Last Review: 04/12/2018

Effective: 11/13/1997 Next Review: 02/14/2019

Review History

Definitions

Clinical Policy Bulletin Notes

Number: 0181

Policy *Please see amendment for Pennsylvania Medicaid at the endof this CPB.

I. Evoked Potential Studies

Aetna considers evoked potential studies medically necessary for the following indications:

A. Somatosensory evoked potentials (SEPs, SSEPs) or dermatosensory evoked potentials (DSEPs) are considered medically necessary for any of the following indications: 1. To assess any decline which may warrant emergent

surgery in unconscious spinal cord injury persons whoshow specific structural damage to the somatosensorysystem, and who are candidates for emergency spinalcord surgery; or

2. To evaluate acute anoxic encephalopathy (within 3days of the anoxic event); or

3. To evaluate persons with suspected brain death; or4. To identify clinically silent brain lesions in multiple

sclerosis suspects in order to establish the diagnosis,where multiple sclerosis is suspected due to presence

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of suggestive neurologic symptoms plus one or more other objective findings (brain plaques on MRI, clinical lesions by history and physical examination, and/or positive CSF (determined by oligoclonal bands detected by established methods (isoelectric focusing) different from any such bands in serum, or by an increased IgG index)); or

5. To localize the cause of a central nervous system deficit seen on exam, but not explained by lesions seen on CT or MRI; or

6. To manage persons with spinocerebellar degeneration (e.g., Friedreichs ataxia, olivopontocerebellar (OPC) degeneration); or

7. Unexplained myelopathy, or 8. Intraoperative SSEPs under certain conditions (see I.

B., below).

SEPs and DSEPs are considered experimental and investigational for all other indications because their effectiveness for indications other than the ones listed above has not been established.

B. Intraoperative somatosensory evoked potentials (SSEPs) performed either alone, or in combination with motor evoked potentials (MEPs) are considered medically necessary for monitoring the integrity of the spinal cord to detect adverse changes before they become irreversible during spinal, intracranial, orthopedic, or vascular procedures, when the following criteria are met:

1. A specially trained physician or a certified professional practicing within the scope of their license, who is not a member of the surgical team contemporaneously interprets the intraoperative evoked potentials during the operation; and

2. The evoked potential monitoring is performed in the operating room by dedicated trained technician; and

3. The clinician who performs the interpretation is monitoring no more than 3 surgical procedures at the

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same time; and 4. The clinician who performs the interpretation may do

so remotely, but must provide direct, immediate communication of intraoperative evoked potential results to the technician and surgeon during the operation.

Intra‐operative SEP monitoring, with or without MEPs, may be appropriate for the following types of surgery (not an all‐inclusive list):

1. Spinal Surgeries:

a. Correction of scoliosis or deformity of the spinal cord involving traction on the cord

b. Decompression of the spinal cord where function of the spinal cord is at risk

c. Removal of spinal cord tumors d. Surgery as a result of traumatic injury to the spinal

cord e. Surgery for arteriovenous (AV) malformation of the

spinal cord

2. Intracranial Surgeries:

a. Chiari malformation surgery b. Correction of cerebral vascular aneurysms (e.g.,

cerebral aneurysm clipping) c. Deep brain stimulation d. Endolymphatic shunt for Meniere's disease e. Microvascular decompression of cranial nerves

(e.g., optic, trigeminal, facial, auditory nerves) f. Oval or round window graft

g. Removal of cavernous sinus tumors h. Removal of tumors that affect cranial nerves i. Resection of brain tissue close to the primary

motor cortex and requiring brain mapping j. Resection of epileptogenic brain tissue or tumor k. Surgery as a result of traumatic injury to the brain

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l. Surgery for intracranial AV malformations m. Surgery for intractable movement disorders n. Vestibular section for vertigo

3. Vascular Surgeries:

a. Arteriography, during which there is a test occlusion of the carotid artery

b. Circulatory arrest with hypothermia (does not include surgeries performed under circulatory bypass such as CABG, and ventricular aneurysms)

c. Distal aortic procedures, where there is risk of ischemia to the spinal cord

d. Surgery of the aortic arch, its branch vessels, or thoracic aorta, including carotid artery surgery (e.g., carotid endarterectomy), when there is risk of cerebral ischemia.

Intra‐operative SSEPs with or without MEPs are considered experimental and investigational for all other indications (e.g., scapula‐thoracic fusion surgery) because their effectiveness for indications other than the ones listed above has not been established.

Note: Depending on the clinical condition being investigated, it may be medically necessary to test several nerves in one extremity and compare them with the opposite limb.

Note: Intra‐operative evoked potential studies have no proven value for lumbar surgery below (distal to) the end of the spinal cord; the spinal cord ends at L1‐L2.

Note: Post‐operative SEP or MEP monitoring is not considered medically necessary for individuals who have undergone intra‐operative SEP or MEP monitoring.

Note: The NIM‐Spine System received 510(k) clearance from the Food and Drug Administration (FDA) in June

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2003. It offers 2 types of monitoring modalities: (i) electromyography, and (ii) MEP. Note on documentation requirements: The physician's SEP report should note which nerves were tested, latencies at various testing points, and an evaluation of whether the resulting values are normal or abnormal. See appendix for additional details on documentation requriements.

II. Visual evoked potentials (VEPs) are considered medically necessary for any of the following indications:

A. To diagnose and monitor multiple sclerosis (acute or chronic phases); or

B. To evaluate signs and symptoms of visual loss in persons who are unable to communicate (e.g., unresponsive persons, etc); or

C. To identify persons at increased risk for developing clinically definite multiple sclerosis (CDMS); or

D. To localize the cause of a visual field defect, not explained by lesions seen on CT or MRI, metabolic disorders, or infectious diseases. Standard or automated VEPs are considered experimental and investigational for routine screening of infants and other persons; evidence‐based guidelines from leading medical professional organizations and public health agencies have not recommended VEP screening of infants. VEPs are considered experimental and investigational for all other indications because their effectiveness for indications other than the ones listed above has not been established.

III. Brain stem auditory evoked response (BAER) ** is considered medically necessary for any of the following:

A. For cerebral vascular surgery; or B. For Chiari malformation surgery; or C. For intra‐operative monitoring during microvascular

decompression of cranial nerve when decompression is

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performed via the intra‐cranial posterior fossa approach; or

D. For intra‐operative monitoring during resection of chordoma , odontoidectomy, decompression of tumor from anterior brainstem/high spinal cord; or

E. To assess brain death or profound metabolic coma in selected cases where diagnosis or outcome is unclear from standard tests (e.g., EEG); or

F. To assess recovery of brainstem function after a lesion compressing the brainstem has been surgically removed; or

G. To diagnose and monitor demyelinating and degenerative diseases affecting the brain stem (e.g., central pontine myelinolysis, olivopontocerebellar (OPC) degeneration, etc.); or

H. To diagnose post‐meningitic deafness in children; or I. To diagnose suspected acoustic neuroma; or J. To evaluate infants and children who have suspected

hearing loss that can not be effectively measured or monitored through audiometry; or

K. To localize the cause of a central nervous system deficit seen on examination, but not explained by CT or MRI; or

L. To screen infants and children under age 5 for hearing loss. Note: For purposes of neonatal screening, only limited auditory evoked potentials or limited evoked otoacoustic emissions are considered medically necessary. Neonates who fail this screening test are then referred for comprehensive auditory evoked response testing or comprehensive otoacoustic emissions. Comprehensive auditory evoked response testing and comprehensive otoacoustic emissions are considered experimental and investigational for neonatal screening because there is a lack of evidence of the value of comprehensive testing over the limited auditory evoked potentials or limited otoacoustic emissions for this indication.

BAERs are considered experimental and investigational for all other indications because their effectiveness for

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indications other than the ones listed above has not been established.

** Also known as auditory evoked potentials (AEPs), brainstem auditory evoked potentials (BAEP), BERA, BSER, and BSRA.

Aetna considers the following studies and indications to be experimental and investigational because they have not been proven necessary to aid in diagnosis or alter the management of the member:

■ Auditory evoked potentials to determine gestational age or conceptual age in pre‐term neonates;

■ BAERs as a test to identify persons at increased risk for developing clinically definite multiple sclerosis (CDMS);

■ BAERs for syringomyelia and syringobulbia; ■ Cervical vestibular evoked myogenic potentials (cVEMP) for

evaluation of vestibular function specifically re lated to the saccule/utricle;

■ cVEMP for the diagnosis of benign paroxysmal positional vertigo, and vestibular neuritis;

■ Cognitive evoked potentials (also known as auditory or visual P300 or P3 cognitive evoked potentials) to diagnose cognitive dysfunction in persons with dementia (e.g., Alzheimer's disease and Parkinson's disease) or to identify the etiology of depression in persons with chronic demyelinating disease;

■ Cortical auditory evoked response (CAER) for the diagnosis of depression, attention deficit/hyperactivity disorder, autism, or any other indication;

■ Event‐related potentials for the diagnosis of attention deficit/hyperactivity disorder (see CPB 0426 ‐ Attention Deficit/Hyperactivity Disorder (../400_499/0426.html)) or post‐traumatic stress disorder, or assessment of amyotrophic lateral sclerosis, brain injury, or evaluation of comatose persons;

■ Evoked potential studies for Kennedy's syndrome/disease; ■ Gustatory evoked potentials for diagnosing taste disorders

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(see CPB 0390 ‐ Smell and Taste Disorders: Diagnosis (../300_399/0390.html));

■ Intraoperative BAER during stapedectomy, tympanoplasty and ossicle reconstruction;

■ Intraoperative MEP during implantation of a spinal cord stimulator;

■ Intraoperative neuromonitoring during adjustment of vertical expandable prosthetic titanium rib;

■ Intraoperative saphenous nerve somatosensory evoked potential for monitoring the femoral nerve during transpoas lumbar lateral interbody fusion;

■ Intraoperative SSEP of the facial nerve for submandibular gland excision or parotid gland surgery, during hip replacement surgery, implantation of a spinal cord stimulator, off‐pump coronary artery bypass surgery, and for thyroid surgery and parathyroid surgery (because they have not been proven necessary to aid in diagnosis or alter the management of individual undergoing surgical treatment);

■ Intraoperative SSEP, with or without MEPs, for cochlear implantation, decompression of the trigeminal nerve, implantation of vagus nerve stimulator, monitoring spinal injections (e.g., epidural injections, facet joint, interlaminar and transforminal epidural), open reduction internal fixation (ORIF) of the finger, radiofrequency ablation of facet medial branch, rotator cuff repair, or wrist arthroscopy repair;

■ Intraoperative visual evoked potentials (e.g., for pituitary surgery, during intra‐cranial surgery for arterio‐venous malformation);

■ Loudness dependence of auditory evoked potentials for monitoring of suicidal persons; Motor evoked potentials for evaluation of Wilson's disease; Motor evoked potentials other than for intraoperative use with SSEPs (e.g., facial MEPs during cerebellopontine angle and skull base tumor surgery);

Ocular vestibular evoked myogenic potentials (oVEMP) for the diagnosis of myasthenia gravis, or vestibular neuritis;

oVEMP for evaluation of vestibular function specifically

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related to the saccule/utricle;

■ SEPs for radiculopathies and peripheral nerve lesions where standard nerve conduction velocity studies are diagnostic (see CPB 0502 ‐ Nerve Conduction Velocity Studies (../500_599/0502.html));

■ SEPs for the diagnosis of carpal tunnel syndrome/ulnar nerve entrapment;

■ SEPs in conscious persons with severe spinal cord or head injuries (the standard neurologic examination is the most direct way to evaluate any deficits);

■ SEPs in diagnosis of cervical spondylytic myeloradiculopathy;

■ SEPs in the diagnosis of thoracic outlet syndrome;

■ SEPs in the diagnosis or management of acquired metabolic disorders (e.g., lead toxicity, B12 deficiency);

■ SEPs in the diagnosis or management of amyotrophic lateral sclerosis (ALS);

■ SEPs for pectus excavatum surgery; ■ SEPs for prostate surgery; ■ VEPs for detecting amnestic mild cognitive impairment; ■ VEPs for evaluation and monitoring of birdshot

chorioretinopathy; ■ VEPs for syringomyelia, syringobulbia, and evaluation of

vigabatrin (Sabril)‐associated retinal toxicity, screening Plaquenil (hydroxychloroquine) toxicity, as prognostic tests in neonates with perinatal asphyxia and hypoxic‐ischemic encephalopathy;

■ Vestibular evoked myogenic potentials (VEMP) (e.g., for diagnosis of Meniere's disease or delayed endolymphatic hydrops; differentiation of Meniere disease from vestibular migraine)

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Background

Evoked potentials measure conduction velocities of sensory pathways in the central nervous system using computerized averaging techniques. Three types of evoked potentials are routinely performed: (i) somatosensory; (ii) visual; and (iii) brainstem auditory In each of these tests a peripheral sense organ is electrically stimulated and conduction velocities are recorded for central somatosensory pathways located in the posterior columns of the spinal cord, brain stem, and thalamus, and the primary sensory cortex located in the parietal lobes. For patients with symptomatic nerve root compression, the accurate identification of the particular nerve root(s) that are causing symptoms is an essential prerequisite to surgical intervention. The history and physical examination may be helpful in identifying the particular peripheral nerve root that is affected, but these are often inconclusive. Patients often have difficulty defining the distribution of pain or sensory symptoms, and the physical examination may be completely normal even in patients with severe pain. Imaging studies may be helpful, but are frequently normal or reveal abnormalities of uncertain clinical relevance. Moreover, because structural abnormalities are commonly seen in imaging studies of normal asymptomatic middle‐aged or elderly subjects, it is difficult to determine whether any such abnormalities that are identified in pain patients are related to their symptoms. In addition, imaging studies may show equivocal changes or anatomic abnormalities at multiple levels, making it impossible to determine which nerve root is responsible for the patient's symptoms. In these circumstances, evoked potentials may be used to measure nerve root function and thereby more accurately identify the precise nerve roots responsible for the patient’s symptoms. Somatosensory evoked potentials (SEPs or SSEPs) (also known as cerebral sensory evoked potentials) augment the sensory examination and are most useful in assessing the spinal nerve roots, spinal cord, or brain stem for evidence of delayed nerve conduction. Dermatomal somatosensory evoked potentials (DSEPs) are elicited by stimulating the skin "signature" areas of specific nerve roots. Both techniques involve production and

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recording of small electrophysiological responses of the central nervous system that follow sequential electrical stimulation of peripheral nerves. These small electrophysiological responses are extracted from the background noise of electroencephalography (EEG), usually by signal averaging techniques. Delays in signal propagation suggest lesions of the central sensory pathways. Although controversial, evoked potentials have been used to assess the prognosis of children with spinal cord lesions, brain malformations, and neurodegenerative diseases, as well as young children who are at risk for brain injury, such as preterm infants. Somatosensory evoked potentials measurements have been used to predict outcome in spinal cord injury; however, signal changes on MRI actually may be more useful in determining the severity of injury. Hemorrhage within the spinal cord is readily identified on MRI, and such hemorrhage is predictive of injury severity. Intra‐operative SSEP measurements are useful in complex neurologic, orthopedic, and vascular surgical procedures as a means of gauging nerve injury during surgery (e.g., resection of cord tumors).

Somatosensory evoked potentials are altered by conditions that affect the somatosensory pathways, including both focal lesions (such as strokes, tumors, cervical spondylosis, syringomyelia) and diffuse diseases (such as hereditary systemic neurologic degeneration, subacute combined degeneration, and vitamin E deficiencies).

Somatosensory evoked potentials may detect clinically silent brain lesions in multiple sclerosis suspects. Although SEP abnormalities alone are insufficient to establish the diagnosis of multiple sclerosis, the diagnosis can be established when there is also other objective findings (brain plaques on MRI, clinical lesions by history and physical examination, and/or positive CSF (determined by oligoclonal bands detected by established methods (isoelectric focusing) different from any such bands in serum, or by an increased IgG index)).

Fifty to 60 % of multiple sclerosis patients have other

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concurrent demyelinating lesions that may not be clinically evident, and SSEP may be helpful in documenting these abnormalities. Somatosensory evoked potentials abnormalities are also produced by other diseases affecting myelin (adrenoleukodystrophy and adrenomyelo‐neuropathy, metachromatic leukodystrophy, Pelizaeus‐Merzbacher disease). In adrenoleukodystrophy and adrenomyeloneuropathy, SSEP abnormalities may be present in asymptomatic heterozygotes. Abnormally large amplitude SEPs, reflecting enhanced cortical excitability, are seen in progressive myoclonus epilepsy, in some patients with photosensitive epilepsy, and in late infantile ceroid lipofuscinosis.

Studies have demonstrated a statistically significant association between abnormal visual evoked potentials (VEPs) and an increased risk of developing clinically definite multiple sclerosis (CDMS). In these studies, patients with suspected MS were 2.5 to 9 times as likely to develop CDMS as patients with normal VEPs. Visual evoked potentials sensitivities ranged from 25 % to 83 %. Visual evoked potentials improved the ability to predict which MS suspects will develop CDMS by as much as 29 %.

