Close Window
Aetna Aetna
Clinical Policy Bulletin:
Evoked Potential Studies
Number: 0181


Policy

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

    1. 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 who show specific structural damage to the somatosensory system, and who are candidates for emergency spinal cord surgery; or
      2. To evaluate acute anoxic encephalopathy (within 3 days of the anoxic event); or
      3. To evaluate persons with suspected brain death; or
      4. To identify clinically silent brain lesions in multiple sclerosis suspects in order to establish the diagnosis, where multiple sclerosis is suspected due to presence 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 forindications other than the ones listed above has not been established.

    2. 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 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:

        1. Correction of scoliosis or deformity of the spinal cord involving traction on the cord
        2. Decompression of the spinal cord where function of the spinal cord is at risk
        3. Removal of spinal cord tumors
        4. Surgery as a result of traumatic injury to the spinal cord
        5. Surgery for arteriovenous (AV) malformation of the spinal cord
           
      2. Intracranial Surgeries:

        1. Chiari malformation surgery
        2. Correction of cerebral vascular aneurysms
        3. Deep brain stimulation
        4. Endolymphatic shunt for Meniere's disease
        5. Microvascular decompression of cranial nerves (e.g., optic, trigeminal, facial, auditory nerves)
        6. Oval or round window graft
        7. Removal of cavernous sinus tumors
        8. Removal of tumors that affect cranial nerves
        9. Resection of brain tissue close to the primary motor cortex and requiring brain mapping
        10. Resection of epileptogenic brain tissue or tumor
        11. Surgery as a result of traumatic injury to the brain
        12. Surgery for intracranial AV malformations
        13. Surgery for intractable movement disorders
        14. Vestibular section for vertigo
           
      3. Vascular Surgeries:

        1. Arteriography, during which there is a test occlusion of the carotid artery
        2. Circulatory arrest with hypothermia (does not include surgeries performed under circulatory bypass such as CABG, and ventricular aneurysms)
        3. Distal aortic procedures, where there is risk of ischemia to the spinal cord
        4. Surgery of the aortic arch, its branch vessels, or thoracic aorta, including carotid artery surgery, 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 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.

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

    1. To diagnose and monitor multiple sclerosis (acute or chronic phases); or
    2. To evaluate signs and symptoms of visual loss in persons who are unable to communicate (e.g., unresponsive persons, etc; or
    3. To identify persons at increased risk for developing clinically definite multiple sclerosis (CDMS); or
    4. 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.

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

    1. For cerebral vascular surgery; or
    2. For Chiari malformation surgery; or
    3. For intra-operative monitoring during microvascular decompression of cranial nerve when decompression is performed via the intra-cranial posterior fossa approach; or
    4. For intra-operative monitoring during resection of chordoma , odontoidectomy, decompression of tumor from anterior brainstem/high spinal cord; or
    5. To assess brain death or profound metabolic coma in selected cases where diagnosis or outcome is unclear from standard tests (e.g., EEG); or
    6. To assess recovery of brainstem function after a lesion compressing the brainstem has been surgically removed; or
    7. To diagnose and monitor demyelinating and degenerative diseases affecting the brain stem (e.g., central pontine myelinolysis, olivopontocerebellar (OPC) degeneration, etc.); or
    8. To diagnose post-meningitic deafness in children; or
    9. To diagnose suspected acoustic neuroma; or
    10. To evaluate infants and children who have suspected hearing loss that can not be effectively measured or monitored through audiometry; or
    11. To localize the cause of a central nervous system deficit seen on examination, but not explained by CT or MRI; or
    12. 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 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;
  • 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) 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 (see CPB 0390 - Smell and Taste Disorders: Diagnosis);
  • Intraoperative BAER during stapedectomy, tympanoplasty and ossicle reconstruction
  • Intraoperative MEP during implantation of a spinal cord stimulator
  • 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 visual evoked potentials (e.g., for pituitary surgery, during intra-cranial surgery for arterio-venous malformation);
  • Motor evoked potentials other than for intraoperative use with SSEPs (e.g., facial MEPs during cerebellopontine angle and skull base tumor surgery);

  • SEPs for radiculopathies and peripheral nerve lesions where standard nerve conduction velocity studies are diagnostic (see CPB 0502 - Nerve Conduction Velocity Studies);

  • 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 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 differentiation of Meniere disease from vestibular migraine)


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 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 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 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.

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 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 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 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 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.

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 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.

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-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 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-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 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 0.97, 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 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 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 anoxic-ischemic 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 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 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-to-baseline 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 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 (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 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 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.

Appendix

Documentation Requirements:

  1. All medical necessity criteria must be clearly documented in the member's medical record and made available upon request.
  2. The member's medical record must contain documentation that fully supports the medical necessity for evoked potential studies. This documentation includes, but is not limited to, relevant medical history, physical examination, the anatomic location of the planned surgical procedure, the rationale for the location and modalities to be monitored, and results of pertinent diagnostic tests or procedures.
  3. For the BAERs, the member’s medical record should document the otologic exam describing both ear canals and tympanic membranes, as well as a gross hearing assessment. The medical record should also include the results of air and bone pure tone audiogram and speech audiometry.
  4. The physician’s evoked potential report should note which nerves were tested, latencies at various testing points, and an evaluation of whether the resulting values are normal or abnormal.
  5. 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 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.
  6. For 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, increments of less than 30 minutes should not be billed. For continuous intraoperative neurophysiology monitoring in the operating room with one on one monitoring requiring personal attendance, increments of less than 8 minutes should not be billed.
 
