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Myofascial trigger point perpetuating factor: metabolic and endocrine inadequacies


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Virtually any condition, which results in hypertonicity, rigidity or spasm, can aggravate trigger points. Chronic or recurrent unresolved pain should always be evaluated for systemic disease or biochemical imbalance. Nutritional and toxicological factors can be preliminarily assessed from case history and interview.

However, the insidious nature of endocrine disorders serving as perpetuating factors are more allusive through their rather nondescript & diffuse symptoms and signs. Frequently, elaborate blood work is required to determine neurotransmitting chemicals and their relationship on hypersensitivity or the manufactured opioids of the body, which dampen pain receptors.

A few basic laboratory tests frequently used for differential diagnosis are referenced in this section. The physician usually orders a SMAC24, or as it’s more recently referenced, an Executive Panel, in addition to an Erythrocyte Sedimentation Rate (ESR). The Executive Panel consists of Complete Blood Count, Complete Metabolic Production, Lipid Panel and Thyroid Panel.

From this basic blood work more specialized testing may be ordered. Chemistries to assess neurotransmission are specialized and require specialty laboratories for testing. Nevertheless, we will discuss neurotransmission as it is imperative to understand their functions as it relates to pain and spasm. 



(Definitions were taken from Dorland’s and Merriam Webster Medical Dictionaries with elaboration by the authors.)


1. Acetylcholine (ACh) a neurotransmitter released at autonomic synapses and neuromuscular junctions, active in the transmission of nerve impulses and formed enzymatically in the tissue from choline. Myasthenia gravis and possibly Alzheimer’s are diseases caused by the interruption of ACh.

Myasthenia gravis is considered an autoimmune disorder and is characterized by muscle weakness especially of the eyes, neck, throat, arms and legs. In addition to an eyelid droop, there can be fatigue with speaking, usually performed with a soft voice, difficulty in swallowing with reflux, dyspnea, and difficulty in climbing stairs and repetitive movement, and possible regurgitation through the nose. Treatment is with corticosteroids to suppress the immune system or surgical removal of the thymus.

Trigger points are not normally associated with Alzheimer’s, a condition normally observed in the elderly and typified by memory loss, agitation and paranoia, the persistent anxiety and fear associated with this condition has psychological implications on the soft tissue. Utilizing manual treatment for the secondary somatic effect of this condition can be uncomfortable and potentially threatening to the individual. Therefore technique should be employed gently, slowly and with constant reassurance. Sudden movement, initiating painful stimuli or failure to repeatedly explain what you will be doing may lead to a verbal explosion or a combative situation.


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2. Catecholamines

...are any of various substances (as epinephrine, norepinephrine, and dopamine) that contain a benzene ring with two adjacent hydroxyl groups and a side chain of ethylamine and that function as hormones or neurotransmitters or both.

      - Dopamine - A monoamine that is a decarboxylated form of dopa and occurs especially as a neurotransmitter in the brain and as an intermediate in the biosynthesis of epinephrine. It is also produced peripherally and acts on peripheral receptors, as in blood vessels. Its association with the malfunction of the basal ganglia is a contributing factor to Parkinson’s disease. A mask like face, muscle rigidity, sluggish movement and foot fixation typifies Parkinsonism. This muscle rigidity obviously can produce numerous triggers secondary to this condition. Parkinson’s disease is typified by tremors, usually unilateral of the hand or arm, later becoming bilateral. As it becomes more progressive there is hyperkyphosis or stooped posture, a flat and emotionless facial expression, and a sluggish gait experiencing foot fixation, which most individuals attempt to release by turning with the occasional burst into small, rapid steps for a short distance to regain balance. Individuals frequently experience depression and a decline in hygienic maintenance. Occasionally, tremors are absent with muscle rigidity being the only initial sign of onset. While reflexes are usually normal, unless affected by tremor or rigidity, the initiating of passive extremity movement may be difficult (lead pipe). The goal is to palliatively relieve rigidity, and perform gentle ROM, and/or joint mobilization. High velocity techniques with these individuals are quite difficult to perform and can be deleterious. 

