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Misdiagnosis of multiple sclerosis
THE LANCET
Jens Peder Bagger Division of Cardiology, Hammersmith Hospital, London W12 0NN, UK
1
2
MacFadyen RJ, Lees KR, Reid JL. Differences in first dose response to angiotensin converting enzyme inhibition in congestive heart failure: a placebo controlled study. Br Heart J 1991; 66: 206–11. Cleland JG, Dargie HJ, McAlpine H, et al. Severe hypotension after first dose of enalapril in heart failure. BMJ 1985; 291: 1309–12.
Misdiagnosis of multiple sclerosis
Department of Neurology, Hope Hospital, Salford Royal Hospitals NHS Trust, Salford M6 8HD, UK
1
Posner CM. Misdiagnosis of multiple sclerosis and -interferon. Lancet 1997; 349: 1916.
Magnetic-resonance imaging of the brain of premature infants SIR—Malcolm Battin and colleagues (June 14, p 1741)1 describe the presence and distribution of the germinal matrix in premature infants with a 1 Tesla magnetic-resonance imaging system. We have imaged 48 infants of between 25 and 44 weeks postmenstrual age (gestational age plus postnatal age) with a 1·5 Tesla Philips Gyroscan NT-ACS (Philips Medical System, Netherlands). Gestational age was determined by routine early antenatal ultrasound. None
of the infants had clinical or radiological evidence of neurological abnormality. The higher field strength and improved signalto-noise ratio of the 1·5 Tesla system has enabled us to supplement Battin’s data on the distribution of the germinal matrix. The germinal matrix was most easily identified as a low-signal-intensity region, adjacent to the lateral ventricles, on T2weighted images (TR 6000 ms, TE 120 ms). In the most premature infants (25–36 weeks), the germinal matrix was seen throughout the subependyma, extending into the posterior horns of the lateral ventricles. Although in more mature infants (32–37 weeks), the germinal matrix is no longer seen in the posterior horns, it could be identified in the anterior horns extending to the caudothalamic notch. In five of nine term infants the germinal matrix was visible at the tip of the anterior horns. Thus, although the germinal matrix involutes with increasing postmenstrual age, it can be easily identified in healthy infants well after 32 weeks (figure). Our findings suggest that brain development is not only a function of postmenstrual age. Other factors in the antenatal, perinatal, and neonatal periods, such as intrauterine growth retardation, are also important. *David J Evans, Anne-Marie Childs, Luca A Ramenghi, Rosemary J Arthur, Malcolm I Levene Division of Paediatrics and Child Health, School of Medicine, University of Leeds, General Infirmary at Leeds, Leeds LS2 9NS, UK
1
Battin M, Maalouf EF, Counsell S, Herilhy AH, Edwards AD. Magnetic resonance imaging of the brain of premature infants. Lancet 1997; 348: 1741.
44
39
34
29
24
ne No
AH
TN +C AH
522
A C Young
H +P TN +C AH
SIR—Charles Poser’s report on the misdiagnosis of multiple sclerosis (June 28, p 1916)1 strikes a chord with many neurologists, particularly those who were trained before the introduction of computed tomography (CT) and magnetic resonance imaging (MRI).The problem is not just one of misdiagnosis but the overzealous and premature diagnosis of multiple sclerosis. I have under my care a man who presented with headaches for which he had MRI, presumably to exclude an intracranial tumour. In fact, MRI revealed multiple white-matter changes, and, although his history and physical examination did not suggest multiple sclerosis, the diagnosis of multiple sclerosis was discussed with him. Not surprisingly, he has been reduced to a psychological cripple, interpreting every physical symptom as a symptom of multiple sclerosis. No neurologist would regret the introduction of non-invasive imaging techniques which have reduced the discomfort and risk for patients of the older procedures and, in some cases, abolished the need for hospital admission. With only invasive investigations available to them, older neurologists had to rely on clinical diagnosis and learn the importance of the passage of time in clarifying a difficult diagnosis. An investigation should not be used simply because it is non-invasive and, at present, there is no benefit to the patient in making an early diagnosis of multiple sclerosis.
Neurologists commonly see patients with minor neurological symptoms, which may well be transient, but have been prematurely investigated and, as Poser indicates, even prematurely treated. A colleague has commented that we have a new syndrome—MR too far. I now instruct my junior staff not to request MRI for patients with neurological symptoms and no signs. This problem extends well beyond neurological practice; for example, it is common practice for patients who present with vertigo to an ear, nose, and throat surgeon to have MRI. Poser rightly draws attention to a serious problem that merits wider discussion.
Postmenstrual age
pressure in the morning after the first dose of the long-acting ACE inhibitor. No carotid bruits were registered before the initiation of the ACE inhibitor and the patient tolerated 1 month of treatment with another ACE inhibitor 4 months before the adverse event. However, 9 months after the event, significant carotid disease was demonstrated by doppler measurements and therefore some degree of carotid atherosclerotic stenosis was probably present at the time of the event. This case report does not question the suitability of perindopril in the treatment of heart failure. It merely draws attention to some precautions to be taken at the initiation of therapy with this drug in a subgroup of patients.
Presence and distribution of germinal matrix Relation between distribution of germinal matrix and postmenstrual age in premature infants AH=anterior horns of lateral ventricles; CTN=caudothalamic notch; PH=posterior horns of lateral ventricles.
