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Diagnosis of ms without lesions, how do i not get angry - Test Out

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According to the McDonald criteria for MS, the diagnosis requires objective evidence of lesions disseminated in time and space. As a consequence there is an important role for MRI in the diagnosis of MS, since MRI can show multiple lesions (dissemination in space), some of which can be clinically occult, and MRI can show new lesions on follow up scans (dissemination in time).
The image on the right is an axial T2 weighted image of the brainstem of an MS-patient, showing typical peripherally located white matter lesions, often in or near the trigeminal tract, or bordering the 4th ventricle.
Even when a patient is clinically suspected of MS, we still have to study the WMLs carefully to decide whether these lesions are indeed suggestive of MS, and not incidental age-related findings. The lesions in the deep white matter (yellow arrow) are nonspecific and can be seen in many diseases. A spinal cord lesion together with a lesion in the cerebellum or brainstem is very suggestive of MS. Spinal cord lesions are uncommon in most other CNS diseases, with the exception of ADEM, sarcoid, Lyme disease and SLE.
On PDW-images the spinal cord has a uniformly low signal intensity (like CSF), which gives the MS lesions a good contrast against the surrounding CSF and normal cord tissue.
The simultaneous demonstration of enhancing and non-enhancing lesions in MS is the radiological counterpart of the clinical dissemination in time and space. The edema will regress and finally only the center will remain as a hyperintense lesion on T2WI. This patien not only has multiple periventricular lesions of which some have the typical Dawson finger aspect (blue arrow), but there is also a juxtacortical lesion.
These enhancing lesions all are new lesions, since Gadolinium enhancement is only visible for about 1 month.
It on MRI presents as a large intra-parenchymal lesion with usually less mass effect than would be expected for its size. These lesions can be distinguished from gliomas or intraparenchymal abscesses, which typically have a closed-ring enhancement. Here T2 and postcontrast T1W images showing a large lesion in the left hemisphere with alternating T2-hyperintense and isointense bands. Think of NMO when there are extensive spinal cord lesions (more than 3 vertebral segments) with low T1-signalintensity and swelling of the cord. Here we see a sagittal T2-weighted image of the spinal cord in a patient with NMO showing a longitudinally extensive cord lesion with marked swelling.
Acute Disseminated Encephalomyelitis (ADEM)is another important differential diagnosis of MS. On MRI there are often diffuse and relatively symmetrical lesions in the supra-and infratentorial white matter which may enhance simultaneously.
The diagnosis of MS requires elimination of more likely diagnoses and demonstration of dissemination of lesions in space and time.
When a patient presents with 2 or more attacks with clinical evidence of 2 or more neurological deficits, there is no need for additional requirements to make the diagnosis of MS, because there is dissemination in place and time. In all other cases (less than 2 attacks or less than 2 clinical lesions) there is a role for MRI to fulfill the diagnostic criteria by demonstrating dissemination in space, in time or both. The McDonald criteria are very specific, because if you want to use MRI for the diagnosis of MS, you have to make sure that the patient really has MS.
You do not want a patient to start treatment daily if there is any doubt about the diagnosis. Gadolinium is administered at the start of the examination because the longer you wait the more enhancement you will see on the T1W images (MS lesions are not spontaneously bright on T1-weighted images without contrast administration). The sagittal FLAIR is ideal for detection of lesions in the corpus callosum and the 3D sequence allows for better detection of smaller and juxtacortical lesions.

The most diagnostic sequence is the conventional SE or FSE (TSE) PDW, because this is the most sensitive technique.
If a patient is clinically suspected of having MS and the MR-images support that diagnosis, than you should not consider the possibility of Lyme's disease and neuro-SLE in the differential diagnosis, because they have such a low prevalence. These diagnoses are only worth mentioning if there are clinical findings that support these diagnoses. Consequently, it is not wise to put MS in the differential diagnosis if the clinician does not suspect the patient of having MS and on the MR incidental WMLs are found. The odds are against the diagnosis of MS, because vascular WMLs are 50-500 times more likely than MS plaques. On the other hand if a patient is clinically suspected of having MS and multiple WMLs are found, our major concern is the differential diagnosis MS versus vascular disease and we have to follow the McDonald criteria.
Borderzone infarctionKey finding: typically these lesions are located in only one hemisphere, either in deep watershed area or peripheral watershed area.
Key findings: Multifocal lesions in WM and basal ganglia 10-14 days following infection or vaccination. On the FLAIR image these lesions are dark, so they follow the intensity of CSF on all sequences (they were hypointense ion the T1WI). On this image we see both very wide VR spaces as well as confluent hyperintense lesions in the WM. Periventricular bands or 'rims' are thin linear lesions along the body of the lateral ventricles and are associated with subependymal gliosis.
The location of these white matter lesions is in the deep white matter and it is important to notice that these lesions are not juxtaventricular, not juxtacortical and not located in the corpus callosum. Given the a priori greater chance of hypoxic-ischemic WM lesions, we must conclude that these WMLs probably have a vascular origin.
Only if the clinical findings strongly direct us towards inflammatory, infectious, toxic or other diseases, should we consider these diagnoses. Suggesting the diagnosis of MS in a patient with these MR findings and with no clinical suspicion for MS would be unwise. Ischemic WMLs present as lacunar infarcts, watershed infarcts or diffuse hyperintense lesions within the deep white matter. Besides lesions in the deep WM, there are some juxtaiventricular lesions and even Dawson finger-like lesions.
Key finding: 2-3mm lesions simulating MS in a patient with skin rash and influenza-like illness. Key finding: subcortical lacunar infarcts with small cystic lesions and leukoencephalopathy in young adults. Department of Diagnostic Radiology, Vrije Universiteit Hospital, Amsterdam, The Netherlands.
Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis. The diagnosis of multiple sclerosis should be made by a physician with experience in identifying the disease. Many investigators view MRI measures as the best prospect for a biological indicator—or biomarker—that can help them understand the disease process, diagnose patients, monitor treatment response, and predict prognosis.
Magnetic resonance imaging with gadolinium contrast, especially during or following a first attack, can be helpful in providing evidence of lesions in other parts of the brain and spinal cord. A second magnetic resonance scan may be useful at least three months after the initial attack to identify new lesions and provide evidence of dissemination over time.
For starters, Meier’s time-lapse movies can’t tell anyone exactly what’s going on inside the patient’s lesions.

