Orthopaedic medicine has a long history and many tools with which to help the patient with musculoskeletal pain. In this Issue I would like to review basic principles regarding Prolotherapy for the benefit of physicians who are developing skills in Prolotherapy (Regenerative Injection Therapy )and PRP and as a review for those already practicing these skills. In order to achieve the greatest success, the procedure should be performed correctly enhancing safe practices and limiting risk for the patients. Several important elements need attention: practice management (consent, documentation, billing and coding issues), assessment and identification of appropriate candidates for the procedure and safe performance of the procedure itself.
Knowledge of the pathology behind the patient’s complaint.
Identify the problem based on history, physical examination and imaging studies. Look for local tender points, as well as distal referral points. Remember, the initial presentation of pain could be referred pain and not necessarily where the problem is. Learn common patterns of referred pain. Become familiar with the diagnosis of instability of joints based on the clinical symptoms and exam findings. Make the correlation between clinical findings and imaging studies. Remember: Imaging studies do not always correlate with clinical findings and vice versa.
Knowledge of anatomy and function. Do your homework before treating the patient. Read anatomy, so you will know what are you are doing. Proficient prolotherapists are perpetual students of anatomy. Have diagrams, posters and anatomical illustrations readily available in your exam rooms. Show your patients where the problem is and how you will treat it.
Informed Consent
Inform the patient about the procedure in detail. Give them realistic expectations of the treatment and prognosis. Explain to the patient that prolotherapy is a PROCESS and requires multiple treatments and time to see results. Give the patient an option to review other possible treatments: Physical therapy, Surgery, OMT, and especially the options offered as standard of care for their particular diagnosis. Informed consent requires that the patient be presented the standard of care alternatives for their diagnosis.
Documentation of Informed Consent is just as important as the signature. Have the patient sign a detailed consent form, explaining all possible side effects and complications. The potential side effects and complications should be discussed and outlined to the patient and documented on the consent form. You may wish to have your forms reviewed by your malpractice carrier to be certain they meet the standards. Encourage the patient to contact you before the scheduled procedure and to ask questions. When examining elderly patients advise them to come with close relatives or friends so that all questions will be answered and not missed. Informed consent must list the standard medical options the patient was informed of and chose not to pursue.
Have the patient sign all medical and financial documents with the co-signature of a witness-your nurse or other office assistant.
Medical Practice/Procedure
Know important medical information pertinent to safe performance of an invasive procedure: Medical history, Medications list, Previous surgeries, Allergies, Presence of prosthesis, hardware, screws and plates. Discuss with referring physician the procedure you are going to perform. If you advise the patient to stop any medications ask the PCP for permission to do so. Do not discontinue medications ordered by other doctors without consulting with them first. Do not criticize other physicians or previous treatments. You also may not be the last doctor. Strive to create a professional and healing atmosphere in your treatment room.
Never use old solutions. All solutions must be mixed on the day of the procedure. Aseptic technique must be taken very seriously. In some cases you may consider prophylactic antibiotics. Proper positioning of the patient is very important. It must be safe for the patient and comfortable for physician performing the procedure. Consider IV line and VS monitoring in some cases. Make sure you are ready for medical emergencies. If you chose to use conscious sedation or pre-medicate your patients be sure they have a driver and that you meet the regulations of your state and malpractice carrier for conscious sedation or premedication.
Prepare skin for procedure. If the skin is inflamed in the area the injections are to be performed it is better to postpone the treatment. Again, know your anatomy and be very careful while injecting:
Midline of the vertebrae: direct needle caudate
Avoid cranial direction.
Be careful injecting midline below L3–Interspinal ligaments could be absent and risk for dural perforation is high.
Always touch the bone.
In some cases, aspirate before injecting, especially the transverse processes of cervical spine.
Be very careful around chest/rib/thoracic injections and lower cervical spine – risk for pneumothorax.
Check the function of the treated area after the procedure: ROM, pulsation, lungs sounds and vital signs.
