We were interested to read the recent case study presented by
Rodrigues and Wild in the current edition of Practical Neurology where
they discussed "Psychogenic non-epileptic seizures in early Huntington's
disease"[1]. The authors gave an in-depth account of the clinical profile
of a 51-year-old male with early Huntington's disease (HD) who presented
with repeated episodes of repetitive, purposeless, c...
We were interested to read the recent case study presented by
Rodrigues and Wild in the current edition of Practical Neurology where
they discussed "Psychogenic non-epileptic seizures in early Huntington's
disease"[1]. The authors gave an in-depth account of the clinical profile
of a 51-year-old male with early Huntington's disease (HD) who presented
with repeated episodes of repetitive, purposeless, complex behaviours,
uncharacteristic of HD and discussed the process they followed before
diagnosing psychogenic non-epileptic seizures. Rodrigues and Wild then
went on to conclude that functional neurological symptoms and dissociative
phenomena are a common feature of early HD, particularly in the period
immediately post-diagnosis.
However, this is very different to our own clinical experience. Although
we have not prospectively undertaken a study to look specifically for
this, we have retrospectively analysed our cohort of over 700 patients
that we have seen over the last 20 years. Over this time we could only
identify two individuals who could be described as having a functional
neurological disorder. Furthermore, upon review of the literature we can
only find one case study reporting a psychogenic movement disorder in
preclinical HD [2] and a further case study of a psychogenic gait disorder
that was presented as a poster at the 2013 Sydney Movement Disorders
Conference.
Therefore, we feel that the claim by Rodrigues and Wild is somewhat
misleading -that this is a common feature of early HD. In our experience a
significant proportion of patients experience psychiatric symptoms in
early HD which can take the shape of increased anxiety and
obsessional/compulsive type behaviours and as such patients can exhibit
repetitive stereotypic actions. They do not however, commonly present with
features that would be consistent with a psychogenic disorder and it is
important that the prevalence of such symptoms is not inflated. We
acknowledge that the behaviors presented in this case study as evidenced
by the video [helpfully included in the supplementary data], are not
consistent with anxiety or OCD, but we consider this to be a relative
rarity in HD. In our opinion, an HD patient presenting with physical,
cognitive or psychiatric features that are not consistent with the common
profile of the disease should be thoroughly investigated to rule out all
possible organic causes and only reluctantly should these symptoms be
attributed to a non-organic process.
References
1. Rodrigues, F.B. and E.J. Wild. Psychogenic non-epileptic seizures
in early Huntington's disease. Pract Neurol 2016.
2. Soltan, W., et al. Abnormal gait and bradykinesia in the preclinical
phase of Huntington's disease - psychogenic movement disorder? Acta
Neuropsychiatr 2011;23(6):315-7.
In his recent Neuromythology article1 on the Babinski sign, Professor
Kiernan repeats the oft quoted recommendation regarding the best method
for testing the plantar response, which is to:
'Run a car key (figure 1; or as some have suggested, a most expensive
motor car key...) along the lateral border of the sole.'
It will not surprise many readers of Practical Neurology to learn
th...
In his recent Neuromythology article1 on the Babinski sign, Professor
Kiernan repeats the oft quoted recommendation regarding the best method
for testing the plantar response, which is to:
'Run a car key (figure 1; or as some have suggested, a most expensive
motor car key...) along the lateral border of the sole.'
It will not surprise many readers of Practical Neurology to learn
that the author of this particular recommendation was the late Professor
Henry Miller and moreover that he was proscriptive with regard to the
precise type of ignition key. In his introduction to the book 'Remembering
Henry'1, reflecting on the remarkable life and career of one of the
undoubted pioneers of modern British neurology (and prolific music
critic), the late Lord Walton of Detchant wrote:
'Books could be (and probably will be) filled with quotations from
his tongue and from his fertile pen, some few of which were hallowed for
posterity as 'Henry Millerisms' in a popular medical journal. Who can
forget such comments as: 'The best instrument for obtaining the plantar
response is the ignition key of a Bentley'; or, 'Hemiplegic multiple
sclerosis is a rarity and is to be diagnosed only by me'?'
Henry George Miller (1913-1976) became Professor of Neurology at
Newcastle University in 1964. This was the second chair in neurology to be
established in the UK (Roger Gilliat having been appointed as professor of
clinical neurology at the Institute of Neurology, Queen Square in 1962).
