“What do you mean by dizziness?”
The first step in evaluating the patient with acute dizziness is to determine precisely what they mean when they tell you they are dizzy. The three sensations that patients describe most commonly when they use the term dizziness are lightheadedness, imbalance, and vertigo. While all three are of potential interest to the neurologist, it is vertigo that is most specific for neurological disease. Lightheadedness and imbalance will therefore be discussed only briefly.
Although lightheadedness or presyncope is usually the province of internists and cardiologists, many patients with frequent, intolerable symptoms are referred to neurologists for evaluation and treatment. After performing a careful history, it is necessary to review the basic assessment, especially electrocardiograms, echocardiograms, and telemetry data, to make sure that there is no medical explanation for the symptoms. Ensure that the patient is not volume depleted and check for any recent changes in antihypertensive medications or sedatives. For patients in whom the cause of lightheadedness is still in question, tilt-table testing and extended cardiac telemetry (i.e. a Holter monitor) may help to distinguish among cardiogenic syncope, orthostatic hypotension, neurally mediated syncope, and paroxysmal tachycardia syndrome.
Arrhythmias, aortic stenosis, and hypertrophic obstructive cardiomyopathy are common and serious cardiogenic causes of presyncope and syncope, which require the attention of a cardiologist.
Orthostatic hypotension is defined as a drop in systolic blood pressure of >20 mmHg or diastolic blood pressure of >10 mmHg that occurs within 3 minutes of standing.1 Orthostatic hypotension is often secondary to antihypertensive medications or volume depletion. Primary neurological conditions that predispose to orthostatic hypotension include multisystem atrophy, pure autonomic failure, and Parkinson’s disease. Conservative measures to treat orthostatic hypotension include adjusting any contributory medications, encouraging adequate hydration, increasing salt intake, and raising the head of the bed at night. Elastic stockings to reduce peripheral venous pooling are another nonpharmacological option, but are poorly tolerated by most patients, especially in the summer. If conservative measures fail, the two main medical options are the mineralocorticoid fludrocortisone (initiated at 0.1 mg qd and titrated to 0.5 mg qd as needed) and the α-adrenergic agonist midodrine (initiated at 2.5 mg tid and increased to 10 mg tid as tolerated). Do not give either agent in the evening, as doing so may produce nocturnal hypertension and worsen daytime hypotension. Both agents may produce supine hypertension as a side effect.
Neurally mediated syncope
Neurally-mediated syncope (the vasovagal response) is a complex and incompletely understood phenomenon. It occurs as a result of peripheral vasodilation and bradycardia secondary to increased vagal output to the sinus node of the heart. Neurally mediated syncope is most often provoked by a painful, stressful, or emotional stimulus. Other common precipitants include urination, defecation, and the Valsalva maneuver. Carotid sinus syncope is a rare form of neurally mediated syncope, which results from pressure in the area of the carotid artery or sudden head turning. Lightheadedness in neurally mediated syncope is often accompanied by weakness, tremulousness, blurred vision, diaphoresis, and nausea. If the diagnosis is not obvious from the history, it may be made with the help of tilt-table testing. Patients with neurally mediated syncope should be educated on how to identify and avoid precipitants of their attacks. Volume expansion and fludrocortisone may be helpful.
Postural tachycardia syndrome
Postural tachycardia syndrome (POTS) is a poorly understood disorder characterized by lightheadedness or fainting that occurs upon standing and is accompanied by tachycardia but not hypotension. Most patients with POTS are young women and, because the symptoms that accompany POTS may resemble panic attacks, patients are often misdiagnosed with anxiety disorders long before the correct diagnosis is contemplated. Postural tachycardia syndrome is diagnosed by finding a symptomatic increase in heart rate of >30 beats/minute without a drop in blood pressure upon assuming an upright position, either by standing in the office or by a tilt table test.2 Unfortunately, treatments such as volume repletion, fludrocortisone, and midodrine usually do not lead to substantial improvement.
