It is a fundamentally important argument for those who are facing the issue of stroke. We have already treated the topic of diaschisis in a generic way in another article, but I felt the need to expand the information also taking into consideration the new scientific contributions on the subject.

Objectives of the article:

1. To show that the initial condition of the patient after suffering a stroke does not correspond to the reality of the injury.
2. A great part of the patient’s recovery, in the first months, is the result of the regression of the diaschisis.
3. To understand the reason why it is erroneously said that after the first six months of a stroke there is no recovery.
4. To explain the mechanisms through which it would be possible to accelerate the recovery while respecting diaschisis.

MOST SERIOUS CONDITION OF REALITY

After a CVA (Cerebrovascular Accident) we put ourselves in a condition that does not correspond exactly to the magnitude of the damage suffered. The effects that we will experience in the coming weeks after cerebral ischemia or cerebral hemorrhage seem notably more devastating from reality than from the brain injury, for a series of reasons that we will develop in more detail.

Perilesional edema
As we know, an ischemia or a cerebral hemorrhage entails suffering to the brain tissue, causing an injury and then cell death.

Just as when we injure a limb with a sharp object, for example, the cells of the directly damaged tissues die, while the areas surrounding the wound, with a reddish tone, are swollen and sore.

Even after an injury to the brain, around the injured area, we find an area involved in edema, however, although this area has not been directly damaged by the stroke, it is in an inactive condition, therefore, it is not capable of performing their duties.

The resolution of the perilesional edema requires up to 2 months, then in this first period, in addition to the evident effects of the brain injury, the patient will demonstrate major disturbances, caused by the inefficiency of the areas around the lesion concerned with the edema. It also follows the recovery demonstrated in these first 2 months, which is not only to be attributed entirely to therapeutic activities, but it must also be considered the physiological absorption of edema as explained by Raymond Lo in this 1986 article on Recovery and Rehabilitation after Stroke.

In the case of cerebral hemorrhages, the patient has a longer resorption period, but the underlying damaged area could be greater with respect to an ischemic event.

It is the area that is not directly involved by the obstruction of the blood vessel, but surrounding it and that reduces blood flow, it is an area with risk of heart attack, but it is salvageable especially in a temporary intervention such as thrombolysis. Also in this case, in addition to the risk of lengthening of the lesion in the absence of a timely therapeutic intervention, the areas concerned by ischemic penumbra see their functionalities altered, once again worsening the initial state shown by the patient. To delve into ischemic penumbra, we return to Domboyy’s 1991 article.

Inhibition of reflexes
After a disturbance of the central nervous system in the acute phases, a still unclear mechanism occurs, leading to a sudden loss of bodily reflexes. In the case of brain injuries after a stroke, we can notice such a phenomenon with the flaccid paralysis that is defined. Recent hypotheses attribute this hyporeflexia to the alteration of the relationship between the motor cortex and the second motor neuron, as explained in this 2013 study by Florman Jeffrey et al. “Lower motor neuron findings after upper motor neuron injury: insights from postoperative supplementary motor area syndrome”.

Diaschisis

So we get to the central argument of this article, diaschisis, the meaning is summarized in an inhibition of nerve structures also at a distance from the area of the injury. Therefore, in the first moments after a brain injury, beyond all the phenomena of neurophysiopathology already described, diaschisis also participates in making the patient’s picture more acute, much more dramatic than the actual result of the injury.
The concept of Diaschisis deserves to be deepened coming from us, since we deal with rehabilitation, because understanding the mechanisms also means understanding how to behave from the point of view of rehabilitation, for the sensory and cognitive motor recovery of the patient who has suffered the stroke. To do a more exhaustive investigation on the subject, we invite the reader, to the look at the writing 2013 of Stanley Finger illustrious professor of psychology at the Washington University of St. Louis: The Monakow Concept of Diaschisis.

