Feeling fed up so wanted a few opinions. Diagnosed wit cerebral APS by Prof D’Cruz at Guys about 18 months ago (possibly more but can’t remember!) so have been in warfarin since then but my mental decline is continuing so a member of his team ordered an MRI and are waiting to get my original MRI (lots of white matter lesions) to compare. I think there are 3 options or diagnosis. 1, Cerebral APS but low INR not stopping micro clots 2, Cerebral APS just continuing my decline despite warfarin, 3 the comparative MRI shows the white matter issues have moved meaning its MS not APS!
I really am beating myself up about this and any insight anyone can offer would be great. My INR is currently between 3-4 or sometimes a little higher if I’ve been naughty! So I don’t think it’s too low even though I used that in one of the options!
Thanks for any help or assistance.
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Greenmil3
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Would you say your memory has declined since diagnosis. I know mine has and see on some of my papers its cerebral.Our symptoms do mirror MS.I am on warfarin and I would say it's not helped at all really
I know they can be active so they shine bright white on the scans and then become not active dull more then 3 months old then black holes which is irreversible damage..
But I have never heard of them moving .. healing but not moving would be a interesting read if you have a link.
Hi Buckley. I am curious about the black holes on the brain. Is it caused by MS or APS? I had an MRI done 3 years ago and my neurologist pointed out to me on the scan a very old black hole on the top right side of my brain. She said it was black because it was filled with iron and most likely caused by a concussion that happened many years ago! A concussion I don’t remember. Now I’m rethinking her thoughts on what it actually could be. Could it be a APS or MS leasion??
Just curious. It’s not like anything can be done about it anyway, but it is interesting!
I am not a Doctor. I have read the difference between MS and APS as to the white matters changing on MR with one of the two illnesses, but now when you talk of it, I am not sure which one it was.
You should absolutely contact Prof d`Cruz and believe in what he has to say as he is said to be very knowledable of APS.
Cerebral APS often needs an INR over 3.5. It should then be taken in a vein and rather often to get a steady and trustable INR-result.
I am the same I don't understand why you have not had a lumbar puncture to determine whether or not you have cfluid to determine a positive test of Ms ? Xx
I would see an MS specialist. They would be able to tell you whether it’s MS or APS. I have cereal APS and it was thought to be MS at first as well. It was and MS specialist that Dx’d me. I was her patient until the white matter stopped changing on the MRIs. Every time it did she increased my therapeutic INR level. I leveled off at 3-3.5.
Then I became the patient of a stroke neurologist and Rheumatologist.
2. Can neurologic manifestations of Hughes (antiphospholipid) syndrome be distinguished from multiple sclerosis? Analysis of 27 patients and review of the literature.
Cuadrado MJ1, Khamashta MA, Ballesteros A, Godfrey T, Simon MJ, Hughes GR.
Author information
Lupus Research Unit, Rayne Institute, St. Thomas' Hospital, London, United Kingdom.
Abstract
Hughes (antiphospholipid) syndrome (APS) can mimic multiple sclerosis (MS). We analyzed the clinical, laboratory, and imaging findings of MS-like expression in a cohort of patients with APS in an attempt to identify parameters that might differentiate the 2 entities. We studied 27 patients who were referred to our unit with the diagnosis of probable or definite MS made by a neurologist. All patients were referred to our lupus clinic because of symptoms suggesting an underlying connective tissue disease, uncommon findings for MS on magnetic resonance imaging (MRI), atypical evolution of MS, or antiphospholipid antibody (aPL) positivity. aPL, antinuclear antibody (ANA), anti-dsDNA, and anti-extractable nuclear antigen (ENA) antibodies were measured by standard methods. MRI was performed in every patient and compared with MRI of 25 definite MS patients who did not have aPL. An index severity score was calculated based on the size and number of increased signal intensity areas in MRI. In the past medical history, 8 patients with primary APS and 6 with APS secondary to systemic lupus erythematosus (SLE) had had symptoms related to these conditions. Neurologic symptoms and physical examination of the patients were not different from those common in MS patients. Laboratory findings were not a useful tool to distinguish APS from MS. When MRI from APS patients was compared globally with MRI from MS patients, MS patients had significantly increased severity score in white matter (p < 0.001), cerebellum (p = 0.035), pons (p < 0.015), and when all areas were taken together (p < 0.001). Patients with APS had significantly increased scores in the putamen (p < 0.01). No differences were noticed in the degree of atrophy. When taken individually, MRI from APS patients could not be distinguished from MRI from MS patients. Most of the patients with primary APS showed a good response to oral anticoagulant treatment. In patients with secondary APS, the outcome was poorer. Hughes syndrome (APS) and MS can be difficult to distinguish. A careful medical history, a previous history of thrombosis and/or fetal loss, an abnormal localization of the lesions in MRI, and the response to anticoagulant therapy might be helpful in the differential diagnosis. We believe that testing for aPL should become routine in all patients with MS.
