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EEG observations in a case with thalamic syndrome
CASE REPORTS EEG O B S E R V A T I O N S IN A CASE W I T H T H A L A M I C S Y N D R O M E 1 GEORG F. HENR1KSEN, M.D., CHASKIEL GaOSSMAN, M.D. and JEROME K. M~RLtS, M.D.
National Veterans Epilepsy Center, Cushing Veterans Administration Hospital, Framingham, Massachusetts There are few data in the literature concerning the electroencephalographic findings in the human with lesions of the thalamus. The few reports available are concerned with tumors of subcortical location. In these cases there are the obvious difficulties of poorly defined anatomical boundaries or localization of the lesion plus the additional complicating factors of increased intracranial pressure, edema, etc. These difficulties may be considered to be minimized in the chronic stage of an intrathalamic thrombosis. W e have recently had the opportunity to study a case with a classical thalamic syndrome, presumably of vascular origin, which presented electroencephalographic findings of interest. W e have followed the case with E E G studies from five weeks to two years after the onset of symptoms. DESCRIPTION
OF T H E CASE
slight left-sided facial paresis and a slight tongue deviation to the left. A slight awkwardness in performing fine movements with the left hand was noted. There were no other disturbances in the motor sphere. During the summer of 1947 the patient began to suffer from severe burning sensations in the left arm, left flank, left testicle and front of the leg. The burning pains were worse at night, interfering with sleep. These pains have continued for two years. During re-examination in June, 1948 and April, 1949, no motor weakness was found but his hemi-hypasthesia for all qualities and his dysesthesia with diminished stereognostic sense of the left hand persisted, as did the spontaneous burning pains. Thus the patient presented a typical picture of thalamic syndrome of D6jerlae-Roussy.
On the night of March 16, 1947 the patient, a 55 year old policeman, suddenly experienced a left facial paresis which he stated cleared up overnight. He found, however, that his left arm and hand had no sense of pain and temperature and he suffered cigarette burns of the fingers as a consequence. He was admitted to the hospital four days later and neurological examination done on admission revealed: left attention hemianopia, left facial paresis of supranuclear type, slight tongue deviation to the left and sensibility to pain, temperature and touch abolished completely on the left side of the face and body. He showed severe burn scars on the fingers of the left hand. Position and vibratory sense were absent in the fingers and wrist of the left hand. On re-examination June 25, 1947, three months after the onset, the patient could appreciate light touch and pin-prick on previously anesthetic parts, but the sensation had an unusual character and although temperature sense had returned to some de. gree it still showed marked impairment, There was a
EEG STUDIES E E G studies were performed on ten different occasions from April, 1947 to April, 19't9, all showing essentially the same findings, The records were obtained with a four channel and later with an eight channel Grass ink-writing machine, using 16 electrode placements and "Monopolar" as well as "Bipolar" tracings. A
I Published with permission of the Chief Medical Director, Department of Medicine and Surgery, Veterans Administration, who assumes no responsibility for the opinions expressed or conclusions drawn by the author.
Fig. 1 Recording with patient awake. A ~ Bilateral symmetrical alpha activity. B - - R u n s of 4 7 per second waves appearing only on the right side.
k0
RO
tO
[ 505 ]
6
t
506
G E O R G F. H E N R I K S E N , C H A S K I E L G R O S S M A N and J E R O M E K. MERLIS
In the waking E E G there ",,,'ere periods of normal, bilaterally symmetrical occipital alpha (fig. IA). However. alpha activity on the right was unstable, with 4 to 7 per sec. slow waves of low to medium voltage appearing in irregular runs (fig. 1B). These waves were also prominent in the parietal leads and much less so in the frontal and temporal leads. This picture resembled closely that seen in the drowsy stage of normal sleep, but it is noteworthy that it appeared only in the right hemisphere. Natural sleep recording was attempted but was unsuccessful because of spontaneous thalamic pains. Sleep was therefore induced with seconal. In the drowsy stage of induced sleep, the right hemisphere manifested the changes described above, these changes appeared in the left hemisphere at a later period, so that the E E G presented the usual picture of the drowsy stage. Durieg the spindle-slow wave stage of sleep, 10 to I I per sec. spindles appeared in the frontal leads and 14 per see. in the parietal, simultaneously. These spindles were markedly reduced or absent in the leads from the right hemisphere (fig. 2).
