Because of the role of the nicotinic cholinergic receptor in autonomic neurotransmission muscle relaxant drugs side effects purchase voveran sr mastercard, autoimmunity to spasms definition cheap 100 mg voveran sr with amex the receptor results in a pandysautonomia spasms parvon plus voveran sr 100 mg with mastercard. Steven Vernino had published a study about autoimmune autonomic neuropathy associated with a circulating antibody to spasms rectal area purchase voveran sr overnight the neuronal nicotinic receptor, which 562 Principles of Autonomic Medicine v. The antibodies interfere with ganglionic neurotransmission, and so post-ganglionic nerve traffic is decreased in the parasympathetic nervous system and the sympathetic noradrenergic and cholinergic systems. Because of parasympathetic cholinergic failure, the patient has decreased salivation, lacrimation, gastrointestinal movements, and bladder tone. Because of sympathetic noradrenergic system failure, the patient has neurogenic orthostatic hypotension. Myasthenia gravis also involves autoimmunity to nicotinic receptors, but these mediate neuromuscular transmission and have different components from the nicotinic receptors mediating autonomic transmission. The closely related Lambert-Eaton syndrome involve autoimmunity to calcium 563 Principles of Autonomic Medicine v. On the other hand, interference with ganglionic neurotransmission would result in decreased post-ganglionic sympathetic nerve traffic. To treat the patient’s chief symptom, dry mouth, we prescribed bethanechol (Urecholine™), which is a muscarinic cholinergic agonist. Bethanechol treatment produced a very gratifying result in our patient—she had a return of her ability to make saliva, alleviating her chief complaint. This sequence suggests that the target of autoimmune attack is post-ganglionic, unmyelinated axons, because parasympathetic post-ganglionic axons are short and 565 Principles of Autonomic Medicine v. Cardiac sympathetic denervation revealed by 18F-dopamine scanning in a patient with autoimmunity-associated autonomic denervation. As the name implies, this syndrome involves episodic painful headache, especially in the area of the eye, with conjunctival injection and tearing on the affected side. Several years ago I evaluated a patient who had attacks of severe pain in the head and face accompanied by conjunctival injection, nasal stuffiness, and local sweating. Injection of edrophonium (Tensilon™), which blocks acetylcholine metabolism, evoked an attack, and ganglion blockade with trimethaphan prevented the Tensilon effects. These findings indicated that the acetylcholine released from autonomic nerves mediated the attacks. Conjunctival injection, tearing and peri-orbital and forehead sweating accompanying pain evoked by edrophonium. Prevention of edrophonium-induced sweating and pain by ganglion blockade with trimethaphan. The cause is disruption of sympathetic nerve fibers, which ascend in the chest and neck alongside the carotid artery. Examples of harlequin syndrome the flushing and sweating occur on the side opposite the sympathetic lesion, presumably because of a form of compensatory activation of the intact sympathetic pathway. Rarely, Horner’s syndrome and the harlequin syndrome occur together; when this happens the ptosis and miosis occur on the same side as the lesion, while the flushing and sweating occur on the opposite side. The images below convey graphically the main visible changes in this rare condition. Patients with erythromelalgia have redness, swelling, and an intense burning sensation in the extremities or face. The symptoms worsen with exposure to heat or exercise and are relieved by local cooling of the skin. Secondary forms of erythromelalgia are associated with other conditions, such as myeloproliferative diseases, autoimmune disorders, Fabry disease, or hypercholesterolemia, or drugs, such as fluoroquinolones (a class of antibiotics), bromocriptine (a dopamine receptor blocker), pergolide (a dopamine receptor 570 Principles of Autonomic Medicine v. Rarely, primary erythromelalgia is inherited as an autosomal dominant trait, results from hyperexcitability of nociceptor C-fibers in the dorsal root ganglion. The channels are activated at more hyperpolarized trans-membrane electrical potentials than normal, so that the channels are open for prolonged periods. Between flare-ups, under resting conditions microcirculatory flow is decreased, and there is blunting of reflexive responses of microcirculatory flow to the Valsalva maneuver and cooling of the opposite extremity. These abnormalities