Thursday, August 29, 2013

The Other Facet of Motor Learning, Part II

Part I, II


Previously, I wrote that motor learning is a trial and error process which consists of making random motor output connections and testing them for fitness. There are two fitness criteria used in motor learning. First, a motor connection must not achieve goals other than the one it is associated with. Second, a motor connection must not cause conflicts with other connections on the same motor neuron. In this post, I explain what a motor conflict is within the context of motor control.

Motor Control

Motor control is a process whereby the brain's cortex sends motor commands to motor neurons in order to effect goal-directed, coordinated behavior. Motor commands are discrete signals of which there are two types, start and stop. These correspond roughly to the excitatory and inhibitory signals that are observed in the motor systems of humans and animals. A start command starts an action (such as contracting a muscle) while a stop command stops an action already in progress.
In the illustration above, the red-filled circle represents the neuron's axonic output to the muscle, the black circle is a stop input synapse and the white circles are start input synapses. Note that the diagram is only meant to illustrate the principles of motor control, not the actual neural mechanisms which can be complicated. The brain has a highly complex structure dedicated to it. It's called the basal ganglia. For our purposes, think of a motor neuron as a little motor that can be turned on or off by multiple pushbutton switches attached to it. When the neuron is on, it continually fires which causes its target muscle to stay contracted. When the neuron is off, it stops firing, allowing the muscle to relax.

An important question is, how does the motor system control the amount of force exerted by the muscles? The answer is that every motor action is serviced by a set of motor neurons and each neuron in the set is pre-wired to exert a different force magnitude. It is up to the motor learning system to determine which ones to activate for a given goal or situation.

Conflict Detection

Since motor neurons are shared by a large number of cortical programs, it is important that the command signals are not in conflict. There are two principles that govern motor coordination.

1. A motor neuron must not receive more than one command at a time.
2. No action can be started if it is already started or stopped if it is already stopped.

During motor learning, motor connections are monitored to see if they violate the coordination rules. Any violation results in the weakening of the conflicting connections. In the end, only the strongest connections survive.


The principles of goal-directed motor learning are simple, powerful and can be easily implemented in a computer. However, they are of no use unless motor signals can be generated in an orderly, predictable and coherent manner. In other words, an intelligent system must have a sophisticated perceptual mechanism before it can even begin to behave sensibly to achieve its goals.

The topic of goals brings us to the notion of motivation. How can an intelligent system have goals unless it is somehow motivated to pursue those goals. Motivation is a huge part of intelligence. In fact, there can be no real intelligence without it. But how can a machine have likes and dislikes? In an upcoming article, I will dig deep into this topic and the importance of motivation to adaptation and survival.

See Also:

The Holy Grail of Robotics
Goal Oriented Motor Learning
Raiders of the Holy Grail
Secrets of the Holy Grail

Tuesday, August 27, 2013

The Other Facet of Motor Learning, Part I

Part I, II


In a previous two-part article titled Goal-Oriented Motor Learning, I wrote the following:
The Two Facets of Motor Learning

I will not go into how the brain learns sensory patterns in this article. I will, one day, but not today. What I will explain in this article is one facet of motor learning, the one that leads to goal-seeking behavior. There is another facet that has to do with eliminating motor conflicts. That, too, will have to await a future article. I just want to explain how the brain finds the right motor connections for goal-seeking behavior. As I wrote previously, I get my understanding of the brain by consulting an ancient oracle (no, I was not joking) and interpreting its message the best I can. Here's what the oracle says about goal-oriented motor learning:

Notwithstanding I have a few things against thee, because thou sufferest that woman Jezebel, which calleth herself a prophetess, to teach and to seduce my servants to commit fornication, and to eat things sacrificed unto idols.
I always burst out laughing every time I read this verse in the book of Revelation. I laugh, not just because I think the wording of the verse is hilarious, but because the choice of metaphors is so exquisitely brilliant. Jezebel is a metaphor for a predictive mechanism. This is why she is called a prophetess. That's an easy one to interpret. But the mechanism is not a good predictor because, during its attempt to achieve various goals, it causes bad things to happen along the way: fornication and idolatry. Fornication is the oracle's metaphor for making connections that cause motor conflicts, a topic for a future article. Idolatry (the worshiping or serving of other gods) symbolizes the making of connections that lead to the wrong goals. Obviously, neither fornication nor idolatry will be tolerated. :-D
I went on to explain that a goal is a pattern and that goal-oriented motor learning consists of choosing the right connections between pattern-associated motor neurons and the target motor effectors. During this trial and error learning process, the idolaters, i.e., the motor connections that fail to satisfy their associated patterns, are simply disconnected. But there is a little bit more to motor learning than just achieving goals. Below, I explain the other facet of motor learning, the one that the oracle metaphorically calls fornication.


Fornication, as used in the Bible, is the act of having sex with a woman who is someone else's wife. It's a conflicting act. In the quoted passage above, the oracle is using fornication as a metaphor for motor conflicts in the brain. Motor conflicts are a problem because there is a fixed number of actuators (i.e., muscles) that must be shared by a huge and growing number of competing sensorimotor entities (neural programs) in the cortex. Obviously, if two or more entities try to use the same actuator simultaneously, conflicts will arise which will cripple any kind of goal-directed behavior.

The Simplicity and Power of Motor Learning

The motor learning system I described above uses a trial and error process to find appropriate motor connections. New connections are made randomly and an error detection mechanism is used to weed out idolaters and fornicators. This system ensures effective and smooth motor coordination. Robots will use it to learn sophisticated motor behavior such as walking, driving, speaking, etc. The simplicity of it all is unnerving, some would say, but its power is in the simplicity. In Part II, I will go into the details of conflict detection and elimination. Coming soon.

See Also:

The Holy Grail of Robotics
Goal Oriented Motor Learning
Raiders of the Holy Grail
Secrets of the Holy Grail

Monday, August 26, 2013

Why Speech Recognition Falls Short

It's Not the Way the Brain Does it

Current speech recognition technology, while impressive, falls short of delivering on the promise of human-like performance. The biggest problem is that speech recognizers are sensitive to noise which makes them pretty much useless if there are several voices speaking at the same time. The reason, of course, is that they do not work like the human brain. We humans have no trouble listening to a friend in a noisy restaurant because, unlike speech recognizers, we have the ability to focus our attention on one voice at a time and we can change our focus in an instant, if we wish. The human brain can also easily adapt to a given situation. A new voice may have an unfamiliar foreign accent but the brain can quickly learn its peculiarities and do a good job at recognizing what is being said.

A New Approach, Rebel Speech

The main reason that current technology falls short is that speech recognizers, unlike the brain, do not learn to recognize speech. They are hand-programmed. In other words, their knowledge (phones, diphones, senones, syllables, words and other speech patterns) is painstakingly compiled and coded by a programmer. This approach, while effective to an extent, is forever doomed to be incomplete. There are important subtleties in speech sounds that can only be detected via direct learning. If we are to make any significant progress in computer speech recognition, then learning and paying attention are key capabilities that we must incorporate into our future recognizers. My hope is that its autonomous ability to learn and to focus its attention on a given voice is what will set Rebel Speech apart from the rest.

See Also:

The Holy Grail of Robotics
Goal Oriented Motor Learning
Raiders of the Holy Grail
Secrets of the Holy Grail
The Myth of the Bayesian Brain

Sunday, August 25, 2013

The Rebel Science Speech Recognition Project

Soon, I plan to go back to work on my ongoing speech recognition project, Rebel Speech [pdf]. The goal of the project is not so much to design a better speech recognition program from scratch but to demonstrate the superiority of the Rebel Science approach to artificial intelligence. Speech recognition will be just one of many applications that use the Rebel Science Intelligence Engine. The latter will serve as the future backbone for any type of AI research project that requires perceptual and motor learning. The key word is learning, which includes adaptation. My ultimate goal is to use it in the design of a brain for a complex autonomous bipedal or quadrupedal robot with many types of sensors and degrees of freedom.