Measurement of visual evoked responses (VERs) is the primary means of objectively testing vision in infants and young children suspected of having disorders of the visual system, where the child is too young to report differences in color vision or to undergo assessment of visual fields and visual acuity. A flashing stroboscope or an alternating checkerboard pattern is presented and the wave patterns are recorded. In an infant, vision may be reliably tested using a flashing light during quiet sleep. Lesions affecting the visual pathways can be localized by noting the presence of decreased amplitudes or increased latencies of VERs, and by determining whether VER abnormalities involve one or both eyes. Visual evoked responses are also useful for testing vision in other persons who are not able to communicate.

Brain stem auditory evoked responses (BAERs) are electrical

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potentials that are produced in response to an auditory stimulus and are recorded from disk electrodes attached to the scalp. Depending on the amount of time elapsed between the "click" stimulus and the auditory evoked response, potentials are classified as early (0 to 10 msec), middle (11 to 50 msec), or late (51 to 500 msec). The early potentials reflect electrical activity at the cochlea, 8th cranial nerve, and brain stem levels; the latter potentials reflect cortical activity. In order to separate evoked potentials from background noise, a computer averages the auditory evoked responses to 1,000 to 2,000 clicks. Early evoked responses may be analyzed to estimate the magnitude of hearing loss and to differentiate among cochlea, 8th nerve, and brainstem lesions.

The clinical utility of BAER over standard auditory testing is due to several of BAER's characteristics: (i) BAER's resistance to alteration by systemic metabolic abnormalities, medications or pronounced changes in the state of consciousness of the patient; and (ii) the close association of BAER waveform abnormalities to underlying structural pathology. Brain stem auditory evoked responses have been proven effective for differentiating conductive from sensory hearing loss, for detecting tumors and other disease states affecting central auditory pathways (e.g., acoustic neuromas), and for noninvasively detecting hearing loss in patients who can not cooperate with subjective auditory testing (e.g., infants, comatose patients). BAER is the test of choice to assess hearing in infants and young children. It is most useful for following asphyxia, hyperbilirubinemia, intracranial hemorrhage, or meningoencephalitis or for assessing an infant who has trisomy. BAER also is useful in the assessment of multiple sclerosis or other demyelinating conditions, coma, or hysteria. Audiometric analysis using multiple sound frequencies is usually preferred over BAER for testing hearing in cooperative patients who are able to report when sounds are heard. Evidence is insufficient at this time to recommend BAER as a useful test to identify patients at increased risk for developing CDMS.

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Studies of cognitive evoked potentials (also known as the P300 or P3 cognitive evoked potentials) have been used in research settings to correlate changes in cognitive evoked potentials with clinical changes in cognitive function in patients with dementia (e.g., Alzheimer's disease and Parkinson's disease) and identify the etiology of depression in patients with chronic demyelinating disease. However, there is insufficient evidence regarding the effectiveness of cognitive evoked potential studies in diagnosing or rendering treatment decisions that would affect health outcomes. Furthermore, there is a lack of studies comparing cognitive evoked potential studies with standard neuropsychiatric and psychometric tests used in diagnosing cognitive dysfunction.

The American Academy of Pediatrics (AAP) Task Force on Newborn and Infant Hearing and the Joint Committee on Infant Hearing (JCIH) endorse the implementation of universal newborn hearing screening. Screening should be conducted before discharge from the hospital whenever possible. Physicians should provide recommended hearing screening, not only during early infancy but also through early childhood for those children at risk for hearing loss (e.g., history of trauma, meningitis) and for those demonstrating clinical signs of possible hearing loss.

The U.S. Preventive Services Task Force (USPSTF) recommends screening for hearing loss in all newborn infants. All infants should be screened before 1 month of age. Those infants who do not pass the newborn screening should undergo audiologic and medical evaluation before 3 months of age for confirmatory testing. Because of the elevated risk of hearing loss in infants with risk indicators (e.g., neonatal intensive care unit admission for 2 or more days; syndromes associated with hearing loss, such as Usher syndrome and Waardenburg syndrome; family history of hereditary childhood hearing loss; craniofacial abnormalities; and congenital infections such as cytomegalovirus, toxoplasmosis, bacterial meningitis, syphilis, herpes, and rubella), an expert panel recommends that these children undergo periodic monitoring for 3 years. The USPSTF

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found good evidence that newborn hearing screening leads to earlier identification and treatment of infants with hearing loss and improves language outcomes. However, additional studies detailing the correlation between childhood language scores and functional outcomes (e.g., school attainment and social functioning) are needed.

Two types of tests are commonly used to screen for congenital hearing loss: (i) otoacoustic emissions (OAEs) and (ii) auditory brainstem response (ABR) (Helfand et al, 2001). Otoacoustic emissions testing evaluates the integrity of the inner ear (cochlea). In response to noise, vibrations of the hair cells in a healthy inner ear generate electrical responses, known as otoacoustic emissions. The absence of OAEs indicates that the inner ear is not responding appropriately to sound. Transient evoked otoacoustic emissions (TEOAEs) are generated in response to wide‐band clicks, while distortion product otoacoustic emissions (DPOAE) are a response to tones. Both stimuli are presented via a light‐weight ear canal probe. A microphone picks up the signal, and multiple responses are averaged to get a specific repeatable waveform. Otoacoustic emissions are used in screening and diagnosis of hearing impairments in infants, and in young children and patients with cognitive impairments (e.g., mental retardation, dementia) who are unable to respond reliably to standard hearing tests. Otoacoustic emissions are also useful for evaluating patients with tinnitus, suspected malingering, and for monitoring cochlear damage from ototoxic drugs.

The ABR is an electrophysiological response generated in the brainstem in response to auditory signals and composed of either clicks or tones. The stimulus is delivered via earphones or an inserted ear probe, and scalp electrodes pick up the signal. Auditory brainstem response evaluates the integrity of the peripheral auditory system and the auditory nerve pathways up to the brainstem and is able to identify infants with normal cochlear function but abnormal 8th‐nerve function (auditory neuropathy). For purposes of neonatal screening, a limited ABR is performed in the nursery using a significantly low

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intensity level (35 to 40 dB) to rule out marked hearing loss (Schwartz and Schwartz, 1990; Scott and Bhattacharyya, 2002). If testing at this level fails to elicit a response, the infant is referred to an audiologic laboratory for a comprehensive ABR, involving testing at many different intensity levels.

Typically, screening programs use a 2‐stage screening approach (either OAE repeated twice, OAE followed by ABR, or ABR repeated twice). Criteria for defining a "pass" or "fail" on the initial screening test vary widely. Comprehensive (diagnostic) OAEs or ABRs are used to diagnose hearing impairments identified by limited (screening) tests.

Auditory brainstem response and OAE have limitations that affect their accuracy in certain patients. Both require a sleeping or quiet child. Middle‐ear effusion or debris in the external canal can compromise the accuracy of these tests. Otoacoustic emissions and ABR test the peripheral auditory system and 8th nerve pathway to the brainstem, respectively. They are not designed to identify infants with central hearing deficits. Therefore, infants with risk factors for central hearing deficits, particularly those who have congenital Cytomegalovirus infection or prolonged severe hypoxia at birth, may pass their newborn hearing screens with either OAE or ABR, but develop profound hearing loss in early infancy.

The newer generation of automated screeners are easy to use and do not require highly trained staff. However, equipping hospitals with equipment and sufficient staff can be costly, the staff must be trained to understand the limitations of the techniques, and ongoing quality control is essential to achieve accurate, consistent test results. The importance of technique is illustrated by the results of multicenter studies of universal screening, in which the rates of false positive and technically inadequate examinations varied 10‐fold among sites.

There are differences between the guidelines with respect to the screening technology that is endorsed. The Joint Committee on Infant Hearing recommends that all infants have

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access to screening using a physiologic measure (either otoacoustic emissions [TEOAE or DPOAE] and/or ABR). The AAPstates that although additional research is necessary to determine which screening test is ideal, EOAE and/or ABR are presently the screening methods of choice. The AAP defers recommending a preferred screening test. The USPSTF recommends a 1‐ or 2‐step validated protocol, stating that OAEs followed by ABR in those who failed the first test is a frequently used protocol. Well‐maintained equipment, thoroughly trained staff, and quality control programs are also recommended to avoid false‐positive tests.

Cortical auditory evoked responses (CAERs) measure the later‐occurring auditory evoked potentials reflecting cortical activity in response to an auditory stimulus (UBC, 2005). Cortical auditory evoked responses have a long latency, compared to the short latency auditory evoked responses; they have been used in clinical research to evaluate the timing, sequence, strength, and anatomic location of brain processes involved with the perception of sounds. Current research underway concerns the use of CAERs to understand the brain processes underlying basic hearing percepts such as loudness, pitch, and localisation, as well as those processes involved with speech perception (UBC, 2005).

Vestibular evoked myogenic potentials (VEMP), also known as click evoked neurogenic vestibular potentials, are presumed to originate in the saccule. They are recorded from surface electrodes over the sternocleidomastoid muscles, and can be activated by means of brief, high‐intensity acoustic stimuli. Papathanasiou et al (2003) stated that VEMP testing is a possible new diagnostic technique that may be specific for the vestibular pathway. It has potential use in patients with symptoms of dizziness, sub‐clinical symptoms in multiple sclerosis, and in disorders specific for the vestibular nerve. There is a lack of reliable evidence from well controlled, prospective studies demonstrating that VEMP testing alters management such that clinical outcomes are improved. Current evidence‐based guidelines on the

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management of neurological disorders from leading medical professional organizations have not incorporated VEMP testing in diagnostic and treatment algorithms. The American Academy of Neurology considered VEMP as an investigational technique (Fife et al, 2000). Guidelines prepared for the State of Colorado (DLE, 2006) state that VEMP "is currently a research tool and is not recommended for routine clinical use." In a review of the literature, Rauch (2006) states that VEMP holds great promise for diagnosing and monitoring Ménière's disease and some other neurotologic disorders. Rauch notes, however, that the methods, equipment, and applications for vestibular evoked myogenic potential testing are not yet standardized, and many aspects of vestibular evoked myogenic potential and its use have not yet been adequately studied or described.

Brantberg et al (2007) studied VEMP in response to sound stimulation (500 Hz tone burst, 129 dB SPL) in 1,000 consecutive patients. Vestibular evoked myogenic potentials from the ear with the larger amplitude were evaluated based on the assumption that the majority of the tested patients probably had normal vestibular function in that ear. Patients with known bilateral conductive hearing loss, with known bilateral vestibular disease and those with Tullio phenomenon were not included in the evaluation. It was found that there was an age‐related decrease in VEMP amplitude and an increase in VEMP latency that appeared to be rather constant throughout the whole age span. Vestibular evoked myogenic potentials data were also compared to an additional group of 10 patients with Tullio phenomenon. Although these 10 patients did have rather large VEMP, equally large VEMP amplitudes were observed in a proportion of unaffected subjects of a similar age group. Thus, the findings of a large VEMP amplitude in response to a high‐intensity sound stimulation is not, per se, distinctive for a significant vestibular hypersensitivity to sounds.

Muyts et al (2007) provided an overview of vestibular function testing and highlights the new techniques that have emerged during the past 5 years. Since the introduction of video­

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oculography as an alternative to electro‐oculography for the assessment of vestibular‐induced eye movements, the investigation of the utricle has become a part of vestibular function testing, using unilateral centrifugation. Vestibular evoked myogenic potentials have become an important test for assessing saccular function, although further standardization and methodological issues remain to be clarified. Galvanic stimulation of the labyrinth also is an evolving test that may become useful diagnostically. The authors concluded that a basic vestibular function testing battery that includes ocular motor tests, caloric testing, positional testing, and earth‐vertical axis rotational testing focuses on the horizontal semicircular canal. Newer methods to investigate the otolith organs are being developed. These new tests, when combined with standard testing, will provide a more comprehensive assessment of the complex vestibular organ.

Magnetic stimulation of the brain and spine elicits so‐called motor evoked potentials (MEPs) (Goetz, 2005). The latency of the motor responses can be measured, and central conduction time can be estimated by comparing the latency of the responses elicited by cerebral and spinal stimulation. Abnormalities have been described in patients with a variety of central disorders including multiple sclerosis, amyotrophic lateral sclerosis, stroke, and certain degenerative disorders. An assessment by the McGill University Health Centre on use of intraoperative neurophysiological monitoring during spinal surgery stated that there is sufficient evidence to support the conclusion that intraoperative spinal monitoring using SSEPs and MEPs during surgical procedures that involve risk of spinal cord injury is an effective procedure that is capable of substantially diminishing this risk (Erickson et al, 2005). The report explained that intra‐operative spinal cord injury during spinal surgery generally compromises both motor and somatosensory pathways; therefore the use of both of these independent techniques in parallel has been proposed and is seen as a safeguard should one of the monitoring techniques fail. Combination of SSEP monitoring with MEP monitoring is also proposed to reduce false‐positive results, and eliminate the

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need for the wake‐up test. The assessment identified 11 studies, all case series, of the combined use of SSEPs and MEPs in neurophysiological monitoring during spinal surgery. The assessment found that, in several reports, combined SSEP and MEP monitoring was shown to have greater sensitivity than SSEP alone. The report also noted that the addition of MEP monitoring where SSEP monitoring is already being performed is considered to be relatively straightforward, adding little to the overall effort and resources employed in intraoperative neurophysiological monitoring.

A study by Schwarz et al (2007) illustrated the advantage of intraoperative monitoring of spinal cord motor tracts directly by recording motor evoked potentials in addition to somatosensory evoked potentials. Investigators reviewed the intraoperative neurophysiological monitoring records of 1121 consecutive patients (834 female and 287 male) with adolescent idiopathic scoliosis (mean age, 13.9 years) treated between 2000 and 2004 at four pediatric spine centers. The same group of experienced surgical neurophysiologists monitored spinal cord function in all patients with use of a standardized multimodality technique with the patient under total intravenous anesthesia. A relevant neurophysiological change (an alert) was defined as a reduction in amplitude (unilateral or bilateral) of at least 50% for somatosensory evoked potentials and at least 65% for transcranial electric motor evoked potentials compared with baseline. The investigators reported that 38 (3.4%) of the 1121 patients had recordings that met the criteria for a relevant signal change (i.e., an alert). Of those 38 patients, 17 showed suppression of the amplitude of motor evoked potentials in excess of 65% without any evidence of changes in somatosensory evoked potentials. In nine of the 38 patients, the signal change was related to hypotension and was corrected with augmentation of the blood pressure. The remaining 29 patients had an alert that was related directly to a surgical maneuver. Three alerts occurred following segmental vessel clamping, and the remaining 26 were related to posterior instrumentation and correction. Nine (35%) of these 26 with an instrumentation­

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related alert, or 0.8% of the cohort, awoke with a transient motor and/or sensory deficit. Seven of these nine patients presented solely with a motor deficit, which was detected by intraoperative monitoring of motor evoked potentials in all cases, and two patients had only sensory symptoms. The investigators reported that somatosensory evoked potential monitoring failed to identify a motor deficit in four of the seven patients with a confirmed motor deficit. Furthermore, when changes in somatosensory evoked potentials occurred, they lagged behind the changes in transcranial electric motor evoked potentials by an average of approximately five minutes. With an appropriate response to the alert, the motor or sensory deficit resolved in all nine patients within one to 90 days.

The clinical utility of MEPs outside of the operative setting, however, is unclear and at the present time the magnetic stimulation of central structures is regarded as investigational (Goetz, 2003; Miller, 2005).

In a prospective consecutive case series study, Lee et al (2009) evaluated the side effects of microvascular decompression (MVD) on hearing and described the main intra‐operative ABR changes. The study included 22 patients who underwent MVD with monitoring of ABRs. The latency prolongation and wave loss were analyzed at each surgical step, which were decided arbitrarily. Patients were divided into 4 groups depending on degree of change of wave V. Group 1 consisted of minimal change, whereas group 4 was permanent loss of wave V. Hearing changes were evaluated in 20 patients in the 4 groups who were available for post‐operative hearing results. Loss of wave I, III, and V occurred with 6 %, 13 %, and 9 % of surgical actions, respectively. Wave III disappearance was identified as the earliest and most sensitive sign and was usually preceded by the disappearance of wave V. The greatest prolongation of wave V at more than 1.0 ms developed statistically significant sensorineural hearing loss in the range of 10 dB. One patient in group 4 experienced deafness. The authors concluded that in addition to the significant delay of wave V, useful recognition of early changes of wave III is possible and enables a change of

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microsurgical maneuvers to favor ABR recovery.

Polo and Fischer (2009) stated that BAEP monitoring is a useful tool to decrease the danger of hearing loss during pontocerebellar angle surgery, particularly in MVD. Critical complications arising during MVD surgery are the stretching of the VIII nerve ‐‐ the main cause of hearing loss ‐‐ labyrinthine artery manipulation, direct trauma with instruments, or a nearby coagulation, and at end of the surgery neocompression of the cochlear nerve by the prosthesis positioned between the conflicting vessel(s) and the VIIth‐VIIIth nerve complex. All these dangers warrant the use of BAEP monitoring during the surgical team's training period. Based on delay in latency of peak V, these investigators established warning thresholds that can provide useful feedback to the surgeon to modify the surgical strategy: the initial signal at 0.4 ms is considered the safety limit. A second signal threshold at 0.6 ms (warning signal for risk) corresponds to the group of patients without resultant hearing loss. The third threshold characterized by the delay of peak V is at 1 ms (warning signal for a potentially critical situation). BAEP monitoring provides the surgeon with information on the functional state of the auditory pathways and should help avoid or correct maneuvers that can harm hearing function. BAEP monitoring during VIIth‐VIIIth complex surgery, particularly in MVD of facial nerves for hemifacial spasm (HFS) is very useful during the learning period.