have been interpreted in terms of decreased cutaneous perfusion combined with reflexive sympathetically mediated vasoconstriction, due to small fiber sympathetic neuropathy and denervation hypersensitivity; however, only a small minority of erythromelalgia patients have small fiber sympathetic 571 Principles of Autonomic Medicine v. Patients I have seen have brought with them small fans to blow against their skin. This should not be used as a form of treatment, however, because of damage to the skin. Tramadol, amitriptyline, mexiletine (a non selective voltage-gated sodium channel blocker), or opioids may give relief. Even at the most sophisticated and knowledgeable centers, the diagnosis often remains uncertain, especially for functional disorders. An agreed upon diagnosis, such as postural tachycardia syndrome, does not necessarily carry with it agreed upon ideas about the mechanism of the condition, the most appropriate treatment, or the long term outcome. On the other hand, there are many treatments for dysautonomias, including non-drug and drug treatments, and there are many coping tactics. Effective management includes learning about situations likely to worsen or improve symptoms. Joining a support group, you can compare notes with others in the same situation and “flip the clinic” by educating clinicians about individual experiences. You also benefit fellow patients and humanity in general by participating in research and in helping train physicians. For instance, postural tachycardia syndrome that comes on soon after a viral infection in an otherwise healthy person may “melt away” over many months or years. First, in patients with chronic orthostatic intolerance, maintaining excellent muscle tone in the anti-gravity muscles of the buttocks, thighs, and calves maximizes the efficiency of muscle pumping to maintain venous return to the heart during orthostasis. Third, it is important in chronic, debilitating disorders for the patient to regain a sense of at least some control over the situation. Sometimes the responses of a patient to a treatment help the doctor determine the diagnosis. Patients with dysautonomias can feel differently from day to day, without any clear reason why. This means that if a treatment is tried, it may take a trial period to decide whether the treatment has helped or not. In patients who have a fall in blood pressure every time they 576 Principles of Autonomic Medicine v. Doctors usually recommend a high salt diet for patients with an inability to tolerate prolonged standing (chronic orthostatic intolerance) or with a fall in blood pressure during standing (orthostatic hypotension). Normally when a person takes in a high salt diet, the kidneys increase the amount of salt in the urine, and this limits the increase in blood volume. After a few days of the same salt intake, the rate of sodium excretion equals the rate of intake. Drugs that promote retention of sodium by the kidneys, such as fludrocortisone, are usually required for high salt intake to increase body fluid volume effectively. Why water drinking should increase the blood pressure in patients with autonomic failure, when doing so does not affect the blood pressure of healthy people, remains unclear. Researchers have proposed the existence of an “osmopressor response,” in which ingested water without solute acts in the gut or liver to increase sympathetic noradrenergic system 577 Principles of Autonomic Medicine v. The osmopressor response may improve orthostatic tolerance in patients with baroreflex failure or autonomically mediated syncope. This habit might indicate a tendency to dehydration and low blood volume, but the pathophysiologic meaning of the “water bottle sign” remains unclear. In people with dizziness or lightheadedness when they stand up 578 Principles of Autonomic Medicine v. Reducing the amounts of sugars or other carbohydrates in meals may help manage symptoms. A substantial proportion of patients with chronic orthostatic intolerance have gastrointestinal symptoms and signs leading to a diagnosis of gastroesophageal reflux, slowed gastric emptying, or irritable bowel syndrome. Gastroenterologists managing these patients should be aware that recommending a high fiber diet might worsen orthostatic intolerance by augmenting shunting of blood to the gut. This can decrease leakage of fluid from the veins into the tissues and decrease swelling of the feet. In patients with veins that fill up or leak excessively during standing, compression garments can improve toleration of prolonged standing. Wearing compression hose may be disappointing in the 579 Principles of Autonomic Medicine v. Inflation of an abdominal binder (which resembles a huge blood pressure cuff) squeezes blood out of the abdomen and increases venous return to the heart. When exposed to the heat, patients with failure of the sympathetic cholinergic system may not sweat adequately to maintain the core temperature by evaporation of the sweat.
