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BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction
Clinical Neurophysiology 112 (2001) 1726±1728
www.elsevier.com/locate/clinph
BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction Joost Nicolai*, Michael J.A.M. van Putten, DeÂnes L.J. Tavy Department of Neurology and Clinical Neurophysiology, Ziekenhuis Leyenburg, Leyweg 275, 2545 CH Den Haag, The Netherlands Accepted 17 May 2001
Abstract Introduction: Akinetic mutism is described as a result of many disorders. Bilateral infarction of the anterior cerebral artery (ACA) territory is reported rarely, however, often leading to akinetic mutism. Case report: We report a 70 year-old man with akinetic mutism due to bilateral ACA infarction. Electroencephalography, 24 h after admission, showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) in the frontal region and diffuse theta and polymorphic delta activity. Discussion: Postanoxic encephalopathy, central nervous system infection and chronic seizure disorders are the major causes of BIPLEDs. However, BIPLEDs may occur in bilateral ACA territory infarction. q 2001 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Akinetic mutism; Anterior cerebral artery; Bilateral independent periodic lateralized epileptiform discharges; Brain infarct; Electroencephalography; Periodic lateralized epileptiform discharges
1. Introduction Akinetic mutism is described as a condition of silent, alert-appearing immobility that characterizes certain subacute or chronic states of altered consciousness in which sleep±wake cycles have returned but externally obtainable evidence for mental activity remains almost entirely absent and spontaneous motor activity is lacking (Plum and Posner, 1980). Several disorders have been described to cause akinetic mutism, such as vascular, toxic, degenerative and infectious disorders. Vascular causes include bilateral occlusions of the anterior cerebral artery (ACA), vasospasm due to subarachnoid haemorrhage from anterior communicating aneurysms and paramedian thalamic or thalamo-mesencephalic strokes (Bassetti and Bogousslavsky, 1995). We describe a 70 year-old man suffering from akinetic mutism due to a bilateral ACA territory infarction with rather uncommon electroencephalography (EEG) ®ndings. 2. Description of a case On 26 October 2000, a 70 year-old man was admitted to our hospital. A few hours before admission, he experienced
acute dif®culty in walking. During transportation to our hospital he started vomiting, lost consciousness and developed bradycardia and hypotension. Examination on admission showed a blood pressure of 130/75 mmHg. There was eye opening to speech only, without limb movements on demand or to pain; verbal responses were absent. The pupils were equal and reactive. Corneal and oculocephalic re¯exes were present. Plantar re¯ex was extensor on both sides. One hour later, consciousness was regained and no paresis was noticed. No metabolic disturbances were found. Computerized tomography (CT) of the brain showed no abnormalities, besides leucoaraiosis. The differential diagnosis included a non-convulsive status epilepticus and a metabolic or postanoxic encephalopathy. Subsequent EEG, recorded 24 h after admission (Fig. 1), showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs). On re-examination, there was eye opening and limb movement to pain, indicating a worsening of his clinical condition. The diagnosis of akinetic mutism was subsequently made, supposed to be due to a bilateral ACA territory infarction. This was con®rmed by magnetic resonance imaging (MRI) on the ®fth day after admission (Fig. 2). Three weeks later, he suddenly died. Autopsy was not allowed.
* Corresponding author. E-mail address: [email protected] (J. Nicolai). 1388-2457/01/$ - see front matter q 2001 Elsevier Science Ireland Ltd. All rights reserved. PII: S13 88-2457(01)0060 2-2
CLINPH 2001548
J. Nicolai et al. / Clinical Neurophysiology 112 (2001) 1726±1728
1727
Fig. 2. Transverse T2-weighted MRI image obtained 4 days after admission, demonstrates bilateral infarction in the ACA territory.
Fig. 1. (A) EEG recording performed approximately 24 h after admission. Shown are PLEDS over the right hemisphere during the ®rst 3 s, indicated by the solid arrows (1) and over the left frontal area in the remaining 3 s, indicated by the dashed arrows (2). Longitudinal bipolar montage. (B). Shown are PLEDS over the left frontal area, indicated by the dashed arrows (2). Initially, periodic discharges are present over the right hemisphere, as well, indicated by the solid arrows (1). Note that the frequency of the PLEDS over the left frontal area changes from about 1.2 to 0.6 Hz. These lower-frequency PLEDS are not present over the contralateral hemisphere.
