Sneaky Seizure Triggers: Pearls & Pitfalls

Author: Rachel Bridwell, MD (@rebridwell, EM Resident Physician, San Antonio, TX) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Clinical Case #1

A 37-year-old female with a history of gestational hypertension and GERD was brought in by EMS seizing. Per EMS report, she told her supervisor at work that she had a headache, and her vision “seemed off”. You note that she was accompanied by her husband and 3-week-old newborn. She has no known seizure history, but her husband said that her blood pressure was high at the end of her pregnancy. Vital signs: T 98.2 F, P 130, RR 18, BP 195/110, SpO291% on 2L NC.In the field she received 2 rounds of 4 mg IM versed with cessation of the seizure.

Clinical Case #2

A 23-year-old female with a history of major depressive disorder, general anxiety disorder, and fibromyalgia was brought in by EMS for altered mental status and agitation. En route, EMS reports she was hard to control and did not have vascular access, but they did find an empty bottle of her bupropion on the counter. After being transferred to the gurney in the resuscitation bay, she seizes. Vital signs en route: T 99.1 F, P 125, RR 22, BP 150/100, Spo2 98% on RA.  ECG reveals sinus tachycardia to 135, QRS 105 ms, QTc 480 ms.


Seizures, both provoked and unprovoked, account for 1% of ED visits annually, and can have a range of etiologies from electrolyte derangements to underlying structural abnormalities, whether from infection or congenital malformation1. The most recent ACEP policy on seizures provides a definition of provoked seizures, which occur at or within 7 days of the inciting derangement, whereas unprovoked seizures lack a provocation2.

The burden of unbroken seizures is associated with high morbidity and mortality. Status epilepticus (SE) is constant or recurrent seizures for > 5 minutes3. The International League Against Epilepsy (ILAE) defines SE at a time of 10 minutes4. However, most consider 5 minutes to be the cutoff, as the vast majority of seizures stop within 1 minute. Refractory status epilepticus has a short-term mortality rate between 16-39%, and a long-term return to neurologic baseline for only 36% of patients, leaving 23% with a lasting neurologic deficit and death in 41% of patients5. Thus, termination of seizures as soon as possible, but especially before the 30-minute mark, is crucial, making recognition of sneaky seizure etiologies paramount.

An excellent approach to seizures has previously been covered in Seizures in the ED. This article will focus on assessing more surreptitious but equally important presentations of seizures. After the blood glucose, pulse oximetry, sodium abnormalities, and benzodiazepine and alcohol withdrawals have been ruled out, what are the next set of concerns and etiologies to consider?

Dangerous Triggers

Intracranial infections

While a rare diagnosis in the ED, meningitis, an inflammation of the dura surrounding the brain, may often initially present non-specifically, culminating in a seizure. Seizures should be treated with benzodiazepines, with consideration for airway protection to minimize aspiration. In the presentation of seizure with elevated core body temperature, stiff neck, or headache, one should have a high index of suspicion for meningitis, with empiric bacterial coverage based on age and risk factors, even if the lumbar puncture cannot be performed prior to the administration of antibiotics7. Viral meningitis rarely presents with seizures, though viral encephalitis has a more pronounced and devastating presentation and effect. For an in depth look on this topic, see this excellent post on meningitis.

Encephalitis, brain parenchymal inflammation, is a rare etiology for seizures in the developed world, with an estimated incidence of 0.7-12.6 per 100,000 persons, 37% of which are idiopathic8. However, HSV encephalitis accounts for 10-15% of annual cases, while VZV is the most common viral encephalitis in the immunocompromised6. Both of these viral etiologies present often with seizure and focal neurologic deficit, which helps determine location. HSV has a predisposition to infect the temporal lobes, which along with seizure, may show personality changes, psychosis, and olfactory and gustatory hallucinations, which may often be mistaken for a psychiatric etiology9. Both of these viral etiologies should be treated ideally within 6 hours with acyclovir 10 mg/kg every 8 hours, though dose should be renally adjusted6,10,11. Acyclovir frequently induces crystalluria, and thus adequate hydration should be maintained to prevent further complication6. A multicenter observational study of 93 patients found that the key factors affecting patient outcome with HSV encephalitis were the patient’s clinical state at presentation and time to initiation of acyclovir. Of these patients, 41% did not have acyclovir started until after 48 hours into their hospital stay12. Other arboviral etiologies required supportive care upon termination of seizures and airway, breathing, and circulation were addressed. Diagnosis of specific encephalitic etiologies can only be confirmed with biopsy8.

