Real the full article here – Electroencephalographic Cerebral Dysrhythmic Abnormalities in the Trinity of Nonepileptic General Population, Neuropsychiatric, and Neurobehavioral Disorders

(The Journal of Neuropsychiatry and Clinical Neurosciences 2008; 20:7?22)

The reporter in this article likely had a TIA… a Transient Ischemic Attack… the temporary insufficiency of vascular flow dynamics to a cortical area providing insufficient local glucose and oxygen for function. This can happen from just flow dynamics due to vasoconstriction, such as seen in hyperventilation or gross over-arousal. This can also happen when blood consistency is not appropriate to allow flow, such as seen with hyperglycemia in diabetics when their blood sugar rises too high.

You may think “what does this have to do with EEG?”… well it is an important EEG area, and not without controversy.

The mid-temporal sharp-slow transients that are seen in EEG are considered neurologically non-specific, and many neurologists do not even comment on them. This is a mistake, as these nonspecific changes are a harbinger of vascular issues, including ischemia (as seen in migraine ischemia and the current discussion of TIAs), or vascular insufficiency, commonly in the vertebro-basillar artery and posterior vascular distributions supplying the hippo-campus (which has a huge metabolic demand load).

No less than Ernst Neidermayer chastises the neurologists doing EEG interpretations for under-reading of these findings. He clearly shows in his paper that these non-specific findings are important.

Recently I had a client who sent in the EEG of his wife, who had experience some word-finding and fluency issues, and it had these “nonspecific” temporal findings on the left… we suggested an MRA (magnetic resonance angiography), and though they had already done the MRI (which was normal), the MRA was done. The MRA showed a 9 millimeter AV malformation, and surgery was done to patch this area so it didn’t burst, saving her life.

These are the sort of waveform distortions that require an experienced EEG interpretation, and preferably an expert with Board qualification in EEG, not just someone licensed to read EEGs. These controversial findings make all the difference, and it is exactly these areas that provide the large difference between interpretation in studies looking at inter-reader visual EEG reliability.

Jay

In modern neuroscience centers, the EEG is still the tool of choice in evaluation of convulsive epilepsy, as well as some other non-convulsive forms, such as staring episodes seen in “absence epilepsy” typically as a 3/second spike and wave dominant anteriorly, or temporal lobe epilepsy, which is seen as a “notched” slow wave discharge fronto-temporally.

The EEG can now be processed through algorithms, such as spike dipole localization software, to identify the “seizure focus” cortically, or spectral averaging to look for changes in the underlying EEG rhythmicity due to the disorder.

One of the difficulty with the two later categories is that they are not always identified as forms of epilepsy, and thus can be mis-diagnosed based on behavior alone as some other disorders, including ADD/ADHD in absence epilepsy “spells” where the attentional process is disturbed by the discharge taking segments of time out of the cognitive streaming of perception, or from discharge in sensory areas.  These segments being removed do not have any conscious awareness of the event for the person experiencing the blips missing from their cognitive process, and they will have trouble tracking on-going events, like driving or listening to a speech or lecture.  Imagine missing a few here and there, to tens of seconds from your awareness, and see if you don’t have “attentional deficits”.

The other major areas of misdiagnosis are of a “schizophrenic” or “psychotic” nature.  This occurs when the discharges are frontal or temporal and disturbing local cortical function, and may be seen as a range of presentations from hallucinations or emotional outbursts of rage, or even “fits of laughter” in “Gelastic seizures”.   Temporal Lobe Epilepsy (TLE) is a particularly difficult one to properly diagnose in the absence of the EEG.

The importance of these missed-diagnoses can be quite severe, with the use of medications to treat the symptoms often being contra-indicated by the epilepsy.  One example of this is TLE that is assumed to be psychosis, since antipsychotic medications lower the seizure threshold, and make the person worse, which can then be responded to with more antipsychotics, spiraling the person into a progressively worsened condition.  The use of stimulants in epilepsy is a controversial area, as the effect of stimulants for inattention in known and treated epileptics may be acceptable, though throwing a stimulant at an undiagnosed epileptic can have severe negative consequences.

The real issue is that IF YOU DO NOT LOOK, YOU WILL NOT SEE… and in epilepsy, looking requires the EEG, as the gold standard.

In surgical approaches, the EEG is used to identify whether there are multiple foci, which generally will preclude a good outcome (you remove the brain tissue and the seizures do not change).

I will post some images of the WIDE variety of morphologic presentation that epilepsy can take, so that some understanding of the task of the Electroencephalographer and Epileptologist can be better appreciated by those who think it is straight-forward.

Thanks for your attention to these obscure issues.

Jay