When the brain struggles to generate alpha waves, it can remain stuck in higher-frequency states such as beta, which are associated with heightened alertness and stress. Without sufficient alpha activity, the brain has difficulty “downshifting” into a more relaxed state. This may present as racing thoughts, persistent mental tension, and difficulty relaxing.
Individuals may also experience trouble staying calm under pressure, brain fog, reduced concentration, mental fatigue, and poor sleep quality. As a result, the stress response—driven by the sympathetic nervous system—can remain activated longer than necessary, placing ongoing strain on both the mind and body.
There are several situations in which alpha brain waves may not be present during an EEG recording. Recording-related issues can contribute to a meaningful number of poor-quality datasets, which in turn may affect diagnostic accuracy and treatment planning.
While EEG equipment manufacturers often provide short training programs, these may not always be sufficient for developing a deep understanding of both the fundamentals and more advanced aspects of EEG interpretation. As a result, some clinicians may benefit from additional training and experience to fully interpret the data with confidence.
Producing reliable EEG recordings requires a solid grasp of electronics and waveform analysis. Without this background, it can be challenging to distinguish artifacts from true EEG signals, understand how filters influence the data, or fully appreciate the strengths and limitations of different montages. In some cases, clinicians may rely heavily on automated or AI-assisted interpretations. While these tools can be helpful, they are most effective when used alongside strong clinical judgment and technical understanding, as automated outputs are not infallible.
Understanding the causes of alpha inhibition is important for effective treatment planning. It is often necessary to consider whether the underlying factors are emotional, stress-related, or neurological. Low alpha activity is commonly associated with increased stress and poor sleep. Sleep quality, in turn, plays a role in physiological processes such as glymphatic function, which supports the clearance of metabolic waste from the brain. When these processes are disrupted, overall brain function may be affected.
High-quality data collection is essential. This includes gathering relevant contextual information such as sleep patterns, stress levels, nutrition, and substance use. Even short-term factors—such as whether a client has eaten recently—can influence the recording and should be considered when interpreting results.
Finally, when EEG data is sent to external processing services, the absence of contextual information can limit the accuracy of interpretations. Details about the recording conditions, client state, and environment are important for ensuring that analyses are as accurate and clinically meaningful as possible.
How False Alpha Dropout Can Occur During an EEG Recording
1. Clinician-Caused Alpha Dropout
- The eyes-closed (EC) condition must be in a dimly room. If the room is too bright, the alpha will be suppressed.
- Drinking coffee, hot chocolate, or having just eaten food will trigger dopamine or norepinephrine in the patient and this will either speed up the alpha into the SMR band or suppress it.
- Too many ambient noises can be distracting to the client.
- Client does not have enough trust and feel safe with clinician.
- Chair may be uncomfortable and cause distraction.
- Thoughts inhibit alpha. Client being asked to relax jaw or face may cause more focus and thinking. Many clients have a degree of obsessive-compulsiveness in their makeup (which shows in their cingulate gyrus). If client shows a muscle tension in the recording, it’s important not to mention relaxing or letting go of thoughts. Best strategy can be not to say anything and simply wait it out. Most of the time, thoughts, and tension will dissipate within 10 minutes.
- A tired patient can slide into theta or fall asleep into delta, and therefore not make alpha.
This example illustrates how external noise during a recording can significantly impact a client’s alpha brainwave activity, as well as increase jaw tension. The startle response triggered a surge of adrenaline and noradrenaline, which altered the EEG to such a degree that the recording was no longer reliable and the appointment had to be rescheduled.
2. Patient-Caused Alpha Dropout:
The biggest cause of patient-caused alpha dropout is from thinking. Many of my clients have all sorts of issues, ranging from health worries to insomnia to mental fog, to strained relationships, fears of losing or having lost their job, and money worries. Some of my clients want to give me a great recording, so they “meditate.” Most people don’t know how to meditate and actually suppress alpha when they should increasing their alpha. Before recording begins, I always watch for alpha bursts on the screen after I have the recording-cap on their head and we are simply being casual, as I often see alpha bursts during this time. But during recording, they cannot make a wavelet of alpha. So, at least this helps me know that we are dealing with psychological issues and not misinterpret this alpha suppression as an actual brain issue.
This EEG recording is from a 42-year-old stressed-out college student with her eyes closed. She has many worries, ranging from school grades to being able to pay her rent. So, the moment she sits quietly, her mind begins to race and she suppresses her alpha. Most of the time, after five minutes, all I have to do is quietly say, “Just let your thoughts go,” and a second or two later, I’ll see a large burst of alpha. This alpha will often last for a minute or two until the client starts thinking again.
