The dissociative mode might be considered a pre-death mode. (For students of physiology, note that the dissociative mode is one of the autonomic modes, but it is not sympathetic mode, nor is it parasympathetic mode. It is a fully autonomic mode in which both the spinal nerves are inhibited and the vagus nerve is inhibited. It is different from sleep mode. It is a bordering-on-death emergency survival mode.)
If a person is able to survive the shock of blood loss and skin perforation, his body should resume somewhat normal function within ten minutes to several days. The dissociative condition is quite rare, but it is a perfectly correct, healthy response to a loss-of-blood or other severe emergency.

Neurotransmitter release is altered during dissociative mode. Dopamine release is severely inhibited. Dopamine, among other roles, regulates a person’s ability to move when the person feels safe. Adrenaline release is also inhibited during dissociative mode. The inhibition of adrenaline release may range from slight to severe. Adrenaline, among other roles, regulates a person’s ability to move when the person thinks that he is in danger.

As an aside, the dissociative condition is very different from the “fight or flight” (sympathetic) mode of the autonomic nervous system. The sympathetic mode enables one to avoid or overcome danger, and is characterized by a surge of adrenaline. The dissociative mode is an automatic, unplanned last-ditch effort that serves to immobilize the injured body. This immobilization can help keep imminent death at bay, potentially benefiting the injured person in a case where rescue and recovery might yet be possible. Also, immobility and lack of consciousness following a severe injury can serve to diminish the interest of a predator who was hunting for sport rather than hunger.
Most of us have seen a mouse become inert after having been caught by a cat. Very often, the cat eventually loses interest in the seemingly dead mouse. When the cat leaves, the mouse may, after about five to ten minutes, return to consciousness and scamper away. His open wounds will have had time to seal over while his heart rate and breathing were nearly stopped. The mouse was not “playing dead.” The mouse had absolutely no control over his body’s autonomic response to being torn by the cat’s talons: the mouse had been in dissociative mode.

In people with Parkinson’s disease or psychogenic parkinsonism, a modified and/or minimized dissociation pattern has become chronic. In people with Parkinson’s, the channel patterns that are fairly rare, but perfectly normal, which is to say the short-term electrical patterns that drive the symptoms of dissociation, have never stopped. Following some injury or emotional trauma, the electrical patterns that drive the symptoms of dissociation have become chronic. In people with Parkinson’s disease, dopamine inhibition, and all the other correct and normal changes that occur during dissociation have become stuck in a long-term holding pattern.

In order to recover from Parkinson’s disease, these patterns must become unstuck. The injuries and or emotional shocks that triggered the electrical patterns of the dissociative mode must be healed. In a person with Parkinson’s, as soon as the injury and the shock is processed and healed, the body steadily reverts back to normal health. The symptoms of Parkinson’s disease decrease, and then cease. The body then heals from the cellular damage and and pathological thought patterns that have usually developed in response to the pathological, long-term use of what should have been a normal, short-term electrical mode.

Idiopathic Parkinson’s disease

In all cases of idiopathic Parkinson’s disease, we have seen evidence of an unhealed foot injury. In a healthy person, a severe foot or leg injury triggers a specific, injured pattern of channel flow. This pattern, in which a specific channel runs backwards from the site of the injury (because the currents cannot traverse the injury site), causes repercussions in the channel system that cause, among other things, inhibition of dopamine, loss of appetite, and other symptoms similar to the dissociative response. The degree of dissociative-like response depends on the severity of the injury. The benefit of these responses is this: the injured person will be able to rest deeply while his injury heals. The injured person will not feel much hunger, pain, or the desire or ability to move quickly. With these inhibitions in place, a person will heal the most quickly. As soon as enough healing has occurred so that the channel current can once again flow unimpeded past the point of injury, the dissociation-like response will cease. Dopamine flow will resume. The person will once again be able to function normally while the limb finishes healing.

Psychogenic parkinsonism

In psychogenic parkinsonism, a somewhat similar electrical pattern presents, but more channels are involved. Even so, the specific channel involved in idiopathic Parkinson’s is the same channel that causes most of the symptoms of psychogenic parkinsonism. In both of these illness patterns, the current in this channel is not flowing correctly. However, in dissociation, the electrical currents do not run backwards. In cases of dissociation, the electrical flow in the channel moves in a rapidly vibrating back-and-forth pattern: the current is going nowhere. Major channel junctions cease to be operational. The body behaves as if many of the channels were standing still. If the electrical signal is weak, it may almost feel as if there is no current running at all in either direction – forwards or backwards – in many of the channels.
In psychogenic parkinsonism, this back and forth movement occurs in the currents flowing in the channels.

