(Acta Paediatr Jpn 1992; 34: 310
- 315)
Case Reports
The Origin of Myoclonus and Periodic Synchronous Discharges in Subacute Sclerosing Panencephalitis Shinichi Yagi, M.D., Yo Miura, M.D., Naoki Kataoka, M.D., Shun Mizuta, M.D., Atsuko Wakunami, M.D. and Tetsuro Morita, M.D. Department of’Pediatrics, Kawasaki Medical School, Okayama
We report here a case of a patient with subacute sclerosing panencephalitis (SSPE) and we have analyzed periodic events using dipole tracing methods to clarify the origin of periodic synchronous discharges and myoclonus. Both source generators were located in the subcortical part of the cerebrum, an area adjacent to the thalamus. Although the pathophysiology of periodic events in SSPE has been controversial, dipole tracing methods may contribute to clarify the origin of periodic events in SSPE. Key Words
SSPE, Periodic events, Dipole tracing methods
Introduction Subacute sclerosing panencephalitis (SSPE) is now widely known as a slow virus infection of the central nervous system due to the measles virus. Since Dawson first reported and described it [I], there have been many neurophysiological and neuroradiological studies and immunological evaluations [2-91. In recent years, treatment with inosiplex andlor interferon a has been widely accepted [lo, 1 I]. but there have been few reports of a favorable outcome in SSPE. Despite recent
Received July 15. 1991 Revised Uovernher 18, 1991 Accepted December 6. 1991 Correspondence address: Shinichi Yagi, M.D., Department of Pediatrics, Kawasaki Medical School, 577 Matsushirna. Kurashiki-city, Okayarna 701-01, Japan
detailed studies, the pathophysiology of periodic synchronous discharges (PSD) on the electroencephalogram (EEG) and correlated myoclonus has been controversial. This study was undertaken to clarify the origin of PSD and myoclonus in SSPE using dipole tracing methods.
Case Report An eight year old girl was referred to us because of a tendency toward clumsiness and memory disturbance of several weeks duration. During the neonatal period, exchange transfusions were performed because of isoimmunization due to Rh incompatibility. At one year of age, she had a natural measles infection complicated by pneumonia which required hospitalization of about one week. Subsequently, she had been healthy until eight
The origin of periodic events in SSPE (53) 31 I years of age. Although she was alert and could follow simple commands on admission, she had an ataxic gait, echolalia and
dysdiadochokinesia dominantly in the left hand. The deep tendon reflexes of the left limbs were increased. A general examination
FPZ Fa F4 c4
T4 P4 T6 02 Fpl F7
F3 c3 T3 P3 T5 01 ECG
Fig. 1 : At the time myoclonus appeared, EEG shows SSPE complexes (arrow heads), and focal spikes and/or sharp waves are seen dominantly in the area of bilateral frontal head area.
Fig. 2: Simultaneous EEG-EMG records; arrow head indicates myoclonus of right thigh.
Vol. 34 No. 3 June 1992
3 I2 (54) Yagi ct al.
including routine hematological and biochemical findings was normal. The diagnosis of SSPE was based on an elevated measles antibody titer, not only in the serum but also in the cerebrospinal fluid (CSF). Her serum measles antibody titers were as follows, HI 256x, CF 512x, NT1024~. CSF measles antibody titers were also elevated to HI 32x, CF 32x, NT 128x and the protein level in the CSF was 52 rng/dl. In addition, oligoclonal IgG bands were strongly detected in the CSF. She had a neurological disability index of 24% and the disease was in clinical stage I. PSD were not seen in her EEG on admission. The patient was treated with inosiplex and interferon (I intrathecally, but she apeared
gradually to deteriorate mentally and neurologically. By the third week after admission dominant myoclonus of the right limbs as well as other involuntary movements had begun. When the myoclous become marked, her EEG revealed PSD. Currently, after a clinical course of six months, her NDI is 56% and the clinical stage of the disease is stage 11. Dipole tracing estimates Scalp potentials generated by concentrated electric sources in the brain are very similar to potentials generated by an electric dipole at the source position. In this sense a concentrated source in the brain is modelled as an electric dipole. Dipole tracing is a method for
Myoclonuscorrelated paroxysmal discharges (100.0 rnsec) LOC.(rnrn) Vec. x= 19.0 -7.31€+05 y= 15.0 -2.01E+05 Z= 6.8 6.12E+05 Mornent=9,74E+05 CH 8 Back
Mag : 0.25
Dipolarity=97.8%
,,A,
I
Axis : Y
Horisontal ,/-.
