Topiramate and Panic Attacks in Patients with Borderline Personality Disorder

 

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The purpose of this letter is to draw attention to a possible occurrence of panic attacks (PA) in patients who take topiramate (TPM). This report describes a 17-year-old woman experiencing repeated PA during treatment with TPM (25 mg daily). A possible causal relationship between adverse side effects and topiramate is supported by the cessation of PA following drug discontinuation and the re-occurrence of attacks after drug resumption. The carbonic anhydrase properties, antiglutamatergic and GABAergic effects of topiramate could trigger PA in susceptible patients.

A 17-year-old woman with borderline personality disorder (BPD) was admitted in the emergency room for a panic attack (PA). The patient had benefited from a combined therapy, integrating interpersonal psychotherapy and 10 mg daily of escitalopram, for the past five months. Clinical evolution was acceptable, except for an important mood instability. Although mood stabilizers are not a recognized indication for BPD and the patient was not diagnosed for a bipolar disorder, the psychiatrist proposed topiramate (TPM) at 25 mg daily. The patient started to have PA several days after the introduction of TPM, but she continued her treatment. One month after TPM introduction, the PA became stronger, and TPM treatment was discontinued, while escitalopram was maintained. The PA stopped entirely several days after discontinuation of TPM, but the treating psychiatrist reintroduced TPM for mood instability. One week after the reintroduction of TPM 25 mg daily, the patient started to re-experience PA, with progressively increasing intensity. This situation culminated with a severe PA requiring a crisis intervention in the emergency room, two weeks after the reintroduction of TPM.

The crisis intervention for the PA in the emergency room consisted of 2.5 mg lorazepam, supportive psychotherapy and a 24-hour hospitalization in the emergency ward. There, the diagnosis of BPD was confirmed by the appropriate section of the Structured Clinical Interview for DSM-IV-Personality Disorders [3]. Axis I comorbidity was assessed with the Mini-International Neuropsychiatric Interview [9]. The patient did not fulfil the diagnostic criteria for bipolar disorder. There was no evidence for any stress factors that could have caused PA at any time. Detailed patient history, as well as clinical and biological routine examination allowed us to exclude interactions with other medication or somatic diseases that could cause PA.

Suspecting a possible TPM induction of PA [2] and taking into account that mood stabilizers are not an indication for BPD, the emergency team proposed the discontinuation of TPM. This advice was accepted by the treating psychiatrist and PA stopped entirely 3 days after discontinuation of TPM. Rather than mood stabilizers, oral [4] [6] [8], or - in an emergency - even intramuscular [1] [7] atypical antipsychotics should be considered for patients with BPD.

This is the third case report concerning the possible implication of TPM in PA. Nevertheless, this is the first time that 25 mg/daily TPM could be associated with PA, instead of 150 mg of TPM or 50 mg TPM associated to 100 mg lamotrigine [2] [5]. One could speculate that patients with BPD might be more sensitive to PA induced by TPM.

Considering the elevated comorbidity of panic disorder associated with bipolar disorders, borderline personality disorders and epilepsy, clinicians from emergency departments should be aware that the use of TPM could induce or increase PA. The carbonic anhydrase retention, antiglutamatergic and GABA-ergic effects of TPM could trigger or generate PA in susceptible patients.

References

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Correspondence

E. ClivazMD 

Geneva University Hospital

24 Rue micheli-du-Crest

1211 Geneva

Switzerland

Email: Emmanuel.clivaz@hcuge.ch