Rating our Effectiveness

Depression

It is noteworthy that depression is among the easiest conditions to treat with EEG biofeedback. These findings cover not only the mild depression that is frequently seen in connection with ADD, such as the dysthymia observed in childhood or the kind of low-grade pervasive depression for which Prozac has become the palliative of choice. They also cover episodes of deep depression, including some which are accompanied by episodes of suicidality, and even reactive depression.

The early effects of the training may be observed in the first few sessions. A person may recover from an excursion into suicidality in just one or two sessions. Full recovery from depression may, however, require on the order of twenty to forty training sessions. The recovery is seen as a restoration of a normal range of physiological arousal. The recovery is not characterized, however, by a numbing of feelings or constriction in affective state (in the event of reactive depression), nor does it interfere with a normal grieving process. The training is usually effective in disrupting patterns of chronic pain that are often seen in depression, although we are not dealing here with an anesthesia. Normal pain sensitivity is retained.

It is noteworthy that with SMR/beta protocols the greatest efficacy for unipolar depression is achieved with beta training on the left hemisphere at sensorimotor cortex. Since the left hemisphere is where language resides, one is aided by the fact that the patient can usually articulate very well the consequences of each training session for left hemisphere function and thus help to guide the process. Matters are different with respect to agitated depression or suicidality. These are attributed to disregulation primarily lodged in the right hemisphere, and require the calming and more stabilizing lower frequency training in the general case. The client may not be in a position to either properly appraise or to articulate his or her own state with respect to right hemisphere dysfunction.

These findings are so startling in their import that perhaps they stretch the credulity of the reader, and are entitled to some further discussion to make this plausible. First of all, this finding of efficacy for depression is concordant with the belief among psychiatrists that depression is rather consistently responsive to electroshock treatment, as already mentioned in the introduction. In many clinical circles, ECT is considered the gold standard of treatment for depression. The severe side effects attendant to that procedure keep it from being employed except as a last resort, and in severe depression. However, the belief is firmly entrenched that depression is expected to respond to shock treatment in the general case. Shock treatment can be seen as a sudden change in the ambient electrical state of brain function. Existing reinforcement patterns of pathological arousal and affect are broken up, and a new homeostasis in terms of arousal level and affect can be quickly established and apparently sustained, often without continuing pharmacological support.

On the other therapeutic extreme, that of non-intervention, it is found that episodes of deep depression quite frequently result in spontaneous remission. Such remission is so commonplace in children and young adults, when deep depression is first observed, that anti-depressant medication has never been shown to be better than placebo (read spontaneous recovery) in children. (Just recently, a first study appeared in which statistical significance was achieved (Emslie, 1997). Yet no one would argue that the nervous system of a child is non-responsive to anti-depressants. The drugs clearly work there as well. It is simply that spontaneous recovery is so robust and commonplace that anti-depressants are not obviously superior statistically in a controlled research setting over a fixed time interval. The mechanisms are clearly in place for a natural recovery to occur in most individuals with a first experience with major depression.

Hence, the claim of efficacy of EEG biofeedback for depression would seem to have the same difficulty vis-a-vis spontaneous recovery that has confounded the drug studies. Not so. In fact, we assert that the mechanisms of spontaneous recovery and of EEG biofeedback are probably identical. The existence of a robust spontaneous recovery capability supports the claim; it does not undermine it. EEG biofeedback can simply induce a systematic re-normalization of arousal function which might also happen randomly all by itself. The difference is that when EEG biofeedback is employed, the response is prompt, predictable, relatively consistent, and more likely to be sustained over the longer term. Moreover, it tracks the specific protocols employed (in terms of electrode placement and reward frequency band). This proposition does not need to await statistical proof (although such proof would be salutary). Simple clinical observation is sufficient (just as it was for shock therapy).

Minor Traumatic Brain Injury

A second category in which rapid, substantial recovery is observed is minor traumatic brain injury. The principal symptoms associated with MTBI are listed in Table 4. Many of these symptoms relate to disregulation of arousal, and of these the majority is depressive in character: depression, inattention, irritability, effort fatigue, chronic pain, and frequent waking. Some relate to overarousal: mania, impulsivity, anxiety and fear, anger, and sleep onset problems. Others relate to cognitive function: dyslexia, loss of short-term memory, articulation problems, word retrieval problems. Other problems relate more to frontal lobe function: behavioral disinhibition, obsessive-compulsive disorder, exacerbated motor and vocal tics, perseveration.

Table 4: Characteristic Symptoms of Minor Traumatic Brain Injury

Headache	Anxiety and Depression	Aphasia
Chronic Pain	Sleep Disturbances	Visuospatial impairments
Dizziness-Vertigo	Irritability	Changes in appetite
Difficulty Concentrating	Mood Swings	Sensitivity to hot and cold
Difficulty with Attention	Personality Changes	Seizures
Difficulty Planning Effort	Hemiparesis
Fatigue	Palsies

Characteristically much of the whole spectrum of MTBI symptoms may be manifested in any one head injury victim. And characteristically also, essentially all of these symptoms remediate with the training at least to some significant degree, although at different rates. The recovery of energy, the restoration of the ability to sleep properly, and the stabilization of mood, are the early markers for EEG training. Subsequently, there is recovery of cognitive function, diminution of pain syndromes, and ultimately even recovery of memory function.