3. Discussion Bilateral infarction in the ACA distribution is presumably rare. In a series of 413 patients with ischaemic infarction, only one case was described (Gacs et al., 1983). In a study of 1490 patients admitted for a ®rst stroke over a period of 7 years, only two cases were found (Bogousslavsky and Regli, 1990). In the period 1930±1999, Minagar found detailed reports of 8 patients with a bilateral ACA infarction causing akinetic mutism in 7 (Minagar and David, 1999). The one exception had no reduction of motor or speech activities but showed complex behavioural changes and a lack of attention (Laplane et al., 1981). Mutism caused by unilateral
infarction of the ACA territory is described as well; 8 out of 16 patients with a left-sided and two out of 9 patients with a right-sided ACA infarction had initial mutism (Bogousslavsky and Regli, 1990). Bassetti and Bogousslavsky state that akinetic mutism caused by bilateral infarction in the ACA distribution is characterized by bifrontal or generalized EEG slowing, with lack of desynchronization following external stimuli (Bassetti and Bogousslavsky, 1995). Ingvar described two cases of akinetic mutism with a normal EEG. However, the precise cause of the akinetic mutism in these two cases is not clear from his description, which makes a comparison dif®cult (Ingvar, 1971). Only in 4 case reports on akinetic mutism due to bilateral ACA infarction are EEG ®ndings discussed, as shown in Table 1. The clinical diagnosis of bilateral ACA infarction can be dif®cult, which is probably due to the presence of reduced consciousness in the initial stage. Coma is reported due to bilateral ACA territory infarction lasting from 1 day (Oomman and Madhusudhanan, 1999) to even 4 weeks (Lipschutz et al., 1991). Coma due to the combination of diabetic ketoacidosis and bilateral ACA infarction lasting for 2 days, resulting in akinetic mutism, is described as well (Freemon, 1971). In several cases reported, the initial diagnosis was brainstem infarction (Minagar and David, 1999) or basilar artery occlusion (Ferbert and Thron, 1992). As in our patient, initial CT scan or MRI scan can be normal. In many reported cases a lumbar puncture was performed (Freemon, 1971; Gugliotta et al., 1989; Lipschutz et al., 1991; Borggreve et al., 1994) on the day of admission, indicating that the clinical picture had not been immediately recognized. In our patient the initial diagnosis was not clear either, the EEG performed 24 h after admission showed a rather unexpected ®nding, i.e. BIPLEDs. BIPLEDs are de®ned as independent, asynchronous periodic lateralized epileptiform discharges (PLEDs) (Pohlmann-Eden et al., 1996) and can be distinguished from
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J. Nicolai et al. / Clinical Neurophysiology 112 (2001) 1726±1728
Table 1 EEG ®ndings reported in akinetic mutism due to bilateral anterior cerebri artery infarction Reference
Sex/age
Clinical picture
EEG made after
Main EEG ®ndings
Freemon (1971) Gugliotta et al. (1989)
M/62 (case 3) M/65
Akinetic mutism Akinetic mutism
Not mentioned At admission 5 days 10 days
Diffuse theta and delta Sporadic 4±7 Hz theta right occipital region Diffuse slow activity, delta right rolandic region Diffuse 7±8 Hz theta, multifocal, intermittent, polymorphic delta Sharp wave and spike and wave complexes, bilaterally central regions Bilateral sharp 4±7 Hz theta, disseminated polymorphic 1±3 Hz delta Diffuse slowing
Spontaneous nocturnal sleep Borggreve et al. (1994)
M/73
Minagar and David (1999)
M/63
Akinetic mutism, almost complete quadriplegia Akinetic mutism
ipsilateral independent PLEDs (Silbert et al., 1996), alternating PLEDs or cerebral bigeminy (Bertolucci and Silva, 1992) and multifocal PLEDs (Lawn et al., 2000). In case of BIPLEDs the complexes are asynchronous and usually differ in morphology, amplitude, repetition rate and the site of maximal involvement (de la Paz and Brenner, 1981). The complexes in BIPLEDs are similar to those that occur with PLEDs: surface-negative bi-, tri-, or polyphasic spike and sharp waves, with an amplitude ranging from 50 to 300 mV, duration ranging from 60 up to 800±1000 ms and periodicity ranging from 0.3 to 4 s (Pohlmann-Eden et al., 1996). Postanoxic encephalopathy, central nervous system (CNS) infection (encephalitis or meningitis) and chronic seizure disorders are reported to be the major causes of BIPLEDs (de la Paz and Brenner, 1981). Thirteen out of 18 patients with BIPLEDs were comatose and mortality was high (61%) in the series described by de la Paz and Brenner. In a series of 5 children with BIPLEDs, 3 had suffered from anoxia and two had a CNS infection (Raroque et al., 1993). Multifocal PLEDs occur independently in 3 or more locations and involve both hemispheres (Lawn et al., 2000). Multifocal PLEDs are associated with vascular lesions, CNS infections, metabolic/toxic disorders, chronic seizure disorders and hypoxic ischaemic insults. Twenty-six out of 35 patients with multifocal PLEDS were comatose and the mortality was high (57%) (Lawn et al., 2000). To our knowledge, this is the ®rst description of a patient with akinetic mutism due to bilateral ACA infarction, showing BIPLEDs on the EEG. References Bassetti C, Bogousslavsky J. Impaired consciousness and sleep. In: Bogousslavsky J, Caplan L, editors. Stroke syndromes, Cambridge: Cambridge University Press, 1995. pp. 108±117. Bertolucci PH, Silva AB. Alternating periodic lateralized epileptiform discharges (cerebral bigeminy). Clin Electroencephalogr 1992;23:177±179.