CPT Codes / HCPCS Codes / ICD-9 Codes
Somatosensory evoked potentials (SEPs, SSEPs):
CPT codes covered if selection criteria are met:
95925
95926
95927
95938
ICD-9 codes covered if selection criteria are met:
333.0 Other degenerative diseases of the basal ganglia [olivopontocerebellar (OPC) degeneration]
334.0 Friedreich's ataxia
336.0 - 336.9 Other diseases of spinal cord [unexplained myelopathy]
340 Multiple sclerosis [with clinically silent lesions]
341.0 - 341.9 Other demyelinating diseases of central nervous system
348.1 Anoxic brain damage
348.82 Brain death
952.00 - 953.9 Spinal cord injury without evidence of spinal bone injury and injury to nerve roots and spinal plexus [unconscious]
ICD-9 codes not covered for indications listed in the CPB (not all-inclusive):
266.2 Other B-complex deficiencies [diagnosis and management of acquired metabolic disorders]
270.0 - 277.9 Other metabolic disorders [diagnosis and management of acquired metabolic disorders]
309.81 Posttraumatic stress disorder
314.00 - 314.01 Attention deficit disorder with or without mention of hyperactivity [ADD or ADHD]
315.10, 315.19 Other and unspecified spinal muscular atrophy [Kennedy's syndrome]
335.20 Amyotrophic lateral sclerosis [ALS]
353.0 Brachial plexus lesions [thoracic outlet syndrome]
354.0 - 355.9 Mononeuritis [radiculopathies, peripheral nerve lesions, carpal tunnel syndrome/nerve entrapment]
721.1 Cervical spondylosis with myelopathy
722.0 - 722.2 Displacement of intervertebral disc without myelopathy
722.70 - 722.73 Intervertebral disc disorder with myelopathy [radiculopathies]
723.4 Brachial neuritis or radiculitis [where standard nerve conduction velocity studies are diagnostic]
724.3 Sciatica [radiculopathies]
724.4 Thoracic or lumbosacral neuritis or radiculitis, unspecified [radiculopathies]
729.2 Neuralgia, neuritis, and radiculitis, unspecified
800.00 - 804.99 Fracture of skull [conscious]
805.00 - 805.9 Fracture of vertebral column [conscious]
806.00 - 806.9 Fracture of vertebral column with spinal cord injury [conscious]
850.00 - 854.19 Intracranial injury, excluding those with skull fracture [conscious]
952.00 - 953.9 Spinal cord injury without evidence of spinal bone injury and injury to nerve roots and spinal plexus [conscious]
961.2 Poisoning by heavy metal anti-infectives
984.0 - 984.9 Toxic effect of lead and its compounds (including fumes)
V80.0 Special screening for neurological conditions [indicates routine exam without signs or symptoms when reported alone]
V82.5 Special screening for chemical poisoning and other contamination [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
95941
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 an all-inclusive):
CPT codes covered if selection criteria are met for intraoperative SEPs:
22210 - 22226
22305 - 22328
22532 - 22819
22840 - 22855
31200 - 31230
33320 - 33335
33400 - 33417
33800 - 33853
33860 - 33877
61000 - 61070
61105 - 61253
61304 - 61576
61600 - 61616
61618 - 61619
61623 - 61626
61680 - 61711
61720 - 61791
61850 - 61888
62000 - 62148
62160 - 62165
62263 - 62319
63001 - 63103
63170 - 63308
63600 - 63615
63700 - 63710
67570
69666
69667
69720
69725
69740
69745
69805
69806
69915
69950
69955
99173
CPT codes not covered for indications listed in the CPB for intraoperative SEPs:
27130 - 27138
33510 - 33548
42410 - 42426
42440
60000 - 60512
61546
61548
62165
63650
Other HCPCS codes related to the CPB:
S8040 Topographic brain mapping
ICD-9 codes covered if selection criteria are met for intraoperative SEPs:
170.0 Malignant neoplasm of bones of skull and face, except mandible
170.2 Malignant neoplasm of vertebral column, excluding sacrum and coccyx
170.6 Malignant neoplasm of pelvic bones, sacrum, and coccyx
191.0 - 191.9 Malignant neoplasm of brain
192.0 - 192.3 Malignant neoplasm of cranial nerves, cerebral meninges, spinal cord, and spinal meninges
198.3 Secondary malignant neoplasm of brain and spinal cord
198.4 Secondary malignant neoplasm of other parts of nervous system
213.2 Benign neoplasm of vertebral column, excluding sacrum and coccyx
213.6 Benign neoplasm of pelvic bones, sacrum, and coccyx
225.0 - 225.4 Benign neoplasm of brain, cranial nerves, cerebral meninges, spinal cord, and spinal meninges
237.5 - 237.6 Neoplasm of uncertain behavior of brain and spinal cord, or meninges
239.6 Neoplasm of unspecified nature of brain
333.0 - 333.99 Other extrapyramidal disease and abnormal movement disorders [intractable]
345.00 - 345.91 Epilepsy [resection of brain tissue or tumor]
348.1 Anoxic brain damage
348.4 Compression of brain
348.5 Cerebral edema
350.8 Other specified trigeminal nerve disorders [compression]
351.8 Other facial nerve disorders [compression]
377.49 Other disorders of optic nerve [compression]
386.00 - 386.04 Meniere's disease [endolymphatic shunt placement]
386.10 - 386.19 Other and unspecified peripheral vertigo [vestibular resection]
386.2 Vertigo of central origin [vestibular resection]
388.5 Disorders of acoustic nerve [compression]
395.0 - 395.9 Diseases of aortic valve
424.1 Aortic valve disorders
440.0 Atherosclerosis of aorta
441.00 - 441.9 Dissection of aorta
442.81 Other aneurysm of artery of neck
443.21 Dissection of carotid artery
444.0 Arterial embolism and thrombosis of abdominal aorta
444.1 Arterial embolism and thrombosis of thoracic aorta
721.41 - 721.42 Thoracic or lumbar spondylosis with myelopathy
722.70 - 722.73 Intervertebral disc disorder, with myelopathy
722.80 - 722.83 Postlaminectomy syndrome
737.30 - 737.39 Kyphoscoliosis and scoliosis [correction involving traction]
737.43 Scoliosis associated with other conditions [correction involving traction]
741.00-741.03 Spina bifida with hydrocephalus
742.0 Encephalocele
742.2 Congenital reduction deformities of brain
747.81 Anomalies of cerebrovascular system [arteriovenous malformation brain]
747.82 Spinal vessel anomaly [arteriovenous malformation spine]
754.2 Congenital musculoskeletal deformities of spine [correction involving traction]
779.2 Cerebral depression, coma, and other abnormal cerebral signs
780.01 Coma [unconscious]
780.39 Other convulsions [resection of brain tissue or tumor]
780.4 Dizziness and giddiness [vertigo NOS]
781.0 Abnormal involuntary movements [intractable movement disorder]
800.00 - 804.99 Fracture of skull
805.0 - 806.9 Fracture of vertebral column
