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New-onset absence status epilepsy presenting as altered mental status in a pediatric patient
CASE REPORT
New-Onset Absence Status Epilepsy Presenting as Altered Mental Status in a Pediatric Patient
From the Department of Emergency Medicine, Madigan Army Medical Center, Fort Lewis, WA*; and Children’s Hospital and Regional Medical Center, Department of Pediatrics, University of Washington, Seattle, WA.‡ Received for publication June 23, 2000. Revision received November 9, 2000. Accepted for publication December 15, 2000. The views expressed herin are those of the authors and do not necessarily reflect the views of the US Army or the US Department of Defense. Address for reprints: Eileen J. Klein, MD, MPH, Children’s Hospital and Regional Medical Center, 4800 Sand Point Way NE, P.O. Box 5371/CH-04, Seattle, WA 98105-0371; 206-528-2708, fax 206-527-3945. 47/1/114093 doi:10.1067/mem.2001.114093
MAJ Peter J. Benson, MD* Eileen J. Klein, MD, MPH‡
Absence status epilepsy (ASE) is an uncommon seizure disorder in children. The primary presentation of new-onset ASE in a pediatric patient is an unusual cause of altered mental status in the emergency department. We describe a previously healthy 8-year-old child who presented with an acutely altered mental state. The patient was awake but confused, with a fluctuating level of alertness and an inability to perform simple routine tasks. The results of general physical and neurologic examination, with the exception of mental status, were normal. Head computed tomography and laboratory test results were normal. Electroencephalographic testing revealed seizure activity consistent with ASE. Administration of intravenous diazepam caused cessation of seizure activity and a return to the patient’s baseline mental function. Although rare, ASE should be considered in the differential diagnosis of altered mental status in children. [Benson PJ, Klein EJ. New-onset absence status epilepsy presenting as altered mental status in a pediatric patient. Ann Emerg Med. April 2001;37:402-405.] INTRODUCTION
Altered mental status is an infrequent presenting complaint in the pediatric population. New-onset or de novo absence status epilepsy (ASE) presents with prolonged altered mental status and impaired cognition that may be very subtle and vary in severity over time. New-onset ASE is particularly uncommon as a primary presentation in the pediatric population. It is seldom considered in the differential diagnosis of altered mental status in patients without a history of seizure disorders. We describe a previously healthy 8-year-old girl with new-onset ASE. CASE REPORT
An 8-year-old girl presented to the emergency department for evaluation of a persisting state of confusion. On
4 0 2
ANNALS OF EMERGENCY MEDICINE
37:4 APRIL 2001
ABSENCE STATUS EPILEPSY IN A CHILD Benson & Klein
the morning of presentation, she was difficult to awaken and remained drowsy after arising. She had difficulty performing routine tasks, such as dressing and eating breakfast. She became angry and combative for a period of 30 minutes, yelling at her mother and resisting attempts to get her prepared for school. She then became calm, sad, and tearful, with decreased speech and purposeful movement. On the way to school, she responded appropriately but remained quiet and withdrawn. At school, she was disoriented and was unable to find her way around the building. She could not comprehend simple classroom instructions or complete routine tasks, such as spelling her name. School staff reported that she did not recognize her teachers or friends. Her parents were called, and she was brought for evaluation to her primary care physician, who found the same altered mental state. The patient was then referred to the ED. The patient’s antenatal and neonatal history were unremarkable. Medical history and review of systems were unremarkable and noncontributory. Detailed questioning, however, revealed a similar event of acute confusion 1 month previously, which lasted 20 minutes and resolved spontaneously, and several episodes of staring spells. No medical evaluation was performed at the time of these events. No other history of prior neurologic disease, head injury, or serious infection was obtained. Possible exposures to medications, illicit drugs, or toxins were explored with the patient and parents. No evidence of intentional or unintentional exposure to toxic or illegal substances was obtained. On examination in the ED, vital signs were blood pressure 104/68 mm Hg, pulse rate 72 beats/min, respiratory rate 20 breaths/min, temperature 36.7°C (98.1°F; tympanic), and weight 26 kg. The patient was a well-appearing school-aged girl who was sitting quietly with her parents. She was awake and oriented to person and place but not to time, events, or situation. She displayed a fluctuating level of alertness and attentiveness. She generally lacked facial expressions, although she would often smile and appear confused when questioned. Her responses to questions were vague and uncertain. The patient had poor recall of preceding daily events. The patient was quite confused and intermittently could not spell simple words but was able to count in sequence. The physical examination was unremarkable, including the neurologic examination, with the exception of her mental status. She had no physical findings suggestive of a toxidrome, including normal pupillary size and reaction to light; normal temperature, heart rate, and blood pressure; and lack of diaphoresis or flushed red skin.
