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A syndrome of isolated gait apraxia has been described with focal degeneration of the medial frontal lobes. In modern classifications of gait disorders, gait apraxia is subsumed into the categories of frontal gait disorder, frontal disequilibrium, and isolated gait ignition failure. Gait apraxia is an important diagnosis to establish since those afflicted generally respond poorly, if at all, to physiotherapy; moreover, because both patient and therapist often become frustrated because of lack of progress, this form of treatment is often best avoided. The neuroanatomical substrates of such decision-making are believed to encompass the prefrontal cortex and the amygdala. Gambling may be defined as pathological when greater risks are taken and potential losses are correspondingly greater; this may be classified as an impulse control disorder. This may occur in psychiatric - 156 - Gaze Palsy G disease such as depression, schizophrenia, and malingering, and sometimes in neurological disease (head injury, epilepsy). A Ganser syndrome of hallucinations, conversion disorder, cognitive disorientation, and approximate answers is also described but of uncertain nosology. Afflicted individuals may also demonstrate paroxysmal hyperpnoea and upbeating nystagmus, suggesting a brainstem (possibly pontine) localization of pathology. The condition should be distinguished from other cranial dystonias with blepharospasm (Meige syndrome). Gaze Palsy Gaze palsy is a general term for any impairment or limitation in conjugate (yoked) eye movements. Preservation of the vestibulo-ocular reflexes may help differentiate supranuclear gaze palsies from nuclear/infranucelar causes. However, this is not a form of impaired muscle relaxation akin to myotonia and paramyotonia. For instance, when lifting the legs by placing the hands under the knees, the legs may be held extended at the knees despite encouragement on the part of the examiner for the patient to flex the knees. Generally, tendon reflexes are normal, plantar responses downgoing, and there is no clonus. Gegenhalten is a sign of bilateral frontal lobe dysfunction, especially mesial cortex and superior convexity (premotor cortex, area 6). It is not uncommon in otherwise healthy elderly individuals with diffuse frontal lobe cerebrovascular disease. Cross References Frontal release signs; Myotonia; Paramyotonia; Rigidity; Spasticity Geophagia, Geophagy Geophagia or geophagy describes earth or clay eating, reports of which dating back to Hippocrates have been found. This may also fall under the rubric of pica, or pagophagia, a morbid craving for unusual or unsuitable food. Besides the obvious risk of infection from ingesting potentially contaminated material, geophagia may be associated with neurological complications. Cases of flaccid quadriparesis and of proximal myopathy associated with profound hypokalaemia in the context of geophagia have been reported, which may lead to walking difficulty. Gerstmann syndrome occurs with lesions of the angular gyrus and supramarginal gyrus in the posterior parietotemporal region of the dominant (usually left) hemisphere, for example, infarction in the territory of the middle cerebral artery. Hence this may be an example of a - 158 - Girdle Sensation G disconnection syndrome. Nonetheless the Gerstmann syndrome remains useful for the purposes of clinical localization. Geste antagoniste consists of a tactile or proprioceptive stimulus, which is learned by the patient, which reduces or eliminates the dystonic posture. For example, touching the chin, face, or neck may overcome cervical dystonia (torticollis), and singing may inhibit blepharospasm. They are almost ubiquitous in sufferers of cervical dystonia and have remarkable efficacy. The phenomenology of the geste antagoniste in primary blepharospasm and cervical dystonia. Cross References Dystonia; Reverse sensory geste; Torticollis Gibbus Angulation of the spine due to vertebral collapse may be due to osteoporosis, metastatic disease, or spinal tuberculosis. Clinical features of the localized girdle sensation of mid-trunk (false localizing sign) appeared [sic] in cervical compressive myelopathy patients. Usually, reflexive blinking in response to tapping habituates quickly, but in extrapyramidal disorders it may not do so. Others conceptualize glossolalia as a form of automatic speech, usually of a pseudolanguage which may be mistaken for a foreign tongue. Such happenings may occur in trance-like states or in pathological states such as schizophrenia. This sign was originally described by Gowers in the context of Duchenne muscular dystrophy but may be seen in other causes of proximal leg and trunk weakness. Graphaesthesia Graphaesthesia is the ability to identify numbers or letters written or traced on the skin, first described by Head in 1920. Loss of this ability (agraphaesthesia, - 161 - G Graphanaesthesia dysgraphaesthesia, or graphanaesthesia; sometimes referred to as agraphognosia) is typically observed with parietal lobe lesions, for example, in conditions such as corticobasal degeneration. Such a cortical sensory syndrome may also cause astereognosis and impaired two-point discrimination. Although categorized as a reflex, it may sometimes be accessible to modification by will (so-called alien grasp reflex). The grasp reflex may be categorized as a frontal release sign (or primitive reflex) of prehensile type, since it is most commonly associated with lesion(s) in the frontal lobes or deep nuclei and subcortical white matter. Clinicoradiological correlations suggest that the cingulate gyrus is the structure most commonly involved, followed by the supplementary motor area. Luria maintained that forced grasping resulted from extensive lesions of premotor region, disturbing normal relationships with the basal ganglia. The incidence of the grasp reflex following hemispheric lesion and its relation to frontal damage. Repetition of the manoeuvre (if the patient can be persuaded to undergo it) causes less severe symptoms (habituation). Central lesions (disorders of the vestibular connections) tend to produce isolated nystagmus which does not fatigue or habituate with repetition. Caloric testing may be required to elicit the causes of dizziness if the Hallpike manoeuvre is uninformative. The pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Benign paroxysmal positioning vertigo: classic descriptions, origins of the provocative positioning technique, and conceptual developments. Cross References Caloric testing; Nystagmus; Vertigo; Vestibulo-ocular reflexes Hallucination A hallucination is a perception in the absence of adequate peripheral stimulus (cf. Visual hallucinations may be normal, especially when falling asleep or waking (hypnogogic, hypnopompic). Auditory hallucinations may be simple (tinnitus) or complex (voices, music) and may be associated with focal pathology in the temporal cortex. Cross Reference Pes cavus Hand Elevation Test this is one of the provocative tests for carpal tunnel syndrome: it is positive if paraesthesia in the distribution of the median nerve develop after raising the hand over the head for up to 2 min. Harlequin sign has on occasion been described in association with multiple sclerosis and superior mediastinal neurinoma. The term Hawthorne effect has come to stand for any situation in which behaviour is altered by observation, or being the object of attention. Guidelines for primary headache disorders in primary care: an "intervention" study. New evidence suggests the Hawthorne effect resulted from operant reinforcement contingencies. It consists of a rapid turning of the head to one side by about 15, sufficiently rapid to ensure that smooth pursuit eye movements do not compensate for head turning. The examiner observes the ability of the subject to maintain fixation on a distant target; if the vestibulo-ocular reflex is intact fixation is maintained.

