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Related Concept Videos

Antiepileptic Drugs: GABAergic Pathway Potentiators01:18

Antiepileptic Drugs: GABAergic Pathway Potentiators

γ-aminobutyric acid or GABA, plays a pivotal role as an inhibitory neurotransmitter in the brain. GABA pathway potentiators, also known as GABAergic drugs, are a class of pharmaceutical agents designed to enhance the functioning of the GABAergic system. These medications primarily treat epilepsy, a neurological disorder characterized by recurrent seizures.
The key GABA pathway potentiators used in epilepsy management are as follows.
Benzodiazepines are a well-known class of drugs used for their...
Antiepileptic Drugs: Calcium Channel Blockers01:17

Antiepileptic Drugs: Calcium Channel Blockers

Calcium channel blockers, a class of antiepileptic drugs, regulate the flow of calcium ions within neurons.
Calcium channel blockers exert their antiepileptic effects by targeting T-type calcium channels, which are integral to transmitting nerve signals in the central nervous system. These channels allow the passage of calcium ions, which are vital for neuronal communication. By inhibiting T-type calcium channels, calcium channel blockers effectively reduce the release of neurotransmitters and...
Antiepileptic Drugs: Glutamate Antagonists01:14

Antiepileptic Drugs: Glutamate Antagonists

Glutamate is a fundamental neurotransmitter in the central nervous system, playing a vital role in neuronal communication and various cognitive processes. Glutamate stands as the principal excitatory neurotransmitter in the brain. Its presence is crucial for the communication between neurons, underpinning essential processes such as synaptic transmission, neuronal excitability, and plasticity. These functions are vital for higher-order cognitive processes, including learning and memory. The...
Antiepileptic Drugs: Potassium Channel Activators01:20

Antiepileptic Drugs: Potassium Channel Activators

Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
Tonsillitis II: Management01:26

Tonsillitis II: Management

This lesson will focus on the different treatment options for managing tonsillitis, which typically depend on the cause and severity.
Epistaxis01:30

Epistaxis

Epistaxis, or nosebleeds, occurs when small, swollen blood vessels in the nasal mucous membrane rupture. Typically, the anterior septum is the primary site of occurrence.
Etiology
Possible causes of this condition include high blood pressure, trauma, low humidity, upper respiratory tract infections, allergies, foreign bodies, nasal inhalation of corticosteroids or illicit drugs, excessive use of decongestant nasal sprays, facial or nasal surgery, anatomic malformation, tumors, or systemic...

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Related Experiment Video

Updated: Jun 18, 2026

Subcutaneous Trigeminal Nerve Field Stimulation for Refractory Facial Pain
09:35

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Published on: May 10, 2017

Intractable epistaxis associated with topiramate administration.

Robert L Page1, Jacquelyn L Bainbridge

  • 1Department of Clinical Pharmacy, Schools of Pharmacy and Medicine, University of Colorado Health Sciences Center, Denver, 80262, USA. robert.page@uchsc.edu

The Annals of Pharmacotherapy
|July 11, 2006
PubMed
Summary

Topiramate therapy can cause severe nosebleeds (epistaxis) in some patients, even leading to hospitalization. Discontinuing the medication typically resolves the epistaxis, suggesting a causal link.

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Area of Science:

  • Neurology
  • Pharmacology
  • Clinical Medicine

Background:

  • Topiramate is a widely used neuromodulator for migraines and seizures.
  • Its therapeutic applications have expanded to various neuropathic conditions.
  • Limited data exist on epistaxis as an adverse effect in older populations.

Observation:

  • A 61-year-old female patient developed severe, intractable epistaxis after initiating topiramate for neuropathy.
  • Epistaxis recurred upon topiramate re-challenge, resolving after discontinuation.
  • The patient required hospitalization and blood transfusion due to epistaxis and anginal pain.

Findings:

  • The Naranjo scale indicated probable causality between topiramate and epistaxis.
  • Topiramate's mechanism may involve modulation of calcium channels, similar to calcium-channel blockers, potentially affecting vascular smooth muscle and platelets.
  • This case suggests a potential association between topiramate and severe epistaxis, especially in conjunction with antiplatelet agents.

Implications:

  • Severe, intractable epistaxis should be considered a potential serious adverse reaction to topiramate.
  • Clinicians should monitor for epistaxis in patients prescribed topiramate, particularly those with cardiovascular disease or on antiplatelet medications.
  • This case highlights the need for vigilance regarding topiramate's side effect profile in diverse patient populations.