ltaL J. NeuroL Sci. 12:207-210, 1991
Complex partial status epilepticus simulating an ischemic insult: case report Musolino R.*, Marabello L.*, De Domenico P.**, Labate C.*, Bruzzese T.*, Galatioto S.*, Gallitto G.* *Clinica Neurologica L Universitit degli Studi, Messina **Servizio di Salute Mentale, USSL 41, Messina
A patientpresenting complexpartial status epilepticus (CPSE) had a clinical history and neurological picture on admission that mimicked a cerebrovascular insult. On admission she was confused and totally unresponsive to verbal stimuli. EEG showed high voltage paroxysmal activity on the left hemisphere, prominent on the temporoccipital leads and tending to spread to the opposite regions. Intravenous diazepam led to resolution of the clinical and EEG picture within 24 hours, only a medium voltage slow wave focus being present on the left temporal regions. CPSE shouM be considered whenever a prolonged impairment of consciousness is present. Only accurate EEG recordings permit correct diagnosis in doubtful cases.
Key-Words: Complex partial status epilepticus - - cerebrovascular insult - - clinical and E EG findings
Introduction Complex partial status epilepticus (CPSE) was first described by Gastaut et al in 1956 [4]. However, to date, despite the high incidence of complex partial seizures (CPS) among populations, only a small number of CPSE has been reported
We report the case of a patient who, three years after a cerebral ischemia, presented CPSE, whose clinical history and neurological picture on admission suggested a cerebrovascular event.
Case report
[8, 10, Ill. Gastaut and Tassinari [5] defined two different types of CPSE: the first consisting in recurrent CPS without complete recovery of consciousness during the interictal period and the second characterized by continuous long-lasting episodes of mental confusion with or withouth automatic behaviour. In both cases the EEG usually shows a continuous focal or secondarily generalized ictal pattern [8]. CPSE occurring in patients with a history of cerebral ischemic insult is infrequent [1, 9].
The patient was a 52 year old woman with no family history of neurological disease. She was born after a normal pregnancy and delivery and her developmental milestones were no contributory. Since the age of 28 she had suffered from essential hypertension; at 37 she had "acute myocardial infarction". At 48 she presented sudden stupor. Hospitalized immediately, she was put on antiedema drug therapy. The impairment of consciousness resolved within 4 days, nominal aphasia and tactile
Received 24 May 1989 -- Accepted 30 September | 990
207
The Italian Journal of Neurological Sciences
agnosia persisting only for about a week. EEG showed the presence of generalized slow waves in the theta-delta range, prominent on the left regions. The cerebral angioscintigram documented a hypercatchment area in the left parieto-temporal region, corresponding to the territory of the sylvian artery. At 49, whilst working, she suddenly appeared "thunderstruck", motionless and, if stimulated, was unable to follow simple commands. Hospitalized immediately, she was found on neurological examination to be in stupor with a right faciobrachiocrural paresis and rotation of her head toward the right side. Further, she presented several focal motor seizures, lasting about I to 2 minutes, involving the right limbs. All these signs disappeared completely within 24 hours. The EEG was characterized by slow waves intermingled with spike waves on the left regions. CT scan of the brain revealed a triangular low density area localized in the left parieto-occipital region. The lateral ventricles were mildly dilated and attracted toward the infarct lesion. A diagnosis of acute left sylvian artery ischemia was made. On discharge she was put on oral phenobarbital (PB) (150 mg daily, plasma level 22 Ixg/ml) and antiplatelet drugs. A year later, when she was 50, she was suddenly found "confused" in bed, disoriented in time and place, unable to speak or follow commands and unresponsive to verbal communication. She was
immediately admitted to a psychiatric unit and, following diagnosis, was transferred to a neurological unit. She appeared to be lethargic, and also presented several episodes characterized by rotation ofthe eyeballs. Put on antiedema drugs, she recovered completely within 36 hours. On "awakening" she was unable to recollect the event. On discharge she continued the previous therapy. She was in good health until the age of 52, when she was hospitalized in our clinic, because of sudden unresponsiveness to any sensory of verbal stimuli. On admission she was confused, disoriented in time and place, totally unresponsive to verbal stimuli. Furthermore she presented hyperactive automatic motor activity. The first EEG performed at that point, during the prolonged confusional state, displayed almost continuous high voltage paroxysmal activity on the left hemisphere, prominent on the temporoccipital regions (Fig. 1). These abnormalities decreased slightly in frequency when a sensory stimulus was applied. She was immediately put on intravenous diazepam (40 mg over the following 12 hours). The level of consciousness rapidly improved and after 6 hours she appeared reasonably responsive to stimuli, carrying out simple commands and expressing short sentences. A second EEG performed revealed slow background activity with medium-high voltage theta-delta waves on the
Fig. 1. High voltage irregular spike and wave complexes are evident on the left regions, prominent on the temporooccipital leads. These abnormalities tend to spread to the opposite regions, where continuous slow wave activity is present.
