OVERVIEW: What every practitioner needs to know
Are you sure your patient has epilepsy? What are the typical findings for this disease?
Epilepsy is one of the most common neurologic disorders. Only Alzheimer’s disease, migraine, and stroke are more common. One in 26 people will be diagnosed with epilepsy at some point in their life. Patients with epilepsy are treated by neurologists including neurologists who specialize in epilepsy (epileptologists).
Definition of epilepsy – history of more than one unprovoked seizure. As an example, febrile seizures are provoked (by fever), so they are not epilepsy. The diagnosis may also be made if a patient has had one unprovoked seizure and has changes on their EEG that indicate a high likelihood of further seizures.
Typical findings for epilepsy
Alteration in consciousness (usually), eye or head deviation, staring, jerking of arms, legs, or trunk. A patient does not always lose consciousness during a seizure and may be confused or have no change in awareness at all.
Confusion after the event, loss of continence of stool or urine (more common), bitten tongue or lip, eye deviation.
Diagnosing and evaluating a seizure
1) What did the event look like (especially at the beginning)? Was there eye deviation? Movement of the body? Change in consciousness?
2) Did it happen unilaterally or bilaterally?
3) Were movements synchronous or asynchronous?
4) How long did it last?
5) How was the patient after the event? Confused? Sleepy? Back to themselves? After the event, was one side of the body weaker than the other?
6) Has this happened before? In the past, were there any other episodes of staring, twitching, jerking?
7) Is there a history of febrile seizures? Brain infections (including meningitis and/or encephalitis)? Brain injury from around the time of birth?
8) Does the patient have a history of epilepsy? Is there a family history of epilepsy?
9) Is the patient on antiseizure medications?
10) Is there any history of something that might have triggered the seizure or lowered the seizure threshold
Alcohol or illicit drug consumption
Missed antiseizure medication dose
Added medications that change anticonvulsant levels (e.g., antibiotics)
Toxin or medication exposures
11) Are there any other medical problems (incl. prematurity) or developmental delays?
What type of seizure does the patient have?
Generalized: Involves the whole body, loss of consciousness. Generalized seizures may start as either a focal seizure or as a generalized one.
Focal: Involves one part of the body, may or may not cause alteration in consciousness (simple if no change in consciousness, complex if there is).
Status epilepticus: Continuous seizure activity (classic definition is greater than 30 minutes, however we now often define status epilepticus as greater than 5 minutes of continuous seizure activity) or multiple seizures in a row without return to baseline.
Non-convulsive status epilepticus: The patient does not appear to be having a clinical seizure but electrographically (on EEG) has continued seizure activity. These patients may be walking and talking and just slower than usual or appear unresponsive.
How do you label the seizure movements?
Generalized tonic-clonic (previously known as ‘grand mal’): Stiffening of limbs (tonic) followed by jerking (clonic), involves the whole brain.
Absence (previously known as ‘petit mal’): Staring. May also include eye fluttering, lip smacking, picking at clothes (automatisms).
Myoclonic: Sudden, rapid, brief jerk of a muscle.
Atonic (drop attack): Abrupt loss of tone, may cause head drop, loss of posture, or complete collapse.
Partial: head, eye deviation, focal jerking or convulsion.
Types of seizures
Sample case: A previously healthy 18-month-old boy presents after a 1 minute generalized tonic clonic seizure. He is febrile to 102 F with upper respiratory infection symptoms. He is sleepy now and crying, but consolable and awake.
Age: 1 month to 6 years (mean: 14 months).
Otherwise normal child.
No evidence of central nervous system infection.
Temperature >38.0 degrees C.
No prior history of afebrile seizures.
Simple febrile seizure.
Less than 15 minutes
Only one seizure within a 24 hour period
Child is normal after the seizure
Complex febrile seizure.
Longer than 15 minutes
More than one seizure within 24 hours
Weakness on one side after the seizure (Todd’s paralysis)
Sample case: Parents of a 7-year-old girl receive a report from her teacher that she is not paying attention in class. She is often caught day dreaming and is falling behind her peers. Mom sometimes has to call her name 5-6 times before she answers.
Onset 4-10 years (childhood) or 8-14 years (juvenile).
Episodes of staring lasting 10-30 seconds in length.
May have automatisms.
No post-ictal state.
Can have up to 100 seizures a day.
