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Adult-onset temporal lobe epilepsy, cognitive decline, multi-antiepileptic drug hypersensitivity, and Hashimoto's encephalopathy: Two case studies.

Sadan O, Seyman E, Ash EL, Kipervasser S, Neufeld MY - Epilepsy Behav Case Rep (2013)

Bottom Line: Hashimoto's encephalopathy is defined by the coexistence of encephalopathy and antithyroid antibodies.We report two cases of adult-onset temporal lobe epilepsy with subacute cognitive decline, high titers of antithyroid antibodies, multi-antiepileptic drug hypersensitivity, and good response to immunomodulatory treatment.The relevance of multidrug hypersensitivity in the setting of adult-onset epilepsy and the importance of searching for autoimmune causes for epilepsy are discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.

ABSTRACT
Hashimoto's encephalopathy is defined by the coexistence of encephalopathy and antithyroid antibodies. We report two cases of adult-onset temporal lobe epilepsy with subacute cognitive decline, high titers of antithyroid antibodies, multi-antiepileptic drug hypersensitivity, and good response to immunomodulatory treatment. The relevance of multidrug hypersensitivity in the setting of adult-onset epilepsy and the importance of searching for autoimmune causes for epilepsy are discussed.

No MeSH data available.


Related in: MedlinePlus

Timeline of Case 2. Clock drawing as a sample of the cognitive assessment before methylprednisolone treatment (A), immediately after the steroid pulse therapy (B), and one month (C) and 7 months (D) following treatment, that begun 5 month after the first admission. These drawings demonstrate progressive improvement. T2 FLAIR axial section at the time of diagnosis (E) and 2 months later (F), showing a progressive periventricular hyperintense signal with increasing atrophy. LMT — lamotrigine, VPA — valproate, LEV — levetiracetam, TPM — topiramate, GBP — gabapentin, MET — methylprednisolone, PRD — prednisone, MoCA — Montreal Cognitive Assessment.
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f0010: Timeline of Case 2. Clock drawing as a sample of the cognitive assessment before methylprednisolone treatment (A), immediately after the steroid pulse therapy (B), and one month (C) and 7 months (D) following treatment, that begun 5 month after the first admission. These drawings demonstrate progressive improvement. T2 FLAIR axial section at the time of diagnosis (E) and 2 months later (F), showing a progressive periventricular hyperintense signal with increasing atrophy. LMT — lamotrigine, VPA — valproate, LEV — levetiracetam, TPM — topiramate, GBP — gabapentin, MET — methylprednisolone, PRD — prednisone, MoCA — Montreal Cognitive Assessment.

Mentions: The neurological examination on admission was notable for disorientation and evident cognitive abnormality as demonstrated by a MoCA score of 12/30 (specifically, abnormal serial seven, immediate memory, and abstraction). She exhibited mild extrapyramidal signs and flapping tremor. An EEG showed focal left frontal intermittent slowing. The lumbar puncture had normal opening pressure and content, and the tau protein level was within the normal range. Routine blood work revealed polycythemia and mild leukocytosis, while the electrolyte levels, liver and kidney functions, thyroid functions, C-reactive protein levels, and neoplastic markers were all normal. Routine rheumatologic tests and antiphospholipid antibodies were normal. The only positive relevant result was very high titers of antithyroglobulin (5564 U/ml) and antithyroid microsomal antibody (> 3000 U/ml). A repeated brain MRI revealed progressive mild atrophy and a hyperintense temporal cortical signal restricted in diffusion. Methylprednisolone (IV, 500 mg/day for 5 days) was administered, and the valproate was switched to levetiracetam (500 mg bid) because of extrapyramidal side effects. She was released from the hospital with instructions to taper the oral prednisone dosage. She returned three weeks later with an allergic drug reaction, manifested through a skin rash and pruritus, while being treated with 30-mg prednisone (during the tapering down) that was attributed to the levetiracetam. Gabapentin was started in addition to topiramate with disappearance of the rash. The repeated MoCA score was 16/30, suggesting mild improvement. At a follow-up visit several months later, the patient and her family reported significant improvement. She had returned to her usual levels of function and normal lifestyle, and she was seizure-free. Although we did not notice a prominent cognitive improvement, she did return to her baseline daily function, and, therefore, we did not suggest further immunomodulatory treatment, except for low prednisone dosage (10 mg daily). Further measurement of the antithyroid antibodies demonstrated a marked reduction (anti-TPO: 349 U/ml, antithyroglobulin: 461 U/ml, Fig. 2).


