Diseases » Balance disorders » Diagnosis

Diagnosis of Balance disorders

Diagnostic Test list for Balance disorders:

The list of medical tests mentioned in various sources as used in the diagnosis of Balance disorders includes:

• Physical examination
• Electronystagmogram (ENG)
• Head/brain scan
• Caloric test
• Posturography

Balance disorders Diagnosis: Book Excerpts

• Ask the Following Questions - SYNCOPE
• Differential Diagnosis - Syncope
• Differential Diagnosis - Dizziness/Lightheadedness & Vertigo
• Differential Diagnosis - Syncope
• Differential Diagnosis - Vertigo
• Approach to the Diagnosis - SYNCOPE
• History and physical examination - Syncope
• History and physical examination - Vertigo
• History and physical examination - Syncope
• History and physical examination - Vertigo
• History - Syncope
• History - Vertigo
• Differential Overview - Syncope
• History - Syncope
• History - Syncope
• History - Vertigo
• Clinical Features and Diagnosis - Vertigo
• Clinical Features and Diagnosis - Syncope and Dizziness
• History and physical examination - Syncope
• History and physical examination - Vertigo
• Approach to the Diagnosis - SYNCOPE

Diagnostic Tests for Balance disorders: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Balance disorders.

SYNCOPE: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Are there convulsive movements or incontinence? The presence of convulsive movements should suggest convulsions, and the differential diagnosis of this is discussed on page 88 . Convulsive movements can occur with other forms of syncope, however.
2. Is the pulse slow or absent? The presence of a slow or absent pulse would suggest heart block, vasovagal syncope, and carotid sinus syncope.
3. Is the pulse rate normal? The presence of a normal pulse rate would suggest anemia, aortic stenosis, aortic insufficiency, and cyanotic congenital heart disease.
4. Is the pulse rate rapid? The presence of a rapid pulse would suggest the various types of ventricular and supraventricular tachycardias, including auricular fibrillation and flutter, and it should also suggest heat exhaustion or heat stroke.
5. If the pulse is rapid, is it regular? The presence of a rapid regular pulse should suggest supraventricular or ventricular tachycardia, heat exhaustion, or heat stroke.
6. Is there a heart murmur? The presence of a heart murmur should suggest aortic stenosis, aortic insufficiency, and cyanotic congenital heart disease.
7. Is there pallor? The presence of pallor should suggest shock or severe anemia and acute bleeding.
8. Are there focal neurologic signs? The presence of focal neurologic signs should suggest cerebral vascular insufficiency, hypoglycemia, and transient ischemic attacks.

DIAGNOSTIC WORKUP

The diagnostic workup includes a CBC, sedimentation rate, urinalysis, chemistry panel, VDRL test, thyroid profile, glucose tolerance test, EKG, and chest x-ray. Several blood pressure recordings in the recumbent and upright positions should be made. If hypoglycemia is suspected, a 72-hr fast and a tolbutamide tolerance test should be done. The drug history should always be reviewed. A toxicology screen may be helpful.

Most cases will require 24-hr Holter monitoring or event Holter monitoring. In addition, other cardiovascular studies, such as echocardiography and His' bundle studies, may need to be done. Exercise tolerance testing is useful when the syncope seems to be exercise induced. An upright-tilt test is helpful when vasodepressor syncope is suspected, especially when combined with isoproterenol infusion. Signal-averaged EKG can be useful if a ventricular arrhythmia is suspected. If transient ischemic attacks are suspected, a carotid scan and cerebral angiography may be necessary. If the syncopal attacks are thought to be due to epilepsy, a wake-and-sleep EEG may need to be done. A CT scan or MRI of the brain may need to be done.

A cardiologist or neurologist should be consulted before ordering expensive diagnostic tests. A psychiatrist may also need to be consulted.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Syncope: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Vasovagal episode
  –Most common cause of syncope
  –May be triggered by heat, fatigue, stress, hunger, alcohol, and severe pain
  –Associated with diaphoresis, weakness, blurry vision, lightheadedness
  –Almost always benign
• Orthostatic hypotension
  –Fall in blood pressure upon standing, due to failure of vasoconstrictor reflexes
  –Precipitated by sudden standing from recumbent position
  –Often associated with antihypertensive medications (diuretics, vasodilators, α - or β-blockers) and dehydration/hypovolemia
  –May occur with autonomic disorders (e.g., Shy-Drager syndrome)
  • Situational syncope
    –Increased intrathoracic pressure (e.g., cough, micturition, defecation) leads to decreased venous return and resulting diminished blood flow to the brain
  • Cardiac arrhythmias
    –Very slow (<30 bpm) or fast (>180 bpm) heart rates may result in decreased cardiac output and resulting diminished blood flow to the brain
• Valvular disease
  –Most commonly due to aortic stenosis
• Myocardial disease
• Cerebrovascular disease
  –Usually due to carotid or vertebrobasilar atherosclerosis
• Hypoglycemia
• Anemia
• Seizure
• Anxiety attack
• Migraine
• Medications (e.g., anticholinergics)
• CVA
• Hemorrhage
• Trauma

