Antiseizure meds Flashcards
Mechanisms of seizures
Paroxysmal discharges –> synchronization and recruitment of large population of cortical/thalamic neurons
Enhanced glutamate/deficient GABA –> propagation of abnormal activity
Seizure sequence
focal epileptogenesis –> synchronization –> propagation
Primary causes of seizure
genetic, idiopathic
Secondary causes of seizure
mechanical (trauma, tumor), metabolic (hypoxia, hypoglycemia, hypocalcemia, alkalosis), withdrawal from CNS depressant, toxins
Tonic-clonic seizures
Grand mal. 30%. High amplitude EEG spikes at 15-40 Hz
loss of postural control; LOC; tonic phase (rigid extension of trunk and limbs), clonic phase (rhythmic contraction of arms and legs)
Tonic-clonic mechanism
Initiation: loss of GABA
Propagation: loss of GABA, increased glu response, Na channel excitation
Absence seizures
petit mal. 3 Hz EEG. Children.
Normal muscle tone; impaired consciousness with staring spells; no postictal state
Absence seizure mechanism
inappropriate activation of low-threshold T-type Ca channels
Simple partial seizure
preserved consciousness
Complex partial seizure
loss/impaired consciousness, psychomotor (limbic, temporal/frontal cortex)
can develop to secondary generalized
Partial seizure mechanism
involves initiation instead of propogation –> more difficult to treat
Primary generalized tonic-clonic seizure drug choice
Valproate or lamotrigine or levetiracetam
Partial seizure treatment
carbamazepine or lamotrigine or levetiracetam
Absence seizure treatment
Ethosuximide or valproate
Atypical absence, myoclonic, atonic seizure treatment
valproate or lamotrigine, or leviteracetam
Use of VSSC blockers
Tonic-clonic seizures. block high-frequency, repetitive firing of APs. Use-dependent
Phenytoin, carbamazepine, lamotrigine, topiramate, valproate,
T-type Ca channel blockers
ethosuximide
Use of high-voltage activated Ca channel blockers (N-type)
blocks neurotransmitter release
Benzos and phenobarbital action
facilitate GABA-mediated opening of Cl channels