© 1988 S. Kargcr AG. Basel 0014-3022/88/0285-025552.75/0 Eur. Neurol. 28: 255-257 (1988) Aphasic Status Epilepticus Alberto Primavera, Gian-Paolo Bo, Simonetta Venturi Clínica Neurologica dell’Uníversitá di Genova, Italia Key Words. Status epilepticus • Complex partial status epilepticus • Aphasia Abstract. We studied a case of focal status epilepticus with aphasia as the sole manifestation, lasting 21 days. A 77-year-old woman developed aphasic seizures followed by aphasic status epilepticus 10 months after a left temporooccipital hemorrhage. The diagnosis was made only after EEG, and seizures were stopped by anticonvulsant medi­ cation. Aphasic status epilepticus may be only a reflection of cerebral irritability, suggesting the possibility of a functional etiology for prolonged language disorders also in adults. Introduction Case Report A 77-year-old woman, right-handed, was hospitalized for lan­ guage disorders, both expressive and receptive on June 15, 1986 (ta­ ble I). Anamnestic data revealed previous hospitalization (10 months earlier) for 'left temporo-occipital intraparenchymal hemorrhage’; speech and motor disorders resulting from this lesion had, in any case, completely regressed. Nearly 15 days prior to the readmission, mixed speech disorders, initially intermittent, reappeared. Relatives reported that, for some minutes, the patient was unable both to understand what was being said to her and to adequately respond. In Table I. Clinical course and 30-min EEG pattern of a 77-year-old woman with aphasic status epilepticus Date (1986) Clinical course EEG pattern Therapy June 1 intermittent speech disorders - - June 2-14 idem, more frequently - - June 15 hospitalization, severe mixed aphasia June 16 unchanged 3 seizures PB. 100 mg June 18 unchanged 4 seizures PB, 100 mg June 20 moderate improvement, mild aphasia 2 seizures PB, 150 mg June 26 normal modest interictal abnormalities PB, 150 mg — Downloaded by: Kings's College London 137.73.144.138 - 11/11/2017 1:45:08 AM Cases of status epilepticus characterized by speech impairment, particularly in the form of aphasia, speech arrest or vocalization, have been pointed out for a con­ siderable time [Penfield and Jasper, 1954; Critchley, 1960; Serafetinides and Falconer, 1963], Nevertheless, reports with aphasia as the sole manifestation of status epilepticus are quite rare [De Pasquet et al., 1976; Ham­ ilton and Matthews, 1979; Dinner et al., 1981; Marrosu et al., 1983; Rosenbaum et al., 1986; Knight and Cooper, 1986]. Here we present the clinical and EEG observation of a patient suffering from aphasic seizures which gave way to a prolonged aphasic status epilepticus. Primavera/Bo/Ventun 256 i i___ i___ i___ i l l J — l— I__ i___ I___l___l___i .......................................... I___ l___ i___ i _ i i___ I___i_ _ l 1 -5 5 -9 2-6 W * i* > + * M S * * .t+ jU * * J* * ' 6 -1 0 12-6 14-10 *#***+*/*>**ik/j* I 50 p V _1____ I____i____I____i____ I------ 1------1------ 1------1------ 1-----1— i------ 1— i i i i i i -I__ I__ i__ I__ I__ I----L 1s yfr-*' i iu\ yv/v^Vi fvA'/ y1 ^^ ^ ^v— the days that followed, such episodes became more frequent and lan­ guage disorders showed no interruption: hospitalization was thus advised. On admission, serious aphasia was apparent as complete abolition of verbal comprehension and reduction of expressiveness to few stereotypes (‘yes, yes’, ‘I don’t know’). Neuropsychological examination showed spontaneous speech, repetition and naming markedly impaired, and comprehension totally abolished. The re­ mainder of the neurological examination was normal, as were princi­ pal laboratory examinations (complete blood count, urinalysis, glu­ cose, creatinine, electrolytes). Computed tomography scan and nu­ clear magnetic resonance findings indicated a vast cystic area in the left temporal lobe, resulting from the old hemorrhagic lesion. During the first EEG, performed on June 16, three electrical seizures were recorded in 30 min, the patient remaining seriously and globally aphasie. Seizures lasted about 2 min each, beginning in the left tem­ poral region, then spreading to the full left hemisphere and partially to the right; they were characterized at first by rapid low-voltage activity, then by spike waves of elevated voltage and finally by slow waves (50-200 pV), intermingled with spike waves (fig. 1). Interictal activity was normal. Treatment with oral phénobarbital (PB) was instituted (100 mg daily). In a second EEG, on June 18, four elec­ trical seizures were seen in 30 min; clinically, the patient was unchanged. After 2 days, a slight global improvement of aphasie symptomatology was observed; the patient began to follow simple orders and express short sentences. Nevertheless, a third EEG