850.00 - 854.19 Intracranial injury, excluding those with skull fracture
952.00 - 953.9 Spinal cord injury without evidence of spinal bone injury and injury to nerve roots and spinal plexus
996.40 - 996.49 Mechanical complication of internal orthopedic device, implant, and graft
996.67 Infection and inflammatory reaction due to other internal orthopedic device, implant, and graft
996.78 Other complications due to other internal orthopedic device, implant, and graft
V54.01 - V54.09 Aftercare involving internal fixation device
ICD-9 codes not covered for indications listed in the CPB for intraoperative SEPs:
142.0 Malignant neoplasm of parotid gland
142.1 Malignant neoplasm of submandibular gland
195.0 Malignant neoplasm of head, face, and neck
210.2 Benign neoplasm of major salivary glands
230.0 Carcinoma in situ of lip, oral cavity, and pharynx
235.0 Neoplasm of uncertain behavior of major salivary glands
239.0 Neoplasm of unspecified nature of digestive system
240.0 - 246.9 Disorders of the thyroid gland
527.0 - 527.9 Diseases of the salivary glands
598.0 - 598.9 Urethral stricture
600.00 - 600.01 Hypertrophy (benign) of prostate
600.10 - 600.11 Nodular prostate
600.20 - 600.21 Benign localized hyperplasia of prostate
600.90 - 600.91 Hyperplasia of prostate, unspecified
754.81 Pectus excavatum
Intra-operative visual evoked potentials monitoring:
CPT codes covered if selection criteria are met:
0333T
95930
+95940
+95941
CPT codes not covered for indications listed in the CPB for intraoperative VEPs:
61680 - 61692
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)
ICD-9 codes not covered for indications listed in the CPB for intraoperative VEPs::
747.81 Congenital anomalies of cerebrovascular system
Visual evoked potentials (VEPs):
CPT codes covered if selection criteria are met:
0333T
95930
ICD-9 codes covered if selection criteria are met (for members > 3 mos of age):
036.81 Meningococcal optic neuritis
054.3 Herpetic meningoencephalitis
055.0 Postmeasles encephalitis
056.01 Encephalomyelitis due to rubella
058.21 Human herpesvirus 6 encephalitis
058.29 Other human herpesvirus encephalitis
062.0 - 064 Mosquito-borne viral encephalitis, tick-borne viral encephalitis, and viral encephalitis transmitted by other and unspecified arthropods
088.81 Lyme disease
094.0 - 094.9 Neurosyphilis
192.0 - 192.9 Malignant neoplasm of other and unspecified parts of nervous system
198.3 - 198.4 Secondary malignant neoplasm of brain and spinal cord
225.0 - 225.9 Benign neoplasm of brain and other parts of nervous system
237.0 - 237.1 Neoplasm of uncertain behavior of endocrine glands and nervous system
237.5 - 237.9 Neoplasm of uncertain behavior of brain and spinal cord, meninges, neurofibromatosis, and other and unspecified parts of nervous system
239.6 Neoplasm of unspecified nature of brain
300.11 Conversion disorder
333.0 Other degenerative diseases of the basal ganglia
334.0 - 334.9 Spinocerebellar disease
340 Multiple sclerosis
341.0 - 341.9 Other demyelinating diseases of central nervous system
342.00 - 342.92 Hemiplegia and hemiparesis
343.0 - 343.9 Infantile cerebral palsy
348.1 Anoxic brain damage
348.2 Benign intracranial hypertension
348.4 Compression of brain
348.5 Cerebral edema
350.1 - 358.9 Trigeminal, facial, and other cranial nerve disorders, nerve root and plexus disorders, mononeuritis, neuropathy, and myoneural disorders
368. 00 - 368.9 Visual disturbances
377.00 - 377.9 Disorders of the optic nerve and visual pathways
386.00 - 386.9 Vertiginous syndromes and other disorders of vestibular system
388.00 - 389.9 Other disorders of ear and hearing loss
430 - 435.9 Subarachnoid hemorrhage, intracerebral hemorrhage, other and unspecified intracranial hemorrhage, occlusion and stenosis of precerebral arteries, occlusion of cerebral arteries, and transient cerebral ischemia
437.3 Cerebral aneurysm, nonruptured
780.01 Coma [unresponsive]
780.03 Persistent vegetative state [unresponsive, unable to communicate]
780.4 Dizziness and giddiness
781.2 - 781.4 Abnormality of gait, lack of coordination, and transient paralysis of limb
784.3 Aphasia [unable to communicate]
794.10 - 794.19 Nonspecific abnormal results of function studies of peripheral nervous system and special senses
850.4 - 853.19 Concussion with prolonged loss of consciousness without return to pre-existing conscious level
907.1 - 907.5 Late effect of 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
950.0 - 950.9 Injury to optic nerve and pathways
ICD-9 codes not covered for indications listed in the CPB (for members > 3 mos of age) (not all-inclusive):
084.0 - 084.9 Malaria
253.0 - 253.9 Disorders of the pituitary gland and its hypothalamic control
290.0 - 290.9 Senile and presenile organic psychotic conditions
291.2 Alcohol induced persisting dementia
292.82 Drug induced persisting dementia
309.81 Posttraumatic stress disorder
314.00 - 314.01 Attention deficit disorder [ADD or ADHD]
331.0 Alzheimer's disease
332.0 - 332.1 Parkinson's disease
336.0 Syringomyelia and syrinobulbia
647.4 Malaria complicating pregnancy, childbirth, or the puerperium
695.4 Lupus erythematosus
710.0 Systemic lupus erythematosus
771.2 Other congenital infections specific to the perinatal period
961.4 Poisoning by antimalarials and drugs acting on other blood protozoa
V20.2 Routine infant or child health check
V70.0 Routine general medical examination at a health care facility
V80.09 Special screening for other neurological conditions
E931.4 Antimalarials and drugs acting on other blood protozoa causing adverse effects in therapeutic use
ICD-9 codes not covered for indications listed in the CPB (for members < 3 mos of age/ neonatal screen):
084.0 - 084.9 Malaria
253.0 - 253.9 Disorders of the pituitary gland and its hypothalamic control
336.0 Syringomyelia and syringobulbia
345.40 - 345.61 Localization-related (focal)(partial) epilepsy and epileptic syndromes with complex partial seizures, and infantile spasms [not covered for vigabatrin (Sabril)-associated retinal toxicity]
695.4 Lupus erythematosus
710.0 Systemic lupus erythematosus
760.0 - 779.9 Certain conditions originating in the perinatal period
768.2 - 768.4 Fetal distress [in neonates]
768.5 - 768.6 Birth asphyxia [in neonates]
768.70 - 768.73 Hypoxic-ischemic encephalopathy [in neonates]
