[:en]In the classical view of Rolfing®, knowledge of the nervous system doesn’t seem to offer much for Rolfers. “It’s that other system.” We know it’s there but we don’t have to talk about it. The sheer complexity is daunting, and most books on neurophysiology leave the reader still very far from useful clinical application. I would like to change that perception.
I’ve been involved in a course of study of clinical application of neurology for over a year now. It’s a chiropractic program and participants are chiropractors and some MD neurophysiologists, so some of the more purely chiropractic applications are not relevant to Rolfing as they involve high velocity thrusts. But so much of what I’m learning is a new way of observing just opening my eyes a little more to what’s right in front of me, that I would like to share with you a distillate of what I’m finding out.
Of course, much of the application is much more “clinical” than most Rolfers are interested in, but when you start to be able to recognize, for instance, cerebellar involvement in a movement disorder and find that you can have an impact on the aberration by having the client move their eyes down and to the right, it alters your understanding of things. It doesn’t even have to be something you ever use; your perception of the human body – the meaning of everyday things – the lid lag on the right, the enlarged pupil, that stop sign up ahead will change. (That’s right, you’ve just entered…)
In the third week of life, processes begin which lead to the development of the nervous system. At this stage of life a body has all the features of a funny little tortilla made of three layers of corn, endocorn, mesocorn and ectocorn. A groove forms in the ectodermal layer, and the lips that form the edge of the groove rise up and join together to form a tube. The tube itself eventually becomes the central canal of the spinal cord, and the cells that line the tube begin to differentiate and migrate outward forming the columns of the spinal cord, the layers of the brain and the peripheral nervous supply eventually forming a system of withering complexity.
As the cells of the neural tube differentiate and divide, they literally climb over one another in a kind of advancing wave, forming first the gray matter at the center of the cord and the white matter farther out. As they reach their final home, as the wave hits the beach so to speak, cells form columns of similar function – called “homologous columns” that stretch sometimes from the midbrain to the caudal end of the cord.
The autonomic nervous system comprises such a column – called the intermedial lateral cell column or IML – that extends from the hypothalamus to the ganglion of impar. The cells of the column were born of the same batch of embryonic brew and rode the same wave (to mix a metaphor or two) to reach a resting ground just lateral to the gray matter of the cord. They have all their brothers and sisters and cousins on either side and all around them and they can talk to each other a lot. This fact accounts for the remarkable adaptability of the neuraxis, for if you can excite members of a column you can excite the whole column. Rather like starting a rumor at the office – well, maybe not your office.
There are some things you have to know about nerve cells and their synaptic relations to make any kind of sense of all this, and there is a profundity to this stuff that I completely missed in my neurology classes in Chiropractic school. Only after my instructors in the post graduate course I’m taking had repeated this mantra 30 or so times did the fundamental importance sink in.
Nerves are dependent on presynaptic input to survive.
Put another way:
Nerve cells die if they are not fired upon.
Or another way:
Along with a fuel supply, neurons need a fairly constant blast of neurotransmitter substance to their dentrites, cell bodies or axon hillocks.
One more try:
The health and well being of a neuron is a direct function of the amount of stimulus, both excitatory and inhibitory, that it receives.
When transmitter substances cross the cell membrane, changes are caused inside the cell. It’s called “cellular immediate early gene response” or CIEG. But you can forget that term now. What it means is that neurotransmitter is like a double cappuccino to a neuron. It initiates RNA replication of protein-5 to build things like microtubules and longer axons. It also increases mitochondrial activity (mitochondria are the little furnaces that transform glucose to raw power). And the protein that is formed – because it is negatively charged – helps to increase the membrane potential of the cell.
I knew that. I’d taken two semesters of neurophysiology, three semesters of neuro anatomy and one of neuromuscular physiopathology, and I got A’s. OK, I didn’t know the RNA part and I’d never heard the long name. But I thought, without knowing that l thought it, that neurons came in strings of A & B, or at most A, B & C. I never thought that we might be talking about an ecosystem – a system where a lack of motor firing to your left leg could cause a diminished sensory response from your leg which might cause a problem in your left cerebellum, and thus the left thalamus and the right side of the brain. I never thought that this lesion in the brain (lesion in this context has nothing to do with leprosy, we’re talking diminished function here) might then have an impact on the autonomic nervous system because o lack of central inhibition of the sympathetics, which might then charge off and make your toes turn blue, or sweat more in one armpit than the other or worse.