Frequently triggered by hyperventilation in the office.
May have generalized tonic-clonic convulsions, as well (more likely in juvenile onset).
EEG finding: 3/second spike and wave, accentuated by hyperventilation.
2) How to differentiate absence from focal seizures with alteration in consciousness (previously termed complex partial seizures)
Focal seizures are:
Longer in duration.
More likely to have automatisms.
There is a post ictal period and there may be an aura (premonition just beforehand that a seizure is about to occur).
They are less frequent.
Sample case: A 6-month old girl comes to the office because her parents note that after eating and waking up from sleep, she has clusters of multiple jerking movements of her arms. Her head will jerk forward with these as well. She is often upset after the episodes.
Age of onset: 3 to 10 months
What do they look like?
Flexor or extensor spasms of the arms and head.
Events often occur around sleep transition.
Children often cry or appear irritable afterwards.
Some children may lose developmental skills once these start.
EEG: Hypsarrhythmia (chaotic high voltage pattern) with brief relative voltage electrodecrements.
Differential diagnosis: Gastro-esophageal reflux, Sandifer syndrome, myoclonic epilepsy of infancy, benign myoclonus of infancy.
Juvenile myoclonic epilepsy
Sample case: A 16-year-old boy presents after having his first generalized tonic-clonic seizure. Mom also reports episodes of zoning out. You ask if he has ever had any jerking episodes in the morning where he will accidently drop something and he says “How did you know?”
Age of onset: 12-18 years.
Types of seizures: Myoclonic (early morning jerking most common, usually bilateral, symmetric and retain consciousness), generalized tonic-clonic, absence.
EEG: Generalized polyspike and wave, 5-7 cps, often induced by photic stimulation on EEG.
Benign epilepsy with centro-temporal spikes (benign Rolandic epilepsy)
Sample Case: An 8-year-old boy comes into his parent’s room at night and has a scared look on his face. He points to the side of his face and his mom sees that it is jerking. He can’t seem to talk.
Most common idiopathic focal epilepsy in childhood.
Age of onset: Between 5 and 10 years.
Often at night.
Hemisensory or motor features on the face.
May involve limbs.
These children may have an increased risk for language dysfunction and migraines.
EEG: Centro-temporal spikes and sharp waves in sleep (may not be present when awake). Horizontal dipole to spikes.
Seizure syndrome with multiple seizure types, specifically tonic and atonic.
Children usually have intellectual disability.
Seizures is usually intractable.
May develop once infantile spasms resolve.
EEG shows slow spike wave activity with slow background.
Myoclonic astatic epilepsy (Doose syndrome)
Atonic and myoclonic seizures.
Can also have tonic, absence, and generalized tonic clonic seizures.
Normal development prior to seizure onset.
Variable outcomes (many do well), some may have mutations in SCN1A or GLUT1 on genetic testing.
What other disease/condition shares some of these symptoms?
Similarities: Loss of consciousness, can have jerking AFTER event (convulsive syncope), eyes roll back in head.
Differences: No eye deviation, feeling of things “going dark,” patient back to baseline almost immediately, may be orthostatic.
2) Breath holding spells:
Similarities: Loss of consciousness, may have jerking movements.
Differences: Occur after child is upset (i.e., provoked), patient pale, back to baseline almost immediately after event.
3) Migraine (with Aura):
Similarities: May present similarly to simple partial seizure with focal sensation change (ex. arm tingling). Some patients develop headache before, after, or during a seizure.
Differences: Focal symptoms develop over minutes as opposed to seconds in a seizure.
4) Psychogenic nonepileptic seizure/event or pseudoseizure:
Similarities: May look just like true seizure. Patient may be unresponsive to painful stimuli.
Differences: Patient usually remembers the event (even if generalized), movements are not stereotyped, eyes closed, event can be triggered, waxing and waning over time, abrupt return to consciousness, thrusting or arching, side to side (“no”) head movements, event interruptible by noxious stimulus.
5) Shuddering attacks:
Similarities: Look like a variety of different types of seizures (ex. myoclonic, may have stiffening).
Differences: Consciousness does not seem to be altered, do not occur during sleep.
What caused this disease to develop at this time?
Predisposing factors: Family history, genetic predisposition, history of head trauma or CNS infection, previous stroke or hemorrhage in the brain, hypoxic ischemic injury (potentially from a premature birth), toxin exposure (including alcohol), certain medications can lower the seizure threshold (e.g., buproprion).