Dizziness of psychological origin
Patients with anxiety and panic disorders may describe a sensation of dizziness that has features distinct from vertigo, including a sensation of floating, lightheadedness, or depersonalization. These patients often come to neurological attention when other symptoms of a panic attack are absent. Careful psychiatric assessment and exclusion of syncope and neurological disorders help to make the diagnosis. Pharmacological and behavioral management of the responsible anxiety or panic disorder may reduce or cure symptoms.
Imbalance is a sensation that is often difficult to describe more specifically than “dizziness.” Some patients will use the term “off balance” or may tell you that they feel as if they are on a ship at sea. Imbalance has a wide variety of etiologies, but, in general, they all have some component of proprioceptive loss secondary to cervical myelopathy, polyneuropathy, or orthopedic conditions. Evaluation and treatment of imbalance is discussed further in Chapter 18.
Evaluation of vertigo
Vertigo is the sensation of environmental movement or rotation produced by dysfunction of the vestibular labyrinth, vestibular nerve, brainstem, or cerebellum. As a general rule, peripheral (labyrinthine and vestibular nerve) dysfunction is benign, while central (brainstem and cerebellar) dysfunction is serious and possibly life-threatening. Distinction between central and peripheral localizations is therefore crucial to determine which patients require further evaluation and monitoring. The most reliable indicator of central vertigo is the presence of accompanying CNS dysfunction such as diplopia, facial numbness, dysarthria, and dysphagia. Features that are more consistent with (but not pathognomonic for) peripheral nervous system pathology include hearing loss, aural fullness, and tinnitus. Several other symptoms may also help to distinguish between central and peripheral nervous system dysfunction, but are less reliable. For example, symptom duration of several minutes is more likely to reflect a central process, whereas symptoms that last for seconds at a time are more consistent with peripheral disease. Occipital or nuchal headaches are more typical of CNS processes such as cerebellar or brainstem hemorrhages. Changes in symptoms with head position are more characteristic of peripheral nervous system disorders. Older patients and those with risk factors for vascular disease are more likely to have central vestibular dysfunction than are younger, otherwise healthy people.
Neurological examination is often more helpful than the history in distinguishing between central and peripheral causes of vertigo. Cranial nerve findings including anisocoria, ocular misalignment, facial numbness, facial weakness, asymmetric hypoactive gag reflex, and tongue deviation favor brainstem pathology (Chapters 7 and 8). Any weakness or sensory deficits in the limbs also point to a brainstem process. Hearing loss more commonly accompanies peripheral causes of vertigo. The following examination techniques are helpful in assessing the vertiginous patient.
For clinical purposes, the cerebellum may be divided roughly into the midline, which coordinates truncal movements, and the hemispheres, which coordinate appendicular movements. A number of examination findings reflect pathology in the cerebellum or its connections within the brainstem and cerebral hemispheres.
Limb dysmetria may be elicited by asking the patient to move their finger rapidly back and forth between their nose and your finger. In order to maximize the yield of this task, instruct the patient to abduct their arm so that the elbow is at shoulder height and place the target an entire arm’s length away from them. A patient with ipsilateral cerebellar hemispheric dysfunction will miss or overshoot the target and may also miss their nose or strike it with excessive force. In some patients with cerebellar system dysfunction, finger-to-nose testing will uncover intention tremor, which is a tremor manifest near the end of a directed movement (Chapter 14).
The overshoot phenomenon is elicited by having the patient attempt to perform mirror movements. Instruct them to align their hand opposite yours and then mirror your hand as you move it rapidly in the vertical or horizontal plane and then stop it abruptly. A patient with an ipsilateral cerebellar hemispheric lesion will not be able to stop in time, terminating their movements several inches past the target.
Ask the patient to extend their arms in front of them with their wrists pronated. Tap the dorsal surfaces of each forearm briskly, observing for abnormal, large amplitude oscillations as the arm returns to its resting position. Rebound also points to an ipsilateral cerebellar hemispheric lesion
Instruct the patient to tap the knee with the opposite heel and then run it up and down the surface of the shin. Clumsiness or an inability to complete this kind of movement points to an ipsilateral cerebellar hemispheric lesion.