, 24 h , 24 h
Bogousslavsky J, Regli F. Anterior cerebral artery territory infarction in the Lausanne Stroke Registry. Clinical and etiologic patterns. Arch Neurol 1990;47:144±150. Borggreve F, De Deyn PP, Marien P, Cras P, Dierckx RA. Bilateral infarction in the anterior cerebral artery vascular territory due to an unusual anomaly of the circle of Willis. Stroke 1994;25:1279±1281. Ferbert A, Thron A. Bilateral anterior cerebral artery territory infarction in the differential diagnosis of basilar artery occlusion. J Neurol 1992;239:162±164. Freemon FR. Akinetic mutism and bilateral anterior cerebral artery occlusion. J Neurol Neurosurg Psychiatry 1971;34:693±698. Gacs G, Fox AJ, Barnett HJ, Vinuela F. Occurrence and mechanisms of occlusion of the anterior cerebral artery. Stroke 1983;14:952±959. Gugliotta MA, Silvestri R, De Domenico P, Galatioto S, Di Perri R. Spontaneous bilateral anterior cerebral artery occlusion resulting in akinetic mutism. A case report. Acta Neurol (Napoli) 1989;11:252±258. Ingvar DH. EEG and cerebral circulation in the apallic syndrome and akinetic mutism. Electroenceph clin Neurophysiol 1971;30:272±273. Laplane D, Degos JD, Baulac M, Gray F. Bilateral infarction of the anterior cingulate gyri and of the fornices. Report of a case. J Neurol Sci 1981;51:289±300. Lawn ND, Westmoreland BF, Sharbrough FW. Multifocal periodic lateralized epileptiform discharges (PLEDs): EEG features and clinical correlations. Clin Neurophysiol 2000;111:2125±2129. Lipschutz JH, Pascuzzi RM, Bognanno J, Putty T. Bilateral anterior cerebral artery infarction resulting from explosion-type injury to the head and neck. Stroke 1991;22:813±815. Minagar A, David NJ. Bilateral infarction in the territory of the anterior cerebral arteries. Neurology 1999;52:886±888. Oomman A, Madhusudhanan M. A case of unpaired anterior cerebral artery occlusion producing akinetic mutism. Neurol India 1999;47:157±158. de la Paz D, Brenner RP. Bilateral independent periodic lateralized epileptiform discharges. Clinical signi®cance. Arch Neurol 1981;38:713±715. Plum F, Posner JB. The diagnosis of stupor and coma, 3rd ed. Philadelphia, PA: F.A. Davis Company, 1980 p. 7±8. Pohlmann-Eden B, Hoch DB, Cochius JI, Chiappa KH. Periodic lateralized epileptiform discharges ± a critical review. J Clin Neurophysiol 1996;13:519±530. Raroque Jr. HG, Wagner W, Gonzales PC, Leroy RF, Karnaze D, Riela AR, Roach ES. Reassessment of the clinical signi®cance of periodic lateralized epileptiform discharges in pediatric patients. Epilepsia 1993;34:275±278. Silbert PL, Radhakrishnan K, Sharbrough FW, Klass DW. Ipsilateral independent periodic lateralized epileptiform discharges. Electroenceph clin Neurophysiol 1996;98:223±226.