That sheds a new light on “Nerves die if not fired upon.” If enough nerves cells die in the right places, people die or are severely limited in their humanism. But it’s much more than just the serious stuff. I’ll explain later how this brain lesion that we’ve hypothethized can cause an imbalance in the musculature of the shoulder which can lead to trigger points on the back of the scapula and thus to lateral epicondylitis and all those wonderful wrist and hand things that keep getting diagnosed as carpal tunnel.
But right now we need to get through a little more cell physiology. We need to have a little excitation and inhibition (it’s everywhere, isn’t it?) before we can start talking about larger systems. And to do this we need to bring up A, B, & C and maybe even X & Y. But I want you to keep in mind, if you weren’t already planning to, that A, B & C could be cells in the basal ganglia, thalamus and cortex and we could be describing Parkinson’s disease or it could be a ventral horn cell in the spinal cord, and inhibitory motor neuron and an alpha motor neuron to the muscles of your toe. And this isn’t like the string between two cans with a kid on either end – this is like fiber optics. This is like sex and death and all that important stuff.
I’m sure you know this, but I’ll start here anyway. Neurons have a voltage differential across their cell membranes; it’s called the membrane potential. It’s not unlike human potential. It’s the ability to make something happen. The membrane potential is created by lots of little protein pumps that take sodium ions and one by one kick them out into this extra-cellular fluid. Kicking out sodium, which are cations, makes the internal milieu negatively charged compared to the external milieu. Protein production makes it even more negative. The resting potential of the normal cell is about -70 millivolts.
The central integrative state of the neuron is dependent upon several factors. We mentioned sodium and protein, and it also depends upon the presynaptic cells that fire onto it. Excitatory impulses cause the cell to depolarize (become less negative), inhibitory input makes it hyperpolarize (get more negative). Depolarization brings cells closer to firing. Obviously hyperpolarization makes it harder to fire. Both excitatory and inhibitory input cause stimulation of protein production and an increase in mitochondrial activity to feed the tiny sodium pumps.
So cells don’t care if they are getting stimulated by excitatory or inhibitory neurons because a stimulated cell is a happy cell. The cells downstream, however, do care. Because if cell A is an inhibitory cell and stimulating the heck out of cell B, cell B may be a very happy cell but it’s not firing much because it’s being inhibited, so cell C, which depends on its input from B, isn’t getting much action. Cell C isn’t able to do its cellular immediate early gene response (I know I told you could forget that term), it has decreased protein production and decreased mitochondrial activity, and soon the cell walls become leaky and sodium starts to come back in faster than the little pumps can kick it out and the cell starts to depolarize. If it depolarizes enough, it will fire all by itself or with only trivial input.
I want to emphasize. the last point, because it will be on the test. When cell C isn’t fired upon, it starts to depolarize. But that’s the same thing that happens when a cell is fired upon. Now you’re starting to see – things aren’t always what they appear. So how can we tell if a cell is firing because it gets a lot of excitation or because it gets a lot of nothing. From the fact that a cell is firing, we can’t tell.
If you are keeping your mind on the eco-view, you may have just had a cold chill down your spine. If you are observing a motor response, that strong response you see might be because the cells are excited and happy and all charged up with new protein and ATP (that’s short for juice), or they might be firing because the sodium pumps can’t keep up with the influx of sodium through the holes in the cell membrane. The ship is going down and there is all this frantic activity on board, but from the distance it looks like a party. Isn’t this grand!
And with cells that aren’t getting enough presynaptic activity, the ship really is going down, because with the collapse of the cell’s internal structure the cell eventually dies. What is even more important from a clinical perspective, if you, as a clinician attempt to induce firing to bring the cell up to normal, it is possible to exceed the already fragile metabolic capacity of the cell and kill it with kindness, so to speak.
Now if you’re bored some evening, you can play some neuron games. You can take an imaginary chain of neurons where A excites B excites C inhibits X inhibits Y excites Z, and you can figure out what happens if the frequency of firing of A is diminished. Or if C is transneurally degenerated, i.e. not doing well. This chain is not unlike the chain from the brain to the alpha motor neurons to the muscles. In fact this is the chain we mentioned earlier where a decrease of cortical output causes problems in a shoulder.
By now it may or may not be clear that a healthy nervous system requires a steady stream of input throughout all of its parts. We mentioned homologous columns earlier on, and these are important here. For it is not necessary that each individual neuron be part of an excitatory or inhibitory pathway all the time. Firing in the neighborhood is all that’s required.