Know the normal physiology of fasting (absorption uterus spasms 38 weeks voveran sr 100mg sale, gluconeogenesis spasms heart purchase voveran sr cheap, glycogenolysis muscle relaxant blood pressure buy voveran sr canada, lipolysis spasms poster generic voveran sr 100 mg with amex, and ketogenesis) 2. Know the history, physical examination, and laboratory findings for glucose-6-phosphate deficiency b. Know the enzyme defects in the syndromes of glucose underproduction and means of testing for them c. Know the diagnosis and treatment of defects in glycogen metabolism (Debrancher enzyme, phosphorylase activation defects, glycogen synthetase) d. Know the clinical findings, diagnosis, and treatment of genetic conditions that result in a functional defect in gluconeogenesis. Know the history, physical examination, and laboratory testing for defects in fatty acid metabolism (defects in fatty acid transport, defects in carnitine metabolism, defects in fatty acid oxidation, defects in amino acid catabolism) g. Know the management and prognosis of children with defects in glycogen metabolism that are relevant to endocrinology h. Know the time to hypoglycemia after eating in disorders of absorption, gluconeogenesis, glycogenolysis, lipolysis, and ketogenesis j. Know age of presentation of hypoglycemia in disorders of absorption, gluconeogenesis, glycogenolysis, lipolysis, and ketogenesis k. Know the laboratory findings in disorders of gluconeogenesis, including the finding of increased lactate concentrations. Recognize that hyperinsulinemia and beta cell hyperplasia are associated with infants of diabetic mothers, erythroblastosis, and Beckwith Wiedemann syndrome 2. Know the treatment of hypoglycemia due to hyperinsulinemia in infants of diabetic mothers, and infants with erythroblastosis and Beckwith Wiedemann syndrome 3. Know the prognosis of hypoglycemia due to hyperinsulinemia in infants of diabetic mothers, or in infants with erythroblastosis and Beckwith Wiedemann syndrome 4. Know that hypoglycemia with hyperinsulinism can be associated with stress and sepsis in newborn infants b. Know that hypoglycemia secondary to hyperinsulinism is due to overutilization and underproduction of glucose 2. Understand the administration of glucagon and significance of blood glucose measurements after its injection in the diagnosis of hypoglycemia 4. Recognize the various names previously used to describe congenital hyperinsulinism (eg, nesidioblastosis, islet cell hyperplasia, islet cell dysplasia, islet cell dysmaturity) represented in the pathological findings of pancreatic beta cells in pancreatic ductal tissue 5. Recognize the clinical settings in which hypoglycemia may be due to islet cell tumors 7. Recognize the clinical findings in hyperinsulinemia, including the requirements for increased glucose infusion 10. Know the most appropriate initial steps in identifying the etiology of hypoglycemia 11. Recognize hyperinsulinemia as a likely cause of intractable hypoglycemia in a neonate 12. Understand the chronic management of hyperinsulinism in young infants and children including mechanisms of action of medications used 14. Know that glutamate dehydrogenase deficiency produces hyperinsulinemic hypoglycemia, and understand the mechanism by which hypoglycemia and hyperammonemia are produced 18. Know the pathophysiology of the genetic mutations that result in congenital hyperinsulinism 20. Understand the difference between focal and diffuse causes of congenital hyperinsulinism and know the diagnostic tests used to differentiate between them 21. Recognize that hypoglycemia secondary to hyperinsulinism may be due to exogenous insulin and sulfonylureas C. Know the biochemistry of glucagon biosynthesis and the factors that regulate glucagon release b. Understand mechanisms of action of glucagon on glycogenolysis and the role of glucagon in the regulation of the blood glucose concentration 2. Understand the use of glucagon as a diagnostic and therapeutic tool in hypoglycemia 2. Know that some extracellular calcium is bound to serum proteins, primarily albumin, while some extracellular calcium is ionized or free 2. Know that in hypoalbuminemia, the total serum calcium concentration is often low