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However cystic acne purchase 30gm elimite amex, as noted earlier acne 8 weeks pregnant elimite 30 gm on line, some of the particles that are deposited in the lung are transported to the gastrointestinal tract (Mena et al acne upper lip buy 30 gm elimite with mastercard. The rate of particle transport from the lungs has not been quantified in humans acne 6 dpo buy elimite 30gm mastercard, but half-times of elimination in animals range from 3 hours to 1 day (Adkins et al acne quitting smoking buy elimite 30gm lowest price. Manganese Levels in Human Serum/Plasma Concentration (g/L) (mean±2 standard deviations) Age 5 Days a Serum c Plasma 0 skin care product reviews buy elimite 30 gm line. No statistically significant differences in manganese concentrations were found between sexes. Increases of 2060% in manganese levels in the kidney and spleen were noted in mice 2448 hours after exposure to manganese dioxide (Adkins et al. Sheep exposed to welding fumes for 3 hours exhibited a 40-fold increase in lung manganese content (Naslund et al. Preferential accumulation of manganese in specific locations of the brain (including the caudate nucleus, globus pallidus, and substantia nigra) was noted in one monkey exposed to an aerosol of manganese chloride (2040 mg/m3) several hours/day for 35 months (Newland et al. This preferential uptake could play a role in the characteristic neurological effects of manganese (see Section 3. This dose also resulted in significantly increased concentrations of manganese in the rat cerebellum (27% increase that approached statistical significance), striatum (205% increase), and cortex (48% increase), compared with control rats. When rats were administered the same amount of manganese under the same dosing regimen, with manganese in the form of manganese dioxide, similar, but less striking, results were observed (Roels et al. Manganese concentrations in the blood were increased by 41%, and in the cerebellum, striatum, and cortex by 31, 48, and 34%, respectively, over the control rats. Radiography data indicated that 1 day after dosing, the olfactory bulb contained 90% of the manganese (measured as g/100g wet weight) in the measured tissues, while the basal forebrain contained 6% of the manganese. Manganese in the cerebral cortex, hypothalamus, striatum, and hippocampus were also maximal at 7 days post-dosing. Manganese values in liver and kidneys were approximately 1% of the total measured for the first 7 days, and then decreased steadily until 12 weeks. These results were compared to distribution of manganese following intraperitoneal injection, in which no brain region showed preferential distribution at 1, 7, or 21 days post-dosing (Tjдlve et al. Injection of 200 g manganese resulted in maximally elevated levels in the olfactory bulb (400% higher than the uninjected side), with levels in the tubercle half that in the bulb within 12 hours post-exposure; these levels remained elevated for 3 days. Two injections of 200 g manganese doubled the level of manganese in the striatum compared to saline-injected controls; single doses did not increase tissue manganese levels. No other brain regions were noted and blood manganese levels were not changed with any treatment. These data indicate that the olfactory mucosa is an important pathway for distribution of manganese into the brain. Exposures lasted for 6 hours/day for either 5 days/week (10 exposures) or 7 days/week (14 exposures). The following tissues were analyzed for manganese content using neutron activation analysis: plasma, erythrocytes, olfactory bulb, striatum, cerebellum, lung, liver, femur, and skeletal muscle. Increased manganese concentrations were reported in olfactory bulb, lung, femur, and skeletal muscle following exposure to 3 mg/m3 (after either dosing regiment); a lower dose of 0. Striatal manganese levels were increased at the two highest doses only after 14 days of exposure. However, concentrations in the cerebellum were similarly elevated, which was interpreted by the authors to indicate that accumulation of manganese was not selective for the striatum. Red blood cell and plasma manganese levels were increased only in rats exposed to the highest dose for the 10-day exposure period. These data indicate that even at lower doses manganese can accumulate in the olfactory bulb and that the neuronal pathway to the brain is significant for inhaled manganese in rodents. Mainstream manganese entry into the brain from blood occurs through capillary endothelial cells of the blood-brain barrier and through the cerebral spinal fluid via the choroid plexuses (Bock et al. A number of transport mechanisms (including facilitated diffusion, active transport, transferrin-mediated transport, divalent metal transporter-1 mediation, store-operated calcium channels) have been proposed to transport manganese across the blood barrier, but current understanding is inadequate to determine the predominant mechanism of transport (Aschner et al. A concern that inhaled manganese, compared with ingested manganese, may more readily result in manganese accumulation in the brain, a principal toxicity target of manganese, has led to recent detailed investigations of manganese concentrations in various brain regions and in other tissues following inhalation exposure of animals to environmentally relevant forms of manganese. The results from these animal studies indicate that tissue manganese concentrations in the brain depended on aerosol concentration, exposure duration, and brain region. Tissue manganese concentrations generally increased with increasing air concentrations and durations of exposure. Comparison of manganese concentrations across tissues shows the following order in exposed maternal rats: liver > pancreas > olfactory bulb > lung > striatum femur > milk > cerebellum >> whole blood (Table 3-9). In young Rhesus monkeys after 65 days of exposure, the order was: bile > olfactory epithelium > pituitary > liver > pancreas globus pallidus > olfactory bulb > kidney > putamen > caudate > cerebellum > heart >skeletal muscle > frontal cortex > lung > parietal bone femur >> blood (Table 3-10). Brain tissues from the monkeys were dissected into more