Seeing a patient for a possible first seizure is an everyday consult in both outpatient and inpatient neurology. It is important to recognize that a first seizure is a time of high stress for the patient and their family. Essentially, they will look to you for five “answers” to the following questions:
1. Why did I have a seizure?
2. Will I have more seizures (i.e., do I have epilepsy)?
a. If I have epilepsy, what kind of epilepsy do I have?
b. If I do not have epilepsy, what is the diagnosis?
3. What kind of testing do I need to undergo?
4. Do I need to take antiseizure medicines (ASMs), and if so, for how long?
5. How will this affect my life?
To answer these questions, you will first need to answer several other questions for yourself through the history from the patient. To make an accurate diagnosis, the questions you will ask yourself are:
1. What history should I take to make a diagnosis?
2. If it is not a seizure, what are other possible diagnoses?
3. What further work up should I order?
4. Do I need to start an ASM?
5. How do I counsel the patient about their questions?
While ordering objective tests is a routine part of neurological care, obtaining an excellent history is the most direct and impactful intervention you can make immediately on seeing the patient. Therefore, this chapter focuses significantly on obtaining a specific epilepsy history that allows you to generate an accurate differential, proceed with an evidence-based evaluation, consider ASM therapy, and provide appropriate counseling to your patient.
Taking the Right History in an Efficient Manner
As with all medical care, obtaining an accurate diagnosis begins with a history. An accurate history can lead to a specific epilepsy diagnosis nearly 50% of the time, compared favorably to the diagnosis rate of electroencephalogram (EEG) at 30% [Reference King, Newton and Jackson1]. An accurate seizure history can be obtained with essentially two critical pieces of information:
Improving Your Seizure History to Efficiently Utilize Your Time
An accurate seizure semiology history can approximate the brain area that produces clinical symptoms during a patient’s seizure, aka the symptomatogenic zone [Reference Rosenow and Lüders2]. Seizure semiology is a description of the patient’s subjective feelings as well as objective behaviors and movements during seizures. Thus, the first symptom in a patient’s seizure description is often, although not always, quite close to where the seizure begins and is of fundamental interest. Therefore, the most important question you can ask a patient is: What is the first thing that happens when you have a seizure? When you ask this question, often a patient will begin at the end of the seizure, typically the tonic clonic portion, and likely the most traumatic part of the first seizure experience to patients and their loved ones alike. It is key to acknowledge the tonic clonic portion as you gently guide the patient back to the beginning of the seizure where often the most localizing history can be obtained.
After establishing the first seizure symptom, it is useful to proceed with questions like: What happens next? This question can be asked multiple times until the patient describes the seizure’s end.
Once the patient’s complete seizure recollection is obtained, one can ask the patient specific questions regarding typical seizure auras (i.e., Do you have strange tastes out of nowhere?) to elicit history of a potential gustatory aura) since many patients do not understand that those symptoms are part of their seizure until identified by you.
Moreover, a history of auras in isolation that precede a first bilateral tonic clonic seizure can establish an epilepsy diagnosis since the patient has already had more than two seizures. Indeed, nearly three-quarters of patients have had “small” seizures prior to a first generalized tonic clonic (GTC) seizure [Reference Hauser, Anderson, Loewenson and McRoberts3]. Identifying this crucial history makes the decision to start ASM therapy straightforward (discussed later in this chapter).
Lastly, clinical history from the period after a seizure concludes (the postictal period) can provide invaluable clues to the patient’s epilepsy diagnosis. Here, questions can probe specific neurological dysfunction, the two most common being postictal weakness and aphasia.
Unilateral postictal weakness (Todd’s paralysis) reliably lateralizes seizure onset to the brain hemisphere contralateral to the weakness. For example, left postictal weakness lateralizes to the right cerebral hemisphere. Postictal aphasia lateralizes to the language-dominant hemisphere, most commonly the left hemisphere [Reference Foldvary-Schaefer and Unnwongse4].
In summary, a neurologist can divide a seizure into four possible phases as the history is obtained. Doing so can provide further organization that makes understanding a patient’s seizure progression more intuitive.
