INTRODUCTION Granulomatous inflammation is a distinctive ...

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SUMMARY better sensitivity and specificity and less time consuming. Looking for new treatments that is more effective and less toxic. More studies about the current and possible treatment regiments for CNS granulomatous disorders instead of focusing studies on the systemic aspects of these disorders. Granulomatous inflammation is a distinctive pattern of chronic inflammation due to infectious or non infectious agents. Its formation is due to the cell mediated immune response to such agents (Mitchell and Cotran, 2003; Dov, 2003). Granulomatous inflammatory disorders involving the CNS have a wide variety of etiologies, clinical presentations, overlapping with each other and with other CNS disorders. And up till now, they have non conclusive investigations results making rapid accurate diagnosis sometimes difficult or impossible without tissue biopsy. Also many medical specialties are involved in the management of such cases, which leads to a lack in comprehensive integrated approach (Metwally, 2006). Tuberculosis remains a major global problem and a public health issue of considerable magnitude, and was declared as a global emergency in 1993 by the World Health Organization (WHO). This was due to spread of HIV and multiple antituberculous drug resistance (Dolin et al., 1994). Common presentations of CNS tuberculosis include basal meningitis, focal cerebral lesions, myelopathy, Pott’s disease, rarely myelitis. In young age it may present with rapid onset encephalopathy (Dastur et al., 1995) Rapid diagnosis of CNS TB is difficult, and usually Treatment is started on clinical assumption. Diagnostic studies, mainly smear examination and culture have low sensitivity and are time consuming (Muralidhar, 2004), while the PCR has higher sensitivity, yet it is not technically and financially available in many endemic areas. Most common imaging studies findings are hydrocephalus and basal meningitis, which is not specific (Chang et al.,1990). Treatment should start with quadruple therapy, and in cases of INH resistance, it should be replaced by Ethambutol. Steroids should be used in cases of clinically or radiological evident of meningoencephalitis or increased CSF pressure to more than 300 cc H2O. Prognosis is related to the severity of meningoencephalitic symptoms at the start of treatment. It should be noted that the most common causes of treatment failure is multiple drug resistance and poor compliance (Daikos et al.,2003). Fungal infections or the CNS has increased recently due to increase prevalence of HIV and immunosuppressive states specially that is related to organ transplantation. Diagnosis is mostly a clinical surprise, and it requires a high index of suspicion. The most common CNS fungal infection is Cryptococcosis. It is specially prevalent in the HIV seropositive population with 20% of HIV mortality cases due to Cryptococcal meningitis. Cryptococcus usually spreads from a pulmonary focus with high tendency to affect the CNS, and is protected from the immune system by a polysaccharide capsule. The most common clinical presentations are headache, fever, increased intracranial tension and blindness. The definitive diagnostic test is CSF examination with India ink stain showing the cryptococci. It is treated with amphotericin B and Flucytosine (Jermey, 2004).
Aspergillosis is another form of fungal infection that can spread to the CNS either hematogenously from the lung or by direct invasion from the nasal sinuses. Unlike cryptococcosis, it is specially prevalent in cases of organ transplantations clinical features vary from diffuse presentation of meningitis and increased ICT to focal lesions. It characteristically invade cerebral vessels and adjacent brain parenchyma, causing thrombosis and secondary haemorrhagic infarcts. It generally has poor prognosis which varies according to patient immunity, in cases of markedly suppressed immunity it is fatal within few weeks, otherwise it may develop to granulomas, abscesses evident as ring enhancing lesions in radiological studies (enhancement = immunity). Definitive diagnosis require brain biopsy. Treatment should be stared as early as possible, and it includes surgical debridement with adequate safety margin (to avoid postoperative cerebrovascular complications) and administration of amphotericin B and flucytosine, in addition to correcting the general condition (immune reconstitution). Recently voriconazole has shown promising results when combined with surgery (Sepkowitz et al., 1997). Rhinocerebral Mucormycosis is a life-threatening fungal infection that occurs in immunocompromised patients, mainly diabetics. These infections are becoming increasingly common, yet survival remains very poor, as many cases are diagnosed late and treatment strategies based on available antifungal and surgical debridement with control of risk factors are not effective (Brad et al., 2005). Invasive candidal CNS infection is more common in premature infants and neonates, and present usually by meningitis with insidious vague clinical picture (lethargy, confusion), and it is also treated with amphotericin B and flucytosine (Burgert et al., 1995). There has been an increased awareness of the parasitic CNS infection in the last few decades. Cysticercosis, on of the common parasitic infections, was frequently under diagnosed due to the lack of adequate diagnostic tools, and even after the advent of modern neuroimaging techniques, it was frequently misdiagnosed as TB. Viable CNS cysticerci don’t induce an immune reaction and are frequently asymptomatic, while the immune system is stimulated by the dying organism, leading to the development of the clinical manifestations of the illness (fits, hydrocephalus). This has provoked an unsettled debate about the necessity of use of parasiticidal drugs in asymptomatic patients. Solid diagnosis is difficult except by tissue biopsy, MRI showing cysts with scolices, or subretinal scolices on fundoscopy. Recently EITB has proved to be 100 % specific (Carpio et al., 1998). Toxoplasmosis is another form of parasitic CNS infection. It commonly presents with afebrile focal cerebral lesions, commonly ganglionic, cerebellar and brain stem. When manifest in an HIV Patient, it presents with encephalitis, fever and disseminated multi organ affection. Diagnosis is difficult, serology and PCR are not sensitive. Radiological studies show multiple brain enhancing lesions which when combined with positive serology empirical treatment (pyrimethamine + leucoverin) should be started and if there is no response in 2 weeks, a tissue biopsy should be obtained (Luis, 2006). In hydatid disease, 5% of cases have CNS affection, in the form of space occupying lesions presenting clinically as increased ICT, fits of focal cerebral lesions. Imaging studies show a cystic brain lesion with no enhancement. Diagnosis rests on the evidence of systemic affection, and ELISA is done in doubtful cases. Treatment is surgical excision under albendazole cover (Eckert et al., 2001). Bilharziasis affect the CNS in 1% of cases, through granulomatous inflammation around ova deposited in brain and spinal cord. It present by myelopathy, meningoencephalitis, optic neuritis and rarely space occupying lesion. It is diagnosed by demonstrating ova in urine, stool or rectal biopsy, also ELISA is 99% specific. Brain imaging reveals central linear enhancement surrounded
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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
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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 and 74: non invasive investigations are not
Page 75: overlapping features however in sar
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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