He is best known for his work on multiple sclerosis (publishing the first
ever therapeutic trial in 19532) and accident neurosis. Henry was
successively Dean of Medicine (1966-1968) and Vice Chancellor (1968-76) of
Newcastle University, served as Secretary-General-Treasurer of the World
Federation of Neurology and Chairman of the medical panel of the MS
Society, and held visiting chairs in Australia, Canada and the USA.
References
1. Remembering Henry. LOCK S, WINDLE H (Editors). BMJ.
The Devonshire Press. 1977.
2. Acute disseminated encephalomyelitis and acute disseminated sclerosis;
results of treatment with ACTH. MILLER HG, GIBBONS JL. BMJ.
1953;2(4850):1345-1348
This sensitive review is very welcome, as in our experience, most
patients with functional disorders are told by specialists what they do
not have. I would be much more inclined to refer patients if this kind of
approach was more common. It is one reason why relatively few of the
patients we see in primary care are referred for specialist attention.
Specialists are seeing only the tip of the primary care functional
iceb...
This sensitive review is very welcome, as in our experience, most
patients with functional disorders are told by specialists what they do
not have. I would be much more inclined to refer patients if this kind of
approach was more common. It is one reason why relatively few of the
patients we see in primary care are referred for specialist attention.
Specialists are seeing only the tip of the primary care functional
iceberg. Referral rates vary widely depending variously on levels of
experience, resilience, tolerance of uncertainty and access to peer or
specialist support.
One advantage GPs have over our specialist colleagues is that we get
to know our patients over many years - which is how long it may take to
discover the biography behind their functional symptoms. A second
advantage we have is a knowledge of their family and social context within
which they experience their symptoms enabling us to take a systemic
approach. We have more in common with Oliver Sacks- who rediscovered the
importance of narratives divulged slowly, and used to visit his patients
at home like his father, a London GP, than we do with our younger
neurological colleagues.
It's worth remembering that a clinical history is not narrative and
biography is not psychology. Stone warns against framing functional
neurological symptoms in psychological terms, which I would agree with -
mental illness, if it co-exists ought to be seen as a co-morbidity rather
than a primary cause. But Stone's approach is still biomedical and lacks
the systemic approach that time, continuity and contextual factors
illuminate. I recently invited older GPs to talk to trainees about their
favourite patients. Many described patients who were struck with their
functional symptoms for years, decades even - in a state of narrative
chaos, before something changed and they found some kind of peace with
themselves and were much better able to live with their symptoms. In
narrative medicine this is a shift from chaos to quest, where making sense
takes over from searching for a cure. There are many ways of making sense
of functional symptoms and my main concern about Stone's approach is that
usually it's most honest to admit we just don't (yet) know.
Title: Romberg's test has stood up to the test of time and should
remain standing
(Neuromythology: Letter to the Editor)
I was Interested to read Professor Martin Turner's article entitled
Romberg's test no longer stands up. In the article Professor Turner
describes the test as "the process of standing unsupported with the eyes
closed and feet together for 30 s" and asserts that "the positive result
is the p...
Title: Romberg's test has stood up to the test of time and should
remain standing
(Neuromythology: Letter to the Editor)
I was Interested to read Professor Martin Turner's article entitled
Romberg's test no longer stands up. In the article Professor Turner
describes the test as "the process of standing unsupported with the eyes
closed and feet together for 30 s" and asserts that "the positive result
is the patient falling to the floor" which he gives as one of his reasons
for abandoning the test. He further states that the test is "neither
highly sensitive nor specific for its original purported purpose".
Furthermore, along with the authors of previous reviews of the test which
he quotes,1,2 he denies Romberg the credit of having linked the positivity
of the test to a dorsal column lesion. I note that Professor Turner
does not reference the 2nd Edition Romberg's Manual, the original source
description3 of the test in and his description of the test or sign does
not corresponded with the original. Romberg3 describes his sign twice in
the Manual. In the second description, at the top of page 396 of Volume
2, Romberg states "If he [the patient with Tabes Dorsalis] is ordered to
close his eyes while in the erect posture, he at once commences to totter
and swing from side to side; the insecurity of his gait also exhibits
itself more in the dark". In the earlier description in Volume 1, on
pages 226-227, he says "I have observed that anaesthesia of the muscles
alone without loss of tactile power, invariably accompanies tabes
dorsalis. A simple experiment suffices to determine the fact. If the
patient is told to shut his eyes while in the erect posture, he
immediately begins to move from side to side, and the oscillations soon
attain such a pitch that unless supported he falls to the ground."
