Phenytoin neuropathy: Structural changes in the sural nerve

Abstract

Phenytoin has been implicated as a causative agent in peripheral neuropathy, although structural changes in nerve have not been characterized. A 47-year-old man was seen with clinical and electrophysiological signs of peripheral neuropathy after 30 years of phenytoin administration. Despite a modest dose of phenytoin (300 mg/day) blood levels were 31 to 38 micrograms/ml. A sural nerve biopsy showed a loss of large myelinated nerve fibers and a nonrandom clustered distribution of segmental demyelination and remyelination. The latter findings were accompanied by axonal shrinkage. Sixteen months after phenytoin was stopped, the patient's clinical and electrophysiological findings reflected improvement. These data indicate that long-term phenytoin administration can cause a reversible neuropathy characterized by axonal shrinkage and secondary demyelination.

B-Vitamin deficiency in patients treated with antiepileptic drugs

“…It is standard clinical practice to supplement isoniazid-treated patients with B6 to avoid the depletion that can otherwise occur via this mechanism. This neuropathic action of isoniazid, and the present findings, are of interest in light of the evidence that PHT may be neuropathic [11,12] .…”

Transient focal lesion in the splenium of the corpus callosum: MR imaging with an attempt to clinical-physiopathological explanation and review of the literature

“…According to the authors, these focal areas could be an expression of transient demyelination, presumably induced by the toxic effects associated with some antiepileptic drugs. According to their findings, Dilantin induces organic cerebellar damage and a distal axonopathy with secondary demyelination in the sural nerve [19,20]. In addition, Dilantin may interfere with the intestinal absorption of dietary folate, causing a deficiency that has been linked to encephalopathy, cerebellar atrophy, myelopathy and peripheral neuropathy [21].…”

“…Secondo gli autori, le aree focali di alterazione deriverebbero da una demielinizzazione transitoria, presumibilmente riconducibile a effetti tossici indotti da alcuni farmaci antiepilettici. Secondo quanto riportato, la dilantina indurrebbe un danno cerebellare organico e un'assonopatia distale con demielinizzazione secondaria del nervo [19,20]. Inoltre il farmaco potrebbe interferire con l'assorbimento intestinale di folati, il cui deficit è stato collegato a encefalopatia, atrofia cerebellare, mielopatia e neuropatia periferica [21].…”

“…The patients, three men and three women, with a mean age of 21 (range [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34] years, underwent brain MRI due to suspected infectious brain disease (n=2), venous sinus thrombosis (n=1) and demyelination disease (n=3). Each patient was studied by brain CT and MRI (Shimadzu…”

Niemann-Pick disease type C: Two cases and an update

“…The common causes of axonal polyneuropathy could not be found, but his longstanding use of phenytoin can be responsible for the polyneuropathy. 12 His hammertoes can be explained by polyneuropathy, but the relationship of cataracts, marfanoid body habitus, and joint laxity to NPC is undetermined. Marfan's or EhlersDanlos syndrome were considered unlikely by rheumatology.…”