Grid Monitoring and Intraoperative Electroencephalography

Number: 0289

Table Of Contents

Policy
Applicable CPT / HCPCS / ICD-10 Codes
Background
References


Policy

Scope of Policy

This Clinical Policy Bulletin addresses grid monitoring and intraoperative electroencephalography.

  1. Medical Necessity

    1. Intraoperative Electroencephalography (EEG)

      Aetna considers intraoperative scalp EEG medically necessary for the following indications:

      1. Monitoring cerebral function during carotid artery surgery; or
      2. Monitoring cerebral function during intracranial vascular surgical procedures; or
      3. Monitoring cerebral function during parietal tumor resection or resection of lesion near the eloquent cortex.

      Note: The use of intraoperative EEG to monitor brain function for anesthetic drug administration in order to determine depth of anesthesia is considered integral to the anesthesia and not separately reimbursed.  In addition, this use of intraoperative EEG is considered experimental, investigational, or unproven.

    2. Grid Monitoring (Electrocorticography, ECoG)

      Aetna considers grid monitoring to determine the location of the epileptogenic focus for possible surgical resection medically necessary for members with intractable seizures when any of the following conditions is met:

      1. Seizures arise from functionally important brain areas; or
      2. Surface (scalp) electroencephalogrphy (EEG) recording did not adequately localize the epileptogenic area, or
      3. There is a discordance between electrophysiological localization and that provided by other neurodiagnostic studies suggesting an abnormality in more than one region of the brain.
    3. Electroencephalography (EEG) monitoring During WADA Testing

      Aetna considers electroencephalography (EEG) monitoring medically necessary during WADA testing.

  2. Experimental, Investigational, or Unproven

    1. Aetna considers intraoperative EEG experimental, investigational, or unproven for open-heart surgery and for all other indications not listed above (e.g., prediction of post-operative delirium) because its clinical value has not been established.
    2. Aetna considers grid monitoring experimental, investigational, or unproven for all other indications not listed above because its clinical value for these indications has not been established.
  3. Policy Limitations and Exclusions

    Note: Grid monitoring is considered appropriate only when used by centers that have expertise and experience, especially with younger persons.

  4. Related Policies


Table:

CPT Codes / HCPCS Codes / ICD-10 Codes

Code Code Description

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

Intra-operative electroencephalographic (EEG) monitoring of cerebral function during intracranial vascular surgical procedures:

CPT codes covered if selection criteria are met:

95812 Electroencephalogram (EEG) extended monitoring; 41-60 minutes
95813     greater than 1 hour
95822 Electroencephalogram (EEG); recording in coma or sleep only)
95940 Continuous intraoperative neurophysiology monitoring in the operating room, one on one monitoring requiring personal attendance, each 15 minutes (List separately in addition to code for primary procedure)
95941 Continuous intraoperative neurophysiology monitoring, from outside the operating room (remote or nearby) or for monitoring of more than one case while in the operation room, per hour (List separately in addition to code for primary procedure)

Other CPT codes related to the CPB:

31200 - 31230, 61000 - 61253, 61304 - 61576, 61590 - 61619, 61623 - 61645, 61680 - 61711, 61720 - 61791, 61850 - 61888, 62000 - 62148, 62160 - 62165, 64716, 67570, 69501 69530, 69601 - 69605, 69635 - 69646, 69666 - 69667, 69720 - 69745, 69805 - 69806, 69910 - 69915, 69950 - 69955 Intracranial vascular surgical procedures

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-10 codes covered if selection criteria are met:

C71.3 Malignant neoplasm of parietal lobe [parietal tumor]
C79.31 Secondary malignant neoplasm of brain [parietal tumor]
D33.0 Benign neoplasm of brain, supratentorial [parietal tumor]
D43.0 Neoplasm of uncertain behavior of brain, supratentorial [parietal tumor]
D49.6 Neoplasm of unspecified behavior of brain [parietal tumor]
G93.89 Other specified disorders of brain [lesion near the eloquent cortex]

Intra-operative electroencephalographic (EEG) monitoring of cerebral function during carotid artery surgery:

CPT codes covered if selection criteria are met:

95955 Electroencephalogram (EEG) during non-intracranial surery (eg, carotid)

Other CPT codes related to this CPB:

37236 - 37237, 37242, 33510, 33889, 33891, 34001, 34151, 35001 - 35002, 35121 - 35122, 35301, 35341, 35390, 35501, 35506, 35508 - 35512, 35515 - 35516, 35518, 35521 - 35523, 35525 - 35526, 35531, 35601, 35606, 35642, 35691, 35694 - 35695, 35701, 36100, 36221 - 36224, 36227 -36228, 36595, 37215 - 37218, 37600, 37605 -37606, 60600, 60605, 61590 - 61592, 61596, 61611, 61710 Carotid artery surgery

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

F05 Delirium due to known physiological condition [post-operative delirium]

Grid Monitoring (Electrocorticography, ECoG) :

CPT codes covered if selection criteria are met:

95829 Electrocorticogram at surgery (separate procedure)

Other CPT codes related to this CPB:

61531 Subdural implantation of strip electrodes through one or more burr or trephine hole(s) for long term seizure monitoring
61533 Craniotomy with elevation of bone flap; for subdural implantation of an electrode array, for long-term seizure monitoring
61535     for removal of epidural or subdural electrode array, without excision of cerebral tissue (separate procedure)
61760 Stereotactic implantation of depth electrodes into the cerebrum for long term seizure monitoring
95812 - 95830 Electroencephalography (EEG)
95954 - 95967 Special EEG Tests
95961 Functional cortical and subcortical mapping by stimulation and/or recording of electrodes on brain surface, or of depth electrodes, to provoke seizures or identify vital brain structures; initial hour of attendance by a physician or other qualified health care professional
+95962     each additional hour of attendance by a physician or other qualified health care professional (List separately in addition to code for primary procedure)

Other HCPCS codes related to the CPB:

S8040 Topographic brain mapping

ICD-10 codes covered if selection criteria are met:

G40.001 - G40.919 Epilepsy and recurrent seizures
R56.1 Post traumatic seizures
R56.9 Unspecified convulsions

Electroencephalography (EEG) monitoring during WADA testing:

CPT codes covered if selection criteria are met:

95812 – 95822 Electroencephalogram (EEG)

Other CPT codes related to this CPB:

95958 Wada activation test for hemispheric function, including electroencephalographic (EEG) monitoring

Background

Standard scalp electroencephalography measures and records the electrical activity of the brain by placing electrodes on the scalp/head; most commonly used when a physician is trying to establish the presence of a seizure disorder.

For patients with intractable seizures, the best surgical outcome is attained after precise localization of the seizure focus. Scalp electroencephalography (EEG) monitoring may be insufficient and invasive subdural EEG monitoring (by means of subdural grid electrodes) has been used. Subdural electrodes provide coverage of large areas of neocortex and are ideally suited for evaluating children with intractable epilepsy and to functionally map critical cortex.

Multi-contact depth electrodes may be implanted into the brain to record electrical activity from deep or superficial cortical structure. Strips or rectangular grid arrays (subdural electrodes) can be placed under the dura to record activity in this region.

Subdural grid electrodes can be used for recording as well as for stimulating neural tissue to identify the underlying function (e.g., language areas, sensation or motor function). These electrodes remain in place for several days to up to 1 to 2 weeks, as needed to record seizures and map brain. They are then removed and epilepsy surgery performed, if findings are favorable for such surgery. In some patients in whom invasive monitoring fails to locate the seizure focus, re-investigation with invasive subdural electrodes can identify the origin of seizure and allow successful surgical treatment.

Invasive EEG monitoring with subdural grid electrodes is associated with significant complications; however, most of them are transient. Higher complication rates are related to an increased number of electrode contacts, increased length of the monitoring period, placement of burr holes in addition to the craniotomy, and multiple cable exit sites.

An American Academy of Neurology Technology Assessment (Nuwer, et al., 1990) stated that electrocorticography (ECog) from surgically exposed cortex can help to define the optimal limits of a surgical resection, identifying regions of greatest impairment. Regions of attenuated or absent EEG, or those with relatively increased slow activity, decrease in fast activity, or abnormal spike discharges help to define regions of cortex that are impaired or abnormal. When used together with long-term EEG/video monitoring, ECoG can help to define the limits of resection for surgery for epilepsy.

An American Academy of Neurology Technology Assessment (Nuwer, et al., 1990) stated that intraoperative scalp EEG monitoring has long been carried out in an effort to safeguard the brain during carotid endarterectomy. The assessment stated that this technique has been shown to be safe and efficacious for such use and for other similar situations in which cerebral blood flow is at high risk. For this purpose, monitoring should be carried out at least at the anterior and posterior regions over each hemisphere. The AAN technology assessment stated that sixteen channels are preferable to identify occasional embolic complications.

A Medicare National Coverage Determination (CMS, 2006) on EEG monitoring during surgical procedures involving the cerebral vasculature states that EEG monitoring may be covered routinely in carotid endarterectomies and in other neurological procedures where cerebral perfusion could be reduced. Such other procedures might include aneurysm surgery where hypotensive anesthesia is used or other cerebral vascular procedures where cerebral blood flow may be interrupted. A Medicare National Coverage Determination on EEG monitoring for open-heart surgery stated that the value of EEG monitoring during open heart surgery and in the immediate post-operative period is debatable because there are little published data based on well designed studies regarding its clinical effectiveness. The NCD states that the procedure is not frequently used for this indication and does not enjoy widespread acceptance of benefit.

One or two channel intraoperative EEG analysis modules have been used by anesthesiologists to gauge depth of anesthesia, such as the Bi-Spectral device (BIS). Such use of limited channel intraoperative EEG for monitoring depth of anesthesia (and level of consciousness) is considered integral to the anesthesia service and not separately reimbursable. In addition, a one or two channel EEG device does not meet the minimal technical requirements for EEG testing as set forth by the American Clinical Neurophysiology Society.