C4 - 0 2 C'~- O~
Ot -Ta
Ta-Ca
.~I
208
, 1 sed
Musolino R.: Complex partial status epilepticus simulating an ischemic insult
temporal regions. Pharmacological fast activities were also evident. No signs of paroxysmal activity were observed (Fig. 2). She recovered consciousness within 12 hours. On this occasion too she was unable to recollect the event. 24 hours later the patient neurological functions were completely normal and the EEG displayed a persistent slow wave focus on the left temporal regions. During the following seven days of hospitalization she had no further episodes. General physical examination was unremarkable. Principal laboratory tests were within normal limits. PB plasma level was within the therapeutic range (24.6 p.g/ml). An electrocardiogram revealed left anterior hemiblock, accompanied by mild disturbances of ventricular repolarization and signs of previous subepicardial ischemia. On digital arteriography the left common carotid artery showed an S pattern but no significant structural alteration. The left internal carotid artery presented diffuse parietal irregularities in its extracranial tract, the right carotid system appeared normal. Brain CT scan was similar to that performed three years previously, showing no signs of recent brain damage. She was discharged in good health, continuing PB (150 mg/die) and antiplatelet therapy.
Discussion
The patient described here had previously presented two episodes of left sylvian artery ischemia, well documented by neuroradiological investigations. During both episodes high arterial blood pressure values were found. Although no ictal EEGs were recorded, the third event appears to have been quite similar, in character to the one we observed. The latter, consisting in a prolonged period of mental confusion, may be regarded as a CPSE, due to activation of a left parietotemporal postischemic focus. Our patient's features fulfil the criteria of Treiman and Delgado-Escueta [10], who defined CPSE, for she presented a prolonged impairment of conseiousness, an epileptiform ictal EEG pattern, a stable interictal EEG focus in the left temporal lobe, a rapid response to intravenous diazepam administration. The relation between brain vascular events and epilepsy has been widely studied by several authors [2, 3]. In particular "tardive" or "cicatricial" epileptic seizures have been observed in about 710% of patients with a history of brain ischemic insult [7]. Further, cerebrovascular damage has been demonstrated in 4-15% of cases of status epilepticus [6]. However, up to now, only a few cases of CPSE secondary to an ischemie cerebral insult have been reported [1, 9], perhaps due to
Fig. 2. Medium-high voltage slow wave activity in the theta-delta range on the left temporal regions.
Slowing of background activity together with pharmacological fast rhythms are also evident. Fp2 - C4
Fpl-C3
C4-02 (::3-0,
0 2 -T4 O1 - T3
T4 - C4
~I
i
,i
209
The Italian Journal of Neurological Sciences
the difficulty of diagnosing CPSE on clinical or E E G features. In fact, patients with CPSE often present strange seizure manifestations (twilight state, long-lasting mental confusion, behavioral abnormalities, automatisms), which may also be observed in other conditions, such as metabolic or vascular insults [10] and psychiatric disorders
[11]. In these cases CPSE may remain unsuspected, especially in the absence o f E E G findings, the symptoms easily lending themselves to misdiagnosis. In the light of these observations very accurate E E G recordings should be always performed in uncertain cases, in order to make a correct diagnosis.
Sommario Viene descritto il caso di una paziente affetta da stato di male parziale complesso, i cui rilievi clinici all'ingresso simulavano un evento cerebrovascolare. La paziente si presentava in stato confusionale, incapace di reagire agli stimoli esterni. L "EEG rivelava un 'attivith parossistica emisferica sinistra, prevalente sulle derivazioni temporooccipitali, tendente a diffondere controlateralmente. La terapia con diazepam per via endovenosa portava alia risoluzione del quadro clinico-EEGrafico entro 24 ore, persistendo soltanto un 'attivith lenta sulle derivazioni temporali di sinistra. Uno stato di male parziale complesso deve essere sospettato ogni qualvoita ci si trova di f r o n t e ad una compromissione della coscienza di lunga durata. Solo una accurata indagine EEGrafica pub permettere diformulare una corretta diagnosi nei cam dubbi.
