Journal o/ the neurological Sciences, 1975, 26:251-257
251
© Elsevier Scientific Publishing Company, Amsterdam - Printed in The Netherlands
The Electrocardiogram in Infratentorial Infarcts BENGT HINDFELT Department o/ Neurology, University Hospital, S-221 85 Lund (Sweden)
(Received 6 March, 1975)
INTRODUCTION The intimate coupling which exists between the brain and the cardiovascular system is well-known. Cardiac activity and vasomotor tone are regulated by central nervous structures, adapting the systemic circulation to immediate needs. Consequently, it is not surprising that intracranial disease is frequently associated with electrocardiographic (ECG) abnormalities (see Wiedler 1974). These may consist of arrhythmias (Reinstein, Gracey and Kline 1972) and/or various kinds of configurational ECG changes , which are sometimes very striking. ECG patterns simulating transmural myocardial infarction have often been observed in patients with subarachnoid haemorrhage and haemorrhagic stroke (Cropp and Manning 1960; Greenhoot and Reichenbach 1969). U-waves, ST-T segment changes and notched T-waves have been reported with raised intracranial pressure (Jachuck, Ramani, Clark and Kalbag 1975) and ischaemic stroke, unaccompanied by increased intracranial pressure, is known to carry a high incidence of arrhythmias (Reinstein et al. 1972), T-wave changes and a left ventricular strain pattern (Fentz and Gormsen 1962; Lavy, Stern, Herishianu and Carmon 1968). The mechanism which causes these ECG abnormalities is obscure though the parasympathetic and sympathetic nervous systems appear to be involved (Manning and Cotton 1962; Gunn, Sevelius, Puiggari and Myers 1968). The ECG changes in cerebrovascular catastrophes, such as subarachnoid haemorrhage, have been thought to be due to the effects of raised intracranial pressure upon brain-stem structures belonging to either of these systems (Takahashi, Mitsuya, Kawamura, Sato, Okamura, Kogure, Kimura, Funaki and Miyamoto 1964). Supporting clinical evidence is sparse but ECG recordings during posterior fossa explorations have revealed a high frequency of cardiac irregularities, consisting predominantly of severe bradyeardia and runs of consecutive ventrieular extrasystoles (Whitby 1963). The infratentorial structures, i.e. the brain-stem and the cerebellum, are interposed between higher integrative centres and the peripheral nervous system. Sympathetic fibers, emanating within the hypothalamus, pass through the brain-stem and im-
252
B. HINDFELT
portant parasympathetic nuclei are located in this region too. Thus, brain-stem lesions would a priori be expected to be associated very frequently with ECG changes. Since, as yet, no clinical study has been published concerning the effect of infratentorial ischaemic lesions on the E C G the present study was done. MATERIALS AND METHODS
Sixty-nine patients with infratentorial infarcts were studied retrospectively. They were admitted to the Department of Neurology, the University Hospital of Lund, during the period 1970-1974. The diagnosis of infarction within the territory of the vertebral and basilar arteries was based on clinical criteria, in a few cases confirmed at autopsy. Angiography was not performed for diagnostic purposes. A lumbar puncture was done in every patient and the cerebrospinal fluid (CSF) was normal with respect to cell count and colour in all patients included in this material. The patients were examined and an E C G was recorded within 24 hr of the stroke. The E C G recording was that used routinely, i.e. a 12-lead ECG consisting of standard and extremity leads (I-III, aVF, aVR and aVL) and the precordial leads V 1 - V 6. Serum transaminases, G O T and GPT, were measured during the subsequent 2 days. Of the 69 patients studied 47 were males and 22 females, Different age groups were represented, the ages ranging from 21 to 86 years with a mean of 63.5 ___ 12.2 years. Student's t-test was used for statistical evaluation. RESULTS
