Seizures and epilepsy (neurological disorder)- AMBOSS.pdf

A is a transient manifestation of abnormal excessive or synchronous electrical brain activity that causes
convulsions, loss of consciousness, and/or lapses of consciousness. The underlying cause of seizures
is a state of
neuronal hyperexcitability, which may be temporary (e.g., due to electrolyte imbalances) or long-lasting (e.g., due to
inherited or acquired neural abnormalities). Provoked occur as a result of various seizures seizure triggers
and
underlying conditions (e.g., stroke, traumatic brain injury, alcohol withdrawal), while unprovoked seizures
occur in the
absence of an identifiable cause. Seizures
can also be classified by onset and degree of CNS involvement (e.g., focal
seizures, ). generalized seizures Epilepsy
is a chronic neurological disorder with diagnostic criteria that are based on
seizure
type, frequency, risk factors, and underlying conditions (e.g., epilepsy syndromes).
Acute complications of seizures
include physical trauma and CNS tissue damage due to hyperthermia, cardiorespiratory
deficits, or excitatory toxicity. Status epilepticus
is a potentially life-threatening condition characterized by continuous
seizure activity for more than 5 minutes that requires immediate management and stabilization. Acute seizures
and
status epilepticus
in adults and children are most oOen initially treated with parenteral benzodiazepines, and then with
the addition of other parenteral antiepileptic drugs (e.g., fosphenytoin) if there is no resolution.
Rapidly reversible causes
of seizures
(e.g., hypoglycemia) should also be managed concurrently. The underlying cause is investigated based on a
combination of clinical evaluation (e.g., , identifying seizure classification seizure triggers
), laboratory studies, and
neuroimaging. Electroencephalography (EEG) can provide additional evidence to support the diagnosis, although a
normal EEG between seizures epilepsy treatment of
does not rule out . Important antiepileptic drugs for the long-term
epilepsy include lamotrigine (first-line treatment in focal seizures), valproate (first-line treatment in generalized seizures
),
and ethosuximide (first-line treatment in absence seizures). Appropriate medical treatment allows the majority of
patients to remain seizure-free in the long term and prevents long-term complications such as psychiatric conditions
(e.g., anxiety, depression, psychosis), sleep disorders, and sudden unexpected death in epilepsy ( ); however,
SUDEP
patients must be monitored for adverse effects of medications (e.g., bone disease). Epilepsy
pregnant individuals, children) also may require specific considerations for management.

1. Seizures and epilepsy
(Seizure disorders)
Last edited: Dec 05, 2024
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Summary
A is a transient manifestation of abnormal excessive or synchronous electrical brain activity that causes
convulsions, loss of consciousness, and/or lapses of consciousness. The underlying cause of is a state of
neuronal hyperexcitability, which may be temporary (e.g., due to electrolyte imbalances) or long-lasting (e.g., due to
inherited or acquired neural abnormalities). occur as a result of various and
underlying conditions (e.g., stroke, traumatic brain injury, alcohol withdrawal), while occur in the
absence of an identifiable cause. can also be classified by onset and degree of CNS involvement (e.g., focal
seizures, ). is a chronic neurological disorder with diagnostic criteria that are based on
type, frequency, risk factors, and underlying conditions (e.g., epilepsy syndromes).
Acute complications of include physical trauma and CNS tissue damage due to hyperthermia, cardiorespiratory
deficits, or excitatory toxicity. is a potentially life-threatening condition characterized by continuous
activity for more than 5 minutes that requires immediate management and stabilization. Acute and
in adults and children are most oOen initially treated with parenteral benzodiazepines, and then with
the addition of other parenteral antiepileptic drugs (e.g., fosphenytoin) if there is no resolution.
(e.g., hypoglycemia) should also be managed concurrently. The underlying cause is investigated based on a
combination of clinical evaluation (e.g., , identifying ), laboratory studies, and
neuroimaging. Electroencephalography (EEG) can provide additional evidence to support the diagnosis, although a
normal EEG between does not rule out . Important antiepileptic drugs for the long-term
include lamotrigine (first-line treatment in focal seizures), valproate (first-line treatment in ),
and ethosuximide (first-line treatment in absence seizures). Appropriate medical treatment allows the majority of
patients to remain seizure-free in the long term and prevents long-term complications such as psychiatric conditions
(e.g., anxiety, depression, psychosis), sleep disorders, and ( ); however,
patients must be monitored for adverse effects of medications (e.g., bone disease). in certain groups (e.g.,
pregnant individuals, children) also may require specific considerations for management.
For information on individual epilepsy syndromes, see “Generalized epilepsy in childhood.”
COLLAPSE NOTES FEEDBACK
Definitions
QBANK SESSION
seizure
seizures
Provoked seizures seizure triggers
unprovoked seizures
Seizures
generalized seizuresEpilepsy
seizure
seizures
Status epilepticus
seizure seizures
status epilepticus
Rapidly reversible causes
of seizures
seizure classification seizure triggers
seizures epilepsy treatment of
epilepsy generalized seizures
sudden unexpected death in epilepsySUDEP
Epilepsy
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TSTUDENT seizures and epilepsy

2. For information on individual epilepsy syndromes, see “Generalized epilepsy in childhood.”
COLLAPSE NOTES FEEDBACK
Definitions

Seizure: an excessive and/or hypersynchronous activity of cortical neurons that results in transient neurological symptoms
Acute symptomatic seizure ( ): a that occurs at the time or soon aAer the onset of an acute systemic
or CNS condition. Examples include:
Within 1 week of stroke, traumatic brain injury (TBI), anoxic encephalopathy, or intracranial surgery
Subdural hematoma
Acute CNS infection
Exacerbation of multiple sclerosis or other autoimmune diseases
Metabolic disturbances
Drug/alcohol intoxication or withdrawal
Reflex seizure: a constantly evoked by a particular stimulus (trigger) that lowers threshold (e.g., flashing lights;
see “ ”)
Unprovoked seizure: a that occurs in the absence of an identifiable cause or beyond the specified interval aAer an
acute CNS condition
Descriptors: the following terms are used to describe events, clinical features, and EEG signs related to
Ictal: occurring during a
Interictal: occurring between the
Postictal: occurring signs aAer a
Epilepsy
: a chronic neurologic disorder characterized by a predisposition to as defined by one of the following:
Two or more unprovoked or separated by more than 24 hours
One unprovoked or in an individual with a high risk of subsequent (e.g., aAer traumatic brain injury,
stroke, CNS infections)
Diagnosis of an epilepsy syndrome: a group of characterized by a set of features typically occurring
together.
Common features include triggers, age of onset, EEG paZerns, radiological findings, and associated conditions (e.g.,
depression and other mood disorders, psychosis, and anxiety disorders)
For more information about individual epilepsy syndromes, see “Generalized epilepsy in childhood.”
Reflex epilepsy: in which are consistently provoked by a certain trigger (e.g., lights, music, hormonal changes
during menstrual cycle). Subtypes can be determined based on the trigger and include:
Photosensitive epilepsy
Musicogenic epilepsy
Catamenial epilepsy
Seizures
[1]
provoked seizureseizure
[2]
seizure seizure
Seizure triggers
seizure
[1]
seizures
[3]
seizure
seizures
seizure
[1]
Epilepsy seizures
[1][4]
reflex seizures
reflex seizure seizures
epileptic disorders
Epilepsy seizures
Seizures and epilepsyDefinitions
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TSTUDENT seizures and epilepsy
A chronic, demyelinating disease of the CNS caused by an immune-mediated inflammatory process. The clinical course is
usually characterized by exacerbations with periods of remission in between. Initial manifestations include internuclear
ophthalmoplegia and retrobulbar neuritis, followed by loss of vibration and touch, upper motor neuron weakness, Charcot's
neurological triad, cranial nerve palsies, and autonomic dysfunction.
High risk is defined as ≥ 60% over the course of 10 years.
a

3. Reflex epilepsy: in which are consistently provoked by a certain trigger (e.g., lights, music, hormonal changes
during menstrual cycle). Subtypes can be determined based on the trigger and include:
Photosensitive epilepsy
Musicogenic epilepsy
Catamenial epilepsy
Drug-resistant epilepsy: in which at least two antiepileptic drugs (administered as sequential monotherapies or as
combination therapy) have failed to prevent
Resolved epilepsy
An age-dependent epilepsy syndrome that has not recurred in individuals who are now past the applicable age.
No recurring for 10 years in individuals who have not taken antiepileptic drugs for at least the last 5 years.
COLLAPSE NOTES FEEDBACK
Epidemiology
Incidence of : 61 per 100,000 population
Incidence of : 79.1 per 100,000 population
Prevalence of : 8.5 per 1,000 population
Epidemiological data refers to the US, unless otherwise specified.
COLLAPSE NOTES FEEDBACK
Etiology
Seizure triggers
are stimuli that can precipitate both in people with and without .
Excessive physical exertion
Alcohol consumption
Fever (febrile seizures)
Sleep deprivation
Flashing lights (e.g., strobe lights, video games)
Music
Hormonal changes (e.g., at different phases of the menstrual cycle, aUer menopause)
Medication-related issues in patients with known : e.g., poor adherence, recent changes in drug doses or formulation,
new medication interactions
Epilepsy seizures
epilepsy
seizures
[5][6]
seizures
A single or multiple provoked or triggered (e.g., febrile seizures) without an underlying
predisposition to do not suffice for the diagnosis of .
seizure seizures
seizures epilepsy
unprovoked seizures
[7]
epilepsy
[8]
epilepsy
[8]
[9]
Seizure triggers seizures epilepsy
[10]
[11]
epilepsy
Seizures and epilepsyDefinitions
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TSTUDENT seizures and epilepsy
Epilepsy in which seizures coincide with certain phases of the menstrual cycle (e.g., periovulatory seizures, perimenstrual seizures)
30% of all epilepsies are drug-resistant.
Fever is the most common trigger in children. Although febrile seizures do not meet the definition of epilepsy, complex febrile seizures and a
particular type of genetic epilepsy, known as “febrile seizure plus,” are associated with an increased risk of developing epilepsy at a later stage.
The pathogenesis of music-induced seizuresis unclear; emotional response to music rather than the sound
itself is suggested to provoke seizures, although pure tones have also been reported as seizure triggers.
I
2
3
4
3
6
7
8