      - Norepinephrine (Noradrenaline) - A catecholamine that is the chemical means of transmission across synapses in postganglionic neurons of the sympathetic nervous system and in some parts of the central nervous system, is a vasopressor hormone of the adrenal medulla, and is a precursor of epinephrine in its major biosynthetic pathway. Norepinephrine elevates metabolic and heart rates. It also causes vasoconstriction, which increases blood pressure. When excessive, it produces sustained “fight or flight” syndrome or hypertension.  Injections of norepinephrine are frequently given when the blood pressure falls to dangerously low levels to avoid shock. Additionally syncope (fainting) can occur with physiologic orthostatic hypotension. This dysfunction is usually observed when an individual rapidly moves from recumbency (lying down) to standing or as a result of self-infliction of the Valsalva maneuver while eliminating.  In addition to using a lying to sitting and standing blood pressure check, the tilt test or as it is sometimes referred to as the tilt table test can assess this condition. Pathological orthostatic hypotension is less frequently observed but is due to adrenocortical insufficiency. In addition to syncope you will observe conditions consistent with depleted sodium (hyponatremia) and elevated potassium (hyperkalemia).  

     - Epinephrine (Adrenaline) - A catecholamine hormone secreted by the adrenal medulla and a neurotransmitter released by some neurons. It is stored in the chromaffin granules and is released in response to hypoglycemia, stress, exercise and severe emotional stimuli such as excitement.  It is a potent stimulator of the sympathetic nervous system and a powerful cardiac stimulant that accelerates the heart rate and increases cardiac output. It also promotes glycogenolysis and exerts other metabolic effects. It is also associated with “fight or flight” syndrome. By constricting the blood vessels in the skin and intestines it enhances blood supply to the muscles, thus causing a pooling of blood in the extremities and pallor of face during situations which require an immediate excitatory response. As a medication it may be used to elevate heart rate in the case of a myocardial infarction or arrhythmia, dilate bronchi in response to an allergic reaction or asthmatic attack or dilate bronchi and constrict blood vessels in response to anaphylactic shock.


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3. Endorphins

A group of neuropeptides that bind to opioid receptors in the brain and have a potent analgesic activity. It is found in the adenohypophysis, hypothalamus and other sites in the brain. One function appears to be the modulation and/or inhibiting of painful stimuli. It is similar in chemical composition to morphine therefore, received its name “endorphin” from endogenous morphine.


4. Enkephalins

Either of two pentapeptides with opiate and analgesic activity that occur naturally in the brain and have a marked affinity for opiate receptors: leucine-enkephalin and methionine-enkephalin. Both enkephalins and endorphins bind to opioid receptors; the two groups derive from functionally and anatomically distinct groups of neurons.  The enkephalins function as neurotransmitters or neuromodulators at many locations in the brain and spinal cord and play a part in pain perception and inhibition, movement, mood, behavior and neuroendocrine regulation. They are also found in nerve plexuses and exocrine glands of the gastrointestinal tract.


5. Gamma-aminobutyric Acid (GABA)

An amino acid that is a neurotransmitter that induces inhibition of neuronal synapses. The medication Baclofen has an agonistic effect with GABA thus serving as an antispasmodic agent. The reduced activity of GABA has been associated with anxiety and epilepsy.


6. Substance P

A neuro poly-peptide that is composed of 11 amino acids and is found in the hypothalamus, substantia nigra, dorsal roots of the spinal nerves, and in special endocrine cells in the gut where it increases the contractions of gastrointestinal smooth muscle and causes vasodilatation, in addition to serving as a neurotransmitter for touch, temperature and released upon the afferent transmission of pain.


7. Glutamate

A salt, ester or anionic form of glutamic acid. Four types of postsynaptic glutamate receptors have been identified: Kainate, AMPA, NMDA and Metabotropic.  Glutamate is a major excitatory transmitter in the brain and spinal cord. 


