Acquired Epileptic Aphasia Medication

  • Author: Eli S Neiman, DO; Chief Editor: Amy Kao, MD   more...
 
Updated: Apr 27, 2011
 

Medication Summary

No drug of choice is known for acquired epileptic aphasia (AEA), but corticosteroids and adrenocorticotropin hormone (ACTH) have become popular despite a lack of controlled trials. One should not treat based on the following information but should reference the most up-to-date literature.

The data presented below, including dosages, are based on how corticosteroids and ACTH have often been prescribed for patients with acquired epileptic aphasia but may be subject to change.

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Corticosteroids

Class Summary

The mechanism of action of immunosuppressant-mediated improvement in acquired epileptic aphasia (AEA) is unknown.

Prednisone

 

Prednisone is effective in improving aphasia in a few reports. Early treatment may be better than late treatment (data from uncontrolled trials).

Corticotropin (H.P. Acthar)

 

Corticotropin is effective in improving aphasia (few reports); early treatment may be better than late treatment (data from uncontrolled trials).

Prednisolone (Millipred, Orapred ODT, Veripred, Prelone)

 

Prednisolone is effective in improving aphasia in a few reports. Early treatment may be better than late treatment (data from uncontrolled trials).

Methylprednisolone (Solu-Medrol)

 

Pulse intravenous (IV) methylprednisolone therapy has been used to induce remission in acquired epileptic aphasia.

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Contributor Information and Disclosures
Author

Eli S Neiman, DO  Assistant Professor of Neurology, Seton Hall University School of Graduate Medical Education, Comprehensive Epilepsy Center, New Jersey Neuroscience Institute-JFK Medical Center, Edison, NJ

Eli S Neiman, DO is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, and American Osteopathic Association

Disclosure: UCB Pharma Honoraria Review panel membership; UCB Pharma Honoraria Speaking and teaching; Cyberonics, Inc Honoraria Speaking and teaching

Coauthor(s)

Michael Seyffert  MD, Assistant Professor or Neurosciences, Seton Hall University School of Graduate Medical Education; Project Advisor, Biomedical Engineering, New Jersey Neuroscience Institute, Neurology and Sleep Medicine, JFK Medical Center

Michael Seyffert is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, and Child Neurology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Robert Stanley Rust Jr, MD, MA  Thomas E Worrell Jr Professor of Epileptology and Neurology, Co-Director of FE Dreifuss Child Neurology and Epilepsy Clinics, Director, Child Neurology, University of Virginia School of Medicine; Chair-Elect, Child Neurology Section, American Academy of Neurology

Robert Stanley Rust Jr, MD, MA is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, American Neurological Association, Child Neurology Society, International Child Neurology Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Chief Editor

Amy Kao, MD  Attending Neurologist, Children's National Medical Center

Amy Kao, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, and Child Neurology Society

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Marcio Sotero de Menezes, MD, to the development and writing of the source article.

References
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Table 1. Long-Term Follow-up of Acquired Epileptic Aphasia
StudyNumber of PatientsMean Follow-up, yNumber of Patients with Normal or Mild Language Problems
Soprano et al[10] (1994) 1283
Mantovani and Landau[15] (1980) 9226
Paquier[16] (1992) 68.13
Rossi[17] (1999) 119.72
Robinson et al[11] (2001) 185.63
Duran et al[13] (2009) 79.51
Total6318 (28.6%)
Table 2. Epileptiform EEG Findings in Autism, Dysphasia, and Epilepsy
SourceDiagnosisNumber of PatientsNumber of Patients with EEGsPatients with Abnormal EEGs (%)
Tuchman et al (1991)Autism with epilepsy424075
Autism without epilepsy1601398
Dysphasia with epilepsy191958
Dysphasia without epilepsy218669
Tuchman and Rapin[22] (1997) PDD or autism585392*NA
With epilepsyNA6659
Without epilepsyNA6659
Without epilepsy but with history of regressionNA15514
Without epilepsy and without history of regressionNA3646
EEG(s) = electroencephalogram(s); NA = not applicable; PDD = personality developmental disorder.



* Sleep EEGs.



Table 3
DiagnosisDeteriorationEEG Patterns
Autistic epileptiform regressionExpressive language, RL, S, verbal and nonverbal communicationCentrotemporal spikes
Autistic regressionExpressive language, RL, S, verbal and nonverbal communicationNormal
Acquired epileptic aphasiaRL, possibly behavioralLeft or right temporal or parietal spikes, possibly ESES
Acquired expressive epileptic aphasiaExpressive language, oromotor apraxiaCentrotemporal spikes
ESESExpressive language, RL, possibly behavioralESES
Developmental dysphasia (developmental expressive language disease)No; lack of expressive language acquisitionTemporal or parietal spikes
Disintegrative epileptiform disorderExpressive language, RL, S, verbal and nonverbal communication, possibly behavioralESES
EEG = electroencephalographic; ESES = electrical status epilepticus of sleep; RL = receptive language; S = sociability.



* Continuous spike and wave of slow-wave sleep (>85% of slow-wave sleep).



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