DIZZINESS AND SYNCOPE Suggestions for Lecturer -1-hour lecture

DIZZINESS AND SYNCOPE Suggestions for Lecturer -1-hour lecture
-Use GRS slides alone or to supplement your own teaching materials. -Refer to GRS for further content. -Refer to Geriatrics at Your Fingertips for updated information. -See GRS7 questions 84, 90, 153, 193, 199, 230, and 235 for additional case vignettes on dizziness and syncope.

OBJECTIVES Know and understand:
The factors that may lead to dizziness and syncope in older adults The elements of evaluation (history, physical examination, testing) of older adults with dizziness and syncope The treatment options for dizziness and syncope

TOPICS COVERED Dizziness Classification and Causes
Prognosis for Older Adults with Dizziness Evaluation and Management Syncope Pathophysiology Causative Factors

IMPORTANCE AND COMPLEXITY OF DIZZINESS
Dizziness is a common symptom in older adults Prevalence in older adults = 4%–30% Prevalence increases 10% for every 5 yr of age Challenges for clinicians Precise classification is difficult Worry about serious causes Specific therapy not available for many 50% of cases have multiple causes

DIZZINESS: CLASSIFICATION BY SYMPTOMS
Vertigo — Rotational sensation Presyncope — Sensation of impending faint Disequilibrium — Feeling of imbalance on standing or walking Other — Lightheadedness, not as specific symptoms Mixed — Most common type

CAUSES OF VERTIGO Peripheral vestibular disorders
Benign paroxysmal positional vertigo (BPPV) Ménière disease Ototoxic medications (eg, aminoglycosides, diuretics, NSAIDs) Acoustic neuroma NSAID = nonsteroidal anti-inflammatory drug

BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV)
Episodic, inner ear disorder Aggravated or brought on by changes in position (eg, turning, rolling over, bending over) Spells are often brief (5–15 sec) Probably results from changes in endolymphatic pressure during head movements resulting from dislodged otoconia in semicircular canal

MÉNIÈRE DISEASE Idiopathic inner ear disorder
Repeated episodes of tinnitus Fluctuating hearing loss with sensation of fullness in ears Severe vertigo Eventual progressive sensorineural hearing loss

BRAIN TUMORS Found in <1% of dizzy patients
Slightly more prevalent (2%–3%) in older patients referred to neurologists Acoustic neuroma Most common tumor associated with dizziness Unilateral cochlear symptoms (tinnitus and hearing loss) predominate, not dizziness Bilateral cochlear symptoms in older persons usually represent presbycusis, not tumor

PRESYNCOPE Sensation of near-fainting
Sign of decreased cerebral perfusion Cardiac causes Electrical: tachy- or bradyarrhythmias Structural, esp. aortic outflow obstruction Vascular causes (eg, orthostatic hypotension, vagal stimulation) Postural change (with or without orthostatic hypotension) Post-prandial hypotension Presyncope, a feeling of faintness or lightheadedness, usually results from a cardiovascular problem causing brain hypoperfusion through postural hypotension. There is no specific definition of postural hypotension in older adults, but it is commonly defined as a drop in systolic arterial blood pressure of at least 20 mmHg and/or a drop in diastolic blood pressure of 10 mmHg after standing up from a supine position. However, older adults commonly describe dizziness on standing from a supine position without any orthostatic changes in blood pressure. Another common condition, postprandial hypotension, is defined as a decrease in systolic blood pressure of ≥20 mmHg in a sitting or standing posture within 1–2 hours of eating a meal.

DISEQUILIBRIUM Sensation of being unsteady when standing or, in particular, walking Many factors can contribute to imbalance: Proprioceptive disorders Visual problems Musculoskeletal disorders Gait disorders Disequilibrium, a feeling of imbalance or unsteadiness on standing or walking, usually results from visual or proprioceptive system abnormalities, with or without vestibular system involvement. Common contributing conditions include vision problems (eg, refractory errors, cataract, macular degeneration), musculoskeletal disorders (eg, arthritis, muscle weakness, deconditioning after prolonged illness), proprioceptive disorders (eg, neuropathies), and gait disorders (eg, cerebrovascular stroke, Parkinson’s disease, cerebellar disorders).

