Journal of neuroimaging : official journal of the American Society of Neuroimaging
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Although conventional magnetic resonance imaging (cMRI) is widely used for diagnosing multiple sclerosis (MS) and monitoring disease activity and evolution, the correlation between cMRI and clinical findings is far from strict. Among the reasons for this "clinical-MRI paradox," a major role has been attributed to the limited specificity of cMRI to the heterogeneous pathological substrates of MS and to its inability to quantify the extent of damage in the normal-appearing tissue. Modern quantitative MRI techniques have the potential to overcome some of the limitations of cMRI. ⋯ Magnetic resonance spectroscopy can add information on the biochemical nature of such changes, with the potential to improve significantly our ability to monitor inflammatory demyelination and axonal injury. Finally, functional MRI might provide new insights into the role of cortical adaptive changes in limiting the clinical consequences of white-matter structural damage. This review outlines the major contributions given by MRI-based techniques to the diagnostic work-up of MS patients, to the understanding of the pathobiology of the disease, and to the assessment of the effects of new experimental treatments.
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Several studies have demonstrated that brain atrophy can be detected over relatively short intervals from the earliest stages of multiple sclerosis (MS). Reviewing the published data, the authors highlight some hypothetical pathological mechanisms proposed as determinants of brain atrophy. ⋯ Examination of the pathological mechanisms proposed in the reviewed studies led the authors to believe that inflammation is only in part responsible for the development of brain atrophy. This conclusion may have an implication for the strategies of tissue protection advocated in the early stages of the RR course and strengthen recent evidence indicating that anti-inflammatory immunomodulatory agents and immunosuppressive treatments, which predominantly act against the inflammatory component of disease activity, may not have similar effects on progressive tissue loss, either in RR or progressive MS.
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Headaches are a universal experience and one of the most common causes for physician consultation. The physician must determine whether a neuroimaging study is warranted to aid in the diagnosis of primary or secondary headaches. ⋯ Neuroimaging has been crucial in the investigation of the pathogenesis of migraine and cluster headaches. Secondary headaches, which may be diagnosed by neuroimaging studies, include subarachnoid hemorrhage, cerebral venous thrombosis, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, aqueductal stenosis, and arterial dissection.
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The authors describe 2 cases of posterior fosa venous infarction. A 56-year-old woman with essential thrombocytemia presented with fluctuating complaints of headache, nausea, vomiting, left-sided numbness-weakness, and dizziness and became progressively stuporous. Cranial magnetic resonance imaging (MRI) showed bilateral parasagittal fronto-parietal and left cerebellar contrast-enhancing hemorrhagic lesions. ⋯ Digital subtraction angiography showed right transverse and sigmoid sinus occlusion. The authors suggest that one should investigate the possibility of venous infarction in the presence of posterior fossa lesions that are often hemorrhagic and are not within any arterial territory distribution but respect a known venous drainage pattern. Recognition of the observed clinical and neuroimaging features can lead to earlier diagnosis and, potentially, more effective management.
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Review Case Reports
Ganglioneurocytoma mimicking a malignant tumor: case report with a literature review of the MRI appearance of neurocytomas and gangliogliomas.
A 14-year-old girl presented with symptoms of increased intracranial pressure after her head was squeezed at a party. MRI demonstrated a mass that was hypointense to brain on T1WI and heterogeneous in signal on PD and T2WI; compression of the ventricle, midline shift, and mild ventriculomegaly also were present. Contrast enhancement was extensive and heterogeneous, mimicking a malignant tumor. Neuropathology revealed a ganglioneurocytoma.