The number of normal and pathological E C G tracings are presented in Table i (A). TABLE 1 PATIENTS W I T H AN INFRATENTORIAL INFARCT AND A NORMAL OR PATHOLOGICAL ELECTROCARDIOGRAM
A. The total numbers of normal and a b n o r m a l records irrespective of the findings in tracings carried out before the cerebrovascular accident Normal Abnormal ECG
Males
Females
Total numbers
17 30
4 18
21 48 69
B. The records reclassified according to whether or not a previous tracing was available N o r m a l or unchanged E C G A b n o r m a l E C G (no previous ECG)
23 24
13 9
36 (group I ) 33 (group II) 69
THE ELECTROCARDIOGRAM IN INFRATENTORIAL INFARCTS
253
A history of pre-existing cardiovascular disease (cardiac disease, arterial hypertension) was obtained in 27 patients. However, more than 2 / 3 of the ECG's were considered abnormal and the proportion of pathological tracings agrees closely with what has been reported in a large series of supratentorial ischaemic infarctions (Lavy e t al. 1968). The main question is which E C G changes, if any, can be attributed to the ischaemic insult p e r se. ECG's recorded prior to the infarct were obtained in a small proportion of the patients, but when these were taken into account more than half of the patients had a normal or unchanged ECG after the infarct (Table 1 B group I). In the remaining cases (Table 1 B - group II) various kinds of E C G abnormalities were observed as shown in Table 2. The dominant abnormalities were arrhythmias, depressed ST-segments, and T-wave inversion. The arrhythmias were clinically benign and did not seriously affect the systemic circulation. Two male patients had an E C G pattern (pathological Q-wave, elevation of the ST-segment) consistent with recent myocardial infarction. In both cases a marked increase in G O T and in the G O T / G P T ratio occurred over the subsequent days after the stroke. TABLE 2 E C G ABNORMALITIES OBSERVED WITH INFRATENTORIAL INFARCTS
ECG abnormality
Numbers o/ cases
Arrhythmia
17
sinus tachycardia (> 100/min) sinus bradycardia (< 60/min) sinus arrhythmia atrial premature beats ventricular premature beats
4 3 4 1 5
ST-segment and T-wave abnormalities
10
Conduction disturbances
12
RBBB LBBB LAHB
5 1 6
Accelerated conduction ( W P W - s y n d r o m e )
1
Acute myocardial inJarction
2
Abbreviations: RBBB and LBBB =
right a n d left b u n d l e
branch block, respectively; LAHB = left anterior hemiblock. Conduction disturbances of various kinds were rather frequently observed, occurring in 12 patients (Table 2). Four of these patients were known to be hypertensive prior to the actual illness. Otherwise evidence of cardio-vaseular disease was lacking.
254
B. HINDFELT
The accompanying neurological symptoms and signs are shown in Table 3. Vertigo was the most common single complaint, followed by motor weakness. Signs of injury to the cortico-spinal tract, nystagmus, and pathological cerebellar tests were the abnormalities most frequently encountered. In Table 3 patients with a normal or unchanged E C G have been separated from those with an abnormal E C G (group II). The two categories were very similar in most respects. The proportions of males and females were similar as were also the average ages within the groups (61.6 ___ 10.6 and 65.4 -+- 13.6 years, group I and II respectively). The E C G changes associated with different brain-stem lesions are presented in Table 4. A wide variation in E C G manifestations with similar neurological lesions is evident and no consistent pattern is revealed.
TABLE 3 NEUROLOGICAL SYMTOMS AND SIGNS WITH INFRATENTORIAL INFARCTS Numbers o/ cases
Neurological symptoms and signs
group 1
group 11
total
21 7 4 3 14 7
25 11 4 3 12 10
46 18 8 6 26 17
3 1 0 9 18 1 1
2 3 3 10 16 4 4
5 4 3 19 34 5 5
19 8 5 5 14
17 11 9 6 15
36 19 14 11 29
Symptoms vertigo diplopia dysarthria dysphagia motor weakness sensory disturbances Signs cranial nerve signs III V VI VII VIII (nystagmus) IX-X XII long tract signs motor sensory sympathetic MFL-lesions cerebellar signs M F L ---- fasciculus longitudinalis medialis.