OTHER FORMS OF DIZZINESS: LIGHTHEADEDNESS
Best reserved as a description for patients who do not experience vertigo, presyncope, or disequilibrium Any cause of dizziness may occasionally produce “lightheadedness” The 2 most prominent considerations: Psychiatric causes (depression, anxiety, somatoform disorders) Idiopathic causes

MEDICATIONS AND DIZZINESS
In older adults, prescription drug toxicity is an important contributor to dizziness Use of 3 medications = dizziness risk factor Certain drugs are more frequently implicated: Those that cause orthostasis or CNS effects Cardiovascular or antihypertensive drugs Psychotropic medications Aminoglycosides NSAIDs

CHARACTERISTICS OF DIZZINESS IN OLDER PERSONS
Usually resolves within days to several months Chronic or recurrent symptoms Multifactorial etiology common Commonly associated with postural hypotension, anxiety and depression, use of 5 or more medications, impaired gait and balance View as geriatric syndrome requiring multifactorial assessment and intervention strategy

EVALUATION OF DIZZINESS: HISTORY
Elicit the patient’s own description of the event without prompting Learn: Whether the dizziness is characterized by any of 3 sensations: spinning, fainting, or falling Whether there is a positional effect on symptoms What other symptoms are associated with dizziness (specifically ask about focal neurological symptoms) What medications the patient is taking The clinical history begins with helping patients to describe their symptoms as precisely as possible, which is potentially daunting for those with multiple sensations. Patients should be encouraged to use their own words and to try distilling the symptoms into specific sensations such as spinning, imbalance or unsteadiness, or fainting. It is also important to document the frequency and duration of dizziness, and whether changing head position exacerbates the dizziness. It is useful to establish whether symptoms peak at any specific time of day, such as after meals or first thing in the morning. Patients should be asked about associated symptoms such as hearing loss, ear fullness, diplopia, dysarthria, and tinnitus. It is also important to elicit the impact on the patient’s quality of life. Patients with Ménière disease complain of recurrent dizziness associated with ear fullness and/or tinnitus along with fluctuating hearing loss. Patients with acoustic neuroma complain of hearing loss and tinnitus but not of ear fullness. Patients with Ménière disease, CNS diseases, and BPPV complain of recurrent dizziness, while patients with psychogenic and central dizziness usually complain of continual dizziness. Inquiring about precipitating factors such as after eating meals (postprandial hypotension), looking down or rolling over in bed (vestibular conditions), or standing from supine position (orthostatic hypotension) can suggest interventions, as well as corroborate timing of symptoms. Any evaluation must include a critical review of medications, including over-the-counter medications.

EVALUATION OF DIZZINESS: PHYSICAL EXAMINATION
Take blood pressure and pulse while patient is supine and after standing for 1 to 2 min Perform a provocative test of vestibular system: Head-thrust test Fukuda stepping test Dix-Hallpike maneuver Perform cardiac examination Observe for balance and gait difficulties The physical examination should begin with measurements of orthostatic changes in blood pressure. Nystagmus should be evaluated; horizontal or rotatory nystagmus usually indicates a peripheral vestibular lesion, while vertical nystagmus is seen in central lesions. Hearing and vision tests should be done, and the cranial nerves examined if vertebrobasilar ischemia or infarction is suspected. The Timed Up and Go test can be performed to look for gait and balance problems. Provocative tests of the vestibular system can be done at the bedside: Head-thrust test: Ask the patient to fixate on the examiner’s nose. The examiner then rotates the head rapidly about 10 degrees to the left or right. In patients with a vestibular deficit, the eyes move away from the target along with the head, followed by a corrective saccade back to the target, while normal eyes remain fixed on the target without a saccade. Fukuda stepping test: Draw a circle on the floor, and ask the patient to stand in the center. Blindfold the patient and ask him or her to take a few steps forward as if walking on a straight line with outstretched arms. The examiner notes the patient’s body sway as the patient takes the steps. In a unilateral vestibular lesion or acoustic neuroma, the patient’s body will sway by >30 degrees toward the affected side. Dix-Hallpike maneuver: This is a useful test for the diagnosis of BPPV. Ask the patient to sit on the examination table with the head rotated 30–45 degrees to one side. Instruct the patient to fix his or her vision on the examiner’s forehead. The examiner holds the patient’s head firmly in the same position, and moves the patient from a seated to a supine position with the head hanging below the edge of the table and the chin pointing slightly upward. The examiner notes the direction, latency, and duration of the nystagmus, if present. The diagnostic criteria for BPPV include 1) paroxysmal vertigo along with a rotatory nystagmus, 2) latency for 1–2 seconds between the completion of the maneuver and the onset of vertigo and nystagmus, and 3) fatigability (decrease in the intensity of the vertigo and nystagmus with repeated testing).

