Megaloblastic anemia associated with the use of anticonvulsant drugs

Long, Michael T.; Childress, Richard H.; Bond, W. H.

doi:10.1212/wnl.13.8.697

Cited by 22 publications

(5 citation statements)

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“…Eisen et al (1974), however, did not observe low serum folate values in their patients. Subnormal folate level has been implicated in the genesis of peripheral neuropathy in association with megaloblastic anaemia and DPH treatment (Long et al, 1963;Hansen et al, 1964). We agree with Lovelace and Horwitz (1968) that there is no association between peripheral nerve dysfunction after DPH treatment and low serum folate level (Table 7).…”

Section: Discussionsupporting

confidence: 74%

Motor nerve conduction study in patients on diphenylhydantoin therapy.

Chokroverty¹,

Sayeed²

1975

Journal of Neurology, Neurosurgery & Psychiatry

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Section: Discussionsupporting

confidence: 74%

Motor nerve conduction study in patients on diphenylhydantoin therapy.

Chokroverty¹,

Sayeed²

1975

Journal of Neurology, Neurosurgery & Psychiatry

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“…Eisen et al[ 22 ] reported a primary axonal shrinkage and secondary demyelination with PHT. Long et al[ 44 ] and Hansen et al[ 45 ] demonstrated that peripheral neuropathy induced by PHT was related to the subnormal serum folate in association with megaloblastic anemia. We suggest that peripheral neuropathy induced by TPM may be related to its anticonvulsant mechanism of action which is multifactorial and involve blockade of voltage-dependent sodium channels (similar to PHT); inhibition of high-voltage-activated calcium channels; potentiation of GABAergic transmission through GABA-A receptors; inhibition of excitatory pathways through an action at α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) AMPA/kainate receptors sites and inhibition of carbonic anhydrase isoenzymes[ 1 ].…”

Section: Discussionmentioning

confidence: 99%

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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“…On the other hand, the relationship between folate levels in the two compartments had been fairly constant through a wide range of values (Reynolds et al, 1972;Frenkel et al, 1973). Peripheral neuropathy occurs rarely in patients with folic acid deficiency anemia induced by antiepileptic drugs (Long et al, 1963;Anand, 1964).…”

Section: Conclusion and Commentsmentioning

confidence: 99%

Adverse Effects of Phenytoin on Peripheral Nerves and Neuromuscular Junction: A Review

Penry

1981

Epilepsia

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Review of the literature shows that long-term phenytoin therapy is associated with peripheral neuropathy and neuromuscular disorder that rarely can be symptomatic. The usual manifestations of the peripheral neuropathy are lower extremity areflexia, sensory deficits, and reduced conduction velocities. The risk for these peripheral nerve abnormalities is greater with increased serum levels or long duration of therapy (usually more than 5 years). The relative risks according to age groups or number and kinds of antiepileptic drugs used are undetermined. It is not known if detected abnormalities are static or slowly progressive. Isolated case reports have claimed the resolution of signs and symptoms after discontinuance of therapy or correction of a state of intoxication. Appropriate measures to prevent the appearance or progression of the complications are discussed in light of the available evidence.

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Megaloblastic anemia associated with the use of anticonvulsant drugs

Cited by 22 publications

References 0 publications

Motor nerve conduction study in patients on diphenylhydantoin therapy.

Motor nerve conduction study in patients on diphenylhydantoin therapy.

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

Adverse Effects of Phenytoin on Peripheral Nerves and Neuromuscular Junction: A Review

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