regions than the rat brains and, immediately following 65 days of exposure to the highest exposure concentration, showed the following order of elevated manganese concentrations: pituitary>globus pallidus>olfactory bulb>putamen>caudate> cerebellum>frontal cortex>trigeminal nerve (see Table 3-10). These results are consistent with the evidence that the human striatum, globus pallidus, and substantia nigra are the primary neurotoxicity target for manganese (Aschner et al. Three- to 5-fold increases (over air control values) in mean manganese tissue concentrations were found in the globus pallidus, putamen, and caudate in monkeys exposed to 1. Comparison with the rat results in Table 3-9 suggests that rodents do not accumulate manganese in the basal ganglia. Recent corroborative findings showed that marmosets, a nonhuman primate, accumulated more manganese in the brain (especially in the basal ganglia and the visual cortex) than rats following intravenous injection of equivalent mg/kg body weight doses of manganese chloride (Bock et al. The mechanisms by which manganese accumulates in the basal ganglia of primates are poorly understood (Aschner et al. Mean (±Standard Error on the Mean) Tissue Manganese Concentrations (µg Manganese/g Tissue Wet Weight) in Young Male Rhesus Monkeys Exposed to Aerosols of Manganese Sulfate (1. In pregnant rats repeatedly exposed to inhaled manganese, the placenta appears to partially limit the transport of manganese to the developing fetus (Dorman et al. The results from this study suggest that the brain in developing fetuses and neonates is partially protected from excess manganese by the placenta, and that the neonatal period, compared with adulthood, is relatively more susceptible to increased manganese concentration in brain tissues with inhalation exposure to manganese sulfate aerosol concentrations between 0. Bar graphs were digitized to obtain numerical estimates of means for male and female offspring combined. No age-related effects were observed on the order of manganese concentrations in the various tissue. These results are consistent with results from 14-day inhalation studies (Dorman et al. These studies show that manganese preferentially accumulates in the basal ganglia, especially the globus pallidus, and the substantia nigra. Rats given a single oral dose of 416 mg manganese/kg body weight (as manganese chloride tetrahydrate) exhibited little tissue accumulation of manganese 14 days later (Holbrook et al. Studies in animals indicate that prolonged oral exposure to manganese compounds results in increased manganese levels in all tissues, but that the magnitude of the increase diminishes over time (Kristensson et al. Table 3-12 provides illustrative data based on rats exposed to 214 mg manganese/kg(body weight)/day (as manganese tetroxide) for up to 224 days. As the data reveal, large increases in tissue levels of manganese compared with the controls occurred in all tissues over the first 24 days, but levels tended to decrease toward the control levels as exposure was continued. This pattern is thought to be due to a homeostatic mechanism that leads to decreased absorption and/or increased excretion of manganese when manganese intake levels are high (Abrams et al. Although the percentage of manganese absorbed decreased, the total amount of manganese absorbed increased when higher levels of manganese were fed. Manganese Levels in Rat Tissue After Oral Exposure Tissue concentrations (percent of control)a 24 Days 60 Days 224 Days 810 430 540 260 137 102 175 125 138 128 125 100 Tissue Liver Kidney Brain Testes a Values presented are the ratio (expressed as a percentage) of tissue levels of manganese in animals receiving 3,550 ppm manganese in the diet (as manganese tetroxide) compared to animals receiving a normal diet (50 ppm). A study measuring the retention of a single oral dose of radiolabeled manganese in adult and neonatal rats indicated that retention of the label 6 days after exposure was much greater in pups (67%) than in adults (0. The distributional differences in rats exposed to either manganese chloride or manganese dioxide by gavage were investigated by Roels et al. Manganese concentrations were significantly elevated in the blood (approximately 83% increase over controls) and the cortex of the brain (approximately 39% increase over controls). Gavage administration of manganese dioxide, by contrast, did not significantly increase the amount of manganese in blood or any section of the brain. In addition, administration of manganese as manganese chloride by gavage caused roughly the same amount of increased manganese in the blood as intratracheal administration of manganese in the same form; it did not cause as significant an increase of manganese in the cortex (Roels et al. These data indicate that inhalation exposure to manganese in the form of manganese chloride or manganese dioxide causes accumulation of manganese in the brain more readily than oral exposure. Acute manganese exposure in drinking water was found to alter brain regional manganese levels in neonatal rats; after 5 days of exposure, the highest level was in the striatum (12. After 10 days, the highest concentrations were in the pons and medulla and the lowest were in the hypothalamus. No studies were located regarding tissue distribution of manganese in humans or animals after dermal exposure to organic manganese. A number of studies have been conducted that investigated various facets of the distribution of inorganic manganese in animal models. The studies utilized a number of routes of administration, and the results suggested that route may play an important role in distribution. In an intraperitoneal study performed in monkeys, manganese was reported in all tissues studied. The highest levels were found in the pancreas, liver, and kidney, and the lowest levels were found in the blood; levels in the central nervous system were found to decrease more slowly than those in other tissues (Dastur et al. Calves injected intravenously with 54Mn were found to have 3-fold higher liver manganese concentrations and 13-fold higher pancreatic manganese concentrations than calves fed manganese (Carter et al. Identical dosing of rats with manganese