CHAPTER 13 ENDOCRINE IMBALANCE
Chapter 13
Clinical Chiropractic: Endocrine Imbalance


From R. C. Schafer, DC, PhD, FICC's best-selling book:

Clinical Chiropractic: Upper Body Complaints

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Clinical Briefing 
  CNS Endocrine Function 
  Normal Effects 
  General Causes of Endocrine
    Imbalance 
  Basic Investigative Approach 
  Adaptation to Stress 
  Associated Complaints 
  Associated Physical Findings 
  Gonadal Dysfunction

Adrenal Dysfunction 

Diabetes Insipidus

Diabetes Mellitus

Hypoglycemia

Goiter

Hyperthyroidism

Hypothyroidism

Parathyroid Dysfunction

Anterior Pituitary Dysfunction

Ovarian Dysfunction

Testicular Dysfunction

Chapter 13: Endocrine Imbalance


     CLINICAL BRIEFING

The nervous and endocrine systems work hand in hand. The nervous system is design to operate body functions when rapid response is necessary. For long-term duty, the endocrines take over and simulate neural activity. These two systems can be compared to an athlete who sprints in a 100-yard dash and another who runs a marathon. They have two different roles but are not entirely independent in either role. They are integrated, synergistic, and facili tating.

Sympathetic stimulation increases the secretion of the adrenals, pancreas (including islets), pineal gland, and thyroid and parathyroids. The parasym pathetics generally have a reverse or unknown effect. See Table 16.18.

The highly integrated system of ductless glands in the body produces internal secretions (hormones) that discharge into circulating blood or lymph to affect remote tissues. Some of these glands also produce external secre tions. The adrenals, isles of Langerhans of the pancreas, thyroid, parathyroid, pituitary (hypophysis) ovaries, and testes are true endocrine glands. The thymus and pineal body have not been shown to produce hormones.


      CNS Endocrine Function

Research of recent years has shown that the brain and spinal cord also secrete many specific and nonspecific hormone-like substances into blood or lymph. Brain endorphins and enkephalins and spinal cord dynorphins and enkephalins are typical examples. Many other similar substances are likely to be discovered as investigation continues. The subtle functions of the nervous system are pioneer fields of study.


      Normal Effects

The endocrine system acts similar to a chemical nervous system. Like the nervous system, self-contained positive and negative feedback mechanisms (essentially hypothalamic, pituitary, or peripheral) are crucial to proper operation and integration of body functions.

Among the physiologic processes influenced by hormones are resistance to disease; rate of systemic metabolism; rate of metabolism of specific substances; rate of growth, development, and repair processes; rate of development and function of the reproductive organs, primary and secondary sexual characteristics, and degree of libido; and the secretory activity of other endocrine glands. Hormonal processes also play an important role in the development and function of the CNS, personality formation, and how the body reacts to stress. Thus, hormones may have a specific effect on a specific organ or tissue or produce a wide systemic effect on the entire body.


      General Causes of Endocrine Imbalance

Endocrine dysfunction may result from inadequate secretion or hypersecretion. Activity is under the control of the nervous system, certain circulating chemical influences, and other hormones. There is barely any pathologic process having a neurologic component that does not involve to some degree parts of the endocrine system. Because of the important role the endocrines have in maintaining homeostasis, the effects of disease, neoplasm, stress, and maladaptation can be widespread. The extent that the imbalance will have on body function depends on the severity and duration of the disturbance.


      Basic Investigative Approach

Certain initial observations in the case history are helpful in determining endocrine imbalance. The significant features of body habitus are often key factors in diagnosis. A patient's general appearance often offers an over view of endocrine function because of the role that the endocrines play in growth and maturity processes, where abnormal signs in body proportion and pattern signal a chronic dysfunction. Endocrine function also exhibits in secondary sexual characteristics, especially of the breast and external genitalia. The skin is especially a mirror of endocrine activity as seen in subcutaneous fat and body hair distribution; in skin color, pigmentation, texture, and thickness; and in hair growth and distribution on the head, face, abdomen, pubis, and extremities. In evaluation of vital signs, it must be remembered that the endocrines are important in temperature regulation, pulse rate, blood pressure, homeostasis, and energy production.


      Adaptation to Stress

An important factor finally receiving recognition in health science is the effect of stress on the body through the endocrines whether the stress originates externally or internally. The effects of excessive stress can be detec- ted in the physical examination and often in laboratory data. However, the identification of the source of stress is usually a function of the case history. It is here that contributing stress factors must be thoroughly discussed and evaluated. These stress factors, singularly or in combination, may be recent or chronic, mild or severe. The quantity and quality of stress and its duration and severity have a profound influence on adequate diagnosis, treat ment, and prognosis.

Total stress on the body is usually a combination of environmental, physical, emotional, and nutritional factors. Emotional stress may be self-imposed or conditioned such as in a self-image of low self-esteem, inferiority, inadequacy, with its unwarranted fears and guilts, and an inability to cope. Poor interpersonal relations result in chronic social stress and finally withdrawal.

Nutritional excesses or deficiencies result in stress from dietary habits. Stress symptoms commonly result from the overuse of drugs, tobacco, tea and coffee, alcohol, and carbonated beverages or other "empty calorie" foods.

Physical stress factors may be involved such as from posture strain, trauma, fatigue, and occupational or athletic strains. Environmental stress factors include water and air pollution, poor ventilation, chemicals ingested-inhaled-contacted, cold and heat exposure, and excessive noise and light expo sure. Stress maladaptation is also the effect of underuse of sleep, rest, relaxation, exercise, and water intake. Poor stress adaptation is always the result when people abuse natural laws.


