Neurology Flashcards
Epinephrine
α-agonist
Decreases IOP by inhibiting synthesis of aqueous humor via vasoconstriction.
Glaucoma
Mydriasis. Do not use in closed-angle glaucoma
Brimonidine
α2-agonist
Decreases IOP by decreasing inhibiting synthesis of aqueous humor
Glaucoma
Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis
Timolol
β-blocker
Decreases IOP by decreasing inhibiting synthesis of aqueous humor
Glaucoma
No pupillary or vision changes
Betaxolol
β-blocker
Decreases IOP by decreasing inhibiting synthesis of aqueous humor
Glaucoma
No pupillary or vision changes
Carteolol
β-blocker
Decreases IOP by decreasing inhibiting synthesis of aqueous humor
Glaucoma
No pupillary or vision changes
Acetazolamide
Decreases IOP by decreasing amount of aqueous humor production via inhibition of carbonic anhydrase
Glaucoma
No pupillary or vision changes
Pilocarpine
Direct cholinomimetic
Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Glaucoma, especially in emergencies. Very effective in opening meshwork into canal of Schlemm
Miosis and cyclospasm (contraction of ciliary muscle)
Carbachol
Direct cholinomimetic
Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Glaucoma
Miosis and cyclospasm (contraction of ciliary muscle)
Physostigmine
Indirect cholinomimetic
Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Glaucoma
Miosis and cyclospasm (contraction of ciliary muscle)
Echothiophate
Indirect cholinomimetic
Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Glaucoma
Miosis and cyclospasm (contraction of ciliary muscle)
Latanoprost (PGF2α)
Decreases IOP by Increasing outflow of aqueous humor
Glaucoma
Darkens iris color (browning)
Morphine
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema, general anesthetic (in combination with other CNS depressants)
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Fentanyl
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema, general anesthetic (in combination with other CNS depressants)
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Codeine
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Methadone
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Maintenance programs for individuals with heroin addiction
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Meperidine
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Dextromethorphan
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Cough suppressant
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Diphenoxylate
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Butorphanol
Mu-opiod receptor partial agonist and kappa-opioid receptor agonist. Produces analgesia.
Severe pain (migraine, labor, etc).
Less respiratory depression than full opioid agonists. Can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors).
Overdose not easily reversed.
Tramadol
Very weak opioid agonist. Also inhibits serotonin and norepinephrine reuptake.
Chronic pain.
Toxicity similar to opioids. Decreases seizure threshold. Serotonin syndrome.
Phenobarbitol
Barbituate
Facilitate GABA-A action by increased duration of Cl channel opening, thus decreasing neuron firing.
Sedate for anxiety, seizures, insomnia.
Respiratory and cardiovascular depression (can be fatal). CNS depression (exacerbated by EtOH use), dependence, drug interactions (induces CYP450). Contraindicated in porphyria.
Overdose treatment is supportive (assist respiration, maintain BP).
Pentobarbital
Barbituate
Facilitate GABA-A action by increased duration of Cl channel opening, thus decreasing neuron firing.
Sedate for anxiety, seizures, insomnia.
Respiratory and cardiovascular depression (can be fatal). CNS depression (exacerbated by EtOH use), dependence, drug interactions (induces CYP450). Contraindicated in porphyria.
Overdose treatment is supportive (assist respiration, maintain BP).
Thiopental
Barbituate
Facilitate GABA-A action by increased duration of Cl channel opening, thus decreasing neuron firing. High potency, high lipid solubility, rapid entry into brain. Decreases cerebral blood flow. Effects terminated by rapid redistribution into tissue and fat.
Induction of anesthesia, short surgical procedures.
Respiratory and cardiovascular depression (can be fatal). CNS depression (exacerbated by EtOH use), dependence, drug interactions (induces CYP450). Contraindicated in porphyria.
Overdose treatment is supportive (assist respiration, maintain BP).
Secobarbital
Barbituate
Facilitate GABA-A action by increased duration of Cl channel opening, thus decreasing neuron firing.
Sedate for anxiety, seizures, insomnia.
Respiratory and cardiovascular depression (can be fatal). CNS depression (exacerbated by EtOH use), dependence, drug interactions (induces CYP450). Contraindicated in porphyria.
Overdose treatment is supportive (assist respiration, maintain BP).
Diazepam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, status epilepticus (first line treatment for acute), eclampsia (after magnesium sulfate), detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazpeine receptor).
Lorazepam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, status epilepticus (first line treatment for acute), eclampsia (after magnesium sulfate), detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazpeine receptor).
Triazolam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Short acting, higher addictive potential.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazpeine receptor).
Temazepam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazpeine receptor).
Oxazepam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Short acting, higher addictive potential.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazpeine receptor).
Midazolam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Short acting, higher addictive potential.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia). Used adjunctively with gaseous anesthetics and narcotics.
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. May cause severe postoperative respiratory depression, hypotension, and anterograde amnesia.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazpeine receptor).
Chlordiazepoxide
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazpeine receptor).
