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Turner and Talbot rightly emphasize that in spite of advances in EMG
techniques and emergence of novel neuroimaging and CSF biomarkers the
diagnosis of motor neuron disease (MND) still remains a clinical one.1
Find upper motor neuron (UMN) and lower motor neuron (LMN) signs in the
same limb and MND should be high up in the differential I recall was
taught to me in medical school. EMG was to be used in atypical cases wher...
Turner and Talbot rightly emphasize that in spite of advances in EMG
techniques and emergence of novel neuroimaging and CSF biomarkers the
diagnosis of motor neuron disease (MND) still remains a clinical one.1
Find upper motor neuron (UMN) and lower motor neuron (LMN) signs in the
same limb and MND should be high up in the differential I recall was
taught to me in medical school. EMG was to be used in atypical cases where
the diagnosis was in doubt. In today's world the pendulum has swung to the
other extreme. UMN and LMN signs in the same limb-->could be MND---
>order a 4 limb EMG making certain that tongue and paraspinal
musculature is examined-->then make the call-->definite MND Vs
probable Vs possible. This over reliance on neuroimaging and
neurophysiological data to make the diagnosis is not unique to MND;
multiple sclerosis (MS) is another causality. Two discreet attacks
separated by time (determined by history) and space (determined by
examination findings) and the diagnosis of MS can be made confidently. No
MRI brain, visual evoked potentials, somatosensory evoked potentials or
oligoclonal bands in CSF are needed. How many of us do that now?
References
1. Turner MR, Talbot K. Motor neurone disease is a clinical
diagnosis. Pract Neurol. 2012 Dec; 12(6):396-7.
Neurophilia can be loosely defined as the love of or fascination for
neurology. Now you may think this is a new recently described exotic
neurological syndrome but dwell into the ancient eastern Hindu and
Buddhist philosophies and you shall quickly realize that the disorder is
as ancient as these civilizations themselves 1. The workings of the brain
and of the mind fascinated these first neurophilia inflicted philosopher...
Neurophilia can be loosely defined as the love of or fascination for
neurology. Now you may think this is a new recently described exotic
neurological syndrome but dwell into the ancient eastern Hindu and
Buddhist philosophies and you shall quickly realize that the disorder is
as ancient as these civilizations themselves 1. The workings of the brain
and of the mind fascinated these first neurophilia inflicted philosophers
and they spent an inordinate amount of time trying to decipher its
secrets. Techniques to control the mind through meditation and
introspection were described and perfected over the years. One can imagine
these neurophiles wondering how this roughly 1400 gram lump of wrinkled
tissue with no moving parts, no joints or valves could function as the
motherboard for all other body systems as well as serve as the seat of the
mind, thoughts, senses; in fact the very essence of the individual. As we
slowly unlock the secrets of the living brain with the aid of
sophisticated imaging techniques, the prevalence of neurophilia has
increased exponentially. One would not be wrong to label it currently as a
pandemic. Identification of this disorder is relatively easy.
Five signs that you may have neurophilia (in no particular order of
importance)
1. You cannot wait for the next book by Oliver Sacks or V.S Ramachandran
to come out.
2. You think Dr. House should only concentrate on neurology cases
henceforth (a variation of this sign was first described by Dr. Fuller)
3. You name your first and only child "Brain"
4. You identify a Queen Square reflex hammer , a tuning fork and a
Wattenberg pin among your priciest possessions
5. You count diagnosing passers-by with Parkinson's disease by mere
observation of their gait as one of your favorite pastimes.
Once inflicted with neurophilia the "disease" course is highly
variable. In some it merely manifests with a curiosity to know more about
the workings of the brain, yet in others (like us neurologists,
neurosurgeons and neuroscientists) it becomes a lifelong obsession to know
everything about the brain both in disease as well as in health. My own
passion for neurology was kindled at a young age by my neurophilia
inflicted neurologist father. Little did I realize that exposure at a
tender age would result in such a passion for the study of the brain. Yes
it is true and I admit it proudly-I have a bad case of neurophilia. Watch
out people it is contagious!