      Associated Complaints

The history and physical examination offer a variety of early, subtle yet sometimes cardinal, symptoms and signs in endocrine dysfunction. For instance, a frequent complaint in Addison's disease is lightheadedness or dizziness on sudden standing from the recumbent position. Fatigue and weakness are often early symptoms of Cushing's and Addison's diseases, hyperparathyroidism, primary aldosteronism, hyper- and hypo-thyroidism, testicular disease, or pitui- tary malfunction. Hyperparathyroidism, primary aldosteronism, and diabetes (mellitus and insipidus) are associated with complaints of an excessive volume of urination. Hypoparathyroidism and primary aldosteronism often present muscle cramps and spasms. Hyperthyroidism manifests an intolerance to heat, and the late stages of hypothyroidism produce an intolerance to cold. Symptoms of headache, fatigue, lightheadedness, muscle cramps, intolerance to heat and cold, and polyuria may point to an endocrine disturbance. A frontal or bitemporal headache is often associated with a pituitary tumor.


      Associated Physical Findings

In the normal male, the shoulders are broad, the hips are narrow, the thighs usually do not touch, and the calves turn inward. In contrast, the shoulders are narrow, the hips are broad, the thighs usually touch, and the calves turn outward in normal female physique. Thus, a general evaluation of body size and proportion, body-type variations, height, weight, fat and hair distribution, relationship between the shoulder and pelvic girdles, and body contours, along with vital signs and other body habitus characteristics may be the first signs of endocrine imbalance.

Impaired peripheral vision, protruded eyes, increased perspiration, hand tremor, excess body hair, forehead hair loss, axillary and pubic hair loss, and excessive skin pigmentation may be the first signs of endocrine malfunction. Impaired peripheral vision results when the optic chiasm becomes compressed by a pituitary tumor. Excessive insulin, thyroid hormone, or epinephrine produce a hand tremor with or without a subjective sense of quivering.

Disorders of the ovary and/or adrenal cortex often produce excessive development of dark body hair. When this state becomes advanced in the female, male-pattern baldness may appear. When advanced androgenic hormone production is decreased in either sex, especially when it is associated with panhypopituitarism, a loss of axillary and pubic hair will be noted.

A frequent sign of Addison's disease is excessive darkening of the skin, and thyrotoxicosis presents a distinct protrusion of the eyes bilaterally. Perspiration is increased in situations of excess insulin, thyroid, epinephrine, or growth hormone activity, while perspiration decreases when the thyroid is subproductive.


      Gonadal Dysfunction

Aberrant sexual development syndromes and gonadal dysgenesis diseases are many and varied. The most common conditions witnessed are those of gonadal failure before and after puberty. Sexual development depends to a large degree on gonadal secretion at puberty. Before puberty, the sexual body habitus of male and female is considered neutral. Testosterone is principally responsible for the development of secondary characteristics in the male, and estrogen is responsible in the female. When these hormones are diminished in quantity or quality, secondary sexual characteristics tend toward the prepuberty neutral state. On the other hand, when these hormones are excessive to the opposite sex, feminization occurs in the male and virilization in the female.



     Adrenal Dysfunction

The adrenal (suprarenal) glands are the major targets of stress stimuli, and this affects to a great extent the body's adaptation or maladaptation to the internal and external environment and its resistance to degeneration and disease.

The medulla of the adrenals (the major adjuster to stress) is under the control of its sympathetic innervation. It synthesizes and stores three catecholamines.

(1) Norepinephrine's primary role is to constrict arterioles and venules, which increases circulatory resistance, produces hypertension, and slows the heart. It is spurred by anticipated action.

(2) Dopamine's chief function is to dilate arteries, increased heart output, and increased the flow of blood to the kidneys.

(3) Epinephrine (called adrenalin in England) constricts cutaneous and splanchnic arteries and arterioles but dilates these vessels in skeletal muscle. It also dilates the bronchi by relaxing bronchial musculature, diminishes G-I activity, increases the amount of blood fatty acid, and increases the level of blood glucose by stimulating the formation of glucose from glycogen in the liver. Extreme stress, expecially that of external stress, spurs the secretion of epinephrine and norepinephrine. The production of any these catecholamines, however, is not limited to the adrenals; they are also produced in other parts of the body.

The cortex of the adrenals is also under the control of the sympathetics. It affects all body systems by synthesizing three groups of hormones (with overlapping function) from cholesterol. Some are glucocorticosteroids that principally act in muscle, bone, G-I, hematologic, carbohydrate, and water metabolism and serve as anti-inflammatory agents. Others are mineralcorticoids that influence the metabolism of sodium and potassium. A third group, the progestins, function in reproduction physiology.


Background

Adrenal Cortex Hyperfunction.   Hyperfunction of the adrenal medulla cortex is features hypertension that is persistent or manifested in paroxysmal attacks, sweating, skin blanching, hand tremor, and dilated pupils that are associated with either tachycardia or bradycardia. The disorder may result from glucocorticoid excess (Cushing's disease), mineralocorticoid excess (primary aldosteronism), or adrenal androgen excess (adrenogenital syndrome). The clinical picture can be the result of steroid treatment or a disorder of an adrenal gland itself (eg, tumor).

Adrenal Medulla Hyperfunction.   A tumor of the adrenal medulla (pheochromocytoma) can produce a state that mimics paroxysmal hypertension, anxiety neurosis, thyrotoxicosis, or diabetes mellitus. Headaches, anorexia, constipation, epitaxis, hyperhidrosis, tremor, weakness, weight loss, pulmonary edema, palpitations, possible tachycardia, postural hypotension, and an increased BMR are commonly associated.

Adrenal Cortex Hypofunction.   Chronic hypofunction of the adrenal cortex (Addison's disease) is characterized by high levels of circulating ACTH, marked muscular weakness, atrophy, fatigue, lassitude, anorexia and weight loss, salt craving, low systolic blood pressure (eg, under 100), narrow pulse pressure, orthostatic hypotension, and tachycardia. A brownish or blue-gray pigmentation of skin creases and mucous membranes that is accentuated in distal areas of the extremities and at pressure points. When severe, areas of vitiligo, decreased axillary and pubic hair, nausea and vomiting, diarrhea, dizziness, dehydration, hypothermia, prostration, and shock manifest in an alarming picture.