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
Is the patient on anticonvulsant medication? If yes, then check medication levels to see if they are adequate and similar to previous levels.
If there is a concern for meningitis then perform a lumbar puncture to look for infection.
Routine laboratory studies are not usually indicated.
How is EEG helpful?
1) When should an EEG be performed?
An EEG should be performed emergently if:
There is a concern that a patient is in non-convulsive status epilepticus
An EEG should be performed urgently if:
There is a concern for infantile spasms
An EEG should be performed on an out patient, non-urgent basis if the patient has:
A first time afebrile seizure
2) What does it mean if there is no epileptiform activity on the EEG?
No epileptiform activity is seen on EEG about 1/2 of the time if the patient has focal seizures. This does not mean that they do not have seizures but just that they were not captured on EEG.
Less frequently (up to 20% of the time) no epileptiform activity is seen on an interictal EEG when someone has a generalized seizure disorder.
3) Certain seizure syndromes have distinct EEG patterns. These include (as described under the seizure disorder above): absence epilepsy, infantile spasms, and benign epilepsy with centro-temporal spikes.
Would imaging studies be helpful? If so, which ones?
Is the seizure generalized and brief (i.e., < 5 min)?
No need for acute imaging unless there are focal findings on exam.
Is the seizure focal? Has the patient returned to baseline?
MRI of the brain with thin cuts through the temporal lobes in a non-urgent fashion is the best modality for imaging to look for focal lesions causing seizure.
Is the seizure focal and the patient has not returned to baseline?
CT of head recommended unless MRI brain can be obtained in an urgent manner.
If you are able to confirm that the patient has epilepsy, what treatment should be initiated?
When should treatment be started immediately?
Status Epilepticus: If a seizure has been continuing for longer than 5 minutes it is less likely to stop on its own and treatment should be initiated.
Steps to treating status epilepticus. Move on to the next step if the one completed has failed to stop the seizures. *Do not use propofol in children due to high risk of propofol infusion syndrome. (See Table I.)
▪ When should treatment be started urgently? (Within 48 hours)
▪ Infantile spasms (See Table II)
▪ Treatment for febrile seizures:
▪ Do not treat with seizure medication
▪ Fever prophylaxis does not help prevent future febrile seizures
▪ Treatment after a single afebrile seizure:
▪ In most circumstances treatment after the first afebrile seizure is not necessary.
▪ Exceptions may include if the patient was in status epilepticus, having another seizure would greatly disrupt life (i.e., the patient is driving), patient has a known underlying lesion that increases the risk for further seizures
▪ Anticonvulsant options for patients with epilepsy: See Table III. in next section.
▪ Non-medication treatments:
▪ Metobolic therapies (diets):
▪ Ketogenic diet – high ratio of fat to carbohydrates + protein (4:1 or 3:1).
▪ Common adverse events – Initial nausea, vomiting, acidosis. Later constipation, growth stunting, kidney stones (decreased risk with supplementation with oral citrate), increased cholesterol (no long term effect known), decreased bone density.
▪ Modified Atkins diet (1-2:1 ratio).
▪ Low glycemic index treatment (restricts carbohydrates and restricts to those with glycemic index <50).
▪ Usually not first line but may be more helpful in certain syndromes (e.g., Doose syndrome, infantile spasms, Dravet syndrome).
▪ IN A MEDICAL EMERGENCY: It is OK to stop the diet if the patient medically requires glucose or glucose-containing products. The diet may then be restarted after the emergent situation has been treated.
▪ If glucose is not medically required then it is preferable to use normal saline solutions for hydration.
▪ Epilepsy surgery:
▪ To be considered after failure of two anticonvulsant medications if possible resectable lesion is present (consider earlier if there is a tumor).
▪ After localization with EEG and imaging, if a resectable lesion is found surgery may be done to remove that lesion.
▪ Adverse events: Bleeding, infection, deficit corresponding to the area of resection.
▪ Vagus nerve stimulator:
▪ Sends pulses of electricity to the brain via the vagus nerve.
▪ Device implanted under the skin on the left chest, electrodes encircle the left vagus nerve.
▪ Electrical pulse may cycle on a set schedule (most commonly every 5 minutes for 30 seconds) and also may be activated by the patient.