The term Diaschisis is brought in the early ‘900 by Constatin Von Monakow Russian neuropathologist.
During the nineteenth century, it had already appeared studies on the depressive effects of nerve structures at a distance from the area of injury, sometimes such temporary “shock” was attributed to edema and alteration of blood flow in the remaining parts of the brain that remained intact, But Von Monakow was the most fruitful author in determining the causes and the modalities by which different nervous structures suffer a depressive effect, even anatomically distant from the area involved in the injury. He defined his theory “Diaschisis” from greek schizien (separation) and Dia (between, from, through).

That theory is based on the concept that a functional system needs cooperation and relationship between its parts and for this reason, when an element of a functional system is damaged, so are the other elements, which are intertwined in functional relationships and then suffer effects.
In our case, understood as results of brain injuries after a stroke, the effects on our functions due to direct injury are added to the depressive effects, also at a distance from other brain structures functionally involved with the injured one, determining a picture even more complex and serious clinical picture.
Von Monakow did not deny the importance of the effects of edema and depressive changes in circulation, but he maintained that these could not sufficiently explain functional alterations and that they should be distinguished from the concept of diaschisis, where instead he alleged that the alterations were of origin neuronal.

The Von Monakow institutions regarding the nervous matrix, based on the functional depression of other nerve structures placed at a distance, were also formed by a study by Gold and Martin Lauritzen of the department of neuroscience of the University of Copenhagen, 100 years later: in 2002.
“Neuronal deactivation explains decreased cerebellar blood flow in response to focal cerebral ischemia or suppressed neocortical function” where the researchers, being able to use powerful diagnostic imaging instruments and studying the deactivation of the contralateral cerebellum after a hemispheric injury, they concluded that the basis of deactivation was a reduction in excitatory activity at the synapse level and that the reduction in metabolism and blood flow was a direct consequence.

With regard to recovery, although Von Monakow did not deny the possibility that some brain structures could functionally substitute for damaged areas, the second concept of vicariation widely spread at that time, he clearly understood that recovery was largely determined by reduction of diaschisis, rather than a cerebral plastic reorganization.

A very interesting contribution of the Russian neuropathologist was identifying different types of diaschisis according to the chosen territory, such as, for example, cerebrospinal or corticospinal diaschisis, where we intuited that remote inhibition after a brain injury also involves other levels, such as that spinal or vice versa spinocerebral diaschisis. In this case, this distinction also allows us to understand the reason why after an injury to the brain, in the acute phase we have a flaccid paralysis with a notable inhibition of the basic reflexes. Another type of individualized and studied diaschisis was the cortico-commissural one, which actually crosses both hemispheres and which also explains the presence of hemiplegia on the same side of the injury, for example language alterations in patients who have suffered an injury of the right hemisphere that should not cause word alterations.

Obviously Constain Von Monakow the different types of diaschisis that could also present simultaneously and different degrees of severity. Another Dane, Høedt-Rasmussen, in 1964 with his study, transneural depression of the cerebral hemisferic metabolism, identified a reduction in metabolism in some areas of the hemisphere contralateral to the lesion, confirming Von Monakow’s intuition regarding cortico-commissural diaschisis.

Recent studies have shown a functional alteration of the areas also located in the opposite hemisphere and not only in terms of inhibition, but also in terms of hyperexcitability. Then, the increase in excitability of certain areas, in response to the reduction of the inhibitory action provided by the lesion area, located particularly in the potentials of the sensorimotor cortex of the cerebral hemisphere opposite the lesion. In the clinic we can observe this phenomenon, noticing the extreme arrogance on the part of the contralateral limb to the one involved in the paralysis in participating in the actions, also when the motor possibilities of the paretic limb are present.

In this 2008 study by Christian Grefkes of the neurology division of the Colonia University, the changes that occur after a brain injury are analyzed, whether in charge of the sensorimotor areas of the same hemisphere involved, than the opposite.

Personally, to make an example, I associate this last type of diaschisis, which involves the contralateral hemisphere to the lesion, to a frequent phenomenon found in my patients with left hemiplegia, where they should not have aphasia problems, but rather the request to name the fingers of one’s own hands has great difficulty, demonstrating a symptom that is instead largely associated with injuries to the opposite hemisphere, that is, the right, where multiple linguistic competences reside.