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8. Histamines

A decarboxylation product of histidine found in all body tissues. Large amounts are found in the pituitary gland, the hypothalamus and particularly in the mast cells and their related blood basophils with the highest concentration being in the lungs. Damaged cells release histamine in injured tissues increasing capillary permeability. Therefore, histamine is responsible for swelling as well as inflammation. In skeletal muscle the release of histamine around trigger points is attributed for their characteristic: increased metabolism, but decreased circulation. Soft tissue manipulation and trigger point injection flushes histamines and metabolites, referenced as noxious stimuli, into the circulatory and lymphatic systems and may result in rebound tenderness. Decreased circulation elicits ischemia and induration of skeletal muscle.

Histamine has several functions, including vassal dilation, which results in a drop of blood pressure; contraction of most smooth muscle tissue, including bronchial smooth muscle of the lung; induces gastric secretion; and acceleration of the heart rate.

It is also implicated as a mediator of the triple response and immediate hypersensitivity. The triple response is a release of histamine typified by erythema, wheals & flare. Based on current research there are two types of histamine: H1 and H2. The H1 receptor mediates the contraction of smooth muscle and the effects on capillaries; the H2 receptor mediates the acceleration of heart rate and the promotion of gastric acid secretion. Both H1 and H2 receptors mediate the contraction of vascular smooth muscle. Histamine has also been postulated to be a neurotransmitter in the central nervous system.


9. Serotonin

In humans it is synthesized in the intestinal chromaffin cells or in central or peripheral neurons and is found in high concentrations in many body tissues, including the intestinal mucosa, pineal body, and central nervous system. Produced enzymatically from tryptophan by hydroxylation and decarboxylation, serotonin has many physiologic properties. It inhibits gastric secretion, stimulates smooth muscle, serves as a central neurotransmitter and is a precursor of melatonin. Melatonin is a popular over the counter sleep aid. However, caution should be used in the recommendation of long-term usage for males. There is preliminary evidence that chronic usage may result in feminine characteristics. While those studies are far from conclusive, the studies pertaining to ecstasy (extasy) an illegal recreational substance which floods the brain with serotonin providing a euphoric state, is conclusive. Permanent irrevocable CNS damage will occur in addition to cardiovascular damage and myologic dysfunction. 



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The CBC or complete blood count consists of the Leukocytes and Erythrocytes. The Leukocytes are the white blood cells or WBC’s. Leukocytes consist of granulocytes, monocytes and lymphocytes. The Erythrocytes are the red blood cells or RBC’s.

White Blood Count (WBC): The function of Leukocytes is to fight infection. Other reasons for Leukocyte elevation or Leukocytosis may be due to stress reactions, inflammation, blood disorders, leukemia, myocardial infarction, anesthesia, burns, hemorrhage, gout, eclampsia, and menstruation.

Leukopenia or a decrease of Leukocytes may occur in a pathologic disorder of the blood (blood dyscrasias).

Viral or bacterial infections perpetuate triggers and give rise to elevated white counts as determined by a CBC. Erythrocytes Sedimentation Rate (ESR) determines inflammation. Elevation over 50mm/h suggests polymyositis, dermatomyositis or Mixed Connective Tissue Disease. Polymyalgia Rheumatica frequently exhibits a value of over 100 mm/h, and is frequently concomitant with Giant Cell Arteritis or Temporal Arteritis, which usually occurs in the population over 50 years of age. Elevated SED rates are also observed in malignancy.

With all of these conditions characteristic muscle pain, headaches, and/or proximal weakness is evident. Trigger point formation should be considered secondary to these insidious conditions. As in Vasculitis there is a hypersensitivity to touch and rebound tenderness. Similar to fibromyalgia a positive 12 of 18 tender point exam can be exhibited. Prompt medical care is needed for suspected malignancies and Temporal Arteritis, which may lead to irreversible blindness.

Elevated ESR’s are usually proportional to the activity of the disease as noted in Systemic Lupus Erythematosus (SLE). Usually observed in young women and children it in can occur in both genders and at all ages. Its initial physical symptomatology is similar to rheumatoid arthritis (RA), which also demonstrates an elevated SED rate. An elevated rheumatoid factor (RF) is not always observed with RA. However, when observed, it is considered an additional indicator of the disease. When the RF titer is extremely elevated it infers a very progressive form of RA, which could elicit nodules, Vasculitis, and pulmonary involvement.     