▪ Adverse events: Cough, hoarseness, infection, battery or device failure.
▪ Anticipatory guidance: Seizure first aid (if someone has a seizure this is what the caregiver should do at home):
▪ Place the patient on the floor. Place something soft under the head, clear the area of objects that could harm the patient.
▪ Do not put anything in the patient’s mouth.
▪ Do not restrain the patient.
▪ Turn the patient on their side to open the airway and allow secretions to drain.
▪ If the seizure lasts longer than 5 minutes or seizure recurs without return to baseline, may use rescue medication (e.g., rectal valium [Diastat]) or call 911.
|Step 1||IV Lorazepam 0.1mg/kg (up to 4mg) orIM Midazolam 10mg for >40kg, 5mg for 13-40kg) orIV Diazepam 0.15-0.2 mg/kg/dose (up to 10mg)||q5 minutes x 2 doses|
|Step 2||Fosphenytoin 20mg/kg (up to 1500mg) orValproic acid 40mg/kg (up to 3000ng) orLevetiracetam 60mg/kg (up to 4500mg)||Avoid valproic acid in children under 2 years|
|Step 3||Consider phenobarbital 15mg/kg|
|Step 4||Consider benzodiazepine drip (midazolam)|
|Put continuous EEG in place|
|Step 5||Barbituate coma vs. general anesthesia*|
|Hormone therapy: Prednisolone or ACTH (Most evidence)|
|Vigabatrin (second most evidence) – use as first line in tuberous sclerosis|
|Medication||Generalized (g) or focal (f)||Standard Dose||Common Adverse Effects||Comment|
|Carbamazepine (Tegretol)||f||7-30mg/kg/day/BID||Sedation||Follow CBC, LFTs|
|Clobazam (Onfi)||g, f||10-20 mg/day/BID||Sedation, irritability||Need to warn about Stevens Johnson syndrome|
|Ethosuximide (Zarontin)||g (absence)||250mg – 1000mg/day/BID||GI upset, headaches|
|Lacosamide (Vimpat)||f||100-200 mg/day/BID (>17 yrs)||Sedation, fatigue, headache|
|Lamotrigine (Lamictal)||g, f||2-15mg/kg/day/BID||Rash||Titrate slowly to prevent Stevens Johnson syndrome|
|Levetiracetam (Keppra)||g, f||20 – 60mg/kg/day/BID||Irritability, behavior change||May use B6 supplementation or lamotrigine for behavior change|
|Oxcarbazepine (Trileptal)||f||8-40mg/kg/day/BID||Sedation, dizziness, hyponatremia||Follow Na level|
|Perampanel (Fycompa)||g, f||8-12 mg/day/QHS||Sedation, headaches, behavior changes|
|Phenobarbital (Luminal, others)||g, f||2-7mg/kg/day||Sedation, cognitive side effects||Mostly in neonates. Wean slowly to prevent withdrawal|
|Phenytoin (Dilantin)||g, f||4-8mg/kg/day/BID||Ataxia, hirsutism, gingival hyperplasia, nystagmus||Used for status epilepticus|
|Topiramate (Topamax)||g, f||3-9mg/kg/day/BID||Cognitive side effects, renal stones, acidosis, weight loss, oligohydrosis, teratogenicity||Consider before using in women of childbearing age|
|Rufinamide (Banzel)||g, f||10-45 mg/kg/day BID||Dizziness||Indicated for LGS|
|Valproic Acid (Depakote)||g, f (more often g)||15-60mg/kg/day/BID||Sedation, weight gain, LFT elevation, tremor, TERATOGENIC||Do not use under 2 years or in women of childbearing age. Follow LFTs, amylase, lipase, and level|
|Vigabatrin (Sabril)||f||50-100 mg/kg/day/BID||Headache, dizziness, tremor, fatigue, swallowing problems||Need special registration to prescribe|
|Zonisamide (Zonegran)||g, f||2-12mg/kg/day/QD-BID||Renal stones, weight loss||Long half-life, can be useful in non-adherent patients|
What are the adverse effects associated with each treatment option?
See Table III. for adverse effects associated with each treatment option.
What are the possible outcomes of epilepsy?
Risk of recurrence after first afebrile seizure:
Rate of recurrence increases if there is a known underlying brain lesion, developmental delays, EEG abnormalities or the first seizure occurred during sleep.