Clearly, our entire nervous system is integrated, and each structure is potentially connected to another, however Von Monakow located nerve structures that are more susceptible to diaschisis than others such as the contralateral cerebellum, the thalamus and the motor cortex, the latter more interested in contrast to that sensitive one that is more resistant to inhibition at a distance, and within the same motor cortex, the parts responsible for the control of the fingers and toes, are more susceptible than others. I think this last observation is more evident in the clinic, for all the operators who are handling the problem of the hemiplegic patient, seeing a notable delay in the recovery of the fingers and toes, with respect to the recovery of the other body segments, such as the back and hips.

What concerns us, given the fact that we deal with post stroke recovery, is the modality with which the diaschisis regresses and inhibits the structures involved in neuronal depression and this is our attempt with this article. The same Von Monakow although he insisted that diaschisis was a process in which resolution always happens spontaneously and passively, and that this can take a lifetime, there are notable variables that participate in the speed and identity of the dissipation that deserve to be deepened.

(2) A GOOD PART OF THE RECOVERY OF THE FIRST MONTHS HAPPENS THANKS TO THE REGRESSION OF THE DIASQUISIS

In this paragraph we will also find the explanation of the phrase that is often said to family members by health professionals in the first days of hospitalization, that is, recovery after a stroke occurs within 6 months or a year of the incident. Answering the question (3) Why does the defined recovery come between 6 months? Obviously it is not just a personal phrase of the employees who say it, but the result of classical clinical experiences and the conclusion of numerous scientific works which has been indicated above, obviously as I have said many times the brain maintains its own plastic capabilities beyond expiration dates. The reason why in the first months after a stroke, we notice a rather rapid recovery and in great part it is due to the spontaneous resolution of the diaschisis. Therefore, the patient who, in the moments following not only the cerebral ischemia or hemorrhage, but also the head trauma or the results of a surgical intervention, shows a particularly serious situation also from the point of view of general health, where not even survival is foreseeable, it represents a clinical picture that is not directly proportional to the brain damage suffered.

As we have seen in the preceding paragraph, our body from the successive moments of the stroke until the first months, puts into action protective actions to guarantee a better recovery.
We have identified this protective action of diaschisis, that is, the remote inhibition of numerous nerve structures in functional connection with the injured area.

It is entirely reasonable for the patient, family members and operators, to think that the recovery obtained in the first months is the result of the quality of the proposed rehabilitation, but as we have seen it is not entirely so, a big part of it it’s about a regression of the inhibitory process, therefore the patient who at the beginning was not able to support the trunk while sitting, who was completely paralyzed or partially on a side and who later manages to stand up, take the first steps, besides the fact that he has worked hard to obtain such results, he owes his achievements largely to spontaneous recovery.

Although if later, at the end of the rehabilitation journey of the first months, these gains in comparison with autonomy are accompanied by undesirable effects such as the appearance of spasticity, the patient and the health system itself, drawing up a balance of the patient’s recovery, cannot think it is positive.
For this reason, afterwards, the patient himself, in view of the enormous progress made in the first months, is led to attribute it to the quality of the rehabilitation operators, no matter whether the physiotherapy consists of a stationary bike, stretching or long forced-walk sessions, everything that was done, led him to rise out of bed while he was completely at the mercy of the disease and then feels saved, also confirming in the successive periods to hospitalization, a type of rehabilitation that led him to stand and tearing him from the bed he lay in.

The fact is that post-stroke recovery, especially in the first months, was largely due to the gradual resolution of the diaschisis, a state intuited by Von Monakow a century ago and later confirmed by numerous researchers, among whom we cite Randolph J. Nudo, researcher and professor of rehabilitation medicine at the University of Kansas, in this study his role of plasticity after a stroke, identifies in the resolution of diaschisis and in vicariation (substitution of the functions linked to the damaged area by other brain structures adjacent or distant) the main keys to the first months recovery of the hemiplegic patient.