Patients with midline cerebellar lesions are unable to sit upright, tending to fall to the side with any perturbation of the trunk. Patients with hemispheric lesions tend to fall to the side of the lesion.
Nystagmus is an abnormal ocular oscillation. Jerk nystagmus is characterized by an abnormal slow movement in one direction followed by a fast corrective movement in the opposite direction. By convention, it is named for the direction of the fast phase. Pendular nystagmus is characterized by eye movements of similar velocity in both directions. Examine for nystagmus in the primary position (with the eyes looking straight ahead) and in all directions of gaze, noting the direction, amplitude, and velocity of nystagmus in each position. Subtle nystagmus is often only observable when visual fixation is removed. The best way to do this at the bedside is to have the patient close one eye while you look into the other eye with an ophthalmoscope. When examining for nystagmus using this method, keep in mind that the fundus moves in the direction opposite to the direction that the eye moves when it is opened. A detailed discussion of the neuroanatomy of nystagmus is beyond the scope of this text. For clinical purposes, the following are several rules of thumb that allow nystagmus to be used in localizing vertigo3:
• Endpoint nystagmus is a low-amplitude, low-frequency nystagmus that occurs with ocular fixation. It fatigues after two to three beats and is usually a normal variant.
• Horizontal and horizontal–torsional nystagmus suggests contralateral peripheral vestibular dysfunction, often vestibular neuritis. This nystagmus may be present in the primary position, but is usually more prominent when looking in the direction of the fast phase of nystagmus.
• Horizontal nystagmus that reverses direction every 2 minutes is called periodic alternating nystagmus and points to dysfunction of the cerebellar midline.
• Horizontal nystagmus that is relatively symmetric in all directions of gaze is usually congenital. People with this form of nystagmus do not actually have oscillopsia (the sensation that objects are moving back and forth). It is important to recognize this form of nystagmus, as it may lead to unnecessary evaluation for serious brainstem pathology if it is misinterpreted.
• Bruns nystagmus suggests a cerebellopontine angle tumor: when gaze is directed towards the side of the tumor, there is a large-amplitude horizontal nystagmus due to brainstem compression, and when the gaze is directed to the contralateral side, there is a small-amplitude horizontal nystagmus away from the tumor due to vestibular paralysis.4
• Downbeating nystagmus in the primary position or with lateral gaze suggests vestibulocerebellar dysfunction, medication toxicity, or a cervicomedullary junction lesion such as a Chiari malformation.5
• Purely upbeating nystagmus also points to drug intoxication or to medullary dysfunction. Unless there is a clear history of intoxication with a medication or drug of abuse, purely vertical nystagmus should prompt imaging of the brainstem.
• Upbeating nystagmus with a torsional component, when it is elicited by the Dix–Hallpike maneuver, is classical for benign paroxysmal positional vertigo.
• Purely torsional nystagmus is uncommon and points to brainstem rather than peripheral vestibular dysfunction.
• Pendular nystagmus also reflects brainstem dysfunction. In some cases, benign congenital nystagmus has a pendular appearance.
• Almost all nystagmus involves both eyes. Causes of true or apparent monocular nystagmus include:
• myasthenia gravis
• internuclear ophthalmoplegia
• congenital monocular blindness
• superior oblique myokymia
The following abnormal eye movements may be misinterpreted as nystagmus:
• Ocular bobbing and dipping are seen in comatose patients with brainstem dysfunction and are discussed further in Chapter 2.
• Square-wave jerks are binocular saccadic movements that occur in the direction opposite to visual fixation and last for a fraction of a second before the eyes return to the primary position. They are frequent in normal subjects,
Figure 9.1 The Dix–Hallpike maneuver for right-sided benign paroxysmal positional vertigo. See text for details.
but may also occur in patients with parkinsonian syndromes, especially progressive supranuclear palsy and multisystem atrophy.6
• Opsoclonus is characterized by irregular, sometimes chaotic, horizontal and vertical eye movements. It is often present in conjunction with myoclonus (Chapter 14), and in this setting is associated with a paraneoplastic syndrome or autoimmune disease.