RF
t P~t C
~c
DISCUSSION The pathology of the thalamic syndrome is well established as being due to involvement of the ventrolateral nuclei. In the case presented the involvement of the face would also indicate pathology in the postero-medial ventral nucleus (Walker'. 1939). The absence of severe motor symptoms and the delay of two months before the onset of thalamic pain indicate the probability that thrombosis rather than hemorrhage was the underlying pathological process. Electroencephalographically the fundamental disturbance in this case appears to be one in the mechanisms for rhythmic activity in the brain. On the side of the lesion there is an early disappearance of alpha, and during deeper sleep a diminution or absence of spindles on the affected side. Rhythmic activity in the cortex appears to be dependent on the integrity of subcortical structures ( W a l t e r and Dovey, 1944; LIlett, 1945) and in particular, upon integration functions of the thalamus (Morison and Bassett, 194"5; Murphy and Gellhorn, 1945; Jasper and Droogleever-Fortuyn, 1947). As pointed out previously, the potentiality for rhythmic activity is present in our patient, for during the waking state alpha rhythm may appear equally bilaterally. It may be considered that the initial disturbance in rhythmical activity appearing on the right during the waking E E G actually represents the earliest manifestation of the drowsy stage of sleep, as though the right cortex is going to sleep before the left. The asymmetry is more definitely evident dur, ing deeper stages of sleep. It is well established that the hypothalamus plays a great role in the sleep mechanism. There is little data on the participation of the hypothalamus in the electrical activity characteristic of sleep. Murphy and Gelthorn have presented evidence that "Dial Bursts" appear synchronously in the hypothalamus, ventrolateral and medial-dorsal nuclei of the thalamus, and the cortex. The same authors report that stimulation of the hypothalamus abolishes the spindles in the cortex of cats. The integration of the thalamus and the hypothalamus in the sleep mechanism would appear to merit further investigation. SUMMARY
RP
i¢,
I
Fig. 2 Recording during seconal induced sleep. 10-11 pet second spindles frontally and 14 per second spindles parietally are reduced in voltage on right side.
A case of thalamic syndrome of the D~jerineRoussy type is presented. E E G studies reveal that although bilaterally symmetrical rhythmic activity may be present when the patient is awake, during drowsiness and deeper sleep a marked asymetry often appears, with early disappearance of alpha activity and reduction or abolition o[ spindles on the side involved.
E E G O B S E R V A T I O N S IN A C A S E W I T H T H A L A M I C S Y N D R O M E Thalamic integration in the sleep mechanism is briefly discussed. REFERENCES JASPER. H. H. and DROOCI.EEVER-FoR'rUYN, ]. Experimental studies on the Functional anatomy ol petit mal. Res. Publ. Ass. neru. inert. Dis., 194'/, 26: 272-298. Moltlsoba R, S. and BASSE'rT, D. L. Electrical activity of the thalamus and basal ganglia in decorticate cats. I. Neuroph!lsiol., 1945, 8: 309-314.
507
MURPHY. ]. P. and GELLHORN, E. Further investigations on diencephalic-cortical relations and their significance for the problem of emotion. ~. Neurophysiol., 194fi, 8: 431-447. Lh.Err. G. Electroencephalogram of dogs with experimental space occupyin o intracranial lesions. Arch. Neurol. Ps~,chiat.. Chica9o, 1945, 54: 1411"t9, WALKER, A. E. The primate thalamus, Chicago, The University of Chicago Press, 1939. 321 pp. V/ALTER, W. G. and DovEY, V. ]. Electroencephalography in cases of subcortical tumor. ]. Neurol. Neurosnr!:]. Psychiat., 1944, 7: 57-65.
