Movement Disorders After Status Epilepticus and Other Brain Injuries William E. Fowler, MD*, Robert L. Kriel, MDT, and Linda E. Krach, MD*
A retrospective medical record review was conducted of 173 consecutive children hospitalized for acquired brain injuries on a specialized pediatric rehabilitation service. The chart review identified children who developed movement disorders with acquired brain injuries: 8 with status epilepticus, 2 with trauma, and 1 with anoxia. Movement disorders were observed more frequently following status epilepticus (8 of 12) than following other causes of acquired brain injury (3 of 161; P = .OOOl).Four additional children had severe neurologic deficits following status epilepticus but did not develop movement disorders. The 11 patients who developed movement disorders had choreiform movements predominantly. Even though status epilepticus is a clinical phenomenon resulting from.a variety of etiologies, the features of movement disorders in these children were strikingly similar. The pathophysiology of this complication is unknown. Fowler WE, Kriel BL, Krach LE. Movement disorders after status epilepticus and other brain injuries. Pediatr Nemo1 1992;8:281-4.
Introduction A number of reports in the literature have examined the etiology, clinical presentation, and outcome of pediatric stat& epilepticus [l-S]. Persistent neurologic deficits attributable to status epilepticus have included the sequelae of recurrent seizures, hemiplegia, mental retardation, and mortality. Inherent in these reports is the acknowledgement that status epilepticus can result from many causes. There has been little mention of movement disorders occurring as a sequela of status epilepticus. In the present study, we describe 11 children who developed movement disorders following acquired encephalopathies. We also attempted to determine the correlation among etiologies of brain injuries or treatment approaches with subsequent development of movement disorders.
From the *Department of Rehabilitation; Gillette Children’s Hospital and the University of Minnesota; and +Department of Pediabic Neurology; Gillette Children’s Hospital; Hennepin County Medical Center; and the University of Minnesota; Minneapo!is, Minnesota.
Methods The records of 173 consecutive children admitted to the pediatric rehabilitation service from June, 1977 through December, 1991 were reviewed. All patients were younger than 18 years of age at the time of brain injury and were hospitalized under the care of one or more of the investigators at Gillette Children’s hospital, a regional specialty hospital for children with disabilities. All children were unconscious longer than 24 hours and had severe motor and/or cognitive impairment persisting longer than 1 week. All patients received intensive rehabilitation therapies usually for several weeks. Of the 173 children, 15 met the basic inclusion criteria of having either acquired, persisting brain injury after status epilepticus (with or without movement disorders) or movement disorders following brain injuries of other causes. These 15 children are the study subjects. The duration of status epilepticus was at least 30 min. Focal or generalized motor manifestations with loss of consciousness, absence status, prolonged single seizures, and recurrent seizure episodes without return of consciousness were included. Movement disorders were defined as gross, nonrhythmic, involuntary movements not correlated with epileptiforrn activity on electroencephalography. Mycclonus. ataxia, and tremors were excluded. Data collected from medical records included age at onset of status epilepticus or brain injury, history of preceding illness, prior neurologic deficits, and seizures. Jnformation regarding status epilepticus and movement disorders was recorded, including the seizure type and duration, description and duration of movement disorders, and the interval between the brain injury and onset of movement disorders. The duration of movement disorders was listed as the time until the movements resolved or until the patient was lost to follow-up. Neuroimaging studies were reviewed by a radiologist who did not know the clinical details and specifically assessed any focal abnotmalities on cranial CT or MRJ.
Results The incidence of movement disorders was higher in the those with status epilepticus than in children with other causes of brain injury (Table 1). There was a trend toward more frequent use of phenytoin in the status epilepticus children who subsequently developed movement disorders than in those who did not (Fisher’s exact test, P = .09>. Barbiturate-induced coma was not related to movement disorders. Mean duration of movement disorders was 6.7 months in the status epilepticus group vs. 3.3 months in the traumatic/anoxic group (t = 0.96, P = 0.36). Status Epilepticus and Movement Disorders. CIini~ttl features and medical therapy used in 8 children with status
Communications should be addressed to: Dr. Kriel; Hennepin County Medical Center, #824-A, 701 Park Avenue South, Minneapolis, MN 55415. Received March 5, 1992; accepted May 8, 1992.