References
1. Fuller GN. Neurophilia: a fascination for neurology--a new syndrome.
Pract Neurol. 2012; 12:276-8.
I enjoyed Fuller's description of 'neurophilia' - we can finally
label this condition afflicting neurologists, and recognise that is
widespread within medicine and the general population.(1) Neurophilia is
probably infectious (i.e. environmental); my personal experience and
informal discussions with neurology colleagues revealed that many chose
neurology as a career following positive experiences during their Senior
Ho...
I enjoyed Fuller's description of 'neurophilia' - we can finally
label this condition afflicting neurologists, and recognise that is
widespread within medicine and the general population.(1) Neurophilia is
probably infectious (i.e. environmental); my personal experience and
informal discussions with neurology colleagues revealed that many chose
neurology as a career following positive experiences during their Senior
House Officer jobs. This emphasizes the suggestion that neurophobia can
be dispelled and neurophilia encouraged through effective, inspirational
teaching, accessible textbooks and journals.
However, I would also like to highlight a potential genetic
contribution. In the UK, I am aware of at least 6 neurological families
- those families where more than one first degree relatives are
neurologists. - many more than would be expected by chance. This does
suggest that neurophilia may have genetic as well as environmental
elements.
Reference
1. Fuller GN. Neurophilia: a fascination for neurology--a new syndrome.
Practical Neurology. 2012;12(5):276-8.
I read with interest the article by Dr. Leach. As things stand at
present, it is not mandatory for physicians in the United States to
discuss about SUDEP with patients or their caregivers. In fact this was
not included in the recently released American Academy of Neurology (AAN)
performance measures for epilepsy 1. Advice about safe recreation and
driving though is included as one of the 8 performance measures. So is...
I read with interest the article by Dr. Leach. As things stand at
present, it is not mandatory for physicians in the United States to
discuss about SUDEP with patients or their caregivers. In fact this was
not included in the recently released American Academy of Neurology (AAN)
performance measures for epilepsy 1. Advice about safe recreation and
driving though is included as one of the 8 performance measures. So is
information about SUDEP useful or too much information (TMI)? Does every
patient with epilepsy warrant this information? What is the ideal time to
impart this information to the patient and the caregivers: first office
visit where this information competes with other "more relevant"
information about anticonvulsant dosing, side-effects and importance of
compliance for the patient's attention or in subsequent office visits when
the patient's seizure semiology and frequency is better characterized? No
two patient's seizure disorder is exactly alike hence the potential risk
of SUDEP varies from patient to patient. So it reasons that information
about SUDEP needs to be customized to the individual patient at hand. Both
Dr. Leach's article and my letter raise more questions than answers. In
the meantime we are all left pondering how to impart this information to
our epilepsy patients and importantly how to do that and take a detailed
history, fulfill the performance measures for epilepsy, exam the patient
and document this all in the 1 hour allocated for a new patient visit.
Reference
1. Fountain NB, Van Ness PC, Swain-Eng R, Tonn S, Bever CT Jr;
American Academy of Neurology Epilepsy Measure Development Panel and the
American Medical Association-Convened Physician Consortium for Performance
Improvement Independent Measure Development Process. Quality improvement
in neurology: AAN epilepsy quality measures: Report of the Quality
Measurement and Reporting Subcommittee of the American Academy of
Neurology. Neurology. 2011 Jan 4;76(1):94-9
The term generalized in EEG is certainly ambiguous and can be a cause
of confusion, especially to a reader who is not formally trained in
neurophysiology. As a neurology resident in training, the importance of
personally reviewing the patient's CT or MRI scan was impressed upon me
time and time again. Do not just take the radiologist's report at face
value, look at the pictures yourself since you after seeing the patient...
