1139
exacerbation of the disease, and a return of reflexes during remission. This pattern has also been recorded by other workers.3-7 There are only two reports of spontaneous remission-one after 4 years with return of tendon reflexes’ and one after 14 years with no comment about reflexes.8 This patient’s wellbeing provides evidence of the benign nature of the disease and stimulates speculation as to the mechanism of the loss of tendon reflexes. If the spontaneous motor fibre activity were not only confined to K fibres but also implicated &bgr; and y fibres to muscle spindles, afferent fibre activity might increase. Suppression of reflexes may then be the result of a central process in a manner analogous to the suppression of reflexes caused by muscle
vibration.9 Department of Neurology, University Hospital of Wales,
Department of Paediatric Neurology, Newcastle General Hospital,
DAVID GARDNER-MEDWIN
1 Gardner-Medwin D, Walton JN. Myokymia with impaired muscular relaxation. Lancet 1969; i: 127-30. 2. Isaacs H. Myokymia with impaired muscular relaxation. Lancet 1969; i: 779. 3. Isaacs H. A syndrome of continuous muscle-fibre activity. J Neurol Neurosurg Psychiatry 1961; 24: 319-25. 4. Isaacs H. Continuous muscle fibre activity in an Indian male with additional evidence of terminal motor fibre abnormality. J Neurol Neurosurg Psychiatry 1967; 30: 126-33. 5. Wallis WE, Poznak AV, Plum F. Generalised muscular stiffness, fasciculations and myokymia of peripheral nerve origin Arch Neurol 1970; 22: 430-39. 6. Irani PF, Purohit AV, Wadia NH. The syndrome of continuous muscle fibre activity. Acta Neurol Scand 1977; 55: 273-88. 7 Lublin FD, Tsairis P, Streletz RA, et al. Myokymia and impaired muscular relaxation with continuous motor unit activity. J Neurol Neurosurg Psychiatry 1979; 42: 557-62. 8. Isaacs H, Heffron JJA. The syndrome of ’continuous muscle fibre activity’ cured. J Neurol Neurosurg Psychiatry 1974; 37: 1231-35. 9 Gillies JD, Lance JW, Neilson PD, et al. Presynaptic inhibition of the monosynaptic reflex by vibration. J Physiol 1969; 205: 329-39.
Photodynamic therapy of localised prostatic cancer
SIR,- The treatment alternatives for localised prostatic cancer are mainly radical surgery or radiotherapy. Both are associated with a considerable morbidity. Since well-differentiated localised prostate carcinoma has a rather benign course,1 treatments with fewer side-effects have been looked for. Nd-YAG laser treatment of the prostatic capsule after radical transurethral resection was introduced in 1982 by Sander and Beisland2 but our experience with this method has been less favourable. Even when our patients were doing well clinically, prostate-specific antigen (PSA) values were still abnormal after the treatment (above 0-5 µg/l [Hybritech kit]); and even if a transrectal ultrasound scan did not show any tumour, we found cancer in random biopsy specimens. Photodynamic therapy (PDT) has been used in the treatment of a variety of malignant tumours with promising results, not least in patients with superficial bladder cancer.3 We have used PDT for 2 years in patients with therapy-resistant carcinoma-in-situ of the bladder. We report here the use of PDT in two patients with
localised prostatic cancer. The work-up before the treatment included routine blood tests, a bone scan, intravenous pyelography, and a transrectal ultrasound scan. The prostate was resected at two sessions, to make the resection as complete as possible. A second ultrasound scan was done 3-4 weeks later to assess how radical the resection had been. 6 weeks after the second resection the patients were injected with 1-5 mg/kg body weight haematoporphyrin derivative (first case) or 2-5 mg/kg ’Photofrin’ (polyporphyrin) (second case) followed by illumination of the prostatic cavity 48-72 h later with laser light (628 mm) through a quartz-fibre with a spherical tip. The calculated energy dose administered to the wall of the prostatic cavity was 15 J/cm2. At follow-up 3 months later random biopsy specimens were free from malignancy. PSA values were 10 and 6 µg/l preoperatively and measurement at PSA,
There
were
no
adverse local effects such
as
the urgency
frequently experienced after PDT for bladder carcinoma. To avoid phototoxicity the two patients with prostatic cancer followed the same regimen as our bladder cancer patients-ie, protection from direct sunlight for 6 weeks. Departments of Urology and Otolaryngology, Orebro Medical Centre Hospital, S-701 85 Orebro, Sweden
TORGNY WINDAHL SWEN-OLOF ANDERSSON LENNART LOFGREN
Johansson J-E, Adami H-O, Anderssen S-O, Bergstrom R, Krusemo UB, Kraaz W. Natural history of localised prostatic cancer. A population based study in 223 untreated patients. Lancet 1989; i: 799-803. 2. Sander S, Beisland HO. Laser treatment of localized prostatic carcinoma.J Urol 1984; 1.