Note firstly that there are arguably two parts to Romberg's test. The
first part, requires no time interval, on the contrary, a positive
Romberg's test is demonstrated by an increased sway that begins "at once"
or "immediately" after the eyes are closed. Furthermore, according to his
second description of the sign, a fall to the floor is not required and
only the now never-undertaken second part of the test, requiring darkness,
is potentially dangerous. Romberg's claim for specificity and
sensitivity is that "it invariably accompanies tabes dorsalis" and "it is
a symptom which I have not observed in other paralyses, nor in
uncomplicated amuarosis; since then [since he first said that he described
the sign 10 years previously], I have found it in a considerable number of
patients [with Tabes Dorsalis] .... and in no case have I found it
wanting." Romberg also states that "some patients mention the
circumstance [increased unsteadiness in the dark, while standing without
support] without being asked about it". It is also interesting that a
little later on in the same description, on page 397 of Volume 2, Romberg
says that as it progresses, "the necessity of employing the eyes becomes
more and more urgent; if he [the patient with Tabes Dorsalis] closes his
eyes, even while sitting, his body begins to sway to and fro" and he "is
no longer able to recognize the position of his own limbs and cannot tell
whether the right leg is crossed over the left, or the reverse". Since
this description of the disease was prior to the discovery of the
causative spirochaete, it quite possibly that Romberg (as well as other
19th century Neurologists) may have included other causes dorsal column
damage and large fibre neuropathy / neuronopathy and among his cases.
Romberg3, correlating the clinical features with the pathology, mentions
on the same page as his sign, that post-mortem findings "almost without
exception show the existence of partial atrophy of the spinal cord" and
that "the contents of the cords of the cauda equina have often been found
to have disappeared to such an extent that nothing but the empty
neurilemmatous sheaths seemed to remain". He further noted that "it is of
especial interest to observe that the posterior, sensory roots are
occasionally alone affected in conjunction with the posterior columns of
the spinal cord, the anterior motor columns and nerves retaining their
normal structure". To my mind, that counts as linking the positivity of
the test to a dorsal column lesion and indeed to a lesion of the sensory
roots and / or nerves which Professor Turner, incidentally, did not
mention as a cause of a positive Romberg's sign.
Sir William Gowers4 in the 1888 American Edition of his textbook cited
Romberg and his test as did the legendary Jean-Martin Charcot5 in his
Tuesday Lectures. It is interesting that Gowers4, referring to Romberg's
test states that "the effect of closure of the eyes is greatest when
sensation in the soles of the feet is defective, but does not depend on
this loss; it may be marked when sensation on the soles of the feet is
perfect". Although the current method of joint position testing in the
Hallux, referred to by Professor Turner, seems unlikely to have been
employed at the time of Gowers, it is certainly my experience that dorsal
column function or peripheral nerve proprioceptive sensory function can be
sufficiently impaired to cause "positive Rombergism" when concurrent
testing of joint position sense in the hallux on both sides is apparently
within normal limits. By way of explanation of this personal observation,
I would suggest that proprioception is likely to be a more complex
predominantly unconscious function of the nervous system, rather than the
simple transmission of the position of the distal phalanx of the hallux to
consciousness. Therefore, I disagree with Professor Turner's assertion
that simply testing joint position test in the Hallux is a substitute for
Romberg's test.
Before dismissing a test proposed by the one of the greatest Neurologists
of the 19th century who was author of the first systematic textbook of
Neurology ever written and who made numerous other seminal contributions
to our subject, I think we should be a little more circumspect. Wilson6
in his classic 1940 textbook also considered Romberg's sign useful and it
is considered an important part of the neurological examination in most
modern textbooks of Neurology. In my view, Romberg's Test is a very
useful part of the neurological examination, because it so beautifully
illustrates and confirms to the clinician and student alike, the degree to
which loss of proprioception contributes to ataxia and impaired balance in
any particular case (whichever of the limited number of underlying
pathophysiologies is responsible). A positive Romberg's test therefore
helps the clinician to attribute ataxia and / or impaired balance to
pathology in the dorsal column of the spinal cord, or in the peripheral
large nerve fibres destined for the dorsal columns, rather than to
pathology in the cerebellum. It is not dangerous and has stood the test
of time. I believe Romberg's test should remain part of the routine
neurological examination taught to all medical students and used by all
Neurologists. I believe that Professor Turner should stand down on this
issue and that Professor Romberg and his test remain upstanding.
