"yada, yada, yada" (Seinfeld and the Hebrew roots of knowledge)

Remember the Seinfeld episode in which George gets bent out of shape because his girlfriend omits some details to a story? She uses the phrase, "Yada, yada, yada" as if to gloss over mundane details with, "you know the rest." George, typical of his neurotic self, becomes obsessed and anxious that she is hiding something very significant from him by employing the yada, yada. The phrase has become common enough that most everyone will have heard or even used it interchangeably with, "Blah, blah, blah." Its etymology is elusive. However, if the phrase has any Jewish roots then it can plainly be linked to the idiom, "You know, you know, you know."

That is a long intro for a post that has nothing to do with Seinfeld and everything to do with the Hebrew verb for to know, "לדעת." Yada, in ancient Hebrew texts has a variety of meanings: to perceive, to understand, to demonstrate skill, to experience physical intimacy. Compare this to the modern sense of the word: assimilating all the data to uncover the object without bias from the subject. Also, compare this to the post modern sense of the word: a commodity exchanged between producers and consumers OR sense making for political expediency. Yada implies neither modern detachment nor post-modern game playing. The Hebrew sense of knowledge portrays a personal knower: from passion to perception to intellect to motor skill. For instance, the primitive metal worker and stone mason, Bezalel, was noted to have "knowledge" in various types of craftsmanship. Knowledge in this case would be a tacitly acquired skill for aesthetic construction. The ancient Hebrew king, David, employed the word "yada" in reference to how the night sky reveals the magnificence of God's glory. Knowledge in this case would be a visual perception of the object (the night sky) transfigured in relation to the subject's creator (see McGrath for this idea of the stars being transfigured into a sacramental mode).

Knowing a fact, knowing a person, knowing a skill, and knowing a feeling all require personal commitment on the part of the knower. The commitment is intellectual, relational, kinesthetic/tactile, and passionate. These functions of knowledge and the knower I hold to be properly basic in epistemology. Next post will focus on fleshing out these functions within my current field of study: epidemiology and yada, yada, yada.

solomon's judgement (or how the p-value is crazy like a fox)

Little Paul (that is me when I was a kid) listened to my father preach and teach many passages from the Bible. One impressionable passage Dad taught from was on King Solomon and his wise judgement when two women came to him claiming the other had stolen her child (I Kings 3:16-28). Being a busy potentate and one not all that interested in hearing the two mother's bicker back and forth all day, King Solomon suggested cutting the baby in half and letting them each take a half. Lo and behold, one woman saw this as a reasonable solution while the other was mortified at the suggestion. King Solomon's verdict: the true mother is the one whose immediate response is to protect the baby. The King was a wise judge; he elicited disparate responses from the two women and ruled based on a good hunch of how a true mother behaves. There is a very small probability that he awarded the baby to the non-biological mother (but, even with such an erroneous judgement he would have given the baby to a woman who wants to protect it and not cut it in half).

This case study in primitive law gets at the center of Fisher's p-value. Fisher, working largely in English agriculture, utilized probabilities (i.e.: p-values) to calculate how likely disparate responses would be among different crop samples under separate conditions for each sample. To do this he had to precede the statistical analysis with assumptions (or hunches) to draw conclusions (or judgments). For Fisher, the foundation was not math, but philosophical commitment to a body of prior learned knowledge that led to a priori presuppositions (beliefs held prior to investigation through which results are interpreted) and a posteriori inductions. Below I will touch lightly on the mathematical reasoning describing these commitments. These commitments are described by two terms: level of significance (a priori commitment) and p-values (a posteriori commitment).

Level of significance is a statistical term that reflects the probability of drawing a false conclusion. The closer the number is to zero, the lower the probability of drawing a false conclusion about groups being different; the closer the number is to one, the higher the probability of drawing a false conclusion. A 0.05 level of significance indicates that their is a 5% chance that a difference has been observed between two groups when in reality no difference exists (referred to as a type I error); a 0.10 level of significance means 10% chance of type I error, etc. This value can also be thought of as a false positive as demonstrated by the below 2 x 2 contingency table of hypothetical results versus hypothetical reality:

	Hypothetical Reality #1: Drug A = Drug B	Hypothetical Reality #2: Drug A ≠ Drug B
Hypothetical Result #1: Drug A ≠ Drug B	False Positive (This is termed “Level of Significance” and is synonymous with a Type I error...observing a difference when no difference truly exists.)	True Positive (This is termed “Power” because it is the power to find a true difference)
Hypothetical Result #2: Drug A = Drug B	True Negative (This is termed “Level of Confidence”)	False Negative (This is the definition of a Type II error...failing to find a difference when one truly exists)

Note that this is all hypothetical. The researcher sets this level of significance prior to the experiment; typically level of significance is set at 0.05. Then the researcher calculates a test statistic called a p-value. Any analysis that yields a p-value of less than 0.05 is considered significant and adds to the evidence that a true difference exists between groups. The p-value can only be obtained by assuming that the condition in box one (false positive) exists. That is, a p-value is calculated based on the assumption that in truth there is no difference between groups who have received different treatments. In other words, if two groups are treated with different diuretic drugs for high blood pressure, the researcher has a hunch that one drug is better than the other. To test the probability that his drug is superior to the other, he either must have access to the truth (which is not available in this kind of research design) or he must assume that there is no difference between the drugs and then test the observed difference against that assumption of no difference. So if he observes that his drug lowers blood pressure 10 points in the experimental groups and the other drug lowers blood pressure only 5 points in the control group, then the difference between the two drugs would be five (that is: 10-5 = 5). Assuming that there truly is no difference (hypothetical condition for box 1 in the above contingency table) he then subtracts the assumed difference (zero) from the observed difference (five) and divides this number by the standard error of the difference between both group means. Remember, standard error is a term used to reflect standard deviation of many experimental/control differences from the true mean if the experiment were repeated with random sampling from the population a large number of times. If the observed difference (5 in our example) is much larger than standard error (lets say standard error is 1 in our example), then the statistic will be large. The statistic can then be utilized to calculate a probability of observing the difference of 5 when the hypothetical reality of no difference is true. This is done by finding the test value on a normal bell curve and determining the area under the curve between that value and the left end of the curve. This area value is then the divided by the value of the entire area under the curve. The results in a probability of finding the difference between the two groups assuming that in truth there is no difference.