The term generalized in EEG is certainly ambiguous and can be a cause
of confusion, especially to a reader who is not formally trained in
neurophysiology. As a neurology resident in training, the importance of
personally reviewing the patient's CT or MRI scan was impressed upon me
time and time again. Do not just take the radiologist's report at face
value, look at the pictures yourself since you after seeing the patient
know what to look for better than the radiologist, was the pearl of wisdom
imparted to me by a seasoned neurologist. While a similar argument can be
made for reviewing the EEG too, interpretation of EEG is a skill which is
not formally taught during residency training. So is there a way out? The
answer is yes and it requires reading the body of the EEG report and not
just the final impression. Is the background frequency normal or slow?
What is the morphology and distribution of the spike wave discharges: slow
spike and wave (secondary generalized seizure disorder) versus 4-6 Hz
polyspike and wave discharges (primary generalized seizure disorder). EEG
reporting truly is like trying to translate a picture into words. One
though needs to see the entire picture and not just the impression at the
end.
Dr. Fuller makes a strong case for coaching in neurology(1). Formal
coaching in neurology usually occurs during residency and fellowship
training. In the United States we have the 360 degree evaluation. The
resident physician in training is evaluated and coached by everyone he
comes in contact with namely the staff attending, nursing staff, other
residents, patient and even the medical student. There...
Dr. Fuller makes a strong case for coaching in neurology(1). Formal
coaching in neurology usually occurs during residency and fellowship
training. In the United States we have the 360 degree evaluation. The
resident physician in training is evaluated and coached by everyone he
comes in contact with namely the staff attending, nursing staff, other
residents, patient and even the medical student. There is little doubt
that this formal coaching is invaluable. Weaknesses and strengths are
identified in a timely fashion and corrective measures are instituted. The
question that needs to be asked by every neurologist is whether this
formal coaching needs to continue in some shape or form throughout one's
professional career. Can I as an assistant professor swallow my pride and
admit that I should have taken a more thorough history? One form of
coaching that has always served me well is the second opinion. When
confronted by a particularly vexing case, I do not hesitate in requesting
a second opinion from a physician whom I respect for his clinical acumen.
The office note which accompanies the patient on his return visit is
always illuminating. If it does not give me the answer I seek, it always
points me in the right direction. Another physician mind has approached
the problem confronting me in a different way. Dr. Fuller is indeed right.
Abundant avenues for coaching already exist in neurology; the trick is to
utilize them in an appropriate and timely fashion.
Reference
1. Fuller G. Do you need a coach? Pract Neurol. 2012;12(1):2-3.
In the Saifee TA et al article (1) regarding the treatment of
"Tardive movment disorders" (TD), the authors recommend the use of
amantadine as second or third line among other possible drugs ("each with
fairly limited evidence for effectiveness" in author?s words).
In 1971, the late Dr. Espejel and I informed for the first time the
benefits of amantadine in drug-induced dyskinesias (2); consequently, I
have f...
In the Saifee TA et al article (1) regarding the treatment of
"Tardive movment disorders" (TD), the authors recommend the use of
amantadine as second or third line among other possible drugs ("each with
fairly limited evidence for effectiveness" in author?s words).
In 1971, the late Dr. Espejel and I informed for the first time the
benefits of amantadine in drug-induced dyskinesias (2); consequently, I
have followed with interest the derived articles. Failures and successes
are reported with the use of this agent. Here, I am interested to comment
the possible cause about the failures in TD treatments with amantadine, to
bring together data that may generate a "personalized" prescription
yielding an increased number of benefited patients.
Drugs-induced dyskinesias are a heterogeneous number of disorders
with different pathophysiological mechanisms in their generation:
presynaptic excess of dopamine formation, postynaptic supersensitive
dopaminergic receptors, or glutamergic overactivity mediated by the N-
methyl-D-aspartic acid (NMDA) receptor, all them grouped in an apparently
homogenous syndrome.
