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Neuroleptic malignant syndrome is variably defined but generally requires fever purchase cheap kamagra gold online erectile dysfunction jokes, alteration of mental status order online kamagra gold erectile dysfunction foundation, and rigidity; many patients have extreme elevations of creatine phosphokinase due to rhabdomyolysis; neuroleptic malignant syndrome may occur at any point once a patient is treated with neuroleptics cheap kamagra gold 100 mg on line erectile dysfunction question, but it usually occurs relatively shortly after drug initiation and dose increase; the onset of neu- roleptic malignant syndrome may be fulminant, progressing to coma over hours, but it usually develops over days; patients develop fever, stiffness, and mental im- pairment with delirium and obtundation; treatment: requires excluding infection, stopping the suspected offending drug, close monitoring of autonomic and respi- ratory parameters, and treatment with dopaminergic replacement (either levodopa or dopamine agonists). Chorea: Irregular, rapid, unsustained, purposeless, jerky involuntary movement that flows randomly from one body part to another A. Etiology (cont’d) Paraneoplastic Postvaccinal Vascular: stroke, venous thrombosis, polycythemia vera Drugs: neuroleptics, levodopa, oral contraceptives, anticholinergics, antihistamines, phenytoin, methylphenidate (Ritalin®), pemoline, methadone, cocaine, etc. Clinical: combines cognitive (subcortical dementia), movement disorders (chorea, dystonia, motor impersistence, incoordination, gait instability, and, in the young, parkinsonism and seizures, also known as Westphal variant), and psychiatric dis- orders (depression with a tendency to suicide, anxiety, impulsivity, apathy, obsessive compulsive disorders, etc. Pathology: the brain is atrophic, with striking atrophy of the caudate nucleus, and, to a lesser degree, the putamen; compensatory hydrocephalus may be seen (box- car-shaped ventricles); microscopically: preferential loss of the medium spiny stria- tal neurons accompanied by gliosis; biochemically: decreased ?-aminobutyric acid, enkephalins, and substance P. Although these disorders have been defined by the presence of red blood cell acanthocytes (deformed erythrocytes with spike-like protrusions), they are not always present and can appear variably during the course of the illness in the same patient, and diagnosis does not require demonstration in peripheral blood smear. Clinical: mean age of onset is 32 years (range, 8–62 years), and the clinical course is progressive, but with marked phenotypic variation. Psychiatric: behavioral disorders, emotional disorders, and psychiatric manifes- tations are common; depression, paranoia, and obsessive-compulsive disorder, self-mutilation behavior; compulsive head banging or biting of tongue, lips, and fingers can lead to severe injury; dementia is often reported. Epilepsy: a considerable proportion of patients have seizures, which may pre- cede onset of movement disorders by many years. Involuntary movement disorders: jerky movements of the limbs; sucking, chew- ing, and smacking movements of the mouth; shoulder shrugs, flinging move- ments of the arms and legs, and thrusting movements of the trunk and pelvis; wild lurching truncal and flinging proximal arm movements; oral-facial dyski- nesias; tic-like, repetitive, and stereotyped movements; involuntary vocaliza- tions are common; occasional patients have primarily dystonia. Disordered voluntary movements: lack of oral-facial coordination is prominent; dysarthria and dysphagia occur in most cases; many patients have a character- istic eating disorder (feeding dystonia) in which food is propelled out of the mouth by the tongue—patients may learn to swallow with the head tipped back, “facing the ceiling,” or place a spoon over the mouth to prevent the food from escaping; bradykinesia in concert with chorea is also common; gait is dis- ordered and features a combination of involuntary movements and poor pos- tural reflexes. Neuromuscular weakness: elevated creatine phosphokinase (in the absence of myopathy); peripheral neuropathy with distal sensory loss and hyporeflexia is common; electrophysiologic studies show increased duration and amplitude of motor unit potentials, indicative of chronic denervation. Paroxysmal dyskinesias: a heterogeneous group of disorders that have in common sudden abnor- mal involuntary movements out of a background of normal motor behavior with complete reso- lution of symptoms in between episodes; may be choreic, ballistic, dystonic, or a combination of these. Myoclonus: Sudden, brief, shock-like involuntary movements caused by muscular contraction (positive myoclonus) or inhibitions (negative myoclonus), usually arising from the central nervous system. Can be classified according to clinical characteristics (body distribution, pattern of movements and relationship to activity), etiology, and area of anatomic origin within the nervous system A. Clinical characteristics: according to relationship to activity, myoclonus