- Email: [email protected]
De novo absence status of late onset following withdrawal of lorazepam: a case report
Seizure 2001; 10: 433–437
doi:10.1053/seiz.2000.0510, available online at http://www.idealibrary.com on
CASE REPORT
De novo absence status of late onset following withdrawal of lorazepam: a case report ´ J. L. FERNANDEZ-TORRE ˜ ´ Asturias, Spain Servicio de Neurofisiolog´ıa Cl´ınica, Hospital de Cabuenes, 33394 Gijon, ´ ˜ Correspondence to: Dr J. L. Fernandez-Torre, Servicio de Neurofisiolog´ıa Cl´ınica, Hospital de Cabuenes, 33394 ´ Asturias, Spain. E-mail: [email protected] Gijon,
The aim of this report is to describe the clinical and electroencephalographic findings seen in an elderly woman without previous history of seizures who developed a nonconvulsive generalized status epilepticus following acute withdrawal of lorazepam. Scalp video-EEG monitoring was obtained using the standard 10/20 system of electrode placement. Cognitive and speech functions were specifically tested during the evaluation. Continuous irregular rhythmic generalized 2.0–2.5 Hz sharp-and-slow wave complexes intermixed with spikes and polyspikes more prominent over the frontocentral areas were seen on the EEG. This epileptic activity was continuous and unmodified by sensory stimulation and eyes opening and closing. Intravenous injection of diazepam caused a rapid normalization of the EEG with disappearance of the clinical manifestations. De novo absence status is a specific epileptic condition that should be suspected in all elderly subjects on chronic treatment with psychotropic drugs presenting in a confusional state. An urgent EEG is essential to confirm the diagnosis. c 2001 BEA Trading Ltd
Key words: nonconvulsive generalized status epilepticus; de novo absence status; benzodiazepine withdrawal; confusional state; electroencephalogram; lorazepam.
INTRODUCTION Most authors recognize two types of nonconvulsive status epilepticus (NCSE) depending on the ictal electroencephalographic changes: generalized (absence status) and complex partial1–14 . In addition, strictly speaking there is also a simple form of status epilepticus which is likely underdiagnosed because of its frequent progression to complex partial status, subtle signs and high proportion of normal electroencephalograms (EEGs)15 . Absence status (AS) is defined by the presence of a prolonged and fluctuating confusional state associated with continuous or nearly continuous generalized 1.5–3.5 Hz spike-and-wave or polyspike-andwave discharges on the EEG1, 3, 4, 7 . This epileptic 1059–1311/01/060433 + 05
$35.00/0
manifestation occurs more frequently in patients having idiopathic or symptomatic generalized epilepsy. However, episodes of AS have also been described in elderly patients without previous history of epilepsy constituting an entity termed de novo absence status of late onset16–18 . As pointed out by Thomas et al.16, 17 , this picture is often provoked by an acute withdrawal of psychotropic drugs. In addition, the confluence of epidemiological, clinical and electroencephalographic features supports the assumption that this epileptic condition may constitute a well-defined type of AS. This report describes an additional case of de novo AS in an elderly woman following withdrawal of lorazepam and adds more evidence sustaining that this type of NCSE is frequently an epileptic event secondary to exogenous factors. c 2001 BEA Trading Ltd
´ J. L. Fernandez-Torre
434
MATERIALS AND METHODS Clinical case A 79-year-old woman was brought to the emergency unit because of an abnormal behavior. She had personal antecedents of hypertension and ischemic cardiopathy on chronic treatment with nitroglycerin and salicylic acid. Moreover, she had been diagnosed as having an anxiety disorder and she was receiving lorazepam (2 mg/24 hours) for several months. There was no history of epilepsy. Fifteen days before admission the patient suffered from fever, cough and expectoration. Her general practitioner established the diagnosis of an upper respiratory tract infection and instituted symptomatic treatment with the unnecessary use of antibiotics. Over the next 12 days, the patient improved and fever and the expectoration disappeared. However, 3 days before admission she developed an abnormal mood and behavior, nausea and vomiting. She looked indifferent and refused to eat. Her speech decreased and she lost sphincter control. In the emergency ward, her temperature was 37.2 ◦ C and blood pressure 140/100 mm Hg. She was confused and disoriented to person, time and place. Her speech was slow and poor and she was only able to perform inconsistently simple orders. On neurological examination, the cranial nerves, visual fields, and motor, sensory, and cerebellar systems were intact. Laboratory tests, including blood cell count, electrolytes, metabolites, urinalysis, chest X-ray and electrocardiogram, were within normal limits. Plasma and urinary levels of benzodiazepines were not determined. A computed tomography (CT) scan of the brain revealed multiple hypodense lesions in the periventricular white matter but was otherwise normal.
