Absence Seizures and the Study of Consciousness

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Absence Seizures and the Study of Consciousness

Epilepsy has intrigued and confused humans for thousands of years. The “sacred disease” was mentioned in 2080 BC in the Hammurabi Laws and the Talmud, and in 400 BC the physician Hippocrates correctly speculated that its origins lie within the brain. Petit mal seizures were not specifically addressed until much later. Despite a seemingly endless amount of research that has been completed within the last century, very little is actually known about petit mal seizures. Their correlation to consciousness is far from clear. Antonio Damasio of the University of Southern California has studied aphasia patients with petit mal epilepsy in great depth. He has concerned himself with the study of behavioral neurology and the origins of consciousness for several decades, working toward a better understanding of the brain’s role in conscious perception, emotion, and awareness. His observations have led him to believe that wakefulness and consciousness are separate, unbound entities. He concludes that consciousness can be associated with brain structure. Furthermore, his studies of patients with petit mal seizures have demonstrated that while consciousness and wakefulness can occur independently of one another, consciousness cannot exist without a sense of self, nor can it be separated from emotion.

A thorough understanding of petit mal epilepsy must be attained before a link can be developed between absence seizures and Damasio’s theories on the origin of conscious perception. From an entirely scientific standpoint, petit mal seizures are brief interruptions of awareness, responsiveness, emotion, and memory. Damasio notes that consciousness, the part of the mind concerned with sense of self and perception, is temporarily impaired. He defines this as “absence without leave… [a] transition between a fully conscious mind and a mind deprived of the sense of self” (Damasio, 6). Petit mal attacks are also referred to as absence seizures because consciousness seems to mysteriously disappear during an attack, even though the patient is still awake. It is estimated that slightly less than two people per 100,000 in the United States are afflicted with petit mal epilepsy. Absence seizures are considered to be fairly safe: there are no evident after-effects or potentially harmful automatisms, and the seizures can be controlled easily once correctly diagnosed. No deaths have been reported as direct results of absence seizures, although epileptics put themselves at serious risk if they choose to drive a car or take part in some other potentially dangerous activity. Some consider petit mal to be the safest way to lose and regain consciousness (Myslobodsky and Mirsky, 1). Children and adolescents are most prone to absence seizures, and cases of an onset later in life are rare. Repeated seizures may indicate a serious seizure disorder known as epilepsy. Thus, petit mal epilepsy results from frequent absence seizures. Although these seizures are not life-threatening, children may withstand hundreds every day.

Absence seizures are fairly short. They typically last less than ten seconds and rarely exceed a minute. There are virtually no warnings prior to a seizure, at least none that are easily detected, and there is really no way of knowing when one will end. The seizures are normally characterized by a short staring spell in which the patient seems to momentarily go blank. Some movement often accompanies a seizure in the form of an automatism, which is an unplanned production of motor behavior that is not accompanied by conscious neural stimulation. A person having an automatism is not aware of his or her actions and has no self control. Automatisms most frequently encountered include blinking, lip smacking, pupil dilation, and slight twitching in the facial muscles. If a person is carrying out a small motor activity such as clenching his or her fist, he or she may maintain a motor response but are incapable of beginning a new one. In some cases all movement is suspended, although ninety-one percent of all reported seizures are accompanied by automatisms. When patients resume consciousness, they are often confused and have absolutely no recollection of what went on during the seizure.

Petit mal, like many other forms of epilepsy, is often passed down genetically (Anderson, 38). Children who have family members with the condition are at a much higher risk of developing petit mal epilepsy, although this is not to say that it is never found in children with no such family history. There are many other factors that could potentially contribute to its onset, such as brain trauma, birth defects, or chemical disturbances resulting from liver or kidney disease. Petit mal epilepsy may be accompanied by other types of seizures, excluding partial seizures, where electrical disturbances are found in only one hemisphere of the brain.

Epileptic seizures are caused by abnormal electrical activity within different regions of the brain. Correct diagnosis cannot be determined solely from studying an individual’s behavior during a seizure, nor can the brain be understood simply by cutting into a person’s skull with the intent of conducting a human brain biopsy. Rather, irregular electrical activity can be monitored and categorized by tracking wave-spike discharges via electrocephalogram (EEG). An EEG is a graphic record produced by a machine that translates the electrical activity within the brain into a series of decipherable waves and spikes. An EEG may be taken to determine whether there are any continuing irregularities in the brain’s electrical activity that could produce seizures (Myslobodsky, 71). Because petit mal seizures are not localized in any one particular region of the brain, sixteen electrodes are placed in different areas of a patient’s scalp. These electrodes, which read minute electrical charges traveling back and forth between nerve cells in the brain, amplify and send the charges to a computer that records and displays brain activity. The changes in electrical activity modify the height of the waves and spikes. An EEG usually takes thirty-five to forty-minutes, although the test will run much longer if the patient is asked to sleep.