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Drug interaction: Blunting of peak aminoglycoside concentration if administered simultaneously with ceftazidime. Indications: Good activity against both gram-negative and gram-positive organisms except for Pseudomonas spp. Precautions: Do not use in gallbladder, biliary tract, liver, or pancreatic disease. Clinical considerations: Do not use as sole therapy for staphylococcal or pseudomonal infections. Ceftriaxone displaces bilirubin from albumin-binding sites, leading to increased free-serum bilirubin levels. Transient formation of gallbladder precipitates characterized by vomiting and cholelithiasis. Precautions: Rectal suppositories are not recommended because of unreliable release characteristics. Drug interactions: Reduced antihypertensive effect with concurrent nonsteroidal anti-inflammatory drug use. Adverse reactions: Hypochloremic alkalosis, prerenal azotemia, volume depletion, blood dyscrasias, decreased serum potassium and magnesium levels, and increased levels of glucose, uric acid, lipids, bilirubin, and calcium. Warnings: Can cause severe and possibly fatal pseudomembranous colitis characterized by severe persistent diarrhea and possibly the passage of blood and mucus. Drug interactions: May potentiate the level and effects of neuromuscularblocking agents. Indications: Anti-inflammatory glucocorticoid used to facilitate extubation and improve lung mechanics. The American Academy of Pediatrics strongly discourages the use of dexamethasone for treatment or prevention of bronchopulmonary dysplasia. Precautions: Hyperglycemia and glycosuria occur frequently after the first few doses. Its use should be avoided except under exceptional clinical circumstances (maximal ventilatory support or high risk of mortality). Positive responses are usually seen within 48 to 72 hours and occur in less than 50% of neonates. Cardioversion or calcium infusion may precipitate ventricular fibrillation in the digoxin-treated neonate (may be prevented by lidocaine pretreatment). Monitoring: Heart rate/rhythm for desired effects and signs of toxicity, serum calcium, magnesium, potassium (especially in neonates receiving diuretics and amphotericin-B, both of which predispose to digoxin toxicity), and renal function. Neonates may have falsely elevated digoxin levels as a result of maternal digoxin-like substances. Contraindications: Atrioventricular block, idiopathic hypertrophic subaortic stenosis, ventricular dysrhythmias, atrial fibrillation/flutter with slow ventricular rates, or constrictive pericarditis. Drug interactions: Amiodarone, erythromycin, cholestyramine, indomethacin, spironolactone, quinidine, verapamil, and metoclopramide. Indications: Treatment of hypoperfusion, hypotension, short-term management of cardiac decompensation. Has more effect on cardiac output than dopamine but less effect on blood pressure. Once 20 to 25 mcg/kg/minute is reached, consideration should be given to adding a second pressor. Contraindications: Pheochromocytoma, tachyarrhythmias, or hypovolemia may increase pulmonary artery pressure. Adverse reactions: Transient or prolonged episodes of hypotension, oliguria, mild nonoliguric renal failure, hypotension in volume-depleted neonates, and hyperkalemia in neonates receiving potassium supplements and/or potassium-sparing diuretics. Time to repeat antifactor Xa level 4 h after next dose 4 h after next dose Before next dose and q12h until antifactor Xa is 0. Contraindications: Avoid or hold in infants who require lumbar puncture to minimize risk of epidural/spinal hematoma. Adverse effects: Fever, edema, hemorrhage, thrombocytopenia, pain/erythema at injection site. High doses of preservative-containing epinephrine will necessitate caution in selection of epinephrine preparations. Correction of acidosis before administration of catecholamines enhances their effectiveness. Indications: Treatment of infections caused by Chlamydia, Mycoplasma, and Ureaplasma; treatment and prophylaxis of Bordetella pertussis and ophthalmia neonatorum; also used as a prokinetic agent. A 10-fold increased risk of hypertrophic pyloric stenosis is seen in neonates under 2 weeks who receive oral erythromycin for pertussis prophylaxis. Drug interactions: Increased blood levels of carbamazepine, digoxin, cyclosporine, warfarin, methylprednisolone, and theophylline. Use of H2 blockers in preterm neonates has been associated with an increased risk of fungal and late-onset bacterial sepsis. Contraindications: Increased intracranial pressure, severe respiratory depression, and severe liver or renal insufficiency. Indication: Prophylaxis for prevention of iron-deficiency anemia in preterm newborns. When ordering, specify the exact amount in mg and clarify whether it is mg of elemental or salt form to avoid over- or under dosing. Iron supplementation may increase hemolysis if adequate vitamin E therapy is not supplied. Contraindications: Peptic ulcer disease, ulcerative colitis, enteritis, hemochromatosis, and hemolytic anemia. Drug interactions: Decreased absorption of both iron and tetracycline when given together. Observe stools (may color the stool black and may cause false-positive guaiac test for blood), and monitor for constipation. Gastric lavage with 1% to 5% sodium bicarbonate or sodium phosphate solution prevents additional absorption of iron. Indications: Treatment of systemic fungal infections, meningitis, and severe superficial mycoses. Alternative to amphotericin-B in patients with preexisting renal impairment or when concomitant therapy with other potentially nephrotoxic drugs is required. Prophylaxis: 3 mg/kg/dose once daily, 2 times/week for the first 2 weeks, then every other day for a total of 4 to 6 weeks (longer duration for infants with birth weight 1,000 g). Possible interference with metabolism of caffeine, midazolam, barbiturates, and phenytoin. Indication: Treatment of megaloblastic and macrocytic anemias as a result of folate deficiency. Clinical considerations: May mask hematologic defects of vitamin B12 deficiency but will not prevent progression of irreversible neurologic abnormalities, despite the absence of anemia. Indications: Management of generalized convulsive status epilepticus refractory to phenobarbital. Consider the amount of phosphate delivered by fosphenytoin in infants who require phosphate restriction. Fosphenytoin and bilirubin compete with phenytoin and displace phenytoin from plasma protein-binding sites. Adverse reactions: Hypotension, vasodilation, tachycardia, bradycardia, fever, hyperglycemia, neutropenia, thrombocytopenia, megaloblastic anemia, osteomalacia, and serious skin reactions. Monitoring parameters: Therapeutic levels: 10 to 20 mg/L total phenytoin or 1 to 2 mg/L unbound (free) phenytoin only. To provide diuresis and improve lung function when a greater diuretic effect than produced by chlorothiazide (Diuril) is needed. For long-term use, consider alternate day therapy or longer (dosing interval q48 to 72 h) in order to prevent toxicities. Monitoring: Follow daily weight changes, urine output, serum phosphate, and serum electrolytes. For infants with neutropenia, an absolute neutrophil count 500 or thrombocytopenia with a platelet count 25,000, use a decreased dose. Adverse reactions: Neutropenia, leukopenia, granulocytopenia, thrombocytopenia, and anemia. At the first sign of significant renal dysfunction, the dose of ganciclovir should be adjusted by either reducing the number of mg/dose or by prolonging the dosing interval. Indications: Active against gram-negative aerobic bacteria, some activity against coagulase-positive staphylococci, ineffective against anaerobes, streptococci.


  • Arthrogryposis multiplex congenita pulmonary hypoplasia
  • Gastrointestinal autonomic nerve tumor
  • Familial hypertension
  • Benzodiazepine withdrawal syndrome
  • Anaplasmosis
  • Chiari type 1 malformation
  • Craniosynostosis, sagittal, with Dandy-Walker malformation and hydrocephalus
  • Refsum disease
  • Cranioectodermal dysplasia

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Newborn infants with Zellweger syndrome have dysmorphic facial features (Table 60. Hepatomegaly with hypoglycemia occurs in gluconeogenesis defects (fructose1,6-bisphosphatase deficiency). Liver failure occurs in galactosemia, hereditary fructose intolerance, tyrosinemia type I, fatty acid oxidation defects, and respiratory chain defects. Cholestatic jaundice occurs in peroxisomal disorders, citrin deficiency, 1antitrypsin deficiency, Byler disease, inborn errors of bile acid metabolism, and Niemann-Pick disease type C. Clinical manifestations include vomiting, diarrhea, feeding difficulties, hypoglycemia, jaundice, hepatosplenomegaly, liver dysfunction, renal tubulopathy, lethargy, irritability, seizures, cataracts, and increased risk of Escherichia coli neonatal sepsis. Galactose is elevated in plasma, and galactose-1-phosphate is elevated in red blood cells. Management consists of substituting a soy-based formula for breastfeeding or for a standard formula, and later, a galactose-restricted diet. An autosomal recessive disorder due to deficiency of fructose-1,6-bisphosphate aldolase (aldolase B), which functions in the catabolic pathway of fructose. Early manifestations include vomiting, hypoglycemia, jaundice, lethargy, irritability, seizures, hepatosplenomegaly, liver dysfunction, renal tubulopathy, and coma. An autosomal recessive disorder due to deficiency of fumarylacetoacetate hydrolase, which functions in the catabolic pathway of tyrosine. It can present in neonatal period with liver failure, vomiting, bleeding, septicemia, hypoglycemia, and renal tubulopathy. Newborn screening programs may screen for tyrosine and/or succinylacetone in the bloodspot to diagnose tyrosinemia; however, many cases may be missed when the screening uses tyrosine alone. It can present in the neonatal period with transient intrahepatic cholestasis, hepatomegaly, liver dysfunction, growth retardation, hemolytic anemia, and hypoglycemia. Elevated plasma concentrations of citrulline, threonine, methionine, and tyrosine. Supplementation with fat-soluble vitamins and use of lactosefree formula and high medium-chain triglycerides. Subsequently, a diet rich in lipids and protein and low in carbohydrates is recommended. When a sibling has a metabolic disorder or symptoms consistent with a metabolic disorder, the following steps should be taken: 1. Planning to deliver the baby in a facility equipped to handle potential metabolic or other complications. Nonmetabolic causes of symptoms such as infection, asphyxia, or intracranial hemorrhage need to be evaluated. The newborn screening program should be contacted for the results of the screening and for a list of the disorders screened. It is important to obtain these specimens