Seizure and Epilepsy Flashcards
(118 cards)
1
Q
Epilepsy
A
The condition of recurrent unprovoked seizures
2
Q
Things that may provoke seizures in non-epileptic patients
A
Acute hypoglycemia, alcohol withdrawal, high fever, and medication or drug toxicity
These are all acute, reversible factors
3
Q
Things that may cause seizures, but do not technically “provoke” them
A
Brain tumors, prior stroke, prior head trauma, prior CNS infection, and cortical malformations
These entities are neither acute nor reversible, and so recurrent seizures due to any of these causes are considered unprovoked. Therefore, patients with recurrent seizures due to brain tumors, prior trauma, prior stroke, prior neurosurgery, prior CNS infection, or any other irreversible underlying seizure focus are considered to have epilepsy and should be treated as such.
4
Q
A patient with seizure(s) will generally present for evaluation in one of three scenarios:
A
- After a first seizure or other spell
- With a history of seizures (or other type of spell)
- Actively seizing
5
Q
Whenever possible when trying to gather history on a suspected seizure, ___ should be obtained.
A
Whenever possible when trying to gather history on a suspected seizure, a clear description of the event by witnesses should be obtained.
6
Q
Seizures are broadly categorized as ___ or ___.
A
Seizures are broadly categorized as generalized seizures or focal seizures.
7
Q
Generalized seizures
A
- Characterized by impaired consciousness and bilateral motor manifestations if motor manifestations are present
- Self-injury, bladder/bowel incontinence, and altered level of consciousness commonly occur with generalized tonic-clonic seizures.
- A postictal state is common after a generalized seizure
- If a patient is found comatose or confused without clear cause and recovers without specific intervention, unwitnessed seizure with a subsequent postictal state should be considered in the differential diagnosis.
- Some generalized seizures produce altered consciousness without motor features, such as absence seizures.
8
Q
Motor manifestations of seizures
A
Motor manifestations can be:
- tonic (stiffening of involved body parts),
- clonic (rhythmic movements),
- tonic-clonic (mix of tonic and clonic),
- myoclonic (brief jerks),
- atonic (loss of postural tone causing drop attacks).
9
Q
Postictal state
A
Characterized by altered consciousness, which can range from confusion to coma depending on the severity and length of preceding seizure activity
In a patient with altered level of consciousness following seizure(s), continued nonconvulsive seizures may be occurring and must be distinguished from a postictal state. EEG is essential to making this distinction, as there may be barely visible motor activity or no motor activity at all.
10
Q
Absence seizures
A
Absence seizures are characterized by brief periods of altered awareness in which patients are unable to communicate or engage with the environment, but have no motor features.
Absence seizures are more common in children.
11
Q
Focal (Partial) Seizures
A
- Focal seizures can occur with impairment of consciousness (complex partial seizures) or with consciousness preserved (simple partial seizures)
- The clinical manifestations depend on the origin of seizure activity within the brain and can include focal motor symptoms (tonic-clonic movements, posturing, head and/or eye deviation), focal sensory symptoms (paresthesias that tend to spread over seconds), visual, auditory, or olfactory hallucinations, and/or psychic phenomena such as déjà vu (a sense of already having experienced a new place or event), jamais vu (a sense of never having been in a familiar place or situation), or a sense of fear.
- A seizure may begin with focal manifestations and secondarily generalize
12
Q
Post-ictal weakness / Todd’s paralysis
A
- May occur in the limb(s) affected by seizure activity
- If a seizure is unwitnessed and a patient is found with focal postictal weakness, the patient may be initially thought to have had a stroke. Therefore, seizure with subsequent postictal paralysis should be considered in the differential diagnosis of acute stroke and transient ischemic attack (TIA) and vice versa.
13
Q
Aspects of history that suggest fall/loss of consciousness is more likely seizure than syncopy
A
- Tonic clonic activity pre-, during, or post-fall
- Tongue biting
- Fecal or urinary incontinence
- Prolonged unconsciousness before awakening
- Prolonged confusion or weakness post-fall
- Preceding aura (foul odor, sense of déjà vu)
- No memory of just before the fall
14
Q
Seizures generally cause ___ while TIAs generally cause ___.
