case_images: PMC6053535_01
case_images: 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;.
case_images: fneur-09-00579-g0001.jpg
case_images: PMC6053535_06_fneur-09-00579-g0001.jpg
case_images: F1
case_images: A 16-year-old girl (patient 6; Figure 1F) presented with FBTCS, eczema and joint pain.
case_images: PMC6053535_02
case_images: 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;.
case_images: fneur-09-00579-g0001.jpg
case_images: PMC6053535_06_fneur-09-00579-g0001.jpg
case_images: F1
case_images: A 16-year-old girl (patient 6; Figure 1F) presented with FBTCS, eczema and joint pain.
case_images: (A) The coronal fluid attenuation inversion recovery (FLAIR) magnetic resonance (MRI) -image taken during the acute stage of the illness shows an abnormally hyperintense and swollen head of the left hippocampus (arrow). (B) Five months later, the finding has mostly resolved, although slight hyperintensity of the left hippocampal head can still be seen (arrow). (C) In a control image, 3 years and 8 months after the acute stage, the abnormal finding has totally resolved (arrow). There are no signs of atrophy in the primarily affected area.
case_images: fneur-09-00579-g0002.jpg
case_images: PMC6053535_02_fneur-09-00579-g0002.jpg
case_images: F2
case_images: A follow-up MRI revealed a novel left temporomesial signal change and edema correlating with the EEG findings (Figure 2).
case_images: PMC6053535_03
case_images: 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;.
case_images: fneur-09-00579-g0001.jpg
case_images: PMC6053535_06_fneur-09-00579-g0001.jpg
case_images: F1
case_images: A 16-year-old girl (patient 6; Figure 1F) presented with FBTCS, eczema and joint pain.
case_images: PMC6053535_04
case_images: 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;.
case_images: fneur-09-00579-g0001.jpg
case_images: PMC6053535_06_fneur-09-00579-g0001.jpg
case_images: F1
case_images: A 16-year-old girl (patient 6; Figure 1F) presented with FBTCS, eczema and joint pain.
case_images: PMC6053535_05
case_images: 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;.
case_images: fneur-09-00579-g0001.jpg
case_images: PMC6053535_06_fneur-09-00579-g0001.jpg
case_images: F1
case_images: A 16-year-old girl (patient 6; Figure 1F) presented with FBTCS, eczema and joint pain.
case_images: PMC6053535_06
case_images: 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;.
case_images: fneur-09-00579-g0001.jpg
case_images: PMC6053535_06_fneur-09-00579-g0001.jpg
case_images: F1
case_images: A 16-year-old girl (patient 6; Figure 1F) presented with FBTCS, eczema and joint pain.