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Main › Hygiene & Health › Health Careers & Profession
 

Staring-Spell Seizures: They're Not All the Same

 
Author: Gary Cordingley

Most people understand that there are multiple types of epileptic seizures. The best known variety--and certainly the most spectacular--is often termed "grand mal," which is French for "major illness." In these attacks the patients lose consciousness, fall to the ground and experience convulsive jerking of their bodies that lasts for 1-2 minutes before subsiding. These attacks are more properly termed tonic-clonic seizures.

A less dramatic form of epilepsy also involves loss of consciousness, but without a fall to the ground or convulsive movements. These attacks are aptly called "staring spells" because the patients stop what they're doing, lose eye-contact with other people, and appear to stare into space. If spoken to during attacks, the patients do not respond.

What is often under-appreciated is that more than one kind of epileptic attack can take the form of a staring spell. And the differences between them can be crucial in understanding the underlying causes as well as the best treatments.

Staring-spell seizures are often lumped together in public awareness under the heading of "petit mal" epilepsy. Petit mal is French for "minor illness," reflecting their more subtle appearance. However, using current terminology, there are two main kinds of staring-spell attacks--absence seizures and partial-complex seizures. Absence attacks correspond to the original "petit mal" designation, while partial-complex seizures were once called "psychomotor seizures" and "temporal lobe epilepsy." The "temporal lobe" label reflects the fact that most seizures of this kind emanate from one of the two temporal lobes, the portions of the brain nearest the tops of the ears.

Although both absence and partial-complex seizures involve staring and unresponsiveness, that's where the similarities end. The attacks differ in the following ways:

  • usual ages of onset
  • duration
  • symptoms recalled by the patients
  • movements or behaviors during the attacks
  • after-effects
  • electroencephalogram (EEG) patterns
  • underlying causes
  • most effective treatments

Absence seizures begin in childhood, and often in the pre-school years. They usually disappear by the time the individuals who have them reach their twenties. Partial complex seizures can begin in either childhood or adulthood, including late in life. So if a middle-aged person has staring-spell seizures, they are almost always of the partial-complex type.

The duration of the attacks also separates the two kinds of seizures. Absence seizures are shorter. Most of them end within 10 seconds, and they almost never continue for 30 seconds. In contrast, partial-complex seizures are longer than 30 seconds, and typically last 2-3 minutes.

Most children with absence seizures are unaware of having them, though might notice a loss of time. The relative lack of symptoms in absence seizures, along with their brevity, can cause them to be overlooked. Teachers, noticing episodic loss of eye-contact, are often the first to detect them. But children and adults experiencing partial-complex seizures often recognize them due to specific, recurrent--and often complex--symptoms. One person with partial-complex seizures might notice a sudden, particular odor that no one else can smell. Another patient might experience a sudden sense of familiarity with their surroundings, a perception that they had been there before (also known as "dj vu," a French term meaning "already seen").

Another point of distinction is that the patient's movements or behaviors during attacks are different. In absence attacks there might be a brief flutter of the eyelids or a minimal shiver, and that's all. In fact, absence seizures are more notable for inactivity than for extra movements. But in partial complex seizures, the behaviors can be elaborate--and complex. There can be facial movements like chewing or puckering of the lips. The patient might repeatedly pick at a button or a pant-leg, or recurrently peer beneath a table. For any one patient with partial-complex seizures the behaviors are the same with each attack.

Yet another difference concerns after-effects. After absence seizures, children resume their preceding conversations or activities as if nothing had happened. There are no after-effects. But following partial-complex seizures, patients can be confused for a few minutes and then often head for bed, complaining of tiredness.

If brain-waves are monitored during attacks, then the two kinds of epilepsy show completely different patterns of abnormality. Absence attacks show characteristic electrical discharges simultaneously generated by both sides of the brain, cycling at a rate of three per second. These can even be induced during an EEG recording by having the child hyperventilate. But in partial-complex seizures, one side of the brain is abuzz with rapid, electrical discharges, while the opposite side is barely affected. Also, hyperventilation is not an effective trigger.

Absence seizures, which occur on both sides of the brain at once, are usually inherited and the underlying problem is invisible to MRI scans. But in patients with partial-complex seizures MRI scans sometimes reveal defects in brain anatomy. Because just one spot in the brain--usually within a temporal lobe--is generating the seizure activity, MRI scans can show defects in the brain near the hot-spot. Some defects, like strokes or tumors, might require treatments of their own. Others, like holes, scars or even just under-developed tissue, have no specific treatments.

Finally, the medications that best control the two kinds of seizures can differ. For example, ethosuximide, also known by its brand name Zarontin, is effective in preventing absence seizures, but has no effect whatsoever on partial-complex seizures. Two other medications--phenytoin (Dilantin) and carbamazepine (Tegretol)--are useful in controlling partial-complex seizures, but can actually worsen absence seizures. So it's important to get it right.

(C) 2005 by Gary Cordingley

Author Bio:

Gary Cordingley

Gary Cordingley graduated from Purdue University with a B.S. in chemistry and biology in 1971. He attended Duke University where he earned a Ph.D. in physiology and pharmacology in 1976, and an M.D. in 1977. He received internship training in internal medicine at the University of Michigan Hospitals 1977-1978, residency training in neurology at the Neurological Institute of Columbia-Presbyterian Medical Center in New York, 1978-1981, and fellowship training as a pharmacology research associate in the National Institute of General Medical Sciences in Bethesda, Maryland, 1981-1983.

He has practiced neurology in Athens, Ohio, since 1983. He is an associate professor of neurology at the Ohio University College of Osteopathic Medicine and a medical staff member of O'Bleness Memorial Hospital in Athens, Ohio.

Dr. Cordingley has been certified in neurology by the American Board of Psychiatry and Neurology. He is a fellow of the American Academy of Neurology and a member of the American Headache Society. He is also a member of the Ohio Academy of Medical History and was president of this organization 1994-1997. Dr. Cordingley's articles on neurology, neuroscience and medical history have appeared in numerous professional and general publications.

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