despite a normal ionized calcium 4. Know that acidosis decreases binding of calcium to serum proteins and thus, in acidosis, the total serum calcium is often low despite a normal ionized calcium 5. Recognize the preanalytical factors (eg, prolonged exposure to air, temperature, excess heparin) which may affect accurate laboratory measurement of ionized calcium b. Understand the difference between passive and active intestinal calcium absorption and identify the factors (calcium load, hormonal regulation) affecting each 2. Recognize that in hyperparathyroidism, hypercalciuria is due to the effect of increased extracellular calcium concentration on the kidney and is not due to increased parathyroid hormone concentration b. Know the effects of thiazide diuretics, corticosteroids, and furosemide on renal excretion of calcium 3. Know that calcium is important for neural function, particularly at the neuromuscular junction, and that decreased extracellular calcium concentration causes increased neuromuscular excitability, accounting for many of the symptoms of hypocalcemia 2. Recognize that phosphate shifts between extracellular and intracellular compartments and know which factors influence this movement 3. Understand that the kidney acts to conserve magnesium during magnesium depletion d. Know that hypocalcemia may be refractory to therapy when serum magnesium concentration is decreased 3. Recognize the suppressive effect of hypermagnesemia on parathyroid hormone secretion B. Be aware that congenital hypoparathyroidism may be inherited as an autosomal dominant, autosomal recessive, or X-linked recessive trait 2. Know that acquired hypoparathyroidism may be a complication of thyroid surgery or, rarely, radioactive iodine therapy 4. Know that hypocalcemia that occurs in hypoparathyroidism is partly due to decreased synthesis of calcitriol 6. Know the clinical features of hypoparathyroidism including ectopic (particularly intracranial) calcification 8. Know that functional hypoparathyroidism can result from activating mutations or antibody-mediated stimulation of the calcium-sensing receptor of the parathyroid cells 10. Know which medications are used to treat children with hypoparathyroidism and how to adjust doses b. Recognize the findings in patients with pseudohypoparathyroidism and in patients with progressive osseous heteroplasia 4. Recognize the laboratory findings, including gene analysis, in patients with pseudohypoparathyroidism 7. Be familiar with the diagnosis of familial hypocalciuric hypercalcemia and know how to distinguish it from other forms of hypercalcemia 2. Know the molecular cause and inheritance pattern for familial hypocalciuric hypercalcemia and its relationship to severe neonatal hyperparathyroidism c. Recognize the biochemical profile consistent with "hungry bone syndrome" after parathyroidectomy for severe hyperparathyroidism 2. Know that vitamin D is produced in the skin by the action of ultraviolet light on 7-dehydrocholesterol 2. Know that the photocatalyzed conversion of 7-dehydrocholesterol to vitamin D proceeds faster in light-skinned persons than dark-skinned persons 3. Know that ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3) can be derived from plant and animal dietary sources respectively and that the two molecules are metabolized similarly b. Understand the regulation of 1-alpha hydroxylase activity by phosphate, parathyroid hormone, and 1,25-dihydroxyvitamin D d. Know that 1-alpha hydroxylase activity exists in some neoplastic and inflammatory monocytes and in macrophages, particularly in sarcoidosis 2. Know that serum 25-hydroxyvitamin D concentrations primarily reflect vitamin D nutritional status b. Know that 1,25-dihydroxyvitamin D concentrations may be elevated in children with rickets due to phosphate or vitamin D deficiency c.
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In cre ase d t im e t o p roce d u re (> 3 d ays) w as sign ifican t ly associated w it h an in cre ase d likelih ood of moderate to spasms in 6 month old baby discount 100 mg voveran sr amex severe neurological deficit spasms catheter cheap voveran sr 100 mg online. Additionally spasms hands and feet 100mg voveran sr amex, the increased morbidity and mortality associated with surgical intervention on patients who present subacutely with evidence of vasospasm on imaging muscle spasms zinc discount voveran sr 100 mg overnight delivery, may be better suited for 79 endovascular intervention. Havin g t h e a n e u r ysm clip p e d p e r m it s u se o f h yp e r d yn a m ic t h e r apy for vasospasm 4. Som e d at a sh ow n o