Case Report
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Dec 16, 2017; 5(12): 446-452
Published online Dec 16, 2017. doi: 10.12998/wjcc.v5.i12.446
Topiramate induced peripheral neuropathy: A case report and review of literature
Sherifa Ahmed Hamed
Sherifa Ahmed Hamed, Department of Neurology and Psychiatry, Assiut University Hospital, Assiut 71516, Egypt
Author contributions: Hamed SA solely contributed to this paper.
Institutional review board statement: This case report was exempt from the Institutional Review Board standards at University of Assiut in Egypt.
Informed consent statement: The patient involved in this study gave her written informed consent authorizing use and disclosure of her protected health information.
Conflict-of-interest statement: The author declared no conflict of interests.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Sherifa Ahmed Hamed, MD, Professor, Consultant Neurologist, Department of Neurology and Psychiatry, Assiut University Hospital, Floor # 7, Room # 4, Assiut 71516, Egypt. sherifa.omran@med.au.edu.eg
Telephone: +20-88-2371820 Fax: +20-88-2333327
Received: June 9, 2017
Peer-review started: June 15, 2017
First decision: August 7, 2017
Revised: August 11, 2017
Accepted: September 3, 2017
Article in press: September 4, 2017
Published online: December 16, 2017
Processing time: 177 Days and 14.3 Hours
Abstract

Drug-induced peripheral neuropathy had been rarely reported as an adverse effect of some antiepileptic drugs (AEDs) at high cumulative doses or even within the therapeutic drug doses or levels. We describe clinical and diagnostic features of a patient with peripheral neuropathy as an adverse effect of chronic topiramate (TPM) therapy. A 37-year-old woman was presented for the control of active epilepsy (2010). She was resistant to some AEDs as mono- or combined therapies (carbamazepine, sodium valproate, levetiracetam, oxcarbazepine and lamotrigine). She has the diagnosis of frontal lobe epilepsy with secondary generalization and has a brother, sister and son with active epilepsies. She became seizure free on TPM (2013-2017) but is complaining of persistent distal lower extremities paresthesia in a stocking distribution. Neurological examination revealed presence of diminished Achilles tendon reflexes, stocking hypesthesia and delayed distal latencies, reduced conduction velocities and amplitudes of action potentials of posterior tibial and sural nerves, indicating demyelinating and axonal peripheral neuropathy of the lower extremities. After exclusion of the possible causes of peripheral neuropathy, chronic TPM therapy is suggested as the most probable cause of patient’s neuropathy. This is the first case report of topiramate induced peripheral neuropathy in the literature.

Keywords: Topiramate; Peripheral neuropathy; Sodium channel blockade; Antiepileptic drugs

Core tip: Peripheral neuropathy is a rare adverse effect of short- or long-term use of antiepileptic drugs (phenytoin, phenobarbital, carbamazepine, valproate, gabapentin, levetiracetam and lacosamide). This is the first case report of topiramate induced peripheral neuropathy (TIPN). Manifestations of TIPN are distal paresthesia, areflexia, sensory deficits and reduced amplitudes and nerve conduction velocities of motor and sensory peripheral nerves of the lower extremities indicating demyelinating and axonal neuropathies. The risk is greater with long-term therapy. The mechanisms of TIPN may involve impairment of nerve function through blocking of sodium voltage channels, enhancement of gamma amino butyric acid inhibitory neurotransmission or others.