If any of you are still reading at this point, no doubt you are waiting for the point. Bottom line, the p-value, when smaller than the pre-set level of significance gives the researcher evidence that drug A truly is more effective than drug B. This is not a mathematical proof of the truth (only because the true situation is unknown), but rather mathematical support (or evidence) for one drug being better than the other. There may be Bayesian tricks (a la Neyman and Pearson) to guess at the true situation (termed prior probability) and then compare the results to this prior probability, however, even prior probability is based on a priori determination of values and so does not escape some personal judgement in the analysis. Fisher's p-value adds evidence one study at a time to slowly and over time produce a reliable body of knowledge. No one study creates definitive knowledge (diagnostic studies excluded). The best stewards of science recognize the valid role of personal judgement in arriving at true knowledge (see Michael Polanyi).

martial arts, global warming, and chance.

Scientific knowledge is produced piece meal through the slow process of research. One particular challenge in this process occurs when a researcher observes a difference between the experimental group and the control group. Did the difference arise because of chance or because of the experimental condition? Consider a child psychologist who is attempting to discern the most effective method for modifying explosive behaviors in children (say, ages 5 to 8). She designs a study in which the control group receives standard family counseling intervention while the treatment group receives standard family counseling plus Aikido martial arts training.

Suppose that the counseling + Aikido group exhibits a greater average reduction in explosive behaviors than the counseling alone group. What should the psychologist conclude? Was the difference really due to martial arts training? Or was there simply random variation between the two groups?

The observable world (a.k.a. the phenomenal or that which is accessible by our five senses) is characterized by variation. The world does have unifying undercurrents, however on the whole a vast multitude of divergent atomic structures abounds. In short, all things are not the same. There are alkali metals, alkaline earth metals, inert transition metals, transition metals and post-transition metals. There are tall people, short people, fat people, skinny people, brown skinned people, olive skinned people, red haired, brown eyed, toothy and toothless. Botanically, there are at least 40 different types of daffodils; each type of daffodil itself has a wide range of variable characteristics. This variation is what statisticians refer to when they use the terms "random error" or "random variation." On the other hand, variation due to some factor (e.g.: medication, exercise, psychotherapy, air pollution, etc) is referred to as explained variation. For example, consider an experiment which showed that lower carbon pollution levels curiously cause increased average temperatures in a simulated atmosphere.

Researchers want to know if this temperature variation is explained by reduced carbon pollution or by error (random variation). A high degree of variation in temperature recordings collected during the experiment may indicate that the average increase in temperature was a chance finding. In other words, if the variation in temperatures is great, then it may be that the researcher simply collected data during a time when temperatures were varying on the high end of the thermometer. Below I will show how the statisticians would answer the question, "Is the temperature rise due to the decreased carbon pollution or due to chance variation?"

When analyzing data sets from an experiment/study, researchers want to know if the observed change is a chance finding or a true reflection of how things really are. To do this they use a statistic called standard error (a quotient of standard deviation divided by the square root of the study sample size) to predict how variable the sample average would be if the experiment were repeated a large number of times. Essentially, the standard error statistic is used to calculate a range of values (termed "confidence interval") in which the researcher can be 95% confident that the true population average lies. Consider the atmospheric temperature study above. If the average temperature increased by 3.0 degrees Celsius, but the 95% confidence interval was -0.3 to 8.2 then it is entirely possible that no temperature change happened whatsoever (note that the value "0" is included in the range...indicating that the true average change in temperature may be 0 degrees Celsius). Such a scenario would indicate that the increase in temperature may truly be due to random variations or chance, not due to reduced carbon pollution.

Further testing can be done viz a viz Fisher's all powerful p-value to determine how insignificant the temperature rise truly is. In fact, selecting levels of significance and calculation of p-values will be the topic of next post. From there I will switch out of statistics mode and into philosophy mode.

descriptive stats revisited

Last post I attempted a brief and somewhat unclear introduction to descriptive statistics. So by way of review I will summarize last post with a graph to help depict things. The three most basic ways of describing a data set are its average, spread and shape. These three concepts are very important as performing statistical analysis depends on these three descriptions of the data being "normal." The average of the data set represents where the majority of the data lie. A normally distributed set of data (referred to as a bell curve when plotted) will have an obvious mean at the peak of that curve. See how on the normal curve below, the line representing the mean divides the curve into two symmetric halves.

The spread of the data indicates to what degree all the data points vary away from the average. Standard deviation is a number that indicates the average distance of all data points from the average. Higher standard deviations indicate that the range of data spread further on either side of the average. See the lines on either side of the central average line on the graph below? The first line on either side of the average line indicates a point that is 1 standard deviation from the mean. The next line indicates a point that is 2 standard deviations away from the mean. Particular to the normal bell curve is the reality that 67% of all data will be only one standard deviation from the mean and 95% of the data only 2 standard deviations away from the mean.

The shape indicates whether the bell curve has a long tail to the left [negative skew], long tail to the right [positive skew], tall curve [leptokurtic], flat cruve platykurtic). Any distortion of the bell curve impacts statistical calculations as basic statistics assume a normal bell curve. See below for depictions of skewed data.

Next post I will answer the following question: how do we know if the difference between two groups or two measurements is due to chance or due to skill or treatment effect?

redlegs and descriptive stats

Honestly, my appreciation of baseball is pathetic. That is a veritable reality (as those acquainted with me can attest). However, as a youth I followed Redlegs baseball compulsively. Sunday mornings were great because the Cincinnati Enquirer would have an expanded sports section with all the breakdown of player and team stats (this was before the dawn of ESPN.com/mlb/statistics....in a former age when all fans waited with baited breath for our information to arrive through the paper delivery man). Batting averages, ERA's, standings, etc. Typical of my analytic approach to things, I would perform my own calculations to see how many hits Hal Morris would need to break .400 over the next 50 at bats. Much has changed since my youth, but I still gain a good deal of satisfaction in performing calculations. For those who might find such a thought foreign or even perverse, I will frame this post on summary statistics around baseball. Perhaps no one will even notice that math is being conducted.

Data collection is the process of compiling bits of information (e.g.: number of hits, innings pitched) in an organized system (I personally prefer Excel for its ubiquitous use). Without doing at least some basic calculations the data are not very meaningful. Summary statistics are employed to describe several qualities of the data: location, spread, and shape. Location captures where the majority of the data lie (e.g.: the team batting average represents a central number around which most of the players on a baseball team are averaging). Spread captures how widely the data varies (e.g.: once the location is known we want to know how big the difference is between the worst batting average and the best batting average). Shape captures how closely a graph of the data resembles a bell shaped curve (e.g.: if the batting average is relatively high compared to the spread of individual batting averages then the shape will be abnormally tall and departs from a normal bell curve). In statistical jargon these three qualities are referred to as: mean, variance and skewness/kurtosis. (WARNING: those who experience anxiety when exposed to mathematical formulas should skip over the next paragraph...you won't miss much).