A
Seizures generally cause “positive” symptoms (i.e., abnormal movements, paresthesias, visual phenomena) while TIAs generally cause “negative” symptoms (i.e., weakness, loss of sensation, visual field deficits).
15
Q
Distinguishing seizure from a migraine with aura
A
- Positive symptoms of migraine auras tend to evolve/spread over minutes, whereas those of seizures generally evolve/spread over seconds.
- Migraine does not lead to alterations in level of consciousness, although it can cause mild confusion in some patients
- A headache is a common (but not universal) accompaniment to migraine with aura, but a headache can also be a component of a seizure aura or postictal state.
16
Q
Distinguishing Seizures From Psychogenic Nonepileptic Spells (Pseudoseizures)
A
- Psychogenic nonepileptic spells (also called pseudoseizures) are generally a manifestation of an underlying psychiatric condition (e.g., conversion disorder)
- Clinical features suggestive of psychogenic nonepileptic spells rather than epileptic seizures include:
- prolonged bilateral movements with preservation of consciousness
- forced eye closure during episodes (eyes are generally open during seizures)
- episodes provoked by stress or other emotional circumstances
- continued events in spite of multiple antiepileptic medications (though this can also occur in refractory epilepsy)
- Remember, patients with epilepsy can have both seizures and nonepileptic spells, and patients with underlying psychiatric conditions can have seizures
17
Q
Five categories of EEG findings
A
- Normal variants not associated with epilepsy but of unclear significance (e.g., small sharp spikes, wicket spikes)
- Findings associated with focal or global cerebral pathology but not necessarily with epilepsy (e.g., focal or generalized slowing, triphasic waves, frontal intermittent rhythmic delta activity [FIRDA])
- Findings indicating cortical irritability and risk of seizures (e.g., spike-wave discharges, periodic lateralized epileptiform discharges [PLEDs], generalized periodic discharges [GPEDs]).
- Seizures
-
Artifact, which can be due to:
- Patient factors (e.g., blinking, movements)
- Technical factors (e.g., electrocardiographic [ECG] artifact, interference from electrical hospital equipment, issues with EEG leads)
18
Q
Sensitivity of a routine EEG in detecting epileptiform activity
A
- Only 50%
- BUT, can be improved by:
- performing the EEG in the sleep-deprived state
- performing EEG within 24 hours of a seizure event
- repeating EEG on multiple occasions
19
Q
Notes on epileptiform activity on EEG
A
- A small proportion of the population may have EEG abnormalities of no clinical significance
- A number of medications can also cause EEG abnormalities
20
Q
The absence of epileptiform discharges ___ and their presence ___
A
The absence of epileptiform discharges does not “exclude” epilepsy and their presence does not “confirm” epilepsy
21
Q
Workup of a patient’s first seizure
A
- Medication/drug history
- Labs (electrolytes, tox screen)
- Neuroimaging (preferably MRI w/ contrast, possibly also arterial/venous imaging)
- Lumbar puncture if CNS disease suspected from clinical picture
22
Q
Epilepsy-protocol MRI
A
- Includes coronal views of the hippocampi to look for asymmetries in size or signal characteristics on T2/FLAIR that may suggest an underlying focus for temporal lobe epilepsy (mesial temporal sclerosis)
- Seizures can produce transient MRI abnormalities, most commonly diffusion restriction (on DWI/ADC sequences) and/or T2/FLAIR hyperintensity in the cortex, splenium, and/or thalamus
- Diffusion restriction on MRI can also be caused by acute stroke
- The pattern of diffusion restriction due to seizure can be distinguished from stroke in that it is often limited to the cortex and can span multiple vascular territories.
23
Q
What is going on in this MRI?
A
Mesial temporal sclerosis
A: Coronal T1-weighted image showing asymmetric hippocampi (smaller left hippocampus). B: Coronal FLAIR image showing increased signal in the left hippocampus.
