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Determining the cause of stress bars is often difficult because they represent a problem that occurred when the feather was developing 100mg lasix. The problem had been pre- Occluded Ear Openings sent since hatching lasix 100 mg, and the aviculturist had been incorrectly told that this was normal and would resolve with age 100 mg lasix. If corrected from Occlusions of the external openings of the ears are hatching lasix 40mg, this problem can be resolved by gently pulling the upper most often seen in macaws 40 mg lasix, (especially Military Ma- beak forward and placing it over the lower beak for about ten caws) lasix 100mg. If allowed to progress 40mg lasix, as in this cockatoo lasix 40 mg, repair requires surgical intervention (see Chapter 42) . This material should be removed by curettage and flushing , cultured for bacteria and fungus, and the ear treated with appropriate topical and systemic antibiotics. Eyelid Malformation Malformation of the eyelids resulting in a narrow aperture is occasionally seen in cockatiels. The bird was being fed a homemade diet with a baby cereal base that was nutritionally reported cases, the aperture closed following treat- deficient. If the canal fails to open, it should be explored with blunt forceps and an opening surgically created if necessary. If a small hole is found, it can often be enlarged by stretching it with the tips of a pair of hemostats. Loxahatchee, Avicultu- Jean Delacour/Intl Foundation for hepatic biliary cyst in a congo African of Cage and Aviary Birds 2nd ed. J Am Vet rum biochemical reference intervals an African grey parrot and an um- Avian Vet 1990, 12-24. J Zoo Wildlife Med rum biochemical reference intervals rots: Methodology and expected 1986, pp 333-340. Clubb K, Clubb S: Management of Breeding and Research Center, 1992, Medicine 1:11-21, 1992. The diet of every avian patient should be carefully evaluated, even if the bird appears clinically to be well nourished. Marginal nutritional inadequacies frequently occur (see Chapter 8), and correcting the 31 diet will improve a bird’s general health and its ability to resist infectious diseases. Gastrointestinal malabsorption, hepatitis or renal disease can in- crease nutrient requirements so that diets that are sufficient in healthy birds may be insufficient for unhealthy birds. Interestingly, free-ranging gra- nivorous birds that are offered both organic (no pes- ticides) and pesticide-treated grains will preferen- tially consume the organic foods. Birds with signs of malnutrition have often devel- oped strong preferences for unbalanced diets. Most seed diets, for example, contain excessive levels of fat and may be deficient in vitamins A, D3, E, B12 and K1, plus riboflavin, pantothenic acid, niacin, biotin, choline, iodine, iron, copper, manganese, selenium, Patricia Macwhirter sodium, calcium, zinc and some amino acids (eg, lysine and methionine). Gradually decreasing the quantity of old food items and increasing the quantity of new foods in the mixture will allow for a smooth transition in the diet. Converting birds housed in large groups to a new diet is often easier than converting individual birds. Ketosis was seen in some Obesity is the most common and the most severe cockatoos that refused to eat during the transition to malnutrition-related problem recognized in avian formulated diets. Obesity occurs if the energy loss, diarrhea, weakness, lethargy and possible vomi- content of the diet is excessive for the energy de- tion. Ketonuria can be demonstrated by a reagent strip mands created by normal metabolic functions and examination of the urine. In some cases, obesity will be trose, supportive alimentation and placing the bird secondary to the over-consumption of food in a bird back on its regular diet. Associated with Malnutrition Because companion birds frequently have limited opportunities for exercise, the energy content of their diet needs to be monitored closely. In species prone to obesity, it is important to avoid offering foods that Avian veterinarians encounter a different type of have high caloric densities and to avoid excessive malnutrition today than was described five to ten quantities of attractive, palatable food. Nutrient deficiencies were historically twice the caloric density of either carbohydrates or common, but with the use of formulated diets in proteins, and foods containing high levels of fats combination with vitamin and mineral supplementa- (such as peanuts or sunflower seeds) should be lim- tion, many malnutrition problems noted today are a ited. Fresh fruit and vegetables have lower calorie densities than dried foods or seeds and should make up a sizable portion of a low-energy diet. Decreasing caloric intake can also be achieved by restricting feeding times (eg, ten minutes in the morning and evening) rather that offering food ad lib. Ideally, com- panion birds should be fed pelleted or extruded foods supplemented with small quantities of fresh fruit and vegetables. Some formulated diets may be helpful in controlling obesity and fatty liver problems. In this case, roidism, thyroxine supplementation is recommended a cockatiel is being used to acclimate a parakeet to a formulated (see Chapter 23). Low Body Weight/Poor Growth Low body weight or poor growth can be the result of inadequate food intake, which in turn can be caused by an insufficient quantity of food, inappropriate diet, unfamiliar food items, infrequent feeding, weaning onto solid foods too early, or loss of appetite, maldigestion or malassimilation of food caused by medical problems. Low body weight or poor weight gain independent of organopathy can generally be corrected by placing the bird on a high-energy diet (high in fat and carbo- hydrates). Digestive enzymes and fiber hemicellu- lose may increase the digestibility and absorbability of the diet. Procedures for calculating daily energy requirements for birds are discussed in Chapter 15. It is important to note that formulas to calculate energy requirements are based on averages, and the nutritional requirements of individual species and individual birds will vary. A bird’s clinical response to a particular diet should be carefully evaluated and adjustments should be made as necessary. The creatic disease may interfere with the absorption of bird was fed a seed diet ad lib and was frequently given treats (eg, crackers, potato chips). Cytologic evaluation of fine-needle aspirates from foods that are easily digested and absorbed to facili- a mass was suggestive of adipose tissue. Abnormal clinical pathol- ogy findings included lipemic serum and hypercholesteremia. Lactose and diographs indicated a diffuse soft tissue mass in the caudal abdo- excessive amounts of green vegetables should be men. Diets should be moderately low in fiber and displacing the abdominal organs cranially (arrow). Note that the cloaca is being compressed and the colon is oriented in a cranial, provide easily digested carbohydrate (eg, canary rather than its normal right lateral position (open arrow). The bird seeds, millet, panicum, corn or hulled oats) and a responded to a diet change (formulated diet, fruits and vegetables moderate amount of highly digestible protein. The addition of A decrease in photoperiod may induce polyphagia digestive