Lacosamide is a novel, sustained-release formulation of the
functionalized amino acid, R-2-acetamido-N-benzyl-3-
methoxypropionamide. It modulates voltage-gated sodium
channels by enhancing slow inactivating states without
afecting the fast inactivation.2 Lacosamide afects neurons only, which depolarized or active for long period
of time, which leads to inhibition of repetitive neuronal
action potential and results in stabilization of hyperexitble
Te drug is rapidly absorbed from the gastrointestinal
tract and has an oral bioavailability of nearly 100%. In
adults, it has low plasma protein binding, which reduces
its potential interaction with other drugs.3 Beyreuther and
colleagues found that lacosamide was efective as an analgesic in rat models for bone cancer pain and chemotherapy-induced neuropathic pain and even reduced hyperalgesia where morphine did not.4 It has also been found
to attenuate thermal and tactile allodynia and mechanical
hyperalgesia in a vincristine-induced neuropathy in rats
and to show a protective efect in a rat model of vincristine
neuropathy.1 Te drug has shown showed efcacy in several short- and long-term phase 2 clinical trials in humans
with diabetic neuropathic pain.5,6 It is used at doses of
200 mg, 400 mg, or 600 mg daily, given as a divided dose.
Lacosamide is generally well tolerated in adult patients in
doses up to 400 mg/day. Te most common side efects are
headache, dizziness, and nausea. Less common side-efects
are diplopia, blurred vision, forgetfulness, discouragement,
and lack of appetite.7
CIPN is a common and often debilitating dose-limiting side efect associated with several commonly used chemotherapeutic agents, including platinum, taxanes, and
vinca alkaloids.8 CIPN occurs in 30%-40% of patients,
but its incidence may be as high as 70%.9 Te symptoms
most commonly associated with it are sensory neuropa-thies, including paresthesia, allodynia, dysthesia, and pain,
which is burning, or electric shock like.10 Te symptoms
often begin in the fngers and toes and spread proximally
in a “glove and socks” distribution.11 CIPN may begin
any time from weeks to months after treatment initiation
and reaches a peak at or after the end of treatment. Te
symptoms get progressively worse over the course of the
Te exact mechanism of CIPN has not been fully
described and can difer within classes of chemotherapeu-
tic agents. In most cases, CIPN is only partially reversible
and can be permanent. Painful symptoms may persist 2-6
months beyond discontinuation of chemotherapy, a phe-
nomenon known as “coasting.”12 In addition, patients who
have had evidence of CIPN, even if signs and symptoms
improved signifcantly after discontinuation of the che-
motherapy, are at increased risk of progressive neuropathic
symptoms if they are exposed to other neurotoxic agents.
Tis may infuence the choice of future chemotherapeutic
agents. As such, CIPN may result in chemotherapy dose
reduction, the selection of less efcacious therapies, or even
cessation of cancer treatment, all of which can be detri-
mental.13 Terefore, it is of great importance to fnd efec-
tive treatment for CIPN in cancer patients.
Findings from randomized, controlled trials with a
variety of drugs with diverse mechanisms of action have
shown there to be no efective treatment for CIPN, with
the exception of duloxetine.14 Few agents – including topi-
cal baclofen-amitriptyline-ketamine gel,15 venlafaxine,16
and pregabalin17 – have preliminary data to support their
use in the treatment of CIPN. It is important to under-
take further investigation into the natural history of CIPN
associated with various classes of neurotoxic chemotherapy
agents. Tis may provide important insight for the devel-
opment of new strategies for the prevention and treatment
Lacosamide may be a promising novel candidate for the
prevention and treatment of cancer pain including chemotherapy-induced peripheral neuropathy. Here we report on
a successful case of cisplatin-induced neuropathy treated
with lacosamide. As far as we know, this is the frst reported
case of its kind. Tere should be further investigation into
the natural history of CIPN associated with various classes
of neurotoxic chemotherapy agents. Tis may provide
important insight for the development of new strategies in
prevention and treatment of CIPN.
1. Geis C, Beyreuther BK, Stöhr T, Sommer C. Lacosamide has protective disease modifying properties in experimental vincristine neuropathy. Neuropharmacology. 2011;61:600-607.
2. Errington AC, Stöhr T, Heers C, Lees G. Te investigational anticonvulsant lacosamide selectively enhances slow inactivation of voltage-gated sodium channels. Mol Pharmacol. 2008;73:157-169.
3. Cawello W, Bökens H, Nickel B, Andreas JO, Halabi A. Tolerability,
pharmacokinetics, and bioequivalence of the tablet and syrup formulations of lacosamide in plasma, saliva, and urine: saliva as a surrogate of pharmacokinetics in the central compartment. Epilepsia.
4. Beyreuther BK, Callizot N, Brot MD, Feldman R, Bain SC, Stöhr T.
Antinociceptive efcacy of lacosamide in rat models for tumor- and
chemotherapy-induced cancer pain. Eur J Pharmacol. 2007;565:98-
5. Wymer JP, Simpson J, Sen D, Bongardt S; Lacosamide SP742 Study
Group. Efcacy and safety of lacosamide in diabetic neuropathic
pain: an 18-week double-blind placebo-controlled trial of fxed-dose
regimens. Clin J Pain. 2009;25:376-385.
6. Rauck RL, Shaibani A, Biton V, Simpson J, Koch B. Lacosamide in
painful diabetic peripheral neuropathy: a phase 2 double-blind placebo-controlled study. Clin J Pain. 2007;23:150-158.
7. Chung S, Ben-Menachem E, Sperling MR, et al. Examining the
clinical utility of lacosamide: pooled analyses of three phase II/III
clinical trials. CNS Drugs, 2010;24:1041-1054.
8. Wolf S, Barton D, Kottschade L, Grothey A, Loprinzi C. Chemotherapy-induced peripheral neuropathy: prevention and treatment