Mean is the sum of the data divided by the number of data points and is denote by the upper case "Y" with a line over it in the equation:

.

Variance is the square of each data points distance from the mean, all summed and divided by total number of data points minus 1. The square root of variance can then be taken to reflect the average distance that data points vary from the mean

.

Skewness is obtained by the cubed value of (the mean subtracted from each data point), summed for all data points and then divided by the product of (total number of data points minus 1) and (the cube of standard deviation). When this number is significantly positive then the data is not normally shaped and is lopsided to the right; when this number is negative then the data is lopsided to the left. Kurtosis is obtained similarly to skewness only the numerator is taken to the 4th power and standard deviation in the denominator is taken to the 4th power . A significantly negative kurtosis number indicates a flat curve and a positive kurtosis number indicates a tall, lanky curve.

Why are descriptive statistics important? There is a phenomenon out there in the sports world known as fanaticism. A true baseball fanatic will go to extreme lengths to stand by her team. It is even conceivable that during pleasant interchange over brews she may overstate or even understate the skill level of her team. In the world of statistics we call this bias. Descriptive statistics help us to reduce the influence of bias and see things more like they really are. No matter how devoted I am to the Redlegs offense, if I compare a variety of reliable offensive indicators to the same indicators for the Cardinals, I will find out the truth of how well they compare. If we compare the two teams and find that the Redlegs have better numbers and that the difference between the two teams is not due to chance, then I may not only brag as a fanatic but as a man who knows the statistical truth ("statistical truth," is that an oxymoron?).

So that raises a question, how would I know if the better Redlegs numbers were due to chance or skill? Tune in to next post for a breathtaking answer.

ents

Last post I mentioned that this post would be a technical one on statistics. However, after studying further on the subject of statistics I quickly realized that I am not qualified to author a technical post on the matter. Instead I will here offer a post that works to hold together statistics and scientific epistemology. Think of scientific epistemology being somewhat like Tolkien's tree Ents that he depicted as gathering around in a counsel to decide on a course of action. They refuse to be rushed in their decision making by the immediacy of danger: rather they thoroughly work the problem over to ensure that their decision places them on the side of good. Likewise with scientific epistemology, establishment of true knowledge occurs slowly and without any deference to the urgent need of human beings. So here ensues an elaboration of Ent-like knowledge building interspersed with pictures of past heroes of statistics (everybody should choose at least one statistical hero...such a thing ought to be as ubiquitous as having a NASCAR driver to root for).

I believe that natural human knowledge is capable of more than a mere approximation of reality. I believe that natural human knowledge can achieve a one-to-one relationship with reality; that is to say that theories of reality (i.e.: how things are) can represent specified slices of reality with perfect accuracy (e.g.: Copernicus and heliocentrism; Newton and gravitational forces, etc.). However, I also believe that the vast majority of natural knowledge produced in a given calendar year is specious at worst (i.e.: false knowledge) and an approximation of reality at best (i.e.: analogous knowledge). Here I refer not to the sort of assertions that pass off as knowledge among the popular pundits, but rather I am referring to critically tested, peer-reviewed scientific knowledge. It is this high level of knowledge that ranges from false to analogous. To characterize this range of knowledge quality I have generated a list of four (4) descriptors beginning with the most basic and contingent sort of knowledge progressing up to true knowledge or "fact" (as science would have us call it).

Ronald Fisher: what's not to like about this statistician? The very incarnation of an Ent.

Possible. Definition: that can be; capable of existing. For example an oval circle is quite possible; an oblong circle is quite possible. However, a square circle could never be a circle (i.e.: essentialistically impossible). An MRI machine that produces only rare cheese could never be an MRI machine (i.e.: nominalistically impossible). Certain things are impossible. Importantly, though, many possible things are not true. For instance, although it is possible for a live cow to go over the moon, if I claim to know that a live cow actually went over the moon last night this would be a false knowledge claim. Although it is possible for the sun to rise in the West and set in the East, this is not the truth of what happens on planet Earth. That which is conceivably possible is not necessarily existentially so. This being held true, there are three possible descriptions of possibilities and existence: existent possibility, nonexistent possibility, nonexistent impossibility. There is no such thing as an existent impossibility.

Karl Pearson: note with what alacrity he wields his pen in noble service of statistics.

Probable. Definition: likely to occur or to be so; that can reasonably be expected or believed on the basis of the available evidence, though not proved or certain. For example, a 2002 study published in Spine journal deduced a clinical prediction rule to identify which patients with low back pain are most likely to be successfully treated with spinal manipulation. The study deduced these 5 parts for a prediction rule: 1) pain onset less than 16 days prior to treatment; 2) no symptoms distal to the knee; 3) Fear Avoidance Behavior Questionnaire score less than or equal to 19; 4) one or more hypomobile segments in the lumbar spine; 5) at least one hip with more than 35 degrees of internal rotation motion. A patient must exhibit at least 4 of the above 5 traits to be considered positive on the rule. A subsequent randomized controlled trial published in 2004 compared patients who satisfy this rule with those who do not. They found that patients positive on the rule and receiving spinal manipulation have an adjusted odds ratio for successful treatment of 60.8 when compared to those negative on the rule and receiving exercise. That is to say, a person who satisfies the prediction rule and is treated with spinal manipulation is 60.8 times more likely to have a successful outcome than someone negative on the rule and receiving exercise. Although adjusted odds ratios are not exactly probabilities, they approximate mathematical probabilities closely when baseline risks are low. Consequently we can say that a person with low back pain who satisfies the prediction rule is very likely to gain significant function after only 2 treatments of spinal manipulation and this functional gain is likely to last for 6 months. But, this is a probability. This means that a small number of people who are positive on the rule and receive spinal manipulation will feel no improvement or worsening symptoms after treatment. So this is a practical example of probabilistic knowledge. The above studies did not elucidate fact, they elucidated pragmatic probabilities to help clinicians, insurance companies and patients make a decision about treatment options.