APRIL 2001
37:4
ANNALS OF EMERGENCY MEDICINE
Laboratory evaluation demonstrated a CBC count with WBC count of 6,800 cells/mm3 with normal differential, hemoglobin level 14.3 mg/dL, and hematocrit level 41%. Platelets were 220,000/µL. Serum sodium level was 142 mEq/L, potassium level was 4.4 mEq/L, chloride level was 105 mEq/L, and bicarbonate level was 25 mEq/L. Blood urea nitrogen level was 12 mg/dL, and creatinine level was 0.5 mg/dL. Serum glucose level was 102 mg/dL. Serum calcium level was 9.9 mg/dL, phosphate level was 5.2 mg/ dL, and magnesium level was 2.3 mg/dL. A toxicology screen was not obtained. A noncontrast computed tomography scan of the head was obtained and interpereted as normal. A neurology consultation was obtained to assess for organic neurologic disease. The neurology consultant concurred with the previous findings and performed an electroencephalograph (EEG). The EEG showed evidence of seizure activity. The patient was treated with 2.5 mg of diazepam administered intravenously. The EEG improved but was still abnormal, with continued evidence of seizure activity. After a second injection of 2.5 mg of diazepam, no further epileptiform activity was noted. The patient’s mental status improved within 8 minutes of the second injection of diazepam, and she became alert and fully oriented and was reported by parents to be “her normal self.” She had poor recall of the preceding events and was without complaint. The patient was admitted for new-onset ASE and a regimen of 250 mg of twice-daily oral ethosuximide was started. She did well and was discharged the next day without further seizure activity or changes in mental status and returned to school 2 days later. Since discharge, the patient has had problems with breakthrough seizures and a change in the character of her seizures from absence to a more complex partial pattern. The patient is currently seizure-free and receiving a combination of valproic acid and topiramate. DISCUSSION
ASE is relatively uncommon, estimated at between 2.2% and 3% of all cases of seizure disorder. It is primarily a disorder of children, rarely commencing before age 3 years or after age 15 years. Episodes consist of brief paroxysmal episodes of altered consciousness lasting from 5 to 30 seconds. These episodes present as sudden staring spells with vacant facies, occasionally with an upward drift to the eyes. A characteristic feature is the lack of prodromal or postictal signs or symptoms. Attacks occur and end abruptly, with the patient almost always able to continue
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ABSENCE STATUS EPILEPSY IN A CHILD Benson & Klein
the interrupted activity. Absence seizures may occur several or up to 100 times daily, often more frequently in the hours after awakening. Absence seizures may be accompanied by fine clonic movements of the eyelids, head, or upper extremities or automatisms, such as chewing, lip smacking, or mumbling.1 ASE, also known as petit mal status, epilepsia minoris continua, or spike wave stupor, is an uncommon presentation of persisting altered mental status.2 ASE was first described by Lennox3 in 1945, who stated that it was rarely encountered. One large series reviewed 17,000 abnormal EEGs, finding 6 that represented ASE, only 1 of which was from a pediatric patient without prior seizure history.4 ASE is known to occur in certain neurologic syndromes. The most common, Lennox-Gastaut syndrome, begins in infancy with severe psychomotor retardation and refractory generalized seizures, including ASE.5,6 In other patients, ASE has been described in those with known childhood absence epilepsy or may occur before or after generalized seizures in patients with a seizure disorder.7 New-onset or de novo ASE has been reported in adult patients, often in association with changes in antiseizure or psychotropic medications or their withdrawal.8-10 A review of the literature reveals that newonset ASE is rare in the pediatric age group.3,4,7,9 ASE is characterized by an acute altered