EVALUATION OF DIZZINESS: DIAGNOSTIC TESTING (1 of 2)
Laboratory In patients with chronic dizziness, check hematocrit, glucose, electrolytes, renal function, vitamin B12, folic acid and thyrotropia Audiometry May help if cochlear symptoms are present (tinnitus, asymmetric hearing loss) Abnormal results may indicate Ménière disease or, rarely, a tumor A small battery of laboratory tests, including hematocrit, glucose, electrolytes, BUN, vitamin B12, folic acid, and thyrotropin, should be performed on all patients with chronic dizziness. An ECG should be done if a cardiac cause is suspected, and a Holter and event monitor only if suspicion of arrhythmia is strong. Tilt-table testing should be done only for select patients with postural hypotension or syncope. Audiometry assists in the evaluation of patients with tinnitus or hearing loss, and helps differentiate between acoustic neuroma and Ménière disease. Suspected vestibular disorders can be evaluated with vestibular function tests such as electronystagmography, rotational testing, and dynamic posturography. These tests are not needed in every patient. Likewise, neuroimaging is not needed in all patients with dizziness. MRI provides better resolution than CT for posterior fossa lesions. However, in a community- based study of adults ≥65 years old, the similar prevalence of MRI abnormalities in the dizzy and nondizzy group led to the conclusion that routine MRI will not identify a specific cause of dizziness in most patients.

EVALUATION OF DIZZINESS: DIAGNOSTIC TESTING (2 of 2)
Vestibular testing Electronystagmography Rotatory chair Dynamic posturography Neuroimaging (CT, MRI) occasionally warranted ECG: if cardiac cause suspected Tilt-table testing only in select patients with postural hypotension or syncope

MANAGEMENT OF DIZZINESS: VERTIGO
Common Causes or Coexisting Conditions Treatment Benign paroxysmal positional vertigo Epley’s maneuver is treatment of choice Ménière disease Salt restriction, diuretics; vestibular suppressants may be helpful during acute attacks; in severe cases, may need surgery, including endolymphatic decompression, vestibular nerve resection, and labyrinthectomy Ototoxic medications, eg, aminoglycosides, diuretics, NSAIDs Discontinue, substitute, or reduce the dosage of offending medication Topic Slide 19

MANAGEMENT OF DIZZINESS: PRESYNCOPE
Common Causes or Coexisting Conditions Treatment Cerebral ischemia secondary to orthostatic hypotension, cardiac causes, dehydration, medications, vasovagal attack, autonomic dysfunction secondary to diabetes, parkinsonism Treatment of specific cause (eg, proper hydration); slow rising from sitting or lying down position; graduated support stockings; PT and/or OT; medications (eg, fludrocortisone, midodrine) as needed Postprandial hypotension Frequent small meals; avoid exertion after meals; slow rising from sitting position; avoid antihypertensive drugs at or near meal time Topic Slide 20

MANAGEMENT OF DIZZINESS: DISEQUILIBRIUM
Common Causes or Coexisting Conditions Treatment Vertebrobasilar ischemia and/or cerebellar infarcts/hemorrhages Low-dose aspirin, clopidogrel, or extended-release dipyridamole; rehabilitation Cerebellopontine angle tumor, eg, acoustic neuroma Surgery Parkinson’s disease Drug therapy, rehab PN secondary to diabetes; vitamin B12 deficiency; idiopathic, etc Treatment of the underlying disease Cervical spine degenerative arthritis, spondylosis Cervical or vestibular rehabilitation; cervical collar; surgery if needed PN = peripheral neuropathy Topic Slide 21

MANAGEMENT OF DIZZINESS: MIXED
Common Causes or Coexisting Conditions Treatment Medications: antianxiety drugs, antidepressants, anticonvulsants, antipsychotics, antihypertensives, anticholinergics Discontinue, substitute, or reduce the dosage of offending medication Combination of any of the above causes Multifactorial intervention Topic Slide 22