Valid. Definition: sound; well grounded on principles or evidence; able to withstand criticism or objection, as an argument. The move from probable knowledge up to valid knowledge is like passing over the Natural Light beer for Kentucky Bourbon Barrel Ale. Like declining the Hostess Snack Cake to save room for Graeter's ice cream. Like operating on the spine with a high precision Medtronic drill instead of a high speed DeWalt house drill. Valid knowledge within medical diagnostics is produced when a new test for diagnosis is measured against a gold standard. Assessing the new test (lets say for detecting prostate cancer) against the gold standard can result in four possible outcomes: true positive, false positive, true negative, and false negative. The box below illustrates this well:

	Gold Standard Negative (no prostate cancer present)	Gold Standard Positive (prostate cancer present)
New Test Positive	False Positive (invalid test result)	True Positive (valid test result)
New Test Negative	True Negative (valid test result)	False Negative (invalid test result)

A variety of statistics are available to describe these results, however I will spare the reader details of these at this time. Let the reader note, though, that validity does not measure probability of departure from truth but rather it measures reality of departure from truth. In this way validity is not a guess at the truth but a true measure of the truth. The greatest mistake in popular conceptions of research occurs when studies analyzed by probabilistic statistics (i.e.: p-values and confidence intervals) are interpreted as if they utilize validity statistics (i.e.: likelihood ratios). In this manner, many studies are presented as valid when they ought truthfully be presented as some grade (e.g.: low, moderate, high grade) of probabilistic evidence for or against a hypothesis.

Thomas Bayes: the right Reverend had a penchant for more than divine truth.

Veritable. Definition: true; real; actual. I am taking the name of this descriptor from the Latin word veritas: truth. How does the descriptor "veritable" differ from the descriptor "valid"? Knowledge that is veritable is perfectly true (1-for-1 correspondence with reality or logic) whereas knowledge that is described by validity is expressed as a degree of departure from truth. Given the above diagnostic example: the new prostate cancer test would be characterized as being valid if it deviates from the gold standard to only a small degree and invalid if it deviates from the gold standard to a large degree. However, the gold standard test is veritable: a container of 100% true knowledge, finding prostate cancer whenever it exists and ruling out prostate cancer whenever it does not exist. Veritable knowledge is not simply produced by a mathematical formula, but is rather arrived at through years of practice, research (statistically analyzed), critical review (e.g.: statistical assessment, construct assessment, etc.), technical reformulation, and even large scale disciplinary enactment (i.e.: use within the guild at large).

Jerzy Neyman: a fierce opponent to Fisher; his calculations were as killer as his Hitler-ish look.

One final cautionary note is due here. Having moved through this post, and engaged with the proposed hierarchical categories of knowledge (low quality "possibility" knowledge up to highest quality "veritable" knowledge) the reader might be tempted to scorn knowledge that is beneath "veritable" in my hierarchical scheme. The purpose of these hierarchies is not to cast aspersion upon "inferior" knowledge, but rather to appropriately characterize the levels of knowledge and their relation to truth. This has very pragmatic implications. Possible knowledge should be utilized with extreme caution and proposed lightly with a ready willingness to believe alternative possibilities; probable knowledge should be utilized discriminantly and defended publicly with openness to evidence to the contrary; valid knowledge should be ubiquitously employed and publicly defended with great vigor and energy; veritable knowledge should be published and re-published with regular frequency as well as being proclaimed with certainty to winsomely disabuse falsehoods consistently where falsehoods appear.

Next post will be devoted to a description of basic statistics and some of their mathematical formulations.

monochrome

Two and one half years have ticked off the mantle top clock since the last post on this blog. Even more embarrassing is a swift look at the goals mentioned in that last post: publishing a case study in the national physical therapy journal (that didn't happen), become a researcher (not much traction on that over 2.5 years), becoming a voice that shapes physical therapy knowledge (I haven't even started talking yet). Alas and alack, my life was actually interesting over the last couple years: job changes, selling/buying a house, first born daughter arrived on the scene, theological growth, starting graduate classes again. No time for the monochrome world of research. I had some life to live. Life is settling down a little now. Hopefully a little more tranquility will invade my work life over the coming months and then I can really begin in earnest tackling scientific epistemology viz a vi statistics and clinical research.

Interestingly enough, my introduction to biostatistics course this summer is a refreshing reminder that learning is fun. My instructors Drs. Shukla and Dwivedi are doing a superb job of instructing the class at a philosophical level. They are engaging questions of statistical certainty within the constraints of probabilistic mathematics (a world they refer to as fuzzy or gray) counterbalancing the clinical drive for a definite answer for ailing patients. The most unique concept I have learned to date is this: hypothesis testing (i.e.: level of significance and p-value) does not result in a mathematical acceptance or rejection of the hypothesis. Rather, hypothesis testing adds or removes weight to an a priori belief that the hypothesis is true. In this manner, statistics are legal procedures. The test statistic is the prosecuting trial attorney arguing the state's case in front of the judge and jury. The data is considered insignificant unless otherwise proven beyond reasonable doubt by the test statistic.

Next post will be a technical one exploring some aspect of statistics and how they relate to contemporary medical knowledge.

Towards publishing...

Adventures excite me. Being a thirty year old white male in America means that any adventure I experience is usually between my ears. My adventure is an intellectual one, no doubt. It is one that I find difficult to share with others. While I might take the nuances of epistemology to be fascinating, most others have heralded it it as the great cure for insomnia. Nonetheless, this blog page is my feeble attempt at bringing my adventure to others in my world.

I am closer to publishing than I was one year ago. I have written over ten papers and am positioning myself to write a case study and attempt to publish it in the national PT journal. This in itself is encouraging.

Recently I have writen several essays for graduate school. The one recurring theme in my essays is my desire to become a researcher. In this career I hope to be able to contribute to the body of knowledge in physical therapy. Research is not an end point in my desire, though. Perhaps more motivating for me is a desire to become a voice that shapes the way in which physical therapy knowledge is intuited, refined, and published as truth.

I would like to follow in the foot steps of Michael Polanyi. Polanyi was a Hungarian physician who went on to become a physical chemist and then philospher. During his career he worked brilliantly to shape scientific epistemology. Through his work he outlined the personal scope of knowledge; he showed that learning knowledge is not some mechanical process, but is rather a personal process. Gaining knowledge involves everything from epiphany to mentorship to critique. And that's what I want to bring to the table in my writing.

My how time flies...

It has been over a month since I last blogged. Time to catch up briefly.

I never did read von Bertalanffy's book. Instead I read and analyzed a bunch of California and Ohio supreme court rulings about duty to warn. For my term paper I chose a California ruling dubbed the Tarasoff rule. This rule holds a mental health professional liable in a situation where a patient confides his intention to harm a third party (that is legal speak for someone with whom the professional has no relationship). The professional is liable only if: 1) the patient ends up harming the third party and; 2) the professional did not warn the third party. I supplemented my case law (case law is court established law) analysis with some statutory law (statutory law is legislatively established law) analysis. I then made some applications for physical therapists. I hope to publish the paper.