at the time of presentation before starting treatment for metabolic disease. Ringer lactate should not be used for fluid or electrolyte therapy in a child with a known or suspected metabolic disorder as this can worsen lactic acidosis. If hypernatremia is a problem, potassium acetate can be used in the maintenance fluid. Caloric consumption during a period of decompensation, in order to support anabolism, should be at least 20% greater than that needed for ordinary maintenance. One must remember that withholding natural protein from the diet also eliminates this source of calories, which should be replaced using other dietary or nutritional (non-nitrogenous) sources. All natural protein should be withheld for 48 to 72 hours while the patient is acutely ill. Special parenteral amino acid solutions and specialized formulas are available for many disorders. Free carnitine levels are low in the organic acidemias because of increased esterification with organic acid metabolites. Pharmacologic doses of appropriate cofactors may be useful in cases of vitamin-responsive enzyme deficiencies. The patient should be monitored closely for any mental status changes, overall fluid balance, evidence of bleeding (if thrombocytopenic), and symptoms of infection (if neutropenic). Anorexia, nausea, and vomiting during the acute crisis period make significant oral intake unlikely. If the patient is not significantly neurologically compromised, consideration should be given to providing the patient (orally or by nasogastric tube) with a modified formula preparation containing all but the offending amino acids. The diet will be individualized for each child and his or her metabolic defect; for example, in galactosemia, the infant should be fed a lactose-free formula. If an infant is dying or has died of what may be a metabolic disease, it is important to make a specific diagnosis in order to help the parents with genetic counseling for future reproductive planning. Sometimes, families that will not permit a full autopsy will allow the collection of some premortem or immediately postmortem specimens that may help in diagnosis. The skin should be well cleaned, but any residual cleaning solution should be washed off with sterile water. The skin can be placed briefly in sterile saline until special media are available. Both premortem samples and generoussize postmortem samples should be flash-frozen to preserve enzyme integrity as well as tissue histology. Depending on the nature of the disease, other tissues such as cardiac muscle, brain, and kidney should be preserved. Photographs can be taken as well as a full skeletal radiologic screening for infants with dysmorphic features. Each state in the United States mandates the disorders evaluated in its own newborn screening program. A list of what each state screens for may be found on the individual state governmental website or in aggregate on the national newborn screening and genetic resource center website genes-r-us. The clinical aspects of newborn screening: importance of newborn screening follow-up. Proceedings of a consensus conference for the management of patients with urea cycle disorders. Consensus statement from a conference for the management of patients with urea cycle disorders. Penoscrotal or perineoscrotal hypospadias, with or without microphallus, even if the testes are descended. Sex assignment depends on anatomy, functional prenatal and postnatal endocrinology, and the potential for sexual functioning and fertility, which may be independent of genetic sex. Until a sex assignment is made, gender-specific names or references should be withheld. Circumcision is contraindicated until a determination is made concerning the need for surgical reconstruction. In general, early undifferentiated structures will develop down the normal female pathway by default, unless specific factors are present that direct differentiation down the male pathway. Genetic sex is determined by the chromosomal complement of the zygote and the presence or absence of specific genes necessary for normal sexual development. Undifferentiated gonads develop in the bilateral genital ridges around 6 weeks of gestation and begin to differentiate by 7 weeks. Testicular descent into the scrotum requires testosterone and generally occurs in the last 6 weeks of gestation.

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Two years prior, he had a similar episode of fever and encephalopathy, which was associated with leftsided focal seizures and left hemiparesis. He was presumptively diagnosed with herpes encephalitis, and received a full course of acyclovir. At his discharge from hospital, he had made a nearly complete recovery, with only mild residual left leg weakness. Over the 2 years leading to his current admission, he continued to have persistent fatigue. Also, it became evident that he was having more difficulty in school than previously, and his grades dropped from As to Cs and Ds. In addition, when reviewing his growth curve, he had dropped several percentiles on his growth curve for both weight and height. According to the parents, the ptosis had slowly developed over the last 2 years and was relatively constant throughout the day, but worsened when he was ill or fatigued. The patient was spontaneously moving all 4 extremities, but had difficulty lifting his right arm and leg against gravity. According to his bedside nurse, his strength was increasing in the right side following his last seizure. His seizures could be spreading to his ipsilateral motor cortex from his temporal lesion, although a second lesion of the motor cortex cannot be excluded. His more chronic, bilateral ptosis with sparing of the pupils and extraocular movements could represent a rostral midbrain lesion affecting the central caudal nucleus, but more likely represents a neuromuscular process (neuromuscular transmission or myopathy). Finally, his pes cavus and hammertoes are possible evidence of a mild chronic polyneuropathy (although the differential diagnosis for these deformities also includes distal myopathy, very chronic myelopathy, inflammatory joint disorders, and familial pes cavus). A chronic toxic exposure could be considered, but there is no history to support this. The acute, recurrent presentation provoked by intercurrent illness suggests a small molecule disorder or disorder of energy metabolism. Another potential metabolic etiology for recurrent strokes with headaches and cognitive decline is homocystinuria, though this is not associated with ptosis, neuropathy, exercise intolerance, or the described systemic involvement and is therefore unlikely. There was local mass effect, but no midline shift or effacement of quadrigeminal or suprasellar cisterns. Lumbar puncture was performed and showed a normal cell count, normal glucose and protein, and a lactate of 5. Antimicrobials were discontinued when all cultures and viral studies returned as negative. There were also smaller, ill-defined areas of high fluid-attenuated inversion recovery signal of varying ages in the right superior temporal gyrus, right occipital lobe, left prefrontal gyrus, left superior temporal gyrus, and left postcentral gyrus. The core features include 1) stroke-like episodes before the age of 40 years, 2) encephalopathy characterized by seizures, dementia, or both, and 3) lactic acidosis, ragged red fibers, or both, and supportive criteria included normal early development, recurrent headache, or recurrent vomiting. Posterior-parietal, temporal, and occipital cortices are preferentially involved, often asymmetrically. It is currently believed that the pathophysiology of these episodes includes both failure of oxidative metabolism at the cellular level in brain tissue itself as well as small vessel vasculopathy from mitochondrial failure in blood vessel endothelium and smooth muscle. Migraine, sensorineural hearing loss, myopathy with exercise intolerance, and peripheral neuropathy are additional common neurologic features. Patients may also have involvement of systemic organs with a high oxidative demand. The respiratory chain enzyme biochemistry may represent the only abnormality present in a child with a mitochondrial disease, and the pattern of abnormal complexes may suggest a particular molecular diagnosis. For a more detailed review of the in-depth investigation of suspected mitochondrial disease, the reader is referred to a recent review article. In general, current management is aimed at slowing neurodegeneration and preventing stroke-like episodes, as well as acutely treating stroke-like episodes. Seizure control should be optimized, since breakthrough seizures may trigger stroke-like episodes. Valproate should be 34 Neurology 79 July 17, 2012 avoided if possible, as it is toxic to mitochondria, inhibits carnitine uptake in cells, and may exacerbate acute metabolic decompensation. There is limited prospective randomized double-blind control study evidence to support the use of any of these, but it is generally believed that there may be a theoretical benefit and little risk of harm in supplementing with these agents. Valproic acid impairs carnitine uptake in cultured human skin fibroblasts: an in vitro model for the pathogenesis of valproic acid-associated carnitine deficiency. He had a history of childhood absence epilepsy that had resolved with antiepileptics discontinued 1 year prior to presentation. Two months prior to admission, the patient had a febrile illness with headache and diarrhea that lasted a few days. Over the ensuing days, however, he developed increasing sleepiness, cognitive slowing with difficulty concentrating, and an illdefined abnormal perception. Alternative potential diagnoses included infectious encephalitis, recurrent seizures, structural lesions in the arousal system involving the diencephalon or the brainstem reticular activating system, or toxic ingestion. Both cytomegalovirus and Coxsackie titers were elevated, and he received a course of ganciclovir with little improvement in his mental status. During hospitalization, it was also noted that he had wide swings of heart rate with intermittent bradycardia. The combination of sleep changes, hypersexual behavior, autonomic dysfunction, and mild confusion with perceptual changes localizes to diencephalic structures, specifically the hypothalamus, as well as cortical associative areas. The differential diagnosis of recurrent hypersomnia also includes structural lesions, as can be seen with brain tumors, traumatic brain injury, or stroke, all ruled out by previous studies. Additional psychiatric considerations include somatic symptom disorder, seasonal affective disorder, and bipolar disease. Although there is no single test to rule out any of these disorders, extensive family and patient interviewing suggested these conditions