Polysomnography
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Nocturnal, laboratory-based polysomnography (PSG) is the most commonly used test in the diagnosis of obstructive sleep apnea syndrome (OSAS). It is often considered the criterion standard for diagnosing OSAS, determining the severity of the disease, and evaluating various other sleep disorders that can exist with or without OSAS. PSG consists of a simultaneous recording of multiple physiologic parameters related to sleep and wakefulness. See the image below. Home-based, limited-channel sleep studies are being used more often to diagnosis obstructive sleep apnea, but they have some limitations.
PSG can directly monitor and quantify the number of respiratory events (ie, obstructive, central, or complex) and the resultant hypoxemia and arousals related to the respiratory events or even independent of the respiratory events. [1]
A single-night PSG is usually adequate to determine if OSAS is present and the degree of the disorder. However, night-to-night variability may exist in patients who have a high probability but a low apnea index. In addition, variability in laboratory equipment, scoring technique, and interscorer reliability may also play roles. As is well known, PSG scoring also usually varies from laboratory to laboratory.
PSG is used to evaluate abnormalities of sleep and/or wakefulness and other physiologic disorders that have an impact on or are related to sleep and/or wakefulness.
Assessment of sleep stages requires 3 studies: electroencephalography (EEG), electrooculography (EOG), and surface electromyography (EMG).
One EEG channel (central channel with an ear reference provides the best amplitude) is used to monitor sleep stage. However, most laboratories use 2 central channels and 2 occipital channels, with ear references as an adjunct to help identify sleep latency and arousals. A 10- to 20-electrode placement system is used to determine the location of these channels. Additional EEG channels can be used, particularly in patients with epilepsy (ie, a full 10-20 montage).
Two EOG channels are used to monitor both horizontal and vertical eye movements. Electrodes are placed at the right and left outer canthi, one above and one below the horizontal eye axis. The electrodes pick up the inherent voltage within the eye; the cornea has a positive charge and the retina has a negative charge. Evaluation of the eye movements is necessary for 2 reasons. First is for documentation of the onset of rapid eye movement (REM) sleep, and second is to note the presence of slow-rolling eye movements that usually accompany the onset of sleep.
One EMG channel (usually chin or mentalis and/or submentalis) is used to record atonia during REM sleep or lack of atonia in patients with REM-related parasomnias. To assess bruxism, the EMG electrodes can be placed over the masseter. The EMG recording from other muscle groups is assessed for other sleep disorders. For example, the anterior tibialis EMG is helpful for assessing periodic limb movements during sleep and the intercostal EMG is used as adjunctive help for determining effort during respiratory events.
Two channels are used for monitoring airflow. One thermistor channel (oral and/or nasal) is used to evaluate the presence or absence of airflow. Any change in temperature as a patient inhales and exhales leads to a normal signal, so this channel is insensitive for partial flow obstruction. Thermistor is the recommended channel for evaluation of apneas. Nasal pressure transducer channel is a more sensitive measure of airflow restriction. Normal breathing has a rounded pattern, while resistance to airflow leads to a squaring off of the flow signal. Pressure transducer is the recommended channel for evaluating hypopneas. It is also used for airflow resistance in upper airway resistance syndrome.
Other parameters that can be monitored in a sleep study include the following:
Electrocardiography
Pulse oximetry
Respiratory effort (thoracic and abdominal)
End tidal or transcutaneous CO2
Sound recordings to measure snoring
Surface EMG monitoring of limb muscles (to detect limb movements, periodic or other)
Continuous video monitoring
Optional parameters that can be monitored in a sleep study include the following:
Core body temperature
Incident light intensity
Penile tumescence
Pressure and pH at various esophageal levels
In 1992, the Office of Technology Assessment of the Agency of Health Care Policy and Research recommended, in an evidence-based assessment, declared two tests as having been studied sufficiently. Both tests are performed in a sleep laboratory.
