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The electroencephalogram in essential hypertension and chronic cerebrovascular disease
T H E E L E C T R O E N C E P H A L O G R A M IN ESSENTIAL HYPERTENSION A N D C H R O N I C C E R E B R O V A S C U L A R DISEASE J. A. RoeEa'rs a n d M.
WALKI~, B.Sc.
Maida Vale Hospital ~or Nervous D/seases, London
(Received for publication: March 22, 1954) INTRODUCTION
in no way different from those observed in In this paper the results are presented of many patients subject to clinical paroxysmal an analysis of 104 patients with essential disturbances. In commenting on this figure hypertension and cerebral arteriosclerosis Cohn et al. pointed out that records with undertaken primarily to correlate the E E G high frequency activity but without slow waves were not considered abnormal in this findings with epilepsy in this disease. The literature on the subject is not exten- series. CASE MATERIAL sive. Bagehi et al. (1950), in 84 patients with essential or malignant hypertension, One hundred and four patients were found moderately or very abnormal E E G s investigated. They fell into 3 groups: 1. Esin 25 per cent as compared with 6 per cent in sential hypertension, 27 cases. 2. Hypertena control group of 52, and these figures were sion with neurological signs and symptoms, statistically significant even after the exclu- 69 cases. 3. Neurological signs and sympsion of cases with a history of eneephalopathy toms without hypertension, 8 cases. The ages or cerebro-vascular accident. No specific E E G of these patients (57 male, 47 female), were pattern was noted and no correlation was from 21 to 78 years with 70 per cent within found with the duration of the condition or the range 45 to 65. The E E G s were taken by the degree of blood pressure nor with any the usual routine methods on 6 or 8 channel signs or symptoms of the disease. Abnormal Ediswan electroencephalographs. records were found more often when there 1. ESSENTIAL HYPERTENSION was a history of cerebro-vascular accident or severe hypertensive encephalopathy; None of the 27 patients in this group had patients with a history of eerebro-vaseular clinical evidence of eerebro-vascular disease accident showing localizing signs in the E E G although in 9 instances there was some degree tended to have a greater background ab- of peripheral or retinal arteriosclerosis. Their normality than those without such localising ages were between 21 and 71 years w i t h an signs. Rohmer ¢t al. (1952), in a series of average of 53. Fourteen or 51.8 per cent had 60 cases of hypertension, found 28 with ab- definitely abnormal EEGs. These were of normal EEG s but of the rest only 7 were many different types but an abnormal definitely abnormal and 12 slightly abnormal amount of slow activity was the most conwhile 13 were doubtful, i.e. a 33 per cent ab- stant feature and in only one trace was it normality. Two of the definitely abnormal minimal. Fast activity was present in widely EEGs were charaeterised by their very low varying relative amounts and amplitudes and potential and prominence of fast activity; in 6 cases was conspicuous or dominant (fig. otherwise the findings were not described in 1). In two of these it occurred at the lower detail. Cohn ¢t al. (1948), investigated a frequency limits as a 14 to 18 c/see, rhythm of large number of patients with arterial hyper- alpha distribution; otherwise it was of higher tension but without evidence of gross cerebral frequency and was generalised or of highest lesions. They found abnormal EEGs in 25 amplitude in the frontal and central leads. per cent of cases. The EEGs usually showed Sharp waves were present in many of the prominent fast and slow activity and were records but were of high potential and uni[ 461 ]
462
J . A . ROBERTS and M. W A L K E R
lateral in only 2. Another trace with unilateral features had runs of 10 c/see. "flattopped" waves in one of the central leads. 2. H Y P E R T E N S I O N W I T H NEUROLOGICAL SIGNS AND SYMPTOMS
No case was included in which there was a family history of epilepsy or in which epilepsy had occurred in early life. In none was there a history of hypertensive encephalopathy or of recent thrombosis or vascular accident.
( a ) Neurological signs and symptoms other than epilepsy The 45 patients in this group presented varying degrees of organic dementia with or
generalised abnormalities fast activity was appreciable in 20; in 5 of these it was prominent and in a further 3 it was dominant and continuous at 12-20 c/sec. Random sharp waves occurred in 10 cases and in 4 were more marked on one side or the other. Three traces were somewhat paroxysmal. Every record showed slow activity but this was not greater in amount or in amplitude than that occurring in some of the simple hypertensives. Many of the patients in this group had clinical evidence of focal cerebral lesions but no EEG correlate of these was apparent. The remaining 10 patients had focal electroencephalographic abnormalities. Of these, 9 had focal slow activity at I to 5 c/sec. (fig. 3), in two instances associated with focal sharp