enzymes to the diet may be useful (see and weight gain in pre-migratory birds. In some cases, feeding a small quantity creased food intake and weight gains appear to be of grit may improve digestion and aid absorption, but mediated by thyroid hormones, prolactin and go- should be supplied only in low quantities to prevent nadotrophins. Cold food, a cold envi- lems are more likely to occur if young birds are ronment or infrequent feeding of large amounts of suddenly introduced to new food items (unhulled food may increase the risk of crop impaction in juve- seeds, particularly). Repeated crop impactions ber of food items at an early age are less likely to may result in an atonic, pendulous crop. Ostriches may eat tion of ventricular musculature has been associated constantly following relocation, leading to foreign with vitamin E and selenium deficiencies and calci- body ingestion and impaction (see Chapter 48). The etiology is Feigned polyphagia, in which a bird hulls seeds and undetermined (see Color 19). Vitamin E and se- foods, particularly highly processed human foods (eg, lenium deficiencies have been suggested as possible cakes, desserts, crackers). When changed to a formulated diet, older, obese budgerigars and cockatiels may lose weight, yet eat Nutritional cases of malabsorption or maldigestion constantly. Obese birds should lose weight slowly to (passing undigested food) include vitamin E and se- prevent hepatopathies associated with overwhelm- lenium deficiencies (sometimes associated with ing fat metabolism. The weight loss can be tempered giardia infection), excess oil in the diet or dehydra- by adding some millet to the diet. A lack of grit has been frequently discussed as a tions and lactulose can be used to suppress progres- cause of maldigestion; however, companion birds on sive hepatopathies in some cases (see Chapter 8). Stud- ies in poultry indicate that the addition of grit in- Polydipsia/Polyuria creases the digestibility of feed by as much as ten percent,14 but similar studies have not been per- Nutritional causes of polydipsia and polyuria include formed in companion birds. Given that obesity is hypovitaminosis A, calcium deficiency, excess pro- more of a problem than maldigestion in companion tein, hypervitaminosis D , excessive dietary salt, dry3 birds, increasing the digestibility of a formulated diet seed diet, formulated diets or a high percentage of that exceeds suggested nutritional requirements is dietary fiber. Charcoal that is used in some grit mixtures may interfere with the absorption of Polyuria alone may occur in birds fed moist foods vitamins A, B2 and K and contribute to deficiencies of such as fruit, vegetables and semi-liquid diets. If offered free choice, some birds may over-con- berries and other fruits can also alter the urine color sume grit, leading to crop, proventricular or ven- (see Color 8). This problem is reported com- monly in North America but appears to be Digestive Disorders uncommon in Australia. The cause for a regional variation in the occurrence of this condition is un- White plaques in the mouth or swelling in the sali- known. Birds showing compulsive grit consumption vary ducts may be associated with hypovitaminosis should be evaluated for hepatopathy, pancreatitis, A (see Colors 8 and 13). Oral paralysis in cockatiels may be related to vita- There is a difference between grit and crushed shell. Crushed shell is almost entirely composed of limestone (calcium car- bonate) and is readily digested by acids in the pro- ventriculus. Crushed shell will provide a source of calcium, and is not effective in aiding in the mechani- cal breakdown of dietary plant material. Heavy met- al toxicity has been associated with feeding crushed shell derived from contaminated sources (oysters raised in polluted waters). The bird was maintained indoors and povitaminosis A leads to squamous metaplasia of had no exposure to sunlight or water for bathing. Horny beak material that is dry and flaky, as well as black discoloration of the epithelial surfaces causing obstruction of respiratory feathers are typical of malnutrition. Dyspnea may be change in diet and daily exposure to direct (unfiltered through caused by calcium or vitamin D deficiency if severe3 glass) sunlight. This can occur if a ciency causes the formation of ragged feathers, while tube is accidentally placed in the trachea when at- a deficiency in growing cockatiels has been associ- tempting crop feeding or if a bird (particularly a weak 46 ated with a lack of contour feathers. The association between diet and feather pigment Plumage Abnormalities has long been recognized by canary breeders. Caro- tene and xanthophyll pigments, which originate from Dark, horizontal lines (stress marks) on feathers plant material, are found in fat globules in the feath- have been associated with nutritional deficiencies ers and give rise to yellow, orange and red colors (see (particularly methionine) and indicate that a release Chapter 24). Birds lacking a dietary source of carote- of corticosteroid hormone occurred while the feather noids may develop muted feather or skin colors, was developing. Stress lines are common in neonates while dietary supplementation of carotenoids in that have had a disrupted feeding schedule or in birds with suitable genetic backgrounds will result in raptors that are molting while in a training period increased depth of color. Molting abnormalities, retained feather sheaths and dry flaking beaks have also been Prolonged feeding of bacon rind and bone marrow associated with overall nutritional deficiencies (Fig- has been associated with an oily feather and stool ure 31. Raptors Feather picking may be initiated by dry, flaky, fed laboratory rats and mice (reduced carotenes) may pruritic skin, which in turn can be caused by nutri- lose the yellow coloration of their cere, feet and legs tional deficiencies, particularly deficiencies of vita- that is characteristic in free-ranging birds. Porphyrins are less sensitive to dietary influ- possible cause of self mutilation (Figure 31. The black feathers in this Amazon parrot resolved with a change in diet Melanin occurs in granules in the skin and feathers (seeds to formulated diet) and correction of chronic active hepatitis. This pigment is derived from tyrosine in an enzy- occurs, melanin granules in the middle of the feather, matic reaction requiring copper. Consequently, defi- if present, would absorb all wave lengths of light, ciencies of tyrosine (or other related amino acids) or giving the visual effect of black (Figure 31. In deficiency, timing of the deficiency in relation to most cases, their occurrence depends on a scattering feather development and the initial color of the af- of light caused by the structure of the keratin in the fected feathers. While lysine deficiency in chickens, spongy layer of the feather rami rather than on the turkeys and quail produces achromatosis, there was presence of pigments. Essential amino acids that no loss of feather color in young cockatiels fed a occur in keratin include methionine, histidine, ly- lysine-deficient diet. However, choline and riboflavin sine, tryptophan, threonine, isoleucine and valine. It deficiencies produced feather changes in young is possible that amino acid deficiencies could alter the cockatiels