Prediction of Post-Operative Delirium

Fritz and colleagues (2016) stated that post-operative delirium is a common complication associated with increased morbidity and mortality, longer hospital stays, and greater health care expenditures.  Intra-operative EEG slowing has been associated previously with post-operative delirium, but the relationship between intra-operative EEG suppression and post-operative delirium has not been investigated.  In this observational cohort study, a total of 727 adult patients who received general anesthesia with planned intensive care unit (ICU) admission were included.  Duration of intra-operative EEG suppression was recorded from a frontal EEG channel (FP1 to F7).  Delirium was assessed twice-daily on post-operative days 1 through 5 with the Confusion Assessment Method for the ICU. Thirty days after surgery, quality of life (QOL), functional independence, and cognitive ability were measured using the Veterans RAND 12-item survey, the Barthel index, and the PROMIS Applied Cognition-Abilities-Short Form 4a survey.  Post-operative delirium was observed in 162 (26 %) of 619 patients assessed.  When these researchers compared patients with no EEG suppression with those divided into quartiles based on duration of EEG suppression, patients with more suppression were more likely to experience delirium (χ(4) = 25, p < 0.0001).  This effect remained significant after these investigators adjusted for potential confounders (odds ratio [OR] for log(EEG suppression) 1.22 (99 % confidence interval [CI]:, 1.06 to 1.40, p = 0.0002] per 1-minute increase in suppression); EEG suppression may have been associated with reduced functional independence (Spearman partial correlation coefficient -0.15, p = 0.02); but not with changes in QOL or cognitive ability.  Predictors of EEG suppression included greater end-tidal volatile anesthetic concentration and lower intra-operative opioid dose.  The authors concluded that EEG suppression is an independent risk factor for post-operative delirium.  Moreover, they stated that future studies should examine if anesthesia titration to minimize EEG suppression decreases the incidence of post-operative delirium.

This study has several major drawbacks:
  1. because this was an observational study, the findings cannot indicate whether the relationship between EEG suppression and delirium is causal.  Delirium was assessed as part of routine clinical care, and such assessments have limited sensitivity despite high specificity,
  2. some patients either left the ICU prior to the first delirium assessment or were sedated at all assessment time points,
  3. the post-discharge outcomes may be limited due to incomplete survey responses, particularly because patients who experienced post-operative delirium were less likely to return the survey,
  4. the Barthel Index was not performed pre-operatively, and thus it was not possible to distinguish whether patients who experienced EEG suppression had reduced functional independence before surgery as well, and
  5. this study also restricted its focus to patients with planned ICU admission after surgery, so care should be taken when applying these results to a broader surgical patient population. 

This  research group is currently conducting the ENGAGES clinical trial (NCT02241655), which may shed further light on the association between intra-operative burst suppression and post-operative delirium.

Prediction of Emergence Agitation After Sevoflurane Anesthesia

Jang and colleagues (2018) noted that emergence agitation (EA) is common after sevoflurane anesthesia, but there are no definite predictors.  In a prospective, predictive study, these researchers examined if intra-operative EEG can indicate the occurrence of EA in children.  EEG-derived parameters (spectral edge frequency 95, beta, alpha, theta, and delta power) were measured at 1.0 minimum alveolar concentration (MAC) and 0.3 MAC of end-tidal sevoflurane (EtSEVO) in 29 patients.  EA was evaluated using an EA score (EAS) in the post-anesthetic care unit on arrival (EAS 0) and at 15 and 30 minutes after arrival (EAS 15 and EAS 30).  The correlation between EEG-derived parameters and EAS was analyzed using Spearman correlation, and receiver-operating characteristic curve analysis was used to measure the predictability.  EA occurred in 11 patients.  The alpha power at 1.0 MAC of EtSEVO was correlated with EAS 15 and EAS 30.  The theta/alpha ratio at 0.3 MAC of EtSEVO was correlated with EAS 30.  The area under the receiver-operating characteristic curve of percentage of alpha bands at 0.3 MAC of EtSEVO and the occurrence of EA was 0.672.  The authors concluded that children showing high-alpha powers and low theta powers (= low theta/alpha ratio) during emergence from sevoflurane anesthesia were at high risk of EA in the post-anesthetic care unit.  These preliminary findings need to be validated by well-designed studies.

Intraoperative Electroencephalography During Parietal Tumor Resection

Mueller et al (1996) examined the usefulness of functional magnetic resonance imaging (fMRI) to map cerebral functions in patients with frontal or parietal tumors.  Charts and images of patients with cerebral tumors or vascular malformations who underwent fMRI with an echoplanar technique were reviewed.  The fMRI maps of motor (11 patients), tactile sensory (12 patients), and language tasks (4 patients) were obtained.  The location of the fMRI activation and the positive responses to intra-operative cortical stimulation were compared.  The reliability of the paradigms for mapping the rolandic cortex was evaluated.  Rolandic cortex was activated by tactile tasks in all 12 patients and by motor tasks in 10 of 11 patients.  Language tasks elicited activation in each of the 4 patients.  Activation was obtained within edematous brain and adjacent to tumors.  fMRI in 3 cases with intra-operative electrocortical mapping results showed activation for a language, tactile, or motor task within the same gyrus in which stimulation elicited a related motor, sensory, or language function.  In patients with greater than 2 cm between the margin of the tumor, as revealed by MRI, and the activation, no decline in motor function occurred from surgical resection.  The authors concluded that fMRI of tactile, motor, and language tasks was feasible in patients with cerebral tumors; fMRI showed promise as a means of determining the risk of a post-operative motor deficit from surgical resection of frontal or parietal tumors.