CNS abscesses typically present with headache, focal neurologic deficit, and fever, though up to half of cases may be afebrile at the time of presentation13. Because symptoms can be indolent and subtle, 25% of cases present with either generalized or focal seizure13. The vast majority of abscesses are secondary to metastatic or contiguous foci of infection, predominantly Streptococcusand Staphylococcusspecies. Mortality rates have decreased from 40% to more recently 10% with improved imaging, treatment options, and antimicrobial regimen. While antibiotic regimen should consider most likely infection nidus, specific antibiotics should be considered as well. Metronidazole has excellent brain abscess penetration, providing anaerobic coverage. Ceftriaxone provides anaerobic and aerobic streptococcal coverage in addition to Enterobacteriaceae, which is a common culprit in brain abscesses secondary to ear infections, sinus infections, and penetrating trauma. In the setting of neurosurgical cases, Pseudomonal coverage can be provided by 4thgeneration cephalosporins and meropenem, though renal dosing is key to prevent antibiotic induced seizures14(see Antibiotics section). Vancomycin should be continued until culture and susceptibility results return.

Special populations:

With the increasing rates of Type 2 Diabetes Mellitus, patients with DM2 have a 2-fold higher risk of bacterial meningitis, which is predominantly S. pneumonia and L. monocytogenes, reflecting their relative immunosuppression15. In examination of this specific cohort, 5% of patients experienced seizure15. Hyperglycemia in bacterial meningitis additionally portends a greater seizure risk16. Seizure in pediatric bacterial meningitis is associated with additional morbidity; in these patients who developed hearing loss, seizure occurs in 10% of cases either prior to or at the time of admission, with an additional 7% experiencing a seizure during their hospital stay17. Further consideration should be taken for those with a ventricular shunt, with increased risk of seizure due to both infection, most commonly seen within the first 6 months postoperatively, and shunt malfunction, producing increased intracranial pressure and hydrocephalus18-19. In a patient with a known shunt, early antibiotics for broad coverage to include skin flora as well as evaluation and relief of mass effect if present are key.

The elderly are uniquely susceptible because they are less likely to mount a systemic response to infection, demonstrate decreased sensitivity and specificity to Kernig’s and Brudzinski’s signs, and are more likely to have altered mental status attributed to age, making them more likely to present with seizure20. After termination of seizures either spontaneously or with benzodiazepines, antibiotics should include coverage for S. pneumoniae, L. monocytogenes, and other gram negative bacteria20-22. Empiric coverage includes triggered ampicillin in addition to usual treatment of vancomycin and ceftriaxone20-22. Additionally, acyclovir should be added with increased prevalence of HSV encephalitis after age 60, and increased mortality in those over 70 years23.

In the immunosuppressed presenting with seizure, CNS infection is a likely cause, secondary to both common CNS infections as well as opportunistic pathogens. In this subset of patients, 15% present with coinfection with depressed cellular immunity, warranting ICU admission and very broad coverage24. Fungal meningitis is generally seen most commonly in this population, triggering initiation of amphotericin B6.

Intracranial hemorrhage 

Seizures secondary to intraparenchymal hemorrhage present within the first few days following bleeding. Typically, they occur more frequently in four clinical situations: large hemorrhage, lobar location, history of epilepsy, and depressed skull fracture25. Additionally, those with hepatic failure, whether pre-existing or due to current clinical status, have an increased risk of seizure26,27. In the setting of decreased level of consciousness or other suspicion of seizure, anticonvulsant therapy is the treatment of choice along with EEG monitoring, though prophylactic anticonvulsants are not recommended; prophylactic treatment of seizures renders fever and worsens functional outcomes28,29. If RSI is planned for airway protection, ensure a good neurologic exam is completed prior to intubation and EEG leads are placed after the paralytic is given to monitor for continued seizure activity.

Subarachnoid hemorrhage management diverges in its consideration of prophylactic phenytoin, working to minimize blood pressure and therefore aneurysm rebleeding risk25. Nonconvulsive seizures and status epilepticus occur more commonly in subarachnoid hemorrhage, triggering routine EEG monitoring26-27. However, phenytoin administration in this clinical setting has demonstrated a dose dependent decrease in functional and cognitive ability28-30. Because a 3-day course of phenytoin has shown equal efficacy to a 14-day course, an abbreviated administration is recommended to minimize these side effects31. Keppra has been shown to have comparable efficacy with significantly reduced side effect profile and presents an alternative regimen32.