I'm curious what my vast readership thinks. Consider a scenario where Bob Jones is being treated by Jack Handy (psychologist) for depression after a rough break-up with his girlfriend. What is the psychologist's duty when Bob makes specific claims that he is "going to bring a knife over to her house and end it all?" According to traditional Anglo-American common law there is no duty to protect between strangers. However, the California Supreme Court made an exception to the common law, stating that when a psychologist enters into a relationship with a patient he then has a duty to protect the public from the patient.

What do you think?

Read, read, read.

Next month's course is on ethics. Yipee!! My professors are both therapists and lawyers. One of them has authored a short book which I am reading on ethical issues in the health care realm. Within the book he made reference to a philosopher that I found enticing--Von Bertalanffy. He was a biologist who developed thought regarding general systems. His writing pertains mostly to the human sciences (e.g. medicine, sociology, psychology, etc). Just to be an overachiever I ordered Von Bertalanffy's book on General System Theory and am going to read it for my class. I hope to quickly take in his thought and analyze it enough to use it in my papers. Here's to the teacher's pet!

Where are my glasses?

I admit that I author a very boring blog. In an attempt to possible hook one or two readers into my blog I have adopted the strategy of using very simple questions as titles (hence, "Where are my glasses?"). Readers beware: my blogs are just as boring as ever. Hopefully my trick will get a few readers to read through at least the first paragraph of my post.

Continuing with my thoughts on epistemology (the philosophy of knowledge) my mind has been lingering on the question of how knowledge is discovered. Particularly I am asking myself about the limits of research to provide useful (or beneficial) information. For any one research study to properly scrutinize the veracity of a principle it must be extremely near-sighted (to use an ophthamolgical metaphor). An exceedingly small part of existence is chosen for study (i.e. patients with acute neck pain referred below the elbow, or adsorption of a particular gas on a solid surface, etc). Years of thorough examination and testing will provide excellent description about the nature of this exceedingly small area replete with evidence for 'behavior' or 'interactions' of variables within the defined scope of study.

However, clinicians and engineers are charged with the task of working within a relatively enormous swath of reality (i.e. restoring functional wholeness to a person after an accident, or designing a subliming animal repellent, etc.). At times the myopic nature of research will prohibit the clinician from generalizing conclusions from research to the treatment of his patient. Perhaps the research literature has not yet broadly examined the problem at hand or perhaps the research has been primarily laboratory oriented without the intrusion of variables which are present in the clinic. Times like this require the clinician to step beyond the research and either rely on a mentor's imparted knowledge or to intuit a new method for treatment. Does this mean that the clinician (or engineer) is definitely making an error? Absolutely not. The clinician is relying on a different skill set to arrive at knowledge.

Whether or not the clinician arrives at erroneous knowledge does not depend on the research, rather the veracity of the clinicians knowledge depends on nothing more than its veracity. Can it get any simpler than that? Intuition leads the clinician down a path that is either mistaken or correct. Absence of research does not determine the falseness of a principle (and often times the presence of research which apparently counters a principle does not definitively determine the falseness of a principle--this is the case when myopic research is over generalized). Rather it is the lack of parallel between principle and reality that determines a principle’s falseness...empiricism teaches us that much.

Considering the research discussed in my last post it is apparent that the authors have gathered treatment methods from various respected schools of thought within the physical therapy community. These schools of thought originated when an individual therapist experienced an epiphany. For example, a veteran therapist experienced an epiphany of understanding, applied principles from the epiphany in the clinic, empirically observed positive outcomes, and began teaching other therapists what she had discovered. As research developed regarding the therapist's principles the task began of verifying what the therapist already knew to be true. Once again, the research does not determine the veracity of a principle...the veracity (or lack thereof) is predetermined by the principle’s parallel to reality. Instead, the research serves to inform the community of the principle's veracity (or lack thereof). Research is merely a matter of opening up the mind to a pre-existing reality of veracity (or lack thereof).

How can I help you?

People who experience neck pain are not always easy to help. As a younger clinician I have found myself frustrated in my attempts to figure out how to help patients with neck pain. Recently I read a research article which helped me immensely with treating the neck. The article offers a treatment-based classification system for patients with neck pain (Fritz JM, Brennan GP. Preliminary examination of a proposed treatment-based classification system for patients receiving physical therapy interventions for neck pain. Physical Therapy. 2007;87:513-524).

Underlying the authors' reasoning is the premise that patients with neck pain should not all be treated the same. Rather, these patients should be grouped into categories based on diagnostic testing and patient history. A good deal of discerning symptom trends and discriminatory placement is involved. Once a patient has been 'placed' in the correct group they can be helped with group-matched treatment. Here are definitions of each category as well as matched treatments (taken from the article verbatim):

1) MOBILITY: younger patients with more acute symptoms and without signs of nerve root compression (e.g. pain down into the arm). These patients benefit from upper thoracic spinal mobilization/manipulation and deep neck flexor exercise.

2) CENTRALIZATION: patients with distal symptoms and signs of nerve root compression (e.g. pain down into the arm). Neck retraction (chin tucking) exercises and traction are used.

3) EXERCISE AND CONDITIONING: patients who have chronic neck pain, but who do not have signs and symptoms of nerve root compression. Strengthening of deep neck flexors and the upper quarter (arm and neck muscles) is recommended.

4) PAIN CONTROL: patients with acute, traumatic onset of neck pain with a whiplash mechanism and with very high levels of pain and disability. Evidence for patients fitting this subgroup recommends mobilization, neck active range-of-motion exercises, and avoidance of immobilization.

5) HEADACHE: patients with a chief complain of headache presumed to originate from structures in the cervical spine. Evidence supports strengthening of the deep neck flexors and upper quarter muscles along with mobilization or manipulation of the cervical spine.

My most recent instructor added the following category:

6) NEURAL TENSIONING: patient with thoracic outlet like symptoms (e.g. numbness and tingling into the arm and potentially compromised arm circulation) as well as patients exhibiting positive neural tension tests. According to my instructor these patients benefit from neural tensioning or sliding, positional training, and spinal mobilization.


Ambiguity has been the number one source of frustration for me as I learn how to help people. And so this classification system has been terrific in providing concrete guidance on how to direct the best treatment to various patients with neck pain. Far from being written in stone as the absolute rule of how to treat the neck, this classification system is however a good beginning at definitively expressing how to treat the neck.