is sponta- neous when it develops at rest, action (or intention) myoclonus when it is action- sensitive, and stimulus-sensitive myoclonus is termed reflex myoclonus; classifica- tion according to body distribution is as follows: focal or segmental (confined to one particular region of the body), multifocal (different parts of the body affected, not necessarily at the same time), or generalized (whole body part affected in a single jerk), pattern of movements may be rhythmic, in which case it is referred to by some as tremor (will usually have a jerky quality), but more typically, it is arrhythmic. Cortical myoclonus (frequently multifocal, rather than focal): the jerks are usu- ally more distal than proximal and more flexor than extensor; usually affects the face and hands; typically, stimulus-sensitive and may be precipitated by sudden loud noise or a visual stimulus; etiology: any type of focal cortical lesion, including tumors, angiomas, and encephalitis, may be associated with focal cortical myoc- lonus. Hereditary cortical myoclonus is usually rhythmic and can be mistaken as a tremor. Lafora body disease: characterized by polyglucosan–Schiff-positive inclusion bodies in the brain, liver, muscle, or skin (eccrine sweat gland) b. Neuronal ceroid lipofuscinosis (Batten disease): presents with seizures, myoc- lonus, and dementia, along with blindness (in the childhood forms); charac- terized by curvilinear inclusion bodies in the brain, eccrine glands, muscle, and gut c. Unverricht-Lundborg disease: characterized by stimulus-sensitive myoclonus, tonic-clonic seizures, a characteristic electroencephalography (paroxysmal generalized spike-wave activity and photosensitivity), ataxia, and mild demen- tia with an onset at around age 5 to 15 years d. Sialidosis: a lysosomal storage disorder associated with a cherry-red spot by funduscopy and dysmorphic facial features 3. Note that there are a number of startle syndromes in certain cultures that are not genetically related to hyperekplexia but also exhibit excessive startle—Jumping Frenchmen of Maine, Latah in Indonesia, and Raging Cajuns of Louisiana. Other causes of subcortical myoclonus include postanoxic myoclonus (also known as Lance-Adams syndrome), myoclonus-dystonia, Friedrich’s ataxia; could also be iatrogenic—medications such as amantadine, levodopa, ver- apamil, monoamine oxidase inhibitors and heavy metal poisoning. It occurs weeks to months after recovery from cardiac arrest and is commonly seen when respiratory dysfunction precedes cardiac arrest. Palatal myoclonus (now palatal tremor): used to be classified as a subcortical my- oclonus; on account of its rhythmic nature has been reclassified as palatal tremor and is discussed in the section on tremors. Spinal segmental myoclonus: affects a restricted body part, usually contiguous muscle groups; is spontaneous, unilateral rhythmic or arrhythmic in nature, and connotes an underlying structural lesion; etiology: inflammatory myelop- athy, cervical spondylosis, tumors, trauma, ischemic myelopathy, and a variety of other causes b. Propriospinal myoclonus involves the trunk and abdomen, is mostly rhythmic, and is worse in the supine position; recently has been found to be psychogenic in a subset of patients. Dystonia: Involuntary movement characterized by sustained or intermittent con- tractions of agonist and antagonist muscles, frequently causing twisting and repetitive movements, abnormal postures, or both; classification now along two axes: A. Axis I: involves identifying the clinical characteristics and allows the dystonia syn- drome to be identified—(i) body distribution: focal (involving a single body part, e. Based on the two axes, dystonias are now classified as either isolated (dystonia is the only feature) or combined (dystonia with other movement disorders); combined dystonias could either be persistent or paroxysmal. When dystonias are associated with neurologic or systemic features, they are referred to as complex dystonias. Should not be missed because the condition is treatable (sensitive to levodopa and effect is sustained). Phenotype can also be seen in other biopterin-deficient states (tyrosine hydroxylase mutations, dopamine-agonist-responsive dystonia due to decarboxylase deficiency). Ataxia: Imbalance or incoordination, usually due to disease of the cerebellum and its connections (can also be afferent in nature from severe proprioceptive dysfunction); acquired (usually acute or subacute in nature) or inherited (insidious onset and usually progressive but could also be paroxysmal) A. The Movement Disorder Society Evidence-Based Med- icine Review update: treatments for the non-motor symptoms of Parkinson’s disease. Commonly accepted pathologic criteria for demyelinating diseases are as follows: 1. Relative sparing of other elements of nervous tissue, such as axis cylinders (may be incomplete) 3. Lack of Wallerian degeneration or secondary degeneration of fiber tracts (due to integrity of the axis cylinders) B. Caveat of criteria: Schilder’s disease and necrotizing hemorrhagic leukoencephalitis may