Those of you who are interested in this topic can brush up on Rebel Science AI by clicking on the following links:

The Holy Grail of Robotics
Goal Oriented Motor Learning
Raiders of the Holy Grail
Secrets of the Holy Grail
The Myth of the Bayesian Brain

I have also created a new forum to start discussing AI and its consequences.

Tuesday, August 20, 2013

ALS, Be Not Proud

Guillermina, my wife, passed away this morning from complications due to ALS. The disease that ravaged her body for over nine years finally won. She fought hard but, in the end, her lungs just stopped working. It is particularly sad because she knew before she died that an effective drug for ALS was just sitting on the hospital shelf, out of reach. A part of me just died but I will continue to fight this horrible disease in her honor.

Tuesday, August 6, 2013

What Really Cured Ted Harada?

Note 1: Mr. Harada correctly pointed out on Twitter that he is not cured. I concur and apologize but it's too late for me to change the title. This does not take away from the spirit of the original message. (8/28/13)

Note 2: This article was written more than a year ago and things have changed drastically. My wife succumbed to ALS almost a year ago. After much study, I have now concluded that it was a combination of the anesthetics and anti-inflammatory drug (dexamethasone) that she received during back surgery years ago that contributed to a near miraculous recovery that lasted almost a month. I would recommend that anybody with ALS take some kind of anti-inflammatory medicine or supplement. Even a non-prescription, over-the-counter drug like Naproxen is likely to help much. Read Anesthetics and Glucocorticoids for ALS for more on this topic. (7/21/2014)

This is a question that must be asked because nobody seems to really know for sure. Ted Harada, an ALS patient, experienced a miraculous recovery after undergoing stem cell treatments in 2011 and 2012 as part of an FDA-approved trial. Neuralstem Inc., the company that derived the stem cells from the spinal cord tissue of a fetus, wasted no time in capitalizing on the apparent success of their technology. Ted Harada became an overnight celebrity.

But not everybody is convinced that Ted Harada got well as a result of the stem cell injections. Some people pointed out that Harada's improvements occurred too quickly after the procedures. The neurotrophic factors in the stem cells do not work that fast. Others noted that his improvements did not correspond to the areas of his spinal cord that received the stem cells. Dr. Angela Genge of the Montréal Neurological Institute and Hospital, expressed doubts according to a January Alzforum article, "suggesting that any benefit might have resulted from the immunosuppressant drugs the participants received, that is, their ability to quell neuroinflammatory pathology."

Dr. Genge had, so to speak, thrown a huge fly in Neuralstem's ointment, so much so that, in May of this year, Neuralstem CEO, Richard Garr was forced to make an interesting admission on his blog:
It is also possible that an “unknown unknown” is responsible for Ted’s long term improvement and the stabilization of the other patients. The argument here is that just because WE can’t figure out what else it might possibly be, doesn't mean there isn't another explanation. However unlikely we feel this could be, it is why large, well-controlled trials are always required and justified. We need to continue and enlarge our clinical trials to refute this argument.
Indeed, in July, Dr. Jonathan Glass and Dr. Christina Fournier of the Emory ALS Center announced plans for a new study in order to eliminate the possibility that Ted Harada might have been cured by the immunosuppressants (anti-rejection drugs) that he received as part of the stem cell procedures. But those of us who have followed ALS research over the years know that it's a useless trial because the outcome is already known: immunosuppressing drugs have already been shown to be ineffective against ALS. So why the study? In my opinion, it's really Mr. Garr's way of calming the fears of his company's investors. Garr plans to wrestle that straw man to the ground and declare victory. He'll be able to triumphantly announce at the next shareholders meeting, "You see, we told you it was our stem cells that cured Ted Harada."

If I were a Neuralstem investor, this is where I would raise my hand and ask, "Uh, are you really sure about that?" I mean, did not Ted Harada receive another powerful immune suppressing drug that has not been tested in this latest study? But of course, he did. Mr. Harada was anesthetized for 5 + hours during each procedure. In other words, he received a massive dose of anesthetics in order to keep him completely immobilized during the delicate operation. Most anesthetics have powerful anti-inflammatory properties. Several ALS patients have asked Mr. Harada to reveal the type of anesthetic he received but he declined to do so. No matter. We can guess that it was probably sevoflurane, isoflurane or a similar volatile anesthetic. Why? Only because these are the anesthetics of choice used to keep a patient perfectly immobilized. So why did those in charge of the new study omit the anesthetics from the list of immunosuppressing drugs to be tested? I am asking because both Glass and Fournier were aware of reports that some ALS patients are seeing improvements after undergoing anesthesia. What's up with that? Inquiring shareholders and all that.