Flu-Related Hypoadrenia.   Hypoadrenia often follows influenza. The symptoms are essentially myasthenic in character, with severe fatigue being the principal element. This asthenia extends to the involuntary muscles to cause heart muscle weakness that is often mistakenly attributed to myocarditis even if there is no structural change in the heart muscle. Vessel walls also lose their tonicity, and low blood pressure follows with evidence of circulatory insufficiency. Actually, any stress-producing situation can produce this syndrome; eg, pregnancy, divorce, lost job, etc.

Postural Blood Pressure Method of Evaluating Adrenal Hypofunction.   This screening test for hypoadrenia measures the body's ability to compensate for the hydrostatic effects of gravity. To understand the significance of this test, remember that the splanchnic veins are without valves and depend on nerve function for their tone. As the tone of the splanchnic nerves is under the primary control of the adrenal system, weak splanchnic veins signify weak splanchnic nerve function and thus weak adrenals. In the healthy person, systolic blood pressure is about 5 to 10 mm higher in the standing position than it is in the recumbent. If, however, blood pressure is lower in the standing position, hypoadrenia can be suspected. Drops of as much as 78 mm have been witnessed, and the degree of drop appears to be directly related to the degree of hypoadrenia present. The test is simply made by recording the systolic pressure in the recumbent and standing positions and then comparing the differences to denote the degree of suggested adrenal hypofunction.

The following protocols have been design primarily for mildmoderate adrenal cortex hypofunction.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood sugar              Plasma renin              Urinalysis
    BMR                      Sedimentation rate        Urine aldosterone
    BUN                      Serum alkaline phospha-   Urine calcium
    CBC and differential      tase                     Urine creatine
    Chest x-ray              Serum bicarbonate         Urine estrogen
    Glucose tolerance test   Serum chloride            Urine hydrocortico-
    Plasma ACTH              Serum gamma globulins      steroids
    Plasma aldosterone       Serum potassium           Urine potassium
    Plasma cortisol          Serum sodium              Urine proteins
    Plasma deoxycortico-     Spinal roentgenography    Urine sodium
     sterone                 Temperature chart         Urine sugar

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check upper-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C1, T12, SI. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments T11L1 for 12 minutes (Table 16.20).


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints GV-10, GV-11, GV-19, CV-15, LI-20, ST-36 (Table 16.21).

  • Treat auriculopoints 13, 22, 51, 55 (Figs 16.3 4).

  • Treat hand points LI-4, SI-3 (Fig. 16.5).

  • If the Valleix adrenal reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the ileo- psoas, latissimus dorsi, lower thoracic multifidi muscles, groin and calf muscles (Tables 16.28-31).

  • If Chapman's adrenal points are tender, deeply massage each to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 13.1.


      Nutritional Therapy

Supplemental adrenal and thyroid extract and ginseng are recommended. The patient should be advised to restrict alcohol, coffee, regular tea, and any other type of diuretic.

Monitor urine sodium and potassium at least weekly. Simple in-office tests are available for this. An important objective during treatment is to obtain an optimal balance of tissue sodium and potassium and to minimize sodium and potassium loss in the urine. Results should be charted.


      Elective Procedures

Other helpful forms of treatment include spinal ultrasound (Table 16.37), vinegar baths (Table 16.46), and suprarenal interferential therapy (Tables 16.39 41) or shortwave diathermy (Table 16.36). Check for a dropped kidney and spasms, adhesions, or taut fascia that might be interfering with the function of the adrenals. In situations of adrenal insufficiency, the patient must avoid exposure to ultraviolet radiation.




     Diabetes Insipidus

In contrast to diabetes mellitus, typically an effect of hypoinsulin secretion in the islands of Langerhans of the pancreas, diabetes insipidus is usually the effect of posterior pituitary hypofunction; ie, a defect of the neurohypophysial system for producing the antidiuretic hormone will produce diabetes insipidus.

Background

The cause may be congenital or acquired via basilar trauma, vascular lesions (autonomic vasospasm), acute or chronic infections, neoplasms, and cysts. Sometimes leukemia, amyloidosis, sarcoidosis, or eosinophilic granulomatosis are involved. However, diabetes insipidus can also be caused by a congenital predisposition or acquired failure of the renal tubules to reabsorb water.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood sugar              Plasma insulin  concen-   Serum chloride
    BMR                       tration                  Serum sodium
    CBC and differential     Renal function tests      Serum growth hormone
    Chest x-ray              Sedimentation rate        Skull x-ray
    Fluid input and out-     Serum alkaline phospha-   Spinal roentgenography
     put monitoring           tase                     Urinalysis
    Glucose tolerance test   Serum calcium             Urine sodium

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check upper-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C1, T11L1. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments T10L2 for 12 minutes (Table 16.20).


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints CV-4, CV-6, SP-6, UB-23, KI-7 (Table 16.21).

  • Treat auriculopoints 28, 55, 95, 99; Left 96 and 98 (Figs 16.3 4).

  • Treat hand points LI-4, HT-7 (Fig. 16.5).

  • If the Valleix pituitary or kidney reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the sternocleidomastoideus, latissimus dorsi, and lower thoracic multifidi muscles (Tables 16.28-31).

  • If Chapman's brain fatigue or kidney points are tender, deeply massage each to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 13.2.


      Nutritional Therapy

Supplemental pituitary and adrenal extract are recommended. Advise the patient to restrict diuretic-acting foods and beverages.


      Elective Procedures

Other helpful forms of treatment include upper thoracic ultrasound (Table 16.37) and mild interferential therapy (Tables 16.39 41) or shortwave diathermy (Table 16.36) to the kidney area. Check for muscle spasms, arteriosclerosis, adhesions, or taut fascia that might interfere with the function of the basilar circulation and the kidneys.