ANTHONY WILTON
Heath Park, Cardiff, UK
Newcastle
postoperatively they were 2-5 ug/1 and 02 µg/1, respectively. One patient died 6 months later from a rapidly progressing cancer of the lung, unknown at the time of PDT. At necropsy residual prostatic tissue was investigated histologically by serial sections and no sign of cancer was found. 5 months
132: 280-81. 3. Benson RC. Treatment of diffuse transitional cell carcinoma in situ by whole bladder haematoporphyrin derivative photodynamic therapy. J Urol 1985; 134: 675-78.
Darwin’s illness SIR,-Professor Field is correct to say that Charles Darwin’s ill-health could not have been due either to hyperventilation or to Chagas’ disease (Sept 29, p 826). However, some of his symptoms are not typical of postviral syndromes such as myalgic encephalomyelitis (ME). (Bowlbyl did not mention symptoms such as rheumatic pain and swollen limbs because they did not fit his theory either; and against all the evidence he strongly doubted the existence of any inherited weakness, because this did not suit his idea of an ad hoc psychological cause.) The only condition that can explain every one of Darwin’s many symptoms is multiple allergy arising from a dysfunctioning immune system.2 The inheritance pattern is there, and evidence of crucial
immunosuppressive encounters. Field’s suggestion is not far off the truth. ME also involves immune system dysfunction. In postviral syndromes the immunosuppressive factors are the initial viruses, capable of non-specific immunosuppression.3Among patients with postviral syndromes, and those with allergy, females predominate, a feature noticeable in other immune dysfunctions too. This is difficult to explain on infective grounds.4 Viruses cannot persist on a sexually selective basis. 55 Manor Place, Edinburgh EH3 7EG, UK
FABIENNE SMITH
1. Bowlby J. Charles Darwin: a new biography. London: Hutchinson, 1990. 2. Smith F. Charles Darwin’s ill health. J History Biol (m press). 3. Roitt I. Essential immunology, 5th ed. Oxford: Blackwell, 1984. 4. David AS, Wessely S, Pelosi AJ. PVFS: time for a new approach. Br Med J 1988; 296: 696-98.
