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Clinical Policy Bulletin:
Quantitative EEG (Brain Mapping)
Number: 0221


Policy

  1. Aetna considers the use of quantitative EEG (brain mapping), also known by the acronym BEAM (Brain Electrical Activity Mapping), medically necessary only as an adjunct to traditional EEG for any of the following:

    1. For screening for possible epileptic spikes or seizures in long-term EEG monitoring; or
    2. For ambulatory recording of EEG to facilitate subsequent expert visual EEG interpretation; or
    3. For continuous EEG monitoring by frequency-trending to detect early, acute intracranial complications in the operating room or intensive care unit (ICU); or
    4. For screening for possible epileptic seizures in high-risk ICU members; or
    5. For topographic voltage and dipole analysis in pre-surgical evaluations for intractable epilepsy; or
    6. For evaluation of certain members with symptoms of cerebrovascular disease whose neuroimaging and routine EEG studies are not conclusive; or
    7. For evaluation of dementia and encephalopathy when the diagnosis remains unresolved after initial clinical evaluation.

  2. In accordance with the American Academy of Neurology / American Clinical Neurophysiology Society's assessment and available evidence, Aetna considers the use of quantitative EEG experimental and investigational for all other indications, including any of the following diagnoses because there is inadequate scientific evidence to prove its clinical usefulness for these indications:

    • Post-concussion syndrome
    • Mild or moderate head injury
    • Learning disability
    • Attention disorders
    • Schizophrenia
    • Depression
    • Alcoholism
    • Drug abuse
    • Tinnitus
    • Predicting response to psychotropic medication.

See also CPB 480 - Tourette Syndrome.



Background

Quantitative EEG, a technique for topographic display and analysis of brain electrophysiological data, has been proposed for use in the diagnosis of various psychiatric disorders.  Clinical studies have demonstrated distinctive forms of brain electrical activity in psychiatric conditions including attention deficit disorder, schizophrenia, major depression, and obsessive-compulsive disorder.  However, the clinical significance of these distinctive patterns of brain wave activity is unknown. Thus the role of quantitative EEG in diagnosis, evaluation of disease progression, and treatment of these conditions has yet to be elucidated.  A report from the American Academy of Neurology and the American Clinical Neurophysiology Society concluded that quantitative EEG remains investigational for clinical use in post-concussion syndrome, mild-to-moderate head injury, learning disability, attention disorders, schizophrenia, depression, alcoholism, and drug abuse.

While there is some evidence that electroencephalograph activity differs between normal control subjects and subjects suffering from tinnitus, additional evidence is needed to evaluate the value of including quantitative EEG in a battery of electrophysiological tests for the clinical identification of a predominantly central type of tinnitus.  In addition, there is little evidence to support the use of quantitative EEG to determine the need for change of medications in the treatment of tinnitus.

Crumbley and associates (2005) examined the use of quantitative EEG in predicting response to psychotropic medication.  The clinical outcomes of two groups of patients were compared: (i) those with prescribed medication regimens that were concordant with the quantitative EEG predictors, and (ii) those whose medication regimens were discordant with the quantitative EEG predictors.  Participants included 70 adolescent inpatients who were administered quantitative EEG upon admission.  The results indicated no significant difference in clinical outcome between the two groups.  The failure of this study to find significant differences in patient outcomes questions this particular use of the quantitative EEG (Crumbley, et al., 2005).

John and Prichep (2006) noted that as quantitative EEG and pharmaco-EEG have evolved, a vast body of facts has been accumulated, describing changes in the EEG or event-related potentials observed in a variety of brain disorders or after administration of a variety of medications.  With some notable exceptions, these studies have tended to be phenomenological rather than analytical.  There has not been a systematic attempt to integrate these phenomena to provide better understanding of how the abnormal behaviors of a particular psychiatric patient might be related to the specific pattern of the deviant electrical activity, nor just how pharmacological reduction of that deviant activity may have resulted in more normal behavior.