Post Procedure: Offer patients fluids and snacks if necessary. Some patients will be light headed or vasovagal from the sympathetic stimulation of the injections. Give patients time for full recovery. All patients must be instructed to come with a designated driver. Make sure that you will be readily available to the patient after the procedure – give them you mobile phone number. It is a very beneficial practice to call your patient the next morning, especially after the first injection session. This is reassuring to the patient and allows you to evaluate their response to the treatment.
Documentation is a necessary part of the job of the physician. Make it simple, but detailed. Forms with diagrams, flow sheets with check boxes or items to circle can ease the documentation process for procedures. The following should always be present:
General information about Prolotherapy for patients as well as their physicians.
Detailed consent form
Medicare waiver
Financial disclosure and agreement
Preparation for Prolotherapy
Procedure protocols
Patient Response to the procedure
Post-procedure instructions
Taking the time to review these processes and implement safe processes and procedures as you introduce new techniques into your practice will facilitate safe practices for you and good outcomes for your patients.
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Article summary Renata Trister DO
Advances in medicine, science and hygiene have allowed modern man to become the longest living humans in history. As life expectancy lengthened, disorders of the nervous system in the aging population are seen more frequently. Dementia, cerebrovascular disease as well as progressive disorders such as peripheral neuropathy and Alzheimer’s are a growing concern for the aging patient. Diseases of the nervous system are being diagnosed in record numbers in the United States: up to 6.8 million suffer from dementia; approximately 4 million have Alzheimer’s disease (AD), and roughly 1.5 million may suffer from Parkinson’s disease (PD), with 50,000 newly diagnosed patients every year. These numbers are projected to continue to increase. Dysfunction in older patients should not be assumed to be the result of the aging process. Although progressive decline in neurologic functioning is a normal aging process, progression to a neurologic disease is not inevitable. Early intervention may prevent and delay the deterioration in these disorders.
Research suggests that a cumulative effect of imbalanced biochemical pathways can greatly impact neurologic cellular decline. Four major biochemical pathways are thought to mediate both aging and premature neurologic decline. By maintaining adequate function in these pathways, it may be possible to achieve optimal neurologic health and brain function.
Environmental factors such as poor diet, toxins and oxidative damage can stress biochemical pathways in the body and accelerate the biological aging of tissue.
Four Biochemical Pathways Implicated in Nervous System Decline
I. Chronic Inflammation—Research suggests that chronic inflammation is a possible mechanism in aging associated neuro-degeneration. Multiple aspects of the inflammatory pathway are capable of propagating premature aging and neuron cell death. Chronic inflammation beyond its protective role, can cause harm to tissue. Epidemiological evidence indicates that populations taking anti-inflammatory drugs for other conditions have a reduced risk of neurodegenerative conditions. Inflammation and oxidation are closely linked. Oxidants serve as signaling agents for the pro-inflammatory factors. Several natural substances offer safe and effective alternatives to anti-inflammatory drugs, which are known to cause various adverse side effects.
II. Mitochondrial Dysfunction—Tissues with a high-energy requirement, such as the brain and heart, have a greater density of mitochondria—the cell’s energy-producers. Since the brain depends so highly on mitochondrial energy supply, dysfunction of mitochondria can affect the central nervous system (CNS) more severely than other tissues. Research suggests two methods of supporting mitochondrial health and function: 1) promoting healthy mitochondrial energy production, and 2) combating free radical production and damage by increasing mitochondrial antioxidants.
III. Endocrine Imbalance—Aging is associated with a reduced ability to adapt to stress and chronic elevations of stress hormones called glucocorticoids (e.g., cortisol).Animal and human data suggest that high levels of glucocorticoids can be particularly detrimental to the hippocampus (the brain structure involved in learning and memory). In addition, changes in glucose and insulin handling during the aging process can lead to neuronal degeneration due to negative effects on nerve cell structure and function. Proper diet, exercise, and nutritional interventions may help reduce glucocorticoid levels, enhance the body’s ability to cope with stress, and improve glucose and insulin metabolism.