mental state caused by recurring, almost continuous, absence spells. The stereotypical appearance is one of confusion, mental dullness, muteness, or monosyllabic speech, with slowness or clumsiness of action. The patient appears disoriented, lethargic, or in a fugue state.8,9,11 This altered mental state varies in intensity and presentation over time and from patient to patient. Patients may be completely alert, with abnormalities of cognition only detected by special neuropsychiatric testing, or the patient may be deeply stuporous.7 In one series, only 19% of patients showed a decrease in level of consciousness.12 The main feature is a decrement in cognition and slowed mental process. Patients frequently have difficulty in tasks requiring sustained attention, sequential planning, or spatial relations.7 Patients are described as disoriented, with defects in planning and reasoning, lack of initiative, and decreased attentiveness and perseverations. Patients may also become excessively emotional, impulsive, or combatative.7 Extreme presentations may display hallucinations or delusions or a catatonic-like state mimicking acute psychosis.7 ASE episodes have a variable time course, lasting minutes to days.9,11 The most important step in the evaluation of these patients is to consider ASE in the differential diagnosis.
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The differential diagnosis of a pediatric patient with altered mental status covers many possible causes; trauma, infection, neoplasm, metabolic cause, toxic cause, temporal lobe seizures, and psychiatric and environmental causes should all be considered. The presentation of ASE is unique in that the altered mental state is generally the most striking and often the only abnormal sign or symptom. Without an obvious organic cause, however, an EEG should be performed to assess for seizure activity as the cause. An EEG performed during an episode of ASE is distinctly abnormal. New-onset ASE appears rare in the pediatric age group, especially without a prior history of seizures. It is rarely reported outside subspecialty journals.9-11 This disorder is much more common both in adults and in those with a prior seizure history. The onset of ASE in adults has been linked to several factors: medication withdrawal or changes, menses, hypoglycemia, hyperventilation, photic stimulation, changes in sleep patterns, emotional stress, and fatigue.13 By inference, the same precipitants may also trigger the onset of ASE in pediatric patients. Treatment of ASE follows standard guidelines for the acute treatment of any status seizure. After ensuring the patient’s safety and vital functions, intravenous benzodiazepines are the treatment of choice. Diazepam and lorazepam may be given intravenously in standard doses. Intravenous valproic acid has also been used with success when benzodiazepine therapy has failed.14-16 Long-term therapy with oral ethosuxamide or valproic acid is successful in more than 80% of children.17 The prognosis for patients with ASE is almost always good, with full recovery without sequelae. Uncomplicated absence seizure activity is generally well controlled with oral medication. ASE, even with prolonged duration, has not been shown to cause any neurologic injury in patients with normal premorbid function.13 New-onset ASE is a rare and treatable cause of altered mental status in the pediatric patient. Its diagnosis and treatment rest largely on being aware of the condition and its unique presentation and considering appropriate EEG testing to confirm clinical suspicion. REFERENCES 1.
Livingstone S, Pruce I. Petit mal epilepsy. Am Fam Physician. 1978;17:107-114.
2.
Moe PG. Spike wave stupor: petit mal status. Am J Dis Child. 1971;121:307-313.
3.
Lennox WG. The petit mal epilepsies. JAMA. 1945;129:1069-1074.
4. Niedermeyer E, Khalifeh R. Petit mal status (“spike-wave stupor”). Epilepsia. 1965;6:250262. 5. Niedermeyer E. The Epilepsies: Diagnosis and Management. Baltimore, MD: Urban & Schwarzenberg; 1990.