VEC. C A L : AVE.
Periodic synchronous discharges EEG DIPOLE -TRACING
p
100.ouv CH
'
Step
f-
,
'
(Vector) 13 Initial mint Dipole No. = 1 (103.2 rnsec) LOC.(rnrn) Vec. X= 14.9 -7.46E+05 Y= 8.3 1.82E+05 Z= 32.7 6.17E+05
Mag : o,25
Mornent=9.85E+05 Dipolarity=97.0%
I 4.42€+05
Axis : Y
Step
VEC. CAL: AVE.
Fig. , 3 : Dipole tracing estimates, top indicates the source generators of myoclonus associated with paroxysmal discharges and bottom shows source generators of SSPE complexes. Both electrical source generators are located in an area adjacent to the thalamus.
Acta Paediatr Jpn
R e origin of periodic events in SSPE (55) 313 estimating the localization and vector moment of electric source generator as an equivalent dipole from the distribution of electric potentials over the scalp. At the time myoclonus appeared, periodic synchronous discharges which occurred every 8 to 10 sec (Fig. 1 arrows) and myoclonus-correlated paroxysmal discharges (Fig. 2) over the scalp recorded on a data recorder were analyzed. EEG was performed with 21 electrodes on the scalp according to the international 10-20 system with the ear reference, and a signal processor 7T18 (NEC-Sanei) was used for these analyses. The dipoles were estimated from 10 points including the peak of each discharge. The location of the electric source generators of the PSD and myoclonusassociated paroxysmal discharges were analyzed using the dipole tracing methods [12]. As shown in Fig. 3, both electric source generators were located in an area adjacent to the thalamus. The source generators of myoclonus-associated paroxysmal discharges tended to be present more on the left side. The dipolarities (the validity of the dipole approximation) for both PSD and myoclonus associated discharges were more than 97%. Therefore these source generators could be expected to reveal optimal dipoles.
Discussion Since Radermecker’s description of periodic EEG patterns Characterizing SSPE [ 131, there have been investigations of the PSD in SSPE. It is well known that periodic EEG patterns occasionally occur in other diseases such as Jakob-Creutzfeldt disease, cerebral lipidosis, severe anoxic-encephalopathy and infections [14]. Many authors have suggested that these EEG abnormalities are caused by a disturbance in the function of certain brain structures. As yet, however, the origin of PSD in SSPE and other diseases has not. been established. In addition myoclonic jerks, one of the characteristic clinical features of SSPE, have been observed during the clinical course of stage 11. Myoclonus is a general term that refers to rapid muscle jerking, but myoclonic jerks in
Vol. 34 No. 3 June 1992
patients with SSPE are often quite prolonged and also show a tendency to be periodic. Although most studies have shown a one to one relationship between myoclonic jerks and PSD in SSPE, some studies based on detailed simultaneous recordings of electromyograms (EMG) and EEGs have revealed variable patterns between PSD and myoclonic jerks [2, 41. Cobb indicated that EMG changes usually began somewhat after the onset of EEG complexes [2]. Celesia, on the other hand, reported that muscle potential tended to precede the EEG complexes by 200-800 msec. in one case. In two other cases, however, there was poor correlation between muscle potentials and EEG [4]. Similar cases were also described by Lombroso [3]. These previous reports involved analysis of simultaneous EMG-EEG records and various kinds of evoked potential, but to our knowledge, there has been no previous attempt to make dipole tracing estimates of the source generators of PSD and myoclonus-associated paroxysmal discharges. The dipole tracing methods are based on a realistic head model which has uniform electrical conductivity [121. Recently, there have been a few studies describing the efficacy of these new techniques for estimating the localization and vector moment of