Hyperuricemia is demonstrated through an elevated Uric Acid Level.  This urate crystal formation is responsible for the joint deposition and peripheral joint pain associated with gout. Osteoarthritis (OA) is typified by a modeling of bone with spicule as exhibited on radiograph. This “modeling” or erosion of lumbar cervical vertebra, hips, shoulders and weight bearing long bones usually has its asymptomatic onset when an individual is in their thirties.  However, it is not uncommon for arthralgia to develop in an individual in there twenties. Rest usually reduces the pain associated with OA, while the pain associated with RA may be reduced by moderate exercise. When either RA or OA is advanced, pain is persistent with only palliative relief being possible.

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Another form of metabolic bone disease is Osteopenia, the precursor for Osteoporosis. Osteopenia is usually represented by 30% reduction or loss of bone mass. Osteoporosis, the more severe form, results in a greater reduction of bone density and usually is attributed to estrogen depletion in women or hypogonadism in men, as observed in Klinefelter’s Syndrome. While this condition is usually radiolucent, bone density studies provide far greater value as it pertains to susceptibility to fracture. This condition is usually associated with aging. However, in addition to the above-mentioned conditions, excessive alcohol consumption, endocrine disease, medications or conditions which would elicit a Vitamin D deficiency, malabsorption syndromes, as well as possible malignancy are primary disease states which could yield secondary Osteoporosis. Osteopenia is frequently asymptomatic; however, Osteoporosis frequently demonstrates diminished height, stooped shoulders, hyperkyphosis, muscle weakness and back pain, in addition to any symptoms associated with the primary disease, when Osteoporosis is secondary. In its more advanced form patient management is more difficult due to the high susceptibility to fracture. Gentle transferring of an individual from gurney to bed could cause fracture. Therefore soft tissue techniques must be performed extremely light with any form of mobilization or joint manipulation being contraindicated. Persons who seem to have the highest prevalence for Osteoporosis are:

  1. Petite Caucasian females over fifty

  2. Obese Caucasian females over fifty

  3. Petite Black females over fifty

  4. Petite Caucasian males over fifty

  5. Obese Black females over fifty

  6. Petite Black males over fifty

  7. Obese Caucasian males over fifty

  8. Obese Black males over fifty

While these rankings have been developed from bone density studies and hold poor qualitative value due to the exclusions of other ethnic groups and limited population, they do provide the manual practitioner with the ability to rapidly discern susceptibility of fracture prior to initiating technique.  Before initiating rigorous treatment protocol with individuals whom are in the top 50% of this survey, whom have had a condition or surgical procedure, which depletes estrogen for a period of more than ten years, regardless of the age, or a family history of Osteoporosis, a bone density study should be performed.

As previously mentioned, with Vitamin D deficiency Osteomalacia and Osteoporosis can coexist.  Osteomalacia, the adult form of Ricketts, is typified through the softening of bone, thinning of vertebra, narrowing of pelvis and bowing of weight bearing long bones.


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Thyroid Dysfunctions

The pituitary gland & hypothalamus controls the function of the thyroid gland. Common thyroid dysfunctions include: Hypothyroidism, hyperparathyroidism, goiters, Graves’ disease, & Hashimoto’s thyroiditis.

Uncommon dysfunctions can be caused by congenital defects, genetic disorders, infection, tumors, other autoimmune disorders, hormonal disorders, nutritional disorders, radiation, and myxedema.

Hypothyroidism occurs in approximately 1% of the population and while it usually afflicts women over the age of 60, it can occur in both genders and at all ages. When it occurs in children it can affect sexual, mental and growth development, if untreated. Additional symptoms are dependent upon deficiency of thyroid hormones. If the deficiency is slight it may be asymptomatic. If more progressive, the individual may possess a coarse voice, fatigue, lethargy, eczema, muscle weakness with periodic cramps resulting in trigger point referral, as well as bradycardia, and when severe, this results in myxedema.

Myxedema is severe hypothyroidism characterized by firm inelastic edema (represented by thickened dry skin), dryness and loss of hair, fatigue, with an increase of fluid accumulation in body cavities, muscle weakness, and retarded tendon reflex. 

