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26 Cards in this Set
- Front
- Back
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partial seizure
- simple |
- seizure onset is Focal in the brain
- no loss of consciousness - often described as "aura" that precedes seizures - Motor - rhythmic shaking of contralateral body, if involving frontal eye fields, eyes also driven contralaterally (toward shaking) - Sensory - a. somatosensory - postcentral gyrus - "breeze" or numbness/tingling b. visual - occipital lobe c. auditory - temporal lobe d. gustatory-olfactory - temporal lobe (UNCUS) - foul odor (ie "burnt rubber") - Autonomic - LIMBIC SYSTEM - Psychic - LIMBIC SYSTEM - deja vu, jamais vu (feeling of unfamiliarity in a familiar place), FEAR (most common), anger |
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partial seizure
- complex - hallmark? |
- Altered level of consciousness!
- *AUTOMATISMS - stereotypic, repetitive actions (lip smacking, chewing, picking at clothes, nose picking) - may begin as partial simple seizures |
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secondary generalization, "grand mal"
- phases - symptoms |
- generalized tonic-clonic seizure which began as a partial simple or partial complex seizure
- phases 1. symptom is a "crying out" - early contrxn of truncal musculature 2. followed by tonic (stiff) phase, often w/ arms elevated and pronated 3. followed by clonic (shaking) phase - in adults are brief, 1-2 minutes - symptoms a. bite their tongue b. lose urine c. may fall and injure themselves d. **postictal period - patients feel sleepy and drowsy for 20-30 mins. Hyperventilation to compensate for the acidosis |
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generalized seizures (seizure onset is Generalized in the brain)
-- absence (petit mal) - which population? - symptoms? - triggers? - **specific dx? |
- exclusively in childhood
- multiple STaring spells (up to hundreds per day) - seizure threshold is reduced by hyperventilation (can be triggered in office by asking to hyperventilate) - ***specific EEG finding of generalized 3Hz SPIKE AND WAVE ACTIVITY |
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generalized seizures
-- primary-generalized seizures - although activity is throughout the cortex, onset occurs where in brain? |
- thalamus! - millions of thalamocortical connections --> cortical neurons simultaneously activated
- lack of focal description (no foul smell, focal shaking, automatisms, etc) |
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generalized seizures
-- atonic |
brief sudden loss of muscle tone
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generalized seizures
-- tonic |
brief episode of stiffening
- most pure atonic/tonic seizures are seen in developmentally delayed children that have multiple seizure types |
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generalized seizures
-- myoclonic |
sudden jerk-like motions w/o loss of consciousness (unlike all other generalized-onset seizures)
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pseudoseizures
- a/w? - features: - physical - timing - trigger - response to meds - postictal phase? - motivation |
- non-epileptic (non-electrical) events
- most a/w psychological factors (ie depression, anxiety, malingering) - features: - atypical movements - wild thrashing, side-to-side head movements, arrhythmic and asynchronous, pelvic thrusting - hours at a time! - triggered by emotional stimulus - never any response to meds! - NO postictal phase - patient has obvious gain (litigation, attention) |
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EYE indications in seizure vs pseudoseizure
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- pts with pseudoseizures CLOSED their eyes
- pts with true seizures OPENED their eyes |
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etiology
- etiology - things to do |
- any structural lesion that involves the CEREBRAL CORTEX (subcortical lesions are unlikely to produce seizures)
- idiopathic very common - children - genetic, high fever, birth trauma - adults - cerebrovascular dz - do: 1. Hx 2. neuro examination 3. *MRI imaging (temporal lobe most common) 4. EEG |
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EEG
- measuring what - good for determing ______ vs ______ |
- EEG generated by inhibitory and excitatory postsynaptic potentials of cortical neurons
- FOCAL vs GENERAL onset - for single EEG, chances of seeing electrical seizure activity on epileptic patient is 50-60%, thus need to repeat. By third EEG, 80-90% - video EEG is gold standard |
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seizure vs syncope
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syncope
- no postictal confusion! - light-headedness prior to spell/passing out |
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MOA for tx of
1. partial onset seizures 2. generalized onset seizures |
1. inactivation of VG Na+ channels (inhibits the sustained, repetitive firing of neurons)
OR enhanced action of GABA 2. blocks VG Ca2+ channel (low-threshold (T) Ca2+ current) |
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list the
- conventional anticonvulsants - newer anticonvulsants |
- conventional
1.phenytoin (dilantin) 2. carbamazepine (tegretol) 3. phenobarbital 4. valproic acid (depakote) 5. benzadiazepine - newer 1. lamotrigine (lamictal) 2. levitiracetam (keppra) 3. topiramate (topamax) |
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takes how many half lives of these drugs to reach steady state in blood?