References
1. Lanska DJ, Goetz CG
Romberg's sign. Development, adoption, and adaptation in the 19th century
Neurology 2000;55:1201-6.
doi:10.1212/WNL.55.8.1201
2. Pearce JM
Romberg and His Sign.
Eur Neurol 2005;53:210-13
doi:10.1159/000086732
3. Romberg MH
A Manual of The Nervous Diseases of Man 2nd Edition 1851 Volumes 1&2 226-
227,396-397.
Translated and edited by Sieveking EH, London: Sydenham Society
Reprint: Alabama: Gryphon Editions Ltd 1983:
4. Gowers WR
A Manual of Diseases of the Nervous System. American Edition P.289
Philadelphia: P.Blakiston, Son & Co 1888
Reprint: Alabama: Gryphon Editions Ltd 1983:
5. Charcot JM
Charcot the Clinician. The Tuesday Lectures
Excerpted and translated case presentations by Goetz CG P143
Raven Press New York 1897
6. Kinnier Wilson SA
Neurology Volume 1 P.494
London: Edward Arnold & Co 1947
"Provenance and peer review. Not commissioned, Externally peer
reviewed. This paper was reviewed by Martin Tuner, Oxford, UK."
I am in general agreement with the notion expressed in Professor
Hawkes' editorial that many patients in
neurology outpatient clinics do not need examination. Certainly, the full
neurological examination has a rather Zen-like quality: it takes a great
deal of work to master it and then one finds one
doesn't really need it. However, I would like
to express a number of disagreements with some of what Professor Hawkes
wr...
I am in general agreement with the notion expressed in Professor
Hawkes' editorial that many patients in
neurology outpatient clinics do not need examination. Certainly, the full
neurological examination has a rather Zen-like quality: it takes a great
deal of work to master it and then one finds one
doesn't really need it. However, I would like
to express a number of disagreements with some of what Professor Hawkes
wrote.
The examination is, of course, not purely diagnostic. I have listed
a number of other features in Box 1.
Fundamentally, Professor Hawkes appears to suggest that the
examination can be replaced by investigation. It could be argued that this
replaces one unnecessary activity (and a relatively cheap one) with
another unnecessary activity (and a much more expensive one). Waiting
times for individuals to be seen in outpatient clinics have been reduced
in recent times. However, there are often significant delays for
necessary investigations, such as MR Imaging and Neurophysiology. One
reason for this is that many arguably unnecessary investigations are
undertaken, particularly imaging for headache, neck pain and back ache.
The majority of patients in general neurology outpatient clinics can in
fact be dealt with by a careful history taking.
On a more specific point, Professor Hawkes states that
"if your patient has a
headache...he or she is going to need a brain
scan". This is an extremely contentious point.
Indeed, Professor Hawkes does imply that this
"need" is for
reassurance rather than for specific diagnostic purposes and, of course,
the majority of causes of headache have normal scans, therefore this
investigation is indeed not diagnostic. He states that no matter how much
one reassures the patient that it is not a serious form of headache, they
will still want a scan. On a purely anecdotal basis, it does seem as
though the desire for brain scans in patients with headaches does vary
greatly, not only from patient to patient but also according to which
clinician they see. One important point is that simple reassurance of a
non-serious cause is not always sufficient: the patient may require a
positive diagnosis. If they accept that diagnosis, they may not wish for a
scan; it is to be hoped that such acceptance depends not simply on the
"charm" of the doctor
(as Professor Hawkes puts it) but also on their perceived competence and
the way they explain the diagnosis.
Professor Hawkes does not deal with the issue of incidental abnormalities.