Efficacy of the biofeedback for MTBI is probably largely attributable to three factors: 1) restoration of appropriate regulation of arousal level; 2) increase in the stability of brain function; and 3) increase in the flexibility of brain function. Commonly in MTBI the EEG exhibits paroxysmal activity, or elevated low frequency activity. Typically also, significant deviations in temporal coherence may be seen between brain regions. These deviations may be in either direction. Too low a coherence would indicate insufficient coupling or communication between brain regions, and too high a coherence would indicate too tight a coupling. It is easy to explain low coherence in terms of axonal shearing or other structural injury attributable to the original trauma. However, that may be too facile.

EEG deviations tend to normalize with the training, as would be expected. However, that is not always the case. Nor does such normalization closely track the recovery of function. Hence the EEG is of limited utility as a measure of recovery of function. Diminishing of paroxysmal activity is attributed to an increase in cortical stability with a strengthening of thalamic regulatory control. Elevated low frequency amplitude could simply be a manifestation of functional disengagement, of low activation and arousal. It can also result from inappropriate cortical-cortical coupling, attributed to insufficient subcortical regulation. The recovery could therefore again be attributed to the strengthening of thalamo-cortical regulatory mechanisms. Finally there are the deviations in coherence themselves. The fact that coherence is likely to recover with training regardless of whether it is low or high indicates that we are dealing largely with functional disorganization rather than structural impediments to function. Again, it is postulated that reassertion of thalamic control of brain rhythms is sufficient to restore appropriate coherence. However, direct cortical-cortical communication surely also plays a role in normalization of coherence.

Recovery from depressive symptoms is attributed to the first factor, renormalization of arousal control. Restoration of cognitive function and short-term memory is attributed to an increase in continuity of brain function, to which the diminution of paroxysmal activity and delta and theta amplitudes are testimony. Paroxysmal activity is very likely to disrupt the temporal relationships by which images, concepts and gestalts are bound together as coherent entities and retained for processing. The subjective experience of this disruption is an inability to organize activities, to make plans, to weigh several competing ideas, to carry mental challenges through to their resolution, and to reliably retain a memory. Finally, the restoration of appropriate coherence leads to recovery of the person's original behavioral flexibility.

MTBI has been listed as responding very quickly and reliably to EEG biofeedback training. This is indeed the case, in the sense that there can be significant recoveries of function even in the first few sessions. A more complete resolution may require as many as 50-100 training sessions, although 20 ' 30 sessions are adequate in most cases. A representative sampling of 16 such cases was reported by Jonathan Walker, of the Neuroscience Centers in Dallas. The results are summarized in Table 5. The average recovery with respect to premorbid functioning, by self- report, was 83%, and the median improvement was 85%. The average number of training sessions was 32, and the median was 30. The EEGs changed in line with the protocol to a statistically significant degree (decrease in theta amplitudes, and an increase in beta amplitudes).

Table 5. Recovery by self-report from symptoms of Minor Traumatic Brain Injury.

There may also be obvious deficits remaining that relate to organic (morphological, structural) injury. In these cases significant recovery is possible as well, but the rate- limiting mechanism is presumably some dendritic regrowth or rearborization. Hence the pace of progress is only partly conditional on the schedule of training. The trainee may continue to make gains by returning to the training episodically, to exploit any new learning opportunity. This phase of training is similar to the experience of Bernard Brucker (1985) in his EMG training for spinal chord injury, where it is found that a limb which did not yield to training on one occasion may readily respond a year later.

When specific organic injury has occurred, it seems more appropriate to include this in the category of major head injury. However, the latter distinction is reserved for those head injuries in which skull fracture or major organic loss has occurred. This is a less meaningful distinction, and often uncorrelated with the severity of deficits incurred. Paradoxically, some head injury that involves skull fracture can be less severe than minor head trauma. Conceivably, this could be due to the fact that the skull fracture, by yielding somewhat on impact, can reduce the g-forces sustained by the brain and the brainstem. For present purposes, organic injury is lumped along with major head injury, and as such appears in the last column of the chart.

The intimate connection of head injury symptomatology with disregulation of arousal seems to have been under-recognized by clinicians, who have by and large retained both a structuralist perspective as well as a focus on the cortex as the locus of injury. When such techniques as CAT scans and structural MRI scans failed to confirm injury, the victim was often declared to be a malingerer and his symptoms discounted. Thus the person became a victim a second time, in this instance of the clinician's myopia. In fact, most head injury involves severe jostling of the head upon its spindly neck, resulting in trauma to the brainstem, from whence arousal is managed. Fortunately, such injury consists more likely of compressional effects such as anoxia rather than of actual axonal shearing. As such, the injury is functional in nature, rather than structural, and turns out to be eminently remediable with our techniques.