Something smells fishy at the Emory ALS Center in Atlanta, Georgia. One wonders what CEO Richard Garr has to say about all this. Join the discussion.

See Also:

Anesthetics and Glucocorticoids for ALS
Treat ALS with Anti-Inflammatory Drugs

Thursday, August 1, 2013

The ALS/Anesthetics Hypothesis

Note: This hypothesis has been revised. Please read Anesthetics and Glucocorticoids for ALS for the latest.

Amyotrophic lateral sclerosis is a rare and fatal neurodegenerative disease that strikes mostly older adults. This hypothesis is based on the finding that ALS is primarily an immune system disorder. Researchers have identified an elevated inflammatory response in ALS patients that is manifested during both presymptomatic and later stages of the disease. This inflammation is thought to be responsible for its rapid progression. Identifying the cause and nature of the inflammatory response is the key to formulating an effective therapy. Even though researchers have known about the innate immune response in ALS patients for more than a decade, attempts at using traditional anti-inflammatory drugs have not been very successful. The reason is that researchers have not yet identified the cause of the inflammation. There are many types of inflammations and many types of anti-inflammatory substances. By identifying the exact cause of ALS inflammation, we can formulate an effective therapy to eliminate it. We believe that eliminating the cause will not only stop progression, but will also bring the disease into full remission, short of regenerating dead motor neurons. We hypothesize that certain anesthetics such as propofol and sevoflurane can fully eliminate the cause of the inflammation.

The Cause of ALS Inflammation

ALS inflammation is caused by a deficiency in certain neurotransmitter receptors (or neuroreceptors), primarily the GABA-A alpha-1 and glycine alpha-1 receptors. A deficiency means that the receptors lack their normal affinity for their neurotransmitters and, as a result, fail to activate properly. These receptors are used extensively by the inhibitory neurons in the brain stem and spinal cord to control the activation of motor neurons. A deficiency causes an abnormal increase in the activity of the motor neurons and this, in turn, leads to a pathological condition known as neuronal excitotoxicity. But, and this is the crux of this argument, the same receptors are also used by innate immune system cells such as monocytes. If monocytic receptors are functioning normally, they respond to the normal level of neurotransmitters in the cerebrospinal fluid and this inhibits the activity of the monocytes. During an infection, messenger immune molecules are used to block the receptors. The ensuing decrease in inhibition activates the monocytes in order to fight the infection. However, if the receptors are deficient, the monocytes are no longer properly inhibited and the result is the chronic and destructive inflammatory response we observe in ALS patients.

The Therapy

An effective ALS therapy must not only suppress ALS inflammation, it must also eliminate the cause. Doing so will kill two birds with one stone because it eliminates neuronal excitotoxicity as well. It just so happens that certain anesthetics, such as propofol and sevoflurane, can potentiate all the known deficient receptors in ALS patients. Potentiation is the key. It consists of increasing a receptor's affinity for its neurotransmitter, restoring it to its normal functioning level. But what sets these anesthetics apart is that the induced potentiation does not disappear after the drug is eliminated from the body. It can last for days and even weeks. Part of this hypothesis is that, by fully eliminating the chronic inflammatory response, the disease can be put into full remission.

Experimental Confirmation

Although no official trials have been conducted to test this hypothesis, at least a dozen patients have reported significant and, at times, spectacular improvements in their symptoms after undergoing anesthesia with the anesthetics propofol and sevoflurane. Based on their reports, we can deduce a number of therapeutic principles. The optimum propofol dose seems to be about 800 mg. Anything below 200 mg does not seem to be very effective. We also have good reasons to believe that a mixture of propofol and sevoflurane is much more effective than propofol alone.