dioxide resulted in significant increases in manganese levels in blood (79%), cerebellum (40%), striatum (124%), and cortex (67%) over those in controls. These data indicate that administration of manganese dioxide by this route resulted in greater accumulation of manganese in the brain than did manganese chloride. The distribution of manganese in the brain was investigated using Cebus (Newland and Weiss 1992; Newland et al. Magnetic resonance images indicated hyper-intensity of the globus pallidus and substantia nigra consistent with an accumulation of manganese in these areas (Newland and Weiss 1992; Newland et al. Substantial accumulation of manganese was also noted in the pituitary at low cumulative doses (Newland et al. Concentrations of manganese in these four tissues was still elevated (~1 mg/kg) at 96 hours post-dosing. The experiment was divided into an acute study (one dose) or a "chronic study" (ten doses). The brain manganese level in the mice administered 10 doses of 11 mg/kg each was 1. The manganese level in brain after manganese chloride exposure followed the same increasing trend over the 24 hour analysis period, but was higher at each time point, with a maximum value of >2. Clinical studies involving cancer patients or healthy volunteers have analyzed the usefulness of mangafodipir as a contrast agent for the identification of certain abdominal tumors. Although these studies do not necessarily quantify the amount of manganese, or mangafodipir, in particular tissues, they are useful tools in identifying the location of the metal; also relative proportions of manganese among two or more tissues that contain the metal can be observed by differences in signal from these imaging studies. Several studies have shown the qualitative presence of manganese in the liver due to increased signal in that organ following mangafodipir administration of 0. The renal cortex was the only other tissue to reach a 100% increase over baseline signal at 0. The signal from the renal cortex at the lower dose had a maximum of 80% over baseline, whereas the signal in the liver at this dose was ~75% of the baseline value (Wang et al. Several studies have determined the distribution of manganese in tissues of animals following intravenous administration of mangafodipir. This maximum value was still observed in the brain 2 weeks post-dosing, but measurements taken at 1 and 3 months post-dosing were below the detection limit. Male and female Sprague-Dawley rats injected with [54Mn] mangafodipir at a dose of 5. Distribution of manganese in tissues of rats injected with labeled manganese chloride was compared to the previous results, and for all tissues, the label was greater after administration with the chloride than from the mangafodipir, with the exception of kidney and large bowel, but these differences were not significant (Elizondo et al. When the bile duct was cannulated, the distribution of an equivalent dose of mangafodipir showed an increased retention of labeled manganese in all organs but the brain (0. By contrast, tissue retention of 14C from radiolabeled mangafodipir was very low: pancreas, 0. These data indicate that manganese dissociates from the fodipir moiety after mangafodipir administration and partitions into the tissues listed above. The tissue distribution of normal and bile-cannulated dogs following administration of [54Mn] or [14C] mangafodipir was also studied (Hustvedt et al. The general pattern of distribution of manganese and carbon was similar to that seen with rats, except the concentrations were increased in the dog. The values for normal dogs were taken 168 hours post-dosing for both forms of labeled mangafodipir; the bile-cannulated dogs were analyzed 24 hours post-dosing. The plasma concentrations declined rapidly with a terminal half-life of approximately 15 minutes. In the normal dog and bile-cannulated dog, the tissue distribution was as follows (the values for the bile-cannulated dog are given in parentheses; all values are in g equivalents of compound/g): liver, 8. The distribution of labeled carbon in normal (or bile-cannulated dogs) was the following: kidneys, 0. These data indicate that in the dog, as in the rat, the manganese cation is retained by the tissues, but the fodipir moiety is not. Distribution of 54Mn and 14C following mangafodipir administration was also studied in the pregnant rat (Hustvedt et al. By 24 hours, fetal livers and bones were clearly seen, but placental radioactivity had decreased substantially. Fat deposits also contained a significant amount of the radioactivity at 24 hours. By contrast, radioactivity from labeled carbon in the mangafodipir was relatively uniformly distributed throughout the pregnant rat at 5 minutes and 1 hour post-dosing, with the highest levels in the kidneys. These studies have shown the liver to accumulate the highest amount of manganese from the administered dose of mangafodipir. This is an important limitation since the brain, the primary target of manganese neurotoxicity, may not accumulate a significant amount of manganese until much later, possibly after the current experiments in humans and animals were truncated. Experiments in rats and dogs, both normal and bile-cannulated, indicate that the brain does not accumulate a significant amount of manganese following administration of mangafodipir at levels much higher than the recommended clinical dose of the agent (Hustvedt et al.