F. age 62, B.P. 260/100. Prominent fast a~tivity in a ease of simple hypertension.
without neurological signs such as hemiplegia, hemianopia, aphasia, pseudo-bulbar palsy or Parkiusonism. Their ages ranged from 38 to 74 years with an average of 58. Thirty seven or 82.2 per cent as compared with 51.8 per cent in the hypertensive group, had abnormal
EEGs. These (fig. 2), were similar to those already described under simple hypertension with the exception of one trace which was grossly abnormal. Of the 26 cases showing
waves and in two others occurring against a background of random delta waves; the last case had focal sharp wave activity only. In 5 of these 10 patients the electroencephalographic focus could be correlated with a cerebral lesion as indicat~l by hemiplegia or aphasia but the other 5 showed no such clinical correlate though the general signs and symptoms of cerebrovaseular disease were severe.
463
E E G I N H Y P E R T E N S I O N AND CEREBROVASCUT,AR D I S E A S E
The grossly abnormal trace was seen in a patient of 67, blood pressure 160/105, who had a history of 7 years mental deteriora-
tion, slowness of movements and dysphasia. Slow activity at frequencies down to 1 c/see. was prominent, the slowest waves often bila-
~opv Fig. 2 M. age 69., B.P. 210/115. Hypertension with mental deterioration. abnormal amount of diffuse slow activity.
~A
M
M
M. age 58, B.P. 200/115. present on the left.
~t
M ~
~
Fig. 3 Hypertension with gross aphasia.
~
The EEG shows an
A
Focal delta
activity is
464
J . A . ROBERTS and M. W A L K E R
terally synchronous and at amplitudes of 65 ~V. ; little activity faster than 8 c/sec, was present (fig. 4).
(b) Epilepsy There were 24 patients in this group. Their ages were between 37 and 76 years with an average of 61 years. In 20 the epilepsy was the only symptom of importance. The remaining 4 presented, in addition to the epilepsy, moderate or severe mental deterioration in one case with widespread focal signs. The epilepsy in 12 cases consisted of grand real attacks which were relatively infrequent,
abnormal. The abnormalities were similar ~ those already described for the cases without epilepsy, except that on the whole they were somewhat more pronounced. Of the 12 patients with grand real, 5 had E E G s with generalised and prominent fast activity while 3 others showed occasional delta waves which in one case were focal. In only 2 E E G s was there any tendency to p ~ r oxysmal build up and spread of potentials. The 2 patients with Jacksonian attacks and 2 of those with psychomotor attacks showed widely varying abnormalities of the types already described. The third psychomotor case
~--4~ Fig. 4 M. age 67, B.P. 160/105. Hypertension. Mental deterioration, slowness of movements and dysphasia. A very abnormal EEG showing diffuse slow activity throughout.
in one instance occurring only in the night; in 3 the attacks were mainly psychomotor and in 2 others were brief sensory Jaeksonian. Seven patients had brief akinetic attacks only. In these, generally when walking, the patient without warning suddenly falls to the ground or on to the knees. He does not remember falling and the loss of consciousness is so brief that he is often doubtful of its occurrence. Recovery is immediate, the patient rising quickly and continuing as before unless h u r t by the fall. All E E G s in this group were
had a more abnormal E E G (fig. 5). Fast activity was present in the central areas; slow activity was prominent and diffuse and occasionally occurred as bilateral and synchronous paroxysms at delta frequencies. In this last ease, where severe mental deterioration was an important clinical feature, the diagnosis of cerebral arteriosclerosis was verified at autopsy. Five of the 7 patients with akinetic attacks had prominent fast activity. In 2 of the 3 cases where it was dominant it was of
465
EEG IN HYPERTENSION AND CEREBROVASCULAR DISEASE highest a m p l i t u d e in the f r o n t a l and central leads (fig. 6), while in the t h i r d it was present as a slower 15 to 16 e/see, r h y t h m of alpha distribution.
Of the r e m a i n i n g 2 patients one showed generalised p a r o x y s m s of slow a n d fast frequencies a n d the other bursts of u n i l a t e r a l i r r e g u l a r delta activity.
) 5o/,v Fig. 5 M. age 66, B.P. 220/120. Hypertension with mental deterioration and psyehomotor epilepsy. Fast activity is prominent in the central leads, slow activity is present diffusely and there are occasional bursts at delta frequencies. .__
•
i
~
*
R
i
¢
,
|
,
I °p
~"h"g. 6 F. are 59, B.P. 170/100. Hypertension and akinetie epilepsy. Fast activity is dominent.