www.elsevier.com/locate/clinph
BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction Joost Nicolai*, Michael J.A.M. van Putten, DeÂnes L.J. Tavy Department of Neurology and Clinical Neurophysiology, Ziekenhuis Leyenburg, Leyweg 275, 2545 CH Den Haag, The Netherlands Accepted 17 May 2001
Abstract Introduction: Akinetic mutism is described as a result of many disorders. Bilateral infarction of the anterior cerebral artery (ACA) territory is reported rarely, however, often leading to akinetic mutism. Case report: We report a 70 year-old man with akinetic mutism due to bilateral ACA infarction. Electroencephalography, 24 h after admission, showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) in the frontal region and diffuse theta and polymorphic delta activity. Discussion: Postanoxic encephalopathy, central nervous system infection and chronic seizure disorders are the major causes of BIPLEDs. However, BIPLEDs may occur in bilateral ACA territory infarction. q 2001 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Akinetic mutism; Anterior cerebral artery; Bilateral independent periodic lateralized epileptiform discharges; Brain infarct; Electroencephalography; Periodic lateralized epileptiform discharges
1. Introduction Akinetic mutism is described as a condition of silent, alert-appearing immobility that characterizes certain subacute or chronic states of altered consciousness in which sleep±wake cycles have returned but externally obtainable evidence for mental activity remains almost entirely absent and spontaneous motor activity is lacking (Plum and Posner, 1980). Several disorders have been described to cause akinetic mutism, such as vascular, toxic, degenerative and infectious disorders. Vascular causes include bilateral occlusions of the anterior cerebral artery (ACA), vasospasm due to subarachnoid haemorrhage from anterior communicating aneurysms and paramedian thalamic or thalamo-mesencephalic strokes (Bassetti and Bogousslavsky, 1995). We describe a 70 year-old man suffering from akinetic mutism due to a bilateral ACA territory infarction with rather uncommon electroencephalography (EEG) ®ndings. 2. Description of a case On 26 October 2000, a 70 year-old man was admitted to our hospital. A few hours before admission, he experienced
acute dif®culty in walking. During transportation to our hospital he started vomiting, lost consciousness and developed bradycardia and hypotension. Examination on admission showed a blood pressure of 130/75 mmHg. There was eye opening to speech only, without limb movements on demand or to pain; verbal responses were absent. The pupils were equal and reactive. Corneal and oculocephalic re¯exes were present. Plantar re¯ex was extensor on both sides. One hour later, consciousness was regained and no paresis was noticed. No metabolic disturbances were found. Computerized tomography (CT) of the brain showed no abnormalities, besides leucoaraiosis. The differential diagnosis included a non-convulsive status epilepticus and a metabolic or postanoxic encephalopathy. Subsequent EEG, recorded 24 h after admission (Fig. 1), showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs). On re-examination, there was eye opening and limb movement to pain, indicating a worsening of his clinical condition. The diagnosis of akinetic mutism was subsequently made, supposed to be due to a bilateral ACA territory infarction. This was con®rmed by magnetic resonance imaging (MRI) on the ®fth day after admission (Fig. 2). Three weeks later, he suddenly died. Autopsy was not allowed.
* Corresponding author. E-mail address: [email protected] (J. Nicolai). 1388-2457/01/$ - see front matter q 2001 Elsevier Science Ireland Ltd. All rights reserved. PII: S13 88-2457(01)0060 2-2
CLINPH 2001548
J. Nicolai et al. / Clinical Neurophysiology 112 (2001) 1726±1728
1727
Fig. 2. Transverse T2-weighted MRI image obtained 4 days after admission, demonstrates bilateral infarction in the ACA territory.
Fig. 1. (A) EEG recording performed approximately 24 h after admission. Shown are PLEDS over the right hemisphere during the ®rst 3 s, indicated by the solid arrows (1) and over the left frontal area in the remaining 3 s, indicated by the dashed arrows (2). Longitudinal bipolar montage. (B). Shown are PLEDS over the left frontal area, indicated by the dashed arrows (2). Initially, periodic discharges are present over the right hemisphere, as well, indicated by the solid arrows (1). Note that the frequency of the PLEDS over the left frontal area changes from about 1.2 to 0.6 Hz. These lower-frequency PLEDS are not present over the contralateral hemisphere.