The most attentive patients, family members and professionals also realize that part of what recovery is defined by is attributable rather to the appearance of developmental processes in certain functions, such as using the entire blocked leg when walking or take greater advantage of the movements of the trunk during the grip, to cover the lack of movement of the upper limb, as explained in this article published on Brain in 2000 by the researchers Cristea and Levin on compensatory strategies during post-stroke recovery.

On this site, we have spoken several times about the plasticity of the brain, and said that recovery after a stroke can go well beyond the first 12 months, since the stroke and now, it might seem strange after evidencing the fact that recovery of the first months is mostly in charge of the spontaneous and compensatory processes put in place by our organism, beyond the rehabilitation carried out.

The reason why we have argued the question in this way is properly to help the reader to become aware that probably the rapid recovery that took him from a state of immobility in bed to the possibility of moving in “autonomy” is not due to the quality or the effectiveness of the proposed rehabilitation, but rather to a process that nature had already planned for our recovery.

Given that most of the rehabilitation proposals of hospitals and clinics are still muscular, however, the injury suffered was responsibility of the brain, we help the reader to reconsider the therapeutic choice, not based on the results obtained so far, but based on the neurophysiological evidence that is the basis of recovery, especially in the first months after the injury.

It is no coincidence, in fact, that most of the patients we have had, begin our rehabilitation journey after a year from the accident, precisely because in the first months they were busy in rehabilitation programs in recovery places and in the following months, rehabilitation continues the same treatment modalities that apparently led us to obtain great results. It is only after a year or so, when the sentence of the end of the recovery expires, that we realize that the last progress obtained was very slow and not properly of quality, added to that an increase in a phenomenon that we did not know such as that of spasticity, due to which there is a progressive increase in muscular rigidity and reinforcement of those compensating movements of which we spoke previously, both in the grip and on the road.

At this point, it is only after long-term use of prosthetics and hand and foot position holders, or after using botulinum hoping that the extremities would soften, we realize that rehabilitation could probably have been addressed to the real problem that has led us in such a state, that is, the brain, and this is the beginning of a neurocognitive journey for many patients. In these cases, most of the rehabilitation work of the first months will be directed to the control and recovery of the pathological compensations created and nurtured in the first year of rehabilitation. We are glad to notice an increase in the population that becomes more quickly aware of the characteristics of the necessary rehabilitation after a stroke, thanks to a growing culture and responsibility, which puts the family in a more leading position on choices related to health, and we have the luck of being able to treat patients in the first months after the stroke, still in a period in which compensations and spasticity have not had the time to feed and establish themselves aggressively, allowing us to proceed with recovery without the need for to correct. In another article we have identified some of the psychological obstacles that families encounter when making a decision as important as modifying rehabilitation.

(3) UNDERSTAND HOW TO TAKE ADVANTAGE OF DIASCHISIS FOR RECOVERY

I realize that this article that we are facing is about a particularly complex issue, unfortunately not only for the reader or for me who wrote it, but also for the entire scientific community that daily faces numerous investigations to discover the aspects of this phenomenon, diaschisis, not yet fully explained.
Unfortunately, although great strides have been made in the matter, thanks also to the evolution of most sophisticated investigation techniques ever compared to what happens in our wonderful brain, many sides of this process are still unclear and unexplored.
In order to translate what we currently know about diaschisis into acts of rehabilitation, we must further deepen the argument and go into detail about the phenomenon.

Diaschisis is a synaptic phenomenon

For many decades it was thought that the inhibition by the nerve structures adjacent and at a distance from the brain injury were a phenomenon linked to the reduction of blood flow, then less blood supply to certain regions of the brain would have determined a reduction in the functionality of the same brain regions. Recent scientific studies have shed light on the nature of such inhibition by keeping it in charge of the synapse and not of blood flow. This paradigm shift for us, who deal with rehabilitation, is of fundamental importance, because it leads us once again to transmit our therapeutic actions in comparison with the nervous processes that can determine a reactivation of the synapses. In this paragraph I will use some important passages highlighted in a 2014 review published on Brain by Giulio Tononi, professor of psychiatry at the University of Wisconsin and Emmanuel Carrera: Diaschisis: past, present, future.