Electrophysiological evaluation The patient was sent to our laboratory for evaluation. Video-EEG monitoring was obtained on a digital Micromed EEG machine (Brain Quick System 2). Scalp electrodes were placed according to the International 10/20 System and a detailed neurological examination was carried out during the recording. Cognitive functions and speech were specifically tested.
RESULTS Scalp video-EEG monitoring showed irregular rhythmic generalized 2.0–2.5 Hz sharp-and-slow wave complexes intermixed with spikes and polyspikes that were more prominent over the frontocentral areas with occasional predominance on the right hemisphere
(Fig. 1(a) and (b)). This epileptic activity was continuous and unalterable by sensory stimulation and eyes opening and closing. The patient had an unexpressive face and a vague look during the evaluation. She was perplexed and confused and was only able to answer simple questions such as ‘what is your name’. Automatisms, rhythmic blinking, clonic twitching or myoclonic jerks were not observed. On the basis of these findings, the diagnosis of a generalized NCSE was made. To confirm this, 10 mg of intravenous diazepam was administrated. Twenty seconds after injection, epileptic activity ceased completely on the EEG (Fig. 1(c)), and the patient experienced a deep sleep. Later on, she woke up and displayed a normal mental status. Subsequently, the patient’s daughter confirmed that her mother had been taking excessive doses of lorazepam that had been reduced acutely without medical or family supervision. Over the following days, she did not have any further confusional episodes and a second EEG showed a normal background without evidence of epileptiform activity. Finally, she was discharged on phenytoin therapy (100 mg/8 hours) and has not experienced more episodes of abnormal behavior for the last 8 months.
DISCUSSION It is quite reasonable to suppose that the patient reported here represents a typical case of de novo AS of late onset. The clinical manifestations, ictal EEG findings and striking response to intravenous diazepam strongly support this hypothesis. She was an old woman without antecedents of epileptic seizures with a history of chronic abuse of benzodiazepines, who discontinued fortuitously the ingestion of psychotropic drugs because of an intercurrent respiratory process. Then, she developed a moderate confusional state with negativism, nausea, vomiting, incontinence and loss of speech. There were no clinical data suggesting the possibility of an epileptic etiology of the clinical condition. Indeed, the diagnosis was delayed for 24 hours and an EEG was finally requested because of the normality of laboratory tests and CT. Although this delay in obtaining an EEG could be attributed to our institution, Kaplan8 observed that diagnostic delay is common in patients with NCSE, even when the patient is referred to a prestigious teaching hospital. Therefore, this fact allows us to emphasize the need for an urgent EEG on all patients showing confusional state. Although the term ‘absence status’ is more often associated with generalized and regular spike-and-wave complexes on the EEG, ictal recordings in patients suffering from de novo AS have been enormously heterogeneous. Indeed, Thomas and Andermann18 stressed
‘De novo’ absence status
435
Fig. 1: Longitudinal (a), and tranversal; (b), montages showing continuous irregular generalized sharp-and-slow wave complexes intermixed with spikes and polyspikes; (c), normalization of EEG 20 seconds after intravenous diazepam.