ANNALS OF EMERGENCY MEDICINE
37:4 APRIL 2001
ABSENCE STATUS EPILEPSY IN A CHILD Benson & Klein
6. Joynt RJ, Griggs RC, eds. Clinical Neurology. Philadelphia, PA: Lippincott Williams & Wilkins; 1998. 7. Guberman A, Cantu-Reyna G, Stuss, D, et al. Nonconvulsive generalized status epilepticus: clinical features, neuropsychological testing and long-term follow-up. Neurology. 1986;36:12841291. 8. Bornstein M, Coddon D, Song S. Prolonged alterations in behavior associated with a continuous electroenceophalopathic (spike and dome) abnormality. Neurology. 1956;6:444-448. 9. Friedlander WJ, Feinstein GH. Petit mal status: epilepsia minoris continua. Neurology. 1956;6:357-363. 10. Thomas PT, Beaumanoir A, Genton, P, et al. ‘De novo’ absence status of late onset: report of 11 cases. Neurology. 1992;42:104-111. 11. Boyd O, Whittingham F, Clements D, et al. Petit mal status: an unusual case of confusion. Br J Hosp Med. 1990;43:230-231. 12. Andelman F, Robb J. Absence status: an appraisal following review of 38 patients. Epilepsia. 1972;13:177-187. 13. Shorvon S, Dreifuss F, Fish D, et al, eds. The Treatment of Epilepsy. Cambridge, MA: Blackwell Science, Ltd; 1996. 14. Yamamoto LG, Yim GK. The role of intravenous valproic acid in status epilepticus. Pediatr Emerg Care. 2000;16:296-298. 15. Chez MG, Hammer MS, Loeffel M, et al. Clinical experience of three pediatric and one adult case of spike-and-wave status epilepticus treated with injectable valproic acid. J Child Neurol. 1999;14:239-242. 16. Alehan FK, Morton LD, Pellock JM. Treatment of absence status with intravenous valproate. Neurology. 1999;52:889-890. 17. Panayiotopoulos CP. Typical absence seizures and their treatment. Arch Dis Child. 1999;81:351-355.
APRIL 2001
37:4
ANNALS OF EMERGENCY MEDICINE
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New-Onset Absence Status Epilepsy Presenting as Altered Mental Status in a Pediatric Patient
From the Department of Emergency Medicine, Madigan Army Medical Center, Fort Lewis, WA*; and Children’s Hospital and Regional Medical Center, Department of Pediatrics, University of Washington, Seattle, WA.‡ Received for publication June 23, 2000. Revision received November 9, 2000. Accepted for publication December 15, 2000. The views expressed herin are those of the authors and do not necessarily reflect the views of the US Army or the US Department of Defense. Address for reprints: Eileen J. Klein, MD, MPH, Children’s Hospital and Regional Medical Center, 4800 Sand Point Way NE, P.O. Box 5371/CH-04, Seattle, WA 98105-0371; 206-528-2708, fax 206-527-3945. 47/1/114093 doi:10.1067/mem.2001.114093
MAJ Peter J. Benson, MD* Eileen J. Klein, MD, MPH‡
Absence status epilepsy (ASE) is an uncommon seizure disorder in children. The primary presentation of new-onset ASE in a pediatric patient is an unusual cause of altered mental status in the emergency department. We describe a previously healthy 8-year-old child who presented with an acutely altered mental state. The patient was awake but confused, with a fluctuating level of alertness and an inability to perform simple routine tasks. The results of general physical and neurologic examination, with the exception of mental status, were normal. Head computed tomography and laboratory test results were normal. Electroencephalographic testing revealed seizure activity consistent with ASE. Administration of intravenous diazepam caused cessation of seizure activity and a return to the patient’s baseline mental function. Although rare, ASE should be considered in the differential diagnosis of altered mental status in children. [Benson PJ, Klein EJ. New-onset absence status epilepsy presenting as altered mental status in a pediatric patient. Ann Emerg Med. April 2001;37:402-405.] INTRODUCTION
Altered mental status is an infrequent presenting complaint in the pediatric population. New-onset or de novo absence status epilepsy (ASE) presents with prolonged altered mental status and impaired cognition that may be very subtle and vary in severity over time. New-onset ASE is particularly uncommon as a primary presentation in the pediatric population. It is seldom considered in the differential diagnosis of altered mental status in patients without a history of seizure disorders. We describe a previously healthy 8-year-old girl with new-onset ASE. CASE REPORT
