Effects of the antiepileptic drugs on peripheral nerve function

Boylu, Ece; Domaç, Füsun Mayda; Mısırlı, Handan; Şenol, Mehmet Güney; Saraçoğlu, Mehmet

doi:10.1111/j.1600-0404.2009.01275.x

Cited by 5 publications

(5 citation statements)

References 22 publications

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“…So far, there are no randomized controlled trials for VP, but the response to treatment with carbamazepine/oxcarbazepine supports the diagnosis [ 14 ]. Although the long-term administration of anticonvulsant drugs in epileptic patients was reported to provoke delayed auditory conduction [ 68 , 69 , 70 ], a normalization of IPL I–III was noticed in our case. Thus, it is possible that the low doses of oxcarbazepine used in VP are less toxic than the higher doses usually required in epilepsy, resulting in a beneficial effect on the narrowed IAC-induced neuropathy.…”

Section: Discussioncontrasting

confidence: 53%

The Narrowed Internal Auditory Canal: A Distinct Etiology of Pediatric Vestibular Paroxysmia

Idriss

Thai‐Van

Altaisan

et al. 2022

JCM

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Vestibular paroxysmia (VP) is a disorder encountered in the pediatric population that etiology has been attributed to neurovascular cross-compression syndrome (NVCC). The purpose of this study was to report a new probable pathological condition, the narrowed internal auditory canal (IAC), which appears to be involved in the development of a clinical picture of VP in the pediatric population. A retrospective descriptive comparative study was conducted to compare clinical, electrophysiological, radiological, and therapeutic outcomes in both etiologies. Overall, 16 pediatric patients suffering from VP were included and divided into two groups: patients with narrowed internal auditory (Group 1) were compared to those with NVCC syndrome (Group 2). Patients in both groups were similar in terms of auditory complaints, as well as hearing, vestibular, and electrophysiological status. A narrowed IAC was encountered in the adolescent age category and females, especially those with rapid growth. The diagnosis requires a careful analysis of the shape and diameters of the IAC. Radiologic measurements in the axial plane do not seem to be sufficient to confirm the diagnosis, and, therefore, an analysis of diameters in the coronal plane is required. Treatment with sodium-channel blockers drugs showed promising results not only by relieving vertigo but also by normalizing the electrophysiological findings. In conclusion, a narrowed IAC can be considered in patients suffering from VP.

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Section: Discussioncontrasting

confidence: 53%

The Narrowed Internal Auditory Canal: A Distinct Etiology of Pediatric Vestibular Paroxysmia

Idriss

Thai‐Van

Altaisan

et al. 2022

JCM

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“…Peripheral neuropathy had been also reported with other AEDs therapy as CBZ[ 26 - 28 ], PB[ 27 ], VPA[ 26 , 29 , 30 ], GPN[ 31 ], LEV[ 32 ] and LCM[ 33 ]. A review of the literature showed that reflex sympathetic dystrophy (RSD) is precipitated by PB in 10%-30% of cases[ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

“…Kapoor et al[ 32 ] reported a case of polyneuropathy induced by LEV which improved with discontinuation of LEV. Boylu et al[ 28 ] reported mild prolongation in the distal latency of median sensory, ulnar sensory and sural nerves with diminished nerve conduction velocities with chronic CBZ therapy but not with VPA, oxcarbazepine (OXC) or TPM. Marusic et al[ 30 ] reported a 26-year-old man with weakness of flexion and abduction of the right arm and loss of sensation in the skin over the lateral upper right arm and reduced amplitude and prolonged latencies in the right axillary nerve because of a suicide attempt with VPA overdose (serum VPA level = 2896 μmol/L; therapeutic range = 350-690 μmol/L).…”

Section: Discussionmentioning

confidence: 99%

“…It had been reported with short-term treatment (hours to weeks) with PHT in toxic[ 15 - 18 ] or non-toxic doses[ 19 - 21 ] and with long-term (≥ 5 years) PHT therapy[ 22 - 25 ]. Peripheral neuropathy had been also reported with therapy with other AEDs as carbamazepine (CBZ)[ 26 - 28 ], phenobarbital (PB)[ 27 ], sodium valproate (VPA)[ 26 , 27 , 29 , 30 ], gabapentin (GPN)[ 31 ], levetiracetam (LEV)[ 32 ] and lacosamide (LCM)[ 33 ]. There is no previous report for peripheral neuropathy induced by TPM.…”

Section: Introductionmentioning

confidence: 99%

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Topiramate induced peripheral neuropathy: A case report and review of literature

Hamed

2017

WJCC

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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.

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“…6 There is also evidence that carbamazepine may result in a peripheral neuropathy. 7 It is uncommon for other ASMs to result in a peripheral neuropathy. Routine neurological exams testing motor function, sensory function, and gait are important to screen for this condition.…”

Section: Nervous System Effectsmentioning

confidence: 99%

Long-Term Effects of Antiseizure Medications

LoPinto-Khoury

2022

Semin Neurol

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Most patients with epilepsy will benefit from seizure control with one of an array of chronic antiseizure medications. Knowledge of the potential long-term effects of these medications is critical to prevent adverse consequences on overall health. Antiseizure medications vary in their capacities to affect the brain and peripheral nerves, hormones, bone mineralization, cardiovascular risk, renal health, hepatic, hematological, and dermatological systems. Understanding of pathophysiology and population risk has evolved, although most of the data available are still on older generation antiseizure medications such as phenytoin, carbamazepine, and valproic acid. The enzyme-inducing properties of some antiseizure medications make their effects on cardiovascular risk and bone health detrimental. Few clear guidelines exist for monitoring long-term effects of medication therapy for epilepsy. When selecting an antiseizure medication, consideration should be given to the individual patient's risks of adverse consequences on other organ systems. During monitoring of patients on chronic therapy, screening tools such as metabolic panels and bone density measurements can help stratify risk and guide management.

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Effects of the antiepileptic drugs on peripheral nerve function

Abstract: Valproic acid, oxcarbazepine and topiramate don't have effects on nerve conduction studies. Mild electrophysiological changes contribute to carbamazepine therapy.

Cited by 5 publications

References 22 publications

The Narrowed Internal Auditory Canal: A Distinct Etiology of Pediatric Vestibular Paroxysmia

The Narrowed Internal Auditory Canal: A Distinct Etiology of Pediatric Vestibular Paroxysmia

Topiramate induced peripheral neuropathy: A case report and review of literature

Long-Term Effects of Antiseizure Medications

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