Huang and colleagues (2009) determined the reliability of: (i) intra‐operative monitoring by stimulated electromyography (EMG) of the facial nerve to predict the completeness of MVD for HFS, and (ii) BAEP to predict post‐operative hearing disturbance. These investigators conducted a prospective study of 36 patients who received MVD for HFS. They confirmed the disappearance of an abnormal muscle response in the facial nerve EMG to predict the completeness of MVD, and performed BAEP monitoring to predict post‐operative hearing disturbance. The sensitivity, specificity and accuracy of facial nerve EMG and BAEP monitoring were evaluated. The sensitivity, specificity and accuracy of facial nerve EMG were

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1.977, 1.0 and 0.97, respectively, and that for BAEP monitoring were 1.0, 0.94 and 0.94, respectively. There was 1 false‐positive result for facial nerve EMG, and 2 false‐positive results for BAEP monitoring. No false‐negative result was encountered for either EMG or BAEP monitoring. Facial nerve EMG correctly predicted whether MVD was successful in 35 out of 36 patients, and BAEP correctly predicted whether there was post‐operative hearing disturbance in 34 out of 36 patients. The authors concluded that intra‐operative facial nerve EMG provides a real‐time indicator of successful MVD during an operation while BAEP monitoring may provide an early warning of hearing disturbance after MVD.

In a systematic review, Fehlings et al (2010) examined if intra‐operative monitoring (IOM) is able to sensitively and specifically detect intra‐operative neurological injury during spine surgery and to assess whether IOM results in improved outcomes for patients during these procedures. Two independent reviewers assessed the level of evidence quality using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) criteria, and disagreements were resolved by consensus. A total of 103 articles were initially screened and 32 ultimately met the pre‐determined inclusion criteria. These researchers determined that there is a high level of evidence that multi‐modal (SSEP and MEP) IOM is sensitive and specific for detecting intra‐operative neurological injury during spine surgery. On the other hand, there is very low evidence from the literature that uni‐modal SSEPS or MEPs are valid diagnostic tests for measuring intra‐operative neurological injury. There is a low level of evidence that IOM reduces the rate of new or worsened peri‐operative neurological deficits (a grade of "low" means that further research is very likely to have an important impact on the confidence in the estimate of effect and is likely to change the estimate). There is very low evidence that an intra‐operative response to a neuromonitoring alert reduces the rate of peri‐operative neurological deterioration (a grade of "very low" means that any estimate of effect is very uncertain). The authors concluded that based on strong evidence that multi‐modality intra‐operative neuromonitoring is sensitive and

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specific for detecting intra‐operative neurological injury during spine surgery, it is recommended that the use of multi‐modality intra‐operative neuromonitoring be considered in spine surgery where the spinal cord or nerve roots are deemed to be at risk, including procedures involving deformity correction and procedures that require the placement of instrumentation. Furthermore, they stated that there is a need to develop evidence‐based protocols to deal with intra‐operative changes in multi‐modality intra‐operative neuromonitoring and to validate these prospectively. Intra‐operative EMG monitoring was not recommended as a means of neurophysiological monitoring during spinal surgery.

Balzer et al (1998) reported on the results of a descriptive case series of the use of somatosensory evoked potentials during lumbrosacral spine surgery. SSEPs and EMG activity were simultaneously recorded for 44 patients who underwent surgical procedures to decompress and stabilize the lumbosacral spine, using pedicle screw instrumentation. Indications included degenerative spondylolisthesis (22), pars fracture with spondylolisthesis (9), failed back syndrome (7), burst/compression fracture (4), and instability from metastasis (2). The specific level of the lumbar spine for each procedure included in this series was not reported. All neurosurgical procedures were performed by a single surgeon. The authors reported that, in two cases, changes in SSEPs and spontaneous EMG activity were noted and were correlated with postoperative patient complaints.

Rothstein (2009) stated that the early recognition of comatose patients with a hopeless prognosis ‐‐ regardless of how aggressively they are managed ‐‐ is of utmost importance. Median SSEP supplement and enhance neurological examination findings in anoxic‐ischemic coma and are useful as an early guide in predicting outcome. The key finding is that bilateral absence of cortical evoked potentials reliably predicts unfavorable outcome in comatose patients after cardiac arrest. The author studied 50 comatose patients with preserved brainstem function after cardiac arrest. All 23 patients with

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bilateral absence of cortical evoked potentials died without awakening. Neuropathological study in 7 patients disclosed widespread ischemic changes or frank cortical laminar necrosis. The remaining 27 patients with normal or delayed central conduction times had an uncertain prognosis because some died without awakening or entered a persistent vegetative state. The majority of patients with normal central conduction times had a good outcome, whereas a delay in central conduction times increased the likelihood of neurological deficit or death. Greater use of SSEP in anoxic­ischemic coma would identify those patients unlikely to recover and would avoid costly medical care that is to no avail.

An UpToDate review on "Hypoxic‐ischemic brain injury: Evaluation and prognosis" (Weinhouse and Young, 2012) states that several ancillary tests have been studied in the period after anoxic injury; these are often helpful at arriving at an earlier prognostic determination than would be possible with clinical testing alone. Somatosensory evoked potentials are the averaged electrical responses in the central nervous system to somatosensory stimulation. Bilateral absence of the N20 component of the SSEP with median nerve stimulation at the wrist in the 1st week (usually between 24 and 72 hours) from the arrest has a pooled likelihood ratio of 12.0 (95 % confidence interval [CI]: 5.3 to 26.6) and a false‐positive rate of zero % for an outcome no better than persistent vegetative state. Repeated testing should be considered when the N20 responses are present in the first 2 to 3 days from the cardiac arrest, as they may later disappear. The clinical operating characteristics of other evoked potentials (brainstem, auditory, visual, middle latency, and event‐related) have not been adequately evaluated. Somatosensory evoked potentials are the best validated and most reliable of the ancillary tests currently available for clinical use.

The Quality Standards Subcommittee of the American Academy of Neurology's Practice Parameter on "Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence‐based review)" (Wijdicks et al, 2006) recommended

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the assessment of poor prognosis can be guided by the bilateral absence of cortical SSEPs (N20 response) within 1 to 3 days (recommendation level B).

Raggi et al (2010) noted that amyotrophic lateral sclerosis (ALS) is increasingly recognized to be a multi‐system disease, involving associative areas in addition to the motor cortex and therefore affecting cognition. Patients with ALS may present with subtle behavioral and executive dysfunctions or, less frequently, with a manifest fronto‐temporal dementia. Event‐related potentials (ERPs) are a high‐temporal resolution technique, which can be used to explore the presence of cognitive dysfunction. All the primary studies reviewed here have shown ERP abnormalities in groups of non‐demented patients affected by sporadic ALS compared to healthy controls. The ERP results support findings of neuropsychological and imaging studies. The authors concluded that prospective studies combining simultaneous neuropsychological and imaging investigations are needed to assess the possible role of ERPs in the early detection and follow‐up of cognitive dysfunction in ALS patients.

The U.S. Preventive Services Task Force (USPSTF) has not recommended vision screening of infants and young children. The 2011 USPSTF recommendation does not support vision screening for children less than 3 years of age, as it concludes that the current evidence is insufficient to assess the balance of benefits and harms to this subpopulation. This position is consistent with the current recommendations of the American Academy of Ophthalmology and the American Association for Pediatric Ophthalmology and Strabismus and other professional organizations.

In a review on "Facial nerve monitoring during cerebellopontine angle and skull base tumor surgery", Acioly et al (2013) stated that intraoperative neuromonitoring has been established as one of the methods by which modern neurosurgery can improve surgical results while reducing morbidity. Despite routine use of intraoperative facial nerve (FN) monitoring, FN

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injury still is a complication of major concern due to severe negative impact on patient's quality of life. Through searches of PubMed, these investigators provided a systematic review of the current literature up to February, 2011, emphasizing all respects of FN monitoring for cerebellopontine angle and skull base tumor surgery from description to current success on function prediction of standard and emerging monitoring techniques. Currently, standard monitoring techniques comprise direct electrical stimulation (DES), free‐running electromyography (EMG), and facial motor evoked potential (FMEP). These researchers included 62 studies on function prediction by investigating DES (43 studies), free‐running EMG (13 studies), and FMEP (6 studies) criteria. DES mostly evaluated post‐operative function by using absolute amplitude, stimulation threshold, and proximal‐to‐distal amplitude ratio, whereas free‐running EMG used the train‐time criterion. The prognostic significance of FMEP was assessed with the final‐to­baseline amplitude ratio, as well as the event‐to‐baseline amplitude ratio and waveform complexity. The authors concluded that although there is a general agreement on the satisfactory functional prediction of different electrophysiological criteria, the lack of standardization in electrode montage and stimulation parameters precludes a definite conclusion regarding the best method. Moreover, studies emphasizing comparison between criteria or even multi‐modal monitoring and its impact on FN anatomical and functional preservation are still lacking in the literature.

Mauguiere et al (1997) examined if abnormalities of central conduction could be detected prospectively in patients with epilepsy treated with vigabatrin (VGB) as long‐term add‐on medication. A total of 201 patients with refractory partial epilepsy were enrolled and monitored for as long as 2 years. Vigabatrin was added to the treatment at an average dose of 2 to 3g/day. Conduction in somatosensory and visual pathways was assessed by median nerve SEP and pattern VEP recordings performed at inclusion and once every 6 months. The upper limit and test‐retest variability of EP latencies were evaluated at time of enrollment in the patient group. Prolonged N13‐N20 or

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P14‐N20 SEP intervals and P100 VEP latency greater than 2.5 SD above the baseline mean, observed on repeated runs in the same session and exceeding the test‐retest variability at enrollment were considered to indicate central conduction slowing. A total of 109 patients completed the 2‐year study period, and 92 discontinued VGB, of whom 37 were monitored with regard to EP until the end of the study. No consistent change in SEP or VEP was observed in the entire group during VGB treatment. The number of occasional EP values outside the baseline range in patients treated with VGB similar to that in patients whose VGB treatment had been discontinued. The authors concluded that they detected no evidence of changes in SEP and VEP attributable to altered neuronal conduction in the CNS during long‐term VGB treatment.

Zgorzalewicz and Galas‐Zgorzalewicz (2000) estimated the effects of VGB as add‐on therapy on VEP and BAEP. The investigation covered 100 epileptic patients from 8 to 18 years of age. The treatment included therapy with carbamazepine (CBZ) or valproate acid (VPA) using slow release formulations of these anti‐epileptic drugs (AEDs). Combination therapy was administered using add‐on VGB in the recommended dose 57.4 +/‐ 26.5 mg/kg body weight/day. VEP and BAEP were recorded by means of Multiliner (Toennies, Germany). The obtained values were compared with age‐matched control group. Compared to control groups, significant differences in epileptic groups emerged in latencies of the peak III, V along with the inter‐peak intervals I‐III of BAEP. Also VEP studies showed the reduction of N75/P100 and P100/N145 amplitudes. The authors concluded that adding VGB did not significantly increase the percentage of pathological abnormalities observed from EPs.

In a prospective cohort study, Zuniga et al (2012) characterized both cervical and ocular vestibular‐evoked myogenic potential (cVEMP, oVEMP) responses to air‐conducted sound (ACS) and midline taps in Meniere disease (MD), vestibular migraine (VM), and controls, and determined if cVEMP or oVEMP responses can differentiate MD from VM. Unilateral definite MD patients

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(n = 20), VM patients (n = 21) by modified Neuhauser criteria, and age‐matched controls (n = 28) were included in this study; cVEMP testing used ACS (clicks), and oVEMP testing used ACS (clicks and 500‐Hz tone bursts) and midline tap stimuli (reflex hammer and Mini‐Shaker). Outcome parameters were cVEMP peak‐to‐peak amplitudes and oVEMP n10 amplitudes. Relative to controls, MD and VM groups both showed reduced click‐evoked cVEMP (p < 0.001) and oVEMP (p < 0.001) amplitudes. Only the MD group showed reduction in tone‐evoked amplitudes for oVEMP. Tone‐evoked oVEMPs differentiated MD from controls (p = 0.001) and from VM (p = 0.007). The oVEMPs in response to the reflex hammer and Mini‐Shaker midline taps showed no differences between groups (p > 0.210). The authors concluded that using these techniques, VM and MD behaved similarly on most of the VEMP test battery. A link in their pathophysiology may be responsible for these responses. The data suggested a difference in 500‐Hz tone burst‐evoked oVEMP responses between MD and MV as a group. However, no VEMP test that was investigated in segregated individuals with MD from those with VM.

Heravian et al (2011) assessed the usefulness of color vision, photo stress recovery time (PSRT), and VEP in early detection of ocular toxicity of hydroxychloroquine (HCQ), in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). A total of 86 patients were included in the study and divided into 3 groups: with history of HCQ use: interventional 1 (Int.1) without fundoscopic changes and Int.2 with fundoscopic changes; and without history of HCQ use, as control. Visual field, color vision, PSRT and VEP results were recorded for all patients and the effect of age, disease duration, treatment duration and cumulative dose of HCQ on each test was assessed in each group. There was a significant relationship among PSRT and age, treatment duration, cumulative dose of HCQ and disease duration (p < 0.001 for all). Color vision was normal in all the cases. P100 amplitude was not different between the 3 groups (p = 0.846), but P100 latency was significantly different (p = 0.025) and for Int.2 it was greater than the others. The percentage of abnormal visual fields for

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Int.2 was more than Int.1 and control groups (p = 0.002 and p = 0.005, respectively), but Int.1 and control groups were not significantly different (p > 0.50). In the early stages of maculopathy, P100 latencies of VEP and PSRT are useful predictors of HCQ ocular toxicity. In patients without ocular symptoms and fundoscopic changes, the P100 latency of VEP predicts more precisely than the others.

Current guidelines from the American Academy of Ophthalmology do not recommend visual evoked potentials for screening or diagnosis of hydroxychloroquine toxicity (Marmor, et al., 2011; Karmel, 2011; Scechtman and Karpecki, 2011). Shechtman and Karpecki (2011) noted that the 2011 testing guidelines for patients on Plaquenil listed: (i) dilated fundus examination, (ii) automated 10‐2 VF, (iii) spectral domain optical coherence tomography (SD‐OCT), fundus autofluorescence (FAF) or multi‐focal electroretinography (mfERG) (if available), and (iv) photography as screening tests. Visual evoked potentials were not mentioned as a screening tool. Furthermore, the screening guidelines on “Hydroxychloroquine toxicity” by Schwartz and Mieler (2011) did not mention the use of VEP. An UpToDate Drug Information on “Hydroxychloroquine” notes that “Ophthalmologic exam at baseline and every 3 months during prolonged therapy (including visual acuity, slit‐lamp, fundoscopic, and visual field exam); muscle strength (especially proximal, as a symptom of neuromyopathy) during long‐term therapy”. Visual evoked potentials were not mentioned as a screening tool. Also, an UpToDate review on “Antimalarial drugs in the treatment of rheumatic disease” (Wallace, 2013) does not mention the use of VEPs.

In a systematic review, van Laerhoven et al (2013) examined the prognostic value of currently used clinical tests in neonatal patients with perinatal asphyxia and hypoxic‐ischemic encephalopathy (HIE). Searches were made on MedLine, Embase, Central, and CINAHL for studies occurring between January 1980 and November 2011. Studies were included if they: (i) evaluated outcome in term infants with perinatal

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asphyxia and HIE, (ii) evaluated prognostic tests, and (iii) reported outcome at a minimal follow‐up age of 18 months. Study selection, assessment of methodological quality, and data extraction were performed by 3 independent reviewers. Pooled sensitivities and specificities of investigated tests were calculated when possible. Of the 259 relevant studies, 29 were included describing 13 prognostic tests conducted 1,631 times in 1,306 term neonates. A considerable heterogeneity was noted in test performance, cut‐off values, and outcome measures. The most promising tests were amplitude‐integrated electroencephalography (sensitivity 0.93, [95 % CI: 0.78 to 0.98]; specificity 0.90 [0.60 to 0.98]), EEG (sensitivity 0.92 [0.66 to 0.99]; specificity 0.83 [0.64 to 0.93]), and VEPs (sensitivity 0.90 [0.74 to 0.97]; specificity 0.92 [0.68 to 0.98]). In imaging, diffusion weighted MRI performed best on specificity (0.89 [0.62 to 0.98]) and T1/T2‐weighted MRI performed best on sensitivity (0.98 [0.80 to 1.00]). Magnetic resonance spectroscopy demonstrated a sensitivity of 0.75 (0.26 to 0.96) with poor specificity (0.58 [0.23 to 0.87]). The authors concluded that this evidence suggested an important role for amplitude‐integrated electroencephalography, EEG, VEPs, and diffusion weighted and conventional MRI. Moreover, they stated that given the heterogeneity in the tests' performance and outcomes studied, well‐designed, large prospective studies are needed.