Alcohol and benzodiazepine withdrawal

The differential diagnosis of alcohol withdrawal syndrome has a myriad of possibilities, but the key factor in optimizing treatment for these patients is maintaining a high index of suspicion early, as the presentation and its precipitation vary broadly. Alcoholic hallucinosis, if wrongly attributed to psychosis, will detrimentally receive antipsychotics, worsening their clinical state33. Errantly administered antipsychotics in this population are additionally associated with increased mortality from QT prolongation and arrhythmia34. In a patient with known epilepsy and alcoholism, the presenting sign of seizure or postictal state may delay care as antiepileptic drug levels are checked rather than treatment of alcohol withdrawal. As outlined in an excellent post,Alcohol Withdrawal, escalating benzodiazepines are the treatment of choice. While diazepam has a more rapid onset and therefore can prevent dose stacking, lorazepam has no active metabolites and therefore is preferred in those with impaired hepatic function, a common comorbidity in chronic alcohol users35,36. Similarly, these alcohol withdrawal syndrome patients who also suffer from hepatic encephalopathy present an ontologic challenge in determining which pathophysiology, if not both, is currently generating these seizures, i.e. did increased hepatic encephalopathy prevent alcohol consumption and precipitate withdrawal or did alcohol use or cessation cause the inciting event in hepatic encephalopathy?  While benzodiazepines are the staple of alcohol withdrawal syndrome, non-hepatically metabolized antiepileptic drugs, e.g. levetiracetam and topiramate, are the treatment of choice in seizures secondary to hepatic encephalopathy37. However, each disease requires specific management, e.g. vitamin supplementation or lactulose, that can be missed without a high index of clinical suspicion.

Additionally, if the seizure occurred prior to the presentation of the patient in alcohol withdrawal, the clinical presentation can be easily misattributed to malignant hypertension and hyperthermia, causing clinical deterioration if blood pressure or temperature control is the focus of resuscitation38.  A variety of toxidromes can present similarly to seizures due to alcohol withdrawal syndrome, further complicated by illicit drug use e.g. sympathomimetics. The obfuscation of hyperthermia and heat related illness with alcohol withdrawal is extremely problematic in both the homeless population or those who render themselves obtunded and subject to weather-related illness.

In trying to identify surreptitious presentation of seizures secondary to alcohol withdrawal syndrome, hypokalemia and thrombocytopenia have been noticed to be associated with seizure activity but unsurprisingly non-specific for this disease state34.

Benzodiazepine withdrawal functions biochemically and clinically similar to alcohol withdrawal, precipitating psychosis and generalized tonic-clonic seizures, which is also treated with benzodiazepines39. Flumazenil, a specific benzodiazepine antagonist, has been shown to reduce withdrawal symptoms in high dose dependent patients who have not taken any benzodiazepines in the past 3 weeks40. However, complications from iatrogenic flumazenil administration have been reported as high as 23.4%, resulting in agitation, dysrhythmia, delirium and seizures41-43. In the setting of a patient with a benzodiazepine ingestion of unknown amount with possible concomitant polypharmacy, supportive care can be administered during the acute benzodiazepine intoxication. However, administration of flumazenil in this same clinical setting can precipitate an avoidable and dangerous seizure.

Posterior Reversible Encephalopathy Syndrome (PRES)

PRES is a reversible disorder marked by vasogenic edema and neurologic symptoms of headaches, visual disturbances, encephalopathy, and seizures. PRES is postulated to be a result of endothelial injury with resulting compromised blood-brain barrier and is closely associated with renal failure, hypertension, sepsis autoimmune disease, chemotherapy, eclampsia, pre-eclampsia, and immunosuppression secondary to solid organ and bone marrow transplant44,45. However, a variety of etiologies have been identified as the inciting factor for PRES, including acute intermittent porphyria, vasculitis, calcineurin inhibitors, and other monoclonal antibodies and tyrosine kinase inhibitors44,46-47.