3. Discussion Bilateral infarction in the ACA distribution is presumably rare. In a series of 413 patients with ischaemic infarction, only one case was described (Gacs et al., 1983). In a study of 1490 patients admitted for a ®rst stroke over a period of 7 years, only two cases were found (Bogousslavsky and Regli, 1990). In the period 1930±1999, Minagar found detailed reports of 8 patients with a bilateral ACA infarction causing akinetic mutism in 7 (Minagar and David, 1999). The one exception had no reduction of motor or speech activities but showed complex behavioural changes and a lack of attention (Laplane et al., 1981). Mutism caused by unilateral
infarction of the ACA territory is described as well; 8 out of 16 patients with a left-sided and two out of 9 patients with a right-sided ACA infarction had initial mutism (Bogousslavsky and Regli, 1990). Bassetti and Bogousslavsky state that akinetic mutism caused by bilateral infarction in the ACA distribution is characterized by bifrontal or generalized EEG slowing, with lack of desynchronization following external stimuli (Bassetti and Bogousslavsky, 1995). Ingvar described two cases of akinetic mutism with a normal EEG. However, the precise cause of the akinetic mutism in these two cases is not clear from his description, which makes a comparison dif®cult (Ingvar, 1971). Only in 4 case reports on akinetic mutism due to bilateral ACA infarction are EEG ®ndings discussed, as shown in Table 1. The clinical diagnosis of bilateral ACA infarction can be dif®cult, which is probably due to the presence of reduced consciousness in the initial stage. Coma is reported due to bilateral ACA territory infarction lasting from 1 day (Oomman and Madhusudhanan, 1999) to even 4 weeks (Lipschutz et al., 1991). Coma due to the combination of diabetic ketoacidosis and bilateral ACA infarction lasting for 2 days, resulting in akinetic mutism, is described as well (Freemon, 1971). In several cases reported, the initial diagnosis was brainstem infarction (Minagar and David, 1999) or basilar artery occlusion (Ferbert and Thron, 1992). As in our patient, initial CT scan or MRI scan can be normal. In many reported cases a lumbar puncture was performed (Freemon, 1971; Gugliotta et al., 1989; Lipschutz et al., 1991; Borggreve et al., 1994) on the day of admission, indicating that the clinical picture had not been immediately recognized. In our patient the initial diagnosis was not clear either, the EEG performed 24 h after admission showed a rather unexpected ®nding, i.e. BIPLEDs. BIPLEDs are de®ned as independent, asynchronous periodic lateralized epileptiform discharges (PLEDs) (Pohlmann-Eden et al., 1996) and can be distinguished from
1728
J. Nicolai et al. / Clinical Neurophysiology 112 (2001) 1726±1728
Table 1 EEG ®ndings reported in akinetic mutism due to bilateral anterior cerebri artery infarction Reference
Sex/age
Clinical picture
EEG made after
Main EEG ®ndings
Freemon (1971) Gugliotta et al. (1989)
M/62 (case 3) M/65
Akinetic mutism Akinetic mutism
Not mentioned At admission 5 days 10 days
Diffuse theta and delta Sporadic 4±7 Hz theta right occipital region Diffuse slow activity, delta right rolandic region Diffuse 7±8 Hz theta, multifocal, intermittent, polymorphic delta Sharp wave and spike and wave complexes, bilaterally central regions Bilateral sharp 4±7 Hz theta, disseminated polymorphic 1±3 Hz delta Diffuse slowing
Spontaneous nocturnal sleep Borggreve et al. (1994)
M/73
Minagar and David (1999)
M/63
Akinetic mutism, almost complete quadriplegia Akinetic mutism
ipsilateral independent PLEDs (Silbert et al., 1996), alternating PLEDs or cerebral bigeminy (Bertolucci and Silva, 1992) and multifocal PLEDs (Lawn et al., 2000). In case of BIPLEDs the complexes are asynchronous and usually differ in morphology, amplitude, repetition rate and the site of maximal involvement (de la Paz and Brenner, 1981). The complexes in BIPLEDs are similar to those that occur with PLEDs: surface-negative bi-, tri-, or polyphasic spike and sharp waves, with an amplitude ranging from 50 to 300 mV, duration ranging from 60 up to 800±1000 ms and periodicity ranging from 0.3 to 4 s (Pohlmann-Eden et al., 1996). Postanoxic encephalopathy, central nervous system (CNS) infection (encephalitis or meningitis) and chronic seizure disorders are reported to be the major causes of BIPLEDs (de la Paz and Brenner, 1981). Thirteen out of 18 patients with BIPLEDs were comatose and mortality was high (61%) in the series described by de la Paz and Brenner. In a series of 5 children with BIPLEDs, 3 had suffered from anoxia and two had a CNS infection (Raroque et al., 1993). Multifocal PLEDs occur independently in 3 or more locations and involve both hemispheres (Lawn et al., 2000). Multifocal PLEDs are associated with vascular lesions, CNS infections, metabolic/toxic disorders, chronic seizure disorders and hypoxic ischaemic insults. Twenty-six out of 35 patients with multifocal PLEDS were comatose and the mortality was high (57%) (Lawn et al., 2000). To our knowledge, this is the ®rst description of a patient with akinetic mutism due to bilateral ACA infarction, showing BIPLEDs on the EEG. References Bassetti C, Bogousslavsky J. Impaired consciousness and sleep. In: Bogousslavsky J, Caplan L, editors. Stroke syndromes, Cambridge: Cambridge University Press, 1995. pp. 108±117. Bertolucci PH, Silva AB. Alternating periodic lateralized epileptiform discharges (cerebral bigeminy). Clin Electroencephalogr 1992;23:177±179.