I had one client who grew up largely abandoned and lonely. He was completely alpha suppressed when the room was quiet. But when either of us were talking about our hobbles, he was flooded with alpha. Quietness pulled up all his fears from a childhood of abandonment, which resulted in acute anxiety and alpha suppression. This effect was very important clinically as it showed his psychologist that we didn’t need to “fix” his brain. We simply needed to heal his mind through talk-therapy and relaxation techniques.
EC Alpha blocking while client was sitting quietly. His mind is racing. He shows mild anxiety-related muscle tension in his forehead and jaw, mainly at FP1, FP2 and T3.
Spectral Graphs of EEG Power Spectra – 4uv
His alpha simply isn’t there. If the clinician missed this and an EEG processing service didn’t know, unnecessary treatments might be recommended.
Here we see lots of large waves that are EC alpha while the client was talking about fixing up his vintage car. Although he is engaged, his mind is very calm. He is in his happy place! There is some jaw muscle activity from talking slowly. It’s amazing what can happen in two minutes.
Spectral Graphs of EEG power spectra-4uv
Here we see that when engaging, he has a proper alpha peak across his entire brain. The frequency is mildly fast at 12 Hz, because this person is sharp and quick when he’s not in fear. This is completely reversed from what would be expected.
3. Neurologically Based Alpha Dropout:
This is the population that I mainly work with and it mostly comprises of those struggling with a previous concussion or severe fever from a viral infection, such as flu. I term this post-concussion syndrome as a Thalamo-Cortical Disconnect (TCD), because there are breaks between the cortex and the thalamus (this loop is where the alpha wave is generated). The alpha rhythm acts like a drummer of sorts, synchronizing the various parts of the brain, such that information retrieval and processing can performed efficiently. The thalamo-cortical loop can provide rhythms in the range from 3 to 16 Hz, with the common range of 8 to12 Hz representing an adult group’s “average”. Hyperpolarization of the thalamus slows the alpha, and hypo-polarization speeds it up until it desynchronizes at about 16 Hz and becomes a low voltage fast EEG in the beta range.
A neurological loss of the alpha rhythm causes extensive cognitive impairments, mainly because the brain struggles to share the various aspects of a memory. This type of TBI seems to not be caused directly by concussions as chronic symptoms often take one or several months to appear-a delayed response. Research suggests that inflammation and long-term, low-grade fever from a concussion or an infection may develop into inflammatory neuropathy, possibly caused by reactive gliosis. Given that the causes of thalamo-cortical disruptions are rarely visible on MRIs, there might not be an actual injury, but more of an interruption or disconnect. The brain might be taking billions of neurons “off-line” as a protective mechanism and then forgets they are there. But, once the neurons go down, the glia go down with it, thus losing neuronal support. Lactate and ATP, the brain’s energy during times of high demand, also shut down. AVE boosts lactate and ATP by 260% in five minutes.
Actively firing neurons are constantly dumping calcium (positive ions) into the surrounding tissue. Calcium (Ca (2+)) is a universal second messenger that regulates the most important activities of all cells. It is of critical importance to neurons as it participates in the transmission of the depolarizing signal and contributes to synaptic activity. Neurons have thus developed extensive and intricate Ca (2+) signaling pathways to couple the Ca (2+) signal to their biochemical machinery. A few DC-based EEG recordings suggest that with the loss of the calcium and other gradients, the brain can develop a highly negative voltage in the order of milli-volts (not micro-volts). So, once the glia goes down, the brain might become hyperpolarized and thalamic gating might result, thus shutting down the alpha rhythm.
It is possible that with a severe TCD, as described in the case below, that 10 billion neurons in the thalamo-cortical loop might have stopped firing. When we consider that the alpha rhythm is close to 10 Hz, and it’s a two-way loop, we could be losing 200 billion action potentials/second, which is a massive loss of calcium, ATP, and lactate boosting activity.
Most of the time, we also see a strip of theta along the cingulate at FZ and CZ, indicating “no brakes” OCD. Most of my clients with this signature are hoarders, counters, cutters, door-closers, ritualists, tappers, anorexics, and committed substance abusers. The severe sleep impairments also cause impaired cerebral spinal fluid circulation within the glymphatic system, and this leads to the development of Alzheimer’s and Parkinson’s over time.
In the diagram below, we see that a non-functioning pathway in either direction breaks the entire alpha rhythm (and information retrieval) in that region of the brain.
In most cases of a TCD, we will see a few EEG channels that show EC alpha. In the case below, this grade 11 youth had been hit on the forehead and both temples with hockey pucks. With the last hit on his right temporal side, he became violent and began to kick in the basement walls. He then threatened to kill some girls at school and his grades dropped from being an honor student to barely passing. Here, we can see that he makes alpha at O2, while all the damaged areas are unable to make any EC alpha. During SMR-Beta randomized AVE, his alpha improved, so this is not produced by the frequency-following response, but other brain systems.