The first is overnight polysomnography (PSG), which is an overnight recording of the patient’s sleep. Typically for a baseline study, the patient is observed sleeping naturally without any treatment, but if a signficant amount of sleep-disordered breathing (AHI> 20–30 events per hour) is seen in the first hours of the study, a split-night study is performed during which positive airway pressure (PAP) is started. Titration studies may also be done with initiation of PAP from the start of the study to determine optimal settings.
The second is multiple sleep latency testing (MSLT), which records multiple naps throughout a day. Maintenance of wakefulness testing (MWT) can also be performed, which determines how long wakefulness can be maintained.
Standard sleep studies usually use the overnight PSG (may be performed over several nights). If daytime sleepiness is an issue and cannot be fully explained by the overnight study results, an MSLT should be performed the next day. Limitations usually stem from the fact that recording conditions may not reflect what happens during a regular night in the patient’s home.
Although diagnosing a sleep problem on the basis of a recording over a single night is common practice, some authorities caution that more than one night of recording may be necessary so the patient can become comfortable with unfamiliar surroundings and sleep more naturally. This effect is greatest on the first night in the sleep laboratory (ie, first-night effect).
Sporadic events may be missed with a single-night PSG. External factors that disturb the subject’s sleep may be present in the home but absent from the controlled environment of the sleep laboratory.
Patient preparation is important so that the patient sleeps naturally. Patient instructions include the following:
Maintain regular sleep-wake rhythm.
Alcohol and sleeping pills may alter the PSG results, but if they are part of the patient’s normal routine, they should not be abruptly stopped.
Avoid stimulants, including medications for narcolepsy.
Avoid strenuous exercise on the day of the PSG.
Avoid naps on the day of the sleep study.
Daytime PSG can be useful for patients who typically sleep during the day. Simplified sleep studies with limited subsets of monitored parameters, such as PAP-NAPs, can be used to help the patient with acclimatization and finding optimal settings.
High costs and long waiting lists have prompted the exploration of alternative methods of evaluation and many insurance companies are requiring home-based, limited-channel sleep studies prior to in-laboratory PSG. Instead of in-laboratory titration, many patients with obstructive sleep apnea can be started on automatically adjusting continuous positive airway pressure (CPAP) and then have the settings adjusted and response monitored through data collected by the device.
In 2008, Medicare approved the use of unattended home sleep monitoring devices of types II, III, or IV (with at least 3 channels) if the patient received a complete clinical evaluation and does not have atypical or complicated symptoms and the studies were read by a trained sleep specialist. [2, 3] The guidelines for using a portable monitor unattended home sleep study device for continuous positive airway pressure (CPAP) therapy include the following:
Type II device: This type of device has a minimum of 7 channels (eg, EEG, EOG, EMG, ECG-heart rate, airflow, respiratory effort, oxygen saturation). This type of device monitors sleep staging so the apnea-plus-hypopnea index (AHI) can be calculated.
Type III device: This device has a minimum of 4 channels, including ventilation or airflow (at least 2 channels of respiratory movement or airflow), heart rate or ECG, and oxygen saturation.
Type IV device: This type of device does not meet requirements for other types, and many measure only 1-2 parameters (eg, oxygen saturation or airflow). For Medicare reimbursement, these devices, including WatchPAT (Itamar Medical Ltd, Caesarea, Israel) can be used if they have a minimum of 3 channels.
The American Academy of Sleep Medicine (AASM) evaluated the literature on unattended sleep monitoring devices to develop their clinical guidelines, published in 2007. [4] These guidelines include the following recommendations and cautions:
Portable monitoring (PM) may be indicated for the diagnosis of obstructive sleep apnea (OSA) in patients for whom in-laboratory PSG is not possible by virtue of immobility, safety, or critical illness. PM may also be indicated to monitor the non-CPAP treatments of sleep apnea including oral appliances, weight loss, and upper airway surgery.
PM is not appropriate for diagnostic evaluation of patients who may have comorbid sleep disorders including central sleep apnea, periodic limb movements, insomnia, parasomnias, circadian rhythm disorders, or narcolepsy.