     Diabetes Mellitus

Subnormal insulin production (diabetes mellitus) eventually leads to hyperglycemia, ketoacidosis, and metabolic disorders manifesting early as polyuria, nocturia, glycosuria, polyphagia, polydipsia, involuntary weight loss, mild tachycardia, intolerance to cold, and sweetness of breath.

Background

The hyperglycemic state expresses as nervousness, fatigue, headache, hyperhidrosis, scrotal or perianal pruritus, boils or rashes, tremor, faintness, diplopia, scotomata, pallor, and irrational behavior. Later, metabolic disorders manifest as weakness and malaise, deep respirations, paresthesia, cramps, intermittent claudication, nausea and vomiting, abdominal and/or chest pain, flank pain, diarrhea, dyspnea, tongue atrophy, dry mucous membranes, vaginal discharge, hypotension, diminished tendon reflexes, progressing tachycardia, softening of the eyeballs, extraocular palsy, cataracts, glaucoma, impotency, pedal ischemia, psychoneurosis, and drowsiness leading to stupor and coma. In the chronic stages, effects on nervous and vascular tissues become pronounced.

The following protocols have been designed for early diabetes mellitus or those cases well controlled by insulin therapy.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood glucose          Glucose tolerance  test  Serum alkaline phospha-
    Blood pH               Plasma acetone            tase
    BMR                    Plasma insulin concen-   Serum electrolytes
    CBC and differential    tration                 Spinal roentgenography
    Chest x-ray            Renal function tests     Urinalysis
    Fluid input and out-   Sedimentation rate
     put monitoring

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check upper-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C1, T7T8. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments T6T8 for 12 minutes (Table 16.20).


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints SP-6, ST-36, PC-6, CV-6, UB-17 (Table 16.21).

  • Treat auriculopoints 22, 76, 77, 96 (Figs 16.3 4).

  • Treat hand points LI-4, SI-3 (Fig. 16.5).

  • If the Valleix pancreas reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the abdominis rectus muscles (Tables 16.28-31).

  • If Chapman's pancreas point is tender, deeply massage to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 13.3. Advise the patient against any activity that might present a danger to himself or others. Urine sugar must be monitored at least once daily. A cooperative arrangement with the patient's family doctor would be ideal so that insulin intake can be gradually reduced.


      Nutritional Therapy

Prescribe a high-protein low-carbohydrate diet. Supplemental pancreas extract or nutrients A, C, B-complex, E, niacin, chromium, manganese, pangamic acid, potassium, and zinc are recommended. Counsel the patient to avoid appropriate antivitamin and antimineral factors (Tables 16.56 and 16.58). Onions and garlic should be eaten frequently; white sugar and white flour should be avoided.


      Elective Procedures

Other helpful forms of treatment include spinal ultrasound (Table 16.37), interferential therapy (Tables 16.39 41) or shortwave diathermy (Table 16.36) to the pancreas area, and local vibration-percussion (Tables 16.19 20). Check for spasms, adhesions, or taut fascia that might be interfering with the function of the pancreas. In conjunction with spinal adjustments and niacin, lumbar interferential therapy will do much to halt and often reverse associated advanced peripheral vascular disease in the lower extremities.



     Hypoglycemia

Insulin and glucagon secretions from the islets have various metabolic effects. Abnormal insulin production is characterized by hypoglycemia and the release of catecholamines that produce hunger, anxiety, tachycardia, dilated pupils, and profuse sweating in the early stages. In late stages, nervous symptoms appear such as severe headache, double vision, disorientation, obtundation, paralysis, convulsions, and possibly coma.

Hypoglycemia, hyperinsulinism, and hypoadrenia are frequently linked in the presenting syndrome. Isolated endocrine dysfunction is not typical.


      Diagnostic Workup

Conduct a complete physical examination, including a thorough analysis of heart sounds, and consider the following workups according to clinical judgment:

    Blood glucose          Glucose tolerance test   Serum alkaline phospha-
    Blood pH               Plasma acetone            tase
    BMR                    Plasma insulin concen-   Serum electrolytes
    CBC and differential    tration                 Spinal roentgenography
    Chest x-ray            Renal function tests     Urinalysis
    Fluid input and out-   Sedimentation rate
     put monitoring

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check upper-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C1, T7T8. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments T6T8 for 12 minutes (Table 16.20).


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints SP-6, ST-36, CV-12, UB-17 (Table 16.21).

  • Treat auriculopoints 18, 22, 55, 96 (Figs 16.3 4).

  • Treat hand points LI-4, SI-3 (Fig. 16.5).

  • If the Valleix pancreas reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the abdominis rectus muscles (Tables 16.28-31).

  • If Chapman's pancreas point is tender, deeply massage to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 13.4.


      Nutritional Therapy

Prescribe a high-protein low-carbohydrate diet. Supplemental pancreas and adrenal extract or nutrients A, C, B-complex, E, niacin, chromium, manganese, pangamic acid, potassium, and zinc are recommended. Counsel the patient to avoid appropriate antivitamin and antimineral factors (Tables 16.56 and 16.58). White sugar and white flour should be avoided. The patient should be advised to eat light main meals with a protein-rich snack between meals.


      Elective Procedures

Other helpful forms of treatment include spinal ultrasound (Table 16.37), interferential therapy (Tables 16.39 41) or shortwave diathermy (Table 16.36) to the pancreas area, and local vibration-percussion (Tables 16.19 20). Check for spasms, adhesions, or taut fascia that might be interfering with the function of the pancreas.



     Goiter

The term goiter in its broad sense means an enlargement of the thyroid gland for whatever reason. Fortunately, most goiters occur in the absence of thyrotoxicosis or cancer. They are called simple or nontoxic goiters.

The cause of goiter may be due to hyperthyroidism or hypothyroidism. Common direct causes of goiters generally include endemic iodine deficiency, follicular hypertrophy, thyroiditis, cyst formation, encapsulated adenomata, and thyroid tumor.