24
Q
When are antiepileptics useful?
A
- If a clear acute, reversible etiology of a patient’s seizure is identified and the patient has returned to normal with treatment of this underlying provoking condition, antiepileptic drug treatment is not necessarily indicated.
- EEG is not particularly helpful in this scenario
- If a structural lesion is also found, anti-epileptics may be used prophylactically
- If there were multiple and/or difficult-to-control seizures due to an underlying acute reversible provoking factor, a short course of antiepileptics may be maintained and later tapered.
- If there is a structural lesion identified in a patient with a first seizure, long-term antiepileptic treatment is generally indicated.
-
After an unprovoked seizure, medium-risk or high-risk patients should be treated immediately with long-term antiepileptic therapy
- For low-risk patients, it is a joint decision between patient and clinician, but data is unclear on benefits.
25
Counseling after first seizure
Patients with active epilepsy or who have just had a first seizure should be **counseled not to drive, operate heavy machinery, work at heights or near fire, bathe/swim alone, or participate in any other activity during which a seizure could lead to significant injury or death**
**Laws vary from state to state** with respect to the seizure-free period necessary before driving, so local regulations should be consulted.
The recommended seizure-free period for driving (**6–12 months in most U.S. states**) can be used as a **rough guide for avoidance of other potentially risky activities.**
26
Antiepileptics sometimes. . .
. . . **make epilepsy worse!!!!**
It is important to know which diseases antiepileptics treat, and which they exacerbate. THESE ARE NOT BENIGN DRUGS.
27
First-line therapy for idiopathic genetic generalized epilepsy syndromes
**Valproate**
*with the exception* of **childhood absence epilepsy**, for which **ethosuximide** is first-line therapy.
28
Valproate should be avoided in. . .
. . . **women of child-bearing age, due to its teratogenicity.**
Same goes for **topiramate.**
It should **also be avoided in children \<2 years of age,** due to **hepatotoxicity** in this population.
29
Carbamazepine is particularly effective for \_\_\_
Carbamazepine is particularly effective for **partial (focal) seizures**
**BUT** may worsen **idiopathic genetic generalized epilepsy syndromes** such as **childhood absence epilepsy**
30
Drug-drug interactions of antiepileptics
* The older AEDs phenobarbital, phenytoin, carbamazepine, and valproate have the most drug–drug interactions
* **Phenobarbital, phenytoin, and carbamazepine** are **enzyme inducers**, **lowering the levels** of other medications, AND **decreasing the effectiveness of oral contraceptives**
* **Valproate** is an **enzyme-inhibitor,** **increasing the levels of other medications.**
31
Side effects of antiepileptics
* Nearly all AEDs can cause **dizziness, double vision, sedation, and/or behavioral changes.** Worse w/ older agents, less so with newer ones.
* Life-threatening toxicities include **hepatic toxicity, agranulocytosis, aplastic anemia,** and **Stevens-Johnson syndrome**
* Initiation of most AEDs requires **evaluation with baseline CBC and hepatic and renal function tests**. Tests are then **followed serially** to monitor for toxicities
* **Carbamazepine and oxcarbazepine** can cause **hyponatremia,** so serum sodium is also monitored for these
* **Lacosamide** can cause **PR interval prolongation**, and so a **baseline ECG** should be obtained with **serial monitoring**
* **Topiramate and zonisamide** can increase the risk of **nephrolithtiasis**
* **Topiramate and valproate are teratogenic**
32
The highest risks of Stevens-Johnson syndrome among antiepileptics are with. . .
. . . **phenytoin, phenobarbital, carbamazepine, and lamotrigine**
The risk of Stephens-Johnson syndrome with **carbamazepine** is higher in **Asian**s with a particular **HLA type (HLA-B\*1502)**, so this should be screened for before starting carbamazepine in patients with Asian ancestry
33
Risk of SJS may be reduced in antiepileptic treatment by. . .
