Seizures Flashcards
Setting: ER
35 year old female
Previously healthy
Right handed
BIBEMS for 1 minute of generalized shaking
Does not recall the event
Woke up in the hospital
Reports pain in her tongue
Witness:
Initially looked confused
Made sounds, pulled at clothing
Looked to her right
Body began to shake
Woke up at hospital
First time this occurred
Preceding déjà vu with smelling burning rubber and taste of iron in her mouth followed by brief confusion from which she needed time to recover
-Vitals:
110/70
HR 75
RR 18/min
Temp 97F
Neuro exam
A&Ox3 now
Normal speech
CN II-XII normal
Motor, sensory, coordination are normal
35 year old woman who presented with 1 minute of generalized shaking preceded by lip smacking and hand picking (automatisms)
Exam significant only for lateral tongue laceration
She was initially confused, and it took time to return to normal mental status
-tonic clonic seizure
-started as a focal -> progressed to bilateral tonic clonic
-focal only has aura
epilepsy definition and clinical definition
Seizure with risk of recurrence: Unprovoked and unpredictable
-Chronic disorder: need lifelong antiseizure meds
- only ~1/3 pts with single unprovoked seizures develop another seizure within 1 yr
-Each type of epilepsy has a distinct form with its own natural history and response to tx
Clinical def:
- at least 2 unprovoked seizures >24hrs apart OR
- 1 unprovoked seizure + high risk of recurrence; > 60% risk by risk stratification with EEG/MRI OR
- Dx of an epilepsy syndrome
seizure definition
-A sudden change in consciousness, movement or behavior
-Caused by electrical hyper-synchronization of neuronal networks in the cerebral cortex!
-Transient event
-May occur only during the course of an acute medical or neurologic illness
epidemiology of seizures
-About 4%of people living up to 74 years of age have at least one unprovoked seizure
6.5 persons per 1000 population with epilepsy = 1-2% of the population
-Highest rates: young children and elderly
-Cause can vary with age
-~60-70% achieve control of their seizures with antiepileptic medications
Mortality
-Risk incurred by underlying disease
-Sudden unexplained death(SUDEP) is 25x more likely in epilepsy patients
transient neurological dysfunction (dont need to know details) Basically: shaking does not equal seizures
-seizures often present with any of the 4 categories
-motor dysfunction/shaking:
-DDX: syncope, movement disorders, ataxia, panic attacks, transient cerebral ischemia, PNES
-non-motor dysfunction (language, vision, sensory changes)
-DDX: migraine with aura, cerebral ischemia
-movements during sleep:
-DDX- REM sleep behavior
-with acute confusion
-DDX- transient global amnesia, syncope, migraine that affects the RAAS
focal seziures: what are the three phases
AURA preceding:
-Experiential phenomena: déjà vu or jamais vu
-Epigastric sensations: stomach butterflies, rising sensation
-Sensory phenomena: abnormal smell or taste
- ipsilateral Automatisms: Lip smacking; pulling of your clothes
ICTUS: shaking
-Abrupt onset
-Rapid progression over ~10 seconds
-Example: Jacksonian march
-Spontaneous termination
POST-ICTAL STATE:
-confusion, lethargy -> Seizure ended but you are confused, tired, “brain just worked a marathon”
- A lot of pts are incontinent post seizure
-focal neuro deficits
-lateral tongue bites
clinical peal: seizure sx are often “stereotypic”: what does this mean?
meaning that it’s the same symptoms in the same person, due to the same neural networks being activated with each seizure
generalized vs focal (partial) seizures: partial seizures types
partial/simple - start in one area -> unilateral shaking and consciousness stays
-complex partial: LOC and shaking
-simple partial: stays in one area -> shaking in left artm
-focal to bilateral tonic-clonic: starts in one areas moves bilaterally + LOC
-only focal has auras
Generalized seizure types
Generalized: whole brain affected, usually central - thalamus, medial
- Tonic clonic: classic - whole body shake
- Motor myoclonic: just body jerking
- Atonic: whole body drops, not moving
non-motor: petit mal
simple partial seizures: sx and clinical picture
-Electrical discharge occurs in limited and circumscribed area of cortex
-Patients interact normally with environment during simple partial seizure
Symptoms widely range depending on foci location
-Subjective (“Aura”)
-Déjà vu, jamais vu, epigastric rising sensation, fear, feeling of unreality or detachment, olfactory hallucination, unilateral sensory disturbance
- auditory hallucination = RARE -> more psychiatric
Physical (observable) manifestation
-Motor movement
-“Jacksonian march” (sometimes):
-Common form: Seizure spreads from the hand, up the arm, to the face, and down the leg; or
-From the foot, the seizure marches up the leg, down the arm, and to the face, usually in a matter of 20 to 30 s.