that resembled achromatosis caused by structure of keratin and consequently alter feather lysine deficiency in poultry. A change in feather color from green to yellow associated with breakage) in feathers may be associ- is usually caused by a loss of structural blue color, ated with a hypovitaminosis B (Figure 31. While this color change is commonly Skin Changes seen in nutritionally deficient Psittaciformes, the exact nature of the deficiency has not been clarified, Plantar corns and pododermatitis have been associ- and it is possible that more than one amino acid could ated with biotin and vitamin A deficiencies, particu- be involved (see Color 24). If a formulated diet is not available, a diet can to black or grey to black in birds that are sick or be supplemented with multivitamins to compensate malnourished. Several kiwis in a with altered keratin structure in the spongy layer New Zealand zoo developed a scaly dermatitis over that prevents normal light scattering. The bird was on an all-seed diet frequently brittle and may break at the site of abnormal coloration. Changing the diet, increasing the exercise (out- door flight enclosure) and standard treatment for grade 4 bumble- ment that was routinely included in their diet was foot were effective in resolving the lesions. The clinical problem resolved when the mul- tivitamin supplement was again added to the diet. Over-supplementation may cause problems with excess vitamin, mineral, fat or protein Tibial dyschondroplasia is characterized by uncalci- consumption. A genetic predisposition along with electro- Demineralized, bent bones and pathologic fractures lyte imbalances involving sodium, potassium and may occur in birds with hypovitaminosis D and cal- chloride are thought to be involved in the develop- cium, phosphorus or magnesium deficiencies or im- ment of tibial dyschondroplasia. Leg paralysis has been associated with calcium, chloride or riboflavin deficiency. Slipped tendon of the hock (perosis) may occur with manganese, biotin, pantothenic acid or folic acid de- Cervical paralysis has been associated with a folic ficiencies (see Color 8). Jerky leg movements have been asso- allowed sufficient exercise and birds fed high-min- ciated with pyridoxine deficiency. There is gross enlargement of the tibiometatarsal joint, twist- Sudden collapse or fainting has been associated with ing and bending of the distal tibia and slipping of the hypoglycemia in raptors or in other species when a gastrocnemius muscle from its condyles. Syncope is naceous birds, cranes and ratites are particularly characteristic of advanced hypocalcemia in African susceptible to this condition. In some cases, surgical correction is possible (see Behavioral changes including aggressiveness (bit- Chapter 46).

Low serum 25-hydroxyvitamin D concentrations are associated with greater all- cause mortality in older community-dwelling women 40 mg lasix. Vitamin D supplementation during pregnancy: double-blind lasix 100 mg, randomized clinical trial of safety and effectiveness lasix 40 mg. Dietary intake and cell membrane levels of long-chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest 100mg lasix. Beneficial effects of long-chain n-3 fatty acids included in an energy-restricted diet on insulin resistance in overweight and obese European young adults lasix 100mg. Specific insulin sensitivity and leptin responses to a nutritional treatment of obesity via a combination of energy restriction and fatty fish intake 100 mg lasix. Insulin action on muscle protein kinetics and amino acid transport during recovery after resistance exercise 40mg lasix. International Journal of Obesity and Related Metabolic Disorders 1993 Dec; 17 suppl 3:S83–S85 lasix 40mg. Insulin’s impact on renal sodium transport and blood pressure in health , obesity , and diabetes. Could mitochondrial efficiency explain the susceptibility to adiposity, metabolic syndrome, diabetes and cardiovascular diseases in South Asian populations? Proceedings of the National Academy of Sciences of the United States of America 1988 Sep; 85(17): 6465–6467. Brain mitochondria as a primary target in the development of treatment strategies for Alzheimer disease. The International Journal of Biochemistry & Cell Biology 2009 Oct; 41(10): 1989–2004. Environmental toxicants inhibit neuronal Jak tyrosine kinase by mitochondrial disruption. Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance. Mitochondrial dysfunction and metabolic syndrome—looking for environmental factors. Chronic levodopa administration alters cerebral mitochondrial respiratory chain activity Annals of Neurology 1993; 34: 715–723. Statin adverse effects: a review of the literature and evidence for a mitochondrial mechanism. Age-related changes in plasma coenzyme Q10 concentrations and redox state in apparently healthy children and adults. Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke. Role of coenzyme Q10 (CoQ10) in cardiac disease, hypertension and Ménière-like syndrome. Supplementation with alkaline minerals reduces symptoms in patients with chronic low back pain. Physical activity and cancer risk: dose-response and cancer, all sites and site-specific. Dietary and nutritional factors and pancreatic cancer: a case-control study based on direct interviews. Breast cancer survival for postmenopausal women who are less overweight and eat less fat. Lung cancer risk in male workers occupationally exposed to diesel motor emissions in Germany. 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Garlic consumption and cancer prevention: meta-analyses of colorectal and stomach cancers. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. A retrospective cohort mortality study of workers exposed to formaldehyde in the garment industry. Genetically based n-acetyltransferase metabolic polymorphism and low-level environmental exposure to carcinogens. Biotransformation of caffeine, paraxanthine, theophylline, and theobromine by polycyclic aromatic hydrocarbon-inducable cytochrome P-450 in human liver microsomes. American Journal of Physiology—Gastrointestinal and Liver Physiology 1990; 259:G524–G529. Effect of ascorbate or N-acetylcysteine treatment in a patient with hereditary glutathione synthetase deficiency. Failure of N-acetylcysteine to reduce low-density lipoprotein oxidizability in healthy subjects. Nutritionally and chemically induced impairment of sulfate activation and sulfation of xenobiotics in vivo. S-adenosyl-L-methionine antagonizes oral contraceptive-induced bile cholesterol supersaturation in healthy women: preliminary report of a controlled randomized trial. Protective effect of methionine against vinyl chloride-mediated depression of non-protein sulfhydryls and cytochrome P-450. Dietary betaine promotes generation of hepatic S-adenosylmethionine and protects the liver from ethanol-induced fatty infiltration. Studies on pharmacodynamics, site and mechanism of action of silymarin, the antihepatotoxic principle from Silybum marianum (L. Selectivity of silymarin on the increase of the glutathione content in different tissues of the rat. Effect of silymarin on chemical, functional, and morphological alteration of the liver. Randomized controlled trial of silymarin treatment in patients with cirrhosis of the liver. Meta-analysis: the efficacy of over-the-counter