Knowing: Critical and Uncritical

In my last post I discussed what I have learned about the mechanics of cervical motion. The information I learned I gained from my text book entitled Management of Common Musculoskeletal Disorders which was edited by Hertling and Kessler. Interestingly, the section from which I took my information has no reference to scientific research. One statement was made that certain cervical mechanics are obvious to observation on dynamic roentgenograms (x-rays). Another reference was made to a text written in the 1970's. Whether the information in this reference was based on research or not is unknown to me.

It appears that I have managed to gain a great deal of knowledge about the mechanical function of the human cervical spine while circumventing modern day scientific practices. How did I do that? I did it in the way that most pupils gain their knowledge--through an uncritical process of information assimilation. I, the learner, uncritically except from my teacher (the text) "factual" information about the spine. The verifiability of this knowledge is not of immediate concern to the novice pupil whose is merely attempting to gain mastery of the teacher's principals. Primary concerns for the pupil pertain to intaking information, assimilating information, learning the teachers story and recreating the teachers story in his words. Doing this process assists the pupil with creating a working theoretical model for interacting with a physical reality. Once this theoretical model is mastered by the student he can interact with the physical reality in various experiments to test the veracity and productivity of the theory.

The philosopher Michael Polanyi compared this uncritical process of learning to a microbiologist who studies the amoeba through a microscope. The microbiologist uncritically looks beyond the lens to critically evaluate the amoeba. His assumption is that the lens has been polished well and the curvature of the lens has been correctly shaped to reflect the image in a non-distorting way. During his crituque of the amoeba it is impossible for him to be critical of the lens. Here the lens is functioning as an extension of his own eye.

And so this is one arguement for personal knowledge in the modern world. I wonder how much knowledge is accumulated in the professional world in this manner?

Description of Neck Motion

One joy particular to the study of human motion is that of characterizing motion in specific human joints. Today's task for me has been developing an internal schema (a sort of mental map) for the motion relations between the base of the skull (occiput) and the first two neck bones--C1 and C2 which are respectively referred to as the atlas (for it's rotational role) and axis (for its phallic process). Below is a diagram of the occiput, atlas, and axis. This diagram depicts from top to bottom: the occiput of the skull (with the back of the skull sawed off), the atlas (with the back side of the atals' ring sawed off), and the axis (with the back side or spine of the axis sawed off). Notice that the dens is hidden by a dense connection of ligaments and proceeds upward from the back side of the axis. The ligaments most relevant to motion are: the alar, the apical, and the cruciform ligaments. Joint surfaces that exist between spinal bones are termed facets. These facet surfaces are planar in topography and glide upon one another to allow neck motion. Each neck bone contains two upper facets and two lower facets. The upper facets of C3-C7 are oriented upward (toward the skull), inward (toward midline) and backward (toward the back of the neck) at roughly 45-degrees from horizontal. The lower facets of C3-C7 are oriented downward (toward the feet), outward (toward the outer neck), and forward (toward the throat) at the same 45-degree angle. Consequently, when considering the component facets motions which make up forward bending of the neck, their motion are described as upward and forward. Likewise, during backward bending of the neck their motions are described as downward and backward. The depiction below is helpful for visualizing these mechanics.Furthermore, rotation of the neck to the left can be characterized as downward glide of the left facet and upward glide of the right fact. Interestingly, side-bending of the neck to the left is characterized by the identical facet motions (left downward glide and right upward glide). As such it is clear that when the neck is bent sideways to the left, rotation to the left occurs (this is termed ipsilateral rotation).

These mechanics do not hold true for the upper cervical spine (occiput, atlas, and axis). During left side bending of the skull on the atlas (C1), the atlas rotates to the opposite (right) side. This occurs to allow room for joint congruency between the concave facet of the right atlas as it travels up the convex surface of the right occiput (Hertling and Kessler 2006: page 714). Side-bending of the occiput is checked by the alar ligament. While viewing the alar ligament in the first diagram presented this checking mechanism can be conceptualized. Additionally, the axis (C2) is rotated to the left during left side bending of the occiput (this also can be visualized from the diagram).

The take home messages go somewhat like this:

C3-C7:

1) Forward bending of the C3-C7 can be diminished by restricted upward gliding at the facet joints.

2) Left side bending of C3-C7 can be diminished by restricted left downward gliding or right upward gliding at the facet joints.

3) Left rotation of C3-C7 can be diminished by restricted left downward gliding or right upward gliding at the facet joints.


Occiput-C2:

1) Forward bending at the occipitoatlanto joint can be diminished by restricted backward glide of the occiput on C1.

2) Backward bending at the occipitoatlanto joint can be diminished by restricted forward glide of the occiput on C1.

3) Left side bending of the occipitoatlanto joint can be diminished by restricted left backward glide or right forward glide of the occiput on C1. It can also be diminished by restricted left rotation of C2 (i.e. restricted inferior glide of left C1 facet on C2 and/or superior glide of superior glide of right C1 facet on C2).

4) Left rotation of atlas (C1) on axis (C2) can be diminished by restricted inferior glide of left facet joints or superior glide of right fact joints.

Neck Pain.

Last weekend I finished a paper on neck pain. I spent over 40 hours reading research and formulating my own analysis. The funny thing about spending all that time on research is that my clinical applications were so succinct. They boiled down to this:

Lots of research has been conducted to show that exercise is helpful in reducing neck pain. Research shows that spinal mobilization increases the pain reducing benefit of exercise. For patients who do not tolerate exercise well, simple chin tucking exercises while lying down are recommended. All exercise routines should be performed over at least a three month period to promote muscle growth. This 3-month training period will promote reduction of neck pain into the long-term.

And that is what 40 hours of research will get you. I have to say that I enjoyed the process of discovery and learning. Especially I enjoyed reflecting on the process of arriving at knowledge.

Pain and its illusory etiology.

Low back pain's etiology (cause) is one great example of the seeming impenetrable nature of reality. Is back pain caused by mechanical failure of discs and boney joints? Or is it caused by hypersensitivity in spinal nerves due to chemicals present with inflammation? Or is low back pain caused remotely by the body's executive center--the brain? Undoubtedly all these tissues and organs take some role in all back pain. But to definitively identify the one tissue or one organ which is principally responsible for back pain in a particular patient is unreasonable.

For example, I recently treated a woman who was diagnosed with a right groin strain. She has a history most significant for leukemia and treatment by radiation and stem cell transplant. Upon evaluation I noted that she was tender to touch over her pubic bones, her groin muscles and her outer hip muscles. Additionally when I had her lie on her back and applied a posterior (backward) shear stress through her right hip joint she complained of increased groin pain. I was immediately concerned about three things:

1) Possible stress fracture in her right hip which would occur due to post-menopausal osteoporosis;
2) Possible cancer metastasis to her pelvic girdle;
3) Possible low back pain referred to the right groin.