Despite the two methods of channel response to trauma – backwards or rapid back-and-forth/going nowhere – the result is the same: inhibition of dopamine, inhibition of movement (unless adrenaline is summoned up through powerful use of will in order to override the inhibition), shunting of blood flow away from the skin and extremities, inhibition of the sensory nerves’s ability to feel pain, and alteration of awareness such that a person feels that he is observing his body from outside himself.

When, because of failure to fully heal from the injury or the shock, either or both of these two patterns become chronic, the result is a movement disorder that is referred to as either idiopathic or psychogenic parkinsonism. To the patient, these disorders look and feel almost the same. The only difference is that symptoms of psychogenic parkinsonism can wax and wane significantly depending on mood and fear level. Symptoms of injury-induced Parkinson’s are somewhat more constant: they are somewhat less subject to mood. The only electrical difference between these two forms of Parkinson’s-type disorders is the nature of the electrical current that is no longer flowing in the usual, healthy direction. In one form of the illness, the channel is running backwards. In the other, the channel is essentially standing still.
MDs do not differentiate between idiopathic Parkinson’s disease and psychogenic parkinsonism when they make a diagnosis. The only time that the diagnosis of psychogenic parkinsonism is made occurs when a person recovers from Parkinson’s. Because Parkinson’s is considered to be incurable, anyone who recovers from Parkinson’s is presumed to have had psychogenic parkinsonism (or to have been misdiagnosed). In truth, both idiopathic Parkinson’s and psychogenic parkinsonism are both illnesses from which a person can recover.

More about idiopathic Parkinson’s disease

The foot injury can become chronic if it fails to fully heal. Failure to heal is usually due to a mental attitude that removes awareness of the injury from normal consciousness, so that the injury heals superficially, but the pain and trauma of the injury remains unprocessed in the brain. If an injury remains unprocessed in the brain, it will remain unprocessed in the channel system. (Brain and heart wave patterns are electromagnetic forces that help drive the electrical systems known as channels.) If the injury is unprocessed, the micromuscle tension at the injury site and/or physical displacement of anatomical structures, together with the brain’s retention of the injury memory in the “unhealed trauma” department of the brain, will cause the channel to continue to run backwards indefinitely. The person will still be able to move, but he will have to rely on creating a constant level of false-emergency to summon up adrenaline to override his chronic dopamine inhibition. Eventually, over decades, as his ability to conjure up the necessary levels of false emergency begin to wane, the symptoms of injury-based dissociation – and sometimes, the symptoms of injury themselves, such as limping – will become physically apparent. These symptoms are synonymous with the symptoms of Parkinson’s disease: dopamine inhibition causing slowness of movement and poor ability to make the quick motor adjustments that allow for balance, and the fear and pain from unhealed injury that correctly cause rigidity and tremor. The locations of the tremor and rigidity, in the early years of Parkinson’s, are even located along the lines of those channels that are most specifically effected by a foot injury.

More about psychogenic parkinsonism

In psychogenic Parkinson, the genuine dissociative state has been triggered, as opposed to the modified form that occurs in response to a channel-blocking injury. Although the dissociative stage is usually triggered by a near-death experience, it can also be triggered by a shock to the emotions. For example, if a person responds to a severe emotional shock by removing from normal consciousness his awareness of the emotional signals that come from his own heart, the dissociative mode can be triggered.
Ordinarily, when a mortally wounded person slides into a dissociative mode, he can no longer feel emotional pain: the pain signals that normally can be sensed, or felt, in the region of the heart cease to be communicated to the brain. The opposite is also true: when a person will not allow the pain signals in his heart to be communicated to the brain, the body slides away from sympathetic (fight, flight, or freeze) mode and moves towards the dissociative mode.
For an illustrative example of psychogenic parkinsonism, let me quickly describe from my own experience a fairly common medical scenario. A patient, female, aged 82, lost her husband of sixty-one years following his two-year battle with cancer. Prior to his death, the patient was physically as functional as might be expected of healthy woman of her age. One week after her husband’s death, three days after his memorial service, the patient was too weak to get up off the sofa by herself. Her posture was hunched. Her sudden-onset rigidity made it hard for her to dress herself or feed herself. Her appetite ceased. Her facial became expressionless. Her hands and feet were very cold. She developed a resting tremor in her hands. Notice that these are similar to the symptoms of Parkinson’s disease.
This sudden-onset condition in response to severe emotional trauma is so common that we have a common name for it: broken heart. The electrical mechanisms by which a “broken heart” triggers the symptoms of Parkinson’s disease creates the same set of channel alterations that occurs during loss-of-blood or near-death dissociation.
The electrical patterns are the same. But with the sudden-emotional-trauma, the method for inducing it is not loss of blood. The method of inducing emotion-based back-and-forth current in the dissociation-causing channel is this: refusal to allow brain communication with the pains being felt in the heart.
Ordinarily, severe-injury dissociation causes communications between the sensory experiences of the heart area and the brain to be cut off. But oppositely, by cutting off heart-brain communications, a person can induce the same dissociation patterns that occur in response to severe injury.