. . . **slowly uptitrating the drug rather than giving the full dose all at once.**
34
Among antiepileptics, ___ both have mood-stabilizing properties, whereas ___ can cause irritability and depression
Among antiepileptics, **valproate and lamotrigine** both have mood-stabilizing properties, whereas **levetiracetam** can cause irritability and depression
35
At each follow-up visit, a patient on AEDs should be assessed for . . .
At each follow-up visit, a patient on AEDs should be assessed for **whether seizure frequency has improved** and **whether there are side effects of the AED(s).**
36
Antiepileptics must always be. . .
. . . **slowly up-titrated and down-titrated, not abruptly started and stopped.**
37
Carbamazepine autoinduction
Unique effect to carbamazepine
Carbamazepine **induces its own metabolism**, and so as a result, the initial **effectiveness may** **decrease around 6 weeks to 2 months** after initiating the medication, **requiring a dose increase.**
38
Refractory epilepsy
* If a patient is **not controlled after adequate trials of two well-tolerated AEDs** (individually or together), the patient is considered to have **refractory (drug-resistant) epilepsy.**
* Such patients should be considered for **vagal nerve stimulator, epilepsy surgery,** and/or the **ketogenic diet**
* ****If surgical resection of the epileptic focus is under consideration and MRI or nuclear medicine study does not reveal the causative lesion, **intracranial EEG** can be used to more precisely localize the epileptogenic lesion
39
Tapering off antiepileptics in seizure-free patients
In patients who have been **seizure free for 2 years**, the question often emerges as to whether AEDs can be titrated off.
**A gradual taper can be attempted**, explaining to the patient that there is about a **40% risk of seizure recurrence**, and that that risk is **greatest during the period of off-titration**. Therefore, during this period, the **patient should not drive, should not swim or bathe unaccompanied, and should not work at heights.**
If a patient has a seizure during the taper, **lifelong AED therapy is generally warranted.**
40
Status epilepticus
defined as **5 or more minutes** of **continuous seizures,** or repeated seizures **without return to consciousness between them.**
41
Aspects of managing status epilepticus
1. **Management of the “ABCs” (airway, breathing, circulation):** Continuous oxygen saturation monitoring and cardiovascular monitoring are essential and intubation/mechanical ventilation may be necessary.
2. **Treatment of seizures in status epilepticus**: Use the status epilepticus treatment algorithm
3. **Search for an underlying cause**: Evaluation for **hypoglycemia, electrolyte abnormalities, drug intoxication or withdrawal, structural lesion, or an infectious or inflammatory etiology** in parallel with treatment. **Glucose and thiamine are generally given immediately** to patients in status epilepticus.
42
Status epilepticus treatment algorithm
1. Serial doses of **benzodiazepines** along with **glucose** and **thiamine**
2. If not under control, **phenytoin load** is given (some practitioners use valproate, phenobarbital, or levetiracetam instead)
3. If not under control, an **additional partial load** of the antiepileptic loaded in the prior step
4. If not under control, **patient is intubated** and **24-hour coma is induced** with **pentobarbitol, midazolam, or propofol.****Continuous EEG**monitoring is generally initiated at this point to guide success of therapy. A**daily maintenance AED** is also initiated.
* This step is generally only taken for **generalized convulsive seizures** but **_not_** **for focal motor status epilepticus**; use of these measures in nonconvulsive status epilepticus is debated
5. **Sedatives are weaned** to see if patient will seize again. If so, **additional AEDs and/or sedative agents** can be added
6. If still not under control, **extreme measures** may include **ketamine, hypothermia, ketogenic diet, immunotherapy** (if there is concern for an autoimmune etiology), **electroconvulsive therapy**, and/or **surgical intervention** (if a seizure focus can be identified).
43
Why do we give glucose and thiamine to patients in status epilepticus?
**Hypoglycemia is a common cause of seizures**, and adding glucose will quickly resolve the seizure. And, even if hypoglycemia isn't the cause, giving glucose is a very cheap and low-risk thing to do.