´ J. L. Fernandez-Torre
436
Fig. 1: Continued
Table 1: Nonconvulsive generalized status epilepticusa : differential diagnosis. Absence status of late onset
Complex partial status epilepticus
Antecedents of psychotropic drug abuse Middle age or elderly subjects Female predominance Prolonged and continuous state Facial myoclonic jerks Complete unresponsiveness unusualb Incontinence described Continuous generalized epileptic activity Dramatic response to benzodiazepines Rare recurrences
Pre-existing partial epilepsy At any age Male/female equal Cyclic evolution Complex automatisms Complete unresponsiveness more frequent Incontinence more rarely reported Recurrent focal epileptiform discharges Variable response to benzodiazepines Frequent episodes of recurrences
a Clinical and EEG features summarized from Refs [3, 4, 8, 13, 16–18]. b Although it has been considered more uncommon, there are cases of AS of late onset with severe impairment of consciousness16 .
the large variability of EEG changes seen in these cases. So, there is a wide range of EEG patterns which may vary from typical spike-and-wave discharges to asymmetric irregular sharp-and-slow wave complexes with frontal or frontocentral maximum. Moreover, under some circumstances, electroencephalographic features can be more atypical, adopting, for instance, triphasic morphology, and this appearance can make it difficult to accurately interpret the EEG of a confused patient4, 14 . To overcome this problem and also to obtain a definitive diagnosis, it is advised to administer intravenous benzodiazepines in the course of the EEG recording. The supression of epileptiform activity associated with a significant improvement in the clinical manifestations will be conclusive. Therefore,
a precise diagnosis requires: first, to keep in mind the possibility of this type of NCSE in all confused elderly subjects taking psychotropic drugs, and second, to recognize that EEG may show variable forms of generalized epileptiform activity which disappears dramatically after the injection of intravenous diazepam. At times, it may be difficult to differentiate between the major categories of NCSE4, 8, 13 . It is wellrecognized that complex partial status, especially complex partial status of frontal origin, may be associated with diffuse EEG anomalies which are the result of a secondary generalization of focal discharges4 . However, there are several clinical and EEG features which have been considered useful for the differential diagnosis (Table 1). The presence of a cyclic evo-
‘De novo’ absence status
lution, complex automatisms, complete unresponsiveness and recurrent focal epileptic activity on the EEG have been described as more typical of complex partial status3, 4, 8, 13 . By contrast, female predominance, antecedents of psychotropic drug abuse, perplexity, facial myoclonic twitches, incontinence and continuous epileptiform dicharges seem to be frequent in AS of late onset16–18 , Nevertheless, the utility of these features is limited and the existence of a confusional state in an old subject taking chronically psychotropic drugs will be the clue to suspect the diagnosis and to carry out an urgent EEG.
ACKNOWLEDGEMENTS The author is indebted to Dr Viteri for his helpful comments and is grateful to Dr Solano for referring the patient.
REFERENCES 1. Anderman, F. and Robb, J. P. Absence status. A reappraisal following review of thirty-eight patients. Epilepsia 1972; 13: 177–187. 2. Celesia, G. G. Modern concepts of status epilepticus. Journal of the American Medical Association 1976; 235: 1571–1574. 3. Belafsky, M. A., Carwille, S., Miller, P., Waddell, G., BoxleyJohnson, J. and Delgado-Escueta, A. V. Prolonged epileptic twilight states: Continuous recordings with nasopharyngeal electrodes and videotape analysis. Neurology 1978; 28: 239–245. 4. Guberman, A., Cantu-Reyna, G., Stuss, D. and Broughton, R. Nonconvulsive generalized status epilepticus: Clinical features, neuropychological testing, and long-term follow-up. Neurology 1986; 36: 1284–1291. 5. Tomson, T., Svanborg, E. and Wedlund, J.-E. Nonconvulsive status epilepticus: high incidence of complex partial status.