Adult-onset temporal lobe epilepsy, cognitive decline, multi-antiepileptic drug hypersensitivity, and Hashimoto's encephalopathy: Two case studies.

Sadan O, Seyman E, Ash EL, Kipervasser S, Neufeld MY - Epilepsy Behav Case Rep (2013)

Timeline of Case 2. Clock drawing as a sample of the cognitive assessment before methylprednisolone treatment (A), immediately after the steroid pulse therapy (B), and one month (C) and 7 months (D) following treatment, that begun 5 month after the first admission. These drawings demonstrate progressive improvement. T2 FLAIR axial section at the time of diagnosis (E) and 2 months later (F), showing a progressive periventricular hyperintense signal with increasing atrophy. LMT — lamotrigine, VPA — valproate, LEV — levetiracetam, TPM — topiramate, GBP — gabapentin, MET — methylprednisolone, PRD — prednisone, MoCA — Montreal Cognitive Assessment.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4150645&req=5

f0010: Timeline of Case 2. Clock drawing as a sample of the cognitive assessment before methylprednisolone treatment (A), immediately after the steroid pulse therapy (B), and one month (C) and 7 months (D) following treatment, that begun 5 month after the first admission. These drawings demonstrate progressive improvement. T2 FLAIR axial section at the time of diagnosis (E) and 2 months later (F), showing a progressive periventricular hyperintense signal with increasing atrophy. LMT — lamotrigine, VPA — valproate, LEV — levetiracetam, TPM — topiramate, GBP — gabapentin, MET — methylprednisolone, PRD — prednisone, MoCA — Montreal Cognitive Assessment.
Mentions: The neurological examination on admission was notable for disorientation and evident cognitive abnormality as demonstrated by a MoCA score of 12/30 (specifically, abnormal serial seven, immediate memory, and abstraction). She exhibited mild extrapyramidal signs and flapping tremor. An EEG showed focal left frontal intermittent slowing. The lumbar puncture had normal opening pressure and content, and the tau protein level was within the normal range. Routine blood work revealed polycythemia and mild leukocytosis, while the electrolyte levels, liver and kidney functions, thyroid functions, C-reactive protein levels, and neoplastic markers were all normal. Routine rheumatologic tests and antiphospholipid antibodies were normal. The only positive relevant result was very high titers of antithyroglobulin (5564 U/ml) and antithyroid microsomal antibody (> 3000 U/ml). A repeated brain MRI revealed progressive mild atrophy and a hyperintense temporal cortical signal restricted in diffusion. Methylprednisolone (IV, 500 mg/day for 5 days) was administered, and the valproate was switched to levetiracetam (500 mg bid) because of extrapyramidal side effects. She was released from the hospital with instructions to taper the oral prednisone dosage. She returned three weeks later with an allergic drug reaction, manifested through a skin rash and pruritus, while being treated with 30-mg prednisone (during the tapering down) that was attributed to the levetiracetam. Gabapentin was started in addition to topiramate with disappearance of the rash. The repeated MoCA score was 16/30, suggesting mild improvement. At a follow-up visit several months later, the patient and her family reported significant improvement. She had returned to her usual levels of function and normal lifestyle, and she was seizure-free. Although we did not notice a prominent cognitive improvement, she did return to her baseline daily function, and, therefore, we did not suggest further immunomodulatory treatment, except for low prednisone dosage (10 mg daily). Further measurement of the antithyroid antibodies demonstrated a marked reduction (anti-TPO: 349 U/ml, antithyroglobulin: 461 U/ml, Fig. 2).

Bottom Line: Hashimoto's encephalopathy is defined by the coexistence of encephalopathy and antithyroid antibodies.We report two cases of adult-onset temporal lobe epilepsy with subacute cognitive decline, high titers of antithyroid antibodies, multi-antiepileptic drug hypersensitivity, and good response to immunomodulatory treatment.The relevance of multidrug hypersensitivity in the setting of adult-onset epilepsy and the importance of searching for autoimmune causes for epilepsy are discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.

ABSTRACT
Hashimoto's encephalopathy is defined by the coexistence of encephalopathy and antithyroid antibodies. We report two cases of adult-onset temporal lobe epilepsy with subacute cognitive decline, high titers of antithyroid antibodies, multi-antiepileptic drug hypersensitivity, and good response to immunomodulatory treatment. The relevance of multidrug hypersensitivity in the setting of adult-onset epilepsy and the importance of searching for autoimmune causes for epilepsy are discussed.

No MeSH data available.


Related in: MedlinePlus