Whether the dissociation channel-shift is brought about by dire injury or severe blood loss, or by shutting down brain communication between the sensations of the heart area and the brain, the result is the same: the dopamine-inhibiting dissociative mode.
In the above example, the “broken heart” emotional shut down was severe and nearly instantaneous (within one week after her husband’s death). But in most cases of psychogenic parkinsonism, the emotional shut down begins as a modest inhibition: a coping mechanism that comes and goes depending on mood and on whether or not the person feels safe. As with injury-based Parkinson’s disease, the movement aspect of this modest level of dissociation can be overridden with adrenaline. A person can teach himself to feel no physical or emotional pain, thus inhibiting dopamine, but he might be able to keep moving by creating the sense of false emergency that triggers the release of adrenaline.
But if, after years or decades, the temptation to emotionally shut-down, thus rendering oneself pain-free, becomes chronic, the person may find himself being diagnosed with Parkinson’s disease. He may notice that his symptoms of Parkinson’s might wax and wane depending upon his mood and how safe he feels. He may also notice that, upon being diagnosed with Parkinson’s disease, his symptoms take an immediate nose-dive. The traumatic news of being diagnosed can cause an increase in his degree of dissociation, coupled with a hopelessness that inhibits even the release of false-emergency adrenaline.

Happily, we have found that, if at some point the person is able to permanently allow heart-area feelings to be once again communicated to the brain, his parkinsonism symptoms will permanently cease. The person will then be diagnosed, after the fact, as having had “only”psychogenic parkinsonism instead of idiopathic Parkinson’s.

As an aside, in our limited experience, an MD will only change a diagnosis to psychogenic parkinsonism if the patient recovers. Also, in our limited experience, when our patients did have idiopathic Parkinson’s disease, if they worked at healing the foot injury and thereby recovered from Parkinson’s symptoms, they were told by their MDs that they had been misdiagnosed, or that they had “only” had psychogenic parkinsonism.
But the main point is this: we have seen patients recover from Parkinson’s disease.
Not only that, but we have seen a similarity in the counterintuitive pain, the infantile movement restoration dystonias, and the post-dissociation emotional-shift changes in all our patients who have recovered from Parkinson’s disease. The sequence and locations of these and other recovery symptoms have helped us form and confirm our hypotheses.

In closing

In our research, we have seen that slightly more than twenty percent of our Parkinson’s patients have foot injury-induced “idiopathic” Parkinson’s disease.
One percent of our patients with symptoms of parkinsonism have no unhealed injury, but do remember having consciously decided, in childhood, in response to severe emotional pain and fear, to “pretend to not have a heart,” and from then on, were able to successfully be numb to any heart-area sensations. These patients, both of whom had been diagnosed with “Parkinson’s disease,” had long-term, chronic dissociations that caused them to eventually, in their late sixties, to develop symptoms of psychogenic parkinsonism.
But nearly eighty percent of our hundreds of patients with idiopathic Parkinson’s disease have both an unhealed foot injury and varying degrees of psychogenic parkinsonism. They have channel flow patterns in the foot that are characteristic of unhealed foot injury. They also have other channel flow patterns that resemble those of dissociation. In these patients, when the foot injury healed and the channel was able to flow correctly, they experienced many symptoms of recovery. These recovery symptoms included return of facial expression, improved sensory awareness in the foot, improved sense of smell, ability to move easily, and other symptoms characteristic of recovery. However, these patients found that, although they might move perfectly normally when they felt safe, they were able to become nearly immobilized if a situation arose that caused them fear or anxiety. Their channel still reverted quickly into back-and-forth movements in these moments. These patients retained dissociation-type channel flow variations that lessened and worsened in response to mood and fear even after the physical injury pattern has been healed. Only after learning to re-associate with heart-area sensations regardless of potentially emotional “risk” were these people able to maintain at all times their newly-won return to normal movement.