Karatas et al (2004) noted that cases with intractable epilepsy may present with multiple lesions in their brains.  Ictal- electroencephalography (EEG) carries a great value in identification of the primary epileptogenic source.  On the other hand, removal of low-grade tumors located around the eloquent cortex may be risky with conventional techniques.  Functional-neuronavigation (f-NN) is the integration of fMRI and stereotactic technologies; and provides interactive data regarding localization of the motor cortex.  This report presented a case with dysembryoplastic neuro-epithelial tumor (DNET), which was removed using f-NN and electrocorticography (ECoG) techniques.  A 19-year old patient with intractable complex partial and secondary generalized seizures was presented; MRI revealed a low-grade tumor located in right parietal region just behind the motor cortex, and a contralateral temporal arachnoid cyst.  Ictal-EEG demonstrated the right parietal origin of the seizures.  The patient underwent a right parietal craniotomy and tumor excision using f-NN and ECoG techniques intraoperatively.  ECoG findings correlated with epileptogenicity of the parietal lesion.  Post-operative course was uneventful; no post-operative deficit was observed.  The patient was seizure-free in 8 months follow-up.  Pathological examination reported the lesion as DNET.  The authors concluded that ictal-EEG had a very important role in identification of the epileptogenic focus in cases with multiple brain lesions.  Preservation of the functional cortex was the most prominent aim during lesional surgery of epilepsy.  Intra-operative mapping using f-NN and ECoG supported the orientation of the neurosurgeon to the functional and epileptogenic cortical areas; and thus, increased the safety and efficacy of surgical procedures.

Maesawa et al (2016) stated that few studies have examined the clinical characteristics of patients with lesions in the deep parietal operculum facing the sylvian fissure, the region recognized as the secondary somatosensory area (SII).  Moreover, surgical approaches in this region are challenging.  These investigators reported on a patient presenting with SII epilepsy with a tumor in the left deep parietal operculum.  The patient was a 24-year old man who suffered daily partial seizures with extremely uncomfortable dysesthesia and/or occasional pain on his right side.  MRI revealed a tumor in the medial aspect of the anterior transverse parietal gyrus, surrounding the posterior insular point.  Long-term video-EEG monitoring with scalp electrodes (for determination of epileptogenesis) failed to show relevant changes to seizures.  Resection with cortical and subcortical mapping under awake conditions was performed.  A negative response to stimulation was observed at the subcentral gyrus during language and somatosensory tasks; thus, the transcortical approach (specifically, a trans-subcentral gyral approach) was used through this region.  Subcortical stimulation at the medial aspect of the anterior parietal gyrus and the posterior insula around the posterior insular point elicited strong dysesthesia and pain in his right side, similar to manifestation of his seizure.  The tumor was completely removed and pathologically diagnosed as pleomorphic xantho-astrocytoma.  His epilepsy disappeared without neurological deterioration post-operatively.  In this case study, 3 points were clinically significant.  First, the clinical manifestation of this case was quite rare, although still representative of SII epilepsy.  Second, the location of the lesion made surgical removal challenging, and the trans-subcentral gyral approach was useful when intra-operative mapping was performed during awake surgery.  Third, intra-operative mapping demonstrated that the patient experienced pain with electrical stimulation around the posterior insular point.  Thus, this report demonstrated the safe and effective use of the trans-subcentral gyral approach during awake surgery to resect deep parietal opercular lesions, clarified electrophysiological characteristics in the SII area, and achieved successful tumor resection with good control of epilepsy.

Yao et al (2018) noted that using intra-operative ECoG to identify epileptogenic areas and improve post-operative seizure control in patients with low-grade gliomas (LGGs) remains inconclusive.  These researchers retrospectively reported on a surgery strategy that was based on intra-operative ECoG monitoring.  A total of 108 patients with LGGs presenting at the onset of refractory seizures were included.  Patients were divided into 2 groups.  In Group I, all patients underwent gross-total resection (GTR) combined with resection of epilepsy areas guided by intra-operative ECoG, while patients in Group II underwent only GTR.  Tumor location, tumor side, tumor size, seizure-onset features, seizure frequency, seizure duration, pre-operative anti-epileptic drug therapy, intra-operative electrophysiological monitoring, post-operative Engel class, and histological tumor type were compared between the 2 groups.  Univariate analysis demonstrated that tumor location and intra-operative ECoG monitoring correlated with seizure control.  There were 30 temporal lobe tumors, 22 frontal lobe tumors, and 2 parietal lobe tumors in Group I, with 18, 24, and 12 tumors in those same lobes, respectively, in Group II (p < 0.05).  In Group I, 74.07 % of patients were completely seizure-free (Engel Class I), while 38.89 % in Group II (p < 0.05).  In Group I, 96.30 % of the patients achieved satisfactory post-operative seizure control (Engel Class I or II), compared with 77.78 % in Group II (p < 0.05).  Intra-operative ECoG monitoring indicated that in patients with temporal lobe tumors, most of the epileptic discharges (86.7 %) were detected at the anterior part of the temporal lobe.  In these patients with epilepsy discharges located at the anterior part of the temporal lobe, satisfactory post-operative seizure control (93.3 %) was achieved after resection of the tumor and the anterior part of the temporal lobe.  The authors concluded that intra-operative ECoG monitoring provided the exact location of epileptogenic areas and significantly improved post-operative seizure control of LGGs.  In patients with temporal lobe LGGs, resection of the anterior temporal lobe with epileptic discharges was sufficient to control seizures.