4. Hormonal changes (e.g., at different phases of the menstrual cycle, a9er menopause)
Medication-related issues in patients with known : e.g., poor adherence, recent changes in drug doses or formulation,
new medication interactions
Causes of
TBI
Stroke
Anoxic encephalopathy
Intracranial surgery
Acute CNS infections (e.g., meningitis, encephalitis)
Electrolyte imbalance (e.g., hypoglycemia, hypocalcemia)
Acute metabolic disturbances (e.g., uremia)
Alcohol withdrawal
Recreational drug use
Prescription drug toxicity
Exacerbations of autoimmune disorders (e.g., SLE)
Common causes of
Genetic
Genetic mutations affecting ion channels or transmiNer receptors (e.g., mutations in KCNQ2 or SCN1A genes)
Chromosomal abnormalities (e.g., Angelman syndrome, Prader-Willi syndrome, ReN syndrome)
Genetic metabolic disorders (e.g., PKU, congenital disorders of glycosylation, lysosomal storage diseases, peroxisomal
biogenesis disorders)
Mitochondrial diseases (e.g., MELAS)
Structural: chronic cerebral lesion or abnormality
Perinatal injury, e.g., hypoxic-ischemic injury
Brain tumors and metastases
Traumatic brain injury (TBI)
Hippocampal sclerosis
Tuberous sclerosis
Congenital cerebral or arteriovenous malformations
Microcephaly, megalocephaly, cortical dysgenesis
Cranial radiation therapy
Metabolic
Inborn errors of metabolism (e.g., organic acidemias, phenylketonuria)
Porphyrias
Immune: autoimmune encephalitides (e.g., anti-NMDA receptor encephalitis), Rasmussen encephalitis
Infectious: chronic CNS infection (e.g., toxoplasmosis, malaria, neurocysticercosis) or complication of acute CNS infection (e.g.,
viral or bacterial meningitis or encephalitis)
epilepsy
acute symptomatic seizures
[2]
epilepsy
[12]
[13]
Seizures and epilepsyEtiology
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TSTUDENT seizures and epilepsy
Traumatic brain injury
Anoxic-ischemic encephalopathy: Global brain injury caused by complete cessation of blood flow (anoxia)
during cardiac arrest. It is the most common cause of death in patients surviving cardiac arrest.
Unintentional drug poisoning is a common cause of seizures in children.
Phenylketonuria: A congenital disorder characterized by the accumulation of phenylalanine in the central nervous system. Can be caused by a defect of phenylalanine hydroxylase
(classic PKU) or deficiency in tetrahydrobiopterin (malignant PKU). Causes psychomotor retardation, seizures, a musty odor, and pale skin/hair (from lack of melanin production).
Seizures starting at least 1 week after the onset of cerebral hypoxia are considered epileptic;
seizures that occur within the first week of perinatal injury are considered acute symptomatic.
Seizures starting at least 1 week after TBI are considered posttraumatic epileptic;
seizuresthat occur within the first week of TBI are considered acute symptomatic
Seizures starting within 1 week of CNS infection are acute symptomatic; seizuresthat occur after 1 week are considered epileptic.

5. Porphyrias
Immune: autoimmune encephalitides (e.g., anti-NMDA receptor encephalitis), Rasmussen encephalitis
Infectious: chronic CNS infection (e.g., toxoplasmosis, malaria, neurocysticercosis) or complication of acute CNS infection (e.g.,
viral or bacterial meningitis or encephalitis)
Causes of according to the age group
COLLAPSE NOTES FEEDBACK
Classification
epilepsy
[14]
MAXIMIZE TABLE TABLE QUIZ
Etiology of in different age groups
Age group at manifestation Causes
Neonates and infants (< 6 months)
Genetic
Congenital structural maldevelopment (e.g., microcephaly, megalocephaly)
Perinatal injury
Perinatal or postnatal infections (e.g., CNS infections)
Metabolic disorders (e.g., hypoglycemia, PKU, hypocalcemia)
In infants aged 1–6 months: West syndrome
Older infants (> 6 months) and children (< 10 years)
Febrile seizures
Genetic (e.g., Rolandic )
Infections
Traumatic brain injury
Congenital brain malformations (e.g., cortical dysgenesis)
Metabolic disorders
Accidental drug poisoning
Adolescents (10–18 years)
Traumatic brain injury
Encephalitis
Genetic disorders
Illicit substance use
Adults (18–60 years)
Alcohol withdrawal
Traumatic brain injury
Illicit substance use
Brain tumors
Infection
Metabolic disorders
Older adults (> 60 years)
Traumatic brain injury
Cerebrovascular disease
Brain tumors
Abscesses
Neurodegenerative diseases
epilepsy
epilepsy
Seizures and epilepsyEtiology
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TSTUDENT seizures and epilepsy
Fever is the most common trigger in children. Febrile seizures are not considered a form of epilepsy;
however, complex febrile seizuresand a particular type of genetic epilepsy, known as febrile seizure
plus, are associated with an increased risk of developing epilepsyat a later stage.

6. Classification
Classification of seizures according to the ILAE 2017 classification
are classified according to localization of abnormal neuronal activity and then further subcategorized based on symptoms and
sometimes level of awareness.
Classification of epilepsy
General considerations
The International League Against (ILAE) recommends a multilevel approach to classifying .
Etiology and comorbidities should be considered at each level of classification.
Levels of classification
For level 1, first determine the type (see “ ” above).
For level 2, then determine the type, which can be:
Focal
The lobe from which originate should be determined.
with focal-to-bilateral is classified as focal.
Generalized: diagnosed in patients with generalized-onset as evidenced by generalized activity (e.g., 3 Hz spike-wave
activity in absence seizures) and/or typical discharges on EEG.
Combined generalized and focal: diagnosed in patients who have both focal-onset and generalized-onset (seen, e.g., in
Dravet syndrome and Lennox-Gastaut syndrome)
Unknown: diagnosed if there is not enough clinical information to classify as focal, generalized, or combined
For level 3, consider epilepsy syndromes (see “Focal seizures and syndromes” and “Generalized epilepsy in childhood” for discussion of
specific syndromes)
[15]
Seizures
MAXIMIZE TABLE TABLE QUIZ
Basic
Focal Generalized Unknown
Location of abnormal
neuronal activity
Originates within the networks of a single hemisphere
Originates from
both hemispheres
Determination of focal or
generalized onset is not possible
Awareness
Aware
Impaired awareness
N/a N/a
Symptoms
Motor onset
Nonmotor onset
Motor
Other motor
Nonmotor
Motor
Other motor
Nonmotor
Other
Focal to bilateral : focal progresses to a paVern
(characteristic of bilateral brain involvement)
N/a Unclassified
* Note: An expanded version of the ILAE 2017 classification also considers further subtypes of motor and nonmotor categories.
classification of seizures
Tonic-clonic Tonic-clonic
tonic-clonic tonic-clonic
[16]
[12]
Epilepsy epilepsy
seizure Classification of seizures
epilepsy
seizures
Epilepsy tonic-clonic seizures
seizures ictal
interictal
seizures
seizures
Seizures and epilepsyClassification
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TSTUDENT seizures and epilepsy
The ILAE recognizes that the
clinical setting and/or patient
presentation does not always
permit a classification across all
three levels. However, classification
at the first level (seizure type)
should always be possible.
Absence seizures: A generalized seizure characterized by transient
unresponsiveness (usually lasting < 20 seconds) without a preceding
aura or postictal lethargy or confusion. Generalized stiffness and
rhythmic jerking seen in tonic-clonic seizures is not seen, but myoclonic
jerks or automatisms of the face may be present. An EEG typically
reveals a spike and wave pattern with a frequency of 2.5-3.5 Hz.
Epilepsy can be
reclassified if
additional
information
becomes available.