The intuition that diaschisis was a synaptic-type phenomenon had long been lodged in the scientific field, as in the case of Ezras Asratovich Asratian, Ivan Pavlov’s apprentice at the Soviet scientific school, a class of scholars among the most fruitful and Illuminated ones of the last century and which investigations and intuition represent until today an incredible theoretical apparatus in respect to the understanding of human behavior. Among the principles of diaschisis described by Asratian in the text Compensatory Adaptation, Reflex Activity, and the Brain, we find the synaptic nature of diaschisis and other principles, which have represented a beacon for the first research on post-stroke recovery by Prof. Perfetti and that have allowed the development of neurocognitive rehabilitation itself.

Understanding that diaschisis and the inhibition of brain areas located at distances from the injury are a phenomenon in charge of the synapse, helps us to understand the mechanisms and why nature has predisposed a phenomenon like this after a cerebral injury. Synapses, as we know, represent the connection and communication point between neurons, and it is thanks to this dense network of nervous communication that faces any task to which we are subjected, that we are able to coordinate the activation of our brain in a complete and harmonious way.

Our actions do not depend on the activation of a dedicated and exclusive area of our brain, but on a combined activation of several areas at the same time that play different roles.
For this reason, the areas involved in the diaschisis, even if placed at a distance from the lesion, are closely related to the damaged area from the functional point of view, meaning they participate with it in the development of some functions.

As we can see in another article by Price from 2001 on functional diaschisis, where the presence of inhibition is observed in some areas facing specific functional requests, published on the Journal of cognitive neuroscience.

The Madrid-based researcher and neuropsychologist Pablo Campo, in an interesting 2011 investigation on working memory after injuries to the middle temporal lobe: “Remote Effects of Hippocampal Sclerosis on Effective Connectivity during Working Memory Encoding: A Case of Connectional Diaschisis?”, identifies an inhibition of brain areas located in the same opposite hemisphere, identifying a neutral network responsible for working memory, which areas involved are not linked to each other by direct connections.

This is a very important observation to understand that the correlation between the areas involved in the diaschisis process do not share an anatomical relationship, but a functional one.

From this we notice how some areas, regions or groups of neurons are not dedicated to a specific function, but they participate being part of different functions in a dynamic way depending on the task and the other areas put into play. An injury to a certain region would then lead to a deactivation of the areas with which certain functions participated during the functions in which the damaged area is involved.
Asking ourselves the reason why nature has chosen to inhibit the areas functionally connected with the damaged one is a must.

“As if the body after the injury had the need to protect the damaged area, also inhibiting the other structures with which it participates in certain functions, in order not to overload them with an information management work that at the moment they would not be able to support but in a reduced and simplified way and at a lower level of complexity”.

An answer to such a question would allow us to individualize with greater precision the typology of stimulus and therefore better experiences to offer our patients, in order to respect the demands of diaschisis and allow a fast regression. This is a second principle assumed by Asratian, who identifies in the “weak stimuli” a way to induce the reduction of diaschisis.

It would therefore make us ask ourselves, in fact, if in the first weeks after a stroke putting the hemiplegic patient on his feet early and facing the complex function of walking, lacking physical condition, is truly an activity that respects the demands of nature declared through the phenomenon of diaschisis.

In short, diaschisis is a synaptic phenomenon and the same synapses allow each neuron to virtually connect with every other neuron, forming a dense network of connections, where individualizing the links between one area of the brain and another during a specific activity makes a very arduous task for the investigator. Here we enter the field of research regarding the “connectome”, that is the map of the nerve connections of our central nervous system. For an interesting overview of the plot, I suggest you to see of the video by Sebstian Seung, taken from a Ted (Technology Entertainment Design) conference.

Von Monakow concludes the explanation of various forms of diaschisis, taking a systematic view, stating that the various forms of diaschisis can be present contemporaneously and in various degrees. A view of the brain as a neural map could help us reason about several forms of diaschisis in a systemic way.