A positive head-thrust test is useful in establishing a unilateral peripheral vestibular lesion.7 To perform the test, instruct the patient to fix their gaze on a target approximately 10 feet away. Next, grasp the head by the vertex and chin, and rotate it horizontally by about 20°. The rotation must be done fairly quickly. In a patient with a unilateral vestibular lesion, rotation of the head towards the affected side will lead to a catch-up saccade opposite to the direction of head rotation. Rotation of the head away from the affected side will be accompanied by normal eye movements without any refixation.
The Dix–Hallpike maneuver is used to elicit nystagmus or reproduce vertigo in patients with benign paroxysmal positional vertigo (BPPV).8 To perform the Dix–Hallpike maneuver, the patient should be seated upright (Figure 9.1A). Warn the patient that the maneuver may lead to intense vertigo. Grasp the head on both sides and quickly turn the head to the side while bringing the patient backwards so that the head lies over the edge of the bed (Figure 9.1B). When the Dix–Hallpike maneuver is performed for patients with the posterior canal variant of BPPV, it produces a torsional upbeat nystagmus beating towards the side of the involved ear. Characteristically, this maneuver fatigues when it is repeated. A less common variant of BPPV involves the horizontal semicircular canal, in which case the nystagmus beats horizontally towards the involved ear. It is important to keep the head turned and hanging over the side of the bed after performing the maneuver, as nystagmus secondary to BPPV is usually associated with a latency of up to 30–45 seconds. If the Dix–Hallpike maneuver is negative when the head is turned to the right, sit the patient upright and repeat the maneuver in the opposite direction.
Imaging of the patient with vertigo
The need for neuroimaging in patients with signs and symptoms of central vertigo is clear cut. The studies of choice are MRI of the brain with magnetic resonance angiography (MRA) of the posterior circulation. CT scans do not provide adequate images of the posterior fossa and are therefore of limited value in evaluating patients with suspected central vertigo. Patients with brief episodes of vertigo and an examination that is normal or shows only horizontal nystagmus and possibly mild gait instability generally do not require neuroimaging. With the rare exception of patients with posterior inferior cerebellar artery infarction, most such patients have peripheral vestibulopathy.9 It is prudent to image older patients and those who have risk factors for vascular disease if any uncertainty remains about the localization after the history and physical examination.
Causes of vertigo
Vertebrobasilar ischemia and infarction
Vertebrobasilar vascular disease is the most dangerous cause of acute-onset vertigo. Symptoms begin suddenly, and some patients have transient ischemic attacks before stroke occurs. Because the blood vessels of the posterior circulation are usually affected in a patchy, irregular manner, there is considerable variability in the presentation of vertebrobasilar strokes. More precisely localizable vertebrobasilar syndromes that are exceptions to this rule include Wallenberg’s syndrome and cerebellar infarction (Chapter 21). Signs and symptoms that accompany vertigo are highly variable and include diplopia, facial pain and numbness, dysarthria, dysphagia, and sensorimotor signs and symptoms in the limbs. The diagnosis of vertebrobasilar infarction is confirmed by MRI. In some cases, MRA may help to identify the responsible vessel. Consider the diagnosis of vertebral artery dissection in patients with posterior circulation strokes accompanied by neck pain, and confirm the diagnosis with MRA or computed tomography angiography (CTA) of the cervical vasculature.
Presumed viral infection of the vestibular nerve is among the most common causes of acute vertigo. A viral prodrome may or may not precede vestibular neuritis. Symptoms usually develop over several hours to days and last for up to a few weeks at a time. Vertigo is typically quite severe and is associated with nausea and vomiting. Some patients have a combination of vestibular neuritis and hearing loss known as neurolabyrinthitis. The nystagmus due to vestibular neuritis is either horizontal or horizontal with a torsional component and directed away from the involved ear. A positive head-thrust test helps to establish the diagnosis in some cases. There is no specific treatment for the underlying cause of vestibular neuritis. Supportive care includes vestibular suppressants such as the antihistamine meclizine (25–50 mg q6h) or the benzodiazepine lorazepam (0.5–1 mg q6h). Patients with severe or persistent symptoms may require vestibular rehabilitation.