1. A beginning portion where the patient is aware (auras; Table 1.1)
2. A portion where the patient is unaware (Tables 1.2 and 1.3)
3. A portion where the seizure propagates throughout the entire brain (secondary generalization with bilateral tonic clonic seizure; Table 1.3)
4. The postictal period (the portion after the seizure concludes).
Table 1.1 Sensory seizuresFootnote a
| Common patient descriptors | Seizure Semiology Classification [Reference Luders, Acharya and Baumgartner5] | 2017 seizure classification [Reference Fisher, Cross and French6,Reference Fisher, Cross and D’Souza7] |
|---|---|---|
| Déjà vu, panic, anxiety, hallucinations, fear, unease | Psychic aura | Focal aware cognitive seizure |
| or | ||
| Focal aware emotional seizure | ||
| Foul smell like rotten eggs, sulfur | Olfactory aura | Focal aware sensory seizure |
| Sometimes foul or metallic taste | Gustatory aura | Focal aware sensory seizure |
| Rising or flipping sensation of the stomach, mild nausea | Abdominal aura | Focal aware sensory seizure |
| or | ||
| Focal aware autonomic seizure | ||
| Flushing, intense nausea, choking sensation, palpitations, hair standing on end | Autonomic aura | Focal aware autonomic seizure |
| Tingling, prickling; less commonly numbness | Somatosensory aura | Focal aware sensory seizure |
| Tones, clicks, basic sounds; less commonly complex sounds like music | Auditory aura | Focal aware sensory seizure |
| Flashing or swirling lights | Visual aura | Focal aware sensory seizure |
Table 1.2 Seizures primarily affecting consciousness/behavior
| Common patient descriptors | Seizure Semiology Classification [Reference Luders, Acharya and Baumgartner5] | 2017 seizure classification [Reference Fisher, Cross and French6, Reference Fisher, Cross and D’Souza7] |
|---|---|---|
| Unresponsiveness, incorrect answers to questions, space out, blank out, repetitive, or simple responses (yeah, no, etc.) | Dialeptic seizure | Focal behavior arrest seizure |
| or | ||
| Unknown onset behavior arrest seizure | ||
| Unresponsiveness, space out, blank out, repetitive, or simple responses (yeah, no, etc.) | Absence seizure | Generalized absence seizure |
| Lip smacking, “acting weird,” repetitive hand/finger movements, drooling, repetitive swallowing | Automotor seizure | Focal automatisms seizure |
| Flailing, running, kicking, boxing, punching, screaming, “crazy” movements | Hypermotor seizure | Focal hyperkinetic seizure |
| Laughing, giggling, “creepy” laugh | Gelastic seizure | Focal emotional seizure |
| Being unable to speak as the primary seizure manifestation with retained awareness | Aphasic seizure | Focal cognitive seizure |
Table 1.3 Seizures with primary motor manifestations
| Common patient descriptors | Seizure Semiology Classification [Reference Luders, Acharya and Baumgartner5] | 2017 seizure classification [Reference Fisher, Cross and French6, Reference Fisher, Cross and D’Souza7] |
|---|---|---|
| Stiffen | Tonic | TonicFootnote a |
| Shake | Clonic | ClonicFootnote a |
| Head turn, eye turn | Versive | VersiveFootnote a |
| Muscle jerk | Myoclonic | MyoclonicFootnote a |
| Stiffen and shake all over, begin with a loud yell (ictal cry) | Tonic clonic | Tonic clonic |
| Fall, “just drop,” head drop | Atonic | AtonicFootnote a |
| Arms stiffen and then hunching over, most commonly in the truncal areas | Epileptic spasm | Generalized onset epileptic spasm |
| or | ||
| Unknown onset epileptic spasm | ||
| Can have any variety of previously described seizure types that evolve to a bilateral tonic clonic seizure | n/aFootnote b | Focal to bilateral tonic clonic seizure |
a The 2017 seizure classification should be preceded by either focal onset or generalized onset as appropriately determined by other testing except for “tonic clonic” and “epileptic spasm,” which can be either generalized or unknown onset while “behavior arrest” can be focal onset or unknown onset.
b The 1998 classification does not have a correlate to “focal to bilateral tonic clonic seizure” as the 1998 classification lists all relevant seizure types from which it evolves. Common patient descriptors and 1998 seizure name should include laterality modifiers when appropriate with options including left, right, axial, or generalized. The 2017 seizure classification does not include laterality modifiers.