Her doctor ordered an MRI of her hips which revealed mild arthritic changes in both hips. Previous MRI of the lumbar spine had revealed mild spondylolisthesis (miniature spine fractures with no to minimal spinal bone displacement) at L4-5 and L5-S1. This data discourages the view that hip fracture is the cause (although MRI's can miss stress fractures) and ruled out a bone tumor. Possible causes of her hip pain would then be:

1) Mild hip arthritis;
2) Referred low back pain;
3) Muscle weakness and imbalance.

The doctor injected her outer hip area with carbocaine (a medicine in the lidocaine family) which immediately relieved that pain. The doctor ruled out low back pain at that point, stating that if it were low back pain the carbocaine would not have helped. Reflecting back on this just now I would beg to differ with his conclusion. Low back dysfunction causes hypersensitivity in sensory nerves distal to the low back. If her tender outer hip is caused by hypersensitive sensory nerves (versus a traditional bursitis or tendonitis) then carbocaine would have the affect of "numbing" these hypersensitive sensory nerves and render them inactive thus blocking the patients outer hip tenderness. In which case her hip pain would be from her back and not from her weak hip.

Medical professionals could spend a lifetime studying this patient and patients like her and may still be unable to determine which tissues or organs are responsible for her pain. Regardless of if we could identify whether it was the patient's back or hip or muscles which are causing her pain the causal question remains unsatisfactorily answered. For instance, if we determine it is muscle weakness on the right side causing her pain we do not definitively know what caused her right hip weakness. Why are both hips not weak? Why does a very active person who regularly exercises have this mysterious unilateral weakness? If we determine that it is her back causing the pain we do not definitively know what it is that causes her back pain. Is it her facet joints? Is it her disc? Is it her spinal nerves? Or, to beat all, is it because she has had this mysterious chronic weakness in the right hip?

And so it goes for the man asking the 'why' and 'how' questions. Just when he thinks he has gained some understanding he realizes that he has merely unearthed ten more questions about the nature of reality.

Back pain and metaphor.

Last February I completed a class on the lumbar spine. One exciting epiphany for me was the thought that pain relief obtained through spinal manipulations are mediated not through mechanical "release" of joints, but rather through neurophysiological inhibition of pain neurons. Chiropractors and therapists in the past explained the efficacy of manipulations referring to poor spinal alignment due to capsular restrictions in the small spinal joints. Manipulations were purported to "adjust" the spine by "freeing" certain capsular restrictions. The idea of manipulations freeing restricted capsules has become decreasingly popular (although I would say at this time not decreasingly tenable) with a paradigm shift toward neurophysiologically decreased spinal pain via manipulations.

In particular two research studies with which I became familiar advanced my own understanding of spinal pain. One study was performed by chiropractors on cats. These cats had force transmitters surgically attached to their 6th lumbar spines. Additionally electrophysiologic readings were obtained from afferent mechanoreceptors (aka: nerves that sense muscle length) of spinal muscles. Oscillations were transmitted to the 6th lumbar spine and as the force on the lumbar bone approached that of a spinal manipulation an abrupt increase was sensed in electrical activity in the afferent mechanoreceptors. Doubtless this increased sensory input to the spianl cord has an effect on regulating the back. I would propose that stimulation of mechanoreceptors could be an initial step of a pathway of spinal reflexes to neurologically block the conduction of local pain sensations. In short, the vibrations from manipulations stimulate sensory nerves in spinal muscles which could in turn block pain conduction and recalibrate muscle resting tone. This theory (commonly referred to as the "gait theory" of pain inhibition) has been well developed in the medical field and there exist substantial scientific data which can be used to validate it.

A second study looked at the use of lumbar spinal manipulations for patients who satisfied a clinical prediction rule. This rule was developed to help clinicians predict which patients would benefit from manipulations. One interesting side note in this study was that each patient was manipulated at the same spinal level regardless of the location of "reduced capsular tightness". The location of the manipulation was not the determining factor in the success of the manipulation. One could conclude that it doesn't mater at which lumbar joint the manipulation was performed. This does not bode well for the older idea of "freeing" capsular restrictions at specific joints to relive pain. It does, however, fit well with the idea of neurophysiological reductions in pain sensation via a mechanically stimulated reduction of resting muscle tone and a lowering of resting membrane potentials in pain neurons.

My parting thoughts relates to truth and metaphor. As mentioned above, chiropractors and therapists used the idea of "freeing" capsular restrictions when performing manipulations. This is a prime example of the use of metaphor to convey powerful meaning to a patient about returning to health. The patient feels that something is "stuck" in her back and the therapist says he is "freeing" that which is "stuck." Regardless of whether or not this metaphor has been a true description of the biomechanical and neurophysiological reality or not, it has been helpful in conveying a sense of efficacy. During my career as a therapist I regularly am asked for explanations about function of the human body. "Why does my leg hurt when I walk?" "Why is my arm muscle weak some days but not others?" The questions are always personal and always difficult to answer in a meaningful and helpful way. Often times I employ metaphor for the purposes of encouraging the patient's understand of procedures and increase motivation towards compliance in therapy. The ethical qualm for me has become, how do I speak in metaphor while honestly tipping my hat to the ambiguity present in human understanding. Currently I am beginning to steer away from answers to 'how' questions and focusing on 'what' questions. I'll give anecdotes of what others have done to successfully overcome spinal pain and just skip over the how altogether. Intellectually these are dull answers but they are more true than any metaphor I can dream up to describe the latest theory. I do not deem the linguistic tool of metaphor to be intrinsically misguiding; rather I deem metaphor that construes fiction as fact to be false in the worst way--deception.

Advocacy: Blood, Sweat and Tears.

Eight months now I have been treating a worker injured on the job. Currently she is at risk of losing workers compensation benefits related to her recent cognitive decline. Losing the benefits would be a devastating blow to this mother of four*. Her husband is unable to work full time due to caring for their six children and now his wife.

She suffered her injuries when a large stack of wooden pallets fell on her causing immediate neck and arm pain. She was admitted to the hospital and discharged shortly thereafter. Subsequently her symptoms became worse, she was re-hospitalized and fell into a coma for several days. Unfortunately diagnostic work-up focused mostly on her neck and shoulder and neglected her brain. She was discharged from the hospital after awaking from her coma. She was able to live at home with her husband and family, but unable to work due to pain.

