674
Journal of the Royal Society of Medicine Volume 83 October 1990
peripheral neuropathy, although nerve conduction studies are not mentioned). This resting tremor is almost invariably accompanied by an additional postural tremor. Although this 'neuropathic' tremor is well recognized in neurological circles, its pathophysiological basis is unclear, since its presence and severity seem to bear no simple relationship to deafferentation, particularly in respect to posterior column sensation'. Indeed, a central, but immunologically mediated, contribution cannot be entirely ruled out. Despite this disagreement concerning the underlying defect, I fully agree that every patient with an unusual tremor and signs of a peripheral neuropathy should have their serum proteins (including immunoglobulin levels) determined. Finally, I suggest that a more appropriate title might be 'Pseudoparkinsonian tremor and dysgammaglobulinaemic polyneuropathy'. N QUINN
Institute of Neurology Queen Square, London WC1N 3BG
Reference 1 Dalakas MC, Teravainen H, Engel WK. Tremor as a feature of chronic relapsing and dysgammaglobulinaemic polyneuropathies. Incidence and management. Arch Neurol 1984;41:711-14
The authors reply below: Dr Quinn provides interesting information regarding tremor in patients with dysgammaglobulinaemic polyneuropathy and he suggests that our patient did indeed have a 'neuropathic' tremor as opposed to a tremor of central origin. While accepting that the chronic sensory lower limb neuropathy in our patient may have been secondary to monoclonal gammopathy, we would stress that the sudden origin of a 'pill-rolling' tremor in the upper limbs coinciding with a grossly elevated plasma viscosity is highly suggestive of a central vascular incident. Dalakas et aLl suggest that there may be a central contribution (immunologically mediated) to the tremor associated with dysgammaglobulinaemic neuropathy. Their patients, however, tended to improve with immunosuppressive therapy whereas the tremor in our patient did not improve with therapy. With regard to Dr Quinn's title suggestion, our term 'Parkinsonian' is used adjectively and provides an acceptable description of the tremor: the prefix 'pseudo' suggests a tremor bearing no resemblance to that associated with Parkinson's disease and this e. In addition, the history would be false in this of longstanding alcohol abuse precludes the use of the suggested latter half of the title, ie 'dysgmmaglobulinaemic neuropathy'. S J MACRURY
Department of General Medicine
R WATKINS K R PATERSON
Royal Infirmary, Glasgow G4 OSF
Reference 1 Dalakas MC, Teravainen H, Engel WK. Tremor as a feature of chronic relapsing and dysgammaglobulinemic polyneuropathies. Incidence and management. Arch
Neurol 1984;41:711-4
Insight and psychosis We read with interest the discussion paper on Insight and Psychosis by Anthony S David (May 1990 JRSM, p 325). We have been attempting to operationalize the concept of insight in schizophrenic patients, and have devised a scale that quantifies insightlessness. Like Dr David, we consider that insight has several dimensions, including attitude to psychiatric illness both past and present, and attitude to treatment. Dr David's inclusion of the ability of the patient to re-label unusual mental events as pathological, as a separate dimension, is, we believe, appropriate. However, compliance with treatment (along with the patient's response to changing symptoms) should be seen not as dimensions of insight, but rather as related events. As Dr David and others have demonstrated1 the correlation between insight and compliance is limited. The mechanisms underlying dimunition of insight remain obscure. Insightlessness may be regarded as: (1) a normal phenomenon, insofar as many people demonstrate limited insight into certain characteristics of their personality and behaviour; (2) a defence mechanism (denial); (3) a delusional phenomenon; (4) a feature of the schizophrenic defect state: and (5) a specific defect of cognition. Given that the direct measurement of components of insightlessness is not possible, our scale attempts to derive an overall measure, based on a semistructured interview, concerning the attitude of the patient to five parameters. These are the appropriateness of clinical management and placement, the treatment prescribed, the existence of a psychiatric disorder, the behaviour in response to symptoms, and the attitude to previous episodes of illness. Preliminary findings indicate that the score so derived correlates well with a global clinical impression of insight based on prior knowledge ofthe patient. M TIMOTHY LAMBERT Academic Department of Psychiatry St Mary's Hosital Medical School DAVID S BALDwm London W2 lNY
Reference 1 Lin IF, Spiga R, Fortsch W. Insight and adherence to medication in chronic schizophrenics. J Clin Psychiatry 1979;40:430-2
From Da Vinci to Harvey J R Novell in his article (June 1990 JRSM, p 396) quotes
my edition of the Anatomical Lectures1 in whose Introduction I gave reasons for the rejection of the date 1616 as that of Harvey's first reference to the circulation of the blood. I gave reasons for believing that the famous passage on f. 80v. which includes the 'two clacks of a water bellows' was an addition to the manuscipt, written at any time up to 10 years later than the main body of the text. Ibelieve that the flow of the handwriting is similar to that of Harvey's treatise De motu locali animalium, dated 1627. This argument, however, is likely to appeal only to palaeographers. The overwhelming argument is that in the whole of the rest of the manuscript, there are no remarks implying or requiring a knowledge ofthe circulation and there are many which reveal ignorance of the circulation. This was Harvey's position in 1616.
