neuronitis) is believed to be caused by an infectious or autoimmune injury to the vestibular portion of the VIIIth cranial nerve (although there is no clear evidence of inflammation, and the exact etiology remains unknown). Patients present with acute-onset vertigo, often associated with nausea, emesis, and mild gait ataxia. When the patient also has acute hearing loss, the syndrome is called labyrinthitis. Patients should not have additional symptoms of focal weakness or sensory changes. Rarely, patients may report diplopia, but this symptom is more concerning for a brainstem infarct or hemorrhage.

On examination, patients have spontaneous unilateral horizontal or torsional nystagmus. The nystagmus can be suppressed with gaze fixation (having the patient fixate on a target). Patients may also have some gait ataxia and typically fall away from the side of the lesion. The head impulse test (HIT) (Fig. 7-3) is used to identify whether there is vestibular impairment, but it does not definitely exclude a central cause.

Vestibular neuritis can mimic a brainstem infarct or, less commonly, a demyelinating lesion (described later). The decision to proceed with a stroke workup is often based on the age and vascular comorbidities of the patient. A magnetic resonance imaging (MRI) of the brain with thin cuts through the brainstem is often warranted in patients with a high risk of stroke.

In patients with an acute onset of symptoms, treatment with a corticosteroid taper can reduce the duration of symptoms. Additional symptomatic treatment with antiemetics and antihistamines may also be helpful.

Ménière disease

Ménière disease is a constellation of symptoms of vertigo, sensorineural hearing loss, and tinnitus. It is believed to be caused by surplus endolymph. The exact cause is unknown, but there are theories that endolymph homeostasis is impaired. It is most common in adults between the ages of 20 and 40 years. Patients may also report gait unsteadiness and nausea, vomiting, or both. Patients typically have phases of exacerbation and remission of the vertigo. Hearing loss remains and often progresses to deafness.

FIGURE 7-3. Head impulse test (HIT) (sometimes referred to as the head thrust test) is a test of vestibular function that can be easily done in bedside examination. It tests the vestibulo-ocular reflex (VOR) and can help to distinguish a peripheral process (e.g., vestibular “neuritis”) from a central one (e.g., a cerebellar stroke). With the patient sitting, the physician instructs him to maintain his gaze on the examiner’s nose. The physician holds the patient’s head steady in the midline (Panel 1) and then turns the head rapidly to about 20 degrees from the midline. The normal response (intact VOR) is for the eyes to stay locked on the examiner’s nose. The abnormal response (impaired VOR) is for the eyes to move with the head (Panel 2) and then to snap back in one corrective saccade to the examiner’s nose (Panel 3). The HIT is usually “positive” (i.e., a corrective saccade is visible) with a peripheral lesion and “normal” (no corrective saccade) with a central lesion (because the VOR pathway does not pass through the cerebellum). Occasionally, patients with small brainstem strokes have a positive test because the VOR pathway does pass through the brainstem.

Because it is the “positive” HIT that is reassuring and the “negative” test worrisome, it is important to use the test only in patients with an acute vestibular syndrome (AVS). If one were to use the HIT in patients with pneumonia or a fractured wrist, it might be “negative” (or worrisome for a central nervous system event). Therefore, it is critical that it be applied only to patients presenting with an AVS. Reprinted with permission from Wolfson AB. Harwood-Nuss’ Clinical Practice of Emergency Medicine. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2014. Figure 14.1.

Ménière disease is diagnosed by the history, while excluding other causes, especially central causes of vertigo (see below). Treatment addresses the symptoms. Patients are counseled to avoid triggers and to have a diet low in sodium and caffeine.

Acoustic Neuroma

An acoustic neuroma (vestibular schwannoma) is a tumor that grows in the vestibular portion of the vestibulocochlear nerves (cranial nerve VIII). Its cells are derived from Schwann cells, usually in the internal auditory canal. The tumor can extend into the posterior fossa and can even cause mass effect on the brainstem. Acoustic neuromas are among the most common tumors in the cerebellopontine angle. They are most common in adulthood and are usually unilateral. They are also common in patients with neurofibromatosis type 2, occurring bilaterally in this condition.

Acoustic neuromas may be asymptomatic and identified as incidental findings on neuroimaging. When patients are symptomatic, they often present with hearing loss and tinnitus. Frank vertigo (i.e., room spinning) is not a common symptom, but feelings of unsteadiness and imbalance are often reported. If there is significant mass effect, the tumor may compress adjacent cranial nerves, and patients may report symptoms of trigeminal neuralgia, a facial nerve palsy, or both.

On examination, patients typically have sensorineural hearing loss on the affected side, but the remainder of the examination is typically normal unless there is significant mass effect impacting other cranial nerves. Patients have hearing impairment on audiometry. The diagnosis is established with an MRI (Fig. 7-4). Treatment is usually surgical resection. In patients who are not surgical candidates, stereotactic radiotherapy may be attempted to reduce the tumor burden. Tumor recurrence is uncommon.

FIGURE 7-4. Magnetic resonance imaging (MRI) of vestibular schwannoma. (A) T1-weighted axial MRI before contrast shows large hypointense mass within the cerebellopontine angle exerting mass effect on the brainstem. (B) T1-weighted axial MRI postcontrast shows a vestibular schwannoma with expansion of the internal auditory meatus. Reprinted with permission from Louis ED, Mayer SA, Rowland LP. Merritt’s Neurology. 13th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2015. Figure 102.1.

Medications

There are numerous medications that cause dizziness as a side effect. Frank vertigo from medications is uncommon, but aminoglycosides are the exception and can cause both cochlear and vestibular toxicity. Patients who develop this side effect have hearing loss from cochlear involvement and vertigo and disequilibrium from the vestibular nerve damage. These side effects are most common in patients on long-term therapy. The exact incidence of ototoxicity from aminoglycosides is not known.

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The Sensory System Head Trauma Neurologic Investigations Neuro-Ophthalmology Demyelinating Diseases of the Central Nervous System Disorders of the Spinal Cord

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