PM is not appropriate for the diagnosis of OSA in patients with significant comorbid medical conditions that may degrade the accuracy of PM. This includes, but is not limited to, severe pulmonary disease, [5] neuromuscular disease, or congestive heart failure. PM is not indicated in the absence of a comprehensive sleep evaluation.
PM is not appropriate for general screening of asymptomatic patients.
At minimum, PM must record airflow, respiratory effort, and blood oxygenation.
The PM device must allow for display of raw data with the capability of manual scoring or editing of automated scoring by a qualified sleep technologist.
A board-certified sleep specialist or an individual who fulfills eligibility criteria for the sleep medicine certification examination must review the raw data from PM using scoring criteria consistent with current published AASM standards.
False negative rates may be as high as 17% in unattended PM studies. If the PM test is technically inadequate or does not provide the expected result, in-laboratory polysomnography should be performed.
AASM does not support type IV devices for home sleep testing.
In 2012, the AASM also published evidence-based practice parameters for the non-respiratory indications for polysomnography and multiple sleep latency testing for children. [6] PSG is indicated for children suspected of having periodic limb movement disorder (PLMD) for diagnosing PLMD. Children with frequent NREM parasomnias, epilepsy, or nocturnal enuresis should be clinically screened for the presence of comorbid sleep disorders and polysomnography should be performed if there is a suspicion for sleep-disordered breathing or PLMD.
Because of the lack of EEG monitoring, Type III devices may underestimate the severity of sleep-disordered breathing. Typically, events must be associated with 3% desaturations to be scored, so patients with events primarily causing arousals may be missed. Additionally, the apnea/hypopnea index (AHI) is calculated by the number of apneas and hypopneas per hours of test rather than hours of sleep, which can also underestimate severity. For these reasons, if a home study is normal in a patient with suspected sleep apnea, an in-laboratory PSG is recommended.
Multiple sleep latency testing (MSLT) is used to assess the degree of daytime sleepiness and to evaluate for possible narcolepsy. MSLT should be performed after a full-night polysomnogram to ensure that at least 6 hours of sleep precede the test and that no other causes for excessive daytime sleepiness are present. A sleep log should be kept for at least 1 week prior to the study, and all medications taken for the 2 weeks prior to the study should be noted. Urine drug testing is often done to evaluate for drugs that may affect study results. Stimulant medications, nicotine, and caffeine can affect the mean sleep latency, and medications (especially selective serotonin reuptake inhibitors [SSRIs]) can affect sleep-onset rapid eye movement (REM) periods. [7] In general, SSRIs and stimulants need to be discontinued at least 2 weeks prior to the test. Small amounts of caffeine do not usually need to be discontinued.
The patient is given 20 minute opportunities to nap every 2 hours for 4 or 5 naps. The first nap should begin within 1.5-3 hours after waking. If the patient falls asleep, he or she is allowed to sleep for 15 minutes. Sleep latency is the time to the first epoch with over 15 seconds of any stage of sleep. The mean sleep latency is determined. A mean sleep latency of 10-15 minutes is consistent with mild sleepiness, 5-10 minutes is consistent with moderate sleepiness, and less than 5 minutes is consistent with severe sleepiness. A series of 2 sleep-onset REM periods (SOREMP) is consistent with the diagnosis of narcolepsy; however, only 80% of patients with narcolepsy and 6.6% of patients without narcolepsy had 2 or more SOREMPs in a review of over 2000 MSLTs.
Maintenance of wakefulness testing (MWT) is used to determine how long a patient is able to maintain wakefulness. The patient should be in a dim room in a semirecumbent position. The 20-min MWT includes 5 20-min tests of wakefulness, and the 40-min MWT includes 4 40-min tests of wakefulness every 2 hours. The first nap should begin within 1.5-3 hours after waking. A preceding PSG is not always necessary. The patient should be instructed to sit still and remain awake as long as possible. The test ends after 20 or 40 minutes if no sleep occurs or if the patient achieves unequivocal sleep, which is determined by either 3 consecutive epochs of stage 1 sleep or 1 epoch of any other stage of sleep. Sleep latency is the time to the first epoch with over 15 seconds of any stage of sleep. The mean sleep latency is determined.