437 Epilepsia 1986; 27: 276–285. 6. Tomson, T., Lindbom, U. and Nilsson, B. Y. Nonconvulsive status epilepticus in adults: thirty-two consecutive patients from a general hospital population. Epilepsia 1992; 33: 829–835. 7. Cascino, G. D. Nonconvulsive status epilepticus in adults and children. Epilepsia 1993; 34 (Suppl. 1): S21–S28. 8. Kaplan, P. W. Nonconvulsive status epilepticus in the emergency room. Epilepsia 1996; 37: 643–650. 9. Treiman, D. M. Electroclinical features of status epilepticus. Journal of Clinical Neurophysiology 1995; 12: 343–362. 10. Treiman, D. M. Status epilepticus. In: Modern Management of Epilepsy. Bailli`ere’s Clinical Neurology. International Practice and Research (Eds M. J. Brodie and D. M. Treiman). London, Bailli`ere Tindall, 1996: Vol. 5, No. 4: pp. 821–839. 11. Salas-Puig, J., Su´arez-Moro, R. and Mateos, V. Status epilepticus. Neurolog´ıa 1996; 11 (Suppl. 4): 108–121. 12. Snead III, O. C., Dean, J. C. and Penry, J. K. Absence status epilepticus. In: Epilepsy: A Comprehensive Textbook (Eds J. Engel and T. A. Pedley). Philadelphia, Lippincott-Raven Publishers, 1997: pp. 701–707. 13. Williamson, P. D. Complex partial status epilepticus. In: Epilepsy: A Comprehensive Textbook (Eds J. Engel and T. A. Pedley). Philadelphia, Lippincott-Raven Publishers, 1997: pp. 681–699. 14. Kaplan, P. W. Assessing the outcomes in patients with nonconvulsive status epilepticus: Nonconvulsive status epilepticus is underdiagnosed, potentially overtreated, and confounded by comorbidity. Journal of Clinical Neurophysiology 1999; 16: 341–352. 15. Wieser, H. G. Simple partial status epilepticus. In: Epilepsy: A Comprehensive Textbook (Eds J. Engel and T. A. Pedley). Philadelphia, Lippincott-Raven Publishers, 1997: pp. 709–723. 16. Thomas, P., Beaumanoir, A., Genton, P., Dolisi, C. and Chatel, M. ‘De novo’ absence status of late onset: Report of 11 cases. Neurology 1992; 42: 104–110. 17. Thomas, P., Lebrun, C. and Chatel, M. De novo absence status as a benzodiazepine withdrawal syndrome. Epilepsia 1993; 34: 355–358. 18. Thomas, P. and Andermann, F. Late-onset absence status epilepticus is most often situation-related. In: Idiopathic Generalized Epilepsies (Eds A. Malafosse, P. Genton, E. Hirsch, C. Marescaux, D. Broglin and R. Bernasconi). London, John Libbey & Company Ltd, 1994: pp. 95–109.
doi:10.1053/seiz.2000.0510, available online at http://www.idealibrary.com on
CASE REPORT
De novo absence status of late onset following withdrawal of lorazepam: a case report ´ J. L. FERNANDEZ-TORRE ˜ ´ Asturias, Spain Servicio de Neurofisiolog´ıa Cl´ınica, Hospital de Cabuenes, 33394 Gijon, ´ ˜ Correspondence to: Dr J. L. Fernandez-Torre, Servicio de Neurofisiolog´ıa Cl´ınica, Hospital de Cabuenes, 33394 ´ Asturias, Spain. E-mail: [email protected] Gijon,
The aim of this report is to describe the clinical and electroencephalographic findings seen in an elderly woman without previous history of seizures who developed a nonconvulsive generalized status epilepticus following acute withdrawal of lorazepam. Scalp video-EEG monitoring was obtained using the standard 10/20 system of electrode placement. Cognitive and speech functions were specifically tested during the evaluation. Continuous irregular rhythmic generalized 2.0–2.5 Hz sharp-and-slow wave complexes intermixed with spikes and polyspikes more prominent over the frontocentral areas were seen on the EEG. This epileptic activity was continuous and unmodified by sensory stimulation and eyes opening and closing. Intravenous injection of diazepam caused a rapid normalization of the EEG with disappearance of the clinical manifestations. De novo absence status is a specific epileptic condition that should be suspected in all elderly subjects on chronic treatment with psychotropic drugs presenting in a confusional state. An urgent EEG is essential to confirm the diagnosis. c 2001 BEA Trading Ltd
Key words: nonconvulsive generalized status epilepticus; de novo absence status; benzodiazepine withdrawal; confusional state; electroencephalogram; lorazepam.