Two to three drops of sterile saline are dropped on the cornea from a height of 4 to 6 inches skin care vitamins and minerals generic 30 gm elimite with amex. However skin care 4men wendy cheap elimite 30gm free shipping, some patients who wear contact lenses may have permanent suppression of the corneal reflex skin care videos order elimite 30gm otc. A small flashlight or bright ophthalmoscope held about 50 cm from the face and shined toward the eyes of the patient should reflect off the same point in the cornea of each eye if the gaze is conjugate delex acne cheap elimite 30gm line. If it is possible to obtain a history acne scar removal buy elimite 30gm with visa, ask about eye movements acne coat order elimite 30 gm online, as a congenital strabismus may be misinterpreted as dysconjugate eye movements due to a brainstem lesion. Slowly roving eye movements are typical of metabolic encephalopathy, and if conjugate, they imply an intact ocular motor system. The head is rotated first in a lateral direction to either side while holding the eyelids open. This can be done by grasping the head on either side with both hands and using the thumbs to reach across to the eyelids and hold them open. The head movements should be brisk, and when the head position is held at each extreme for a few seconds, the eyes should gradually come back to midposition. The head is then rotated in a vertical plane (as in head nodding) and the eyes are observed for vertical conjugate movement. In an awake patient, the voluntary control of gaze overcomes this reflex response. However, in patients with impaired consciousness, the oculocephalic reflex should predominate. There may also be a small contribution from proprioceptive afferents from the neck,112 which also travel through the medial longitudinal fasciculus. Because these pathways overlap extensively with the ascending arousal system (see Figure 28), it is quite unusual for patients with structural causes of coma to have a normal oculocephalic examination. In contrast, patients with metabolic encephalopathy, particularly due to hepatic failure, may have exaggerated or very brisk oculocephalic responses. Eye movements in patients who are deeply comatose may respond sluggishly or not at all to oculocephalic stimulation. In such cases, more intense vestibular stimulation may be obtained by testing caloric vestibulo-ocular responses. With appropriate equipment, vestibulo-ocular monitoring can be done using galvanic stimulation and video-oculography. The ear canal is first examined and, if necessary, cerumen is removed to allow clear visualization that the tympanic membrane is intact. The head of the bed is then raised to about 30 degrees to bring the horizontal semicircular canal into a vertical position so that the response is maximal. If the patient is merely sleepy, the canal may be irrigated with cool water (158C to 208C); this usually induces a brisk response and may occasionally cause nausea and vomiting. Fortunately, in practice, it is rarely necessary to use caloric stimulation in such patients. If the patient is deeply comatose, a maximal stimulus is obtained by using ice water. An emesis basin can be placed below the ear, seated on an absorbent pad, to catch the effluent. The ice water is infused at a rate of about 10 mL/minute for 5 minutes, or until a response is obtained. After a response is obtained, it is necessary to wait at least 5 minutes for the response to dissipate before testing the opposite ear. To test vertical eye movements, both external auditory canals are irrigated simultaneously with cold water (causing the eyes to deviate downward) or warm water (causing upward deviation). The cold water induces a downward convection current, away from the ampulla, in the endolymph within the horizontal semicircular canal. The effect of the current upon the hair cells in the ampulla is to reduce tonic discharge of the vestibular neurons. The left-hand side shows the responses to oculocephalic maneuvers (which should only be done after the possibility of cervical spine injury has been eliminated). The right-hand side shows responses to caloric stimulation with cold or warm water (see text for explanation). Normal brainstem reflexes in a patient with metabolic encephalopathy are illustrated in row (A). The patient shown in row (B) has a lesion of the right side of the pons (see Figure 28), causing a paralysis of gaze to that side with either eye. Row (E) illustrates a patient with a midbrain infarction eliminating both the oculomotor and trochlear responses, leaving only bilateral abduction responses. Hearing was intact, as were facial, oropharyngeal, and tongue motor and sensory responses. Motor and sensory examination was also normal, tendon reflexes were symmetric, and toes were downgoing. At that point, the pupils were pinpoint and the patient was unresponsive with flaccid limbs. The sudden onset of bilateral impairment of eye movements on the background of clear consciousness is rare, and raised the possibility of a brainstem injury even without unconsciousness. Any activation of the anterior canal (which activates the ipsilateral superior rectus and the contralateral inferior oblique muscles) and the posterior canal (which activates the ipsilateral superior oblique and contralateral inferior rectus muscles) by caloric stimulation cancel each other out. When caloric stimulation is done in an awake patient who is trying to maintain fixation. This mnemonic can be confusing for inexperienced examiners, as the responses seen in a comatose patient with an intact brainstem are the opposite: cold water induces only tonic deviation (there is no little or no corrective nystagmus), so the eyes deviate toward the ear that is irrigated. The presence of typical vestibular nystagmus in a patient who is unresponsive indicates a psychogenic cause of unresponsiveness. The absence of a response to caloric stimulation does not always imply brainstem dysfunction. Bilateral vestibular failure occurs with phenytoin or tricyclic antidepressant toxicity. Aminoglycoside vestibular toxicity may obliterate the vestibular response, but oculocephalic responses may persist, the neck muscles supplying the afferent information. Finally, if there has been head trauma, one or more eye muscles may become trapped by a blowout fracture of the orbit. It is important to distinguish this cause of abnormal eye movements from damage to neural structures, either peripherally or centrally. This is generally done by an ophthalmologist, who applies topical anesthetics to the globe and uses a fine, toothed forceps to tug on the sclera to attempt to move the globe (forced duction). Inability to move the globe through a full range of movements may indicate a trapped muscle and requires evaluation for orbital fracture. Patient 21 A 56-year-old man with a 20-year history of poorly controlled hypertension came to the emergency department with a complaint of sudden onset of severe dizziness. On examination, he was fully Interpretation of Abnormal Ocular Movements