There are publications indicating that brain scanning in cases of headache
uncovers incidental abnormalities in a proportion of patients, causing
additional anxiety and greater use of medical time 1,2,3. As a taxpayer,
I might feel somewhat aggrieved if my financial support for the headache
patient with extends over dismaying a series of cost events: a general
practice consultation, a neurological consultation, a high-tech
investigation, further investigation because of doubtful abnormalities on
the first test and, finally, additional consultation time to deal with the
uncovered incidental abnormalities. Professor Hawkes states that patients
may wish to pay for a scan "in the private
sector". (As an aside here, all NHS
consultations are indeed private. I think Professor Hawkes is referring
here to the commercial sector.) If indeed a patient requires a medically
unnecessary scan, then it might be reasonable for them to pay for it - providing that all subsequent matters arising
from the scan, including reassurance about abnormal results, are also
dealt with in the commercial sector.
As a final point, Professor Hawkes discusses the issues of
"video clinics". I
can understand that this is a potential way of dealing with certain
problems. However, there is an irreducible human element in the medical
consultation and face-to-face consultations can be extremely important,
allowing interaction, assessment and reassurance that is simply not
possible through remote video or audio connection.
References
1. Computed Tomography in the headache patient: Is routine evaluation
really necessary? Mitchell et al Headache 1993 33:82-86
2. Incidental Findings in magnetic resonance imaging of the brains of
healthy young men. Weber & Kopf J Neurol Sci 2006 240:81-84
3. Incidental findings on brain magnetic resonance imaging: systematic
review and meta-analysis. Morris et al BMJ In Press
Box 1
Non-diagnostic aspects of the examination
o To give the clinician time to think
o To help establish doctor/patient relationship
o To allow the patient to volunteer aspects of the history not given
during direct enquiry
o To demonstrate to the patient features which are important in their
management
o Non specific therapeutic effect of examination
Sometimes it is necessary to make a point with overemphasis and we
believe that was done in the letter by Chris Hawkes. We agree that it is
essential to talk to a patient and to watch them and observe how they
speak, what they are saying and what they are doing with their body as
they walk in and out of a room. However, to exclude the examination is a
form of conceit. The only reason that a very senior neurologist can
o...
Sometimes it is necessary to make a point with overemphasis and we
believe that was done in the letter by Chris Hawkes. We agree that it is
essential to talk to a patient and to watch them and observe how they
speak, what they are saying and what they are doing with their body as
they walk in and out of a room. However, to exclude the examination is a
form of conceit. The only reason that a very senior neurologist can
observe so much is from a long period of diligently examining all patients
and slowly learning shortcuts by pattern recognition. But you
can't teach neurology that way. Students must
first be taught the discipline of a routine in order to learn which part
of the routine can be discarded in individual patients. When a TIA is
caused by atrial fibrillation a finger on the pulse will lead you to the
ECG as the first test. A stethoscope on the neck will suggest that a
Doppler should happen immediately. When resources are limited (which
occurs in much more than half the world) it is important to direct your
tests sensibly rather than blindly ordering a battery. If a student
can't distinguish between an upper and lower
motor lesion then the differential of a paralysed limb trebles and an EMG
as well as an MRI needs to be done routinely. We are not against spending
more time talking to a patient, even if it means less time examining, but
don't eliminate the examination.
It's like throwing the baby out with the
bathwater. When in doubt the most cost effective investigation is to
retake the history and to examine the patient. We
mustn't forget that an essential part of any
consultation is to gain the trust and respect of the patient; if a patient
doesn't trust the consultant they are unlikely
to accept the diagnosis and treatment plan. We have all seen patients for
second and third opinions when on completing the examination they
complement you on how thorough you have been and inform you that their
previous consultants hadn't bothered to examine
them. The "laying on of
hands" is as essential to
today's consultation as it was in the past. In
today's litigious environment not examining a
patient would be welcomed by the opposing legal team with glee. We doubt
any expert witness would support the notion of not examining a patient as
standard clinical practice. In the new era of revalidation admitting to
your peers that you do not examine your patients would be inviting an
early retirement or a change in career.
In the referring doctor vs consultant neurosurgeon interaction(1),
there is, sometimes, a reversal of roles with the result that it is the
patient(often elderly) who is confronted with the reality that he or she
is not suitable candidate for acceptance by the neurosurgeon. For a
succesful referral to take place the referring doctor(often a harassed
trainee) has to make the patient marketable(2) to tertiary care, using...
