> Table of Contents > Seizure Disorder, Partial
Seizure Disorder, Partial
Noel Dunn, MD
David Haight, MD
image BASICS
DESCRIPTION
  • Seizures occur when abnormal synchronous neuronal discharges in the brain cause transient cortical dysfunction.
  • Generalized seizures involve bilateral cerebral cortex from the seizure's onset.
  • Partial seizures originate from a discrete focus in the cerebral cortex.
  • Partial seizures are further divided into simple and complex subtypes:
    • If consciousness is impaired during a partial seizure, it is classified as complex.
    • If consciousness is preserved, it is a simple partial seizure.
EPIDEMIOLOGY
Prevalence
Partial seizures occur in 20/100,000 persons in the United States.
ETIOLOGY AND PATHOPHYSIOLOGY
  • Partial seizures begin when a localized seizure focus produces an abnormal, synchronized depolarization that spreads to a discrete portion of the surrounding cortex.
  • The area of cortex involved in the seizure determines the symptoms; for example, an epileptogenic focus in motor cortex produces contralateral motor symptoms.
  • In some cases, etiology is related to structural abnormalities that are susceptible to epileptogenesis. Most common etiologies vary by life stage:
    • Early childhood: developmental/congenital malformation, trauma
    • Young adults: developmental, infection, trauma
    • Adults 40 to 60 years of age: cerebrovascular insult, infection, trauma
    • Adults >60 years of age: cerebrovascular insult, trauma, neoplasm
  • Complex partial seizures: A common cause is mesial temporal sclerosis.
Genetics
Benign rolandic epilepsy, a form of partial seizure disorder, has an autosomal dominant inheritance pattern with penetrance depending on multiple factors.
RISK FACTORS
  • History of traumatic brain injury (1)[B]
  • Children exposed to a thiamine-deficient formula (2)[C].
COMMONLY ASSOCIATED CONDITIONS
Epilepsy patients have a higher incidence of depression than the general population.
image DIAGNOSIS
  • Seizure activity usually stereotyped.
  • Duration: Seconds to minutes, unless status epilepticus develops; status epilepticus may present as focal/generalized convulsions/altered mental status without convulsions.
  • Simple partial seizures
    • Simple partial seizures are characterized by localized symptoms. The patient is conscious. Symptoms may involve motor, sensory, or psychic systems.
    • Motor: Seizure activity in motor strip causes contraction (tonic) or rhythmic jerking (clonic) movements that may involve one entire side of body or may be more localized (i.e., hands, feet, or face).
      • Jacksonian march: As discharge spreads through motor cortex, tonic-clonic activity spreads in predictable fashion (i.e., beginning in hand and progressing up arm and to the face).
    • Sensory/psychic
      • Todd paralysis: after motor seizure, residual, temporary weakness in the affected area
      • Parietal lobe: sensory loss/paresthesias, dizziness
      • Temporal lobe: déjà vu, rising sensation in epigastrium, auditory hallucinations/forced memories, unpleasant smell/taste
    • Occipital: visual hallucinations
  • Complex partial seizures
    • Impaired consciousness by definition
    • May have aura; this is start of seizure.
  • Amnesia for the event, postictal confusion
    • Most often, focus in complex partial seizures is temporal/frontal.
    • Motor manifestations may include dystonic posturing/automatisms (i.e., simple, repetitive movements of face and hands such as lip smacking, picking, or more complex actions such as purposeless walking).
    • Frontal lobe seizure is characterized by brief, bilateral complex movements, vocalizations, often with onset during sleep.
PHYSICAL EXAM
Include neurologic exam, with attention to lateralizing signs suggestive of structural lesion.
DIFFERENTIAL DIAGNOSIS
  • Nonepileptic seizure
  • Syncope/postanoxic myoclonus
  • Hypoglycemia
  • For hemiparesis following event
    • Transient ischemic attack
    • Hemiplegic migraine
DIAGNOSTIC TESTS & INTERPRETATION
EEG: spikes/sharp waves over seizure focus
  • Yield of EEG is increased by being obtained in the first 24 hours following seizure and by sleep deprivation.
  • Frontal lobe seizure focus may be difficult to detect by routine EEG.
  • If difficulty with diagnosis, continuous video-EEG monitoring may be appropriate.
  • Serum electrolytes, including calcium, magnesium, phosphorus; hepatic function panel; CBC; drugs of abuse urine drug screen
  • Elevated prolactin, if measured within 10 to 20 minutes of suspected seizure, or elevated creatine phosphokinase; if measured within 6 to 24 hours, may help to differentiate generalized/complex partial seizure from psychogenic seizure (3)[B].
  • CSF exam if infection is suspected.
  • Urinalysis, chest x-ray, levels of antiepileptic drugs for breakthrough seizure
  • Technologic advances in neuroimaging are usually directed at the diagnosis and prognosis for seizure control (4)[C].
  • Emergency evaluation of new seizure: CT scan to screen for hemorrhage and stroke
  • After emergency evaluation, MRI with thin cuts through area of interest
  • If planning epilepsy surgery, positron emission tomography (PET) scan and/or interictal singlephoton emission computed tomography (SPECT) may be of value.