Reference: HENRIKSEN, G. F., GROSSMAN, C. and MERLIS, J. K. EEG observations in a case with thalamic syndrome. EEG
Clin. Neurophgsiol.,
1949, 1: 505-507.
National Veterans Epilepsy Center, Cushing Veterans Administration Hospital, Framingham, Massachusetts There are few data in the literature concerning the electroencephalographic findings in the human with lesions of the thalamus. The few reports available are concerned with tumors of subcortical location. In these cases there are the obvious difficulties of poorly defined anatomical boundaries or localization of the lesion plus the additional complicating factors of increased intracranial pressure, edema, etc. These difficulties may be considered to be minimized in the chronic stage of an intrathalamic thrombosis. W e have recently had the opportunity to study a case with a classical thalamic syndrome, presumably of vascular origin, which presented electroencephalographic findings of interest. W e have followed the case with E E G studies from five weeks to two years after the onset of symptoms. DESCRIPTION
OF T H E CASE
slight left-sided facial paresis and a slight tongue deviation to the left. A slight awkwardness in performing fine movements with the left hand was noted. There were no other disturbances in the motor sphere. During the summer of 1947 the patient began to suffer from severe burning sensations in the left arm, left flank, left testicle and front of the leg. The burning pains were worse at night, interfering with sleep. These pains have continued for two years. During re-examination in June, 1948 and April, 1949, no motor weakness was found but his hemi-hypasthesia for all qualities and his dysesthesia with diminished stereognostic sense of the left hand persisted, as did the spontaneous burning pains. Thus the patient presented a typical picture of thalamic syndrome of D6jerlae-Roussy.
On the night of March 16, 1947 the patient, a 55 year old policeman, suddenly experienced a left facial paresis which he stated cleared up overnight. He found, however, that his left arm and hand had no sense of pain and temperature and he suffered cigarette burns of the fingers as a consequence. He was admitted to the hospital four days later and neurological examination done on admission revealed: left attention hemianopia, left facial paresis of supranuclear type, slight tongue deviation to the left and sensibility to pain, temperature and touch abolished completely on the left side of the face and body. He showed severe burn scars on the fingers of the left hand. Position and vibratory sense were absent in the fingers and wrist of the left hand. On re-examination June 25, 1947, three months after the onset, the patient could appreciate light touch and pin-prick on previously anesthetic parts, but the sensation had an unusual character and although temperature sense had returned to some de. gree it still showed marked impairment, There was a
EEG STUDIES E E G studies were performed on ten different occasions from April, 1947 to April, 19't9, all showing essentially the same findings, The records were obtained with a four channel and later with an eight channel Grass ink-writing machine, using 16 electrode placements and "Monopolar" as well as "Bipolar" tracings. A
I Published with permission of the Chief Medical Director, Department of Medicine and Surgery, Veterans Administration, who assumes no responsibility for the opinions expressed or conclusions drawn by the author.
Fig. 1 Recording with patient awake. A ~ Bilateral symmetrical alpha activity. B - - R u n s of 4 7 per second waves appearing only on the right side.
k0
RO
tO
[ 505 ]
6
t
506
G E O R G F. H E N R I K S E N , C H A S K I E L G R O S S M A N and J E R O M E K. MERLIS
In the waking E E G there ",,,'ere periods of normal, bilaterally symmetrical occipital alpha (fig. IA). However. alpha activity on the right was unstable, with 4 to 7 per sec. slow waves of low to medium voltage appearing in irregular runs (fig. 1B). These waves were also prominent in the parietal leads and much less so in the frontal and temporal leads. This picture resembled closely that seen in the drowsy stage of normal sleep, but it is noteworthy that it appeared only in the right hemisphere. Natural sleep recording was attempted but was unsuccessful because of spontaneous thalamic pains. Sleep was therefore induced with seconal. In the drowsy stage of induced sleep, the right hemisphere manifested the changes described above, these changes appeared in the left hemisphere at a later period, so that the E E G presented the usual picture of the drowsy stage. Durieg the spindle-slow wave stage of sleep, 10 to I I per sec. spindles appeared in the frontal leads and 14 per see. in the parietal, simultaneously. These spindles were markedly reduced or absent in the leads from the right hemisphere (fig. 2).