So, it is important to know if the patient we are treating are within
the glutamergic overactivity mediated by the NMDA receptor subset, since
only in these patients will obtain good results when treated with drugs
like amantadine or other well-tolerated NMDA receptor antagonist (3).
However, how do we can investigate this phenotypic feature? Brain MRI
spectroscopy can reveal the NMDA receptors excess but its high cost may
limit its routine use. However, if we bear in mind that patients with low
NMDA activity are clinically hypoactive and anhedonic and have exaggerated
extrapiramidal sensitivity (4), they will be prone to suffer TD amantadine
-resistant. Therefore, give amantadine in affected TD patients with
hyperactivity preferentially (or at least with normal motor activity) to
obtain better responses.
References:
1. Saifee TA, Edwards MJ. Tardive movement disorders: a practical
approach. Pract Neurol 2011;11:341-348
2. Vale S, Espejel MA. Amantadine for dyskinesia tarda. N Engl J Med.
1971;284:673.
3. Del Dotto P, Pavese N, Gambaccini G, Bernardini S, Metman LV,
Chase TN, Bonuccelli U. Intravenous amantadine improves levadopa-induced
dyskinesias: an acute double-blind placebo-controlled study. Mov Disord.
2001;16:515-20.
4. Telfer S, Shivashankar S, Krishnadas R, McCreadie RG, Kirkpatrick
B. Tardive dyskinesia and deficit schizophrenia. Acta Psychiatr Scand.
2011;124:357-62.
Geraint Fuller's neurological reflections describe the Dunning Kruger
effect (1). This is one expression of illusory superiority, the cognitive
bias that makes us over-rate our attributes (2). Apart from Shakespeare,
whom the author quoted, other eminent people have noted that the less
skilled and less educated are usually unaware of their inadequacy. Charles
Darwin for example says: 'ignorance more frequently begets confi...
Geraint Fuller's neurological reflections describe the Dunning Kruger
effect (1). This is one expression of illusory superiority, the cognitive
bias that makes us over-rate our attributes (2). Apart from Shakespeare,
whom the author quoted, other eminent people have noted that the less
skilled and less educated are usually unaware of their inadequacy. Charles
Darwin for example says: 'ignorance more frequently begets confidence than
does knowledge'. Bertrand Russell has a slightly longer expression: 'one
of the painful things about our time is that those who feel certainty are
stupid, and those with any imagination and understanding are filled with
doubt and indecision'. My own personal favourite is: 'often wrong, but
never in doubt', attributed to Ivy Baker Priest.
Closely allied to the Dunning Kruger effect is the fundamental
attribution error- the tendency to blame personal failures on
circumstances, and to ascribe successes to inherent factors. Paradoxically
this rule is inverted when attributing the achievements and shortcomings
of others. The outcome of this is a failure to learn from personal
mistakes and from errors committed by others.
The author has rightly highlighted the implications of the Dunning
Kruger effect on self assessment in medical training and revalidation.
Just as worrying is the effect on patient safety. The obvious solution is
self awareness and introspection. Everyone needs to be conscious of how
well they know what they know- the concept of knowledge calibration (3).
To avoid the consequences of misplaced confidence, we should aspire to be
well-calibrated. To succeed in this, we must not assume immunity from the
Dunning Kruger effect.
1. Fuller, G. Ignorant of ignorance? Pract Neurol 2011; 11:365
2. http://en.wikipedia.org/wiki/Illusory_superiority
3. Cook RI and Woods DD. Operating at the sharp end. In: Bogner MS, ed.
Human error in medicine. Lawrence Erlbaum Associates, Hove. 1994: 264.
As a long term and avid reader of Practical Neurology I was somewhat
surprised by the article and correspondence suggesting that the
stethoscope is now an irrelevancy to clinical neurologists (Practical
Neurology 2010;10:344) On the contrary, I believe neurologists should
still use their stethoscopes. Heres why.
