A newsletter reader has kindly sent me a long-lost paper by the great Russian neurophysiologist, AD Speransky, entitled "Past traumatic contractures". This paper was published in 1944 and had escaped my notice despite many years of searching for more information by and about this remarkable man.
As reader regular readers of this newsletter know, I refer to Speransky frequently and consider knowledge of his theories to be essential to understanding how neural therapy works. However access to his work is complicated by language barriers (publications in French, Russian and English) and the political, economic and military turmoil in Russia during the 1930s and 1940s.
When I asked my correspondent, Steve Walton DC, how he had found this article, his answer was this:
I was at one time Chairman of the Principles and Practice Department of Cleveland Chiropractic College, Los Angeles. I had the good fortune to have an extremely intelligent and skilled mentor, Dr. RJ Watkins (first Clinic Director at Canadian Memorial Chiropractic College).
He turned me on to Speransky, and that led me into the bowels of the UCLA BioMed Library where I went through the entire Index Medicus at the time (1983) to see if I could find some refutation of Speransky and his theories: I couldn't... every article I could find (there weren't that many) referred to him as an authority.
I left LA in 1985 and moved to Hawaii. I brought my library and file cabinet with me. That's where I found the article, sitting forgotten (by me) for almost 30 years.
It is amazingly on point for those in our professions. If I read it right, then relatively brief periods of adaptation to trauma leave a permanent trace in the neural circuitry. These traces may produce atypical responses when the system is under stress. (The importance of a good history.) Also, it gives a good rationale for treating the "good side" when approaching extremities. Not shocking when we think about how "mirror-box" therapy resolves phantom limb issues, though.
I've been incorporating neurofeedback into my practice, and it seems that all of us who address the role of the nervous system in health/disease wrestle with the same issues. So, I enjoy reading your thoughts from the neural therapy point of view.
Anyway, I'm glad you enjoyed the article, and thanks for sharing your insights online.
So here is the article published in American Review of Soviet Medicine, Oct. 1946, Vol IV. #1:
A. D. SPERANSKI
Studies were undertaken on the nature of posttraumatic contractures. The neural or reﬂex origin of contractures has been taken for granted since the reﬂex character of posttraumatic contractures has been proved by careful clinical experiments of Molotkov, Novotelnov, Leriche, and Shamov. The source of the pathologic reﬂex contracture may lie in the sympathetic or spinal nerves. An analysis of the available literature suggests that both points of view are probably correct. Some posttraumatic contractures are not the result of scars, and ﬁnally, others occur after superﬁcial soft tissue wounds without injury to large nerves. These are called "hysterical" contractures. They may also occur after protracted immobilization, especially in plaster casts. In the ﬁrst case, deep irritation is apparently absent; in the second, the local disturbances follow pressure and irritation from interrupted circulation in tendons, muscles, and joints.
Work was carried on for several years on dystrophic processes in the nervous system produced by various methods. New facts have been gathered by S. I. Frankshtein in the prewar period. The study was based on the Sherrington pattern of "decerebrate rigidity." The cat was used because decerebrate rigidity is pronounced in this animal. The animal was anesthetized, skull trephined, carotids ligated, and blunt separation of the brain done in the region of the tentoriurn. Such interference produces contracture of an extensor type due to disturbance of normal tonicity. This may last hours and days. The whole phenomenon is attributed to irritation of the "red nucleus" (Sherrington, Magnus), or its removal (Beritov).
Both central and peripheral irritation was investigated in order to ascertain in what manner extensor rigidity was intensiﬁed after external inﬂuences. It was noted that the side on which the animal lies is always under greater tension than the opposite. We investigated other forms of peripheral irritation likewise related to the proprioceptor but of a more specialized character. A local inﬂammatory process might be such an irritation.
Experimental procedure: 1-2 drops of turpentine was injected subcutaneously on the posterior surface of one paw. An abscess developed and within 3‐5 days the cat "favored" the injured paw and walked on three legs. The abscess sometimes reached considerable size and ulcerated.
After decerebration, the body and extremities were affected with extensor rigidity with the exception of the injured part. The affected paw either remained soft and pliable in all its joints or developed ﬂexor rigidity. Prolonged observation revealed an intermittent relaxation of spasticity, not only in the affected paw but in the homolateral one. This can be explained only by the fact that the irritation spreading through the nervous system is of a reciprocal character. A peripheral inﬂammatory process, therefore, involves the neural segments. This involvement occurs also in decerebration when a conscious "protective" reﬂex is nonexistent.
The unconscious "protective" reﬂex as seen in a decapitated frog was studied in the following experiment. Cats were given subcutaneous turpentine injections in the front or hind paws. Decerebration was postponed until the abscess healed and the functions of the extremity restored. After decerebration, rigidity developed in all parts of the body with the exception of the paw that had recently been inﬂamed.
The following case is characteristic. Decerebration was performed on a normal cat but for some unexplained reason, decerebrate rigidity did not affect one of the hind legs. It remained ﬂaccid during the whole experiment. When the cat died postmortem examination revealed an old healed fracture of the corresponding hip.
It may be assumed that peripheral trauma or inﬂammation produces irritation of the nervous system which in turn acts as a source of further irritation. This source of nervous irritability is always manifest in the intact animal because the unusual mobility of the nervous system favors rapid compensation for any functional disturbance. In other words, the animal becomes functionally compensated sooner than the complete healing of the injury.