EPLEY’S MANEUVER Self-treatment of BPPV using Epley’s maneuver
Perform the maneuver 3 times a day until free of BPPV for 24 hours. Use the positions shown here when the right ear is affected. Reverse all positions (left instead of right) when the left ear is affected. The affected ear is the ear that when turned downward during the Dix-Hallpike test triggers vertigo or nystagmus, or both. Each maneuver consists of the following steps (numbered to match the illustrations): 1. Sit on the bed with a pillow far enough behind you to be under your shoulders when you lie back. Turn your head 45 degrees to the left. 2. Holding your head in the turned position, lie back quickly so that your shoulders are supported on the pillow and your head is reclined on the bed. Hold this position for 30 seconds. 3. Remain prone on the bed and turn your head 90 degrees to the right. Hold this position for 30 seconds. 4. Turn your head and body another 90 degrees to the right; you should now be looking down at the bed. Hold this position for 30 seconds. 5. Sit up, facing to the right.

SYNCOPE: INTRODUCTION Sudden, transient loss of postural tone and consciousness (not due to trauma) with spontaneous full recovery Accounts for: ~3% of emergency department visits 2% to 6% of hospital admissions 80% of those hospitalized for syncope are aged 65+ Causes Generally by reduced cerebral perfusion In older adults, may be multifactorial Possible causes are numerous

NORMAL REFLEXES THAT PREVENT SYNCOPE
1/3 of blood volume pools in legs while standing Reflex pathways facilitate venous return and increase cardiac output Baroreceptor reflex: ↑ autonomic sympathetic tone  peripheral vasoconstriction and ↑ heart rate Renal nerve: ↑ renin release from juxtaglomerular apparatus  angiotensin II (causes vasoconstriction) and aldosterone (causes sodium retention) Atrial natriuretic factor: reduced upon standing, further facilitating vasoconstriction

PATHOPHYSIOLOGY OF SYNCOPE: EFFECTS OF AGING
Reflex mechanisms are less responsive ↓ ability to increase heart rate in response to sympathetic stimulation ↑ sensitivity to effects of dehydration and vasodilator drugs Comorbidities that affect postural responses are common (eg, diabetes mellitus) Drugs may further impair postural reflexes (eg, vasodilators, antidepressants-blockers, -blockers, tricyclic antidepressants)

SYNCOPE: NATURAL HISTORY
Altered systemic blood pressure or Increased cerebral vascular resistance Reduced cerebral perfusion Syncope Causes may be benign or life-threatening Causes may be multiple

COMMON CAUSES OF SYNCOPE IN OLDER ADULTS
Arrhythmia Aortic stenosis Carotid sinus hypersensitivity Dehydration Hypoglycemia Medications (β-blockers, diuretics, vasodilator tricyclics) Myocardial infarction Orthostatic hypotension Postprandial hypotension Postmicturition Psychogenic causes Pulmonary embolism (large) Vasovagal faint

Intermediate, generally favorable
SYNCOPE: PROGNOSIS Type of syncope 1-year mortality Cardiac 18%–33% Noncardiac 6% Unknown cause (1/3 to 1/2 of patients) Intermediate, generally favorable

SYNCOPE EVALUATION: HISTORY (1 of 2)
Precipitants? Eating Urinating Coughing Medication Emotional stress Physical exertion Turning head Prodromal symptoms? Chest pain Palpitations Dyspnea Diaphoresis Presyncope Nausea Vomiting

SYNCOPE EVALUATION: HISTORY (2 of 2)
Medications? How, when taken, what doses Relationship to meals and activities Recent changes Any witnesses? Duration of event Appearance of patient during event (flaccid tone and motionless or increased tone and motion?) Comorbid conditions? Eg, coronary artery disease, diabetes mellitus

SYNCOPE CAUSED BY ARRHYTHMIA
Prior to event Occurs in any position, <5 sec warning No precipitant; palpitations rare During event Flaccid tone; pulse faint or absent Blue, ashen skin Incontinence (rare) Recovery Rapid and complete

VASOVAGAL SYNCOPE Prior to event During event Recovery
Aborted if person lies flat Seconds to minutes of warning Precipitant present; nausea/diaphoresis common Visual changes During event Motionless; relaxed tone; slow, faint pulse Pale color; dilated, reactive pupils Recovery Fatigue, nausea and diaphoresis common No retrograde amnesia

SYNCOPE CAUSED BY SEIZURE
Prior to event Occurs in any position No warning or prodrome During event Rigid tone; rapid pulse; elevated BP Tonic eye deviation common Frothing at mouth Recovery Slow, incomplete Disorientation; focal neurologic findings