An 8-year-old girl presented to the emergency department for evaluation of a persisting state of confusion. On
4 0 2
ANNALS OF EMERGENCY MEDICINE
37:4 APRIL 2001
ABSENCE STATUS EPILEPSY IN A CHILD Benson & Klein
the morning of presentation, she was difficult to awaken and remained drowsy after arising. She had difficulty performing routine tasks, such as dressing and eating breakfast. She became angry and combative for a period of 30 minutes, yelling at her mother and resisting attempts to get her prepared for school. She then became calm, sad, and tearful, with decreased speech and purposeful movement. On the way to school, she responded appropriately but remained quiet and withdrawn. At school, she was disoriented and was unable to find her way around the building. She could not comprehend simple classroom instructions or complete routine tasks, such as spelling her name. School staff reported that she did not recognize her teachers or friends. Her parents were called, and she was brought for evaluation to her primary care physician, who found the same altered mental state. The patient was then referred to the ED. The patient’s antenatal and neonatal history were unremarkable. Medical history and review of systems were unremarkable and noncontributory. Detailed questioning, however, revealed a similar event of acute confusion 1 month previously, which lasted 20 minutes and resolved spontaneously, and several episodes of staring spells. No medical evaluation was performed at the time of these events. No other history of prior neurologic disease, head injury, or serious infection was obtained. Possible exposures to medications, illicit drugs, or toxins were explored with the patient and parents. No evidence of intentional or unintentional exposure to toxic or illegal substances was obtained. On examination in the ED, vital signs were blood pressure 104/68 mm Hg, pulse rate 72 beats/min, respiratory rate 20 breaths/min, temperature 36.7°C (98.1°F; tympanic), and weight 26 kg. The patient was a well-appearing school-aged girl who was sitting quietly with her parents. She was awake and oriented to person and place but not to time, events, or situation. She displayed a fluctuating level of alertness and attentiveness. She generally lacked facial expressions, although she would often smile and appear confused when questioned. Her responses to questions were vague and uncertain. The patient had poor recall of preceding daily events. The patient was quite confused and intermittently could not spell simple words but was able to count in sequence. The physical examination was unremarkable, including the neurologic examination, with the exception of her mental status. She had no physical findings suggestive of a toxidrome, including normal pupillary size and reaction to light; normal temperature, heart rate, and blood pressure; and lack of diaphoresis or flushed red skin.
APRIL 2001
37:4
ANNALS OF EMERGENCY MEDICINE
Laboratory evaluation demonstrated a CBC count with WBC count of 6,800 cells/mm3 with normal differential, hemoglobin level 14.3 mg/dL, and hematocrit level 41%. Platelets were 220,000/µL. Serum sodium level was 142 mEq/L, potassium level was 4.4 mEq/L, chloride level was 105 mEq/L, and bicarbonate level was 25 mEq/L. Blood urea nitrogen level was 12 mg/dL, and creatinine level was 0.5 mg/dL. Serum glucose level was 102 mg/dL. Serum calcium level was 9.9 mg/dL, phosphate level was 5.2 mg/ dL, and magnesium level was 2.3 mg/dL. A toxicology screen was not obtained. A noncontrast computed tomography scan of the head was obtained and interpereted as normal. A neurology consultation was obtained to assess for organic neurologic disease. The neurology consultant concurred with the previous findings and performed an electroencephalograph (EEG). The EEG showed evidence of seizure activity. The patient was treated with 2.5 mg of diazepam administered intravenously. The EEG improved but was still abnormal, with continued evidence of seizure activity. After a second injection of 2.5 