INTRODUCTION Most authors recognize two types of nonconvulsive status epilepticus (NCSE) depending on the ictal electroencephalographic changes: generalized (absence status) and complex partial1–14 . In addition, strictly speaking there is also a simple form of status epilepticus which is likely underdiagnosed because of its frequent progression to complex partial status, subtle signs and high proportion of normal electroencephalograms (EEGs)15 . Absence status (AS) is defined by the presence of a prolonged and fluctuating confusional state associated with continuous or nearly continuous generalized 1.5–3.5 Hz spike-and-wave or polyspike-andwave discharges on the EEG1, 3, 4, 7 . This epileptic 1059–1311/01/060433 + 05
$35.00/0
manifestation occurs more frequently in patients having idiopathic or symptomatic generalized epilepsy. However, episodes of AS have also been described in elderly patients without previous history of epilepsy constituting an entity termed de novo absence status of late onset16–18 . As pointed out by Thomas et al.16, 17 , this picture is often provoked by an acute withdrawal of psychotropic drugs. In addition, the confluence of epidemiological, clinical and electroencephalographic features supports the assumption that this epileptic condition may constitute a well-defined type of AS. This report describes an additional case of de novo AS in an elderly woman following withdrawal of lorazepam and adds more evidence sustaining that this type of NCSE is frequently an epileptic event secondary to exogenous factors. c 2001 BEA Trading Ltd
´ J. L. Fernandez-Torre
434
MATERIALS AND METHODS Clinical case A 79-year-old woman was brought to the emergency unit because of an abnormal behavior. She had personal antecedents of hypertension and ischemic cardiopathy on chronic treatment with nitroglycerin and salicylic acid. Moreover, she had been diagnosed as having an anxiety disorder and she was receiving lorazepam (2 mg/24 hours) for several months. There was no history of epilepsy. Fifteen days before admission the patient suffered from fever, cough and expectoration. Her general practitioner established the diagnosis of an upper respiratory tract infection and instituted symptomatic treatment with the unnecessary use of antibiotics. Over the next 12 days, the patient improved and fever and the expectoration disappeared. However, 3 days before admission she developed an abnormal mood and behavior, nausea and vomiting. She looked indifferent and refused to eat. Her speech decreased and she lost sphincter control. In the emergency ward, her temperature was 37.2 ◦ C and blood pressure 140/100 mm Hg. She was confused and disoriented to person, time and place. Her speech was slow and poor and she was only able to perform inconsistently simple orders. On neurological examination, the cranial nerves, visual fields, and motor, sensory, and cerebellar systems were intact. Laboratory tests, including blood cell count, electrolytes, metabolites, urinalysis, chest X-ray and electrocardiogram, were within normal limits. Plasma and urinary levels of benzodiazepines were not determined. A computed tomography (CT) scan of the brain revealed multiple hypodense lesions in the periventricular white matter but was otherwise normal.
Electrophysiological evaluation The patient was sent to our laboratory for evaluation. Video-EEG monitoring was obtained on a digital Micromed EEG machine (Brain Quick System 2). Scalp electrodes were placed according to the International 10/20 System and a detailed neurological examination was carried out during the recording. Cognitive functions and speech were specifically tested.
RESULTS Scalp video-EEG monitoring showed irregular rhythmic generalized 2.0–2.5 Hz sharp-and-slow wave complexes intermixed with spikes and polyspikes that were more prominent over the frontocentral areas with occasional predominance on the right hemisphere
(Fig. 1(a) and (b)). This epileptic activity was continuous and unalterable by sensory stimulation and eyes opening and closing. The patient had an unexpressive face and a vague look during the evaluation. She was perplexed and confused and was only able to answer simple questions such as ‘what is your name’. Automatisms, rhythmic blinking, clonic twitching or myoclonic jerks were not observed. On the basis of these findings, the diagnosis of a generalized NCSE was made. To confirm this, 10 mg of intravenous diazepam was administrated. Twenty seconds after injection, epileptic activity ceased completely on the EEG (Fig. 1(c)), and the patient experienced a deep sleep. Later on, she woke up and displayed a normal mental status. Subsequently, the patient’s daughter confirmed that her mother had been taking excessive doses of lorazepam that had been reduced acutely without medical or family supervision. Over the following days, she did not have any further confusional episodes and a second EEG showed a normal background without evidence of epileptiform activity. Finally, she was discharged on phenytoin therapy (100 mg/8 hours) and has not experienced more episodes of abnormal behavior for the last 8 months.