A recent case review found that 59% of patients with confirmed PRES presented with an epileptic seizure, while 57% presented with encephalopathy, and only one third of patients presented with headache48. Within this study population, hypertension and chemotherapy carried odds ratios of 5.89 and 3.04, respectively, with renal failure and immune suppression especially post transplant as other associated risk factors48. Further complicating the presenting seizure, intracranial hemorrhage and/or subarachnoid hemorrhage complicate up to 30% of cases, adding to multifaceted etiologies for seizures in these patients49. CT may show vasogenic edema in parieto-occipital regions, but FLAIR MRI is optimal to show the characteristic T2 signal abnormalities, which is typically asymmetrically bilateral44.

PRES has no specific treatment but resolves with the treatment of the underlying disorder. It is recommended that seizures secondary to PRES are treated with antiepileptics, though no specific recommendations are currently available44. In the setting of drug induced PRES e.g. immunomodulators, these causative agents should be discontinued acutely; failure to discontinue these medications results in prolongation of PRES50. Additionally, treatment of hypertension is key, though no specific antihypertensive is currently recommended. Similar to hypertensive emergency, the mean arterial pressure should be reduced by 25% in the first few hours, with efforts to avoid large undulations in blood pressure51. 

Occult head trauma

While major trauma is commonly associated with seizure from mass effect, depressed skull fractures, and other sequelae, occult head trauma represents a surreptitious etiology of seizures. In children, seizures can present as a late finding of non-accidental trauma. Patients aged between 2-24 months who presented with seizures without neuro-radiological abnormalities, were found to have retinal hemorrhage as a result of non-accidental trauma52. SIADH is often seen in traumatic brain injury patients due to damage to the pituitary stalk or posterior pituitary53. This can result in seizures secondary to hyponatremia, both acutely and chronically54,55. Additionally, chronic subdural hematoma is one of the most common neurosurgical conditions, usually secondary to trivial trauma56. Generally occurring in the elderly as well as those on anticoagulation or on hemodialysis, it can present with seizures and CN III palsy56. As with many neurosurgeries, evacuation of the hematoma may generate postoperative seizures, though prophylaxis with antiepileptic drugs remains controversial57.


Special Seizure Etiologies

Heavy metals

Heavy metals such as lead, thallium, zinc, arsenic, and copper initially present with GI irritation and can later lead to CNS manifestations, the late stages of which are seizures. Additionally, platinum in the form of cisplatin can result in blindness and seizures58. Lead is more commonly associated with seizures, with vague and subtle CNS symptoms such as headache, insomnia, ataxia, and restlessness prior to this late finding of repetitive tonic-clonic seizures59. Often found in old paint as well as herbal remedies, lead can cross the placenta freely, with intrauterine lead exposure potentially generating neonatal seizures60. If high clinical suspicion for lead exposure in neonates or children exists, radiographs can show radio-opaque dense bands at the epiphysesof long bones while low serum levels of 10 mcg/dL result in mild cognitive impairment60. Chronic lead exposure can also produce a thiamine deficiency, further lowering the seizure threshold in this population. Chelating agents include EDTA as well as succimer; in patients with CNS symptoms, these two drugs are combined in order to reduce lead levels, with the addition of steroids and mannitol if cerebral edema develops61.

Both mercury and tin can cause seizures after acute and chronic ingestion. Mercury, though commonly associated with game fish and shark ingestion, can be found in skin whitening cream, cosmetics, and laxatives, as well as environmental exposures, though vapors are most dangerous62. Acute mercury poisoning generates multi-organ system failure within hours, with CNS manifestations most commonly including visual symptoms, tremors, and tonic clonic seizures secondary to astrocyte damage preventing glutamate reuptake63. Chelating agents, such as DMPS, may be effective in treating acute toxicity to remove mercury deposits. Chronic poisoning more closely resembles the symptomatology of lead poisoning with irritability, headaches, apathy, and insomnia, though neuropsychological symptoms such as delirium and personality changes are more prominent, progressing to recurrent seizures64-66. In addition to standard seizure treatment, DMPS should be added to chelate approximately 1 mg of Hg/day67.

Tin toxicity usually occurs secondary to occupational exposure, with similar generalized CNS symptoms of memory deficits, ataxia, and notably with disturbed sexual behavior68. Those who work in tin factories as well as agrochemicals, dyes, glass, and PVC heat stabilizers are at risk. If persistent, tin toxicity can cause epilepsy requiring long term administration of AEDs68.