gastro-oesophageal reflux disease therapies. Influence of gastric acidity on bacterial and parasitic enteric infections: a perspective. Gastric secretion of acid and intrinsic factor in patients with hyper and hypothyroidism. An investigation into the gastric secretion of a hundred normal persons over the age of sixty. Estimation of gastric residence time of the Heidelberg capsule in humans: effect of varying food composition. Gastroesophageal reflux disease and Helicobacter pylori: what may be the relationship? Occurrence and significance of gastric colonization during acid-inhibitory therapy. High acid secretion may protect the gastric mucosa from injury caused by ammonia produced by Helicobacter pylori in duodenal ulcer patients. Helicobacter pylori infection and gastric juice vitamin C levels: impact of eradication. Vitamin E concentrations in the human stomach and duodenum: correlation with Helicobacter pylori infection. Effects of flavonoids on parietal cell acid secretion, gastric mucosal prostaglandin production and helicobacter pylori growth. Effect of colloidal bismuth subcitrate on symptoms and gastric histology in non-ulcer dyspepsia: a double blind placebo controlled study. Efficacy and tolerability of a fixed combination of peppermint oil and caraway oil in patients suffering from functional dyspepsia. Systematic review: efficacy and safety of pancreatic enzyme supplements for exocrine pancreatic insufficiency. Pancreatic enzyme replacement therapy: comparative effects of conventional and enteric-coated microspheric pancreatin and acid-stable fungal enzyme preparations on steatorrhoea in chronic pancreatitis. Mortality from all causes and from coronary heart disease related to smoking and changes in smoking during a 35-year follow-up of middle-aged Finnish men. Relationship of cigarette smoking to blood pressure and serum lipids and lipoproteins in men. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. An analysis of the effectiveness of interventions intended to help people stop smoking. Trends in leisure-time physical inactivity by age, sex, and race/ethnicity— United States, 1994–2004. Low grade inflammation and coronary heart disease: prospective study and updated meta-analysis. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. The emerging role of Mediterranean diets in cardiovascular epidemiology: monounsaturated fats, olive oil, red wine or the whole pattern? N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials. Dose-response effects of omega-3 fatty acids on triglycerides, inflammation, and endothelial function in healthy persons with moderate hypertriglyceridemia. Serum cholesterol ester fatty acids and their relation with serum lipids in elderly men in Crete and the Netherlands. Eicosapolyenoic acids of serum lipids of Japanese islanders with low incidence of cardiovascular diseases. Nut consumption and risk of coronary heart disease: a review of epidemiologic evidence. A walnut diet improves endothelial function in hypercholesterolemic subjects: a randomized crossover trial. C-reactive protein concentration and concentrations of blood vitamins, carotenoids, and selenium among United States adults. Acute effect of drinking red and white wines on circulating levels of inflammation-sensitive molecules in men with coronary artery disease. Moderate alcohol intake and lower risk of coronary heart disease: meta-analysis of effects on lipids and haemostatic factors. Polyphenolic compounds from red grapes acutely improve endothelial function in patients with coronary heart disease. European Journal of Cardiovascular Prevention & Rehabilitation 2005; 12(6): 596–600. Effects of pomegranate juice consumption on myocardial perfusion in patients with coronary heart disease. Concentrated pomegranate juice improves lipid profiles in diabetic patients with hyperlipidemia. Use of antioxidant vitamins for the prevention of cardiovascular disease: meta- analysis of randomised trials. Carotenoid composition and antioxidant potential in subfractions of human low-density lipoprotein. Inverse correlation between plasma vitamin E and mortality from ischemic heart disease in cross- cultural epidemiology. 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Research in cognitive neuropsychology has also produced many new assessment tech- niques: while these were originally designed to explore theoretical models they are now used for clinical assessments as well 100 mg lasix. In parallel with these developments and complementary to them 40 mg lasix, re- habilitation medicine and the clinical neurosciences have highlighted the ecological value of cognitive assessment lasix 40 mg. Patient examinations have demonstrated that it is necessary to take into account the influence of en- vironment and real-life conditions on cognitive functioning 40mg lasix, as well as the influence of cognitive deficits on every day functioning lasix 100 mg. A test may be defined as an observa- tional technique which “elicits behavior samples in a standardized 100mg lasix, replic- able lasix 40mg, and more or less artificial and restricted situation (4) lasix 100mg. Psychometric tests generate quantitative data well-suited for statistical evaluation tech- niques . Standard scores , for example, are raw scores scaled according normative data based on scores from a demographically defined popula- tion sample. Depending on their scores, patients’ performances may also be classified in reference to a corresponding division (e. For tests with a normal (gaussian, parametric) raw score distribution, a score is considered abnormal when it falls one- and-one-half to two or more standard deviations below the mean of the reference groups. In the ideal situation, the same process with the same patient would always result in the same performance, so that the same meaning might be attributed to the same scores – whether from one pa- tient to another or from one examination to another. Some collections of tests (often termed batteries) such as the Wechsler Adult Intelligence Scales (which is updated about every 15 years) or the Halstead-Reitan Battery (which has remained unchanged for decades) contain different tasks for examining a number of cognitive dimensions (8,9). In the past, scores for these different tests were summed into one or several scores, presumably communicating something about the ephemeral concept “intelligence”, or the presence of a brain disorder. However, current knowledge of the complexities of brain function have rendered these summation procedures obsolete (4). Most individual tests actually examine a number of functions – not least being the ability to un- derstand instructions or keep them in mind. A drawing task, for example, in examining the ability to copy a design, will provide information on the patient’s fine motor control, visuospatial orientation, visual concept for- mation, perceptual accuracy, attention to details, among other capacities. Comput- erized tests are now available in which items are always delivered in the same format, automatic scoring takes into account reaction times and re- sponse delays, and the data are automatically recorded and evaluated. The main strengths of psychometric tests are their precision, their re- liability, and their generally good construct validity which allows examin- ers to generalize