source generators from the distribution of electric potentials over the scalp, such as focal spikes in epilepsy and/or evoked potentials [15, 161. There are certain problems involved in estimating the accuracy of the source generators analyzed by the dipole tracing methods. There are two major difficulties inherent in this method such as that the low electric conductivity of the skull causes systematic shifts of the optimal dipoles positions from the true position of concentrated sources and/or the optimal dipoles cannot specify diffuse source positions. Therefore, Homma and Musha have proposed that dipolarities of 98% are required for optimal dipoles [171. In the present case, both source generators were surprisingly located in the subcortical part of the cerebrum, an area adjacent to the
3 I4 ( 5 6 ) Yagi et a/. thalamus, and both generators had dipolarities of over 97%. The authors assumed that analyzed paroxysmal discharges accompanied by myoclonic jerks correlate closely with individual myoclonus. Thus. we believe that the present source generators which were analyzed during discharges of myoclonic jerks also reflect the origin of myoclonus in this case. It seems possible that electrical periodic events take place in all parts of the brain. Celesia suggested that a severe impairment of the cortical-subcortical structures is necessary for SSPE complexes to appear [4]. Fenyo and Hasznos on the other hand, indicated that such periodic events have a brain stem origin which they confirmed by pharmacological studies [ 181. They noted that regular complexes may be replaced by irregular delta activities after the administration of mephenesin, a drug which blocks the diffuse thalamic system. Cobb also proposed the brain stem as the site of the origin of electrical periodic events and assumed that these periodic events require a functional cortex rather than severe cortical damage [2]. Neuropathologically, Ohya tends to believe that the SSPE complexes are indicative of relative preservation of the cortex and later severe cortical damage seems to cause disappearance of the SSPE complexes [19]. Of additional interest have been studied regarding the association between ocular jerks and both peripheral EMG and EEG discharges reported by Lombroso [3]. He noted the occurrence of ocular jerks 500 to 1,200 msec. before myoclonic limbs jerks and/or the PSD on EEG. Such a timelag suggests that the initial electrical event originates from the reticular formation of the pons and/or midbrain. Subsequently, eye movement secondary to excitation of the oculomotor nuclei and. later, myoclonic limb jerks and PSD may be observed. The author wishes to emphasize the importance of the existence of variable neurological conditions in SSPE individually. Although further studies are required, the dipole tracing methods may contribute to clarification of the pathophysiology of the characteristic periodic events in SSPE.
Acknowledgements The autKors wish to thank Miss Eiko Matsuda and Miss Yoko Tetsukura for their excellent technical assistance.
References I. 2. 3. 4.
5. 6.
7.
8.
9.
10.
1 I.
12.
13. 14. 15. 16.
17.
Dawson J.R. Cellular inclusions in cerebral lesions of epidemic encephalitis. Arch. Neurol. Psychiatry 1934: 31: 685-700. Cobb W. The periodic events of subacute sclerosing leukoencephalitis. Electroenceph. Clin. Neurophysiol. 1966; 21: 278-94. Lombroso C.T. Remarks on the EEG and movement disorder in SSPE. Neurol. 1968; 18-part 2: 69-75. Celesia G.G. Pathophysiology of periodic EEG complexes in subacute sclerosing panencephalitis (SSPE). Electroenceph. Clin. Neurophysiol. 1973: 35: 293-300. Markand 0 . N . & Pans7i J.G. The electroencephalogram in subacute sclerosing panencephalitis. Arch. Neurol. 1975; 32: 719-26. Miyake S., Yoshida H., lnoue H., et al. Subacute sclerosing panencephalitis. A clinical and electroencephalographic study. No To Hattatsu 1985: 17: 29-36 (in Jpn). Lum (3.9.. Williams J.P., Dyken P.D., et al. Magnetic resonance and CT imaging correlated with clinical status in SSPE. Pediatr. Neurol. 