It is no surprise when insurance companies find ways to restrict what they will cover as a service for their clients, whether flood insurance liability insurance, or any other branch of this financial industry.  This is especially true for medical insurance companies, which are always finding reasons to restrict payments.

This decision restricts the payment for a qEEG to be an extension of the analysis of an EEG analysis, which makes the qEEG a medical procedure requiring licensure adequate to provide credentials to do a medical EEG interpretation. If further restricts the payments to applications that match the American Academy of Neurology position paper, which approves the technique in vascular cases, encephalopathies such as dementia cases, or for epilepsy, as well as longer term EEG monitoring, where quantitative analysis allows the selection of segments for review visually, assisting the electroencephalographer in eliminating long time segments from detailed analysis.

Specifically restricted from payment are these applications:

• Alcoholism
• Asperger’s syndrome and other autism spectrum disorders
• Attention disorders
• Depression
• Drug abuse
• Fibromyalgia
• Hypoxic ischemic encephalopathy
• Insomnia
• Learning disability
• Mild or moderate head injury
• Panic disorder
• Post-concussion syndrome
• Predicting response to psychotropic medication
• Schizophrenia
• Tinnitus

The list above is not an appropriate reason to do an EEG medically… at least not on the surface. In many of these cases the clinical decision may include ruling our an encephalopathy, a a vascular or epileptic process. As an example of this, approximately 30% of those with autism have undiscovered epileptiform discharges in the EEG, and respond well to anticonvulsants. An EEG is the only way to rule out epilepsy in such a case, and this may be allowed under the coverage listed, if the testing is ordered appropriately and the chart supports the order for the testing.

This is generally the same for TBI, where a post-traumatic vascular issue or epileptiform response to the TBI may be suspected, such as with contusion or post traumatic edema/ischemia.
In atypical clinical presentation, an alcoholic can be evaluated for dementia (Korsakov’s syndrome), as well as epilepsy (PLEDS are a common withdrawal pattern in chronic alcoholics). The chart needs to support the evaluation diagnostically for ruling out any of these covered categories.

The report can comment on medication implications, even if the testing was not done for that purpose diagnostically.

Attentional and affective disorders will not be covered, but if the physician is trying to rule out epilepsy (absence can mimic ADD) or an encephalopathy or dementia as the etiology of the psychiatric changes, then the insurance may cover the EEG and subsequent qEEG examination.

The important thing is to have the documentation in the chart to support the diagnostic/treatment question being posed with the testing.

The fact that they cover any of the qEEG at all is only due to the AAN position paper’s support for these areas. As the neuroscience is done to support more applications, then the carriers will have to amend their coverage statements. It is up to us to do the hard work to open these other areas up to payment…. and to argue for some other licenses to be covered for payment.

Concussion is a common consequence of trauma to the head in contact sports, estimated by the Centers for Disease Control and Prevention to occur three million times in the United States each year. Among people aged 15 to 24 years, sports are now second only to motor vehicle accidents as the leading cause of traumatic brain injury. While the majority of concussions are self-limited injuries, catastrophic results can occur and the long-term effects of multiple concussions are unknown.

Members of the AAN specialize in treating disorders of the brain and nervous system, and some members have particular interest and experience caring for athletes and are best qualified to develop and disseminate guidelines for managing athletes with sports-related concussion. Based on the clinical experience of these experts, the AAN supports the implementation of policy that supports the following recommendations:

Recommendations

1. Any athlete who is suspected to have suffered a concussion should be removed from participation until he or she is evaluated by a physician with training in the evaluation and management of sports concussions
2. No athlete should be allowed to participate in sports if he or she is still experiencing symptoms from a concussion.
3. Following a concussion, a neurologist or physician with proper training should be consulted prior to clearing the athlete for return to participation.
4. A certified athletic trainer should be present at all sporting events, including practices, where athletes are at risk for concussion.
5. Education efforts should be maximized to improve the understanding of concussion by all athletes, parents, and coaches.

Position Statement History
Approved by the AAN Sports Neurology Section, Practice Committee, and Board of Directors
October 2010 (AAN Policy 2010-36).

How can we live a fuller and healthier lifestyle as we get older? Perhaps keeping our body and brain engaged can help. That seems to be the case in Japan where the number of centegenarians is greater than 20,000.

THE ART OF AGING:THE LIMITLESS POTENTIAL OF THE BRAIN introduces a number of these “super-seniors” who lead healthy lives at nearly 100-years-old and, through them,searches for the “keys” to living a healthy and vital life regardless of age.

Click here to view the embedded video.

I’d like to just throw out there a few other findings that were discovered in a few exploratory investigations while working on some studies with our colleague Alicia Townsend, at the time at Univ. of North Texas. Lexicor funded these projects and now the arrangements are such that I can’t disclose more than was published in the abstracts from our talks at ISNR and AAPB.  I did at least want to point to these very preliminary findings because theoretically they are in concert with your explanations.

First, we explored 10 participants between the ages of 65 and 85 were recruited at the University of North Texas Health Science Center.  Each was diagnosed by the Alzheimer’s Disease Assessment Scale and a medical interview.  The aim of the study was to identify current source density markers in AD.  EEG recording of the eyes closed condition of an AD group was compared to an age-sex matched control group using within-subject multiple t-test procedures. sLORETA difference maps in nine frequency bands were investigated. Interestingly the results showed that there was a significant increase in current source density in the delta and theta bands in the Brodmann Area (BA) 39 of the right temporal lobe and BA 31, the cingulate gyrus respectively.  Additionally there were decreases in alpha in the BA 21 of the right temporal lobe and right inferior parietal lobule (Sherlin, Townsend & Hall, 2006).