Workup and Diagnosis

• History and physical exam will often suggest the underlying etiology
  –Note pre- and postsyncopal symptoms (e.g., chest pain, dizziness, lightheadedness, nausea/vomiting, headache, diaphoresis, blurry vision, blindness)
  –Full HEENT, neurologic, and cardiovascular exam
  –Examine for trauma following syncope
  –Record BP in supine, sitting, standing, and in both arms
  –Strategically attempt to reproduce syncope by Valsalva maneuver (e.g., coughing, deep breathing for 2–3 min)
• Initial labs should include CBC, electrolytes, calcium, magnesium, glucose, toxicology screens, and ECG
• Further cardiovascular testing may include cardiac enzymes if ischemia is suspected, 24-hour Holter monitor, echocardiogram, stress testing, and/or invasive cardiac monitoring
• Head CT to rule out cerebral disease
• Doppler ultrasound of carotids if bruit is heard
• EEG may be useful if seizure disorder is suspected
• Tilt table test may induce vasovagal episode
• Plasma aldosterone/mineralocorticoid levels to evaluate for hypovolemia due to adrenocortical insufficiency

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Source: In a Page: Signs and Symptoms, 2004

Dizziness/Lightheadedness & Vertigo: Differential Diagnosis
(In a Page: Signs and Symptoms)

Dizziness/lightheadedness

• Transiently decreased cerebral blood flow
  –Hyperventilation
  –Vasovagal response
  –Congestive heart failure
  –Aortic stenosis
  –Hypertrophic cardiomyopathy
  –Hemorrhage
  –Dehydration or hypotension
  –Carotid sinus pressure
  –Cerebral artery thrombosis or embolism
  –Cardiac arrhythmia
  –Autonomic dysfunction (e.g., Shy-Drager syndrome)
  –TIA
  –Hypoxemia
  –Anemia

• Primary CNS dysfunction not associated with decreased blood flow
  –Migraine
  –Seizure
  –Severe electrolyte disturbance
  –Elevated intracranial pressure
• Panic attack
• Hyperventilation and/or anxiety
• Ictal aura
• Basilar migraine
• Drug intoxication (e.g., alcohol, sedatives, centrally-acting α-blockers)
• Allergic reactions
• Postconcussion syndrome
• Carbon monoxide poisoning
  Vertigo
• Peripheral vertigo (inner ear pathology)
  –Benign positional vertigo (>20% of cases)
  –Ménière's disease
  –Labyrinthine trauma
  –Labyrinthitis (viral)
  –Nonspecific or recurrent vestibulopathy
  –Bilateral vestibular loss
  –Acoustic neuroma
  –Autoimmune inner ear disease
• Central vertigo (CNS pathology)
  –Multiple sclerosis
  –Brainstem tumors
  –Labyrinthine trauma
  –Epileptic vertigo
  –Vertebrobasilar insufficiency
  –Tabes dorsalis
  –Friedreich's ataxia

Workup and Diagnosis

• A complete history and physical exam should include signs of dehydration, questions about excessive pressure on the neck, headaches, palpitations, history of heart disease, hearing loss, cardiac auscultation, orthostatic blood pressures, and complete ENT (including Weber's and Rinne's tests) and neurologic exams (gait)
• Laboratory evaluation may include CBC, electrolytes, calcium, glucose, BUN/creatinine, BNP, ESR, carbon monoxide level, pulse oximetry and/or arterial blood gas, eosinophil count, and stool occult blood testing
• Further testing may include ECG, 24-hour ECG monitoring, echocardiography, electronystagmography, hearing evaluation, head CT, EEG, MRI (head and/or labyrinth) and/or MRA (head or vertebrobasilar circulation)
• Vertigo may be evaluated with several specific maneuvers
  –Dix-Hallpike maneuver: Patient is sitting; rapidly move to supine position with head over back of table; observe for nystagmus (type and duration); repeat with head facing to the left and right (nystagmus that does not fatigue or is vertical is unlikely to be BPV)
  –Barany maneuver (Nylan-Barany maneuver) is similar to the Dix-Hallpike maneuver, but less sensitive

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Source: In a Page: Signs and Symptoms, 2004

Syncope: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Vasovagal
  –Most common etiology (more than 50%)
  –Also known as neurocardiogenic or vasodepressor syncope
  –Typical in adolescents; greater in females
  –Occurs after prolonged standing in a warm place; with emotional upset, pain, hunger, the sight of blood; crowded places

• Postural/orthostatic hypotension
  –Occurs when standing up quickly
• Micturation syncope (a rare form)
• Breath-holding spells
  –Usually at ages 1–5 years
  –Two types: Cyanotic (80%) vs pale (20%)
  –Cyanotic spells start with crying
  –Provoked by anger, frustration, or pain, or used as an attention-getting behavior
  –May have generalized clonic jerks
  • Cardiac etiologies (less common)
    –Arrhythmias
    –Supraventricular tachycardia is the most common cause
    –Long QT syndrome (QTc >0.44 seconds): Causes ventricular arrhythmias, Romano-Ward (autosomal dominant), Jervell and Lange-Nielsen (autosomal recessive with deafness)
    –Medications (e.g., cisapride)
    –Sinus node dysfunction and atrioventricular block may lead to bradyarrhythmias
    –Post-op congenital lesions and dilated cardiomyopathy lead to arrhythmias
    –Structural cardiac disease
    –Severe obstructive lesions (e.g., hypertrophic obstructive cardiomyopathy, aortic stenosis, pulmonic stenosis, atrial myxomas, and pulmonary hypertension)
  • Hysterical fainting
  • Migraine
  • Hyperventilation
  • Pregnancy
  • Anemia or hypovolemia
  • Hypoglycemia
  • Carbon monoxide poisoning
  • Medications and drugs of abuse
  • Electrolyte abnormalities
  • Intracranial hypertension
  • Epilepsy may mimic syncope
  • Adrenal insufficiency