466
J . A . ROBERTS and M. W A L K E R
CEREBRAL ARTERIOSCLEROSIS WITHOUT HYPERTENSION
Few patients of this type are seen in neurological clinics and only 8 in our series fell definitely into this group. A brief statement of the E E G findings is given for comparison with the other cases but it is realized that a study of larger numbers drawn from special hospitals for the aged might give a different picture. These patients were between 51 and 74 years with an average of 61. All had evidence of retinal or peripheral arteriosclerosis. The diagnosis of cerebral arteriosclerosis was made on the basis of focal cerebral thrombosis or a history of progressive dementia or epilepsy for which no other cause could be demonstrated. In every case the E E G was abnormal and on the whole slow activity was the most prominent feature. Of the 4 cases without epilepsy the abnormalities were not marked in 2 where only a temporary weakness of a limb had occurred, but in 2 others with symptoms of progressive dementia and paralysis agitans respectively slow activity at frequencies down to 2 c/sec. was widespread and dominant. Two of the remaining 4 patients had akinetic attacks and 2 had grand mal attacks. The trace in one of the grand mal cases was slightly paroxysmal but otherwise there were no features of note. DISCUSSION
In this study of the E E G in hypertension and chronic cerebro-vascular disease an 80 per cent incidence of abnormality is reported. This is much higher than that described in other papers but all cases included in our series are without doubt abnormal by our criteria. The E E G abnormalities described here and elsewhere do not merit detailed discussion. It would appear reasonably well established that in simple hypertension a generalized abnormality consisting of irregularity of the alpha r h y t h m with excess of fast and slow waves may be found in 25 to 50 per cent of cases. Fast activity is sometimes a prominent feature and occasionally theta and delta frequencies are dominant. More rarely there is paroxysmal synchronization.
As pointed out by Bagchi et al. (1950), there is no correlation between the h y p e r t e m sion and the E E G abnormality, indeed, in some patients with long standing and high blood pressure, the records are within normal limits. W h e n there is vascular damage to the brain in addition to the hypertension the incidence of electroencephalographic abnormality increases greatly (90 per cent in our series). A focal electroeneephalographic abnormality, when present, can sometimes be correlated with a thrombotic lesion, but frequently no clinical signs of a gross structural lesion can be found in the presence of ~ definite electroencephalographic focus. It would appear that the greater the ccrebrovascular disturbance, as evidenced by clinical symptoms, the greater is the likelihood of an abnormal E E G pattern. The factual basis for this generalisation is strengthened by the occurrence of a very abnormal E E G in a patient with progressive mental deteriora~ tion of 7 years duration, and the presence o[ considerable abnormality in all 8 cases of cerebral arteriosclerosis without hypertension. Nevertheless, it must be emphasized that, in 8 patients with hypertension and definite signs of cerebral damage normal E E G s were recorded, and no noteworthy difference could be detected between the clinical history in these cases and those with the abnormal EEGs. In this series of 104 patients with hypertension and cerebrovascular disease, 77 had neurological signs and symptoms. Of these 24 or 36 per cent had epilepsy. This figure emphasizes the importance of epilepsy as a symptom in cerebro-vascular disease. With the possible exception of typical petit mal the epileptic manifestations may be of any type, but grand mal attacks and akinetic attacks appear to be the most common. There is a 100 per cent E E G abnormality in these patients with epilepsy. The patterns are, on the whole, similar in type to those without epilepsy and in only 4 cases (one akinetic and 3 grand mal) was there a n y tendency to paroxysmal synchronization. The findings then in these patients bear out the statement of Strauss and Greenstein (1948), that ep-
EEG IN HYPERTENSION AND CEREBROVASCULARDISEASE ilepsy in eerehro-vas~ular disease is not assoeiated with characteristic interseizure patterns in the EEG. A consideration of the findings in this series makes evident that the E E G abnormalities, despite their absence in a considerable number of cases, must be directly attributed to the vascular disease. This is suggested by the high initial incidence of abnormality and by the fact that repeat recordings in 12 patients, at long intervals, showed increasing abnormality. I f this is so, then 2 questions arise. What is the significance of the EEG abnormalities, and why arc they absent in a large number of eases .