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    Epilepsy Treatment1

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    kkaallhumm
    The document discusses treatment for epilepsy through anti-epileptic drugs (AEDs). It explains that the main mechanisms of action for AEDs include blocking sodium channels, inhibiting calcium currents, enhancing GABA, and blocking glutamate. It provides examples of specific AEDs that work through each of these mechanisms, such as carbamazepine which blocks sodium channels and valproate which inhibits calcium currents and enhances GABA. It also discusses using AEDs to treat status epilepticus.

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    Epilepsy Treatment1

    Uploaded by

    kkaallhumm
    8 views19 pages
    The document discusses treatment for epilepsy through anti-epileptic drugs (AEDs). It explains that the main mechanisms of action for AEDs include blocking sodium channels, inhibiting calcium currents, enhancing GABA, and blocking glutamate. It provides examples of specific AEDs that work through each of these mechanisms, such as carbamazepine which blocks sodium channels and valproate which inhibits calcium currents and enhances GABA. It also discusses using AEDs to treat status epilepticus.

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    Epilepsy treatment1

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    The document discusses treatment for epilepsy through anti-epileptic drugs (AEDs). It explains that the main mechanisms of action for AEDs include blocking sodium channels, inhibiting calcium currents, enhancing GABA, and blocking glutamate. It provides examples of specific AEDs that work through each of these mechanisms, such as carbamazepine which blocks sodium channels and valproate which inhibits calcium currents and enhances GABA. It also discusses using AEDs to treat status epilepticus.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    8 views19 pages

    Epilepsy Treatment1

    Uploaded by

    kkaallhumm
    The document discusses treatment for epilepsy through anti-epileptic drugs (AEDs). It explains that the main mechanisms of action for AEDs include blocking sodium channels, inhibiting calcium currents, enhancing GABA, and blocking glutamate. It provides examples of specific AEDs that work through each of these mechanisms, such as carbamazepine which blocks sodium channels and valproate which inhibits calcium currents and enhances GABA. It also discusses using AEDs to treat status epilepticus.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    of 19

    ‫بسم هللا الرمحن الرحيم‬

    ‫ كلية الطب‬- ‫جامعة اجلزيرة‬

    Epilepsy (2)
    By Dr. Mahmoud Hussien
    Salih
    MBBS- MRCP- clinical MD internal medicine. MD neurology

    2020
    Contents:

    ◼ How do we treat epilepsy?


    ➢ Mechanism of action of anti Epileptic Drugs.
    ➢ Specific AEDs
    ◼ status Epilepticus.
    Treatment
    Anti Epileptic Medications
    ( first line)
    Sodium Valproate Carbamazepine
    Broad-spectrum Narrow spectrum

    Active against generalized and Active against focal seizures


    focal seizures

    Active against photosensitive More effective in foal seizure than


    seizure valproate

    Unlikely to be the first line drug May exacerbate generalized


    for female approaching child seizures
    bearing age
    Mechanism of action:

    ◼ The main groups include:


    ➢ Sodium channel blockers.
    ➢ Calcium current inhibitors.
    ➢ GABA enhancers.
    ➢ Glutamate blockers.
    1.Sodium channel blockers
    ◼ EDs that target the sodium channels prevent the
    return of these channels to the active state by
    stabilizing them in the inactive state. In doing so,
    they prevent repetitive firing of the axons.
    ◼ Sodium channel blockers are :
    ➢ Carbamazepine
    ➢ Phenytoin
    ➢ Lamotrigine
    2.Calcium channel
    blockers
    ◼ Calcium channels function as the " pacemakers "
    of normal rhythmic brain activity. This is particularly
    true of the thalamus.
    ◼ T-calcium channels have been known to play a
    role in absence seizures.
    ◼ AEDs that inhibit these T-calcium channels are:
    ➢ Ethosuximide.
    ➢ Valproate.
    3. GABA enhancers
    ◼ Gamma-aminobutyric acid (GABA) has 2 types of
    receptors, A and B.
    ◼ When GABA binds to a GABA-A receptor, the
    passage of chloride, a negatively charged ion, into
    the cell is facilitated via chloride channels.
    ◼ This influx of chloride increases the negativity of
    the cell ( a more negative resting membrane
    potential).
    ◼ This causes the cell to have greater difficulty
    reaching the action potential.
    ◼ The GABA system can be enhanced by :
    ➢ binding directly to GABA-A receptors
    ➢ blocking presynaptic GABA uptake
    ➢ inhibiting the metabolism of GABA by GABA
    transaminase
    ➢ increasing the synthesis of GABA.
    ◼ GABA is produced by decarboxylation of glutamate
    mediated by the enzyme glutamic acid
    decarboxylase (GAD). Some AEDs may act as
    modulators of this enzyme, enhancing the
    production of GABA and down-regulating
    glutamate .
    ◼ Some AEDs function by blocking the reuptake of
    GABA (tiagabine [TGB]) or by inhibiting its
    metabolism by GABA transaminase (vigabatrin
    [VGB]), resulting in increased accumulation of
    GABA at the postsynaptic receptors.
    4. Glutamate blockers
    ◼ Glutamate receptors bind glutamate, an excitatory
    amino acid neurotransmitter. Upon binding
    glutamate, the receptors facilitate the flow of both
    sodium and calcium ions into the cell, resulting in
    excitation.

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