961.4 Poisoning by antimalarials and drugs acting on other blood protozoa
V20.2 Routine infant or child health check
V20.31 - V20.32 Health supervision for newborn under 8 days old to 28 days old
V27.0 - V27.9 Outcome of delivery
V29.0 - V39.2 Observation and evaluation of newborns and infants for suspected condition not found or liveborn infants according to type of birth
V72.0 Examination of eyes and vision [indicates routine screen without signs or symptoms when reported alone]
V80.09 Special screening for other neurological conditions
V80.2 Special screening for other eye conditions [indicates routine screen without signs or symptoms when reported alone]
E931.4 Antimalarials and drugs acting on other blood protozoa causing adverse effects in therapeutic use
Intra-operative brain stem auditory evoked response (BAER) monitoring:
CPT codes covered if selection criteria are met:
92585 - 92586
+95940
+95941
Intra-operative brain stem auditory evoked response (BAER) monitoring may be appropriate for the following types of surgery:
22100
+22101
22110
+22116
22220
+22226
22548
61343
61575
61576
62164
62165
63001
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
ICD-9 codes covered if selection criteria are met:
170.0 Malignant neoplasm of bones of skull and face, except mandible
170.2 Malignant neoplasm of vertebral column, excluding sacrum and coccyx
191.7 Malignant neoplasm of brain stem
192.2 Malignant neoplasm of spinal cord
756.0 Congenital anomalies of skull and face bones
Brain stem auditory evoked response (BAER), comprehensive:
CPT codes covered if selection criteria are met:
92585
CPT codes not covered for indications listed in the CPB:
69631 - 69633
69660 - 69662
ICD-9 codes covered if selection criteria are met (members > 3 mos of age):
036.81 Meningococcal optic neuritis
046.3 Progressive multifocal leukoencephalopathy
054.3 Herpetic meningoencephalitis
055.0 Postmeasles encephalitis
056.01 Encephalomyelitis due to rubella
058.21 Human herpesvirus 6 encephalitis
058.29 Other human herpesvirus encephalitis
062.0 - 064 Mosquito-borne viral encephalitis, tick-borne viral encephalitis, and viral encephalitis transmitted by other and unspecified arthropods
088.81 Lyme disease
094.0 - 094.9 Neurosyphilis
191.0 - 191.9 Malignant neoplasm of brain
192.0 - 192.9 Malignant neoplasm of other and unspecified parts of the nervous system
198.3 - 198.4 Secondary malignant neoplasm of brain and spinal cord
225.0 - 225.9 Benign neoplasm of brain and other parts of nervous system
237.0 - 237.1 Neoplasm of uncertain behavior of endocrine glands and nervous system
237.5 - 237.9 Neoplasm of uncertain behavior of brain and spinal cord, meninges, neurofibromatosis, and other and unspecified parts of nervous system
239.6 Neoplasms of unspecified nature of brain
300.11 Conversion disorder
326 Late effects of intracranial abscess or pyogenic infection
333.0 Other degenerative diseases of the basal ganglia
334.0 - 334.9 Spinocerebellar disease
340 Multiple Sclerosis
341.0 - 341.9 Other demyelinating diseases of the central nervous system
342.0 - 342.92 Hemiplegia and hemiparesis
343.0 - 343.9 Infantile cerebral palsy
348.0 Cerebral cysts
348.1 Anoxic brain damage
348.2 Benign intracranial hypertension
348.4 Compression of brain
348.5 Cerebral edema
348.82 Brain death [for members >3 months of age]
350.1 - 358.9 Trigeminal, facial, and other cranial nerve disorders, nerve root and plexus disorders, mononeuritis, neuropathy, and myoneural disorders
368. 00 - 368.9 Visual disturbances
377.00 - 377.9 Disorders of the optic nerve and visual pathways
386.00 - 386.9 Vertiginous syndromes and other disorders of vestibular system
388.00 - 389.9 Other disorders of ear and hearing loss
430 - 435.9 Subarachnoid hemorrhage, intracerebral hemorrhage, other and unspecified intracranial hemorrhage, occlusion and stenosis of precerebral arteries, occlusion of cerebral arteries, and transient cerebral ischemia
437.1 - 437.2 Other generalized ischemic cerebrovascular disease or hypertensive encephalopathy
437.3 Cerebral aneurysm, nonruptured
741.00 -741.03 Spina bifida with hydrocephalus
742.0 Encephalocele
742.2 Congenital reduction deformities of brain
763.0 - 763.9 Fetus or newborn affected by other complications of labor and delivery
779.2 Cerebral depression, coma, and other abnormal cerebral signs
780.01 Coma
780.03 Persistent vegetative state
780.4 Dizziness and giddiness
781.2 - 781.4 Abnormality of gait, lack of coordination, and transient paralysis of limb
794.10 - 794.19 Nonspecific abnormal results of function studies of peripheral nervous system and special senses
850.4 - 853.19 Concussion with prolonged loss of consciousness without return to pre-existing conscious level
907.1 - 907.5 Late effect of 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
950.0 - 950.9 Injury to optic nerve and pathways
V20.1 - V20.2 Health supervision of other healthy infant or child receiving care or routine infant or child health check
V58.62 Long-term (current) use of antibiotics [damage due to ototoxic drugs]
V58.69 Long-term (current) use of other medications [damage due to ototoxic drugs]
V72.11 Encounter for hearing examination following failed hearing screening
ICD-9 codes not covered for indications listed in the CPB (members > 3 mos of age) (not all-inclusive):
290.0 - 290.9 Senile and presenile organic psychotic conditions
291.2 Alcohol induced persisting dementia
292.82 Drug induced persisting dementia
293.9 Unspecified transient mental disorder in conditions classified elsewhere
294.10 - 294.9 Other organic psychotic conditions (chronic)
295.20 - 295.25 Schizophrenic disorders, catatonic
295.90 - 295.95 Unspecified schizophrenia
296.00 - 296.99 Episodic mood disorders
298.0 Depressive type psychosis
299.00 - 299.01 Autistic disorder
300.4 Dysthymic disorder
309.81 Posttraumatic stress disorder
311 Depressive disorder, not elsewhere classified
314.00 - 314.01 Attention deficit disorder [ADD or ADHD]
331.0 Alzheimer's disease
331.11 Pick's disease
331.19 Other frontotemporal dementia
331.82 Dementia with Lewy bodies
332.0 - 332.1 Parkinson's disease
335.10, 335.19 Other and unspecified spinal muscular atrophy [Kennedy's syndrome]
336.0 Syringomyelia and syringobulbia
781.1 Disturbances of sensation of smell and taste
V21.0 - V21.9 Constitutional states in development