Fowler
et
al:StatusEpilepticus,288
Table 1. Incidence encephalopathies
of movemelt
Etiology
disorders
in acquired
Extrapyramidal Yes No
Movements Total
Status epilepticus
s*
4
12
Trauma and anoxicmetabolic
3*
1.58
161
162
173
Total:
11
* Fisher I-tailed test, P = .GOOl.
epilepticus who developed movement disorders are presented in Table 2. Patient 4 had positive fluorescent antibody testing for herpes simplex antigen from brain biopsy, implicating this agent as a probable cause of status epilepticus. Patient 6 had been hospitalized 1 week prior to onset of status epilepticus due to presumed viral encephalitis. Brain biopsy demonstrated a lymphocytic infiltrate without identification of an infectious organism. Patient 8 had a nonprogressive hemiparesis and Patient 5 had febrile seizures before status epilepticus. Patient 1 (brother of Patient 2) subsequently was found to have nonspecific amino acid abnormalities. All children with status epilepticus and movement disorders received a minimum of 2 antiepileptic and/or anesthetic agents acutely, with most receiving 4 or more. All were given phenytoin and phenobarbital; 5 also were treated with pentobarbital-induced coma. All children had persisting cognitive and motor deficits. Six became nonverbal after status epilepticus. Most patients had severe, generalized atrophy documented on neuroimaging studies performed during the period of movement disorders; 3 had focal lesions (Table 2). Status Epilepticus without Movement Disorders. The clinical features and therapy of these children are listed in Table 2. Patient 11 had acutely elevated liver function tests with nonspecific abnormalities on liver biopsy. Patient 12 had chorea which resolved within 24 hours and was not included in the group with movement disorders. Patients 9 and 10, who were developmentally delayed prior to status epilepticus, developed new, severe neurologic deficits. Two of 4 patients became nonverbal and nonambulatory. The other 2 patients are in special education classes.
Movement Disorders After Anoxic%Traumatic Brain Injury. A summary of the clinical features of these 3 children is presented in Table 2. Hospital records indicated no occurrence of seizures in the immediate post-injury period. These children also had profound neurologic impairment: Patient 13 requires a self-contained classroom; Patient 14 is nonverbal and nonambulatory; and Patient 15 is in a persistent vegetative state.
Discussion Since the description by Aicardi and Chevrie in 1970 of 239 cases [5], a growing body of literature has described
282 PEDIATRIC NEUROLOGY
Vol. 8 No. 4
the epidemiology, etiology, clinical presentation, and outcome of pediatric status epilepticus [l-5]. Although more recent studies have demonstrated an apparent decrease in the mortality in children, pediatric status epilepticus remains a serious medical emergency with significant morbidity and mortality [3,4]. Because status epilepticus is caused by a variety of disorders, debate continues as to the specific etiology of brain damage caused by or coincident with status epilepticus. Prolonged seizure activity may cause brain injury independent of ischemia, hypoxia, or other metabolic factors [6-91. In the presence of acute neurologic illness, duration of status epilepticus, age of the child, and other individual factors may also affect outcome [l-5]. Although neurologic sequelae, such as recurrent seizures, hemiplegia, and mental retardation, have been observed following status epilepticus, relatively little mention has been made of movement disorders developing after status epilepticus. Aicardi and Chevrie observed that neurologic sequelae were present in 42% of 2 12 surviving children with status epilepticus [5]. The sequelae included hemiplegia, dystonia, and athetosis; 54% had mental retardation. In the group without pre-existing neurologic disorders, 20% had acquired deficits following status epilepticus, most commonly hemiplegia. The patients were relatively young (73% younger than age 3 years). The duration of status epilepticus was at least 60 min. Dunn reported persisting neurologic deficits, including motor dysfunction, in 18 of 97 children after status epilepticus [2]. Maytal et al. reported persistent motor deficits in 7.5% of their pediatric patients experiencing status epilepticus [3]. The mean patient age was 5 years and minimum duration of status epilepticus was 30 min. Motor deficits were observed, including hemiparesis, diparesis, and pseudobulbar findings. In these series, young age [1,2] and etiology of status epilepticus [3] were correlated with adverse outcome. In all series, including our report, no identifiable cause of status epilepticus was found in approximately one-half of the patients. Movement disorders have occurred following prolonged seizures. Osorio and Reed reported disabling side effects after pentobarbital coma and high-dose phenytoin [lo]. These side effects included temporary neurologic deficits with confusion, weakness, hypotonia, ataxia, and oculomotor dysfunction. Filloux and Thompson described 4 children younger than 2 years of age with no prior significant neurologic disease who developed transient chorea when treated with phenytoin for a febrile episode of status epilepticus, despite nontoxic phenytoin levels [ 111. In the present study, all 8 of 12 children with status epilepticus who developed movement disorders had received both phenytoin and phenobarbital. The use of barbiturate-induced coma did not correlate with the development of movement disorders. Because of the much higher incidence of movement disorders following status epilepticus than anoxic injuries in our series, we believe that possible anoxia during pro-
Table
2.
