Partial Epilepsies Differential Diagnoses

  • Author: Alberto Figueroa Garcia, MD; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Jun 7, 2011
 
 

Diagnostic Considerations

Understanding the conceptual difference between seizure and epileptic syndrome is important. An epileptic seizure is defined as a transient neurologic dysfunction resulting from an excessive abnormal electrical discharge of cerebral neurons. The clinical manifestations are numerous, including disturbances of consciousness, changes in emotions, changes in sensation, abnormal movements, and changes in visceral functions or behavior.

Epilepsy is a group of disorders characterized by chronic, recurrent, paroxysmal changes in neurologic function caused by abnormalities in electrical activity of the brain. Differentiation of the specific disorders is important for the following reasons:

  • It permits determination of prognosis
  • It is essential to choosing appropriate drug therapy
  • It is essential for surgical treatment

Clinically, seizures may be simple partial or complex partial, with or without secondary generalization. Interictal EEG shows focal spikes or sharp waves, and ictal EEG shows a focal or regional discharge at onset.

Benign epilepsy syndromes are characterized below.

Neonates

In neonates, seizures that occur during sleep manifest as head banging and benign neonatal myoclonus. Seizures during wakefulness may have the following manifestations:

  • Jitteriness
  • Head banging
  • Masturbation
  • Benign myoclonus of epilepsy
  • Spasmodic torticollis
  • Spasms nutans
  • Opsoclonus
  • Rumination
  • Startle disease or hyperexplexia
  • Shuddering attacks
  • Alternating hemiplegia
  • Infantile apnea
  • Cyanotic breath-holding spells
  • Pallid syncope

Children

In children, seizures that occur during sleep manifest as hypnagogic paroxysmal dystonia, nightmares, night terrors, and sleep walking. Seizures during wakefulness may have the following manifestations:

  • Chorea
  • Tics
  • Paroxysmal choreoathetosis
  • Stereotypical movements
  • Head nodding
  • Headache
  • Recurrent abdominal pain
  • Rage attacks

Differential diagnostic considerations in these cases include confusional migraine, benign paroxysmal vertigo, stool-withholding activity,[1] and Munchausen syndrome by proxy.

Late childhood

Seizures during wakefulness may manifest as syncope, narcolepsy and/or cataplexy, basilar migraine, tremor, or panic disorder.

Mesial temporal epilepsy

The most common cause of temporal lobe epilepsy in candidates for epilepsy surgery in adults is hippocampal sclerosis. In children, etiologies are dominated by cortical dysplasias and low-grade neoplasms. Seizures typically are complex partial with automatisms, often preceded by a simple partial phase with sensory symptoms (ie, aura).

Auras commonly observed in temporal lobe epilepsy are epigastric (abdominal) and psychic auras, including déjà-vu or jamais-vu and fear.

Complex partial seizures of temporal lobe origin are semiologically automotor, with fine distal automatisms involving hands and/or fingers and orobuccal movements.

Interictal EEG typically shows temporal sharp waves maximal at anterior temporal or sphenoidal electrodes. Ictal EEG often shows well-defined rhythmic theta seizure patterns.

Diagnosis of mesial temporal lobe epilepsy often is confirmed by high-resolution MRI using dedicated epilepsy protocols. Localization by MRI is a strong predictor of a favorable surgical outcome, especially when concordant with ictal EEG, so much so that performing successful temporal lobectomies without ictal recordings may be possible. The availability and high sensitivity of MRI in this setting has greatly reduced the need for invasive EEG.

Neocortical seizures

Neocortical seizures may be simple partial or complex partial, with symptoms depending on the area of cortex affected. Interictal EEG typically shows sharp waves or spikes outside of the anterior temporal region. Ictal EEG often shows regional or widespread discharges.

In general, localization of the epileptogenic zone by surface EEG (interictal and ictal) is less reliable for neocortical than for mesiotemporal epilepsy. Epileptiform discharges can be absent on surface EEG when the focus is deep, as in supplementary sensorimotor area epilepsy.

Frontal discharges can spread rapidly and mimic primary generalized spike-wave complexes. This is referred to as secondary bilateral synchrony (with interictal epileptiform discharges that appear to be generalized but are in reality secondarily generalized focal discharges). Strict criteria are required to attribute generalized discharges to secondary bilateral synchrony, focal or lateralized epileptiform discharges, or a structural lesion.