jacksonian march seizure: what type of seizure and what characteristic
Found in SIMPLE partial focal seizures
Common form:
- Seizure spreads from the hand, up the arm, to the face, and down the leg; or
-From the foot, the seizure marches up the leg, down the arm, and to the face, usually in a matter of 20 to 30 s.
- pearl: the first sx correlates to the focus of the seizure
Levetiracetam: moa, indication, dose, adrs
MOA: largely unknown
use:
- first line monotherapy for most focal and gernalized seizures
- status epiletpicus: mc second line tx
- seizure prophylaxis after neuro surgery, bleed, TBI
dose: oral
- 500 mg BID; titrate every 2 wks by 1000 mg
- max dose: 4000mg QD
- no monitoring required
ADRs
- relatively well tolerated
- FATIGUE, SOMNOLENCE
- dizziness
Good because it works immediately (compare with lamotrigine)
Tends to be well tolerated but there are cognitive ADRs: irritable, feeling off -> self discontinue
focal seizures with impaired awareness: main sxs
-Previously called “complex” focal seizures
-Impaired consciousness!
Ipsilateral Automatism:
-Repetitive, complex, purposeless motor activity
-Lip-smacking, repeated swallowing, chewing, picking motions with hands (temporal lobe epilepsy)
-Hypermotor, frenetic activity (Frontal lobe epilepsy)
Staring
location: TEMPORAL LOBE
- 70-80% of complex partial seizures arise from temporal lobes
-Remainder arise from frontal and occipital lobes
generalized onset motor seizures (tonic-clonic) (grand-mal) general presentation and post-ictal sx
-ABRUPT LOC with little to no warning (no prodrome)
-Fall to the floor that often results in facial/bodily injuries
-ictal cry: Loud vocalization as air forced across contracted vocal cords
-May bite the lateral margin of the tongue
-tonic: Bilateral tonic STIFFENING of muscles - extension of trunk and limbs
-clonic: Synchronous muscle JERKING
-Apnea/cyanotic: may turn light blue/purple, breathing stopped
-Pupils: dilated and unresponsive to light
-Bladder incontinence can occur during the seizure or post-ictally
Post-ictally:
-Unarousable, then lethargic / confused / bewildered / possibly agitated
-Prefer to sleep, wont remember anything said in the post-ictal time
generalized onset motor seizures (tonic-clonic) (grand-mal)- EEG tracing
Initially movement artifact obscures tracing
- May seen early spike-wave discharges lasting a few seconds followed by 10s period of 10Hz spikes
Clonic phase: spikes mix with slow waves then assumes a polyspike and wave pattern
-As movements cease: isoelectric then resumes pre-seizure pattern
general onset non-motor seizures (absence) (petit mal) presentation
presentation:
-Brief, rapid onset, rapid cessation, without warning
-KIDS MC (4 yrs -puberty): stop what they are doing and zone out; May have several hundred episodes in a day
-Momentary lapses in awareness lasting 2-10s
-To an onlooker: Motionless staring with behavioral arrest
-May have fine myoclonic movements of eyelids, facial muscles,
-May have minor automatisms—in the form of lip-smacking, chewing, and fumbling movements of the fingers
-No postictal period!!!!!!!!!
