The article on a neurological MRI menagerie by Jonathan Schott1 was a good read. I would like to highlight an important and potentially treatable differential diagnosis for the “eye of the tiger” sign, highlighted by Professor Patrick Chinnery in his interesting talk at the 29th Advanced Clinical Neurology Course in Edinburgh in May this year and recently published in Brain. Neuroferritinopathy produce...
The article on a neurological MRI menagerie by Jonathan Schott1 was a good read. I would like to highlight an important and potentially treatable differential diagnosis for the “eye of the tiger” sign, highlighted by Professor Patrick Chinnery in his interesting talk at the 29th Advanced Clinical Neurology Course in Edinburgh in May this year and recently published in Brain. Neuroferritinopathy produces similar neuroradiological changes to pantothenate kinase-associated neurodegeneration. In males and non-menstruating females, the serum ferritin will help to distinguish panthotenate kinase deficiency from neuroferritinopathy.
Sui H Wong
References
1. Schott JM. A neurological MRI menagerie. Pract Neurol 2007;7:186–90.
2. Chinnery PF. Clinical features and natural history of
neuroferritinopathy caused by the GTL1160InsA mutation. Brain 2007;130:110–19.
I am impressed that Ridsdale et al has done justice to a topic that has been on many minds. I cannot but hail this wonderful masterpiece of theirs and hope that all in the medical profession having anything to do with the
Nervous System would lay their hands on this article.
I was a patient of Neurophobia until the third year in my residency when during my second rotation in Neurology, i develo...
I am impressed that Ridsdale et al has done justice to a topic that has been on many minds. I cannot but hail this wonderful masterpiece of theirs and hope that all in the medical profession having anything to do with the
Nervous System would lay their hands on this article.
I was a patient of Neurophobia until the third year in my residency when during my second rotation in Neurology, i developed a lot of interest in Cerebral Palsy. We had a brilliant neurologist then (she did not wear bow ties!)who believed in making things very simple for all to understand. This became the first time i began to perceive Neorology differently. Later in the year, i became a DAAD* fellow during which i spent one year
at the Child Neurology Department of the University Children's Hospital, Eberhard-Karl University, Tuebingen,Germany. I found here that Neurology could not only be as interesting as Cardiology, but could indeed appeal to all clinicians.
With Neurological diseases and related conditions posing some of the most outstanding medical challenges worldwide today, efforts like this laudable one by Ridsdale and group, aimed at dissolving the debilitating neurology myth among medical students and doctors, would certaily be of
great value. This is even more so in the developing world where i live and practice, where Neurophobia among medical students and doctors is not only dangerously costly, but seems to negatively impact the future since less and less residents are showing interest in Neurology. I am fired by this article to renew my resolve to aid the upcoming generation of clinicians in overcoming Neurophobia.
Thank you.
Uzochukwu E Egere
References
1. Preventing neurophobia in medical students, and so future doctors. Leone Ridsdale, Roger Massey, and Lucy Clark. PRACTICAL NEUROLOGY 2007; 7: 116-123 (Teaching neurology)
I fully agree with the comeents made by Prof Warlow on current medical research. How often have we found ourselves proven wrong with time, of what we thought marvellous treatments. This trend will continue
and will expand with the trend to find out modest benefits of treatment effects by large trials. We may say the same of such trials one day and I wonder if Prof Warlow would agree....
I fully agree with the comeents made by Prof Warlow on current medical research. How often have we found ourselves proven wrong with time, of what we thought marvellous treatments. This trend will continue
and will expand with the trend to find out modest benefits of treatment effects by large trials. We may say the same of such trials one day and I wonder if Prof Warlow would agree. For instance trying to find out whether aspirin is better than clopidogrel or vice versa. However big the
trial is, we know that the end result would show only a marginal benefit and probably not relevant clinically. But before this conclusion is made, millions will be spent and a huge effort and time will be wasted.
Probably it is time to revert back to smaller trials, so that the treatments tested will have to have a bigger significant effect to come up with positive or negative results. Our reliance on statistics have contributed immensely to this time wasting, and expensive pastime of
academics of organising large trials to weed out marginal, clinically irrelevant benefits.