This concept was demonstrated experimentally many years ago but met with strong objections. Surgeons pointed out that in operations on various parts of the body and for various injuries they had not observed focal disturbances in the nervous system. It seems that were it not for the compensating capacity which a complex organism possesses, thanks to its nervous system, contemporary surgery would hardly be possible.
In other experiments, mechanical pressure was produced by a plaster of paris bandage, applied for 3‐8 days. After removal of the plaster cast the cat was decerebrated. The results were the same as in the ﬁrst series of experiments. Extensor decerebrate rigidity occurred in the body and extremities but not in the one that had been immobilized by the plaster. A modiﬁcation of the experiments consisted in applying the plaster to a ﬂexed or extended leg. The bandage was removed in 8‐5 days. The cat quickly began to walk and ran normally making equal use of all legs. Decerebration at this point produced rigidity similar to the pattern following inﬂammation. It appears that brief plaster immobilization involves not only local tissue disturbance but a permanent change in the corresponding parts of the nervous system.
A "protective" reaction was not formed because the animal had recovered its functions before the experiment. It is only possible to assume an after effect of irritation and to speak of the changes in the nervous system as a result of inadequate proprioceptive irritation.
The experiments show that there was a change in the nervous system, developing progressively from the periphery. The effect on the nervous system is either dissipated with varying rapidity or persists depending on the duration and degree of intensity of the irritation.
Similar experiments were then done on dogs. This was undertaken to analyze the capacity of the nervous system for compensatory activity as worked out by Anokhin and Asratyan. Inflammation was produced by 2‐3 drops of turpentine injected under the skin of the front or hind paw posteriorly. In a very short time the dog drew in the paw and moved about on three legs. When another injury was inflicted on the animal in the same region of the opposite paw, the animal almost immediately began to use all four extremities freely, without limping. This occurred in several cases where repeated symmetrical irritation produced less effect than the previous unilateral injury.
It appears that the so-called protective reaction does not play any role. Corroboration was obtained by the following experiments. A plaster of paris bandage was applied to a cat in an extended position, not only on one, but on both front legs. After five days the bandage was removed and the animal was decerebrated. Decerebrate rigidity was uniform but extensor rigidity of the front legs alternated with flexor rigidity.
Similar clinical and experimental observations were known but no explanation offered. Trendelenburg noted that motor disorders in dogs after decortication disappeared rapidly if a bilateral operation were done on the brain. P. K. Anolchin noted the same phenomenon after bilateral section of the posterior radicles. A. Kharitonov observed a more rapid recovery of functions in animals when total rather than partial removal of the cerebellum was done. Finally, Gubich observed that motor functions are restored more readily in a dog when bilateral cutting of the sciatic nerves was performed instead of unilateral. These facts become clear when it is realized that neural processes are interwoven and interacting and occur to a marked degree in the same or neighboring segments.
Conclusions and suggestions: Incipient "reflex" contractures or other affections such as causalgia lacking clearly defined organic changes should be counterirritation in a symmetrical part of the body. This stimulation may be the quartz lamp, roentgen rays, mustard poultice, cantharidin or, as recommended by Davidenkov, novocaine. Probably different combinations are called for in various cases. This treatment does not hold any danger for the patient.
Voprosy neirokhirurgii 1944,
Vol. 8, No. 3, pp. 3-7
Much to think about from this paper!
I absolutely agree about sciatica and that Hackett and Travell and Simons are essential to treating leg pain. There is another type of leg pain due to irritated cutaneous nerves, often irritated as they emerge from fascia eg the cluneal nerves over the top if the iliac crests (I'd never hear of them either but they are there in Google images if you want to have a look) and the lateral femoral cutaneous nerves, and sural and saphenous nerves. This is a true neuropathy with burning pain mediated by the capsaicin sensitive nerves, and the nerves are tender to palpate, in fact it makes the patient gasp, unlike referred pain which is not tender to palpation. The doctor who pioneered this is John Lyftogt from NZ and his workshops are amazing ‐ full of fascinating research and demonstrations ‐ teaching simple 1cc injections of 5% glucose, no lignocaine! Think of all those patients with lateral hip pain that is worse when they lie on it at night. Some of it is of course glut minimus trigger point referral pain, but not the ones where the tenderness goes all down the lateral thigh. One of the doctors who did his first workshop with me in 2009, has done a randomised trial of the use of 5% glucose in caudal epidurals ‐ much better than steroid. See his website http://www.doctorliftoff.co.nz/ I think you'll be fascinated. I can cure lots more pain using all 3 approaches now.
Margaret Taylor MD
Dear Dr Kidd;
I enjoyed your article so much. I just wanted to share my humble experience in that matter. I worked for 10 years at the VA system and I had the privilege to do enormous amounts of SI prolotherapy and PRP under X ray guidance. Surprisingly around 5 % of these patients did not respond to prolo therapy and I send them for EMG and almost everybody had S1 Radiculopathy. The genius Dr Cyriax had discovered this long time ago and he mentioned that main differential diagnosis of SI pain is S1 Radiculopathy .
Hope this was helpful and thank you again for your wonderful contribution in the field of neural therapy.
Little Rock AR
Very interesting!!!!! And I absolutely agree.
Some patients like to hear they have sciatic problems. It is difficult to explain to them that some leg pains are not sciatic pain.
Very common interference field are tonsils or very close areas.
Robert F. Kidd, MD, CM