Most neck bruits indicate underlying arterial disease. For instance,
in a study comparing the 'blind...
As a long term and avid reader of Practical Neurology I was somewhat
surprised by the article and correspondence suggesting that the
stethoscope is now an irrelevancy to clinical neurologists (Practical
Neurology 2010;10:344) On the contrary, I believe neurologists should
still use their stethoscopes. Heres why.
Most neck bruits indicate underlying arterial disease. For instance,
in a study comparing the 'blinded' findings at auscultation on asymptomatic
patients with cervical bruits also assessed by Doppler ultrasound, there
was a highly significant correlation. In most cases, bruits represented
arterial stenosis (Neurology 1985;35:742). When examining patients with a
suspected transient ischaemic attack, the finding of bruits in the neck,
abdomen and groins is also a useful index of underlying arteriopathy.
I recently saw a patient referred with an unexplained 'swishing'
sound in her head, already dismissed as probably 'non organic'. No one had
listened with a stethoscope. May be they didn't have one. If they had,
they would have confirmed the existence of a loud bruit over the right
side of the
head, later confirmed as an intracranial arteriovenous malformation.
Although it is true that, in patients with suspected meningitis, a
CSF:plasma glucose of >0.5 suggests a viral aetiology(1),
underrecognition of the fact that the ratio may sometimes fall below 0.5
has led to inclusion of a CSF:plasma ratio > 0.5 among the "clinical
case definitions" of aseptic meningitis(2), notwithstanding the fact that
CSF:plasma glucose ratios below 0.5(and even as low as 0.26) may be
encounte...
Although it is true that, in patients with suspected meningitis, a
CSF:plasma glucose of >0.5 suggests a viral aetiology(1),
underrecognition of the fact that the ratio may sometimes fall below 0.5
has led to inclusion of a CSF:plasma ratio > 0.5 among the "clinical
case definitions" of aseptic meningitis(2), notwithstanding the fact that
CSF:plasma glucose ratios below 0.5(and even as low as 0.26) may be
encountered in viral meningitis(3), and in viral encephalitis(4).
In one study, among 22 patients with enterovirus meningitis, the
CSF:plasma glucose ratio fell within the range 0.26-0.76. In the same
study, among 8 patients with varicella zoster virus meningitis the ratio
fell within the range 0.4-0.73, and within the range 0.47-0.57 among 8
patients with herpes simplex type 2 meningitis(3). Even in viral
encephalitis, patients have been encountered with CSF:plasma glucose
ratios < 0.5, as was the case in a multicentre population-based
prospective study of patients in England(4). In that study among 18
subjects with herpes simplex virus encephalitis in whom the CSF;plasma
ratio was evaluated , there were five with a ratio < 0.5. Among 6 with
varicella zoster virus encephalitis in whom the ratio was evaluated there
were two in whom the ratio fell below 0.5(4). Given the fact that some
subtypes of viral meningitis are amenable to treatment(3), and the fact
that management of this disorder may be suboptimal, in part due to its
underrecognition(5), it is important to stress to frontline medical staff
that the diagnosis should be entertained even when the CSF:plasma glucose
ratio falls within the range where the differential diagnosis includes
tuberculous meningitis.