In evaluating seizing pregnant patients, eclampsia occupies a high priority in the differential; however, eclampsia, defined as generalized tonic-clonic seizures in pre or postpartum women not caused by epilepsy, can occur up to 8 weeks postpartum69. Postpartum eclampsia is subdivided into early and late phases, which occurs within the first 48 hours after delivery and greater than 48 hours after delivery, respectively70. Eclampsia, both pre- and postpartum, is one of the most common causes of morbidity and mortality worldwide, with an incidence of 1.6-10 cases per 10,000 deliveries in developed nations, increasing ten-fold in developing nations70.

One study examined the clinical manifestations and biomarkers associated with both pre-partum and postpartum eclampsia. Multiparity, mild to moderate hypertension, and headache were identified as the most pertinent key features in postpartum eclampsia70. As compared to prepartum eclampsia patients, postpartum eclamptic women did not have significant proteinuria or thrombocytopenia, which are anticipated laboratory derangements70. However, postpartum patients presented more consistently with elevated AST and anemia, versus their prepartum counterparts70. Thus, in a postpartum patient with complaints of a headache, pre-eclampsia and eclampsia must generate a high index of suspicion in the face of the more common and benign postdural puncture headache.

While pre-partum pre-eclampsia was not found to be a predictor of late postpartum eclampsia, gestational hypertension was found to be a risk factor, as well as patients presenting with headaches, the most common presenting symptom, and visual changes71. In multiple cases, late postpartum eclampsia can present only with these two features in the absence of the anticipated edema, proteinuria, and hypertension until just proximate to the seizure event72. Additionally, hyperreflexia is the most common clinical sign, seen in up to 80% of cases73. While eclampsia in a postpartum patient must stay high on the differential of not-to-miss diagnoses, the differential also includes electrolyte abnormalities, uremia, meningitis, encephalitis, trauma or intracranial bleeding, and hypertensive encephalopathy.

First line treatment is intravenous magnesium. Dosing includes a load with 4-6g IV over 30 minutes, followed by an infusion of 2 g/h. This can also be given 10 mg IM. Patient must be monitored for magnesium toxicity, specifically respiratory depression and diminished DTRs. For patient with renal insufficiency, the loading dose of Mg is only 2g74.

Lithium toxicity

Lithium toxicity can occur in both acute and chronic intoxication, which can be directly affected by the patient’s kidney function. In one review, seizures occurred in equal amounts of chronic and acute toxicity, which then received extracorporeal treatment management75. GI symptoms are generally not present in chronic toxicity, whereas in acute poisoning they are prominent early75.  Mild poisoning may cause CNS symptoms of vomiting, tremors, agitation, and muscle weakness, which can then progress to seizure, myoclonus, and coma76-77. Intermittent hemodialysis is the ideal treatment, but CRRT is a backup if HD is unavailable. Lithium is an ideal substrate for HD, as it is not bound to serum proteins and has a low volume of distribution. Lithium does not bind to activated charcoal, and whole bowel irrigation and gastric lavage do not have data to show efficacy in decontamination78. Permanent neurologic sequelae include short-term memory deficits, choreoathetosis, and truncal or limb ataxia79.

Sympathomimetic use

While withdrawal from GABA potentiating drugs can be associated with seizures, sympathomimetics increase monoamine release at synaptic nerve terminals, which can present with agitation, increased HR/BP, hyperthermia, and later, seizures68.  With widespread accessibility to these substances through both prescribed and illegal means, sympathomimetic-induced seizure can account for a significant portion of these, with 4% of Australian patients presenting for a first-time seizure secondary to amphetamine use28. Cocaine additionally can cause generalized seizures, both in first time presentations as well by lowering the seizure threshold in those with a known epileptic disorder. Seizures secondary to cocaine have been reported between as high as 40% of presentations, though notably with a female predominance29-30. Cocaine when smoked has been reported to precipitate complex partial status epilepticus, originally attributed to cocaine psychosis, thus requiring a very low index of suspicion to investigate and treat seizure activity in known intoxication31. Once status epilepticus occurs with both cocaine and MDMA, seizures are particularly difficult to treat and require immediate management and typically ICU admission with EEG monitoring after paralysis28. In these patients, the usual seizure and supportive care with benzodiazepines is recommended, though associated multi-organ system failure, must be considered with these global excitatory states. Both cocaine and MDMA can cause acute CNS catastrophes with massive hemorrhage, both subarachnoid and intraparenchymal, as well as ischemic stroke due to profound vasoconstriction, which can in turn generate seizures32-33. In the setting of MDMA overdose, hyperthermia, hyponatremia, and rhabdomyolysis must also be considered and appropriately managed if diagnosed68.