SYNCOPE EVALUATION: PHYSICAL EXAMINATION (1 of 2)
Pulse in supine and standing positions Orthostatic vital signs: Measure BP in both arms, 1 min after standing and again after standing for 3 min Carotid pulse examination Delayed upstroke and low volume may identify aortic stenosis Perform carotid massage only with continuous ECG and resuscitation equipment available Contraindicated with carotid bruit, CVD, recent MI

SYNCOPE EVALUATION: PHYSICAL EXAMINATION (2 of 2)
Cardiac examination for murmurs, extra heart sounds Stool for occult blood Neurologic examination for focal deficits

SYNCOPE EVALUATION: TESTING (1 of 2)
ECG for all syncopal older adults; assess for: Acute or remote MI Conduction abnormalities and pre-excitation Sinus bradycardia Prolonged QT interval Ambulatory ECG Among patients able and willing to operate loop recorders, diagnostic yield is ~25% Implantable loop recorders May increase ability to establish diagnosis in syncope patients who do not have structural heart disease Unfortunately, the occurrence of symptoms during ambulatory ECG monitoring is relatively rare in most patients with syncope that remains unexplained after a history, physical examination, and ECG. On average, studies examining the diagnostic yield of ambulatory ECG report an arrhythmia correlating with symptoms in approximately 4% of patients. In another 15% of patients studied, an arrhythmia was excluded by the presence of symptoms during the recording, but without evidence of an arrhythmia; in approximately 14% of patients, arrhythmias were found to be present but without concomitant symptoms. These patients may represent a diagnostic dilemma. However, certain arrhythmias, even asymptomatic ones, such as nonsustained ventricular tachycardia, second- and third-degree AV block, and sinus pauses in excess of 3 seconds, are rare in persons without heart disease. Their presence, even if asymptomatic, in a patient with a history of syncope indicates the need for further evaluation. Subcutaneous implantable loop recorders have been developed; these devices are placed in the prepectoral region under local anesthesia. The devices have long-term memories and a battery life of approximately 14–18 mo. Generally, no patient intervention is required for the device to store recordings, but the patient can also trigger the device to record and retain an ECG if symptoms occur. In a randomized study of patients with recurrent syncope who did not have evidence of structural heart disease, implantable loop recorders significantly increased the ability to establish a diagnosis.

SYNCOPE EVALUATION: TESTING (2 of 2)
Echocardiography Tilt-table testing Electrophysiologic (EP) studies Neurologic testing (MRI and CT, plus EEG) if focal neurologic signs or symptoms are present, or if the history suggests seizure Two-dimensional echocardiography has a low yield in the absence of features suggestive of heart disease by history, physical examination, or ECG. It is most useful in confirming a specific diagnosis suspected after other assessment. However, unsuspected findings on echocardiography are reported in approximately 5% to 10% of unselected patients. Occult coronary artery disease is also prevalent among elderly persons. In some patients, particularly those with the suggestion of structural cardiac abnormalities and ischemia, it is efficient to perform stress echocardiography as a single procedure. Tilt-table testing is useful for patients suspected of having vasovagal syncope and those with unexplained syncope who are not suspected of having a cardiac cause. The test is considered positive if the patient has a cardioinhibitory or vasodepressor response, or both. A positive tilt-table result occurs in approximately 11% of normal elderly persons and does not ensure that a vasovagal event is the cause of syncope. It is generally recommended that men over the age of 45 and women over the age of 55 have stress testing prior to tilt- table testing so that a positive tilt-table test result does not delay diagnosis of coronary ischemia when that is the true culprit. Guidelines suggest that invasive EP testing should be used to evaluate patients with structural heart disease who have unexplained syncope. There is also agreement that EP testing should not be employed if the results would not influence treatment or if a cause of syncope has been established. The role of EP testing in patients with recurrent syncope with no structural heart disease and negative tilt-table studies remains undefined. EP testing is most sensitive for detecting ventricular arrhythmias in the setting of ischemic heart disease and is less sensitive for the detection of ventricular arrhythmias in dilated nonischemic cardiomyopathies. Its sensitivity for detecting most bradyarrhythmias is also low.