RF
t P~t C
~c
DISCUSSION The pathology of the thalamic syndrome is well established as being due to involvement of the ventrolateral nuclei. In the case presented the involvement of the face would also indicate pathology in the postero-medial ventral nucleus (Walker'. 1939). The absence of severe motor symptoms and the delay of two months before the onset of thalamic pain indicate the probability that thrombosis rather than hemorrhage was the underlying pathological process. Electroencephalographically the fundamental disturbance in this case appears to be one in the mechanisms for rhythmic activity in the brain. On the side of the lesion there is an early disappearance of alpha, and during deeper sleep a diminution or absence of spindles on the affected side. Rhythmic activity in the cortex appears to be dependent on the integrity of subcortical structures ( W a l t e r and Dovey, 1944; LIlett, 1945) and in particular, upon integration functions of the thalamus (Morison and Bassett, 194"5; Murphy and Gellhorn, 1945; Jasper and Droogleever-Fortuyn, 1947). As pointed out previously, the potentiality for rhythmic activity is present in our patient, for during the waking state alpha rhythm may appear equally bilaterally. It may be considered that the initial disturbance in rhythmical activity appearing on the right during the waking E E G actually represents the earliest manifestation of the drowsy stage of sleep, as though the right cortex is going to sleep before the left. The asymmetry is more definitely evident dur, ing deeper stages of sleep. It is well established that the hypothalamus plays a great role in the sleep mechanism. There is little data on the participation of the hypothalamus in the electrical activity characteristic of sleep. Murphy and Gelthorn have presented evidence that "Dial Bursts" appear synchronously in the hypothalamus, ventrolateral and medial-dorsal nuclei of the thalamus, and the cortex. The same authors report that stimulation of the hypothalamus abolishes the spindles in the cortex of cats. The integration of the thalamus and the hypothalamus in the sleep mechanism would appear to merit further investigation. SUMMARY
RP
i¢,
I
Fig. 2 Recording during seconal induced sleep. 10-11 pet second spindles frontally and 14 per second spindles parietally are reduced in voltage on right side.
A case of thalamic syndrome of the D~jerineRoussy type is presented. E E G studies reveal that although bilaterally symmetrical rhythmic activity may be present when the patient is awake, during drowsiness and deeper sleep a marked asymetry often appears, with early disappearance of alpha activity and reduction or abolition o[ spindles on the side involved.
E E G O B S E R V A T I O N S IN A C A S E W I T H T H A L A M I C S Y N D R O M E Thalamic integration in the sleep mechanism is briefly discussed. REFERENCES JASPER. H. H. and DROOCI.EEVER-FoR'rUYN, ]. Experimental studies on the Functional anatomy ol petit mal. Res. Publ. Ass. neru. inert. Dis., 194'/, 26: 272-298. Moltlsoba R, S. and BASSE'rT, D. L. Electrical activity of the thalamus and basal ganglia in decorticate cats. I. Neuroph!lsiol., 1945, 8: 309-314.
507
MURPHY. ]. P. and GELLHORN, E. Further investigations on diencephalic-cortical relations and their significance for the problem of emotion. ~. Neurophysiol., 194fi, 8: 431-447. Lh.Err. G. Electroencephalogram of dogs with experimental space occupyin o intracranial lesions. Arch. Neurol. Ps~,chiat.. Chica9o, 1945, 54: 1411"t9, WALKER, A. E. The primate thalamus, Chicago, The University of Chicago Press, 1939. 321 pp. V/ALTER, W. G. and DovEY, V. ]. Electroencephalography in cases of subcortical tumor. ]. Neurol. Neurosnr!:]. Psychiat., 1944, 7: 57-65.
Reference: HENRIKSEN, G. F., GROSSMAN, C. and MERLIS, J. K. EEG observations in a case with thalamic syndrome. EEG
Clin. Neurophgsiol.,
1949, 1: 505-507.