Implications of rehabilitation

Every time we bother the neurosciences and we challenge neurophysiology in the world of rehabilitation, we must do it with a very precise intention, that is, to translate current knowledge about the functioning of our organism into true and proper acts of rehabilitation. Together we observe the behavior of recovery after a stroke and then the modality with which the diaschisis gradually tends to regress. After a first phase of post-stroke, when the reflexes are also absent, these ones begin to appear and it is at this point that the neurologist generally affirms that the diaschisis is coming out. Therefore one of the Asratian principles, by which the diaschisis is freed from the circuits with the least number of synapses in addition to getting space in the field of rationality, is observable in the clinic every day.

In addition to the basic reflexes, including those physiological, such as the one that allows us to empty the bladder, we find ourselves facing the awakening of the reflexes to muscle stretching, and those that make us move our leg to understand ourselves as when the neurologist gives us a small hit to the knee. However, the nature of these muscle and tendon reflexes, in case of hemiplegia, have a small threshold, therefore conditions are also manifested in which the muscle is not subjected to stretching, determining what we know as hypertone; stiffness of the muscles which is one of the components of spasticity.

The same behavior of the body caused by the appearance and increase of spasticity could not be accidental, the decision of nature to close the hand and limit the exposure to the acquisition of information that at that time could not be managed, there could be a correlation with the organism’s need to face experiences from the informational point of view in a gradual manner and compatible with the degree of convalescence, that is, to question groups of neurons with a gradually increasing number of synapses, starting from the most elementary ones and proceeding bit by bit to a brain activation towards higher levels of complexity.

Involve the patient’s cognitive processes

Being diaschisis a synaptic type of phenomenon, then the rehabilitation experiences that could positively influence it, accelerating regression, are those that consider brain functions and then the activation of these same connections. Therefore, a physiotherapy work directed towards the mobilization of the passive extremities might not be the most intelligent solution in this first phase. Brain activation occurs when the patient participates actively, triggering attention, perception, memory and the ability to solve problems through the body, as occurs for example in tactile recognition or body positioning exercises.

Avoid excessive physical stimulation

Being a protective phenomenon, diaschisis would play a fundamental role in guiding the organism towards the best convalescence. Respecting the diaschisis could mean offering our patients rehabilitation experiences of increasing complexity, starting with simple stimulations, both in motor terms and in cognitive terms. Although in the first months of cure, where the patient is hospitalized in physiotherapy structures, where the periods of times unfortunately are not always compatible with those that the body would need to recover from a brain injury, whether it has the need to offer the greatest autonomy to the patient by getting him to his feet as soon as possible and making him wander autonomously, this exposition might not be the most suitable decision in light of such knowledge about diaschisis.

We are in fact aware of the results of such decisions, which in many cases produce an aggravation of spasticity, then stiffness of the arm and leg, afterwards requesting pharmacological interventions such as botulinum or orthotics such as the use of the ones that block the joints to allow the autonomy of certain functions such as walking. In this regard, given that in any case also after the first period of rehabilitation guaranteed by hospitals and clinics, the patient will continue his recovery journey, because he has not yet achieved a satisfactory recovery, it could have been made therapeutic decisions that did not compromise the quality of the successive recovery, without the consolidation of the activation of the neural populations that are in front of a reduced number of synapses (reflexes) or the appearance of compensations.

When we see the first steps of a hemiplegic patient, in a too early phase, we can notice that instead of using the knee and ankle, the leg is raised being blocked, starting with a sideways movement, although in this case, we can speak of a motor organization that is facing a simpler brain activation and then, with a lower number of synaptic integrations. By encouraging this way of walking, you could make it more difficult to access more evolved and integrated forms of movement.

As we have seen in fact, the tendency of diaschisis is to inhibit the more complex synthetic circuits from releasing chronologically starting with the simpler ones. In light of these studies, it seems as if it was our organism itself through diaschisis that offers us a fair scale of work, considering also that the phenomenon of diaschisis can last a lifetime if it is not skilfully interpreted.