DISCUSSION
Infratentorial ischaemic lesions are associated with a high incidence of ECG abnormalities (Table 1A). About 700/0 of the patients had a pathological ECG within
THE ELECTROCARDIOGRAM
255
IN INFRATENTORIAL INFARCTS
TABLE 4 THE OCCURRENCE OF VARIOUS E C G CHANGES W I T H DIFFERENT LESIONS WITHIN THE BRAIN-STEM
Level o/ the lesions cranial nerve
ECG changes 111
Sinus tachycardia
x
Sinus bradycardia Sinus arrhythmia
V
V1
x
M F L eympathetic tract
VII
VIII
X
X
x
IX-X
X
Xll
X
X
X
X X
X
X
X
X X
X X
X X
X
X
X X X
X
Atrial premature beats Ventricular premature beats ST-T abnormalities LBBB RBBB
x x
X
x x
LAHB WPW-syndrome Acute myocardial infarct
X x
X
X X
X
X
X X
X
X
X
Abbreviations as in Tables 2 and 3.
24 hr of the stroke. This incidence is in perfect agreement with the corresponding data obtained in a large series of cerebral infarcts (Lavy et al. 1968). Furthermore, the kinds of E C G abnormality that accompany supra- and infratentorial infarctions are similar. This raises the question as to whether the E C G changes are a predisposing factor for an ischaemic insult or if they are secondary to the infarct, or the result of an imbalance between various nervous influences upon the heart and the vascular system. Yet another possibility is that infarct and the E C G abnormalities are merely coincidental, both being the consequence of atheroma. The brain may suffer from ischaemic insults due to arrhythmias, induced either by embolization or by a failing systemic circulation. The arrhythmias observed in this material were all benign forms and were unlikely to have affected the cerebral perfusion pressure. Nor were the arrhythmias of the kind which carry a high risk of embolization, such as atrial fibrillation or flutter. No episode with loss of consciousness was reported, thus ruling out a failing systemic circulation as a pathogenetic factor. Thus, it seems reasonable to conclude that the E C G abnormalities observed could not be considered to be important in the pathogenesis of infratentorial infarction. If the E C G changes observed with cerebral infarcts were the consequence of the brain lesion per se, lesions within the brain-stem would be anticipated to carry a much higher incidence of E C G changes, since all nervous stimuli to and from the cerebrum must pass through this region. Furthermore, infarcts within the territory of the basilar artery are typically scattered, extending over different parts of the
256
B. HINDFELT
brain-stem; this may well increase the incidence of damage to neuro-fibres which influence the cardio-vascular system. However, comparison of our findings with those of Lavy et al. (1968) suggests that infratentorial infarcts are not associated with ECG changes more frequently than are supratentorial ischaemic lesions, in this material less than half of the patients had ECG abnormalities which theoretically may be attributed to the infarct. If prior ECG's had existed in all cases, a comparison with the postinfarct ECG's would probably have considerably lowered this incidence. From a neurological point of view the two groups with normal (or unchanged) and pathological ECG's were comparable. This challenges the concept that any of the observed ECG abnormalities were triggered by the infarct. The wide variety of ECG changes with similar neurological deficits does also suggest that the relationship between the location of the infarct and the accompanying ECG changes was not close. Consequently, the present results suggest that the ECG abnormalities observed with ischaemic lesions within the central nervous system are merely coincidental, reflecting other effects of vascular disease and not the damage to the nervous system. The occurrence of ECG changes with intracranial disease associated with increased intracranial pressure is a somewhat different matter. In that situation the nervous pathways are intact and homeostatic mechanisms are attempting to preserve optimal conditions for cerebral perfusion by raising the arterial blood pressure. Under these circumstances ECG abnormalities may be induced by nervous activity (Jachuck e t al. 1975). However, many of the ECG changes encountered can probably be attributed to the superimposed load on the heart, unmasking subclinical pathology within the myocardium and the conduction system. Since these questions have considerable clinical relevance they deserve much further study. SUMMARY
Sixty-nine patients with infratentorial infarcts were studied with respect to associated electrocardiographic (ECG) abnormalities. ECG changes were encountered in about 70% of the patients, the most frequent abnormalities being arrhythmias, conduction disturbances and ST-T changes. No relationship was found between the localization of the brain-stem lesion and the accompanying ECG pattern. It is concluded that ischaemic lesions within the central nervous system do not p e r se affect the ECG and that associated ECG changes are merely coincidental, reflecting the same basic vascular disease. REFERENCES
CROPP, G. J. AND G. W. MANNING (1960) Electrocardiographic changes simulating myocardical ischemia and infarction associated with spontaneous intracranial hemorrhage, Circulation, 22: 25-38. FENTZ, V. AND J. GORMSEN (1962) Electrocardiographic patterns in patients with cerebrovascular accidents, Circulation, 25: 22-28. GREEN-HOOT, J. H. AND D. D. REICHENBACH(1969) Cardiac injury and subarachnoid haemorrhage - A clinical, pathological and physiological correlation, 1. Neurosurg., 30: 521-531.