Seizure Classification Systems
After obtaining the seizure semiology history, you should have a clear narrative of how the patient and bystanders perceived the seizure from beginning to end. You then “translate” the described movements/behaviors of a seizure into specific seizure types from which you can more easily make a localization.
There are two seizure classification systems for seizure semiology that over time have increased in similarity [Reference Luders, Acharya and Baumgartner5, Reference Fisher, Cross and French6]. The Seizure Semiology Classification (SSC) uses semiology on its own without reference to imaging or electrophysiologic data. In essence, the SSC recognizes semiology as its own discrete data point with significant potential to inform a specific epilepsy diagnosis [Reference Luders, Acharya and Baumgartner5].
The International League Against Epilepsy (ILAE) system by contrast combines the seizure type with an electrophysiologic implication (generalized versus focal) as part of the classification itself [Reference Fisher, Cross and French6]. Still, removing the electrophysiologic implication from the ILAE seizure classification yields a similar description to the SSC; hence why overlap is increasing.
The SSC additionally benefits from emphasizing the progression of seizure symptoms [Reference Lüders, Akamatsu and Amina8]. For instance, people with temporal lobe epilepsy can have a classic progression of metallic taste (gustatory aura) to unresponsiveness with lip smacking and pill-rolling finger movements (automotor seizure) to a bilateral tonic clonic seizure (aka grand mal seizure, GTC). By contrast, the ILAE system defines each seizure separately without reference to progression, potentially obscuring key information that informs a specific epilepsy diagnosis. The earlier described seizure would be termed a focal to bilateral tonic clonic seizure, unfortunately losing some of the rich description that allows for the localization process so familiar to all neurologists.
Accordingly, a third key difference is that the SSC encourages establishment of a specific anatomic localization whereas the ILAE system, by definition, limits to one of three localizations: focal, generalized, and unknown [Reference Fisher, Cross and French6].
All of those factors reviewed, the authors assert that epilepsy patients benefit from a specific and actionable localization or syndrome diagnosis, similar to any neurological diagnosis. Since the SSC urges the neurologist to establish a localization, we will primarily discuss that classification. However, we do appropriately reference the most current ILAE system in Tables 1.1–1.5 recognize that many neurologists use the ILAE system in everyday practice. As noted, it is worth being conversant in both classifications in case patients or other physicians alike use those seizure types. In the end, what is most important is that the patient receives a specific and actionable diagnosis, whether epilepsy, nonepileptic events, or a nonneurological diagnosis like syncope.
Evolution of ILAE Seizure Terminology
Before further discussing the SSC, it is worth reviewing the evolution of the ILAE seizure classification since previous terminology continues in widespread use. Perhaps the best-known ILAE classification remains the 1981 version [9], which introduced the terms “simple partial” and “complex partial.” The 2017 version changes verbiage without substantive change in meaning (Table 1.4). Thus, it is worth being fluent in the 1981 and 2017 ILAE systems since both are used.
Table 1.4 1981 and 2017 ILAE terminology
| 1981 terms [9] | 2017 terms [Reference Fisher, Cross and French6] |
|---|---|
| Partial | Focal |
| Simple | Aware |
| Complex | Impaired awareness or unaware |
| Secondary generalization | Focal to bilateral tonic clonic |
Seizure Semiology Classification System
The SSC utilizes common localization elements from other neurological diagnoses like stroke while expanding on localizations specific to epilepsy [Reference Luders, Acharya and Baumgartner5]. It is useful to break down seizures into four main categories, with the fourth category being less common than the first three:
1. Sensory – commonly called auras; these are subjective experiences of which only the patient is aware (Table 1.1)
2. Consciousness – changes in patient behavior or responsiveness that can be objectively observed and, at times, variably noted by the patient. One novel term of note, dialeptic, is introduced by the SSC and means altered awareness/consciousness as the only manifestation of the seizure. An intuitive alternate term to use here is dyscognitive (Table 1.2)
3. Motor – specific stereotyped movements that can be observed and, at times, noted by the patient (Table 1.3)
4. Autonomic – a less common seizure type where symptoms affect the autonomic nervous system, whether subjective (considered an aura, i.e., palpitations) or objective (then considered a seizure, i.e., tachycardia).