This was corroborative previous findings of increased delta and theta and decreased alpha from a single case study of AD I analyzed with Tom Budzynski  (Budzyski, Budzynski, & Sherlin, 2002).  Results varied from previous studies that showed diffuse differences although the temporal lobe slowing is replicated.  We recognized that the proximity of the significant locations to the precuneus and fusiform gyrus which are both important in facial recognition and processing social information.  The precuneus is also involved in episodic memory retrieval and imagery of motor functions. A correlation study found similar patterns with sLORETA.

I believe that future investigation for patterns in different types of dementia (vascular vs. alzheimer’s vs. frontal lobe vs. mild cognitive impairment) may increase our ability to differentially diagnose.

The second study we completed was to examine the relationship between memory loss and brain electrical activity that was not AD diagnosable. Eighty-four participants between the ages of 50 and 85 were recruited for the original study. Participants were administered the Alzheimer’s Disease Assessment Scale – Cognitive (ADAS-Cog), a QEEG, and a clinical interview. The cross spectra was averaged and LORETA correlation maps.  Correlations were computed for each individual’s ADAS-Cog score compared to each voxel (7×7x7 mm) of their baseline sLORETA.

What we found were significant positive correlations between ADAS-Cog scores and frontal and parietal delta activity, and theta activity in the precuneus. Significant negative correlations were found between ADAS-Cog scores and temporal alpha. This corroborated prior findings and further alluded that as our memory continues to become impaired we expect frontal and parietal delta as well as anterior midline theta to increase. And that alpha will decrease as impairment grows (Townsend, Sherlin & Hall, 2006). This is exactly as you reported as expectations in the EEG.

Budzinski, T., Budzinski, H., & Sherlin, L. (2002).  Short and Long Term effects of Audio Visual Stimulation (AVS) on an Alzheimer’s Patient as documented by Quantitative Electroencephalography (QEEG) and Low Resolution Electromagnetic brain Tomography (LORETA) [Abstract].  Journal of Neurotherapy. Vol 6:1.

Sherlin, L. ,Townsend, A., & Hall, J. (2006). LORETA Analysis of Alzheimer’s Disease. [Abstract].  Journal of Neurotherapy. Vol 9:4.

Townsend, A., Sherlin, L., & Hall, J.  (2006).  LORETA and QEEG Correlations with the Alzheimer’s Disease Assessment Scale. [Abstract].  Journal of Neurotherapy. Vol 9:4.

Whenever a client presents with the question of dementia, all other forms of
dementia need to be ruled out before you are left with the diagnosis of AD.
There are many EEG signatures of various forms of dementia, all of which are
helpful in evaluating a client’s presentation of dementia.

Done by experts in EEG in dementia, the EEG and qEEG may be of substantial
additive value in the differential diagnosis puzzle that all cases of
dementia represent clinically.

One EEG pattern seen in dementia is the presence of periodic triphasic
slowing in the EEG, which is actually diagnostic of subacute sclerosing
panencephalitis (SSPE). SSPE is a “spongiform encephalopathy” where the
brain becomes like “Swiss cheese”, with holes scattered throughout. This
periodic triphasic finding is differentiated from MULTIFOCAL triphasics
which are diagnostic of Crutzfeld-Jacob Syndrome (CJD), which in lay terms
is a form of mad cow disease in humans.

Other helpful EEG signatures include PAFA (periodic anterior fast activity)
which is seen in many with Pick’s disease (a fronto-temporal dementia),
FIRDA (frontal intermittent rhythmic delta activity) or in children OIRDA
(an occipital variant), and also diffuse slowing patterns are all reported
in those with hypoxic/anoxic encephalopathies… as well as the rather
differentiation of multi-infarct dementia (MID) versus AD, where the
difference is seen in coherence, which in AD is seen as anterior posterior
hypocoherence, and from MID, which is seen as fronto-temporal hypocoherence.

This doesn’t speak to more common dementias where non-specific slowing is
seen, like Korsakov’s Syndrome, and Binswanger’s Disease, and some
interesting ones that have more specific EEG signatures, like atypical
frontal and/or temporal Status Epilepticus, which in EEG terms may be seen
as PLEDS (periodic lateralized epileptiform discharges) which is also common
in chronic alcohol related presentation of an “acute dementia”.

The progressive slowing of the alpha peak and increased slower content may
be seen in normo-tensive hydrocephalus, which is a reversible dementia.
This is reversed with the simple surgical placement of a V-P shunt
(ventricular-periteneal) which drains the cerebrospinal fluid accumulation
into the abdominal cavity where it is absorbed.

One other EEG finding that has a virtually diagnostic EEG signature is a
hepatic encephalopathy, where the classic EEG pattern was called a “liver
wave”. This is a triphasic slow wave, with an anterior-to-posterior phase
lead of 100-150 milliseconds. The reason I said “virtually” is that some
with less experience have mistaken triphasic slowing s from anoxia/hypoxia,
and the previously noted periodic and multifocal forms of triphasic slowing,
but this doesn?t have the phase change anterior-posteriorly seen with the
hepatic related findings.

Some point to qEEG measures of “theta” correlating with more severe AD in
the older qEEG literature, but it is really slowed alpha that shows up as
theta in broad band databases… see the work on AD by Brain Resource
Company (BRC)… increased delta with advanced severity, also with decreased
faster activity, and most importantly slowing of the alpha peak which is
more severe with advancing AD.

The EEG is very useful in dementia, but only in the hands of those expert
enough to have seen these patterns in the clinical EEG in full detail.

Jay