d i erence in surgical complications in good and bad grade patients with 122 anterior circulation aneurysms 3. This is usually accomplished by excluding the aneurysm from the circulation with a clip across its neck. Placing the clip too low on the aneurysm neck may occlude the parent vessel, while too distal placement may leave a so-called “aneurysmal rest” which is not benign since it may enlarge (see below). A “dog-ear” occurs when a clip is angled to leave part of the neck at one end, and obliter ates the neck at the other. Rests are not innocuous, even if only 1–2mm, because they may later 124 expand and possibly rupture years later, especially in younger patients. Patients should be followed w ith serial angiography, and any increase in size should be treated by reoperation or endovascular techniques if possible. Bo o k i n g t h e c a s e: Cr a n i o t o m y f o r a n e u r y s m Als o s e e d e fa u lt s & d is c la im e r s (p. The oxygen deficiency pre cludes aerobic glycolysis and oxidative phosphorylation. Surrounding this central core is the penum bra, where collateral flow (usually through leptom eningeal vessels) provides m arginal oxygenation w hich m ay impair cellular function w ithout im m ediate irreversible dam age. However, after adjustment for age, this association was no longer statistically signifi cant. Because of the potential danger of hypoxic injury to brain and other organs (including areas of impaired autoregulation as well as normal areas), some surgeons avoid this method. Th e follow in g fa ct o r s m ay m a n d a t e t h e u se o f t e m p o r a r y clip s (a n d a ss o cia t e d t e ch n iq u e s o f ce r e bral protection): giant aneurysm, calcified neck, thin/fragile dome, adherence of dome to critical structures, vital arterial branches near the aneurysm neck, intraoperative rupture. Aside from giant aneurysms, most of these factors may be di cult to identify pre-op. Therefore, Solom on provides some degree of cerebral protection to all patients undergoing aneurysm surgery. Re s u lt s a r e p r e lim in a r y, fu r t h e r in ve s t ig a t io n is n e e d e d t o d e m o n s t r a t e t h e d e g r e e o f n e u r o p r o t e c 137 tion. Has been reported at doses 170 mcg/kg/min for neuroprotection (if tolerated) but this may be risky. Sid e e ects: possible anaphylactic reaction with angioneurotic edema (angioedema) of the air 138 ways, Propofol Infusion syndrom e (p. Alt h o u gh r u p t u r e r a t e m ay b e 141 142 higher in early surgery than with late surgery, other series found no di erence. Prevent ion of intraoperat ive rupture Presented as a list here to be incorporated into general operative techniques. Brain can become surprisingly tight even when bleeding seems to be into open subar achnoid space. Use the same modality for each follow-up to facilitate accurate com parison may shrink down with repeated low current strokes with the bipolar (avoid the temptation to use continuous high current) 3. Bleeding worsens as clip blades become approximated prompt opening and removal of clip at the first hint of bleeding may minimize the extent of the tear utilize 2 suckers to determine if definitive clipping can be done, or what is more common, to allow temporary clipping (see above) b) poor technical clip application: tends to abate as clip blades become approximated. Inspect the blade tips for the following: to be certain that they span the breadth of the neck. If not, a second longer clip is usually applied parallel to the first, which may then be advanced to verify that they are closely approximated. If not, tandem clips may be necessary, and sometimes multiple clips are needed 79. Th is in clu d es an eu r ysm s t h at are clipped or coiled w here there is still aneurysm filling, as well as a persistent aneurysm rest or a neck (p. W hile m ost aneurysm rests appear to be stable, there is a sm all subset that m ay enlarge or 144 rupture. Ad d it io n a lly, e ve n a n a n e u r ysm t h a t h a s b e e n co m p le t e ly o b lit e r a t e d m a y r e cu r, a n d t h e r e fo r e one has to consider the durability of treatment. Frequency natural history, clinical outcome, and risks of sur of incidental intracranial aneurysms in neurofi gical and endovascular treatment. Cerebral aneurysms in child Polycystic Kidney Disease Would Benefit from hood and adolescence. Ne w Yo r k: In tracran ial an eurysm s in autosom al dom inan t Grun e an d Stratton; 1958:17–22 polycystic kidney disease. Philadelphia matic Intracranial Aneurysm in a Patient with 1990 Au t o so m a l Do m in a n t Po lycyst ic Kid n e