I may have posted this already, apologies if repeating
http://www.epilepsy.com/newsletter/...de092e-Epilepsy_News_8_08_12&utm_medium=email
In the May issue of the journal, Archives of Neurology, Drs. Quek and colleagues from both Mayo Clinic in Rochester, Minnesota and Scottsdale, Arizona present a retrospective observational case series looking at patients with autoimmune-based epilepsy. The goal of the study was to assess and characterize the number of patients who have positive antibodies that can cause epilepsy and then classify the clinical features associated with their epilepsy and response to treatment.
Thirty-two patients with an exclusive or predominant seizure presentation in which an autoimmune cause was suspected on the basis of positive autoantibodies, inflammatory spinal fluid or an MRI suggesting inflammation were studied and investigated. All of these patients had partial seizures, 81% had failed treatment with two or more seizure drugs and had daily seizures, and 38 had seizures that were from multiple locations and/or changed with time. In 47% of patients the MRI was normal. EEG abnormalities ranged from mild slowing to spike wave discharge and seizures. Specific antibodies included voltage-gated potassium channels in 56%, contactin-associated protein-like 2 specific antibody in one patient, glutamic acid decarboxylate 65 in 22%, collapsin response mediated protein antibody in 6% and an NMDA receptor and ganglionic acetylcholine receptor one patient each. Treatment with methylprednisolone, IV immune globulin, and combinations of these including plasmapheresis or cyclophosphamide were tried.
Eighty-one percent of patients reported improvement after initiation of immunotherapy treatment with 18 becoming seizure free. The median time from onset of seizures to starting therapy was four months in patients who responded and 22 months for those who did not. All voltage-gated potassium channel complex antibody positive patients reported an initial or lasting benefit. One voltage-gated potassium channel patient was seizure free after detection of a thyroid cancer with surgical removal of that tumor and another patient responded to antiseizure drug alone.
This study is important because the authors found if an autoimmune cause for seizures is found in patients who have epilepsy then starting treatment with an immune-based option such as steroids, IVIG, plasmapheresis or other immune modulating therapies is likely a better approach to the management of these patients as opposed to those who do not have these antibodies. This study is important because it once again highlights another potential way in which epilepsy can occur and helps to delineate potential new treatment options for the management of epilepsy that may not often be considered by many individuals. An accompanying editorial by Dr. Bergey suggests that we need to make certain that in patients with epilepsy we consider autoimmune cause of epilepsy and appropriately institute therapy when those causes are suspected or found.
http://www.epilepsy.com/newsletter/...de092e-Epilepsy_News_8_08_12&utm_medium=email
In the May issue of the journal, Archives of Neurology, Drs. Quek and colleagues from both Mayo Clinic in Rochester, Minnesota and Scottsdale, Arizona present a retrospective observational case series looking at patients with autoimmune-based epilepsy. The goal of the study was to assess and characterize the number of patients who have positive antibodies that can cause epilepsy and then classify the clinical features associated with their epilepsy and response to treatment.
Thirty-two patients with an exclusive or predominant seizure presentation in which an autoimmune cause was suspected on the basis of positive autoantibodies, inflammatory spinal fluid or an MRI suggesting inflammation were studied and investigated. All of these patients had partial seizures, 81% had failed treatment with two or more seizure drugs and had daily seizures, and 38 had seizures that were from multiple locations and/or changed with time. In 47% of patients the MRI was normal. EEG abnormalities ranged from mild slowing to spike wave discharge and seizures. Specific antibodies included voltage-gated potassium channels in 56%, contactin-associated protein-like 2 specific antibody in one patient, glutamic acid decarboxylate 65 in 22%, collapsin response mediated protein antibody in 6% and an NMDA receptor and ganglionic acetylcholine receptor one patient each. Treatment with methylprednisolone, IV immune globulin, and combinations of these including plasmapheresis or cyclophosphamide were tried.
Eighty-one percent of patients reported improvement after initiation of immunotherapy treatment with 18 becoming seizure free. The median time from onset of seizures to starting therapy was four months in patients who responded and 22 months for those who did not. All voltage-gated potassium channel complex antibody positive patients reported an initial or lasting benefit. One voltage-gated potassium channel patient was seizure free after detection of a thyroid cancer with surgical removal of that tumor and another patient responded to antiseizure drug alone.
This study is important because the authors found if an autoimmune cause for seizures is found in patients who have epilepsy then starting treatment with an immune-based option such as steroids, IVIG, plasmapheresis or other immune modulating therapies is likely a better approach to the management of these patients as opposed to those who do not have these antibodies. This study is important because it once again highlights another potential way in which epilepsy can occur and helps to delineate potential new treatment options for the management of epilepsy that may not often be considered by many individuals. An accompanying editorial by Dr. Bergey suggests that we need to make certain that in patients with epilepsy we consider autoimmune cause of epilepsy and appropriately institute therapy when those causes are suspected or found.