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.

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.

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.

Identification of myofascial trigger point syndromes: a case of atypical facial neuralgia.

Myofascial trigger points (TPs) in a muscle are usually activated by acute or chronic overload of the muscle. They are identified by objective and subjective findings. Objective signs include a palpably firm, tense band in the muscle, production of a local twitch response, restricted stretch range-of-motion, weakness without atrophy, and no neurologic deficit.

Effects of ergometrine (ergonovine) on the isolated atherosclerotic heart of the cholsterol-fed rabbit.

Ergometrine usually depresses the S-T segment as in coronary insufficiency, when injected intravenously in rabbits with experimental coronary atherosclerosis and in patients with effort angina, but not in normal animals and man. To explain this difference, we carried out Langendorff perfusion studies in 32 normal and 29 atherosclerotic isolated rabbit hearts. Preliminary tests with ergometrine were done to ensure that advanced coronary atherosclerosis had developed in the rabbits fed a cholesterol diet; pathological examination of the heart after perfusion confirmed the result of the final test with ergometrine.