Hashimoto’s Thyroiditis is an autoimmune disorder whereby the body develops antibodies towards its own thyroid gland, which results in hypothyroidism and the same symptomatic manifestations associated with that disease.

Goiter is an enlargement of the thyroid gland, which may occur from iodine deficiency leading to thyroxine insufficiency or as a result of toxicity (thyrotoxicosis), which usually is observed from the medication for hyperparathyroidism or birth control pills. Thyrotoxicosis is also observed in Graves’ disease. However, goiter may be seen in all ages or as a result of pregnancy. Frequently, goiter is idiopathic (cause unknown) with no evidence of thyroid dysfunction.

Graves Disease or Hyperthyroidism is an autoimmune disorder resulting in the overproduction of thyroid hormones. It is typified by a toxic goiter, thyrotoxicosis, bulging eyeballs (exophthalmos), and drooping eyelids, usually accompanied with appetite irregularities and weight loss.  Other systemic symptoms include tachycardia, palpitations, muscle weakness, and tremors with possible atrophy, heat intolerance, hyperactivity, insomnia, blank stare, and excessive perspiration or fever. Graves’ disease is the most common form of hyperthyroidism; however, thyroid nodules or tumors can also elicit elevated thyroid hormones.

Hyperparathyroidism is a result of the parathyroid and thyroid glands producing excessive hormones, which elevates the level of calcium in the blood (hypercalcemia). The cause is usually attributed to either enlargement of the parathyroid gland (cause unknown) or a benign tumor on the glands.  These hormones pull calcium from the bone resulting in osteoporosis or osteomalacia as well as muscle aches and pain. When the body attempts to eliminate this excess calcium from the blood, renal calculi frequently form resulting in dysfunction and possible renal failure. Serum calcium, phosphorus and hormone levels in addition to bone density studies and radiograph are needed to determine cause and extent of this disease. You will seldom see the above-mentioned symptoms to the exclusion of a host of other orthopedic, gastrointestinal, endocrine, and neuropsychological complaints.


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Adrenal Dysfunctions

As previously mentioned with the thyroid glands, the adrenal glands are also controlled by the hypothalamus and pituitary glands. The adrenal glands, also known as suprarenal glands are located directly above the kidneys. Thus, they derive their name adrenal. These triangular shaped glands consist of two major components. The cortex, which surrounds the medulla, is responsible for the production of hydrocortisone, corticosterone, and androgenic hormones, with the medulla responsible for the production of epinephrine and norepinephrine.

When the cortex is examined under microscopy three zones can be observed. The most superficial or outermost zone is responsible for the manufacture of the aldosterone hormone, which inhibits sodium excretion and regulates blood pressure and volume. The two deeper zones are responsible for the manufacture of hydrocortisone, corticosterone, and androgen hormones. Hydrocortisone controls the digestion of protein, fats and carbohydrates, and collectively with corticosterone assists in the suppression of inflammation and enhancing the immune system.  The androgen hormones are also referred to as testoids due to the fact they are the masculinizing hormone and have influence on body shape and hair.

The medulla produces epinephrine and norepinephrine, and as previously discussed are neurotransmitters which have numerous functions, the most significant being regulation of heart rate, blood volume and pressure and responsible for the “fight or flight syndrome”.

Dysfunctions of the adrenal glands may be due to pituitary dysfunction, which could cause over production of hydrocortisone (Cushing’s syndrome) or under production (adrenal failure). Tumors in the adrenal glands, which are rare, could result in excess hormone production causing Aldosteronism, masculinizing hormones in females, high blood pressure, or neuroblastoma.

Autoimmune disorders or infection may cause adrenal failure or deficiency of hormone production resulting in Addison’s disease.

Cushing’s syndrome is caused by the overproduction of hydrocortisone. Its symptoms include rounded “moon” face with a red appearance. There is obesity of the trunk with “buffalo hump”; the distal extremities and fingers are usually quite slender. Muscle atrophy and weakness are present. The skin is thin and easily bruised with poor wound healing. Purple stretch marks may appear on the abdomen, breasts and thighs. Menstrual irregularities, osteoporosis, glucose intolerance, hypertension, renal calculi, reduced resistance to infection, and psychiatric disturbances are common.