~ It is clear from what has been said that epilepsy as a symptom is in no way a significant factor. The presence of considerable abnormality in the cases of simple hypertension suggests that E E G changes can result from abnormal functioning of the cerebral vessels or from variation in blood flow within the arteriole and capillary bed. Here the observations of Darrow and Graf (1945), are of interest. These workers were able to show by careful experimental technique that vasodilatation of the cerebral vessels was associated with increase in frequency and potential of the fast waves whereas vasoconstriction decreased the frequency and increased the potential of the slow waves. It is probable, therefore, that widespread variations in the functional state of the cerebral vessels may give rise in some way to the combination of diffuse excess of fast and slow activity which so often characterises the EEG in cerebro-vascular disorders. Further support is given to this conception by the work of Engel et al. (1944), who found focal slow activity in the occipital regions during an experimentally produced migraine-like syndrome, when a circulatory disturbance of some kind was almost certainly present. It would be useless in the present state of knowledge to speculate as to how the circulatory disturbances act. Many chemical changes in the external milieu of the neurones
467
must occur as a result of even slight vascular changes and it is reasonable to suppose that these can alter the pattern of the electrotonic potentials of the brain, potentials which, in any ease, are possibly only an indirect sign of neural functioning. It may be that the severe abnormalities seen in some of the eases of simple hypertension are caused by more intense local circulatory changes producing, in some eases, minimal brain haemorrhage or ischemia. When there is widespread hyaline necrosis of the vessels with cerebral damage in addition to the hypertension, as might be expected the percentage abnormality increases greatly (90 per cent for groups 2 and 3). Sometimes the EEG changes may be very marked and in such cases the clinical disturbance of function, both mental and physical, is often severe. The importance of cerebral damage is further suggested by the presence of fairly severe EEG abnormalities in every one of our 8 cases of cerebro-vascular disease without hypertension. There remains the difficult problem of the normal EEG, not only in the simple hypertensive, but also in the cases of hypertension with neurological signs and symptoms where in 8 such patients the clinical histories did not differ significantly from those with abnormal EEGs. Bagchi et al. (1950), have suggested that certain hypertensives differ from non-hypertensives by some structural or physiological factors, constitutional or otherwise, which are not understood and which reveal themselves in the EEG. In this idea there may well be some truth. Just as the E E G varies widely from person to person so may its stability when subject to changes in the neuronal environment. Thus with circulatory stress the more abnormal is the EEG likely to be. When the vascular abnormality is severe and the clinical disturbance of function great the incidence of EEG abnormality will be higher and the greater will be the likelihood of a grossly abnormal pattern in any individual ease.
468
J . A . ROBERTS and M. W A L K E R SUMMARY
1. A study of the routine EEG findings in 104 patients with cerebro-vascular disease is reported. 2. Abnormal EEGs were found in 52 per cent of cases of simple hypertension, 82 per cent of cases with hypertension and cerebrovascular disease and 100 per cent of these cases if epilepsy was a symptom. 3. Throughout the whole series the EEG abnormality varied widely in type and severity and was no way specific for any subgroup. Paroxysmal activity was occasionally present in both epileptic and non-epileptic patients. 4. In the epileptic group grand mal and akinetic attacks were the most common. 5. The significance of the findings is briefly discussed. We have pleasure in thanking Dr. Nevin for his help in the clinical analysis of the cases.
REFERENCES BAQCHX, B. K., Koob K. A., HOOBLEa, S. W. and P ~ T , M. M. Electroencephalographie findings in hypertension: 1. Correlation with clinical status. Univ. of Michigan Med. Bull., 19r~a, I6: 92. BAGCHI, B. K., gooI~ K. A., HOOBLER,S. W. and I~ET, M. M. Electroencephalographic findings in h y pertension: II. Correlation with operative risk and pest-operative course. Univ. of Michigan Med. Bull., 1950b, 16: 117-126. COHN, R., RAINES, G. N., MULDER, D. W. and NEUMANLY, N. A. Cerebral vascular lesions. Arch. Neurol. Psychiat., Chicago, 19~, 60: 165-181. DARROW, C. W. and GRA~, C. G. : Relation of electroencephalogram to photometrically observed vasomotor changes in the brain. J. Neurophysiol., 1946, 8: 449-461. EN(]EL, G., WEBB, J., FERRIS, E., ROMANO, J., RYDER, H. and BLANKENHORN,M. A migraine like syndrome complicating decompression sickness. War Medicine, 1944, 5: 304-314. ROHMER, F., GASTAUT, Y. et DELL, M. B. L ' E E G dans la pathologie vasculaire du cerveau. Rev. Neurot. 1952, 87: 93-114. SVRAUSS, H. and GREENSTEIN, L. The electroencephalogram in cerebrovaseular disease. Arch. l~eurol. Psychiat., Chicago, 1948, 59: 395-403.