TREATMENT OF SYNCOPE (1 of 3)
Focus on treating the underlying disorder In older patients, treatment of multiple possible causes is often necessary Discontinuation of medications that increase the risk of syncope is always an early step

Cause Treatment Myocardial ischemia Revascularization or aggressive medical therapy Valvular heart disease (esp. aortic stenosis) Usually surgery, avoid preload reduction Symptomatic SVT Medical therapy or electrophysiology ablation Significant ventricular tachyarrhythmia Implanted defibrillator or medical therapy Bradyarrhythmia Usually pacemaker SVT = supraventricular tachycardia

Cause Treatment Orthostatic hypotension Adjust medications, ensure adequate volume, other conservative measures Vasovagal syncope Avoidance of triggers; medical therapy is somewhat controversial (-blockers, clonidine, paroxetine, midodrine) Carotid sinus hypersensitivity Avoid stimulating factors (tight collars or rapid neck movements); pacemaker Postprandial hypotension Avoid alcohol and high-carbohydrate meals; remain recumbent after meals Conservative measures that may help reverse orthostatic hypotension include the use of waist-high compression stockings, squatting, and sleeping in a head-up position. Avoidance of excessively warm environment and activities associated with straining (Valsalva) may also be beneficial. If autonomic dysfunction is present and hypertension, heart failure, and hypokalemia are not concerns, then low-dose fludrocortisone may be effective.

RECURRENT SYNCOPE WITHOUT IDENTIFIABLE CAUSE
Help patients avoid harm to themselves or others Consider recommending against driving for several months and resuming if patient remains recurrence-free (American Heart Association guidelines) Many states have reporting or restricting laws regarding driving with a history of syncope

SUMMARY (1 of 2) Precise classification of dizziness into vertigo, presyncope, disequilibrium, and lightheadedness is often difficult, and multiple causes of the same symptoms are common Most dizziness resolves within days to several months Key physical exam steps include checking for orthostatic hypotension, performing the head-hanging (Dix-Hallpike) test, and observing gait

SUMMARY (2 of 2) In older adults the cause of syncope is often multifactorial Most diagnostic procedures for syncope are expensive and have a low yield unless findings from the H & P suggest a particular cause The absence of cardiac disease strongly suggests that the cause of syncope is not cardiac Treatment of dizziness and syncope focuses on treating the underlying disorder

CASE 1 (1 of 4) A 68-year-old woman is brought to the ED because she woke up from an afternoon nap with a sudden onset of rotational vertigo and clumsiness of the right arm. She feels as though the world is tilting toward the right. She is unable to walk even with assistance, and she has a headache. History includes hypertension and type II insulin- dependent diabetes. Her medications include lisinopril, metformin, and aspirin.

CASE 1 (2 of 4) On examination, the patient’s temperature is 37.5°C (99.5°F). Blood pressure is 180/95 mmHg, pulse is 80 beats per minute, and respiratory rate is 16 breaths per minute. She has horizontal nystagmus and a negative head thrust test. She has difficulty both with making rapid alternating movements with the right arm and with toe-tapping or heel-to-shin movements on the right leg. Slide 46 46

CASE 1 (3 of 4) Which of the following is the most likely diagnosis?
(A) Cerebellar infarct (B) Dorsolateral medullary stroke (C) Ménière disease (D) Herpes zoster infection of the inner ear (Ramsay Hunt syndrome) (E) Benign paroxysmal positional vertigo Slide 47 47

CASE 1 (4 of 4) Which of the following is the most likely diagnosis?
(A) Cerebellar infarct (B) Dorsolateral medullary stroke (C) Ménière disease (D) Herpes zoster infection of the inner ear (Ramsay Hunt syndrome) (E) Benign paroxysmal positional vertigo ANSWER: A The sudden onset of vertigo with other focal neurologic symptoms makes a stroke most likely. A diagnosis of cerebellar or posterior fossa infarction should be considered in any patient with acute onset of vertigo. The patient should undergo immediate imaging, especially given her history of headache. In the event of posterior fossa hemorrhage, surgical evaluation may be lifesaving. The nystagmus in a cerebellar infarct may look similar to a peripheral nystagmus (horizontal torsional). A head thrust test (or head impulse test) can help distinguish vestibular neuritis from stroke. With rapid, passive head rotation as the patient fixes on a central target, the normal response (ie, a negative test) is an equal and opposite eye movement that keeps the eyes stationary in space. The inability to maintain fixation after head rotation that requires a corrective gaze shift is abnormal (ie, a positive test). Vertigo with a negative head thrust test suggests central stroke. A positive head thrust test suggests a peripheral cause but does not absolutely exclude a stroke. Patients can also present with an ocular tilt reaction that can be on the same side or on the opposite side of the cerebellar infarct. Dorsolateral medullary stroke (Wallenberg’s syndrome) is usually accompanied by other focal neurologic signs and symptoms, including ipsilateral Horner’s pupil, ipsilateral facial pain and loss of temperature sensation, ipsilateral central facial (lower face only) weakness, and contralateral pain and loss of temperature sensation in the arms and legs. It is often associated with artery-to- artery emboli from vertebral artery atherosclerosis to the posterior inferior cerebellar artery. Ménière disease, Ramsay Hunt syndrome, and benign paroxysmal positional vertigo do not present with clumsiness of the extremities.

