INTRODUCTION Granulomatous inflammation is a distinctive ...

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Treatment The treatment of choice for CNS hydatid disease is surgical removal. In the case of E. granulosus, care must be taken not to rupture the cyst with resultant spread of the protoscolexes. This is more readily accomplished if the diagnosis is made before surgery. Antiparasitic drugs, particularly albendazole, are routinely recommended before surgery in hepatic cases. However, the role of preoperative antiparasitic drugs in CNS infection has not been clearly defined. Recent data, however, suggest that adjuvant chemotherapy is associated with an improved outcome (Altinors et al., 2000). The practice of aspirating the cyst and injecting scolicidal agents is no longer recommended because of the increased risk of spillage of the protoscolexes (David et al., 2004). In the case of E. multilocularis, CNS involvement is often a manifestation of advanced disease. Few cases of alveolar hydatid disease can be cured with surgery alone, so chemotherapy is now routinely recommended postoperatively. In patients in whom the lesion is completely resected, albendazole is recommended for 2 years after surgery. In other patients, albendazole should be continued indefinitely (Schmid et al., 1998). The dose of albendazole for patients weighing more than 60 kg is 400 mg PO twice daily for 28 days. A dose of 15 mg/kg of body weight daily in 2 divided doses (not to exceed total daily dose of 800 mg) has been suggested for patients weighing less than 60 kg. For CE, the 28-day course may be repeated after 14 days without treatment to a total of 3 treatment cycles (Metwally, 2006-1). Schistosomiasis Schistosomiasis is caused by Schistosoma hematobium, Schistosoma mansoni, Schistosoma japonicum and. Two other species (Schistosoma mekongi and Schistosoma intercalatum) can also cause human infection in circumscribed foci in Southeast Asia and Africa, respectively. Human contact with water is necessary for infection by schistosomes (David et al., 2004). Epidemiology Schistosomiasis affects more than 200 million people worldwide. S. mansoni is found in Africa, Southwest Asia, the Caribbean, the Middle East, and South America. S. hematobium is found in Africa, the Middle East, and Southwest Asia. S. japonicum is found in Japan, China, the Philippines, and Southeast Asia. No nonhuman reservoirs have been found for S. mansoni and S. hematobium, although these species are rarely found in other hosts. Domestic animals are important reservoirs for S. japonicum (King, 2001). Pathology Schistosoma is a trematode, with man as a definitive host. When the parasite eggs are passed into freshwater, they can release ciliated miracidia, which swim and penetrate freshwater snails. Once inside the snail, the miracidium is able to mature into a mother sporocyst which can produce motile daughter sporocysts that target the snail's hepatic and gonadal tissues. The daughter sporocysts develop into cercariae within the snails hepatic and gonadal tissues, migrate to the vascular sinuses, and exit through the mantle. Humans, particularly children and adolescents, become infected when released motile cercariae attach to and penetrate skin. The cercariae shed their forked tail and develop into the schistosomula, which migrates to the heart, lung, and the liver. From the liver, each Schistosoma species is able to migrate to its preferred sites and to its residence in venules. Nevertheless, the parasites occasionally migrate to other sites (Sturrock, 2001). The adult worms of the Schistosoma live in the human vasculature. S. mansoni lives in the inferior
mesenteric veins draining the large intestine, S. hematobium lives in the venous plexus surrounding the bladder and in the rectal venules, and S. japonicum lives in the superior mesenteric veins draining the small intestine. After the adult worms mate in the blood vessels, the female worm (7 to 20 mm) travels against the flow of the blood to reach the vessels surrounding the intestine or bladder. There, she releases hundreds to thousands of eggs in the small venules of the portal and periportal systems (David et al., 2004). Early in the course of infection, adult worms may localize in the spinal cord vasculature or cerebral vessels (Pittella, 1997). More commonly and later in the course of infection, CNS schistosomiasis results from ectopic deposition of the parasite eggs. In heavy infection, the ova are able to reach the CNS by retrograde flow from the iliac veins and inferior vena cava by the valveless venous plexus of Batson. Eggs reach the brain and spinal cord by embolization from this vertebral venous plexus. Egg size may have an effect on deposition (Scrimgeour and Gajdusek, 1985). Cerebral schistosomiasis is thought to be more common with S. japonicum because S. japonicum releases small eggs, which are able to reach the brain. The eggs of S. mansoni are larger, containing a lateral spine, and are found more commonly in the spinal cord. The eggs of S. hematobium are