Thiamine is given with glucose so as to prevent development of **Wernicke’s encephalopathy** in potentially at-risk patients
44
Nonconvulsive status epilepticus
Status epilepticus seizure activity without frank convulsions.
**Subtle motor signs** (e.g., eye deviation or nystagmus, eyelid or facial twitching, extremity twitching) may be present, but some patients may only have **alterations in level of consciousness** ranging from confusion to coma
**The diagnosis is made definitively by EEG.** Continuous EEG for **at least 24 hours** is generally required to evaluate for NCSE, since seizures may be intermittent. If EEG is ambiguous, a **benzodiazepine trial** can be undertaken to see if there is both electrographic and clinical improvement.
45
\_\_\_ should be considered in patients who fail to recover consciousness after one or more seizures
**NCSE** should be considered in patients who fail to recover consciousness after one or more seizures
46
Diagnostic criteria for epilepsy
* An epilepsy syndrome
* OR, 1 seizure with \>60% risk of another
* OR, 2 seizures \>24 hr apart
47
\_\_\_% of people will develop epilepsy at some point in their lifetime.
**3%** of people will develop epilepsy at some point in their lifetime.
48
\_\_% of people will have a seizure in their lifetime
**10%** of people will have a seizure in their lifetime
49
#1 cause of epilepsy worldwide
**Infection**
* **Neurocysticercosis** (Taenia solium, aka pork tapeworm)
* **HIV**
* **TB**
* **ToRCHeS** infections
50
Childhood Absence epilepsy syndrome
* During childhood, ages ~4-8
* 3 Hz spike wave pattern on EEG (shown)
* Normal neurologic exam
* Treated w/ ethosuxamide with good prognosis
51
West epilepsy syndrome
* Begins in infancy
* EEG has hypsarrhythmia (shown)
* Intellectual dysfunction on exam
* Treated w/ ACTH, variable prognosis
52
Juvenile Myoclonic epilepsy syndrome
* Begins in late teens
* Fast, spike wave discharges (shown)
* Neuro exam normal
* Treated w/ broad-spectrum antiepileptics, prognosis requires lifelong antiepileptic therapy
53
Mesial temporal sclerosis
Very common finding on MRI that can produce focal elilepsy
54
Convulsive syncopy
Phenomenon where syncopy **can produce convulsions.**
However, people still regain consciousness rapidly. Important to know that this does exist and can be very difficult to differentiate from a seizure. Even more confusing, syncopy can sometimes trigger a true seizure.
55
Drugs that are IV ABD oral options for epilepsy
* Levetiracetam
* Lacosamide
* Valproate
* Phenytoin
* Phosphenytoin
56
Trigeminal neuralgia is ___ and is therefore treated with \_\_\_
Trigeminal neuralgia is **a focal seizure** and is therefore treated with **carbamazepine**
57
Oral agents good for focal seizures
**Carbamazepine** (makes generalized seizures worse)
**Oxcarbazepine** (makes generalized seizures worse)
**Lamotragine** (can cause SJS, used in women of child bearing age due to good data in pregnancy)
58
Treatment of choice for absence seizure
Ethosuximide
59
Oral only agents good for generalized seizures
**Clobazam**: A benzodiazepine. Has typical benzo side effects (drowsiness). Some patients love it, some cannot tolerate the drowsiness.
**Zonisamide**: Good for general or focal seizures. Risk of kidney stones. History of nephrolithiasis is a contraindication.
60
Which two antiepileptics CANNOT be used in combination?
Carbamazepine and valproic acid
61
Main downside of Lacosamide
Prolongs the PR interval.
An already prolonged PR interval is a contraindication.
62
Practical contraindications of levetiracetam
Levetiracetam can cause psychosis, irritability, or suicidal ideation.
Psych diagnoses are not themselves contraindications to levetiracetam, but prior experience of these symptoms or exacebation while ON levetiracetam is.