  Workup and Diagnosis

  • History: Most important aspect to guide diagnostic workup
    –Vasovagal syncope: Prodromal symptoms (e.g., cold, clammy skin; pallor; nausea; blurry vision; yawning; dizziness; lightheadedness; palpitations; hyperventilation)
    –Duration: Vasovagal syncope is short (seconds to minutes)
    –Inciting situations
    –Lightheadedness: In orthostatic hypotension
    –Syncope at rest or recumbent in seizure or arrhythmia; syncope without prodrome or with exercise/exertion in cardiac etiology
    –Auras in migraine headaches
    –Seizures may have incontinent or post-ictal state or generalized tonic-clonic movements
    –Family history: Sudden or unexplained deaths, cardiac abnormalities, seizures, or deafness
  • Physical exam
    –Orthostatic blood pressures and pulse
    –Perform a thorough cardiac and neurologic exam
  • Extensive laboratory workup is not usually needed
    –Most clinicians would do an ECG
    –Tilt-table testing to diagnose vasovagal syncope is controversial as it is not very reproducible
    –Labs might include CBC, glucose, electrolytes, drug screen, carboxyhemoglobin, EEG, or head CT as guided by history; if cardiac abnormalities are suspected, may get a chest X-ray, Holter monitoring, or exercise testing

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Source: In A Page: Pediatric Signs and Symptoms, 2007

Vertigo: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Benign paroxysmal positional vertigo (BPPV)
  –Each episode lasts seconds to minutes
• Vestibular neuritis
  –Viral infection of the vestibular nerve
• Otitis media
• Migraine
  –Vertigo may precede, follow, or present with the headache and aura
• Acute labyrinthitis
  –Acute onset with nausea and vomiting
  –Lasts for days and slowly resolves
  –45% cluster with viral infections
• Posttraumatic
  –Perilymphatic fistula
  –Labyrinthine concussion
  –Associated with postconcussive syndrome
  –Worsened by change in head position, cough, sneeze, swallow, straining, and airplane travel
• Cerebellar tumors
  –Tumors may be associated with tinnitus, facial weakness, and nystagmus
• Toxins/drugs: Antibiotics (aminoglycosides), salicylates, alcohol, phenytoin, quinine, arsenic, tricyclic antidepressants
• Autoimmune: Collagen vascular disease, Wegener granulomatosis
• Posterior circulation dissection
  –Often associated with a history of neck extension or rotational injury
• Cerebellar hemorrhage: Acute onset of vertigo, headache, nausea, and vomiting
• Multiple sclerosis
  –Vertigo is the presenting symptom in 5%
  –Hearing loss rare
  –Most common in young women
• Temporal lobe or complex partial seizures
• Ménière disease
• Familial periodic ataxia syndromes
  –Recurrent bouts of vertigo brought on by emotional stress or physical exertion
• CNS infection: Syphilis, Lyme disease
• Motion sickness
• Vertigo mimics: Presyncope, disequilibrium from decreased vision or proprioception
• Psychogenic
  –Panic or anxiety disorder

Workup and Diagnosis

• History
  –Duration, headache, nausea, vomiting, worsening with activity or movement (postural hypotension, hyperventilation)
  –Nausea and vomiting are classically more prominent with peripheral vertigo
  –Associated neurologic deficits (extremity weakness, numbness, incoordination, dysarthria, diplopia, tinnitus, hearing loss, loss of consciousness)
  –Facial numbness/weakness
  –History of autoimmune disease, hyperlipidemia, stroke, migraine, seizure, cancer, prior ear surgery

• Physical exam may be normal in asymptomatic periods
• Cardiac and peripheral vascular examination for murmurs, arrhythmias, orthostatic changes in pulse and blood pressure (±ECG, Holter, Echo, Doppler)
• Nystagmus, truncal ataxia, and limb incoordination are sometimes found in cerebellar infarction or neoplasm
• Vertigo of a panic attack can sometimes be elicited by having the patient hyperventilate
• Dix-Hallpike maneuver: Rapidly lay the patient down from sitting allowing the head to hang over the side of the bed while turning to the left or right; positive test shows vertigo with rotatory nystagmus within 30 seconds; if the etiology is peripheral, the nystagmus shows extinction with positioning maneuvers
• MRI and MRA can help evaluate the posterior circulation

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Source: In A Page: Pediatric Signs and Symptoms, 2007

SYNCOPE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Clinical differentiation of the various forms of syncope is made by combinations of symptoms. Thus, syncope with marked sweating and tachycardia is more likely due to hypoglycemia. Syncope with sweating and bradycardia is more likely due to vasovagal syncope. Focal neurologic signs during the attack suggest transient cerebral ischemia (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia). A family history of syncope suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong possibility in the young, whereas heart block is more likely in the aged. Consequently, an EEG and Holter monitoring are useful in the workup.

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Source: Differential Diagnosis in Primary Care, 2007

Syncope: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Vertigo: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he’s moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he’s ever fallen. Ask if he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history, and note any evidence of alcohol abuse.

Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient’s gait and posture for abnormalities.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Syncope: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Vertigo: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he’s moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he’s ever fallen. Ask if he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history, and note any evidence of alcohol abuse.

Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient’s gait and posture for abnormalities.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Syncope: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. What are the symptoms or circumstances related to the syncope?

1. Dizziness preceding syncope is highly associated with a psychological cause (24%) versus syncope without preceding dizziness (5%) (3). Dizziness with syncope can also be associated with arrhythmia.

2. Important history includes palpitation, duration of prodrome and recovery, and presence of postural or exertional symptoms.

3. Related environmental factors include heat, dehydration, and alcohol.

B. Which disease, risk factor, or family history is present?

1. Organic heart disease is associated with arrhythmia and increased risk of death.

 2. Psychiatric illnesses most commonly associated with syncope are major depression (12.2%), alcoholism (9.2%), generalized anxiety disorder (8.6%), and panic disorder (4.3%). These correlate with a higher rate of recurrent syncope, younger age, and a more benign course (4) (Chapters 3.1 and 3.3).

 3. Older age (>60 years) is more highly associated with arrhythmias, orthostatic hypotension, medication side-effects, and situational (e.g., micturition) syncope.

 4. Ask about diabetes mellitus, neuropathy, anemia, and other chronic diseases.

 5. Inquire about a family history of sudden death, hypertrophic cardiomyopathy, or other organic heart disease.

C. What medicines does the patient take? The most commonly implicated are antihypertensives and antidepressants. Others include antianginals, analgesics, and sedatives.

Physical examination

What are the essential aspects to cover?

A. General: mental status, temperature, hydration status, pallor, or cyanosis.

 B. Vital signs: tachycardia, bradycardia, irregularity, or orthostatic hypotension.

 C. Cardiovascular: heart sounds, murmurs, bruits, edema, rales, and pulses.

 D. Neurologic: cranial nerves, reflexes, strength and sensation, tremor, Romberg’s sign, gait, and cerebellar signs.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Vertigo: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

The patient’s age, underlying comorbidities, and symptom classification category will help limit the diagnostic possibilities. Further specificity is gained by eliciting the following:

A. Temporal pattern. Are the symptoms episodic or continuous? If episodic, how long do they last? Peripheral origin vertigo is often intermittent and of sudden onset compared with the usual, more gradual onset of central vertigo. A continuous history suggests CNS pathology, drug or toxin effects, metabolic dysfunction, or psychiatric disease. BBPV episodes last less than a minute; vertebrobasilar transient ischemic attacks last minutes to an hour; Ménière’s disease persists 1 to 24 hours; and vestibular neuronitis or acute labyrinthitis continues several days.

 B. Precipitating or exacerbating factors. Has there been recent head trauma (implying perilympathic fistula) or viral illness (labyrinthitis)? What is the relationship to sudden head movement or turning over in bed (BPPV), coughing or sneezing (perilymphatic fistula), postural changes (orthostasis), exercise (arrhythmias), foods (salty meals exacerbating Ménière’s), walking and turning (multiple sensory deficits), micturition or pain (vasovagal reaction), and emotional upset (hyperventilation)?

C. Associated symptoms. Marked nausea, vomiting, diaphoresis, aural fullness, and recruitment (perception of sounds being too loud) are typical of peripheral vestibular disorders. Episodic vertigo associated with tinnitus and gradual (unilateral) hearing loss involving low frequencies preferentially suggests Ménière’s disease. Asymmetric weakness, cranial nerve or cerebellar dysfunction, diplopia, or dysarthria suggests brainstem or CNS disease. Headache, scotomata, or tunnel vision points to migraine. Numbness or paresthesias may indicate neuropathy contributing to multiple sensory deficits (Chapter 4.6). A single, abrupt episode of severe vertigo with negative Dix-Hallpike (DH) testing (section III.A) that gradually subsides over days implies labyrinthitis (if hearing is affected) or vestibular neuronitis (if hearing is unaffected). Mild vertigo with prominent tinnitus, unilateral hearing loss, and loss of corneal reflex is worrisome for an acoustic neuroma.

 D. Medications or toxins. Many medications can cause “dizziness,” although few (aminoglycosides, lead, mercury) cause vertigo. Assess toxin exposure by exploring job and recreational activities.

Physical examination (PE)

This will emphasize orthostatic vital signs, the eyes, ears, and neurologic and cardiovascular systems.

 A. Detection of nystagmus is critical because it is the only objective sign of vertigo (5). Nystagmus can occur spontaneously or in response to changes in eye or body position. Peripheral vestibular disorders usually cause horizontal or rotatory nystagmus, whereas CNS pathology is reflected by vertical nystagmus—an ominous sign. In true vertigo caused by BPPV, DH maneuvers will often confirm the diagnosis (sensitivity 60% to 90%, specificity 90% to 95%) (2,3). The patient is moved rapidly from a sitting to a supine position with the head turned at a 30-degree angle, first to one side and then to the other. A positive DH test includes precipitation of vertigo, latency of onset by a few seconds, rotational nystagmus, resolution within a minute, and lessened symptoms and nystagmus with prolonged latency on repeated testing (i.e., fatiguability). Lack of latency and fatiguability characterize vertigo caused by serious central lesions.