Summary
Patient NoJAge at Itiuv Ws, mos)fex Status
Epilepticus
of patient Cause of Brain Injury
characteristics
Prior Seizure History
Encephalopathy
and treatments
status Type of Seizure with Movement
Medications Used to Treat Status Epilepticus Seizure
Barbiturate Coma in APT
Interval from Injury to Movement Disorder (wks)
+
7
Disorder Duration
New Focal Lesions on CT or MFU
Chor
10
-
4
Chor, MC
10
-
Disorders
I /3,4/M
SE
+
GTC
VPA, PB, PUT, PA, DZ. LZ, cz
2/l ,9/F
SE
+
TC
PB, PHT, DZ, VPA. PA, ACTH
3/5,0/F
SE
TC
DZ, CZ, PB, LZ. CMP, VPA, PHT, PA
+
4
Chor, hemiballismic, Atb
2
4/3.7/F
SE
GTC
DZ, PHT, PA, PB, LD, PC
+
2
Chor, ballismic
N+)
+*
5/5,9/F
SE
+
TC
PHT, PB, DZ
6
Chor, Ath, ballismic
1
-
6/ll,l/M
SE
+
GTC
PB, PHT, PC
-
8
Dystonic posturing
N+)
++
ll7,llF
SE
GTC
MZ, PB, PUT, CMP, PT
+
7
Chor
4(+)
-
8/6,1/M
SE
NCV
PHT, PB, VPA
+
4
Char, Ath
1
+$
Movement
Disorders
Status
Epilepticus
+
Encephalopathy
without
9/6,10/F
SE
+
GTC
DZ, PA
10/7,4/M
SE
+
PM
PB, VPA, PA, MX, LZ
11/0,10/F
SE
GTC
PB. PHT, DZ
1217.1 l/F
SE
GTC
PHT, PB, VPA
Other
Acquired
-
Encephalopathy
with Movement
VPA.
NA
NA
NA
-5
+
NA
NA
NA
-
-
NA
NA
NA
-
+I
NA
NA
NA
Disoniers
13/5,8/M
Trauma
-
NA
NA
-
8
14/8,4/F
Trauma
-
NA
NA
+”
11
15/1,0/F
Anoxia
-
NA
NA
* + $ 5 1 A **
I
Chor, Atb MC
+-
Hemiballismic
+**
Chor, MC
-
Left temporal lobe edema acutely: left posterior temporal-occipital lobe focal encephalomalacia later. Left frontal lobe and left basal ganglia infarcts acutely: more generalized progressing atrophy later. Focal right internal capsule degeneration with generalized atrophy, more pronounced in right hemisphere. Generalized cerebral and cerebellar atrophy, also found to have Dandy Waker complex. Barbiturate-induced coma with thiopentothal. Focal infarcts in bilateral frontal lobes and globus pallidus, and in left occipital lobe. Barbiturate-induced coma with thiopentothal as treatment of elevated intracranial pressure.. Right lenticulate and caudate nucleus encephalomalacia, with generalized atrophy, more pronounced in right hemisphere
Abbreviations: = Yes = No (+I = Time at which follow-up was lost hormone ACTH = Admnocorticotropic Ath = Athetoid Chor = Choreiform CMP = Carbamazepine cz = Clonazepam DZ = Diazepam
+
Movement
GTC LD LZ MC MZ NCV NA PA
= = = = = = = =
Generalized tonic-clonic Lidocaine Lorazepam Myoclonic Midazolam Nonconvulsive Not applicable Paraldehyde
PB PC PHT PM PT SE TC VPA
= = = = = = = =
Phenobarbital Pancuronium bromide Phenytoin Petit mal Sodium thiopental Status epilepticus Tonic-clonic Valproic acid
Fowler
et al: Status Epilepticus
283
A retrospective medical record review was conducted of 173 consecutive children hospitalized for acquired brain injuries on a specialized pediatric rehabilitation service. The chart review identified children who developed movement disorders with acquired brain injuries: 8 with status epilepticus, 2 with trauma, and 1 with anoxia. Movement disorders were observed more frequently following status epilepticus (8 of 12) than following other causes of acquired brain injury (3 of 161; P = .OOOl).Four additional children had severe neurologic deficits following status epilepticus but did not develop movement disorders. The 11 patients who developed movement disorders had choreiform movements predominantly. Even though status epilepticus is a clinical phenomenon resulting from.a variety of etiologies, the features of movement disorders in these children were strikingly similar. The pathophysiology of this complication is unknown. Fowler WE, Kriel BL, Krach LE. Movement disorders after status epilepticus and other brain injuries. Pediatr Nemo1 1992;8:281-4.