Benign paroxysmal positional vertigo
This is characterized by brief (<30–60 seconds), episodic vertigo, which occurs with changes in head position, often when turning over in bed or bending the head backwards while reaching for something on a high shelf. Because of the intensity of the episodes, patients may report that symptoms last for up to a few minutes at a time. Precipitating factors include head trauma, vestibular neuritis, and a perilymph fistula. The pathophysiology of BPPV involves excessive stimulation of the cupula by otoconial debris in the semicircular canal, which in turn leads to increased firing of the ampullary nerve, resulting in the characteristic vertigo and nystagmus. The diagnosis is established via the Dix–Hallpike maneuver (see above). In patients with the posterior semicircular canal variant, this maneuver produces nystagmus that is upbeating and torsional towards the lower ear. In patients with the less common horizontal canal variant, the nystagmus is horizontal and also beats towards the lower ear. Nystagmus may occur in the opposite direction in patients recovering from acute BPPV, or may be absent entirely.
Figure 9.2 The Epley maneuver for right posterior canal variant benign paroxysmal positional vertigo. See text for details.
The Epley or particle-repositioning maneuver is an effective treatment for patients with the posterior semicircular canal variant of BPPV (Figure 9.2):10
1. The patient should be seated upright (Figure 9.2A).
2. Instruct them to turn their head 45° towards the symptomatic side (Figure 9.2B).
3. Next, the patient should bring their head backwards so that they are lying over the edge of the bed (Figure 9.2C). They should wait 30 seconds in this position.
4. Next, they should rotate their head 90° so that they are facing in the opposite direction (Figure 9.2D). Wait 30 seconds in this position.
5. Instruct the patient to rotate the entire head and body 90° toward the unaffected side and wait for 30 seconds in this position (Figure 9.2E).
6. Finally, instruct the patient to sit up while keeping the head rotated 45° with respect to the body. Wait 30 seconds in this position (Figure 9.2F).
In some patients with BPPV, the vertigo may be so severe that the Epley maneuver is poorly tolerated. These patients may benefit from pretreatment with vestibular suppressants such as meclizine. Because symptoms tend to recur over time, give patients written instructions or pictures on how to perform the Epley maneuver so that they may treat themselves at home without delay.
Treat the horizontal variant of BPPV with the barbecue-spit maneuver (Figure 9.3).11 The patient lies supine (Figure 9.3A) and then rotates 90° so that the affected ear is facing downwards (Figure 9.3B). Instruct them to wait for 30 seconds in this position. The patient then completes three successive 90° rotations, waiting for 30 seconds in between each rotation (Figures 9.3C–E).
Ménière’s disease is thought to occur as a consequence of endolymphatic fluid buildup in the inner ear. The classical symptom cluster of Ménière’s disease is recurrent, spontaneous vertigo, sensorineural hearing loss, aural fullness, and tinnitus.12 The diagnosis may be missed in its early stages when vertigo is the sole symptom. Episodes of vertigo last for between 20 minutes and a few hours. Several days of milder imbalance may follow the intense vertiginous spells. During attacks, low-frequency hearing loss may be detected with a 256 Hz tuning fork, although formal audiometric testing is usually required. Hearing loss progresses with recurrent attacks. Prophylaxis for Ménière’s disease includes salt restriction and diuretics such as hydrochlorthiazide (50 mg qd) or acetazolamide (500 mg bid). Acute attacks respond to vestibular suppressants. Patients with symptoms that are refractory to medical treatment should be referred to an otorhinolaryngologist for consideration of endolymphatic sac surgery, transtympanic gentamicin, or labyrinthectomy.13
When vertigo occurs as a migraine aura (Chapter 19), the diagnosis is straightforward. More difficult from a
Figure 9.3 The barbecue-spit maneuver for right horizontal canal variant benign paroxysmal positional vertigo. See text for details.
diagnostic perspective, however, are attacks of vertigo in migraineurs that last for hours to days and occur independently of the headaches. Patients with such episodes are often diagnosed with Ménière’s disease or chronic undifferentiated dizziness. Overall, migraine-associated dizziness accounts for only 2% of episodic dizziness, and other more common conditions should be excluded prior to committing to this diagnosis.14 Migraine abortive and prophylactic agents may help stop these attacks and reduce the frequency with which they recur.