 B. Neurologic examination serves to detect brainstem or CNS pathology.

C. Otoscopy can detect otitis media or cholesteatoma. Nystagmus with vertigo following positive or negative pressure applied to the tympanic membrane (pneumatic otoscopy) suggests a perilymphatic fistula.

D. Other provocative tests (forced hyperventilation, vestibulo-ocular reflex testing, vigorous horizontal head shaking) are not routinely helpful.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Syncope: Differential Overview
(Field Guide to Bedside Diagnosis)

Orthostatic/Autonomic

❑ Neurally mediated hypotension

❑ Volume depletion

❑ Cough syncope

❑ Anemia

❑ Autonomic insufficiency

Cardiac/Obstructive

❑ Myocardial infarction

❑ Pulmonary embolism

❑ Aortic stenosis

❑ Hypertrophic obstructive cardiomyopathy

❑ Aortic dissection

❑ Cardiac tamponade

❑ Left atrial myxoma

Cardiac/Dysrhythmic

❑ Complete heart block

❑ Sick sinus syndrome

❑ Tachyarrhythmia

❑ Carotid sinus hypersensitivity

Neurologic

❑ Vertebrobasilar ischemia

❑ Hypoglycemia

❑ Unwitnessed seizure

❑ Subclavian steal syndrome

Psychologic

❑ Hyperventilation

❑ Hysterical faint

Diagnostic Approach

The cause of syncope is usually evident after a careful history and physical exam. Identification of a cardiac cause is critical because it portends a poor prognosis (1-year mortality 18% to 33%). In patients with heart disease, the most specific predictors of a cardiac cause are syncope in the supine position or during effort, blurred vision, and convulsive syncope. In patients without heart disease, palpitations are the only significant predictor of a cardiac cause.

Focus on preceding events and witness description. Sudden loss of consciousness without warning is usually due to an arrhythmia. Syncope with chest pain mandates that aortic dissection, myocardial infarction, and pulmonary embolism be ruled out. Syncope with exertion suggests aortic stenosis, hypertrophic obstructive cardiomyopathy, or bradycardia. Events after the syncope, such as confusion, lethargy, or neurological symptoms suggest a seizure.

Consider syncope as the cause of unexplained trauma such as hip fracture or MVA.

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Source: Field Guide to Bedside Diagnosis, 2007

Syncope: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Ask the patient for information about the fainting episode. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he stand quickly from a sitting or prone position? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

Physical examination

Perform a complete cardiac and neurologic examination. Provide continuous cardiac monitoring. Next, take the patient’s vital signs and examine him for injuries that may have occurred during his fall.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Syncope: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Vertigo: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he’s moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he has ever fallen. Ask if he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history. Note any evidence of alcohol abuse.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Vertigo: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Peripheral Vestibular Dysfunction

Labyrinthitis

Acute otitismedia is most common cause of labyrinthitis in childhood. The infection mayextend directly into labyrinth, or inflammatory toxins may causelabyrinthine disturbance.

Viral infections (e.g., mumps, measles,and infectious mononucleosis) also may cause labyrinthitis.

History of infection followed by vertigoand hearing loss suggests diagnosis. Exam often reveals spontaneousnystagmus with fast component directed toward normal ear.

Motion Sickness

Can occur with land, sea, or air travel.Nausea and vomiting are common findings, but vertigo and nystagmusalso can occur.

Head Trauma

May causelabyrinthine injury with or without temporal bone fracture.

Frequent findings are falling towardaffected side and hearing loss.

Skull radiography and CT of temporalbone are useful in diagnosis. Caloric testing usually reveals decreasedlabyrinthine response on affected side.

Drugs

Several drugs, including aminoglycosides,ethacrynic acid, and quinine, may cause hearing loss, but rarelyvertigo.

Benign Paroxysmal Vertigo

Usuallyoccurs in children 2–6 yrs and is characterized by recurrentepisodes of vertigo that occur without warning.

Child appears pale, anxious, and unableto maintain upright position.

Nystagmus also may occur.

Results of neurologic exam are normalbetween episodes.

Vestibular Neuronitis

Most frequentcause of vestibular neuronitis, which usually occurs in adolescents,is viral upper respiratory infection.

Onset is acute, with nausea, vomiting,vertigo, and nystagmus. Hearing loss does not occur.

Episodes are self-limited but may recur.

Caloric stimulation produces decreasedor absent response on affected side.

Middle Ear and Temporal Bone Masses

Middle earand temporal bone masses (e.g., cholesteatoma and acoustic neuroma) maydamage labyrinth and produce vertigo and hearing loss.

CT and MRI locate mass and define itsextent.

See Bellet et al. (1992) for furtherdiscussion.

Perilymphatic Fistula

Head trauma or sudden change in barometricpressure (flying or diving) may cause rupture of round or oval windowinto vestibule, creating fistula and producing vertigo and hearingloss (see Chap. 26, Hearing Lossand Deafness).

Ménière Disease

Uncommon disorder in children characterizedby recurrent episodes of vertigo, fluctuating hearing loss, andtinnitus. Caloric testing usually reveals reduced vestibular responseon involved side.

Central Vestibular Dysfunction

Head Trauma

Concussion or brain contusion with shearingforces may damage vestibular nuclei and produce vertigo. Calorictesting reveals diminished caloric responses.