V27.0 - V27.9 Outcome of delivery
V29.0 - V39.2 Observation and evaluation of newborns and infants for suspected condition not found or liveborn infants according to type of birth
V72.19 Other examination of ears and hearing [indicates routine exam without signs or symptoms when reported alone]
V80.3 Special screening for ear diseases [indicates routine exam without signs or symptoms when reported alone]
ICD-9 codes not covered for indications listed in the CPB (for members < 3 mos of age/ neonatal screen):
336.0 Syringomyelia and syringobulbia
760.0 - 779.9 Certain conditions originating in the perinatal period
V20.0 - V21.9 Health supervision of infant or child or constitutional states of development [neonatal screen]
V27.0 - V27.9 Outcome of delivery
V29.0 - V39.2 Observation and evaluation of newborns and infants for suspected condition not found or liveborn infants according to type of birth
V72.19 Other examination of ears and hearing [indicates routine exam without signs or symptoms when reported alone]
V80.3 Special screening for ear diseases [indicates routine exam without signs or symptoms when reported alone]
Brain stem auditory evoked response (BAER), limited:
CPT codes covered if selection criteria are met:
92586
CPT codes not covered for indications listed in the CPB:
69631 - 69633
69660 - 69662
ICD-9 codes covered if selection criteria are met:
036.81 Meningococcal optic neuritis
054.3 Herpetic meningoencephalitis
055.0 Postmeasles encephalitis
056.01 Encephalomyelitis due to rubella
058.21 Human herpesvirus 6 encephalitis
058.29 Other human herpesvirus encephalitis
062.0 - 064 Mosquito-borne viral encephalitis, tick-borne viral encephalitis, and viral encephalitis transmitted by other and unspecified arthropods
088.81 Lyme disease
094.0 - 094.9 Neurosyphilis
191.0 - 191.9 Malignant neoplasm of brain
192.0 - 192.9 Malignant neoplasm of other and unspecified parts of the nervous system
225.0 - 225.9 Benign neoplasm of brain and other parts of the nervous system
237.0 - 237.1 Neoplasm of uncertain behavior of endocrine glands and nervous system
237.5 - 237.9 Neoplasm of uncertain behavior of brain and spinal cord, meninges, neurofibromatosis, and other and unspecified parts of nervous system
239.6 Neoplasms of unspecified nature of brain
300.11 Conversion disorder
326 Late effects of intracranial abscess or pyogenic infection
333.0 Other degenerative diseases of the basal ganglia
334.0 - 334.9 Spinocerebellar disease
341.0 - 341.9 Other demyelinating diseases of the central nervous system
342.0 - 342.92 Hemiplegia and hemiparesis
343.0 - 343.9 Infantile cerebral palsy
348.0 Cerebral cysts
348.1 Anoxic brain damage
348.2 Benign intracranial hypertension
348.4 Compression of brain
348.5 Cerebral edema
350.1 - 358.9 Trigeminal, facial, and other cranial nerve disorders, nerve root and plexus disorders, mononeuritis, neuropathy, and myoneural disorders
368.00 - 368.9 Visual disturbances
388.00 - 389.9 Other disorders of ears and hearing loss
430 - 435.9 Subarachnoid hemorrhage, intracerebral hemorrhage, other and unspecified intracranial hemorrhage, occlusion and stenosis of precerebral arteries, occlusion of cerebral arteries, and transient cerebral ischemia
437.1 - 437.2 Other generalized ischemic cerebrovascular disease or hypertensive encephalopathy
437.3 Cerebral aneurysm, nonruptured
741.00 - 741.03 Spina bifida with hydrocephalus
742.0 Encephalocele
742.2 Congenital reduction deformities of brain
763.0 - 763.9 Fetus or newborn affected by other complications of labor and delivery
779.2 Cerebral depression, coma, and other abnormal cerebral signs
780.01 Coma
780.03 Persistent vegetative state
780.4 Dizziness and giddiness
781.2 - 781.4 Abnormality of gait, lack of coordination, and transient paralysis of limb
794.10 - 794.19 Nonspecific abnormal results of function studies of peripheral nervous system and special senses
850.4 - 853.19 Concussion with prolonged loss of consciousness without return to pre-existing conscious level
907.1 - 907.5 Late effect of 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
950.0 - 950.9 Injury to optic nerve and pathways
V20.1 - V20.2 Routine infant or child health check [*note - per ICD-9 guidelines - this is the correct code for hearing screen of infant or child over 28 days old as category V72 excludes routine hearing exam of infant or child]
V20.31 - V20.32 Health supervision for newborn under 8 days old to 28 days old [*note - per ICD-9 guidelines - this is the correct code for neonatal hearing screen as category V72 excludes routine hearing exam of newborn]
V27.0 - V27.9 Outcome of delivery
V29.0 - V39.2 Observation and evaluation of newborns and infants for suspected condition not found or liveborn infants according to type of birth
V58.62 Long-term (current) use of antibiotics [damage due to ototoxic drugs]
V58.69 Long-term (current) use of other medications [damage due to ototoxic drugs]
V72.11 Encounter for hearing examination following failed hearing screening
ICD-9 codes not covered for indications listed in the CPB:
335.10 - 335.19 Other and unspecified spinal muscular atrophy [Kennedy’s syndrome]
336.0 Syringomyelia and syringobulbia
Evoked otoacoustic emissions:
CPT codes covered if selection criteria are met:
92587
92588
ICD-9 codes not covered for indications listed in the CPB (for comprehensive exam only for members < 3 mos. of age/ neonatal screen):
760.0 - 779.9 Certain conditions originating in the perinatal period
V20.0 - V21.9 Health supervision of infant or child or constitutional states of development
V27.0 - V27.9 Outcome of delivery
V29.0 - V39.2 Observation and evaluation of newborns and infants for suspected condition not found or liveborn infants according to type of birth
V72.19 Other examination of ears and hearing [indicates routine exam without signs or symptoms when reported alone]
V80.3 Special screening for ear diseases [indicates routine exam without signs or symptoms when reported alone]
Motor evoked potentials (other than intraoperative with SSEPs and billed with 95925, 95926, or 95927, in conjunction with add-on code 95920):
CPT codes not covered for indications listed in the CPB:
95928
95929
95938
95939
Motor evoked potentials not covered intraoperatively:
CPT codes not covered for indications listed in the CPB:
63650