IV. Hypomethylation—Methylation, the transfer of a methyl group (CH3) from one molecule to another, is required for numerous biochemical reactions vital to good health. However, insufficient levels of folate and vitamins B6 and B12 can cause reduced methylation, or hypomethylation, which in turn can produce elevated levels of the amino acid homocysteine (Hcy). Elevated Hcy levels are strongly linked to cognitive decline and irreversible dementia. See tables below.
Nutritional Modulation of the Four Pathways
Fortunately, interventions begun in the initial stages of the disease process may prevent or delay the course of neurologic deterioration, resulting in an overall improvement. The following nutrients may help prevent and interrupt the damaging cascade that contributes to neurologic decline.
Niacinamide—Niacinamide, a form of the B vitamin niacin, is a potent inhibitor of inflammatory cascade. In animal models, administration of niacinamide resulted in reduced brain damage and reduced neurologic functional losses.
Essential Fatty Acids—Fish oils, which contain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are well known for their anti-inflammatory activity. Furthermore, DHA is required for normal brain function in adults. Decreases in brain DHA content are associated with age-related cognitive decline, dementia, and AD.
Resveratrol—Resveratrol is a polyphenol found in the skins of red grapes and various other plants. In vitro, animal, and epidemiologic research suggests that resveratrol may protect against inflammation and CNS disorders. It is also a potent antioxidant.
N-Acetylcysteine (NAC)—The protective effect of NAC is likely related its restoration of brain glutathione (GSH) levels.GSH is central to antioxidant defenses in the brain and cellular detoxification of free radicals. In addition, NAC has been shown to support proper mitochondrial function.
Alpha-Lipoic Acid (ALA)—ALA is a cofactor in the synthesis of ATP (energy required for tissue function) and improves overall mitochondrial function. ALA is also an excellent antioxidant agent in neurodegenerative diseases due to the fact that it can interrupt free radical damage at several points. Animal research has shown that ALA supplementation elevates antioxidants in various brain regions and improves memory in aged mice.In addition, ALA supports healthy blood glucose levels and insulin activity.
Acetyl-L-Carnitine (ALC)—ALC is a vitamin-like substance that may improve energy production within brain cells via its effect on mitochondria.An analysis of studies reports that persons with dementia given 1.5 to 3 grams of ALC daily have shown improvement in numerous clinical measures of cognitive function such as memory, depression, and mental deterioration.
Magnesium & Thiamin—Magnesium plays an important role in maintaining the integrity and permeability of the mitochondrial membrane as well as assisting in energy-producing machinery of the mitochondria. Thiamin is a cofactor needed for mitochondrial energy production.
Coenzyme Q10 (CoQ10)—CoQ10 is a mitochondrial antioxidant cofactor that has been shown to be neuro-protective. In addition to being a potent free radical scavenger, CoQ10 is also critical for energy production by the mitochondria. CoQ10 supplementation has proven effective in a wide variety of age-related conditions.
Vitamin E—Vitamin E is the primary antioxidant found in all tissues. Low vitamin E levels are consistently associated with an increased risk and occurrence of neurologic disease, including AD and Parkinson’s. In a study of patients with AD, treatment with 2000 IU of vitamin E per day for 2 years was beneficial in delaying the primary outcome (time to the occurrence of death, institutionalization, loss of ability to perform activities of daily living, and severe dementia) of disease progression.
Ginkgo (Ginkgo biloba)—Ginkgo biloba extract (GBE) is an approved treatment for dementia in Germany, and it is the only nonprescription substance considered a treatment for dementia in Canada. Many clinical studies have demonstrated the effectiveness of GBE in the treatment of patients with dementia, AD, and age-associated memory and cognitive impairment. In addition, GBE may also prevent changes in mitochondrial structure and function associated with aging of the brain.
Adaptogenic herbs—Adaptogens are plants that help to decrease cellular sensitivity to stress. Herbs with adaptogenic properties may be beneficial in ameliorating the decreased ability to handle stress and the increased levels of glucocorticoids associated with aging and neurodegeneration. Ayurvedic herbs such as ashwagandha (Withania somnifera), holy basil (Ocimum sanctum), and brahmi (Bacopa monniera) have a positive influence on stress response, mental function, and cognition.