Address reprint requests to: Dr.ssa Rosa Musolino Clinica Neurologica I Policlinico Universitario 98013 Contesse (Messina)
References [I] BEHRENSJ.: Psychomotor status epilepticus masking as a stroke. Postgrad Med 68:223-226, 1980. [2] DE CAROUSP., D'ALESSANDROR., FERRARAR., ANDREOLI m., SACQUEGNAT AND LUGARESI E.: Late seizures in patients with internal carotid and middle cerebral artery occlusive disease following ischemic events. J. Neurol. Neurosurg. Psychiatry 47:1345-1347, 1984. [3] FAVALEF.:Cerebral ischemia as a cause of epileptic seizures. In: Loeb C. (ed) Studies in cerebrovascular disease. Masson, Milano: 121-140, 1981. [4] GASTAUTH., ROJERJ., ROGERA. :Sur la signification de certains fugues dpileptiques: Apropos d'une observation (lectroclinique d'dtat de real temporal. Rev. Neurol. 94:293-301, 1956. [5] GASTAUTH., TASS1NARIC.: Status epilepticus. In: Gastaut H. (ed) Handbook of electroencephalography and clinical neurophysiology, vol 13 A, Amsterdam, Elsevier: 39-45, 1975. [6] HAUSERW.A.: Epidemiology. morbidity and mot-
210
tality of status epilepticus. Presented at the International Symposium on Status Epileptieus, Santa Monica, California, 1980. [7] LOISEAUP.: Les dpilepsies vasculaires. In: Loiseau P., Jallon P. (eds) Les 6pilepsies, Masson, Paris: 155-160, 1981. [8] MAYEtJXR., LUEDERSH.: Complex partial status epilepticus: case report and proposal for diagnostic criteria. Neurology 28:957-96 !, 1978 [9] TOMSONT., SVANBARGE. AND WEDLUNGJE.: Nonconndsive status epilepticus: high incidence of complex partial status. Epilepsia 27 (3): 276-285, 1986. [10] TREIMAN DM., DELGADO-EscUETAAV.: Complex partial status epilepticus In: Delgado-Escueta AV., Wasterlain CG., Treiman DM., Porter ILl. (eds) Advances in Neurology, vo134 Status epilepticus. New York, Raven Press: 69-81, 1983. [I 1] VAN ROSSUMJ., GROENVELD-OCKUYSENAAW, ARTS RJHM.: Psychomotor status. Arch. Neurol. 42:989-993, 1985.
Complex partial status epilepticus simulating an ischemic insult: case report Musolino R.*, Marabello L.*, De Domenico P.**, Labate C.*, Bruzzese T.*, Galatioto S.*, Gallitto G.* *Clinica Neurologica L Universitit degli Studi, Messina **Servizio di Salute Mentale, USSL 41, Messina
A patientpresenting complexpartial status epilepticus (CPSE) had a clinical history and neurological picture on admission that mimicked a cerebrovascular insult. On admission she was confused and totally unresponsive to verbal stimuli. EEG showed high voltage paroxysmal activity on the left hemisphere, prominent on the temporoccipital leads and tending to spread to the opposite regions. Intravenous diazepam led to resolution of the clinical and EEG picture within 24 hours, only a medium voltage slow wave focus being present on the left temporal regions. CPSE shouM be considered whenever a prolonged impairment of consciousness is present. Only accurate EEG recordings permit correct diagnosis in doubtful cases.
Key-Words: Complex partial status epilepticus - - cerebrovascular insult - - clinical and E EG findings
Introduction Complex partial status epilepticus (CPSE) was first described by Gastaut et al in 1956 [4]. However, to date, despite the high incidence of complex partial seizures (CPS) among populations, only a small number of CPSE has been reported
We report the case of a patient who, three years after a cerebral ischemia, presented CPSE, whose clinical history and neurological picture on admission suggested a cerebrovascular event.
Case report
[8, 10, Ill. Gastaut and Tassinari [5] defined two different types of CPSE: the first consisting in recurrent CPS without complete recovery of consciousness during the interictal period and the second characterized by continuous long-lasting episodes of mental confusion with or withouth automatic behaviour. In both cases the EEG usually shows a continuous focal or secondarily generalized ictal pattern [8]. CPSE occurring in patients with a history of cerebral ischemic insult is infrequent [1, 9].