y Dise a se. Physical Factors in the Initiation, Saccu lar In tracran ial An eu r ysm s in Au tosom al Grow th, an d Rupture of Hum an In tracran ial Saccu Dom inant Polycystic Kidney Disease. Spontane cranial Aneurysms: Determining the Site of Rup ous Thrombosis of an Intracranial Aneurysm. Dis lar Hemorrhage from Ruptured Aneurysm: Retro appearance of a Cerebral Aneurysm: An Unusual spective Analysis of 91 Cases. Cere Hemorrhage due to Aneurysms of the Distal Poste bral Aneurysm Thrombosis, Shrinkage, Then Dis rior Inferior Cerebellar Artery. The Clinical bral Artery Aneurysm with Angiographic Reap Spect rum of Unruptured In tracran ial An eur ysm s. Thunderclap Headache: Symp Th erap y in th e Acu the Period Follow in g An eu r ysm al tom of Unruptured Cerebral Aneurysm. Subarach n oid Hem orrhage: Prelim in ar y Observa 1986; 2:1247–1248 tions from the Cooperative Aneurysm Study. Bilateral Giant Intra in the Treatment of Unclippable Cerebral Aneur cavernous Aneurysms: Technique of Unilateral ysm. Fam In operable Carotid An eu r ysm s w ith En d ovascu lar ilial association of intracranial aneurysms and Ca r o t id Occlu sion Aft e r Ext r a cr a n ia l In t r a cr a n ia l multiple congenital anomalies. The Management of Ruptured Intra ruptured intracranial aneurysms: a systematic cranial Aneurysms. Com parison bet w een clipping and coil Follow in g An eu r ysm Wrap p in g: A 10-Year Follow ing on the incidence of cerebral vasospasm after Up Review of Clipped and Wrapped Aneurysm s. Subse 2007; 30:22–30; discussion 30-1 quent Bleeding from Ruptured Intracranial Aneur  Jones J, Sayre J, Chang R, Tian J, Szeder V, Gonzalez ysms Treated by Wrapping or Coating: A Review of N, Jahan R, Vinuela F, Duckwiler G, Tateshim a S. Ce reb ra l va sosp a sm p a t t e rn s fo llow in g an e u r ys 1993; 32:344–347 mal subarachnoid hemorrhage: an angiographic  Minakawa T, Koike T, Fujii Y, et al. J Neurointerv Re su lt s of Ru p t u re d An e u r ysm s Tr e a t e d b y Coa t Surg. Ge o gr a p h ic va r ia t io n a n d r e gio n a l Hydrocephalus in Aneurysmal Subarachnoid Hem trends in adoption of endovascular techniques for orrhage Patients. Outcomes of early endo hydrocephalus after occlusion of ruptured intra vascular versus surgical treatment of ruptured cranial aneurysms by surgical clipping or endovas cerebral aneurysms. A prospective randomized cular coiling: a single-institution series and meta study. Clip p in g or coilin g o f r u p t u r e d ce r eb r a l gical clipping versus endovascular coiling in 2143 aneurysms and shunt-dependent hydrocephalus. Outcomes of of intracranial aneurysms: a prospective study of endovascular coiling versus surgical clipping in the the influence of treatment modality. Th e Barrow mal subarachnoid hemorrhage by enhancement of Ru p tu red An eu r ysm Tr ial. Hyd r o ce p h a lu s: co m p a r iso n o f clip p in g a n d cranial aneurysms has no significant advantage embolization in aneurysm treatment. Rationale reducing shunt-dependent hydrocephalus follow for treatin g un ruptured in tracran ial aneur ysm s: ing aneurysmal subarachnoid hemorrhage: a sys actuarial analysis of natural history risk versus tematic review. Pa t ie n t o u t co m es a r e b e t t e r fo r u n r u p 2000; 93:379–387 tured cerebral aneurysms treated at centers that  Tsutsumi K, Ueki K, Morita A, Kirino T. Risk of rup preferentially treat with endovascular coiling: a ture from incidental cerebral aneurysms. Unru p surgery improves the cure of aneurysm-induced tured intracranial aneurysms: incidence of rupture oculmotor palsy. Co m p a r iso n o f m icr o su r ge r y a n d e n d o va scu la r surgeon reimbursement at the university of Flori treatment on clinical outcome following poor da.
As in man muscle relaxant for children cheap 100 mg voveran sr overnight delivery, the reaction leads to muscle relaxant not working order voveran sr from india the formation of inflammatory foci spasms throughout body cheap voveran sr amex, granulomas back spasms 32 weeks pregnant cheap 100mg voveran sr with mastercard, fibroses, and ultimately, the obstruction of portal irrigation. The chronic disease occurs in animals that have been repeatedly exposed to infections with large numbers of cercariae, and the principal manifestations are emaciation, anemia, eosinophilia, and hypoalbuminemia (Soulsby, 1982). Unlike man, animals do not appear to be susceptible to splenomegaly or esophageal varices, but the presence of dead parasites can cause them to develop enlarged follicles or lymph nodes, as well as venous thromboses, with infarct of the organ. In addition