In a retrospective analysis of a case series, Silverstein et al (2014) described a novel technique to monitor femoral nerve function by analyzing the saphenous nerve SSEP during transpsoas surgical exposures of the lumbar spine. Institutional review board approval was granted for this study and the medical records along with the intraoperative monitoring reports from 41 consecutive transpsoas lateral interbody fusion procedures were analyzed. The presence or absence of intraoperative changes to the saphenous nerve SSEP was noted and the post‐operative symptoms and physical examination findings were noted. Changes in SSEP were noted in 5 of the 41 surgical procedures, with 3 of the patients waking up with a femoral nerve deficit. None of the patients with stable SSEP's

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developed sensory or motor deficits post‐operatively. No patient in this series demonstrated intraoperative EMG changes indicative of an intraoperative nerve injury. The authors concluded that saphenous nerve SSEP monitoring may be a beneficial tool to detect femoral nerve injury related to transpsoas direct lateral approaches to the lumbar spine. These preliminary findings need to be validated by well‐designed studies.

Fix and colleagues (2015) noted that amnesic mild cognitive impairment (MCIa) is often characterized as an early stage of Alzheimer's dementia (AD). The latency of the P2, an electroencephalographic component of the flash VEP (FVEP), is significantly longer in those with AD or MCIa when compared with controls. In a pilot study, these investigators examined the diagnostic accuracy of several FVEP‐P2 procedures in distinguishing people with MCIa and controls. The latency of the FVEP‐P2 was measured in participants exposed to a single flash condition and 5 double‐flash conditions. The double‐flash conditions had different inter‐stimulus intervals between the pair of strobe flashes. Significant group differences were observed in the single‐flash and 2 of the double‐flash conditions. One of the double‐flash conditions (100 ms) displayed a higher predictive accuracy than the single‐flash condition, suggesting that this novel procedure may have more diagnostic potential. Participants with MCIa displayed similar P2 latencies across conditions, while controls exhibited a consistent pattern of P2 latency differences. These differences demonstrated that the double stimulation procedure resulted in a measurable refractory effect for controls but not for those with MCIa. The authors concluded that the pattern of P2 group differences suggested that those with MCIa have compromised cholinergic functioning that resulted in impaired visual processing. They stated that results from the present investigation lend support to the theory that holds MCIa as an intermediate stage between normal healthy aging and the neuropathology present in AD; and measuring the FVEP‐P2 during several double stimulation conditions could provide diagnostically useful information about the health of the

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cholinergic system.

Loudness-Dependence of Auditory Evoked Potentials:

In a pilot study, Uhl and colleagues (2012) measured serotonergic activity in a follow‐up study of suicidal patients. In particular, these researchers examined if suicide attempts or suicidal states cause changes in the loudness dependence of auditory evoked potentials (LDAEP). A total of 13 patients (6 males; mean age of 40.9 ± 11.3 years; range of 20 to 61) with a major depressive episode who had attempted suicide or had suicidal plans (Hamilton Depression Rating Scale item 3 [suicidality] greater than or equal to 3) were included in the study; LDAEP and psychometric measurements took place about 2, 5, 9 and 16 days after attempted suicide or suicidal action. On day 9, LDAEP was significantly higher compared to day 2 and day 16; there was a similar tendency compared to day 5. Instability of central serotonergic function was suggested resulting in reduced serotonergic activity about 1 week after suicide attempt. The authors concluded that further studies are needed that include larger samples in order to distinguish between different psychiatric diseases and to consider confounding factors like gender, medication, smoking, impulsivity or lethality of suicidal action.

GraBnickel et al (2015) stated that differences in central serotonergic function due to affective disorders and due to extraordinary situations like suicidality may be visualized using the LDAEP. A total of 20 patients (11 males; mean age of 43.25 ± 10.85, age range of 20 to 61) suffering from a major depressive episode who had either acutely attempted suicide or who had suicidal plans and behavior, which were reflected by item 3 of Hamilton Depression Rating Scale greater than or equal to 3 (suicidality), were included in the study. Furthermore, these researchers compared subjects’ LDAEP to those of non‐suicidal depressed patients as well as to healthy volunteers, each matched according to age and gender; LDAEP measurement and psychometric tests took place about 2, 5, 9, 16 and 30 days after acute suicidal action or suicide attempts.

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In contrast to previous results, significant differences in LDAEP could not have been shown in between the suicidal group, or by comparing results of suicidal patients to non‐suicidal depressed patients or to healthy volunteers. However, when the LDAEP of non‐suicidal depressed patients were compared to healthy volunteers, there was a trend for a higher LDAEP in the healthy volunteers. The authors concluded that further studies are needed to ascertain further influences on serotonergic function and confounding factors like medication, smoking, age, gender, co‐morbidities and methods of suicidal attempt.

Pak et al (2015) noted that the relationship between suicidality and the LDAEP remains controversial. These investigators reviewed the literature related to the LDAEP and suicide in patients with major depressive disorder, and suggested future research directions. Serotonergic dysfunction in suicidality seems to be more complicated than was originally thought. Studies of suicide based on the LDAEP have produced controversial results, but it is possible that these were due to differences in study designs and the smallness of samples. For example, some studies have evaluated suicide ideation and the LDAEP, while others have evaluated suicide attempts and the LDAEP. Furthermore, some of the latter studies enrolled acute suicide attempters, while others enrolled those with the history of previous suicide attempts, irrespective of whether these were acute or chronic. Thus, a more robust study design is needed in future studies (e.g., by evaluating the LDAEP immediately after a suicide attempt rather than in those with a history of suicide attempts and suicide ideation in order to reduce bias). Moreover, the authors stated that genuine suicide attempt, self‐injurious behaviors, and faked suicide attempt need to be discriminated in the future.

Intraoperative Motor Evoked Potentials during Descending and Thoraco-Abdominal Aortic Aneurysm Repair:

Fok and colleagues (2015) stated that paraplegia remains the most feared and a devastating complication after descending

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and thoraco‐abdominal aneurysm operative repair (DTA and TAAAR). Neuro‐monitoring, particularly use of MEPs, for this surgery has gained popularity. However, ambiguity re mains regarding its use and benefit. These researchers systematically reviewed the literature to evaluate the benefit and applicability of neuro‐monitoring in DTA and TAAAR. Electronic s earches were performed on 4 major databases from inception until February 2014 to identify relevant studies. Eligibility decisions, method quality, data extraction, and analysis were performed according to predefined clinical criteria and end‐points. Among the studies matching the inclusion criteria, a total of 1,297 patients had MEP monitoring during DTA and TAAAR. In‐ hospital mortality was low (6.9 % ± 3.6). Immediate neurological deficit was low (3.5 % ± 2.6). In 1/3 of patients (30.4 % ± 14.2), the MEPs dropped below threshold, which were 30.4 % and 29.4 % with threshold levels of 75 % and 50 %, respectively. A range of surgical techniques were applied after reduction in MEPs. Most patients whose MEPs dropped and remained below threshold had immediate permanent neurological deficit (92.0 % ± 23.6). Somatosensory‐evoked potentials were reported in 1/3 of papers with little association between loss of SEPs and permanent neurological deficit (16.7 % ± 28.9 %). The authors concluded that they demonstrated that MEPs are useful at predicting paraplegia in patients who lose their MEPs and did not regain them intra‐operatively. Moreover, they stated that to date, there is no consensus regarding the applicability and use of MEPs; current evidence does not mandate or support MEP use.

Motor Evoked Potentials for Evaluation of Wilson's Disease:

Bembenek et al (2015) stated that Wilson's disease (WD) is a metabolic brain disease resulting from improper copper metabolism. Although pyramidal symptoms are rarely observed, sub‐clinical injury is highly possible as copper accumulates in all brain structures. The usefulness of MEPs in pyramidal tracts damage evaluation still appears to be somehow equivocal. These investigators searched for original papers examining the value of transcranial magnetic stimulation

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(TMS) elicited MEPs with respect to motor function of upper and lower extremity in WD. They searched PubMed for original papers evaluating use of MEPs in WD using key words: "motor evoked potentials Wilson's disease" and "transcranial magnetic stimulation Wilson's disease". These researchers found 6 articles using the above key words. One additional article and 1 case report were found while viewing the references lists; thus, these investigators included 8 studies. Number of patients in studies was low and their clinical characteristic was variable; there were also differences in methodology. Abnormal MEPs were confirmed in 20 to 70 % of study participants; MEPs were not recorded in 7.6 to 66.7 % of patients. Four studies reported significantly increased cortical excitability (up to 70 % of patients). Prolonged central motor conduction time was observed in 4 studies (30 to 100 % of patients); 1 study reported absent or prolonged central motor latency in 66.7 % of patients. The authors concluded that although MEPs may be abnormal in WD, this has not been thoroughly assessed. Moreover, they stated that further studies are needed to evaluate MEPs' usefulness in evaluating pyramidal tract damage in WD.

Somatosensory Evoked Potentials as Prognostic Tests in Neonates with Hypoxic-Ischemic Encephalopathy:

Garfinkle and colleagues (2015) noted that SEPs were reported to have high positive‐predictive value (PPV) for neuro­developmental impairment (NDI) in neonates with moderate or severe hypoxic‐ischemic encephalopathy (HIE). These researchers evaluated if this predictive value remains high with the use of therapeutic hypothermia. A cohort of HIE neonates treated with hypothermia was recruited between September 2008 and September 2010; SEPs were elicited after hypothermia and classified as bilateral absent N19, abnormal N19 (i.e., delayed or unilateral absent), or normal. Qualitative evaluation of MRI was also performed. The primary outcome was moderate or severe NDI around 2 years of age. Somatosensory evoked potentials were performed after hypothermia in 26 of 34 neonates submitted to hypothermia

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with adequate follow‐up at a median day of life 11 (inter­quartile range [IQR]: 9 to 13). Twenty‐three (88 %) had moderate encephalopathy; 11 neonates (42 %) had bilateral absent N19, 4 of whom had NDI, while 15 neonates (58 %) had either abnormal or normal N19, of whom only 1 had NDI. Somatosensory evoked potentials thus had a PPV of 0.36 (4/11) and a negative‐predictive value (NPV) of 0.93 (14/15). Eighteen neonates (69 %) had brain injury on MRI; thus, MRI had a PPV of 0.28 (5/18) and an NPV of 1.00 (8/8). The authors concluded that neonates with HIE treated with hypothermia with bilateral absent N19 potentials may have a better prognosis than reported in the pre‐hypothermia era; MRI also had a low PPV and high NPV. They stated that SEPs should be interpreted with caution in this new population and need to be re‐evaluated in larger studies.

Visual Evoked Potentials for Evaluation of Birdshot Chorioretinopathy:

Tzekov and Madow (2015) noted that birdshot chorioretinopathy (BSCR) is a rare form of autoimmune posterior uveitis that can affect the visual function and, if left untreated, can lead to sight‐threatening complications and loss of central vision. These investigators performed a systematic search of the literature focused on visual electrophysiology studies, including ERG, electrooculography (EOG), and VEP, used to monitor the progression of BSCR and estimate treatment effectiveness. Many reports were identified, including using a variety of methodologies and patient populations, which made a direct comparison of the results difficult, especially with some of the earlier studies using non‐standardized methodology. Several different electrophysiological parameters, such as EOG Arden's ratio and the mfERG response densities, are reported to be widely affected. However, informal consensus emerged in the past decade that the full‐field ERG light‐adapted 30‐Hz flicker peak time is one of the most sensitive electrophysiological parameters. As such, it has been used widely in clinical trials to evaluate drug safety and effectiveness and to guide therapeutic decisions in clinical practice. The

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authors concluded that despite its wide use, a well‐designed longitudinal multi‐center study to systematically evaluate and compare different electrophysiological methods or parameters in BSCR is still lacking; but would benefit both diagnostic and therapeutic decisions.

Intraoperative Neuromonitoring During Adjustment of Vertical Expandable Prosthetic Titanium Rib:

Skaggs and colleagues (2009) stated that the vertical expandable prosthetic titanium rib (VEPTR) device is used in the treatment of thoracic insufficiency syndrome and certain types of early‐onset spinal deformity. These researchers evaluated the risk of neurologic injury during surgical procedures involving use of the VEPTR and determined the effectiveness of intra‐operative spinal cord neuro‐monitoring (IONM). Data were collected prospectively during a multi‐center study. Surgical procedures were divided into 3 categories: (i) primary device implantation, (ii) device exchange, and (iii) device lengthening. Further retrospective evaluation was undertaken in cases of neurologic injury or changes detected with neuro‐monitoring. There were 1,736 consecutive VEPTR procedures at 6 centers: 327 (in 299 patients) consisted of a primary device implantation, 224 were a device exchange, and 1,185 were a device lengthening. Peri‐operative clinical neurologic injury was noted in 8 (0.5 %) of the 1,736 cases: these injuries were identified after 5 (1.5 %) of the 327 procedures for primary device implantation, 3 (1.3 %) of the 224 device exchanges, and none of the 1,185 device‐lengthening procedures. Of the 8 cases of neurologic injury, 6 involved the upper extremity and 2 involved the lower extremity. The neurologic deficit was temporary in 7 patients and permanent in 1 patient, who had persistent neurogenic arm and hand pain; IONM demonstrated changes during 6 (0.3 %) of the 1,736 procedures: 5 (1.5 %) of the 327 procedures for primary device implantation and 1 (0.08 %) of the 1,185 device‐lengthening procedures. The surgery was altered in all 6 cases, with resolution of the monitoring changes in 5 cases and persistent signal changes and a neurologic deficit (upper‐extremity brachial plexopathy) in 1; 2

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patients had false‐negative results of monitoring of SEPs, and 1 had false‐negative results of monitoring of SEPs and MVPs during implant surgery; 2 had a brachial plexopathy and 1 had monoplegia post‐operatively, with all 3 recovering. The authors concluded that neurologic injury during VEPTR surgery occurred much more frequently in the upper extremities than in the lower extremities. The rates of potential neurologic injuries (neurologic injuries plus instances of changes detected by monitoring) during primary implantation of the VEPTR (2.8 %) and during exchange of the VEPTR (1.3 %) justified the use of IONM of the upper and lower extremities during those procedures. As neuro‐monitoring did not demonstrate any changes in children without a previous VEPTR‐related monitoring change and there were no neurologic injuries during more than 1,000 VEPTR‐lengthening procedures, IONM may not be necessary during those procedures in children without a history of a neurologic deficit during VEPTR surgery.

Intraoperative Somatosensory Evoked Potentials for Cochlear Implantation:

American Academy of Neurology’s “Principles of Coding for Intraoperative Neurophysiologic Monitoring (IOM) and Testing” did not mention cochlear implantation.

American Speech‐Language‐Hearing Association (ASHA)’s Technical Report on “Cochlear Implants” did not mention somatosensory evoked potentials (SSEPs) as a management tool.

Motor Evoked Potentials for Evaluation of Wilson's Disease:

Bembenek and colleagues (2015) noted that Wilson's disease (WD) is a metabolic brain disease resulting from improper copper metabolism. Although pyramidal symptoms are rarely observed, sub‐clinical injury is highly possible as copper accumulates in all brain structures. The usefulness of MEPs in pyramidal tracts damage evaluation still appears to be

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somehow equivocal. These investigators searched for original papers assessing the value of transcranial magnetic stimulation elicited MEPs with respect to motor function of upper and lower extremity in WD. They searched PubMed for original papers evaluating the use of MEPs in WD using key words: "motor evoked potentials Wilson's disease" and "transcranial magnetic stimulation Wilson's disease”. These investigators found 6 articles using the above key words; 1 additional article and 1 case report were found while viewing the references lists. Thus, a total of 8 studies were included in this analysis; number of participants in studies was low and their clinical characteristic was variable. There were also differences in methodology. Abnormal MEPs were confirmed in 20 to 70 % of study participants; MEPs were not recorded in 7.6 to 66.7 % of patients; 4 studies reported significantly increased cortical excitability (up to 70 % of patients). Prolonged central motor conduction time was observed in 4 studies (30 to 100 % of patients). One study reported absent or prolonged central motor latency in 66.7 % of patients. The authors concluded that although MEPs may be abnormal in WD, this has not been thoroughly assessed. They stated that further studies are needed to evaluate MEPs' usefulness in assessing pyramidal tract damage in WD.

Ocular Vestibular Evoked Myogenic Potentials for the Diagnosis of Myasthenia Gravis:

In a case‐control, proof‐of‐principle study, Valko and colleagues (2016) examined if ocular vestibular evoked myogenic potentials (oVEMP) can be used to detect a decrement in the extra‐ocular muscle activity of patients with myasthenia gravis (MG). A total of 27 patients with MG, including 13 with isolated ocular and 14 with generalized MG, and 28 healthy controls were included in this study. These investigators applied repetitive vibration stimuli to the forehead and recorded the activity of the inferior oblique muscle with 2 surface electrodes placed beneath the eyes. To identify the oVEMP parameters with the highest sensitivity and specificity, these researchers evaluated the decrement over 10 stimulus repetitions at 3

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different repetition rates (3 Hz, 10 Hz, and 20 Hz). Repetitive stimulation at 20 Hz yielded the best differentiation between patients with MG and controls with a sensitivity of 89 % and a specificity of 64 % when using a unilateral decrement of greater than or equal to 15.2 % as cut‐off. When using a bilateral decrement of greater than or equal to 20.4 % instead, oVEMP allowed differentiation of MG from healthy controls with 100 % specificity, but slightly reduced sensitivity of 63 %. For both cut­offs, sensitivity was similar in isolated ocular and generalized MG. The authors concluded that the findings of this study demonstrated that the presence of an oVEMP decrement is a sensitive and specific marker for MG. This test allowed direct and non‐invasive examination of extra‐ocular muscle activity, with similarly good diagnostic accuracy in ocular and generalized MG. They stated that oVEMP represents a promising diagnostic tool for MG. This study provided Class III evidence that oVEMP testing accurately identifies patients with MG with ocular symptoms (sensitivity 89 %, specificity 64 %). Well‐designed studies are needed to confirm the diagnostic utility of oVEMP in clinical practice.