The healthy, correct electrical channel shifts that are supposed to occur during channel blockage from injury or from physical or emotional trauma – and which are supposed to be very short term, measured in minutes or days – seem to have become “locked in,” to varying degrees, in people with Parkinson’s disease. Also, people breezily diagnosed with “Parkinson’s disease” may actually have one, or another, or most often both, of two distinct channel patterns.

Finally, and most importantly, people have been able to recover from Parkinson’s disease using the treatment plans that we have developed. Parkinson’s disease is not, and never has been, an incurable illness. Parkinson’s disease is the result of perfectly normal emergency body processes becoming locked into a chronic mode. In the early years of pathological retention of these patterns, the dopamine-inhibition and immobility can be overridden by mentally-induced adrenaline. This willful summoning up of adrenaline in the place of dopamine can cause the person to appear healthy and normal – even faster, stronger, and smarter than normal, but usually much less able to relax. However, the chronic dopamine inhibition and relentless use of adrenaline eventually leads to the appearance of the symptoms of Parkinson’s disease.
But if the injury and/or turned-off heart are successfully treated and cured, the symptoms of Parkinson’s do go away.

Please note: our research has not been used to address the conditions that develop in drug- or toxin-induced parkinsonism. These pathologies do not cause backwards or back-and-forth flowing current in channels, nor are they treatable via the techniques that we have developed. MDs do not bother to differentiate between idiopathic Parkinson’s disease, psychogenic parkinsonism, or drug- or toxin-induced parkinsonism. This is because there exists no mechanism other than autopsy that allows an MD to differentiate between these illnesses. However, a person who can perform channel-based diagnoses will be able to differentiate between these patterns. A book on channel theory, and how to feel channels, is underway. When it is finished, it will be posted on this website.

Our non-profit organization, The Parkinson’s Recovery Project, is dedicated to research on Parkinson’s and disseminating the results of our research. The above introduction is extremely brief. Highly detailed information, with everything we have discovered about Parkinson’s and how to treat it, is available on this website.

The above description of the long-term shifts in the autonomic nervous system that lead to Parkinson’s disease is very short: a mere webpage introduction. This brief introduction should raise more questions than it answers: Does a person with Parkinson’s need to work with a trained professional in order to recover? (No.) Does everyone who studies Asian medicine know about this? (No.) What sort of recovery statistics do we have for our project? Are there any objective methods for measuring the brain changes in Parkinson’s or during recovery? What is channel energy? How can a person learn to detect it? (Read the book Trouble Afoot.)
To answer as many of these questions as possible, Janice Walton-Hadlock has written Trouble Afoot: Tracking Down the Causes and Cures of Parkinson’s Disease. This book, in its current form, is, in large part, a chronology of the research of the Parkinson’s Recovery Project. A person can work from this book and undertake his own recovery from Parkinson’s disease. This book includes enormous amounts of detail about both the pertinent Asian medicine and the most up-to-date western understanding of Parkinson’s disease – including new research information that many “Parkinson’s specialists” have not kept up with.
Hopefully, in the years to come, another book will be released which is shorter, and is more of a simple how-to book for recovering from Parkinson’s disease. However, because we are still researching the most effective, most direct methods of recovering, that how-to book has not yet been written. Until then, we are using the chronologically based Trouble Afoot book as our main publication for helping people recover from Parkinson’s disease. A person who reads the story of our research, the details of what our patients do, and what happens when they do it, will be able to understand the principles behind our findings. If he has Parkinson’s disease, he may be able to use those principles, and the techniques described in Yin Tui Na, The Science of Asian Light-Touch Therapy by Janice Walton-Hadlock, to replicate the results we have gotten.
Since the non-profit Project was founded in 1998, the findings of the Project have been written up and posted on this website. The book has steadily grown and changed over the years as more pieces of the Parkinson’s puzzle have fallen into place. Even the name of the book has changed from one edition to the next, in order to reflect our ever-deepening understanding of Parkinson’s disease.
This website is our primary method for disseminating the results of our research. Our books are available for free download at the publications page of this website.

Please note: we are not affiliated in any way with any of the recently created programs and websites that have used variations on our name “Parkinson’s Recovery” in order to draw attention to their mercenary programs: programs that, so far as we can tell, are not based on hard science or on research.