Dementia & Alzheimer’s Disease (AD)

I often get questions about Alzheimer’s Disease (AD) and the EEG.

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.


1 thought on “Dementia & Alzheimer’s Disease (AD)”

  1. Jay,
    Thanks for this post. Not only to you explain what we should expect and evaluate in the EEG you have provided some EEG theory to some previous work. This inspired me to write a post on some of the LORETA findings in dementia and AD from a couple of preliminary studies a few years back. See my 05/09/09 post on Dementia and Alzheimer’s Disease: LORETA findings.


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