Standardized criteria for the staging of sleep were published first in 1968 by Rechtschaffen and Kales. A revised version was published in 2007 by the American Academy of Sleep Medicine. [8] The chief revision was the consolidation of stages 3 and 4 into a single stage N3 (slow wave sleep). Previous stages 1 and 2 were renamed N1 and N2. Both systems are reflected below, with the expectation that the discontinued stages will be omitted from future revisions of this article.
Alpha EEG
Frequency of 8-13 Hz
Produced in occipital region
Crescendo-decrescendo appearance
Theta EEG
Frequency of 3-7 Hz
Produced in the central vertex region
No amplitude criteria
Most common sleep frequency
Delta EEG
EEG frequency of 0.5-2 Hz
Seen predominantly in frontal region
Amplitude of greater than 75 microvolts
See the list below:
Frequency of 12-14 Hz
Produced in central-vertex region
Greater than 0.5-3 seconds in duration
0.5-second spindles with 6-7 cycles
Indicative of stage 2 sleep
See the list below:
Sharp, slow waves with a negative, then positive, deflection
No amplitude criteria
Duration must be at least 0.5 seconds
Predominantly produced in central-vertex region
Indicative of stage 2 sleep
May occur with or without stimuli
See the list below:
Greater than 50% of each epoch contains alpha activity
Eye blinks at a frequency of 0.5-2 Hz
Reading eye movements
Irregular conjugate rapid eye movements associated with normal or high chin tone.
See the list below:
Greater than 50% of the epoch contains theta activity (4-7 Hz) with slowing of the background rhythms greater than or equal to 1 Hz from those of stage wake
Vertex sharp waves
Slow-rolling eye movements in EOG channels
Relatively high submental EMG tone
See the list below:
Theta activity (4-7 Hz)
K-complexes and sleep spindles occur episodically
High tonic submental EMG
See the list below:
Greater than 20% of each epoch must contain delta activity
Amplitude of 75 microvolts or greater
Submental muscle tone may be slightly reduced
See the list below:
Between 20-50% of each epoch must contain delta activity
Amplitude of 75 microvolts or greater
Submental muscle tone may be slightly reduced
See the list below:
Greater than 50% of the epoch has scorable delta activity
Amplitude of 75 microvolts or greater
Submental EMG activity slightly reduced from that of light sleep
See the list below:
Rapid eye movements
Low amplitude, mixed frequency EEG (similar to awake pattern)
Atonia or the lowest tonic submental EMG
May see saw-tooth waves
In 2015, the AASM updated scoring rules, making changes to scoring of apneas, hypopneas, Cheyne Stokes respiration, and hypoventilation.
The event duration starts at the nadir preceding the first breath that is clearly reduced to the beginning of the first breath that approximates the baseline breathing amplitude. Events terminate if there is a clear and sustained increase in breathing or if there is a desaturation, when there is a re-saturation of at least 2%.
Polysomnography reports should report an apnea/hypopnea index (AHI), which, for an in-lab study, is the number of apneas and hypopneas per hour of sleep. For portable studies, the AHI is the number of apneas and hypopneas per hour of test. It is important to know what criteria was used for the events as there have been many changes to the scoring criteria for hypopneas, which may have led patients who were scored with desaturation criteria only to have significantly underestimated sleep apnea. In general, an AHI > 5 is considered significant sleep apnea. Some polysomnography report respiratory disturbance index (RDI), which is typically the number of apneas plus hypopneas plus respiratory-related arousals.