THE ELECTROCARDIOGRAM IN INFRATENTORIAL INFARCTS
257
GUNN, C. G., G. SEVELIUS, M. J. Puiggari AND F. K. MYERS (1968) Vagal cardiomotor mechanisms in the hindbrain of the dog and cat, Amer. I. Physiol., 214: 258-262. JACHUCK, S. J., P. S. RAMANI, V. CLARK AND R. M. KALBAG (1975) Electrocardiographic abnormalities associated with raised intracranial pressure, Brit. reed. J., 1: 242--244. LAVY, S., S. STERN, Y. HERISHIANU AND A. CARMON (1968) Electrocardiographic changes in ischaemic stroke, ./. neurol. Sci., 7: 409-415. MANNING, G. W. AND M. COTTON (1962) Mechanisms of cardiac arrhythmia induced by diencephalic stimulation, Amer. 1. Physiol., 203: 1120-1124. REINSTEIN, L., J. G. GRACEY AND J. A. KLINE (1972) Cardiac monitoring of the acute stroke patient, Arch. phys. Med., 53: 311-314. TAKAHASHI, T., S. MITSUYA, H. KAWAMURA,Y. SATO, T. OKAMr.mA, T. KOGURE, Y. KIMUR:., M. FUNAKI AND S. MIYAMOTO, (1964) Electrocardiograms in cerebrovascular accidents. In: Proceedings of the 3rd Asian-Pacific Congress of Cardiology, Vol. 1, Kyoto, p. 355. WHrrBy, J. D. (1963) Electrocardiography during posterior fossa operations, Brit..1. Anaesth., 35: 624-630. WlEDLER, D. J. (1974) Myocardial damage and cardial arrhythmias after intracranial hemorrhage - A critical review, Stroke, 5: 759-764.
251
© Elsevier Scientific Publishing Company, Amsterdam - Printed in The Netherlands
The Electrocardiogram in Infratentorial Infarcts BENGT HINDFELT Department o/ Neurology, University Hospital, S-221 85 Lund (Sweden)
(Received 6 March, 1975)
INTRODUCTION The intimate coupling which exists between the brain and the cardiovascular system is well-known. Cardiac activity and vasomotor tone are regulated by central nervous structures, adapting the systemic circulation to immediate needs. Consequently, it is not surprising that intracranial disease is frequently associated with electrocardiographic (ECG) abnormalities (see Wiedler 1974). These may consist of arrhythmias (Reinstein, Gracey and Kline 1972) and/or various kinds of configurational ECG changes , which are sometimes very striking. ECG patterns simulating transmural myocardial infarction have often been observed in patients with subarachnoid haemorrhage and haemorrhagic stroke (Cropp and Manning 1960; Greenhoot and Reichenbach 1969). U-waves, ST-T segment changes and notched T-waves have been reported with raised intracranial pressure (Jachuck, Ramani, Clark and Kalbag 1975) and ischaemic stroke, unaccompanied by increased intracranial pressure, is known to carry a high incidence of arrhythmias (Reinstein et al. 1972), T-wave changes and a left ventricular strain pattern (Fentz and Gormsen 1962; Lavy, Stern, Herishianu and Carmon 1968). The mechanism which causes these ECG abnormalities is obscure though the parasympathetic and sympathetic nervous systems appear to be involved (Manning and Cotton 1962; Gunn, Sevelius, Puiggari and Myers 1968). The ECG changes in cerebrovascular catastrophes, such as subarachnoid haemorrhage, have been thought to be due to the effects of raised intracranial pressure upon brain-stem structures belonging to either of these systems (Takahashi, Mitsuya, Kawamura, Sato, Okamura, Kogure, Kimura, Funaki and Miyamoto 1964). Supporting clinical evidence is sparse but ECG recordings during posterior fossa explorations have revealed a high frequency of cardiac irregularities, consisting predominantly of severe bradyeardia and runs of consecutive ventrieular extrasystoles (Whitby 1963). The infratentorial structures, i.e. the brain-stem and the cerebellum, are interposed between higher integrative centres and the peripheral nervous system. Sympathetic fibers, emanating within the hypothalamus, pass through the brain-stem and im-
252
B. HINDFELT
portant parasympathetic nuclei are located in this region too. Thus, brain-stem lesions would a priori be expected to be associated very frequently with ECG changes. Since, as yet, no clinical study has been published concerning the effect of infratentorial ischaemic lesions on the E C G the present study was done. MATERIALS AND METHODS