Mixed Carotenoids—Carotenoids are a class of naturally occurring plant pigments that provide the bright red, orange, and yellow colors of fruits and vegetables. A balanced intake of mixed carotenoids, as found in a healthy diet, provides the best protection against oxidative damage. In addition, the carotenoids lutein and zeaxanthin are found concentrated in the retina of the eye where they offer protection from conditions such as age-related macular degeneration.
Folate, Vitamin B6, and Vitamin B12—Folate and vitamins B6 and B12 are needed for proper methylation and to keep Hcy within a normal range.Insufficiencies of these nutrients may result in forgetfulness, memory loss, confusion, depression, dementia, and mood and sensory changes.
Conclusion
Healthcare professionals and their patients must take a preventative stance against neurologic decline. Due to the great deal of interest and research in this area, information about appropriate nutritional supplementation is constantly evolving. By looking for early warning signs and providing nutritional guidance that simultaneously addresses chronic inflammation, mitochondrial dysfunction, endocrine imbalance, and hypomethylation, perhaps more people can live out their most rewarding years with mind and body intact.
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Article Summary
Renata Trister DO
Estrogens affect the growth, differentiation, and function in various organs and tissues. Although commonly known as the “female hormone”, estrogen plays an important role in bone health, protects the cardiovascular system, and influences behavior and mood. Estrogen also affects male organs such as prostate and testes. While appropriate levels of estrogens are essential for good health, excessive estrogen exposure can lead to health problems such as premenstrual syndrome (PMS), endometriosis, fibrocystic breasts and breast cancer.
Lifestyle and environmental factors can greatly influence estrogen production, metabolism, and balance. These factors include poor diet, obesity, excess alcohol consumption, high insulin levels, medications such as hormone replacement therapy and birth control pills, overexposure to chemicals found in pesticides and industrial chemicals, and agricultural hormones in animal products consumed by humans.
Nutritional Support of Optimum Estrogen Metabolism
Diet and nutrition play an important role in influencing estrogen metabolism and detoxification. Incorporating dietary changes with the addition of beneficial nutrients and herbs can profoundly affect estrogen balance.
Dietary modulation of estrogen metabolism
Consumption of cruciferous vegetables like cabbage and broccoli, and foods such as soy can significantly increase the 2-hydroxylation of estrogen. Dietary fiber intake can promote the excretion of estrogen by binding estrogens in the digestive tract and also increases sex hormone binding globulin (SHBG), thus reducing levels of free estradiol. Complex carbohydrates, such as those found in vegetables and whole grains, are more effective in optimizing estrogen metabolism than simple carbohydrates, which can raise blood glucose and insulin levels, resulting in secondary adverse influences on sex hormone balance.
Phytoestrogens — These plant compounds are similar in shape to the estrogen molecule and can bind to estrogen receptors (ERs). They are much weaker than endogenous estrogens and, through competitive inhibition, have been shown to prevent the receptor binding of “stronger”, more stimulating estrogens. Phytoestrogens are currently under extensive investigation as a potential alternative therapy for a range of conditions associated with estrogen imbalance, including menopausal symptoms, PMS, endometriosis, prevention of breast and prostate cancer, and protection against heart disease and osteoporosis.
The two main classes of phytoestrogens are isoflavones and lignans. Soy is perhaps the most common food source of isoflavones, but other excellent sources include legumes, clover, and kudzu root. Higher intakes of soy products and isoflavones, such as consumed in traditional Japanese diets, are associated with low rates of hormone-dependent cancers. Lignans are compounds found in fiber-rich foods such as flaxseeds, whole grains, legumes, and vegetables. Lignans stimulate the production of SHBG in the liver, and therefore reduce the levels of free estrogen in circulation. They also inhibit aromatase, an enzyme that synthesizes estrogen.