For each seizure type, one should describe the localization of the behavior/movement as well as the laterality, if applicable. We provide four examples of how you would translate a patient history into a seizure type with its commensurate localization.
1. A patient tells you their right arm tingles at seizure onset. You would note a right arm somatosensory seizure, which concisely localizes to the left parietal lobe (Tables 1.1 and 1.5).
2. A patient describes flashing lights in the left peripheral vision. You “translate” to a left visual aura with a most likely localization to the right occipital lobe (Tables 1.1 and 1.5).
3. You observe a seizure with stereotyped posture of the left arm extended and the right arm raised/flexed. This seizure type is concisely described as a left asymmetric tonic seizure (since the left arm is extended), which often localizes to the right frontal lobe, but at the least lateralizes to the right hemisphere (Tables 1.3 and 1.5).
4. A patient is observed to have bilateral stiffening of their arms and legs followed by rhythmic shaking of the arms and legs. This would be classified as a GTC seizure or bilateral tonic clonic seizure. It would not have localizing or lateralizing value (Tables 1.3 and 1.5).
Table 1.5 Typical lateralization and localizations of seizure types and postictal symptoms
| Common patient descriptors | Seizure Semiology Classification [Reference Luders, Acharya and Baumgartner5] | Localization [Reference Foldvary-Schaefer and Unnwongse4] |
|---|---|---|
| Déjà vu, panic, anxiety, hallucinations, fear, unease | Psychic aura | Temporal lobe; can consider parietal or frontal lobe |
| Foul smell like rotten eggs, sulfur | Olfactory aura | Temporal lobe; can consider orbitofrontal lobe |
| Sometimes foul or metallic taste | Gustatory aura | Temporal lobe |
| Rising or flipping sensation of the stomach; mild nausea | Abdominal aura | Temporal lobe |
| Flushing, intense nausea, choking sensation, palpitations, hair standing on end | Autonomic aura | Insula |
| Tingling, prickling; less commonly numbness, far less commonly painful | Somatosensory aura | Contralateral parietal lobe; can consider insula, particularly if painful |
| Tones, clicks, basic sounds; less commonly complex sounds like music | Auditory aura | Temporal lobe |
| Flashing or swirling lights | Visual aura | Contralateral occipital lobe |
| Unresponsiveness, incorrect answers to questions, space out, blank out, repetitive, or simple responses (yeah, no, etc.) | Dialeptic seizure | Not particularly localizing; should consider absence epilepsy in a child |
| Lip smacking, “acting weird,” repetitive hand/finger movements, drooling, repetitive swallowing | Automotor seizure | Temporal lobe is most likely, although this seizure type has been seen in all localizations |
| Flailing, running, kicking, boxing, punching, screaming, “crazy” movements | Hypermotor seizure | Frontal lobe, although can be from alternate localizations; if dystonia is present, it will localize contralateral to the dystonia |
| Laughing, giggling, “creepy” laugh | Gelastic seizure | Hypothalamic hamartoma; frontal lobe if mechanical laugh; temporal lobe if “emotional” |
| Stiffen | Tonic seizure | Contralateral motor cortex or supplemental motor area |
| Shake | Clonic seizure | Contralateral motor cortex |
| Head turn, eye turn | Versive seizure | Frontal lobe (frontal eye fields) |
| Muscle jerk | Myoclonic seizure | Generalized |
| Stiffen and shake all over, begin with a loud yell (ictal cry) | Tonic clonic seizure | If primary seizure type, generalized epilepsy |
| Otherwise, does not localize | ||
| Fall, “just drop,” head drop | Atonic seizure | Generalized |
| Arms stiffen and then hunching over, most commonly in the truncal areas | Epileptic spasm | Can be generalized or focal |
Symptoms and 1998 seizure name should include laterality modifier when appropriate with options including left, right, axial, or generalized.
