There are many in the field of Neurotherapy who do not perform qEEGs prior to designing a clinical intervention. These people are currently practicing well within the standard of practice for this rapidly evolving field. Many within this group have standard protocols which are used on all clients, with various alterations to respond to the client’s reported experiences during the treatment.
Diffuse slowing, with slower alpha
The ascending reticular activating system stimulates the diffuse thalamic projection system and sets the general arousal level of the brain. With an increase in the CNS arousal level, there is an increase in the mean frequency of alpha and a decreased slowing. With decreases in arousal there is a slowing of the alpha, as well as eventually an increase in diffusely distributed slowing ( a mixture of diffuse lower voltage delta and theta, usually with a weak vertex prominence in linked ear montages).
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.
This brief summary will discuss the various EEG findings seen in head injury when it results in a brain injury, though any given head injury may or may not result in traumatic brain injury. When an injury is incurred by the brain there are a few varieties of findings seen in the EEG, ranging from spectral changes associated with either white or gray matter damage, to the changes in “connectivity”, seen as changes in coherence or correlation measured across the cortex, or between more distant functionally related areas.
Identifying subtypes of specific disorders is an attractive exercise, as it expands our understanding of the individual’s response to therapy, but it remains attached to the approach based on the Diagnostic and Statistical Manual of Mental Disorders (DSM), which is rooted in behavior and frequently does not predict therapeutic response by any individual within the DSM grouping. Phenotypes are an intermediate step between genetics and behavior. These proposed electroencephalography (EEG) phenotypes are semistable states of neurophysiological function. The author proposes a framework allowing one to describe much of the observed EEG variance with a small number of phenotypical categories. These groupings cut across the DSM categories, and unlike the DSM, the phenotypes predict the individual’s response to therapy, for neurofeedback as well as for medication.