to the liver, the schistosome eggs can settle in the intestinal wall, lungs, kidneys, blad der, and other organs, where they cause damage and symptoms in proportion to the parasite burden. Cattle have also been reported to have obstructive phlebitis caused by the presence of adult parasites in the veins. While some areas are making progress through vigorous control campaigns, the infection is spreading to others in the wake of new irrigation projects or carried by individuals. Moreover, the geo graphic range of the intermediate hosts is greater than that of the human infection. The Aswan Dam in Egypt provides an example of how environmental change can impact on the disease. Although construction of the dam has resulted in important economic benefits for the country, it has also brought about profound ecological changes in the region and created favorable conditions for the survival of the mol lusks that act as intermediate hosts of S. The dam reduced the flow rate of the Lower Nile and held back the alluvial sediment, thereby favoring penetration of the mollusks by the miracidia and also facilitating human contact with the cercariae that emerge from them. At the same time, there was an increase in human activities, such as fishing and washing clothes and utensils, along the Nile River. The ecology of Lower Egypt (the Nile Delta) also underwent changes favorable to the vectors of this parasitosis. The absence of alluvial sediment promoted the growth and spread of aquatic plants as well as the microflora on which the mollusks feed, with a consequent increase in their popula tion and greater possibility of transmission of the parasite to the human host (Malek, 1975). The situation in Egypt, which has been repeated in several other countries of Africa, the Americas, and Asia, shows that knowledge of ecological conditions is essential to understanding the variability of the human infection. The growing rate at which dams are being constructed in the developing countries, sometimes with out prior ecologic and epidemiologic studies to serve as a basis for implementing disease prevention measures, is helping to bring about the spread and intensification of schistosomiasis. These mollusks become infected when their water becomes contaminated with fecal matter from definitive hosts, especially humans, or urine in the case of S. Man acquires the infection by the cutaneous route by entering water that contains mollusks infected with the parasite. Studies in endemic areas have shown that the prevalence of infection in the snails concerned is generally lower than 5% and that the density of free-liv ing cercariae is extremely low because they are dispersed over a large volume of water. These low rates sug gest that the intense infections needed to cause disease require relatively prolonged exposure to contaminated water. In some regions, schistosomiasis is also an occupational disease of farm laborers who work in irrigated fields (rice, sugarcane) and fisherman who work in fish culture ponds and rivers. Another highly exposed group is the village women who wash clothing and utensils along the banks of lakes and streams. The infection can also be contracted while bathing, swimming, or playing in the water. Studies in the Americas have shown that rodents alone cannot maintain prolonged environmental contamination, but perhaps baboons (Papio spp. These species play an important epidemiologic role because they contaminate the water, enabling man to become infected. It has been observed that persons infected with abortive animal schistosomes or those that have little pathogenicity for man develop a degree of cross-resistance that protects them against subsequent human schistosome infections. It is even thought that resistance produced by abortive infections of the zoonotic strain S. In light of this heterologous or cross-immunity, some researchers have proposed vaccinating humans with the antigens or parasites of animal species (zooprophylaxis). The influence of factors involving the parasite, host, and environment on the per sistence of schistosomiasis has been studied using S. Diagnosis: Schistosomiasis is suspected when the characteristic symptoms occur in an epidemiologic environment that facilitates its transmission. The ease with which their presence is confirmed depends on the intensity and duration of the infection; mild and long-standing infections produce few eggs. Whenever schistosomiasis is suspected, samples should be examined over a period of several days, since the passage of eggs is not continuous. The Kato-Katz thick smear technique offers