The patient was a 52 year old woman with no family history of neurological disease. She was born after a normal pregnancy and delivery and her developmental milestones were no contributory. Since the age of 28 she had suffered from essential hypertension; at 37 she had "acute myocardial infarction". At 48 she presented sudden stupor. Hospitalized immediately, she was put on antiedema drug therapy. The impairment of consciousness resolved within 4 days, nominal aphasia and tactile
Received 24 May 1989 -- Accepted 30 September | 990
207
The Italian Journal of Neurological Sciences
agnosia persisting only for about a week. EEG showed the presence of generalized slow waves in the theta-delta range, prominent on the left regions. The cerebral angioscintigram documented a hypercatchment area in the left parieto-temporal region, corresponding to the territory of the sylvian artery. At 49, whilst working, she suddenly appeared "thunderstruck", motionless and, if stimulated, was unable to follow simple commands. Hospitalized immediately, she was found on neurological examination to be in stupor with a right faciobrachiocrural paresis and rotation of her head toward the right side. Further, she presented several focal motor seizures, lasting about I to 2 minutes, involving the right limbs. All these signs disappeared completely within 24 hours. The EEG was characterized by slow waves intermingled with spike waves on the left regions. CT scan of the brain revealed a triangular low density area localized in the left parieto-occipital region. The lateral ventricles were mildly dilated and attracted toward the infarct lesion. A diagnosis of acute left sylvian artery ischemia was made. On discharge she was put on oral phenobarbital (PB) (150 mg daily, plasma level 22 Ixg/ml) and antiplatelet drugs. A year later, when she was 50, she was suddenly found "confused" in bed, disoriented in time and place, unable to speak or follow commands and unresponsive to verbal communication. She was
immediately admitted to a psychiatric unit and, following diagnosis, was transferred to a neurological unit. She appeared to be lethargic, and also presented several episodes characterized by rotation ofthe eyeballs. Put on antiedema drugs, she recovered completely within 36 hours. On "awakening" she was unable to recollect the event. On discharge she continued the previous therapy. She was in good health until the age of 52, when she was hospitalized in our clinic, because of sudden unresponsiveness to any sensory of verbal stimuli. On admission she was confused, disoriented in time and place, totally unresponsive to verbal stimuli. Furthermore she presented hyperactive automatic motor activity. The first EEG performed at that point, during the prolonged confusional state, displayed almost continuous high voltage paroxysmal activity on the left hemisphere, prominent on the temporoccipital regions (Fig. 1). These abnormalities decreased slightly in frequency when a sensory stimulus was applied. She was immediately put on intravenous diazepam (40 mg over the following 12 hours). The level of consciousness rapidly improved and after 6 hours she appeared reasonably responsive to stimuli, carrying out simple commands and expressing short sentences. A second EEG performed revealed slow background activity with medium-high voltage theta-delta waves on the
Fig. 1. High voltage irregular spike and wave complexes are evident on the left regions, prominent on the temporooccipital leads. These abnormalities tend to spread to the opposite regions, where continuous slow wave activity is present.
C4 - 0 2 C'~- O~
Ot -Ta
Ta-Ca
.~I
208
, 1 sed
Musolino R.: Complex partial status epilepticus simulating an ischemic insult
temporal regions. Pharmacological fast activities were also evident. No signs of paroxysmal activity were observed (Fig. 2). She recovered consciousness within 12 hours. On this occasion too she was unable to recollect the event. 24 hours later the patient neurological functions were completely normal and the EEG displayed a persistent slow wave focus on the left temporal regions. During the following seven days of hospitalization she had no further episodes. General physical examination was unremarkable. Principal laboratory tests were within normal limits. PB plasma level was within the therapeutic range (24.6 p.g/ml). An electrocardiogram revealed left anterior hemiblock, accompanied by mild disturbances of ventricular repolarization and signs of previous subepicardial ischemia. On digital arteriography the left common carotid artery showed an S pattern but no significant structural alteration. The left internal carotid artery presented diffuse parietal irregularities in its extracranial tract, the right carotid system appeared normal. Brain CT scan was similar to that performed three years previously, showing no signs of recent brain damage. She was discharged in good health, continuing PB (150 mg/die) and antiplatelet therapy.
Discussion
The patient described here had previously presented two episodes of left sylvian artery ischemia, well documented by neuroradiological investigations. During both episodes high arterial blood pressure values were found. Although no ictal EEGs were recorded, the third event appears to have been quite similar, in character to the one we observed. The latter, consisting in a prolonged period of mental confusion, may be regarded as a CPSE, due to activation of a left parietotemporal postischemic focus. Our patient's features fulfil the criteria of Treiman and Delgado-Escueta [10], who defined CPSE, for she presented a prolonged impairment of conseiousness, an epileptiform ictal EEG pattern, a stable interictal EEG focus in the left temporal lobe, a rapid response to intravenous diazepam administration. The relation between brain vascular events and epilepsy has been widely studied by several authors [2, 3]. In particular "tardive" or "cicatricial" epileptic seizures have been observed in about 710% of patients with a history of brain ischemic insult [7]. Further, cerebrovascular damage has been demonstrated in 4-15% of cases of status epilepticus [6]. However, up to now, only a few cases of CPSE secondary to an ischemie cerebral insult have been reported [1, 9], perhaps due to
Fig. 2. Medium-high voltage slow wave activity in the theta-delta range on the left temporal regions.
