INTRODUCTION Granulomatous inflammation is a distinctive ...

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Figure 20. Sarcoidosis axial T2W and gadoliniumenhanced T1W brain images with multiple, extensive white-matter periventricular and subcortical enhancing lesions, some of which are large (arrowed). ( Zajicek et al., 1999) White matter lesions can mimic lesions seen in multiple sclerosis (Smith et al., 1989). In contrast to multiple sclerosis, linear enhancement along blood vessels in the region of white matter changes is seen in neurosarcoidosis. These signal changes along the Virchow-Robin spaces suggest that lesions infiltrate the brain through perivascular Virchow-Robin spaces, and are believed to be the result of infarctions caused by granulomatous vasculitis (Corse and Stem, 1990). Non inhancing brain parenchmal lesions is best seen on the MRI T2 and FLAIR studies and is seen as confluent or nonconfluent hyperintense patches, that do not show contrast enhancement and have no mass effect. These lesions tend to occur in the periventricular white matter but may also occur in the brain stem and basal ganglia and the corticomedullary junction. Periventricular lesions are nonspecific and can occur in association with multiple sclerosis, hypertension, and vasculitis. Theoretically, they can result from periventricular granulomas or from small areas of infarction caused by granulomatous angiopathy. The exact nature of these lesions has not been identified in the literature. Symptomatic improvement usually did not correspond to improvement on MR imaging studies. This behavior differed from that of enhancing brain lesions for which symptoms often correlated with imaging findings and symptomatic improvement correlated with regression on MR images. These facts also imply that the nonenhancing brain parenchymal lesions and the enhancing lesions have different pathophysiologic mechanisms (Greg et al., 1999). Involvement of cranial nerves have been described in association with sarcoidosis. Most frequently, the facial nerve is involved clinically. Imaging, however, revealed that the optic nerve and/or chiasma are the most frequently affected cranial nerves (Zajicek et al., 1999). Spinal Cord and Nerve Root Involvement manifest as cord swelling, with increased signal intensity on T2-weighted images and a pattern of enhancement on T1-weighted contrast-enhanced images (Figure 21), that predominates in the periphery of the cord but includes patchy multifocal enhancement of the cord. Imaging findings are thus nonspecific and can mimic multiple sclerosis, cord tumor, vacuolar myelopathy, TB, or fungal infection (Gideon and Mannino, 1996).
Patients with spinal cord sarcoidosis progress in four phases, which begin with a linear leptomeningeal pattern of enhancement and progress to a phase in which there is cord enlargement with faint enhancement or no enhancement. Enhancement then progresses but the cord begins to reduce in size until it reaches a final stage of atrophy without any enhancement. Although it is fairly evident that patients who present with cord atrophy will most likely not respond to steroid treatment, it is unclear whether the degree of enhancement plays a role in treatment response (Greg et al., 1999). Figure 21. Sarcoidosis. T1W gadolinium-enhanced sagittal MRI of the thoracic spinal cord showing focal contrast enhancement and expansion of the cord at T6–T7 level (arrowed). ( Zajicek et al., 1999) In general, resolution of lesions on MR imaging lags behind resolution of clinical symptoms. The role of MR imaging in neurosarcoidosis is to confirm clinical suspicion, establish subclinical disease, and document the response of pathologic lesions to treatment (Zylberberg et al., 2001). Neurophysiological Studies Evoked potential (EP) studies may be of value in supporting the diagnosis and monitoring the course of the disease. VEPs and brainstem auditory evoked potentials (BAEPs) tend to be abnormal in about one third of the patients with neurosarcoidosis. Somatosensory evoked potentials tend to show abnormalities less frequently. All 3 modalities of EPs can show abnormalities in patients before the appearance of clinical signs (Oksanen, 1986). EMG/nerve conduction studies can be used to confirm neuropathy or myopathy. The most characteristic electrodiagnostic finding is mononeuropathy multiplex, showing axonal degeneration and segmental demyelination. With treatment and clinical improvement, motor, sensory and mixed nerve conduction tend to improve. In cases of myopathy, the EMG shows myopathic potentials (Ando et al., 1985). Nuclear studies Gallium 67 citrate scans often are supportive when typical findings are lacking. This is especially true in neurosarcoidosis or uveitis when biopsy may not be feasible. Gallium 67 scanning may help demonstrate sites of inflammation. Positive scans secondary to increased uptake can identify asymptomatic lesions. Though the test can be positive in any inflammatory or neoplastic lesions,
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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
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: Occasionally, granulomas coalesce t
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 and 76: overlapping features however in sar
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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