7. specific syndromes)
COLLAPSE NOTES FEEDBACK
Clinical features
Focal seizures (formerly partial seizures)
Originate in one brain hemisphere
Usually caused by focal structural abnormalities
Symptoms depend on the anatomical location of the lesion or disturbance within the brain.
For more information about the etiology and symptoms of originating from the cortex of particular brain lobes, see “Focal
seizures and syndromes.”
[10][15][17]
[18]
seizures
MAXIMIZE TABLE TABLE QUIZ
Clinical features of focal seizures
Type Awareness
Focal
May manifest with intact
or impaired awareness
Focal seizures with
impaired awareness
most frequently
originate from the
temporal lobe.
Prodromal symptoms: aura
Neuropsychiatric symptoms (e.g., anxiety, fear, déjà vu)
Usually lasts seconds to minutes
Aware and with impaired awareness are possible
Motor symptoms
Automatisms (e.g., lip smacking, blinking, tapping, exploratory movements with
hands)
Abrupt loss of tone in a muscle group ( )
Myoclonus: brief involuntary twitching of muscle groups
Clonic, involuntary, repetitive movements of the contralateral limbs or facial
muscles.
Tonic contraction of the contralateral limbs
Jacksonian march (march of convulsions): progressive involvement of different
muscle groups
Irregular large amplitude movements such as pedaling, jumping, pelvic
thrusting (hyperkinetic )
Nonmotor symptoms
Autonomic (e.g. flushing, sweating)
Behavioral arrest
Cognitive (e.g., dyslexia, aphasia, anomia, anterograde amnesia)
Emotional (e.g., laughing, crying, feeling fear)
Sensory
Visual (e.g., hallucinations, micropsia, macropsia)
Somatosensory (e.g., paresthesias)
Vestibular (e.g., vertigo)
Auditory (i.e., hearing simple sounds like ringing)
Olfactory (e.g., unusual or intense smells)
Gustatory hallucinations
See “Focal seizures and syndromes” for features according to cortical origin.
Residual transient neurologic
deficits depending on the affected
cerebral region
Todd paralysis:
or paralysis of the involved limb or
facial muscles (can last for minutes
or up to 36 hours)
Prodromal aura may be present.
Starts as unilateral, localized focal symptoms that then progress into a bilateral
Ictal Postictal
[19]
seizuresseizures
atonic seizure
seizure
postictal weakness
Seizures and epilepsyClinical features
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TSTUDENT seizures and epilepsy
The term “partial” has been replaced with the term “focal” to describe seizures that
develop from neurological networks in one hemisphere of the brain.
For more information
about the features of
such seizures, see
“Temporal lobe
epilepsy” in the
“Focal seizures and
syndromes” article.
Aura results from abnormal activity in the brain regions where the seizure originates., and is
currently considered an onset of seizure rather than a distinct phenomenon; however, it is still
regarded as “prodromal” in the literature.
Focal seizures with
impaired awareness
most frequently
originate from the
temporal lobe.
Purely tonic contraction is possible but rare.
Less common than clonic contractions
Abnormal electric activity spreads to neighboring
regions of the same precentral gyrus.
The spreading of
paresthesia or uncontrolled
motor activity during a
simple partial seizure from
a distal part of the body
toward a more proximal
part. Results from seizure
activity that progresses to
the motor cortex.
These deficits can
be easily mistaken
for symptoms of
TIA or stroke.
The exact mechanism of Todd paralysis
is not established yet but is thought to
be caused by focal hypoperfusion, the
prolonged refractory period after cell
depolarization, and prolonged local
inhibition.
-

8. Generalized-onset seizures
Involve one/both hemispheres
Start with loss of consciousness.
Patients do not recall the .
Olfactory (e.g., unusual or intense smells)
Gustatory hallucinations
See “Focal seizures and syndromes” for features according to cortical origin.
Focal to
bilateral
Progresses to loss of
consciousness
Prodromal aura may be present.
Starts as unilateral, localized focal symptoms that then progress into a bilateral
generalized phase: Initial focal symptoms may go unnoticed if the condition
progresses rapidly, leading to a potential misdiagnosis of
and inappropriate therapy.
Bilateral generalized phase
Loss of consciousness
Motor symptoms: See “ ” in the table below.
Bladder or bowel incontinence
Confusion
Drowsiness
Agitation
Fatigue
May not recall the focal onset
tonic-
clonic
generalized-onset
seizures
Tonic-clonic seizure
If focal to bilateral type progresses rapidly to the bilateral generalized phase, initial focal symptoms may go
unnoticed, leading to a potential misdiagnosis of and inappropriate therapy.
tonic-clonic
generalized-onset seizures
[10][20][21]
seizure
MAXIMIZE TABLE TABLE QUIZ
Clinical features of
Type
Generalized motor
Tonic-clonic seizure ( )
Prodromal symptoms may occur up to hours before onset (e.g., sleep disturbances,
lightheadedness, mood changes, anxiety/irritability, impaired concentration)
Loss of consciousness (sudden and without warning)
Motor symptoms
1.
Tonic phase
Generalized muscle contractions: rotated eyes, apnea, lateral tongue biting, pooled oral
secretions, cyanosis, and characteristic loud moan ( cry)
Increased sympathetic tone: dilated, unresponsive pupils, ↑ heart rate, ↑ blood pressure
2.
Clonic phase: rhythmic muscle twitching
Bladder or bowel incontinence
Tongue-bite lacerations
Usually lasts 1–3 minutes
Unresponsiveness
Confusion
Amnesia of the event
Aphasia
Fatigue
Muscular flaccidity and
muscle pain
Headache
Hypersalivation with or
without airway obstruction
Clonic seizure
Loss of consciousness
Bilateral rhythmic jerking (of the entire body or only a part)
Amnesia of the event
Tonic seizure
OXen occurs when the patient is drowsy, asleep, or aXer waking
Loss of consciousness
Muscle stiffening (extension or flexion of the head, trunk, and/or extremities)
Contraction can be bilateral or unilateral
Can be accompanied by autonomic symptoms (e.g., tachycardia, flushing)
Can be followed by atypical absence seizure
Amnesia of the event
Drowsiness or confusion
may occur
generalized seizures
Ictal Postictal
seizure
grand mal
seizure
ictal
Seizures and epilepsyClinical features
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TSTUDENT seizures and epilepsy
Formerly referred to as
“secondarily generalized
tonic-clonic seizure.”
Patient usually falls to the ground.
Caused by the contraction of the
respiratory and laryngeal muscles
Movements during a clonic seizure can resemble
serial myoclonic seizures. A clonic seizure can be
distinguished from a prolonged or repetitive
myoclonic seizure by its rhythmicity and regularity
(i.e., jerking occurs in the same muscles with the
same temporal pattern).
Unilateral contraction results in forced deviation of the affected
part of the body to one side. This deviation is called “versive” if it
affects eyes, head, and/or trunk.
May last
a few
seconds
or up to
an hour
Due to tonic
muscle
contraction
&
-
-

9. COLLAPSE NOTES FEEDBACK
Diagnosis
The following addresses evaluation following the resolution of an acute . See “
” for actively seizing patients.
Confirmation of
History
Tonic seizure
O<en occurs when the patient is drowsy, asleep, or a<er waking
Loss of consciousness
Muscle stiffening (extension or flexion of the head, trunk, and/or extremities)
Contraction can be bilateral or unilateral
Can be accompanied by autonomic symptoms (e.g., tachycardia, flushing)
Can be followed by atypical absence seizure
Amnesia of the event
Drowsiness or confusion
may occur
Myoclonic seizure
Positive myoclonus: sudden jerk-like muscle twitching
Negative myoclonus: a brief loss of muscle activity during tonic contraction of a muscle
Myoclonus can affect the entire body or only a part.
are nonrhythmic (i.e., jerks occur at different intervals) and irregular (i.e.,
jerks are asymmetric and may change laterality)
Amnesia of the event
Myoclonic-atonic seizure
Myoclonus followed by a brief loss of tone
Myoclonic-tonic seizure
Myoclonus followed by a brief increase in tone
Atonic seizure (also known as “
” or “drop aLack”)
Sudden loss of muscle tone: sudden head drop or collapse (lasts < 15 seconds)
Frequently mistaken for syncope
Generalized nonmotor (absence seizure)
Typical
Interrupted motion or activity, blank stare, unresponsiveness
Can occur several hundred times a day and usually lasts < 10 seconds
Subtle (o<en go unnoticed): lip-smacking, eye fluXering, or head nodding are
common.
Sudden onset and stop
Triggers: hyperventilation, flashing lights
None
Consciousness returns
rapidly, without any
impairment
Amnesia is common
Atypical
Interrupted motion or activity, blank stare
Patients may be responsive
: lip-smacking, eye fluXering, chewing
Small hand movements (e.g., rubbing of the fingers)
Longer than typical form (10–30 seconds)
Gradual onset and stop
Myoclonic seizures
drop
seizure
seizure
automatisms
Automatisms
It is important to distinguish between focal/bilateral and , as they
manifest similarly but are managed differently.
tonic-clonic seizuresgeneralized tonic-clonic seizures
seizure Management of acute seizures and status
epilepticus
seizure
Seizures and epilepsyClinical features
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TSTUDENT seizures and epilepsy
Associated with epilepsy syndromes, e.g.,
juvenile myoclonic epilepsy, Lennox-Gastaut
syndrome, progressive myoclonic epilepsy
An involuntary muscle twitch caused by a contraction of muscle fibers. Seen in metabolic encephalopathies, epilepsy, and traumatic brain injury.
A brief loss of muscle activity during tonic contraction. Seen in metabolic encephalopathies (e.g., hepatic encephalopathy) and epilepsy.
Negative myoclonus can
also be nonepileptic, e.g. in
hepatic encephalopathy.
Associated with epilepsy syndromes, e.g., Lennox-
Gastaut syndrome, Dravet syndrome
Common feature of childhood epilepsy syndromes
Often mistaken for day-dreaming
&