-Seizure can be induced with hyperventilation
general onset non-motor seizures (absence) (petit mal)- EEG and tx
Characteristic EEG finding during seizure :
- 3 Hz generalized spike-and- wave!!!!!**
Treatment:
- Ethosuximide!!!! is 1st line! (PANCE)
- others: Valproate**, lamotrigine, divalproex
-Attacks tend to diminish in adolescence then disappear
-Some children will be at increased risk of generalized motor seizure later on
myoclonic seizures definition and variations
-Rapid brief (50-100ms) muscle jerk
Variations:
-Bilaterally, synchronously
-Unilaterally, asynchronously
-can or can not have post ictal; NO LOC
-Myoclonic jerks range from isolated small movements of face, arm or leg to massive bilateral jerks
atonic seizure
-drop attacks
-sudden loss of muscle tone resulting in fails
febrile seizure: presentation, what age group
-Specific to infants and children between 6 months – 5 years old
-Benign condition and uncomplicated~!
-Single, generalized motor seizure during the peak of a fever + lasts no more than a few minutes
-Seizure should not recur during the same episode of fever
-Return to baseline
-Risk of developing epilepsy later in life is almost zero above gen pop
-Do not miss: acute encephalitis, meningitis, complex febrile convulsions
-LOOK towards/away LESION FOR STROKE
-LOOK towards/away FROM LESION FOR SEIZURES
-LOOK TOWARDS LESION FOR STROKE
-LOOK AWAY FROM LESION FOR SEIZURES
what sx are associated with frontal lobe partial seizures vs temporal lobe seizures
Frontal:
- intense fear
- gaze/head deviation contralaterally
-tonic posturing
Temporal:
- deja vu
- epigastric sensation
- smell/taste sx
- automatism
localization of seizures:
35 year old woman
Prior déjà vu with burnt smell and metallic taste
Followed lip smacking and hand picking
Followed by looking to her right side
Followed by generalized shaking
35 year old woman
Prior déjà vu with burnt smell and metallic taste
Followed lip smacking and hand picking
Followed by looking to her right side
Followed by generalized shaking
-LOOK TOWARDS LESION FOR STROKE
-LOOK AWAY FROM LESION FOR SEIZURES
-Began in TEMPORAL lobe
-LEFT SIDE
- FOCAL THAT Spread to bilateral tonic clonic
estimate risk of seizure recurrence: unprovoked vs provoked
Unprovoked seizure:
-Whatever lesion or network that caused the first seizure.. Is likely to happen again!!
Provoked seizure = low risk
-Drug-induced- Antibiotics, illicit drugs
-Cerebrovascular - Acute strokes
-Toxic or metabolic disorders- Hyponatremia
-Traumatic brain injury
-CNS infections- Meningitis, encephalitis
etiology and pathophysiology of provoked seizures
Vascular
-Acute ischemic stroke
-Intracerebral hemorrhage
-Subarachnoid hemorrhage
-Hypertensive encephalopathy (PRES)
-Anoxic brain injury
Infectious causes
-Encephalitis
-Meningitis
-Abscess
-Traumatic causes
-Epidural hematoma
-Subdural hematoma
-Autoimmune causes
-Systemic lupus erythematous (SLE)
-Paraneoplastic syndromes
Metabolic causes:
-B1 (Thiamine) deficiency! - ALCOHOL
-Hypoglycemia
-Hyponatremia (sometimes hyper-)
-Hypocalcemia
-Hypomagnesemia
-Hypophosphatemia
-Uremia (BUN)
-Hyperammonemia (liver damage)
-Hyperthyroidism (T3 T4)
-Idiopathic causes- Epilepsy
-Neoplastic causes
-Drug causes (see next slide)
-Eclampsia
-Everything else - Fevers can trigger esp. in children
-Genetic diseases- Phenylketonuria (PKU)
-Is it a provoked or unprovoked seizure?
No reported meds
Negative urine tox
Non-contrast CT head negative
CBC, CNP, UA is normal
No evidence or history suggestive of brain injury or head trauma
No fever or evidence of CNS infection
No reported meds
Negative urine tox
Non-contrast CT head negative
CBC, CNP, UA is normal
No evidence or history suggestive of brain injury or head trauma
No fever or evidence of CNS infection
Likely had an unprovoked seizure!
first unprovoked seizure: risk factors for developing epilepsy
-Prior neurological insult, such as neurological deficits from birth (e.g. Mental Retardation Cerebral Palsy) = most powerful and consistent predictor of recurrence****
-Partial (focal) seizure- means you already has some lesion or scar in the brain -> likely to happen again
-Abnormal EEG
-Febrile seizures- minor
-Status Epilepticus
-Postictal (Todd’s) paralysis- seizure that occurs and takes out half the body
- only ~25% of pts have second seizure in next 2 yrs
Evaluation of first seizure: AAN guidelines
Neuroimaging (CT, MRI)
-Yield cause in about 10%
-Always perform for focal seizures -> there has to be something there to cause seizure (lesions)
-May lead to the diagnosis of brain tumor, stroke, cysticercosis (parasitic infection of central nervous system), or other structural lesions.