Alprazolam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazpeine receptor).
Zolpidem (Ambien)
Non-benzodiazepine hypnotic
Act via BZ1 subtype of the GABA receptor.
Insomnia.
Ataxia, headaches, confusion. Short duration of action because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Less dependence risk than benzodiazepines.
Effects reversed by flumazenil.
Zaleplon
Non-benzodiazepine hypnotic
Act via BZ1 subtype of the GABA receptor.
Insomnia.
Ataxia, headaches, confusion. Short duration of action because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Less dependence risk than benzodiazepines.
Effects reversed by flumazenil.
Eszopiclone
Non-benzodiazepine hypnotic
Act via BZ1 subtype of the GABA receptor.
Insomnia.
Ataxia, headaches, confusion. Short duration of action because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Less dependence risk than benzodiazepines.
Effects reversed by flumazenil.
Halothane
Inhaled anesthetic.
Unknown mechanism.
Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
Hepatotoxicity, malignant hyperthermia.
Enflurane
Inhaled anesthetic.
Unknown mechanism.
Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
Proconvulsant, malignant hyperthermia.
Isoflurane
Inhaled anesthetic.
Unknown mechanism.
Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
Malignant hyperthermia.
Sevoflurane
Inhaled anesthetic.
Unknown mechanism.
Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
Malignant hyperthermia.
Methoxyflurane
Inhaled anesthetic.
Unknown mechanism.
Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
Nephrotoxicity, malignant hyperthermia.
Nitrous oxide
Inhaled anesthetic.
Unknown mechanism.
Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
Expansion of trapped gas in a body cavity.
Ketamine
Arylcyclohexylamine
PCP analog that acts as dissociative anesthetic. Blocks NMDA receptors. Cardiovascular stimulant.
Disorientation, hallucination, bad dreams. Increases cerebral blood flow.
Propofol
Potentiates GABA-A.
Rapid anesthesia induction, used for short procedures. Used for sedation in ICU. Less postoperative nausea than thiopental.
Procaine
Local anesthetic. Ester.
Block Na channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na channels, so most effective in rapidly firing neurons.
Minor surgical procedures, spinal anesthesia. Used in patients with amide allergy.
CNS excitation, hypertension, hypotension.
Cocaine
Local anesthetic. Ester.
Block Na channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na channels, so most effective in rapidly firing neurons.
Minor surgical procedures, spinal anesthesia. Used in patients with amide allergy.
CNS excitation, hypertension, hypotension, arrhythmias.
Tetracaine
Local anesthetic. Ester.
Block Na channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na channels, so most effective in rapidly firing neurons.
Minor surgical procedures, spinal anesthesia. Used in patients with amide allergy.
CNS excitation, hypertension, hypotension.
Lidocaine
Local anesthetic. Amide.
Block Na channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na channels, so most effective in rapidly firing neurons. Tertiary amines penetrate membrane in uncharged form, then bind to ion channels in charged form.
Minor surgical procedures, spinal anesthesia.
CNS excitation, hypertension, hypotension, allergy (use esters instead).
Mepivacaine
Local anesthetic. Amide.
Block Na channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na channels, so most effective in rapidly firing neurons. Tertiary amines penetrate membrane in uncharged form, then bind to ion channels in charged form.
Minor surgical procedures, spinal anesthesia.
CNS excitation, hypertension, hypotension, allergy (use esters instead).
Bupivacaine
Local anesthetic. Amide.
Block Na channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na channels, so most effective in rapidly firing neurons. Tertiary amines penetrate membrane in uncharged form, then bind to ion channels in charged form.
Minor surgical procedures, spinal anesthesia.
CNS excitation, severe cardiovascular toxicity, hypertension, hypotension, allergy (use esters instead).
Succinylcholine
Depolarizing neuromuscular blocking agent.
Strong Ach receptor agonist. Produces sustained depolarization and prevents muscle contraction.
Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
Phase I: Prolonged depolarization, no antidote. Block is potentiated by anticholinesterases.
Phase II: Repolarized but blocked. Antidote is cholinesterase inhibitors.
Hypercalcemia, hyperkalemia, malignant hyperthermia.
Tubocurarine
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Atracurium
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Mivacurium
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Pancuronium
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Vecuronium
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Rocuronium
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Dantrolene
Prevents the release of Ca from the sarcoplasmic reticulum of skeletal muscle.
Used to treat malignant hyperthermia and neuroleptic malignant syndrome (toxicity of antipsychotic drugs).
Succinylcholine
Depolarizing neuromuscular blocking agent.
Strong Ach receptor agonist. Produces sustained depolarization and prevents muscle contraction.
Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
Phase I: Prolonged depolarization, no antidote. Block is potentiated by anticholinesterases.
Phase II: Repolarized but blocked. Antidote is cholinesterase inhibitors.
Hypercalcemia, hyperkalemia, malignant hyperthermia.
Tubocurarine
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Atracurium
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Amantadine
May increase dopamine release. Antiviral against influenza A and rubella.