to be less likely. Reinforcing this interpretation were his cycling aspect, the lack of clear stressors, and other clinically relevant symptoms that compound diagnostic criteria in these conditions. His perceptual changes, expressed by a sensation that "things did not feel or look right, as if I was not there," are signs of derealization. On the first day of medication, he started to have limited conversations with staff. On the second day, he was able to get out of bed and normalized his sleep/wake routine, although he still expressed a sense of derealization. However, he went on to have 3 more relapses over the course of 4 months and was switched to lithium. Although hypersomnolence, hyperphagia, and hypersexuality have been previously considered mandatory diagnostic criteria, the more recent diagnostic framework reflects the fact that most patients do not have all symptoms but rather some combination. This underscores the shift in diagnosis to the presence of hypersomnia with at least one of confusion, apathy, or derealization. A systematic review suggests that based on case reports, stimulant drugs may improve sleepiness (but not other symptoms) and lithium significantly reduces duration of episodes and decreases relapses, with anticonvulsants having less robust data as preventive medications. This case exemplifies the difficulties in the diagnosis and management of a syndrome that went underrecognized until appropriate treatment was instituted. Maski: analysis and review of case discussion, suggestions to differential diagnosis and conclusion. All authors were directly involved in the care of the patient reported in this article. Recurrent hypersomnia (recurrent episodes of sleepiness lasting from 2 days to 4 weeks; episodes recur at least once per year; alertness, cognitive function, and behavior are normal between episodes; the hypersomnia is not better explained by another sleep, neurologic, or mental disorder or substance abuse); and at least one of the following: Cognitive abnormalities. Relationship between Kleine-Levin syndrome and upper respiratory infection in Taiwan. Sleep polygraphic studies as an objective method for assessing the therapeutic result 8.

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Compensation and cost You will not be paid for your blood sample and there will be no charge to you for the shipping or testing of your blood. I have been given the opportunity to ask questions and my questions have been answered. Printed or typed name Signature Date Addendum Since some neurodegenerative diseases cause dementia, the subjects themselves may not be able to provide informed consent. In that event, the legal guardian, next of kin or individual with health care power of attorney for the subject can provide the consent and any other necessary information. Printed name of legal guardian Signature Date Printed name of person administering consent Signature Date Use of translator Fill in this section if the subject is not fluent in English and a translator was used to obtain consent: Print name of translator: Signature of translator: Date: Date: An oral translation of this document was administered to the subject in. In some health care situations, as described in Chapter 6, one of the following less effective methods may be preferred. Wherever possible, instruments and other materials subject to reuse should be kept moist between the time of exposure to infectious materials and subsequent decontamination and cleaning. If it can be done safely, removal of adherent particles through mechanical cleaning will enhance the decontamination process. The following recommendations are based on the best available evidence at the time of the Consultation and are listed in order of more or less severe treatments. Unless otherwise noted, the recommended concentration is 20 000 ppm available chlorine. In worse-case scenarios (brain tissue bake-dried on to surfaces) infectivity will be largely but not completely removed. Porous load autoclaves are optimized for sterilization of clean instruments, gowns, drapes, towelling, and other dry materials required for surgery. Be familiar with and observe safety guidelines for working with sodium hypochlorite. Household or industrial-strength bleach is sold at different concentrations in different countries, so that a standard dilution cannot be specified. Efficacy depends upon the concentration of available chlorine and should be 20 000 ppm available chlorine. If solid precursors of hypochloric acid are available, then stock solution and working solutions can be prepared fresh for each use. However, in practice some formulations of stainless steel can be damaged (including some used for surgical instruments). It is advisable to test a sample or consult with the manufacturer before dedicating a large number of instruments to decontamination procedures. If hypochlorite is used to clean or soak an instrument, it must be completely rinsed from the surfaces before autoclaving. Other decontamination methods may need testing, or consultation with the manufacturer, to verify their effect on the instrument. In addition, recipients of dura mater are largely unaware of the fact, making identification of many of the dura mater recipients unlikely. Countries not applying appropriate control measures cannot assume similarly low levels of current risk among tissue recipients. Cautions regarding hazardous materials In all cases, hazardous materials guidelines must be consulted. Hypochlorite solutions continuously evolve chlorine and so must be kept tightly sealed and away from light. The amount of chlorine released during inactivation may be sufficient to create a potential respiratory hazard unless the process is carried out in a well-ventilated or isolated location. Discrimination against such persons and legal implications regarding their access to insurance, employment and health care were described by several participants in the Consultation. It was proposed that such discrimination would inevitably lead to a harm that exceeded any evidence of risk posed by them to others. Others argued that if a familial risk were identified, more stringent levels of infection control could be adopted, even in the absence of firm evidence of risk, particularly during procedures involving highinfectivity tissues. Scientific resolution of these issues was impossible because of a lack of precise information about tissue infectivity during the preclinical phase of human disease. A more conservative approach may be taken for interventions involving surgical procedures, or when handling tissues and body fluids in the laboratory. It is noted that considerable safety is afforded through the measures described above and in Annex 4. Professor Pierluigi Gambetti, Institute of Pathology, Case Western Reserve University School of Medicine, 10900 Euclid Ave. Infection Control Guidelines: for the prevention of transmission of infectious diseases in the health care setting. The following persons contributed to it and sections of their original work may remain in this version. Their contribution to the previous version and to this version is acknowledged with gratitude. Departments of Human Genetics and Neurology, University of Pittsburgh, Pittsburgh, Pennsylvania Ryan L. Department of Human Genetics, University of Pittsburgh, Pittsburgh, Pennsylvania M. Department of Human Genetics, University of Pittsburgh, Pittsburgh, Pennsylvania Ronald L. Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania Cyril H. Departments of Pathology and Epidemiology, University of Pittsburgh, Pittsburgh, Pennsylvania Reprint requests: Bennet I. This case draws attention to the need for further studies in the cohort of retired National Football League players to elucidate the neuropathological sequelae of repeated mild traumatic brain injury in professional football. A complete autopsy with a comprehensive neuropathological examination was performed on the retired National Football League player approximately 12 years after retirement. The brain demonstrated no cortical atrophy, cortical contusion, hemorrhage, or infarcts. Chronic traumatic encephalopathy was evident with many diffuse amyloid plaques as well as sparse neurofibrillary tangles and -positive neuritic threads in neocortical areas. There were no neurofibrillary tangles or neuropil threads in the hippocampus or entorhinal cortex. The prevalence and pathoetiological mechanisms of these possible adverse long-term outcomes and their relation to duration of years of playing football have not been sufficiently studied. We recommend comprehensive clinical and forensic approaches to understand and further elucidate this emergent professional sport hazard. Despite this recommendation, which was made many years ago, the possible long-term cognitive and neurodegenerative sequelae of professional football as well as the underlying histological changes and pathobiological cascades associated with and likely induced by the trauma of professional football are little understood. This is especially true for the neuropathological changes, because no cases have come to autopsy. This case draws attention to a disease that remains inadequately studied in the cohort of professional football players, with unknown true prevalence rates. Although clinical assessments can determine encephalopathy and dementia, and new neuroimaging methods may aid in the detection of amyloid plaques (23), autopsy examination is required to confirm the neuropathological basis of these changes. The pericardium revealed diffuse fibrocalcific and adhesive pericardioepicarditis. The cardiovascular system revealed dilated cardiomyopathy with severe cardiomegaly (855 g), severe bilateral atrioventricular dilation; biventricular hypertrophy; and patchy subendocardial, endocardial, and valvular fibrosis. There was evidence of cardiogenic shock with centrilobular hepatocellular coagulative necrosis. There was severe atherosclerosis of the proximal and distal right coronary artery and the left anterior descending coronary artery, with approximately 95% multifocal intraluminal occlusion. The proximal left circumflex coronary artery revealed moderate atherosclerosis with 50 to 75% focal intraluminal occlusion. A metal intraluminal surgical stent was identified in the proximal right coronary artery. The respiratory system revealed moderate acute pulmonary edema and congestion with patchy, acute, and terminal bronchopneumonia. The formalin-fixed whole brain weighed 1565 g, whereas the cerebellum and brainstem weighed 220 g. There was moderate cerebral edema but no evidence of uncal or cerebellar tonsillar herniation. The cerebral blood vessels and circle of Willis revealed focal mild eccentric atherosclerosis of the left vertebral artery without aneurysms or other anomalies.