In an editorial that accompanied the afore‐mentioned study, Prasad and Halmagyi (2016) stated that cohort studies are needed to evaluate the value of oVEMP in clinical practice, where a broader range of diagnostic possibilities leaves the clinician uncertain.

Vestibular Evoked Myogenic Potentials for the Diagnosis of Meniere's Disease or Delayed Endolymphatic Hydrops:

Akkuzu et al (2006) examined the role of VEMP in benign paroxysmal positional vertigo (BPPV) and Meniere's disease, and ascertained if this type of testing is valuable for assessing the vestibular system. The 62 participants included 17 healthy controls and 45 other subjects selected from patients who presented with the complaint of vertigo (25 diagnosed with BPPV and 20 diagnosed with Meniere's disease). Vestibular evoked myogenic potentials were recorded in all subjects and findings in each patient group were compared with control

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findings. Vestibular evoked myogenic potentials for the 30 affected ears in the 25 BPPV patients revealed prolonged latencies in 8 ears and decreased amplitude in 1 ear (9 abnormal ears; 30 % of total). The recordings for the 20 affected ears in the Meniere's disease patients revealed 4 ears with no response, 6 ears with prolonged latencies (10 abnormal ears; 50 % of total). Only 2 (5.9 %) of the 34 control ears had abnormal VEMP. The rate of VEMP abnormalities in the control ears was significantly lower than the corresponding rates in the affected BPPV ears and the affected Meniere's ears that were studied (p = 0.012 and p < 0.001, respectively). The results suggested that testing of VEMP is a promising method for diagnosing and following patients with BPPV paroxysmal positional vertigo and Meniere's disease.

Egami and associates (2013) estimated the sensitivity and specificity of VEMPs in comparison with caloric test in diagnosing MD among patients with dizziness. Data were retrospectively collected from 1,170 consecutive patients who underwent vestibular tests. Among them, 114 patients were diagnosed as having unilateral definite MD; VEMPs in response to clicks and short tone burst stimulation as well as caloric tests were performed. The sensitivity and specificity of each test were evaluated. The results of each test were compared with hearing level and staging of MD. The sensitivity and specificity of VEMPs were 50.0 % and 48.9 %, while those of the caloric test were 37.7 % and 51.2 %, respectively. There was no significant difference in hearing level between patients appropriately or inappropriately identified by VEMPs, whereas there was a significant difference in those of the caloric test. Combined use of VEMP and caloric test increased the sensitivity to 65.8 %. The authors concluded that although the sensitivity and specificity of VEMPs in diagnosing MD were not high, they were comparable to those of caloric test. They stated that VEMPs as well as caloric testing may give additional information as part of a diagnostic test battery for detecting vestibular abnormalities in MD.

In a systematic review and meta‐analysis, Zhang and colleagues

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(2015) evaluated the clinical diagnostic value of VEMPs for endolymphatic hydrops (EH). The pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio (OR) and area under summary receiver operating characteristic curves (AUC) were calculated. Subgroup analysis and publication bias assessment were also conducted. The pooled sensitivity an d the specificity were 49 % (95 % CI: 46 % to 51 %) and 95 % (95 % CI: 94 % to 96 %), respectively. The pooled positive likelihood ratio was 18.01 (95 % CI: 9.45 to 34.29) and the pooled negative likelihood ratio was 0.54 (95 % CI: 0.47 to 0.61); AUC was 0.78 and the pooled diagnostic OR of VEMPs was 39.89 (95 % CI: 20.13 to 79.03). The authors concluded that the findings of the present meta‐analysis showed that VEMPs test alone is not sufficient for the diagnosis of MD or delayed EH, but that it might be an important component of a test battery for diagnosing MD or delayed EH. Moreover, VEMPs, due to its high specificity and non‐invasive nature, might be used as a screening tool for EH.

Furthermore, an UpToDate review on “Meniere disease” (Moskowitz and Dinces, 2016) states that “Meniere disease is a clinical diagnosis. Although not diagnostic, patients should undergo audiometry, vestibular testing, and MRI to rule out other causes of symptoms. The vestibular evoked myogenic potential (VEMP) test may be useful for monitoring disease progression”.

Intraoperative Somatosensory Evoked Potentials During Cervical Facet Injections:

An UpToDate review on “Subacute and chronic low back pain: Nonsurgical interventional treatment” (Chou, 2017) does not mention “neuroimaging or intraoperative monitoring” for facet joint injection.

Intraoperative Somatosensory Evoked Potentials During Decompression of the Trigeminal Nerve:

An UpToDate review on “Trigeminal neuralgia” (Bajwa et al,

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2017) does not mention intraoperative monitoring or intraoperative SSEP monitoring.

Intraoperative Somatosensory Evoked Potentials During Rotator Cuff Repair:

An UpToDate review on “Management of rotator cuff tears” (Martin and Martin, 2017) does not mention intraoperative SSEP monitoring.

Cervical and Ocular Vestibular Evoked Myogenic Potential Testing:

On behalf of the American Academy of Neurology (AAN), Fife and colleagues (2017) reviewed the evidence and made recommendations regarding the diagnostic utility of cervical and ocular vestibular evoked myogenic potentials (cVEMP and oVEMP, respectively). Four questions were asked: (i) does cVEMP accurately identify superior canal dehiscence syndrome (SCDS)? (ii) does oVEMP accurately identify SCDS? (iii) for suspected vestibular symptoms, does cVEMP/oVEMP accurately identify vestibular dysfunction related to the saccule/utricle? and (iv) for vestibular symptoms, does cVEMP/oVEMP accurately and substantively aid diagnosis of any specific vestibular disorder besides SCDS? The guideline panel identified and classified relevant published studies (January 1980 to December 2016) according to the 2004 AAN process. The following recommendations were provide:

Level C positive: Clinicians may use cVEMP stimulus threshold values to distinguish SCDS from controls (2 Class III studies) (sensitivity 86 % to 91 %, specificity 90 % to 96 %). Corrected cVEMP amplitude may be used to distinguish SCDS from controls (2 Class III studies) (sensitivity 100 %, specificity 93 %). Clinicians may use oVEMP amplitude to distinguish SCDS from normal controls (3 Class III studies) (sensitivity 77 % to 100 %, specificity 98 % to 100%). oVEMP threshold may be used to aid in distinguishing SCDS from controls (3 Class III studies) (sensitivity 70 % to 100 %,

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specificity 77 % to 100 %). Level U: Evidence is insufficient to determine whether cVEMP and oVEMP can accurately identify vestibular function specifically related to the saccule/utricle, or whether cVEMP or oVEMP is useful in diagnosing vestibular neuritis or Meniere disease. Level C negative: It has not been demonstrated that cVEMP substantively aids in diagnosing benign paroxysmal positional vertigo, or that cVEMP or oVEMP aids in diagnosing/managing vestibular migraine.

Appendix

Documentation Requirements:

I. All medical necessity criteria must be clearly documented in the member's medical record and made available upon request.

II. The member's medical record must contain documentationthat fully supports the medical necessity for evokedpotential studies. This documentation includes, but is notlimited to, relevant medical history, physical examination,the anatomic location of the planned surgical procedure, therationale for the location and modalities to bemonitored, and results of pertinent diagnostic tests orprocedures.

III. For the BAERs, the member’s medical record shoulddocument the otologic exam describing both ear canals andtympanic membranes, as well as a gross hearing assessment.The medical record should also include the results of air andbone pure tone audiogram and speech audiometry.

IV. The physician’s evoked potential report should note whichnerves were tested, latencies at various testing points, andan evaluation of whether the resulting values are normal orabnormal.

V. Baseline testing prior to intraoperative neuromonitoring requires contemporaneous interpretation prior to the surgical procedure. To qualify for coverage of baseline testing, results of testing of multiple leads for signal

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strength, clarity, amplitude, etc., should be documented in the medical record. The time spent performing or interpreting the baseline electrophysiologic studies performed prior to surgery should not be counted as intraoperative monitoring, but represents separately reportable procedures. Testing performed during surgery does not qualify as baseline testing and is not a separately reportable procedure.

VI. For continuous intraoperative neurophysiology monitoring,from outside the operating room (remote or nearby) or formonitoring of more than one case while in the operatingroom, increments of less than 30 minutes should not bebilled. For continuous intraoperative neurophysiologymonitoring in the operating room with one on onemonitoring requiring personal attendance, increments ofless than 8 minutes should not be billed.

CPT Codes / HCPCS Codes / ICD‐10 Codes

Information in the [brackets] below has been added for clarification purposes. Codes requiring a 7th character are represented by "+":

Code Code Description

Somatosensory evoked potentials (SEPs, SSEPs):

CPT codes covered if selection criteria are met:

95925 Short‐latency somatosensory evoked potential study, stimulation of any/all peripheral nerves or skin sites, recording from the central nervous system; in upper limbs

95926 in lower limbs

95927 in the trunk or head

95938 Short‐latency somatosensory evoked potential study, stimulation of any/all peripheral nerves or skin sites, recording from the central nervous system; in upper and lower limbs

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Code Code Description

ICD‐10 codes covered if selection criteria are met:

G11.1 Early‐onset cerebellar ataxia [Friedreich's ataxia]

G23.8 Other specified degenerative diseases of basal ganglia [olivopontocerebellar (OPC) degeneration]

G35 Multiple sclerosis [with clinically silent lesions]

G36.0 ­G37.9

Other demyelinating diseases of central nervous system

G93.1 Anoxic brain damage, not elsewhere classified

G93.82 Brain death

G95.9 Diseases of spinal cord [unexplained myelopathy]

ICD‐10 codes not covered for indications listed in the CPB (not all‐inclusive):

E53.8 Deficiency of other specified B group vitamins [diagnosis and management of acquired metabolic disorders]

F43.10 ‐ F43.12

Posttraumatic stress disorder

E70.0 ­ E89.89

Metabolic disorders [diagnosis and management of acquired metabolic disorders]

F90.0 ­ F90.9

Attention‐deficit hyperactivity disorders [ADD or ADHD]

G12.21 Amyotrophic lateral sclerosis

G12.8 ­ G12.9

Other and unspecified muscular atrophies

G54.0 Brachial plexus disorders [thoracic outlet syndrome]

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Code Code Description

G56.00 ‐ G59

Mononeuropathies of upper and lower limbs [radiculopathies, peripheral nerve lesions, carpal tunnel syndrome/nerve entrapment]

M47.11 M47.13

Cervical spondylosis with myelopathy

M50.00 ‐M50.13, M51.04 M51.17

Intervertebral disc disorder with myelopathy [radiculopathies]

M50.10 ‐ M50.13 M54.11 M54.13

Brachial neuritis or radiculitis [where standard nerve conduction velocity studies are diagnostic]

M50.20 M50.23 M51.24 ­ M51.27

Cervical disc displacement without myelopathy

M51.14 ­ M51.17 M54.14 ­ M54.17

Thoracic or lumbosacral neuritis or radiculitis, unspecified [radiculopathies]

M54.10, M54.18, M79.2

Neuralgia, neuritis, and radiculitis, unspecified

M54.30 ­ M54.42

Sciatica

S02.0xx+ ­ S02.42x+ S02.600+ ­ S02.92x+

Fracture of skull and facial bones [conscious]

S06.0x0+ ‐ S06.9x9+

Intracranial injury

­

­

­

­

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Code Code Description

S12.000+ S12.9xx+ S22.000+ S22.089+ S32.000+ S32.2xx+

Fracture of vertebral column [conscious]

S14.0xx+ S14.159+ S24.0xx+ S24.159+ S34.01x+ ­ S34.139+

Spinal cord injury [conscious]

T37.8x1+ T37.8x4+

Poisoning by other specified systemic anti­ infectives

T56.0x1+ T56.0x4+

Toxic effect of lead and its compounds (including fumes)

Z13.850 Z13.858

Encounter for screening for nervous system disorders [indicates routine exam without signsor symptoms when reported alone]

Z13.88 Encounter for screening for disorder due to exposure to contaminants [indicates routine exam without signs or symptoms when reported alone]

Intra‐operative somatosensory evoked potentials (SSEPs) performed either alone, or in combination with motor evoked potentials (MEPs):

CPT codes covered if selection criteria are met:

95940 Continuous intraoperative neurophysiology monitoring in the operating room, one on one monitoring requiring personal attendance, each 15 minutes (List separately in addition to code for primary procedure)

­

­

­

­

­

­

­

­

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Code Code Description

95941 Continuous intraoperative neurophysiology monitoring, from outside the operating room (remote or nearby) or for monitoring of more than one case while in the operating room, per hour (List separately in addition to code for primary procedure

HCPCS codes covered if selection criteria are met:

G0453 Continuous intraoperative neurophysiology monitoring, from outside the operating room (remote or nearby), per patient, (attention directed exclusively to one patient) each 15 minutes (list in addition to primary procedure

Intra‐operative SEP monitoring, with or without MEPs, may be appropriate for the following types of surgery (not all‐inclusive):

CPT codes covered if selection criteria are met for intraoperative SEPs:

22210 22212, 22216 22222, 22226

Osteotomy of spine

22305 22319, 22326 22328

Treatment of fracture and/or dislocation of vertebrae

22513 Percutaneous vertebral augmentation, including cavity creation (fracture reduction and bone biopsy included when performed) using mechanical device (eg, kyphoplasty), 1 vertebral body, unilateral or bilateral cannulation, inclusive of all imaging guidance; thoracic

­

­

­

­

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Code Code Description

+22515 each additional thoracic or lumbar vertebral body (List separately in addition to code for primary procedure)

22532, 22534 ­ 22556, 22585, 22590 ­ 22610, 22614, 22800 ­ 22819

Arthrodesis [not covered for monitoring the femoral nerve during transpsoas lumbar lateral interbody fusion]

22840 ­ 22855

Spinal instrumentation

22856 Total disc arthroplasty (artificial disc), anterior approach, including discectomy with end plate preparation (includes osteophytectomy for nerve root or spinal cord decompression and microdissection); single interspace, cervical

+22858 second level, cervical (List separately in addition to code for primary procedure)

31200 ‐ 31230

Ethmoidectomy and maxillectomy

33320 ­ 33335

Repair of aorta or great vessels

33400 ­ 33417

Aortic valve procedures

33800 ­ 33853

Aortic anomalies procedures

33860 ­ 33877

Thoracic aortic aneurysm repair

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Code Code Description

61000 61070

Injection, drainage, or aspiration of skull meninges, and brain

61105 61253

Twist drill, burr hole(s), or trephine

61304 ‐ 61345, 61480 61576

Craniectomy or craniotomy

61600 61616

Definitive procedures of skull base

61618 61619

Repair and/or reconstruction of surgical defects of skull base

61623 ‐ 61626

Endovascular therapy

61680 61711

Surgery for aneurysm, arteriovenous malformation or vascular disease

61720 ‐ 61791

Stereotaxis, intracranial

61850 ‐ 61888

Neurostimulators (intracranial)

62000 62148

Repair of skull

62160 ‐ 62165

Neuroendoscopy

62263 62327

Injection, drainage, or aspiration of spine and spinal cord

­

­

­

­

­

­

­

­

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Code Code Description

63001 63003, 63015 63016, 63020, 63035 63040, 63043, 63045 63046, 63048 63055, 63057 63101, 63103

Exploration/decompression of spinal cord

63170 63199, 63250 63266, 63270 63271, 63275 63276, 63280 63281, 63285 63302, 63304 63306, 63308

Incision/excision intraspinal

63600 ‐ 63615

Stereotaxis, spinal

63700 63710

Repair (spinal)

­

­

­

­

­

­

­

­

­

­

­

­

­

­

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Code Code Description

64716 Neuroplasty and/or transposition; cranial nerve (specify)

67570 Optic nerve decompression (e.g., incision or fenestration of optic nerve sheath)

69666 Repair of oval window fistula

69667 Repair of round window fistula

69720 Decompression facial nerve, intratemporal; lateral to geniculate ganglion

69725 including medial to geniculate ganglion

69740 Suture facial nerve, intratemporal, with or without graft or decompression; lateral to geniculate ganglion

69745 including medial to geniculate ganglion

69805 Endolymphatic sac operation; without shunt

69806 with shunt

69915 Vestibular nerve section, translabyrinthine approach

69950 Vestibular nerve section, transcranial approach

69955 Total facial nerve decompression and/or repair (may include graft)

99173 Screening test of visual acuity, quantitative, bilateral

CPT codes not covered for indications listed in the CPB for intraoperative SEPs:

0195T Arthrodesis, pre‐sacral interbody technique, disc space preparation, discectomy, without instrumentation, with image guidance, includes bone graft when performed; L5‐S1 interspace

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Code Code Description

0196T L4‐L5 interspace (List separately in addition to code for primary procedure)

0213T Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or

nerves innervating that joint) with ultrasound guidance, cervical or thoracic; single level

+0214T second level

++0215T third and any additional level(s)