Additional History Vital in the Context of a Potential First Seizure
While the semiology history is the bulk of seizure-specific history, there are multiple risk factors that you should assess. In essence, these risk factors revolve around ascertaining if your patient has had any brain trauma, whether acquired or developmental. Straightforward questions you can ask the patient include [Reference Gavvala and Schuele10]:
1. Was there any difficulty with your birth?
2. Did you develop normally as a child?
3. Have you had any brain or spine infections?
4. Have you had a head injury with loss of consciousness (LOC) and, if so, how long were you unconscious?
5. Is there anyone in your family with epilepsy or seizures?
Infections can predispose to seizures and epilepsy. Early seizures can be seen in 22% of viral encephalitis cases and 10% of patients present with seizures later. Likewise, early seizures can be seen in 13% of patients with bacterial meningitis and 2.4% of patients on a more chronic basis [Reference Annegers, Hauser, Beghi, Nicolosi and Kurland11].
Head injury can be classified as mild, moderate, or severe. These are determined by length of amnesia or LOC. Mild is <30 minutes, moderate is 0.5–24 hours, and severe is >24 hours. Rate of epilepsy after mild head injury was 1.5 and not statistically significant compared to 2.9 and 17 times more likely for moderate and severe, respectively [Reference Annegers, Hauser, Coan and Rocca12]. It is worth remembering that people with nonepileptic events more commonly had mild head injury [Reference Barry, Krumholz and Bergey13].
There is a hereditary nature to some epilepsy. Generalized epilepsy can be passed from either the mother or father. For focal epilepsy, the risk is limited more specifically to the mother [Reference Peljto, Barker-Cummings and Vasoli14]. Still, in general, most people with epilepsy do not inherit it.
Besides risk factors intrinsic to the patient, you should assess external causes of a seizure, otherwise known as a provoked seizure. Some medications (bupropion, tramadol, cefepime, benzodiazepine rapid/acute withdrawal) are well known to cause isolated seizures [Reference Beleza15, Reference Sutter, Rüegg and Tschudin-Sutter16].
Is It Really a Seizure? The Differential Diagnosis of a First-Time Seizure
Patients who present for evaluation of a possible first seizure most typically have alteration of consciousness. Alternate symptoms can include specific transient neurological dysfunctions such as numbness, visual disturbance, weakness, or difficulty speaking. When discussing the differential of a first seizure, it bears recalling typical features of seizures as discussed earlier. This will help to compare and contrast with alternate diagnostic possibilities.
Differential #1: Nonepileptic Events
Nonepileptic events are covered extensively in Chapter 10 of this manual. In brief, these are paroxysmal episodes with some resemblance to epilepsy, but with some key differences. Patients with nonepileptic events are more likely [Reference Gavvala and Schuele10, Reference French and Pedley17]:
To have asymmetric movements
To have a start/stop quality to the events themselves
To have events that last longer than seizures (often >5 minutes compared to the <2 minutes for seizures)
To have their eyes closed during the episodes
Suggestible to the event starting and stopping
Differential #2: Syncope
Syncope is an acute LOC or near LOC. The key difference is that syncope is due to globally decreased cerebral blood flow whereas a seizure is due to abnormal coordinated brain electrical activity [Reference Gavvala and Schuele10].
A common confounder is when people have convulsive movements during a seizure. This is by no means uncommon as myoclonic movements are noted in 60% of patients in one well-documented cohort [Reference van Dijk, Thijs and van Zwet18]. Nearly all patients had their eyes open with syncope [Reference van Dijk, Thijs and van Zwet18] in similarity to epilepsy but in contrast to nonepileptic events.
From a historical perspective, syncope patients expectedly have autonomic symptoms such as pallor, change in heart rhythm, or sweating [Reference van Dijk, Thijs and van Zwet18, Reference McKeon, Vaughan and Delanty19]. As discussed previously, autonomic symptoms can be present in epilepsy, but are less common compared to syncope in general.
Differential #3: Transient Ischemic Attack
A focal acute loss of cerebral perfusion can cause a transient ischemic attack (TIA). Crucially, the initial symptom is more likely to be a loss of function due to hypoactivity of the brain compared to the relative “gain of function” due to electrical hyperactivation of the brain region during a seizure. One well-documented exception is the limb-shaking TIA. This is seen as episodic limb-shaking episodes contralateral to the occluded carotid artery [Reference Yanagihara, Piepgras and Klass20]. Prompt consideration of limb-shaking TIAs in the work up of “EEG negative” focal seizures is indicated.
