Magnetic resonance imaging (MRI) of the brain and spinal cord plays a central role in establishing the diagnosis of multiple sclerosis (MS), in monitoring disease activity, and as a key outcome measure in clinical trials of new MS therapies. Conventional MRI continues to evolve, reflecting advances in imaging hardware and software. These advances have led to important new insights into MS disease pathophysiology and can be used to improve patient management. Despite these improvements, standard MRI continues to capture only a small portion of the underlying changes that occur during the course of the disease.
"The MRI can detect changes in inflammatory activity but for quantification of intact myelin and remyelination, magnetization transfer imaging has been proposed. Diffusion tensor imaging can be used to monitor tract-specific changes that may be more closely linked to clinical measures and may be particularly powerful when combined with functional measures, such as functional MRI [10,11]. "
[Show abstract][Hide abstract] ABSTRACT: Background
Demyelinating diseases cause destruction of the myelin sheath, while axons are relatively spared. Pathologically, demyelination can be the result of an inflammatory process, viral infection, acquired metabolic derangement and ischemic insult. Three diseases that can cause inflammatory demyelination of the CNS are: Multiple sclerosis (MS), Acute disseminated encephalomyelitis (ADEM) and Acute hemorrhagic leucoencephalitis. Differentiation is not always easy and there is considerable overlaping. Data about adults with acute demyelination requiring ICU admission is limited.
A 17 year old Greek female was hospitalised in the ICU because of acute respiratory failure requiring mechanical ventilation. She had a history of febrile disease one month before, acute onset of paraplegia, diplopia, progressive arm weakness and dyspnea. Her consciousness was not impaired. A demyelinating central nervous system (CNS) disease, possibly post infectious encephalomyelitis (ADEM) was the underlying condition. The MRI of the brain disclosed diffused expanded cerebral lesions involving the optic nerve, basal ganglia cerebellum, pons and medulla oblongata. There was also extended involvement of the cervical and thoracic part of the spinal cord. CSF leukocyte count was elevated with lymphocyte predominance. The patient required mechanical ventilation for two months. Then she was transferred to a rehabilitation centre. Three years later she remains paraplegic. Since then she has not suffered any other demyelination attack.
Demyelinating diseases can cause acute respiratory failure when the spinal cord is affected. Severe forms of these diseases, making necessary ICU admission, is less frequently reported. Intensivists should be aware of the features of these rare diseases.
BMC Research Notes 01/2013; 6(1):22. DOI:10.1186/1756-0500-6-22
[Show abstract][Hide abstract] ABSTRACT: To assess the reliability of new magnetic resonance imaging (MRI) lesion counts by clinicians in a multiple sclerosis specialty clinic.
An observational study.
A multiple sclerosis specialty clinic.
Eighty-five patients with multiple sclerosis participating in a National Institutes of Health–supported longitudinal study were included.
Each patient had a brain MRI scan at entry and 6 months later using a standardized protocol.
The number of new T2 lesions, newly enlarging T2 lesions, and gadolinium-enhancing lesions were measured on the 6-month MRI using a computer-based image analysis program for the original study. For this study, images were reanalyzed by an expert neuroradiologist and 3 clinician raters. The neuroradiologist evaluated the original image pairs; the clinicians evaluated image pairs that were modified to simulate clinical practice. New lesion counts were compared across raters, as was classification of patients as MRI active or inactive.
Agreement on lesion counts was highest for gadolinium-enhancing lesions, intermediate for new T2 lesions, and poor for enlarging T2 lesions. In 18% to 25% of the cases, MRI activity was classified differently by the clinician raters compared with the neuroradiologist or computer program. Variability among the clinical raters for estimates of new T2 lesions was affected most strongly by the image modifications that simulated low image quality and different head position.
Between-rater variability in new T2 lesion counts may be reduced by improved standardization of image acquisitions, but this approach may not be practical in most clinical environments. Ultimately, more reliable, robust, and accessible image analysis methods are needed for accurate multiple sclerosis disease-modifying drug monitoring and decision making in the routine clinic setting.
[Show abstract][Hide abstract] ABSTRACT: The pathophysiological correlates and the contribution to persisting disability of hypointense T1-weighted MRI lesions, black holes (BH), in multiple sclerosis (MS) are still unclear. In order to study the in vivo functional correlates of this MRI finding, we used 11C-PK11195 PET (PK-PET) to investigate changes in microglial activity. Ten relapsing and 9 progressive MS subjects had a PK-PET scan and a MRI scan alongside a full clinical assessment, including the expanded disability status scale (EDSS) for evaluation of disability. We studied the PK binding potential of the specifically bound radioligand relative to the non-displaceable radioligand in tissue (BPND) in T1 BHs. Out of a total of 1,242 BHs identified, 947 were PK enhancing. The PKBPND was correlated with the EDSS (r = 0.818; p < 0.05) only in the progressive group. In the relapsing patients there was an inverse correlation between PKBPND and BH total lesion volume in whole brain (r = − 0.781; p < 0.05). When progressive patients were grouped according to the disability outcome at 2 years from the PK-PET scan, the total PKBPND in BHs was found to be a significant outcome predictor of disability (p < 0.01). Our findings show that relapsing and progressive patients have heterogeneous patterns of PKBPND in T1 BHs and indicate that BHs are not just “holes” representing loss of axons and myelin, but display inflammatory activity in the form of activated microglia. The significant association between PKBPND, neurological impairment and outcome in progressive subjects supports a role for activated microglia in disability progression.
Neurobiology of Disease 05/2014; 65. DOI:10.1016/j.nbd.2014.01.018 · 5.08 Impact Factor
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