4. Significant number of patients misdiagnosed as having MS
Researchers report that many patients are diagnosed with multiple sclerosis (MS) when in fact they may have systemic lupus erythematosus (SLE) or antiphospholipid syndrome (APS). In a review article published in the April 2005 issue of Rheumatology, investigators say that this lapse could have an important effect on quality of life and mortality [ 1 ]. "As seems evident from the literature and from the everyday practice of those working with APS and SLE, a significant number of these patients are probably mislabeled as MS," comment the researchers, led by Dr Susana Ferreira (S Joao Hospital, Porto, Portugal). "Transverse myelitis and multifocal white-matter lesions seem to be the most common confounding factors."
Multiple sclerosis-like features: Some people with Hughes Syndrome develop MS-like features, such as loss of part of the field of vision and difficulty walking. As a result, Hughes syndrome may be wrongly diagnosed as MS.
Multiple sclerosis (MS) and antiphospholipid syndrome (APS) share common clinical, laboratory and radiological features. We reviewed all the English papers on MS and APS published in the literature from 1965 to 2014 using PubMed and Google Scholar. We found that APScan mimic antiphospholipid antibodies (aPL)-positive MS in many ways in its clinical presentation. Nevertheless, APS diagnosis, clinical manifestations and management differ from those of MS. aPL were found in MS patients with titers ranging from 2% to 88%. The distribution and volume of lesions on magnetic resonance imaging (MRI) may help to differentiate MS from primary APS. In addition, atypical MS presentation can guide physicians toward an alternative diagnosis, especially when features of thrombosis and/or history of connective tissue disease are present. In that case, an anticoagulation trial could be worthwhile.
I Uthman1, MHA Noureldine2, A Berjawi2, M Skaf2, AA Haydar2, M Merashli3and GRV Hughes41
Division of Rheumatology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; 2 Lebanese American University, Faculty of Medicine, Beirut, Lebanon; 3 Rheumatology SpR, The Royal London Hospital, London, UK; and 4 Graham Hughes Lupus Research Laboratory,The Rayne Institute, Lambeth Wing, St Thomas’ Hospital, London, UK
(18) (PDF) Hughes syndrome and Multiple sclerosis. Available from: researchgate.net/publicatio... [accessed Aug 31 2019].
We reviewed all the English papers on MS and APS published in the literature from 1965 to 2014 using PubMed and Google Scholar. We found that APS can mimic antiphospholipid antibodies (aPL)-positive MS in many ways in its clinical presentation. Nevertheless, APS diagnosis, clinical manifestations and management differ from those of MS. aPL were found in MS patients with titers ranging from 2% to 88%. The distribution and volume of lesions on magnetic resonance imaging (MRI) may help to differentiate MS from primary APS. In addition, atypical MS presentation can guide physicians toward an alternative diagnosis, especially when features of thrombosis and/or history of connective tissue disease are present. In that case, an anticoagulation trial could be worthwhile.
I hope this is helpful. IMHO, you need to see someone like Professor David D'Cruz at St Thomas;' Hospital. Neurologists are not experts in APS/Hughes Syndromer.
2. Can neurologic manifestations of Hughes (antiphospholipid) syndrome be distinguished from multiple sclerosis? Analysis of 27 patients and review of the literature.
Cuadrado MJ1, Khamashta MA, Ballesteros A, Godfrey T, Simon MJ, Hughes GR.
Author information
Lupus Research Unit, Rayne Institute, St. Thomas' Hospital, London, United Kingdom.