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They are made of a mass of protoplasm differentiated in to cytoplasm and nucleoplasm. The ectoplasm function in protection, locomotion, ingestion of food, excretion, respiration. The protozoa of medical importance to humans include Amoebas, Flagellates, Ciliates, Coccidia, sporozoa and Microsporidia. However, they may be For this reason the difficult to differentiate from pathogenic species. Protozoa may colonize or infect intestinal tract, pharynx, and the uro-genital tract of humans. The majority of this parasite belongs to the Amoeba or Flagellate; however infection with Ciliate, Coccidian or Microsporidian parasite may also be encountered. These organisms are generally of world wide distribution and almost are acquired by fecal- oral contamination. In review of stool specimens examined for intestinal parasite in United State, non pathogenic protozoa were detected in 10. The protozoa of blood and tissues include the sporozoan parasites Plasmodium, Babesia and Toxoplasma gondii; the hemoflagellates Leishmania and Trypanosoma; and the free living amoeba Naegleria and Acathamoeba. The protozoa causing tissue infections cause significant damage to specific organs such as the eyes (toxoplasmosis, acanthamoeba, keratitis), the brain (toxoplasmosis, amoebic meningoencephalitis, African sleeping sickness), the heart (toxoplasmosis, chagas disease),or gastrointestinal tract (chagas disease). Pneumocystis carnii primarily causes pneumonia; however invasion of other sites such as the eye have been reported. As a parasite protozoa play a double role; they can attack man and cause disease or they can affect him economically by attacking domestic Parasitology 28 animals. The general procedures utilized for diagnosis of the protozoa vary according to where the parasite is found in the body. The malarial parasites and blood or tissue flagellates (Trypanosome or Leishmania) are usually detected in stained smears of blood or tissue. In the case of the blood or tissue flagellates cultivation procedures and animal inoculations are often important tools. The intestinal and atrial parasites, with few exceptions, may be found in stool as a motile trophozoite stage or a non-motile, resistant cyst stages. One of them is found in the oral cavity and the remaining six species are found in the large intestine, these include: Entamoeba histolytica, E. Coli, Endolimax nana, Iodamoeba butschlii and Entamoeba polecki; of these only one, i. All human intestinal amoebae have: 1) a trophozoite from which is motile organism, feed, and reproduce, and, 2) a cystic form which is the nonfeeding, non motile, dormant stage of protozoa. The trophozoite stage consists of a shapeless mass of moving cytoplasm which is divided into granular endoplasm and clear ectoplasm. Before going into structural details here for each of them, their nuclear character for identification is considered: E. Habitat:-Trophozoite:- Large intestine, liver abscesses and other extraintestinal organs Cyst:- found in the stools of chronic dysenteric patients and carriers. Morphology Trophozoite: Size:Shape:12 to 35m, Usually as long as 3 or 4 red blood cells. Motility:Active, Progressive, directional amoeboid motility in fresh warm stool specimen. Stored food: Sausage shaped chromatoidal bars with blunt ends and glycogen mass in immature cysts with one or two nuclei. Life cycle: Entamoeba histolytica requires a single host to complete its life cycle. When mature tetra-nucleated cyst from contaminated food or drink or form hands contaminated with feces is ingested it excysts in the small intestine to produce metacystic trophozoite by a process of binary fission. The immature trophozoites migrate to the colon and grow to become mature trophozoite stage, multiply by binnary fission to invade the mucus membrane of the large intestine. Some times it can perforate the intestinal wall causing extra-intestinal amoebiasis. After a period of growth and multiplication, encystment occurs in the large intestine. In the process of cyst formation, the trophozoite discharge undigested food appears spherical in shape and condense to become pre-cyst. The pre-cyst secrets cyst wall to form a mono-nucleated cyst which is followed by a nuclear division to produce a bi-nucleated and then a tetra-nucleated mature cyst. Cyst and precyst will also pass in semi- formed or formed stool, where cyst is infective if it is ingested by any means of transmission. Clinical Features and Pathology May be asymptomatic or exhibit amoebic dysentery or extra-intestinal amoebiasis in the liver, brain, spleen, lung, etc. Amoebic dysentery occurs when E histolytica trophozoites invade the wall of the large intestine and multiply in the submucosa, forming large flask shaped ulcers. Amoebic Liver Abscess: Occasionally amoeba is carried to the liver in the portal circulation and form abscesses, usually in the right lobe. There is pain & tenderness over the liver, wasting and fever with chills & night sweats. Laboratory Diagnosis Laboratory diagnosis of intestinal amoebiasis is based on: 1) Examination of a fresh diarrheic or dysenteric faecal specimen or rectal scraping for motile amoebae using saline, or 2) Examination of formed or semi-formed faeces for cyst stages. Such stool can be examined by direct saline and/or iodine smear, and Zinc sulphate floatation or centrifugal floatation method. Charcot-Leyden crystals, representing the crystallized contents of granules from eosinophil leukocytes may also be found in a fecal smear. Specimens must be examined without delay otherwiseidentification of the trophozoites becomes impossible because the amoeba lose containing red cells, round up With the recognition that E. A wider range in prevalence has been reported from community surveys in other parts of the country. Twelve percent of 698 school-aged children in 17 rural communities in the highlands of Showa were infected (Kloos H et al. Low to intermediate levels of amoebiasis prevalence have been reported from towns, apparently due to the effect of urbanization on transmission; 0. The highest prevalence of amoebiasis in Ethiopia was found the potential for nosocomial infections in Ethiopian health institutions (Editorial, Ethiop Med J, 1972). In a relatively recent country wide survey of amoebiasis, a totalof 12,457 persons in 97 communities was stool examined by formol ether concentration technique. So far as our survey goes, the influence of altitude on the prevalence of amoebiasis appeared not to be significant. Health education,improvement of sanitationand personal hygiene are suggested as realistic measures toreducethe transmissionof the parasite (Erko B, et al. Tetranucleated cystMetacystMetacystic trophozoiteTrophozoitePrecystUninucleated cyst Mode of Transmission Through contaminated food or drink, or from hands contaminated with faeces. Pathology:- Harmless commensal Parasitology 39 Laboratory Diagnosis: Finding the characteristic trophozoite and cyst stages in stool specimen. Habitat Both trophozoite and cysts in the large intestine of man Morphology Trophozoite:Size: 15-50m(average 25m), usually bigger than E. Thick nuclear membrane lined with coarse chromatin granules and eccentric karyosome. Nucleus: 1-8 nuclei; thick irregular nuclear membrane large, diffuse,often eccentric karyosome Parasitology 40 Cytoplasm: bright pale yellow in iodine stained smear. Octanucleated cyst Metacyst Metacystic Trophozoite Trophozoite precyst unincleated cyst binucleated cyst Tetranucleated cyst Mode of transmission Ingestion of contaminated food or drink by infective cyst. Laboratory diagnosis:Finding the characteristic trophozoite and cyst stages in stool specimen. Entamoeba gingivalis Geographical distribution: world wide distribution Habitat: Oral cavity Morphology:-Has trophozoite stage only, no cyst stage Trophozoite:Size:-10-20 nm Motility: sluggish Cytoplasm: well differentiate into ectoplasm and endoplasm Pseudopodia:- multiple Nucleus:- single, delicate nuclear membrane lined with fine chromatin granules and Small central karyosome. Parasitology 41 Life cycle:-It is reproduced by binary fission and transmitted from one person to another through kissing, droplets spray from the mouth,contaminated spoons or cups. Pathology: non pathogenic commensal amoebae Laboratory Diagnosis:-Finding the characteristic trophozoite stage from swab of the oral cavity. It should be differentiated from Trichomonas tenax which belong to flagellates and found in oral cavity.