The above policy is based on the following references:
  1. Schmid UD, Hess CW, Ludin HP. Somatosensory evoked responses following nerve and segmental stimulation do not confirm cervical radiculopathy with sensory deficit. J Neurol Neurosurg Psychiatry. 1988;51(2):182-187.
  2. American Academy of Neurology. Assessment: Dermatomal somatosensory evoked potentials. Report of the American Academy of Neurology's Therapeutics and Technology Assessment Subcommittee. Neurology. 1997;49(4):1127-1130.
  3. Galla JD, Ergin MA, Lansman SL, et al. Use of somatosensory evoked potentials for thoracic and thoracoabdominal 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 evoked potentials 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 in acute and chronic spinal canal compromise. Spine. 1999;24(10):1029-1033.
  6. Medical Services Advisory Committee (MSAC). Oto-acoustic emission audiometry. Final Assessment Report. MSAC Application 1002. Canberra, ACT: MSAC; 1999.
  7. Bejjani GK, Nora PC, Vera PL, et al. The predictive value of intraoperative somatosensory evoked potential monitoring: Review of 244 procedures. Neurosurgery. 1998;43(3):491-500.
  8. Kresch EN, Levitan ML, Baran EM, et al. Correlation analysis 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 and electrophysiologic characteristics of compressed lumbar nerve roots. Spine. 1997;22(18):2100-2105.
  10. Eisen A, Hoirch M, Moll A. Evaluation of radiculopathies by segmental stimulation and somatosensory evoked potentials. Can J Neurol Sci. 1983;10:178-182.
  11. Aminoff MJ, Goodin DS, Barbaro NM, et al. Dermatomal somatosensory evoked potentials in unilateral lumbosacral radiculopathy. Ann Neurol. 1985;17:171-176.
  12. Aminoff MJ, Goodin DS, Parry GJ, et al. Electrophysiologic evaluation of lumbosacral radiculopathies: Electromyography, late responses, and somatosensory evoked potentials. Neurology. 1985;35:1514-1518 .
  13. Seyal M, Sandhu LS, Mack YP. Spinal segmental somatosensory evoked potentials in lumbosacral radiculopathies. Neurology. 1989;39:801-805.
  14. Scarf TB, Dallmann DE, Toleikis JR, et al. Dermatomal somatosensory evoked potentials in the diagnosis of lumbar root entrapment. Surg Forum. 1981;32:489-491.
  15. Katifi HA, Sedgwick EM. Evaluation of the dermatomal somatosensory evoked potential in the diagnosis of lumbosacral root compression. J Neurol Neurosurg Psychiatry. 1987;50:1204-1209.
  16. Walk D, Fisher MA, Doundoulakis SH, et al. Somatosensory evoked potentials in the evaluation of lumbosacral radiculopathy. Neurology. 1992;42:1197-1202.
  17. Aminoff MJ, Goodin DS. Dermatomal somatosensory evoked potentials in lumbosacral root compression. J Neurol Neurosurg Psychiatry. 1988;51:740-741.
  18. Katifi HA, Sedgwick EM. Dermatomal somatosensory evoked potentials in lumbosacral root compression (a reply). J Neurol Neurosurg Psychiatry. 1988;51:741-742.
  19. Fisher MA. Dermatomal/segmental somatosensory evoked potential evaluation of L5/S1 radiculopathies. Muscle Nerve. 1997;20(3):392-393.
  20. Dreyfuss P, Dumitru D. Dermatomal/segmental somatosensory evoked potential evaluation of L5/S1 radiculopathies (a reply). Muscle Nerve. 1997;20:392-393.
  21. Dumitru D, Dreyfuss P. Dermatomal/segmental somatosensory evoked potential evaluation of L5/S1 unilateral/unilevel radiculopathies. Muscle Nerve. 1996;19(4):442-449.
  22. American Academy of Neurology. Practice parameters for determining brain death in adults (summary statement). The Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 1995;45(5):1012-1014.
  23. American Academy of Pediatrics. Joint committee on infant hearing 1994 position statement. American Academy of Pediatrics Joint Committee on Infant Hearing. Pediatrics. 1995;95(1):152-156.
  24. McClelland RJ, Watson DR, Lawless V, et al. Reliability and effectiveness of screening for hearing loss in high risk neonates. BMJ. 1992;304(6830):806-809.
  25. Stapells DR, Kurtzberg D. Evoked potential assessment of auditory system integrity in infants. Clin Perinatol. 1991;18(3):497-518.
  26. Hyde ML, Riko K, Malizia K. Audiometric accuracy of the click ABR in infants at risk for hearing loss. J Am Acad Audiol. 1990;1(2):59-66.
  27. Acoustic Neuroma Association (ANA). Detection and diagnosis of acoustic neuromas. [Web Site]. Atlanta, GA: ANA, 1998. Available at: http://www.anausa.org/detect.htm. Accessed January 10, 2001.
  28. Gronseth GS, Ashman EJ. Practice parameter: The usefulness of evoked potentials in identifying clinically silent lesions in patients with suspected multiple sclerosis (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2000;54(9):1720-1725.
  29. Rothstein TL. The role of evoked potentials in anoxic-ischemic coma and severe brain trauma. J Clin Neurophysiol. 2000;17(5):486-497.
  30. Medical Services Advisory Committee (MSAC). Visual electrodiagnosis. MSAC Application 1005. Canberra, ACT: MSAC; 2001.
  31. Noordeen MH, Taylor BA. Somatosensory evoked potentials. J Bone Joint Surg Am. 2000;82-A(10):1517-1518.
  32. American Association of Electrodiagnostic Medicine (AAEM), American Academy of Neurology (AAN), and American Academy of Physical Medicine and Rehabilitation (AAPMR). Recommended Policy for Electrodiagnostic Medicine. Rochester, MN: AAEM; 1995-2001. Available at: http://www.aaem.net/position_statements/
    recommended_policy.htm. Accessed January 18, 2001.
  33. Reeves RR. The effects of donepezil on the P300 auditory and visual cognitive evoked potentials of patients with Alzheimer's disease. Am J Geriatr Psychiatry. 1999;7:349-352.
  34. Pallanti S, Quercioli L, Pazzagli A. Basic symptoms and P300 abnormalities in young schizophrenic patients. Compr Psychiatry. 1999;40(5):363-371.
  35. Thomas A, Iacono D, Bonanni L, et al. Donepezil, rivastigmine, and vitamin E in Alzheimer's disease: A combined P300 event-related potentials/neuropsychological evaluation over 6 months. Clin Neuropharmacol. 2001;24(1):31-42.
  36. Erenberg A, Lemons J, Sia C, Trunkel D, Ziring P. Newborn and infant hearing loss: Detection and intervention. American Academy of Pediatrics. Task Force on Newborn and Infant Hearing, 1998-1999. Pediatrics. 1999;103(2):527-530.
  37. Joint Committee on Infant Hearing. Year 2000 position statement. Principles and guidelines for early hearing detection and intervention programs. Am J Audiol. 2000;9(1):9-29.
  38. U.S. Preventive Services Task Force. Newborn hearing screening: Recommendations and rationale. Am Fam Physician. 2001;64(12):1995-1999.
  39. Helfand M, Thompson DC, Davis R, et al. Newborn hearing screening. Systematic Evidence Review Number 5. Contract 290-97-0018 to the Oregon Health & Science University Evidence-based Practice Center, Portland, Oregon. AHRQ Publication No. 02-S001. Rockville, MD: Agency for Healthcare Research and Quality (AHRQ); October 2001.