Intracranial Infection

Vertigo may sometimes occur with meningitis,encephalitis, and brain abscess. These disorders are discussed in Chap. 3, Alteration in Consciousness.

Seizure Disorder

Vertigo may occur as part of initial manifestationof complex partial seizure.

Basilar Artery Migraine

In this type of migraine, vertigo may precedeor accompany throbbing occipital headache (see Chap. 25, Headache).

Neoplasm

Posteriorfossa tumors may cause vertigo, ataxia, and nystagmus, whereas brainstem gliomasmay cause vertigo, double vision, hearing loss, nystagmus, and cranialnerve dysfunction (III–VIII).

MRI is diagnostic study of choice.

Histologic diagnosis is definitive.

Psychologic Disturbance

Anxiety,depression, conversion reaction, or malingering may produce vertigo.

History and physical exam suggest diagnosis.Results of vestibular function testing, electroencephalography,and CT are normal.

Diagnostic Approach

Once presenceof vertigo has been established, next step is to determine whetherdisturbance is in peripheral or central vestibular system or whetherit is psychologic.

Important information is age of child;whether vertigo is acute, recurrent, or chronic; presence of hearingloss, ear pain, or tinnitus; and any history of recent trauma ordrug ingestion.

Complete physical exam should be performed,focusing on otologic and neurologic exams.

Vertigo caused by disturbance of peripheralvestibular system often occurs suddenly, lasts short time, and isunassociated with loss of consciousness. Sudden change in head positionfrequently precipitates episode. Nausea, vomiting, tinnitus, hearingloss, and swaying or falling toward affected side are common findings.Nystagmus is inhibited by visual fixation and may change with headposition.

Disturbance in central vestibular systemcan cause recurrent or chronic vertigo, which may be accompaniedby cranial nerve deficits, pyramidal signs, and cerebellar signs.If nystagmus occurs, it does not change with head position, noris it inhibited by visual fixation.

The history and physical exam are diagnosticin many cases of vertigo. Audiologic testing or brainstem evokedresponses should be performed with suspected hearing loss.

CT should be performed if there ishistory of acute head trauma. Otherwise, MRI is study of choiceif neuroimaging is indicated. Electroencephalography is useful ifseizures are suspected.

» READ BOOK EXCERPT ONLINE »

Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Syncope and Dizziness: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Cardiovascular Syncope

Neurocardiogenic Syncope (Common Faint)

Most commontype of syncope in childhood and adolescence.

Often a response to anxiety, fear,pain, or other emotional stress.

Also may occur after extreme fatigue,prolonged standing, or fasting.

Pathogenesis involves vasodilatationof skeletal muscle vasculature and failure of heart rate and strokevolume to maintain cardiac output for adequate cerebral blood flow.

Dizziness, nausea, sweating, and abdominaldiscomfort may precede syncope. Interruption of cerebral perfusionfor 2–3 secs produces dizziness, but lying down duringpresyncopal phase may prevent syncopal episode.

If cerebral perfusion is interruptedfor >10 secs, syncope occurs.

Onset is sudden with hypotension (vasodepressorresponse), and BP decreases to ≤60 mm Hg. Bradycardia usuallyoccurs, and often junctional rhythm or period of asystole (cardioinhibitory response)may follow.

Most episodes are associated with uprightposition, and child becomes limp and falls to ground. Loss of consciousnessusually lasts <1 min.

Seizures are unusual but may occurwith prolonged syncope.

Once individual is horizontal, BP,heart rate, and color return toward normal.

History and physical exam are usuallydiagnostic. Individuals with this form of syncope do not need furthertesting unless syncope is recurrent, when tilt table testing mayconfirm its presence.

Both tussive and micturition syncopeare now considered forms of neurocardiogenic syncope.

Tussive syncopehas been attributed to large increase in intrathoracic pressure,which decreases venous return to the heart. It may occur after significantcoughing of any cause, but especially after severe paroxysmal coughingwith pertussis.

Micturition syncope is most commonin elderly men, but it can occur in older adolescents. Syncope usuallyoccurs at the end of micturition. The mechanism is unclear, buta full bladder causes peripheral vasoconstriction, and with emptying,peripheral vasodilatation occurs, which in the erect posture mayproduce syncope.

Cardiac Syncope

Congenital and Acquired Heart Disease

Syncopemay occur with outflow obstruction of left ventricle (LV) (valvar,subvalvar, or supravalvar aortic stenosis; hypertrophic cardiomyopathy),outflow obstruction of right ventricle (RV) (pulmonic stenosis,primary pulmonary artery hypertension, pulmonary vascular disease),inflow obstruction of LV (mitral stenosis, atrial myxoma), and inflowobstruction of RV (cardiac tamponade). More likely to occur duringor just after physical exertion, when cardiac output cannot increaseenough to meet demands of oxygen delivery to brain.

Syncope also may occur with cardiomyopathy,myocarditis, and endocarditis as a result of decreased cardiac output.

Another cause is myocardial ischemia,which may occur with coronary artery anomalies, especially anomalousorigin of left coronary artery from pulmonary artery and abnormalcourse of left coronary artery between aortic and pulmonary trunkswith compression of artery during exercise. Coronary artery aneurysmsand thrombosis found in Kawasaki disease also may produce myocardialischemia and syncope.

In most cases, history, physical exam,chest radiograph, ECG, and 2-D echocardiogram are diagnostic.