still indicated two focal seizures during a 30-min registration; PB therapy was then increased to 150 mg daily. Improvement continued in suc­ cessive days with progressive remission of aphasie symptoms. The last EEG, taken on June 26, showed only modest interictal abnormal­ ities (slow waves at medium voltage) in the left temporal region. The patient was discharged on PB therapy ( 150 mg daily, plasma level 25.2 pg/ml). After 12 months no seizures have been seen. Downloaded by: Kings's College London 137.73.144.138 - 11/11/2017 1:45:08 AM Fig. 1. The EEG, recorded during status epilcpticus, showed epileptiform discharges starting with paroxysmal fast activity in the left temporal region (a) which became generalized and was then replaced by spikes and waves of elevated voltage (b). Aphasie Status Epilepticus According to Mayeux and Lueders [ 1978] and Dinner et al. [ 1981 ], we can define complex partial status epilep­ ticus as ‘an electroclinical syndrome of prolonged or repetitive complex partial seizures, with persistence of some or all of the complex symptoms in the interictal period’. The EEG seizure patterns may be either focal (frequently temporal lobe), or secondarily generalized from a focal lesion; seizures may be continuous or recur­ rent, as apparent in our subject [Lugaresi et al., 1971; Wieser, 1980; Ballenger et al., 1983]. In the last case, the persistence of the symptoms in the interictal period is obviously essential to the diagnosis of ‘status epilepti­ cus’, independently from the nature of the seizures [Gastaut, 1970]. Our patient presented status epilepticus in which ictal and interictal symptomatology was mani­ fested only by a mixed type of aphasia. We hold that the posthemorrhagic cyst of the temporal lobe caused a focal epileptogenic lesion in the left hemisphere, but it cannot be responsible for the persistence of aphasia in the inter­ ictal period. In fact, speech and motor disorders conse­ quent to the hemorrhagic lesion had completely re­ gressed; the reappearance of speech impairment oc­ curred successively, culminating in status epilepticus; serious aphasia lasted as long as recurrent seizures ex­ isted, but disappeared simultaneously with the control of seizures; more than 12 months after dismissal, the pa­ tient is neurologically normal. In conclusion, this case of aphasic status epilepticus with a clear clinical-EEG cor­ relation shows that, also in adults, prolonged language disorders may be only a reflection of cerebral irritation. Although prolonged aphasia is usually seen in associa­ tion with acute brain damage or tumors, since the treat­ ments are strikingly different, focal status epilepticus should be considered in the differential diagnosis, when a known etiology is not clearly demonstrated. References Ballenger, C.E.; King, D.W.; Gallagher, B.B.: Partial complex status epilepticus. Neurology 33: 1545-1552 (1983). Critchley, M.: Troubles de la parole dans les cas d’épilepsie. Encé­ phale 49: 134-137 (1960). De Pasquet, E.D.; Gaudin, E.S.; Bianchi, A.; De Mendilaharsu, S.: Prolonged and monosymptomatic dysphasic status epilepticus. Neurology 26: 244-247 (1976). Dinner, D.S.; Lueders, H.; Lederman, R.; Gretter, T.E.: Aphasic status epilepticus: a case report. Neurology 31: 888-890 (1981). Gastaut, H.: Clinical and electroencephalographic classification of epileptic seizures. Epilepsia 11: 102-113 (1970). Hamilton, N.G.; Matthews, M.D.: Aphasia: the sole manifestation of focal status epilepticus. Neurology 29: 745-748 (1979). Knight, R.T.; Cooper, J.: Status epilepticus manifesting as reversible Wernicke’s aphasia. Epilepsia 27: 301-304 (1986). Lugaresi, E.; Pazzaglia, P.; Tassinari, C.A.: Differentiation of ‘ab­ sence status’ and ‘temporal lobe status’. Epilepsia 12: 77-87 (1971). Marrosu, F.; Brundu, A.; Rachele, M.G.; Marrosu, G.: Epileptic aphasia as dynamic disturbance: a case report. Acta neurol. 5: 43-46 (1983). Mayeux, R.; Lueders, H.: Complex partial status epilepticus: case report and proposal for diagnostic criteria. Neurology 28: 957961 (1978). Penfield, W.; Jasper, H.: Epilepsy and the functional anatomy of the human brain (Little, Brown, Boston 1954). Rosenbaum. D.H.; Siegel, M.; Barr, M.A.; Rowan, A.J.: Epileptic aphasia. Neurology 36: 822-825 (1986). Serafetinides, E.A.; Falconer, M.A.: Speech disturbance in temporal lobe seizures. Brain 86: 333-346 (1963). Wieser, H.G.: Temporal lobe or psychomotor status epilepticus: a case report. Electroenceph. clin. Neurophysiol. 48: 558-572 (1980). Received: July 21, 1987 Accepted: October 26, 1987 Dr. Alberto Primavera Clinica Neurologica deH’Universita Via De Toni, 5 16132 Genova (Italy) Downloaded by: Kings's College London 137.73.144.138 - 11/11/2017 1:45:08 AM Discussion 257