Introduction A number of reports in the literature have examined the etiology, clinical presentation, and outcome of pediatric stat& epilepticus [l-S]. Persistent neurologic deficits attributable to status epilepticus have included the sequelae of recurrent seizures, hemiplegia, mental retardation, and mortality. Inherent in these reports is the acknowledgement that status epilepticus can result from many causes. There has been little mention of movement disorders occurring as a sequela of status epilepticus. In the present study, we describe 11 children who developed movement disorders following acquired encephalopathies. We also attempted to determine the correlation among etiologies of brain injuries or treatment approaches with subsequent development of movement disorders.
From the *Department of Rehabilitation; Gillette Children’s Hospital and the University of Minnesota; and +Department of Pediabic Neurology; Gillette Children’s Hospital; Hennepin County Medical Center; and the University of Minnesota; Minneapo!is, Minnesota.
Methods The records of 173 consecutive children admitted to the pediatric rehabilitation service from June, 1977 through December, 1991 were reviewed. All patients were younger than 18 years of age at the time of brain injury and were hospitalized under the care of one or more of the investigators at Gillette Children’s hospital, a regional specialty hospital for children with disabilities. All children were unconscious longer than 24 hours and had severe motor and/or cognitive impairment persisting longer than 1 week. All patients received intensive rehabilitation therapies usually for several weeks. Of the 173 children, 15 met the basic inclusion criteria of having either acquired, persisting brain injury after status epilepticus (with or without movement disorders) or movement disorders following brain injuries of other causes. These 15 children are the study subjects. The duration of status epilepticus was at least 30 min. Focal or generalized motor manifestations with loss of consciousness, absence status, prolonged single seizures, and recurrent seizure episodes without return of consciousness were included. Movement disorders were defined as gross, nonrhythmic, involuntary movements not correlated with epileptiforrn activity on electroencephalography. Mycclonus. ataxia, and tremors were excluded. Data collected from medical records included age at onset of status epilepticus or brain injury, history of preceding illness, prior neurologic deficits, and seizures. Jnformation regarding status epilepticus and movement disorders was recorded, including the seizure type and duration, description and duration of movement disorders, and the interval between the brain injury and onset of movement disorders. The duration of movement disorders was listed as the time until the movements resolved or until the patient was lost to follow-up. Neuroimaging studies were reviewed by a radiologist who did not know the clinical details and specifically assessed any focal abnotmalities on cranial CT or MRJ.
Results The incidence of movement disorders was higher in the those with status epilepticus than in children with other causes of brain injury (Table 1). There was a trend toward more frequent use of phenytoin in the status epilepticus children who subsequently developed movement disorders than in those who did not (Fisher’s exact test, P = .09>. Barbiturate-induced coma was not related to movement disorders. Mean duration of movement disorders was 6.7 months in the status epilepticus group vs. 3.3 months in the traumatic/anoxic group (t = 0.96, P = 0.36). Status Epilepticus and Movement Disorders. CIini~ttl features and medical therapy used in 8 children with status
Communications should be addressed to: Dr. Kriel; Hennepin County Medical Center, #824-A, 701 Park Avenue South, Minneapolis, MN 55415. Received March 5, 1992; accepted May 8, 1992.