See the list below:
Greater than 90% reduction in oronasal thermistor amplitude for more than 10 seconds
The duration of the 90% drop is greater than or equal to 10 seconds
Often associated with increasing respiratory effort; usually seen as paradoxical
AASM recommendation
Reduction in nasal pressure amplitude by greater than 30% lasting for at least 10 seconds
Associated with SaO2 drop of at least 3% from pre-event baseline or an arousal
Obstructive hypopneas can be scored if any of the following are present: Snoring, increased inspiratory flattening of the nasal pressure, or associated thoracoabdominal paradox during the event but not pre-event
Central hypopneas can be score if none of above findings is present
Medicare definition
Reduction in pressure amplitude greater than 30% of baseline value
Asocciated with SaO2 decrease of greater than 4%
See the list below:
Greater than 90% reduction in thermistor flow for greater than 10 seconds
Total absence of respiratory effort at the beginning of the event, followed by a gradual increase in effort, which eventually breaks the apnea (usually paradoxical)
See the list below:
Greater than 90% reduction in thermistor flow for greater than 10 seconds
Complete absence of respiratory effort
See the list below:
Greater than 10 breaths with increasing respiratory effort or flattening of the nasal pressure followed by an arousal
Does not meet criteria for hypopnea or apnea
See the list below:
At least 3 consecutive cycles
Cyclical crescendo and decrescendo change in breathing amplitude
Either 5 per hour of sleep or duration greater than 10 minutes
Cycle length > 40 seconds
See the list below:
Increase in CO2 levels (ETCO2 or TCCO2) to > 55 mmHg for greater than or equal to 10 minutes or
Increase in CO2 levels (ETCO2 or TCCO2) by at least 10 mmHg (from awake supine value) to > 50 mmHg for greater than or equal to 10 minutes
See the list below:
Each jerk more than 0.5 seconds but less than 10 seconds in duration
Minimum amplitude is an 8 mV increase in EMG voltage above resting EMG
Must have 4 jerks separated by no less than 5 seconds and no more than 90 seconds
No associated respiratory event within 0.5 seconds
See the list below:
Abrupt shift of EEG frequency including alpha, theta, and/or frequencies greater than 16 Hz (but not spindles)
Greater than 3 seconds of changed frequency on EEG
At least 10 seconds of stable sleep preceding the change
In REM sleep, increase in submental EMG for at least 1 second
See the list below:
At least twice the amplitude of baseline chin EMG activity
At least 3 elevations of 0.25-2 seconds of increased chin EMG activity
One elevation of greater than 2 seconds of increased chin EMG activity
Standard analysis still consists of reviewing each of the parameters recorded. Overnight parameters (eg, times of lights on/off, total time in bed, total sleep time, sleep latency, REM latency) are collected. The overnight recording is divided into epochs of approximately 30 seconds. The standard EEG, EMG, and EOG recordings are evaluated, and the predominant stage of sleep (according to the AASM 2007 scoring manual) is then assigned to the entire epoch. In 2015, the AASM changed the recommended scoring criteria of most events including now recommending using 3% desaturation or arousal for criteria for hypopneas. Medicare guidelines, however, still use the not-recommended 4% desaturation criteria that can miss many patients with signficant obstructive sleep apnea.
Total time and relative proportion of the night spent in each of the stages and in REM and non-REM sleep are calculated. Latencies to REM and slow-wave sleep are reported.
Stages of sleep, any abnormalities noted with EEG, and periodic limb movements are reported. Respiratory activity (eg, apneic or hypopneic episodes, oxygen desaturations) is correlated with sleep stages. Other parameters, such as body position, are recorded. If needed, esophageal pH or penile tumescence can also be recorded.
Once sleep apnea is diagnosed with either a portable limited-channel stud or an in-laboratory PSG, a patient can either be started with autotitrating CPAP at home or an in-laboratory titration study can be done. In-laboratory titration is recommended if there are other breathing disorders than obstructive sleep apnea, including hypopnea, hypoventilation, or central sleep apnea, as devices other than CPAP are often needed.