10. COLLAPSE NOTES FEEDBACK
Diagnosis
The following addresses evaluation following the resolution of an acute . See “
” for actively seizing patients.
Confirmation of
History
History of present illness: description of the event by the patient (aware ) and/or witnesses ( with impaired awareness)
Potential triggers (e.g., sleep deprivation, excessive alcohol intake)
Prodromal symptoms (e.g., aura)
symptoms
symptoms
Past medical history
History of (including current antiepileptic drugs and adherence)
History of other potential underlying conditions (e.g., head trauma, stroke, tumor, CNS infection)
Physical examination: aHention should be paid to visual inspection (e.g., for bruises from falls, tongue bites, phakomatosis-specific skin
manifestations) and evaluation for cardiovascular disorders
EEG
Performed in individuals who present with first , with insufficient information for , and/or
treatment-refractory
Characteristic EEG findings help to establish the diagnosis of ; the absence of such findings cannot, however, rule out
.
During the ()
Epileptiform discharges (e.g., spikes, sharp waves, spike waves) are usually detected.
Certain types of conditions characterized by have characteristic discharge paHerns (e.g., hypsarrhythmia in West
syndrome, 3 Hz spike-and-wave in typical absence seizures, burst suppression in anoxic encephalopathy or barbiturate
administration)
If no epileptiform discharges are detected during a , alternative diagnoses (e.g., ) should
be considered.
ATer a or between ( or )
ODen normal findings (even aTer provocation via sleep deprivation, hyperventilation, or visual stimuli)
May show epileptiform activity (bursts of abnormal discharges featuring spikes and/or sharp waves, hypsarrhythmia in West
syndrome)
Video-EEG telemetry in hospitalized patients
Continuous EEG in ambulatory patients
manifest similarly but are managed differently.
seizure Management of acute seizures and status
epilepticus
seizure
seizure seizure
Ictal
Postictal
epilepsy
seizure seizure classification
seizures
epilepsy
epilepsy
seizureictal
seizures
seizure psychogenic nonepileptic seizures
seizure seizurespostictalinterictal
is diagnosed based on the clinical presentation (e.g., changes in behavior and/or mental
status from baseline) and the demonstration of activity on EEG.
Nonconvulsive status epilepticus
seizure
Seizures and epilepsyDiagnosis
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy

11. Continuous EEG in ambulatory patients
Evaluation for underlying conditions
ECG: Rule out cardiogenic causes (e.g., cardiac arrhythmias resulting in cerebral hypoxia) in all patients with loss of consciousness during
a .
MRI: Modality of choice for investigating potential underlying structural abnormalities.
All patients with first-time focal seizures
Exception: children with history and examination suggestive of benign or characteristic epilepsy syndrome
CT: May be used if MRI is not available, but is less sensitive for identifying soG-tissue lesions
Angiography: if vascular cause (e.g., cerebral arteriovenous malformation) is suspected
Laboratory screening: to identify metabolic disorders and infectious diseases, if suspected
Blood
CBC
Glucose
Electrolytes
Prolactin
Toxicology screening
ESR
Rapid plasma reagin
Creatine kinase
Renal and liver function tests
Antiepileptic drug levels (e.g., phenytoin, carbamazepine, phenobarbital)
Urinalysis
Bacterial cultures
Cerebrospinal fluid analysis
Endocrine studies
Thyroid function tests
Adrenal function tests
Pituitary function tests
is diagnosed based on the clinical presentation (e.g., changes in behavior and/or mental
status from baseline) and the demonstration of activity on EEG.
Nonconvulsive status epilepticus
seizure
Anterior temporal
spikes and sharp
waves
seizure
[24]
seizure
[24]
[25]
Seizures and epilepsyDiagnosis
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
Increased levels for ∼ 15 min after tonic-clonic or, in some cases, focal seizures
To rule out syphilis infection
Peaks ∼ 6 hrs after a tonic‑clonic seizure
Interpret antiepileptic drug (AED) levels with caution as therapeutic ranges vary and spot serum
levels may not adequately reflect adherence. Some AED levels may not be routinely measurable
by hospital laboratories. Consult a specialist and local protocols where available.
?

12. Antiepileptic drug levels (e.g., phenytoin, carbamazepine, phenobarbital)
Urinalysis
Bacterial cultures
Cerebrospinal fluid analysis
Endocrine studies
Thyroid function tests
Adrenal function tests
Pituitary function tests
COLLAPSE NOTES FEEDBACK
Differential diagnoses
[25]
Arteriovenous mal-
formation
Arteriovenous an-
gioma (arteriovenous
malformation)
Arteriovenous mal-
formation (angioma)
In adults, an isolated unprovoked focal or focal to bilateral typically indicates a structural or metabolic
origin and should receive further evaluation.
tonic-clonic seizure
MAXIMIZE TABLE TABLE QUIZ
Differential diagnosis of epilepsy
Condition Risk factors and triggers Clinical features Duration Diagnostics
Focal-onset
seizure
Prior
Excessive physical exertion
Sleep deprivation
Flashing lights
Aura is common
Symptoms variable, depending on
location of epileptogenic focus
Jacksonian march
Usually < 2 minutes
EEG: may show
abnormal brain activity
EEG: focal repetitive spikes
or sharp waves, with or without
slow waves
MRI: may demonstrate structural
lesion
Generalized-
onset motor
Aura is uncommon
Loss of consciousness
Tongue biting
Bladder and bowel incontinence
: confusion,
amnesia, fatigue
Eyes oUen open or do not resist
opening
Usually < 5 minutes
EEG: usually normal
EEG: generalized
spike-and-wave complex
MRI: usually normal
Simple (∼ 70% of cases)
seizure
Postictal paralysis
Interictal
Ictal
seizure Postictal phase
Interictal
Ictal
Seizures and epilepsyDiagnosis
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
The spreading of paresthesia or uncontrolled motor
activity during a simple partial seizure from a distal
part of the body toward a more proximal part.
Results from seizure activity that progresses to the
motor cortex.
Abnormal patterns may be seen in some
epileptic syndromes, e.g. hypsarrhythmia
in West syndrome.
&
>
>
⑤
E
-
#-
&
·

13. incontinence
: confusion,
amnesia, fatigue
Eyes o2en open or do not
resist opening
EEG: generalized
spike-and-wave complex
MRI: usually normal
Febrile
seizure
Young age (6 months to 5 years)
Genetic predisposition
High fever (> 40°C/104°F)
Viral infection (e.g., HHV-6,
influenza)
Postimmunization fever
Simple febrile seizure
Usually
No further apparent
neurologic disorders
Complex febrile seizure
Focal
May be followed by a
postical phase
See “Clinical features of febrile
seizures.”
Simple (∼ 70% of cases)
15 minutes
1 per
24 hours
Complex (∼ 25% of
cases)
≥ 15 minutes
> 1 per
24 hours
Febrile status
epilepticus (∼ 5% of
cases)
> 30 minutes
Series of
lasting > 30 minutes
in total without full
recovery in between
Tests to determine the cause
of fever (e.g., blood and/or
urine culture, lumbar puncture)
See “Diagnosis of febrile
seizures.”
Psychogenic
nonepileptic
seizure
( )
Female sex
Psychiatric disorders (e.g.,
obsessive-compulsive disorder,
posbraumatic stress disorder)
History of physical or sexual
maltreatment
Substance use
Usually occur in presence of
eyewitnesses
Generalized asynchronous
motor activity
Eyes are usually closed and
resist being opened
Tongue-biting, other types of
self-injury, and incontinence
are rare.
Awareness is usually
unimpaired
Aura and vocalizations are
common
Individuals with can
recall the event
is uncommon
Typically > 5 minutes
Video-EEG monitoring (gold
standard): normal electrical
brain activity during a
nonepileptic seizure
Panic a7ack
Genetic predisposition
Anxiety disorders
Stress
Palpitations
Chest pain
Sweating
Dyspnea
Dizziness
Fear of losing control and/or
dying
Seconds to hours History
Syncope
Emotional stress
Pain
Sudden changes in body position
Dehydration
Heart disease (e.g., atrial
fibrillation)
Medications (e.g., β-blockers,
clonidine, serotonin reuptake
inhibitors)
Prodromal symptoms
Dizziness
Palpitations
Pallor
Sweating
Transient loss of consciousness
and muscle tone
Possible myoclonic jerks
No or minimal post-event
symptoms
1–2 minutes
History
ECG
Blood tests
Supine and orthostatic blood
pressure measurements
seizure
Postictal phase
Ictal
generalized tonic-
clonic seizure
seizure
seizure
seizures
PNES
[26][27]
PNES
Postictal phase
[28]
[29]
Seizures and epilepsyDifferential diagnoses
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy

14. The differential diagnoses listed here are not exhaustive.
COLLAPSE NOTES FEEDBACK
Acute management
Acute management steps are determined by the time from onset and include patient stabilization, identification and treatment of
reversible acute , and pharmacotherapy to terminate the .
Approach
Start as needed.
Identify and treat .
Implement phased-based .
Heart disease (e.g., atrial fibrillation)
Medications (e.g., β-blockers,
clonidine, serotonin reuptake
inhibitors)
Transient loss of consciousness
and muscle tone
Possible myoclonic jerks
No or minimal post-event
symptoms
Supine and orthostatic blood
pressure measurements
Stroke/TIA
Hypertension
Hypercholesterolemia
Smoking
Diabetes
Cardiovascular disease
Symptoms variable, depending on
the location of the stroke or TIA
Usually negative symptoms (e.g.,
weakness, visual loss)
Consciousness preserved
TIA: Minutes to hours
Stroke: Days to years,
oOen permanent damage
History
MRI/MRA
CTA
Migraine
aura
Genetic predisposition
Female sex
Hormonal changes
Life stress
Typically positive symptoms (e.g.,
hallucinations) followed by
negative ones (e.g., anesthesia)
Gradual onset
Consciousness preserved
Auras followed by headache
≤ 1 hour History
Breath-
holding spell
Young age (6 months to 6 years)
Iron deficiency anemia
Distress due to strong emotions
(e.g., anger, frustration, tantrums) or
injury
Episodes of prolonged expiratory
apnea
Transient paroxysms of cyanosis
or pallor
Possibly generalized stiffness and
jerky movements of the limbs
Post-event syncope
Vigorous cry:
< 15 seconds
Cessation of breathing:
≤ 1 minute
Recovery: ≤ 1 minute
History
Self-
stimulatory
behavior
Associated with
neurodevelopmental disorders,
autism, and a]ention deficit
hyperactivity disorder (ADHD)
Repetitive movements performed
to stimulate one's own senses
Examples of behaviors include
tapping on a desk, twirling a lock
of hair, and/or rocking back and
forth.
Variable History
Masturbation
in children
Normal behavior in children
5 months to 8 years
Dystonic posturing with rocking,
grunting, and sweating
Median frequency:
7/week
Median duration: 2.5
minutes
History
[30]
seizure
causes of seizures seizure
[31][32][33]
initial stabilization steps for acute seizures
rapidly reversible causes of seizures
acute seizure management
Seizures and epilepsyDifferential diagnoses
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
Apnea and subsequent decrease in
blood pressure and heart rate result in
brief cerebral hypoxia, triggering a
seizure.
#

15. Approach
Start as needed.
Identify and treat .
Implement phased-based .
If < 5 minutes from onset: monitor and prepare for benzodiazepine administration.
If the lasts ≥ 5 minutes (i.e., ):
Urgently administer a parenteral benzodiazepine.
If no response to benzodiazepines: Start a parenteral antiepileptic drug.
COLLAPSE NOTES FEEDBACK
Initial stabilization for acute seizures
Call for help and remove or control hazards (e.g., remove sharp objects in the patient's vicinity).
Perform an ABCDE assessment; if needed, perform cardiopulmonary resuscitation.
Initiate basic airway maneuvers, start oxygen therapy, and place the patient in the recovery position.
Check POC glucose and vital signs.
COLLAPSE NOTES FEEDBACK
Phase-based acute seizure management
The following addresses in adults and children. For other patient groups see “ ”,
“Eclampsia”, or “Febrile seizures.”
[31][32][33]
initial stabilization steps for acute seizures
rapidly reversible causes of seizures
acute seizure management
seizure
seizure status epilepticus
[34]
is a life-threatening condition. If not interrupted, it can lead to cerebral edema, hyperthermia,
rhabdomyolysis, and cardiovascular failure. If the time from onset is unknown, begin management for
.
Status epilepticus
seizure status
epilepticus
Acute are oXen self-limited and may not require immediate pharmacological intervention.seizures
[34]
acute seizure management Neonatal seizures
[31]
MAXIMIZE TABLE TABLE QUIZ
Overview of pharmacotherapy for acute
Pharmacotherapy
phase (time from onset) Preferred agents Alternatives
Early (0–5 minutes) OXen self-limited; pharmacotherapy is usually not indicated.
Early (5–20 minutes): first-line therapy
IV benzodiazepine (lorazepam OR diazepam)
Intranasal midazolam
Buccal midazolam
seizures
[31][34][37]
Seizure seizure
seizure
status epilepticus
Seizures and epilepsyAcute management
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
Status epilepticus is less likely to resolve spontaneously. Early initiation of medical treatment is
associated with a higher probability of seizure termination and a better prognosis.
Preferred: IV lorazepam or IV diazepam
Preferred: IV fosphenytoin, IV valproic acid, or IV levetiracetam
To prevent aspiration
and ensure adequate
oxygenation
&
&

16. COLLAPSE NOTES FEEDBACK
Management of rapidly reversible causes of seizures
Pharmacotherapy
phase (time from onset) Preferred agents Alternatives
Early (0–5 minutes) O"en self-limited; pharmacotherapy is usually not indicated.
Early (5–20 minutes): first-line therapy
Repeat every 5–10 minutes if no response.
IV benzodiazepine (lorazepam OR diazepam)
IM midazolam if IV access is NOT available
Intranasal midazolam
Buccal midazolam
Rectal diazepam
Persistent (20–40 minutes): second-line
therapy
IV fosphenytoin
IV valproic acid
IV levetiracetam
IV phenobarbital
Refractory (40–60 minutes)
Options include repeat second-line therapy or induction of coma (e.g., with IV propofol, thiopental, midazolam, or
pentobarbital).
Seizure seizure
seizure
status epilepticus
status epilepticus
status epilepticus
Concurrently manage (e.g., hypoglycemia, hyponatremia, hypocalcemia) without
delay.
rapidly reversible causes of seizures
Treatment of status
epilepticus
MAXIMIZE TABLE TABLE QUIZ
Management of
Cause Recommended initial interventions
Hypoglycemia
Give IV dextrose.
Consider concurrent thiamine if there is evidence of significant chronic alcohol use and/or poor nutritional status.
Electrolyte
imbalance
Hyponatremia Rapid correction with IV hypertonic saline bolus: e.g., 3% NaCl
Hypocalcemia Urgent IV calcium repletion
Hypomagnesemia
Urgent magnesium repletion with IV magnesium sulfate
Start pharmacological .
rapidly reversible causes of seizures
[31]
[31][34][39]
[40]
[41]
[45]
[46]
management of acute seizure by seizure phase
Seizures and epilepsyAcute managementPhase-based acute seizure management
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
Patients treated for suspected thiamine deficiency require ongoing treatment for days to weeks.
-

17. COLLAPSE NOTES FEEDBACK
Long-term management
Long-term management following an isolated seizure
Remove cause or provoking factors (e.g., cessation of recreational drug use, treatment of underlying disorders).
Assess for risk of recurrence; patients with a CNS insult or lesion , abnormality on brain imaging or EEG, or nocturnal are at
higher risk of recurrence.
Low risk of recurrence: shared decision-making with the patient; expectant management is usually appropriate.
High risk of recurrence: .
Long-term management of epilepsy
Electrolyte
imbalance
Hypocalcemia Urgent IV calcium repletion
Hypomagnesemia
Urgent magnesium repletion with IV magnesium sulfate
Hyperthermia
Start pharmacological .
For heatstroke: Immediately initiate cooling measures.
For febrile seizures: Consider antipyretics and a cooling blanket.
Eclampsia
Immediately start magnesium sulfate.
Monitor for signs of magnesium toxicity.
Start antihypertensives for urgent blood pressure control in pregnancy.
Hypertensive encephalopathy
Start in conjunction with intravenous antihypertensives for the treatment of
hypertensive crisis.
Alcohol withdrawal
Immediately administer a parenteral fast-acting benzodiazepine: e.g., diazepam
If there is no response to benzodiazepines, administer anticonvulsants for alcohol withdrawal syndrome.
Consider concurrent IV thiamine.
Poisoning
Modify to treat toxic seizures.
Use a benzodiazepine as first-line therapy and avoid phenytoin
[41]
[45]
[46]
management of acute seizure by seizure phase
[47]
management of acute seizure by seizure phase
[48]
[49]
phase-based acute seizure management
[31][32][33]
seizure
[32][33]
Treat as epilepsy
Long-term medical therapy following a first is not required unless the patient meets the criteria for
or is at high risk of recurrence.
unprovoked seizure
epilepsy
AWer the confirmation of diagnosis with video-EEG, anticonvulsants should be withdrawn under medical supervision.PNES
Patients with may benefit from cognitive behavioral therapy. PNES
[53]
[31][32][33]
Seizures and epilepsyAcute managementManagement of rapidly reversible causes of seizures
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
Consider in patients with a
history of medication (e.g.,
tricyclic, salicylate, isoniazid,
lithium) or recreational drug use
(e.g., cocaine, MDMA).
Phenytoin can worsen the cardiotoxic effects of certain drugs
(tricyclic antidepressants, theophylline, and cocaine) and is
ineffective in seizures caused by withdrawal or isoniazid.
E.g., traumatic brain injury, stroke, infection
However, the risk of recurrence declines with the use of antiepileptic
drugs. Therefore, patients may prefer to take antiepileptic drugs to
avoid any potential disruption caused by further seizures.