Fowler
et
al:StatusEpilepticus,288
Table 1. Incidence encephalopathies
of movemelt
Etiology
disorders
in acquired
Extrapyramidal Yes No
Movements Total
Status epilepticus
s*
4
12
Trauma and anoxicmetabolic
3*
1.58
161
162
173
Total:
11
* Fisher I-tailed test, P = .GOOl.
epilepticus who developed movement disorders are presented in Table 2. Patient 4 had positive fluorescent antibody testing for herpes simplex antigen from brain biopsy, implicating this agent as a probable cause of status epilepticus. Patient 6 had been hospitalized 1 week prior to onset of status epilepticus due to presumed viral encephalitis. Brain biopsy demonstrated a lymphocytic infiltrate without identification of an infectious organism. Patient 8 had a nonprogressive hemiparesis and Patient 5 had febrile seizures before status epilepticus. Patient 1 (brother of Patient 2) subsequently was found to have nonspecific amino acid abnormalities. All children with status epilepticus and movement disorders received a minimum of 2 antiepileptic and/or anesthetic agents acutely, with most receiving 4 or more. All were given phenytoin and phenobarbital; 5 also were treated with pentobarbital-induced coma. All children had persisting cognitive and motor deficits. Six became nonverbal after status epilepticus. Most patients had severe, generalized atrophy documented on neuroimaging studies performed during the period of movement disorders; 3 had focal lesions (Table 2). Status Epilepticus without Movement Disorders. The clinical features and therapy of these children are listed in Table 2. Patient 11 had acutely elevated liver function tests with nonspecific abnormalities on liver biopsy. Patient 12 had chorea which resolved within 24 hours and was not included in the group with movement disorders. Patients 9 and 10, who were developmentally delayed prior to status epilepticus, developed new, severe neurologic deficits. Two of 4 patients became nonverbal and nonambulatory. The other 2 patients are in special education classes.
Movement Disorders After Anoxic%Traumatic Brain Injury. A summary of the clinical features of these 3 children is presented in Table 2. Hospital records indicated no occurrence of seizures in the immediate post-injury period. These children also had profound neurologic impairment: Patient 13 requires a self-contained classroom; Patient 14 is nonverbal and nonambulatory; and Patient 15 is in a persistent vegetative state.
Discussion Since the description by Aicardi and Chevrie in 1970 of 239 cases [5], a growing body of literature has described
282 PEDIATRIC NEUROLOGY
Vol. 8 No. 4
the epidemiology, etiology, clinical presentation, and outcome of pediatric status epilepticus [l-5]. Although more recent studies have demonstrated an apparent decrease in the mortality in children, pediatric status epilepticus remains a serious medical emergency with significant morbidity and mortality [3,4]. Because status epilepticus is caused by a variety of disorders, debate continues as to the specific etiology of brain damage caused by or coincident with status epilepticus. Prolonged seizure activity may cause brain injury independent of ischemia, hypoxia, or other metabolic factors [6-91. In the presence of acute neurologic illness, duration of status epilepticus, age of the child, and other individual factors may also affect outcome [l-5]. Although neurologic sequelae, such as recurrent seizures, hemiplegia, and mental retardation, have been observed following status epilepticus, relatively little mention has been made of movement disorders developing after status epilepticus. Aicardi and Chevrie observed that neurologic sequelae were present in 42% of 2 12 surviving children with status epilepticus [5]. The sequelae included hemiplegia, dystonia, and athetosis; 54% had mental retardation. In the group without pre-existing neurologic disorders, 20% had acquired deficits following status epilepticus, most commonly hemiplegia. The patients were relatively young (73% younger than age 3 years). The duration of status epilepticus was at least 60 min. Dunn reported persisting neurologic deficits, including motor dysfunction, in 18 of 97 children after status epilepticus [2]. Maytal et al. reported persistent motor deficits in 7.5% of their pediatric patients experiencing status epilepticus [3]. The mean patient age was 5 years and minimum duration of status epilepticus was 30 min. Motor deficits were observed, including hemiparesis, diparesis, and pseudobulbar findings. In these series, young age [1,2] and etiology of status epilepticus [3] were correlated with adverse outcome. In all series, including our report, no identifiable cause of status epilepticus was found in approximately one-half of the patients. Movement disorders have occurred following prolonged seizures. Osorio and Reed reported disabling side effects after pentobarbital coma and high-dose phenytoin [lo]. These side effects included temporary neurologic deficits with confusion, weakness, hypotonia, ataxia, and oculomotor dysfunction. Filloux and Thompson described 4 children younger than 2 years of age with no prior significant neurologic disease who developed transient chorea when treated with phenytoin for a febrile episode of status epilepticus, despite nontoxic phenytoin levels [ 111. In the present study, all 8 of 12 children with status epilepticus who developed movement disorders had received both phenytoin and phenobarbital. The use of barbiturate-induced coma did not correlate with the development of movement disorders. Because of the much higher incidence of movement disorders following status epilepticus than anoxic injuries in our series, we believe that possible anoxia during pro-
Table
2.