References
(1)Davies N ., Thwaites G
Infections of the nervous system
Practical Neurology 2011:11:121-131
(2) Michael BD., Sidhu M., Stoeter D et al
Acute central nervous system infections in adults-a retrospective cohort
study in the NHS Northwest region
QJ Med 2010;103:749-758
(3)Ihekwaba UK., Kudesia G., McKendrick MW
Clinical features of viral meningitis in adults: significant differences
in cerebrospinal fluid findings among herpes simplex virus, varicvella
zoster virus, and enterovirus infections
Clinical Infectious Diseases 2008;47:783-789
(4) Granerod J., Ambrose HE., Davies NWS et al
Causes of encephalitis and differences in their clinical presentations in
England: a multicentre, population-based prosepctive study
Lancet Infectious diseases 2010;10:835-844
(5)Landrey ML., Greenwold J., Vikram HR
Herpes simplex type-2 meningitis: presentation and lack of standardised
therapy
American Journal of Medicine 2009;122:688-691
Turner and Talbot rightly emphasize that in spite of advances in EMG techniques and emergence of novel neuroimaging and CSF biomarkers the diagnosis of motor neuron disease (MND) still remains a clinical one.1 Find upper motor neuron (UMN) and lower motor neuron (LMN) signs in the same limb and MND should be high up in the differential I recall was taught to me in medical school. EMG was to be used in atypical cases wher...
Neurophilia can be loosely defined as the love of or fascination for neurology. Now you may think this is a new recently described exotic neurological syndrome but dwell into the ancient eastern Hindu and Buddhist philosophies and you shall quickly realize that the disorder is as ancient as these civilizations themselves 1. The workings of the brain and of the mind fascinated these first neurophilia inflicted philosopher...
I enjoyed Fuller's description of 'neurophilia' - we can finally label this condition afflicting neurologists, and recognise that is widespread within medicine and the general population.(1) Neurophilia is probably infectious (i.e. environmental); my personal experience and informal discussions with neurology colleagues revealed that many chose neurology as a career following positive experiences during their Senior Ho...
I read with interest the article by Dr. Leach. As things stand at present, it is not mandatory for physicians in the United States to discuss about SUDEP with patients or their caregivers. In fact this was not included in the recently released American Academy of Neurology (AAN) performance measures for epilepsy 1. Advice about safe recreation and driving though is included as one of the 8 performance measures. So is...
The term generalized in EEG is certainly ambiguous and can be a cause of confusion, especially to a reader who is not formally trained in neurophysiology. As a neurology resident in training, the importance of personally reviewing the patient's CT or MRI scan was impressed upon me time and time again. Do not just take the radiologist's report at face value, look at the pictures yourself since you after seeing the patient...
Dear Editor,
Dr. Fuller makes a strong case for coaching in neurology(1). Formal coaching in neurology usually occurs during residency and fellowship training. In the United States we have the 360 degree evaluation. The resident physician in training is evaluated and coached by everyone he comes in contact with namely the staff attending, nursing staff, other residents, patient and even the medical student. There...
In the Saifee TA et al article (1) regarding the treatment of "Tardive movment disorders" (TD), the authors recommend the use of amantadine as second or third line among other possible drugs ("each with fairly limited evidence for effectiveness" in author?s words).
In 1971, the late Dr. Espejel and I informed for the first time the benefits of amantadine in drug-induced dyskinesias (2); consequently, I have f...
Geraint Fuller's neurological reflections describe the Dunning Kruger effect (1). This is one expression of illusory superiority, the cognitive bias that makes us over-rate our attributes (2). Apart from Shakespeare, whom the author quoted, other eminent people have noted that the less skilled and less educated are usually unaware of their inadequacy. Charles Darwin for example says: 'ignorance more frequently begets confi...
As a long term and avid reader of Practical Neurology I was somewhat surprised by the article and correspondence suggesting that the stethoscope is now an irrelevancy to clinical neurologists (Practical Neurology 2010;10:344) On the contrary, I believe neurologists should still use their stethoscopes. Heres why.
Most neck bruits indicate underlying arterial disease. For instance, in a study comparing the 'blind...
Although it is true that, in patients with suspected meningitis, a CSF:plasma glucose of >0.5 suggests a viral aetiology(1), underrecognition of the fact that the ratio may sometimes fall below 0.5 has led to inclusion of a CSF:plasma ratio > 0.5 among the "clinical case definitions" of aseptic meningitis(2), notwithstanding the fact that CSF:plasma glucose ratios below 0.5(and even as low as 0.26) may be encounte...
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