1986; 2: 75-9. Huber M., Herholtz K., Pawlik G., et al. Cerebral glucose metabolism in the course of subacute sclerosing panencephalitis. Arch. Neurol. 1989; 46: 97TIOO. Dhib-Jalbut S., Jacobson S., McFarlin D.E., et al. Impaired human leukocyte cytotoxic T-cell response in subacute sclerosing panencephalitis. Ann. Neurol. 1989; 25: 272-80. Dyken P.R., Swift A. & DuRant R.H. Long-term follow-up of patients with subacute sclerosing panencephalitis treated with inosiplex. Ann. Neurol. 1982; I 1 : 359--64. Steiner I., Wirguin I., Morag A. & Abramsky 0. Intraventricular interferon a treatment for subacute sclerosing panencephalitis. J. Child. Neurol. 1989; 4: 20-3. Homma S., Nakajima Y., Musha T., et al. Dipoletracing method applied to human brain potentials. J. Neuroscience Methods 1987: 21: 195-200. Radermecker J . & Poser C.M. The significance of repetitive paroxysmal electroencephalographic patterns. World Neurol. 1960: 1: 422-31. Kuroiwa S. & Celesia G.G. Clinical significance of periodic EEG patterns. Arch. Neurol. 1980: 37: 1520. Yoshinaga H.. Amano R. & Ohtahara S. Dipole tracing in childhood epilepsy with special reference to rolandic epilepsy. Brain Topography 1990; 3: 220. Tsutsui J. Dipole tracing on visual evoked potentials. Rinsho Noha 1991; 33: 6- 10 (in Jpn). Musha T. & Homma S. D o optimal dipoles obtained by dipole tracing methods always suggest true source locations? Brain Topography 1990: 3: 143--50.
Acta Paediatr Jpn
The origin 03 perzoatc events in SSPE (57) 3 15 18. Fenyo E. & Hasznos T. Periodic EEG complexes in subacute sclerosing panencephalitis: Reactivity, response to drugs and respiratory relationships. Electroencepha. Clin. Neurophysiol. 1964; 16: 44658.
Vol. 34 No. 3 June 1992
19. Ohya T., Martinez A.J., Jabbour J.T., et al. Subacute sclerosing panencephalitis, correlation of clinical, neurophysiologic and neuropathologic findings. Neurol. 1974; 24: 211-8.
- 315)
Case Reports
The Origin of Myoclonus and Periodic Synchronous Discharges in Subacute Sclerosing Panencephalitis Shinichi Yagi, M.D., Yo Miura, M.D., Naoki Kataoka, M.D., Shun Mizuta, M.D., Atsuko Wakunami, M.D. and Tetsuro Morita, M.D. Department of’Pediatrics, Kawasaki Medical School, Okayama
We report here a case of a patient with subacute sclerosing panencephalitis (SSPE) and we have analyzed periodic events using dipole tracing methods to clarify the origin of periodic synchronous discharges and myoclonus. Both source generators were located in the subcortical part of the cerebrum, an area adjacent to the thalamus. Although the pathophysiology of periodic events in SSPE has been controversial, dipole tracing methods may contribute to clarify the origin of periodic events in SSPE. Key Words
SSPE, Periodic events, Dipole tracing methods
Introduction Subacute sclerosing panencephalitis (SSPE) is now widely known as a slow virus infection of the central nervous system due to the measles virus. Since Dawson first reported and described it [I], there have been many neurophysiological and neuroradiological studies and immunological evaluations [2-91. In recent years, treatment with inosiplex andlor interferon a has been widely accepted [lo, 1 I]. but there have been few reports of a favorable outcome in SSPE. Despite recent
Received July 15. 1991 Revised Uovernher 18, 1991 Accepted December 6. 1991 Correspondence address: Shinichi Yagi, M.D., Department of Pediatrics, Kawasaki Medical School, 577 Matsushirna. Kurashiki-city, Okayarna 701-01, Japan
detailed studies, the pathophysiology of periodic synchronous discharges (PSD) on the electroencephalogram (EEG) and correlated myoclonus has been controversial. This study was undertaken to clarify the origin of PSD and myoclonus in SSPE using dipole tracing methods.