  40. Schwartz DM, Schwartz JA. Auditory evoked potentials in clinical pediatrics. In: Hearing Assessment. 2nd ed. WF Rintelmann, ed. Austin, TX: ProEd Press Publishers; 1990.
  41. Scott ME, Bhattacharyya N. Auditory brainstem response audiometry. eMedicine J. 2002;3(5). Available at: http://www.emedicine.com/ent/topic473.htm. Accessed July 16, 2002.
  42. Anyanwu E, Campbell AW, High W. Brainstem auditory evoked response in adolescents with acoustic mycotic neuroma due to environmental exposure to toxic molds. Int J Adolesc Med Health. 2002;14(1):67-76.
  43. Ikui A. A review of objective measures of gustatory function. Acta Otolaryngol Suppl. 2002;(546):60-68.
  44. Barry RJ, Johnstone SJ, Clarke AR. A review of electrophysiology in attention-deficit/hyperactivity disorder: II. Event-related potentials. Clin Neurophysiol. 2003;114(2):184-198.
  45. Aminoff MJ, Eisen AA. AAEM minimonograph 19: Somatosensory evoked potentials. Muscle Nerve. 1998;21(3):277-290.
  46. Hayes D. Screening methods: Current status. Ment Retard Dev Disabil Res Rev. 2003;9(2):65-72.
  47. Hausmann ON, Boni T, Pfirrmann CW, et al. Preoperative radiological and electrophysiological evaluation in 100 adolescent idiopathic scoliosis patients. Eur Spine J. 2003;12(5):501-506.
  48. Haghighi SS, Baradarian S, Zhang R. Diagnostic utility of somatosensory and motor evoked potentials in a patient with thoracic outlet syndrome. Electromyogr Clin Neurophysiol. 2003;43(6):323-327.
  49. Gillard J, Perez-Cousin M, Hachulla E, et al. Diagnosing thoracic outlet syndrome: Contribution of provocative tests, ultrasonography, electrophysiology, and helical computed tomography in 48 patients. Joint Bone Spine. 2001;68(5):416-424.
  50. Cakmur R, Idiman F, Akalin E, et al. Dermatomal and mixed nerve somatosensory evoked potentials in the diagnosis of neurogenic thoracic outlet syndrome. Electroencephalogr Clin Neurophysiol. 1998;108(5):423-434.
  51. Komanetsky RM, Novak CB, Mackinnon SE, et al. Somatosensory evoked potentials fail to diagnose thoracic outlet syndrome. J Hand Surg [Am]. 1996;21(4):662-666.
  52. Mackinnon SE, Novak CB. Evaluation of the patient with thoracic outlet syndrome. Semin Thorac Cardiovasc Surg. 1996;8(2):190-200.
  53. Passero S, Paradiso C, Giannini F, et al. Diagnosis of thoracic outlet syndrome. Relative value of electrophysiological studies. Acta Neurol Scand. 1994;90(3):179-185.
  54. Veilleux M, Stevens JC, Campbell JK. Somatosensory evoked potentials: Lack of value for diagnosis of thoracic outlet syndrome. Muscle Nerve. 1988;11(6):571-575.
  55. Fife TD, Tusa RJ, Furman JM, et al. Assessment: Vestibular testing techniques in adults and children: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2000;55(10):1431-1441.
  56. Cone-Wesson B, Wunderlich J. Auditory evoked potentials from the cortex: Audiology applications. Curr Opin Otolaryngol Head Neck Surg. 2003;11(5):372-377.
  57. Papathanasiou E, Zamba-Papanicolaou E, Pantziaris M, et al. Click evoked neurogenic vestibular potentials (NVESTEPs): A method of assessing the function of the vestibular system. Electromyogr Clin Neurophysiol. 2003;43(7):399-408.
  58. Neuloh G, Schramm J. Motor evoked potential monitoring for the surgery of brain tumours and vascular malformations. Adv Tech Stand Neurosurg. 2004;29:171-228.
  59. Mazzini L. Clinical applications of event-related potentials in brain injury. Phys Med Rehabil Clin N Am. 2004;15(1):163-175.
  60. Olichney JM, Hillert DG. Clinical applications of cognitive event-related potentials in Alzheimer's disease. Phys Med Rehabil Clin N Am. 2004;15(1):205-233.
  61. Bomba MD, Pang EW. Cortical auditory evoked potentials in autism: A review. Int J Psychophysiol. 2004;53(3):161-169.
  62. National Collaborating Centre for Chronic Conditions. Multiple sclerosis. National clinical guideline for diagnosis and management in primary and secondary care. London, UK: National Institute for Clinical Excellence (NICE); 2004.
  63. Goetz CG. Textbook of Clinical Neurology. 2nd ed. St. Louis, MO: W.B. Saunders Co.; 2003.
  64. Miller RD. Miller's Anesthesia. 6th ed. Edinburgh, UK: Churchill Livingstone; 2005.
  65. University of British Columbia (UBC), School of Auditory and Speech Sciences, Human Auditory Physiology (HAP) Laboratory. What are auditory evoked potentials? HAP Lab Website. Vancouver, BC: UBC; March 2005. Available at: http://www.audiospeech.ubc.ca/haplab/aep.htm. Accessed April 22, 2005.
  66. Erickson L, Costa V, McGregor M. Intraoperative neurophysiological monitoring during spinal surgery. Montreal, QC: Technology Assessment Unit of the McGill University Health Centre (MUHC); 2005:1-39.
  67. Joint Committee on Infant Hearing (JCIH). Year 2000 Position Statement: Principles and guidelines for early hearing detection and prevention programs. Pediatrics. 2000;106(4):798-817. Available at:www.jcih.org/jcih2000.pdf. Accessed June 6, 2006.
  68. Cunningham M, Cox EO. Hearing assessment in infants and children: Recommendations beyond neonatal screening. Pediatrics. 2003;111(2):436-440.
  69. Swedish Council on Technology Assessment in Health Care (SBU). Universal newborn hearing screening - early assessment briefs (Alert). Stockholm, Sweden: Swedish Council on Technology Assessment in Health Care (SBU); 2004.
  70. Pichon Riviere A, Augustovski F, Bardach A, et al. Otoacoustic emissions. Clinical applications. Report IRR No. 41. Buenos Aires, Argentina: Institute for Clinical Effectiveness and Health Policy (IECS); 2005.
  71. State of Colorado, Department of Labor and Employment (DLE), Division of Workers' Compensation. Traumatic brain injury. Medical Treatment Guidelines. Denver, CO: DLE; 2006. 
  72. Karl A, Malta LS, Maercker A. Meta-analytic review of event-related potential studies in post-traumatic stress disorder. Biol Psychol. 2006;71(2):123-147.
  73. Rauch SD. Vestibular evoked myogenic potentials. Curr Opin Otolaryngol Head Neck Surg. 2006;14(5):299-304.
  74. Kane NM, Butler SR, Simpson T. Coma outcome prediction using event-related potentials: P(3) and mismatch negativity. Audiol Neurootol. 2000;5(3-4):186-191.
  75. Laureys S, Perrin F, Schnakers C, et al. Residual cognitive function in comatose, vegetative and minimally conscious states. Curr Opin Neurol. 2005;18(6):726-733.
  76. Young GB, Shemie SD, Doig CJ, Teitelbaum J. Brief review: The role of ancillary tests in the neurological determination of death. Can J Anaesth. 2006;53(6):620-627. 
  77. Akkuzu G, Akkuzu B, Ozluoglu LN. Vestibular evoked myogenic potentials in benign paroxysmal positional vertigo and Meniere's disease. Eur Arch Otorhinolaryngol. 2006;263(6):510-517.