CASE 2 (1 of 4) A 70-year-old man comes to the office because he has difficulty walking, especially in the dark, and he is unable to read street signs during car rides because the environment appears to be “jumping up and down.” History includes diabetes mellitus, peripheral neuropathy, and renal insufficiency. The patient was recently discharged after hospitalization for cellulitis in his legs, for which he received intravenous gentamicin and nafcillin.

CASE 2 (2 of 4) While he was hospitalized, the patient reported a continuous sense of imbalance, but he did not have vertigo. He did not notice any tinnitus, aural fullness, or hearing loss. Examination is normal except that gait is somewhat wide-based and unsteady, and a Romberg test is positive. Slide 50 50

CASE 2 (3 of 4) Which of the following is the most likely cause of the patient’s imbalance? (A) Aminoglycoside ototoxicity (B) Vestibular neuritis (C) Benign paroxysmal positional vertigo (D) Ménière disease (E) Perilymph fistula Slide 51 51

CASE 2 (4 of 4) Which of the following is the most likely cause of the patient’s imbalance? (A) Aminoglycoside ototoxicity (B) Vestibular neuritis (C) Benign paroxysmal positional vertigo (D) Ménière disease (E) Perilymph fistula ANSWER: A Gentamicin often causes isolated vestibular toxicity. In a study of 35 patients with aminoglycoside ototoxicity, 33 reported oscillopsia (having a sense of the environment “jumping” when in a moving car or when walking); only 3 noted a change in hearing. There are no pre- or post-treatment pharmacologic interventions to attenuate aminoglycoside ototoxicity. Kidney function should be measured before beginning any potentially ototoxic medication. Major risk factors include impaired renal function, high drug serum concentrations, prior use of ototoxic medications, treatment course >14 days, preexisting sensorineural hearing loss, and age >65 years. Patients should be referred for vestibular rehabilitation, which includes learning compensatory strategies for loss of vestibular input. Patients with peripheral neuropathy generally have more difficulty compensating for bilateral vestibular loss. Vestibular neuritis typically presents with subacute onset of spontaneous vertigo. In benign paroxysmal positional vertigo, episodes are brief and associated with positional change only. Ménière disease presents with aural fullness, hearing loss, tinnitus, and vertigo. Perilymph fistula typically presents with hearing loss and episodic vertigo.

CASE 3 (2 of 2) Which of the following is an age-related physiologic change that predisposes older adults to syncope? (A) Inability to excrete a dilute urine (B) Increased baroreflex control of arterial vasoconstriction (C) Reduced baroreflex control of heart rate (D) Increased relaxation of the left ventricle Slide 53 53

CASE 3 (2 of 2) Which of the following is an age-related physiologic change that predisposes older adults to syncope? (A) Inability to excrete a dilute urine (B) Increased baroreflex control of arterial vasoconstriction (C) Reduced baroreflex control of heart rate (D) Increased relaxation of the left ventricle ANSWER: C Syncope is a sudden, transient loss of consciousness and postural tone with relatively rapid and spontaneous recovery. Transient cerebral hypoperfusion is the underlying pathophysiologic event. Older adults are particularly vulnerable because of age-related physiologic changes in heart rate and blood pressure regulation, structure and function of the left ventricle, and ability to preserve sodium and water. Changes in physiologic function are also related to comorbidity, medical conditions such as hypertension and atherosclerosis, reduced thirst, autonomic dysfunction, and use of medications that affect blood pressure regulation. Normal aging is characterized by 1) reduced baroreflex control of the heart rate and peripheral vascular resistance in response to an orthostatic stress; 2) reduced left- ventricular compliance, which can exacerbate preload-induced changes in blood pressure; and 3) changes in renal function that impair salt and water handling and predispose to dehydration.