During randomized SMR-Beta AVE (about 30 minutes), his alpha improved to some extent, particularly the alpha spindling.
We can see in his Entropy analysis that his Entropy intake lacks alpha (the blue heads) and has excessive theta and delta (the pink heads). Although he was given SMR-Beta AVE, his theta and delta are much less and his alpha has improved. This means that we were affecting neuronal systems not tied to the frequency-following response.
Pre AVE Entropy Post 20-Minutes SMR-beta AVE
He was given a DAVID Delight Plus and instructed to use the SMR-Beta sessions in the Brain Boosting category. His grades improved enough in June to pass with a B grade. He had improved so much by the next fall (Grade 12) that he qualified for a student exchange program in Germany!
This case illustrates the severest loss of EC alpha that I have ever seen.
Case TZ
Closed-head injury from a childhood fall. This is a 31-year-old male who has become a binge alcoholic. He cannot seem to learn a skill and or maintain an intimate relationship. He is reclusive and lives in a friend’s basement suite. He does odd jobs such as helping people move and other manual labor jobs.
History (as described by client)
Grade 1: Slide accident with major trauma to my left skull. Caved it in about 1 inch. I was in and out of consciousness. I don’t feel like it has affected me and my life has been normal since. I’ve always lacked motivation.
We were in an inner-tube being pulled by a skidoo. My leg got caught in the middle of the tube and I was sucked under. I was knocked unconscious.
Since high school: Trouble socializing - often a loner and binge drinking on weekends and then later on during the week.
2013 - Lost my license in July from a DUI.
2014 - I spent 6 months at a treatment center.
2015 - 7 weeks in rehab - snuck in alcohol and was kicked out.
2016 - I spent five days in detox. Shortly there afterwards, I began drinking again.
Raw EEG - EC
In this case, every channel is suppressed across all bands. So I don’t know if this is the result of TZ obsessing on life situation or neurologically based alpha suppression. During the setting up process, I didn’t see a hint of alpha, which is one indicator of neurological suppression. Also, at five minutes, I gently asked him to “let his thought go.” There was no change, which is another indicator of neurological suppression.
Entropy – 2 SD
Here we see a great deal of delta plus a severe alpha dropout (blue heads at 8 to 11 Hz), as is consistent with post-concussion inflammation.
He was put on our Mood Booster session, which is a mixture of right-brain alpha and left-brain Beta AVE. Quite quickly, his alpha spindles began to surge, and by 15 minutes into the session, he was producing substantial alpha spindles (that were a bit fast). No longer needing to self-medicate. Ten days later, he had not had a drink of alcohol. Between October and December, he was able to control his alcohol intake and only drank socially. On New Year’s, he quit drinking completely and joined AA.
The post entropy was misleading, given that our client was so tired and so had fallen asleep, thus making ample delta, along with fast alpha. So this image is not included.
Three-years Post Treatment
As is typical with our post-concussed clients, once we fire the thalamus (and alpha generation) back up, the brain continues to function fine and improve over time. Following three months of alpha-beta AVE, our client continued to show beautiful EC alpha spindles.
QEEG in 1 Hz Bins (2.3uv)
In the left image, we see the pink strip down his cingulate gyrus, indicating his obsessive-compulsive (OC) behaviors around consuming alcohol. He also doesn’t show an alpha peak in the left image. On the right side, we see the OC behavior has cleared up, and we have an alpha peak at 8 to 9 Hz (pink areas).
Pre Treatment 3-Years Post Treatment
Our client shared with us that he received his Five Years of Sobriety key-chain award. He could not have done this without a brain filled with wonderful, healthy alpha!
Conclusion:
Alpha brainwave production plays a vital role in overall brain health and the functioning of its support systems and is closely linked\ to an individual’s mental health and quality of life. Clinicians must have sufficient experience and certainty—not guesswork—when determining whether recorded alpha activity, or the absence of it, has been properly interpreted. This includes considering the individual’s mental state, the recording environment, and the clinician–patient interaction, all of which can influence alpha production during assessment.
This article highlights how elusive “normal” alpha activity can be in a recording context. When making a diagnosis, any conclusions about alpha inhibition must be based on clear, well-supported evidence.
For a more in-depth discussion of the many factors that can affect EEG recordings, please watch my YouTube lecture here:
For further detail on how thalamo-cortical dropout can occur—and practical approaches to address it—please view these lectures:
https://youtu.be/QBp2Qr665gk?si=5Pe8LM9wLEA4jUpM
https://youtu.be/C7Haz2Ge7hM?si=j_vIh_oHBJu4ksIE
This video is about how to help your glymphatic system clean waste material from your brain by circulating cerebral spinal fluid:
Dave Siever is the founder of Mind Alive Inc. Dave is a researcher and lecturer on the topic of neuromodulation.