Journal of the Royal Society of Medicine Volume 83 October 1990
This manuscript is a collection of lecture notes, used many times and has various additions which refer to editions of books which appeared between 1616 and 1628. An important addition is a reply to Riolan's Anthropographiae of 1626 in which Riolan said that blowing into the uterine veins will distend the arteries. At that date, Harvey's tentative comment was 'Or does the reverse occur?' Subsequently in De Generatione Harvey confidently asserts that only the reverse does occur, a strong argument for the truth of the circulation. Obviously establishing this truth must have taken many months, perhaps years, and it seems likely that Harvey was not certain of all the ramifications of his discovery even in 1626. Oxford GWENETH WHrTTERIDGE References 1 Whitteridge G. The anatomical lectures of William Harvey. Edinburgh: Livingstone, 1964 2 Whitteridge G. Disputations touching the generation of animals. Oxford: Blackwell, 1981
Postviral syndrome Dr D J D Perrins writes (June 1990 JRSM, p 413) of the difficulty in making a definitive diagnosis of postviral syndrome (myalgic encephalomyelitis, ME) echoing the paper by Dr Bowman et aL (December 1988 JRSM, p 712) and goes on to affirm 'the clinical pattern of ME has much in common with multiple sclerosis'. No neurologist of experience would agree with this statement. Dr Perrins admits that some of the patients he himself reported upon may in fact have had MS. Seven out of 10 MS patients will tell you the diagnosis if you listen carefully (the late Henry Miller); 'a blind neurologist is better than a deaf one' (Mumenthaler, Berne). The clinical course of ME and MS is usually quite different, though occasional 'difficult' similarities may be met with. Fortunately an objective test exists which determines the patient with MS diathesis. Those who have not got an MS diathesis cannot develop MS; those who have, may develop MS or any other illness (including ME). Briefly the test depends on the alteration in absolute electrophoretic mobility of well washed red blood cells (RBC) after exposure to emanation from a 0.5 mW He-Ne laser guarded by a Zeiss filter'. After irradiation linoleic acid (LA) is added to a final concentration of 0.08 mg/ml and RBC mobility is measured. As control ethanol is used (since LA is made up in ethanol). If the RBC came from a patient with MS diathesis then they travel more rapidly than control, until at some point between 104 and 110 s exposure to the irradiation there is a sudden transition to control value. Patients with destruction of central nervous system (CNS) tissue from any cause other than MS (other neurological disease, OND) reach break point somewhere between 74 and 81 s, whilst cells from normals do so at 70 s exposure'. The simplest differentiation is to make an exposure of 90 s which is too long for normals or OND and so the 'break' occurs; but not high enough for MS to break. If the clinical history is consonant with ME then a diagnosis of this disease as an organic lesion of the CNS is clear.
A long-term substantiation of this simple differential diagnosis is obtainable by exhibition of essential fatty acids which will convert the MS result to normal in about 9 months, whilst the ME type result scarcely changes.' A real difficulty arises when a patient with MS diathesis picks up ME, for an MS diathesis takes precedence over an OND, but such cases are rare. Full details are available in 'Multiple Sclerosis: a conceptual reappraisal with heuristic implications'2. E J FIELD Honorary Director Naomi Bramson Medical Research The Science Park, University of Warwick Coventry CV4 7EZ
References 1 Field EJ, Joyce G, Field D. Multiple sclerosis: further observations on the effect of He-Ne laser on erythrocytes. IRCS Med Sci 1984;12:717-18 2 Field EJ. Multiple sclerosis: a conceptual reappraisal with heuristic implications. Springfield, llinois: Thomas, 1989
According to D J D Perrins's letter (June 1990 JRSM, p 413) hyperbaric oxygen was used for treatment on the postviral syndrome (myalgic encephalomyelitis) without apparent knowledge of underlying physiology. If one considers a few of the other labels that have been used to describe the disorder, DaCosta's syndrome, soldier's heart, effort syndrome, neurocirculatory asthenia and hyperventilation syndrome1 and their known physiology2 the logic of using hyperbaric pressure becomes clear. In one of his 1919 papers3 describing the cause of the disorder J S Haldane states 'In fact the patients are in the same state as a normal individual at high altitudes where diminished oxygen tension of the inspired air produces the same series of effects'. If symptoms are compared to those of acute mountain sickness the lists appear interchangeable4. A hyperbaric environment without oxygen enrichment has been shown to be a successful treatment for the disorder in its more extreme form where neurocirculatory collapse is life threatening5. Its successful use results from accumulating carbon dioxide and carbonic acid which is detrimental for underwater or hyperbaric work6 but represents simple replacement for an individual in a hypobaric condition due to a compensated alkalosis7. Increased lactic acid production not a result of exercise has been shown to be directly and inversely related to the diminished bicarbonate levels that characterize this disorder7 8. Use of 100% oxygen appears inadvisable9 and unnecessar9 where inadequate oxygen is secondary to reduced carbon dioxide levels (Bohr effect)2 and physical exertion is not a factor. It would appear that longer treatment times, at higher pressure, without additional oxygen would produce faster and better
results5. B EWING
14401 SE Petravinski Rd, F-204, Renton, Washington 98058, USA
References 1 King JC. Hyperventilation - a therapist's point of view: discussion paper. J R Soc Med 1988;81:532-6 2 Magaian GJ, Middaugh DA, in DH. Hyperventilation
syndrome: a diagnosis begging for recognition. West J Med 1983;138:733-6
675
Journal of the Royal Society of Medicine Volume 83 October 1990
peripheral neuropathy, although nerve conduction studies are not mentioned). This resting tremor is almost invariably accompanied by an additional postural tremor. Although this 'neuropathic' tremor is well recognized in neurological circles, its pathophysiological basis is unclear, since its presence and severity seem to bear no simple relationship to deafferentation, particularly in respect to posterior column sensation'. Indeed, a central, but immunologically mediated, contribution cannot be entirely ruled out. Despite this disagreement concerning the underlying defect, I fully agree that every patient with an unusual tremor and signs of a peripheral neuropathy should have their serum proteins (including immunoglobulin levels) determined. Finally, I suggest that a more appropriate title might be 'Pseudoparkinsonian tremor and dysgammaglobulinaemic polyneuropathy'. N QUINN
Institute of Neurology Queen Square, London WC1N 3BG
Reference 1 Dalakas MC, Teravainen H, Engel WK. Tremor as a feature of chronic relapsing and dysgammaglobulinaemic polyneuropathies. Incidence and management. Arch Neurol 1984;41:711-14