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Shortterm longitudinal trends in cognitive performance in older adults with type 2 diabetes. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. The relationship between impaired glucose tolerance, type 2 diabetes, and cognitive function. Neuropsychological functioning in older people with type 2 diabetes: the effect of controlling for confounding factors. Hippocampal damage and memory impairments as possible early brain complications of type 2 diabetes. Hypothalamicpituitary-adrenal axis dysregulation and memory impairments in type 2 diabetes. Brain magnetic resonance imaging correlates of impaired cognition in patients with type 2 diabetes. The impact of diabetes mellitus on cognitive decline in the oldest of the old: a prospective population-based study. Is diabetes associated with cognitive impairment and cognitive decline among older women? Metabolic and vascular determinants of impaired cognitive performance and abnormalities on brain magnetic resonance imaging in patients with type 2 diabetes. Diabetes and function in different cognitive systems in older individuals without dementia. Cognitive impairment, physical disability and depressive symptoms in older diabetic patients: the Fremantle cognition in diabetes study. Cognitive dysfunction in older subjects with diabetes mellitus: impact on diabetes self-management and use of care services. Investigation on the relationship between diabetes mellitus type 2 and cognitive impairment. Cognitive decline and dementia in diabetes-systematic overview of prospective observational studies. Changes in cognitive abilities over a 4-year period are unfavorably affected in elderly diabetic subjects. Type 2 diabetes mellitus contributes to cognitive decline in old age: a longitudinal population-based study. Structural and functional brain complications in obese adolescents with type 2 diabetes mellitus. Type 2 diabetes mellitus and cognitive decline in two large cohorts of community-dwelling older adults. Relationships between hyperglycemia and cognitive performance among adults with Type 1 and Type 2 diabetes. Better cognitive performance following a low-glycaemic-index compared with a high-glycaemic-index carbohydrate meal in adults with type 2 diabetes. Acute hyperglycemia alters mood state and impairs cognitive performance in people with type 2 diabetes. Why is learning and memory dysfunction in type 2 diabetes limited to older adults? Improving metabolic control leads to better working memory in adults with type 2 diabetes. Association of type 2 diabetes with depression, brain atrophy, and reduced fine motor speed in a 60- to 64-year-old community sample. Incidence and risk factors of silent brain infarcts in the populationbased Rotterdam scan study. The brain in the age of old: the hippocampal formation is targeted differentially by diseases of late life. Comorbid type 2 diabetes mellitus and hypertension exacerbates cognitive decline: evidence from a longitudinal study. Comorbid depression is associated with increased health care use and expenditures in individuals with diabetes. Depression: an important comorbidity with metabolic syndrome in a general population. Chapter 23 Neuropsychological Functioning of Endocrinology Disorders: Gonadotropic Hormones and Corticosteroids Michelle M. Normative levels of estrogen and testosterone as well as homeostatic levels of corticosteroids are required for optimal cognitive functioning. The present review will focus on the neuropsychological sequelae of conditions resulting from elevated or insufficient levels of the primary sex hormones and corticosteroids as well as post-treatment neuropsychological response. Sex Hormones Estrogen Overview of Sex Hormones Estrogen and testosterone are the two primary sex hormones that influence neurons, brain structures, and cognition. Clinically low levels of each are relatively common in different medical conditions. Estrogen and testosterone each can influence neurons as neuromodulators and permanently change synapse structure [7]. Each hormone Estrogen impacts cognition via the hippocampus and its effect on synapse formation, cell morphology, cell signaling, and neuronal excitability [2]. Estrogen increases neural spine density in the rat hippocampus; correspondingly, ovariectomy decreases the density of hippocampal dendritic spines [10]. Congruently, administration of estradiol to ovariectomized monkeys increases synaptic density in the hippocampus by up to 35% [12]. In rodents, estrogen impacts neurotransmitters and electrophysiology by activating cell signaling in hippocampal neurons [13]. Following estrogen administration, memory improvement occurs only in younger, but not older, rats [15, 16]. Second, few studies assess or control the effect of age such that developmental confounds may occur with test ceiling effects. Randomized trials reveal a range of improved cognitive abilities following hormone replacement. Better executive functioning [24], nonverbal reasoning, visuospatial and visuomotor skills [4, 25], and general cognitive functioning [26] are also reported. Women awaiting hysterectomy and ovariectomy received neuropsychological tests preoperatively; following surgery, women randomly received either estradiol valerate, testosterone, estradiol and testosterone, or placebo [35]. Women with any of the hormonal treatments maintained verbal memory postoperatively, while women on placebo showed a decline in skills [35]. Others find that transdermal estradiol alone relates to better visual memory and spatial ability [37], and orally administered estradiol combined with progesterone relates to better verbal memory in postmenopausal women [25]. All of these factors are known to be influential confounds with cognitive outcomes [43]. Careful control of educational and socioeconomic status will be important in future studies. Positive effects were found on global cognitive functioning and selected tests of verbal delayed recall, quantitative working memory, and speed of 23 Neuropsychological Functioning of Endocrinology Disorders 433 information processing; no significant effects were found for visual memory or general language [44]. Interestingly, the two Hogervorst [17, 44] analyses found inconsistent duration effects; some cognitive improvements became significant after a length of time, while others lost significance with elapsed time. A review of genetic contributions to the neurocognitive phenotype is beyond the scope of this chapter; refer instead to Ross et al. Some investigations find equivalent deficits in visual and spatial aspects of working memory [67], while others suggest that the challenging components of nonverbal skills change across development [52, 56]. Specifically, errors of commission or increased impulsivity occurs in sustained attention tasks [56].