Summary
Patient NoJAge at Itiuv Ws, mos)fex Status
Epilepticus
of patient Cause of Brain Injury
characteristics
Prior Seizure History
Encephalopathy
and treatments
status Type of Seizure with Movement
Medications Used to Treat Status Epilepticus Seizure
Barbiturate Coma in APT
Interval from Injury to Movement Disorder (wks)
+
7
Disorder Duration
New Focal Lesions on CT or MFU
Chor
10
-
4
Chor, MC
10
-
Disorders
I /3,4/M
SE
+
GTC
VPA, PB, PUT, PA, DZ. LZ, cz
2/l ,9/F
SE
+
TC
PB, PHT, DZ, VPA. PA, ACTH
3/5,0/F
SE
TC
DZ, CZ, PB, LZ. CMP, VPA, PHT, PA
+
4
Chor, hemiballismic, Atb
2
4/3.7/F
SE
GTC
DZ, PHT, PA, PB, LD, PC
+
2
Chor, ballismic
N+)
+*
5/5,9/F
SE
+
TC
PHT, PB, DZ
6
Chor, Ath, ballismic
1
-
6/ll,l/M
SE
+
GTC
PB, PHT, PC
-
8
Dystonic posturing
N+)
++
ll7,llF
SE
GTC
MZ, PB, PUT, CMP, PT
+
7
Chor
4(+)
-
8/6,1/M
SE
NCV
PHT, PB, VPA
+
4
Char, Ath
1
+$
Movement
Disorders
Status
Epilepticus
+
Encephalopathy
without
9/6,10/F
SE
+
GTC
DZ, PA
10/7,4/M
SE
+
PM
PB, VPA, PA, MX, LZ
11/0,10/F
SE
GTC
PB. PHT, DZ
1217.1 l/F
SE
GTC
PHT, PB, VPA
Other
Acquired
-
Encephalopathy
with Movement
VPA.
NA
NA
NA
-5
+
NA
NA
NA
-
-
NA
NA
NA
-
+I
NA
NA
NA
Disoniers
13/5,8/M
Trauma
-
NA
NA
-
8
14/8,4/F
Trauma
-
NA
NA
+”
11
15/1,0/F
Anoxia
-
NA
NA
* + $ 5 1 A **
I
Chor, Atb MC
+-
Hemiballismic
+**
Chor, MC
-
Left temporal lobe edema acutely: left posterior temporal-occipital lobe focal encephalomalacia later. Left frontal lobe and left basal ganglia infarcts acutely: more generalized progressing atrophy later. Focal right internal capsule degeneration with generalized atrophy, more pronounced in right hemisphere. Generalized cerebral and cerebellar atrophy, also found to have Dandy Waker complex. Barbiturate-induced coma with thiopentothal. Focal infarcts in bilateral frontal lobes and globus pallidus, and in left occipital lobe. Barbiturate-induced coma with thiopentothal as treatment of elevated intracranial pressure.. Right lenticulate and caudate nucleus encephalomalacia, with generalized atrophy, more pronounced in right hemisphere
Abbreviations: = Yes = No (+I = Time at which follow-up was lost hormone ACTH = Admnocorticotropic Ath = Athetoid Chor = Choreiform CMP = Carbamazepine cz = Clonazepam DZ = Diazepam
+
Movement
GTC LD LZ MC MZ NCV NA PA
= = = = = = = =
Generalized tonic-clonic Lidocaine Lorazepam Myoclonic Midazolam Nonconvulsive Not applicable Paraldehyde
PB PC PHT PM PT SE TC VPA
= = = = = = = =
Phenobarbital Pancuronium bromide Phenytoin Petit mal Sodium thiopental Status epilepticus Tonic-clonic Valproic acid
Fowler
et al: Status Epilepticus
283