Petit mal epilepsy is easily identified with an EEG during a seizure due to the uniform nature of electrical activity within the brain. Pure forms of absence seizures are accompanied by wave-spikes (WS) with a frequency of three cycles per second (3-cps). The wave-spike rhythm begins instantaneously and ends with just as little of a warning. WS discharges do not show any major evolution in the course of a seizure. 3-cps WS emissions as shown by an EEG

The discharges are widespread throughout the brain; electrical activity appears to shift between the two hemispheres on a millisecond-by-millisecond basis. Scientists can look for atypical interactions between neuronal populations and abnormal firing patterns. Individual neurons at the single cell level do not demonstrate any irregular behavior in a WS discharge, so all abnormality must stem from mass integration of neuronal systems.

Although the beginning of abnormal electrical brain activity is abrupt, cognitive processing is not immediately impaired. A person suffering from petit mal epilepsy has full mental capabilities until moments before the onset of a WS burst, when their consciousness appears to progressively deteriorate. Neuronal activity in the cortex and thalamus, which control higher nervous functions, is impaired once the WS paroxysms start. A person’s conscious perception declines exponentially during petit mal and may disappear entirely. Recovery is a mirror process and occurs quickly once all electrical irregularities have subsided.

People suffering from absence seizures have considerable hope for being cured of their condition due to anti-epileptic drugs. While many epileptics find that the forms of medication they take are ineffective, patients with petit mal seizures have been found to respond positively to very specific drugs. Anti-absence medication is aimed at eliminating seizures by countering generalized wave-spike discharges. Since the origin of a wave-spike pattern is unknown, doctors strive to “treat the EEG” (Porter, 12) to combat the onset of further seizures. Excluding atypical cases where electrical activity in the brain deviates from the archetypal 3-cps wave-spike pattern taken by EEG, all petit mal seizures are similar enough such that most patients respond well to the same medications (Porter, 4). Valproic Acid (Depakene) and ethosuximide (Zarontin) are the most widely acknowledged drugs used to fight absence epilepsy. Some newer drugs include lamotrigine (Lamictal) and topiramate (Topamax). While both Depakene and Zarontin are incredibly effective in pure cases, they have a wide array of side effects. Patients are often troubled by gastrointestinal pain, headaches, and weight gain. Impairment of cognitive functions can result from extensive use in extreme cases.

Monotherapy, the prescription of a single drug rather than numerous medications, usually works once a patient has been diagnosed. These drugs must often be administered twice or three times a day, which when compared to medications used to combat other forms of epilepsy, is not too frequent. Such drugs generally have a very short half-life (the period of time in which the drug is effective) while ethosuximide has a reported half-life of over twenty-four hours. Thus, patients undergoing monotherapy with Zarontin do not need to take a pill at every meal. Despite the success rate of current seizure medication, a correct diagnosis of a person’s condition is crucial due to the highly specific nature of the administered drugs. While many patients might opt for surgery, petit mal seizures are not localized in one specific area of the brain. There is no agreed-upon surgical target (Mirsky and Grady, 285). This eliminates the possibility of preventing further seizures by identifying and removing a portion of the brain.

Alternatives to pharmacological therapy have been discussed within the scientific community over the past few decades since not all side effects are clear. Many of the side effects that are known, such as gastrointestinal discomfort and possible birth defects, are regarded as generally unsafe for patients. There has been some debate over whether an electronic prosthesis could be created to counter absence seizures. A detector turned to preburst signals, possibly placed in the ear like a hearing aid, could theoretically interrupt wave-spike bursts and stop seizures at their onset. However, much more research much be conducted before any serious resolutions can be made regarding the practicality and feasibility of such a device.

Scientists’ knowledge of absence epilepsy is far from complete. Although many medications are readily available to combat a seizure, the aspects of absence epilepsy pertaining to conscious perception are still mysteries. There is some debate as to whether patients are truly unconscious during a petit mal seizure. Many scientists conclude from their studies of aphasia patients that a person has not lost all contact with reality if he or she is still able to perform a specific task (Myslobodsky, 71). While many parts of the brain are affected by an absence seizure, some neural circuits are left intact and continue to perform their functions. For instance, a certain degree of sensation is not blocked during absence. The V1 may still take static pictures during a WS wave, but it is unknown as to whether the frontal lobe can actively create conscious representations of the environment. One patient in particular is able to play piano during a petit mal seizure and feels “that her ability to use fingers on the piano [is] better than average because she [is] not at all concerned with the music she produces” (Andermann and Robb, 88). Many scientists argue that her ability to play piano is a matter of muscle memory and has nothing to do with conscious perception.