Uremia can be an etiology of seizures both in patients with CKD who develop symptomatic seizures as well as in individuals with known seizure disorders who later develop CKD, thus lowering their seizure threshold. In the CKD population, the incidence of seizures is approximately 10%86.

Uremic encephalopathy tends to begin with vague neurologic symptoms such as fatigue or apathy and can progress to asterixis and then myoclonus and seizures87. Generalized seizures are more common in ARF, whereas a host of factors can cause cortical irritability in CKD88; secondary hyperparathyroidism, which is secondary to CKD, increases calcium in the CNS, generating neuronal excitability and therefore augmented depolarization89-90. Treatment with EPO for anemia in CKD patients was previously associated with seizures, but this has since be questioned87. Additionally, antibiotics can lower the seizure threshold in septic patients with CKD, with particular focus on cefepime, which requires renally adjusted dosing91-92. Uremic patients have underlying platelet dysfunction; in the setting of potential head trauma, their underlying coagulopathy needs to be addressed. Treatment focuses on terminating the seizure and reversing the underlying cause, which in this case indicates hemodialysis.


Bupropion (Wellbutrin, Zyban) is a selective norepinephrine and dopamine reuptake inhibitor used to treat depression as well as smoking cessation, though it has risen to be the most common cause of drug-induced seizures for which Poison Control is consulted93. Patients will present altered with hallucinations, agitation, seizures, and a variety of cardiovascular effects. Bupropion is proposed to have an alternative mechanism of action of myocardial depression, in which gap junction leakage occurs, widening the QRS and prolonging the QTc with decreased contractility94-96.  While it is not a true sodium channel blockade, bupropion overdose is often treated with sodium bicarbonate administration initially, which has been shown to partially reverse the QRS prolongation96-97. ECG may show sinus tachycardia or bradycardia as well as conduction delays94. Non-cardiovascular effects of bupropion overdose also include transaminitis98.

Some patients who crush and snort bupropion receive immediate parenteral absorption without extended release. However, multiple metabolites are still active and epileptogenic97,99. Even if the patient appears well at the time of presentation, observe for 24 hours because of the extended-release formulation and previous discussion of metabolites. Benzodiazepines and supportive care are recommended for agitation, seizure, and hallucination control, but avoid antipsychotics as they decrease the already lowered seizure threshold 98. Administration of intravenous lipid emulsion can be considered to combat cardiovascular and CNS toxicity in conjunction with a medical toxicologist100.


A variety of antibiotics can be the etiology of sneaky seizures, especially carbapenems. Cephalosporins of all generations can cause both tardive and myoclonic seizures, whereas penicillins cause tardive seizures, exacerbated by any condition that impairs renal clearance101. Additionally, pre-existing CNS conditions have been associated with seizures after cephalosporin administration102. The adverse effects of novel fluoroquinolone derivatives, notably moxifloxacin and levofloxacin, manifest often with delirium and extrapyramidal side effects, which if unaddressed can progress to seizures 103-104. Finally, metronidazole has cerebellar toxicity, presenting as ataxia and dysarthria, with T2 hyperintense lesions on MRI, in patients actively taking the drug and shortly thereafter, though with resolution after cessation; this can then progress to encephalopathy and seizures105. Treatment involves discontinuation of the antibiotic and alteration of regimen, seizure management, and consideration of HD versus CVVHF101.

Cefepime should also be specifically highlighted, as it is known to cause non-convulsive status epilepticus (NCSE), especially in those with CKD106. NCSE is defined as epileptiform activity on EEG without seizures with an alteration of consciousness for greater than 30 minutes106. In patients with renal dysfunction, either ARF or CKD, a 6-10 day course of cefepime accounted for many neurologic symptoms to include NCSE in one study92.


In seizure patients, sodium derangement is often the first electrolyte considered, but a more surreptitious cause of seizures is hypomagnesemia. Magnesium has CNS membrane-stabilizing effects in NMDA glutamate receptors and calcium channels. Levels lower than 1.2 mEq/L cause mild to moderate disturbances while levels<0.8mEq/L are considered severe, most commonly caused by diarrhea, abuse of laxatives, and a variety of drugs to include aminoglycosides, amphotericin B, foscarnet, cyclosporine, tacrolimus as well as both loop and thiazide diuretics107-108. Additionally, any patients with malabsorptive issues, e.g. inflammatory bowel disease, are also prone to hypomagnesemia109. More importantly, remember if hypokalemia is present, hypomagnesemia is as well.