A wide range of eye movements may be seen, both at rest and during vestibular stimulation. Each presents clues about the nature of the insult that is causing the impairment of consciousness. Table 23 lists some of the spontaneous eye movements that may be observed in unconscious patients. Most individuals have a mild degree of exophoria when drowsy and not maintaining active fixation. However, other individuals have varying types of strabismus, which may worsen as they become less responsive and no longer attempt to maintain conjugate gaze. Hence, it is very difficult to determine the meaning of dysconjugate gaze in a stuporous or comatose patient if nothing is known about the presence of baseline strabismus. On the other hand, certain types of dysconjugate eye movements raise suspicion of brainstem injury that may require further examination for confirmation. For example, injury to the oculomotor nucleus or nerve produces exodeviation of the involved eye. In skew deviation,114 in which one eye is deviated upward and the other downward, there typically is an injury to the brainstem (see below). A destructive lesion involving the frontal eye fields causes the eyes to deviate toward the side of the lesion (away from the side of the associated hemiparesis). An irritative lesion may cause deviation of the eyes away from the side of the lesion. These eye movements represent seizure activity, and often there is some evidence of quick, nystagmoid jerks toward the side of eye deviation indicative of continuing seizure activity. Hemorrhage into the thalamus may also produce ``wrong-way eyes,' which deviate away from the side of the lesion. Damage to the lateral pons, on the other hand, may cause loss of eye movements toward that side (gaze palsy, Figure 29). The lateral gaze deviation in such patients cannot be overcome by vestibular stimulation, whereas vigorous oculocephalic or caloric stimulation usually overcomes lateral gaze deviation due to a cortical gaze paresis. Absence of abduction of a single eye suggests injury to the abducens nerve either within the brainstem or along its course to the orbit. However, either increased intracranial pressure or decreased pressure, as occurs with cerebral spinal fluid leaks,121 can cause either a unilateral or bilateral abducens palsy, so the presence of an isolated abducens palsy may be misleading. Isolated loss of adduction of the eye contralateral to the head movement implies an injury to the medial longitudinal fasciculus. Bilateral lesions of the medial longitudinal fasciculus impair adduction of both eyes as well as vertical oculocephalic and vestibulo-ocular eye movements, a condition that is distinguished from bilateral oculomotor nucleus or nerve injury in the comatose patient by preservation of the pupil- lary light responses. Typically, there may also be severe ptosis on that side (so that if the patient is awake, he or she may not be aware of diplopia). In rare cases with a lesion of the oculomotor nucleus, the weakness of the superior rectus will be on the side opposite the other third nerve muscles (as these fibers are crossed) and ptosis will be bilateral (but not very severe). This occurs most often when the paresis is due to ischemia of the oculomotor nerve (the smaller pupilloconstrictor fibers are more resistant to ischemia), such as in diabetic occlusion of the vasa nervorum. Such patients are also typically awake and alert, whereas third nerve paresis due to brainstem injury or compression of the oculomotor nerve by uncal herniation results in impairment of consciousness and early pupillodilation. Trochlear nerve impairment causes a hyperopia of the involved eye, often with some exodeviation. If awake, the patient typically attempts to compensate by tilting the head toward that shoulder. Because the trochlear nerve is crossed, a trochlear palsy in a comatose patient suggests damage to the trochlear nucleus on the opposite side of the brainstem. In some cases, the eye that is elevated may alternate from side to side depending on whether the patient is looking to the left or the right. As in sleeping individuals who typically have some degree of exophoria, the eye positions may not be quite conjugate, but the ocular Examination of the Comatose Patient 71 excursions should be conjugate. Most roving eye movements are predominantly horizontal, although some vertical movements may also occur. Most patients with roving eye movements have a metabolic encephalopathy, and oculocephalic and caloric vestibulo-ocular responses are typically preserved or even hyperactive. The roving eye movements may disappear as the coma deepens, although they may persist in quite severe hepatic coma. Roving eye movements cannot be duplicated by patients who are awake, and hence their presence indicates that unresponsiveness is not psychogenic. A variant of roving eye movements is periodic alternating or ``ping-pong' gaze,126 in which repetitive, rhythmic, and conjugate horizontal eye movements occur in a comatose or stuporous patient. The eyes move conjugately to the extremes of gaze, hold the position for 2 to 3 seconds, and then rotate back again. The episodic movements of the eyes may continue uninterrupted for several hours to days. Periodic alternating eye movements have been reported in patients with a variety of structural injuries to the brainstem or even bilateral cerebral infarcts that leave the oculomotor system largely intact, but are most common during metabolic encephalopathies. Spontaneous nystagmus is uncommon in coma because the quick, saccadic phase is generally a corrective movement generated by the voluntary saccade system when the visual image drifts from the point of intended fixation. However, continuous seizure activity with versive eye movements may give the appearance of nystagmus. In addition, several unusual forms of nystagmoid eye movement do occur in comatose patients. Retractory nystagmus consists of irregular jerks of both globes back into the orbit, sometimes occurring spontaneously but other times on attempted upgaze. Electromyography during retractory nystagmus shows that the retractions consist of simultaneous contractions of all six extraocular muscles. Convergence nystagmus often accompanies