In the referring doctor vs consultant neurosurgeon interaction(1),
there is, sometimes, a reversal of roles with the result that it is the
patient(often elderly) who is confronted with the reality that he or she
is not suitable candidate for acceptance by the neurosurgeon. For a
succesful referral to take place the referring doctor(often a harassed
trainee) has to make the patient marketable(2) to tertiary care, using
"streetwise" strategies and wiles best borrowed from Sir Alan Sugar's
"Apprentice" programme(3). In the clinical context less unsavoury
strategies include an aptitude for lateral thinking, exemplified by
acting(by requesting computerised tomography) on the hitherto unvalidated
suspicion that chronic treatment with antiplatelet agents(even without
coprescription of warfarin) might be a risk factor for subdural
haematoma(SDH) in patients with head injury(4). That is the easy bit. The
real challenge is to convince tertiary care that, notwithstanding evidence
from potentially outdated observational studies suggesting certain care
pathways for elderly patients with SDH(5), even a 75 year old SDH patient
with either pupillary dilatation or extensor motor responses might be a
suitable candidate for neurosurgical intervention. On a more serious note,
although I have used the Editorial(1) as a pretext, the two observational
studies(4)(5) that I have mentioned seriously need to be followed up by
well designed prospective studies so as to enhance the clinical quality
and intellectual rigour of management of SDH.
References
(1) Haines SJ
How to choose your neurosurgeon
Practical Neurology 2010;10:2-3
(2) Nagus P., Bridges J., Braithwaite J
Selling patients
BMJ 2009;339:19-26
(3) Harding J
Show business
The Times June 13, 2007, pages 4-5
(4) Major J., Reed MJ
A restrospective review of patients with head injury with coexistent
anticoagulant and antiplatelet use admitted from a UK emergency department
Emerg Med J 2009;26:871-6
(5) Jamjoom A., Nelson R., Stranjalis G et al
Outcome following surgical evacuation of traumatic intracranial haematomas
in the elderly
British Journal of Surgery 1992;6:27-32
In the presence of risk factors for thromboembolism, a focal
neurological episode which has a sudden onset should be assumed to be
embolic until proved otherwise. Whether or not that episode is purely
ischaemic, or whether or not it undergoes subsequent hamorrhagic
transformation is a separate issue which should not detract from the
urgency to identify the embolic source by means of echocardiography. That
is why I am so...
In the presence of risk factors for thromboembolism, a focal
neurological episode which has a sudden onset should be assumed to be
embolic until proved otherwise. Whether or not that episode is purely
ischaemic, or whether or not it undergoes subsequent hamorrhagic
transformation is a separate issue which should not detract from the
urgency to identify the embolic source by means of echocardiography. That
is why I am so surprised that echocardiography was not performed as a
matter of urgency in this patient(1). The "mantra" of "thromboembolism
until proved otherwise" is one which has stood the test of time in other
contexts, notably in the context of acute abdominal pain(attributable to
mesenteric embolism) in the presence of risk factors for thromboembolism
such as atrial fibrillation, myocardial infarction, and infective
endocarditis(2). "Frequently, [however], acute occlusive mesenteric
ischemia remains unrecognised, initially, so that specific treatment is
delayed for > 24 hours"(3). This is, arguably, attributable, at least
in part, to underrecognition of the diagnostic utility of the "mantra",
and the same might be true of the delayed recognition of the embolic
nature and the embolic source in the case reported by the authors(1).
Where the index of suspicion is sufficiently high, it should also be
recognised that normal intensity anticoagulation is no bar to
thromboembolism, as shown by the graph depicting occurence of embolic
stroke despite chronic anticoagulat therapy in patients with non valvular
atrial fibrillation, some of whom had international normalized ratios in
the range 2-3.4(4)
References
(1) Nieuwkamp DJ., Kirkels JH., Rinkel GJE
Multiple intracerebral haematomas during normal intensity anticoagulation
Practical Neurology 2010;10:45-47
(2)Jolobe,O
Intestinal ischaemia(letter)
British journal of Hospital Medicine 2002;63:695
(3)Menke J., Luthje L., Kastrup A., Larsen J
Thromboembolism in atrial fibrillation
Am J Cardiol 2010;105:502-10
(4)Hylek EM., Skates SJ., Sheehan MA., Singer DE
An analysis of the lowest effective intensity of prophylactic
anticoagulation for patients with non rheumatic atrial fibrillation
N Engl J Med 1996;335:540-6
Many thanks to Ramadan and his colleagues for this article about
neurology in the land of Mesopotamia. I have few notes:
1. The author has not mentioned other neurologists who participated
substantially in the creation of the subject "neurology in Iraq," and
these are Muhammed Tawfiq, Fadhil Al-Hadithy, and Adnan Al-Araji; Ajeeb
Ali practiced neurology in a city in the north of Iraq and was away from
the teachi...