Diagnosis of primary pulmonary hypertensionusually requires lung biopsy to exclude pulmonary venoocclusivedisease. Although pulmonary vascular disease may be diagnosed clinicallywith support of echocardiography, cardiac catheterization and angiographycan confirm these findings.

Hypercyanotic Episodes

Consistof intense cyanosis and hyperpnea. Occur most commonly with tetralogyof Fallot but also can occur with tricuspid atresia, transpositionof great arteries with pulmonary stenosis, and pulmonary vasculardisease.

Children who can walk may squat duringepisode, which increases systemic vascular resistance and decreasesright-to-left shunt.

Occasionally episodes may be prolongedand associated with syncope and seizures. During episode, murmuris less intense or disappears.

Several factors seem to play a role:prolonged crying with decreased venous return, constriction of RVinfundibulum, decreased systemic vascular resistance secondary toimmobilization or spontaneous vasomotor changes, relative anemia,and increased physical activity with higher oxygen requirement.

Arrhythmias in Structurally Normal Heart

Syncopemay occur from sinus bradycardia, junctional bradycardia, second-and third-degree (atrioventricular) AV block with low ventricularrate, supraventricular tachycardia, atrial flutter, or ventriculartachycardia.

Atrial fibrillation with rapid ventricularresponse over the accessory pathway may be associated with syncopeor near syncope in Wolff-Parkinson-White (WPW) syndrome. Diagnosisis usually confirmed by ECG, which shows short PR interval and deltawave.

Syncope also may occur with prolongedQT interval, in which variable recovery time with reentry depolarizationmay cause torsade de pointes ventricular tachycardia.

ProlongedQT interval has a number of genetic causes. Hypokalemia, hypocalcemia, andhypomagnesemia also may cause QT interval prolongation. Tricyclicantidepressants and phenothiazines have been associated with prolongedQT interval, and so have overdoses of quinidine, procainamide, anddisopyramide.

Prolonged QT interval can be diagnosedby measuring this interval on routine ECG, but it must be correctedfor heart rate. 1 method for correction of QT interval is to measureQT interval (in secs) and divide by the square root of the RR interval(in secs). In 95% of individuals, the corrected QT interval is <0.45secs.

Sympathomimetic drugs when taken inlarge doses or from idiosyncratic reaction may produce supraventricularor ventricular tachycardia. Cocaine also may produce ventriculartachycardia and syncope. Metabolic derangements (e.g., hyperkalemia,hypoglycemia, and hypercalcemia) also may result in syncope by producingarrhythmias, but this is rare.

ECG may be diagnostic of these arrhythmias.If syncopal episodes are frequent, Holter monitoring may be useful;if they occur during exercise, maximal exercise testing may be diagnostic.Otherwise, event recorder or implanted loop recorder should be considered.

If syncope still remains unexplained,electrophysiologic studies should be performed.

Arrhythmias in Structurally Abnormal Heart

Childrenwho have congenital or acquired heart disease are at risk for arrhythmias thatmay produce syncope. These include sinus bradycardia, sick sinussyndrome, supraventricular tachycardia, atrial fibrillation, atrialflutter, ventricular tachycardia, ventricular fibrillation, andcomplete heart block.

WPW syndrome and supraventricular tachycardiaare occasionally associated with Ebstein anomaly.

Complete heart block may be associatedwith ventricular inversion and transposition of great arteries.

Ventricular tachycardia may occur fromarrhythmogenic RV dysplasia, although echocardiography may not bediagnostic because a heavily trabeculated RV may be indistinguishablefrom dysplasia. Recurrent ventricular tachycardia, especially exercise-induced,and left bundle branch pattern suggest this diagnosis, which canbe confirmed by MRI.

Children who have had surgical repairof a cardiac defect are also at risk for development of arrhythmias.An incision in the ventricle is a risk factor for ventricular tachycardia.Supraventricular tachycardia, atrial fibrillation, atrial flutter,sick sinus syndrome, and ventricular tachycardia may occur after Mustardor Senning procedure for repair of transposition of great arteries.Surgical manipulation in the area of sinus or AV nodes in repairof AV canal defects, posterior ventricular septal defects, or tunnelaortic stenosis may predispose to development of sinus bradycardiaand heart block.

ECG may be diagnostic of these arrhythmias.Holter monitoring and maximal exercise testing also may be helpfulin diagnosis.

If these tests are normal consideringhigher risk of life-threatening events in children with structurallyabnormal hearts, electrophysiologic studies should be considered.

Vascular Syncope

Orthostatic Syncope

Occurs whenindividual assumes upright posture and systolic arterial BP decreasesby ≥15 mm Hg.

Possible causes include

Decreasedblood volume (blood loss, GI fluid loss, excessive diuretic use)

Failure of normal postural reflexes(suddenly standing up after prolonged bedrest, familial dysautonomia,spinal cord lesions)

Drugs (vasodilators, tricyclic antidepressants,sedatives, opiates, cocaine)

Supine and standing BPs should be measuredin any individual with unexplained syncope.

Cerebrovascular Syncope

This typeof syncope may be due to excessive vagal stimulation, which causessevere bradycardia or AV block.

Examples include intubation, placementof nasogastric tube or esophageal overdrive pacing catheter, removalof pleural or peritoneal fluid, and distention of viscera.