CASE 4 (1 of 4) A 75-year-old woman comes to the office because she has had repeated episodes of profound dizziness and syncope, along with at least 2 episodes in which she found herself on the floor but was unaware of how she fell. Each episode has been preceded by a prodrome during which she feels warm and is diaphoretic and progressively lightheaded. The episodes are most likely to occur when she has been standing for a long time, such as during church services.

CASE 4 (2 of 4) The patient’s history includes hypertension, for which she takes hydrochlorothiazide daily. Blood pressure is 142/84 mmHg while supine and 110/70 mmHg while upright. Heart rate is 76 beats per minute while supine and 80 beats per minute while upright. There is no jugular venous distension or carotid bruit. Lungs are clear. Carotid upstroke is slightly delayed, with a II/VI systolic murmur at the base; the second heart sound is intact, and there is no gallop.

CASE 4 (3 of 4) Which of the following is the most appropriate next step? (A) Stop hydrochlorothiazide. (B) Begin oral midodrine 5 mg three times daily (about 4 h apart, not too close to bedtime). (C) Begin fludrocortisone 0.1 mg q12h. (D) Obtain tilt-table test.

CASE 4 (4 of 4) Which of the following is the most appropriate next step? (A) Stop hydrochlorothiazide. (B) Begin oral midodrine 5 mg three times daily (about 4 h apart, not too close to bedtime). (C) Begin fludrocortisone 0.1 mg q12h. (D) Obtain tilt-table test. ANSWER: A Physical examination of this patient reveals orthostatic hypotension, an important cause of syncope in older adults. When a standing position is assumed, gravity induces pooling of blood in the lower extremities. Blood pressure is normally maintained by vasoconstriction and increased heart rate when circulatory volume is decreased. The incidence and prevalence of orthostatic hypotension in older adults are affected by numerous age-related changes in cardiovascular structure and function, such as impaired baroreflex function, diastolic dysfunction, higher prevalence of disorders that directly or indirectly impair autonomic function, common use of vasoactive medications, and impaired salt and water balance. The most commonly accepted definition of orthostatic hypotension is a decrease of >20 mmHg in systolic blood pressure or >10 mmHg in diastolic blood pressure on standing. In most patients with orthostatic hypotension, the drop in blood pressure is detected within 2 min of assuming an upright posture. Some patients, however, have delayed orthostatic intolerance, and blood pressure falls progressively over 15–45 min. This dysautonomic response to upright posture can be detected during a tilt-table test. In this particular patient, the diagnosis of orthostatic hypotension is apparent on physical examination, which eliminates the need for the tilt-table test. Initial treatments for orthostatic hypotension include withdrawal of potentially exacerbating medications; accordingly, stopping hydrochlorothiazide is the best option in this patient. If necessary, physiologic interventions should be introduced next (eg, compressive devices such as stockings or abdominal bands, counterpressure maneuvers like squatting or leg crossing). Pharmacologic therapy (eg, fludrocortisone and midodrine) should be used only if other measures fail. Patients should be 1) reassured that the problem can be controlled; 2) taught to avoid predisposing factors and triggering events, such as volume depletion and prolonged upright posture; and 3) taught maneuvers to abort an episode of orthostasis. In older adults, supine hypertension can coexist with and be exacerbated by treatment of orthostatic hypotension. Some degree of supine hypertension may have to be tolerated to minimize the short-term risk of orthostasis and associated falls.

ACKNOWLEDGMENTS Copyright © 2010 American Geriatrics Society
Editor: Annette Medina-Walpole, MD GRS6/GRS7 Chapter Authors: David Bush, MD Kurt Kroenke, MD Aman Nanda, MD GRS7 Question Writers: Gail Ishiyama, MD Mathew Maurer, MD Pharmacotherapy Editor: Judith L. Beizer, PharmD Medical Writers: Beverly A. Caley Faith Reidenbach Managing Editor: Andrea N. Sherman, MS Copyright © 2010 American Geriatrics Society

DIZZINESS AND SYNCOPE Suggestions for Lecturer -1-hour lecture

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DIZZINESS AND SYNCOPE Suggestions for Lecturer -1-hour lecture

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