0216T Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or

nerves innervating that joint) with ultrasound guidance, lumbar or sacral; single level

+0217T second level

+0218T third and any additional level(s)

0309T Arthrodesis, pre‐sacral interbody technique, including disc space preparation, discectomy,

with posterior instrumentation, with image guidance, includes bone graft, when performed,

lumber, L4‐L5 interspace (List separately in addition to code for primary procedure)

11646 Excision, malignant lesion including margins, face, ears, eyelids, nose, lips; excised diameter over 4.0 cm

13132 Repair, complex, forehead, cheeks, chin, mouth, neck, axillae, genitalia, hands and/or feet; 2.6 cm

to 7.5 cm

14060 Adjacent tissue transfer or rearrangement, eyelids, nose, ears and/or lips; defect 10 sq cm or

less

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Code Code Description

15100 Split‐thickness autograft, trunk, arms, legs; first 100 sq cm or less, or 1% of body area of infants and children (except 15050)

15120 Split‐thickness autograft, face, scalp, eyelids, mouth, neck, ears, orbits, genitalia, hands, feet, and/or multiple digits; first 100 sq cm or less, or

1% of body area of infants and children (except 15050)

15260 Full thickness graft, free, including direct closure of donor site, nose, ears, eyelids, and/or lips; 20 sq cm or less

15275 Application of skin substitute graft to face, scalp, eyelids, mouth, neck, ears, orbits, genitalia,

hands, feet, and/or multiple digits, total wound surface area up to 100 sq cm; first 25 sq cm or

less wound surface area

15732 Muscle, myocutaneous, or fasciocutaneous flap; head and neck (eg, temporalis, masseter muscle,

sternocleidomastoid, levator scapulae)

15760 Graft; composite (eg, full thickness of external ear or nasal ala), including primary closure,

donor area

15770 derma‐fat‐fascia

20680 Removal of implant; deep (eg, buried wire, pin, screw, metal band, nail, rod or plate)

20900 Bone graft, any donor area; minor or small (eg, dowel or button)

20926 Tissue grafts, other (eg, paratenon, fat, dermis)

+20985 Computer‐assisted surgical navigational procedure for musculoskeletal procedures, image‐less (List separately in addition to code for

primary procedure)

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Code Code Description

21235 Graft; ear cartilage, autogenous, to nose or ear (includes obtaining graft)

21554 Excision, tumor, soft tissue of neck or anterior thorax, subfascial (eg, intramuscular); 5 cm or greater

21556 Excision, tumor, soft tissue of neck or anterior thorax, subfascial (eg, intramuscular); less than 5 cm

22214 Osteotomy of spine, posterior or posterolateral approach, 1 vertebral segment; lumbar

22224 Osteotomy of spine, including discectomy, anterior approach, single vertebral segment; lumbar

22325 Open treatment and/or reduction of vertebral fracture(s) and/or dislocation(s), posterior approach, 1 fractured vertebra or dislocated segment; lumbar

22514 Percutaneous vertebral augmentation, including cavity creation (fracture reduction and bone biopsy included when performed) using mechanical device (eg, kyphoplasty), 1 vertebral body, unilateral or bilateral cannulation, inclusiveof all imaging guidance; lumbar

22533 Arthrodesis, lateral extracavitary technique, including minimal discectomy to prepare interspace (other than for decompression); lumbar

22558 Arthrodesis, anterior interbody technique, including minimal discectomy to prepare interspace (other than for decompression); lumbar

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Code Code Description

22586 Arthrodesis, pre‐sacral interbody technique, including disc space preparation, discectomy, with posterior instrumentation, with image guidance, includes bone graft when performed, L5‐S1 interspace

22612 Arthrodesis, posterior or posterolateral technique, single level; lumbar ( with lateral transverse technique, when performed)

22630 Arthrodesis, posterior interbody technique, including laminectomy and/or discectomy to prepare interspace (other than for decompression), single interspace; lumbar

+22632 each additional interspace (List separately in addition to code for primary procedure)

22633 Arthrodesis, combined posterior or posterolateral technique with posterior interbody technique including laminectomy and/or discectomy sufficient to prepare interspace (other than for decompression), singleinterspace and segment; lumbar

+22634 each additional interspace and segment (List separately in addition to code for primary procedure)

22899 Unlisted procedure, spine

23700 Manipulation under anesthesia, shoulder joint, including application of fixation apparatus (dislocation excluded)

27130 27138

Total hip arthroplasty (includes conversion and revision to previous surgery)

27280 Arthrodesis, open, sacroiliac joint, including obtaining bone graft, including instrumentation, when performed

­

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Code Code Description

27360 Partial excision (craterization, saucerization, or diaphysectomy) bone, femur, proximal tibia

and/or fibula (eg, osteomyelitis or bone abscess)

27437 Arthroplasty, patella; without prosthesis

27443 Arthroplasty, femoral condyles or tibial plateau(s), knee; with debridement and partial synovectomy

27446 Arthroplasty, knee, condyle and plateau; medial OR lateral compartment

27447 medial AND lateral compartments with or without patella resurfacing (total knee

arthroplasty)

29843 29847

Wrist arthroscopy repair

29848 Endoscopy, wrist, surgical, with release of transverse carpal ligament

29999 Unlisted procedure, arthroscopy

31525 Laryngoscopy direct, with or without tracheoscopy; diagnostic, except newborn

31536 Laryngoscopy, direct, operative, with biopsy; with operating microscope or telescope

31575 Laryngoscopy, flexible fiberoptic; diagnostic

31610 Tracheostomy, fenestration procedure with skin flaps

31622 Bronchoscopy, rigid or flexible, including fluoroscopic guidance, when performed; diagnostic, with cell washing, when performed

(separate procedure)

33510 33548

Coronary artery bypass surgery

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Code Code Description

35301 Thromboendarterectomy, including patch graft, if performed; carotid, vertebral, subclavian, by

neck incision

36556 Insertion of non‐tunneled centrally inserted central venous catheter; age 5 years or older

37799 Unlisted procedure, vascular surgery

38500 Biopsy or excision of lymph node(s); open, superficial

38510 Biopsy or excision of lymph node(s); open, deep cervical node(s)

38720 Cervical lymphadenectomy (complete)

38724 Cervical lymphadenectomy (modified radical neck dissection)

4110F Internal mammary artery graft performed for primary, isolated coronary artery bypass graft

procedure (CABG)

41120 Glossectomy; less than one‐half tongue

42410 42426

Excision of parotid tumor or parotid gland

42440 Excision of submandibular (submaxillary) gland

43191 Esophagoscopy, rigid, transoral; diagnostic, including collection of specimen(s) by brushing

or washing when performed (separate procedure)

51785 Needle electromyography studies (EMG) of anal or urethral sphincter, any technique

60000 60512

Thyroid and parathyroid surgery

60699 Unlisted procedure, endocrine system

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Code Code Description

61450 Craniectomy, subtemporal, for section, compression, or decompression of sensory root

of gasserian ganglion

61458 Craniectomy, suboccipital; for exploration or decompression of cranial nerves

61460 for section of 1 or more cranial nerves

61546 Craniotomy for hypophyesctomy or excision of pituitary tumor, intracranial approach

61548 Hypophyesctomy or excision of pituitary tumor, transnasal or transseptal approach, nonsterotatic

61796 Stereotactic radiosurgery (particle beam, gamma ray, or linear accelerator); 1 simple cranial lesion

+61797 each additional cranial lesion, simple (List separately in addition to code for primary procedure)

61798 Stereotactic radiosurgery (particle beam, gamma ray, or linear accelerator); 1 complex cranial

lesion

+61799 each additional cranial lesion, complex (List separately in addition to code for primary procedure)

+61800 Application of stereotactic headframe for stereotactic radiosurgery (List separately in

addition to code for primary procedure)

62165 Neuroendoscopy, intracranial; with excision of pituitary tumor, transnasal or trans‐sphenoidal approach

62320 62327

lnterlaminar epidural injections ­

61 of 114

Code Code Description

63005 Laminectomy with exploration and/or decompression of spinal cord and/or cauda equina, without facetectomy, foraminotomy or discectomy (eg, spinal stenosis), 1 or 2 vertebral segments; lumbar, except for spondylolisthesis

63011 sacral

63012 Laminectomy with removal of abnormal facets and/or pars inter‐articularis with decompressionof cauda equina and nerve roots for spondylolisthesis, lumbar (Gill type procedure)

63017 Laminectomy with exploration and/or decompression of spinal cord and/or cauda equina, without facetectomy, foraminotomy or discectomy (eg, spinal stenosis), more than 2 vertebral segments; lumbar

63030 Laminotomy (hemilaminectomy), with decompression of nerve root(s), including partialfacetectomy, foraminotomy and/or excision of herniated intervertebral disc; 1 interspace, lumbar

63042 Laminotomy (hemilaminectomy), with decompression of nerve root(s), including partialfacetectomy, foraminotomy and/or excision of herniated intervertebral disc, reexploration, single interspace; lumbar

+63044 each additional lumbar interspace (List separately in addition to code for primary procedure)

63047 Laminectomy, facetectomy and foraminotomy (unilateral or bilateral with decompression of spinal cord, cauda equina and/or nerve root[s], [eg, spinal or lateral recess stenosis]), single vertebral segment; lumbar

62 of 114

Code Code Description

63056 Transpedicular approach with decompression of spinal cord, equina and/or nerve root(s) (eg,

herniated intervertebral disc), single segment; lumbar (including transfacet, or lateral

extraforaminal approach) (eg, far lateral herniated intervertebral disc)

63102 Vertebral corpectomy (vertebral body resection), partial or complete, lateral extracavitary

approach with decompression of spinal cord and/or nerve root(s) (eg, for tumor or

retropulsed bone fragments); lumbar, single segment

63200 Laminectomy, with release of tethered spinal cord, lumbar

63267 Laminectomy for excision or evacuation of intraspinal lesion other than neoplasm, extradural; lumbar

63268 sacral

63272 Laminectomy for excision of intraspinal lesion other than neoplasm, intradural; lumbar

63273 sacral

63277 Laminectomy for biopsy/excision of intraspinal neoplasm; extradural, lumbar

63278 extradural, sacral

63282 intradural, extramedullary, lumbar

63283 intradural, sacral

63303 Vertebral corpectomy (vertebral body resection), partial or complete, for excision of intraspinal lesion, single segment; extradural, lumbar or

sacral by transperitoneal or retroperitoneal approach

63 of 114

Code Code Description

63307 intradural, lumbar or sacral by transperitoneal or retroperitoneal approach

63650 Percutaneous implantation of neurostimulator electrode array, epidural

63655 Laminectomy for implantation of neurostimulator electrodes, plate/paddle,

epidural

63685 Insertion or replacement of spinal neurostimulator pulse generator or receiver,

direct or inductive coupling

64479 ‐ 64484

Transforaminal injections

64490 Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or

nerves innervating that joint) with image guidance (fluoroscopy or CT), cervical or thoracic; single level

64491 second level

64492 third and any additional level(s) level

64493 Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or

nerves innervating that joint) with image guidance (fluoroscopy or CT), lumbar or sacral;

single level

64494 second level

64495 third and any additional level(s) level

64580 Incision for implantation of neurostimulator electrode array; neuromuscular

64600 Destruction by neurolytic agent, trigeminal nerve; supraorbital, infraorbital, mental, or

inferior alveolar branch

64 of 114

Code Code Description

64605 second and third division branches at foramen ovale

64610 second and third division branches at foramen ovale under radiologic monitoring

64633 Destruction by neurolytic agent, paravertebral facet joint nerve(s), with imaging guidance

(fluoroscopy or CT); cervical or thoracic, single facet joint

+64634 each additional facet joint (List separately in addition to code for primary procedure)

64708 Neuroplasty, major peripheral nerve, arm or leg, open; other than specified

64713 brachial plexus

64718 Neuroplasty and/or transposition; ulnar nerve at elbow

64721 median nerve at carpal tunnel

+64727 Internal neurolysis, requiring use of operating microscope (List separately in addition to code

for neuroplasty) (Neuroplasty includes external neurolysis)

64742 Transection or avulsion of; facial nerve, differential or complete

64784 Excision of neuroma; major peripheral nerve, except sciatic

64790 Excision of neurofibroma or neurolemmoma; major peripheral nerve

64886 Nerve graft (includes obtaining graft), head or neck; more than 4 cm length

64905 Nerve pedicle transfer; first stage

65 of 114

Code Code Description

64910 Nerve repair; with synthetic conduit or vein allograft (eg, nerve tube), each nerve

64999 Unlisted procedure, nervous system

69140 Excision exostosis(es), external auditory canal

69145 Excision soft tissue lesion, external auditory canal

69310 Reconstruction of external auditory canal (meatoplasty) (eg, for stenosis due to injury,

infection) (separate procedure)

69320 Reconstruction external auditory canal for congenital atresia, single stage

69436 Tympanostomy (requiring insertion of ventilating tube), general anesthesia

69440 Middle ear exploration through postauricular or ear canal incision

69620 Myringoplasty (surgery confined to drumhead and donor area)

69631 Tympanoplasty without mastoidectomy (including canalplasty, atticotomy and/or middle

ear surgery), initial or revision; without ossicular chain reconstruction

69632 with ossicular chain reconstruction (eg, postfenestration)

69633 with ossicular chain reconstruction and synthetic prosthesis (eg, partial ossicular

replacement prosthesis [PORP], total ossicular replacement prosthesis [TORP])

69635 Tympanoplasty with antrotomy or mastoidotomy (including canalplasty, atticotomy, middle ear

surgery, and/or tympanic membrane repair); without ossicular chain reconstruction

66 of 114

Code Code Description

69636 with ossicular chain reconstruction

69637 with ossicular chain reconstruction and synthetic prosthesis (eg, partial ossicular replacement prosthesis [PORP], total ossicular replacement prosthesis [TORP])

69641 Tympanoplasty with mastoidectomy (including canalplasty, middle ear surgery, tympanic membrane repair); without ossicular chain reconstruction

69642 with ossicular chain reconstruction

69643 with intact or reconstructed wall, without ossicular chain reconstruction

69644 with intact or reconstructed canal wall, with ossicular chain reconstruction

69645 radical or complete, without ossicular chain reconstruction

69646 radical or complete, with ossicular chain reconstruction

69650 Stapes mobilization

69660 Stapedectomy or stapedotomy with reestablishment of ossicular continuity, with or without use of foreign material;

69661 with footplate drill out

69662 Revision of stapedectomy or stapedotomy

69930 Cochlear device implantation, with or without mastoidectomy

Other HCPCS codes related to the CPB:

S8040 Topographic brain mapping

67 of 114

Code Code Description

ICD‐10 codes covered if selection criteria are met for intraoperative SEPs:

C41.0 Malignant neoplasm of bones of skull and face [except mandible]

C41.2 Malignant neoplasm of vertebral column [excluding sacrum and coccyx]

C41.4 Malignant neoplasm of pelvic bones, sacrum, and coccyx

C70.0 ­ C70.9 C72.0 ­ C72.9

Malignant neoplasm of cranial nerves, cerebral meninges, spinal cord, and spinal meninges

C71.0 ­ C71.9

Malignant neoplasm of brain

C79.31, C79.49

Secondary malignant neoplasm of brain and other parts of nervous system [spinal cord]

C79.32 Secondary malignant neoplasm of cerebral meninges

D16.6 Benign neoplasm of vertebral column [excluding sacrum and coccyx]

D16.8 Benign neoplasm of pelvic bones, sacrum, and coccyx

D32.0 D33.4

­ Benign neoplasm of brain, cranial nerves, cerebral meninges, spinal cord, and spinal meninges

D42.0 ‐ D43.2 D43.4

Neoplasm of uncertain behavior of brain and spinal cord, or meninges

D49.6 Neoplasm of unspecified behavior of brain

G10 Huntington's disease

68 of 114

Code Code Description

G23.0 ‐ G26

Extrapyramidal and movement disorders [intractable]

G40.001 G40.919

Epilepsy [resection of brain tissue or tumor]

G50.8 Disorders of trigeminal nerve [compression]

G51.8 Other disorders of facial nerve [compression]

G93.1 Anoxic brain damage, not elsewhere classified

G93.5 Compression of brain

G93.6 Cerebral edema

H47.091 H47.099

Other disorders of optic nerve, not elsewhere classified [compression]

H81.01 H81.09

Meniere's disease [endolymphatic shunt placement]

H81.391 H81.399

Other and unspecified peripheral vertigo [vestibular resection]

H81.41 H81.49

Vertigo of central origin [vestibular resection]

H93.3x1 H93.3x9

Disorders of acoustic nerve [compression]

I06.0 I06.9

Diseases of aortic valve

I35.0 ‐ I35.9

Nonrheumatic aortic valve disorders

I70.0 Atherosclerosis of aorta

I71.00 I71.9

Dissection of aorta

I72.0 Aneurysm of carotid artery (common) (external) (internal, extracranial portion)

­

­

­

­

­

­

­

­

69 of 114

Code Code Description

I74.01 I74.09

Embolism and thrombosis of abdominal aorta

I74.11 Embolism and thrombosis of thoracic aorta

I77.71 Dissection of carotid artery

M41.00 M41.05,

M41.112 M41.115,

M41.122 M41.125,

M41.26 M41.27, M41.30 M41.35,

M41.82 M41.85,

M96.5

Idiopathic and thoracogenic scoliosis and kyphoscoliosis [correction involving traction]

