David Noton, PhD
The Forest Institute
Two studies of premenstrual syndrome (PMS), EEG, and photic stimulation have recently been completed at the Royal Postgraduate Medical School, Hammersmith Hospital, London (UK). In a preliminary trial of photic stimulation as a treatment for PMS seventeen women with PMS were treated with a take-home flashing light device for 15 to 20 minutes per day throughout their cycle. At the end of three months of treatment the median reduction in PMS symptoms for the 17 patients was 76% and twelve of the 17 patients technically no longer had PMS. Separately, an EEG study of six women with PMS demonstrated that, when they were premenstrual, their EEGs showed more slow (delta) activity and slower P300 evoked response than when they were mid-cycle. These results are discussed in the context of other known “slow brainwave” disorders, such as ADD and Minor Head Injury, and various theoretical explanations are proposed.
Preliminary Trial of Photic Stimulation for PMS
A preliminary trial of photic stimulation (flashing light therapy) as a treatment for PMS was recently completed by Duncan Anderson and his associates at the Royal Postgraduate Medical School, Hammersmith Hospital, London (UK). It was an open study of 17 women, all of whom had confirmed, severe, and long-standing PMS.
The flashing light device is similar to the device previously used for treatment of migraine (Anderson 1989). It consists of a mask, which covers the eyes shutting out all light. Mounted in the mask are red LED lamps, one over each eye, which flash alternately in left and right eyes. The device is portable and designed to be used by the patient at home. The brightness of the light and the frequency of flashing are controlled by the patient, with ranges of approximately 10 to 45 mcd and 0.5 to 50 Hz respectively (one frequency cycle consisting of light in the left eye for half the cycle and then light in the right eye for half the cycle). The patients were instructed to start at the brightest setting and at the flicker-fusion point (around 30 Hz) and then adjust the brightness and frequency for best comfort. The patients were asked to use the device for 15 minutes per day, every day throughout their menstrual cycle. The patients recorded their symptoms daily for two menstrual cycles before treatment, three cycles during treatment, and one cycle after treatment was stopped.
At the end of treatment the median reduction in PMS symptoms for the 17 patients was 76%. Twelve of the 17 patients technically no longer had PMS. Although the results of an open trial are subject to placebo effects, the results were so large and persistent that it is unlikely that placebo can fully explain them. The complete results of this trial are published in detail elsewhere (Anderson et al. 1997).
Study of EEG during PMS
A study of EEG during PMS was recently completed by Istra Toner and her associates at the Royal Postgraduate Medical School in London (Toner et al. 1995). Six women with self-reported PMS had 21 channel QEEG recordings and P300 evoked potentials measured during mid-cycle and premenstrually. Ages ranged from 30 to 43 and all were taking no treatment for PMS.
A significant increase in delta activity during PMS was observed (p=0.043) along with a suggestive, but not necessarily significant, decrease in beta activity. This is consistent with previous reports of increased slow activity and decreased fast activity during PMS (Harding et al. 1976, Lamb et al. 1953).
P300 evoked potential was elicited using an odd-tone procedure with a frequent tone (1000 Hz) and an odd tone (2000 Hz) presented in the ratio 4:1 at a rate of 1 per second. Using global field power averaging, a significant increase in P300 latency during PMS was observed (p=0.027).
DISCUSSION AND INTERPRETATION
PMS is a “Slow Brainwave” Disorder
It is proposed that there is a group of disorders characterized by excessive low frequency EEG activity. For example:
|Disorder||Abbr.||Reported Brainwave Characteristic|
|Attention Deficit||ADHD||Excess theta/beta ratio (Lubar 1991, etc.)|
|Chronic Fatigue Syndr||CFS||Slow alpha, excess theta (Lindenfeld et al 1996)|
|Minor Head Injury||MHI||Diffuse slow activity (Duffy et al. 1989, Ayers 1987, both also quoted in Byers, 1995)|
|Toxic Trauma||TT||Excess slow activity (Heuser 1994)|
|Premenstrual Syndrome||PMS||Excess delta, slow P300 (Toner 1995reported above)|
Treatment of Slow Brainwave Disorders with Photic Stimulation
The preliminary trial reported above shows the efficacy of photic stimulation as a treatment for PMS. The treatment of ADHD with photic stimulation has been developed extensively by Harold Russell and his associates, using frequencies of 18 Hz and 10 Hz alternating for two minute periods, with demonstrable improvements in IQ scores and behavior (Russell and Carter, 1993). Many clinicians appear to be using photic stimulation informally for ADHD and the other slow brainwave disorders, with anecdotal reports of successful treatment but with very few published results.
Treatment of Slow Brainwave Disorders with Neurofeedback
Many neurofeedback (EEG biofeedback) practitioners report successful treatment of some or all of these slow brainwave disorders. For example, the Lubar’s have for many years worked with children with ADHD, training them with beta frequency biofeedback, with excellent results (Lubar 1991 and 1989); the Othmer’s have a long history of success with beta frequency biofeedback with patients with all of the disorders in this group (Othmer 1994); and there are many other practitioners using this approach. Generally the feedback protocol involves positive reinforcement of beta frequencies and negative reinforcement of theta frequencies, though various other protocols are also used successfully.
The Brainwave Frequency Hypothesis
A reasonable explanation that is commonly proposed for the above experimental and clinical results is that the key to treating these disorders (all characterized by excessive slow brainwave activity) is to speed up the brainwave frequency. It is proposed that this can be accomplished either by training the patients to speed up their own brainwaves (beta-training neurofeedback) or by entraining the patients’ brainwaves with a photic stimulation device flashing at beta frequencies.
Problems with the Brainwave Frequency Hypothesis
Unfortunately there is evidence, both from photic stimulation research and from neurofeedback training, that undermines this brainwave frequency hypothesis.
In the trial of PMS and photic stimulation reported above, the patients were free to adjust the frequency of the flashing light at will, between 0.5 Hz and 50 Hz. A frequency of around 30 Hz (high beta) was suggested, based on previous clinical results, but the patients were free to change this at any time in any session. Of those patients who achieved a greater than 50% reduction in symptoms, about half chose to operate the flashing light in the range of 5 to 10 Hz, ie, theta-alpha frequency, not beta frequency.
Furthermore, some neurofeedback clinicians report equally good results when treating slow brainwave disorders with frequency protocols quite different from the beta enhancement/theta reduction protocol discussed above. In fact, Hoffman et al. (1995) list six different neurofeedback protocols (including alpha training) that have been used successfully for minor head injury.
Apparently “speeding up” the brainwaves with photic stimulation or neurofeedback at beta frequencies is not an adequate explanation for the successful treatment of these disorders.
The Cerebral Blood Flow Hypothesis
Many studies have shown that excessive slow brainwave activity is closely associated with hypoperfusion, ie, insufficient cerebral blood flow. These studies have been collected and summarized by Toomim (1994). Looking at the individual “slow brainwave” disorders we see that in each case there is some evidence for hypoperfusion: