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ACUPUNCTURE ANÆSTHESIA
417 a history of exposure to asbestos there was patient with pulmonary asbestosis. (There was apical pulmonary fibrosis in five other cases, but this is unlikely to be related to asbestos exposure.) The explanation of this apparent anomaly seems to be that heavy industrial exposure in the past has in most cases resulted in severe asbestosis and early death before the patient could survive long enough for cancer to develop. With the introduction of modern precautions for the protection of asbestos workers, there has been a fall in the incidence of
noma
only
with
one
asbestosis and an increase in the number of cases of asbestos-associated cancer.6 This would be in keeping with a long latent period, of say 30 years, as in our patients. The patients’ smoking-habits were similar, irrespective of their exposure to asbestos. As expected, however, there were more smokers among the patients than among the controls.5 It may be that smoking is a cofactor in the development of laryngeal carcinoma, but, as previously pointed out/ it is unlikely to be very important, since the incidence of laryngeal carcinoma in the twentieth century has declined slightly in the face of an enormous increase in tobacco
consumption.
Hypothesis ACUPUNCTURE ANÆSTHESIA
G. M. BULL Medical Research Council Clinical Research Centre, Watford Road, Harrow, Middlesex HA1 3UJ
A possible mechanism to explain acupuncture anæsthesia is presented which takes into consideration the fact that acupuncture needles have to be vibrated or rotated and which is not invalidated by the lack of correlation between the traditional acupuncture sites and the It is anatomy of the peripheral nervous system. suggested that rhythmic stimulation causes areas of the cerebral cortex to become " locked on" to the stimulating rhythm and thus " busy " and unable to react to stimuli in the normal way.
Summary
Two hypotheses are currently favoured to explain how acupuncture might induce anaesthesia.1 The one is hypnotism and the other is the so-called <
We intend to perform histological examinations for asbestos bodies in patients with laryngeal carcinoma. not many specimens are available because the vast majority of patients with laryngeal carcinoma are treated by radiotherapy. Even if the tumour recurs and the larynx becomes available for study after laryngectomy, it is doubtful whether asbestos bodies could be found-presumably they would lie at the centre of the tumour and thus be sloughed off as the tumour ulcerated during its growth. Even if they survived this insult, they would almost certainly slough out in the healing process after radiotherapy. As a pilot study, we examined serial sections from one larynx, but no asbestos bodies were
Unfortunately, however,
found. Requests for reprints should be addressed
to
P. M. S.
REFERENCES 1. 2.
Buchanan, W. D. Ann. N.Y. Acad. Sci. 1965, 132, 507. Wagner, J. C., Sleggs, C. A., Marchand, P. Br. J. ind. Med. 1960, 17, 260.
3. Whitwell, F., Rawcliffe, R. M. Thorax, 1971, 26, 6. 4. Stell, P. M., McGill, T. Lancet, 1973, i, 678. 5. Stell, P. M. ibid. 1972, i, 617. 6. Selikoff, I. T., Hammond, I. C., Churg, J. J. Am. med. Ass. 1968, 204, 106.
the limb proximally in the " path " of the ascending * sensory or motor disturbance.3,4 It is postulated that this stimulus causes the cortex in the area surrounding the dysrhythmic focus to become sufficiently refractory to block the spread of the dysrhythmia to the rest of the cortex. The " busy " area of the cortex is partly refractory to further stimulation. There is another circumstance in which the cortex can be made refractory to random impulses, and that is when a rhythmic stimulus is fed in through a sensory channel. This is most easily demonstrated in the case of the visual cortex, where photic stimulation at appropriate rates may induce a wide variety of subjective experiences not only in the visual fields but also in other sensory modalities. In many subjects fits of varying sorts may be induced and demonstrated electroencephalographically or seen clinically. This forms the basis of the use of photic stimulation in diagnostic electroencephalography. The phenomenon is not confined to the visual pathways, and similar effects can be demonstrated electroencephographically and occasionally clinically with rhythmic stimulation of the periphery or of the auditory pathways. The rate of stimulation appears to be critical and to vary between about 1 and 25 cycles per second. Moreover, the interval between volleys of stimulation appears to be important in determining the response. Voluntary inhibition or augmentation of the responses can be demonstrated both electroencephalographically and subjectively.5.6 It appears that, when a sensory stimulus recurs at an appropriate frequency, large " to that areas of the cortex may become " locked on or a harmonic of it and that its normal frequency function may be thereby disturbed. The analogy with acupuncture anaesthesia is close. The frequency of vibration or rotation of the acupuncture needles is within the appropriate range to
418 " lock on " the cortical rhythm and could thereby of the cortex to be " busy ". The lack of correlation between the traditional acupuncture sites and the anatomy of the peripheral nervous system would not invalidate this hypothesis. One could postulate that the acupuncture sites happen to be supplied by nerves which, by reason of appropriate lengths and pathways, have time constants of transmission which " tune " them to the
to
cause areas
stimulating frequency. This hypothesis is moreover not inconsistent with a participation of hypnotic effects. The mechanism of hypnosis has never been adequately explained. Perhaps it facilitates establishment of a " busy " cortex just as with voluntary inhibition or augmentation of rhythmic responses mentioned above. The " busy cortex" hypothesis could be studied by varying the frequency of acupuncture-needle vibration while assessing the pain threshold and correlating the findings with the electroencephalographic pattern. One could also predict from this hypothesis that an enhancement of the anaesthetic effect would be likely if larger areas of the cortex were recruited to the dominant rhythm by synchronous photic or auditory stimulation.
factor which increases either PS. S or RA.V., and it is suggested therefore that the general term " reduced C.S.F. absorption syndrome " should replace " benign intracranial hypertension" and similar terms. INTRODUCTION
SINCE the early descriptions of Gowers, Quincke, Nonne, and others over 75 years ago 1-3 there have been many clinical reports of the condition now commonly termed benign intracranial hypertension.’ Typically, in this condition, there is raised intracranial pressure with no apparent cause, no associated neurological abnormalities, and normal investigative findings-in particular, a normal ventricular system.’’ The cause of the intracranial hypertension remains unknown; indeed even which intracranial compartment (brain, blood, or c.s.F.) is involved is uncertain. In addition a wide variety of Eetiological agents have been linked to the condition,6,7 although without knowledge of the underlying pathophysiology it is impossible to say how these factors are related to The present the increase in intracranial pressure. the intracranial is advanced to hypothesis explain to a more hypertension, suggest appropriate term for this condition, and to show how it is related to known astiological agents.
REFERENCES 1. 2. 3. 4. 5.
Lancet, 1973, i, 1372. Melzack, R., Wall, P. D. Science, 1965, 150, 971. Jackson, J. Hughlings. Lancet, 1868, i, 618. Wilson, S. A. Kinnier. Neurology. London, 1940. Walter, V. J., Walter, W. Grey. J. Electroenceph. clin. Neurophysiol. 1949, 1, 1. 6. Kiloh, L. G., McComas, A. J., Osselton, J. W. Clinical Electroencephalography. London, 1972.
REDUCED C.S.F. ABSORPTION SYNDROME Reappraisal of Benign Intracranial Hypertension and Related Conditions IAN
JOHNSTON
Department of Neurosurgery, Hospital for Sick Children, Toronto
A reduced
cerebrospinal-fluid (C.S.F.) absorption syndrome has been defined by considering the factors controlling C.S.F. absorption; the pressure-gradient between the subarachnoid space and the superior sagittal sinus (PC..S.F.-PS.S.), and the resistance to flow across the absorptive channels (RA.V.). The hypothesis is advanced that this syndrome is the same as that previously described by various terms (benign intracranial hypertension, pseudotumour cerebri, otitic hydrocephalus, &c.), since the clinical evidence favours an increase in C.S.F. volume due to impaired absorption as the cause of the intracranial hypertension. In known such as occlusion addition, ætiological agents of the sagittal sinus or the major neck veins (increasing PS.S) or acute steroid withdrawal (increasing RA.V.) have been shown experimentally to cause a marked reduction in C.S.F. absorption. Clinically the syndrome may be produced by any Summary
HYPOTHESIS
It is suggested that the syndrome is due to a reduction in c.s.F. absorption causing an increase in c.s.F. volume. It is this increase in volume, which is accommodated in a distended subarachnoid space, that is responsible for the increase in intracranial pressure. The reduction in c.s.F. absorption is due to a change in the relation between the factors which control the passage of C.S.F. across the arachnoid villi. This relation may be formulated as follows:
where FC.8.F. represents flow of C.S.F. across the arachnoid villi (i.e., absorption), PC.S.F. the c.s.F. pressure within the subarachnoid space, Pgs. the sagittal-sinus pressure, and R.y. the resistance to flow across the arachnoid villi. Any factor which leads to a sufficient increase in sagittal-sinus pressure or in the resistance across the arachnoid villi may, therefore, cause the syndrome provided that c.s.F. production remains relatively constant. c.s.F. absorption under these circumstances will depend on the resultant increase in PC.S.F. compensating for the increase in either P88g or R.B..v. In addition, alternative pathways of c.s.F. absorption may be utilised. CLINICAL
EVIDENCE
The most direct clinical evidence in favour of this concept is the demonstration of delayed c.s.F. flow and reduced absorption on isotope studies of patients with benign intracranial hypertension.8,9 In particular, two patients in the latter study showed a normal clearance of c.s.F. from the ventricles but had a marked delay in flow through the subarachnoid space. Evidence of an increase in c.s.F. volume includes the common finding of distended subarachnoid spaces," low c.s.F.
noma
only
with
one
asbestosis and an increase in the number of cases of asbestos-associated cancer.6 This would be in keeping with a long latent period, of say 30 years, as in our patients. The patients’ smoking-habits were similar, irrespective of their exposure to asbestos. As expected, however, there were more smokers among the patients than among the controls.5 It may be that smoking is a cofactor in the development of laryngeal carcinoma, but, as previously pointed out/ it is unlikely to be very important, since the incidence of laryngeal carcinoma in the twentieth century has declined slightly in the face of an enormous increase in tobacco
consumption.
Hypothesis ACUPUNCTURE ANÆSTHESIA
G. M. BULL Medical Research Council Clinical Research Centre, Watford Road, Harrow, Middlesex HA1 3UJ
A possible mechanism to explain acupuncture anæsthesia is presented which takes into consideration the fact that acupuncture needles have to be vibrated or rotated and which is not invalidated by the lack of correlation between the traditional acupuncture sites and the It is anatomy of the peripheral nervous system. suggested that rhythmic stimulation causes areas of the cerebral cortex to become " locked on" to the stimulating rhythm and thus " busy " and unable to react to stimuli in the normal way.
Summary
Two hypotheses are currently favoured to explain how acupuncture might induce anaesthesia.1 The one is hypnotism and the other is the so-called <
We intend to perform histological examinations for asbestos bodies in patients with laryngeal carcinoma. not many specimens are available because the vast majority of patients with laryngeal carcinoma are treated by radiotherapy. Even if the tumour recurs and the larynx becomes available for study after laryngectomy, it is doubtful whether asbestos bodies could be found-presumably they would lie at the centre of the tumour and thus be sloughed off as the tumour ulcerated during its growth. Even if they survived this insult, they would almost certainly slough out in the healing process after radiotherapy. As a pilot study, we examined serial sections from one larynx, but no asbestos bodies were
Unfortunately, however,
found. Requests for reprints should be addressed
to
P. M. S.
REFERENCES 1. 2.
Buchanan, W. D. Ann. N.Y. Acad. Sci. 1965, 132, 507. Wagner, J. C., Sleggs, C. A., Marchand, P. Br. J. ind. Med. 1960, 17, 260.
3. Whitwell, F., Rawcliffe, R. M. Thorax, 1971, 26, 6. 4. Stell, P. M., McGill, T. Lancet, 1973, i, 678. 5. Stell, P. M. ibid. 1972, i, 617. 6. Selikoff, I. T., Hammond, I. C., Churg, J. J. Am. med. Ass. 1968, 204, 106.
the limb proximally in the " path " of the ascending * sensory or motor disturbance.3,4 It is postulated that this stimulus causes the cortex in the area surrounding the dysrhythmic focus to become sufficiently refractory to block the spread of the dysrhythmia to the rest of the cortex. The " busy " area of the cortex is partly refractory to further stimulation. There is another circumstance in which the cortex can be made refractory to random impulses, and that is when a rhythmic stimulus is fed in through a sensory channel. This is most easily demonstrated in the case of the visual cortex, where photic stimulation at appropriate rates may induce a wide variety of subjective experiences not only in the visual fields but also in other sensory modalities. In many subjects fits of varying sorts may be induced and demonstrated electroencephalographically or seen clinically. This forms the basis of the use of photic stimulation in diagnostic electroencephalography. The phenomenon is not confined to the visual pathways, and similar effects can be demonstrated electroencephographically and occasionally clinically with rhythmic stimulation of the periphery or of the auditory pathways. The rate of stimulation appears to be critical and to vary between about 1 and 25 cycles per second. Moreover, the interval between volleys of stimulation appears to be important in determining the response. Voluntary inhibition or augmentation of the responses can be demonstrated both electroencephalographically and subjectively.5.6 It appears that, when a sensory stimulus recurs at an appropriate frequency, large " to that areas of the cortex may become " locked on or a harmonic of it and that its normal frequency function may be thereby disturbed. The analogy with acupuncture anaesthesia is close. The frequency of vibration or rotation of the acupuncture needles is within the appropriate range to
418 " lock on " the cortical rhythm and could thereby of the cortex to be " busy ". The lack of correlation between the traditional acupuncture sites and the anatomy of the peripheral nervous system would not invalidate this hypothesis. One could postulate that the acupuncture sites happen to be supplied by nerves which, by reason of appropriate lengths and pathways, have time constants of transmission which " tune " them to the
to
cause areas
stimulating frequency. This hypothesis is moreover not inconsistent with a participation of hypnotic effects. The mechanism of hypnosis has never been adequately explained. Perhaps it facilitates establishment of a " busy " cortex just as with voluntary inhibition or augmentation of rhythmic responses mentioned above. The " busy cortex" hypothesis could be studied by varying the frequency of acupuncture-needle vibration while assessing the pain threshold and correlating the findings with the electroencephalographic pattern. One could also predict from this hypothesis that an enhancement of the anaesthetic effect would be likely if larger areas of the cortex were recruited to the dominant rhythm by synchronous photic or auditory stimulation.
factor which increases either PS. S or RA.V., and it is suggested therefore that the general term " reduced C.S.F. absorption syndrome " should replace " benign intracranial hypertension" and similar terms. INTRODUCTION
SINCE the early descriptions of Gowers, Quincke, Nonne, and others over 75 years ago 1-3 there have been many clinical reports of the condition now commonly termed benign intracranial hypertension.’ Typically, in this condition, there is raised intracranial pressure with no apparent cause, no associated neurological abnormalities, and normal investigative findings-in particular, a normal ventricular system.’’ The cause of the intracranial hypertension remains unknown; indeed even which intracranial compartment (brain, blood, or c.s.F.) is involved is uncertain. In addition a wide variety of Eetiological agents have been linked to the condition,6,7 although without knowledge of the underlying pathophysiology it is impossible to say how these factors are related to The present the increase in intracranial pressure. the intracranial is advanced to hypothesis explain to a more hypertension, suggest appropriate term for this condition, and to show how it is related to known astiological agents.
REFERENCES 1. 2. 3. 4. 5.
Lancet, 1973, i, 1372. Melzack, R., Wall, P. D. Science, 1965, 150, 971. Jackson, J. Hughlings. Lancet, 1868, i, 618. Wilson, S. A. Kinnier. Neurology. London, 1940. Walter, V. J., Walter, W. Grey. J. Electroenceph. clin. Neurophysiol. 1949, 1, 1. 6. Kiloh, L. G., McComas, A. J., Osselton, J. W. Clinical Electroencephalography. London, 1972.
REDUCED C.S.F. ABSORPTION SYNDROME Reappraisal of Benign Intracranial Hypertension and Related Conditions IAN
JOHNSTON
Department of Neurosurgery, Hospital for Sick Children, Toronto
A reduced
cerebrospinal-fluid (C.S.F.) absorption syndrome has been defined by considering the factors controlling C.S.F. absorption; the pressure-gradient between the subarachnoid space and the superior sagittal sinus (PC..S.F.-PS.S.), and the resistance to flow across the absorptive channels (RA.V.). The hypothesis is advanced that this syndrome is the same as that previously described by various terms (benign intracranial hypertension, pseudotumour cerebri, otitic hydrocephalus, &c.), since the clinical evidence favours an increase in C.S.F. volume due to impaired absorption as the cause of the intracranial hypertension. In known such as occlusion addition, ætiological agents of the sagittal sinus or the major neck veins (increasing PS.S) or acute steroid withdrawal (increasing RA.V.) have been shown experimentally to cause a marked reduction in C.S.F. absorption. Clinically the syndrome may be produced by any Summary
HYPOTHESIS
It is suggested that the syndrome is due to a reduction in c.s.F. absorption causing an increase in c.s.F. volume. It is this increase in volume, which is accommodated in a distended subarachnoid space, that is responsible for the increase in intracranial pressure. The reduction in c.s.F. absorption is due to a change in the relation between the factors which control the passage of C.S.F. across the arachnoid villi. This relation may be formulated as follows:
where FC.8.F. represents flow of C.S.F. across the arachnoid villi (i.e., absorption), PC.S.F. the c.s.F. pressure within the subarachnoid space, Pgs. the sagittal-sinus pressure, and R.y. the resistance to flow across the arachnoid villi. Any factor which leads to a sufficient increase in sagittal-sinus pressure or in the resistance across the arachnoid villi may, therefore, cause the syndrome provided that c.s.F. production remains relatively constant. c.s.F. absorption under these circumstances will depend on the resultant increase in PC.S.F. compensating for the increase in either P88g or R.B..v. In addition, alternative pathways of c.s.F. absorption may be utilised. CLINICAL
EVIDENCE
The most direct clinical evidence in favour of this concept is the demonstration of delayed c.s.F. flow and reduced absorption on isotope studies of patients with benign intracranial hypertension.8,9 In particular, two patients in the latter study showed a normal clearance of c.s.F. from the ventricles but had a marked delay in flow through the subarachnoid space. Evidence of an increase in c.s.F. volume includes the common finding of distended subarachnoid spaces," low c.s.F.