Cerebral venous thrombosis and demyelinating diseases: report of a case in a clinically isolated syndrome suggestive of multiple sclerosis onset and review of the literature

2005 ◽  
Vol 11 (2) ◽  
pp. 242-244 ◽  
Author(s):  
Maurizia Maurelli ◽  
Roberto Bergamaschi ◽  
Elisa Candeloro ◽  
Alessandra Todeschini ◽  
Giuseppe Micieli

Cerebral venous thrombosis (CVT) has been described in several cases of clinically definite multiple sclerosis (MS). In the majority of these, lumbar puncture followed by intravenous corticosteroid treatment was suspected as the cause. We report what is, to our knowledge, the first case of a patient with a multifocal clinically isolated syndrome suggestive of MS onset, who developed multiple CVT after lumbar puncture and during high-dose i.v. corticosteroid treatment. We conclude that the sequence ‘lumbar puncture followed by corticosteroid treatment’ may be a contributory risk factor for the development of CVT when associated with other risk factors.

2002 ◽  
Vol 47 (1) ◽  
pp. 57-58 ◽  
Author(s):  
Dilek Ince Gunal ◽  
Nazire Afsar ◽  
Nese Tuncer ◽  
Sevinc Aktan

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Jasem Yousef Al-Hashel ◽  
Samar Farouk Ahmed ◽  
K. J. Alexander ◽  
Walaa Ahmed

Background. The association between cerebral venous thrombosis (CVT) and multiple sclerosis (MS) has already been reported in patients with clinically definite MS in relation to intravenous methylprednisolone (IVMP) or previously performed lumbar puncture (LP).Case Summery. We report a 29-year-old Indian female who presented with a clinically isolated spinal cord syndrome according to the revised 2010 McDonald Criteria. She developed CVT after a lumbar puncture and two days of finishing the course of IVMP.Conclusion. We conclude that the sequence of doing lumbar puncture followed by high-dose IVMP may increase the risk of CVT. A prophylactic anticoagulation may be indicated in this setting.


2013 ◽  
Vol 35 (6) ◽  
pp. 602-605 ◽  
Author(s):  
Anna Presicci ◽  
Vincenza Garofoli ◽  
Marta Simone ◽  
Maria Gloria Campa ◽  
Anna Linda Lamanna ◽  
...  

2014 ◽  
Vol 29 (5) ◽  
pp. 315-316
Author(s):  
M. Sillero Sánchez ◽  
N. Rodriguez Fernandez ◽  
L. Sánchez Vera ◽  
B. Gómez González ◽  
J.J. Asencio Marchante

2019 ◽  
Vol 12 ◽  
pp. 175628641987211 ◽  
Author(s):  
Jeremias Motte ◽  
Janina Kneiphof ◽  
Katrin Straßburger-Krogias ◽  
Kalliopi Pitarokoili ◽  
Anna Lena Fisse ◽  
...  

The cblC defect is the most common inborn error of cobalamin (Cbl) metabolism. Clinical severity and presentation of the cblC defect ranges from death to mild disability. Only 71 cases of late-onset cblC defect have been described in the literature. We provide the 41-year follow up of two siblings with a late-onset cblC defect, first described after initial diagnosis in 1996. While one of the siblings showed initial symptoms resembling multiple sclerosis with a good response to corticosteroids, the other sister showed only subclinical signs of the disease. The course of the first case was characterized by a severe deterioration and intensive-care therapy after respiratory failure. After diagnoses and Cbl treatment, the patient survived and showed a pronounced improvement of the symptoms. Both sisters have an active life and gave birth to healthy children. The reason for the initial improvement after corticosteroids could not be explained by the classical metabolic pathways of Cbl. Recent studies have suggested that Cbl plays an important role as a regulator of the balance between neurotrophic and neurotoxic factors in the central and peripheral nervous system (CNS and PNS). This first long-term follow up revealed that ultra-high-dose intramuscular Hydroxocobalamin (OH-Cbl) treatment can effectively protect patients from disease progression. It underlines the importance of diagnostic vigilance and laboratory work up even in cases without typical hematologic signs of Cbl deficiency. Cbl-related diseases are often a chameleon and must always be considered in the differential of demyelinating diseases of the PNS and CNS. The case supports the theory that it is not only the classical biochemical pathways that play a key role in Cbl deficiency, especially with regard to neurological symptoms.


2001 ◽  
Vol 2 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Andrea Giorgetti ◽  
Maria Vittoria Calloni ◽  
Roberto Freschi ◽  
Giuseppe Mariani ◽  
Patrizia Perrone ◽  
...  

2003 ◽  
Vol 10 (1) ◽  
pp. 63-66 ◽  
Author(s):  
N. Vandenberghe ◽  
M. Debouverie ◽  
R. Anxionnat ◽  
P. Clavelou ◽  
S. Bouly ◽  
...  

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