Vitamin E and Magnesium — Low serum vitamin E is associated with elevated estrogen levels, and may negatively affect estrogen detoxification. Women with PMS have experienced improvements of their symptoms when given supplemental vitamin E. Magnesium promotes estrogen detoxification by promoting methylation and glucuronidation, key estrogen detoxification pathways. Ovarian hormones influence magnesium levels, triggering decreases at certain times during the menstrual cycle as well as altering the calcium to magnesium ratio. These cyclical changes can produce many of the well-known symptoms of PMS in women who are deficient in magnesium and/or calcium.
Indole-3-Carbinol (I3C) – I3C is a naturally occurring compound derived from cruciferous vegetables that actively promotes the breakdown of estrogen via the beneficial 2-OH pathway. Therefore, I3C is protective to estrogen-sensitive tissues and may be beneficial to those with health issues related to excessive estrogen. Not only does I3C promote healthier estrogen metabolism, it may also act as a “weak” or anti-estrogen in a similar fashion to isoflavones.
B Vitamins — B12, B6 and folate function as important cofactors for enzymes involved in estrogen detoxification; thus, decreased levels of B vitamins can lead to increased levels of circulating estrogens. Vitamin B6 can also modulate the effects of estrogen by decreasing the cell’s response when estrogen binds to the estrogen receptor. B vitamins are also important for DNA synthesis and repair.
Beneficial Phytonutrients and Herbs
Many other compounds can promote healthy estrogen metabolism. Curcumin, a compound found in the herb turmeric (Curcuma longa) increases the phase II detoxification of estrogens; chrysin, a bioflavonoid that inhibits aromatase activity, thus reducing the synthesis of estrogen; D-limonene from citrus fruits promotes the detoxification of estrogen and shows promise in the prevention and treatment of breast and other cancers. Antioxidants can reduce the oxidation of the 2-OH and 4-OH estrogen metabolites. Antioxidants include vitamin C, N-acetyl cysteine, selenium, and green tea. Traditional medicines from many cultures have relied on a variety of hormone-modulating herbs in treating women’s health conditions. These include black cohosh, chaste berry, ginseng, dong quai, and licorice.
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By Jon Trister, MD
Gastrointestinal Physiology.
It is important to understand GI function.
Neurological consideration.
Glossopharyngeal nerve (Cranial nerve IX): mixed, sensory and motor nerve.
Sensory function:Oropharynx,Eustachian tube,Middle ear,Posterior third of the tongue,Carotid sinus, Carotid body, Taste to posterior third of the tongue, Supplies parasympathetic fibers to the parotid gland via otic ganglion,contribute to the pharyngeal plexus.
Motor function: Stylopharyngeus muscle.
Vagus nerve (Cranial nerve X):
a)Parasympathetic control of the heart, lungs, gastrointestinal tract.
b)Sympathetic control of the peripheral chemoreceptors.
Nuclei:
Dorsal nucleus of the vagus nerve:Parasympathetic output to the intestines;
Nucleus ambiguus:Parasympathetic output to the heart;
Solitary nucleus:Receives afferent taste information and afferent info from visceral organs.
Spinal trigeminal nucleus:afferent impulses arising from the outer ear, the dura of the posterior cranial fossa and mucosa of the larynx.
Accessory nerve ( Cranial nerve XI):Originates in the C1-C2 segments): Innervates sternocleidomastoid and trapezius muscles.
It enters the scull via foramen magnum, travels along the inner wall toward jugular foramen and leave the scull again fia Jugular foramen together with IX and X nerves.
Cranial nerves IX-X-XI provide neurological regulation of the gastrointestinal function.
They pass through jugular foramen which has very complex anatomy.JUgular foramen is formed by the anterolateral part of the temporal bone and posteromedial part of the occipital bone.
Its subdivided into larger posterolateral compartment ( pars venosa) containing the jugular bulb and tenth and eleventh cranial nerves and a smaller anteromedial compartment ( pars nervosa) containing the ninth cranial nerve.These two parts are usually separated by a fibrous bridge connecting the jugular spine of the petrous temporal bone to the jugular process of the occipital bone.This bridge could be osseos or fibrous.