have massive damage to axis cylinders as well as myelin. Subacute combined degeneration, tropical spastic hemiparesis, progressive multi- focal leukoencephalopathy, central pontine myelinolysis, and Marchiafava-Bignami disease were not included because of their known etiology—they are part of either viral or nutritional deficiency; metabolic deficiencies with white-matter involve- ment are also excluded. Neuroimmunology Pluripotent stem cells Lym phoid lineage M yeloid lineage T-cells B-cells Eosinophils Neutrophils M acrophages Basophils Natural killer cells Figure 13. B-lymphocytes: develop in the bone marrow; acquire immunoglobulin (Ig) recep- tors that commit them to a specific antigen; express IgM on the surface; after antigen challenge, T-lymphocytes assist B-lymphocytes either directly or indirectly through secretion of helper factors to differentiate and form mature antibody-secreting plasma cells. Igs: glycoproteins; secretory products of plasma cells; the heavy chain on Fc portion determines class: IgM, IgD, IgG, IgA, and IgE; activates complement cascade: IgM, IgG1, and IgG3. Formation of antigen-antibody complex, which inhibits B-cell differentiation and proliferation 3. Idiotypic regulation: variable region on Ig molecule expresses proteins that are new and can act as antigens. Also known as disseminated sclerosis, sclerose en plaques: protean clinical mani- festations; usually a course of remission and relapse, but occasionally intermittently progressive or steadily progressive (especially in those >40 years old (y/o)) affecting white (more common) and gray matter and spinal cord B. Pathology: grossly numerous pink-gray (due to myelin loss) lesions scattered sur- rounding white matter; vary in diameter; do not extend beyond root entry zones of cranial or spinal nerves 1. Periventricular localization: characteristic, in which subependymal veins line ventricles 2. Other favored structures: optic nerves, chiasm, spinal cord; distributed randomly through brainstem, spinal cord, cerebellar peduncles 3. Astrocytic reaction: perivascular infiltration with mononuclear cells and lympho- cytes; sparing of axis cylinders prevents Wallerian degeneration.
Metabolic abnormalities include with benzodiazepines results in a decrease in anxiety order discount kamagra gold on-line erectile dysfunction doctor manila. Peripheral tinnitus is associated with symmetric hearing assess for progression of symptoms discount kamagra gold 100 mg impotence juice recipe. As hearing loss increases order 100 mg kamagra gold fast delivery common causes erectile dysfunction, tinnitus Treatment for tumors depends on the size, location, increases. In patients with hearing loss that is not pathologic condition of the external and middle ear, treatable by a surgical procedure, a hearing aid may malignancy, glomus tumor, and cholesteatoma. Symptoms of an acoustic neuroma of tinnitus patients: report of a randomized clinical trial and clinical prediction of bene?t. Approximately 50% of the 16 million Americans who when the patient is a young adult. Hearing loss can It may result from viral infections during pregnancy be conductive when sound is impeded through the external (e. Profound loss is associated with poor medications; recent upper respiratory infection; and as- prognosis for recovery. Examination of the ear includes otoscopy to look for longitudinal fracture results in middle ear damage and otitis externa, foreign body, cerumen impaction, canal is associated with a conductive hearing loss. Transverse cholesteatoma, exostosis (osteochondroma), tympanic fracture may damage the facial nerve and labyrinth and membrane perforation, and effusions (hemorrhagic, result in a sensorineural de?cit. In the past when the cause was not normal result or bilaterally symmetric sensorineural or found, bed rest, head elevation, avoidance of loud conductive defects. Controlled studies handle of a vibrating tuning fork against the mastoid of steroid therapy for idiopathic sudden-onset hearing process and having the patient signal when he or she loss show a statistically signi?cant improvement in can no longer hear it. Sudden near the ear and have the patient signal when sound is idiopathic sensorineural hearing loss is an urgent situa- no longer audible. Heavy lifting may result twice as long as bone conduction but not in a conduc- in a leak of inner ear ?uid from a membranous rupture tive hearing loss. Vascular causes include vertebrobasilar insuf?ciency, greater than air conduction thresholds. In mixed de?