[joopoele]

The chickens of our neighbour and some ideas concerning Parkinson’s Disease

Joop Oele, May 22nd 2009

Our neighbour kept chickens. I still remember very well how I was the hesitating witness of the last moments of their life. On the chopping block they were stripped of their heads, protesting loudly. With an axe it was. I try to remember the technique he used, but while other memories are quite vivid, I seem to have missed this one. The next thing I recall is that he throws a couple of chicken legs to me, while laughing joyfully. He once showed me that the claws could still move if you pulled the tendons. I found it in fact rather distasteful but with such a moving claw you could impress the sea-scoutss who occassionaly visited the remote place where we lived at the time. And so I stood in front of those macho boys, chicken leg in my hand. Make sure the claw is open and than pul the tendon, hardly missing a nose, causing a nervous laughter.

Kinesia paradoxa, thus called Oliver Sacks the phenomenon that people with Parkinson’s, who could not move under normal circumstances, were able to catch a ball thrown at them. Mohammed Ali comes running into the ring with his well-known ali-shuffle dealing blows to the cameraman and other invisibly foes. If the show is over, he stiffens. A tennis tournament for parkies. Picking up the balls is more difficult than playing. Sometimes if I can no longer walk I’m still able to run back home.

Dopamine, serotonine and acetylcholine are examples of neurotransmitters. These chemical compounds influence the way signals travel through our nerve system. In a way they function like a series of switches in a railroad system. To simply transfer one single signal you wouldn’t need a neurotransmitter. A direct electrical signal to the proper nerve would be sufficient. A neurotransmitter however opens certain pathways, and closes others. This way, for example, certain muscles are grouped and behave in the same coordinated manner. A mode is set. This doesn’t only apply to musclesgroups but also to other nerve driven systems and thus it also influences our way of thinking. Lots of drugs function as neurotransmitters and as such change the way we think. While we perceive the same things, the way we interprete this information changes.

What is the difference between hitting a ball and picking it up from the ground? If you pick up a ball or if you make any other refined movement, some muscles are contracted (agonists) while others are released (antagonists). This all happens with a certain timing. When hitting a ball or dealing a blow certain muscles are contracted, but there is no controlled release. The function of the antagonist muscles is done by the slowness of the tissue. This way of moving resembles the way those chicken legs move using the tendons.
Using different neurotransmitters, you can define different groups of the same nerves. This gives a very complicated structure with a fragile balance.

At highschool I had to cycle eight kilometres to school and than again eight kilometres back. It happened one day that I forgot to lock my bike. I thought about it only when I was in the classroom. After the lessons were done I ran to the cycle shed to see if my bicycle was still there. Fortunately it still was there. So I tried to pick up my bike only to find that it was locked. And the keys were gone! Some funny nose had locked my bike and had taken my key too. So I decided to drag my bike along. But anyone who has tried this before will confirm it. If you drag a bike that is locked, the rear wheel will start bouncing.

One of the symptoms people with Parkinson’s disease have, is the cogwheel phenomenon. This rythmic pattern of changing resistance can be observed when you move the joint of an arm of a person with parkinson’s disease. If a movement is initiated supposing the antagonist will release, and it doesn’t do that, the resistence of this antagonist has to be overcome. My bike illustrated that this makes the wheel bounce. Resistance is always overcome in shocks.

Resistance also is dependent on the speed of the movement. That’s why it is often easier if movements are performed fast. Slow movements always have a lot of friction. The antagonist muscles can help to overcome the friction, by forcing a movement in a different direction.

Experiment:
Tie a long rubber band to the ear of a cup. Tie the other end to the table using some tape. Make sure there is so much tension on the rubber band that the cup just doesn’t move. Also tie a piece of rope to the ear. If you gently pull that rope in any direction, the friction will be overcome and the cup will be pulled in by the rubber band. This way the antagonist (the rope) will help to overcome the friction for the agonist (the rubber band).

I’m playing tennis and want to pick up a ball. My cramped lower back muscles have to give way, but they don’t. I try to bent my knees instead but allthough gravity is on my site I have to use the musclepower to force my leggs in a bended position. After I have picked up the ball, I have to get up. This happens in a very cramped way too. My lower back muscles are contracted at full speed just like the muscles that straighten my legs. The result is that I get up with a sort of jump.
What goes wrong with Parkinon’s disease, is not so much the contracting of the agonist muscles, but rather the releasing of the antagonists.

If the system of cooperation of two opposing mucles doesn’t work properly, there is still a way to give some relief.

Sometime in evolution a species needed a more sophisticated way of moving. The simple system witch one muscle contracting no longer could meet the demands. To make small and precise movements, the friction had to be overcome gradually. To accomplish this task the antagonist, who already had been developed to drive movement in the opposite direction, was now used to overcome friction. Actually we know two kinds of transmission, one fast and one slow. The slow transmission is responsible for what is also called neuromodulation.

Friction is the main problem in performing precise movements. This could also explain why whole-body-vibrations have a positive effect on some of the parkinson’s symptoms especially rigidity (Christiaan Haas, The effects of Whole-body-vibrations on motor control in Parkinson’s disease).

[reverett123]

Along a similar line, I wonder about the psychic underpinnings that go with this mess.

"Freezing" for example, is not confined to PD nor humans. A rabbitt freezes in the lights of an approaching car. A rat dropped into the middle of an "open field" test freezes before seeking the safety of the margin. Both are defensive behaviors in reaction to the anxiety of an unfamiliar situation. If the rat has been exposed in the womb to certain things he freezes for a longer time than otherwise.

Freezing is the locking up of all those muscles for a moment. Same mechanism whether rabbitt or PWP. Are the stimuli triggering it related?

Another response to anxiety is to seek control. A sense of control, even illusory, reduces anxiety. In the work environment that response can lead to success. Part of the PD Personality?