of intermediate size and are found more commonly in the brain parenchyma compared to S. mansoni but less commonly than S. japonicum. (Ferrari, 1999). Schistosoma eggs have been identified in leptomeninges, parietal, occipital and temporal lobes, basal ganglia, hippocampus, brainstem, cerebellum, choroid plexus, and spinal cord. Eggs that localize to the brain or spinal cord may cause inflammation with perivascular infiltration of lymphocytes, eosinophils, and macrophages, focal and diffuse vasculitis, microinfarction, or granuloma formation (Pittella, 1997). Clinical picture Involvement of the CNS occurs in about 1% to 2% of patients, but most patients do not have neurologic symptoms (Pittella and Lana, 1981). Neurologic symptoms include mental confusion, meningitis, encephalitis, headache, vertigo, seizures, coma, visual changes, optic neuritis, papilledema, hemiplegia, opisthotonos and tremors. Schistosomal myelopathy is characterized by lumbar pain (often radicular), followed by muscle weakness, sensory deficits, and loss of sphincter control (Gomes et al., 2002). Other spinal cord involvement includes multiple nodules on the spinal cord, cord compression, and cord necrosis and less likely involvement of the cauda equina and thoracic portion of the spinal cord. Additional CNS syndromes include cerebellar and vestibular syndromes, tumor-like mass lesions, cerebral edema, and intracerebral and subarachnoid hemorrhage(Ferrari, 1999). Diagnosis Peripheral blood eosinophilia may occur, but other general laboratory studies are not particularly helpful. The CSF may show pleocytosis typically with a lymphocyte predominance. Eosinophils are present only in a few patients. Protein concentrations are increased, glucose concentrations are normal, and ICP may be increased (Ferrari, 1999). CSF from patients with schistosomal myelopathy may be xanthochromic. CT and MRI scans of the brain may show cerebral edema or atrophy. Many patients present with large granulomas, which can cause focal latencies, enhancing lesions and tumor-like lesions (Pittella et al., 1996; Sanelli et al., 2001). Some patients display a characteristic central linear enhancement surrounded by multiple enhancing punctate nodules. This tree like pattern is thought to be highly suggestive of schistosomiasis. Myelography with CT may show schistosomiasis involvement with intramedullary cord swelling and partial or complete spinal cord block. MRI images reveal lesions that are isointense to cord in T1-weighted images and patchy
Page 1 and 2: INDEX Master degree thesis presente
Page 3 and 4: Necrosis usually minimal and focal,
Page 5 and 6: Most tuberculous infections of the
Page 7 and 8: A predominantly spinal form of tube
Page 9 and 10: neuroimaging characteristics. Evide
Page 11 and 12: PCR assay The advent of detection p
Page 13 and 14: Figure 2. CT scan in a patient with
Page 15 and 16: Treatment of CNS tuberculosis In co
Page 17 and 18: Presence of tuberculomas Basilar e
Page 19 and 20: aspergillosis was the most common c
Page 21 and 22: There are few reported cases of pat
Page 23 and 24: growth (Geol et al., 1996; Nadkarni
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Page 29 and 30: (Talmi et al., 2002). Although evid
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Page 33 and 34: immunocompetent patients. Symptoms
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Page 41 and 42: Despite the lower sensitivity of CT
Page 43: Diagnosis is primarily made by imag
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Page 49 and 50: sequentially in approximately one t
Page 51 and 52: Furthermore, the majority of the pa
Page 53 and 54: Imaging Studies Chest x-rays have b
Page 55 and 56: Occasionally, granulomas coalesce t
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Page 59 and 60: Monthly tapering after 8 months ove
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Page 63 and 64: weighted contrast-enhanced spin-ech
Page 65 and 66: identified within the CNS (Calabres
Page 67 and 68: Balancing control of the disease wi
Page 69 and 70: Two major patterns of white matter
Page 71 and 72: By MRI, cholesteatomas are hypointe
Page 73 and 74: non invasive investigations are not
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Page 81 and 82: 24. Behri M, Raj M, Ahuja GK et al
Page 83 and 84: 56. Carol A Langford (2003), Wegene
Page 85 and 86: Infectious Diseases;26:781-805 89.
Page 87 and 88: 119. Feely M, Sternberg M (1977). A
Page 89 and 90: Press :675-705. 151. Hadi M, Boncoe
Page 91 and 92: 182. Jones Richard E. ; Chatham W.
Page 93 and 94: Medicine; 76: 423-31 214. Levy RM,
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278. Oksanen V, Salmi (1986). Visua
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enhanced MR images; AJNR;. 11:915-9
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transplantation patients: CT and MR
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INTRODUCTION Granulomatous inflammation is a distinctive ...

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