Vol 350 • August 16, 1997
Jens Peder Bagger Division of Cardiology, Hammersmith Hospital, London W12 0NN, UK
1
2
MacFadyen RJ, Lees KR, Reid JL. Differences in first dose response to angiotensin converting enzyme inhibition in congestive heart failure: a placebo controlled study. Br Heart J 1991; 66: 206–11. Cleland JG, Dargie HJ, McAlpine H, et al. Severe hypotension after first dose of enalapril in heart failure. BMJ 1985; 291: 1309–12.
Misdiagnosis of multiple sclerosis
Department of Neurology, Hope Hospital, Salford Royal Hospitals NHS Trust, Salford M6 8HD, UK
1
Posner CM. Misdiagnosis of multiple sclerosis and -interferon. Lancet 1997; 349: 1916.
Magnetic-resonance imaging of the brain of premature infants SIR—Malcolm Battin and colleagues (June 14, p 1741)1 describe the presence and distribution of the germinal matrix in premature infants with a 1 Tesla magnetic-resonance imaging system. We have imaged 48 infants of between 25 and 44 weeks postmenstrual age (gestational age plus postnatal age) with a 1·5 Tesla Philips Gyroscan NT-ACS (Philips Medical System, Netherlands). Gestational age was determined by routine early antenatal ultrasound. None
of the infants had clinical or radiological evidence of neurological abnormality. The higher field strength and improved signalto-noise ratio of the 1·5 Tesla system has enabled us to supplement Battin’s data on the distribution of the germinal matrix. The germinal matrix was most easily identified as a low-signal-intensity region, adjacent to the lateral ventricles, on T2weighted images (TR 6000 ms, TE 120 ms). In the most premature infants (25–36 weeks), the germinal matrix was seen throughout the subependyma, extending into the posterior horns of the lateral ventricles. Although in more mature infants (32–37 weeks), the germinal matrix is no longer seen in the posterior horns, it could be identified in the anterior horns extending to the caudothalamic notch. In five of nine term infants the germinal matrix was visible at the tip of the anterior horns. Thus, although the germinal matrix involutes with increasing postmenstrual age, it can be easily identified in healthy infants well after 32 weeks (figure). Our findings suggest that brain development is not only a function of postmenstrual age. Other factors in the antenatal, perinatal, and neonatal periods, such as intrauterine growth retardation, are also important. *David J Evans, Anne-Marie Childs, Luca A Ramenghi, Rosemary J Arthur, Malcolm I Levene Division of Paediatrics and Child Health, School of Medicine, University of Leeds, General Infirmary at Leeds, Leeds LS2 9NS, UK
1
Battin M, Maalouf EF, Counsell S, Herilhy AH, Edwards AD. Magnetic resonance imaging of the brain of premature infants. Lancet 1997; 348: 1741.
44
39
34
29
24
ne No
AH
TN +C AH
522
A C Young
H +P TN +C AH
SIR—Charles Poser’s report on the misdiagnosis of multiple sclerosis (June 28, p 1916)1 strikes a chord with many neurologists, particularly those who were trained before the introduction of computed tomography (CT) and magnetic resonance imaging (MRI).The problem is not just one of misdiagnosis but the overzealous and premature diagnosis of multiple sclerosis. I have under my care a man who presented with headaches for which he had MRI, presumably to exclude an intracranial tumour. In fact, MRI revealed multiple white-matter changes, and, although his history and physical examination did not suggest multiple sclerosis, the diagnosis of multiple sclerosis was discussed with him. Not surprisingly, he has been reduced to a psychological cripple, interpreting every physical symptom as a symptom of multiple sclerosis. No neurologist would regret the introduction of non-invasive imaging techniques which have reduced the discomfort and risk for patients of the older procedures and, in some cases, abolished the need for hospital admission. With only invasive investigations available to them, older neurologists had to rely on clinical diagnosis and learn the importance of the passage of time in clarifying a difficult diagnosis. An investigation should not be used simply because it is non-invasive and, at present, there is no benefit to the patient in making an early diagnosis of multiple sclerosis.
Neurologists commonly see patients with minor neurological symptoms, which may well be transient, but have been prematurely investigated and, as Poser indicates, even prematurely treated. A colleague has commented that we have a new syndrome—MR too far. I now instruct my junior staff not to request MRI for patients with neurological symptoms and no signs. This problem extends well beyond neurological practice; for example, it is common practice for patients who present with vertigo to an ear, nose, and throat surgeon to have MRI. Poser rightly draws attention to a serious problem that merits wider discussion.
Postmenstrual age
pressure in the morning after the first dose of the long-acting ACE inhibitor. No carotid bruits were registered before the initiation of the ACE inhibitor and the patient tolerated 1 month of treatment with another ACE inhibitor 4 months before the adverse event. However, 9 months after the event, significant carotid disease was demonstrated by doppler measurements and therefore some degree of carotid atherosclerotic stenosis was probably present at the time of the event. This case report does not question the suitability of perindopril in the treatment of heart failure. It merely draws attention to some precautions to be taken at the initiation of therapy with this drug in a subgroup of patients.
Presence and distribution of germinal matrix Relation between distribution of germinal matrix and postmenstrual age in premature infants AH=anterior horns of lateral ventricles; CTN=caudothalamic notch; PH=posterior horns of lateral ventricles.
Vol 350 • August 16, 1997