The authors reply below: Dr Quinn provides interesting information regarding tremor in patients with dysgammaglobulinaemic polyneuropathy and he suggests that our patient did indeed have a 'neuropathic' tremor as opposed to a tremor of central origin. While accepting that the chronic sensory lower limb neuropathy in our patient may have been secondary to monoclonal gammopathy, we would stress that the sudden origin of a 'pill-rolling' tremor in the upper limbs coinciding with a grossly elevated plasma viscosity is highly suggestive of a central vascular incident. Dalakas et aLl suggest that there may be a central contribution (immunologically mediated) to the tremor associated with dysgammaglobulinaemic neuropathy. Their patients, however, tended to improve with immunosuppressive therapy whereas the tremor in our patient did not improve with therapy. With regard to Dr Quinn's title suggestion, our term 'Parkinsonian' is used adjectively and provides an acceptable description of the tremor: the prefix 'pseudo' suggests a tremor bearing no resemblance to that associated with Parkinson's disease and this e. In addition, the history would be false in this of longstanding alcohol abuse precludes the use of the suggested latter half of the title, ie 'dysgmmaglobulinaemic neuropathy'. S J MACRURY
Department of General Medicine
R WATKINS K R PATERSON
Royal Infirmary, Glasgow G4 OSF
Reference 1 Dalakas MC, Teravainen H, Engel WK. Tremor as a feature of chronic relapsing and dysgammaglobulinemic polyneuropathies. Incidence and management. Arch
Neurol 1984;41:711-4
Insight and psychosis We read with interest the discussion paper on Insight and Psychosis by Anthony S David (May 1990 JRSM, p 325). We have been attempting to operationalize the concept of insight in schizophrenic patients, and have devised a scale that quantifies insightlessness. Like Dr David, we consider that insight has several dimensions, including attitude to psychiatric illness both past and present, and attitude to treatment. Dr David's inclusion of the ability of the patient to re-label unusual mental events as pathological, as a separate dimension, is, we believe, appropriate. However, compliance with treatment (along with the patient's response to changing symptoms) should be seen not as dimensions of insight, but rather as related events. As Dr David and others have demonstrated1 the correlation between insight and compliance is limited. The mechanisms underlying dimunition of insight remain obscure. Insightlessness may be regarded as: (1) a normal phenomenon, insofar as many people demonstrate limited insight into certain characteristics of their personality and behaviour; (2) a defence mechanism (denial); (3) a delusional phenomenon; (4) a feature of the schizophrenic defect state: and (5) a specific defect of cognition. Given that the direct measurement of components of insightlessness is not possible, our scale attempts to derive an overall measure, based on a semistructured interview, concerning the attitude of the patient to five parameters. These are the appropriateness of clinical management and placement, the treatment prescribed, the existence of a psychiatric disorder, the behaviour in response to symptoms, and the attitude to previous episodes of illness. Preliminary findings indicate that the score so derived correlates well with a global clinical impression of insight based on prior knowledge ofthe patient. M TIMOTHY LAMBERT Academic Department of Psychiatry St Mary's Hosital Medical School DAVID S BALDwm London W2 lNY
Reference 1 Lin IF, Spiga R, Fortsch W. Insight and adherence to medication in chronic schizophrenics. J Clin Psychiatry 1979;40:430-2
From Da Vinci to Harvey J R Novell in his article (June 1990 JRSM, p 396) quotes
my edition of the Anatomical Lectures1 in whose Introduction I gave reasons for the rejection of the date 1616 as that of Harvey's first reference to the circulation of the blood. I gave reasons for believing that the famous passage on f. 80v. which includes the 'two clacks of a water bellows' was an addition to the manuscipt, written at any time up to 10 years later than the main body of the text. Ibelieve that the flow of the handwriting is similar to that of Harvey's treatise De motu locali animalium, dated 1627. This argument, however, is likely to appeal only to palaeographers. The overwhelming argument is that in the whole of the rest of the manuscript, there are no remarks implying or requiring a knowledge ofthe circulation and there are many which reveal ignorance of the circulation. This was Harvey's position in 1616.