~efereace : ROBwaTS,J. A. and WaL~m~_, M. The electroencephalogram in essential hypertension and chronic cerebrovaseular disease. ]~BG ~ , t . Neurolohy~o|. , 19N, 6: 461-468.
WALKI~, B.Sc.
Maida Vale Hospital ~or Nervous D/seases, London
(Received for publication: March 22, 1954) INTRODUCTION
in no way different from those observed in In this paper the results are presented of many patients subject to clinical paroxysmal an analysis of 104 patients with essential disturbances. In commenting on this figure hypertension and cerebral arteriosclerosis Cohn et al. pointed out that records with undertaken primarily to correlate the E E G high frequency activity but without slow waves were not considered abnormal in this findings with epilepsy in this disease. The literature on the subject is not exten- series. CASE MATERIAL sive. Bagehi et al. (1950), in 84 patients with essential or malignant hypertension, One hundred and four patients were found moderately or very abnormal E E G s investigated. They fell into 3 groups: 1. Esin 25 per cent as compared with 6 per cent in sential hypertension, 27 cases. 2. Hypertena control group of 52, and these figures were sion with neurological signs and symptoms, statistically significant even after the exclu- 69 cases. 3. Neurological signs and sympsion of cases with a history of eneephalopathy toms without hypertension, 8 cases. The ages or cerebro-vascular accident. No specific E E G of these patients (57 male, 47 female), were pattern was noted and no correlation was from 21 to 78 years with 70 per cent within found with the duration of the condition or the range 45 to 65. The E E G s were taken by the degree of blood pressure nor with any the usual routine methods on 6 or 8 channel signs or symptoms of the disease. Abnormal Ediswan electroencephalographs. records were found more often when there 1. ESSENTIAL HYPERTENSION was a history of cerebro-vascular accident or severe hypertensive encephalopathy; None of the 27 patients in this group had patients with a history of eerebro-vaseular clinical evidence of eerebro-vascular disease accident showing localizing signs in the E E G although in 9 instances there was some degree tended to have a greater background ab- of peripheral or retinal arteriosclerosis. Their normality than those without such localising ages were between 21 and 71 years w i t h an signs. Rohmer ¢t al. (1952), in a series of average of 53. Fourteen or 51.8 per cent had 60 cases of hypertension, found 28 with ab- definitely abnormal EEGs. These were of normal EEG s but of the rest only 7 were many different types but an abnormal definitely abnormal and 12 slightly abnormal amount of slow activity was the most conwhile 13 were doubtful, i.e. a 33 per cent ab- stant feature and in only one trace was it normality. Two of the definitely abnormal minimal. Fast activity was present in widely EEGs were charaeterised by their very low varying relative amounts and amplitudes and potential and prominence of fast activity; in 6 cases was conspicuous or dominant (fig. otherwise the findings were not described in 1). In two of these it occurred at the lower detail. Cohn ¢t al. (1948), investigated a frequency limits as a 14 to 18 c/see, rhythm of large number of patients with arterial hyper- alpha distribution; otherwise it was of higher tension but without evidence of gross cerebral frequency and was generalised or of highest lesions. They found abnormal EEGs in 25 amplitude in the frontal and central leads. per cent of cases. The EEGs usually showed Sharp waves were present in many of the prominent fast and slow activity and were records but were of high potential and uni[ 461 ]
462
J . A . ROBERTS and M. W A L K E R
lateral in only 2. Another trace with unilateral features had runs of 10 c/see. "flattopped" waves in one of the central leads. 2. H Y P E R T E N S I O N W I T H NEUROLOGICAL SIGNS AND SYMPTOMS
No case was included in which there was a family history of epilepsy or in which epilepsy had occurred in early life. In none was there a history of hypertensive encephalopathy or of recent thrombosis or vascular accident.
( a ) Neurological signs and symptoms other than epilepsy The 45 patients in this group presented varying degrees of organic dementia with or
generalised abnormalities fast activity was appreciable in 20; in 5 of these it was prominent and in a further 3 it was dominant and continuous at 12-20 c/sec. Random sharp waves occurred in 10 cases and in 4 were more marked on one side or the other. Three traces were somewhat paroxysmal. Every record showed slow activity but this was not greater in amount or in amplitude than that occurring in some of the simple hypertensives. Many of the patients in this group had clinical evidence of focal cerebral lesions but no EEG correlate of these was apparent. The remaining 10 patients had focal electroencephalographic abnormalities. Of these, 9 had focal slow activity at I to 5 c/sec. (fig. 3), in two instances associated with focal sharp