LP:
-Helpful in febrile patients or afebrile immunocompromised patients
Toxicology screening:
-~ 3% of all seizures in the ER: drug intoxication (e.g., cocaine, other stimulants)
anti-seizure drug levels labs: when is it indicated, factors that affect drug level targets, and what type of drug levels can be checked
-recommended for any pt with known epilepsy/seizure disorder who has a change in their seizure pattern
Factors that affect drug levels and dictate target drug levels include:
-Their usual target drug level
-Drug compliance
-Any new meds that may interact with the anti-seizure medication (eg antibiotics, Wellbutrin)
-Change in frequency, duration or features of the seizure
-Intercurrent illness that may lower the the seizure threshold
Anti-seizure drug concentration assays available to most EDs include: phenytoin, valproate, phenobarbital and carbamazepine.
Drug levels that are not immediately available in the ED but may be useful for our neurology colleagues in follow-up include: lamotrigine, levetiracetam (Keppra) and clobazam
-breakthrough seizures
drugs that may lower seizure threshold
If you are susceptible - you may get seizure
Regular person should be fine
temporal lobe epilepsy onset, seizure types
“Mesial temporal sclerosis”
-Age of onset: 7-20
-Often refractory to medication
-± History of febrile seizure as infant
seizure types:
-Simple partial (“aura”)- one part moving w/o loss of consciousness
-Complex partial seizure (LOC): 70-80%
-Secondarily generalized tonic clonic
temporal lobe epilepsy: EEG findings and MRI structural abnormality
Characteristic EEG finding: Focal interictal spikes over temporal lobe- just know its over temporal lobe
MC structural abnormality on MRI: mesial temporal lobe sclerosis
35 year old woman with a single unprovoked 1 minute seizure
MRI and EEG revealed a confirmed left temporal epileptogenic focus
MRI and EEG revealed a confirmed left temporal epileptogenic focus
FOCAL TEMPORAL LOBE EPILEPSY due to a structural lesion (mesial sclerosis)
identifiable causes of epilepsy based on age:
- neonate to 3 yrs
- 3 - 20 yrs
-20 -60 yrs
- 60+ yrs
what to do if somenoes having a seizure
-Don’t panic!
-dont restrain
-Keep them safe
-Time the seizure
-Turn on side for recovery position -> after the seizure
initial tx of epilepsy based on special populations/comorbidities: Female of Childbearing Age, elderly, depression, hepatic renal
Female of childbearing age with either genetic generalized epilepsy or focal epilepsy: Lam and Lev for Ladies
- LAMotrigine
- LEVetiracetam
- DO NOT GIVE VALPROATE (X)
-LONG TERM THERAPY
elderly: 3 Ls for elderly
- Lamotrigine
- Levetiracetam
- Lacosamide
depression:
- focal (LaLaOx): Lamotrigine, Lacosamide, Oxcarbazepine
- Genetically mediated epilepsy (LV): Lamotrigine, Valproate
Liver: Lets Go Liver
- Levetiracetam, Gabapentin, Lacosamide
Kidney = LOL
- Lamotrigine, Oxcarbazepine, Levetiracetam
Focal Epilepsy: first line tx
“LL-O-CL for Focal”
Lamotrigine****
Levetiracetam
Oxcarbazepine
Carbamazepine
Lacosamide
Genetically mediated generalized epilepsies syndrome with mainly generalized tonic-clonic seizures and Genetically mediated generalized epilepsy syndrome with myoclonic seizures tx
“L-L-V-T-Z for Generalized Tonic-Clonic”:
- Lamotrigine
- Levetiracetam
- Valproate
- Topiramate
- Zonisamide
Myoclonic: “Leaps and Violent Zaps”
- Levetiracetam
- Valproate
- Zonisamide
Absence Seizures: first line tx
“EVL”: Absence Seizures (“Evil Absences”)
- ETHOSUXIMIDE!!!!!