  • Magnetoencephalography (MEG) is an evolving technology for localizing seizure focus.
image TREATMENT
GENERAL MEASURES
  • Ask the patient to maintain a seizure diary.
  • Note potential triggers, such as stress, sleep deprivation, drug use, discontinuation of alcohol/benzodiazepines, menses.
MEDICATION
  • Current guidelines do not recommend for or against starting an antiepileptic drug (AED) after a single unprovoked seizure. Patients should be counseled that AEDs will reduce risk of repeat seizure over 2 years but have no effect on long-term remission (5)[C].
  • AEDs act on voltage-gated ion channels, affect neuronal inhibition via enhancement of &ggr;-aminobutyric acid (GABA, an inhibitory neurotransmitter), or decrease neuronal excitation. End result is to decrease the abnormal synchronized firing and to prevent seizure propagation.
  • 50% of those with newly diagnosed partial seizures respond to, and tolerate, first AED trial. Up to 50% of those who fail the first AED trial will also fail a second AED trial (6)[B].
  • Choose AED based on seizure type, side effect profile, and patient characteristics. Increase dose until seizure control is obtained/side effects become unacceptable.
  • Attempt monotherapy, but many patients will require adjunctive agents.
  • Refractory to medications is defined as failure of at least three anticonvulsants to achieve adequate control.
  • AEDs may prevent seizures after a traumatic brain injury (TBI) in the short-term, although they provide no efficacy in long-term prevention (7)[B].
  • Several AEDs induce/inhibit cytochrome P450 enzymes (watch for drug interactions).
First Line
  • Carbamazepine: Affects sodium channels; side effects include GI distress, hyponatremia, diplopia, dizziness, rare pancytopenia/marrow suppression, and exfoliative rash.
  • Oxcarbazepine: Affects sodium channels; side effects include dizziness, diplopia, hyponatremia, and headache.
  • Lamotrigine: Affects sodium channels.
    • Side effects include insomnia, dizziness, and ataxia.
    • Risk of Stevens-Johnson reaction (potentially fatal exfoliative rash), especially when given with valproate, requires slow titration.
  • Levetiracetam: multiple mechanisms; side effects include sedation, ataxia, and irritability.
P.957

Second Line
  • Phenytoin: Affects sodium channels; side effects include ataxia, dizziness, diplopia, tremor, GI upset, gingival hyperplasia, and fever.
  • Phenobarbital: multiple mechanisms; side effects include sedation and withdrawal seizures.
  • Valproate: multiple mechanisms; side effects include GI upset, weight gain, alopecia, and tremor; less common, thrombocytopenia, hepatitis, pancreatitis
  • Topiramate: multiple mechanisms; side effects include anorexia, cognitive slowing, sedation, nephrolithiasis, and anhidrosis.
  • Gabapentin: multiple mechanisms; side effects include sedation, dizziness, and ataxia.
  • Pregabalin: Affects calcium channels; side effects include sedation, dizziness, and weight gain.
  • Zonisamide: Affects sodium channels.
    • Side effects include sedation, anorexia, nausea, dizziness, ataxia, anhidrosis, and nephrolithiasis.
    • Cross-reaction with sulfa allergy
Pregnancy Considerations
  • Folate should be prescribed for all women of childbearing age who are taking AEDs. AED therapy during the 1st trimester is associated with doubled risk for major fetal malformations (6% vs. 3%).
  • Phenytoin in pregnancy may result in fetal hydantoin syndrome.
  • Valproate is associated with neural tube defects.
  • Fetal insult from seizures following withdrawal of therapy also may be severe. Risk-to-benefit balance should be evaluated with high-risk pregnancy and neurology consultations. Most patients remain on anticonvulsants.
  • Consider vagal nerve stimulator during pregnancy (8)[B].
ISSUES FOR REFERRAL
For refractory seizures, consider referral to an epilepsy specialist (9)[B].
ADDITIONAL THERAPIES
  • Vagal nerve stimulator provides periodic stimulation to vagus nerve; may induce hoarseness, cough, and dysphagia. High-frequency stimulation in adults provides greater reduction in seizure frequency than low-frequency stimulation but also has greater rates of side effects (10)[B].
  • Deep brain stimulation may decrease seizure frequency in medically refractive epilepsy but its efficacy varies by seizure source location (11)[B].
  • Repetitive magnetic transcranial stimulation may reduce the frequency of seizures in individuals with refractory focal seizures (12)[B].
SURGERY/OTHER PROCEDURES
  • For refractory partial complex seizures with identifiable focus
  • Preoperative testing, such as Wada test, should be done to decrease likelihood of inducing aphasia and memory loss.
  • 34-74% will be seizure-free after temporal lobe surgery. Prognosis varies for surgical resection of extratemporal foci (13)[B].
  • Goal of surgical intervention is to reduce reliance on medications; most patients remain on anticonvulsants postoperatively.
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
Admit for unremitting seizure (partial/secondary generalized status epilepticus).