There may be just a gnawing question lingering in the back of your brain, viz., if neurons don’t fire unless fired upon (normally), i.e. it presynaptic stimulation is a necessary ingredient for neuron health and happiness, how do we get the whole train of events started? What is the neuronal Prime Mover?
The answer, of course, is receptor cells do it. Receptor cells are specialized cells that are fired by various stimuli, such as light, sound, chemicals, pressure, temperature, and changes in tension. Receptor cells are also important avenues for producing change, because you can, for example, shine a light in someone’s eyes and improve their life. You have to know when and how to shine the light, but that’s minor stuff. All the sensory modalities are potential paths to producing change in nervous system function.
There are, however, two basic classes of receptors, those which are non constant – which fire only when being stimulated by a particular stimulus and those which fire all the time, or constant receptors. Constant receptors are the ones that respond to the force of gravity, which, as we know, never sleeps. These include muscle spindle, Golgi tendon organs and joint mechanoreceptors. Obviously, not all these receptors are firing all the time. However, some of the receptors are firing all the time. Spindle cell fire along one pathway when they are under stretch and via a different one when they aren’t being stretched.
Thus far we’ve said:
Nerve cells need activation to survive.
Activation comes either from presynaptic cells or from receptor cells.
If neurons are stimulated by excitatory synapses they are healthy and happy and move closer to depolarization and firing.
If neurons are stimulated by inhibitory synapses they are healthy and happy and move farther from depolarization.
If neurons don’t get either stimulation they get unhealthy and don’t make protein, and their cells walls get leaky, and they move closer to depolarization and firing.
This is a term that is critical to the whole concept of neural function. It occupies the same place that “balance” does in a discussion of Rolfing – and means about the same thing, only the opposite. Hemisphericity refers to the imbalance in neural function that occurs between the two sides of the brain. I hear it mostly in clinical contexts, because stimulation of the side that’s already doing better can have serious consequences for the lessioned side.
Now that we understand the rules, let’s meet the players.
The top of the heap is the cerebral cortex – the brain. We won’t worry that there are six layers of cerebral cortex, that there’s neocortex and paleocortex or that the older structures under the cortex, like the thalamus and the basal ganglia probably also qualify as brain. For our purposes brain means cortex. The cortex is situated in such a way that if there is a lesion of some kind in the cortex, there is certainly going to be a diminution of function somewhere else in the neuraxis and possibly also an increase of function somewhere else as a result of the previous diminution. Moreover, if there is a problem anywhere in the sensory system, we can be certain that it will have some effect on cortical function, though not necessarily a measurable one.
Brain has its fingers in many functions and many of the functions are inhibitory ones. (Note: the output of the brain itself is all excitatory, but it fires into inhibitory centers to accomplish its task.) Among its inhibitory tasks, 1) brain inhibits sympathetic activity, 2) it inhibits an inhibitory interneuron that terminates on the ventral horn cells. I’ll say that more simply: the brain inhibits a cell that dampens motor activity. Without the brain’s inhibition, that cell can make the muscle go weak. Do you think that might be important to Rolfers? 3) The brain also systematically inhibits muscles on the front of the body above T6 and on the back of the body below T6. This has the function of balancing the anterior muscles which get the majority of the action with the back muscles, or of balancing the hamstrings which do more of the work in locomotion with the quadriceps.
From the number of times those three inhibitory functions have come up in the past year, one would get the idea that they might be important. The brain also has another inhibitory function which if it is lost causes muscle to become spastic, which is what you see in stroke victims and other upper motor neuron lesions. But that one is a little outside the field of what I’ll be writing about. The other three are involved in conditions we see all the time, and they are conditions which it is possible to affect, in most cases, without fear of damaging the neuraxis. Which is to say, if you do the same thing you’ve always done, and do it a little differently, you might have a different effect.
Directly under the brain is the mesencephalon – the midbrain. The mesencephalon houses several important structures, including the nuclei f cranial nerves 3 and 4 which control movements of the eye, and are major summation centers for the optical and auditory nerves. Cranial nerves are important windows into the neuraxis, in part because the locations of their nuclei are well circumscribed, the distances they travel are relatively small (compared to a motor neuron to the toe), and very importantly, because it is possible to measure their output much more precisely. The pupillary response, which measures the central integrative state of a mesencephalic nucleus of cranial nerve III, is one of the more important windows for that reason.