Sixty-nine patients with infratentorial infarcts were studied retrospectively. They were admitted to the Department of Neurology, the University Hospital of Lund, during the period 1970-1974. The diagnosis of infarction within the territory of the vertebral and basilar arteries was based on clinical criteria, in a few cases confirmed at autopsy. Angiography was not performed for diagnostic purposes. A lumbar puncture was done in every patient and the cerebrospinal fluid (CSF) was normal with respect to cell count and colour in all patients included in this material. The patients were examined and an E C G was recorded within 24 hr of the stroke. The E C G recording was that used routinely, i.e. a 12-lead ECG consisting of standard and extremity leads (I-III, aVF, aVR and aVL) and the precordial leads V 1 - V 6. Serum transaminases, G O T and GPT, were measured during the subsequent 2 days. Of the 69 patients studied 47 were males and 22 females, Different age groups were represented, the ages ranging from 21 to 86 years with a mean of 63.5 ___ 12.2 years. Student's t-test was used for statistical evaluation. RESULTS
The number of normal and pathological E C G tracings are presented in Table i (A). TABLE 1 PATIENTS W I T H AN INFRATENTORIAL INFARCT AND A NORMAL OR PATHOLOGICAL ELECTROCARDIOGRAM
A. The total numbers of normal and a b n o r m a l records irrespective of the findings in tracings carried out before the cerebrovascular accident Normal Abnormal ECG
Males
Females
Total numbers
17 30
4 18
21 48 69
B. The records reclassified according to whether or not a previous tracing was available N o r m a l or unchanged E C G A b n o r m a l E C G (no previous ECG)
23 24
13 9
36 (group I ) 33 (group II) 69
THE ELECTROCARDIOGRAM IN INFRATENTORIAL INFARCTS
253
A history of pre-existing cardiovascular disease (cardiac disease, arterial hypertension) was obtained in 27 patients. However, more than 2 / 3 of the ECG's were considered abnormal and the proportion of pathological tracings agrees closely with what has been reported in a large series of supratentorial ischaemic infarctions (Lavy e t al. 1968). The main question is which E C G changes, if any, can be attributed to the ischaemic insult p e r se. ECG's recorded prior to the infarct were obtained in a small proportion of the patients, but when these were taken into account more than half of the patients had a normal or unchanged ECG after the infarct (Table 1 B group I). In the remaining cases (Table 1 B - group II) various kinds of E C G abnormalities were observed as shown in Table 2. The dominant abnormalities were arrhythmias, depressed ST-segments, and T-wave inversion. The arrhythmias were clinically benign and did not seriously affect the systemic circulation. Two male patients had an E C G pattern (pathological Q-wave, elevation of the ST-segment) consistent with recent myocardial infarction. In both cases a marked increase in G O T and in the G O T / G P T ratio occurred over the subsequent days after the stroke. TABLE 2 E C G ABNORMALITIES OBSERVED WITH INFRATENTORIAL INFARCTS
ECG abnormality
Numbers o/ cases
Arrhythmia
17
sinus tachycardia (> 100/min) sinus bradycardia (< 60/min) sinus arrhythmia atrial premature beats ventricular premature beats
4 3 4 1 5
ST-segment and T-wave abnormalities
10
Conduction disturbances
12
RBBB LBBB LAHB
5 1 6
Accelerated conduction ( W P W - s y n d r o m e )
1
Acute myocardial inJarction
2
Abbreviations: RBBB and LBBB =
right a n d left b u n d l e
branch block, respectively; LAHB = left anterior hemiblock. Conduction disturbances of various kinds were rather frequently observed, occurring in 12 patients (Table 2). Four of these patients were known to be hypertensive prior to the actual illness. Otherwise evidence of cardio-vaseular disease was lacking.