Differential #4: Migraine with Aura or Basilar Migraine
Migraine with aura can have a variety of neurological symptoms including most commonly visual aura as well as less commonly numbness, speech difficulty, weakness, and vertigo. Compared to epilepsy, migraine symptoms are more prolonged and there is of course the subsequent headaches in the majority of migraine patients [Reference Gavvala and Schuele10].
Differential #5: Metabolic Derangements
Alteration of consciousness, encephalopathy, and provoked seizures are commonly seen in periods of either hepatic or uremic encephalopathy [Reference Beleza15]. Acute hypoglycemia with blood sugars below 20 can cause GTC seizures and is a particularly relevant consideration in patients with diabetes.
Do I Need to Order Labs, EEG, or Imaging?
While the previously mentioned semiology and epilepsy-specific history is the most accessible way to make a specific diagnosis in a first seizure patient, additional testing is indicated.
Lab Work
Lab work in general is also covered in Chapter 6. In brief here, routine lab work such as complete metabolic profile (CMP) or complete blood count (CBC) should be obtained to assess for any infection or metabolic derangement. Urinalysis with or without urine toxicology may also be obtained as clinically appropriate. Many first-time seizure patients are otherwise healthy so the routine lab work may be more useful if considering ASM initiation [Reference French and Pedley17].
An ammonia level >80 µmol/L drawn ≤60 minutes after the seizure can correctly classify 80% of episodes between a generalized seizure and focal seizure or nonepileptic event [Reference Albadareen, Gronseth and Landazuri21]. Given the specific timing requirements, ammonia levels would be of limited utility and not recommended unless drawn within 1 hour of the seizure.
Prolactin is a desired biomarker for seizures, but is only useful if there is a baseline prolactin level >6 hours prior to the episode. In that rare scenario, an elevated prolactin level can distinguish between a generalized and focal seizure, but crucially not between a seizure and syncope or a seizure and a nonepileptic event [Reference Gavvala and Schuele10]. As these are the two more common clinical questions being assessed as well as the rare presence of a prolactin level >6 hours prior, we do not recommend prolactin measurement.
Electroencephalogram
Patients with a first seizure should have EEG performed. Data do support an increased epileptiform yield if done within 24 hours of the first seizure [Reference King, Newton and Jackson1]. When strongly suspecting an epilepsy diagnosis, data also indicate that a >1 hour study will increase the likelihood of capturing an epileptiform finding. Moreover, the same study increased capture of events (epileptic or nonepileptic) after 30 minutes of recording [Reference Burkholder, Britton and Rajasekaran22]. The utilization of EEG in epilepsy care is covered expansively in Chapter 4.
Imaging
The utility of imaging in a first seizure is twofold: rule out a neurological emergency and potentially identify the cause of the patient’s seizure. To rule out a neurological emergency such as stroke or intracranial hemorrhage, computed tomography (CT) of the head is adequate. To identify more subtle causes of epilepsy like focal cortical dysplasia, hippocampal sclerosis, and so on, a 3 tesla (3T) magnetic resonance imaging (MRI) with an epilepsy protocol has shown to be superior [Reference Knake, Triantafyllou and Wald23, Reference von Oertzen, Urbach and Jungbluth24]. Thus, if considering MRI, it is worth verifying your facility performs 3T with an epilepsy protocol to enhance the diagnosis rate of the MRI study. Imaging in new onset and chronic epilepsy is covered extensively in Chapter 5.
Do I Need to Start an ASM?
The decision to start an ASM can be more accurately stated “Do I think the patient has epilepsy?” If you do not think that the patient has epilepsy, an ASM will have no clinical benefit. For instance, if a patient has had recurrent seizures due to alcohol withdrawal, the best treatment would be to address the alcoholism. Epilepsy is defined as one of the three following conditions [Reference Fisher, Acevedo and Arzimanoglou25]:
1. At least two unprovoked seizures >24 hours apart
2. One unprovoked seizure with a >60% chance of seizure recurrence within 10 years
3. A recognized epilepsy syndrome.
For condition #1, it is critical to consider all of the patient’s seizure types. For instance, the patient has had multiple episodes of déjà vu over the past months and comes to you after a first tonic clonic seizure; that patient has had more than two seizures. The epilepsy definition does not require multiple tonic clonic seizures.