Approximately four months after her injury the patient's husband noticed a rapid change in her behavior: drowsiness, paranoia, memory loss, inappropriate speech. A neurologist was consulted and he recommended physical and occupational therapy. My evaluation revealed marked deficits in the patient's neck and shoulder function and acute onset of vertigo with neck motion. Interestingly I found the patient's cognitive deficits to be more profound than her orthopaedic deficits. Those deficits matched those of a brain injured patient: poor attention span, short-term memory loss, decreased executive function. Apparently no MRI was performed on her brain and so I was unable to understand what was the underlying cause for this patient's decline.

She has made excellent progress with her shoulder and neck function. Sadly, though, her cognitive status prevents her from being safe when unattended and will possibly prevent her from ever being able to work again. Workers compensation is looking to deny any coverage for cognitive related disabilities claiming that her cognitive decline is not associated with the accident, but is rather a combination of the patient's diabetes and her poor diet since the injury. Neuropsychiatric evaluation revealed that the patient does have profound cognitive deficits in the realms of attention span, short term memory, safety judgement. In their conclusion, the psychiatrists stopped short of directly implicating her work injury for this patient's cognitive decline. I plan on advocating for workers compensation coverage for this patient. Below is the beginning of my line of argument.

Rational for explaining my patient's cognitive decline boil down to two: 1) traumatic brain injury with chronic cognitive sequela; 2) diet induced diabetic encephalopathy. I will develop the former rational as workers compensation is developing the later.

Traumatic brain injury typically results in an immediate and significant cognitive loss followed by a steady but small cognitive decline over the life of the patient. Given that my patient experienced a coma after her injury she likely suffered at least mild brain injury if not moderate or severe. Unfortunately no MRI is available from that time period and no MRI has been performed since. Consequently brain damage cannot be assessed. The lack of an MRI is very surprising in a case such as this one. A brain MRI has not been performed either due to medical mismanagement or due to the patient's haste to exit the hospital (she has expressed a strong phobia of dying in the hospital due to past family experience). Because no MRI is available certain brain injury diagnoses can not be ruled out and therefore should be considered as possible causes.

My patient experienced significantly increased appetite after her work injury. Increased appettite is associated with injury to the ventro-medial aspect of the hypothalamus. In such a case the patient's increased appetite (and subsequent diabetic encephalopathy) would then be a direct result from the work related injury. Magnetic resonance imaging of the brain would reveal the status of my patients hypothalamus. Damage in the hypothalamus means that the patient's increased appetite is a symptom as well as a cause. Increased food consumption would lead to diabetic encephalopathy. This entire process would then be a work related injury. Workers compensation would then be warranted for her cognitive issues.

Should the MRI demonstrate no damage to the hypothalamus I would argue that the patient's appetite changes are at the least an indirect symptom of depression related to her injury. Depression, unless treated, leads to increased appetite and hence the diabetic encephalopathy. Additionally, brain damage from the accident would predispose the patient toward onset of encephalopathy due to uncontrolled glucose levels. In other words, had she not had a brain injury, diabetic encephalopathy would be no where near as pronounced as it is now.


*I have changed various non-medical details about this patient to ensure privacy.

How will it all come out...

So I've thought a little bit tonight as I walked downtown. I was wondering about my adolescent experience during a summer spent in the inner city with children doing puppet shows, games and Bible lessons. Kids I encountered had names like Squeaky and MJ (short for Michael Jordan) and James (there was a family of at least 4 boys named James). They were different from me in so many ways. They were all black. Few of them had involved fathers. They rarely showered. Each child possessed a key to his or her house because Mom wouldn't come home until after dark. But, they were not all that different. Lanky and pubescent as I was, they would climb all over my body like I was an animated jungle gym. Eye to eye, we would have conversations as they climbed. "My favorite food is..." "I love to run fast..." "On hot days I like to drink..."

I cherish those memories of time spent with innocent children from such a sad space of Cincinnati inner-city. Tonight those memories were so strong as I walked down alley-ways alone. I was thinking about how since those days I have not made contact with those children or children like them. So an episode of nostalgia like none other is hitting me tonight, replete with its feelings of "those grand old days" and "it will never be the same."

And I have this horrible thought. What if I spend my whole life consumed with getting the last little detail of my house fixed. What if when I'm old I will have only a life of academic achievements to reflect on. What if I die without having poor black children feel like my little brothers or sisters. I can so clearly see myself letting my ambitions and my possessions lead me down that path swiftly. Life devoid of many rich charities in the blink of an eye.

Like I said, I have a serious case of nostalgia tonight. Probably it is skewing my thoughts just a little. But I can think of at least one small way that I'd like to choose a different path for myself. I'd like to give more of my time. Ridiculous amounts of time that I devout to my house could be shared on others around me who could benefit from my youth, companionship, skills and resources. God, grant me grace to live well.

A Fresh Start.

One years worth of blogging is now under my belt. My friends and I started out on an intellectual challenge to write something and get it published within the next 7 years. And so I began writing on the topic of pacifism; I persisted on that topic for exactly one year. Really, I lasted longer than I thought I would. Writing for a year on one topic is impressive for me. I suppose it is a tribute to the level of my interest in the topic. Unfortunately I am unable to finish my thoughts on the topic largely due to beginning graduate school for an altogether unrelated field--physical therapy.

Now I begin again on this new topic. My overall topical focus will be on treating pain in and from the spine. Additionally, though, my writing will include topics that range beyond the boundary of the spine. I will pursue answers to questions like these:

-How does the mind influence spinal pain?
-How is pain generate from the spinal structures?
-Why does back pain persist?
-What function do various muscles play in supporting the spine?
-What are the neurophysiological benefits of touch, joint manipulation and exercise?
-What are the mechanical benefits of touch, joint manipulation and exercise?

I hope to learn some very specific data about spinal pain and effective treatment options. But more than this I hope to build a foundation from which I can launch some ever more exciting questions such as:

-What is pain?
-What is perception?
-Is a basic level of consciousness prerequisite to perception?
-How is the body controlled by the mind?

If I can spend the next 20 years asking these questions I would be happy. In fact after that I would not be content to stop. After 20 years of asking scientific questions I would love to then draw on my experience to begin asking philosophical questions:

-How is human knowledge produced in the scientific community?
-What are the limits and constraints on human knowledge?
-Does theory ever perfectly match reality and if so how would we know?
-To what extent is correct knowledge a prerequisite for helpful application?
-To what degree can incorrect knowledge lead to beneficial treatment?