Janet Travell

Myofascial origins of low back pain: 1. Principles of diagnosis and treatment

Myofascial trigger points (TPs) are frequently overlooked sources of acute and chronic low back pain. An active myofascial TP is suspected by its focal tenderness to palpation and by restricted stretch range of motion. The restricted lengthening of the muscle is due to the tense band of muscle fibers in which the TP is located. The presence of a TP is confirmed by a local twitch response and by reproduction of its known pattern of referred pain, which matches the distribution of the patients pain. Only an active TP causes a clinical pain complaint; a latent TP does not. The pain can be relieved by the stretch-and-spray procedure, ischemic compression, or precise injection of the TP with procaine solution. Relief is usually long lasting only if mechanical and systemic perpetuating factors are corrected.

Myofascial origins of low back pain. 3. Pelvic and lower extremity muscles.

Gluteal, pelvic, and lower extremity muscles are common sites of origin of myofascial low back pain. Trigger points (TPs) in the gluteus maximus and medius muscles refer pain locally to the gluteal and sacral regions, while those in the gluteus minimus are likely to refer pain down the lower extremity as far as the ankle on the same side. TPs in intrapelvic muscles refer pain chiefly to the pelvic region. Besides producing referred myofascial pain, TPs in the piriformis muscle can cause symptoms of entrapment of the peroneal portion or all of the sciatic nerve. TPs in the soleus muscle may refer pain to the sacroiliac joint.

Postural vertigo due to trigger areas in the sternocleidomastoid muscle.

Summary In an 11-year-old girl, attacks of postural vertigo and headache were traced to their source in trigger areas in the sternocleidomastoid muscle, the chief balancing muscle of the head. This is the first case of this syndrome to be reported in the pediatric literature. Etiological factors, diagnosis, treatmentby local measures directed at interrupting the trigger mechanism, and the pathophysiology of the sternocleidomastoid syndrome are discussed. A concept of the myofascial triggerarea as a physical sign with predictable patterns of referred pain and reflex autonomic concomitants is presented. Every patient with headache, posturalvertigo or dizziness, and imbalance should be examined routinely for related trigger areas in the sternocleidomastoid muscles. A therapeutic trial with ethyl chloride spray and procaine infiltration of the trigger areas should be made. Temporary or partial relief implies either insufficient treatment or reactivation of the trigger mechanism reflexly by remote disease.

ABSORPTION OF NICOTINE FROM VARIOUS SITES

That hydrogen ion concentration is important in determining permeability of cell membranes to nicotine was established decades yet this principle is still slighted in current texts of pharmacology if, indeed, they mention it at all. For this reason, it is pertinent to review our early experiments and some unpublished data on the role of the pH in the absorption of alkaloids from various tissues.

Myofascial origins of low back pain. 2. Torso muscles.

Trigger points (TPs) in muscles of the lower torso associated with the spine are an important cause of low back pain. The quadratus lumborum is the muscle most commonly involved, but TPs located there are often overlooked because of inadequate physical examination techniques. TPs in the lower rectus abdominis refer pain horizontally across the low back, and those in the iliopsoas refer pain in a vertical pattern, parallel to the lumbosacral spine. The pain pattern of TPs in the serratus posterior inferior is noted in the region of the muscle itself.

Effect of heparin in effort angina

ELIEF of angina pectoris by heparin was R first reported in 1951 by Graham and his co-workers.’ This finding was incidental to an investigation of the effects of heparin on the concentration of the serum lipoproteins (S, 1 Z-20 and 20-l 00). Efficacy of heparin in effort angina has since been reported by Engelberg, 2 while, on the other hand, no significant benefits were found by Russek3 or by Miller, Zinn and Griffith.4 The present study was undertaken first to evaluate heparin in effort angina by the double blindfold method and the daily report card system for collecting data,6 and secondly, to determine at the same time the effect of a course of heparin on the concentration of serum lipoproteins of the S, 12-20 and S, 20-l 00 classes.

Role of somatic trigger areas in the patterns of hysteria.

AMONG several hundred patients with muscular pain and associated disturbances of function, and with trigger areas in the voluntary muscles, we had the opportunity to study a few subjects who exhibited the classical patterns of hysteria. These patterns included disorders of vision, respiration, motor power, and cutaneous sensation. Briefly, our data indicate first, that the phenomena of hysteria which we observed were in each instance mediated by afferent neural impulses from trigger areas in the skeletal muscles. Secondly, similarly located trigger areas produced the same pattern of clinical effects whether the trigger mechanism was activated in one person by psychogenic stress or in another person by some other factor such as physical trauma. These observations are important since they suggest one basic physiologic mechanism to correlate the bizarre and apparently unrelated signs and symptoms which coexist in the hysterical syndromes.