  78. Pollak L, Kushnir M, Stryjer R. Diagnostic value of vestibular evoked myogenic potentials in cerebellar and lower-brainstem strokes. Neurophysiol Clin. 2006;36(4):227-233.
  79. Wuyts FL, Furman J, Vanspauwen R, Van de Heyning P. Vestibular function testing. Curr Opin Neurol. 2007;20(1):19-24.
  80. Brantberg K, Granath K, Schart N. Age-related changes in vestibular evoked myogenic potentials. Audiology & Neuro-Otology. 2007;12(4):247-253.
  81. U.S. Preventive Services Task Force. Universal screening for hearing loss in newborns: U.S. Preventive Services Task Force Recommendation Statement. Pediatrics. 2008;122(1):143–148.
  82. Lee SH, Song DG, Kim S, et al. Results of auditory brainstem response monitoring of microvascular decompression: A prospective study of 22 patients with hemifacial spasm. Laryngoscope. 2009;119(10):1887-1892.
  83. Polo G, Fischer C. Intraoperative monitoring of brainstem auditory evoked potentials during microvascular decompression of cranial nerves in cerebellopontine angle. Neurochirurgie. 2009;55(2):152-157.
  84. Huang BR, Chang CN, Hsu JC. Intraoperative electrophysiological monitoring in microvascular decompression for hemifacial spasm. J Clin Neurosci. 2009;16(2):209-213.
  85. Fehlings MG, Brodke DS, Norvell DC, Dettori JR. The evidence for intraoperative neurophysiological monitoring in spine surgery: Does it make a difference? Spine. 2010;35(9 Suppl):S37-S46.
  86. American Academy of Audiology. Intraoperative neurophysiological monitoring. Scope of Practice. Reston, VA: American Academy of Audiology; updated January 2004.
  87. Wijdicks EF, Hijdra A, Young GB, et al, Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2006;67(2):203-210.
  88. American Academy of Ophthalmology. Policy Statement. Vision screening for infants and children. A Joint Statement of the American Association for Pediatric Ophthalmology and Strabismus and the American Academy of Ophthalmology. March 2007. Available at: http://one.aao.org/printerfriendly.aspx?cid=0ad11e02-6a8b-437e-8d01-f45eb18bc0b6. Accessed January 24, 2012.
  89. Rothstein TL. The utility of median somatosensory evoked potentials in anoxic-ischemic coma. Rev Neurosci. 2009;20(3-4):221-233.
  90. Raggi A, Iannaccone S, Cappa SF. Event-related brain potentials in amyotrophic lateral sclerosis: A review of the international literature. Amyotroph Lateral Scler. 2010;11(1-2):16-26.
  91. U.S. Preventive Services Task Force. Screening for visual impairment in children ages 1 to 5 years. January 2011. Available at: http://www.uspreventiveservicestaskforce.org/uspstf11/vischildren/vischildrs.htm. Accessed January 26, 2012.
  92. Acioly MA, Liebsch M, de Aguiar PH, Tatagiba M. Facial nerve monitoring during cerebellopontine angle and skull base tumor surgery: A systematic review from description to current success on function prediction. World Neurosurg. 2013;80(6):e271-e300.
  93. Weinhouse GL, Young GB. Hypoxic-ischemic brain injury: Evaluation and prognosis. Last reviewed January 2012. UpToDate, Inc. Waltham, MA.
  94. Nuwer MR, Emerson RG, Galloway G, et al. Evidence-based guideline update: Intraoperative spinal monitoring with somatosensory and transcranial electrical motor evoked potentials: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and the American Clinical Neurophysiology Society. Neurology 2012;78;585-589.
  95. Novitas Solutions, Inc. LCD L32640 - Medicine: Neurophysiology Evoked Potentials (NEPs). Contractor Type: MAC Type A & B. Camp Hill, PA: Novitas Solutions; revised November 19, 2012.
  96. Mauguiere F, Chauvel P, Dewailly J, Dousse N. No effect of long-term vigabatrin treatment on central nervous system conduction in patients with refractory epilepsy: Results of a multicenter study of somatosensory and visual evoked potentials. PMS Study Multicenter Group. Epilepsia. 1997;38(3):301-308.
  97. Zgorzalewicz M, Galas-Zgorzalewicz B. Visual and auditory evoked potentials during long-term vigabatrin treatment in children and adolescents with epilepsy. Clin Neurophysiol. 2000;111(12):2150-2154.
  98. Zuniga MG, Janky KL, Schubert MC, Carey JP. Can vestibular-evoked myogenic potentials help differentiate Ménière disease from vestibular migraine? Otolaryngol Head Neck Surg. 2012;146(5):788-796.
  99. Heravian J, Saghafi M, Shoeibi N, et al. A comparative study of the usefulness of color vision, photostress recovery time, and visual evoked potential tests in early detection of ocular toxicity from hydroxychloroquine. Int Ophthalmol. 2011;31(4):283-289.
  100. Karmel M. Retina screening. Rx side effects: New Plaquenil guidelines and more. Clinical Update. EyeNet. San Francisco, CA: American Academy of Ophthalmology; May 2011:23-25. Available at: http://www.aao.org/publications/eyenet/201105/upload/CUComp-May-2011.pdf. Accessed February 18, 2013.
  101. Shechtman DL, Karpecki PM. New Plaquenil guidelines. Here is a look at the 2011 testing guidelines for patients on Plaquenil guidelines. Review of Optometry, April 20, 2011. Available at: http://www.revoptom.com/content/c/27904/. Accessed February 18, 2013.
  102. Schwartz SG. Mieler WF. New screening guidelines for hydroxychloroquine toxicity. Experts explain their role in clinical practice. Retinal Physician, March 1, 2011. Available at: http://www.retinalphysician.com/articleviewer.aspx?articleid=105383. Accessed February 18, 2013.
  103. Wallace DJ. Antimalarial drugs in the treatment of rheumatic disease. UpToDate [online serial]. Waltham, MA: UpToDate; reviewed November 2013.
  104. van Laerhoven H, de Haan TR, Offringa M, et al. Prognostic tests in term neonates with hypoxic-ischemic encephalopathy: A systematic review. Pediatrics. 2013;131(1):88-98.
  105. Marmor MF, Kellner U, Lai TY, et al.; American Academy of Ophthalmology. Revised recommendations on screening for chloroquine and hydroxychloroquine retinopathy. Ophthalmology. 2011;118(2):415-422.
  106. Balzer JR, Rose RD, Welch WC, Sclabassi RJ. Simultaneous somatosensory evoked potential and electromyographic recordings during lumbosacral decompression and instrumentation. Neurosurgery. 1998;42(6):1318-1324; discussion 1324-1325.
  107. Schwartz DM, Auerbach JD, Dormans JP, et al. Neurophysiological detection of impending spinal cord injury during scoliosis surgery. J Bone Joint Surg Am. 2007;89(11):2440-2449.
  108. Nuwer MR, Emerson RG, Galloway G, et al.; Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology; American Clinical Neurophysiology Society. Evidence-based guideline update: Intraoperative spinal monitoring with somatosensory and transcranial electrical motor evoked potentials: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and the American Clinical Neurophysiology Society. Neurology. 2012;78(8):585-589.


email this page   


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.
Aetna
Back to top