Maesawa et al (2018) stated that epilepsy surgery aims to control epilepsy by resecting the epileptogenic region while preserving function.  In some patients with epileptogenic foci in and around functionally eloquent areas, awake surgery is implemented.  These investigators analyzed the surgical outcomes of such patients and discussed the clinical application of awake surgery for epilepsy.  They examined a total of 5 consecutive patients, in whom these researchers performed lesionectomy for epilepsy with awake craniotomy, with post-operative follow-up of greater than 2 years.  All patients showed clear lesions on MRI in the right frontal (n = 1), left temporal (n = 1), and left parietal lobe (n = 3).  Intra-operatively, under awake conditions, sensorimotor mapping was performed; primary motor and/or sensory areas were successfully identified in 4 cases, but not in 1 case of temporal craniotomy.  Language mapping was performed in 4 cases, and language areas were identified in 3 cases.  In 1 case with a left parietal arterio-venous malformation (AVM) scar, language centers were not identified, probably because of a functional shift.  Electrocorticograms (ECoGs) were recorded in all cases, before and after resection; ECoG information changed surgical strategy during surgery in 2 of 5 cases.  Post-operatively, no patient demonstrated neurological deterioration.  Seizure disappeared in 4 of 5 cases (Engel class 1), but recurred after 2 years in the remaining patient due to tumor recurrence.  Therefore, for patients with epileptogenic foci in and around functionally eloquent areas, awake surgery allowed maximal resection of the foci; intra-operative ECoG evaluation and functional mapping allowed functional preservation.  This led to improved seizure control and functional outcomes.

Electroencephalography (EEG) Monitoring During WADA Testing

Tu et al (2015) noted that the intra-carotid amobarbital or Wada procedure is a component of the pre-surgical evaluation for refractory epilepsy, during which monitoring the onset and offset of transient anesthetic effects is critical.  These researchers characterized changes of 8 quantitative measures during 26 Wada tests, which included alpha, beta, theta, and delta powers, alpha/delta power ratio, beta/delta power ratio, median amplitude-integrated EEG, and 90 % spectral edge frequency (SEF90), and correlated them with contralateral hemiplegia.  They found that on the side of injection, delta and theta powers, alpha/delta power ratio, beta/delta power ratio, and SEF90 peaked within 1 min following injection of 70 to 150 mg amobarbital or 4 to 7 mg methohexital.  When contralateral arm strength returned to 3/5, delta power and amplitude-integrated EEG decayed on average 24 % and 19 %, respectively, for amobarbital, similar to that of methohexital (27 % and 18 %).  The authors concluded that because delta power resolution most closely mirrored that of the hemiplegia and amplitude-integrated EEG had the highest signal/noise ratio, these quantitative values appeared to be the best measures for decay of anesthetic effects.  Moreover, these researchers stated that increase in alpha power persisted longest; thus, may be the best measure of late residual anesthetic effects.

Passarelli et al (2015) examined the effect of contralateral electrographic involvement on memory performance (measured by neuropsychological and Wada memory testing) in patients with epilepsy associated with unilateral mesial temporal sclerosis (MTS).  These investigators studied 51 patients with medically-refractory epilepsy associated with unilateral MTS (27 women, 30/51, left MTS) submitted to prolonged non-invasive video-EEG monitoring and bilateral Wada testing.  According to ictal electrographic involvement, patients were classified as: Contralateral ictal involvement, when 1 or more seizures evolved with rhythmic activity in the temporal region contralateral to the MTS or exclusive ipsilateral ictal involvement if all seizures showed ictal EEG activity exclusively on the MTS side.  Wada testing involved a 12-item memory paradigm.  Wada memory asymmetry score was calculated for each patient subtracting the number of recalled items after injection on the lesion side from the number of recalled items after contralateral injection.  Expected asymmetry (EA) was considered if Wada memory asymmetry > 0, and Symmetrical or Reversed memory asymmetry (S-RA) when ≤ 0.  Neuropsychological testing was applied in the 51 patients and in 40 healthy controls (HCs).  Verbal Memory was examined with the Rey Auditory Verbal Learning Test (RAVLT), considering the number of recalled items on immediate recall after the initial 5 consecutive encoding trials (RAVLT 6), a post-interference delayed (30 mins) recall (RAVLT 7), and recall after 7 days.  Non-verbal memory was tested with Wechsler Memory Scale-III (WMS-III) Faces subtests 1 e 2.  Groups did not differ in demographic, clinical and video-EEG monitoring variables.  S-RA was observed more frequently in the group with contralateral ictal involvement (57.2 % versus 27.0 %; p: 0.03).  Logistic regression analysis considering demographic, clinical, hippocampal volume and video-EEG monitoring variables showed contralateral ictal involvement as the only independent variable associated with S-RA (coefficient = 1.32, p = 0.029, OR of 3.77; 95 % CI: 1.1 to 12.47).  Furthermore, the patient group with contralateral ictal EEG involvement displayed worse verbal and nonverbal memory scores compared to HCs.  The authors concluded that in this cohort of unilateral MTS patients, contralateral ictal involvement was associated with decreased memory performance on Wada and on neuropsychological testing.