a good balance between simplicity and sensitivity, and it is commonly used in the field (Borel et al. Among the feces concentration techniques, formalin-ether sedimentation is con sidered one of the most efficient. In chronic cases with scant passage of eggs, the rectal mucosa can be biopsied for high-pressure microscopy. Also, the eclosion test, in which the feces are diluted in unchlorinated water and incubated for about four hours in a centrifuge tube lined with dark paper, can be used. At the end of this time, the upper part of the tube is illuminated in order to concentrate the miracidia, which can be observed with a magnifying glass. In addition to the mere presence of eggs, it is important to determine whether or not the miracidia are alive (which can be seen from the movement of the miracidium or its cilia) because the immune response that leads to fibrosis is triggered by antigens produced by the miracidium. In cases of prepatent, mild, or long-standing infection, the presence of eggs is difficult to demonstrate, and diagnosis therefore usually relies on finding specific antigens or antibodies (Tsang and Wilkins, 1997). However, searching for parasite antigens is not a very efficient approach when the live parasite burden is low. The circumoval precipitation, cercarien-Hullen reaction, miracidial immobilization, and cercarial fluorescent antibody tests are reasonably sensitive and specific, but they are rarely used because they require live parasites. Hence, the reaction of this antigen to IgM antibodies may be a marker of acute disease (Valli et al. A questionnaire administered to students and teachers from schools in urinary schistosomiasis endemic areas revealed a surprisingly large number of S. In many cases, cen trifugation and examination of the urine sediment is sufficient to find eggs, although filtration in microporous membranes is more sensitive. Examination of the urine sediment for eosinophils reveals more than 80% of all infections. The use of strips dipped in urine to detect blood or proteins also reveals a high number of infections, even though the test is nonspecific. Also, there are now strips impregnated with spe cific antibodies that reveal the presence of S. Searching for antibodies or antigens in serum was substantially more sensitive than looking for eggs in urine (Al-Sherbiny et al. Chemotherapy of infected individuals is not only curative but also preventive in that it halts the production of eggs that contaminate the environment. In a three-year study carried out in Madagascar, 289 individuals from a village in which S. In most cases, it is not recom mended to treat the entire community; a more effective approach is to perform par asitologic examinations and treat only the infected individuals. When the intensity of infection declines in a given population, it may be necessary to resort to serologic diagnosis, which is more sensitive. In communities that have a high prevalence of infection but limited economic resources, treatment can be restricted to the groups with the highest parasite burdens, such as children between 7 and 14 years old. Health education consists essentially in teaching people to avoid contact with con taminated water and not to contaminate water with their own excreta. However, many of the populations most affected by schistosomiasis are communities with low levels of schooling and such limited resources that they often have no alternative but to use contaminated water or to contaminate the environment with their excreta. The intermediate hosts have been controlled in a number of areas by draining or filling in swampland, removing vegetation from water bodies, and improving irrigation systems. In Japan, excellent results were achieved by lining irrigation canals with concrete. The use of molluscicides, though expensive, is a rapid and effective means of reducing transmission if it is combined with other prevention measures, espe cially chemotherapy. The cost-benefit ratio is more favorable where the volume of water to be treated is small, and for rivers or lakes where transmission is focal (lim ited to a relatively small habitat). Selection of the molluscicide to be used should take into account the nature of the snail’s habitat, the cost of the chemical com pound, and any harmful effects it might have on fish and other forms of aquatic life. The introduction of snails that compete with the intermediate hosts of the schisto some has been successful in some areas. In Puerto Rico, for example, introduction of the snail Marisa cornuarietis, coupled with chemical control, has eliminated B.