Size of the right jugular foramen is usually larger than the left.
Dura over the jugular foramen had a two perforations forming a glossopharyngeal meatus through ninth nerve passed to enter the pars nervosa and vagal meatus through which vagus and accessory nerves entered the anteromedial part of the pars venosa and jugular bulb.The glossopharyngeal and vagal meati consistently separated by a dural septum.(Albert Rhoton etc, J.Neurosurgery/Volume 42/May 1975).
This complex anatomical entity is a subject to somatic dysfunction as the result of trauma, congenital abnormalities, tumors,dural strains, inter- and intraosseous strains of the temporal and occipital bones.
Those pathologies may alter anatomical relationship of the structures occupying the jugular foramen and subsequently to their physiological dysfunction.
Digestion begins with imaginary stimulation: thinking , seeing and smelling food send signals to the brain via afferent nerves. In the brain processing of information is occurs and efferent pathway-parasympathetic- glossopharyngeal nerve is activated to stimulate salivary glands to produce saliva rich in digestive enzymes-amylase ( initial breakdown of carbohydrates) and lipase (initial breakdown of triglycerides).
Glossopharyngeal nerve ( IX)
[originates in upper medulla, passes through the Jugular foramina]: Stimulate salivary glands.
Vagus (X) [Originate in medulla oblongata and passes through the Jugular foramina] Control digestive tract from the esophagus to the mid-colon.
Accessory nerve (XI) [Originate at the junction of medulla oblongata and spinal cord and passes via jugular foramen with IX and X nerves]
1.Mastication stimulates production of the saliva by oral salivary glands (IX).Mastication stimulates gastric secretion of Pepsin and water (X).
Stomach:Distention of the esophagus stimulates the oral salivary glands.Distention of the gastric fundus stimulates secretion of the Pepsin,HCL, Intrinsic Factor and water.
Distention of the antrum stimulates Gastrin secretion. In addition, the cells lining the stomach secrete a thick mucus coating that protects the stomach from acid and pepsin.
Distention of the duodenum stimulates secretion of the Pepsin, HCL, Intrinsic Factor and water. Pepsin is active in acidic environment. Pepsin is very specific in digestive capability: it break down only [protein linkages containing certain amino acids : tryptophan , tyrosine, Methionine and leucine.
The presence of food stimulates the vigorous contraction of the muscles of the stomach wall, mixing of the food particles with digestive juices and push semi digested food into duodenum.
Antral drainage inhibit secretion of the Pepsin, HCL, Intrinsic Factor and water
Gastrin amplifies antral production of the HCL, Intrinsic Factor, Pepsinogen and water
Gastrin amplifies duodenal secretion of Cholecystokinin
Gastrin is produced by G cells of antrum, in the duodenum, small intestine and pancreas.
HCL inhibit production of Gastrin.HCL stimulates secretion of Secretin by duodenum
Duodenum very complex process and regulated by nervous system and hormones:
Gastrin stimulate the formation of the Cholecystokinin.Lipids in the jejunum stimulate secretion of the Cholecystokinin.Carbohydrates and HCL in duodenal bulb stimulate secretion of the Cholecystokinin.Cholecystokinin induce gallbladder contraction and opening of the hepato-pancreatic ampulla.
Cholecystokinin stimulates production of the Insulin, HCO3, Glucagon in the pancreas
Cholecystokinin inhibit antral secretions and bulbar acidity.Secretin reduce HCL production and stimulate HCO3 production by pancreas which protect duodenal bulb from acid.Secretin stimulate Insulin release and inhibit Glucagon release.Duodenum also secretes mucus for protection from destructive effect of HCL.
Hypertonic Glucose solutions, Acidity in the bulb, Lipids in the jejunum limit the formation of the HCL and diminish gastric motility.If Lipids, proteins and carbohydrates evacuated at the same time disturbing of digestive function might occurs.
Enterokinase in duodenum convert into Trypsin and inhibit Action of the biliary salts.Biliary salts (weak concentration) stimulate Lipase secretion and inhibit (strong concentration) Lipase secretion.