Bogaarts et al (2016) stated that the Wada test is commonly used to evaluate language and memory lateralization in candidates for epilepsy surgery.  The spatial Brain Symmetry Index (BSI) quantifies inter-hemispheric differences in the EEG; and its use has been shown to be feasible during Wada testing.  These researchers developed a method for the quantification of EEG asymmetry that matches visual assessments of the EEG better than BSI.  A total of 53 patients' EEG data, with a total of 85 injections were analyzed.  In a step-wise, data-driven manner, multiple electrode and frequency band combinations were examined.  Eventually, BSI, calculated using only the frontal electrodes F3 and F4, was combined with a temporal measure of delta power in the central electrodes, C3 and C4, into a new measure: cBSI.  Using the area under the ROC curve (AUC), these investigators showed that cBSI performed significantly better relative to BSI (median AUC of 0.98 versus 0.96, p = 0.0015, Wilcoxon signed rank test).  The authors concluded that these findings showed that asymmetry detection was significantly improved by combining temporal with spatial qEEG measures.  These researchers noted that in the future, their combined quantitative EEG (qEEG) measure could allow for a more objective way of monitoring EEG asymmetry; thus, increasing the feasibility of using EEG as a monitoring tool during the Wada test.  These investigators stated that future studies are needed to validate their cBSI method in real time in the operating room or radiology suite.  The authors listed the following highlights of this study:

  • A qEEG measure combining temporal and spatial EEG changes during Wada testing better agrees with visual assessment of EEG slowing.
  • Quantification of EEG changes per EEG channel and frequency band during the Wada test can reduce subjectivity of EEG interpretation.
  • Not all EEG electrodes and frequency bands are equally important for the detection of EEG slowing during Wada testing

Danoun et al (2021) stated that the Wada test is used to evaluate language lateralization and memory performance following inactivation of an isolated cerebral hemisphere.  Methohexital, a short-acting barbiturate, has been employed for induction of inter-ictal discharges during intra-operative corticography.  In a retrospective study, these investigators reported a new finding of activation of lateralized periodic discharges (LPDs) following methohexital injection.  They reviewed 174 consecutive adult patients who underwent Wada testing in preparation for epilepsy surgery (n = 129, 74 %) or brain tumor resection (n = 45, 26 %) at the University of Michigan to determine the frequency of induced periodic discharges by methohexital.  A total of 4 epilepsy patients (2.29 %) had methohexital-induced LPDs within a median of 2 s (1 to 99 s) of the injection and lasting a median of 4 mins (3 to 10 mins) after a total of 7 injections.  All LPDs occurred ipsilateral to the injection hemisphere in the known region of inter-ictal epileptiform discharges.  LPDs were not induced in brain tumor patients.  In 1 patient, LPDs occurred during memory testing, and this patient's memory performance was below expectation based on pre-test neuropsychological testing.  The authors concluded that methohexital could induce LPDs in ipsilateral hemisphere and that could potentially affect memory performance.  These investigators stated that this observation demonstrated that concurrent EEG monitoring during the Wada test is important and that induced discharges should be considered when interpreting Wada test results.

Castro-Lima et al (2023) compared memory outcomes after surgery for unilateral hippocampal sclerosis (HS)-associated epilepsy in patients with unilateral and bilateral ictal electrographic involvement.  These researchers prospectively evaluated HS patients, aged 18 to 55 years and IQ of 70 or higher.  Left (L) and right (R) surgical groups underwent non-invasive video-EEG monitoring and Wada test.  They classified patients as ipsilateral if ictal EEG was restricted to the HS side, or bilateral, if at least 1 seizure onset occurred contralaterally to the HS, or if ictal discharge evolved to the opposite temporal region.  Patients who declined surgery served as controls.  Memory was assessed on 2 occasions with Rey Auditory-Verbal Learning Test and Rey Visual-Design Learning Test.  Baseline neuropsychological test scores were compared between groups.  Pre- and post-operative scores were compared within each group.  Reliable change index Z-scores (RCI) were obtained using controls as references, and compared between surgical groups.  These investigators evaluated 64 patients.  Subjects were classified as: L-ipsilateral (n = 9), L-bilateral (n = 15), L-control (n = 9), R-ipsilateral (n = 10), R-bilateral (n = 9), and R-control (n = 12).  On pre-operative evaluation, memory performance did not differ among surgical groups.  Right HS patients did not present post-operative memory decline.  L-ipsilateral group presented post-operative decline on immediate (p = 0.036) and delayed verbal recall (p = 0.011), while L-bilateral did not decline.  L-ipsilateral had lower RCI Z-scores, indicating delayed verbal memory decline compared to L-bilateral (p = 0.012).  The authors concluded that dominant HS patients with bilateral ictal involvement presented less pronounced post-operative verbal memory decline compared to patients with exclusive ipsilateral ictal activity.  Surgery was indicated in these patients regardless of memory impairment on neuropsychological testing, since resection of the left sclerotic hippocampus could result in cessation of contralateral epileptiform activity, and, thus, improved memory function.


References

The above policy is based on the following references:

  1. Adelson PD, Black PM, Madsen JR, et al. Use of grids and strip electrodes to identify a seizure locus in children. Pediatr Neurosurg. 1995;22(4):174-180.
  2. American Academy of Neurology (AAN). Electroencephalography (EEG) —routine (95812-95827). Coding FAQs. Rochester, MN: AAN; 2011. Available at: http://www.aan.com/go/practice/coding/faqs. Accessed August 17, 2011.
  3. Ballotta E, Dagiau G, Saladini M, et al. Results of electroencephalographic monitoring during 369 consecutive carotid artery revascularizations. Eur Neurol. 1997;37(1):43-47.
  4. Bogaarts G, Gommer E, Hilkman D, et al. An improved qEEG index for asymmetry detection during the Wada test. Epilepsy Behav. 2016;62:40-46.
  5. Brewster DC, O'Hara PJ, Darling RC, Hallett JW Jr. Relationship of intraoperative EEG monitoring and stump pressure measurements during carotid endarterectomy. Circulation. 1980;62(2 Pt 2):I4-I7.
  6. Burkholder DB, Sulc V, Hoffman EM, et al. Interictal scalp electroencephalography and intraoperative electrocorticography in magnetic resonance imaging-negative temporal lobe epilepsy surgery. JAMA Neurol. 2014;71(6):702-709.
  7. Byer JA, Henzel JH, Dexter JD. Correlation of intraoperative electroencephalography with neurologic deficit after carotid endarterectomy. South Med J. 1979;72(8):956-958.
  8. Castro-Lima H, Passarelli V, Ribeiro ES, et al. Bilateral ictal EEG is associated with better memory outcome after hippocampal sclerosis surgery. Epilepsia Open. 2023;8(4):1532-1540.
  9. Centers for Medicare and Medicaid Services (CMS). Electroencephalographic monitoring during surgical procedures involving the cerebral vasculature. National Coverage Determination. Medicare Coverage Issues Manual Section 35-37. CMS Manual Section 160.8, Publication No. 100-3. Baltimore, MD: CMS; effective June 19, 2006.
  10. Centers for Medicare and Medicaid Services (CMS). Electroencephalographic (EEG) monitoring during open-heart surgery. National Coverage Determination. CMS Manual Section 160.9, Publication No. 100-3. Baltimore, MD: CMS; 2010.
  11. Chang R, Reddy RP, Sudadi S, et al. Diagnostic accuracy of various EEG changes during carotid endarterectomy to detect 30-day perioperative stroke: A systematic review. Clin Neurophysiol. 2020;131(7):1508-1516.
  12. Cho I, Smullens SN, Streletz LJ, Fariello RG. The value of intraoperative EEG monitoring during carotid endarterectomy. Ann Neurol. 1986;20(4):508-512.
  13. Danoun OA, Beimer N, Buchtel H, et al. Methohexital -- Induced lateralized periodic discharges during Wada test. Clin Neurophysiol Pract. 2021;6:225-228.
  14. Ding L, Chen DX, Li Q. Effects of electroencephalography and regional cerebral oxygen saturation monitoring on perioperative neurocognitive disorders: A systematic review and meta-analysis. BMC Anesthesiol. 2020;20(1):254.
  15. Fiol ME, Gates JR, Mireles R, et al. Value of intraoperative EEG changes during corpus callosotomy in predicting surgical results. Epilepsia. 1993;34(1):74-78.
  16. Fountas KN, Smith JR. Subdural electrode-associated complications: A 20-year experience. Stereotact Funct Neurosurg. 2007;85(6):264-272.
  17. Fritz BA, Kalarickal PL, Maybrier HR, et al. Intraoperative electroencephalogram suppression predicts postoperative delirium. Anesth Analg. 2016;122(1):234-242.
  18. Hamer HM, Morris HH, Mascha EJ, et al. Complications of invasive video-EEG monitoring with subdural grid electrodes. Neurology. 2002;58(1):97-103.
  19. Jang YE, Jeong SA, Kim SY, et al. The efficacy of intraoperative EEG to predict the occurrence of emergence agitation in the postanesthetic room after sevoflurane anesthesia in children. J Perianesth Nurs. 2018;33(1):45-52.
  20. Johnston JM Jr, Mangano FT, Ojemann JG, et al. Complications of invasive subdural electrode monitoring at St. Louis Children's Hospital, 1994-2005. J Neurosurg. 2006;105(5 Suppl):343-347.
  21. Jones TH, Chiappa KH, Young RR, et al. EEG monitoring for induced hypotension for surgery of intracranial aneurysms. Stroke. 1979;10(3):292-294.
  22. Karatas A, Erdem A, Savas A, et al. Identification and removal of an epileptogenic lesion using Ictal-EEG, functional-neuronavigation and electrocorticography. J Clin Neurosci. 2004;11(3):343-346.
  23. Kutsy RL, Farrell DF, Ojemann GA. Ictal patterns of neocortical seizures monitored with intracranial electrodes: Correlation with surgical outcome. Epilepsia. 1999;40(3):257-266.
  24. Lagerlund TD, Cascino GD, Cicora KM, Sharbrough FW. Long-term electroencephalographic monitoring for diagnosis and management of seizures. Mayo Clin Proc. 1996;71(10):1000-1006.
  25. Liubinas SV, Cassidy D, Roten A, et al. Tailored cortical resection following image guided subdural grid implantation for medically refractory epilepsy. J Clin Neurosci. 2009;16(11):1398-1408.
  26. Maesawa S, Fujii M, Futamura M, et al. A case of secondary somatosensory epilepsy with a left deep parietal opercular lesion: Successful tumor resection using a transsubcentral gyral approach during awake surgery. J Neurosurg. 2016;124(3):791-798.
  27. Maesawa S, Nakatsubo D, Fujii M, et al. Application of awake surgery for epilepsy in clinical practice. Neurol Med Chir (Tokyo). 2018;58(10):442-452.