Case Report An eight year old girl was referred to us because of a tendency toward clumsiness and memory disturbance of several weeks duration. During the neonatal period, exchange transfusions were performed because of isoimmunization due to Rh incompatibility. At one year of age, she had a natural measles infection complicated by pneumonia which required hospitalization of about one week. Subsequently, she had been healthy until eight
The origin of periodic events in SSPE (53) 31 I years of age. Although she was alert and could follow simple commands on admission, she had an ataxic gait, echolalia and
dysdiadochokinesia dominantly in the left hand. The deep tendon reflexes of the left limbs were increased. A general examination
FPZ Fa F4 c4
T4 P4 T6 02 Fpl F7
F3 c3 T3 P3 T5 01 ECG
Fig. 1 : At the time myoclonus appeared, EEG shows SSPE complexes (arrow heads), and focal spikes and/or sharp waves are seen dominantly in the area of bilateral frontal head area.
Fig. 2: Simultaneous EEG-EMG records; arrow head indicates myoclonus of right thigh.
Vol. 34 No. 3 June 1992
3 I2 (54) Yagi ct al.
including routine hematological and biochemical findings was normal. The diagnosis of SSPE was based on an elevated measles antibody titer, not only in the serum but also in the cerebrospinal fluid (CSF). Her serum measles antibody titers were as follows, HI 256x, CF 512x, NT1024~. CSF measles antibody titers were also elevated to HI 32x, CF 32x, NT 128x and the protein level in the CSF was 52 rng/dl. In addition, oligoclonal IgG bands were strongly detected in the CSF. She had a neurological disability index of 24% and the disease was in clinical stage I. PSD were not seen in her EEG on admission. The patient was treated with inosiplex and interferon (I intrathecally, but she apeared
gradually to deteriorate mentally and neurologically. By the third week after admission dominant myoclonus of the right limbs as well as other involuntary movements had begun. When the myoclous become marked, her EEG revealed PSD. Currently, after a clinical course of six months, her NDI is 56% and the clinical stage of the disease is stage 11. Dipole tracing estimates Scalp potentials generated by concentrated electric sources in the brain are very similar to potentials generated by an electric dipole at the source position. In this sense a concentrated source in the brain is modelled as an electric dipole. Dipole tracing is a method for
Myoclonuscorrelated paroxysmal discharges (100.0 rnsec) LOC.(rnrn) Vec. x= 19.0 -7.31€+05 y= 15.0 -2.01E+05 Z= 6.8 6.12E+05 Mornent=9,74E+05 CH 8 Back
Mag : 0.25
Dipolarity=97.8%
,,A,
I
Axis : Y
Horisontal ,/-.
VEC. C A L : AVE.
Periodic synchronous discharges EEG DIPOLE -TRACING
p
100.ouv CH
'
Step
f-
,
'
(Vector) 13 Initial mint Dipole No. = 1 (103.2 rnsec) LOC.(rnrn) Vec. X= 14.9 -7.46E+05 Y= 8.3 1.82E+05 Z= 32.7 6.17E+05
Mag : o,25
Mornent=9.85E+05 Dipolarity=97.0%
I 4.42€+05
Axis : Y
Step
VEC. CAL: AVE.
Fig. , 3 : Dipole tracing estimates, top indicates the source generators of myoclonus associated with paroxysmal discharges and bottom shows source generators of SSPE complexes. Both electrical source generators are located in an area adjacent to the thalamus.
Acta Paediatr Jpn
R e origin of periodic events in SSPE (55) 313 estimating the localization and vector moment of electric source generator as an equivalent dipole from the distribution of electric potentials over the scalp. At the time myoclonus appeared, periodic synchronous discharges which occurred every 8 to 10 sec (Fig. 1 arrows) and myoclonus-correlated paroxysmal discharges (Fig. 2) over the scalp recorded on a data recorder were analyzed. EEG was performed with 21 electrodes on the scalp according to the international 10-20 system with the ear reference, and a signal processor 7T18 (NEC-Sanei) was used for these analyses. The dipoles were estimated from 10 points including the peak of each discharge. The location of the electric source generators of the PSD and myoclonusassociated paroxysmal discharges were analyzed using the dipole tracing methods [12]. As shown in Fig. 3, both electric source generators were located in an area adjacent to the thalamus. The source generators of myoclonus-associated paroxysmal discharges tended to be present more on the left side. The dipolarities (the validity of the dipole approximation) for both PSD and myoclonus associated discharges were more than 97%. Therefore these source generators could be expected to reveal optimal dipoles.
