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Topiramate Relieves Idiopathic and Symptomatic Trigeminal Neuralgia

2001; Elsevier BV; Volume: 21; Issue: 5 Linguagem: Inglês

10.1016/s0885-3924(01)00275-5

1873-6513

Claudio Solaro, Michele Messmer Uccelli, Giampaolo Brichetto, Claudio Gasperini, Gianluigi Mancardi,

Trigeminal Neuralgia and Treatments

To the Editor: Topiramate (TPM) is a new antiepileptic drug (AED) recently approved for the treatment of partial seizures. It has a broad spectrum of anticonvulsant actions that may result from actions on voltage-gated Na channels and Ca channels, as well as on GABA and glutamate channels.1Glauser T.A Topiramate.Epilepsia. 1999; 40: S71-S80Crossref PubMed Scopus (141) Google Scholar Recently, TPM was found to be effective for several neuralgic symptoms, including intercostal neuralgia,2Bajwa ZH, Sami N, Warfield CA, Wootton J. Topiramate relieves refractory intercostal neuralgia. Neurology 1999;52:1917.Google Scholar cluster headache,3Wheeler S.D Carrazana E.J Topiramate-treated cluster headache.Neurology. 1999; 53: 234Crossref PubMed Google Scholar and infantile spasms.4Glauser T.A Clark P.O Strawburg R A pilot study of topiramate in the treatment of infantile spasms.Epilepsia. 1998; 39: 1324-1328Crossref PubMed Scopus (157) Google Scholar Trigeminal neuralgia (TN) is a sudden recurrent pain in the distribution of the fifth cranial nerve. It may be essential or secondary to demonstrable structural lesions, such as aneurysm or multiple sclerosis (MS). In MS patients, TN is likely due to an ephaptic transmission between demyelinated axons at the fifth root entry zone in the pons. Carbamazepine (CBZ) is the first choice medication for TN. Many patients are resistant to this drug, however, or cannot tolerate it. This is most likely when other neurological symptoms are present, such as in MS. Recently, other AEDs, such as lamotrigine (LMT) and gabapentin (GBP),5Solaro C Lunardi G.L Capello E et al.An open label trial of gabapentin treatment of paroxysmal symptoms in multiple sclerosis patients.Neurology. 1998; 51: 609-611Crossref PubMed Scopus (117) Google Scholar have been shown to be effective for treating TN, both in essential and in secondary cases. We report 4 subjects, 1 with essential TN and 3 with secondary TN, who were resistant or intolerant of other AEDs, but could be successfully treated with TPM. In each case, subjective pain level was rated utilizing a previously described three-point scale: 0 = no pain, 1 = mild, 2 = moderate, 3 = severe.5Solaro C Lunardi G.L Capello E et al.An open label trial of gabapentin treatment of paroxysmal symptoms in multiple sclerosis patients.Neurology. 1998; 51: 609-611Crossref PubMed Scopus (117) Google Scholar Titration began with 25 mg/daily and was increased by 25 mg every three days until pain relief was achieved or dosage reached 300 mg daily. The trial was conducted at the Department of Neurological Sciences and Vision, University of Genoa and S. Camillo Hospital, Rome and written informed consent was obtained from all subjects. A 57-year-old woman had essential TN for more than 15 years. Brain MRI was normal. She was previously treated with CBZ (1600 mg/day), phenytoin (PHT) (300 mg/day), lamotrigine (300 mg/day) and GBP (2400 mg/day), with which she experienced only transient pain relief. The patient was successfully treated with TPM at a dose of 300 mg daily, and was pain-free after six months of treatment. A 35-year-old man underwent a surgical intervention for arteriovenous malformation in the posterior fossa, had residual cerebellar and pyramidal signs, and later developed lancinating paroxysmal pain in the trigeminal area. He was intolerant to low dose CBZ and GBP due to worsening cerebellar signs, and he developed a skin rash with LMT. He was successfully treated with 150 mg of TPM. A 58-year-old woman had clinically definite MS and TN, and was previously treated with CBZ, PHE, LMT, and GBP without benefit or adverse effects. The patient was successfully treated with TPM at 200 mg daily. A 39-year-old woman with TN related to clinically definite MS was previously treated with CBZ, but this treatment was interrupted due to skin rash. GBP was ineffective at a dosage of 900 mg and it was not possible to increase the dosage due to worsening neurological symptoms. The patient was successfully treated with TPM at 200 mg daily. Table 1 provides patient characteristics, TPM dosage levels, and pain scores at T0 (pre-treatment), T1 (pain relief achieved), and T2 (after six months of treatment). Patients presented with a classic TN with trigger points and pain described as electrical discharges within the fifth nerve distribution. Only Patient 2 experienced sensory impairment in the trigeminal area. During the treatment period, no significant adverse effects were reported by any patient. Patient 3 complained of mild asthenia and dry mouth.Table 1Clinical Characteristics and Drug RegimenPatientDiseaseAgeGenderDisease duration (yr)TN durationTPM dosageT0T1T21Essential57F1518 y3003112AVM35M32 y1502003MS58F3215 y2002004MS39F91 y200200T0 = Pre-treatment score; T1 = Post-treatment; T2 = six months score; AVM = arteriovenous malformation; MS = multiple sclerosis. Open table in a new tab The varied mechanisms of action of TPM, which act at different neural transmission levels, such as sodium channels and enhancing GABA concentration, may explain the antinociceptive action of TPM on TN. Other advantages of TPM include the lack of relevant adverse effects and few interactions with other drugs. AEDs such as CBZ, LMT, or GBP are reported to decrease neuropathic pain, although many patients either do not achieve optimal pain relief or are unable to reach high dosage levels, due to adverse effects. For these patients, TPM can represent a new therapeutic option.