exam2 Flashcards
describe the 2 phases in a generalized motor onset seizure
- tonic-clonic: bilateral stiffening and jerking (1-3min)
- post ictal (min to hrs) : lethargic, deep/slow breaths
describe the symptoms of a non-motor generalized onset seizure
- absence phase (s): behavioral arrest
- no post ictal phase
which type of generalized onset seizure is most often occuring in children?
non-motor/absent seizures
what are the 2 types of focal onset seizures?
- aware/motor
- unaware/non motor
a focal motor onset seizure….
- occurs in?
- symptoms ?
- post ictal phase
- duration
- frontal lobe
- unilateral arm/face/leg jerking activity and stiffened posture
- none
- 45s to 4min
which type of seizure is associated with the jacksonian march
focal motor
a focal non-motor onset seizure….
- occurs in?
- symptoms ?
- post ictal phase
- duration
- temporal lobe
- aura/automatism/non-purposeful movements
- confusion and amnesia to event
- 45s to 4min
why is it hard to diagnose a seizure correctly if its onset is unilateral but spreads bilaterally
symptoms will mimic a generalized onset seizure and potentially be misdiagnosed
what are the three main childhood epilepsy syndromes? at what ages do they typically occur?
infancy - west syndrome
infancy/early childhood - dravet syndrome
childhood - lennox gastaut syndrome
list some key concepts about lennox gastaut syndrome
- can be many seizure types
- cognitive impairment occurs
- slow spikes on EEG signify presence of syndrome
list some key concepts about dravet syndrome
- Na+ channel mutation
- cardiac morbidities
- worsens with fever
- can be many seizure types
lennox gastaut and dravet syndromes are associated in what way?
they are both ineffective with most medicine, but have similar symptoms that can be improved with CBD
name the seizure type that is typically resolved by early adolescence and describe some key features
childhood absence seizures
- normal neurodevelopment
- treated with Ethosuximide
- 5-7yrs old
- generalized non motor seizures
- 3Hz spike on EEG is present
name the seizure type that is typically resolved by mid teenage years and describe some key features
Rolandic Epilepsy (centrotemporal)
- 7-8yrs old
- nocturnal, focal hemi-clonic seizures
- treatment is a risk benefit discussion
Juvenile Myoclonic Epilepsy symptoms include?
- tonic clonic phase
- occasional absence seizures
- photsensitivity
Juvenile Myoclonic Epilepsy is triggered by and describe the medication.
triggered by:
- sleep deprivation
- alcohol
medications are effective but life long
febrile seizures can be ___1.___ if theyre less than 15 minutes long or ___2.____ if they are longer than 15 minutes. This peaks at __3.____. Treatments are typically __4._____. Children who have febrile seizures have a ____5.____ % chance of developing epilepsy if they have ___6.___ seizures.
- simple non-focal
- complex focal
- 18 months
- supported
- 2-5
- complex
Which childhood epilepsy syndromes do not resolve as children get older
lennox gastaut, dravet, west
west syndrome is a type of childhood epilepsy syndrome that can be described by
- infantile spasms
- developmental aggression
- hypsarrhythmia (extreme disorganization)
seizures fall into which two categories
provoked and unprovoked
which type of seizure (provoked/unprovoked) are more likely to recur
unprovoked
describe a provoked seizure
- acute symptoms
- less than 7 days between
- caused by stroke, infection, TBI
describe an unprovoked seizure
- remote symptoms
- more than 7 days between
- caused by random events or tumors
if someone has 2 unprovoked seizures, their chances of recurring are up to _____%
60
what are the 4 etiologies of seizures?
- metabolics
- substances
- structural insults
- genetics
genetic factors are involved in about how many seizure cases?
2/3
Whole exome sequencing is helpful….
for precision medicine
describe seizure progression
Aura, ictal, post ictal, interictal, repeat
describe the DSM-5 criteria for diagnosing someone with schizophrenia
- must experience at least two - delusions, hallucinations, disorganized speech, catatonic behavior, negative symptoms
- decrease in level of function
- continuous signs of disturbance for more than 6 months
- ruled out schizoaffective and mood disorders
- not caused by substances or other medical conditions
- diagnosis only if prominent delusions or hallucinations are present in patients with autism
what percent of people are diagnosed with schizophrenia?