[cervical, thoracic, thoracolumbar]

M41.41 ­ M41.45,

M41.52 ­ M41.55

Neuromuscular and other secondary scoliosis [correction involving traction] [cervical, thoracic,

thoracolumbar]

M47.14 ­ M47.15

Other spondylosis with myelopathy, thoracic and thoracolumbar region

M50.00 ‐ M50.03,

M51.04 ­ M51.05

Intervertebral disc disorder, with myelopathy

M96.1 Postlaminectomy syndrome, not elsewhere classified

P91.0 ­ P91.1 P91.3 ­ P91.5

Other disturbances of cerebral status of newborn

­

­

­

­

­

­

­

70 of 114

Code Code Description

Q01.0­ Q01.9

Encephalocele

Q04.0 ­ Q04.3

Congenital reduction deformities of brain

Q07.00 ‐ Q07.03

Arnold‐Chiari syndrome

Q28.2 Arteriovenous malformation of cerebral vessels

Q28.8 Other specified congenital malformations of circulatory system [arteriovenous malformation spine]

Q67.5, Q76.3 Q76.425 ­Q76.429

Congenital musculoskeletal deformities of spine [correction involving traction]

R25.0 ­ R25.9

Abnormal involuntary movements [intractable movement disorder]

R40.20 ­ R40.236

Coma [unconscious]

R42 Dizziness and giddiness [vertigo NOS]

R56.9 Unspecified convulsions [resection of brain tissue or tumor]

S02.0xx+ ­ S02.42x+ S02.600+ ­ S02.92x+

Fracture of skull and facial bones [conscious]

S06.0x0+ ‐ S06.9x9+

Intracranial injury

71 of 114

Code Code Description

S12.000+ S12.9xx+ S22.000+ S22.089+

S32.000+ S32.2xx+

Fracture of vertebral column

S14.0xx+ S14.159+ S24.0xx+ S24.159+ S34.01x+ ­ S34.139+

Spinal cord injury

T84.010+ T84.59x+

Complication of internal orthopedic prosthetic devices, implants, and grafts

T84.50x+ T84.7xx+

Infection and inflammatory reaction due to otherinternal orthopedic device, implant, and graft

T84.81x+ T84.9xx+

Other specified complications of internal orthopedic devices, implants, and grafts

Z47.2 , Z51.89

Aftercare involving internal fixation device

ICD‐10 codes not covered for indications listed in the CPB for intraoperative SEPs:

C07 Malignant neoplasm of parotid gland

C08.0 Malignant neoplasm of submandibular gland

C76.0 Malignant neoplasm of head, face, and neck

D00.0 D00.08

Carcinoma in situ of lip, oral cavity, and pharynx

D11.0 ­ D11.9

Benign neoplasm of major salivary glands

D37.030 ­D37.039

Neoplasm of uncertain behavior of major salivaryglands

­

­

­

­

­

­

­

­

­

72 of 114

Code Code Description

D49.0 Neoplasm of unspecified behavior of digestive system

E00.0 ­ E07.9

Disorders of the thyroid gland

K11.0 K11.9

Diseases of the salivary glands

M41.06 M41.08, M41.116 M41.119,M41.126 M41.129,M41.20, M41.26 M41.27, M41.80, M41, 86 M41.87

Idiopathic scoliosis [lumbar, sacral, unspecified]

M41.40, M41.46 M41.47, M41.50, M41.56 M41.57

Neuromuscular and other secondary scoliosis [lumbar, sacral, unspecified]

M43.26 M43.28

Fusion of spine, lumbar, lumbosacral, sacral or sacrococcygeal region

M47.16 Other spondylosis with myelopathy, lumbar region

M47.26 M47.28

Other spondylosis with radiculopathy, lumbar, lumbosacral, sacral or sacrococcygeal region

M47.816 ‐M47.818

Spondylosis without myelopathy or radiculopathy, lumbar, lumbosacral, sacral, or sacrococcygeal region

­

­

­

­

­

­

­

­

­

­

73 of 114

Code Code Description

M47.896 M47.898

Other spondylosis, lumbar, lumbosacral, sacral or sacrococcygeal region

M51.06 Intervertebral disc disorder with myelopathy, lumbar region

M51.16 ‐ M51.17

Intervertebral disc disorders with radiculopathy, lumbar or lumbosacral region

M51.26 M51.27

Other intervertebral disc displacement, lumbar or lumbosacral region

M51.36 M51.37

Other intervertebral disc degeneration, lumbar or lumbosacral region

M51.86 M51.9

Other and unspecified intervertebral disc disorders, lumbar, lumbosacral, sacral or

sacrococcygeal region

M53.2X6 M53.2X9

Spinal instabilities, lumbar, lumbosacral, sacral or sacrococcygeal region

M53.3 Sacrococcygeal disorders, not elsewhere classified

M53.86 M53.9

Other specified and unspecified dorsopathies, lumbar, lumbosacral, sacral or sacrococcygeal

region

M54.05 Low back pain

M54.16 ‐ M54.18

Radiculopathy, lumbar, lumbosacral, sacral or sacrococcygeal region

N35.010 N35.9 N99.110 N99.12

Urethral stricture

N40.0 N40.1

Enlarged prostate

­

­

­

­

­

­

­

­

­

74 of 114

Code Code Description

N40.2 ­N40.3

Nodular prostate

Q67.6 Pectus excavatum

Intra‐operative visual evoked potentials monitoring:

CPT codes covered if selection criteria are met:

95930 Visual evoked potential (VEP) testing central nervous system, checkerboard or flash

+95940 Continuous intraoperative neurophysiology monitoring in the operating room, one on one monitoring requiring personal attendance, each

15 minutes (List separately in addition to code for primary procedure)

+95941 Continuous intraoperative neurophysiology monitoring, from outside the operating room

(remote or nearby) or for monitoring of more than one case while in the operating room, per hour (List separately in addition to code for

primary procedure)

CPT codes not covered for indications listed in the CPB for intraoperative VEPs:

0333T Visual evoked potential, screening of visual acuity, automated

61680 ­ 61692

Surgery of intracranial arteriovenous malformation

HCPCS codes covered if selection criteria are met:

G0453 Continuous intraoperative neurophysiology monitoring, from outside the operating room

(remote or nearby), per patient, (attention directed exclusively to one patient) each 15 minutes (list in addition to primary procedure)

75 of 114

Code Code Description

ICD‐10 codes not covered for indications listed in the CPB for intraoperative VEPs:

Q28.3 Other malformations of cerebral vessels

Visual evoked potentials (VEPs):

CPT codes covered if selection criteria are met:

95930 Visual evoked potential (VEP) testing central nervous system, checkerboard or flash

CPT codes not covered for indications listed in the CPB:

0333T Visual evoked potential, screening of visual acuity, automated [not covered for screening]

ICD‐10 codes covered if selection criteria are met (for members > 3 mos of age):

A39.82 Meningococcal retrobulbar neuritis

A52.10 A52.19

Symptomatic neurosyphilis

A69.20 Lyme disease, unspecified

A83.0 ‐ A84.9 A85.2

Mosquito‐borne viral encephalitis, tick‐borne viral encephalitis, and viral encephalitis

transmitted by other and unspecified arthropods

B00.4 Herpesviral encephalitis

B05.0 Measles complicated by encephalitis

B06.01 Rubella encephalitis

B10.01 Human herpesvirus 6 encephalitis

B10.09 Other human herpesvirus encephalitis

C70.0 ­ C70.9 C72.0 ­

C72.9

Malignant neoplasm of other and unspecified parts of nervous system

­

76 of 114

Code Code Description

C79.31, C79.49

Secondary malignant neoplasm of brain and spinal cord

D32.0 D33.9

Benign neoplasm of brain and other parts of nervous system

D42.0 D43.9

Neoplasm of uncertain behavior of brain and spinal cord, meninges, and other and unspecified

parts of nervous system

D44.3 D44.5

Neoplasm of uncertain behavior of endocrine glands [pituitary gland, craniopharyngeal duct, pineal gland]

D49.6 Neoplasm of unspecified behavior of brain

F44.4 F44.7 F44.89 ­ F44.9

Conversion disorder

G11.0 G11.9

Hereditary ataxia

G23.0 G23.9

Other degenerative diseases of the basal ganglia

G35 Multiple sclerosis

G36.0 G37.9

Other demyelinating diseases of central nervous system

G45.0 G45.2 G45.8 ­ G45.9

Transient cerebral ischemic attacks and related syndromes

G50.0 ‐ G70.9

Trigeminal, facial, and other cranial nerve disorders, nerve root and plexus disorders,

mononeuritis, neuropathy, and myoneural disorders

­

­

­

­

­

­

­

­

77 of 114

Code Code Description

G80.0 G80.9

Cerebral palsy

G81.00 ‐ G81.94

Hemiplegia and hemiparesis

G93.1 Anoxic brain damage, not elsewhere classified

G93.2 Benign intracranial hypertension

G93.5 Compression of brain

G93.6 Cerebral edema

H47.011 H47.9

Disorders of the optic nerve and visual pathways

H53.001 H53.9

Visual disturbances

H81.01 H83.2x9

Disorders of vestibular function

H83.3 H94.83

Other disorders of ear and hearing loss

I60.00 ‐ I66.9

Subarachnoid hemorrhage, intracerebralhemorrhage, other and unspecified intracranial hemorrhage, occlusion and stenosis of precerebral arteries, and occlusion of cerebral

arteries

I67.1 Cerebral aneurysm, nonruptured

Q85.00 ‐ Q85.09

Neurofibromatosis (nonmalignant)

R26.0 ‐ R27.9 R29.5

Abnormality of gait, lack of coordination, and transient paralysis of limb

R40.20 R40.236

Coma [unresponsive]

­

­

­

­

­

­

78 of 114

Code Code Description

R40.3 Persistent vegetative state [unresponsive, unable to communicate]

R42 Dizziness and giddiness

R47.01 Aphasia [unable to communicate]

R94.110 ­R94.138

Nonspecific abnormal results of function studies of peripheral nervous system and special senses

S04.011+ ­ S04.9

Injury to optic nerve and pathways

S04.011s­ S04.9 S14.0xxs­ S14.9xxs S24.0xxs­ S24.9xxs S34.01xs­ S34.9xxs S44.00xs­ S44.92xs S54.00xs­ S54.92xs S64.00xs­ S64.92xs S74.00xs­ S74.92xs S84.00xs­ S84.92xs S94.00xs­ S94.92xs

Injury to cranial nerve, spinal cord, nerve root(s), spinal plexus(es), and other nerves of trunk, peripheral nerve of shoulder girdle and upper limb, or peripheral nerve of pelvic girdle and lower limb, sequela

S06.0x6+ Concussion with prolonged loss of consciousness without return to pre‐existing conscious level

ICD‐10 codes not covered for indications listed in the CPB (for members > 3 mos of age) (not all‐inclusive):

79 of 114

Code Code Description

B50.0 B54

Malaria

E22.0 ‐ E23.7

Hyperfunction, hypofunction and other disorders of the pituitary gland

F01.50 ­ F03.91,

F05

Dementia and delirium

F10.27 Alcohol dependence with alcohol‐induced persisting dementia

F10.97, F11.22, F13.27, F18.17

F18.27, F18.97, F19.17, F19.27

F19.97

Drug induced persisting dementia

F90.0 F90.9

Attention‐deficit hyperactivity disorder

G20 G21.9

Parkinson's disease

G30.0 G30.9

Alzheimer's disease

G31.84 Mild cognitive impairment, so stated [amnestic]

G95.0 Syringomyelia and syringobulbia

H30.90 H30.93

Unspecified chorioretinal inflammation [birdshot chorioretinopathy]

L93.0 L93.2

Lupus erythematosus

­

­

­

­

­

­

80 of 114

Code Code Description

M32.0­ M32.9

Systemic lupus erythematosus

O98.611 ‐ O98.63

Protozoal diseases complicating pregnancy, childbirth and the puerperium [malaria]

P35.0 P35.9

Congenital viral disease [specific to the perinatal period]

T37.2X1+ T37.2X6+

Poisoning by antimalarials and drugs acting on other blood protozoa

ICD‐10 codes not covered for indications listed in the CPB (for members < 3 mos of age/ neonatal screen):

B50.0 B54

Malaria

E22.0 ‐ E23.7

Hyperfunction, hypofunction and other disorders of the pituitary gland

G40.201 G40.219

Localization‐related (focal) (partial) symptomatic epilepsy and epileptic syndromes with complex

partial seizures, intractable or not intractable, with and without status epilepticus

G95 Syringomyelia and syringobulbia

L93.0 L93.2

Lupus erythematosus

M32.0­ M32.9

Systemic lupus erythematosus

P00.0 P96.9

Certain conditions originating in the perinatal period

P19.0 P19.9

Metabolic acidemia in newborn

P84 Other problems with newborn [birth asphyxia]

P91.60 ‐ P91.63

Hypoxic ischemic encephalopathy [HIE]

­

­

­

­

­

­

­

81 of 114

Code Code Description

T37.2X1+ ­T37.2X6+

Poisoning by antimalarials and drugs acting on other blood protozoa

Z00.110 Health examination for newborn under 8 days old

Z00.121 ­Z00.129

Encounter for routine child health examination with or without abnormal findings

Z01.00 ­Z01.01

Encounter for examination of eyes and vision [indicates routine screen without signs or symptoms when reported alone]

Z13.5 Encounter for screening for eye and ear disorders [indicates routine screen without signs or symptoms when reported alone]

Z13.858 Encounter for screening for other nervous system disorders

Z37.0 ­Z37.9

Outcome of delivery

Z38.00 ­Z38.8

Liveborn infants according to place of birth and type of delivery

Intra‐operative brain stem auditory evoked response (BAER) monitoring:

CPT codes covered if selection criteria are met:

92585 Auditory evoked potentials for evoked response audiometry and/or testing of the central nervous system; comprehensive

92586 Auditory evoked potentials for evoked response audiometry and/or testing of the central nervous system; limited

82 of 114

Code Code Description

+95940 Continuous intraoperative neurophysiology monitoring in the operating room, one on one monitoring requiring personal attendance, each 15 minutes (List separately in addition to code for primary procedure)

+95941 Continuous intraoperative neurophysiology monitoring, from outside the operating room (remote or nearby) or for monitoring of more than one case while in the operating room, per hour (List separately in addition to code for primary procedure)

HCPCS codes covered if selection criteria are met:

G0453 Continuous intraoperative neurophysiology monitoring, from outside the operating room (remote or nearby), per patient, (attention directed exclusively to one patient) each 15 minutes (list in addition to primary procedure

Intra‐operative brain stem auditory evoked response (BAER) monitoring may be appropriate for the following types of surgery:

22100 Partial excision of posterior vertebral component (eg, spinous process, lamina or facet) for intrinsic bony lesion, single vertebral segment; cervical

+22103 each additional segment (List separately in addition to code for primary procedure)

22110 Partial excision of vertebral body, for intrinsic bony lesion, without decompression of spinal cord or nerve root(s), single vertebral segment; cervical

+22116 each additional vertebral segment (List separately in addition to code for primary procedure)

83 of 114

Code Code Description

22210 Osteotomy of spine, posterior or posterolateral approach, 1 vertebral segment; cervical

+22216 each additional vertebral segment (List separately in addition to code for primary procedure)

22220 Osteotomy of spine, including discectomy, anterior approach, single vertebral segment; cervical

+22226 each additional vertebral segment (List separately in addition to code for primary procedure)

22548 Arthrodesis, anterior transoral or extraoral technique, clivus‐C1‐C2 (atlas‐axis), with or without excision of odontoid process

61343 Craniectomy, suboccipital with cervical laminectomy for decompression of medulla and spinal cord, with or without dural graft (eg, Arnold‐Chiari malformation)

61575 Transoral approach to skull base, brain stem or upper spinal cord for biopsy, decompression or excision of lesion

61576 requiring splitting of tongue and/or mandible (including tracheostomy)

62164 Neuroendoscopy, intracranial; with excision of brain tumor, including placement of external ventricular catheter for drainage

62165 with excision of pituitary tumor, transnasal or trans‐sphenoidal approach

84 of 114

Code Code Description

63001 Laminectomy with exploration and/or decompression of spinal cord and/or cauda

equina, without facetectomy, foraminotomy or discectomy, (eg, spinal stenosis), one or two

vertebral segments; cervical

ICD‐10 codes covered if selection criteria are met:

C41.0 Malignant neoplasm of bones of skull and face

C41.2 Malignant neoplasm of vertebral column

C71.7 Malignant neoplasm of brain stem

C72.0 Malignant neoplasm of spinal cord

Q75.0 Q75.9

Other congenital malformations of skull and face bones

Brain stem auditory evoked response (BAER), comprehensive:

CPT codes covered if selection criteria are met:

92585 Auditory evoked potentials for evoked response audiometry and/or testing of the central nervous system; comprehensive

CPT codes not covered for indications listed in the CPB:

69631 ‐ 69633

Tympanoplasty & ossicle chain reconstruction

69660 ­ 69662

Stapedectomy

ICD‐10 codes covered if selection criteria are met (members > 3 mos of age):

