NURS 5461 Seizures New Exam With Complete
Solutions 100% Verified
Pathophysiology - ANSWER Much of the excitatory activity in the brain is via
glutamatergic synapses, and increasing the amount or the effect of glutamate in the
brain—which predisposes one to seizures Glutamate depolarizes neurons by activating
specific receptors that open channels for small cations [Na+ and K+]—referred to as
ionotropic receptors CNS contains at least 3 different ionotropic glutamate receptors
High levels of agonists [cocaine; angel dust] can induce seizures These agonists bind to
receptors and activate it to produce the seizure
Pathophysiology - ANSWER Much of the inhibitory messages that occur in the brain
occurs via gamma-aminobutyric acid [GABA] synapses Neurons use GABA to prevent
spread of abnormal bursts of neuron discharge Reducing GABA predisposes one to
seizures—drugs that interfere with synthesis of GABA, lack of Vitamin B6, which helps
biosynthesize GABA can cause epilepsy Drugs that interfere with GABA receptors or
with GABA binding to receptors [bicuculline, PCN, picrotoxin] can cause seizures
Gabapentin and Pregabalin - ANSWER drugs to increase GABA,GABA agonists have the
opposite effect—counteract the tendency to have a seizure
GABA agonists - ANSWER Benzodiazepines, Barbiturates
* Tiagabine and Vigabatrin both work to enhance GABA mediated inhibitory circuits
kindling - ANSWER Abnormal metabolic activities that occur with seizures can produce
long-term changes in brain circuits that make future seizures more likely
Subjective Presentation - ANSWER With new onset seizures Any recent headache?
Recent illness/trauma? Focal neuro deficit? Lightheadedness? History of
TIA/stroke?Description is important! Any warning of event? Gastric sensation Feeling of
déjà' vu Suggest **temporal lobe seizure
, Any of these suggest true epileptic seizure - ANSWER Incontinence Injury Tongue biting
Lateral weakness Headache Post ictal confusion
Post ictal state is the end of a seizure - ANSWER Represents transition from seizure
back to normal Recovery period for the brain Lasts seconds to hours
Objective Presentation - ANSWER If exam is within minutes or hours of event—are
postictal signs present—confusion, depressed LOC or Todd's paralysis If exam done
some time after last seizure—main goal is to determine if there is any baseline
neurological dysfunction [suggesting a brain legion]; assess for papilledema, cardiac
murmur or arrhythmia [that could suggest syncope]
Clinical Manifestations of Focal Seizures with Impaired Consciousness [CPS] - ANSWER
Temporal Epigastric sensation Déjà' vu Altered LOC Oral, hand automatisms Moderate
postictal confusion 75-85%
Frontal Dizziness or fear Abrupt onset, rapid clearing Frenetic behavior Sexual
automatisms Most occur during sleep 10-15%
Parietal Sensory With or without altered LOC Often begins with numbness, tingling or
pain Rare
Occipital Visual May begin with eye twitching May include visual hallucinations May
include ictal blindness 5-15%
Diagnostics - ANSWER Tests may include: EKG CBC Glucose Electrolytes [including
LFTs] Ca++ UA Drug screen / blood alcohol level. Blood levels to assess AED levels [if
the patient is taking AEDs] Serum prolactin-will be high in true sz.CK Lactate **Those
with a first-time seizure should have a CT or MRI to look for a structural lesion
EEG - ANSWER Many patients with partial seizures show no EEG abnormality; therefore,
normal recording does not rule out epilepsy Generalized seizures often produce spike
and wave activity or generalized slowing If diagnosis of seizure disorder cannot be
made after H/P, EEG +/- imaging studies, referral to an epilepsy center should be
ordered
If infection suspected - ANSWER LP indicated in Patient has history of CA that could met
to meninges Rule out structural lesion 1st
Solutions 100% Verified
Pathophysiology - ANSWER Much of the excitatory activity in the brain is via
glutamatergic synapses, and increasing the amount or the effect of glutamate in the
brain—which predisposes one to seizures Glutamate depolarizes neurons by activating
specific receptors that open channels for small cations [Na+ and K+]—referred to as
ionotropic receptors CNS contains at least 3 different ionotropic glutamate receptors
High levels of agonists [cocaine; angel dust] can induce seizures These agonists bind to
receptors and activate it to produce the seizure
Pathophysiology - ANSWER Much of the inhibitory messages that occur in the brain
occurs via gamma-aminobutyric acid [GABA] synapses Neurons use GABA to prevent
spread of abnormal bursts of neuron discharge Reducing GABA predisposes one to
seizures—drugs that interfere with synthesis of GABA, lack of Vitamin B6, which helps
biosynthesize GABA can cause epilepsy Drugs that interfere with GABA receptors or
with GABA binding to receptors [bicuculline, PCN, picrotoxin] can cause seizures
Gabapentin and Pregabalin - ANSWER drugs to increase GABA,GABA agonists have the
opposite effect—counteract the tendency to have a seizure
GABA agonists - ANSWER Benzodiazepines, Barbiturates
* Tiagabine and Vigabatrin both work to enhance GABA mediated inhibitory circuits
kindling - ANSWER Abnormal metabolic activities that occur with seizures can produce
long-term changes in brain circuits that make future seizures more likely
Subjective Presentation - ANSWER With new onset seizures Any recent headache?
Recent illness/trauma? Focal neuro deficit? Lightheadedness? History of
TIA/stroke?Description is important! Any warning of event? Gastric sensation Feeling of
déjà' vu Suggest **temporal lobe seizure
, Any of these suggest true epileptic seizure - ANSWER Incontinence Injury Tongue biting
Lateral weakness Headache Post ictal confusion
Post ictal state is the end of a seizure - ANSWER Represents transition from seizure
back to normal Recovery period for the brain Lasts seconds to hours
Objective Presentation - ANSWER If exam is within minutes or hours of event—are
postictal signs present—confusion, depressed LOC or Todd's paralysis If exam done
some time after last seizure—main goal is to determine if there is any baseline
neurological dysfunction [suggesting a brain legion]; assess for papilledema, cardiac
murmur or arrhythmia [that could suggest syncope]
Clinical Manifestations of Focal Seizures with Impaired Consciousness [CPS] - ANSWER
Temporal Epigastric sensation Déjà' vu Altered LOC Oral, hand automatisms Moderate
postictal confusion 75-85%
Frontal Dizziness or fear Abrupt onset, rapid clearing Frenetic behavior Sexual
automatisms Most occur during sleep 10-15%
Parietal Sensory With or without altered LOC Often begins with numbness, tingling or
pain Rare
Occipital Visual May begin with eye twitching May include visual hallucinations May
include ictal blindness 5-15%
Diagnostics - ANSWER Tests may include: EKG CBC Glucose Electrolytes [including
LFTs] Ca++ UA Drug screen / blood alcohol level. Blood levels to assess AED levels [if
the patient is taking AEDs] Serum prolactin-will be high in true sz.CK Lactate **Those
with a first-time seizure should have a CT or MRI to look for a structural lesion
EEG - ANSWER Many patients with partial seizures show no EEG abnormality; therefore,
normal recording does not rule out epilepsy Generalized seizures often produce spike
and wave activity or generalized slowing If diagnosis of seizure disorder cannot be
made after H/P, EEG +/- imaging studies, referral to an epilepsy center should be
ordered
If infection suspected - ANSWER LP indicated in Patient has history of CA that could met
to meninges Rule out structural lesion 1st