You may recall I left you with a question of how to distinguish the firing of a cell which received a lot of excitatory stimulation from a cell that was firing because it was in the throes of degeneration – the party on the boat vs. the boat that was sinking. Both cells fire rapidly and strongly. How can you tell them apart? The difference is fatigue rate. The healthy cell fires rapidly and continues to fire. The degenerated cell fires rapidly because depolarization has pushed it close to firing threshold and very little stimulus causes it to fire, but it rapidly exhausts its capacity.
The mesencephalon is also the most rostral portion of the IML – remember way back page 1, the IML is the cell column that carries the autonomic fibers. So the mesencephalon and the general state of the surrounding structures within the mesencephalon, have a large effect on the functioning of the sympathetic nervous system. If I do papillary reflexes and an ophthalmic exam on someone whose cortex is not doing a good job of inhibiting the sympathetics, I can boost their heart rate 10 points in a matter of seconds. The man who designed the neurology course that I am taking, works regularly with coma patients (and has returned over 500 such patients to consciousness) and attaches a pulse meter when examining the eyes so he can monitor the response he is having on the autonomics.
PONS AND MEDULLA
The pons and medulla share a kind of double billing. The pons is the potbelly that hangs over the belt at the top of the medulla. Together the pons and medulla receive 90% of the output from the brain. The mesencephalon receives the other 10%. Ponto-medullary centers turn the excitatory output of the brain into inhibition of centers down the spinal cord.
The three inhibitory jobs we listed under the brain are actually carried out by the ponto-medullary centers. So that you don’t have to look back, those were 1) Inhibit the sympathetics, 2) Inhibit the inhibitory interneuron of ventral horn cells, and 3) inhibit anterior musculature above T6 and posterior musculature below T6.
What would be the point of mentioning that these functions are carried out by ponto-medullary tracts? Isn’t it enough to know that the brain initiates them and we have ways to stimulate brain activity? There are several sensory pathways into the pons and medulla via the cranial nerves, which are excellent ways to facilitate these activities. For example, anything that stimulates the cerebellum has pathways into the pons, and the centers for the carotid-baro receptors lie in the medulla. Both systems have an effect on reducing sympathetic output.
For a more everyday example, consider what happens it you spin around a few times rapidly. Your eyes water and your stomach gets upset. The input from the semi-circular canals in your inner ear, which are stimulated by the spinning, fires by way of the cerebellum into the pons to areas that a closely related spatially to the nucleus of the facial nerve which controls tear production and to the motor nucleus of the vagus nerve, which among other things stimulates peristalsis. This is a case of a sensory tract stimulation increasing activity in a neighboring motor tract though there is no direct connection between the two.
This same pathway, semi-circular canals to cerebellum to pons, has more interesting implications with regard to Rolfing. The vestibular centers in the pons are where the information synapses are hardwired to the nuclei of the extraocular muscles and to the deep axial muscles of the spine. Movements of the head cause reflexive movement of the eyes in the opposite direction as well as reflexive contraction of the deep spinal muscles. And it works the other way too. Movements of the eyes also cause contraction of the deep spinal muscles.
I have a demo I like to do with clients to illustrate the power of these neural pathways. When I do my neuro exam, I often discover small problems with the extra-ocular muscles. These are called saccades, and they are small interruptions or glitches in the eye movement during the test of the cardinal fields of gaze. What they indicate generally is a functional lesion in one of the cerebelli. Almost without exception the arm and leg opposite the problematic cerebellum will test weak. I have the client move their eyes in the direction in which the saccades occurred, and retest the leg or arm. Almost without except the limb will now test strong. Of course, the clients can feel the difference instantly, and it’s much more dramatic and effective than my talking about neural function.
I think the cerebellum will turn out to be the Rolfer’s friend. It has its fingers in most motor activity – either initiating movement in the somatic muscles of the body or in terminating movement in the eyes. It grades and modulates muscular activity. On the sensory side it receives fibers from all the mechanoreceptors of the body and relays that information to the brain. Input to the cerebellum also comes from vestibular centers which are critical to overall balance.
South of the medulla is the spinal cord, which is comprised largely of tracts running in both directions between the periphery and the higher centers. But research continues to uncover a larger role of the cord in motor activity, so fortunately there are still a couple things to be learned about the nervous system.
In future installations I plan to discuss the cerebellum in much more detail and to present a section on the autonomic nervous system. These are windows into the health of our clients. It takes some learning to use the windows, but we all use windows all the time – the outward signs that let us know about inward states.