Background

Palpation of a goiterous thyroid will reveal enlargement. One or masses (cysts or tumors) or firm nodes may be felt, and pulsations are sometimes sensed.

Early differentiation between a toxic and nontoxic goiter is important. Thyrotoxicosis, sometimes called thyroid "storm" or thyroid crisis when severe, resembles the normal state following severe prolonged physical exertion such as after a fast long run. The skin is hot, flushed, and sweaty. There are obvious signs of tension, weakness, and fatigue. The respiratory rate is rapid, the pulse is fast and bounding, and the eyes appear to bulge. The chronic signs include nervousness, irritability, hyperkinesia, mild fever, fine tremors, and polyphagia with weight loss. Diarrhea is common. There are a diminished tolerance to warm temperatures, proximal muscle weakness, and possible signs of osteoporosis or myasthenia gravis. The syndrome is commonly related to either toxic nodular goiter or Graves' disease:

Thyrotoxicosis is commonly related to toxic nodular goiter and Graves' disease:

(1) Besides thyrotoxicosis, the only other major physical signs in toxic nodular goiter are a lumpy thyroid on palpation and a moderate exophthalmos.

(2) In Graves' disease, signs besides thyrotoxicosis include distinct exophthalmos, a diffusely enlarged thyroid gland, possible infiltration under the skin of the shins, finger clubbing, and a systolic bruit may be heard over the thyroid.

The protocols described below have been designed for the treatment of non-toxic and noncancerous goiter.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood sugar              Sedimentation rate        Serum thyroxine
    BMR                      Serum alkaline phospha-   Serum total lipids
    CBC and differential      tase                     Spinal roentgenography
    Chest x-ray              Serum calcium             Temperature chart
    Fluid input and out-     Serum carotene            Urinalysis
     put monitoring          Serum cholesterol         Urine ketosteroids
    Glucose tolerance test   Serum electrolytes        Urine sugar

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check upper-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C2C4, T1. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments C7T4 for 12 minutes (Table 16.20).


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints LI-11, LU-7, SP-3, SP-6 (Table 16.21).

  • Treat auriculopoints 17, 22, 45, 55 (Figs 16.3 4).

  • Treat hand points LI-4, SI-3 (Figs 16.3 4). (Fig. 16.5).

  • If the Valleix thyroid reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the sterno- cleidomastoideus, digastric, and pterygoid muscles (Tables 16.28-31).

  • If Chapman's thyroid point is tender, deeply massage to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 13.5.


      Nutritional Therapy

Supplemental thyroid and parotid extract and iodine are recommended. Counsel the patient to avoid appropriate antimineral factors (Tables 16.58).


      Elective Procedures

Other helpful forms of treatment include upper-thoracic ultrasound (Table 16.37) or interferential therapy (Tables 16.39 41). Check for spasms, adhesions, or taut fascia that might be interfering with the function of the thyroid. It is common to find taut fascia or binding adhesions between the anterior border of the sternocleidomastoideus and the thyroid.



     Hyperthyroidism

Iodine deficiency, neoplastic disease, and inflammatory disease may produce a thyroid gland that is diffusely swollen, nodular, and sometimes cystic. There are three major inflammatory diseases of the thyroid gland: Hashimoto's disease (autoimmune thyroiditis), De Quervain's disease (subacute thyroiditis), and Riedel's disease (woody thyroiditis). Thyrotoxicosis, however, may be evident when enlargement is not palpable.

Background

A hum, systolic bruit, or thrill will often be noted because of the increased blood flow. The associated hypermetabolism produces weight loss and deficient subcutaneous fat, nervousness and hand tremor, exaggerated tendon reflexes, protruding eyes, high and bounding pulse rate, elevated systolic pressure, hyperactive heart sounds, and a skin that is warm, moist, and smooth.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood sugar              Sedimentation rate        Serum thyroxine
    BMR                      Serum alkaline phospha-   Serum total lipids
    CBC and differential      tase                     Spinal roentgenography
    Chest x-ray              Serum calcium             Temperature chart
    Fluid input and out-     Serum carotene            Urinalysis
     put monitoring          Serum cholesterol         Urine ketosteroids
    Glucose tolerance test   Serum electrolytes        Urine sugar

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check upper-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Importance of a Temperature Chart

The thyroid sets the thermostat of the body's energy production. Thus, body temperature is the simplest indicator of thyroid function. A patient with a thyroid disorder of any nature should be instructed to maintain a temperature chart showing temperature on arising in the morning, noon, 6 pm, and just before sleep. This is useless, however, unless the patient is carefully instructed in how and when to take an oral or axillary temperature. Females should note the first and last day of their menstrual period on the chart.



      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C2C4, T1. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep high-velocity percussion spondylotherapy over segments C7T4 for 34 minutes (Table 16.20).


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints UB-11, SP-3, SP-6, CV-15, GV-19, LI-20 (Table 16.21).

  • Treat auriculopoints 22, 28, 45, 55 (Figs 16.3 4).

  • Treat hand points LI-4, SI-3 (Figs 16.3 4). (Fig. 16.5).

  • If the Valleix thyroid reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the teres minor, sternocleidomastoideus, digastric, and pterygoid muscles (Tables 16.28-31).

  • If Chapman's thyroid point is tender, deeply massage to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 13.6.


      Nutritional Therapy

Supplemental thyroid, thymus, and pituitary extract or B6, PABA, iodine, niacin, and potassium are recommended. Counsel the patient to avoid appropriate antimineral factors (Tables 16.58).


      Elective Procedures

Other helpful forms of treatment include upper-thoracic ultrasound (Table 16.37) or interferential therapy (Tables 16.39 41). Check for spasms, adhesions, or taut fascia that might be interfering with the function of the thyroid.