In their article on neurophobia, or fear of the neural sciences and clinical neurology, Ridsdale et al highlight an important phenomenon, i.e. the misperception that clinical neurology is difficult and only understood
by those who are “brilliant, forgetful” with bulging crania and loud bow ties [1], an impression which may have been encouraged by neurologists who thrive on perpetuating this myth of omn...
In their article on neurophobia, or fear of the neural sciences and clinical neurology, Ridsdale et al highlight an important phenomenon, i.e. the misperception that clinical neurology is difficult and only understood
by those who are “brilliant, forgetful” with bulging crania and loud bow ties [1], an impression which may have been encouraged by neurologists who thrive on perpetuating this myth of omniscience.
In addition, neurophobia may be engendered by non-neurologist tutors, who may themselves be neurophobic, hiding their lack of understanding of the topic by giving their students vague non-answers, which only add to
their confusion. Ridsdale et al describe a programme adopted at King’s College, comprising small group teaching by neurologists, neurosurgeons, neurology residents and paramedical staff, which emphasises topics commonly seen by general practitioners, as well as core neurology
examination skills [1]. We would like to applaud their attempts to demystify and simplify neurology, and to highlight our own under- and postgraduate educational programmes in neurology at the National University of Singapore. Upon commencing clinical training, our medical
undergraduates undergo a refresher course in clinical neuroanatomy, followed by a lecture on neurologic localisation, replete with videotaped vignettes of proper neurologic examination techniques, normal and abnormal
clinical signs. Subsequently, they are taught the core neurology examination skills in groups of 6-8, first conducting the examinations on their fellow undergraduate volunteers, before progressing to bedside tutorials on progressively more complicated and interesting “live”
patients [2]. In 2003, we introduced a “neurological localisation course” for our postgraduate trainees preparing for the MRCP PACES (Practical Assessment of Clinical Examinations Skills) examination. During the
course, trainees are observed by accredited neurologist tutors whilst they examine a series of patients with good clinical signs or interesting neurological conditions, after which their examination techniques are critiqued, and they are taught to ascertain the level of the neurological lesion by analysing the clinical signs elicited [3]. The success of this course has prompted us to organise tutorials for our medical undergraduates along similar lines.
Finally, in order to simplify abstruse concepts, we have sought to explain the workings of the brain and sense organs in terms of familiar everyday objects [4]. For example, by likening the eye to a security camera, we have been able to explain how conjugate movements of both eyes
allow us a wider field of vision, enable us to adjudge distance (stereoscopy) and how dysconjugate movements cause split images (binocular diplopia). In addition, by extending the analogy to include problems in the gears (i.e. extraocular muscles) that drive the cameras, we have
managed to explain gaze palsies from cranial neuropathies, myasthenia gravis and dysthyroid ophthalmopathies. By using the same “familiarity breeds comprehension” concept, and likening the brain and spinal cord to the central processing unit (CPU) of a computer and its electrical
conduits, we have been able to discuss lesions in the central and peripheral nervous systems and somatotopic representation [4]. We are heartened that neurologists are recognising the invidious disease that is neurophobia and attempting to eradicate it through education.
References
1. Ridsdale L, Massey R, Clark L. Preventing neurophobia in medical students, and so future doctors. Practical Neurology 2007;7:116-23.
2. Lim EC, Ong BK, Seet RC. Using videotaped vignettes to teach medical students to perform the neurologic examination. J Gen Intern Med 2006;21:101.
3. Lim EC, Seet RC, Ong BK. Neurological localisation course for postgraduate candidates. Med Educ 2006;40:487-8.
4. Lim EC. Familiarity breeds comprehension: going with what you know. Acad Med 2006;81:270.
I must thank Dr Smith for his entertaining and informative case study of van Gogh. (1) It pains me to ask for caution to be used when interpreting his findings, (particularly as I love a good pun for a title).
Arnold and Loftus in 1991 calculated that one must drink 182 litres of absinthe to induce xanthopsia. (2,3,4) After that lethal load, one can only speculate that it may be difficult for Mr V...
I must thank Dr Smith for his entertaining and informative case study of van Gogh. (1) It pains me to ask for caution to be used when interpreting his findings, (particularly as I love a good pun for a title).