retractory nystagmus and also is typically seen in patients with dorsal midbrain lesions. The patients were comatose and the movements were not affected by caloric vestibular stimulation. The initially described patients had caudal pontine injuries or compression, although later reports described similar eye movements in patients with obstructive hydrocephalus, uncal herniation, or even metabolic encephalopathy. A variety of related eye movements have been described including inverse bobbing (rapid elevation of the eyes, with bobbing downward back to primary position) and both dipping (downward slow movements with rapid and smooth return to primary position) and inverse dipping (slow upward movements with rapid return to primary position). Seesaw nystagmus describes a rapid, pendular, disjunctive movement of the eyes in which one eye rises and intorts while the other descends and extorts. It is most commonly seen during visual fixation in an awake patient who has severe visual field defects or impairment of visual acuity, and hence is not in a coma. Seesaw nystagmus appears to be due in most cases to lesions near the rostral end of the periaqueductal gray matter, perhaps involving the rostral interstitial nucleus of Cajal. Rather than testing power in specific muscles, it is focused on assessing the overall responsiveness of the patient (as measured by motor response), the motor tone, and reflexes, and identifying abnormal motor patterns, such as hemiplegia or abnormal posturing. Paratonia is often seen in patients with dementia and is normally found in infants between the second and eighth weeks of life, suggesting that it represents a state of disinhibition of forebrain control as the level of consciousness becomes depressed. As patients become more deeply stuporous, muscle tone tends to decrease and these pathologic forms of rigidity are less apparent.
Eggs hatch miracidium Eggmiracidium sporocystRediaercariae metacercariaeAdult Parasitology 158 Sheep acne tretinoin cream 005 buy cheap elimite 30 gm online, cattle skin care questions and answers purchase elimite 30 gm mastercard, man and other herbivorous animals are definitive host and species of Lymanae snails are intermediate hosts acne scar removal trusted 30gm elimite. Following ingestion acne 4 weeks pregnant discount elimite 30 gm otc, the metacercariae excyst in the duodenum and the young flukes migrate in to the peritoneal cavity acne blemishes buy elimite 30 gm with mastercard. They reach the bile ducts of the liver by penetrating through the liver capsule and become adult worms acne location order elimite 30gm without a prescription. The egg develops in fresh water and hatches miracidium which enter snails of the genus Lymnaea. In the snail, the miracidium develop in to sporocyst and produces generation of rediae and then cercariae. The cercaria is shaded from the snail host and undergoes encystation on water vegetation to become metacercariae. Man acquires infection by eating wild water cress or other water vegetation on which metacercariae have encysted. Clinical Manifestation Light infections are usually asymptomatic In heavy infection · Local irritation during migration of the young warms to the liver Fever, Sweating, abdominal pain, Colic & Obstructive jaundice Acute epigastria pain & abdominal tenderness Persistent diarrhea In the bile duct flukes cause inflammation Prevention and Control 1. Avoid eating uncooked water plants Treating infected animals Destroying snail hosts Sanitary disposal of faeces Treating infected individuals and giving health education Parasitology 159 Laboratory Diagnosis: Finding 1. Eggs in the faces in chronic infection Eggs in aspirates & in bile if eggs are absent in stool. Serological diagnosis by testing serum for antibodies is particularly valuable in the early stages of infection when the immature flukes are migrating through the liver and causing serious symptoms but not yet producing eggs. Note: If eggs are found in human faces it must be confirmed that they are present due to a Fasciola infection & not from eating animal liver containing fascioliasis eggs (false fascioliasis) False Fascioliasis - due to ingestion of animal liver containing Fasciola egg, with the passage of eggs in stool, is at time mistaken for actual infection Rules out keep the patient on liver free diet for three days. Relevance to Ethiopia the parasite does not play an important role in human health in Ethiopia. There are only as few reported cases of the disease; even those reports may have been the result of finding eggs in the stools of people who had consumed infected liver of sheep or cattle. Parasitology 160 Fasciola giagantica (The giant liver fluke) Geographical Distribution:-Widely distributed in tropical Africa including Ethiopia, and Far East, south and south East Asia. Habitat:-Adult: In the bile duct of sheep, goat, cattle; it is a relatively commonparasite of hebivorous mammals Egg: In faeces All larva stages: Fresh water snail Metacercaria: on water vegetations Morpology: Similar to F. However, its infection in cattle leads to considerable economic loss especially in some African countries. Destroying snail habitats when feasible Proper sanitary disposal of faeces Treating infected individuals and giving health education Cultivating watercress in water free from fecal pollution Laboratory Diagnosis: 1. Clonorchis sinesis (The Chinese Liver fluke) Geographical Distribution:-Far East, Japan, Korea, Taiwan, High infection rates are found especially in those parts of china where fish are cultured in pond that are fertilized with human or animal feaces. Habitat: Adult: bile duct of man and fish eating animals including cat, dog, pig, etc. Eggs: In the faeces Metacercariae: under the scale of fresh water fish Morphology: Adult- Size: 10-25 mm by 3-5 mm Parasitology 162 Boat shaped, Smooth cuticle with out spine Oral sucker is larger than ventral sucker Simple unbranched caeca Egg- Size: 25-30m Colour: shell; yellowish brown; contents pale yellow Fine and smooth shell Operculum: At the narrow end of the egg, fitting into thickened rim of the shell. A small knob-like boss at the wide end of the egg Contains a well organized ciliated embryo Life cycle: Eggmiracidium