, 24 h , 24 h
Bogousslavsky J, Regli F. Anterior cerebral artery territory infarction in the Lausanne Stroke Registry. Clinical and etiologic patterns. Arch Neurol 1990;47:144±150. Borggreve F, De Deyn PP, Marien P, Cras P, Dierckx RA. Bilateral infarction in the anterior cerebral artery vascular territory due to an unusual anomaly of the circle of Willis. Stroke 1994;25:1279±1281. Ferbert A, Thron A. Bilateral anterior cerebral artery territory infarction in the differential diagnosis of basilar artery occlusion. J Neurol 1992;239:162±164. Freemon FR. Akinetic mutism and bilateral anterior cerebral artery occlusion. J Neurol Neurosurg Psychiatry 1971;34:693±698. Gacs G, Fox AJ, Barnett HJ, Vinuela F. Occurrence and mechanisms of occlusion of the anterior cerebral artery. Stroke 1983;14:952±959. Gugliotta MA, Silvestri R, De Domenico P, Galatioto S, Di Perri R. Spontaneous bilateral anterior cerebral artery occlusion resulting in akinetic mutism. A case report. Acta Neurol (Napoli) 1989;11:252±258. Ingvar DH. EEG and cerebral circulation in the apallic syndrome and akinetic mutism. Electroenceph clin Neurophysiol 1971;30:272±273. Laplane D, Degos JD, Baulac M, Gray F. Bilateral infarction of the anterior cingulate gyri and of the fornices. Report of a case. J Neurol Sci 1981;51:289±300. Lawn ND, Westmoreland BF, Sharbrough FW. Multifocal periodic lateralized epileptiform discharges (PLEDs): EEG features and clinical correlations. Clin Neurophysiol 2000;111:2125±2129. Lipschutz JH, Pascuzzi RM, Bognanno J, Putty T. Bilateral anterior cerebral artery infarction resulting from explosion-type injury to the head and neck. Stroke 1991;22:813±815. Minagar A, David NJ. Bilateral infarction in the territory of the anterior cerebral arteries. Neurology 1999;52:886±888. Oomman A, Madhusudhanan M. A case of unpaired anterior cerebral artery occlusion producing akinetic mutism. Neurol India 1999;47:157±158. de la Paz D, Brenner RP. Bilateral independent periodic lateralized epileptiform discharges. Clinical signi®cance. Arch Neurol 1981;38:713±715. Plum F, Posner JB. The diagnosis of stupor and coma, 3rd ed. Philadelphia, PA: F.A. Davis Company, 1980 p. 7±8. Pohlmann-Eden B, Hoch DB, Cochius JI, Chiappa KH. Periodic lateralized epileptiform discharges ± a critical review. J Clin Neurophysiol 1996;13:519±530. Raroque Jr. HG, Wagner W, Gonzales PC, Leroy RF, Karnaze D, Riela AR, Roach ES. Reassessment of the clinical signi®cance of periodic lateralized epileptiform discharges in pediatric patients. Epilepsia 1993;34:275±278. Silbert PL, Radhakrishnan K, Sharbrough FW, Klass DW. Ipsilateral independent periodic lateralized epileptiform discharges. Electroenceph clin Neurophysiol 1996;98:223±226.