- embolism, hypercoagulable states, and basilar mi- cits air conduction, both are depressed. Salicylate withdrawal results in genital abnormality, or it may be an acquired de?cit. Patients with chronic otitis media, tuberculosis, otoscle- insuf?ciency, autoimmune disease, infection, degenera- rosis, skull fractures, and penetrating injury of the ear; tive disorder, and neoplasm. Although the most common Wegener’s granulomatosis; and squamous cell carci- cause of hearing loss in the elderly is presbycusis, a sym- noma all have been observed to have a mixed conduc- metric, progressive decrease in hearing, it is a diagnosis tive and sensorineural de?cit in advanced disease. Conductive hearing loss, de?ned as a lesion involving cludes an evaluation for diabetes mellitus, hyperthyroid- the outer and middle ear to the level of the oval ism and hypothyroidism, anemia, hyperlipidemia, renal window, results from mechanical disruption of the disease, infection, and syphilis. Review exposures to transmitted sound through the external auditory canal, medications that are commonly known to cause hearing tympanic membrane, and ossicle. Direct observation of the external canal during the lates and others such as quinine, chloroquine, and anti- examination allows evaluation of conditions causing neoplastics such as cisplatinum. Acoustic stapedius re?ex testing for ?xation of the sta- nodosum, and Wegner’s granulomatosis. Neoplasms such pedius is part of the evaluation of conductive hearing as acoustic neuromas and metastatic carcinoma of the loss. Acous- of conductive hearing loss, is diagnosed with this test tic neuromas can present with bilateral hearing loss in up and treated with stapedectomy. Cholesteatoma, glomus tumor, and nasopharyngeal Degenerative disorders include presbycusis, noise-in- malignancies (squamous cell carcinoma, adenocarcino- duced hearing loss, and Meniere’s disease. Therapy of the underlying problem may surgery, radiation, or chemotherapy for a neoplasm; improve the conductive hearing loss: removal of the surgical repair of a membrane rupture; and antibiotics foreign body or cerumen, antituberculous drugs, tym- and steroids for syphilis. Acoustic trauma requires sur- panoplasty, ossiculoplasty, stapedectomy, and removal gical evaluation, whereas hearing aids are the treat- of excessive cartilage (exostosis). Treatments of masses ment of choice for presbycusis and disorders not im- within the middle ear depend on the site, pathologic proved by medical or surgical intervention. Med Clin North Am does not reveal an abnormality, continue surveillance 1991;75:1239. First, patients guidelines for cardiac revascularization as do all who require emergent surgery clearly do not bene?t from other patients. Second, Beta blockers are often routinely prescribed to re- preoperative evaluation does not “clear” a patient for sur- duce perioperative cardiac risk. Preopera- suggests that only those at high risk bene?t from beta tive evaluation provides an assessment of medical risk and blockers. Those at moderate risk did not bene?t, and the identi?cation of measures to reduce that risk. Third, those at low risk actually experienced increased mortal- consultants need to have a clear understanding of their role ity. The goal of perioperative cardiac risk assessment more frequently than cardiac events. Such events is to identify those patients with unstable cardiac dis- include atelectasis, bronchospasm, pneumonia, pro- ease for whom further study and treatment warrants longed mechanical ventilation, and exacerbation of the risk of surgical delay. Arozullah and colleagues have the American College of Cardiology are summarized published a respiratory failure index that predicts the in the algorithm. Stress testing is unnecessary in pa- risk of respiratory failure based on the type of surgery, tients with adequate functional capacity (e. Moreover, such testing should not is not surprising that patients with established lung be recommended unless patients are willing to post- disease are at higher risk for perioperative pulmonary pone surgery so as to proceed with cardiac revascular- complications. Such delay may itself be harmful in the patient patients with reversible pulmonary pathology who who is bedridden and thus at risk for decubitus ulcers, would bene?t from preoperative intervention. The results of such testing can then be sation of these agents risks in-stent restenosis. Con- used to determine disease-speci?c therapy, which, in tinuation of these agents risks perioperative bleeding. Those Discuss these issues with patients and their families with previously identi?ed pulmonary pathology and before ordering a stress test. The same American Col- baseline symptomatology do not require investigation lege of Cardiology guidelines also state that there is no or change in management. The Ameri- tients with stable coronary disease do not benefit can Diabetes Association has endorsed the following from preoperative revascularization. Exclusion cri- goals for glycemic control in hospitalized patients: 90 teria to this study included those with 50% left to 130 preprandial blood sugars and 180 postpran- main disease, an ejection fraction 20%, and se- dial blood sugars. When managing patients with renal failure, because to be aware that hypoglycemia may be a greater threat thromboembolism is a signi?cant cause of avoidable than hyperglycemia in the acute setting of hospitaliza- hospital morbidity and mortality, consultants should tion. Thus, such testing is graduated compression stockings and intermittent discouraged unless there is a high suspicion of thyroid pneumatic compression. The available data suggest that there is mini- considered insuf?cient thromboprophylaxis for any mal additional surgical risk in those with mild or mod- category of surgical patient. Surgery in those with severe Patients should be routinely asked about alcohol in- hypothyroidism (i.
