Reversible cerebral vasoconstriction syndrome associated with fingolimod treatment in relapsing–remitting multiple sclerosis three months after childbirth

2015 ◽  
Vol 21 (11) ◽  
pp. 1473-1475 ◽  
Author(s):  
Markus Kraemer ◽  
Ralph Weber ◽  
Michèle Herold ◽  
Peter Berlit
Keyword(s):  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
Magnetic Resonance Angiography ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Reversible Cerebral Vasoconstriction Syndrome ◽  
Conventional Angiography ◽  
Cerebral Vasoconstriction ◽  
Relapsing Remitting ◽  
Relapsing Remitting Multiple Sclerosis

Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by acute thunderclap headache, evidence of vasoconstriction in conventional angiography or magnetic resonance angiography and reversibility of these phenomena within 12 weeks. Some triggering factors, for example drugs such as selective serotonin reuptake inhibitors, sumatriptan, tacrolimus, cyclophosphamide and cocaine, or states such as pregnancy, puerperium or migraine have been described. We describe the case of a 29-year-old woman with RCVS associated with fingolimod three months after childbirth. This case represents the first report of RCVS in fingolimod treatment.

scholarly journals DIAGNOSTICS OF REVERSIBLE CEREBRAL VASOCONSTRICTION SYNDROME: CLINICAL MANIFESTATION AND IMAGING PATTERNS

2018 ◽  
pp. 50-55
Author(s):  
E. G. Klocheva ◽  
V. V. Goldobin
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Angiography ◽  
Clinical Manifestation ◽  
Thunderclap Headache ◽  
Reversible Cerebral Vasoconstriction Syndrome ◽  
Treatment Modification ◽  
Cerebral Vasoconstriction

Data of 130 patients with thunderclap headache are presented. The data include clinical manifestation analysis and neuroimaging results (magnetic resonance angiography). Magnetic resonance angiography was performed 15 days after acute clinical manifestation and permitted to verify cerebral vasoconstriction, that led to treatment modification with clinical and neuroimaging signs of vasoconstriction reverse.

Progressive Cerebellar Ataxia After Natalizumab Treatment

2021 ◽  
pp. 65-68
Author(s):  
Michel Toledano
Keyword(s):  
Magnetic Resonance Imaging ◽  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
Polyoma Virus ◽  
Resonance Imaging ◽  
Disease Modifying Therapy ◽  
Relapsing Remitting ◽  
Disease Modifying ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis

A 47-year-old woman with a history of relapsing-remitting multiple sclerosis (MS) receiving natalizumab therapy sought a second opinion regarding a recent diagnosis of secondary progressive disease. She was first diagnosed with multiple sclerosis 8 years earlier. While taking natalizumab, she was monitored for the development of antibodies to JC polyoma virus. Nine months before our evaluation, anti-JC polyoma virus antibodies became positive, with an increased index of 1.1. Given sustained remission, she was continued on natalizumab with increased surveillance and a plan to switch to a different disease-modifying therapy after 24 months. Five months later she noted subacute onset of slurred speech and right upper extremity incoordination. Over the next 4 months she continued to have clinical decline. On examination she had moderate ataxic dysarthria and right greater than left appendicular ataxia. She relied on a wheelchair for transportation and required 1-person assist to stand. Reflexes were brisk with bilateral Babinski sign. This patient with relapsing-remitting multiple sclerosis on natalizumab had a new subacute progressive cerebellar syndrome without radiographic evidence of disease activity. Repeated magnetic resonance imaging showed worsening cerebellar atrophy, right sided greater than left sided, and evolving T2 hyperintensity in the brainstem without enhancement or mass effect. JC polyoma virus polymerase chain reaction was positive. The patient was diagnosed with JC polyoma virus granule cell neuronopathy. Natalizumab was discontinued, and she was treated with 4 of 5 planned cycles of plasma exchange. After her 4th cycle, worsening symptoms developed. Magnetic resonance imaging showed gadolinium enhancement in the brainstem supportive of immune reconstitution inflammatory syndrome. She received high-dose intravenous methylprednisolone followed by a prednisone taper. Her disability progression stabilized. JC polyoma virus central nervous system infection, 1 of several infections reported among treated patients with multiple sclerosis, occurs almost exclusively in immunosuppressed patients, including those receiving disease-modifying therapy for multiple sclerosis.

Axonal metabolic recovery and potential neuroprotective effect of glatiramer acetate in relapsing-remitting multiple sclerosis

2005 ◽  
Vol 11 (6) ◽  
pp. 646-651 ◽  
Author(s):  
Omar Khan ◽  
Yimin Shen ◽  
Christina Caon ◽  
F en Bao ◽  
Wendy Ching ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
Glatiramer Acetate ◽  
Axonal Injury ◽  
Neuronal Marker ◽  
Metabolic Recovery ◽  
Relapsing Remitting ◽  
Treatment Naïve ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis

Glatiramer acetate (GA) is a disease-modifying therapy for relapsing-remitting multiple sclerosis (RRMS) with several putative mechanisms of action. Currently, there is paucity ofin vivo human data linking the well-established peripheral immunologic effects of therapy with GA to its potential effects inside the central nervous system (CNS). Brain proton magnetic resonance spectroscopy (MRS) allows in vivo examination of axonal integrity by quantifying the resonance intensity of the neuronal marker N-acetylaspartate (NAA). In a pilot study to investigate the effect of GA on axonal injury, we performed combined brain magnetic resonance imaging (MRI) and MRS studies in 18 treatment naïve RRMS patients initiating therapy with GA at baseline and annually for two years on therapy. A small group of four treatment naïve RRMS patients, electing to remain untreated, served as controls. NAA/Cr was measured in a large central brain volume of interest (VOI) as well as the normal appearing white matter (NAWM) within the VOI. After two years, NAA/Cr in the GA-treated group increased significantly by 10.7% in the VOI (2.179±0.26 versus 1.969±0.24, P=0.03) and by 7.1% in the NAWM (2.239±0.26 versus 2.089±0.31, P=0.04). In the untreated group, NAA/Cr decreased by 8.9% at two years in the VOI (2.019±0.16 versus 1.839±0.21, P=0.03) and 8.2% in the NAWM (2.079±0.24 versus 1.909±0.29, P=0.03). Our data shows that treatment with GA leads to axonal metabolic recovery and protection from sub-lethal axonal injury. These results support an in situ effect of GA therapy inside the CNS and suggest potential neuroprotective effects of GA.

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