Discussion Since Radermecker’s description of periodic EEG patterns Characterizing SSPE [ 131, there have been investigations of the PSD in SSPE. It is well known that periodic EEG patterns occasionally occur in other diseases such as Jakob-Creutzfeldt disease, cerebral lipidosis, severe anoxic-encephalopathy and infections [14]. Many authors have suggested that these EEG abnormalities are caused by a disturbance in the function of certain brain structures. As yet, however, the origin of PSD in SSPE and other diseases has not. been established. In addition myoclonic jerks, one of the characteristic clinical features of SSPE, have been observed during the clinical course of stage 11. Myoclonus is a general term that refers to rapid muscle jerking, but myoclonic jerks in
Vol. 34 No. 3 June 1992
patients with SSPE are often quite prolonged and also show a tendency to be periodic. Although most studies have shown a one to one relationship between myoclonic jerks and PSD in SSPE, some studies based on detailed simultaneous recordings of electromyograms (EMG) and EEGs have revealed variable patterns between PSD and myoclonic jerks [2, 41. Cobb indicated that EMG changes usually began somewhat after the onset of EEG complexes [2]. Celesia, on the other hand, reported that muscle potential tended to precede the EEG complexes by 200-800 msec. in one case. In two other cases, however, there was poor correlation between muscle potentials and EEG [4]. Similar cases were also described by Lombroso [3]. These previous reports involved analysis of simultaneous EMG-EEG records and various kinds of evoked potential, but to our knowledge, there has been no previous attempt to make dipole tracing estimates of the source generators of PSD and myoclonus-associated paroxysmal discharges. The dipole tracing methods are based on a realistic head model which has uniform electrical conductivity [121. Recently, there have been a few studies describing the efficacy of these new techniques for estimating the localization and vector moment of source generators from the distribution of electric potentials over the scalp, such as focal spikes in epilepsy and/or evoked potentials [15, 161. There are certain problems involved in estimating the accuracy of the source generators analyzed by the dipole tracing methods. There are two major difficulties inherent in this method such as that the low electric conductivity of the skull causes systematic shifts of the optimal dipoles positions from the true position of concentrated sources and/or the optimal dipoles cannot specify diffuse source positions. Therefore, Homma and Musha have proposed that dipolarities of 98% are required for optimal dipoles [171. In the present case, both source generators were surprisingly located in the subcortical part of the cerebrum, an area adjacent to the
3 I4 ( 5 6 ) Yagi et a/. thalamus, and both generators had dipolarities of over 97%. The authors assumed that analyzed paroxysmal discharges accompanied by myoclonic jerks correlate closely with individual myoclonus. Thus. we believe that the present source generators which were analyzed during discharges of myoclonic jerks also reflect the origin of myoclonus in this case. It seems possible that electrical periodic events take place in all parts of the brain. Celesia suggested that a severe impairment of the cortical-subcortical structures is necessary for SSPE complexes to appear [4]. Fenyo and Hasznos on the other hand, indicated that such periodic events have a brain stem origin which they confirmed by pharmacological studies [ 181. They noted that regular complexes may be replaced by irregular delta activities after the administration of mephenesin, a drug which blocks the diffuse thalamic system. Cobb also proposed the brain stem as the site of the origin of electrical periodic events and assumed that these periodic events require a functional cortex rather than severe cortical damage [2]. Neuropathologically, Ohya tends to believe that the SSPE complexes are indicative of relative preservation of the cortex and later severe cortical damage seems to cause disappearance of the SSPE complexes [19]. Of additional interest have been studied regarding the association between ocular jerks and both peripheral EMG and EEG discharges reported by Lombroso [3]. He noted the occurrence of ocular jerks 500 to 1,200 msec. before myoclonic limbs jerks and/or the PSD on EEG. Such a timelag suggests that the initial electrical event originates from the reticular formation of the pons and/or midbrain. Subsequently, eye movement secondary to excitation of the oculomotor nuclei and. later, myoclonic limb jerks and PSD may be observed. The author wishes to emphasize the importance of the existence of variable neurological conditions in SSPE individually. Although further studies are required, the dipole tracing methods may contribute to clarification of the pathophysiology of the characteristic periodic events in SSPE.