sporocystRediaercariae metacercariaeAdult Definitive host: man Intermediate hosts: Primary intermediate host is Bulimus snail. Man acquires infection from eating raw or inadequately cooked fresh water fish containing metacerariae. The metacercariae excysts in the intestine and migrates to the liver to become adult worm. The cercariae swim resides under the scales of fresh water fish and become metacercariae. Pathology: Causes clonorchiasis Major symptoms are diarrhea, jaundice, cirrhosis, biliary obstruction, hepatomegally Parasitology 163 Prevention and Control 1. Avoid eating raw fish Sanitary disposal of faeces and not using faeces as a night soil Destroy the snails Inspection of fish Treating infected person and giving health education Laboratory Diagnosis Finding: 1. They are hermaphrodite Fasciolopsis buski (The giant intestinal fluke) Geographical Distribution China, Taiwan, Thailand, Vietnam, Indonesia, etc. Habitat: Adults: small intestine of man, pig, dog, Eggs: In the faeces of man Pig, dog, Larval forms: Fresh water snails Metacercariae: encysted on certain aquatic vegetation. Parasitology 164 Morphology: Adult: Size: 20-75mm by 8-20mm Large, fleshy, flat worm Has no cephalic cone and shoulder Oral sucker is smaller than the ventral sucker Intestinal caeca is not branched Tests are highly branched and in tandem position Egg: Size: 130 - 140 (m by 80 - 85(m pale yellow-brown in colour Shape: oval Small operculum Unembroynate Life Cycle: Eggmiracidium sporocystRediaercariae metacercariaeAdult Definitive host: Man Intermidate host: Segmentina species which are fresh water snails Man gets infection by feeding on infected water vegetation containing metacercariae. Pathology: Diarrhae, Ulceration and inflammation of the intestine, malabsorption, eosinophilia. Treating infected individuals and giving health education Laboratory Diagnosis Finnding 1. Heterophyes heterophyes Geographical Distribution: China, Japan, Egypt, Korea, Taiwan Habitat:-Adult: In small intestine of man, cat, dog, fox Egg: In the faeces Larval forms: In fresh water snails Metacercariae: fresh water fish Morphology: Adult: Size: 1-2mm Shape: elongated pyriform Has three suckers; oral, ventral and genital suckers. Tests are ova and side by side Numerous integumantary scales / spines Egg: Similar to the egg of Clonorchis sinensis Size: 25-30m Shape: more oval, the operculum does not overlap Yellow to dark brown in colour Shell: Slightly thicker than that of Clonorchis sinensis Contain developed miracidium Parasitology 166 Life Cycle: Eggmiracidium sporocystRediaercariae metacercariaeAdult Requires three hosts to complete its life cycle. Definitive host: Man Intermediate host: First intermediate host: Fresh water snail such as Pirenella Second intermediate host: Brackish water fish such as Tilapia, mullet. Avoid eating raw or undercooked fish Proper waste disposal of faeces in latrine Avoid use of human faces as a fertilizer Destroy snails and their habitat Inspection of fish for metacercariae Treating infected individuals and giving health education Laboratory Diagnosis Finding the characteristics eggs in the faeces 3. Lung Fluke Paragonimus westermani (Oriental lung fluke) Geographical Distribution:-Extensively distributed in the Far East, and focally in West African countries such as Zaire, Nigeria, Cameroon and also in South America. Parasitology 167 Habitat: Adults: In the lung of man Eggs: In the sputum of man Metacercariae: Fresh water crabs and crayfish Morphology: Adult: Size: 7. Avoid eating raw or uncooked crabs and crayfish Avoid contamination of water with sputum or faeces Destroy snails and their habitat Inspecting crabs and crayfish for metacercariae Treating infected individuals and giving health education Laboratory Diagnosis 1. Eggs in aspirates of pleural fluid and occasionally in faeces Parasitology 169 Review Questions Trematoda 1. Illustrate the classification of trematodes according to their habitat in human host. What hosts are required to complete the life cycle of medically important lung flukes? The most common nematode of medical importance are those inhabiting the intestinal tract. Most of these have a direct life cycle and their presence may be confirmed by detecting the characteristics eggs in feces. The filarai are long, slender round worms that parasitize the blood, lymph, subcutaneous and connective tissue of humans. All of the filaria are transmitted by insect vectors and most produce larva called microfilaria that may be demonstrated in the blood, lymph or connective tissue of the human host. Non segmented cylindrical or round worms Possess a shiny cuticle which may be smooth, spined, or ridged Mouth is surrounded by lips or papillae Sexes are separate with the male worms being smaller than the female 5. In the male there is a testis at the distal end of a long tube which terminates in copulatory organs consisting of one or two projections called spicules 6. Copulatory bursa, caudal alae or genital papillae Females are either viviparous (produce larvae) or oviparous (lay eggs) 8. Tissue nematodes are transmitted mainly by insect vectors and most intestinal nematodes are feco-oral route and soil transmitted. Adult worms live in the intestinal tract Female worms are oviparous (lay eggs) Humans are the only or the most significant hosts Most species are soil transmitted Before becoming adults in their human host, the larvae of A. Habitat: Adult: In the small intestine Egg: In the faeces Morphology:-Adult: colour: pinkish Male: size: about 15cm curved tail and two copulatory spicules of unequal size Female: size 2-25cm, with a straight tail. Fertilized Egg With Double Shell Size: about 70mShape: oval, or some times round Shell: the two layer are distinct, rough, brown, covered with little lumps external shell and smooth, thick, colourless Parasitology 172 internal shell. Unfertilized Egg With Double Shell size: 80-90m shape; more elongated (elliptical) shell: brown, puffy external shell and thin internal shell. Semi-decorticated Fertilized Egg Similar to Type A but With out the External Shell shell: single, smooth, thick and colourless or very pale yellow. Semi-Decorticated Unfertilized Egg Shell: a single smooth thin colourless shell (double line) Content: large rounded colourless refractile granules. Infection occurs by ingestion of the infective egg in contaminated food or drink, from contaminated hand. Following ingestion the larvae hatch in the small intestine and penetrate blood vessels in the small intestinal wall. After mating the female produces large number of eggs (200,000 eggs/day/ female) which are passed in the feces. Parasitology 175 -Its infection in children is known to affect gastrointestinal function. Infected children are often Vitamin A deficient and have low serum albumin levels. Frequent exposure to infection may result in impairment of physical and intellectual development. Prevent soil contamination by sanitary latrines and avoid disposal of faeces in the use of night soil as a fertilizer and washing hands before eating 2. Finding the eggs in faeces Identifying adult worms expelled through the anus or mouth. Relevance to Ethiopia: Ascaris lumbricoides is one of the commonest and most widespread human parasites in the world. Highest rates of infection are recorded from children in the age group 5 to 9 years old. Parasitology 176 Ascariasis is found in practically every Ethiopian community and is probably the most common communicable disease in the country, particularly in the malaria -free highlands. The most extensive survey of ascariasis in Ethiopia reported 44% of 32,276 persons, two thirds of them school children, infected. The overriding role of climate is also indicated by the distinct geographical distribution of the infection. Thus, between 50% and 75% of the children examined in Kefa, Gojam, Welega, and Gonder were infected; between 10% and 40% in Ilubabor, Sidamo, Wello, Tigray, Gamo Gofa, Shewa, Bale, and Arsi; and below 10% in the semiarid regions of Eritrea and Harerge. Prevalence rate of Ascaris lumbricoides in recent studies conducted in Ethiopia ranges from 17% to 77. Entrobius vermicularis (Pin Worm) Geographical Distribution:-Cosmopolitant more common in temperate and cold climates than in warm climates more commonly infected than adults. Habitat: Adult: small intestine (terminal ileum) Parasitology 177 Gravid female: Caecum and rectum Eggs: In faeces or deposited on perianal skin Morphology: Adults: Color: yellow white Male: Size 2-5mm Coiled tailed with a single spicule. Female: 8-13mm, thin pointed tail wing like expansion of cervical alae Egg: Size: 50-60m Shape: oval but flattened on one side, rounded on the other side Smooth and thin but with double shell Content: either a small granular mass or a small curved up larvae. Following ingestion of infective eggs, the larvae hatch in the intestine and develop into adult worms in the large intestine. Man also acquires infection from clothing, bedding, air borne eggs autoinfection or retroinfection. Finding eggs from perianal skin using cellulose adhesive tape Finding eggs in the faeces Finding adult worms in the faeces. Relevance to Ethiopia Most past surveys of intestinal parasitism have reported low Enterobius vermicularis infection rates largely because it is underreported due to failure of routine stool examination methods to detect the eggs in infected Parasitology 179 persons. The finding that 5% of 569 school children in rural communities in Gonder region had E. Recent studies done using routine stool examination method, a prevalence rate up to 1% were reported (Erko B, 1993 and Assefa T, 1998) Trichuris trichiura (The Whipworm) Geographical Distribution:-Cosmopolitan: more common in moist warm climates. Habitat Adult: large intestine (caecum) and vermiform appendix Eggs: In the faeces, not infective when passed Morphology Adults: whip-like shape, anterior 3/5th of the warm resembles a whip & hence the name the posterior 2/5th are thick. Male: Size 30-45 mm, coiled tail with a single spicule Female: 35-50mm, straight thick tail. Egg: Size: 50-54m Shape: barrel-shaped with a colorless protruding mucoid plug at each end Shell: fairly thick and smooth, with two stained Color: yellow brown layers; & bile Parasitology 180 Content: a central granular mass which is unsegmented ovum Life Cycle Figure 3. The infective eggs are ingested and the larva hatch and penetrate the villa of the small intestine. In young children, severe infection can cause chronic diarrhea, intestinal ulceration with blood and mucus being passed in the feces, iron deficiency anemia, failure to develop at the normal rate, weight loss and prolapse of the rectum. Sanitary disposal of faeces in latrine Avoid the use of night soil as a fertilizer Treatment of infected individuals and health education. Relevance to Ethiopia:In a national survey in which 28, 696 stool specimens were examined, 36. As with the other intestinal helminths, pathology depends on worm burden, light infections being asympotomatic, this parasite commonly occurs together with A. Bure (Gojam) had a prevalence of 100% Whereas Mendida (shewa) was found to be free of trichuriasis (Kloos M et al. A similar pattern also has also been noted between the prevalence of infection due to A. Strongyloides stercoralis (The dwarf thread worm) Geographical Distribution: world wide distribution in the warm moist climates of tropical and subtropical countries. Habitat: Has both free living and parasitic generations Parasitic Adults: buried in the mucosal epithelium of the small intestine of man. Rhabditiform larvae: Passed in the faeces and external environments Filariform larvae: soil and water the infective stage Morphology: Adult Male (free living):-size = 1. In parasitic way of life, usually man acquires infection by filariform larva penetrating the skin. Following penetration, the larvae enter blood Parasitology 185 vessels and undergo a heart lung migration to develop. After migrating up the trachea, the larvae are swallowed and they mature in the intestinal tract. The rhabditiform larve hatch out in the intestine and either develop in the intestine in to infective larvae causing autoinfection or they are passed out in the faeces. The rhabditiform larvae which are expelled in the faeces can follow free living way of life if the external environment is suitable or it develop in to the infective stage called filariform larvae.
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Diseases