from test data to real-life predictions. Their chief limita- tions include difficulty in interpreting scores generated by tests of com- plex behaviors (e. Test users must realize that reliance on test scores alone loses very important qualitative aspects of patients’ per- formances; e. Significant idiosyncrasies of speech and pragmatics will al- so remain undocumented. Moreover, the development, standardization, and validation of a new test takes a long time – around ten years on aver- age – yet knowledge about cognition advances more rapidly. By missing a critical component discovered after their development is underway, some tests may be out of date even before their publication. Clinical scales and symptom inventories derived from classical neu- rology are also used for assessing impairment, both cognitive and behav- ioral. Tasks and items are designed to elicit data specific for one or an- other pathological symptom or syndrome. Since symptoms are not nor- mally distributed in either the patient or the general population, the usu- al normative approach is not relevant to standardization. For instance, the well-known Boston Diagnostic Aphasia Examination (11) is a standardized and quantitative examination of aphasia signs, not a test of language skills. Clinical scales are often used in preliminary investigations to be supplemented, as needed, by more spe- cific tests. Cognitive neuropsychology has also devised methodologically sophis- ticated research protocols that can identify specific cognitive functions. Using similar methods, relationships between brain structures or brain pathology and highly specific cognitive functions or dysfunctions have al- so been elucidated. To identify specific cognitive functions – or dysfunc- tions, this methodology requires two or more tasks with known properties in a cognitive domain. For example, if two cognitive functions A and B are independent (for instance, reading words aloud via a direct, lexical route, or reading via a grapheme/phoneme conversion process in a phonological route) it should be possible to find two tasks X and Y (in this example, reading aloud non-words and reading irregular words) such that success on task X and failure on task Y would be characteristic of the impairment of A and of the integrity of B; and conversely, success on Y and failure on X would be characteristic of the impairment of B and the integrity of A. Rather, the assessment is tailored for each patient, with tasks improvised accord- ing to the hypotheses to be tested. Selective attention, working memory, written language, visual perception, and agnosia in stroke patients are some of the domains in which this kind of procedure has proven fruitful. Advantages are coherence with theoretical models and refined under- standing of the specificity and brain relationships of many cognitive func- tions – and disorders, which had proven useful for therapy. However, this complex and time-consuming methodology, while important for research, has poor ecological validity, i. Questionnaires, checklists, and rating scales based on observation or in- terview are the most usual forms of assessment. Self-administered questionnaires ask patients for their opinions about their own abilities and behavior. These questionnaires have the ad- vantage of documenting self-awareness and the extent to which patients perceive their own limits with regard to cognitive skills. Conversely, they may not provide an objective or accurate account of the patient’s cogni- tive status. Items commonly included in such scales deal with abilities to read and write documents (e. Other items inquire about the patient’s self-sufficiency at home, such as taking prescribed medications without help or managing money (e. The Catherine Bergego Scale, which addresses the difficulties that pa- tients with unilateral inattention (neglect) are faced with in daily living is another example (14). Communication abilities, which are often impaired in brain damaged patients, need specific assessments. Recently these au- thors developed the Bordeaux Verbal Communication Scale, an ordinal scale rated from a structured interview, to document the efficacy of the aphasic patient’s communication in daily living and social activities: e. Some disability scales are scored according to the degree and type of help needed to per- form the task, which provides useful data for planning services (e. It is the visible product of the interaction between the person and the envi- ronment in a given situation. So it depends on many parameters, such as speed and accuracy in processing information coming from the external world, mental states about the situation (degree of awareness, affect, mo- tivation), previous goal-directed schemes and life styles (influence of cul- ture, education, previous experiences), and, of course, attitudes and reac- tions of other persons participating in the situation. Obviously it would be impossible to create an assessment tool which would take into account all these parameters. So behavioral assessment is necessarily global and de- scriptive, as is disability assessment. Questionnaires, check lists, and ordinal scales include brief descriptions of symptoms or behaviors that may be observed during the course of the condition, or lists of behaviors consid- ered abnormal with respect to social standards or compared to premor- bid behavior. More recently devel- oped scales contain many more behavioral tasks with graduated scores in- dicating task difficulty and degree of patient independence. The fine gra- dations of some instruments may permit the data to be treated much as scales with continuous variables (16, 18). Some ask for reports on correct or usual behaviors, which immediately raises the major questions: what is normal behavior? Many check lists ask for frequency or severity data for each item which gives quantifiable data for ordinal scaling. The goal of these instruments is to be more comprehensive by gathering cognitive, af- fective, and behavioral data in the same interview. Like cognitive ability scales, it developed mostly under the influence of rehabilitation medicine and pragmatic inquiry into the ecological validity of classical testing: e. And to what extent are the memory processes involved in a test the same as those required for everyday activities? Despite a general relationship be- tween memory test scores and daily functioning (4), good scores do not necessarily predict satisfactory behavioral adjustment or ability to return to work. Conversely, some patients with effective coping strategies may function well even though memory test performance is severely impaired. Three kinds of techniques for improving the ecological validity of cognitive assessment have been used. Putting the laboratory in real life settings (21) involves observing pa- tient behavior at home, during usual activities, with relatives and associ- ates. Although observation in the natural setting provides data that is most likely to be valid, it is both costly and very time-consuming. The re- liability of these observations may also be questioned as the data are not collected in a standardized manner: the examiner may have observed an atypical situation or the patient in a not usual state. Simulating real life in the laboratory requires examiners to design