Excessive vagal tone also may occurin normal adolescents or well-trained athletes, and a further increasein vagal tone may worsen bradycardia or AV block enough to causesyncope.

Carotid Sinus Syncope

Pressure on baroreceptors in carotid sinusmay cause carotid sinus syncope. Uncommon in children but can occurwith excessive pressure on neck (e.g., wearing tight collar).

Noncardiovascular Syncope

Breath-Holding

Common inchildren 6 mos–6 yrs of age. Precipitating factors includepain, frustration, and anger.

Pallid breath-holding, which is nowthought to be variation of neurocardiogenic syncope, usually followsacute pain or injury. The infant or child becomes pale and losesconsciousness. Complete recovery occurs in 1–2 mins.

More common is cyanotic breath-holdingspell in which infant or child cries, holds breath during expiration,and turns dusky until breathing begins again. Loss of consciousnessand tonic-clonic movements may occur with prolonged episode.

Hyperventilation

Frequentcause of dizziness but rare cause of syncope.

Common in adolescent girls and usuallydue to emotional stress.

Frequent complaints include lightheadedness,blurred vision, difficulty breathing, choking, smothering, chesttightness, and numbness or tingling of fingers, toes, and face.Individuals who are hyperventilating appear anxious and have fastand deep respirations.

Rebreathing into paper bag and thoughtfulreassurance usually lessen hyperventilation, so that individualscan begin talking about what is upsetting them.

Migraine

Severe migraine headache may cause syncopalepisode, especially if basilar arterial system is affected (see Chap. 25, Headache).

Metabolic

Hypoxia Including Anemia

Severe hypoxia or severe anemia of any causemay result in syncope. See Chap.45, Pallor (Anemia), and Chap. 56, Respiratory Distress and Apnea.

Hypoglycemia

Often causesfaintness and dizziness, but syncope is exceedingly rare. Othermanifestations of hypoglycemia include headache, hunger, sweating,and jitteriness, which may progress to confusion, seizures, andcoma.

Low blood glucose level confirms presenceof hypoglycemia.

With administration of oral or intravenousglucose, symptoms resolve.

See further discussion of hypoglycemiain Chap. 59, Seizures.

Psychologic

Acute stressmay produce anxiety and syncope with or without hyperventilation. Commonstresses are witnessing a tragic event or hearing news of the deathof close friend or relative.

Hysteria is common cause of recurrentfainting in adolescents, especially in those with hysterical personalities.

In this typeof episode, which almost always occurs in presence of other people,hysterical person falls or slumps in dramatic way but avoids injury.Fainting also may occur while lying or sitting down. There is noprodrome or change in heart rate, BP, or skin color.

Diagnosis of psychologic causes ismade from history, physical exam, and clinical observation.

Diagnostic Approach

Neurocardiogenicsyncope, vascular syncope, breath-holding, hyperventilation, and psychologicdisturbances can usually be distinguished by history and physicalexam.

If syncopal episode occurs on assumingupright posture, BP should be measured in supine and upright positions.Postural difference in systolic pressure of >15 mm Hg confirmsdiagnosis of orthostatic syncope.

Individuals with recurrent syncope,family history of sudden death, or syncope occurring during intensiveexercise need further evaluation.

If recurrent syncope occurs, tilt testingmay determine whether syncope is neurocardiogenic.

Family history of syncope and suddendeath suggests hypertrophic cardiomyopathy or long QT interval syndrome.

Syncope during intense exercise mayoccur with hypertrophic cardiomyopathy, severe aortic stenosis,anomalous left coronary artery from pulmonary artery, primary pulmonaryhypertension, or exercise-induced atrial fibrillation associatedwith WPW syndrome.

Diagnosis of cardiac disorders canbe made from history, physical exam, chest radiograph, ECG, and2-D echocardiogram. Cardiac catheterization and angiography maybe necessary to make definitive diagnosis and to determine severityof lesion. Arrhythmia may be suspected from history, and routine ECGwith rhythm strip may be diagnostic. Otherwise, further testingmay be needed (e.g., Holter monitoring, maximal exercise testing,event recorder or implanted loop recorder monitoring, and electrophysiologictesting).

With syncopal episode of unknown cause,ECG should be initially performed searching for WPW syndrome, longQT interval syndrome, or LV hypertrophy with T-wave changes indicativeof cardiomyopathy.

>>

» READ BOOK EXCERPT ONLINE »

Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Syncope: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur? Obtain a complete drug history.

Next, take the patient's vital signs and examine him for any injuries that may have occurred during his fall. Place him on a cardiac monitor and assess his heart rhythm for abnormalities. Assess cardiac and respiratory status. Monitor pulse oximetry. Perform a neurologic examination.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Vertigo: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he's moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he has ever fallen. Ask whether he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history, and note evidence of alcohol abuse.

Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient's gait and posture for abnormalities.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

SYNCOPE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Clinical differentiation of the various forms of syncope is made by combinations of symptoms. Thus, syncope with marked sweating and tachycardia is more likely due to hypoglycemia. Syncope with sweating and bradycardia is more likely due to vasovagal syncope. Focal neurologic signs during the attack suggest transient ischemia attack (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia). Transesophageal echocardiography is the procedure of choice to find a cardiac source. A family history of syncope suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong possibility in the young, whereas heart block is more likely in the aged. Consequently, an EEG and Holter monitoring are useful in the workup.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

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