Journal of the Royal Society of Medicine Volume 83 October 1990
This manuscript is a collection of lecture notes, used many times and has various additions which refer to editions of books which appeared between 1616 and 1628. An important addition is a reply to Riolan's Anthropographiae of 1626 in which Riolan said that blowing into the uterine veins will distend the arteries. At that date, Harvey's tentative comment was 'Or does the reverse occur?' Subsequently in De Generatione Harvey confidently asserts that only the reverse does occur, a strong argument for the truth of the circulation. Obviously establishing this truth must have taken many months, perhaps years, and it seems likely that Harvey was not certain of all the ramifications of his discovery even in 1626. Oxford GWENETH WHrTTERIDGE References 1 Whitteridge G. The anatomical lectures of William Harvey. Edinburgh: Livingstone, 1964 2 Whitteridge G. Disputations touching the generation of animals. Oxford: Blackwell, 1981
Postviral syndrome Dr D J D Perrins writes (June 1990 JRSM, p 413) of the difficulty in making a definitive diagnosis of postviral syndrome (myalgic encephalomyelitis, ME) echoing the paper by Dr Bowman et aL (December 1988 JRSM, p 712) and goes on to affirm 'the clinical pattern of ME has much in common with multiple sclerosis'. No neurologist of experience would agree with this statement. Dr Perrins admits that some of the patients he himself reported upon may in fact have had MS. Seven out of 10 MS patients will tell you the diagnosis if you listen carefully (the late Henry Miller); 'a blind neurologist is better than a deaf one' (Mumenthaler, Berne). The clinical course of ME and MS is usually quite different, though occasional 'difficult' similarities may be met with. Fortunately an objective test exists which determines the patient with MS diathesis. Those who have not got an MS diathesis cannot develop MS; those who have, may develop MS or any other illness (including ME). Briefly the test depends on the alteration in absolute electrophoretic mobility of well washed red blood cells (RBC) after exposure to emanation from a 0.5 mW He-Ne laser guarded by a Zeiss filter'. After irradiation linoleic acid (LA) is added to a final concentration of 0.08 mg/ml and RBC mobility is measured. As control ethanol is used (since LA is made up in ethanol). If the RBC came from a patient with MS diathesis then they travel more rapidly than control, until at some point between 104 and 110 s exposure to the irradiation there is a sudden transition to control value. Patients with destruction of central nervous system (CNS) tissue from any cause other than MS (other neurological disease, OND) reach break point somewhere between 74 and 81 s, whilst cells from normals do so at 70 s exposure'. The simplest differentiation is to make an exposure of 90 s which is too long for normals or OND and so the 'break' occurs; but not high enough for MS to break. If the clinical history is consonant with ME then a diagnosis of this disease as an organic lesion of the CNS is clear.
A long-term substantiation of this simple differential diagnosis is obtainable by exhibition of essential fatty acids which will convert the MS result to normal in about 9 months, whilst the ME type result scarcely changes.' A real difficulty arises when a patient with MS diathesis picks up ME, for an MS diathesis takes precedence over an OND, but such cases are rare. Full details are available in 'Multiple Sclerosis: a conceptual reappraisal with heuristic implications'2. E J FIELD Honorary Director Naomi Bramson Medical Research The Science Park, University of Warwick Coventry CV4 7EZ
References 1 Field EJ, Joyce G, Field D. Multiple sclerosis: further observations on the effect of He-Ne laser on erythrocytes. IRCS Med Sci 1984;12:717-18 2 Field EJ. Multiple sclerosis: a conceptual reappraisal with heuristic implications. Springfield, llinois: Thomas, 1989
According to D J D Perrins's letter (June 1990 JRSM, p 413) hyperbaric oxygen was used for treatment on the postviral syndrome (myalgic encephalomyelitis) without apparent knowledge of underlying physiology. If one considers a few of the other labels that have been used to describe the disorder, DaCosta's syndrome, soldier's heart, effort syndrome, neurocirculatory asthenia and hyperventilation syndrome1 and their known physiology2 the logic of using hyperbaric pressure becomes clear. In one of his 1919 papers3 describing the cause of the disorder J S Haldane states 'In fact the patients are in the same state as a normal individual at high altitudes where diminished oxygen tension of the inspired air produces the same series of effects'. If symptoms are compared to those of acute mountain sickness the lists appear interchangeable4. A hyperbaric environment without oxygen enrichment has been shown to be a successful treatment for the disorder in its more extreme form where neurocirculatory collapse is life threatening5. Its successful use results from accumulating carbon dioxide and carbonic acid which is detrimental for underwater or hyperbaric work6 but represents simple replacement for an individual in a hypobaric condition due to a compensated alkalosis7. Increased lactic acid production not a result of exercise has been shown to be directly and inversely related to the diminished bicarbonate levels that characterize this disorder7 8. Use of 100% oxygen appears inadvisable9 and unnecessar9 where inadequate oxygen is secondary to reduced carbon dioxide levels (Bohr effect)2 and physical exertion is not a factor. It would appear that longer treatment times, at higher pressure, without additional oxygen would produce faster and better
results5. B EWING
14401 SE Petravinski Rd, F-204, Renton, Washington 98058, USA
References 1 King JC. Hyperventilation - a therapist's point of view: discussion paper. J R Soc Med 1988;81:532-6 2 Magaian GJ, Middaugh DA, in DH. Hyperventilation
syndrome: a diagnosis begging for recognition. West J Med 1983;138:733-6
675