Abstract
Hughes (antiphospholipid) syndrome (APS) can mimic multiple sclerosis (MS). We analyzed the clinical, laboratory, and imaging findings of MS-like expression in a cohort of patients with APS in an attempt to identify parameters that might differentiate the 2 entities. We studied 27 patients who were referred to our unit with the diagnosis of probable or definite MS made by a neurologist. All patients were referred to our lupus clinic because of symptoms suggesting an underlying connective tissue disease, uncommon findings for MS on magnetic resonance imaging (MRI), atypical evolution of MS, or antiphospholipid antibody (aPL) positivity. aPL, antinuclear antibody (ANA), anti-dsDNA, and anti-extractable nuclear antigen (ENA) antibodies were measured by standard methods. MRI was performed in every patient and compared with MRI of 25 definite MS patients who did not have aPL. An index severity score was calculated based on the size and number of increased signal intensity areas in MRI. In the past medical history, 8 patients with primary APS and 6 with APS secondary to systemic lupus erythematosus (SLE) had had symptoms related to these conditions. Neurologic symptoms and physical examination of the patients were not different from those common in MS patients. Laboratory findings were not a useful tool to distinguish APS from MS. When MRI from APS patients was compared globally with MRI from MS patients, MS patients had significantly increased severity score in white matter (p < 0.001), cerebellum (p = 0.035), pons (p < 0.015), and when all areas were taken together (p < 0.001). Patients with APS had significantly increased scores in the putamen (p < 0.01). No differences were noticed in the degree of atrophy. When taken individually, MRI from APS patients could not be distinguished from MRI from MS patients. Most of the patients with primary APS showed a good response to oral anticoagulant treatment. In patients with secondary APS, the outcome was poorer. Hughes syndrome (APS) and MS can be difficult to distinguish. A careful medical history, a previous history of thrombosis and/or fetal loss, an abnormal localization of the lesions in MRI, and the response to anticoagulant therapy might be helpful in the differential diagnosis. We believe that testing for aPL should become routine in all patients with MS.
4. Significant number of patients misdiagnosed as having MS
Researchers report that many patients are diagnosed with multiple sclerosis (MS) when in fact they may have systemic lupus erythematosus (SLE) or antiphospholipid syndrome (APS). In a review article published in the April 2005 issue of Rheumatology, investigators say that this lapse could have an important effect on quality of life and mortality [ 1 ]. "As seems evident from the literature and from the everyday practice of those working with APS and SLE, a significant number of these patients are probably mislabeled as MS," comment the researchers, led by Dr Susana Ferreira (S Joao Hospital, Porto, Portugal). "Transverse myelitis and multifocal white-matter lesions seem to be the most common confounding factors."
Multiple sclerosis-like features: Some people with Hughes Syndrome develop MS-like features, such as loss of part of the field of vision and difficulty walking. As a result, Hughes syndrome may be wrongly diagnosed as MS.
Multiple sclerosis (MS) and antiphospholipid syndrome (APS) share common clinical, laboratory and radiological features. We reviewed all the English papers on MS and APS published in the literature from 1965 to 2014 using PubMed and Google Scholar. We found that APScan mimic antiphospholipid antibodies (aPL)-positive MS in many ways in its clinical presentation. Nevertheless, APS diagnosis, clinical manifestations and management differ from those of MS. aPL were found in MS patients with titers ranging from 2% to 88%. The distribution and volume of lesions on magnetic resonance imaging (MRI) may help to differentiate MS from primary APS. In addition, atypical MS presentation can guide physicians toward an alternative diagnosis, especially when features of thrombosis and/or history of connective tissue disease are present. In that case, an anticoagulation trial could be worthwhile.
I Uthman1, MHA Noureldine2, A Berjawi2, M Skaf2, AA Haydar2, M Merashli3and GRV Hughes41
Division of Rheumatology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; 2 Lebanese American University, Faculty of Medicine, Beirut, Lebanon; 3 Rheumatology SpR, The Royal London Hospital, London, UK; and 4 Graham Hughes Lupus Research Laboratory,The Rayne Institute, Lambeth Wing, St Thomas’ Hospital, London, UK
(18) (PDF) Hughes syndrome and Multiple sclerosis. Available from: researchgate.net/publicatio... [accessed Aug 31 2019].
We reviewed all the English papers on MS and APS published in the literature from 1965 to 2014 using PubMed and Google Scholar. We found that APS can mimic antiphospholipid antibodies (aPL)-positive MS in many ways in its clinical presentation. Nevertheless, APS diagnosis, clinical manifestations and management differ from those of MS. aPL were found in MS patients with titers ranging from 2% to 88%. The distribution and volume of lesions on magnetic resonance imaging (MRI) may help to differentiate MS from primary APS. In addition, atypical MS presentation can guide physicians toward an alternative diagnosis, especially when features of thrombosis and/or history of connective tissue disease are present. In that case, an anticoagulation trial could be worthwhile.
I hope this is helpful. IMHO, you need to see someone like Professor David D'Cruz at St Thomas;' Hospital. Neurologists are not experts in APS/Hughes Syndromer.
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