F. age 62, B.P. 260/100. Prominent fast a~tivity in a ease of simple hypertension.
without neurological signs such as hemiplegia, hemianopia, aphasia, pseudo-bulbar palsy or Parkiusonism. Their ages ranged from 38 to 74 years with an average of 58. Thirty seven or 82.2 per cent as compared with 51.8 per cent in the hypertensive group, had abnormal
EEGs. These (fig. 2), were similar to those already described under simple hypertension with the exception of one trace which was grossly abnormal. Of the 26 cases showing
waves and in two others occurring against a background of random delta waves; the last case had focal sharp wave activity only. In 5 of these 10 patients the electroencephalographic focus could be correlated with a cerebral lesion as indicat~l by hemiplegia or aphasia but the other 5 showed no such clinical correlate though the general signs and symptoms of cerebrovaseular disease were severe.
463
E E G I N H Y P E R T E N S I O N AND CEREBROVASCUT,AR D I S E A S E
The grossly abnormal trace was seen in a patient of 67, blood pressure 160/105, who had a history of 7 years mental deteriora-
tion, slowness of movements and dysphasia. Slow activity at frequencies down to 1 c/see. was prominent, the slowest waves often bila-
~opv Fig. 2 M. age 69., B.P. 210/115. Hypertension with mental deterioration. abnormal amount of diffuse slow activity.
~A
M
M
M. age 58, B.P. 200/115. present on the left.
~t
M ~
~
Fig. 3 Hypertension with gross aphasia.
~
The EEG shows an
A
Focal delta
activity is
464
J . A . ROBERTS and M. W A L K E R
terally synchronous and at amplitudes of 65 ~V. ; little activity faster than 8 c/sec, was present (fig. 4).
(b) Epilepsy There were 24 patients in this group. Their ages were between 37 and 76 years with an average of 61 years. In 20 the epilepsy was the only symptom of importance. The remaining 4 presented, in addition to the epilepsy, moderate or severe mental deterioration in one case with widespread focal signs. The epilepsy in 12 cases consisted of grand real attacks which were relatively infrequent,
abnormal. The abnormalities were similar ~ those already described for the cases without epilepsy, except that on the whole they were somewhat more pronounced. Of the 12 patients with grand real, 5 had E E G s with generalised and prominent fast activity while 3 others showed occasional delta waves which in one case were focal. In only 2 E E G s was there any tendency to p ~ r oxysmal build up and spread of potentials. The 2 patients with Jacksonian attacks and 2 of those with psychomotor attacks showed widely varying abnormalities of the types already described. The third psychomotor case
~--4~ Fig. 4 M. age 67, B.P. 160/105. Hypertension. Mental deterioration, slowness of movements and dysphasia. A very abnormal EEG showing diffuse slow activity throughout.
in one instance occurring only in the night; in 3 the attacks were mainly psychomotor and in 2 others were brief sensory Jaeksonian. Seven patients had brief akinetic attacks only. In these, generally when walking, the patient without warning suddenly falls to the ground or on to the knees. He does not remember falling and the loss of consciousness is so brief that he is often doubtful of its occurrence. Recovery is immediate, the patient rising quickly and continuing as before unless h u r t by the fall. All E E G s in this group were
had a more abnormal E E G (fig. 5). Fast activity was present in the central areas; slow activity was prominent and diffuse and occasionally occurred as bilateral and synchronous paroxysms at delta frequencies. In this last ease, where severe mental deterioration was an important clinical feature, the diagnosis of cerebral arteriosclerosis was verified at autopsy. Five of the 7 patients with akinetic attacks had prominent fast activity. In 2 of the 3 cases where it was dominant it was of
465
EEG IN HYPERTENSION AND CEREBROVASCULAR DISEASE highest a m p l i t u d e in the f r o n t a l and central leads (fig. 6), while in the t h i r d it was present as a slower 15 to 16 e/see, r h y t h m of alpha distribution.
Of the r e m a i n i n g 2 patients one showed generalised p a r o x y s m s of slow a n d fast frequencies a n d the other bursts of u n i l a t e r a l i r r e g u l a r delta activity.
) 5o/,v Fig. 5 M. age 66, B.P. 220/120. Hypertension with mental deterioration and psyehomotor epilepsy. Fast activity is prominent in the central leads, slow activity is present diffusely and there are occasional bursts at delta frequencies. .__
•
i
~
*
R
i
¢
,
|
,
I °p
~"h"g. 6 F. are 59, B.P. 170/100. Hypertension and akinetie epilepsy. Fast activity is dominent.