Snyder and Hall (2006) performed a meta-analysis on the use of quantitative EEG in evaluating patients with attention-deficit hyperactivity disorder (ADHD).  The 9 eligible studies (n = 1498) observed quantitative EEG traits of a theta power increase and a beta power decrease, summarized in the theta/beta ratio with a pooled effect size of 3.08 (95 % confidence interval, 2.90, 3.26) for ADHD versus controls (normal children, adolescents, and adults).   These investigators concluded that this meta-analysis supports that a theta/beta ratio increase is a commonly observed trait in patients with ADHD relative to normal controls.  Moreover, they noted that since it is known that the theta/beta ratio trait may arise with other conditions, a prospective study covering differential diagnosis would be needed to determine generalizability to clinical applications.  Furthermore, standardization of the quantitative EEG technique is also needed, specifically with control of mental state, drowsiness, and medication.

 
CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes covered if selection criteria are met:
95961
+ 95962
Other CPT codes related to the CPB:
95812 - 95830
HCPCS code covered if selection criteria are met:
S8040 Topographic brain mapping
ICD-9 codes covered if selection criteria are met (not all-inclusive):
046.0 - 046.9 Slow virus infection of central nervous system
290.0 - 290.9 Senile and presenile organic psychotic conditions
294.10 Dementia in conditions classified elsewhere without behavioral disturbance
294.11 Dementia in conditions classified elsewhere with behavior disturbance
294.8 Other persistent mental disorders due to conditions classified elsewhere
323.7 Toxic encephalitis, myelitis, and encephalomyelitis
345.00 - 345.91 Epilepsy
348.1 Anoxic brain damage
348.30 - 348.39 Encephalopathy, not elsewhere classified
349.82 Toxic encephalopathy
433.00 - 438.9 Occlusion and stenosis of precerebral arteries, occlusion of cerebral arteries, transient cerebral ischemia, acute, but ill-defined cerebrovascular disease, other and ill-defined cerebrovascular disease, and late effects of cerebrovascular disease
780.39 Other convulsions
984.0 Toxic effect of inorganic lead compound
997.00 - 997.09 Nervous system complications
ICD-9 codes not covered for indications listed in the CPB:
291.0 - 291.9 Alcoholic induced mental disorders
292.0 - 292.9 Drug induced mental disorders
295.00 - 295.95 Schizophrenic disorders
296.00 - 296.99 Episodic mood disorders
298.0 Depressive type psychosis
299.00 - 299.91 Psychoses with origin specific to childhood
300.4 dysthymic disorder
303.00 - 303.93 Alcohol dependence syndrome
304.00 - 305.93 Drug dependence and nondependent abuse of drugs
310.2 Post-concussion syndrome
311 Depressive disorder, not elsewhere classified
314.00 - 314.9 Attention deficit disorder
315.00 - 315.9 Learning difficulties
388.30 - 388.32 Tinnitus
850.00 - 854.19 Intracranial injury, excluding those with skull fracture
959.01 Head injury, unspecified