Slowing of background activity together with pharmacological fast rhythms are also evident. Fp2 - C4
Fpl-C3
C4-02 (::3-0,
0 2 -T4 O1 - T3
T4 - C4
~I
i
,i
209
The Italian Journal of Neurological Sciences
the difficulty of diagnosing CPSE on clinical or E E G features. In fact, patients with CPSE often present strange seizure manifestations (twilight state, long-lasting mental confusion, behavioral abnormalities, automatisms), which may also be observed in other conditions, such as metabolic or vascular insults [10] and psychiatric disorders
[11]. In these cases CPSE may remain unsuspected, especially in the absence o f E E G findings, the symptoms easily lending themselves to misdiagnosis. In the light of these observations very accurate E E G recordings should be always performed in uncertain cases, in order to make a correct diagnosis.
Sommario Viene descritto il caso di una paziente affetta da stato di male parziale complesso, i cui rilievi clinici all'ingresso simulavano un evento cerebrovascolare. La paziente si presentava in stato confusionale, incapace di reagire agli stimoli esterni. L "EEG rivelava un 'attivith parossistica emisferica sinistra, prevalente sulle derivazioni temporooccipitali, tendente a diffondere controlateralmente. La terapia con diazepam per via endovenosa portava alia risoluzione del quadro clinico-EEGrafico entro 24 ore, persistendo soltanto un 'attivith lenta sulle derivazioni temporali di sinistra. Uno stato di male parziale complesso deve essere sospettato ogni qualvoita ci si trova di f r o n t e ad una compromissione della coscienza di lunga durata. Solo una accurata indagine EEGrafica pub permettere diformulare una corretta diagnosi nei cam dubbi.
Address reprint requests to: Dr.ssa Rosa Musolino Clinica Neurologica I Policlinico Universitario 98013 Contesse (Messina)
References [I] BEHRENSJ.: Psychomotor status epilepticus masking as a stroke. Postgrad Med 68:223-226, 1980. [2] DE CAROUSP., D'ALESSANDROR., FERRARAR., ANDREOLI m., SACQUEGNAT AND LUGARESI E.: Late seizures in patients with internal carotid and middle cerebral artery occlusive disease following ischemic events. J. Neurol. Neurosurg. Psychiatry 47:1345-1347, 1984. [3] FAVALEF.:Cerebral ischemia as a cause of epileptic seizures. In: Loeb C. (ed) Studies in cerebrovascular disease. Masson, Milano: 121-140, 1981. [4] GASTAUTH., ROJERJ., ROGERA. :Sur la signification de certains fugues dpileptiques: Apropos d'une observation (lectroclinique d'dtat de real temporal. Rev. Neurol. 94:293-301, 1956. [5] GASTAUTH., TASS1NARIC.: Status epilepticus. In: Gastaut H. (ed) Handbook of electroencephalography and clinical neurophysiology, vol 13 A, Amsterdam, Elsevier: 39-45, 1975. [6] HAUSERW.A.: Epidemiology. morbidity and mot-
210
tality of status epilepticus. Presented at the International Symposium on Status Epileptieus, Santa Monica, California, 1980. [7] LOISEAUP.: Les dpilepsies vasculaires. In: Loiseau P., Jallon P. (eds) Les 6pilepsies, Masson, Paris: 155-160, 1981. [8] MAYEtJXR., LUEDERSH.: Complex partial status epilepticus: case report and proposal for diagnostic criteria. Neurology 28:957-96 !, 1978 [9] TOMSONT., SVANBARGE. AND WEDLUNGJE.: Nonconndsive status epilepticus: high incidence of complex partial status. Epilepsia 27 (3): 276-285, 1986. [10] TREIMAN DM., DELGADO-EscUETAAV.: Complex partial status epilepticus In: Delgado-Escueta AV., Wasterlain CG., Treiman DM., Porter ILl. (eds) Advances in Neurology, vo134 Status epilepticus. New York, Raven Press: 69-81, 1983. [I 1] VAN ROSSUMJ., GROENVELD-OCKUYSENAAW, ARTS RJHM.: Psychomotor status. Arch. Neurol. 42:989-993, 1985.