Neocortical extratemporal epilepsies may be difficult to localize precisely. Precise localization is important only when considering surgical treatment.

Certain syndromes are well characterized, including frontal, supplementary sensorimotor, parietal, and occipital lobe epilepsies.

Frontal seizures are brief, stereotypical, and often occur in clusters and in sleep. They include behaviors such as bicycling, sexual automatisms, vocalizations, asymmetric tonic extension of proximal extremities, and gestural automatisms. Consciousness may be spared. Owing to the bizarre behaviors, clinically these are often confused as psychogenic nonepileptic attacks.

Parietal seizures often spread to other regions quickly. Somatosensory symptoms such as pain, thermal sensation, or paresthesias contralateral to site of origin are often reported.

Occipital lobe seizures often include vision loss, elementary (flashing white/colored lights) or complex hallucinations, and illusions.[2, 3]

Most adult-onset localization-related epilepsies do not have an identifiable etiology (ie, MRI is most often normal). When a cause is found, it can include various structural lesions (eg, traumatic scars, neoplasms, vascular malformations, strokes, neuronal heterotopias).

Differential Diagnoses

Proceed to Workup
 
 
Contributor Information and Disclosures
Author

Alberto Figueroa Garcia, MD  Resident Physician, Department of Neurology, University of South Florida College of Medicine

Alberto Figueroa Garcia, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Coauthor(s)

Vikas K Agrawal, MD  Attending Neurologist, Medical Director of Stroke Unit, Bronx Lebanon Hospital Center; Clinical Instructor, Albert Einstein College of Medicine

Vikas K Agrawal, MD is a member of the following medical societies: American Academy of Neurology and American Medical Association

Disclosure: Nothing to disclose.

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Specialty Editor Board

Claude G Wasterlain, MD  Chair, Department of Neurology, VA Greater Los Angeles Health Care System; Distinguished Professor and Vice-Chair, Department of Neurology, University of California, Los Angeles, David Geffen School of Medicine

Claude G Wasterlain, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Federation for Medical Research, American Neurological Association, Royal Society of Medicine, and Society for Neuroscience

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Jose E Cavazos, MD, PhD, FAAN  Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center, University Hospital System; Director of the San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

Jose E Cavazos, MD, PhD, FAAN is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, and American Neurological Association

Disclosure: GXC Global, Inc. Intellectual property rights Medical Director - company is to develop a seizure detecting device. No conflict with any of the eMedicine articles that I wrote or edited.

Chief Editor

Helmi L Lutsep, MD  Professor, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

References
  1. Cohn A. Stool withholding presenting as a cause of non-epileptic seizures. Dev Med Child Neurol. Oct 2005;47(10):703-5. [Medline].

  2. Rudzinski LA, Shih JJ. The Classification of Seizures and Epilepsy Syndromes. CONTINUUM: Lifelong Learning in Neurology. Jun 2010;16(3):15-35. [Full Text].

  3. Sveinbjornsdottir S, Duncan JS. Parietal and occipital lobe epilepsy: a review. Epilepsia. May-Jun 1993;34(3):493-521. [Medline].

  4. Naritoku DK, Warnock CR, Messenheimer JA, Borgohain R, Evers S, Guekht AB, et al. Lamotrigine extended-release as adjunctive therapy for partial seizures. Neurology. Oct 16 2007;69(16):1610-8. [Medline].

  5. Richy FF, Banerjee S, Brabant Y, Helmers S. Levetiracetam extended release and levetiracetam immediate release as adjunctive treatment for partial-onset seizures: an indirect comparison of treatment-emergent adverse events using meta-analytic techniques. Epilepsy Behav. Oct 2009;16(2):240-5. [Medline].

  6. Powell G, Saunders M, Marson AG. Immediate-release versus controlled-release carbamazepine in the treatment of epilepsy. Cochrane Database Syst Rev. Jan 20 2010;CD007124. [Medline].

  7. Benbadis SR. Evaluation for surgical treatment of partial epilepsy: an overview. Wis Med J. 1995;94(9):500-4. [Medline].

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This graph illustrates the 2 peaks of incidence of epilepsy: early and late in life.
 
 
 
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