18. Long-term management of epilepsy
Start, continue, or optimize long-term antiepileptic drugs.
Monotherapy is preferred unless the are not adequately controlled.
may be managed with nonpharmacological methods (e.g., surgery, neurostimulation, ketogenic diet).
Pharmacotherapy (antiepileptic drugs or AEDs)
AEDs reduce the risk of future by raising the threshold, which is pathologically lowered in individuals with .
Criteria for the choice of antiepileptic drugs:
type
Patient age
Comorbidities
Treatment regimen
Monotherapy should be maintained if possible.
If initial monotherapy is ineffective, increase the dosage of the single agent or switch to an alternative agent before initiating
combination therapy.
Approx. ⅔ of patients become -free with monotherapy.
Combination therapy should only be given if monotherapy fails.
In this case, drugs from different classes and/or with different pharmacologic modes of action should be tried.
Combining two or three of the standard antiepileptic drugs is usually safe.
Patients with may benefit from cognitive behavioral therapy. PNES
[53]
[31][32][33]
seizures
Drug-resistant epilepsy
[54]
seizures seizure epilepsy
Seizure
MAXIMIZE TABLE TABLE QUIZ
Pharmacotherapy for
type First line Second line
Focal
Lamotrigine
Levetiracetam
Phenytoin
Carbamazepine
Oxcarbazepine
Phenobarbital (children)
Gabapentin
Valproate
Pregabalin
Topiramate
Generalized
Lamotrigine
Valproate
Phenobarbital (children)
Carbamazepine
Zonisamide
Typical absence
Ethosuximide
Valproate
Lamotrigine
Clonazepam
Atypical absence
Valproate
Lamotrigine
Topiramate
Clonazepam
Felbamate
Myoclonic
Atonic
epilepsy
Seizure
Tonic-clonic
epilepsy seizure
[55]
Seizures and epilepsyLong-term management
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
Including focal to bilateral tonic-clonic
An advantage of levetiracetam
treatment is that uptitration is not
necessary.
Zonisamide is given
as an adjunct therapy.
Treatment of new-onset epilepsy with multiple agents increases the risk of pharmacological resistance.
I
2
!
3
-
Y
!
~
3
I
-
-
-
=> -

19. combination therapy.
Approx. ⅔ of patients become -free with monotherapy.
Combination therapy should only be given if monotherapy fails.
In this case, drugs from different classes and/or with different pharmacologic modes of action should be tried.
Combining two or three of the standard antiepileptic drugs is usually safe.
Failure of combination therapy : Consider nonpharmacological therapy.
Termination of treatment
Evaluated on a case-by-case basis
May be considered if the patient meets all of the following:
< 2 /year
An inconspicuous provocation EEG
Normal psychological findings
No hereditary predisposition
Generally possible aIer 2–5 seizure-free years with normal EEG results
Medications should be tapered with caution.
Adverse effects of AEDs
See “Overview of AEDs” for agent-specific adverse effects.
Neurocognitive changes (e.g., sedation, headache, dizziness, tremor, memory impairment)
Skin disorders (e.g., rash, SJS, DRESS)
Psychiatric symptoms (e.g., depression, psychosis)
Laboratory abnormalities (e.g., hyponatremia, neutropenia, thrombocytopenia)
Gastrointestinal symptoms (e.g., nausea, vomiting, constipation)
Weight gain or loss
Nonpharmacological therapy
Indications:
Surgery
Resection (surgical removal of pathological lesions)
Patients with temporal lobe epilepsy (e.g., due to hippocampal sclerosis): resection of the anteromedial temporal lobe or of the
amygdala and the hippocampus
Patients with severe intractable due to structural cerebral abnormalities confined to one hemisphere: resection of an entire
hemisphere (hemispherectomy)
Disconnection (surgical section of neuronal circuits)
Callosotomy: section of the corpus callosum
Initially: partial disconnection only (usually the anterior ⅔)
If persist: complete disconnection
Hemispherotomy: disconnection of the cortex of one hemisphere from the ipsilateral subcortical structures and cortex of the other
hemisphere without removal of the affected hemisphere
Stimulation techniques: vagus nerve stimulation, deep brain stimulation
Dietary measures: ketogenic diet
epilepsy seizure
[55]
[56]
seizures
[57][58]
pharmacoresistant epilepsy
seizures
[60]
seizures
[61]
[62]
Successful therapy depends on determining whether the patient has focal or and prescribing
medication accordingly.
epilepsy generalized seizures
Seizures and epilepsyLong-term management
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
Only 15–30% of patients on combination therapy become seizure‑free.
In patients with liver disease, hepatically metabolized anticonvulsants (e.g., valproic acid,
phenytoin, felbamate, lamotrigine) should be avoided or dose adjusted.
Evidence regarding effectiveness is limited, but studies suggest that a ketogenic diet may reduce seizure
frequency, especially in children and those with West syndrome or Dravet syndrome.
I
2
3
4
I
A
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E
C

20. COLLAPSE NOTES FEEDBACK
Complications
Acute
Hyperthermia, cardiorespiratory deficits, and excitatory toxicity, which can cause irreversible tissue damage, especially to the CNS (e.g.,
cortical laminar necrosis) and, in turn, increase the risk of further
Postictal lactic acidosis: transient anion gap metabolic acidosis with increased lactic acid and reduced serum bicarbonate
(usually resolves spontaneously within 60–90 minutes aGer activity stops)
Physical trauma, such as:
Tongue biting
Posterior dislocation of the glenohumeral joint due to falling
Polytrauma from a car accident
Long term
Psychiatric
Anxiety
Depression and risk of suicide
Cognitive impairment
Psychosis (interictal psychosis, postictal psychosis, or secondary to antiepileptic drugs)
Psychosocial distress (e.g., at the workplace)
Sleep disturbances and insomnia
Bone disease (osteomalacia, osteoporosis) associated with antiepileptic drugs
Sudden unexpected death in epilepsy ( )
The sudden death of a person with diagnosed that cannot be aNributed to trauma or drowning and occurs with or without
evidence of preceding in the absence of any underlying medical conditions that could explain the event
Usually occurs while the patient is asleep
Is more common in patients with intractable , frequent (especially ), and early age of onset
We list the most important complications. The selection is not exhaustive.
medication accordingly.
seizures
postictal
seizure
Status epilepticus
Cortical laminar
necrosis
[63]
[64]
SUDEP
[65]
epilepsy
seizure
epilepsy seizures tonic-clonic seizures
Seizures and epilepsyComplications
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
Lactic acidosis results from
excess muscle exertion in
the setting of inadequate
oxygen delivery.
Approx. 20% of affected individuals patients with seizures experience them only at night, and another 35% have seizures both during the day and at night.
One potential mechanism is related to the induction of the cytochrome P450 system by antiepileptic
drugs, leading to increased catabolism of vitamin D to inactive metabolites and a subsequent rise in
parathyroid hormone, which increases bone turnover.
I

21. We list the most important complications. The selection is not exhaustive.
COLLAPSE NOTES FEEDBACK
Prognosis
Risk of recurrence
A6er the first
With no underlying brain insult (stroke, trauma, or CNS infection): ∼ 40–50% within 2 years
80% of recurrences occur within 2 years of the initial .
Occurring a6er at least 1 week a6er a brain insult: ∼ 65% over the next 10 years
A6er the second : 60% within 1 year
A6er an : ∼ 19% over the next 10 years
Treatment outcomes
60–70% of all treated patients become -free at 10 years a6er first
60–90% of children and 35–57% of adults remain -free a6er discontinuing medical therapy following a 2-year -free
period on antiepileptic drugs.
Legal regulations: State laws vary with regard to the requirements for individuals with to operate vehicles and heavy
machinery.
Mortality
Risk of all-cause mortality is 1.6–3 times higher in individuals with than in the general population.
The worldwide incidence of is 1.2–6.3 per 1,000 individuals with .
COLLAPSE NOTES FEEDBACK
Status epilepticus
Definition
is a that lasts ≥ 5 minutes or a series of in rapid succession without full neurological recovery in the
period, which increases the risk of long-term consequences such as neuronal injury and functional deficits.
The time threshold a6er which a is considered differs according to the type of :
: ≥ 5 minutes
Focal seizures with impaired consciousness: ≥ 10 minutes
Absence seizures: 10–15 minutes
Etiology
Withdrawal from antiepileptic drugs
Electrolyte imbalance (e.g., hyponatremia, hypocalcemia)
Metabolic disturbances (e.g., hypoglycemia, uremia, porphyria)
Structural brain lesions and/or injury (e.g., tumors, trauma, stroke)
seizure
unprovoked seizure
[66][67]
seizure
unprovoked seizure
acute symptomatic seizure
[68]
seizure seizure
seizure seizure
epilepsy
[69]
[70]
epilepsy
SUDEP epilepsy
[31][71]
Status epilepticusseizure seizures
interictal
seizure status epilepticus seizure
Tonic-clonic seizures
[72]
Seizures and epilepsyPrognosis
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
↑

22. Withdrawal from antiepileptic drugs
Electrolyte imbalance (e.g., hyponatremia, hypocalcemia)
Metabolic disturbances (e.g., hypoglycemia, uremia, porphyria)
Structural brain lesions and/or injury (e.g., tumors, trauma, stroke)
Anoxic brain injury
Alcohol withdrawal
Recreational drug use
Drug toxicity (e.g., from tricyclic antidepressants, isoniazid)
CNS infections (e.g., cerebral malaria, neurocysticercosis, viral encephalitis, prion diseases)
Late-stage neurodegenerative diseases (e.g., Alzheimer disease)
Classification
With prominent motor features
Convulsive ( )
Myoclonic (with or without coma)
Focal motor
Tonic
Hyperkinetic
Without prominent motor features: nonconvulsive status epilepticus (NCSE)
With coma
Without coma
Absence
Focal (e.g., aphasia, impaired consciousness, ongoing autonomic or sensory symptoms)
Management
See “ .”
Maintain a high level of suspicion for NCSE.
Prognosis
Mortality is bimodal, with the highest risk in neonates (25–39%) and patients > 80 years of age (> 50%).
Overall infant and child mortality: 3.6%
Overall adult mortality: 15.9%
COLLAPSE NOTES FEEDBACK
Epilepsy in pregnancy
[71]
tonic-clonic
Management of acute seizures and status epilepticus
Consider NCSE in patients with persistently altered mental status following a or with otherwise unexplained altered
mental status, bizarre behavior, autonomic dysfunction, or sensory symptoms.
seizure
[73][74]
[75]
[75]
Seizures and epilepsyStatus epilepticus
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
Motor features may diminish during the course of the event, but seizure activity will still be visible on EEG.
Subtle motor features, such as eyelid or orofacial myoclonus, may be present.