63
Main two antiepileptics that CAN cause SJS
1. Lamotragine
2. Valproate
64
Contraindication to valproate
Highly teratogenic
Causes neural tube defects
65
Side effects of phenytoin
* Older medication
* Now used mosty in status epilepticus
* Long-term use is associated with **gingival hypertrophy, hypotension, and bradycardia**
* Phosphenytoin still causes gingival hypertrophy, but is less likely to cause hypotension and bradycardia
66
Status protocol, per Sydni
1. **Lorazepam (ativan)**
* In kids, weight based dosing
* In adults, sequential 2 mg pushes
2. **Levetiracetam, valproate, OR phosphenytoin**
* All noninferior to benzos and to one another
3. **Propofol + intubation**
4. If all else fails, **phenobarbital (barbiturates)**
67
Two categories of generalized seizures
Motor seizures
Absence seizures
68
Generalized motor seizure progression
Starts as tonic, lasting several seconds
Followed by clonic phase, which typically lasts 1-2 minutes and is more or less symmetrical
Toward the end of the clonic phase, jerking stops and the body becomes flaccid
69
Common trigger of absence seizures
Hyperventilation
70
Antiepileptics in febrile seizures
Start them for complex, not for simple
Remember: Complex febrile seizure is an unmasking of underlying epilepsy due to the epileptogenic state of fever in the developing brain
71
Infantile Spasms aka West syndrome
* **NOT A TRUE SEIZURE**, it is a seizure mimic
* Patient will be **\< 1 year old** and present with **bilateral symmetric jerking**
* Will NOT be generalized and there will be NO fever
* Dx: **Interictal EEG** showing **hypsarrhythmia**
* Treat with **ACTH**
* Often associated with **developmental delay** and **tuberous sclerosis**
72
Tuberous sclerosis
* Genetic disease
* Patient will typically be **\< 2 years old**, have **ash leaf spots** (visible w/ Wood's lamp) and **angiofibromas** on skin, afebrile or complex febrile **seizures**
* On brain imaging, **cortical tubers**
* Diagnose w/ CT or MRI of brain
* Treatment of supporting
* Risk of d**evelopment of benign tumors anywhere in body**
74
Special features of absence epilepsy
* Loss of consciousness, but **no loss of tone**
* **No post-ictal state**
* Hundreds to thousands of seizures per day
* "Spacing out" or "ADHD"
* Diagnose with EEG, treat w/ ethosuximide (valproate as backup or if combined generalized seizures)
75
Prerequisite to genetic screening for intellectual disability disorder
Mother must be willing to terminate
Otherwise, the procedure only puts both mom and fetus at risk
76
Diagnosis of intellectual disability disorder
Clinical diagnosis based upon loss of adaptive functioning
77
Stereotypy
Doing the same thing over and over, repetitive behaviors
Symptom of autism spectrum
78
Tic disorder diagnosis and treatment
* Consistent vocal or motor tic
* Patient \< 18 years of age
* Duration \> 1 year
* Clinical diagnosis
* Treatment is D2 antagonist and cognitive-behavioral therapy
79
Febrile seizures
* Most common cause of seizure in a child (3-9% prevalence)
* Occur between 6 months and 5 years
* Setting of febrile illness without evidence of itnracranial infection
* Generalized in onset with no neurologic deficits and no post-ictal state
80
Presence of Todd's paralysis suggests what about the onset of a seizure?
It was focal in onset, even if not apparent to observers present at the time
81
Lennox-Gastaut syndrome
* Seizure disorder of **childhood**
* Tonic, atonic, myotonic, generalized tonic-clonic, or absence
* Associated with **major cognitive impairment and disability**
* EEG shows **slow (1-2 per second) spike-and-wave discharges**
* Treat w/ valproic acid, lamotragine, felbamate, rufinamide, or clobazam
82
Focal motor seizure (eg benign rolandic epilepsy)
* Seizure syndrome of childhood
* Aware, focal seizure involving mouth and face, infrequently as generalized tonic clonic seizures
* Associate with a **nocturnal preponderance of seizures**
* EEG: **Centrotemporal spikes**
* Treat w/: Carbamazepine, sometimes no treatment is necessary
83
Absence epilepsy
* Seizure disorder of childhood and adolescence
* Mostly absence seizures, sometimes tonic clonic seizures
* **Hyperventilation** is a common trigger
* EEG: **3 per second generalized spike wave**
* Treat w/: Ethosuximide. Second line is valproate or lamotrigine.