254
B. HINDFELT
The accompanying neurological symptoms and signs are shown in Table 3. Vertigo was the most common single complaint, followed by motor weakness. Signs of injury to the cortico-spinal tract, nystagmus, and pathological cerebellar tests were the abnormalities most frequently encountered. In Table 3 patients with a normal or unchanged E C G have been separated from those with an abnormal E C G (group II). The two categories were very similar in most respects. The proportions of males and females were similar as were also the average ages within the groups (61.6 ___ 10.6 and 65.4 -+- 13.6 years, group I and II respectively). The E C G changes associated with different brain-stem lesions are presented in Table 4. A wide variation in E C G manifestations with similar neurological lesions is evident and no consistent pattern is revealed.
TABLE 3 NEUROLOGICAL SYMTOMS AND SIGNS WITH INFRATENTORIAL INFARCTS Numbers o/ cases
Neurological symptoms and signs
group 1
group 11
total
21 7 4 3 14 7
25 11 4 3 12 10
46 18 8 6 26 17
3 1 0 9 18 1 1
2 3 3 10 16 4 4
5 4 3 19 34 5 5
19 8 5 5 14
17 11 9 6 15
36 19 14 11 29
Symptoms vertigo diplopia dysarthria dysphagia motor weakness sensory disturbances Signs cranial nerve signs III V VI VII VIII (nystagmus) IX-X XII long tract signs motor sensory sympathetic MFL-lesions cerebellar signs M F L ---- fasciculus longitudinalis medialis.
DISCUSSION
Infratentorial ischaemic lesions are associated with a high incidence of ECG abnormalities (Table 1A). About 700/0 of the patients had a pathological ECG within
THE ELECTROCARDIOGRAM
255
IN INFRATENTORIAL INFARCTS
TABLE 4 THE OCCURRENCE OF VARIOUS E C G CHANGES W I T H DIFFERENT LESIONS WITHIN THE BRAIN-STEM
Level o/ the lesions cranial nerve
ECG changes 111
Sinus tachycardia
x
Sinus bradycardia Sinus arrhythmia
V
V1
x
M F L eympathetic tract
VII
VIII
X
X
x
IX-X
X
Xll
X
X
X
X X
X
X
X
X X
X X
X X
X
X
X X X
X
Atrial premature beats Ventricular premature beats ST-T abnormalities LBBB RBBB
x x
X
x x
LAHB WPW-syndrome Acute myocardial infarct
X x
X
X X
X
X
X X
X
X
X
Abbreviations as in Tables 2 and 3.
24 hr of the stroke. This incidence is in perfect agreement with the corresponding data obtained in a large series of cerebral infarcts (Lavy et al. 1968). Furthermore, the kinds of E C G abnormality that accompany supra- and infratentorial infarctions are similar. This raises the question as to whether the E C G changes are a predisposing factor for an ischaemic insult or if they are secondary to the infarct, or the result of an imbalance between various nervous influences upon the heart and the vascular system. Yet another possibility is that infarct and the E C G abnormalities are merely coincidental, both being the consequence of atheroma. The brain may suffer from ischaemic insults due to arrhythmias, induced either by embolization or by a failing systemic circulation. The arrhythmias observed in this material were all benign forms and were unlikely to have affected the cerebral perfusion pressure. Nor were the arrhythmias of the kind which carry a high risk of embolization, such as atrial fibrillation or flutter. No episode with loss of consciousness was reported, thus ruling out a failing systemic circulation as a pathogenetic factor. Thus, it seems reasonable to conclude that the E C G abnormalities observed could not be considered to be important in the pathogenesis of infratentorial infarction. If the E C G changes observed with cerebral infarcts were the consequence of the brain lesion per se, lesions within the brain-stem would be anticipated to carry a much higher incidence of E C G changes, since all nervous stimuli to and from the cerebrum must pass through this region. Furthermore, infarcts within the territory of the basilar artery are typically scattered, extending over different parts of the
256
B. HINDFELT