Many thanks to Ramadan and his colleagues for this article about
neurology in the land of Mesopotamia. I have few notes:
1. The author has not mentioned other neurologists who participated
substantially in the creation of the subject "neurology in Iraq," and
these are Muhammed Tawfiq, Fadhil Al-Hadithy, and Adnan Al-Araji; Ajeeb
Ali practiced neurology in a city in the north of Iraq and was away from
the teaching environment of Baghdad. All of them were Members/Fellows of
the Royal Colleges of Physicians. One only, Khalid Ibrahim (who was
assassinated during the period of sectarian violence in Iraq, 2006) was
certified by the Arab board of Medicine. Therefore, the three names
mentioned in the article were not alone and the credit should also be
given to their neurology colleagues.
2. The so-called Scientific Council of Neurology (which is part of
the Iraqi Board of Medical Specializations; IBMS) collapsed totally in
late 2006 (the peak of the sectarian violence) after the immigration of
its founding members. Its post-graduate students were left alone facing
their unknown future; many of its trainees left Iraq. The IBMS then
brought three names to fill in the gap within 2 years; all of them were
locally trained and certified. One might ask, "Three individuals only
train, supervise researches, and examine 10 (more or less) post-graduate
students?"; misuse and abuse of those trainees occurred and occurs for
several reasons, which are beyond the scope of this article.
4. One of the authors himself (which is a neurologist) fled Iraq just
few months prior to the US-lead war against Iraq in 2003 and returned back
for unknown reasons in 2006; he did not return to his previous hospital,
but to a city in the north of Iraq. Some neurologists left Iraq after 2003
not because of the current disastrous situation in Iraq, but as part of
the immigration wave, which started in 2005 to deliberately empty Iraq
from its resources.
In short, adult clinical neurology in Iraq, instead of moving forward
after the "liberation of Iraq," has regressed profoundly and declined in
efficiency to a very counterproductive way. Many people travel to a nearby
country if they get a neurological disease; simply, they don't trust the
"new generation of Iraqi neurologists."
By no means, this article or any eLetter would cover this subject.
Anyway, as the author said, we hope that Iraq will re-take its position in
the lead.
Larner wrote an interesting article on morning headaches.1 We would
like to react to the statement 'Onset of subarachnoid haemorrhage during
sleep is extremely rare, if it occurs at all.'
In October 2008 a 62 year old woman was seen on the emergency department.
She reported moderately severe headache on awakening with chills and a
slight dizziness. There was a history of ulcerative colitis and she smoked
5 cigarettes a da...
Larner wrote an interesting article on morning headaches.1 We would
like to react to the statement 'Onset of subarachnoid haemorrhage during
sleep is extremely rare, if it occurs at all.'
In October 2008 a 62 year old woman was seen on the emergency department.
She reported moderately severe headache on awakening with chills and a
slight dizziness. There was a history of ulcerative colitis and she smoked
5 cigarettes a day. General, neurological, and laboratory examinations
were unremarkable. Because of the chills a possible viral infection with
headache was presumed. The patient was reassured and went home. The next
morning her husband found her in bed unresponsive and took her to the
emergency department urgently. She was comatose, with a Glasgow Coma Scale
Score of E1M3V1, fixed dilated pupils and bilateral extensor plantar
responses. CT showed a massive subarachnoid haemorrhage with intracerebral
and subdural blood and CTA a middle cerebral artery aneurysm. Despite
surgical decompression with clipping of the aneurysm, the patient died the
next day.
Our patient had an aneurysmal bleeding during sleep in two successive
nights. Although aneurysmal subarachnoid haemorrhage often is considered
to be triggered by strenuous activities, onset during non-strenous
activities and even sleep is not rare. In a series of 141 patients, onset
of SAH occurred during sleeping, resting, sitting, eating, or drinking in
38 patients ( 27%).2 In a series of 513 patients it occurred during
sleeping or resting in 41 (8%),3 and in a series of 500 patients during
sleep in 45 (9%).4
In conclusion, onset of subarachnoid haemorrhage during sleep is not
extremely rare. Not considering aneurysmal subarachnoid haemorrhage in
patients awakening with unusual headache is dangerous.