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A titre of log23 is indicative of protection and a titre of log26 or more suggests a recent infection by the virus. If no vaccination has taken place, diagnosis of the infection can be made on this basis, although it cannot be determined exactly when it took place. Sequential samples taken at different times can indicate whether the titre is rising - indicative of a recent infection - or declining [28]. The La Sota antigen has been found to be unsuitable for this purpose when vaccination is done by the same strain as it results in an overestimation of protective serum antibody titres [31]. This anti-chicken antibody is conjugated to an enzyme that catalyzes a reaction, causing a change of colour which can then be read quantitatively on a photo spectrometer designed to read microtitration plates. A cotton-covered stick is inserted into the trachea or cloaca, and then put into a vial containing phosphate buffered saline plus penicillin and streptomycin. Although cloacal swabs or faeces should always be sampled, virus can also be isolated from homogenized organs from dead birds, chosen to reflect the clinical signs. This proves infection of the bird by the virus, but does not indicate whether the virus is a pathogenic or avirulent strain [4]. This involves the inoculation of virus derived from fresh infective allantoic fluid into the brain of ten day-old chicks from specific pathogen-free parents. Each bird is examined at 24-hour intervals for eight days and graded zero if normal, one if sick and two if dead. Hygiene includes measures such as cleaning, disinfection, limiting access to wild birds, and personal hygiene of the farm staff. However, after the 1933 outbreak in England, an attenuated live vaccine was produced which was called strain H. It is the purpose of this chapter to present an overview of the different kinds of vaccine available. It is not the intention to recommend a particular vaccine, but rather to try and outline the relative advantages and limitations of each, with particular reference to its use in the village situation and giving examples of how the different vaccines are employed. Copyright@ Tewodros Alemneh probably, as serological surveys have shown where they have been carried out [38], that antibodies to the virus are already present in the village poultry as a result of previous infection by the wild virus. The principle of vaccination against a viral disease is wellknown: to elicit an immunological response against the virus in a way that does not cause the disease. The simplest way to do this is to take the virus, kill it, and then inject it into the bird. Another approach is to select a naturally occurring virus that is not virulent enough to cause serious disease and infect the birds with this virus. This latter approach can be taken further by taking a non-virulent natural virus and selecting a clone from the virus population with desirable properties, such as lack of vaccinal reactions, or heat tolerance. Finally, it is possible to genetically engineer a vaccine by, for example, taking part of the genetic material of the virus that codes for a surface antigen, and inserting this into another, different, virus to produce a recombinant vaccine [18]. Live lentogenic vaccines are usually derived from field viruses that have been shown to have low pathogenicity for poultry but produce an adequate immune response. However, these viruses have been frequently subjected to selection pressures by manufacturers in order to improve their immunogenicity or to enable their use by a particular method of application [18]. An adjuvant, such as mineral oil, is usually then added to make the inactivated virus more immunogenic. Since the vaccine is no longer capable of replication or spread, it has to be injected individually into every bird needing vaccination. It is normally injected into the back of the thigh muscle (sometimes the breast muscle is used), using 0. This requires some training, and cannot be done by every keeper of chickens without prior demonstration. In intensive poultry production, inactivated vaccines are usually applied after an initial priming vaccination with a live vaccine. In village poultry, however, good results in the absence of an initial vaccination with live vaccine have been reported [37]. The reason for this is Inactivated vaccines have been used extensively in village poultry, for example, in a successful project in Burkino Faso [39]. Although inactivated vaccine gives good protection, it is relatively expensive to produce. While inactivated vaccines are, to some extent, heat sensitive, they are much less so than conventional live vaccines which makes transporting them to villages more feasible [36]. Live vaccines differ from inactivated vaccines in that they can replicate in the host. It is an advantage in that it is not necessary to vaccinate every bird individually; the vaccinal virus can spread on its own from one bird to another. It is, however, a disadvantage in that, since an infection with a live virus is involved; this may result in clinical signs because of the innate virulence of the vaccine virus or by exacerbating other organisms that may be present, especially in the respiratory tract. The severity of this reaction depends therefore on the particular vaccinal strain used [40] and the presence or otherwise of concurrent infection with other pathogens. Another advantage of live vaccines compared to inactivated vaccines, is their ease of application as they can be applied to the drinking water or with an eye-dropper. These have been classified, in order of increasing pathogenicity, into asymptomatic enteric, lentogenic, mesogenic and velogenic strains. The majority of live vaccines are derived from asymptomatic enteric or lentogenic strains, although some vaccines derived from mesogenic strains are still in use [36]. La Sota produces moderate vaccinal reactions, especially in immunologically naive birds and is not usually recommended for primary vaccination. In theory, La Sota would also be unsuitable for vaccinating a multi-age population, including young chicks which are inevitably seen in the village situation. This is because the virus spreads and it is not practical to isolate the adults from the chicks. In practice, the degree of reaction from La Sota as a primary vaccine depends on the residual level of antibodies, which could protect the birds from vaccinal reactions, and on the extent of other concurrent infections, such as Mycoplasma spp, pathogenic E. In intensive systems, vaccination using spray delivery systems which produce small particle sizes may also exacerbate the vaccine reaction [18]. All conventional live vaccines have the disadvantage of needing to be kept at low temperatures to maintain their efficacy. This is not a problem for intensive poultry production in an industrial setting, but the maintenance of the "cold chain" during distribution can be very difficult in village settings, particularly where there is high ambient temperature. Another problem that is often encountered when using commercial vaccines in the village situation is that they are sold in vials containing 1000 or 500 doses, many more than the average village farmer needs. In fact, the packaging is a major component of the cost of manufacturing them, because a vial containing a smaller number of doses would not necessarily reduce the cost proportionally. Oil adjuvant, normally used with inactivated vaccines to improve immunogencicity, has also been tested with live vaccines and found to improve immunogenicity [41], but this combination has not been tested with village chicken is not advisable in situations where chickens are without any immune protection against the virus. Normally mesogenic vaccines, such as Komarov [51] and Mukteswar [52] are used as secondary vaccines after a primary vaccination with a lentogenic vaccine [18]. The genes coding for either of these can be inserted into a different kind of virus to make a recombinant vaccine. Another advantage is that antigens for multiple different pathogens can be inserted into the same host virus to produce a single vaccine against several different diseases. Perhaps the most significant advantage for field use is that it is possible to monitor the response to the vaccine independently of the wild virus but in its presence, and conversely, it is possible to detect antibodies against the wild virus in the presence of vaccination. A disadvantage of recombinant vaccines is that where they have been developed commercially the cost is high [18]. Copyright@ Tewodros Alemneh Recombinant Vaccines Some asymptomatic enteric viruses have been noted for their greater heat resistance than more conventional lentogenic viruses. This property has been enhanced by selection and cloning in the laboratory to produce heat tolerant vaccines. These have a distinct advantage in the village situation because it is possible to transport the vaccine without a cold chain. The application was in feed, which, because of its thermo-stability, it was possible to pre-coat with the vaccine.

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Participants 21 years of age and older are not eligible for routine eye exams, eyeglasses, and contact lenses unless otherwise noted. A prior authorization request with supporting documentation must be submitted for review. References: Age Restrictions a) Idaho Medicaid Publications "Attention: Optometrists, Ophthalmologists and Other Vision Service Providers. It must be proven safe, effective and accepted as a medical practice or treatment for the condition being addressed. December 16, 2020 Page 12 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. Authorization numbers are automatically generated for eligible participants if the item does not require prior approval. Federal Regulations Prescribed Drugs, Dentures, Prosthetic Devices, and Eyeglasses, 42 C. December 16, 2020 Page 13 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services Contact Lenses Contact lenses will be covered for participants under the age of 21 with extreme myopia or hyperopia requiring a correction equal to, or greater than, minus or plus ten (10. Participants over the age of 21 are eligible for contact lenses when necessary to prevent further degradation of vision. Orders for contacts should be made through Classic Optical by completing the Contact Lens Order Form (available for download at December 16, 2020 Page 14 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services d) State Regulations "Lenses. December 16, 2020 Page 15 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. Contact Lens Bandage Idaho Medicaid covers the fitting of contact lens for treatment of ocular surface disease for children and adults. December 16, 2020 Page 16 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. Prior authorization requests should include the contact lens prior approval form and physician documentation to support the diagnosis of Keratoconus. When requesting custom lenses, note on the request form "custom made contacts for keratoconus, diagnosis H18. You may reach Classic Optical at 1-888-522-2020 and a customer service representative will assist you, or by faxing a request to 1 (888) 522-2022. Fitting kits for Rose K, Jupiter, Custom Stable, McGuire or Dyna Intra Limbal gas permeable lenses are available. After the trial fit, please clean and disinfect the lenses before returning the kit. There is a warranty period on custom lenses, during which time you may exchange the contacts. Participants over the age of 21 are only eligible for eyeglasses once every four years, when necessary to prevent further degradation of vision. Replacement of broken, lost, or missing glasses is the responsibility of the participant. December 16, 2020 Page 18 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services c) Idaho State Plan Alternative Benefit Plan. December 16, 2020 Page 19 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. Children under the age of three (3) may qualify with documentation of multiple V2020 frames trialed that do not fit. December 16, 2020 Page 20 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services Eyeglass Lenses Participants under the age of 21 are eligible for one set of single vision or bifocal lenses once every four (4) years without a prior authorization, except when there is a minimum Rx of 0. Participants over the age of 21 necessary to prevent further necessary; please refer to the submit a request. December 16, 2020 Page 22 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. December 16, 2020 Page 23 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. Both spherical and cylindrical prescription may be added together for the same eye if both numbers are a minus (-). December 16, 2020 Page 24 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. Both the spherical and cylindrical prescription may be added together for the same eye if both numbers are a plus (+) or a minus (-). December 16, 2020 Page 25 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. December 16, 2020 Page 26 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. December 16, 2020 Page 27 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. Other conditions might be aniridea, aphakia, migraine headaches, retinitis pigmentosa, severe blepharospasm, corneal injury, or congenital abnormalities. Tint can be applied to a solid lens or as a gradient to the lens and based upon a percentage. Requests for a special therapeutic rose-colored tint F41 may be submitted under V2799. December 16, 2020 Page 28 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 4. December 16, 2020 Page 29 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services Eye Glasses for Cataract Surgery One pair of eyeglasses is covered for all ages following a recent cataract surgery. The Department follows the Medicare Coverage Determination Guidelines for cataract surgery. December 16, 2020 Page 32 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services Non-Covered Services Participants who desire additional features non-covered by Medicaid due to not being medically necessary may pay for them separately. The Medicaid contractor will bill the provider separately, and the provider may bill their usual and customary charge to the participant. If the participant cannot adapt to new lenses that were not originally covered by Medicaid, the participant is responsible for any additional charges. See the General Information and Requirements for Providers, Idaho Medicaid Provider Handbook for information on billing a participant. December 16, 2020 Page 33 of 149 Idaho Medicaid Provider Handbook Eye and Vision Services 5. Covered Services and Limitations: Examinations and Diagnostics Idaho Medicaid requires the appropriate eye exam procedure code to be billed for routine eye exams. Instrument-based ocular screening (photo screening) may be used as part of a vision exam but is not separately reimbursable unless performed by a physician or a non-physician practitioner. If the participant requests a copy of their prescription, it must be provided to the participant. Vision exams and testing are allowed once every 365 days without a prior authorization for participants under the age of twenty-one (21). Examinations and vision testing are only covered for participants over twenty-one (21) when necessary to monitor a chronic medical condition that may damage the eye such as diabetes or for acute conditions that, if left untreated, may cause permanent or chronic damage to the eye. A list of preapproved chronic and acute condition diagnosis codes is listed in Appendix A, no prior authorization is necessary. Idaho Medicaid Publications "Attention: Optometrists, Ophthalmologists and Other Vision Service Providers. Office of the Administrative Rules Coordinator, Division of Financial Management, State of Idaho, adminrules.