84
Juvenile myoclonic epilepsy
* Seizure disorder of adolescence and young adulthood
* Myoclonic, absence, or generalized tonic clonic seizures
* Associated with an **early morning preponderance of seizures**
* EEG: **4-6 second polyspike-and-wave**
* Treat w/: Valproate, lamotrigine, or levetiracetam
85
Topiramate
Can be used for focal or generalized seizures
Side effects: Word finding difficulty, renal stones, weight loss
86
When there is no witness of a seizure, ___ may be a clue to tonic-clonic activity
When there is no witness of a seizure, **diffuse muscle aches** may be a clue to tonic-clonic activity
87
Adult-onset seizure is caused by ___ until proven otherwise
Adult-onset seizure is caused by **tumor or stroke** until proven otherwise
88
Technically, an aura is. . .
. . . **a focal seizure with preserved awareness**
That may or may not precede a more generalized seizure
89
3/4 of focal seizures with impaired awareness emanate from. . .
. . . **the temporal lobe**
90
\_\_\_ is always on the ddx for absence seizure
The two can be differentiated by. . .
**Focal seizure with imparied awareness** is always on the ddx for absence seizure
The two can be differentiated by **the presence or absence of an aura and post-ictal state,** which occur **only with focal seizures** and **not with absence seizures**
91
Atypical absence seizures
Absence seizures with **poorly defined beginning and end** and/or with **tonic and autonomic components.**
These usually occur in **cognitively impaired children with epilepsy** or in patients with an **epileptic encephalopathy,** like **Lennox-Gastaut syndrome.**
92
Prognosis for absence seizures
Quite good.
For those beginning in childhood (basically all of them), **70% will resolve by age 18.**
93
Longer absence seizure vs atypical absence seizure
When an absence seizure lasts **beyond 10 seconds**, there may be **small stereotyped movements** such as eye blinking or lip smacking.
However, this should not be confused with atypical absence seizures, which have more dramatic motor components.
94
Automatisms
**Repetitive, stereotyped, unconscious motor or verbal behaviors** that commonly accompany **focal seizures with impaired awareness (aka complex partial seizures).**
If an automatism is unilateral, the seizure is likely originating in the contralateral hemisphere
95
Complex partial seizures often begin with. . .
. . . **simple partial seizures! (in the form of an aura)**
96
Internationally, __ is a common cause of focal seizures
Internationally, **cystericercosis** is a common cause of focal seizures
97
Sudden unexpected death in epilepsy (SUDEP)
Occurs with no apparent cause
Most common among patients with **frequent, medically intractable seizures** who are **noncompliant with antiepileptic medications**
98
\_\_\_ is always indicated for a complex partial seizure
**MRI of the brain** is always indicated for a complex partial seizure
Since many have a focal, anatomic etiology. MRI may reveal a tumor or may reveal mesial temporal sclerosis -- **both of which can be resected to cure the epilepsy.**
Add gadolinium contrast if a neoplasm or vascular malformation is suspected.
99
Anticonvulsants and pregnancy summary
* Many listed as unsafe in pregnancy, but use is often warranted anyway if necessary to control seizures
* Always use high dose (4 mg) folic acid for PNV for women on antiepileptics during pregnancy
* Valproate and phenobarbital are most likely to cause NTDs in a dose-related fashion (moreso than other anticonvulsants)
* Lamotrigine is safest for pregnancy
100
Laboratory abnormalities often observed on anticonvulsant therapy that are screened for those on regular regimen
Liver enzyme elevation
Blood cell count depressions
101
Potential surgeries for refractory epilepsy
* There are MANY:
* Temporal lobectomy
* Extratemporal resections
* Corpus callostomy
* Placement of vagus nerve stimulator
* Hemispherectomy
* Multiple subpial transections
102
What is the MOST common type of seizure in an adult?