Arnold and Loftus in 1991 calculated that one must drink 182 litres of absinthe to induce xanthopsia. (2,3,4) After that lethal load, one can only speculate that it may be difficult for Mr VG to find his muse until the affects of green liquid had thoroughly worn off.
Arnold and Loftus do make a good case for acute intermittent porphyria. (5) However as mentioned by Dr Smith, the presence of digitalis in not one but two portraits of his physician, Gachet, just seems too
perfect to ignore.
Rhys Thomas
Medical SHO, Gloucestershire Royal Hospital
Competing Interests: I have enjoyed a glass of absinthe in Prague - but it did not cloud my judgement.
References
1. Smith PEM, Absinthe attacks, Practical Neurology 2006;6:376-381
2. Wolf P, Creativity and chronic disease Vincent van Gogh (1853-1890) West J Med. 2001 November; 175(5): 348
3. Arnold WN and Loftus LS, Xanthopsia and van Gogh's yellow palette,Eye. 1991;5 (Pt 5):503-10
4. Arnold W, The Illness of Vincent Van Gogh, Journal of the History of the Neurosciences, 2004, Vol 14: No 1, pp 22-43
5. Loftus LS and Arnold WN, Vincent van Gogh's illness: acute intermittent porphyria? BMJ. 1991 December 21; 303(6817): 1589–1591
I very much enjoyed Dr Stewart’s informative article on ulnar
neuropathies in the August issue of the journal,1 which included images of
Rodin’s The Thinker to demonstrate that elbow flexion may increase the
likelihood of nerve damage.
May I suggest the painting of Saint Bartholomew of 1661 (see fig) by
Rembrandt van Rijn (1606–69) in the J Paul Getty Museum, Los Angeles, as a
possible exam...
I very much enjoyed Dr Stewart’s informative article on ulnar
neuropathies in the August issue of the journal,1 which included images of
Rodin’s The Thinker to demonstrate that elbow flexion may increase the
likelihood of nerve damage.
May I suggest the painting of Saint Bartholomew of 1661 (see fig) by
Rembrandt van Rijn (1606–69) in the J Paul Getty Museum, Los Angeles, as a
possible example of ulnar neuropathy? Wasting of the first dorsal
interosseous muscle seems evident in the apostle’s left hand.
In the differential diagnosis of ulnar neuropathy, camptodactyly (bent
little finger) might also be included. Although there are no motor or
sensory signs, patients may sometimes be referred for neurophysiological
studies to exclude ulnar neuropathy because of the clawed hand posture.2
REFERENCES
1. Stewart J. Ulnar neuropathies: where, why, and what to do? Practical
Neurology 2006;6:218–29.
2. Larner AJ. Camptodactyly in a neurology outpatient clinic. Int J Clin
Pract 2001;55:592–5.
I felt rather uncomfortable with some of the articles in the August
2006 issue of the Practical Neurology and it was not because I was reading
the journal in a sultry afternoon of Indian summer.
Andrew Chancellor was
wrong in invoking a clinical diagnosis of multiple sclerosis in his fourth
problem (Test Yourself, p260). The diagnosis of multiple sclerosis (MS)
cannot be made without objecti...
I felt rather uncomfortable with some of the articles in the August
2006 issue of the Practical Neurology and it was not because I was reading
the journal in a sultry afternoon of Indian summer.
Andrew Chancellor was
wrong in invoking a clinical diagnosis of multiple sclerosis in his fourth
problem (Test Yourself, p260). The diagnosis of multiple sclerosis (MS)
cannot be made without objective clinical findings, even if objective
paraclinical findings are in place (1). In the given case, one would only
suspect the possibility of demyelination or a "clinically vague syndrome"
(1).
We should be aware of the inherent pitfall of overdiagnosis of MS
and its consequences. In their commentary, Gold and Hohfield (2) avoided
the key issue of selection of MS patients for monoclonal antibody based
interventions in clinical practice. Given the unknown risks of long-term
therapy, the benefit would seem less certain in patients with low
disability and relatively stable disease (3). However, nearly two-thirds
of recruited patients in natalizumab trials (1801 and 1802) had low
disability (Kurtzke’s EDSS score 0-2.5), only a minority had serious
clinical relapses during treatment (7 and 13% in the treated and placebo
arms respectively in the monotherapy trial), and absolute reduction of
disease progression was rather modest (between 6 and 12%). I am uncertain
if the trial data can be extrapolated to the general population of the MS
clinic notwithstanding the regulatory approval of the drug.