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Reducing substances in urine can be used as screening for galactosemia; however, this test is not very reliable because of high false-positive and false-negative rates. In neonates, the presence of ketonuria is always abnormal and an important sign of metabolic disease. Recognition of patterns of abnormalities is important in the interpretation of the results. Urine organic acid analysis is indicated for patients with unexplained metabolic acidosis, seizures, hyperammonemia, hypoglycemia, and/or ketonuria. Carnitine transports long-chain fatty acids across the inner mitochondrial membrane. An elevation of carnitine esters may be seen in fatty acid oxidation defects, organic acidemias, and ketosis. The presence or absence of ketosis in metabolic acidosis can narrow the differential diagnosis. An autosomal recessive disorder due to deficiency of branched-chain -keto acid dehydrogenase. Branched-chain amino acids metabolism and enzyme defects associated with inborn errors of metabolism. Note that propionic acid inhibits glycine cleavage enzyme and N-acetylglutamate synthetase resulting in elevated glycine and hyperammonemia in propionic acidemia. Increased plasma levels of branched-chain amino acids (leucine, isoleucine, alloisoleucine, and valine) with perturbation of the normal 1:2:3 ratio of isoleucine:leucine:valine, low plasma alanine, and presence of urine branched-chain keto and hydroxyacids on urine organic acid analysis. Hemofiltration/hemodialysis is indicated for quick removal of leucine, which is neurotoxic. Treatment after recovery from the acute state requires a special low branched-chain amino acid diet. Organic acidurias are disorders of branched-chain amino acid metabolism with accumulation of intermediate carboxylic acids. Organic acidurias can present in the neonatal period with lethargy, poor feeding, vomiting, and truncal hypotonia with limb hypertonia, myoclonic jerks, hypothermia, unusual odor, cerebral edema, coma, and multiorgan failure. Laboratory testing usually reveals high anion gap metabolic acidosis, and occasionally, hyperammonemia, hypoglycemia, neutropenia, thrombocytopenia, and pancytopenia are seen. An autosomal recessive disorder due to deficiency of isovaleryl-CoA dehydrogenase. Elevated hydroxypropionic acid and methylcitric acid in urine and propionylcarnitine (C3) in plasma. Glycine is elevated in plasma due to the suppression of the glycine cleavage enzyme system by propionate; hyperammonemia Metabolism 777 is due to propionate suppression of N-acetylglutamate synthetase. Biotin is a cofactor for propionyl-CoA carboxylase and may be beneficial in rare patients. Chronic treatment includes a diet low in amino acids that produce propionic acid (isoleucine, valine, methionine, and threonine). Elevated methylmalonic and methylcitric acids in urine; and increased propionylcarnitine (C3) and glycine in plasma. Vitamin B12 (adenosylcobalamin) is a cofactor for methylmalonyl-CoA mutase and hydroxycobalamin injection (1 mg daily) should be given as a trial or until a disorder of cobalamin transport or synthesis can be excluded (Note: a normal serum B12 level does not exclude these disorders). Chronic treatment includes a diet low in amino acids that produce propionic and methylmalonic acids (isoleucine, valine, methionine, and threonine). The pyruvate dehydrogenase complex is encoded by genes on autosomes and on the X chromosome. Severe lactic acidosis, hypotonia, feeding and breathing abnormalities, seizures, encephalopathy, white matter abnormalities, brain malformation, and dysmorphic facial features (Table 60. Enzyme studies and/or mutational analysis are necessary for a definitive diagnosis. Treatment is usually not very effective, particularly when compared with urea cycle defects and organic acidurias. Deficiency of this enzyme causes malfunction of all carboxylases, including propionyl-CoA, acetyl-CoA, 3-methylcrotonyl-CoA, and pyruvate carboxylases. Affected infants become symptomatic in the first few weeks of life with respiratory distress, hypotonia, seizures, vomiting, and failure to thrive. Skin manifestations include generalized erythematous rash with exfoliation and alopecia totalis. These infants may also have an immunodeficiency manifested by a decrease in the number of T cells. Lactic acidosis, ketosis, organic acids (methylcrotonylglycine, 3-hydroxyisovaleric, 3-hydroxypropionic, and methylcitric acids), and hyperammonemia. Hypoglycemia associated with ketosis suggests an organic acidemia or a defect of gluconeogenesis such as glycogen storage disease type I or fructose-1,6-diphosphatase deficiency. Nonketotic or hypoketotic hypoglycemia is the hallmark of fatty acid oxidation defects. Fatty acid oxidation defects can present in neonatal period with hypoketotic hypoglycemia, lactic acidosis, cardiomyopathy, and hepatopathy. Fructose-1,6-bisphosphatase deficiency can present with neonatal lactic acidosis, ketosis, hypoglycemia, hepatomegaly, coma, and seizure. Glycogen storage disease type 1 may present as hypoglycemia in the newborn period, but more typically presents at 3 to 6 months of age with poor Metabolism 779 Table 60. Decreased total carnitine; and elevated C16 (hexadecanoylcarnitine) and C18:1 (octadecenoylcarnitine). Laboratory findings include lactic acidosis, hypertriglyceridemia, and hyperurecemia. Treatment includes the avoidance of fasting through frequent and/or continuous feeding. The presence of respiratory alkalosis or metabolic acidosis can help in guiding the evaluation. Transient hyperammonemia can be seen in premature neonates with respiratory distress. In neonates, rapidly progressive symptoms appear in the first few days of life after a short symptom-free interval. These patients may develop seizures, apnea, coma, coagulopathy, and increased intracranial pressure unless hyperammonemia is diagnosed and treated promptly. Other laboratory abnormalities may include mild serum liver enzyme elevations and coagulopathy. Plasma amino acid analysis and urinary orotic acid can pinpoint the metabolic defect and provide a diagnosis. Intravenous ammonia-scavenging drugs (Ammonul) should be started for ammonia levels above 300 mol/L. Ammonul (sodium benzoate 100 mg/mL and sodium phenylacetate 100 mg/mL) is given as loading dose of 2. A repeat loading dose of Ammonul can be given in neonates with severe illness not sooner than 24 hours of the first loading dose. Hemofiltration/hemodialysis is the only means for rapid removal of ammonia from blood in acute neonatal hyperammonemia. Hemodialysis is preferred over peritoneal dialysis because it is much more effective.


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