     Hypothyroidism

Thyroid deficiency during infancy causes cretinism, characterized by its distinctive facial expression, mental and physical retardation, and hoarse cry. In the child, dwarfism may result from hypothyroidism that features childish proportions. In the adult or child, prolonged severe hypothyroidism results in myxedema, characterized by a puffy face and eyelids, a boggy non-pitting edema in the hands and feet, thick tongue and lips, slowed speech, and deepened voice. The skin is thick, dry, cool, and has a rough texture. The hair is dry, coarse, brittle, and thinning on the scalp and eyebrows. Speech, thought, and actions are slow. Other signs include anorexia, subnormal temperature, diminished tolerance to cold, slow pulse rate, possible angina and/or palpitations, normal to slightly high blood pressure, soft and muffled heart sounds, hypoactive tendon reflexes that are slow to recover, menorrhagia, anemia, increased cholesterol levels, a flattened glucose tolerance curve, low ECG voltage, and late dementia.

Common Subclinical Forms

Most cases of hypothyroidism will not show such overt signs. Subclinical hypothyroidism is far more common than generally suspected. The first signs will be cool hands, a slightly subnormal body temperature, teres minor weakness, frequent colds, constipation, abnormal hair loss (as observed in the hairbrush), memory deficits, an odd taste in the mouth, unusual procrastination to duties, easily provoked to crying, and self-isolation from social events and crowds. A "what's the use, to hell with it all" attitude is common.

The general apathy and forgetfulness so often seen with the hypothyroid patient can easily be confused with early senile dementia in the elderly or depression in younger patients.

Normal temperature variances are in the 97.8F98.2F range. Mild hypo-thyroid patients will show daily temperatures varying between 97F and 97.6F; severe hypothyroidism, 95.8F to 96.6F.


Hypothyroidism vs Hyperthyroidism

Symptoms of lassitude, weakness, constipation, menorrhagia, or weight gain point toward hypothyroidism. As advanced thyroid diseases cause profound metabolic effects, symptoms of diarrhea, weight loss, oligomenorrhea, fatigue, or tremor are suspicious of hyperthyroidism. The hyperthyroid patient tends to be heat tolerant; the hypothyroid patient, cold tolerant. In shaking hands, the hyperthyroid patient will present a hand that is warm and moist; the hypothyroid patient, one that is cool and dry. The hypothyroid patient may be overly dressed on a warm day; the hyperthyroid patient may wear a light jacket on a cold winter day. Obese female patients who do not have a demonstrable thyroid condition may have a low tolerance to heat. Hypothyroidism is often secondary to pituitary or hypothalamic disease and other glandular diseases. Prior thyroid treatment and surgery should be carefully evaluated.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood sugar              Sedimentation rate        Serum thyroxine
    BMR                      Serum alkaline phospha-   Serum total lipids
    CBC and differential      tase                     Spinal roentgenography
    Chest x-ray              Serum calcium             Temperature chart
    Fluid input and out-     Serum carotene            Urinalysis
     put monitoring          Serum cholesterol         Urine ketosteroids
    Glucose tolerance test   Serum electrolytes        Urine sugar

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check upper-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C2C4, T1. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments C7T4 for 12 minutes (Table 16.20).


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints LI-20, ST-10, GV-16 (Table 16.21).

  • Treat auriculopoints 22, 28, 45, 55 (Figs 16.3 4).

  • Treat hand points LI-4, SI-3 (Figs 16.3 4). (Fig. 16.5).

  • If the Valleix thyroid reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the sterno- cleidomastoideus, teres minor, pectoralis major, sternalis, digastric, and pterygoid muscles (Tables 16.28-31).

  • If Chapman's thyroid point is tender, deeply massage to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 13.7.


      Nutritional Therapy

Supplemental thyroid, parotid, adrenal, and pituitary extract or amino acids, potassium, niacin, pangamic acid, and iodine are recommended. Counsel the patient to avoid appropriate antivitamin and antimineral factors (Tables 16.56 and 16.58).


      Elective Procedures

Other helpful forms of treatment include upper-thoracic ultrasound (Table 16.37) or interferential therapy (Tables 16.39 41). Check for spasms, adhe sions, or taut fascia that might be interfering with the function of the thyroid.



     Parathyroid Dysfunction


Hyperparathyroidism has hypercalcemic, normocalcemic, and hypocalcemic forms. Hypercalcemia is associated with renal disease, kidney stones, peptic ulcers, and emotional disturbances. Normocalcemic hyperparathyroidism is seen with renal disease, kidney stones, pregnancy, and rickets or osteomalacia. Renal disease and pseudohypoparathyroidism can produce hypocalcemic states. Typical hyperparathyroidism features the manifestations of hypercalcemia and accompanying bone disease such as muscular hypotonia, general weakness, disorientation, obtundation, a faint corneal band of calcium deposits, eyelid conjunctival calcium flecks, eardrum calcification, height loss from vertebral collapse, long bone fractures from demineralization, and sometimes palpable bone tumors and cysts in the jaw and at the ends of long bones. Constipation and fatigue are commonly associated, and polyuria and secondary polydipsia are almost always associated because the hypercalcemia creates a loss of renal concentrating ability. A patient will become insidiously disabled from the hypercalcemia associated with a parathyroid tumor.

Hypoparathyroidism features hypocalcemic manifesta tions such as carpopedal spasm, as elicited by Trousseau's sign, and other overt signs of tetany. A positive Chvostek's sign (elicited in 10% of normal people) may manifest. Other characteristics of chronic hypoparathyroidism are cataracts, papilledema, defective teeth enamel, brittle nails, thin and patchy body hair, and a dry scaly skin.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood sugar                Hemoglobin level       Serum growth hormone
    BMR                        Kidney x-ray           Serum phosphorus
    Bone-age roentgenography   Sedimentation rate     Serum uric acid
    CBC and differential       Serum alkaline phos-   Skull x-ray
    Chest x-ray                 phatase               Spinal roentgenography
    Fluid input and out-       Serum calcium          Urinalysis
     put monitoring            Serum electrolytes     Urine calcium
    Glucose tolerance test     Serum globulins        Urine phosphorus

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check upper-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and per form tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C2C4, T1. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments C7T4 for 12 minutes (Table 16.20).