My disappointment did not get any better with the review of ulnar
neuropathy by John Stewart (4). Worldwide, probably the commonest cause of
ulnar neuropathy -and its disabling serious motor complication-is leprosy,
not habitual elbow leaning. Leprosy only appears at the tail of Table 2,
with no mention about its clinical diagnosis and management, and the fact
that leprosy is possibly the only example of peripheral (ulnar) nerve
abscess. A picture of Hansen, rather than the sculpture of Rodin would
have been more appropriate, but I have enclosed a picture (courtesy: World
Health Organisation) of an ulnar
neuropathic hand of leprosy after reconstruction surgery. Maybe the
editor would commission an article on this topic in the future to rectify
the omission. As one of the junior colleagues has written it, I would
prefer not commenting on some of the misconceptions regarding the immunity
of Guillain-Barre syndrome (GBS)(5).
Passive transfer of anti-ganglioside
antibodies has never capitulated the nerve pathology of GBS and anti-GQ1b
antibody does not explain the known pathology of cerebellar ataxia in
Miller Fisher syndrome. It may also be important to draw the attention
of the readers to the not-so-infrequent findings of liver function test
abnormalities and the commonly overlooked association of GBS with acute
glomerulonephritis(6-10). Plasma exchange or human intravenous
immunoglobulin should be started in an eligible patient once the diagnosis
is clinically secure and treatment must not be delayed for peripheral
nerve electrophysiology (Figure 3, p214). The risk of relapsing GBS is
also higher in treated patients but the relapses respond well to
treatment.
Rather than writing individual responses, I thought it might not be
inappropriate to write a jobbing neurologist’s feedback to the editor and
I hope to be excused if my response falls outside the rules of the book.
Figure
References
1. Polman CH, Reingold SC, Edan G, et al. Diagnostic criteria for
multiple sclerosis: 2005 revisions to the "McDonald criteria". Ann Neurol
2005; 58: 840-6.
2. Gold R, Hohlfield R. Multipe sclerosis therapy: new agents carry
new risks. Practical Neurology 2006; 6: 248-51.
3. Chaudhuri A. Lessons for clinical trials from natalizumab in
multiple sclerosis. BMJ 2006; 332: 416-419.
4. Stewart J. Ulnar neuropathies: where, why and what to do. Practical
Neurology 2006; 6: 218-229.
5. Pritchard J. What’s new in Guillain-Barre syndrome? Practical
Neurology 2006; 6: 218-217.
6. Behan PO, Lowen stein LM, Stilmant M, Sax DS. Landry-Guillain-
Barre-Strohl syndrome and immune-complex nephritis. Lancet 1973; 1: 850-4.
7. Talamo TS, Borochovitz D. Membranous glomerulonephritis associated
with the Guillain-Barre syndrome. Am J Clin Pathol 1982; 78: 563-6.
8. Bettinelli A, Giani M, Rossi L, et al. Ex novo episodes of acute
glomerulonephritis and Guillain-Barre syndrome: a case report. Clin
Nephrol 1989; 31: 269-73.
9. Olbricht CJ, Stark E, Helmchen U, Sculze M, Brunkhorst R, Koch KM.
Glomerulonephritis associated with inflammatory demyelinating
polyradiculoneuropathy: a case report and review of the literature.
Nephron 1993; 64: 139-41.
10. Emsley HC, Molloy J. Inflammatory demyelinating polyneuropathy
associated with membranous glomerulonephritis and thrombocytopenia. Clin
Neurol Neurosurg 2002; 105: 23-6.
I read with interest this work ..indeed nerve
ultrasonography has other parameters more than cross section area
measurements in detection of the pathological changes and prediction of
outcome of the treatment (medical or surgical}...the normal nerve as seen
by high resolution ultrasonography is:
1- oval shaped or round with high
ability to change its shape in response to applied pressure easi...