1%
what 4 pathways play a role in schizophrenia - describe each
- mesolimbic - behavior regulation + cause delusions/hallucinations when overactive
- nigrostriatal - controls movement, EPS when dopamine is blocked
- mesocortical - executive fxn, - symptoms when dopamine is blocked
- tuberoinfundibular - regulates prolactin release, increases w/dopamine blocked and is where side effects originate from treatments
what are some generalized side effects from schizophrenia treatments and which drug groups treat them
- parkinsonism - tremor - treated w/anticholinergic meds
- acute dystonia - involuntary spasm - treated w/ intramuscular benztropine
- akathisia - restlessness - treated w/hydrophobic b-blockers
the dopamine hypothesis suggests
- dopamine mimetics worsen symptoms (cocaine)
- dopamine receptor antagonists improve symptoms
- schizophrenia is caused by overabundance of dopamine
what are some key receptors involved in schizophrenia and what generally do each do
D2, D3, D4 - inhibitory
D1, D5 - stimulatory
describe how epilepsy differs in women
estrogen is a proconvulsant and progesterone is an anticonvulsant so medications need to be monitored and adjusted
describe how epilepsy differs in eldery
- mostly focal and staticus seizures with prolonged post-ictal phases
- 1.7 year average time from symptom onset to diagnosis due to misinterpretation of symptoms in elderly
what are some treatment challenges with elderly epilepsy
- removing or adding inhibitory/inducing medications impacts everything
- medicine interactions and efficacy in elderly are impacted
what are some of the genes susceptible to mutation in schizophrenia
DISC1, dysbindin, neureglin
what are the big ideas behind glutamate drug treatments for schizophrenia
they looked promising in clincal phases early, but the most promising even failed in phase 3
describe a general overview of the progression of treatment for schizophrenia
- 1900-1950s frontal lobotomy and ECT were main treatments
- in the 1950s chlorpromazine was the first drug to be productive at treatments
- in 1960s typical antipsychotic drugs were developed but had bad side effected
- in the 1990s atypical antipsychotic drugs were developed but some side effects prolonged after usaged
- 2000s developed next gen atypical antipsychotics that are used today
typical antipsychotics
- which receptors
- induce what side effects
- example
- relationship with dopaminergic neurons
-D2
- induced EPS and tardive dyskinesia - elevate serum prolactin
- haloperidol
- induce depolarization blockade of S.Nigra and VTA dop neurons
atypical antipsychotics
- which receptors
- induce what side effects
- example
- relationship with dopaminergic neurons
- 5HT2A/D2
- no EPS or tardive dyskinesia or serum elevation - longer lasting than typical
- clozapine
- induce depolarizations blockade of VTA dop neurons
what does the glutamatergic deficiency tell us about schizophrenia
the decrease in dendritic spines, increase in glutamatergic tone leading to cell death, and decreased inhibition of GABA causing excessive stimulation could be the closest thing to pathology for schizophrenia
key differences because epilepsy and orthostatic hypertension
OH- triggered by position changes, quick recovery, negative motor and brief myoclonus, light headed vague aura and orthostatic vital signs, low volume status and autonomic dysfunction history
key differences because epilepsy and transient ischemic attack
TIA- lasts min to days, negative motor and sensory, no aura, vascular risk factors
key differences because epilepsy and PNES
PNES- anxiety or stress inducing, last 5-30min, headache following, forced eye closure, prior history of trauma or psychiatric disease
key differences because epilepsy and migraines
M - triggered by food or smells, last hours to days, aura followed by headache, family history of migraines
key differences because epilepsy and vasovagal syncope
VS- triggered by needles, negative motor symptoms and myoclonus for a few seconds, vague aura of light headedness and palpitations, no neurological risk factors
key differences because epilepsy and cardiac arrhythmia
CA- negative motor symptoms, family history of cardiac syndromes, last seconds to minutes and similar recovery time