Aldosteronism or Conn’s Syndrome is caused by the overproduction of aldosterone. Symptoms are over excretion of potassium, excessive thirst, and high blood pressure, due to elevated sodium levels, muscle fatigue, weakness, and kidney dysfunction.

Pheochromocytoma is a nonmalignant tumor on the adrenal medulla causing over secretion of epinephrine and norepinephrine resulting in high blood pressure, which is the main symptom. Pressure on the tumor can cause symptoms such as headache, nausea, vomiting, rapid heart rate, hypertension, palpitations, or impending morbidity.

Neuroblastoma, usually found in children under the age of ten, is a tumor in the adrenal gland or sympathetic nervous system. They begin in the abdomen, thorax, neck, pelvis, or very rarely as a primary CNS tumor.  Due to the secretion of excessive epinephrine and norepinephrine hypertension, diarrhea, skin flushing, and fight or flight response may be present.  Symptoms vary due to the sight of tumor; however, symptoms may include paleness, general aches and pains, weight loss, and irritability. Respiratory problems may occur with thorax involvement. As the tumor metastasizes along the sympathetic nerve path, the symptoms become more extreme with bone pain, liver enlargement, anemia, petechiae, and focal neurologic deficits due to metastases of the spinal canal.

Ganglioneuroma is a benign form of neuroblastoma occurring in adults. While it does not metastasize it has pertinence to the manual medicine practitioner as it can easily be mistaken as biomechanical peripheral nerve compression. Symptomatology will vary dependent upon the ganglia, which are affected.  Thoracic and retroperitoneal involvement is difficult to assess even though they are frequently palpable when large. Occasionally a test for fremitus will reveal thoracic involvement. 

Addison’s disease was once considered fatal with its primary cause being tuberculosis. This rare disease results in the underproduction of hydrocortisone and aldosterone, and can now be treated with hormone replacement. Its usual causation is autoimmune disorder. If this is the cause it is chronic and insidious. Addisonian crises are acute and are caused by infection, injury, or stress. The most specific indication is an unusual darkening of the skin, predominantly in the creases of the palms, elbows, and plantar surface of the feet. However with the popularity of tanning beds these indications can be deceptive. Therefore for the suspicious practitioner, examine for darkening of the bucco mucosa of the mouth, especially when this discoloration is accompanied with extreme muscle weakness, hypotension, dehydration, confusion, or coma. Utilizing the pinch test for dehydration should be invoked in the physical exam sequence to avert dyer consequence.

Diabetes Insipidus, although not affecting the adrenal glands themselves, is worthy of mention in this section. It usually results from the failure of the pituitary gland to secrete antidiuretic hormones, which causes excessive amounts of water being passed by the kidneys thereby depleting the constant dilution of the blood.  Constant thirst and excessive urination are the only symptoms. The output of urine must be matched by intake of water or the signs and symptoms of dehydration will appear leading to confusion, stupor and coma. Congenital diabetes insipidus usually called nephrogenic diabetes insipidus is due to lack of the kidneys responding to normal levels of ADH and may result in pyelonephritis (kidney disease).


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Pancreatic dysfunction

The pancreas is located behind the stomach at the back of the abdomen with the head, or right-hand end lying in the loop of the duodenum while the tapered end, or tail ends near the spleen. This elongated, tapered gland consists of exocrine tissue that holds nests of endocrine cells called the islets of Langerhans. Digestive enzymes and bicarbonate are secreted by the exocrine cells and are carried into the main pancreatic duct, which connects to the common bile duct to form the ampulla of Vater chamber. This chamber opens into the duodenum where the enzymes are then activated by other enzymes, which break down fats, proteins, carbohydrates, and nucleic acids. The islets of Langerhans endocrine cells secrete insulin and glucagon hormones into the blood vessels by which they are surrounded. These hormones regulate the level of glucose in the blood.

Cancer, diabetes, cystic fibrosis, trauma, poisons, drugs, and autoimmune disorders cause the major dysfunctions of the pancreas. There is suspicion that chronic pancreatitis could be hereditary.