brain-stem; this may well increase the incidence of damage to neuro-fibres which influence the cardio-vascular system. However, comparison of our findings with those of Lavy et al. (1968) suggests that infratentorial infarcts are not associated with ECG changes more frequently than are supratentorial ischaemic lesions, in this material less than half of the patients had ECG abnormalities which theoretically may be attributed to the infarct. If prior ECG's had existed in all cases, a comparison with the postinfarct ECG's would probably have considerably lowered this incidence. From a neurological point of view the two groups with normal (or unchanged) and pathological ECG's were comparable. This challenges the concept that any of the observed ECG abnormalities were triggered by the infarct. The wide variety of ECG changes with similar neurological deficits does also suggest that the relationship between the location of the infarct and the accompanying ECG changes was not close. Consequently, the present results suggest that the ECG abnormalities observed with ischaemic lesions within the central nervous system are merely coincidental, reflecting other effects of vascular disease and not the damage to the nervous system. The occurrence of ECG changes with intracranial disease associated with increased intracranial pressure is a somewhat different matter. In that situation the nervous pathways are intact and homeostatic mechanisms are attempting to preserve optimal conditions for cerebral perfusion by raising the arterial blood pressure. Under these circumstances ECG abnormalities may be induced by nervous activity (Jachuck e t al. 1975). However, many of the ECG changes encountered can probably be attributed to the superimposed load on the heart, unmasking subclinical pathology within the myocardium and the conduction system. Since these questions have considerable clinical relevance they deserve much further study. SUMMARY
Sixty-nine patients with infratentorial infarcts were studied with respect to associated electrocardiographic (ECG) abnormalities. ECG changes were encountered in about 70% of the patients, the most frequent abnormalities being arrhythmias, conduction disturbances and ST-T changes. No relationship was found between the localization of the brain-stem lesion and the accompanying ECG pattern. It is concluded that ischaemic lesions within the central nervous system do not p e r se affect the ECG and that associated ECG changes are merely coincidental, reflecting the same basic vascular disease. REFERENCES
CROPP, G. J. AND G. W. MANNING (1960) Electrocardiographic changes simulating myocardical ischemia and infarction associated with spontaneous intracranial hemorrhage, Circulation, 22: 25-38. FENTZ, V. AND J. GORMSEN (1962) Electrocardiographic patterns in patients with cerebrovascular accidents, Circulation, 25: 22-28. GREEN-HOOT, J. H. AND D. D. REICHENBACH(1969) Cardiac injury and subarachnoid haemorrhage - A clinical, pathological and physiological correlation, 1. Neurosurg., 30: 521-531.
THE ELECTROCARDIOGRAM IN INFRATENTORIAL INFARCTS
257
GUNN, C. G., G. SEVELIUS, M. J. Puiggari AND F. K. MYERS (1968) Vagal cardiomotor mechanisms in the hindbrain of the dog and cat, Amer. I. Physiol., 214: 258-262. JACHUCK, S. J., P. S. RAMANI, V. CLARK AND R. M. KALBAG (1975) Electrocardiographic abnormalities associated with raised intracranial pressure, Brit. reed. J., 1: 242--244. LAVY, S., S. STERN, Y. HERISHIANU AND A. CARMON (1968) Electrocardiographic changes in ischaemic stroke, ./. neurol. Sci., 7: 409-415. MANNING, G. W. AND M. COTTON (1962) Mechanisms of cardiac arrhythmia induced by diencephalic stimulation, Amer. 1. Physiol., 203: 1120-1124. REINSTEIN, L., J. G. GRACEY AND J. A. KLINE (1972) Cardiac monitoring of the acute stroke patient, Arch. phys. Med., 53: 311-314. TAKAHASHI, T., S. MITSUYA, H. KAWAMURA,Y. SATO, T. OKAMr.mA, T. KOGURE, Y. KIMUR:., M. FUNAKI AND S. MIYAMOTO, (1964) Electrocardiograms in cerebrovascular accidents. In: Proceedings of the 3rd Asian-Pacific Congress of Cardiology, Vol. 1, Kyoto, p. 355. WHrrBy, J. D. (1963) Electrocardiography during posterior fossa operations, Brit..1. Anaesth., 35: 624-630. WlEDLER, D. J. (1974) Myocardial damage and cardial arrhythmias after intracranial hemorrhage - A critical review, Stroke, 5: 759-764.