- Valproate
- Lamotrigine
lamotrigine:MOA, indication, adrs
MOA: Not completely understood
Indication:
-Focal onset seizures, generalized onset seizures (usually add on)
-3rd line for absence seizures
ADR:
Dizziness, headache, !rash (rare SJS)!, nausea!, diplopia
High number of CYP450 interactions
carbamazepine: moa, indication, dose, adrs
MOA: sodium channel blocker
-Slow oral absorption but enters brain rapidly because of its high lipid solubility
-Induces P-450 system
-narrow spectrum
Indication:
-First line med for trigeminal neuralgia
-FOCAL SEIZURES: Simple partial, complex partial, and secondarily generalized seizures
( Not used for generalized epilepsy)
Dose:
-Usual adult dose: 800-1600 mg/day
-Half-life: 8-22 hrs
Common side effects: drowsiness, vertigo, ataxia, blurred vision, low sodium.
ADRs:
-SIADH - HYPONATREMIA!! -> can cause seizures
-Hepatotoxicity
- SJS
valproate acid: MOA, indication, dose, adr
MOA: multiple
- suppresses voltage gated Na+ channels
- increases effects of GABA (inhibitory neurotransmitter)
Indication:
- myoclonic
- absence
- generalized tonic-clonic seizures/epilepsy
Dosing:
- adult: 1000-3000 mg/day
- half -life: 15 hrs
common side effects:***
- n/v
- tremors
- WT GAIN -> young pt hate this
- hair loss
ADRs: tbh use only in refractory seizures bc of adrs
- teratogenic*
- pancreatitis
- hepatotoxicity
- thrombocytopenia (easy bruising)
Patient was started on Keppra due to its low side effect profile and was doing well
Many months later…
Patient became ill with suspected food poisoning with multiple bouts of vomiting
She smelt the familiar burning rubber
Developed bilateral tonic-clonic seizure
Followed by another…
And another …
EMS was called
status epilepticus
status epilepticus
-TIME IS BRAIN
-Immediate management andstabilization
-Pharmacological and non-pharmacological interventions
-longer you are seizing the worser off
-Seizure activity >30 minutes causes permanent brain damage
ADrs of anti-seizure meds
classic definition off status epilepticus
-continuous seizure lasting > 5 mins
->= 2 seizures occurring in close succession (<5cm) without returning to neurological baseline in between
-permanent damage after
convulsive status epilepticus!! epidemiology
-Medical Emergency “Seizure -> Coma -> Death”
-65,000 cases each year in US
-Remember, most seizures resolve spontaneously in 1-3 minutes!
-Seizure activity >30 minutes causes permanent brain damage
-> 50% affected do not have history of epilepsy
convulsive status epilepticus: acute causes
-Low antiseizure medication levels
-Cerebrovascular disorders (CVA) or hypoxia
-Systemic metabolic derangement or alcohol related
-Drug abuse
-Head trauma
-Infection
-Tumor
-Fevers in children 6mo-5yo
Convulsive status epilepticus: focused hx and goals
Focused history:
-History of seizures?
-What anti-epileptic meds are they on?
-Anything that could have provoked the seizure?
-If they have had status before, what worked?
Goals:
-Stop seizure
-Treat underlying medical or neurological disorder
Convulsive Status Epilepticus: why is it a medical emergency
Metabolic and Physiologic Stresses: Prolonged seizures cause complications like
- hyperthermia
- hypoxia
- lactic acidosis
- hypoglycemia
- HTN encephalopathy
Mortality Risk: Death from the underlying cause
Immediate life threats in convulsive status epilecticus: what is the treatment
Hypoxemia (O2)
hypertensive encephalopathy (labetolol, nitroprusside)
- dont lower BP >25% -> can cause ischemic stroke
severe hyperthermia (cooling)
Metabolic: hypoglycemia (glucose), hyponatremia (hypertonic saline), hypomagnesemia (Mg), hypocalcemia (Ca)
Toxicologic:
- anticholinergics (HCO3)
- isoniazid (pyridoxine)
- lipophilic drug overdose (lipid emulsion)
Eclampsia:
- Occurs typically >20 weeks of pregnancy and up to 8 weeks postpartum
- tx: IV MgSO4 4-6 g over 15-20 min, then infusion 1-2 g/h
protocol for status epilepticus: first 0-10 minutes
0-10 min: Recognize status epilepticus immediately
-ABC DEFG (airway breathing circulation) (Don’t Ever Forget the Glucose!!!)
