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Partial Epilepsies Clinical Presentation

  • Author: Alberto Figueroa Garcia, MD; Chief Editor: Helmi L Lutsep, MD  more...
 
Updated: Feb 22, 2016
 

History

Obtaining a description of the seizures from the patient and any witnesses is critical. The description needs to include a description of the patient’s state of consciousness during the seizure. Consciousness usually is assessed by the ability of the patient to respond to external stimuli (ie, responsiveness).

Partial seizures are divided into simple, complex, and those that evolve into secondary generalized seizures. Simple and complex seizures are distinguished solely on the basis of the state of consciousness. This is intact in simple partial seizures and impaired in complex partial seizures.

Simple partial seizures

Simple partial seizures are subdivided into 4 categories, according to whether the symptoms are motor, sensory, autonomic, or psychic.

Motor symptoms can vary. They may include motor signs with or without march, versive movements, posturing, and phonatory symptoms.

Sensory symptoms include all 5 senses and a vertiginous sensation. With the exception of vertigo, these usually are characterized by elementary hallucinations.

Autonomic symptoms include the common rising epigastric sensation (typically observed in mesial temporal lobe epilepsy). Less frequent symptoms are vasomotor phenomena and mydriasis.

Psychic symptoms are characterized by various experiences involving memory (déjà-vu, jamais-vu), affect (fear, pleasure), or other complex psychic phenomena such as illusions.

Complex partial seizures

Complex partial seizures include some complex symptomatology (ie, automatisms) and, by definition, an impairment of consciousness. Automatisms consist of involuntary but coordinated motor activity, which tends to be purposeless and repetitive. Common automatisms include lip smacking, chewing, fidgeting, and walking.

Complex partial seizures can begin as simple partial seizures and seizures with impaired consciousness at onset. Complex partial seizures are not subdivided according to coexisting symptoms, no matter how prominent.

Partial seizures that evolve into generalized seizures

The third type of partial seizure evolves into a generalized seizure. This is divided further according to what precedes generalization (simple partial seizure only, complex partial seizure only, simple partial seizure evolving into complex partial seizure). For clinical purposes, however, the partial phase of the seizure often is missed and many patients simply present with a convulsion (secondarily generalized tonic-clonic seizures).

Genetic partial epilepsies

Three genetic partial epilepsies are recognized, as follows:

  • Childhood epilepsy of occipital paroxysms
  • Benign childhood epilepsy with centrotemporal spikes
  • Autosomal dominant nocturnal frontal lobe epilepsy

Childhood epilepsy of occipital paroxysms

Age of onset is 15 months to 17 years. One third of patients have a family history of epilepsy, especially rolandic epilepsy.

Symptoms of attacks include the following:

  • Visual hallucination
  • Blindness
  • Hemianopia
  • Visual illusions (eg, micropsia, macropsia, metamorphopsia)
  • Loss of consciousness
  • Unilateral clonic seizure followed by migraine like headache

These attacks can occur while the child is awake or sleeping. They tend to occur during the transition period between wakefulness and sleep.

Benign childhood epilepsy with centrotemporal spikes

Age of onset is 2-12 years, with a strong peak at 8-9 years.

Characteristic ictal symptoms include the following:

  • Guttural vocalizations
  • Hypersalivation
  • Drooling
  • Sensations or movements of the mouth
  • Dysphasia
  • Speech arrest

Though these focal seizures are the most characteristic seizure types, they can be quite subtle and are missed easily. The most common mode of presentation is a nocturnal (secondary) generalized tonic-clonic seizure during sleep.

Neurologic examination is normal. The natural history is benign. This syndrome has an excellent prognosis regardless of treatment, with spontaneous remission by age 14-16 years. If treatment is required, options may include carbamazepine, gabapentin, or valproate. Antiepileptic drugs (AEDs) should always be weaned by age 14-16 years.

Autosomal dominant nocturnal frontal lobe epilepsy

Autosomal dominant nocturnal (ADNFLE) is a recently described syndrome. Onset is early in life.

ADNFLE is caused by mutation in the neuronal nicotinic acetylcholine receptor alpha4 subunit (CHRNA4) gene. Several mutations of this gene have been identified as causes of ADNFLE. Despite its established genetic basis, the genetic findings are variable (locus heterogeneity); thus, definite diagnosis is difficult and largely one of exclusion.

Seizures are nocturnal and occur in clusters, mimicking parasomnias. They mostly are brief tonic seizures and rare tonic-clonic convulsions, often preceded by a nonspecific aura.

Seizures often subside with age and may even disappear at adulthood. They usually are controlled with carbamazepine.

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Physical Examination

In most focal epilepsies, physical examination is unrevealing. A neurologic examination should be done to elicit any cortical abnormality or dysfunction, which would depend on etiology and lesion site.

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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)

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 Medical Association, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics; Eisai; Glaxo Smith Kline; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics; Lundbeck; Sepracor; Sunovion; UCB; Upsher-Smith.

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, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, Assistant Dean for the MD/PhD Program, 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, San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

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

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Brain Sentinel, consultant.<br/>Stakeholder (<5%), Co-founder for: Brain Sentinel.

Chief Editor

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

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

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Additional Contributors

Claude G Wasterlain, MD, MSc 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, MSc 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, Society for Neuroscience

Disclosure: Nothing to disclose.

References
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  8. Krauss GL, Serratosa JM, Villanueva V, Endziniene M, Hong Z, French J, et al. Randomized phase III study 306: Adjunctive perampanel for refractory partial-onset seizures. Neurology. 2012 May 1. 78(18):1408-15. [Medline].

  9. Hufnagel A, Ben-Menachem E, Gabbai AA, Falcão A, Almeida L, Soares-da-Silva P. Long-term safety and efficacy of eslicarbazepine acetate as adjunctive therapy in the treatment of partial-onset seizures in adults with epilepsy: results of a 1-year open-label extension study. Epilepsy Res. 2013 Feb. 103(2-3):262-9. [Medline].

  10. Halász P, Cramer JA, Hodoba D, Czlonkowska A, Guekht A, Maia J, et al. Long-term efficacy and safety of eslicarbazepine acetate: results of a 1-year open-label extension study in partial-onset seizures in adults with epilepsy. Epilepsia. 2010 Oct. 51(10):1963-9. [Medline].

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