DISCUSSION It is quite reasonable to suppose that the patient reported here represents a typical case of de novo AS of late onset. The clinical manifestations, ictal EEG findings and striking response to intravenous diazepam strongly support this hypothesis. She was an old woman without antecedents of epileptic seizures with a history of chronic abuse of benzodiazepines, who discontinued fortuitously the ingestion of psychotropic drugs because of an intercurrent respiratory process. Then, she developed a moderate confusional state with negativism, nausea, vomiting, incontinence and loss of speech. There were no clinical data suggesting the possibility of an epileptic etiology of the clinical condition. Indeed, the diagnosis was delayed for 24 hours and an EEG was finally requested because of the normality of laboratory tests and CT. Although this delay in obtaining an EEG could be attributed to our institution, Kaplan8 observed that diagnostic delay is common in patients with NCSE, even when the patient is referred to a prestigious teaching hospital. Therefore, this fact allows us to emphasize the need for an urgent EEG on all patients showing confusional state. Although the term ‘absence status’ is more often associated with generalized and regular spike-and-wave complexes on the EEG, ictal recordings in patients suffering from de novo AS have been enormously heterogeneous. Indeed, Thomas and Andermann18 stressed
‘De novo’ absence status
435
Fig. 1: Longitudinal (a), and tranversal; (b), montages showing continuous irregular generalized sharp-and-slow wave complexes intermixed with spikes and polyspikes; (c), normalization of EEG 20 seconds after intravenous diazepam.
´ J. L. Fernandez-Torre
436
Fig. 1: Continued
Table 1: Nonconvulsive generalized status epilepticusa : differential diagnosis. Absence status of late onset
Complex partial status epilepticus
Antecedents of psychotropic drug abuse Middle age or elderly subjects Female predominance Prolonged and continuous state Facial myoclonic jerks Complete unresponsiveness unusualb Incontinence described Continuous generalized epileptic activity Dramatic response to benzodiazepines Rare recurrences
Pre-existing partial epilepsy At any age Male/female equal Cyclic evolution Complex automatisms Complete unresponsiveness more frequent Incontinence more rarely reported Recurrent focal epileptiform discharges Variable response to benzodiazepines Frequent episodes of recurrences
a Clinical and EEG features summarized from Refs [3, 4, 8, 13, 16–18]. b Although it has been considered more uncommon, there are cases of AS of late onset with severe impairment of consciousness16 .
the large variability of EEG changes seen in these cases. So, there is a wide range of EEG patterns which may vary from typical spike-and-wave discharges to asymmetric irregular sharp-and-slow wave complexes with frontal or frontocentral maximum. Moreover, under some circumstances, electroencephalographic features can be more atypical, adopting, for instance, triphasic morphology, and this appearance can make it difficult to accurately interpret the EEG of a confused patient4, 14 . To overcome this problem and also to obtain a definitive diagnosis, it is advised to administer intravenous benzodiazepines in the course of the EEG recording. The supression of epileptiform activity associated with a significant improvement in the clinical manifestations will be conclusive. Therefore,
a precise diagnosis requires: first, to keep in mind the possibility of this type of NCSE in all confused elderly subjects taking psychotropic drugs, and second, to recognize that EEG may show variable forms of generalized epileptiform activity which disappears dramatically after the injection of intravenous diazepam. At times, it may be difficult to differentiate between the major categories of NCSE4, 8, 13 . It is wellrecognized that complex partial status, especially complex partial status of frontal origin, may be associated with diffuse EEG anomalies which are the result of a secondary generalization of focal discharges4 . However, there are several clinical and EEG features which have been considered useful for the differential diagnosis (Table 1). The presence of a cyclic evo-
‘De novo’ absence status
lution, complex automatisms, complete unresponsiveness and recurrent focal epileptic activity on the EEG have been described as more typical of complex partial status3, 4, 8, 13 . By contrast, female predominance, antecedents of psychotropic drug abuse, perplexity, facial myoclonic twitches, incontinence and continuous epileptiform dicharges seem to be frequent in AS of late onset16–18 , Nevertheless, the utility of these features is limited and the existence of a confusional state in an old subject taking chronically psychotropic drugs will be the clue to suspect the diagnosis and to carry out an urgent EEG.