Risk of recurrence after the second afebrile seizure:
Risk of recurrence of first febrile seizure:
▪ 1/3 of children will recur
▪ 1/2 of those will recur in the first 6 months
▪ 3/4 of those will recur in one year
▪ 90% of those will recur within 2 years
▪ Factors predictive of recurrence:
▪ Age <18 months
▪ Temperature <40 C
▪ Brief duration of fever (<1hr)
▪ First degree relative with febrile seizures
Prognosis of common seizure syndromes
Infantile spasms: Nearly all patients will stop having spasms, but many will develop other seizure types and have developmental delay.
Absence epilepsy: Childhood absence: 80% outgrow them by 20 yrs of age, may have continuing attentional and cognitive problems; juvenile absence: less likely to outgrow (50%).
Benign epilepsy with centro-temporal spikes: Outgrown around puberty, some may go on to have other seizure types.
Juvenile myoclonic epilepsy: Most need life long treatment but typically easily controlled with a small dose of medication.
Intractable epilepsy: Failure of 2 anticonvulsant medications with adequate (time and dose) trials to stop seizures.
▪ 33% of patients will be intractable to medical treatment
When do we discontinue medications?
Consider discontinuation of medication after 2 years of seizure freedom in most cases.
May consider EEG prior to discontinuation if there is concern for ongoing seizure activity.
What causes this disease and how frequent is it?
▪ ~10% of people will have at least one seizure in their life
▪ 1/26 of people have epilepsy during their life
▪ 0.8% of people have active epilepsy at any one time
▪ Causes of seizure:
▪ Seizure syndrome/genetic
▪ Congenital lesion (e.g., dysplasia, malformation of cortical development)
▪ Toxin exposure
▪ Electrolyte disturbance
▪ Previous stroke (ischemic or hemorragic)
▪ Many idiopathic epilepsies appear to have genetic basis as seen in linkage studies and family studies. A few epilepsies have known genetic defects associated with particular syndromes.
▪ KCNQ2, KCNQ3 – benign familial neonatal convulsions.
▪ CHRNA4, CHRNB2 – Autosomal dominant nocturnal frontal lobe epilepsy.
▪ SCN1A, SCN1B, GABRG2 – Dravet syndrome, generalized epilepsy with febrile seizures plus a syndrome where the patient has febrile seizures but continues to have them after 6 years of age and may go on to have afebrile seizures as well (this categorization includes Dravet syndrome).
How do these pathogens/genes/exposures cause the disease?
▪ Causes of seizure:
▪ Traumatic: Injury to the brain can lead to scarring leading to seizure activity.
▪ Seizure syndrome/genetic – genetic abnormalities lead to seizure disorder either because of channelopathy or some other unknown mechanism.
▪ Congenital lesion (e.g., dysplasia, malformation of cortical development): abnormalities in brain circuitry development lead to a seizure focus.
▪ Toxin exposure.
▪ Electrolyte disturbance: Leads to change in electrical activity and conduction and can lead to seizure.
▪ Previous stroke (ischemic or hemorrhagic): Injury to the brain can lead to a focus for seizure activity.
▪ Infectious/meningitis: Any irritation to the brain can potentially lead to seizure activity.
What complications might you expect from the disease or treatment of the disease?
Side effects for medications and other treatments may be seen above.
Mortality in those with chronic epilepsy is 2-3x greater than the general population and 24x greater in healthy young adults.
▪ SUDEP: Sudden unexplained death in epilepsy.
▪ 5%-18% of epilepsy deaths.
▪ Incidence: 3.5:10,000.
▪ Usually unwitnessed.
▪ 45% found in bed.
▪ 50% have signs of having a seizure.
▪ Most have a history of generalized tonic-clonic seizures.
▪ The patient has epilepsy.
▪ Death occurs unexpectedly while the patient is in reasonably good health.
▪ Death occurs over minutes.
▪ Death occurs in benign circumstances during normal activities.
▪ No other cause found at autopsy.
▪ Death was not the direct result of a seizure or status epilepticus.
▪ Risk factors:
▪ Young adults.
▪ Intellectual disability.
▪ Prone posture.
▪ Males >Female.
▪ Ongoing seizure activity, most commonly GTC.
▪ Increased seizure frequency.