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints SP-6, ST-36, LV-3, UB-11, KI-27 (Table 16.21).

  • Treat auriculopoints 22, 45, 51, 55 (Figs 16.3 4).

  • Treat hand points LI-4, SI-3 (Figs 16.3 4). (Fig. 16.5).

  • If the Valleix thyroid or cervical spine reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the sternocleidomastoideus, digastric, and pterygoid muscles (Tables 16.28-31).

  • If Chapman's thyroid point is tender, deeply massage to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 13.8.


      Nutritional Therapy

Supplemental C, D, calcium, niacin, pangamic acid, magnesium, and potassium are recommended. Counsel the patient to avoid appropriate antivitamin and antimineral factors (Tables 16.56 and 16.58).


      Elective Procedures

Other helpful forms of treatment include upper-thoracic ultrasound (Table 16.37) or interferential therapy (Tables 16.39 41). Check for spasms, adhesions, or taut fascia that might be interfering with the function of the parathyroids.



     Anterior Pituitary Dysfunction


Anterior Pituitary Hyperfunction.   Situations involving overt malfunction of the anterior pituitary are rarely seen in the chiropractic office, yet signs of possible giantism, acromegaly, dwarfism, and hypopituitarism may be found in screening procedures. Growth is increased with normal body proportions in giantism and acromegaly. In common giantism, a pituitary adenoma is usually the cause of the excessive production of growth hormone before the epiphyses are closed. A pituitary adenoma is also often at the root of acromegaly, which is characterized by overgrowth of bone, cartilage, and soft tissues. Early signs and symptoms include excessive sweating; the soft tissues of the hands are warm, moist, and spongy; the forehead and facial bones become prominent; the nose becomes broad and enlarged, and the nasolabial folds are accentuated.

Anterior Pituitary Hypofunction.   Nongenetic dwarfism such as that from a pituitary hypofunction is rare. It is characterized by normal body proportions, childish features, subnormal sexual development, and deficient function of other endocrines. Adult hypopituitarism is also associated with a wide-spread hypoendocrine decrease such as moderate myxedema, hair loss, postural hypotension, weight loss, emaciation, asthenia, pallor, a dry smooth skin, and skin depigmentation associated with a difficulty to suntan.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood sugar                Glucose tolerance test   Serum phosphorus
    BMR                        Sedimentation rate       Skull x-ray
    Bone-age roentgenography   Serum ACTH               Spinal roentgenography
    CBC and differential       Serum alkaline phos-     Urinalysis
    Chest x-ray                 phatase                 Urine gonadotrophins
    Fluid input and out-       Serum electrolytes
     put monitoring            Serum growth hormone

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check upper-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal major will likely be found at C1. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments T1T4 for 12 minutes (Table 16.20).

      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoint LI-20, PC-6, LV-3 (Table 16.21).

  • Treat auriculopoints 22, 25, 28, 55 (Figs 16.3 4).

  • Treat hand points LI-4, HT-7, PC-10 (Fig. 16.5).

  • If the Valleix pituitary reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the sterno- cleidomastoideus muscles (Tables 16.28-31).

  • If Chapman's brain fatigue points are tender, deeply massage each to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 13.9.


      Nutritional Therapy

Supplemental pituitary and adrenal extract and nutrients niacin and panga mic acid are recommended. Counsel the patient to avoid appropriate antivitamin and antimineral factors (Tables 16.56 and 16.58).


      Elective Procedures

Other helpful forms of treatment include spinal ultrasound (Table 16.37), and upper thoracic interferential therapy (Tables 16.39 41) or shortwave diathermy (Table 16.36). Check for cervical spasms, arteriosclerosis, adhe sions, or taut fascia that might be interfering with basilar circulation.



     Ovarian Dysfunction

It is sometimes difficult to differentiate between ovarian dysfunction and adrenal dysfunction in the adolescent female. Androgen effects can be noted by the development of external vaginal tissues, pubic and axillary hair, and acne. Estrogen effects contribute to the development of female breast tissues, internal vaginal tissues, and the uterus and ovaries. Poor development of these structures suggests subnormal production of the respective hormones, while early development indicates premature hormonal production. Early or late hormonal production, or abnormalities in quantity or quality, affects both sexual development and stature (epiphyseal influence).

Background

Delayed Puberty in the Female.   Retarded menstruation, pubic and axillary hair growth, breast development, nipple pigmentation, genital growth, and thickening of the vaginal epithelium usually have adrenal, physiologic, or familial etiologies, especially in the presence of obesity. Chronic infections, thyroid disorders, renal failure, and diabetes mellitus may be contri buting factors. In true ovarian failure (eg, tumor, cyst, trauma, congenital absence), delayed epiphyseal fusion will lead to overgrowth of the long bones.

Virilization.   In virilization (female body habitus tending toward the male), the patient expresses many male secondary sexual characteristics such as a receding hairline on the scalp, a deepening of the voice, and axillary hair growth on the face, abdomen, chest, and back. The frontal recession of hereditary male pattern baldness, influenced by testosterone, helps to distinguish virilization in the female from hirsutism or from the unusual pattern of alopecia secondary to toxic or drug effects upon hair follicles. The cause may be either ovarian or adrenal in origin.

Skin texture in virilization becomes coarse and waxy, and acne is usually present. Strength and muscle development increases, especially in the shoulder girdle. Hip fat deposition decreases. Pubic hair increases and usually extends up the abdomen and sometimes into the chest. There is little change in breast size, but areolae tend to flatten. The clitoris becomes enlarged and unusually erectile. Vulva atrophy may be noted.