A linear streak of traumatic subarachnoid blood is visible at the base of the frontal lobe () kamagra gold 100 mg fast delivery erectile dysfunction in diabetes medscape. His mental status gradually patients with minor head trauma who are neurologically normal improved over the next several days generic kamagra gold 100mg with amex erectile dysfunction forums. The patient therefore had described three cases of delayed subdural hematoma occurring during his hospital stay: delayed intracra- 1–3 months after minor head trauma discount kamagra gold 100 mg on-line fda approved erectile dysfunction drugs. In some instances, nasal trauma involves more mechanism of injury is a direct blow to this region, as was sus- extensive injury. How- ever, interpreting these injuries as “bilateral tripod fractures” would be incorrect. Bilateral midface fractures are the hallmark of a complex of fractures that were ?rst described by Rene Le Fort in 1901. Compiled by nearly two dozen contributors and edited by four leading neurologists from the Cleveland Clinic, this comprehensive point form review presents the latest research, data, and knowledge on all aspects of neurology that you need to know to succeed on these exams. The frst section covers basic neurosciences, including neurochemistry, clinical neuroanatomy, and genetics. The next section discusses clinical neurology, with chapters devoted to the major diseases and disorders including stroke, head trauma, dementia, epilepsy, and movement disorders, among others. Each chapter has been fully reviewed, revised, and updated to refect current knowledge and practice and presents the information in an outline format, ideal for test preparation. Crucial topics and high-yield data are highlighted in bold or italic for maximal retention. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the publisher. Research and clinical experience are continually expanding our knowledge, in particular our understanding of proper treatment and drug therapy. The authors, editors, and publisher have made every effort to ensure that all information in this book is in accordance with the state of knowledge at the time of production of the book. Nevertheless, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the contents of the publication. Every reader should examine carefully the package inserts accompanying each drug and should carefully check whether the dosage schedules mentioned therein or the contraindications stated by the manufacturer differ from the statements made in this book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. The authors and editors have tried hard to include the most up-to-date material while keeping the verbiage to a minimum. We have followed a point form outline style where possible, also including tables and lists where long paragraphs would be problematic. A brief Cheat Sheet at the end of most chapters provides a simple quick study section for key facts or potential “board question” information, often those tricky eponyms that we all learn and rapidly forget. We have included some suggested readings for those who want to dive deeper into a review, but have not exhaustively referenced the chapters for the sake of space and clarity. Finally, there are 50 all-new questions with answers and explanations at the end of the book for self-assessment. The editors hope this text will provide a useful tool to students of neurology at multiple levels, and will help in review for whatever neurological examination looms in the future for the reader. Fernandez ix Acknowledgments the editors would like to acknowledge the support of Christine Moore, our editorial assistant, who valiantly assisted in organizing authors, managing editors, modifying manuscripts, and generally making the entire con- traption function. Thanks go to our authors, who carefully reviewed and updated the chapters to reflect recent changes in understanding of disease and approaches to treatment within the bounds of the Ultimate review format. We would like to acknowledge the support of the leadership of the Neurological Institute at the Cleveland Clinic for encouraging our authors and editors to contribute to clinical pedagogy. We would also like to thank our editor, Beth Barry, at Demos for her assistance and support during the edit- ing of this third edition of Ultimate Review for the Neurology Boards. The editors would also like to thank their loving wives (Mary Bruce, Ritika, Divya, and Cecilia) and their wonderful children (Michael, Tucker, George, Sasha, Jordan, and Annella Marie) for their unconditional support and understanding during this process. How to Use This Book Neurology covers a broad spectrum of disease processes and complex neuroanatomy, neurophys- iology, and neuropathology. Moreover, your certification examination will also include