▪ Polydrug therapy (i.e., multiple anticonvulsants).
▪ With controlled epilepsy there is not known to be an increased risk.
▪ Comorbid conditions:
▪ Headache/migraine (more common in specific syndromes such as benign epilepsy with centro-temporal spikes and juvenile myoclonic epilepsy, but over all increased prevalence in epilepsy).
▪ Psychiatric disorders (especially depression and anxiety): 20%-50% of epilepsy population.
▪ Learning problems.
▪ Attentional problems (including attention deficit hyperactivity disorder).
▪ Behavioral and emotional problems.
▪ Sleep disorders.
▪ Physical injury as a result of seizure.
Are additional laboratory studies available; even some that are not widely available?
Genetic testing is available for some of the known genes that may lead to certain seizure syndromes.
How can epilepsy be prevented?
Many types of epilepsy are thought to be genetically determined. Few have single gene diagnoses identified (see above for those that do). Genetic counseling may be helpful in selected situations (i.e., Dravet syndrome, due to prognosis, therapeutic options, and decreased need for other expensive work-up).
What is the evidence?
Berg, AT, Shinnar, S, Darefsky, AS, Holford, TR, Shapiro, ED, Salomon, ME. “Predictors of recurrent febrile seizures. A prospective cohort study”. Arch Pediatr dolesc Med.. vol. 151. 1997. pp. 371-8. (Examines the likelihood of recurrence of febrile seizures and what predisposing factors increase that risk.)
Berg, AT. “Identification of pharmacoresistant epilepsy”. Neurol Clin. vol. 27. 2009. pp. 1003-13. (Discusses intractable and refractory epilepsy definitions and consequences.)
Ficker, DM, So, EL, Shen, WK, Annegers, JF, O’Brien, PC, Cascino, GD, Belau, PG. “Population-based study of the incidence of sudden unexplained death in epilepsy”. Neurology. vol. 51:5. 1998. pp. 1270-4. (Examines risk factors for SUDEP.)
Glauser, TA, Cnaan, A, Shinnar, S, Hirtz, DG, Dlugos, D, Masur, D. “Childhood Absence Epilepsy Study Group. Ethosuximide, valproic acid, and lamotrigine in childhood absence epilepsy”. N Engl J Med.. vol. 362. 2010. pp. 790-9. (This study evaluates the three most common treatments for absence epilepsy based on efficacy and side effect profile.)
Glauser, Tracy. “Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society”. Epilepsy Currents. vol. 16:1l. 2016. pp. 48-61. (Presents a treatment algorithm for convulsive status epilepticus.)
Haut, SR, Shinnar, S. “Considerations in the treatment of a first unprovoked siezure”. Seminars in Neurology. vol. 28. 2008. pp. 289-296. (Discusses risks and benefits of treating a first seizure.)
Kossoff, EH, Zupec-Kania, BA, Rho, JM. “Ketogenic Diets: An update for child neurologists”. J Child Neurol. vol. 24. 2009. pp. 979-988. (An overview of the ketogenic diet, how and when it is used, benefits, and side effects.)
Muthugovindan, D, Hartman, AL. “Pediatric epilepsy syndromes”. Neurologist. vol. 16. 2010. pp. 223-37. (Discusses many pediatric epilepsy syndromes, characterization, treatment and prognosis of these syndromes. Includes a table showing evidence for different treatments.)
Ongoing controversies regarding etiology, diagnosis, treatment
There is still much research to be done to determine why some people develop epilepsy and some people do not. While some treatment mechanisms are understood many are not and determining why they work may help us further treat and potentially cure epilepsy.
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- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has epilepsy? What are the typical findings for this disease?
- What other disease/condition shares some of these symptoms?
- What caused this disease to develop at this time?
- What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
- Would imaging studies be helpful? If so, which ones?
- If you are able to confirm that the patient has epilepsy, what treatment should be initiated?
- What are the adverse effects associated with each treatment option?
- What are the possible outcomes of epilepsy?
- What causes this disease and how frequent is it?
- How do these pathogens/genes/exposures cause the disease?
- What complications might you expect from the disease or treatment of the disease?
- Are additional laboratory studies available; even some that are not widely available?
- How can epilepsy be prevented?
- What is the evidence?
- Ongoing controversies regarding etiology, diagnosis, treatment