tests and tasks that resemble real life conditions and cognitive demands. Self-administered questionnaires and disability rating scales, of course, can only be used with patients who never left their home or have returned. Some laboratory techniques have the patient watch and react to videotapes or computerized virtual surroundings (see, for instance, 22). Others involve role-playing in which patient and examiner act out a fic- tive communication situation such as shopkeeper and customer or pa- tient and physician’s secretary (23, 24). Last, and the most difficult to check and score, some ecological tests take place in the real environment: e. In route-finding tests patients have to find their way to a goal in complex and unfamiliar surroundings (e. Al- though devised to have ecological validity, these tests can be difficult to use because of standardization, scoring, and reliability problems. Anoth- er weakness is that they provide little if any information about the under- lying mechanisms of impairment. These tests are best used in association with other tests of cognitive functioning. Mostly they tell about the prac- tical needs for setting the goals and assessing the efficacy of rehabilitation programs. However, disability level may change with differ- ent situations and in different environments. This changing nature of participation restriction (handicap), by itself, makes it difficult to stan- dardize these assessments. For instance, a baker with mild aphasia suf- fers a restriction of his social role when he sells bread in his shop, al- though this restriction disappears (or diminishes greatly ) when he is alone baking in front of his oven, and may even be less when he deals with a familiar customer than with a stranger. In this case it is neither the aphasia nor communication ability that should be assessed, but the situation of this patient selling in this shop. Some evaluation instruments have been developed by occupational therapists to take into account these factors (28, 29). Cognitive symptoms can be opaque and ambiguous: the same surface manifestation may be subtended by different mechanisms. For example, Nespoulous and Soum outline some reasons for the weak relationships between apha- sia symptoms and the underlying impairments (31): A symptom may be attributed to either of two different mechanisms depending on the sensi- tivity of the assessment technique and depth of analysis (e. A symptom may be related either to an impairment or to a compensation process (speak- ing slowly may result from difficulty encoding the forthcoming word or from a voluntary control of phonetic production. A symptom may be ex- plained by a single condition or may have arisen from multiple impair- ments, and so on. Moreover, great variability characterizes language or- ganization from one person to another (32), so that the same symptom may be related to different lesions sites in different persons. Thus one must be very careful before generalizing data from one patient to anoth- er. Similar questions, relevant for all domains of cognition, are of major importance when preparing a therapy program. A score is nothing more than a numerical value on a conven- tional scale, attributed to a patient’s answer or reaction to more or less standardized questions or stimuli by an examiner following a set of scor- ing rules. Each individual test performance should be evaluated in the light of the patient’s demography, history, education, and medical condi- tion. General and non-cognitive factors may interfere with the validity of the assessment. Health problems: pain, fatigue, sleep disorders, and med- ications can impair response speed and important aspects of attention and memory. Mood disorders, anxiety, poor motivation, fear of testing, and – most of all – depression, can impair cognitive performance. On the other hand, deliberately poor performance (malingering) in the course of a medico-legal assessment is usually easy to identify as unexpectedly low performances when evaluated in the context of daily functioning, or when errors do not make sense either in terms of usual patient test perfor- mances or knowledge of the condition presumably being evaluated. For example, when recall of the second and third trial of a word list are worse than the first, or when scores are by far better for rare items than com- monplace ones in a confrontation naming test, the examiner’s suspicions of poor motivation should be aroused. However, most patients want to preserve their dignity and perform at their best, even when monetary re- wards for impairment are anticipated. Other interpretation problems may come from the design of the tests themselves (4). Many ques- tionnaires and check lists generate a summed score based on points for positive answers. While this one-dimensional quantitative variable is readily accessible to statistical treatment, it may hide different – and sometimes, very different – answers. Cognitive measures should be related to naturalistic ob- servations in so far as possible. In case of disagreement between test scores and daily observations, believe the last. It also includes a qualitative dimension that takes into account all the factors that make sense of the score, including the patient’s examina- tion behavior and qualitative aspects of the test performances. For exam- ple, assessing cognitive strategies, that is, understanding how a patient performs a task, is often as important as finding out what the patient knows or can do (33).

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Anxiety differs from fear in that while fear is a rational response to a real danger lasix 100mg, anxiety usually lacks a clear or realistic cause lasix 100 mg. Though some anxiety is normal and even healthy 40 mg lasix, higher levels of anxiety not only are uncomfortable but also can lead to significant problems lasix 40 mg. The most common symptoms relate to the chest 100mg lasix, such as heart palpitations (awareness of a more forceful or faster heart beat) lasix 40mg, throbbing or stabbing pains 100 mg lasix, a feeling of tightness or inability to take in enough air 40mg lasix, and a tendency to sigh or hyperventilate . Tension in the muscles of the back and neck often leads to headaches , back pains, and muscle spasms. Other symptoms can include excessive sweating, dryness of the mouth, dizziness, digestive disturbances, and the constant need to urinate or defecate. Anxious individuals usually have a constant feeling that something bad is going to happen. They may fear that they have a chronic or dangerous illness—a belief that is reinforced by the symptoms of anxiety. Inability to relax may lead to difficulty in getting to sleep and constant waking in the night. Panic Attacks Severe anxiety will often produce what are known as “panic attacks”—intense feelings of fear. Panic attacks may occur independently of anxiety but are most often associated with generalized anxiety or agoraphobia. Causes Clinical anxiety, including panic attacks, can be produced by psychological problems as well as by biochemical factors such as caffeine, certain other drugs, and the infusion of lactate into the blood. The fact that these compounds can produce anxiety and panic attacks can be put to good use in understanding the underlying biochemical features of