PHARMACOLOGY OF STIMULANT LAXATIVES

I have been asked to contribute this paper, not because of any extensive investigations of cathartic drugs, but because of our interest in rational therapeutics, expressed in our Cornell Conferences on Therapy’ which dealt with the rational use of cathartic agents. At the conference on which this monograph is based, emphasis was placed on the need of the abnormal colon for rest in general and, in particular, for relief from irritation by cathartics. With respect to chronic constipation, or functional bowel stasis, such rest is admittedly desirable. Presently, however, I shall quote some figures on the amounts of stimulant laxatives actually prescribed which suggest that ideal therapy of this condition is not always attained. In view of their widespread use, salient points in the pharmacology of these drugs merit review, especially since, in recent years, the stimulant laxatives have received less attention than the bulk laxatives. The scope of this paper does not permit discussion of the place of stimulant cathartics in chronic constipation. In acute constipation, however, it is clear that legitimate indications often do exist for giving these preparations; for instance, during administration of constipating drugs, such as codeine, morphine, and ephedrine, during bedrest and hospitalization, after dietary indiscretions, and after certain vermifuges. Also, preparation of the patient for roentgen examination of the abdomen usually includes catharsis by one of this group. The stimulant cathartics comprise several widely different types of compounds, mainly of vegetable origin: (1) anthraquinone derivatives contained in cascara sagrada, aloe, senna, and rhubarb; (2) phenolphthalein, and other phthaleins and coal tar dyesf (3) ricinoleic acid liberated from castor oil; (4) the hydragogue “drastics,” potent resins and alkaloids of podophyllum, jalap, colocynth, elaterin, gamboge, and croton oil; ( 5 ) sulfur; and (6) calomel. Mode of actiorz. The “stimulant ”or “irritant” cathartics, as they have been termed, are to be contrasted with the “mechanical” laxatives: the gums, salines, liquid petrolatum, and water, which promote peristalsis mainly by increasing the bulk or altering the consistency of the stool. These cathartics are also to be distinguished from “systemic” agents which stimulate intestinal motility only after absorption into the blood stream; for example, picrotoxin, vasopressin, and the cholinergic drugs. Unlike the latter, the irritant cathartics are believed to act only when they are present within the lumen of the intestinal tract. This action occurs even when evacuation is induced by their parenteral administration. For instance, emodin (tri-hydroxymethyl-anthraquinone) causes catharsis when injected intravenously. The effect is thought to depend 011 the excretion of the drug into the colon. In fact, by common usage the terms “laxative,” cathartic,” and “purgative” always imply a local site of action within the gut. On the other hand, in

Cardiac effects of nicotine in the rabbit with experimental coronary atherosclerosis.

Groups of male Dutch rabbits about 2 kg. in weight were started contemporaneously either on a stock diet or on the stock diet to which 2 per cent cholesterol, or 2 per cent cholesterol in 6 per cent corn oil, had been added.3 Serial electrocardiographic ergonovine tests3 s 4 z 5 were performed at monthly intervals to insure that coronary atherosclerosis had developed a t the time of coronary perfusion with nicotine. After intravenous ergonovine maleate (0.05 mg./kg.), positivity of the test is indicated by sagging depression of the S-T segment in about 3 to 5 min. In 16 such ergonovine-positive cholesterol-fed rabbits, nicotine was injected intravenously in a dose of 0.05 mg./kg., and the electrocardiogram followed for 30 min. Electrocardiographic effects of nicotine were similarly observed in 12 control rabbits fed the stock diet. Intravenous pentobarbital sodium

Influence of pH on Absorption of Nicotine from Urinary Bladder and Subcutaneous Tissues

in a dose of 10 to 15 mg./kg. was adequate to keep the animal quiet fbr electrocardiography if it was not disturbed during this period of observation. For stabilization of heart rate and blood pressure, a t least 20 min. was allowed to elapse between intravenous injections of pentobarbital and nicotine. Perfusion studies. Langendorff coronary perfusion was carried out on 16 ergonovine-positive atherosclerotic and 14 normal isolated hearts. The heart was removed for perfusion under anesthesia with pentobarbital sodium, 15 to 20 mg./kg., intravenously. Single injections of drugs in a volume of 2 cc. were made into the perfusion system to simulate the peak concentration of an intravenous injection in the intact animal. Observations were made for 4 min. afterward, or longer if the effects lasted longer. The modified apparatus and method have been described in detaiL3