-Airway: Lateral decubitus (minimize aspiration risk) or head-up with suction/nasal trumpets
-Give oxygen as needed
-Obtain IV access; get VBG, CBC, CMP, mag, phos, tox screen, beta-HCG, CK, AED levels, trop
-Begin EKG monitoring
First line meds: are BENZOS (FOR ALL ACTIVE SEIZURES)
- IV Lorazepam (Ativan) 2-4 mg; repeat once 4 minutes later (max 0.1mg/kg)
-If no rapid IV access: Midazolam (Versed) 10 mg IM
-Other options: Diazepam 20 mg per rectum, Diazepam IV 0.15mg/kg, Phenobarbital IV: 15 mg/kg
-Consider thiamine 100 mg IV; 50 ml of D50 IV unless adequate glucose known
- biggest pitfall: underdosing or dosing too late… time is way more important than chose of benzo or route
protocol for status epilepticus: 10-15 mins, second tx phase
10-15 min: Prepare to intubate via RSI
If seizures persist, begin 2nd line options as a single dose: LVFL
-Levetiracetam (Keppra) - MC
-Valproic acid
-Fosphenytoin (Cerebyx) or Phenytoin: Avoid in toxicogical causes of seizure (drugs) it can cause cardiovascular collapse, Continuous ECG monitoring
-Lacosamide 400mg IV - dont need to know
-IF YOU BROKE THE SEIZURE WITH A BENZO TILL GIVE THESE MEDS AFTER!!!!!!!!!!!!
status epilepticus protocol- 15-20mins
15-20 min: If seizures persist after 1st and 2nd line medications = refractory status epilepticus
-the longer they are in it the harder it is to get them out
Medication options in refractory status epilepticus:
continuous infusion general anesthesias + paralytics:
-Midazolam (Versed) 0.2 mg/kg IV, then infusion of 0.05-2mg/kg/hr
-Propofol 2-5 mg/kg IV, then infusion of 50-80 mcg/kg/min (3-5 mg/kg/hr)
- pt will stop moving -> need EEG to see active seizure
others:
-Ketamine 0.5-3 mg/kg IV, then infusion of 0.3-4mg/kg/hr
-Lacosamide 400 mg IV over 15min, then maintenance of 200mg q12h PO/IV
-Phenobarbital 15-20mg/kg IV at 50-75mg/min
-Begin EEG monitoring ASAP if patient does not rapidly awaken, or if any continuous IV treatment is used
-you cant tell if they are still seizuring if you give anesthetics or paralytics!!!! -> MONITOR EEG
-If stable for imaging: CT head to rule out space occupying lesions or intracranial hemorrhage
Paramedics administered 10mg Midazolam IM
Received 4mg lorazepam and 3.5 grams of levetiracetam in the ER
Seizures stopped
Intubated for airway protection
Continue midazolam drip
Continuous EEG -> no further seizure activity
-she prob went into status bc of vomiting up her pills
-load up on keppra
non-convulsive status epilepticus (NCSE) definition and presentation, dx
-Status epilepticus without convulsions!
-brain is seizuring but not the body
-Frequently unrecognized and difficult to diagnose
-MC: middle-aged or elderly w/ no prior history of epilepsy
Continuous altered mental status and behavioral changes
-Can last days
-Examples: Inattentive, dull, change in affect, bizarre behavior, hallucinations
DX: ictal pattern on EEG while the patient is symptomatic
delaying tx in status epilepticus: young pts and tx consequences
-Young: Mortality increased from 36% in those whose NCSE was diagnosed within 30 minutes to 75% in those in whom the diagnosis was delayed 24 hours.