Gastrin Stimulates: HCL and Water secretion by stomach; secretion of Pepsin, Secretion of Intrinsic Factor, Secretion of Cholecystokinin in the duodenum.
HCL: Inhibits secretion of Gastrin; Stimulates secretion of Secretin; Stimulates production of pepsin from pepsinogen.Anti-bacterial function; Converts Ferric iron to Ferrous iron(absorbable)
Cholecystokinin: Stimulates action of biliary salts, Contraction of Gallbladder, dilatation of choledocho-pancreatic ampula,inhibit gastrin and HCL production; stimulates HCO3, insulin and glucagon release
Secretin: Inhibit HCL, Glucagon, stimulate Insulin release ,stimulates HCO3 production by Pancreas
Pancreas:
Endocrine function:
Alpha cells produce and secrete Glucagon, which pancreas release in response to low blood sugar in the serum.Glucagon stimulates breakdown of glycogen ( liver and muscles) to glucose , which is released into bloodstream to serve as a source of cellular energy.
Beta cells secrete insulin in response to high glucose level in the serum.Insulin ( among other functions) drive glucose into muscles and liver to store in the form of glycogen.
Delta cells produce and secrete somatostatin , a complex hormone that is also produced by intestinal lining cells as well as certain neurons in the brain.In the pancreas somatostatin can inhibit release of insulin and glucagon (!?!) to help maintain blood sugar level in a very narrow range.
Exocrine function:
The cells of exocrine pancreas arranged in acini- special clusters along the network of channels forming pancreatic duct-to secrete pancreatic enzymes.
Proteolytic enzymes:Trypsin, Chymotrypsin, Carboxypeptidase A, Carboxypeptidase B,Elastase, Amynopetodases, Dipeptidases, Tripeptidases,Pepsin.
Each of these enzymes has precise and specific function.
Trypsin will break down a protein only at amino acid linkages containing either arginine or lysine.
Chymotripsyn will break down a protein at amino acid linkages containing tryptophan,phenylalanine, tyrosine.
DIpeptidase will break down a protein consisting two amino acids
Tripeptidase will break down a protein consisting three amino acids
All of these enzymes are produced in in-active forms to prevent self-destruction:
Trypsinogen, Chymotripsynogen,Procarboxypeptidase,Prodipeptidases,Protripeptidases
The acing cells also secrete multiple lipases and amylases.
The acinar cells store the inactive precursors in little sacs, or vacuoles, in the cytoplasm, until they are needed for digestion.As ling as these pre-enzymes remain in their inactive form, they pose no threat to the pancreas themselfs.
The body has a remarkable mechanism for signaling the acinar cells of the pancreas to begin manufacturing and secreting stored precursor enzymes.
First, the presence of the food in the mouth and in the stomach stimulate vagal nerve to release its neurotransmitter-Acetylcholine which stimulate release of pre-enzymes into the common space of cul-de-sac.
The presence of food in duodenum stimulates lining cells of duodenum to secrete the hormone Cholecystokinin into bloodstream. This hormone like vagus nerve stimulates the acinar cells to produce and release stored enzymes into duct of Wirsung and than empty pre-enzymes into the duodenum via Vater papilla.
The cells lining the small intestine produce proteolytic enzyme calle enteropeptidase, whose function is specifically to cleave off the six-amino-acid tail of trypsinogen, leaving the active and very powerful trypsin.
Trypsin activates other proteolytic enzymes making them active, to digest protein-cascade reactions.
This semiliquid food boluses that make their way from the stomach to intestine are extremely acidic, from stomach HCL.But Trypsin and Chemotrypsin can perform their digestive function only in an alkaline environment.To solve this problem, lining cells of small intestine sense the load of incoming food, they release another hormone, Secretin into the bloodstream.Secretin stimulate pancreas to produce NaHCO3, powerful antacid quickly neutralizes acid produced earlier by stomach.Now, the activated Enzymes have an ideal environment in which to begin digestive work.