mg of diazepam, no further epileptiform activity was noted. The patient’s mental status improved within 8 minutes of the second injection of diazepam, and she became alert and fully oriented and was reported by parents to be “her normal self.” She had poor recall of the preceding events and was without complaint. The patient was admitted for new-onset ASE and a regimen of 250 mg of twice-daily oral ethosuximide was started. She did well and was discharged the next day without further seizure activity or changes in mental status and returned to school 2 days later. Since discharge, the patient has had problems with breakthrough seizures and a change in the character of her seizures from absence to a more complex partial pattern. The patient is currently seizure-free and receiving a combination of valproic acid and topiramate. DISCUSSION
ASE is relatively uncommon, estimated at between 2.2% and 3% of all cases of seizure disorder. It is primarily a disorder of children, rarely commencing before age 3 years or after age 15 years. Episodes consist of brief paroxysmal episodes of altered consciousness lasting from 5 to 30 seconds. These episodes present as sudden staring spells with vacant facies, occasionally with an upward drift to the eyes. A characteristic feature is the lack of prodromal or postictal signs or symptoms. Attacks occur and end abruptly, with the patient almost always able to continue
4 0 3
ABSENCE STATUS EPILEPSY IN A CHILD Benson & Klein
the interrupted activity. Absence seizures may occur several or up to 100 times daily, often more frequently in the hours after awakening. Absence seizures may be accompanied by fine clonic movements of the eyelids, head, or upper extremities or automatisms, such as chewing, lip smacking, or mumbling.1 ASE, also known as petit mal status, epilepsia minoris continua, or spike wave stupor, is an uncommon presentation of persisting altered mental status.2 ASE was first described by Lennox3 in 1945, who stated that it was rarely encountered. One large series reviewed 17,000 abnormal EEGs, finding 6 that represented ASE, only 1 of which was from a pediatric patient without prior seizure history.4 ASE is known to occur in certain neurologic syndromes. The most common, Lennox-Gastaut syndrome, begins in infancy with severe psychomotor retardation and refractory generalized seizures, including ASE.5,6 In other patients, ASE has been described in those with known childhood absence epilepsy or may occur before or after generalized seizures in patients with a seizure disorder.7 New-onset or de novo ASE has been reported in adult patients, often in association with changes in antiseizure or psychotropic medications or their withdrawal.8-10 A review of the literature reveals that newonset ASE is rare in the pediatric age group.3,4,7,9 ASE is characterized by an acute altered mental state caused by recurring, almost continuous, absence spells. The stereotypical appearance is one of confusion, mental dullness, muteness, or monosyllabic speech, with slowness or clumsiness of action. The patient appears disoriented, lethargic, or in a fugue state.8,9,11 This altered mental state varies in intensity and presentation over time and from patient to patient. Patients may be completely alert, with abnormalities of cognition only detected by special neuropsychiatric testing, or the patient may be deeply stuporous.7 In one series, only 19% of patients showed a decrease in level of consciousness.12 The main feature is a decrement in cognition and slowed mental process. Patients frequently have difficulty in tasks requiring sustained attention, sequential planning, or spatial relations.7 Patients are described as disoriented, with defects in planning and reasoning, lack of initiative, and decreased attentiveness and perseverations. Patients may also become excessively emotional, impulsive, or combatative.7 Extreme presentations may display hallucinations or delusions or a catatonic-like state mimicking acute psychosis.7 ASE episodes have a variable time course, lasting minutes to days.9,11 The most important step in the evaluation of these patients is to consider ASE in the differential diagnosis.
