14. Seizure

Question 1

Seizure defen

Answer 1

incr excitation or impaired inhibition of neurons resulting in abnormal firing and synconization of neighboring neurons

Question 2

Why do seizures typically terminate alone?

Answer 2

• neuronal exhaustion<br></br>-alteration of local balance NT ach and glutamate with inhibitory GABA

Question 3

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Question 4

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Question 5

<span> Automatisms usually include oral or finger stereotypic movements such as lip smacking, yawning, repetitive vocalizations, or picking at sheets or clothing; these automatisms can be complex and often arise from a frontal seizure focus.</span>

Question 6

<span>Seizures impairing distinct cognitive domains such as language (e.g., aphasia) or abnormal thoughts and perceptions (e.g., dèjá vu, hallucinations, illusions, or perceptual distortions)—often referred to as “auras”―are now termed “cognitive seizures.” </span>

Question 7

<span>These cognitive seizures commonly arise from the orbital frontal region manifesting as olfactory hallucinations, or from the temporal lobe, which classically manifests as epigastric rising sensation, auditory hallucinations, and increased fear or impending doom.</span>

Question 8

Seizure history important points

Answer 8

• sequence of events<br></br>- itctal events have 5 properties: abrupt onset with triggers, brief duration, altered consciousness, purposeless/stereotypic/non-suppressible, postictal state (exc abscence)

Question 9

<span>Autonomic discharges and bulbar muscle involvement may result in urinary or fecal incontinence, vomiting (with aspiration risk), lateral tongue biting, and airway compromise in the peri-ictal period. All of these signs are helpful discriminators in the differential evaluation of seizure-like episodes</span>

Question 10

<span>The history should focus on clinical factors known to decrease the seizure threshold, such as recent illness or trauma, drug or alcohol use, sleep deprivation, potential adverse drug-drug interactions with antiseizure drugs, medication noncompliance, recent change in dosing regimens, or change in ictal pattern or characteristics. </span>

Question 11

<span>After the seizure activity has ceased, resting vital signs are evaluated. Fever and underlying infection can cause seizures, although there may be a low-grade temperature elevation immediately after a generalized convulsive seizure. Tachypnea, tachycardia, fever, or an abnormal blood pressure that persists beyond the immediate postictal period may indicate toxic exposure, hypoxia, infection, or an acute central nervous system lesio</span>

Question 12

<span>A persistent focal deficit after a seizure (e.g., Todd paralysis) often indicates the focal origin of the event but also may suggest underlying structural injury, such as ischemic or hemorrhagic strokes</span>

Question 13

<span>The higher-risk population for ongoing nonconvulsive status epilepticus include those with acute or remote brain injury (including prior violations of the intracranial cavity with craniotomies), toxic exposure, sepsis, or renal or liver failure.</span>

Question 14

<span>The patient with persistent altered consciousness should be carefully examined for signs of ongoing subtle convulsive or nonconvulsive seizures, such as abnormal eye movements and facial myoclonus.</span>

Question 15

Lab tests for seizure

Answer 15

wo = pregn<br></br>- BG<br></br>- CK and lactic acid if >2 mins to assess rhabdo, acute metabolic acido<br></br>- adv age, comorbid or ill appearing: extended metabolic panel, <br></br>- persistent AG after 1 hour (as seizure itself can cause lactic AG) suggestive sepsis, ketosis or poisoning<br></br>- liver enzymes ast and alt for chronic disease<br></br>- consider levels of previous seizure med if on (phenyt, phenobarb, VPA, carbamez most commonly available with quick turn around);<br></br>- test Li level as can cause<br></br>- tox screen if sub abuse or OD expected <br></br>-cbc for wbc<br></br>- febrile: consider LP and viral tests after CT

Question 16

Imaging in seizures:<br></br>previous dx vs new

Answer 16

no need<br></br>need <br></br>OR need if have following:<br></br>- age >40<br></br>- coma<br></br>-immcomp<br></br>-clot disorder<br></br>-hx ICH or malignancy<br></br>-severe thunderclap headache<br></br>- status epilepticus, convuls/not<br></br>- stigmata neurocut syndrome<br></br>- suspected trauma 

Question 17

Consider CT perfusion (contrast enh with arterial phase and postsignal processing of imaging helpful if transient neuro deficit like Todd paralysis)

Question 18

<div>For pediatric considerations, refer to Chapter 169); in brief, emergent neuroimaging in children presenting with seizures is indicated in the setting of an abnormal neurologic exam or medical or surgical comorbidities and in those younger than 3 years with focal or prolonged seizures.</div>

Question 19

<span>EEG is useful to diagnose nonconvulsive status epilepticus, monitor seizure activity, guide third-line therapies after intubation and neuromuscular blockade, and help differentiate seizures from other nonepileptic presentations. ED-based EEG may assist with the prompt diagnosis of epilepsy in patients with new-onset seizures and decision making on the initiation of secondary seizure prophylaxis; however, studies demonstrating its cost-effectiveness are lacking. </span>¹<span> New devices with limited montage or assembly that can be performed at the point of care in select cases may be of value and expedite EEG in the emergent setting but are not routinely recommended.</span>

Question 20

<span>An electrocardiogram (ECG) is also an early screen for drug toxicity. Tricyclic cardiotoxicity may manifest as a QRS complex lasting more than 0.1 second or a rightward shift of the terminal 40 ms of the frontal plane QRS complex (a prominent R wave in lead aV </span>_R<span> ). The ECG can also identify a prolonged QT, a delta wave, Brugada pattern, or heart block, which might contribute further clues to the seizure etiology. Electrocardiographic changes are common in the peri-ictal period and range from sinus tachycardia to more concerning features such as ST segment depression and T wave inversion. Prolongation of intervals on ECG is common in the peri-ictal period, which may challenge differentiating seizures from a primary cardiac related etiology of syncope.</span>