The most common pancreatic dysfunction is caused by Diabetes.

Diabetes Mellitus is caused by the lack of insulin produced by the pancreas. Insulin is a protein hormone that is essential for the metabolism of carbohydrates, lipids, and proteins. It regulates blood sugar levels by facilitating the uptake of glucose into tissues and promoting its conversion into glycogen, fatty acids, and triglycerides. It also reduces the release of glucose from the liver. Lack of insulin causes glucose to remain in the body in excessive amounts, which causes constant thirst, hunger, excessive urination, fatigue, and weight loss. Diabetes mellitus causes degeneration of small blood vessels and lipid metabolism disorder. In early stages the symptoms of diabetes mellitus are similar to diabetes insipidus; however, that is the only correlation. Bronze diabetes or hemochromatosis is rare and can be the precursor for diabetes mellitus

Type I diabetes mellitus (juvenile onset) results from no production of insulin by the pancreas and is the more severe type of diabetes. Type I DM usually occurs in people under the age of 35 and most commonly between the ages of 10 and 16. While inherited genes can be a factor in causing Type I diabetes mellitus, it is more commonly caused by a viral infection resulting in an immune response, which destroys the cells in the pancreas that secrete insulin. A complication of type I DM is ketosis (ketoacidosis) caused by fat being used by the body for energy instead of glucose. When the fatty acids are released into the blood, excessive amounts of ketones, such as acetone are produced. Sweet smelling breath, nausea, vomiting, loss of appetite and abdominal pain are the symptoms of ketosis and when left untreated can result in death.  Without insulin injections on a regular basis, coma, and death will occur.

Type II diabetes mellitus (mature or adult onset) is caused by the gradual onset of the pancreas not producing enough insulin and is usually only found with a physical examination. While usually occurring in people over the age of 40, they may be asymptomatic and never diagnosed with type II diabetes mellitus. Patients with type II DM may develop nonketotic coma.  However, when progressive, complications may occur of the large and small vessels as well as muscle wasting (atrophy). Large vessel involvement includes coronary artery disease (CAD) and peripheral vascular disease (PVD). Small vessel involvement includes renal disease (nephropathy), peripheral and autonomic disease or neuropathy and retinal disease (retinopathy). The onset of neuropathy is usually noticed by the loss of sensation in the hands and feet and persons state that they feel as if they are walking on cotton.  This loss of sensation effects proprioception and when severe, makes the individual oblivious to foot trauma which can either damage skin or joints (Charcot’s joints). While usually painless, Charcot’s joints can palpate similar to a bag of rocks, with the joints being freely mobile. Also in the more progressive form of this disease, cranial neuropathy can ensue. If the gene is inherited and the person is overweight, it usually is contracted. Other causes of type II diabetes mellitus are pregnancy, infections, pancreatitis, thyrotoxicosis, certain prescription medications such as corticosteroids and diuretics.

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It is possible for diabetics to lead a normal lifestyle through the regulation of diet and possibly the use of oral medication and proper foot care; however, when complications occur they can be severe. Severe complications can include minor skin breaks of the feet resulting in amputation, coronary artery disease resulting in heart attack, kidney disease resulting in renal shutdown, and retinopathy resulting in total blindness. The clinician usually receives the first indication through symptoms derived from history or interview. As this disease is insidious the individual frequently attributes their physical change to the aging process. Symptoms most frequently stated are weight loss, fatigue, weakness, polyuria, nocturia, emotional outbursts with little or no provocation, erectile dysfunction or impotency in men, recurrent vaginal itching or candida in females, cramping of calves with muscle ischemia and triggers, cold hands or feet, numbness, tingling or burning of toes, feet or hands which have a glove and stocking distribution, dizziness resulting in a staggered gait, and/or blurred vision. As vascular insufficiency is the cause for poor wound healing, decreased ability to fight off infection, visual phenomena, claudification, and hypoesthesia; the individual may seek the initial care of a manual medicine practitioner. As peripheral vascular disease and vascular thrombosis are secondary to this condition, the practitioner should avoid utilizing any manual technique, which could dislodge a clot or compromise a blood vessel. However, after a vascular work up has been performed, soft tissue manipulation can be quite beneficial in promoting vassal circulation thus offsetting the negative effects of this disease or to serve as a mechanical pump to push medications such as Topamax or Neurontin to assist in the sensory deprivation.  Due to this sensory deprivation, hot packs, heating pads, and exceedingly warm whirlpools are contraindicated as well as any manipulation around wounds or bruises.

