Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, April 12, 2022

Incidence, clinical spectrum, and immunotherapy of non-ischemic cerebral enhancing lesions after endovascular therapy

 So you described a problem, but did nothing to solve it. USELESS!

Incidence, clinical spectrum, and immunotherapy of non-ischemic cerebral enhancing lesions after endovascular therapy

First Published January 31, 2022 Research Article 

Symptomatic and asymptomatic delayed non-ischemic cerebral enhancing (NICE) lesions in magnetic resonance imaging (MRI) have been reported as a rare complication after endovascular therapy (EVT) in recent years with incidence rates between 0.05% and 0.9% in most studies. Information on long-term clinical course and immunotherapies is scarce or has not been reported in detail in the literature.

Aims of our study were to assess the incidence of NICE lesions in patients after cerebral EVT over a period of more than 12 years, describe clinical and EVT characteristics, and immunotherapies applied.

A retrospective chart review of all patients treated by endovascular therapy for symptomatic or asymptomatic aneurysms at the University Hospital of Augsburg from May 1, 2008 to December 31, 2020 was performed. Patients were identified retrospectively and followed-up prospectively where appropriate. In addition, one case treated at another institution was included.

Five out of 746 patients, 0.67%, developed NICE lesions after EVT, all with non-ruptured aneurysms and all symptomatic upon detection of NICE lesions by MRI. In total, the disease course of 6 female patients is reported. Symptoms occurred after a mean time of 15 days (±13.42, SD) after EVT with headache (6/6 patients), focal neurological signs (6/6 patients), epileptic seizures (2/6 patients) and cognitive deficits (3/6 patients). All 6 patients received glucocorticosteroids (GCS), 1/6 azathioprine (AZA), 4/6 mycophenolate mofetil (MMF), 1/6 methotrexate (MTX), 1/6 rituximab (RTX), 2/6 cyclophosphamide (CYC) and 3/6 tocilizumab (TCZ). A treatment response could be observed for GCS, TCZ and MMF (in two of four cases), RTX and AZA did not result in disease stabilization.

Delayed NICE lesions are a rare complication after EVT, requiring immunotherapies in all patients reported here. Physicians should be aware(What good does being aware do if there is no solution to the problem? Oh you have this problem, but I know nothing about treating it.) of this disorder in case of new symptoms or contrast enhancing lesions after EVT.

Standard of care for treatment of cerebral aneurysms has been dominated by endovascular therapy (EVT) in recent years. Main complications of endovascular coiling are procedural aneurysm perforations and thromboembolic events.1 Delayed non-ischemic cerebral enhancing (NICE) lesions in magnetic resonance imaging (MRI) have rarely been reported as a complication after EVT.28 Punctate, nodular or annular foci of leptomeningeal, cortical, and subcortical enhancements and perilesional edema8 in the territory of the endovascular access of EVT represent characteristics of NICE lesions. The disorder has also been termed as delayed cerebral hypersensitivity,4 leukoencephalopathy9 or descriptively as reversible intracranial parenchymal changes.7 Incidence rates after EVT are reported to be as high as 0.05%10 to 0.9%,11 except for one study reporting a higher incidence rate of 2.3%.12 Several studies have been published on the pathogenesis of NICE lesions: Besides foreign body emboli, in some patients identified as hydrophilic polymer coating emboli, and subsequent granulomatous reactions,2,3,5,6,8,13,14 cerebral metallic hypersensitivity and nickel allergy4,7,15 have been reported. Successful treatment with glucocorticosteroids (GCS) has been described in many cases, other immunosuppressants like mycophenolate mofetil (MMF) or azathioprine (AZA) in few cases only.13,16,17 However, data on long-term follow-up and response to long-term treatments are scarce and have not been reported in detail in many cases.

Main aims of our study were (a) to compute the incidence of NICE lesions in patients undergoing cerebral EVT over 12 years and 8 months, (b) describe clinical and EVT characteristics of patients affected, and (c) immunotherapies used, including long-term follow-up.

More at link.

 

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