HIV seropositive populations have a predilection for hypomagnesemia sensitivity with resultant seizures, stressing the importance of checking magnesium levels in these patients and to consider this electrolyte in an HIV seropositive seizing patient110. It should also be considered in pediatric patients with renal disorders, e.g. Gitelman’s, who present seizing108. Additionally, proton pump inhibitors have a notable side effect of hypomagnesemia, with cases of seizures secondary to hypomagnesemia in both acute and chronic PPI users111-112.


Camphor, also known as kapoor, has traditionally been used as an insect repellant with case reports starting as early as the mid-20thcentury, but it more commonly is utilized as the solvent for essential oils and salves. With the rise of essential oil use for both aromatic and medicinal purposes, camphor toxicity with resultant seizures has also increased113. Toxicity from overdose affects both adults and children, including those who have accidentally ingested the oil as well as those given a supratherapeutic dose. Camphor can be rapidly absorbed both enterically and transcutaneously, with the toxic level reported to be 50 mg/kg114. Case reports have also shown that it is used intranasally for allergic rhinitis, PO to aid digestion, topically for arthritis, and vaporized for respiratory conditions115. Toxicity presents with irritability and hyperreflexia, but often the first presenting sign may be grand mal seizures, especially if ingested without any obvious lab abnormality at presentation114,116. The mainstay of treatment is benzodiazepines for seizures, though supportive care after resolution of seizures is required for potential hepatotoxicity and neurotoxicity117. Death is usually secondary to convulsions or respiratory failure, stressing the importance of terminating the seizure with benzodiazepines and providing an advanced airway early118.

Camphor is the most common culprit, but this also highlights the stealthy role herbal medications and supplements can play in lowering a patient’s seizure threshold. Medication lists should be evaluated for caffeine-containing substances, valerian, ephedra, chamomile, and kava, which can also have similar effects to camphor119.


Case Conclusion #1

The patient was loaded with 6 g of magnesium over 30 minutes with a follow up infusion of 2g/h. The initial magnesium load broke her seizure, after which she was intubated and admitted for postpartum eclampsia.

Case Conclusion #2

The patient received 10 mg IV lorazepam and was intubated using propofol, fentanyl, and rocuronium. A sodium bicarbonate gtt was initiated in response to the widened QRS, and she was transferred to the ICU for further management with consults to medical toxicology and psychiatry.

Key Points

-Always address ABCs to include cardiac monitoring of the patient, as there is a risk of dysautonomia in a subset of seizure patients.

-In the setting of seizure with personality changes, psychosis, and olfactory or gustatory hallucinations, consider encephalitis; do not reflexively attribute this to an underlying psychiatric disorder.

-Assess the more common causes of seizure first such as hypoxia, hyper/hyponatremia, hypoglycemia, inadequate control of their seizure disorder (breakthrough seizure vs AED non-compliance), EtOH/benzo/barbiturate withdrawal.

-If clinically suspicious for meningitis, do not delay antibiotic administration for LP and strongly consider if acyclovir administration is warranted.

-In the setting of an unknown amount of benzodiazepine overdose, exercise extreme caution in flumazenil reversal, with a great risk of precipitating seizures.

Consider heavy metals, exposures, supplements, renal clearance, and antibiotics, all of which can play a role in triggering seizures or lower the seizure threshold.

-In the extremes of life as well as hypocoagulable states, trivial and unnoticed trauma can generate chronic subdural hematoma, which can present with seizure.

-In the setting of intoxication, consider polypharmacy of both SNRIs (venlafaxine, duloxetine) and bupropion predominantly as well as tramadol, antihistamines, and antibiotics. Additionally, not only ingestion but withdrawal from substances can trigger seizures.

-If seizures are refractory to multiple treatments and RSI is considered or if concerned for NCSE, EEG placement is crucial for continued monitoring of seizure activity after paralytics are administered.

-50% of “initial presentation” seizures had a previous event.120


References/Further Reading

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  6. Dorsett, Maia, and Stephen Y. Liang. Diagnosis and Treatment of Central Nervous System Infections in the Emergency Department.Emergency medicine clinics of North America34.4 (2016): 917–942. PMC. Web. 2 Oct. 2018.
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