psychiatry and other neurologic subspecialties such as neuro-ophthalmology, neuro-otology, and neuroen- docrinology, to name a few. Covering all of the possible topics for these boards is not only impos- sible, it is impractical. Although this book is entitled Ultimate Review for the Neurology Boards, it is not intended to be your single source of study material in preparing for your examination. Rather, it presumes that throughout your residency training, or at the very least, several months before your board examination date, you will have already read primary references and textbooks (and, therefore, carry a considerable fund of knowledge) on the specific broad categories of neurology. Because you cannot possibly retain all the information you have assimilated, we offer this book as a convenient way of tying it all together. The point-form information will help you recall specific facts, associations, and clues that may help with answering questions correctly. Ultimate Review for the Neurology Boards contains detailed chapters on subjects included on the neurology board examination. For maximal retention within the shortest amount of time, we have used an expanded outline format in this manual. A few phrases or a short paragraph is spent on subtopics that we think are of particular importance. We suggest that you first read the entire chapter, including the brief sentences on each subtopic. After the first reading, you should go back a second time, focusing only on the headings and subtopics in bold and the italicized words within the outline. If you need to go back a third time to test yourself, or, alternatively, if you feel you already have a solid fund of knowledge on a certain topic, you can just concentrate on the backbone outline in bold to make sure you have, indeed, retained everything. Whenever appropriate, illustrations are liberally sprinkled throughout the text to tap into your “visual memory. We have added a few suggested readings where pertinent to help you extend your learning both for the exams and for your education. For example, some diseases discussed in the chapter on pediatric neu- rology and the chapter on neurogenetics can also be found in the individual chapters of the Clinical Neurology section. We have included 50 questions at the end of the book to help you practice for the tests. One of the best preparation methods for taking exams is practicing the exam situation over and over. We hope these questions will give you a chance to try out your hand at answering questions. Preparing for Your Board Examination Although most residents initially feel that after a busy residency training it is better to “take a break” and postpone their certification examination, we believe that, in general, it is best to take your examination right after residency, when “active” and “passive” learning are at their peak. There will never be “a perfect time” (or “enough time”) to review for your boards. The board examination is a present-day reality that you will need to prepare for whether you are exhausted, in private practice, expecting your first child, renovating your newly purchased 80-year-old house, or burning candles in your research laboratory. Luckily, all the others taking these tests are in the same boat, so you are not alone! Although most res- idency programs are clinically oriented and have a case-based structure of learning, here are some suggestions as to how you can create an “active” learning process out of your clinical training, rather than just passively learning from your patients and being content with acquiring clinical skills.
Distances were recorded before the supplementation program and again ten days later order kamagra gold with a visa erectile dysfunction doctor memphis. Twelve somewhat out-of-shape participants were asked to take either the flower pollen or our own formula purchase 100 mg kamagra gold with visa impotence blood pressure medication, and then initiate an n exercise program of weights and running generic kamagra gold 100 mg online erectile dysfunction icd 9 code 2013. After three days participants were asked to rate the muscle pain and strain that they experienced from exercise. Ability to flex Results the results of experiment #1 showed conclusively that the Bee Pollen formula, versus the control and the Flower Pollen, was able to put oxygen into cells. The results of experiment #2 showed an increase of approximately one tenth of a mile in performance of the athletes versus control or Bee Pollen. The participants in this experiment were members of the Cleveland Browns and in the next five years they will all but one make the all pro list. A friend of mine was a high altitude bike athlete who was not so good at his sport. After two weeks of the formula he placed second in a race then he had three consecutive wins. He told me it seemed like he could run the race again, instead of being wasted at the end. Results of experiment #3 showed that the homeopathic combination formulas were able to help patients to control the aches and pains of starting a sports program. But bound 