ACKNOWLEDGEMENTS The author is indebted to Dr Viteri for his helpful comments and is grateful to Dr Solano for referring the patient.
REFERENCES 1. Anderman, F. and Robb, J. P. Absence status. A reappraisal following review of thirty-eight patients. Epilepsia 1972; 13: 177–187. 2. Celesia, G. G. Modern concepts of status epilepticus. Journal of the American Medical Association 1976; 235: 1571–1574. 3. Belafsky, M. A., Carwille, S., Miller, P., Waddell, G., BoxleyJohnson, J. and Delgado-Escueta, A. V. Prolonged epileptic twilight states: Continuous recordings with nasopharyngeal electrodes and videotape analysis. Neurology 1978; 28: 239–245. 4. Guberman, A., Cantu-Reyna, G., Stuss, D. and Broughton, R. Nonconvulsive generalized status epilepticus: Clinical features, neuropychological testing, and long-term follow-up. Neurology 1986; 36: 1284–1291. 5. Tomson, T., Svanborg, E. and Wedlund, J.-E. Nonconvulsive status epilepticus: high incidence of complex partial status.
437 Epilepsia 1986; 27: 276–285. 6. Tomson, T., Lindbom, U. and Nilsson, B. Y. Nonconvulsive status epilepticus in adults: thirty-two consecutive patients from a general hospital population. Epilepsia 1992; 33: 829–835. 7. Cascino, G. D. Nonconvulsive status epilepticus in adults and children. Epilepsia 1993; 34 (Suppl. 1): S21–S28. 8. Kaplan, P. W. Nonconvulsive status epilepticus in the emergency room. Epilepsia 1996; 37: 643–650. 9. Treiman, D. M. Electroclinical features of status epilepticus. Journal of Clinical Neurophysiology 1995; 12: 343–362. 10. Treiman, D. M. Status epilepticus. In: Modern Management of Epilepsy. Bailli`ere’s Clinical Neurology. International Practice and Research (Eds M. J. Brodie and D. M. Treiman). London, Bailli`ere Tindall, 1996: Vol. 5, No. 4: pp. 821–839. 11. Salas-Puig, J., Su´arez-Moro, R. and Mateos, V. Status epilepticus. Neurolog´ıa 1996; 11 (Suppl. 4): 108–121. 12. Snead III, O. C., Dean, J. C. and Penry, J. K. Absence status epilepticus. In: Epilepsy: A Comprehensive Textbook (Eds J. Engel and T. A. Pedley). Philadelphia, Lippincott-Raven Publishers, 1997: pp. 701–707. 13. Williamson, P. D. Complex partial status epilepticus. In: Epilepsy: A Comprehensive Textbook (Eds J. Engel and T. A. Pedley). Philadelphia, Lippincott-Raven Publishers, 1997: pp. 681–699. 14. Kaplan, P. W. Assessing the outcomes in patients with nonconvulsive status epilepticus: Nonconvulsive status epilepticus is underdiagnosed, potentially overtreated, and confounded by comorbidity. Journal of Clinical Neurophysiology 1999; 16: 341–352. 15. Wieser, H. G. Simple partial status epilepticus. In: Epilepsy: A Comprehensive Textbook (Eds J. Engel and T. A. Pedley). Philadelphia, Lippincott-Raven Publishers, 1997: pp. 709–723. 16. Thomas, P., Beaumanoir, A., Genton, P., Dolisi, C. and Chatel, M. ‘De novo’ absence status of late onset: Report of 11 cases. Neurology 1992; 42: 104–110. 17. Thomas, P., Lebrun, C. and Chatel, M. De novo absence status as a benzodiazepine withdrawal syndrome. Epilepsia 1993; 34: 355–358. 18. Thomas, P. and Andermann, F. Late-onset absence status epilepticus is most often situation-related. In: Idiopathic Generalized Epilepsies (Eds A. Malafosse, P. Genton, E. Hirsch, C. Marescaux, D. Broglin and R. Bernasconi). London, John Libbey & Company Ltd, 1994: pp. 95–109.