Hypoglycemia is the abnormally low amount of glucose in the blood. While symptoms vary with the cause it usually is typified by weakness, tremor, coma, and even death. The most frequently observed causes originate from fasting, or elevated levels of insulin in the body. Skipping meals, especially breakfast, can produce hypoglycemia, which is usually mild but can be easily remedied by sugar intake. Insulin dependent diabetics must eat after taking a prescribed dosage otherwise, their glucose can drop to dangerously low levels. In addition to insulin injections resulting in elevated insulin levels and depleted blood sugar; pancreatic stimulants must also be considered when symptoms of hypoglycemia are experienced. There are numerous medications on the market that either suppress glucose production or enhance the level of insulin. Reactive hypoglycemia usually occurs as a result of the overproduction of insulin due to the rapid consumption and processing of a meal.  This usually occurs 2-4 hours following a meal and is known as a “dumping syndrome”.  It also is referenced as a post gastrectomy syndrome due to its reaction of rapid passing of food through the elementary tract with persons whom have had a hemi-gastrectomy.

Fasting hypoglycemia as previously mentioned, frequently occurs with persons whom have self-imposed starvation, such as Anorexia Nervosa. The symptoms of weakness and vertigo normally persist for over four hours after eating. However, pancreatic tumor, adrenal insufficiency, alcohol consumption, or renal failure, as well as hepatic disease and pregnancy, especially in the first trimester, may also cause these symptoms.   Drug induced hypoglycemia is frequently observed with insulin dependent type I diabetics. Occasionally, type II or non-insulin dependent diabetics experience hypoglycemia in the early onset of this disease. Symptoms of hypoglycemia include headache, veracious appetite, visual disturbances, proprioceptive dysfunction, anxiety, agitation and if untreated, delirium, coma, and death.

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Pancreatitis is the inflammation of the pancreas usually caused by gallstones or alcoholism. However, viral infections, trauma to the abdomen or injury to the biliary tract are uncommon causes. In an acute pancreatic attack symptoms include severe upper abdominal and possible back pain, nausea, vomiting, and pain from movement.  Acute pancreatitis, which can lead to chronic pancreatitis, causes disturbances of the functions of the pancreas, which usually returns to normal within a few days. However, if the gland is damaged severely it may lead to hypotension, heart and renal failure, respiratory failure, abdominal fluid accumulation (ascites), cysts or abscesses. Chronic pancreatitis is usually caused by alcoholism or hemochromatosis (Bronze Diabetes). Although symptoms are usually the same as for acute pancreatitis, the episodes last much longer and become more frequent as the condition progresses. Pain is not always a symptom; sometimes malabsorption syndrome or diabetes mellitus are the first clinical indications of chronic pancreatitis. However, it is not uncommon for trigger points to develop in the rectus abdominis or mid thoracic region secondary to this condition. Additionally, a mid thoracic peripheral nerve compression (pseudo GI syndrome) can elicit the same physical manifestations to include abdominal distention. Bile duct obstruction and aortic aneurysm must also be considered prior to initiating manual care. Chronic pancreatitis does result in permanent damage to the pancreas as well as releasing pancreatic enzymes into the blood. Complications of chronic pancreatitis are the development of ascites and cysts, Cholecystitis, diabetes mellitus, splenic thrombosis, or the antecedent manifestation of pancreatic carcinoma.

Pancreatic Cancer can be the result of chronic pancreatitis, heavy smoking, alcoholism and high amounts of fat in the diet; however the actual causes are unknown. Symptoms include boring abdomen pain that radiates to the back, indigestion, loss of appetite and weight, nausea, vomiting, diarrhea, jaundice and fatigue. However, by the time symptoms appear, the disease has usually spread to the liver, stomach, or lungs. 


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