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5 half lives!
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phenytoin (dilantin)
- MOA - half-life - *unique properties - *acute sfx - chronic sfx |
- inhibits VG Na+ channels
- 24 hours (5 days to reach SS) - ***NONLINEARITY OF ELIMINATION KINETICS results in a disproportionate rise in the phenytoin blood level with a small increase in the dose!!! - can be loaded IV (good for hospital use) - acute = *cerebellar/vestibular toxicity - ataxia, nausea/vomiting, vertigo, NYSTAGMUS - rapid IV loading - cardiac arrhythmias and hypotension - chronic = GINGIVAL hyperplasia, peripheral neuropathy, osteomalacia |
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carbamazepine (tegretol)
- MOA - **sfx |
- inhibits VG Na+ channels
- *diplopia - *aplastic anemia (requires periodic blood testing) - *SIADH with hyponatremia (syndrome of inappropriate ADH hypersecretion) - check sodium/electrolyte levels! |
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phenobarbital
- MOA - half-life - *sfx |
- increases GABA-A receptor-mediated currents
- 96 hours! (3 weeks for SS) - can be given IV - *sedation and slowed mentation (primary reason it's not used) - bad for children |
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primidone (unique drug!!)
- MOA - DOC |
- metabolized to phenobarbital and phenylethylmalonamide (PEMA)
- rarely used for epilepsy - one of the two DOCs for *ESSENTIAL TREMOR! |
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valproic acid (depakote)
- MOA - *unique properties - sfx |
- MOA several: (and thus, effective for BOTH general & partial seizures)
1. inhibits VG Na+ channels 2. reduces low-threshold (T) Ca2+ current 3. elevated GABA lvls in brain - like phenytoin, highly protein bound --> displace phenytoin from albumin --> SYMPTOMS of phenytoin toxicity --> although, phenytoin blood levels MAY BE NORMAL --> requires assessment of FREE phenytoin levels - TREmor, stimulation of appetite with weight gain, fatal fulminate hepatitis (many have elevated liver enzymes), acute pancreatitis and hyperammonemia |
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benzodiazepines (lorazepam, and diazepam [valium])
- exclusively for tx of: - very short half-life, not effective in prevention of seizures - MOA - sfx |
- status epilepticus (medical emergency, prolonged seizure)
- enhancement of GABA-mediated inhibition - sfx - SEDation - excessive dosing = death due to respiratory sedation |
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ethosuximide
- MOA - *used for? |
- VG T-type Ca2+ channel blocker
- ABSENCE seizures in children |
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lamotrigine
- MOA - **strong interaction with other drug? - DOC - disadvantage |
- inhibits VG N+ channels; may also inhibit glutamate release
- *VPA greatly increases plasma [lamotrigine]. thus, must be started on smaller dose if pt is already on VPA - DOC as anticonvulsant during pregnancy - takes 4 weeks to reach a therapeutic range |
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levitiracetam (keppra)
- advantage - MOA - sfx* |
- therapeutic blood lvls reached much sooner than with lamotrigine
- not clear; but effective for BOTH partial and generalized onset - available IV, good for tx of status epilepticus - irritability and behavioral complaints (caution in patients with underlying depression) |
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topiramate (topamax)
- MOA - **sfx |
- inhibits VG N+ channels; also enhances postsynaptic GABA currents, and limits action of glutamate R
- since is weak carbonic anhydrase inhibitor, numbness and tingling - most common reason for d/c - CONFUSION/DULL THINKING - *** "WORD FINDING DIFFICULTY" - Weight loss! |