  28. McKinsey JF, Desai TR, Bassiouny HS, et al. Mechanisms of neurologic deficits and mortality with carotid endarterectomy. Arch Surg. 1996;131(5):526-532.
  29. Meneghetti G, Deriu GP, Saia A, et al. Continuous intraoperative EEG monitoring during carotid surgery. Eur Neurol. 1984;23(2):82-88.
  30. Michaelides C, Nguyen TN, Chiappa KH, et al. Cerebral embolism during elective carotid endarterectomy treated with tissue plasminogen activator: Utility of intraoperative EEG monitoring. Clin Neurol Neurosurg. 2010;112(5):446-449.
  31. Mueller WM, Yetkin FZ, Hammeke TA, et al. Functional magnetic resonance imaging mapping of the motor cortex in patients with cerebral tumors. Neurosurgery. 1996;39(3):515-520.
  32. Nuwer M, Aminoff M, Chatrain G, et al. Assessment: Intraoperative neurophysiology. Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 1990;40(11):1644-1646.
  33. Nuwer MR. Intraoperative electroencephalography. J Clin Neurophysiol. 1993;10(4):437-444.
  34. Onal C, Otsubo H, Araki T, et al. Complications of invasive subdural grid monitoring in children with epilepsy. J Neurosurg. 2003;98(5):1017-1026.
  35. Otsubo H, Shirasawa A, Chitoku S, et al. Computerized brain-surface voltage topographic mapping for localization of intracranial spikes from electrocorticography. Technical note. J Neurosurg. 2001;94(6):1005-1009.
  36. Ozlen F, Asan Z, Tanriverdi T, et al. Surgical morbidity of invasive monitoring in epilepsy surgery: An experience from a single institution. Turk Neurosurg. 2010;20(3):364-372.
  37. Passarelli V, Castro-Lima Filho H, Adda CC, et al. Contralateral ictal electrographic involvement is associated with decreased memory performance in unilateral mesial temporal sclerosis. J Neurol Sci. 2015;359(1-2):241-246.
  38. Pinkerton JA Jr. EEG as a criterion for shunt need in carotid endarterectomy. Ann Vasc Surg. 2002;16(6):756-761.
  39. Plestis KA, Loubser P, Mizrahi EM, et al. Continuous electroencephalographic monitoring and selective shunting reduces neurologic morbidity rates in carotid endarterectomy. J Vasc Surg. 1997;25(4):620-628.
  40. Reuter NP, Charette SD, Sticca RP. Cerebral protection during carotid endarterectomy. Am J Surg. 2004;188(6):772-777.
  41. Shah AK, Fuerst D, Sood S, et al. Seizures lead to elevation of intracranial pressure in children undergoing invasive EEG monitoring. Epilepsia. 2007;48(6):1097-1103.
  42. Siegel AM, Jobst BC, Thadani VM, et al. Medically intractable, localization-related epilepsy with normal MRI: Presurgical evaluation and surgical outcome in 43 patients. Epilepsia. 2001;42(7):883-888.
  43. Siegel AM, Roberts DW, Thadani VM, et al. The role of intracranial electrode reevaluation in epilepsy patients after failed initial invasive monitoring. Epilepsia. 2000;41(5):571-580.
  44. Simon SL, Telfeian A, Duhaime AC. Complications of invasive monitoring used in intractable pediatric epilepsy. Pediatr Neurosurg. 2003;38(1):47-52.
  45. Smith MC, Buelow JM. Epilepsy. Dis Mon. 1996;42(11):729-827.
  46. Sperling MR, Bucurescu G, Kim B. Epilepsy management: Issues in medical and surgical treatment. Postgrad Med. 1997;102(1):102-104, 109-112, 115-118, passim.
  47. Spire WJ, Jobst BC, Thadani VM, et al. Robotic image-guided depth electrode implantation in the evaluation of medically intractable epilepsy. Neurosurg Focus. 2008;25(3):E19.
  48. Tan TW, Garcia-Toca M, Marcaccio EJ Jr, et al. Predictors of shunt during carotid endarterectomy with routine electroencephalography monitoring. J Vasc Surg. 2009;49(6):1374-1378.
  49. Tu B, Assassi NJ, Bazil CW, et al. Quantitative EEG is an objective, sensitive, and reliable indicator of transient anesthetic effects during Wada tests. J Clin Neurophysiol. 2015;32(2):152-158.
  50. Van Gompel JJ, Meyer FB, Marsh WR, et al. Stereotactic electroencephalography with temporal grid and mesial temporal depth electrode coverage: Does technique of depth electrode placement affect outcome? J Neurosurg. 2010;113(1):32-38.
  51. Van Gompel JJ, Worrell GA, Bell ML, et al. Intracranial electroencephalography with subdural grid electrodes: Techniques, complications, and outcomes. Neurosurgery. 2008;63(3):498-505; discussion 505-506.
  52. Vendrame M, Kaleyias J, Loddenkemper T, et al. Electroencephalogram monitoring during intracranial surgery for moyamoya disease. Pediatr Neurol. 2011;44(6):427-432.
  53. Wassmann H, Fischdick G, Jain KK. Cerebral protection during carotid endarterectomy--EEG monitoring as a guide to the use of intraluminal shunts. Acta Neurochir (Wien). 1984;71(1-2):99-108.
  54. Wiggins GC, Elisevich K, Smith BJ. Morbidity and infection in combined subdural grid and strip electrode investigation for intractable epilepsy. Epilepsy Res. 1999;37(1):73-80.
  55. Wong CH, Birkett J, Byth K, et al. Risk factors for complications during intracranial electrode recording in presurgical evaluation of drug resistant partial epilepsy. Acta Neurochir (Wien). 2009;151(1):37-50.
  56. Yao P-S, Zhen S-F, Wang F, et al. Surgery guided with intraoperative electrocorticography in patients with low-grade glioma and refractory seizures. J Neurosurg. 2018;128(3):840-845.