Contributions
Abstract: EP1697
Type: Poster Sessions
Abstract Category: Therapy - Symptomatic treatment
Introduction: Tumefactive multiple sclerosis (TMS) is characterized by demyelinating lesions that are greater than 2 cm in diameter with associated peri-lesional edema, which radiographically resembles a mass lesion and rarely mimics an acute ischemic stroke.
Objective:To present a case of intravenous tissue plasminogen activator (IV tPA) being used as treatment for an acute MS exacerbation
Results: A 33-year-old woman with a history of TMS presented with sudden onset of aphasia and right sided facial droop while 8 weeks pregnant. Prior to pregnancy, she was stable on fingolimod which had been discontinued 16 weeks prior to presentation. CT head showed no hemorrhage or mass effect in the corresponding left frontal area. As she was within 3 hours of symptom onset, she was given IV tPA. Over the next 8 hours, her expressive aphasia improved to only mild word finding difficulty. This profound improvement, however, did not persist on re-assessment the following morning. MRI brain showed a 2 cm ovoid T2-hyperintense lesion in the left corona radiata with associated restricted diffusion consistent with acute demyelination. She was then treated with 5 days of IV methylprednisolone with partial improvement in aphasia noted 3 weeks later.
Discussion: Stroke and MS differ in their etiology but previous studies have shown impaired fibrinolysis in MS. Moreover, the role of the plasminogen activator system has been implicated in neuroinflammation for both diseases. tPA is a serine protease approved for acute ischemic stroke but it has also been investigated for its effect in MS. Endogenous tPA is released from endothelium and astroglia and acts on the blood brain barrier (BBB) and other neuroinflammatory cells. tPA protects oligodendrocytes from apoptosis and facilitates the migration of oligodendrocyte progenitor cells (OPCs) across the BBB in the experimental autoimmune encephalomyelitis (EAE) model. While the tPA‐plasmin cascade can promote neurodegeneration via excitotoxin‐induced neuronal death, in inflammatory conditions with BBB disruption, it can play a protective role by removing fibrin, which exacerbates axonal injury. Therefore, tPA, by promoting fibrinolysis has the potential to decrease axonal damage in MS.
Conclusion: This is the first reported case of tPA being given to a pregnant woman who presented with a MS relapse resulting in a transient, but profound, reversal of symptoms.Further research is needed to consider whether tPA is a potential “rescue” option for acute MS relapse.
Disclosure: Brian Barry: nothing to disclose
Shala Moghbel: nothing to disclose
Mary Carter Denny: nothing to disclose
Carlos Mora: nothing to disclose
Faria Amjad: On the speakers bureau for Teva, Biogen Idec, Novartis and Sanofi Genzyme
Abstract: EP1697
Type: Poster Sessions
Abstract Category: Therapy - Symptomatic treatment
Introduction: Tumefactive multiple sclerosis (TMS) is characterized by demyelinating lesions that are greater than 2 cm in diameter with associated peri-lesional edema, which radiographically resembles a mass lesion and rarely mimics an acute ischemic stroke.
Objective:To present a case of intravenous tissue plasminogen activator (IV tPA) being used as treatment for an acute MS exacerbation
Results: A 33-year-old woman with a history of TMS presented with sudden onset of aphasia and right sided facial droop while 8 weeks pregnant. Prior to pregnancy, she was stable on fingolimod which had been discontinued 16 weeks prior to presentation. CT head showed no hemorrhage or mass effect in the corresponding left frontal area. As she was within 3 hours of symptom onset, she was given IV tPA. Over the next 8 hours, her expressive aphasia improved to only mild word finding difficulty. This profound improvement, however, did not persist on re-assessment the following morning. MRI brain showed a 2 cm ovoid T2-hyperintense lesion in the left corona radiata with associated restricted diffusion consistent with acute demyelination. She was then treated with 5 days of IV methylprednisolone with partial improvement in aphasia noted 3 weeks later.
Discussion: Stroke and MS differ in their etiology but previous studies have shown impaired fibrinolysis in MS. Moreover, the role of the plasminogen activator system has been implicated in neuroinflammation for both diseases. tPA is a serine protease approved for acute ischemic stroke but it has also been investigated for its effect in MS. Endogenous tPA is released from endothelium and astroglia and acts on the blood brain barrier (BBB) and other neuroinflammatory cells. tPA protects oligodendrocytes from apoptosis and facilitates the migration of oligodendrocyte progenitor cells (OPCs) across the BBB in the experimental autoimmune encephalomyelitis (EAE) model. While the tPA‐plasmin cascade can promote neurodegeneration via excitotoxin‐induced neuronal death, in inflammatory conditions with BBB disruption, it can play a protective role by removing fibrin, which exacerbates axonal injury. Therefore, tPA, by promoting fibrinolysis has the potential to decrease axonal damage in MS.
Conclusion: This is the first reported case of tPA being given to a pregnant woman who presented with a MS relapse resulting in a transient, but profound, reversal of symptoms.Further research is needed to consider whether tPA is a potential “rescue” option for acute MS relapse.
Disclosure: Brian Barry: nothing to disclose
Shala Moghbel: nothing to disclose
Mary Carter Denny: nothing to disclose
Carlos Mora: nothing to disclose
Faria Amjad: On the speakers bureau for Teva, Biogen Idec, Novartis and Sanofi Genzyme