Question 21

DDX Seizures:<br></br>Cardiac - 3<br></br>Neuro -5 <br></br>tox - 3<br></br>metabolic- 4<br></br>infx - 2<br></br>pysch - 3

Answer 21

vagal syncope, orthost, cardiogenic syncope<br></br>stroke or TIA, complic migraine, movement disorder with chorea/dystonia/myclonus/tremor, parasomnias, ext/flexor posture from herniation syndr<br></br>intox, inebriation, over sedation or over analgesia, extrapyramidal sx<br></br>low BG or high, thyrotoxicosis, DT<br></br>meningoencephalitits, tetanus<br></br>Psych: PNES, conversion disorder, panic att, cataplexy 

Question 22

I<span>n patients suspected of having had a seizure, the first step is to determine whether the history from the patient or bystander(s) supports the diagnosis. <b>Critical causes of seizures with specialized treatments include eclampsia, toxic ingestion (e.g., isoniazid, lithium, tricyclic antidepressants), hypoglycemia, hyponatremia, and increased intracranial pressur</b></span>

Question 23

<b>Critical causes of seizures with specialized treatments include eclampsia, toxic ingestion (e.g., isoniazid, lithium, tricyclic antidepressants), hypoglycemia, hyponatremia, and increased intracranial pressur</b>

Question 24

Emergent dx seizure 

Answer 24

infection<br></br>acute brain injury - ischemic or hemorrhagic, tbi, cerebral venous thrombosis<br></br>serious mimics of seizure activity 

Question 25

Question 26

Answer 26

Question 27

 For example, isoniazid overdose can cause prolonged seizures refractory to benzodiazepines and requires pyridoxine to terminate the seizures.

Question 28

In seizing female patients of childbearing age, eclampsia may be the cause, and IV magnesium is the treatment of choic

Question 29

clamptic seizures refractory to magnesium may respond to benzodiazepines or barbiturates, with or without second-line therapy. 

Question 30

Children and psychiatric patients at risk for water intoxication may be hyponatremic and require hypertonic saline therapy. 

Question 31

Recurrence of seizures following first-time unprovoked seizures is highest in the first 2 years

Question 32

The description of the episode of loss of consciousness with associated cyanosis, and tonic-clonic convulsions is highly suspicious for a generalized tonic-clonic seizure. The patient has not returned to baseline mentation as demonstrated by GCS of 10 and is displaying subtle signs of potentially ongoing seizures (nystagmus); thus the most likely diagnosis is nonconvulsive status epilepticus, which can be diagnosed only with an electroencephalogram. The elevated blood pressure along with hypodensities in the posterior cortical region on CTH are highly suggestive of posterior reversible encephalopathy syndrome, a form of hypertensive emergency. The patient has acute encephalopathy and the stem of the question does not display findings suggestive of cortical blindness (preserved pupillary light reflex with complete binocular vision loss). Lack of prodrome of headache and confusion, fever, and meningismus make meningoencephalitis less likely. The episode happened towards the end of hemodialysis section, so profound uremia is unlikely.

Question 33

Although all the answers reflect conditions that can be considered seizure mimics, nonepileptic spells, or pseudoseizures, represent the most common differential diagnosis for generalized convulsive status epilepticus with an incidence of approximately 10% of subjects enrolled in clinical trials. Nonepileptic spells tend to last greater than 5 minutes, thus meeting criteria for convulsive status epilepticus by duration of events, and be resistant to high doses of benzodiazepines. Neuroleptic malignant syndrome is also associated with prolonged spells of abnormal movement, but the type of involuntary movement (typically tonic extension of all extremities, opisthotonos and rigors) and associated hyperthermia, tachycardia, and diaphoresis can distinguish these disorders. Complex migraine typically manifests as lateralizing dysesthesia in association with severe throbbing headache with phono/photophobia, and not with prolonged convulsions. Convulsions associated with cardiogenic syncope usually occur in the setting of hypoperfusion and are brief, unlike this case.

Question 34

• Which additional features may assist in the diagnosis of nonepileptic spells?
  • a. 
    Disproportionally short postictal confusional state
  • b. 
    Normal lactic acid and creatine kinase
  • c. 
    Lack of reactive leukocytosis
  • d. 
    All of the above

Answer: d. 

Question 35

What is the typical period for the development of preeclampsia and eclampsia?

Answer 35

20 weeks of gestational age until 8 weeks postpartum

Question 36

Intravenous magnesium 4 to 6 g is first-line therapy in the pregnant patient experiencing new-onset seizures

Question 37

Neuroimaging should be considered if neurologic deficits persist, prolonged loss of consciousness or coma, advanced age, immunocompromised state, coagulopathy (including anticoagulant drugs) or hypercoagulability, history of malignancy, preceding severe thunderclap headache, status epilepticus, in patients with stigmata of neurocutaneous syndromes, and suspected trauma.

Question 38

Adults presenting with a first seizure should undergo cranial computed tomography and evaluation of serum electrolyte and glucose levels because abnormalities would likely influence disposition while identifying potentially life-threatening conditions. For otherwise healthy adults with normal findings after evaluation, early outpatient follow-up can be considered. In some cases, initiation of antiepileptic drugs can be considered after a first seizure; however, this should be done in consultation with the neurologist responsible for outpatient follow-up.