I read with interest this work ..indeed nerve
ultrasonography has other parameters more than cross section area
measurements in detection of the pathological changes and prediction of
outcome of the treatment (medical or surgical}...the normal nerve as seen
by high resolution ultrasonography is:
1- oval shaped or round with high
ability to change its shape in response to applied pressure easily seen by
dynamic study during flexion and extension of the limbs
2- the nerve
according to the number of fascicles has a normal fascicular pattern
3- it
has the ability to change its position according to the force applied on
it during limb movement this excursion can be calculated by the dynamic
study
4- in response to exercise it reacts in the form of increase its
cross section area and increase signals from its blood vessels
5- in
response to the applied pressure the cross section area is reduced by 20-30% with flattening of the contour so by applying all these parameters the
subtle changes can be detected first = the loss of fascicular pattern which
seen with long standing pathology can be detected and its length can be
measured = second the loss of compressibility by applied pressure [most
probably due to fibrosis and new short nerve fiber growth] can be easily
measured and the less the compressibility the poorer the outcome of
treatment third = loss of normal nerve excursion during limb movement on
the dynamic study due either intrinsic changes or surrounding fibrosis
fourth the focal nerve changes can be estimated and the change in the
volume by measuring the affected segment length and the cross section area
can calculated and used for follow up ....so the cross section area as
single criterion do not explain the recurrent cases of the operated
cubital tunnel syndrome or the poor response to the operation in
conservative cases finally to use the gray ultrasound alone the
echotexture of the nerve with applied stress compressibility test together
with the cross sectional area in rest and on dynamic stress condition
should be used in all examined cases thanks
Dear Editor,
The article on a neurological MRI menagerie by Jonathan Schott1 was a good read. I would like to highlight an important and potentially treatable differential diagnosis for the “eye of the tiger” sign, highlighted by Professor Patrick Chinnery in his interesting talk at the 29th Advanced Clinical Neurology Course in Edinburgh in May this year and recently published in Brain. Neuroferritinopathy produce...
Dear Editor,
I am impressed that Ridsdale et al has done justice to a topic that has been on many minds. I cannot but hail this wonderful masterpiece of theirs and hope that all in the medical profession having anything to do with the Nervous System would lay their hands on this article.
I was a patient of Neurophobia until the third year in my residency when during my second rotation in Neurology, i develo...
Dear Editor,
I fully agree with the comeents made by Prof Warlow on current medical research. How often have we found ourselves proven wrong with time, of what we thought marvellous treatments. This trend will continue and will expand with the trend to find out modest benefits of treatment effects by large trials. We may say the same of such trials one day and I wonder if Prof Warlow would agree....
Dear Editor,
In their article on neurophobia, or fear of the neural sciences and clinical neurology, Ridsdale et al highlight an important phenomenon, i.e. the misperception that clinical neurology is difficult and only understood by those who are “brilliant, forgetful” with bulging crania and loud bow ties [1], an impression which may have been encouraged by neurologists who thrive on perpetuating this myth of omn...
Dear Editor,
I must thank Dr Smith for his entertaining and informative case study of van Gogh. (1) It pains me to ask for caution to be used when interpreting his findings, (particularly as I love a good pun for a title).
Arnold and Loftus in 1991 calculated that one must drink 182 litres of absinthe to induce xanthopsia. (2,3,4) After that lethal load, one can only speculate that it may be difficult for Mr V...
Dear Editor
I very much enjoyed Dr Stewart’s informative article on ulnar neuropathies in the August issue of the journal,1 which included images of Rodin’s The Thinker to demonstrate that elbow flexion may increase the likelihood of nerve damage.
May I suggest the painting of Saint Bartholomew of 1661 (see fig) by Rembrandt van Rijn (1606–69) in the J Paul Getty Museum, Los Angeles, as a possible exam...
Dear Editor,
I felt rather uncomfortable with some of the articles in the August 2006 issue of the Practical Neurology and it was not because I was reading the journal in a sultry afternoon of Indian summer.
Andrew Chancellor was wrong in invoking a clinical diagnosis of multiple sclerosis in his fourth problem (Test Yourself, p260). The diagnosis of multiple sclerosis (MS) cannot be made without objecti...
Dear Editor,
I read with interest this work ..indeed nerve ultrasonography has other parameters more than cross section area measurements in detection of the pathological changes and prediction of outcome of the treatment (medical or surgical}...the normal nerve as seen by high resolution ultrasonography is:
1- oval shaped or round with high ability to change its shape in response to applied pressure easi...
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