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. 2018 Jul 13;9:579. doi: 10.3389/fneur.2018.00579

Figure 1.

Figure 1

Individual characteristics of treatment responses and therapies provided in the studied GAD-epilepsy patients are shown. X-axis shows the time-points in months starting from symptom onset. The blue line displays seizures / no seizures. Dotted lines refer to the interventions. Orange dots are GAD65 antibody levels. Discontinuation of therapies is shown in parenthesis. 4 wk means 4-week intervals. Patient 1 (A) responded well to early initiation of immunotherapy. With patient 2 (B), there was longer delay before immunotherapy and she continued to experience seizures even after several AED and immunotherapy trials. However, her MRI pathology resolved. Patient 3 (C) responded well to immunoadsorption with decreasing of GAD65 antibody levels after every trial. Patients 4–6 (D–F) did not respond to late immunotherapy. In patient 4, a vagus nerve stimulator ultimately reduced seizure levels. In patient 6, AED modification reduced her seizure levels. AED, antiepileptic drugs; AZM, acetazolamide; AZP, azathioprine; CBZ, carbamazepine; CLB, clobazam; CP, Cyclophosphamide; ECZ, eslicarbazepine; GAD65, Glutamic acid decarboxylase 65-kilodalton isoform; HCQ, hydroxychloroquine; IA, immunoadsorption; IVIG, intravenous immunoglobulin; LCM, lacosamide; LEV, levetiracetam; LZP; lorazepam; MMF, mycophenolate mofetil; MP, methylprednisolone; OCZ, oxcarbazepine; PEH, phenytoin; PR, prednisolone; RTX, rituximab; SAH, selective amygdalohippocampectomy; TPM, topiramate; VNS, vagus nerve stimulation: wk, week; VLP, sodium valproate; ZNS, zonisamide;.