Roger J. Porter of the University of Nebraska says that there are different degrees of impairment of consciousness. He notes that most of the patients he observes are “dull and confused, responsiveness in the large majority will be neither normal nor totally lacking but somewhere in between” (Porter, 31). A patient may retain some sense of awareness, but he or she could potentially be losing the ability to monitor himself or herself and the environment. Patients could potentially be conscious throughout the entire seizure and yet unable to express themselves. Some have even proposed that waking up could produce an amnesia effect (Chatrian et al, 89). Thus, all verbal reports attained from patients could be incomplete. Naturally, these theories are entirely speculative. WS discharges need to be studied more to establish a stronger link between loss of awareness and seizures.

Damasio refutes the entire idea of consciousness without a sense of self. A person may maintain wakefulness during an absence seizure, but he or she cannot be conscious. Damasio writes that during an epileptic fit, “there would have been no sense of self, no identifiable person with a past and an anticipated future – specifically, no core self and no autobiographical self” (Damasio, 98). Core consciousness, the base for extended consciousness, is regenerated every moment. It results from the interaction of the body with the outside environment or memories within the mind. This interaction is referred to as a first-order representation. First-order maps, which are unconscious and constantly changing, are detected in the different regions of the brain and tracked by second-order representations. Changes in second-order representations lead to pulses of core consciousness. Qualia (a distinctive feeling and quality of self-knowing, of what it is like to be you) and memories developed through pulses of consciousness are compiled over time to produce extended consciousness, which creates the autobiographical self. There is no core self and no autobiographical self during a petit mal seizure because second-order representations are not functional. They are unable to detect changes in first-order maps. Thus, core consciousness is temporarily defective during an absence seizure. No pulses of consciousness can arise from defective core consciousness (Damasio, 100), and if there are no pulses of consciousness, there can be no qualia. Consciousness cannot exist without a sense of self.

While in a state of wakefulness, a person still maintains first-order representations. He or she is still capable of creating neural patterns and sufficient mapping of images. The operational first-order representations enable the individual to keep low-level attention. Thus, operations that are committed to muscle memory may be carried out during a seizure. Low level attention enables the brain to work sensory images and signal different neural groups. Additionally, the lack of high-level planning and attention that accompanies a seizure prohibits an individual from experiencing emotion. Emotion and consciousness are inseparable entities (Damasio, 131). When a person is without consciousness, as is the case during sleep (excluding REM sleep) or a seizure, no emotions can be felt because pulses of core consciousness are not operating or creating qualia. There is no feeling or experience and no second-order representations tracking changes within first-order representations. Consciousness is unmistakably accompanied by emotion and vice versa. What is not known, however, is the point at which emotion leaves an individual who falls into a state of unconsciousness.

Some tests with definitive results have been devised to determine the point at which consciousness is lost during an absence seizure. The CPT, or Continuous Performance Test, devises simple tasks that a petit mal patient must carry out on a momentary basis. Simple motor tasks switch constantly and measure the patient’s ability to avoid omission errors (Mirsky, 312). In a word, the CPT is an excellent gauge of the presence of consciousness. Generalized WS bursts are highly correlated with a decrease in conscious perception. Similar tests have found that if WS emissions last longer than one second, patients will respond more slowly or not at all to certain motor stimuli due to a decreased capacity to process information. An individual’s ability to give correct responses primarily diminishes a half-second prior to the onset of a WS paroxysm.

Absence seizures are understood well enough to counter with medication but there is still much left to be learned. Damasio concludes his studies when he writes, “absence seizures are of great value to the student of consciousness, and the typical variety of absence seizure is in fact one of the most pure examples of loss of consciousness” (Damasio, 96). All that has been learned about petit mal epilepsy thus far is contributing greatly to the fields of psychology and neurobiology, as well as adding some insight to the still mysterious picture of conscious perception. In the realm of consciousness, at least from Damasio’s point of view, conscious perception is lost when abnormal electrical activity within the brain prohibits pulses of consciousness from being produced. Second-order representations cannot monitor and map first-order representations. While the person suffering from a petit mal seizure maintains wakefulness, he or she does not retain consciousness, thereby losing emotion as well. Absence seizures stand as neurological proof of all of these concepts. We can hope that further exploration of seizures and similar brain lesions will lead to more definite conclusions regarding the unity between the physical brain and the mind.

Damasio, Antonio. Decartes’ Error. New York: G. P. Putnam’s Sons, 1994.

Damasio, Antonio. The Feeling of What Happens. Florida: Harcourt Inc., 1999.

Myslobodsky, Michael S. and Allan F. Mirsky. Elements of Petit Mal Epilepsy.

New York: Peter Lang Publishing, Inc., 1988.

Nervous System: Petit Mal Seizure. 21 June 2005. Mayoclinic.com.

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Raichle, Marcus. The Scientific American Book of the Brain: Visualizing the Mind.

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Segan, Scott. Absence Seizures. 12 September 2005. Emedicine. 30 November 2006.


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Loyola University Medical Education Network. 7 December 2006.


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