-Status epilepticus becomes harder to treat the longer it continues!!!
surgical tx for epilepsy with focal source: brain surgery risks vs benefits
Risks of surgical resection:
-Temporal lobe damage, Visual field defects, Aphasia, Memory loss, Depression
-Perioperative risks: Bleeding, infection etc.
Benefits:
-65% of patients are essentially cured of seizures
-90% have at least signficiant decrease in seizures
-Decreased mortality -> Ppl usually die from the hypoxia due to choking form seizures
-recommend for pts that are refractory to tx
surgical tx - neuromodulation- non-resection options
Responsive neurostimulation (RNS)
-Closed loop system that detects electrical activity with internal EEG and sends signals to modulate
Deep brain stimulation (DBS)
-Open loop therapy that gives continuous electric therapy to the thalamus to increase the seizure threshold
Vagal nerve stimulator (VNS)
-Delivers intermittent electrical pulses to the left vagus nerve
-not as good as resection as of now
A 39-year-old man presents to the emergency department due to abnormal movement of his left arm. These involuntary abnormal movements last a few minutes and he is aware during these episodes. He also endorses right-sided headaches that are worse in the morning. Medical history is unremarkable. He reports increased stress due to co-parenting for his newborn baby two months ago.
Physical examination is normal.
-What type of seizure is this patient having?
-What are you concerned for?
- What imaging tests would you order? + where would you expect to find something
What type of seizure is this patient having?
-partial focal seizure
What are you concerned for?
-positional postural headache - brain tumor
-infection- fever, nuchal rigidity
-new meds
-drugs
-falls? -> subdural hematoma
-stroke
-ADMs
What imaging tests would you order?
-CT non-contrast
-MRI with contrast
Where would you expect to find something?
-right sided motor cortex temporal lobe side
discharge instructions and mandatory reporting for seizures
Good discharge instructions can be lifesaving. Instruct that they CANNOT
- SWIM
- DRIVE: seizure with impaired awareness -> must wait 12 months from last seizure
- bathe alone or a baby in a bathtub
- climb heights
- operate heaving machinery
Check your local regulations and policies for laws regarding mandatory reporting.
-In NY: NOT required to report a seizure to the DMV. Individuals with epilepsy are expected to provide that information
-In Ontario: mandatory to report anyone 16+ yrs who has had a seizure to the Ministry of Transportation regardless even if they don’t have a driver’s license
A 25 y/o male presents with a witnessed tonic-clonic seizure. His past medical history is significant for epilepsy. He has been off all medications for 6 months. His vitals and labs in the ED are normal, his neurological exam is normal, there are no signs of head injury, and he is at his baseline neurologic status. Which of the following is the MOST appropriate next step and rationale?
!!!!!!!C. Administer Levetiracetam 1500 mg PO, no neuroimaging required in ED. Leviteracetam loading is unlikely to cause severe side effects which may prolong length of stay in the ED compared to IV phenytoin loading.
A 40 year old man presents to the ER during summer after a syncopal episode with loss of consciousness with generalized body shaking
He reports walking and having a sensation that he was about to faint, including feeling dizzy and nauseous. The next thing he remembers is waking up.
Witnesses report his body shaking after he hit the floor, but he woke up quickly afterwards. There was brief confusion after awakening but he quickly returned to baseline.
Is this seizure?
NOT A SEIZURE - What imaging tests would you order?
syncope vs seizure
-absence has no post ictal
-vitals arent helpful
- Eyes are open in seizure and look away and eyes closed in syncope
Mrs L, who is a 55 years old, presents with episodes of light-headedness, unresponsiveness, olfactory hallucinations, and occasional motor weakness that had been occurring for approximately 1 year, as well as more recent onset of stammering speech.
PMH: Obesity, HTN, Pre-DM
Social history reveals severely stressful life events; abuse as a child, several recent family deaths. No alcohol or ilicit drug use.
Extensive neurological workups, including inpatient evaluations in 2 university epilepsy monitoring units, failed to reveal a cause of these symptoms
psychogenic non-epileptic seizures (PNES)!!!!