SIR,-Professor Field’s letter makes sense only if it is assumed that myalgic encephalomyelitis (ME) is different from chronic hyperventilation. This assumption is commonly made in the mistaken belief that chronic hyperventilation is the outcome of hysterical overbreathing and by those who do not include capnography in their investigation of chronic fatigue. The loss of ability to make and sustain effort in association with Darwin’s symptoms of pain around the heart, gastric symptoms, remissions and aggravation by psychological factors, diurnal variability, panic attacks, failure of performance, hyperacusis, and the adoption of the disorders by family members are common amongst the physiological instability and the derangements caused by hypocapnia and chronic respiratory alkalosis. 1-3 Our study of patients thought to have ME shows that almost all were made worse by hyperventilation, and its symptoms were evident for an average of two years before any virus infection.4 We have two contenders for an identical group of symptoms. The traditional physician calls it effort syndrome or Da Costa’s syndrome caused by chronic hyperventilation and provides
exacerbation of the disease, and a return of reflexes during remission. This pattern has also been recorded by other workers.3-7 There are only two reports of spontaneous remission-one after 4 years with return of tendon reflexes’ and one after 14 years with no comment about reflexes.8 This patient’s wellbeing provides evidence of the benign nature of the disease and stimulates speculation as to the mechanism of the loss of tendon reflexes. If the spontaneous motor fibre activity were not only confined to K fibres but also implicated &bgr; and y fibres to muscle spindles, afferent fibre activity might increase. Suppression of reflexes may then be the result of a central process in a manner analogous to the suppression of reflexes caused by muscle
vibration.9 Department of Neurology, University Hospital of Wales,
Department of Paediatric Neurology, Newcastle General Hospital,
DAVID GARDNER-MEDWIN
1 Gardner-Medwin D, Walton JN. Myokymia with impaired muscular relaxation. Lancet 1969; i: 127-30. 2. Isaacs H. Myokymia with impaired muscular relaxation. Lancet 1969; i: 779. 3. Isaacs H. A syndrome of continuous muscle-fibre activity. J Neurol Neurosurg Psychiatry 1961; 24: 319-25. 4. Isaacs H. Continuous muscle fibre activity in an Indian male with additional evidence of terminal motor fibre abnormality. J Neurol Neurosurg Psychiatry 1967; 30: 126-33. 5. Wallis WE, Poznak AV, Plum F. Generalised muscular stiffness, fasciculations and myokymia of peripheral nerve origin Arch Neurol 1970; 22: 430-39. 6. Irani PF, Purohit AV, Wadia NH. The syndrome of continuous muscle fibre activity. Acta Neurol Scand 1977; 55: 273-88. 7 Lublin FD, Tsairis P, Streletz RA, et al. Myokymia and impaired muscular relaxation with continuous motor unit activity. J Neurol Neurosurg Psychiatry 1979; 42: 557-62. 8. Isaacs H, Heffron JJA. The syndrome of ’continuous muscle fibre activity’ cured. J Neurol Neurosurg Psychiatry 1974; 37: 1231-35. 9 Gillies JD, Lance JW, Neilson PD, et al. Presynaptic inhibition of the monosynaptic reflex by vibration. J Physiol 1969; 205: 329-39.
Photodynamic therapy of localised prostatic cancer
SIR,- The treatment alternatives for localised prostatic cancer are mainly radical surgery or radiotherapy. Both are associated with a considerable morbidity. Since well-differentiated localised prostate carcinoma has a rather benign course,1 treatments with fewer side-effects have been looked for. Nd-YAG laser treatment of the prostatic capsule after radical transurethral resection was introduced in 1982 by Sander and Beisland2 but our experience with this method has been less favourable. Even when our patients were doing well clinically, prostate-specific antigen (PSA) values were still abnormal after the treatment (above 0-5 µg/l [Hybritech kit]); and even if a transrectal ultrasound scan did not show any tumour, we found cancer in random biopsy specimens. Photodynamic therapy (PDT) has been used in the treatment of a variety of malignant tumours with promising results, not least in patients with superficial bladder cancer.3 We have used PDT for 2 years in patients with therapy-resistant carcinoma-in-situ of the bladder. We report here the use of PDT in two patients with
localised prostatic cancer. The work-up before the treatment included routine blood tests, a bone scan, intravenous pyelography, and a transrectal ultrasound scan. The prostate was resected at two sessions, to make the resection as complete as possible. A second ultrasound scan was done 3-4 weeks later to assess how radical the resection had been. 6 weeks after the second resection the patients were injected with 1-5 mg/kg body weight haematoporphyrin derivative (first case) or 2-5 mg/kg ’Photofrin’ (polyporphyrin) (second case) followed by illumination of the prostatic cavity 48-72 h later with laser light (628 mm) through a quartz-fibre with a spherical tip. The calculated energy dose administered to the wall of the prostatic cavity was 15 J/cm2. At follow-up 3 months later random biopsy specimens were free from malignancy. PSA values were 10 and 6 µg/l preoperatively and measurement at PSA,
There
were
no
adverse local effects such
as
the urgency
frequently experienced after PDT for bladder carcinoma. To avoid phototoxicity the two patients with prostatic cancer followed the same regimen as our bladder cancer patients-ie, protection from direct sunlight for 6 weeks. Departments of Urology and Otolaryngology, Orebro Medical Centre Hospital, S-701 85 Orebro, Sweden
TORGNY WINDAHL SWEN-OLOF ANDERSSON LENNART LOFGREN
Johansson J-E, Adami H-O, Anderssen S-O, Bergstrom R, Krusemo UB, Kraaz W. Natural history of localised prostatic cancer. A population based study in 223 untreated patients. Lancet 1989; i: 799-803. 2. Sander S, Beisland HO. Laser treatment of localized prostatic carcinoma.J Urol 1984; 1.