See the list below:
Circadian rhythm disorders
Narcolepsy
Idiopathic hypersomnia
Inadequate sleep hygiene
Sleep-wake misperception
Sleep-related respiratory disorders
Sleep apnea syndrome
Upper airway resistance syndrome
Obesity hypoventilation syndrome
Central sleep apnea
See the list below:
Disorders of arousal
Disorders of sleep-wake transition
Disorders that occur during REM sleep
Nightmares
REM behavior disorder
Medical-psychiatric sleep disorders
Medical – Sleep-related asthma
Psychiatric – Depression, panic disorder
Neurologic – Sleep-related epilepsy
Others
Bruxism [9]
Restless legs syndrome and periodic limb movement disorder
Treatment is determined by the disorder diagnosed using polysomnography, multiple sleep latency testing, or both.
For excellent patient education resources, visit eMedicineHealth’s Sleep Disorders Center. In addition, see eMedicineHealth’s patient education article Disorders That Disrupt Sleep (Parasomnias).
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Palinkas M, De Luca Canto G, Rodrigues LA, Bataglion C, Siéssere S, Semprini M, et al. Comparative Capabilities of Clinical Assessment, Diagnostic Criteria, and Polysomnography in Detecting Sleep Bruxism. J Clin Sleep Med. 2015 Nov 15. 11 (11):1319-25. [Medline].
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Chesson AL Jr, Ferber RA, Fry JM, et al. The indications for polysomnography and related procedures. Sleep. 1997 Jun. 20(6):423-87. [Medline].
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Parrino L, Ferrillo F, Smerieri A, et al. Is insomnia a neurophysiological disorder? The role of sleep EEG microstructure. Brain Res Bull. 2004 Jun 30. 63(5):377-83. [Medline].
Rechtschaffen A, Kales A. A Manual of Standardized Terminology, Techniques and Scoring System for Sleep Stages of Human Subjects. Washington, DC: US Government Printing Office, US Public Health Service. 1968.
Rodsutti J, Hensley M, Thakkinstian A, et al. A clinical decision rule to prioritize polysomnography in patients with suspected sleep apnea. Sleep. 2004 Jun 15. 27(4):694-9. [Medline].
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Zonato AI, Bittencourt LR, Martinho FL, et al. A comparison of public and private obstructive sleep apnea clinics. Braz J Med Biol Res. 2004 Jan. 37(1):69-76. [Medline].
Carmel Armon, MD, MSc, MHS Chair, Department of Neurology, Assaf Harofeh Medical Center, Tel Aviv University Sackler Faculty of Medicine, Israel
Carmel Armon, MD, MSc, MHS is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American College of Physicians, American Epilepsy Society, American Medical Association, American Neurological Association, American Stroke Association, Massachusetts Medical Society, Sigma Xi
Disclosure: Received research grant from: Neuronix Ltd, Yoqnea’m, Israel<br/>Received income in an amount equal to or greater than $250 from: JNS – Associate Editor. UpToDate – Author Royalties.
Karin Gardner Johnson, MD Assistant Professor of Medicine, Tufts University Medical School; Attending Neurologist, Baystate Medical Education and Research Foundation, Baystate Medical Center
Karin Gardner Johnson, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine
Disclosure: Nothing to disclose.
Asim Roy, MD Clinical and Research Associate, Ohio Sleep Medicine Institute
Asim Roy, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Academy of Sleep Medicine
Disclosure: Nothing to disclose.
William J Nowack, MD Associate Professor, Epilepsy Center, Department of Neurology, University of Kansas Medical Center
William J Nowack, MD is a member of the following medical societies: American Academy of Neurology, Biomedical Engineering Society, American Clinical Neurophysiology Society, American Epilepsy Society, EEG and Clinical Neuroscience Society, American Medical Informatics Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Norberto Alvarez, MD Assistant Professor, Department of Neurology, Harvard Medical School; Consulting Staff, Department of Neurology, Boston Children’s Hospital; Medical Director, Wrentham Developmental Center
Norberto Alvarez, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society
Disclosure: Nothing to disclose.
Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;Preacute Population Health Management;The Physicians Edge<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; for: Rxblockchain;Bridge Health.
Anthony M Murro, MD Professor, Laboratory Director, Department of Neurology, Medical College of Georgia, Georgia Regents University
Anthony M Murro, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society
Disclosure: Nothing to disclose.
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