anxiety. Perhaps the most significant biochemical disturbance noted in people with anxiety and panic attacks is an elevated blood lactic acid level and an increased ratio of lactic acid to pyruvic acid. Lactate (the soluble form of lactic acid) is the final product in the breakdown of blood sugar (glucose) when there is a lack of oxygen. To illustrate how lactic acid is produced, let’s take the classic example of the exercising muscle. Muscles prefer to use fat as their energy source, but when you exercise vigorously there isn’t enough oxygen, so the muscle must burn glucose. Without oxygen, there is a buildup of lactic acid within the muscle; this is what causes muscle fatigue and soreness after exercise. Lactic Acid Conversion to Pyruvic Acid or Glucose The first few steps of normal glucose breakdown can occur without oxygen, until pyruvic acid is produced. The next steps require oxygen and end in the complete breakdown of pyruvic acid to carbon dioxide and water. Because the exercising muscle needs energy, the muscle cells continue to convert glucose to pyruvic acid in a process referred to as anaerobic metabolism. With good circulation, the lactic acid is removed from the muscle and transported to the liver, where it can be turned back into pyruvic acid or even glucose if needed. All of this biochemistry plays a role in anxiety, because individuals with anxiety have elevated blood levels of lactate and a higher ratio of lactic acid to pyruvic acid when compared with normal controls. Furthermore, if people who get panic attacks are injected with lactate, severe panic attacks are produced. Reducing the level of lactate is a critical goal in the treatment of anxiety and panic attacks. Therapeutic Considerations The natural approach to anxiety builds upon the recommendations given for stress in the chapter “Stress Management. If you suffer from mild anxiety, follow all of the recommendations given in that chapter for diet, exercise, nutritional supplementation, calming the mind and body, and taking an adrenal adaptogen. If you suffer from moderate to severe anxiety, follow all of the recommendations in that chapter as well as those discussed below; substitute kava for the adrenal adaptogen. Lactate Levels As pointed out previously, increased lactic acid levels may be an underlying factor in panic attacks and anxiety. The goal is to prevent the conversion of pyruvic acid to lactic acid and to improve the conversion of lactic acid back to pyruvic acid. There are at least six nutritional factors that may be responsible for elevated lactate levels or ratios of lactic acid to pyruvic acid:1 1. Food allergens By avoiding alcohol, caffeine, sugar, and food allergens, people with anxiety can go a long way toward relieving their symptoms. This recommendation may seem too simple to be valid, but substantial clinical evidence indicates that in many cases it is all that is necessary. For example, one study dealt with four men and two women who had generalized anxiety or panic disorder. Follow-up exams 6 to 18 months afterward indicated that five out of the six patients were completely without symptoms; the sixth patient became asymptomatic with a very low dose of Valium. By following the guidelines in the chapter “A Health-Promoting Diet,” as well as the recommendations for nutritional supplementation given in the chapter “Supplementary Measures,” you will provide your body with the kind of nutritional support it needs to counteract the biochemical derangements found in patients with anxiety and panic attacks. Nutritional Supplements Omega-3 Fatty Acids Anxiety and depression appear to be linked to lower levels of omega-3 fatty acids. A high intake of omega-6 fatty acids (found in corn-fed animal products, dairy products, and common vegetable oils such as corn, soy, safflower, and sunflower) and a low intake of omega-3 fatty acids (found in fish, fish oils, and flaxseed oil) can lead to an amplification in the production of these cytokines. So increasing the intake of omega-3 fatty acids and lowering the intake of omega-6 fatty acids may help to reduce anxiety and depression. The positive results seen with fish oil supplements in clinical depression are well documented. In regard to anxiety, one clinical study showed that fish oil supplementation decreased feelings of anger and anxiety in substance abusers. In one study, three out of four patients with a history of agoraphobia for 10 or more years improved within two to three months after taking flaxseed oil at a dosage of 2 to 6 tbsp per day, in divided doses depending upon response. Kava The area of Oceania—the island communities of the Pacific, including Micronesia, Melanesia, and Polynesia—is one of the few geographic areas in the world that did not have alcoholic beverages before European contact in the 18th century. However, these islanders did possess a magical drink that was used in ceremonies and celebrations because of its calming effect and ability to promote sociability. The drink, called kava, is still used today in this region, where the people are often referred to as the happiest and friendliest in the world. Preparations of kava root (Piper methysticum) gained popularity in Europe and the United States up until 2001, when safety concerns (discussed below) derailed their popularity. Several clinical trials utilized a special kava extract standardized to contain 70% kavalactones. However, this high percentage of kavalactones may be sacrificing some of the other constituents that may contribute to the pharmacology of kava. More important than the actual percentage of kavalactones is the total dosage of the kavalactones and the assurance that the full range of kavalactones is present. In one of the first double-blind studies, a 70% kavalactone extract was shown to exhibit significant therapeutic benefit in patients suffering from anxiety. Therapeutic effectiveness was evaluated using several standard psychological assessments, including the Hamilton Anxiety Scale. The results of this four-week study indicated that individuals who took kava extract had a statistically significant reduction in symptoms of anxiety, including feelings of nervousness and somatic complaints such as heart palpitations, chest pains, headache, dizziness, and feelings of gastric irritation. Studies have also compared the effects of a kava extract with antianxiety drugs such as buspirone and opipramol. In one double-blind study, 129 patients with generalized anxiety disorder were given either 400 mg kava (30% kavalactones), 10 mg buspirone, or 100 mg opipramol per day for eight weeks. Detailed analysis showed that no significant differences could be observed in terms of efficacy and safety. About 75% of patients were classified as responders (at least a 50% reduction of the anxiety score) in each treatment group, and about 60% achieved full remission. The group receiving the kava extract demonstrated significant improvement at the end of the very first week of treatment. In addition to symptoms of stress and anxiety, a number of other symptoms also improved. Most notably there was an overall improvement in subjective well-being, mood, and general symptoms of menopause, including hot flashes. Additional studies have shown that unlike benzodiazepines (Valium-like drugs), alcohol, and other drugs, kava