Once definite disability develops, it may be too late to treat that component of the disease.The ability to diagnose and treat MS has improved considerably in the past 10 years because of the availability of MRI and partially effective immunomodulating therapies. Intuition tells us that lesions, or plaques, can’t be good for the brain, but their meaning for a person’s functional status and future is unclear.
Although brain lesions often don’t correlate with clinical symptoms, that discrepancy can partly be understood as a function of where in the nervous system those plaques hit, experts say, and of whether anatomical redundancies and adaptive mechanisms in a given person’s brain can compensate. For instance, a white spot (or hyperintensity) on a T2 brain scan means excess water, which accompanies inflammation or swelling that can result from various causes, such as a tumor or infection—or an MS lesion. In MS, lesions arise when white blood cells, having crossed the blood-brain barrier, infiltrate an area and fuel inflammation that strips the fatty myelin insulation from the axon nerve fiber, thus letting additional water in to fill the breach, on top of the fluid of the initial swelling. With the 2001 criteria, however, that diagnosis could be clinched if brain images taken a few months apart revealed that new lesions had formed. In a small study, Guttmann and colleagues in Boston and Amsterdam found that two-thirds of MS patients showed no Gd-enhanced lesions at their initial visit or 1 year later (Liguori et al., 2011).
If clinicians relied on Gd-enhanced scans as a primary indicator of active disease, they might conclude that those patients were stable, Guttmann says; although doctors also look for whether new lesions have formed on T2 scans since the previous year’s visit, he adds, they tend to eyeball the images in a cursory manner.
But many of those lesions can heal in such a way that they disappear from that record, according to unpublished results from Naismith and Stuart Cook of the University of Medicine and Dentistry of New Jersey in Newark (Qian et al., 2011). In a phase-II clinical trial,33 this drug appeared promising in that it reduced active MRI lesions by 90 percent and decreased MS relapses by more than 50 percent. However, an examination of tissue integrity within those lesions—using DTI—revealed that traces of injury persisted (although leaving less damage than in permanent FLAIR lesions).
Many of his own MS patients on treatments look good, feel good, and have T2 lesions that appear stable on MRI from year to year, but they could have plaques “coming and going, coming and going, and I just didn't catch 'em,” he says. Clinical trials have shown that when drugs reduce relapses of MS symptoms, lesion activity on scans decreases, says neurologist Daniel Reich, chief of the translational neuroradiology unit at NINDS.
Evidence indicates that on average, people with MS who suffer many clinical attacks or show a large burden of lesions on MRI early in their disease tend to fare worse, years later, than those who don’t. The answer is “no” for changes in T2 lesion volume and Gd-enhanced lesions, say Ebers and Martin Daumer, director of the nonprofit Sylvia Lawry Centre for Multiple Sclerosis Research in Munich. For example, those who originally received a placebo treatment were later offered interferon; any differences in MRI lesions that the drug triggered between the treated and untreated groups during the trial’s 3 years would tend to disappear, since everyone ended up on interferon. As many studies, including Sormani’s work, have shown, inflammation-inhibiting medications such as interferon that suppress new lesions on conventional MRI generally curb the number of relapses in the 2- to 3-year time frame of clinical trials.
That being the case, Sicotte says, an experimental anti-inflammatory agent that fails to reduce new Gd-enhanced lesions in small, early-stage studies might not be developed further. It’s possible that some novel therapies might not inhibit MRI lesion activity, yet could still quell flare-ups by, say, counteracting the downstream consequences of the plaques; or they could protect neurons in a way that prevents disease progression. The findings suggest that structural damage unfolds independently in the two areas—meaning that even when no new changes show up on brain scans, MS could be progressing in the spinal cord without the patient knowing it, Bakshi says.
It was only by using FLAIR scans (which adjust T2 scans for the brightness of background water signals from fluid in nearby brain ventricles) that investigators first noticed cortical lesions. The latest version of MRDSS will factor in white-matter abnormalities by measuring T2 lesion and T1 black hole volumes as well as diffuse damage (as detected by diffusion tensor imaging).
The complete story, encompassing an entire gangster ring, would entail not just whether and where T2 or Gd-enhanced lesions are present, but also whether other kinds of damage are ravaging the brain or spinal cord. MRI technology has transformed the practice of medicine for MS in accelerating diagnoses and helping to inform some treatment decisions, but it “doesn’t show us everything, and sometimes it shows us things that are not important,” says UT Southwestern’s Greenberg.

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