Used to be pseudoseizures =. Bad rep
* Usually reaction to stressful events and pt will feel like they have a seizure
The way they present is different
* Asynchronous thrashing
* Forcefully close eye
CK levels could rise in seizures but wont here
Don’t accuse them of lying - CBT is intense tx
psychogenic non-epileptic seizures (PNES) DSM 5, pearls, red flags
DSM-5 diagnosis: Functional neurologic disorder and behavioral response to underlying emotional or psychological distress
-Often underlying conversion disorder and rarely, malingering
-manifestation of brain- brain hyperactivity is not there
-Episodes that simulate seizures (pseudoseizures) but are not a result of neuronal discharge
- 60% of pts with PNES also have hx of epileptic seizures…when in doubt, assume true seizure
Red flags for PNES:
-Treatment resistant “epilepsy” with normal cognitive function and normal brain imaging
-Unconventional motor display: asynchronous thrashing of limbs, side-to-side movements of the head, striking at the staff, hand biting, kicking, forcefully closed eyes, screaming or even talking during the episode
-Rapid breathing (tonic-clonic usually are apneic)
-Lack of a post-ictal period
-Normal serum creatine kinase levels post seizure
These patients suffer from morbid psychiatric illness. The treatment of these patients requires a patient, nonjudgmental, and multidisciplinary approach with the goal of reducing disability and hospital admission and eliminating unnecessary medications. CBT is the only proven therapy for PNES.
-CK levels wont rise
-sympathize with them
Which of the following statements is the MOST accurate regarding the comparison of migraines and seizures?
!!!!!C. Seizure symptoms typically progress to maximum intensity over seconds while migraine symptoms typically progress to maximum intensity over several minutes
D. Both migraines and seizures typically produce negative neurological symptoms
A 32 y/o G2P2 who is 1 week postpartum presents to the Emergency Department after a witnessed seizure. She received 1 dose of IM Lorazepam with EMS. Her triage vitals are BP 179/105 HR 92 SpO2 96% Glucose 102. She seizes again in the Emergency Department. Which of the following is the BEST next step in management?
C. Administer Magnesium Sulfate IV bolus
syncope: definition and common causes
Def: Sudden, transient loss of consciousness due to inadequate cerebral nutrient flow -> SX not DS!!!
Common causes: !Vasovagal (reflex)!, Arrhythmias, Aortic Stenosis, Carotid Sinus Hypersensitivity, Myocardial Infarction, Hypoglycemia, Orthostatic Hypotension, Postprandial Hypotension, Psychogenic, Pulmonary Embolus, Seizures, Intoxications, Metabolic Disorders
syncope Hx: presyncope sx, position before syncope, precipitating factors, post syncope sx
Presyncope: lightheadedness, warm/cold feeling, sweating, palpitations, pallor, nausea, visual blurring, diminution of hearing and/or unusual (often “whooshing”) sounds
Position before syncope:
- !prolonged standing!, sudden change in posture, supine
Precipitating factors:
- exertion, meds, !coughing/micturition/urination/defecation, emotional stress!, head movement / shaving / tight collars
-Prodrome: !Neurally mediated (vasovagal) = abdominal pain, diaphoresis, nausea, blurry vision, dizziness, lightheadedness.! SAH=HA. Cardiac = palpitations, chest pain, dyspnea
Post syncope symptoms: Seizure = amnesia, eyes closed, tonic-clonic movement, prolonged confusion, tongue biting. Immediate recovery = cardiac, psychogenic. Neuro deficit = CVA/TIA. !Vasovagal = fatigue, nausea, vomiting, myoclonic movement, transient disorientation!
-*Bolded = more likely neurally mediated = vasovagal, orthostatic, or carotid sinus
syncope dx
Diagnostic studies are determined by history and exam
-ECG: always get this first, top differential is arrhythmia**
-Labs: CBC for anemia, HCG for pregnancy
-Holter monitor, Echo (TTE): arrhythmias and cardiac causes
- Tilt-table testing: suspect vasovagal or orthostatic causes
-EEG, CT, MRI brain: ONLY if neurological causes suspected
vasovagal syncope: overview, sx, tx
MC syncope:
- typically benign
- clear disposing factors: prolonged standing, emotional distress, pain
- prodrome is neurally mediated : nausea, abdominal pain, blurred vision, or diaphoresis before fainting
- recovery occurs quickly when lying down.
tx:
- assist pt to supine with leg elevated to avoid injury
- avoid triggers: prolonged standing, straining, stressful situation