Parkinson disease.
Toxicity leads to ataxia.
Selegiline
Selective type B MAO inhibitor.
Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5HT, thereby increasing dopamine availability.
Parkinson disease. Adjunctive agent to L-dopa.
May enhance adverse effects of L-dopa.
Vecuronium
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Rocuronium
Nondepolarizing neuromuscular blocking agent.
Competitive antagonists at Ach receptors.
Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Dantrolene
Prevents the release of Ca from the sarcoplasmic reticulum of skeletal muscle.
Used to treat malignant hyperthermia and neuroleptic malignant syndrome (toxicity of antipsychotic drugs).
Levodopa/carbidopa
Increases level of dopamine in brain. Unlike dopamine, L-dopa can cross BBB and is converted by dopa decarboxylase in CNS to dopamine. Carbidopa is a peripheral decarboxylase inhibitor, and is given with L-dopa to increase the bioavailability of L-dopa in the brain and to limit peripheral side effects.
Parkinson disease
Arrhythmias from increased peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration (“on-off” phenomenon), akinesia between doses.
Memantine
NMDA receptor antagonist. Helps prevent excitotoxicity (mediated by Ca)
Alzheimer disease
Dizziness, confusion, hallucinations
Ropinirole
Non-ergot dopamine agonist.
Parkinson disease.
Amantadine
May increase dopamine release. Antiviral against influenza A and rubella.
Toxicity leads to ataxia.
Entacapone
COMT inhibitor. Prevents L-dopa degradation, increasing dopamine availability.
Parkinson disease.
Tolcapone
Prevents L-dopa degradation, increasing dopamine availability.
Parkinson disease.
Benztropine
Antimuscarinic. Curbs excess Ach.
Improves tremor and rigidity in Parkinson disease. Little effect on bradykinesia.
Donepezil
AchE inhibitor
Alzheimer disease
Nausea, dizziness, insomnia
Galantamine
AchE inhibitor
Alzheimer disease
Nausea, dizziness, insomnia
Rivastigmine
AchE inhibitor
Alzheimer disease
Nausea, dizziness, insomnia
Tetrabenazine
Inhibits vesicular monoamine transporter (VMAT), limits dopamine vesicle packaging and release
Huntington disease
Reserpine
Inhibits vesicular monoamine transporter (VMAT), limits dopamine vesicle packaging and release
Huntington disease
Haloperidol
Dopamine receptor antagonist
Huntington disease
Sumatriptan
5HT-1B/1D agonist. Inhibits trigeminal activation; prevents vasoactive peptide release. Induces vasoconstriction. Half life < 2 hours. Acute migraine, cluster headache attacks Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild tingling.
Ethosuximide
Antiepileptic
Blocks thalamic T-type calcium channels
Absence seizures
GI distress, fatigue, headache, urticaria, Steven-Johnson syndrome.
Phenytoin
Antiepileptic
Increases Na channel inactivation. Fosphenytoin for parenteral use.
Simple, complex, tonic-clonic (first line) seizures and status epilepticus (first line prophylaxis)
Zero order kinetics. Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, teratogenesis, SLE-like syndrome, cytochrome P-450 induction, lymphadenopathy, Stevens-Johnson syndrome, osteopenia
Carbamazepine
Antiepileptic
Increases sodium channel inactivation
First line treatment for simple, complex, and tonic-clonic seizures and first-line treatment for trigeminal neuralgia
Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450, SIADH, Stevens-Johnson syndrome.
Valproic acid (valproate)
Antiepileptic
Increases sodium channel inactivation and increases GABA concentration by inhibiting GABA transaminase
Simple, complex, tonic-clonic (first line), myoclonic, and absence seizures. Bipolar disorder.
GI dress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects, tremor, weight gain, contraindicated in pregnancy.
Gabapentin
Antiepileptic
Primarily inhibits high voltage-activated calcium channels. Designed as a GABA analog.
Simple, complex, and tonic-clonic seizures. Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, and bipolar disorder.
Sedation, ataxia.
Phenobarbital
Antiepileptic
Increases GABA-A action
Simple, complex, and tonic-clonic seizures. First line in neonates.
Sedation, tolerance, dependence, induction of cytochrome P-450, cardiorespiratory depression
Topiramate
Antiepileptic
Blocks Na channels, increases GABA action
Simple, complex, and tonic-clonic seizures. Also used for migraine prevention.
Sedation, mental dulling, kidney stones, weight loss.
Lamotrigine
Antiepileptic
Blocks voltage-gated Na channels. Simple, complex, tonic-clonic, and absence seizures.
Stevens-Johnson syndrome. Titrate slowly.
Levetiracetam
Antiepileptic
Unknown mechanism. Possibly related to modulation of GABA and glutamate release.
Simple, complex, and tonic-clonic seizures.
Tiagabine
Antiepileptic
Increases GABA by inhibiting reputake
Simple and complex seizures
Vigabatrin
Antiepileptic
Increases GABA by inhibiting reuptake
Simple and complex seizures