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Physicians practicing Orthopaedic Medicine must be able to utilize different clinical findings for identification of the pathological processes.
Restriction of the ROM, pain, changes in the texture of the structures, autonomic manifestations ( sweating, temperature, color changes, etc) will indicate the involvement of different structures in the pathological process. All of these processes indicate disruption of Bio-tensegrity.
I will present several examples:
Sciatica.
Entrapment of the sciatic nerve may occur at various areas along its course and may be difficult to differentiate from a herniated disc.Detailed history and examination may give a clue to the source of the problem.In most cases, sciatica develops at the area of pelvic musculo-tendinous junction.
Piriformis syndrome is an example of the above.
The sciatic nerve may have a high division and may pass through the Piriformis muscle.
In such cases compression of the nerve by surrounding musculature may give rise to neuropathy.
The following muscles can contribute to the symptoms of “Sciatica”
Piriformis.
Attachments:Sacrum & greater trochanter.Function: lateral rotation.Innervation : L5-S1S2
Quadratus femoris.Attachments: Ischial tuberosity & intertrochanteric crest
Function: lateral rotation
Innervation:L4-L5-sacral plexus
Gemelli inferior.
Attachments: Ischial tuberosity &
Obturator interns tendon.Function:lateral rotation.Innervation:L4-L5
Gemelli superior.
Attachments: Ischium spine & Obturator interns tendon
Function: lateral rotation
Innervation:S1-S2-S3
Obturator internus.
Attachments: Ischiopubic ramus & Greater trochanter.Function: Lateral rotation
Inneravation: L5-S1-S2
All of the above muscles go into contractual state as the result of ligamental instability of the pelvic ligaments: the most important include: sacro-iliac , sacro-tuberous, ilio-lumbar ligaments, as well as the posterior ligamentous and tendinous structures of the hip.
Clinical symptoms of muscular involvement/ compensation will be pain, restricted mobility and external rotation of the leg.
Ligamental relaxation develop as the result of various etiologies including: trauma, overuse, metabolic /infectious processes resulting in muscle contractures. (Clinical manifestation of the ligamental laxity and examination pearls described in details in G.Hackett Prolotherapy text).
This lead to compression of the neighboring neuro-vascular structures by the muscles and tendons: initially only capillary network, leading to chronic ischemia of the corresponding nerves and later to compression of the nerves with symptoms of neuropathy.
Fascial distortion leads to fascial shifts and mechanical injury of the cutaneous nerves and neurogenic inflammation.Contractures of surrounding musculature are secondary to ligamental laxity of the joint leading to a decrease in range of motion of the corresponding joints, which are “aiding” in its stability.
The major concept of Prolotherapy and Orthopaedic medicine is stabilization of the joints via restoration of the ligaments. This will lead to restoration of muscle, blood flow, & nerve decompression thereby restoring its function.In the case of sciatica the targets of Prolotherapy will be Ilio-lumbar, sacroiliac, sacro-tuberous, sacro-ischial ligaments and posterior hip capsule.
Osteopathic manipulative therapy may facilitate normal anatomical realignment .
Peri-neural subcutaneous injection of the D5W (Neuroprolo) will help to reduce neurogenic inflammation and restore fascial distortion.Acupuncture will also assist in regulation of the viscera-somatic aspects of ligamental laxity.Similar principle will be applicable in the other anatomical areas:
Lateral elbow pain:
Laxity of the annular radial ligament and resulting increase in superior translation of the radius will lead to compensatory spasms and contractures of the proximal forearm muscle; the most important-supinator.
These will lead to compression of the posterior interosseous nerve at the Arcade of Frohse.
Thoracic outlet syndrome in some cases is a manifestation of ligamental laxity. It occurs as a result of abnormal muscle tone, postural changes, and compression of the neurovascular structures.
These examples indicates the importance of the meticulous clinical examination and imaging studies for confirmation of the possible pathological processes.
Orthopaedic medicine is a life long affair. Please, be persistent and patient.
Jon Trister MD
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