extract is not associated with depressed mental function or impairment in driving or the operation of heavy equipment. Like other benzodiazepines, oxazepam inhibited the recognition of both new and old words. In contrast, kava allowed a slightly greater recognition rate and a larger difference between old and new words. In this case, it relieves anxiety, but unlike standard antianxiety drugs, kava actually improves mental function and, at the recommended levels, does not promote sedation. In 2009, the first documented human clinical trial assessing the antianxiety and antidepressant efficacy of a water-based extract of kava was published. The kava preparation produced significant antianxiety and antidepressant activity and raised no liver toxicity or safety concerns at the dose and duration studied. Specifically, kava reduced participants’ Hamilton Anxiety Scale score in the first controlled phase by –9. Pooled analyses also revealed highly significant relative reductions in other anxiety and depression scale scores. As a result of clinical studies, the recommendation for anxiety-relieving effects is 45 to 70 mg kavalactones three times per day. For sedative effects, the same daily quantity (135 to 210 mg) can be taken as a single dose one hour before retiring. To put the therapeutic dosage in perspective, it is important to point out that a standard bowl of traditionally prepared kava drink contains approximately 250 mg kavalactones, and several bowls may be consumed at one sitting. In November 2001, German health authorities announced that 24 cases of liver disease (including hepatitis, liver failure, and cirrhosis) associated with the use of kava had been reported; of the affected individuals, one died and three required a liver transplant. Food and Drug Administration began advising consumers of the potential risk of severe liver injury associated with the use of kava-containing dietary supplements. Kava was subsequently withdrawn form the market in the European Union, the United Kingdom, and Canada. In the initial report the true nature of kava-induced liver damage was clouded by the fact that in 18 of these cases, conventional prescription or over-the-counter pharmaceutical drugs with known or potential liver toxicity were also being used. Proponents of kava quickly argued that it was entirely possible that the use of kava by these individuals was a coincidence rather than the cause of the liver problem. As of 2007 of the approximately 100 cases of liver toxicity that had been reported worldwide, only in 14 cases was causality deemed to be “probable. The existing data are complex, but it looks as if the major factor in any kava-induced liver toxicity was the use of non-root parts such as stems and leaves as well as stem peelings. Up until that development, the only parts of the kava plant that were traditionally used throughout its 3,000-year history were the roots, never the peelings or the leaves. A survey of 400 German medical practices showed that 78% of the kava prescriptions that were written prior to 2001 significantly exceeded the recommended intake. Measures suggested to address the liver toxicity issue include (1) use of a noble kava cultivar that is at least five years old at time of harvest, (2) use of peeled and dried rhizomes and roots, (3) dosage recommendation of ≤250 mg kavalactones per day (for medicinal use), and (4) manufacturer quality control systems enforced by strict policing. It should be mentioned that while it has been suggested that traditional aqueous extracts should be used instead of alcoholic or acetonic extracts, the toxicity is linked to the kava plant itself, possibly with a low-quality plant or wrong plant part, rather than the method of extraction or solvent. Use of kava for more than four weeks requires close monitoring of liver enzymes once every four to six weeks. Patients should be instructed to discontinue use of kava if symptoms of jaundice (e. Nonspecific symptoms of liver disease include nausea, vomiting, light-colored stools, unusual tiredness, weakness, stomach or abdominal pain, and loss of appetite. Kava has the potential to interact with a wide range of medications and may also potentiate the effects of benzodiazepines, barbiturates, and prescription sedative drugs (sleeping pills). In that regard, it is important to follow these recommendations: • Reduce or eliminate the use of stimulants. Note: If you are currently taking a sedative-hypnotic or antidepressant drug, you will need to work with a physician to get off the drug. Stopping the drug on your own can be dangerous; you absolutely must have proper medical supervision. Withania somnifera (ashwagandha), equivalent to Sensoril: 125 to 250 mg per day22 Kava (Piper methysticum): dosage equivalent to 45 to 70 mg kavalactones three times per day Asthma • Recurrent attacks of shortness of breath, cough, and coughing up thick mucus • Prolonged expiration phase with generalized wheezing and abnormal breath sounds • Laboratory signs of allergy (increased levels of eosinophils in blood, increased serum IgE levels, positive food and/or inhalant allergy tests) Asthma is a breathing disorder characterized by spasm and swelling of the bronchial airways along with excessive excretion of a viscous mucus that can also make breathing difficult. Asthma affects approximately 7% of the population of the United States and causes 4,210 deaths per year. There is a 2:1 male-to-female ratio among affected children, which equalizes by the age of 30. Reasons often given to explain the rise in asthma include the following: • Increased stress on the immune system due to factors such as greater chemical pollution in the air, water, insect allergens (mostly from dust mites), and food • Earlier weaning and earlier introduction of solid foods to infants • Food additives • Higher incidence of obesity2 • Genetic manipulation of plants, resulting in food components with greater allergenic tendencies In addition, certain genetic variables may make certain individuals more susceptible to asthma. Extrinsic or atopic asthma is generally considered an allergic condition with a characteristic increase in IgE—the antibody produced by white blood cells that can bind to specialized white blood cells, known as mast cells, and cause the release of mediators such as histamine. Intrinsic asthma is associated with a bronchial reaction that is due not to an allergy but rather to such factors as chemicals, cold air, exercise, infection, and emotional upset. If you are suffering from an acute attack, consult your physician immediately or go to an emergency room. Causes Asthma is caused by a complex interaction of environmental and genetic factors. The strongest risk factor for developing asthma is a history of allergies such as eczema (atopic dermatitis) and hay fever. The presence of atopic dermatitis increases the risk of asthma three- to fourfold. The specific imbalance is an increase in the number or function of specialized white blood cells known as Th2 helper T cells. These cells ultimately lead to an increase in the release of compounds that heighten the allergic response. They are either preformed in little packets (granules) within mast cells or generated from fatty acids that reside in cell membranes.

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