Complex partial seizure
NOT grand mal
103
Catamenial epilepsy
Accounts for **1/3 of women with epilepsy**
## Footnote
**Seizure timing is dependent upon menstrual cycle.**
104
Things that cause withdrawal seizures
Benzodiazepines
Alcohol
105
If someone presents with hallucinations which then get *worse* on antipsychotics, what is probably going on?
They are not psychotic, they are having occipital lobe seizures.
Get an EEG. Then take them off the antipsychotic and put them on an antiepileptic.
106
Two clinical definitions of status epilepticus
Seizure lasting longer than 5 minutes
Failure to return to baseline for \> 20 minutes following a seizure
107
Classic picture of an atonic seizure
Preserved consciousness, but loss of tone
"These are the kids who walk around with football helmets"
They lose tone and fall. They are conscious the whole time, but can't do anything about it.
Treat w/ valproic acid
108
Picture of a myoclonic seizure
There is no loss of consciousness, but brief jerking spasms of a muscle or muscle group
Can look a lot like a tic. Some of these people also get atonic seizure, which look a lot like syncope.
Treat w/ valproate.
109
Four treatments for specific seizure disorders that should be reflex:
* Trigeminal neuralgia:
* Absence:
* Atonic:
* Myoclonic:
* Trigeminal neuralgia: Carbamazepine
* Absence: Ethosuximide
* Atonic: Valproate
* Myoclonic: Valproate
110
Syndrome of trigeminal neuralgia
**Unilateral, burning/electric pain** coming from the trigeminal nerve, which **starts near the top of the ear** and splits in three, toward the **eye, cheek and jaw.**
111
Postictal ___ on BMP supports a diagnosis of generalized tonic-clonic seizure
Postictal **acidosis** on BMP supports a diagnosis of generalized tonic-clonic seizure
Resolves within ~2 hours
112
Cortical laminar necrosis
Type of brain damage caused by prolonged epileptic activity
Characterized by permanent neurologic deficit following status epilepticus
113
Idiopathic forms of focal epilepsy
* **Benign rolandic epilepsy**
* **Temporal lobe epilepsy**
* Both have a strong genetic component
114
"t1" and "t2" for generalized convulsive status epilepticus
**t1: 5 minutes.** The time at which a seizure is **assumed to be status epilepticus** with continuous seizure activity
**t2: 30 minutes.** The time at which a patient is at **risk for long-term neurologic consequences** of status epilepticus
115
Four most common epilepsy syndromes in children
* Febrile convulsions (simple febrile seizures, resolves spontaneously at age ~5)
* Benign rolandic epilepsy (resolves spontaneously)
* Childhood absence epilepsy (resolves spontaneously)
* Juvenile myoclonic epilepsy
116
Primary focal epilepsy syndromes should be treated with. . .
. . . **phenytoin or carbamazepine**
117
A patient arrives at the ED following a seizure. The seizure lasted ~6 minutes, then the patient became unresponsive. They have remained unresponsive since this time. What is the next step in management?
Order an EEG, but **initiate benzodiazepines or phenytoin immediately**
If there is high suspicion of non-convulsive status epilepticus, **you should NOT wait for EEG confirmation**. As with acute stroke, **time is brain** in status epilepticus.
118
Temporal lobe epilepsy is often poorly responsive to \_\_\_, but responds well to \_\_\_
Temporal lobe epilepsy is often poorly responsive to **antiepileptics**, but responds well to **surgery**
119
Breath holding spell
* May be **simple, cyanotic** (turning blue), or **pallid** (turning pale)
* Simple and cyanotic typically caused by **frustration**
* Pallid typically caused by **pain**
* Child **(6-18 months) holds their breath until they lose consciousness**, then wake back up without a post-ictal state
* Treatment is just reassurance
