INTRODUCTION Granulomatous inflammation is a distinctive ...

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CNS granulomas, MRI may show multiple infarctions, with hemorrhage in 50%. The CSF exam and culture carries the main brunt for diagnosing the fungal etiology affecting CNS if positive. Moreover, CNS affection due to fungi may affect immunocompetent patients, mainly Cryptococcus. And the therapeutic yield is variable according to the type of organism and the immune status of the patient. The emergence and rapid development in the neuroradiology has offered many clues yet insufficient to diagnose and differentiate the causative disorder. As a result, it is worth mentioning a postulated guideline to differentiate CNS granulomas based on the relatively specific radiological findings (Figure 29). Figure 29. Postulated guidelines to differentiate common CNS granulomas in immunocompetent patients Common CNS granulomatous disorders in immunocompetent patients include TB, sarcoidosis, cysticercosis, Wegener granulomatosis, Langerhans cell histiocytosis, primary CNS angiitis, bilharziasis, and echinococcus granulosus. Clinically, these disorders have varying systemic manifestations that are helpful in guiding the diagnosis. Neurologically, there are some
overlapping features however in sarcoidosis the most common features is cranial nerve affection, in cysticercosis the patients usually present by fits, in bilharziasis most cases involve the spinal cord, and hydatid disease behave as a space occupying lesion. Regarding the investigations, Sarcoidosis is best diagnosed by tissue biopsy yet recently the combination of gallium scan and serum ACE level is not invasive and has shown specificity of 83- 99%. There are common MRI findings which are suggestive of certain diagnosis. large cystic lesions, not surrounded by edema, is suggestive of hydatid disease, while Cysticercosis shows multiple cysts, surrounded by variable degrees of edema, and may show scolices or enhancement. Multiple small vessel infarcts are suggestive of Wegener granulomatosis, which present also with meningeal enhancement, while evidence of beading of cerebral arteries on angiography is suggestive of primary CNS angiitis. Despite of this accumulation of data regarding the individual disorders causing granulomatous CNS affection, it is still far beyond doubt that reaching the definite diagnosis for these disorders is still lacking. This is attributed to heterogeneity of clinical presentation of the disorders on one hand, with lack of awareness among the medical stuff through their various specialities on the other hand. Adding to this hinders, the yield of investigational work up is still many steps behind reaching a rapid conclusive final diagnosis. Owing to the difficulty in diagnosis and the high morbidity and fatality of these conditions, a comprehensive approach for management of suspected cases should be formulated. This approach includes an integrated multidisciplinary team from different medical specialities, to achieve the following objectives: to avoid missing cases with mainly systemic presentations and to formulate an integrated management plan tackling all the systems involved. Even in cases presenting only with neurological symptomatology proper management is sometimes hindered by the immunocompromised status of the patient, and therefore involvement of other relevant medical specialities would maximize the therapeutic yield. On the other hand cases without overt neurological affection should still warrant a neurological consultation. The neurologist can help elicit subtle neurological deficits and guide the diagnostic investigations concerning CNS involvement to help reach a rapid early diagnosis, leading to early start of treatment and better prognosis. RECOMMENDATIONS Clinical Research Forming integrated multidisciplinary team from different medical specialities to detect and manage patients of CNS granulomas. Formulating defined investigational channels to guide clinicians to a definitive diagnosis. Establishing treatment protocols specific for CNS granulomas to replace those based on systemic granulomatous disorders. Preparing training course to clinicians and neurologists illustrating clinical picture and clues for diagnosis of CNS granulomas to increase awareness with these disorders, and provide a higher index of suspicion to diagnoses patients early. Searching and testing new diagnostic tools and investigations that would provide
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INDEX Master degree thesis presente
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Necrosis usually minimal and focal,
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Most tuberculous infections of the
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A predominantly spinal form of tube
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neuroimaging characteristics. Evide
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PCR assay The advent of detection p
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Figure 2. CT scan in a patient with
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Treatment of CNS tuberculosis In co
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Presence of tuberculomas Basilar e
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aspergillosis was the most common c
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There are few reported cases of pat
Page 23 and 24: growth (Geol et al., 1996; Nadkarni
Page 25 and 26: Neuroimaging The imaging findings r
Page 27 and 28: emains very poor (Brad et al., 2005
Page 29 and 30: (Talmi et al., 2002). Although evid
Page 31 and 32: disease and can be used as a basis
Page 33 and 34: immunocompetent patients. Symptoms
Page 35 and 36: Table 4. Diagnostic criteria for ne
Page 37 and 38: Giant cysts, measuring more than 50
Page 39 and 40: Toxoplasmosis is caused by an intra
Page 41 and 42: Despite the lower sensitivity of CT
Page 43 and 44: Diagnosis is primarily made by imag
Page 45 and 46: mesenteric veins draining the large
Page 47 and 48: Sarcoidosis Sarcoidosis is a granul
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
Page 57 and 58: Patients with spinal cord sarcoidos
Page 59 and 60: Monthly tapering after 8 months ove
Page 61 and 62: patients with spinal cord involveme
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: non invasive investigations are not
Page 77 and 78: Aspergillosis is another form of fu
Page 79 and 80: cyclophosphamide (Scolding et al.,
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,
Page 95 and 96: 245. Metwally Y.(2006-4); Neurologi
Page 97 and 98: 278. Oksanen V, Salmi (1986). Visua
Page 99 and 100: 311. Ribes, J. A., C. L. Vanover-Sa
Page 101 and 102: enhanced MR images; AJNR;. 11:915-9
Page 103 and 104: 373. Tuzun M, Altinors N, Arda IS,
Page 105: transplantation patients: CT and MR
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INTRODUCTION Granulomatous inflammation is a distinctive ...

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