23. Overall adult mortality: 15.9%
COLLAPSE NOTES FEEDBACK
Epilepsy in pregnancy
Information on other disorders that can occur in pregnancy (e.g., eclampsia, ) is detailed
separately.
Epidemiology
Approximately 1.5 million female individuals of reproductive age in the US have .
Approximately 24,000 female individuals with become pregnant per year.
In the majority of cases, pregnancy does not affect frequency.
Etiology
Factors associated with an increased risk of during pregnancy include:
Reduced plasma concentration of AEDs due to physiologic changes in pregnancy (e.g., steroid-hormone induced hepatic
enzyme induction, increased renal clearance)
Psychosocial stress
Sleep deprivation
Hormonal changes (e.g., increased estrogen:progesterone ratio)
Management
Reduce AED-associated risk of major congenital malformations (MCMs).
AEDs with low teratogenic risk: lamotrigine and levetiracetam
AEDs with high teratogenic risk: valproate (highest risk), phenobarbital, topiramate, and phenytoin
In patients planning pregnancy
Measure AED levels before conception (if possible)
During pregnancy
Measure AED levels regularly.
Adjust target levels as needed.
[75]
Folic acid supplementation is recommended in all individuals capable of pregnancy.
[81]
seizure acute symptomatic seizure
[82][83][84]
epilepsy
epilepsy
seizure
epileptic seizures
[77][82][84][85]
Intrapartum exposure to teratogenic AEDs is associated with a 2–3 fold increase in the likelihood of major
congenital malformations.
[76]
[82]
[77][82]
Seizures and epilepsyEpilepsy in pregnancy
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
20–35% of pregnant female individuals with epilepsy experience an increased seizurefrequency.

24. AEDs with high teratogenic risk: valproate (highest risk), phenobarbital, topiramate, and phenytoin
In patients planning pregnancy
Measure AED levels before conception (if possible)
During pregnancy
Measure AED levels regularly.
Adjust target levels as needed.
Complications
Fetal complications
Increased risk of low birth weight and small size for gestational age due to maternal
Teratogenic effects of AEDs (e.g., congenital malformations, abnormal neurocognitive development)
Maternal complications: increased risk of the following
Preterm delivery
Need for cesarean section
Preeclampsia
Severe postpartum hemorrhage
Death during delivery
COLLAPSE NOTES FEEDBACK
Related One-Minute Telegram
One-Minute Telegram 61-2022-1/3: Restock your aspirin and laceration repair kits - it’s almost Halloween!
Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and
links” below.
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Tips and Links
[82]
[7][82]
[77][87]
seizures
One-Minute Telegram
Free CDC Application to Assist Contraception Selection According to the USMEC category
2020 ACOG Commi`ee Opinion on Gynecologic Management of Adolescents and Young Women With Seizure Disorders
2019 International League Against Epilepsy Task Force on Women and Pregnancy:Management of Epilepsy in Pregnancy (E
xecutive Summary)
2016 AES Guideline on the Treatment of Convulsive Status Epilepticus in Children and Adults
Youtube video "Understanding generalized seizures"
Youtube video "Understanding partial epilepsy"
Seizures and epilepsyEpilepsy in pregnancy
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT seizures and epilepsy
-

25. An 8-year-old boy is brought to the emergency department 3 hours a8er having a 2-minute episode of violent, jerky
movements of his right arm at school. He was sweating profusely during the episode and did not lose consciousness.
He remembers having felt a chill down his spine before the episode. Following the episode, he experienced weakness
in the right arm and was not able to li8 it above his head for 2 hours. Three weeks ago, he had a sore throat that
resolved with over-the-counter medication. He was born at term and his mother remembers him having an episode of
jerky movements when he had a high-grade fever as a toddler. There is no family history of serious illness, although
his father passed away in a motor vehicle accident approximately 1 year ago. His temperature is 37.0°C (98.6°F),
pulse is 98/min, and blood pressure is 94/54 mm Hg. Physical and neurologic examinations show no abnormalities. A
complete blood count and serum concentrations of glucose, electrolytes, calcium, and creatinine are within the
reference range. Which of the following is the most likely diagnosis?
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HINT USED
Transient focal following an episode of jerky movements is consistent with the syndrome known as
, which is associated with a particular diagnosis.
GIVE FEEDBACK
SHOW ALL EXPLANATIONS RESET QUESTION HIDE STATS
KEY INFO ATTENDING TIP LABS
weakness Todd
paralysis
22%A Sydenham chorea
3%B Sporadic transient tic disorder
6%C Conversion disorder
4%D Hemiplegic migraine
65%
A focal seizure may occur with or without dyscognitive features (e.g., loss of consciousness) and can manifest
with a variety of positive and negative symptoms, including focal motor activity that may be followed by
transient weakness in the affected limb. Focal seizures may arise in the seWing of hippocampal sclerosis,
infection, trauma, or perinatal injury, among others. The majority of affected patients also experience an aura,
with higher cortical sensations such as déjà vu and fear that precede the focal seizure. This patient
experienced violent, jerky arm movements preceded by a “chill down his spine” and followed by temporary
focal paresis without residual effects (Todd paralysis) upon presentation to the emergency department, which
is consistent with the diagnosis of a focal seizure without impairment of consciousness, previously referred to
as a simple partial seizure.
Seizures and epilepsy GIVE FEEDBACK
E Focal seizure
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TSTUDENT Ctrl+K
movements of his right arm
chill down his spine
violent
,
jerky
weakness
inthe
rightdr

26. HINT USED
An 18-month-old boy is brought to the emergency department by his mother 25 minutes a:er an episode of loss of
consciousness. The child began crying a:er his 4-year-old brother snatched a toy from him. The brief shrill cry was followed
by a period of expiration; he then turned blue, became unconscious, and briefly lost his muscle tone, before he stiffened and
had jerky movements of his arms and legs for 15 seconds. A:er this episode, he immediately regained consciousness. He had
a similar episode 2 weeks ago when his father refused to give him a juice box. He has been healthy and has met all of his
developmental milestones. He is alert and active. Vital signs are within normal limits. Cardiopulmonary examination shows no
abnormalities. Neurologic examination shows no focal findings. Which of the following is the most appropriate next step in
management?
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HINT USED
This patient's episode of with following emotional upset (i.e., frustration) and vigorous crying is
indicative of a .
GIVE FEEDBACK
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KEY INFO ATTENDING TIP LABS
cyanosisloss of consciousness
breath-holding spell
3%A CT scan of the head
12%B Echocardiography
12%D Electroencephalography
0%E Lumbar puncture
1%F Tilt table test
73%
Breath-holding spells most commonly manifest between the age of 6–18 months and are typically triggered by
emotional distress. Most patients outgrow this benign condition between 4 and 8 years of age; usually, reassurance
and follow-up are sufficient and no further treatment is required. The typical sequence includes crying, exhalation,
and breath-holding, followed by cyanosis and loss of consciousness. Patients usually resume breathing and regain
consciousness in less than 1 minute. Diagnosis is typically based on the clinical features and a detailed description of
the episode. Parents should be made aware of the triggers of breath-holding spells, such as tantrums, minor injuries,
and distress. However, no special precautions must be taken to avoid these triggers. Because several studies suggest
an association between breath-holding spells and iron-deficiency anemia, confirmatory tests (e.g., CBC, serum ferritin)
may be considered. Iron supplements may decrease the frequency of breath-holding spells.
See “Differential diagnosis of epilepsy” table.
Seizures and epilepsy GIVE FEEDBACK
C Reassurance
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TSTUDENT Ctrl+K
brief shrill cry was followed
immediately regained consciousness
lossof
consciousness
by
a
period
ofexpiration
turnedblue
jerky
movements
ofhisarms
andlessfor15seconds
EEG

27. A 9-year-old girl is brought to the physician by her father because of multiple episodes of staring and facial grimacing that
have occurred over the past 3 weeks. There are no precipitating factors for these episodes and they last for several minutes.
She does not respond to her family members during these episodes. One week ago, her brother witnessed an episode in
which she woke up while sleeping, stared, and made hand gestures. She does not remember any of these episodes but does
recall having a vague muddy taste in her mouth prior to the onset of these symptoms. AAer the episode, she feels lethargic
and is confused. Physical and neurologic examinations show no abnormalities. Which of the following is the most likely
diagnosis?
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HINT USED
This patient likely experienced an with (muddy ) preceding the onset of her motor
symptoms, which suggests that the pathology arises within the .
GIVE FEEDBACK
SHOW ALL EXPLANATIONS RESET QUESTION HIDE STATS
KEY INFO ATTENDING TIP LABS
aura gustatory hallucinationstaste
medialtemporal lobe
1%A Generalized tonic-clonic seizures
1%B Atonic seizure
1%C Focal aware seizure
22%D Absence seizure
0%F Syncope
0%G Breath-holding spell
0%H Narcolepsy
3%I Myoclonic seizure
71%
This patient's presentation is most consistent with recurrent focal seizures with impaired awareness (formerly
complex partial seizure), which are caused by abnormal electrical activity arising within the temporal lobe. The muddy
taste in her mouth (gustatory aura) marks the onset of the seizure. The ictal phase consists of her staring,
nonresponsiveness to external stimuli, and automatisms such as facial grimacing and hand gestures. The ictal phase is
typically followed by postictal confusion, lethargy, and amnesia.
See “Differential diagnosis of epilepsy” table.
Seizures and epilepsy GIVE FEEDBACK
E Focal seizure with impaired awareness
EXIT SESSION PREVIOUS NEXT
TSTUDENT Ctrl+KAsk a medical question
multiple episodes of staring and facial grimacing
muddy taste in her mouth prior After the episode, she feels lethargic
and is confused
X
X
X
#
L
&
L
G