All my life, when in a restaurant or bar, I seek a seat looking out into the room. "Back to the wall" reflects caution. And desperation. Anxiety response?

I seek new things but only in a controlled manner. Never have been comfortable seeking adventure. Well, not quite true. Very uncomfortable seeking adventure when I felt responsible for the safety of, say, my wife. Same situation with a group of my "mates" however, totally different and at ease. Reflection of the anxious "hero child" perhaps?

How deep does it go, this clinging to the safety of the status quo? This illusion of equilibrium as safety? Normal cortisol levels fluctuate in a wide and predictable pattern each day. High in the morning to wake us up. Low in the evening to prepare for sleep. But not so for the PWP. Our levels seek the middle ground and stay there. Clinging to the mean.

There is a clue here somewhere.

[joopoele]

Hi Rick, Thank you

What causes freezing has puzzled us both. I think you once wrote it was caused by information overload.
From the inside, to me it feels like I want to move but something won’t let me. This might be caused by friction of the joint. It helps if you choose to make a fast impulsive movement. This would support the theory that friction is the problem.
I have no clue however what the relation with anxiety, stress or information overload could be. I’m convinced however there is a relation.

Joop

[reverett123]

Joop-

I don't know if you were around when Anne Frobert and I were experimenting with the effects a simple cloth band around a leg or arm or even forehead on tremor and control. This led to the realization that there is another component to the action of a muscle group beyond simply "activate-release", namely sensory feedback informing the brain that the indicated action has taken place.

Perhaps there is a clue there. Maybe a process such as-
1) Signal muscle "A" to contract;
2) Receive confirmation that action is taking place;
3) Signal muscle "B" to relax;
4) Receive confirmation that action etc.

Blockage at step 2 would result in both muscles being contracted, thus freezing.

There is some interesting stuff at http://scienceweek.com/2004/sb040813-2.htm

[chasmo]

How does the fact that a laser spot on the floor enables us to get moving by stepping on it tie in to this thesis? I have often thought that it has something to do with the utilization of different neuro pathways.

I should wake up before I comment any further!!

Charlie

[joopoele]

Chasmo, I really don't know. I can only guess.
What I want to say in essence is that if you want precise movement (as a species) you have to solve the friction problem. What I think is, that the kind of movement that is not functioning any longer in Parkinson's disease, is our answer to that problem. I hope someone will come up with a really good idea. Something like "If you attach a vibrating device to a patient, this will reduce rigidity". That's why I mentioned Haas' research.

[Ronhutton]

Hi Joopoele,
Hoe gaat U? Heel moi veer vindt je niet?
I think that acetyl choline and dopamine need to be in balance, acetyl choline contracts muscles, dopamine releases the contraction. In PD, the balance is disturbed by an inability to make dopamine so we need to add the precurser levodopa or block acetyl choline to some extent to get the balance right.
I am not sure why you think a slow movement has more friction than a fast movement, or what evidence there is for this. When I am "off", my leg muscles are stretched and I can't release them to walk due to lack of sufficient dopamine, (and excess acetyl choline). When I take levodopa and it moves to the brain and boosts my level of dopamine, getting the balance back to normal with acetyl choline, I can walk.
When I try to cross a busy road, the stress causes an increase in the blood-brain barrier (BBB) permeability, and my small supply of dopamine is dumped to the bloodstream. The result, I freeze. Dopamine does not pass a healthy BBB, but it is a smaller molecule than levodopa which does pass the BBB, so it does not need much of an increase in the permeability in order to pass. The result, a freeze is the same situation as when I am off, ie an imbalance in the dopamine/acetyl choline level, with high acetyl choline and low dopamine.
I think this explains what we observe rather than the "friction" idea.
There isn't really friction in moving muscles, it is the signal to move that is lost. If there was muscle friction, you would not easily pull the tendons on your chicken leg and move the claw. It would be rigid.
Ron

[reverett123]

Let me complicate things a little more. My understanding is that rigidity and increased muscle tone are the same. And that is what I experience, except first thing in the morning waiting for meds to kick in. There is a period of low muscle tone of about 30 minutes. Anyone else?

[joopoele]

Hi Ron,

Het is hier inderdaad prachtig weer ik wou dat het in mijn hoofd net zo zonnig was. Misschien toch maar over schakelen op engels. Lijkt me op deze site beter..

I’m familiar with this theory of the balance of dopamine and acetyl choline. Whether dopamine induces or inhibits is dependant on the kind of receptors in the specific synapse. But I don’t disagree on this.

It is a matter of mechanics that in slow movements friction is higher than in fast movements. In the human body joints are lubricated. This makes friction low once moving. Compare it to sliding on a slippery floor. One moment you stand steady and the next moment the friction is gone. There is always the problem that if you want to make a controlled movement, there are certain stages you cannot avoid. Put a cup on the table and tie a rubber band to its ear. Increase the stress. You can stretch the rubber for say 30 centimetres and than suddenly it starts to move real fast. You can imagine this is not very accurate. This is a problem that has to be solved if you want to design a system that can perform accurate movements.

I’m not stating that we cannot move because of friction. We cannot move because the system that was designed to make better controlled movements, doesn’t function any more.

You say: “dopamine does not pass a healthy BBB, but it is a smaller molecule than levodopa which does pass the BBB, so it does not need much of an increase in the permeability in order to pass. “ I think that the transport mechanism of the BBB functions or it does not. If it functions it does not discriminate on size but on the presence of the methyl-group. It is not a matter of size as far as I know but a matter of polarity.

Joop

[joopoele]

Rick, I experence the same relaxed 30 minute period. This is the only period that I feel like I used to. It's quite different from the relaxed feeling I get from ldopa.

Joop