466
J . A . ROBERTS and M. W A L K E R
CEREBRAL ARTERIOSCLEROSIS WITHOUT HYPERTENSION
Few patients of this type are seen in neurological clinics and only 8 in our series fell definitely into this group. A brief statement of the E E G findings is given for comparison with the other cases but it is realized that a study of larger numbers drawn from special hospitals for the aged might give a different picture. These patients were between 51 and 74 years with an average of 61. All had evidence of retinal or peripheral arteriosclerosis. The diagnosis of cerebral arteriosclerosis was made on the basis of focal cerebral thrombosis or a history of progressive dementia or epilepsy for which no other cause could be demonstrated. In every case the E E G was abnormal and on the whole slow activity was the most prominent feature. Of the 4 cases without epilepsy the abnormalities were not marked in 2 where only a temporary weakness of a limb had occurred, but in 2 others with symptoms of progressive dementia and paralysis agitans respectively slow activity at frequencies down to 2 c/sec. was widespread and dominant. Two of the remaining 4 patients had akinetic attacks and 2 had grand mal attacks. The trace in one of the grand mal cases was slightly paroxysmal but otherwise there were no features of note. DISCUSSION
In this study of the E E G in hypertension and chronic cerebro-vascular disease an 80 per cent incidence of abnormality is reported. This is much higher than that described in other papers but all cases included in our series are without doubt abnormal by our criteria. The E E G abnormalities described here and elsewhere do not merit detailed discussion. It would appear reasonably well established that in simple hypertension a generalized abnormality consisting of irregularity of the alpha r h y t h m with excess of fast and slow waves may be found in 25 to 50 per cent of cases. Fast activity is sometimes a prominent feature and occasionally theta and delta frequencies are dominant. More rarely there is paroxysmal synchronization.
As pointed out by Bagchi et al. (1950), there is no correlation between the h y p e r t e m sion and the E E G abnormality, indeed, in some patients with long standing and high blood pressure, the records are within normal limits. W h e n there is vascular damage to the brain in addition to the hypertension the incidence of electroencephalographic abnormality increases greatly (90 per cent in our series). A focal electroeneephalographic abnormality, when present, can sometimes be correlated with a thrombotic lesion, but frequently no clinical signs of a gross structural lesion can be found in the presence of ~ definite electroencephalographic focus. It would appear that the greater the ccrebrovascular disturbance, as evidenced by clinical symptoms, the greater is the likelihood of an abnormal E E G pattern. The factual basis for this generalisation is strengthened by the occurrence of a very abnormal E E G in a patient with progressive mental deteriora~ tion of 7 years duration, and the presence o[ considerable abnormality in all 8 cases of cerebral arteriosclerosis without hypertension. Nevertheless, it must be emphasized that, in 8 patients with hypertension and definite signs of cerebral damage normal E E G s were recorded, and no noteworthy difference could be detected between the clinical history in these cases and those with the abnormal EEGs. In this series of 104 patients with hypertension and cerebrovascular disease, 77 had neurological signs and symptoms. Of these 24 or 36 per cent had epilepsy. This figure emphasizes the importance of epilepsy as a symptom in cerebro-vascular disease. With the possible exception of typical petit mal the epileptic manifestations may be of any type, but grand mal attacks and akinetic attacks appear to be the most common. There is a 100 per cent E E G abnormality in these patients with epilepsy. The patterns are, on the whole, similar in type to those without epilepsy and in only 4 cases (one akinetic and 3 grand mal) was there a n y tendency to paroxysmal synchronization. The findings then in these patients bear out the statement of Strauss and Greenstein (1948), that ep-
EEG IN HYPERTENSION AND CEREBROVASCULARDISEASE ilepsy in eerehro-vas~ular disease is not assoeiated with characteristic interseizure patterns in the EEG. A consideration of the findings in this series makes evident that the E E G abnormalities, despite their absence in a considerable number of cases, must be directly attributed to the vascular disease. This is suggested by the high initial incidence of abnormality and by the fact that repeat recordings in 12 patients, at long intervals, showed increasing abnormality. I f this is so, then 2 questions arise. What is the significance of the EEG abnormalities, and why arc they absent in a large number of eases .