References
1. Larner AJ. Not all morning headaches are due to brain tumours. Pract
Neurol 2009;9:80-84
2. Ferro JM, Pinto AN. Sexual activity is a common precipitant of
subarachnoid hemorrhage. Cerebrovasc Dis 1994;4:375
3. Matsuda M, Watanabe K, Saito A, Matsumura K, Ichikawa M. Circumstances,
activities, and events precipitating aneurysmal subarachnoid hemorrhage. J
Stroke Cerebrovasc Dis 2007;16:25-29
4. Schievink WI, Karemaker JM, Hageman LM, van der Werf DJM. Circumstances
surrounding aneurysmal subarachnoid hemorrhage. Surg Neurol 1989;32:266-272
Dear Editor,
We were interested to read the recent case study presented by Rodrigues and Wild in the current edition of Practical Neurology where they discussed "Psychogenic non-epileptic seizures in early Huntington's disease"[1]. The authors gave an in-depth account of the clinical profile of a 51-year-old male with early Huntington's disease (HD) who presented with repeated episodes of repetitive, purposeless, c...
Dear Editor,
In his recent Neuromythology article1 on the Babinski sign, Professor Kiernan repeats the oft quoted recommendation regarding the best method for testing the plantar response, which is to:
'Run a car key (figure 1; or as some have suggested, a most expensive motor car key...) along the lateral border of the sole.'
It will not surprise many readers of Practical Neurology to learn th...
This sensitive review is very welcome, as in our experience, most patients with functional disorders are told by specialists what they do not have. I would be much more inclined to refer patients if this kind of approach was more common. It is one reason why relatively few of the patients we see in primary care are referred for specialist attention. Specialists are seeing only the tip of the primary care functional iceb...
Title: Romberg's test has stood up to the test of time and should remain standing (Neuromythology: Letter to the Editor)
I was Interested to read Professor Martin Turner's article entitled Romberg's test no longer stands up. In the article Professor Turner describes the test as "the process of standing unsupported with the eyes closed and feet together for 30 s" and asserts that "the positive result is the p...
I am in general agreement with the notion expressed in Professor Hawkes' editorial that many patients in neurology outpatient clinics do not need examination. Certainly, the full neurological examination has a rather Zen-like quality: it takes a great deal of work to master it and then one finds one doesn't really need it. However, I would like to express a number of disagreements with some of what Professor Hawkes wr...
Sometimes it is necessary to make a point with overemphasis and we believe that was done in the letter by Chris Hawkes. We agree that it is essential to talk to a patient and to watch them and observe how they speak, what they are saying and what they are doing with their body as they walk in and out of a room. However, to exclude the examination is a form of conceit. The only reason that a very senior neurologist can o...
In the referring doctor vs consultant neurosurgeon interaction(1), there is, sometimes, a reversal of roles with the result that it is the patient(often elderly) who is confronted with the reality that he or she is not suitable candidate for acceptance by the neurosurgeon. For a succesful referral to take place the referring doctor(often a harassed trainee) has to make the patient marketable(2) to tertiary care, using...
In the presence of risk factors for thromboembolism, a focal neurological episode which has a sudden onset should be assumed to be embolic until proved otherwise. Whether or not that episode is purely ischaemic, or whether or not it undergoes subsequent hamorrhagic transformation is a separate issue which should not detract from the urgency to identify the embolic source by means of echocardiography. That is why I am so...
Many thanks to Ramadan and his colleagues for this article about neurology in the land of Mesopotamia. I have few notes:
1. The author has not mentioned other neurologists who participated substantially in the creation of the subject "neurology in Iraq," and these are Muhammed Tawfiq, Fadhil Al-Hadithy, and Adnan Al-Araji; Ajeeb Ali practiced neurology in a city in the north of Iraq and was away from the teachi...
Larner wrote an interesting article on morning headaches.1 We would like to react to the statement 'Onset of subarachnoid haemorrhage during sleep is extremely rare, if it occurs at all.' In October 2008 a 62 year old woman was seen on the emergency department. She reported moderately severe headache on awakening with chills and a slight dizziness. There was a history of ulcerative colitis and she smoked 5 cigarettes a da...
Pages