A39.82 Meningococcal retrobulbar neuritis

A52.10 ­ A5219

Symptomatic neurosyphilis

A69.20 Lyme disease, unspecified

­

85 of 114

Code Code Description

A81.2 Progressive multifocal leukoencephalopathy

A83.0 A84.9,

A85.2

Mosquito‐borne viral encephalitis, tick‐borne viral encephalitis, and viral encephalitis

transmitted by other and unspecified arthropods

B00.4 Herpesviral encephalitis

B05.0 Measles complicated by encephalitis

B06.01 Rubella encephalitis

B10.01 Human herpesvirus 6 encephalitis

B10.09 Other human herpesvirus encephalitis

C70.0 ­ C70.9

C72.0 ­ C72.9

Malignant neoplasm of other and unspecified parts of the nervous system

C71.0 ­ C71.9

Malignant neoplasm of brain

C79.31, C79.49

Secondary malignant neoplasm of brain and spinal cord

D32.0 D33.9

Benign neoplasm of brain and other parts of nervous system

D42.0 D43.9

Neoplasm of uncertain behavior of brain and spinal cord, meninges, and other and unspecified

parts of nervous system

D44.3 D44.5

Neoplasm of uncertain behavior of endocrine glands [pituitary gland, craniopharyngeal duct, pineal gland]

D49.6 Neoplasms of unspecified behavior of brain

F44.4 F44.7 F44.89 ­

F44.9

Conversion disorder

­

­

­

­

­

86 of 114

Code Code Description

G09 Sequelae of inflammatory disease of central nervous system

G11.0 G11.9

Hereditary ataxia

G23.0 G23.9

Other degenerative disease of basal ganglia

G35 Multiple Sclerosis

G36.0 G37.9

Other demyelinating diseases of the central nervous system

G45.0 ‐ G45.2 G45.8 ‐ G45.9

Transient cerebral ischemic attacks and related syndromes

G50.0 ‐ G70.9

Trigeminal, facial, and other cranial nerve disorders, nerve root and plexus disorders,

mononeuritis, neuropathy, and myoneural disorders

G80.0 G80.9

Cerebral palsy

G81.00 ‐ G81.94

Hemiplegia and hemiparesis

G93.0 Cerebral cysts

G93.1 Anoxic brain damage, not elsewhere classified

G93.2 Benign intracranial hypertension

G93.5 Compression of brain

G93.6 Cerebral edema

G93.82 Brain death [for members >3 months of age]

H47.011 H47.9

Disorders of the optic nerve and visual pathways

­

­

­

­

­

87 of 114

Code Code Description

H53.001 H53.9

Visual disturbances

H81.01 H83.2x9

Disorders of vestibular function

H83.3 H94.83

Other disorders of ear and hearing loss

I60.00 ‐ I66.9

Subarachnoid hemorrhage, intracerebral hemorrhage, other and unspecified intracranial hemorrhage, occlusion and stenosis of precerebral arteries, occlusion of cerebral

arteries

I67.1 Cerebral aneurysm, nonruptured

I67.4 Hypertensive encephalopathy

I67.81 I67.82

I67.89

Acute cerebrovascular insufficiency, cerebralischemia and other cerebrovascular disease

I67.841 I67.848

Cerebral vasospasm and vasoconstriction

P03.0 P03.9

Newborn (suspected to be) affected by other complications of labor and delivery

P91.0 P91.1 P91.3 P91.5

Other disturbances of cerebral status of newborn

Q01.0 ‐ Q01.9

Encephalocele

Q04.0 Q04.3

Congenital reduction deformities of brain

Q07.00 ‐ Q07.03

Arnold‐Chiari syndrome

­

­

­

­

­

­

­

­

­

88 of 114

Code Code Description

R26.0 ‐ R27.9, R29.5

Abnormality of gait, lack of coordination, and transient paralysis of limb

R40.20 R40.236

Coma

R40.3 Persistent vegetative state

R42 Dizziness and giddiness

R94.110 R94.138

Nonspecific abnormal results of function studies of peripheral nervous system and special senses

S04.011+ S04.9

Injury to optic nerve and pathways

S04.011s­ S04.9 S14.0xxs­ S14.9xxs S24.0xxs­ S24.9xxs S34.01xs­ S34.9xxs S44.00xs­ S44.92xs S54.00xs­ S54.92xs S64.00xs­ S64.92xs S74.00xs­ S74.92xs S84.00xs­ S84.92xs S94.00xs­ S94.92xs

Injury to cranial nerve, spinal cord, nerve root(s), spinal plexus(es), and other nerves of trunk, peripheral nerve of shoulder girdle and upper limb, or peripheral nerve of pelvic girdle and lower limb, sequela

­

­

­

S06.0x6+ Concussion with prolonged loss of consciousness without return to pre‐existing conscious level

89 of 114

Code Code Description

Z01.110 Encounter for hearing examination without abnormal findings

Z76.1 ­Z76.2

Encounter for health supervision of foundling and other healthy infant or child

Z79.2 Long‐term (current) use of antibiotics [damage due to ototoxic drugs]

Z79.891 ­Z79.899

Long‐term (current) use of opiate analgesic and other drug therapy [damage due to ototoxic drugs]

ICD‐10 codes not covered for indications listed in the CPB (members > 3 mos of age) (not all‐inclusive):

F01.50 ­F03.91, F05

Dementia and delirium

F02.80 ­F02.81

Dementia in other diseases classified elsewhere with or without behavioral disturbance

F06.8 Other specified mental disorders due to known physiological condition

F10.27 Alcohol dependence with alcohol‐induced persisting dementia

F10.97, F11.22, F13.27, F18.17 F18.27, F18.97, F19.17, F19.27 F19.97

Drug induced persisting dementia

F20.2 Catatonic schizophrenic

F20.9 Schizophrenia, unspecified

90 of 114

Code Code Description

F30.10 ­ F33.9

Episodic mood disorders

F34.1 Dysthymic disorder

F43.10 ‐F43.12

Posttraumatic stress disorder

F84.0 Autistic disorder

F90.0 90.9

Attention‐deficit hyperactivity disorder

G12.8 G12.9

Other and unspecified muscular atrophies [Kennedy's syndrome]

G20 G21.9

Parkinson's disease

G30.0 G30.9

Alzheimer's disease

G31.01 Pick's disease

G31.09 Other frontotemporal dementia

G31.83 Dementia with Lewy bodies

G95.0 Syringomyelia and syringobulbia

P00.2 P00.3

P00.89 P00.9

Newborn (suspected to be) affected by maternal conditions that may be unrelated to present pregnancy

R43.0 R43.9

Disturbances of smell and taste

T14.91 Suicide attempt

Z00.2 ­ Z00.3,

Z00.8

Constitutional states in development

­

­

­

­

­

­

­

91 of 114

Code Code Description

Z01.110 Encounter for examination of ears and hearing without abnormal findings [indicates routine exam without signs or symptoms when reported alone]

Z13.5 Encounter screening for ear disease [indicates routine exam without signs or symptoms when reported alone]

Z37.0 ­Z37.69

Outcome of delivery

Z38.00 ­Z38.8

Liveborn infants according to place of birth and type of delivery

Z76.1 Encounter for health supervision and care of foundling

Z76.2 Encounter for health supervision and care of other healthy infant and child

ICD‐10 codes not covered for indications listed in the CPB (for members < 3 mos of age/ neonatal screen):

G95.0 Syringomyelia and syringobulbia

P00.0 ­P96.9

Certain conditions originating in the perinatal period

Z00.2 ­Z00.3, Z00.8 Z76.1 ­Z76.2

Health supervision of infant or child or constitutional states of development [neonatal screen]

Z01.110 ­Z01.118

Other examination of ears and hearing [indicates routine exam without signs or symptoms when reported alone]

Z13.5 Encounter for screening for ear diseases [indicates routine exam without signs or symptoms when reported alone]

92 of 114

Code Code Description

Z37.0 ­ Z37.9

Outcome of delivery

Z38.00 ‐ Z38.8

Liveborn infants according to place of birth and type of delivery

Brain stem auditory evoked response (BAER), limited:

CPT codes covered if selection criteria are met:

92586 Auditory evoked potentials for evoked response audiometry and/or testing of the central nervous system; limited

CPT codes not covered for indications listed in the CPB:

69631 ‐ 69633

Tympanoplasty & ossicle chain reconstruction

69660 69662

Stapedectomy

ICD‐10 codes covered if selection criteria are met:

A39.82 Meningococcal retrobulbar neuritis

A52.10 ­ A52.19

Symptomatic neurosyphilis

A69.20 Lyme disease, unspecified

A83.0 ‐ A84.9, A85.2

Mosquito‐borne viral encephalitis, tick‐borne viral encephalitis, and viral encephalitis transmitted by other and unspecified arthropods

B00.4 Herpesviral encephalitis

B05.0 Measles complicated by encephalitis

B06.01 Rubella encephalitis

B10.01 Human herpesvirus 6 encephalitis

B10.09 Other human herpesvirus encephalitis

­

93 of 114

Code Code Description

C70.0 ­ C70.9

C72.0 ­ C72.9

Malignant neoplasm of other and unspecified parts of the nervous system

C71.0 ­ C71.9

Malignant neoplasm of brain

D32.0 D33.9

Benign neoplasm of brain and other parts of the nervous system

D42.0 D43.9

Neoplasm of uncertain behavior of brain and spinal cord, meninges, and other and unspecified

parts of nervous system

D44.3 D44.5

Neoplasm of uncertain behavior of endocrine glands [pituitary gland, craniopharyngeal duct, pineal gland]

D49.6 Neoplasms of unspecified behavior of brain

F44.4 F44.7

Conversion disorder

G09 Sequelae of inflammatory disease of central nervous system

G11.0 G11.9

Hereditary ataxia

G23.0 G23.9

Other degenerative disease of basal ganglia

G36.0 G37.9

Other demyelinating diseases of the central nervous system

G45.0 G45.2,

G45.8 G45.9

Transient cerebral ischemic attacks and related syndromes

­

­

­

­

­

­

­

­

­

94 of 114

Code Code Description

G50.0 G70.9

Trigeminal, facial, and other cranial nerve disorders, nerve root and plexus disorders,

mononeuritis, neuropathy, and myoneural disorders

G80.0 G80.9

Cerebral palsy

G81.00 G81.94

Hemiplegia and hemiparesis

G93.0 Cerebral cysts

G93.1 Anoxic brain damage, not elsewhere classified

G93.2 Benign intracranial hypertension

G93.5 Compression of brain

G93.6 Cerebral edema

H53.001 H53.9

Visual disturbances

H83.3 H94.83

Other disorders of ears and hearing loss

I60.00 I66.9

Subarachnoid hemorrhage, intracerebral hemorrhage, other and unspecified intracranial hemorrhage, occlusion and stenosis of precerebral arteries, occlusion of cerebral arteries

I67.1 Cerebral aneurysm, nonruptured

I67.4 Hypertensive encephalopathy

I67.81 I67.89

Other specified cerebrovascular diseases

­

­

­

­

­

­

­

95 of 114

Code Code Description

Numerous options

Injury to cranial nerve, spinal cord, nerve root(s), spinal plexus(es), and other nerves of trunk,

peripheral nerve of shoulder girdle and upper limb, or peripheral nerve of pelvic girdle and lower limb, sequela

P00.2 P00.3

P00.89 P00.9

Newborn (suspected to be) affected by maternal conditions that may be unrelated to present pregnancy

P03.0 P03.9

Newborn (suspected to be) affected by other complications of labor and delivery

P91.0 P91.1 P91.3 P91.5

Other disturbances of cerebral status of newborn

Q01.00 ‐ Q01.9

Encephalocele

Q04.0 Q04.3

Congenital reduction deformities of brain

Q07.00 ‐ Q07.03

Arnold‐Chiari Syndrome

R26.0 R27.9, R29.5

Abnormality of gait, lack of coordination, and transient paralysis of limb

R40.20 R40.236

Coma

R40.3 Persistent vegetative state

R42 Dizziness and giddiness

R94.110 R94.138

Nonspecific abnormal results of function studies of peripheral nervous system and special senses

­

­

­

­

­

­

­

­

­

96 of 114

Code Code Description

S04.011+ ­S04.9

Injury to optic nerve and pathways

S06.0x6+ Concussion with prolonged loss of consciousness without return to pre‐existing conscious level

Z00.110 Health examination for newborn under 8 days old

Z00.111 Health examination for newborn under 8 to 28 days old

Z00.121 ­Z00.129

Encounter for routine child health examination with/without abnormal findings [over 28 days]

Z01.110 Encounter for hearing examination following failed hearing screening

Z37.0 ­Z37.9

Outcome of delivery

Z38.00 ‐Z38.8

Liveborn infants according to place of birth and type of delivery

Z76.2 Encounter for health supervision and care of other healthy infant and child

Z79.2 Long‐term (current) use of antibiotics [damage due to ototoxic drugs]

Z79.891 ­Z79.899

Long‐term (current) use of opiate and other drug therapy [damage due to ototoxic drugs]

ICD‐10 codes not covered for indications listed in the CPB:

G12.8 ­G12.9

Other and unspecified muscular atrophies [Kennedy's syndrome]

G95.0 Syringomyelia and syringobulbia

T14.91 Suicide attempt

Evoked otoacoustic emissions:

CPT codes covered if selection criteria are met:

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Code Code Description

92558 Evoked otoacoustic emissions, screening (qualitative measurement of distortion product or transient evoked otoacoustic emissions), automated analysis

92587 Evoked otoacoustic emissions; limited (single stimulus level, either transient or distortion products)

92588 comprehensive or diagnostic evaluation (comparison of transient and/or distortion product otoacoustic emissions at multiple levels and frequencies [not covered for routine screening of neonates]

ICD‐10 codes not covered for indications listed in the CPB (for comprehensive exam only for members < 3 mos. of age/ neonatal screen):

P00.0 ­P96.9

Certain conditions originating in the perinatal period

Z00.2 ­Z00.3, Z00.8 Z76.1 ­Z76.2

Health supervision of infant or child or constitutional states of development [neonatal screen]

Z01.10 ­Z01.118

Encounter for examination of ears and hearing without abnormal findings

Z01.110 ­Z01.118

Encounter for examination of ears and hearing without abnormal findings [indicates routine exam without signs or symptoms when reported alone]

Z13.5 Encounter for screening for ear diseases [indicates routine exam without signs or symptoms when reported alone]

98 of 114

Code Code Description

Z37.0 ­ Z37.9

Outcome of delivery

Z38.00 ‐ Z38.8

Liveborn infants according to place of birth and type of delivery

Z76.1 Encounter for health supervision and care of foundling

Z76.2 Encounter for health supervision and care of other healthy infant and child

Motor evoked potentials (other than intraoperative with SSEPs):

CPT codes not covered for indications listed in the CPB:

95928 Central motor evoked potential study (transcranial motor stimulation); upper limbs

95929 lower limbs

95939 Central motor evoked potential study (transcranial motor stimulation); in upper and lower limbs

ICD‐10 codes not covered for indications listed in the CPB:

E83.01 Wilson's disease

Motor evoked potentials not covered intraoperatively:

CPT codes not covered for indications listed in the CPB:

63650 Percutaneous implantation of neurostimulator electrode array, epidural

Vestibular evoked myogenic potentials or ocular vestibular evoked myogenic potentials ‐ no specific code:

The above policy is based on the followingreferences:

99 of 114

1. Schmid UD, Hess CW, Ludin HP. Somatosensory evokedresponses following nerve and segmental stimulation donot confirm cervical radiculopathy with sensory deficit. JNeurol Neurosurg Psychiatry. 1988;51(2):182‐187.

2. American Academy of Neurology. Assessment:Dermatomal somatosensory evoked potentials. Report ofthe American Academy of Neurology's Therapeutics andTechnology Assessment Subcommittee. Neurology.1997;49(4):1127‐1130.

3. Galla JD, Ergin MA, Lansman SL, et al. Use ofsomatosensory evoked potentials for thoracic andthoracoabdominal aortic resections. Ann Thorac Surg.1999;67(6):1947‐1952.

4. Guerit JM, Witdoeckt C, Verhelst R, et al. Sensitivity,specificity, and surgical impact of somatosensory evokedpotentials in descending aorta surgery. Ann Thorac Surg.1999;67(6):1943‐1946.

5. Norcross‐Nechay K, Mathew T, Simmons JW, et al.Intraoperative somatosensory evoked potential findings inacute and chronic spinal canal compromise. Spine.1999;24(10):1029‐1033.

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7. Bejjani GK, Nora PC, Vera PL, et al. The predictive value ofintraoperative somatosensory evoked potentialmonitoring: Review of 244 procedures. Neurosurgery.1998;43(3):491‐500.

8. Kresch EN, Levitan ML, Baran EM, et al. Correlationanalysis of somatosensory evoked potential waveforms:Clinical applications. Arch Phys Med Rehabil.1998;79(2):184‐190.

9. Matsui H, Kanamori M, Kawaguchi Y, et al. Clinical andelectrophysiologic characteristics of compressed lumbarnerve roots. Spine. 1997;22(18):2100‐2105.

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11. Aminoff MJ, Goodin DS, Barbaro NM, et al. Dermatomal

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Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.

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AETNA BETTER HEALTH® OF PENNSYLVANIA

Amendment to Aetna Clinical Policy Bulletin Number: 0181 Evoked Potential Studies

There are no amendments for Medicaid.

www.aetnabetterhealth.com/pennsylvania revised 04/12/2018