Acknowledgements The autKors wish to thank Miss Eiko Matsuda and Miss Yoko Tetsukura for their excellent technical assistance.
References I. 2. 3. 4.
5. 6.
7.
8.
9.
10.
1 I.
12.
13. 14. 15. 16.
17.
Dawson J.R. Cellular inclusions in cerebral lesions of epidemic encephalitis. Arch. Neurol. Psychiatry 1934: 31: 685-700. Cobb W. The periodic events of subacute sclerosing leukoencephalitis. Electroenceph. Clin. Neurophysiol. 1966; 21: 278-94. Lombroso C.T. Remarks on the EEG and movement disorder in SSPE. Neurol. 1968; 18-part 2: 69-75. Celesia G.G. Pathophysiology of periodic EEG complexes in subacute sclerosing panencephalitis (SSPE). Electroenceph. Clin. Neurophysiol. 1973: 35: 293-300. Markand 0 . N . & Pans7i J.G. The electroencephalogram in subacute sclerosing panencephalitis. Arch. Neurol. 1975; 32: 719-26. Miyake S., Yoshida H., lnoue H., et al. Subacute sclerosing panencephalitis. A clinical and electroencephalographic study. No To Hattatsu 1985: 17: 29-36 (in Jpn). Lum (3.9.. Williams J.P., Dyken P.D., et al. Magnetic resonance and CT imaging correlated with clinical status in SSPE. Pediatr. Neurol. 1986; 2: 75-9. Huber M., Herholtz K., Pawlik G., et al. Cerebral glucose metabolism in the course of subacute sclerosing panencephalitis. Arch. Neurol. 1989; 46: 97TIOO. Dhib-Jalbut S., Jacobson S., McFarlin D.E., et al. Impaired human leukocyte cytotoxic T-cell response in subacute sclerosing panencephalitis. Ann. Neurol. 1989; 25: 272-80. Dyken P.R., Swift A. & DuRant R.H. Long-term follow-up of patients with subacute sclerosing panencephalitis treated with inosiplex. Ann. Neurol. 1982; I 1 : 359--64. Steiner I., Wirguin I., Morag A. & Abramsky 0. Intraventricular interferon a treatment for subacute sclerosing panencephalitis. J. Child. Neurol. 1989; 4: 20-3. Homma S., Nakajima Y., Musha T., et al. Dipoletracing method applied to human brain potentials. J. Neuroscience Methods 1987: 21: 195-200. Radermecker J . & Poser C.M. The significance of repetitive paroxysmal electroencephalographic patterns. World Neurol. 1960: 1: 422-31. Kuroiwa S. & Celesia G.G. Clinical significance of periodic EEG patterns. Arch. Neurol. 1980: 37: 1520. Yoshinaga H.. Amano R. & Ohtahara S. Dipole tracing in childhood epilepsy with special reference to rolandic epilepsy. Brain Topography 1990; 3: 220. Tsutsui J. Dipole tracing on visual evoked potentials. Rinsho Noha 1991; 33: 6- 10 (in Jpn). Musha T. & Homma S. D o optimal dipoles obtained by dipole tracing methods always suggest true source locations? Brain Topography 1990: 3: 143--50.
Acta Paediatr Jpn
The origin 03 perzoatc events in SSPE (57) 3 15 18. Fenyo E. & Hasznos T. Periodic EEG complexes in subacute sclerosing panencephalitis: Reactivity, response to drugs and respiratory relationships. Electroencepha. Clin. Neurophysiol. 1964; 16: 44658.
Vol. 34 No. 3 June 1992
19. Ohya T., Martinez A.J., Jabbour J.T., et al. Subacute sclerosing panencephalitis, correlation of clinical, neurophysiologic and neuropathologic findings. Neurol. 1974; 24: 211-8.