4 0 4
The differential diagnosis of a pediatric patient with altered mental status covers many possible causes; trauma, infection, neoplasm, metabolic cause, toxic cause, temporal lobe seizures, and psychiatric and environmental causes should all be considered. The presentation of ASE is unique in that the altered mental state is generally the most striking and often the only abnormal sign or symptom. Without an obvious organic cause, however, an EEG should be performed to assess for seizure activity as the cause. An EEG performed during an episode of ASE is distinctly abnormal. New-onset ASE appears rare in the pediatric age group, especially without a prior history of seizures. It is rarely reported outside subspecialty journals.9-11 This disorder is much more common both in adults and in those with a prior seizure history. The onset of ASE in adults has been linked to several factors: medication withdrawal or changes, menses, hypoglycemia, hyperventilation, photic stimulation, changes in sleep patterns, emotional stress, and fatigue.13 By inference, the same precipitants may also trigger the onset of ASE in pediatric patients. Treatment of ASE follows standard guidelines for the acute treatment of any status seizure. After ensuring the patient’s safety and vital functions, intravenous benzodiazepines are the treatment of choice. Diazepam and lorazepam may be given intravenously in standard doses. Intravenous valproic acid has also been used with success when benzodiazepine therapy has failed.14-16 Long-term therapy with oral ethosuxamide or valproic acid is successful in more than 80% of children.17 The prognosis for patients with ASE is almost always good, with full recovery without sequelae. Uncomplicated absence seizure activity is generally well controlled with oral medication. ASE, even with prolonged duration, has not been shown to cause any neurologic injury in patients with normal premorbid function.13 New-onset ASE is a rare and treatable cause of altered mental status in the pediatric patient. Its diagnosis and treatment rest largely on being aware of the condition and its unique presentation and considering appropriate EEG testing to confirm clinical suspicion. REFERENCES 1.
Livingstone S, Pruce I. Petit mal epilepsy. Am Fam Physician. 1978;17:107-114.
2.
Moe PG. Spike wave stupor: petit mal status. Am J Dis Child. 1971;121:307-313.
3.
Lennox WG. The petit mal epilepsies. JAMA. 1945;129:1069-1074.
4. Niedermeyer E, Khalifeh R. Petit mal status (“spike-wave stupor”). Epilepsia. 1965;6:250262. 5. Niedermeyer E. The Epilepsies: Diagnosis and Management. Baltimore, MD: Urban & Schwarzenberg; 1990.
ANNALS OF EMERGENCY MEDICINE
37:4 APRIL 2001
ABSENCE STATUS EPILEPSY IN A CHILD Benson & Klein
6. Joynt RJ, Griggs RC, eds. Clinical Neurology. Philadelphia, PA: Lippincott Williams & Wilkins; 1998. 7. Guberman A, Cantu-Reyna G, Stuss, D, et al. Nonconvulsive generalized status epilepticus: clinical features, neuropsychological testing and long-term follow-up. Neurology. 1986;36:12841291. 8. Bornstein M, Coddon D, Song S. Prolonged alterations in behavior associated with a continuous electroenceophalopathic (spike and dome) abnormality. Neurology. 1956;6:444-448. 9. Friedlander WJ, Feinstein GH. Petit mal status: epilepsia minoris continua. Neurology. 1956;6:357-363. 10. Thomas PT, Beaumanoir A, Genton, P, et al. ‘De novo’ absence status of late onset: report of 11 cases. Neurology. 1992;42:104-111. 11. Boyd O, Whittingham F, Clements D, et al. Petit mal status: an unusual case of confusion. Br J Hosp Med. 1990;43:230-231. 12. Andelman F, Robb J. Absence status: an appraisal following review of 38 patients. Epilepsia. 1972;13:177-187. 13. Shorvon S, Dreifuss F, Fish D, et al, eds. The Treatment of Epilepsy. Cambridge, MA: Blackwell Science, Ltd; 1996. 14. Yamamoto LG, Yim GK. The role of intravenous valproic acid in status epilepticus. Pediatr Emerg Care. 2000;16:296-298. 15. Chez MG, Hammer MS, Loeffel M, et al. Clinical experience of three pediatric and one adult case of spike-and-wave status epilepticus treated with injectable valproic acid. J Child Neurol. 1999;14:239-242. 16. Alehan FK, Morton LD, Pellock JM. Treatment of absence status with intravenous valproate. Neurology. 1999;52:889-890. 17. Panayiotopoulos CP. Typical absence seizures and their treatment. Arch Dis Child. 1999;81:351-355.
APRIL 2001
37:4
ANNALS OF EMERGENCY MEDICINE
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