The above policy is based on the following references:
  1. American Academy of Neurology.  Assessment: EEG brain mapping.  Report of the American Academy of Neurology, Therapeutics and Technology Assessment Subcommittee.  Neurology. 1989;39(8):1100-1101.  
  2. American Psychiatric Association.  Quantitative electroencephalography: A report on the present state of computerized EEG techniques.  American Psychiatric Association Task Force on Quantitative Electrophysiological Assessment.  Am J Psychiatry. 1991;148(7):961-964.  
  3. Kahn EM. Imaging of brain electrophysiologic activity: Applications in psychiatry. Gen Hosp Psychiatry. 1992;14(2):99-106. 
  4. Stam CJ, Jelles B, Achtereekte HA, et al. Diagnostic usefulness of linear and nonlinear quantitative EEG analysis in Alzheimer's disease. Clin Electroencephalography. 1996;27(2):69-77.  
  5. Kuperman S, Johnson B, Arndt S, et al. Quantitative EEG differences in a nonclinical sample of children with ADHD and undifferentiated ADD. J Am Acad Child Adolesc Psychiatry. 1996;35(8):1009-1017.  
  6. Nuwer M. Assessment of digital EEG, quantitative EEG, and EEG brain mapping: Report of the American Academy of Neurology and the American Clinical Neurophysiology Society. Neurology. 1997;49(1):277-292.  
  7. Hoffman DA, Lubar JF, Thatcher RW, et al. Limitations of the American Academy of Neurology and American Clinical Neurophysiology Society paper on QEEG. J Neuropsychiatry Clin Neurosci. 1999;11(3):401-407.  
  8. Small JG, Milstein V, Malloy FW, et al. Clinical and quantitative EEG studies of mania. J Affect Disord. 1999;53(3):217-224.  
  9. Hughes JR, John ER. Conventional and quantitative electroencephalography in psychiatry. J Neuropsychiatry Clin Neurosci. 1999;11(2):190-208.  
  10. Claus JJ, Kwa VI, Teunisse S, et al. Slowing on quantitative spectral EEG is a marker for rate of subsequent cognitive and functional decline in early Alzheimer disease. Alzheimer Dis Assoc Disord. 1998;12(3):167-174.  
  11. Mai R, Facchetti D, Micheli A, et al. Quantitative electroencephalography in amyotrophic lateral sclerosis. Electroencephalogr Clin Neurophysiol. 1998;106(4):383-386.  
  12. Claus JJ, Ongerboer de Visser BW, Walstra GJ, et al. Quantitative spectral electroencephalography in predicting survival in patients with early Alzheimer disease. Arch Neurol. 1998;55(8):1105-1111.  
  13. Drake ME, Padamadan H, Newell SA. Interictal quantitative EEG in epilepsy. Seizure. 1998;7(1):39-42.  
  14. Ebersole JS. New applications of EEG/MEG in epilepsy evaluation. Epilepsy Res Suppl. 1996;11:227-237.  
  15. Jacobs MP, Fischbach GD, Davis MR, et al. Future directions for epilepsy research. Neurology. 2001;57(9):1536-1542.  
  16. Procaccio F, Polo A, Lanteri P, et al. Electrophysiologic monitoring in neurointensive care. Curr Opin Crit Care. 2001;7(2):74-80.  
  17. Wallace BE, Wagner AK, Wagner EP, et al. A history and review of quantitative electroencephalography in traumatic brain injury. J Head Trauma Rehabil. 2001;16(2):165-190. 
  18. Barry RJ, Clarke AR, Johnstone SJ.  A review of electrophysiology in attention-deficit/hyperactivity disorder: I. Qualitative and quantitative electroencephalography. Clin Neurophysiol. 2003;114(2):171-183.
  19. Weiler EW, Brill K, Tachiki KH, Wiegand R. Electroencephalography correlates in tinnitus. Int Tinnitus J. 2000;6(1):21-24.
  20. Shulman A, Goldstein B. Quantitative electroencephalography: Preliminary report--tinnitus. Int Tinnitus J. 2002;8(2):77-86.
  21. Chabot RJ, di Michele F, Prichep L. The role of quantitative electroencephalography in child and adolescent psychiatric disorders. Child Adolesc Psychiatr Clin N Am. 2005;14(1):21-53, v-vi.
  22. Nuwer MR, Hovda DA, Schrader LM, Vespa PM. Routine and quantitative EEG in mild traumatic brain injury. Clin Neurophysiol. 2005;116(9):2001-2025.
  23. Crumbley JA, DeFilippis NA, Dsurney J, Sacco A. The neurometric-quantitative electroencephalogram as a predictor for psychopharmacological treatment: An investigation of clinical utility. J Clin Exp Neuropsychol. 2005;27(6):769-778.
  24. John ER, Prichep LS. The relevance of QEEG to the evaluation of behavioral disorders and pharmacological interventions. Clin EEG Neurosci. 2006;37(2):135-143.
  25. Snyder SM, Hall JR. A meta-analysis of quantitative EEG power associated with attention-deficit hyperactivity disorder. J Clin Neurophysiol. 2006;23(5):440-455.
  26. Bares M, Brunovsky M, Kopecek M, et al. Changes in QEEG prefrontal cordance as a predictor of response to antidepressants in patients with treatment resistant depressive disorder: A pilot study. J Psychiatr Res. 2007;41(3-4):319-325.


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