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
  • Most states have restrictions on driving for those with seizure disorders.
  • Depending on seizure manifestation, may also recommend against activities such as swimming, climbing to heights, or operating heavy machinery
Patient Monitoring
AED levels if concern over toxicity, noncompliance, or for breakthrough seizures
DIET
Ketogenic or low-glycemic index diet may improve seizure control in some patients but is not welltolerated (14)[B].
PATIENT EDUCATION
Avoid potential triggers such as alcohol or drug use and sleep deprivation.
PROGNOSIS
  • Risk of seizure recurrence: ˜30% after first seizure; of these, 50% will occur in the first 6 months; 90% in the first 2 years.
  • Depends on seizure type; rolandic epilepsy has a good prognosis; temporal lobe epilepsy is more likely to be persistent.
  • ˜25-30% of all seizures are refractory to current medications.
  • AEDs initiated after an initial seizure have been shown to decrease the risk of seizure over the first 2 years but are not demonstrated to reduce longterm risk of recurrence.
  • The potential for AEDs to confer neuroprotection is under investigation.
  • The risk of developing seizure after mild TBI remains high for a long period (>10 years) (1)[B].
REFERENCES
1. Christensen J, Pedersen MG, Pedersen CB, et al. Long-term risk of epilepsy after traumatic brain injury in children and young adults: a population-based cohort study. Lancet. 2009;373(9669):1105-1110.
2. Fattal-Valevski A, Bloch-Mimouni A, Kivity S, et al. Epilepsy in children with infantile thiamine deficiency. Neurology. 2009;73(11):828-833.
3. Brigo F, Igwe SC, Erro R, et al. Postictal serum creatine kinase for the differential diagnosis of epileptic seizures and psychogenic non-epileptic seizures: a systematic review. J Neurol. 2015;262(2):251-257.
4. Gaillard WD, Cross JH, Duncan JS, et al. Epilepsy imaging study guideline criteria: commentary on diagnostic testing study guidelines and practice parameters. Epilepsia. 2011;52(9):1750-1756.
5. Krumholz A, Wiebe S, Gronseth GS, et al. Evidence-based guideline: management of an unprovoked first seizure in adults: report of the Guideline Development Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology. 2015;84(16):1705-1713.
6. Bonnett LJ, Smith CT, Donegan S, et al. Treatment outcome after failure of a first antiepileptic drug. Neurology. 2014;83(6):552-560.
7. Thompson K, Pohlmann-Eden B, Campbell LA, et al. Pharmacological treatments for preventing epilepsy following traumatic head injury. Cochrane Database Syst Rev. 2015;(8):CD009900.
8. Houser MV, Hennessy MD, Howard BC. Vagal nerve stimulator use during pregnancy for treatment of refractory seizure disorder. Obstet Gynecol. 2010;115(2, Pt 2):417-419.
9. Hemb M, Velasco TR, Parnes MS, et al. Improved outcomes in pediatric epilepsy surgery: the UCLA experience, 1986-2008. Neurology. 2010;74(22):1768-1775.
10. Panebianco M, Rigby A, Weston J, et al. Vagus nerve stimulation for partial seizures. Cochrane Database Syst Rev. 2015;(4):CD002896.
11. Sprengers M, Vonck K, Carrette E, et al. Deep brain and cortical stimulation for epilepsy. Cochrane Database Syst Rev. 2014;(6):CD008497.
12. Sun W, Mao W, Meng X, et al. Low-frequency repetitive transcranial magnetic stimulation for the treatment of refractory partial epilepsy: a controlled clinical study. Epilepsia. 2012;53(10): 1782-1789.
13. Jobst BC, Cascino GD. Resective epilepsy surgery for drug-resistant focal epilepsy: a review. JAMA. 2015;313(3):285-293.
14. Levy RG, Cooper PN, Giri P. Ketogenic diet and other dietary treatments for epilepsy. Cochrane Database Syst Rev. 2012;(3):CD001903.
Additional Reading
&NA;
  • Walker LE, Mirza N, Yip VL, et al. Personalized medicine approaches in epilepsy. J Intern Med. 2015;277(2):218-234.
  • Wilden JA, Cohen-Gadol AA. Evaluation of first nonfebrile seizures. Am Fam Physician. 2012;86(4): 334-340.
Codes
&NA;
ICD10
  • G40.109 Local-rel symptc epi w simp prt seiz,not ntrct, w/o stat epi
  • G40.209 Local-rel symptc epi w cmplx prt seiz,not ntrct,w/o stat epi
  • G40.119 Local-rel symptc epi w simple part seiz, ntrct, w/o stat epi
Clinical Pearls
&NA;
  • It is controversial whether AED treatment is indicated after a first seizure. Treatment should be strongly considered when a clear structural cause is identified/risk of injury from seizure is high (e.g., osteoporosis, anticoagulation).
  • Consider vagus nerve stimulation in pregnancy and in patients with medically refractory seizures.
  • Postictal elevation in prolactin and CPK levels can help distinguish physiologic from psychogenic seizures.