ANTHONY WILTON
Heath Park, Cardiff, UK
Newcastle
postoperatively they were 2-5 ug/1 and 02 µg/1, respectively. One patient died 6 months later from a rapidly progressing cancer of the lung, unknown at the time of PDT. At necropsy residual prostatic tissue was investigated histologically by serial sections and no sign of cancer was found. 5 months
132: 280-81. 3. Benson RC. Treatment of diffuse transitional cell carcinoma in situ by whole bladder haematoporphyrin derivative photodynamic therapy. J Urol 1985; 134: 675-78.
Darwin’s illness SIR,-Professor Field is correct to say that Charles Darwin’s ill-health could not have been due either to hyperventilation or to Chagas’ disease (Sept 29, p 826). However, some of his symptoms are not typical of postviral syndromes such as myalgic encephalomyelitis (ME). (Bowlbyl did not mention symptoms such as rheumatic pain and swollen limbs because they did not fit his theory either; and against all the evidence he strongly doubted the existence of any inherited weakness, because this did not suit his idea of an ad hoc psychological cause.) The only condition that can explain every one of Darwin’s many symptoms is multiple allergy arising from a dysfunctioning immune system.2 The inheritance pattern is there, and evidence of crucial
immunosuppressive encounters. Field’s suggestion is not far off the truth. ME also involves immune system dysfunction. In postviral syndromes the immunosuppressive factors are the initial viruses, capable of non-specific immunosuppression.3Among patients with postviral syndromes, and those with allergy, females predominate, a feature noticeable in other immune dysfunctions too. This is difficult to explain on infective grounds.4 Viruses cannot persist on a sexually selective basis. 55 Manor Place, Edinburgh EH3 7EG, UK
FABIENNE SMITH
1. Bowlby J. Charles Darwin: a new biography. London: Hutchinson, 1990. 2. Smith F. Charles Darwin’s ill health. J History Biol (m press). 3. Roitt I. Essential immunology, 5th ed. Oxford: Blackwell, 1984. 4. David AS, Wessely S, Pelosi AJ. PVFS: time for a new approach. Br Med J 1988; 296: 696-98.
SIR,-Professor Field’s letter makes sense only if it is assumed that myalgic encephalomyelitis (ME) is different from chronic hyperventilation. This assumption is commonly made in the mistaken belief that chronic hyperventilation is the outcome of hysterical overbreathing and by those who do not include capnography in their investigation of chronic fatigue. The loss of ability to make and sustain effort in association with Darwin’s symptoms of pain around the heart, gastric symptoms, remissions and aggravation by psychological factors, diurnal variability, panic attacks, failure of performance, hyperacusis, and the adoption of the disorders by family members are common amongst the physiological instability and the derangements caused by hypocapnia and chronic respiratory alkalosis. 1-3 Our study of patients thought to have ME shows that almost all were made worse by hyperventilation, and its symptoms were evident for an average of two years before any virus infection.4 We have two contenders for an identical group of symptoms. The traditional physician calls it effort syndrome or Da Costa’s syndrome caused by chronic hyperventilation and provides