Condition #2 arose to better manage patients in clinical situations such as a first seizure and neuroimaging demonstrating a brain tumor concordant with semiology history. Logically, one should not withhold ASM treatment for the patient to have a second seizure just to fulfill the criteria for condition #1.
When you have decided that the patient does have epilepsy, you should start an ASM. While the topic of which ASM and what dose to use will be covered extensively in Chapter 3, data indicate that lamotrigine, zonisamide, and carbamazepine are reasonable options for focal epilepsy whereas valproate is the most effective choice for generalized epilepsy [Reference Marson, Burnside and Appleton26, Reference Marson, Burnside and Appleton27]. However, valproate’s teratogenic risk and side effect profile certainly influences the selection of valproate as initial therapy [Reference Perucca and Tomson28, Reference Tomson, Battino and Bonizzoni29].
In general, patients who are seizure free tend to be so at lower doses, so you do not need to target the highest dose to achieve a seizure-free outcome [Reference Kwan and Brodie30].
How Do I Counsel Patients after a First Seizure?
This brings us back to the initial questions that patients will ask you in consultation of a first seizure.
Why Did I Have a Seizure?
Ideally a combination of history, lab work, and imaging can help provide this answer. You first should establish that the patient really did have a seizure and then provide an etiology if it is known at that time. If you do not know an etiology, it is perfectly acceptable to tell the patient that the cause of the seizure is not determined at this point.
Will I Have More Seizures?
Again, you should be able to clearly tell the patient if they have epilepsy. If you do think that they have epilepsy, you are likely starting a seizure medicine and you can tell them that around 50% of people with epilepsy are seizure free with their first ASM [Reference Chen, Brodie, Liew and Kwan31]. For patients with a clear first-time seizure, a metaanalysis of five prospective studies has indicated that the risk is 40% for seizure recurrence [Reference Berg and Shinnar32] – coincidentally why most patients with an isolated first seizure are not started on an ASM.
What Kind of Testing Do I Need to Undergo?
You can counsel patients that they should have a thorough history, an EEG (ideally within 24 hours if feasible), and a 3T MRI with an epilepsy protocol.
Do I Need to Take ASMs, and if so, for How Long?
This question is essentially asking: “Will I have more seizures, or do I have epilepsy?” If you think that they have epilepsy, your patient should take ASMs. The length of ASM treatment depends on your certainty that they have epilepsy and the specific diagnosis that you have made. For instance, childhood absence epilepsy is a common diagnosis in children that most commonly resolves, so you could counsel the patient that they will likely be able to come off medications. Alternately, a patient who has had a stroke and a year later has a first seizure consistent with the area of brain injury, you would counsel that it is less likely that they will come off medications due to the static nature of the injury.
How Will This Affect My Life?
Answering this question requires sensitivity coupled with straightforwardness, no doubt a delicate balance.
The first specific thing that patients often want to know about is driving. Laws regarding driving after a seizure differ between countries and states. Commonly, patients may resume driving after being 6 months seizure free, although this length may be longer or shorter depending on location. You should ascertain your local laws. You can discuss that seizure freedom at 6 months, 12 months, and 18 months are associated with a relapse rate of 44%, 32%, and 17%, respectively [Reference Hart, Sander, Johnson and Shorvon33]. This can help some patients understand the local laws who are understandably frustrated about the revocation of their driving privileges.
A straightforward way to discuss precautions taken at the time of first seizure are to note that they are made to prevent injury. Thus, in addition to driving, patients are not recommended to take a bath or swim alone (risk of drowning), use power tools (risk of bodily injury), or cook with open flames (risk of fire and burns) until they are 6 months seizure free. Scuba diving and sky diving are commonly restricted completely in the event of an epilepsy diagnosis [Reference Fountain and May34].
Life events that can be encouraged include having a family [Reference Pennell, French and Harden35]. In the United States, epilepsy is a protected disability by the American with Disabilities Act and workplace accommodations should be made for these patients [Reference Krumholz, Hopp and Sanchez36].