~ It is clear from what has been said that epilepsy as a symptom is in no way a significant factor. The presence of considerable abnormality in the cases of simple hypertension suggests that E E G changes can result from abnormal functioning of the cerebral vessels or from variation in blood flow within the arteriole and capillary bed. Here the observations of Darrow and Graf (1945), are of interest. These workers were able to show by careful experimental technique that vasodilatation of the cerebral vessels was associated with increase in frequency and potential of the fast waves whereas vasoconstriction decreased the frequency and increased the potential of the slow waves. It is probable, therefore, that widespread variations in the functional state of the cerebral vessels may give rise in some way to the combination of diffuse excess of fast and slow activity which so often characterises the EEG in cerebro-vascular disorders. Further support is given to this conception by the work of Engel et al. (1944), who found focal slow activity in the occipital regions during an experimentally produced migraine-like syndrome, when a circulatory disturbance of some kind was almost certainly present. It would be useless in the present state of knowledge to speculate as to how the circulatory disturbances act. Many chemical changes in the external milieu of the neurones
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must occur as a result of even slight vascular changes and it is reasonable to suppose that these can alter the pattern of the electrotonic potentials of the brain, potentials which, in any ease, are possibly only an indirect sign of neural functioning. It may be that the severe abnormalities seen in some of the eases of simple hypertension are caused by more intense local circulatory changes producing, in some eases, minimal brain haemorrhage or ischemia. When there is widespread hyaline necrosis of the vessels with cerebral damage in addition to the hypertension, as might be expected the percentage abnormality increases greatly (90 per cent for groups 2 and 3). Sometimes the EEG changes may be very marked and in such cases the clinical disturbance of function, both mental and physical, is often severe. The importance of cerebral damage is further suggested by the presence of fairly severe EEG abnormalities in every one of our 8 cases of cerebro-vascular disease without hypertension. There remains the difficult problem of the normal EEG, not only in the simple hypertensive, but also in the cases of hypertension with neurological signs and symptoms where in 8 such patients the clinical histories did not differ significantly from those with abnormal EEGs. Bagchi et al. (1950), have suggested that certain hypertensives differ from non-hypertensives by some structural or physiological factors, constitutional or otherwise, which are not understood and which reveal themselves in the EEG. In this idea there may well be some truth. Just as the E E G varies widely from person to person so may its stability when subject to changes in the neuronal environment. Thus with circulatory stress the more abnormal is the EEG likely to be. When the vascular abnormality is severe and the clinical disturbance of function great the incidence of EEG abnormality will be higher and the greater will be the likelihood of a grossly abnormal pattern in any individual ease.
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J . A . ROBERTS and M. W A L K E R SUMMARY
1. A study of the routine EEG findings in 104 patients with cerebro-vascular disease is reported. 2. Abnormal EEGs were found in 52 per cent of cases of simple hypertension, 82 per cent of cases with hypertension and cerebrovascular disease and 100 per cent of these cases if epilepsy was a symptom. 3. Throughout the whole series the EEG abnormality varied widely in type and severity and was no way specific for any subgroup. Paroxysmal activity was occasionally present in both epileptic and non-epileptic patients. 4. In the epileptic group grand mal and akinetic attacks were the most common. 5. The significance of the findings is briefly discussed. We have pleasure in thanking Dr. Nevin for his help in the clinical analysis of the cases.
REFERENCES BAQCHX, B. K., Koob K. A., HOOBLEa, S. W. and P ~ T , M. M. Electroencephalographie findings in hypertension: 1. Correlation with clinical status. Univ. of Michigan Med. Bull., 19r~a, I6: 92. BAGCHI, B. K., gooI~ K. A., HOOBLER,S. W. and I~ET, M. M. Electroencephalographic findings in h y pertension: II. Correlation with operative risk and pest-operative course. Univ. of Michigan Med. Bull., 1950b, 16: 117-126. COHN, R., RAINES, G. N., MULDER, D. W. and NEUMANLY, N. A. Cerebral vascular lesions. Arch. Neurol. Psychiat., Chicago, 19~, 60: 165-181. DARROW, C. W. and GRA~, C. G. : Relation of electroencephalogram to photometrically observed vasomotor changes in the brain. J. Neurophysiol., 1946, 8: 449-461. EN(]EL, G., WEBB, J., FERRIS, E., ROMANO, J., RYDER, H. and BLANKENHORN,M. A migraine like syndrome complicating decompression sickness. War Medicine, 1944, 5: 304-314. ROHMER, F., GASTAUT, Y. et DELL, M. B. L ' E E G dans la pathologie vasculaire du cerveau. Rev. Neurot. 1952, 87: 93-114. SVRAUSS, H. and GREENSTEIN, L. The electroencephalogram in cerebrovaseular disease. Arch. l~eurol. Psychiat., Chicago, 1948, 59: 395-403.
~efereace : ROBwaTS,J. A. and WaL~m~_, M. The electroencephalogram in essential hypertension and chronic cerebrovaseular disease. ]~BG ~ , t . Neurolohy~o|. , 19N, 6: 461-468.