02s are continually shaking loose from their sites in the presence of trace minerals such as zinc. Equilibrium is reached when the number being bound just equals the number shaking loose. In Hb, this equilibrium is reached very fast, anc its position is determined largely by the P02. The higher the P02 (the more concentrated the 02), the more frequent the collision with Hb and the more frequently an 02 will bind. As the 02 concentration increases, more and more binding sites are filled, until finally every site is filled, with each Hb molecule containing four bound 02 molecules. At this point, we say the Hb is 100% saturated; when only half are occupied, the Hb is 50% saturated. Hb takes up 02 at the partial pressures that exist in the lungs and in the tissues. Hb will unload 02 in the tissues where P02 averages about 40 mm Hg and may fall even lower to 20 mm Hg in active muscles. There is a difference between the percentage of Hb saturation of blood just after leaving the lungs and the percentage of Hb saturation in the tissues. This oxygenation cycle is the base of all life and the best indicator of wellness. The supply of the methyl donor pamgamin and the other high end B vitamins boost and enhance the carbohydrate utilization curve via the oxygen cycle. The additional rare minerals and bee pollen components also have oxygen stimulation effects. Hb “works” because its saturation curve is S shaped; it unloads most of its 02 in a very narrow range of P02 between 20 and 40 mm Hg. This behavior is due to the fact that Hb is made of four interacting subunits that “cooperate” in binding Oz. The first portion of the curve at very low P02 is flat because Hb is in the tense state and not receptive to 02. As more 02 molecules are introduced, the likelihood of one of them binding goes up. Once it binds, it influences the other vacant binding sites on the same Hb molecule, increasing the probability of binding a second 02, which will increase the chances for a third, etc. Thus, the binding (saturation) curve rises very steeply and fortunately in just the right region! Contrast this behaviour with that of myoglobin, the 02 storage protein in muscle cells. It is similar to Hb, but it contains only one subunit; one molecule binds only one 02, and there is no possibility of a T state or of cooperative binding. Its binding curve is not S shaped, and rather than giving up its 02 at the P02 found in the venous blood, it takes it up. But this fits its function; myoglobin stores 02 and will give it up in the tissues only when the P02 falls very low. There are several percentage of saturation curves for Hb under different conditions. In one of them, the concentration of C02 has increased, and the 02 saturation curve for Hb has shifted to the right (i. In this case, a higher P02 is required to achieve the same percentage of saturation, and this means the Hb has a lower affinity for 02. If the Hb were just sitting there, exposed to a constant P02, and C02 suddenly increased, shifting the curve to the right, then the Hb would release some of its 02. This actually happens as blood passes through a capillary, and C02 diffuses into the blood from the tissues. These each bind at separate locations on the Hb molecule, but they all act in similar ways by strengthening linkages between Hb subunits, which promotes the tense state with low 02 affinity. When the curve is shifted to the left, above the “normal” curve, the Hb has more affinity for 02; it takes some up. As a result, the 02 saturation curve for fetal Hb lies above the curve for maternal Hb, showing that fetal Hb has a greater affinity for 02. This is an advantage for the fetus because when fetal Hb comes in proximity to maternal Hb (in the placenta), it will draw 02 from the maternal blood. Rather, its level can vary considerably, and it is involved in regulating 02 transport in both health and disease. Its level rises when 02 uptake in the lungs is compromised, and this helps the Hb unload a larger portion of the 02 that it does carry when it gets to the tissues. The word Xrroid is defined as the testing of a patient Electro Physiological Reactivity to thousands of substances at biological speeds. Biological speeds are defined as those approaching the ionic exchange speed of a persons’ electrical reaction to the items in their immediate environment. The Xrroid is the process of measuring a patients’ reaction to such items as vitamins, homeopathics, enzymes, hormones, allersodes, isodes, nosodes, etc. The Xrroid has been used on millions of patients around the world for over a decade. The process has been clinically tested with results being published in medical journals and articles being presented in several world wide medical conferences. The users of the systems have sent in thousands of testimonials and reports of dramatic success come in daily. The users use the device as directed, which means seeing a patient once a week at best. For over a decade occasionally someone with an overly suspicious mind will try to use the device not as directed but on someone repeatedly in the same day.