Vestibulotoxic medications that commonly produce vertigo include aminoglycosides, anticonvulsants, sedatives, and cisplatin. In some but not all cases, discontinuing the responsible medication may reverse the symptoms.
This condition results from a leakage of perilymph fluid through the labyrinthine membrane. The classic constellation of symptoms is a popping sound in the ear accompanied by a combination of sudden hearing loss, tinnitus, and vertigo. Symptoms are precipitated by sneezing, straining, and coughing. The diagnosis is established by finding a positive fistula sign: symptoms are reproduced when the patient attempts to “pop” his or her ears while squeezing the nose closed. Instruct patients with perilymph fistula to avoid precipitating activities and to take vestibular suppressants such as meclizine during acute attacks. Refer patients with refractory symptoms to an otorhinolaryngologist for definitive treatment.
In rare circumstances, a sudden brief feeling of instability or frank vertigo may be a seizure manifestation, usually pointing to a focus in the posterior–superior temporal lobe.15 Epileptic dizziness or vertigo should be considered only after more common conditions are thoroughly excluded. Because it so uncommon, epileptic dizziness must be confirmed with an EEG demonstrating epileptiform discharges during an episode.
Cerebellopontine angle tumors
Acoustic neuromas and meningiomas are the most common tumors of the cerebellopontine angle (CPA) (Chapter 23). These tumors generally grow slowly, and compensation from the contralateral vestibular system makes acute vertigo uncommon.16 Other signs and symptoms of CPA tumors include facial numbness, facial weakness, hearing loss, and disequilibrium. Surgical intervention should be considered for patients with progressive symptoms or evidence of tumor expansion on serial neuroimaging studies.16
Chronic undifferentiated dizziness
This diagnosis may represent a forme fruste of migraine, Ménière’s disease, or vestibular neuritis. Many patients with this condition are dismissed as having psychiatric disorders. A viral prodrome or mild head trauma frequently precedes symptom onset by several weeks, but it is hard to prove that either process is really responsible for the symptoms. Most patients describe a sense of being off balance rather than frank vertigo. They do not usually have hearing problems, ocular motility disorders, or falls. Examination is normal with the possible exception of subtle horizontal nystagmus. Chronic undifferentiated dizziness is ultimately a diagnosis of exclusion. A thorough evaluation should include electronystagmography, caloric testing, neuroimaging studies, and lumbar puncture. Some patients respond to vestibular rehabilitation and vestibular suppressant medications. I have found that agents used for migraine prophylaxis are helpful to a small minority.
Postconcussion syndrome and posttraumatic dizziness
Post concussion syndrome includes headache, irritability, forgetfulness, poor concentration, and dizziness (Chapter 4). The dizziness is often due to labyrinthine trauma or BPPV. In many cases, however, the dizziness of postconcussion syndrome is a vague sense of imbalance rather than true vertigo.
Demyelinating lesions involving the cerebellum or its connections within the brainstem may lead to vertigo (Chapter 22). As a presenting complaint of MS, however, vertigo is uncommon.
Paraneoplastic cerebellar degeneration
The most common antibodies that lead to paraneoplastic cerebellar degeneration are anti-Yo (breast and ovarian cancers), anti-Hu (small-cell lung cancer), anti-Tr (Hodgkin’s lymphoma), and anti-Ri (breast and ovarian cancers).17Treatment should focus on the underlying cancer. Unfortunately, the cerebellar degeneration associated with these syndromes is progressive, and most patients lose the ability to ambulate.
The episodic ataxias are a group of uncommon channelopathies characterized (as their name suggests) by recurrent bouts of ataxia.18 Episodic ataxia type 2 in particular may cause episodic vertigo and headaches that are precipitated by stress and fatigue and which may last for hours or days at a time. Acetazolamide (500–1000 mg) reverses the symptoms of an acute attack.
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