28. HINT USED
A 17-year-old boy is brought to the emergency department by his brother a8er losing consciousness 1 hour ago. The brother
reports that the patient was skateboarding outside when he fell on the ground and started to have generalized contractions.
There was also some blood coming from his mouth. The contractions stopped a8er about 1 minute, but he remained
unconscious for a few minutes a8erward. He has never had a similar episode before. There is no personal or family history of
serious illness. He does not smoke or drink alcohol. He does not use illicit drugs. He takes no medications. On arrival, he is
confused and oriented only to person and place. He cannot recall what happened and reports diffuse muscle ache, headache,
and fatigue. He appears pale. His temperature is 37.0°C (98.6°F), pulse is 80/min, and blood pressure is 130/80 mm Hg.
There is a small wound on the le8 side of the tongue. A complete blood count and serum concentrations of electrolytes, urea
nitrogen, and creatinine are within the reference ranges. Toxicology screening is negative. An ECG shows no abnormalities.
Which of the following is the most appropriate next step in management?
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HINT USED
Generalized muscle contractions, biting, and concurrent followed by confusion and fatigue are
consistent with a . This patient's protracted 1 hour a=er the event is especially
concerning.
GIVE FEEDBACK
SHOW ALL EXPLANATIONS RESET QUESTION HIDE STATS
KEY INFO ATTENDING TIP LABS
tongue loss of consciousness
tonic-clonic seizure altered mental status
1%A Lorazepam therapy
6%B Reassurance and follow-up
11%C MRI of the head
0%D Lumbar puncture
2%E Lamotrigine therapy
22%G Electroencephalography
57%
A noncontrast CT scan of the head is indicated in patients with an unprovoked first seizure if an intracranial process
(e.g., hemorrhage) is suspected. This patient's protracted altered mental status (continued disorientation, headache) in
the seZing of a fall raises concern for intracranial hemorrhage. A8er ruling out any life-threatening bleeding via CT
scan, the patient should also receive an EEG to assess whether his altered mental status is a result of continued
seizure activity and an MRI to identify anatomic causes of the seizures.
Seizures and epilepsy GIVE FEEDBACK
F CT scan of the head
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TSTUDENT Ctrl+KAsk a medical question
confused and oriented only to person and place
some blood coming from his mouth
losing consciousness 1 hour ago
generalized contractions
diffuse muscle ache
On arrival, he is
headache
&
L
~
L
X
EEG
X

29. A previously healthy 10-year-old boy is brought to the emergency department 15 minutes a:er he had a seizure. His mother
reports that he complained of sudden nausea and seeing “shiny lights,” a:er which the corner of his mouth and then his face
began twitching. Next, he let out a loud scream, dropped to the floor unconscious, and began to jerk his arms and legs as well
for about 2 minutes. On the way to the hospital, the boy regained consciousness, but was confused and could not speak
clearly for about 5 minutes. He had a fever and sore throat one week ago which improved a:er treatment with
acetaminophen. He appears lethargic and cannot recall what happened during the episode. His vital signs are within normal
limits. He is oriented to time, place, and person. Deep tendon reflexes are 2+ bilaterally. There is muscular pain at aMempts to
elicit deep tendon reflexes. Physical and neurologic examinations show no other abnormalities. Which of the following is the
most likely diagnosis?
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HINT USED
What type of is initially limited to the face and then involves the entire body?
GIVE FEEDBACK
SHOW ALL EXPLANATIONS RESET QUESTION HIDE STATS
KEY INFO ATTENDING TIP LABS
seizure
3%B Focal seizure with dyscognitive features
1%C Convulsive syncope
4%D Sydenham chorea
8%E Generalized myoclonic seizure
27%F Generalized tonic-clonic seizure
57%
A focal to bilateral tonic-clonic seizure (formerly called partial seizure with secondary generalization) is a seizure that
begins in a limited area of one hemisphere of the brain and progresses to involve both hemispheres. O:en, these
seizures begin with an aura that may include feelings of nausea or seeing shiny lights. This patient's initial facial
twitching and muscle contractions are characteristic of a focal seizure (repetitive movements on one side). The
bilateral tonic-clonic portion of the seizure then manifests with loss of consciousness and rhythmic jerking of the
extremities. A:er tonic-clonic seizures, consciousness usually returns slowly and a postictal phase (in this case,
lethargy and confusion) begins. This patient's muscle pain on examination is likely due to the tonic muscle
contractions during his seizure.
Seizures and epilepsy GIVE FEEDBACK
A Focal to bilateral tonic-clonic seizure
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TSTUDENT Ctrl+KAsk a medical question
sudden nausea and seeing “shiny lights, the corner of his mouth and then his face
dropped to the floor unconscious, and began to jerk his arms and legs as wellbegan twitching
for about 2 minutes
clearly for about 5 minutes
was confused and could not speak

30. HINT USED
A previously healthy 7-year-old boy is brought to the emergency department by his parents because of a 1-day history of high
fever. His temperature prior to arrival was 40.0°C (104°F). There is no family history of serious illness. Development has been
appropriate for his age. He is administered rectal acetaminophen. While in the waiting room, he becomes unresponsive and
starts jerking his arms and legs back and forth. A fingerstick blood glucose concentration is 86 mg/dL. AOer 5 minutes, he
continues having jerky movements and is unresponsive to verbal and painful stimuli. Which of the following is the most
appropriate next step in management?
ADD NOTES MARK GET ANKI CARDS
HINT USED
movements and unconsciousness for > 5 minutes indicate , which is a ! If
not interrupted as soon as possible, it can lead to , , , and/or cardiovascular
failure!
GIVE FEEDBACK
KEY INFO ATTENDING TIP LABS
Tonic-clonic status epilepticus medical emergency
cerebral edemahyperthermiarhabdomyolysis
8%A Intravenous administration of valproate
11%C Intravenous administration of phenobarbital
Obtain blood cultures
61%
Parenteral benzodiazepines (e.g., lorazepam, midazolam) are the first-line treatment for early status epilepticus (i.e.,
seizure activity lasting 5–20 minutes). Benzodiazepines increase GABAergic transmission, thereby decreasing neuronal
excitability and aborting the seizure. If IV access cannot be obtained, other routes of benzodiazepine administration
(e.g., intramuscular, rectal, buccal, nasal) should be used. If initial pharmacotherapy is unsuccessful, benzodiazepine
administration should be repeated every 5–10 minutes. Rapidly reversible causes of seizures (e.g., hypoglycemia,
hyponatremia, hypocalcemia) should be investigated and, if present, managed immediately.
In persistent status epilepticus (i.e., seizure activity lasting 20–40 minutes), second-line treatment with intravenous
fosphenytoin, levetiracetam, or valproate is indicated. Refractory status epilepticus (i.e., seizure activity lasting > 40
minutes) may be addressed with repetition of second-line therapy or induction of coma (e.g., with IV propofol,
thiopental, midazolam, pentobarbital).
Seizures and epilepsy GIVE FEEDBACK
B Intramuscular administration of midazolam
Treatment of
status
…
epilepticus
EXIT SESSION PREVIOUS SEE ANALYSIS
TSTUDENT Ctrl+KAsk a medical question
continues having jerky movements and is unresponsive
After
5minutes
,
he
Not
haveIV
Access
S
S
&
X

31. movements and unconsciousness for > 5 minutes indicate , which is a ! If
not interrupted as soon as possible, it can lead to , , , and/or cardiovascular
failure!
GIVE FEEDBACK
SHOW ALL EXPLANATIONS RESET QUESTION HIDE STATS
Tonic-clonic status epilepticus medical emergency
cerebral edemahyperthermiarhabdomyolysis
8%A Intravenous administration of valproate
11%C Intravenous administration of phenobarbital
2%D Obtain blood cultures
2%E Perform electroencephalogram
2%F Rectal administration of ibuprofen
4%G Repeat rectal administration of acetaminophen
2%H Rectal administration of lamotrigine
8%I Intravenous administration of fosphenytoin
61%
Parenteral benzodiazepines (e.g., lorazepam, midazolam) are the first-line treatment for early status epilepticus (i.e.,
seizure activity lasting 5–20 minutes). Benzodiazepines increase GABAergic transmission, thereby decreasing neuronal
excitability and aborting the seizure. If IV access cannot be obtained, other routes of benzodiazepine administration
(e.g., intramuscular, rectal, buccal, nasal) should be used. If initial pharmacotherapy is unsuccessful, benzodiazepine
administration should be repeated every 5–10 minutes. Rapidly reversible causes of seizures (e.g., hypoglycemia,
hyponatremia, hypocalcemia) should be investigated and, if present, managed immediately.
In persistent status epilepticus (i.e., seizure activity lasting 20–40 minutes), second-line treatment with intravenous
fosphenytoin, levetiracetam, or valproate is indicated. Refractory status epilepticus (i.e., seizure activity lasting > 40
minutes) may be addressed with repetition of second-line therapy or induction of coma (e.g., with IV propofol,
thiopental, midazolam, pentobarbital).
Seizures and epilepsy GIVE FEEDBACK
B Intramuscular administration of midazolam
Treatment of
status
…
epilepticus
EXIT SESSION PREVIOUS SEE ANALYSIS
TSTUDENT Ctrl+K
X
L
&
X
&
&