The following protocols are designed for ovarian dysfunction. Adrenal dysfunction is described in a separate section.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood sugar              Plasma androsterone      Skull x-ray
    BMR                      Plasma cortisol          Spinal roentgenography
    CBC and differential     Plasma estrogen          Urinalysis
    Chest x-ray              Plasma gonadotrophins    Urine gonadotropins
    Fluid input and out-     Plasma testosterone      Urine estrogen
     put monitoring          Sedimentation rate       Urine ketosteroids
    Glucose tolerance test   Serum electrolytes
    Pap smear                Serum growth hormones

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check lower-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C1, T11T12. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments T10L1 for 12 minutes (Table 16.20). It should be noted that low levels of estrogen (such as seen in early menopause) are closely linked to hypoadrenia.


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints SP-6, CV-6, ST-36 (Table 16.21).

  • Treat auriculopoints 22, 55, 58 (Figs 16.3 4).

  • Treat hand points LI-4, HT-7, SI-3 (Fig. 16.5).

  • If the Valleix pelvic organs reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the lower abdominis rectus, lower thoracic multifidi, piriformis, and gluteii muscles (Tables 16.28-31).

  • If Chapman's uterus point is tender, deeply massage to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 12.10.


      Nutritional Therapy

Supplemental ovary and adrenal extract or nutrients B6, E, niacin, pangamic acid, and iodine are recommended. Counsel the patient to avoid appropriate antivitamin and antimineral factors (Tables 16.56 and 16.58).


      Elective Procedures

Other helpful forms of treatment include spinal ultrasound (Table 16.37), and thoracolumbar junction interferential therapy (Tables 16.39 41) or short wave diathermy (Table 16.36). Check for spasms, adhesions, or taut fascia that might be interfering with the function of the ovaries. These are common especially if pelvic or abdominal surgery has been performed.



     Testicular Dysfunction

It is often difficult to differentiate between testicular dysfunction and adrenal dysfunction in the adolescent male. Androgen effects can be noted in the development of the penis and testes, wrinkling of the scrotum, pubic and axillary hair, prostate development, and voice depth, along with seborrhea and acne development.

Background

Delayed Puberty in the Male.   A delay in the development of pubic and axillary hair, facial hair, testicular development, scrotal darkening with folds, genital growth, and deepening of the voice usually have familial adrenal or gonadal (rare) etiologies. Secondary endocrine manifestations and debilitating illnesses can also delay puberty in the male.

Feminization.   If feminization occurs (male body habitus tending toward the female), scalp hair is fine with no recession at the hair line, and facial hair is scanty, requiring infrequent shaving. The voice is high pitched. Strength and muscles are poorly developed, especially in the shoulder girdle. Chest, pubic, and extremity hair is scanty. The skin has a fine texture, and there is little or no acne. Fat deposition around the hips plus narrow shoulders contribute to the classic female appearance. Excessive development of the male mammary glands (gynecomastia) is noted, even to the functional state in some cases. If feminization occurs after puberty, most of the signs described will be absent or greatly minimized. There may be some reduction in shaving and some excessive hip fat deposition. The only clinical finding may be gynecomastia.

The following protocols are designed for testicular dysfunction. Adrenal dysfunction is described in a separate section.


      Diagnostic Workup

Conduct a thorough physical examination and consider the following workups according to clinical judgment:

    Blood sugar                Sedimentation  rate      Spinal roentgenog-
    BMR                        Semen analysis            raphy
    Bone-age roentgenography   Serum alpha-fetoprotein  Urinalysis
    CBC and differential       Serum electrolytes       Urine gonadotropins
    Chest x-ray                Serum growth hormone     Urine ketosteroids
    Plasma testosterone        Skull x-ray

Motion palpate the spine, and relate findings with the patient's complaints. Confirm findings with appropriate orthopedic and neurologic tests (Table 16.16; Fig. 16.1). Check pertinent tendon and superficial reflexes (Tables 16.2), and grade the reaction (Table 16.3). Check lower-extremity joint motion and muscle strength against resistance, and grade resistance strength (Table 16.9). Interpret resisted motion signs (Table 16.6), and perform tests for autonomic imbalance (Table 16.7).


      Eclectic Diagnostic Aids

Check alarm points (Table 16.15), visceral Valleix areas of the foot (Fig. 16.2), Chapman's points (Fig. 16.6), and potential contributing trigger points (Tables 16.28 16.31).


      Articular Adjustment

Spinal majors will likely be found at C1, T11T12. After relaxing the tissues and adjusting the subluxated/fixated segments, apply deep low-velocity percussion spondylotherapy over segments T10L1 for 12 minutes (Table 16.20).


      Adjunctive Therapy

To restore further neurologic homeostasis and enhance healing:

  • Treat acupoints CV-6, SP-6, ST-36 (Table 16.21).

  • Treat auriculopoints 22, 55, 58 (Figs 16.3 4).

  • Treat hand points LI-4, HT-7, SI-3 (Fig. 16.5).

  • If the Valleix pelvic organs reflex areas in the feet are tender, massage each to patient's tolerance for 20 seconds (Fig. 16.2).

  • Treat trigger points discovered, especially those found in the lower abdominis rectus, lower thoracic multifidi, piriformis, and gluteii muscles (Tables 16.28-31).

  • If Chapman's urethra, rectal, or adrenal points are tender, deeply massage each to patient's tolerance for 10 seconds while simultaneously holding firm fingertip contact against the respective spinal area with your other hand (Fig. 16.6).

These points are summarized in Figure 12.11.


      Nutritional Therapy

Supplemental testis and adrenal extract or nutrients B6, E, niacin, pangamic acid, iodine, and zinc are recommended. Counsel the patient to avoid ap- propriate antivitamin and antimineral factors (Tables 16.56 and 16.58).


      Elective Procedures

Other helpful forms of treatment include spinal ultrasound (Table 16.37), and thoracolumbar junction interferential therapy (Tables 16.39 41) or short wave diathermy (Table 16.36). Check for spasms, adhesions, or taut fascia that might be interfering with the function of the scrotum. These are common especially if pelvic or abdominal surgery has been performed.

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