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.
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.
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.
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.
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
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.
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.
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.
The borderland between functional diseases and neurological diseases
gets blurred especially when the patient presents with a myriad of
symptoms which do not localize to any one level of the neural axis.1 If in
addition the neurological examination is normal (especially the lack of
'hard' neurological signs such as upgoing plantars, cranial nerve signs,
definite asymmetry of the deep tendon reflexes, cerebellar signs and...
The borderland between functional diseases and neurological diseases
gets blurred especially when the patient presents with a myriad of
symptoms which do not localize to any one level of the neural axis.1 If in
addition the neurological examination is normal (especially the lack of
'hard' neurological signs such as upgoing plantars, cranial nerve signs,
definite asymmetry of the deep tendon reflexes, cerebellar signs and gait
disorder) the question of a functional disease certainly crosses the mind.
In my mind there are two ways to approach such patients. One way is to
order an exhaustive battery of tests including laboratory, neurophysiology
and neuroimaging studies. This "fishing" for an answer approach rarely if
ever yields the answer and risks reinforcing the sick role in the
patient's and caregiver's psyche ("I must have a horrible and terrible
illness which the doctor is trying hard to find"). The other approach is
one I have adopted in my practice. If after a thorough history,
examination and relevant investigations the answer still eludes me and I
am reasonably certain (though not 100% sure) that the patient's
presentation is unlikely on account of an organic neurological disease, I
adopt a policy of wait and watch after reassuring the patient that if new
symptoms were to appear or if the current symptoms were to change in
frequency or intensity, I would consider re approaching the diagnosis. The
patient at this point may or may not be ready to see a psychiatrist but I
do suggest that consulting one may be helpful.
References
1. Stone J, Reuber M, Carson A. Functional symptoms in neurology:
mimics and chameleons. Pract Neurol 2013; 13:104-13.
We enjoyed the review by our colleagues Finlayson et al 1 from the
United Kingdom, Congenital Myasthenic service, covering all aspects of the
congenital myasthenic syndromes. We would, however, suggest that the
section on neurophysiology could have been expanded and elaborated more.
To state that the neurophysiological findings in congenital myasthenic
syndromes are similar to those in autoimmune myasthenia gravis is corr...
We enjoyed the review by our colleagues Finlayson et al 1 from the
United Kingdom, Congenital Myasthenic service, covering all aspects of the
congenital myasthenic syndromes. We would, however, suggest that the
section on neurophysiology could have been expanded and elaborated more.
To state that the neurophysiological findings in congenital myasthenic
syndromes are similar to those in autoimmune myasthenia gravis is correct
perhaps with respect to repetitive nerve stimulation but when talking
about single fibre EMG (SFEMG) it should be emphasised for accuracy that
it is stimulated single fibre EMG (StimSFEMG) that should be used in
children, certainly under the age of eight years or in the intensive care
setting, and not the voluntary SFEMG technique, which requires significant
levels of patient cooperation. Furthermore, with most congenital
myasthenic syndromes (CMS) having symptoms at birth, which do not always
include ptosis, the use of StimSFEMG should be encouraged as it has
superior sensitivity in comparison to repetitive nerve stimulation, which
makes it the better screening test. The test is well tolerated and is
usually performed in the outpatient setting with the child awake. The
problem of the specificity of StimSFEMG can be addressed if the technique
is used as part of a more wide-ranging neurophysiological examination
including nerve conduction studies and EMG examination of limb and bulbar
muscles. As an example, demonstration of significant myopathic changes in
other muscles will direct the clinician more to the diagnosis of a
myopathy with associated secondary neuromuscular transmission defect
rather than a primary myasthenic syndrome.
We do not hesitate to use Stim SFEMG, which is well tolerated even by the
youngest of infants, and consequently we have seen a decrease in both the
age at referral for investigation and subsequent diagnosis over the years.
This approach has to be encouraged as in several studies it is clear that
in many children with CMS, symptoms have been present from birth, which
are often non-specific, such as feeding difficulties 2 or stridor 3. Many
of us have experienced the consequences of delayed diagnosis, regrettably
including sibling death, and we feel that the liberal use of this
excellent technique has been a major factor in preventing this by
providing an early diagnosis. In an article for a wide readership it is
perhaps an omission not to use this opportunity to advertise this
technique, available at many Neurophysiological centres (including those
of the authors). Hopefully this letter will in part address this
oversight.
Reference List
1 Finlayson S, Beeson D, Palace J. Congenital myasthenic syndromes:
an update. Pract Neurol 2013;13:80-91.
2 Kinali M, Beeson D, Pitt MC, et al. Congenital Myasthenic
Syndromes in childhood: Diagnostic and management challenges 1. J
Neuroimmunol 2008 15;201-202:6-12.
3 Jephson CG, Mills NA, Pitt MC, et al. Congenital stridor with
feeding difficulty as a presenting symptom of Dok7 congenital myasthenic
syndrome. Int J Pediatr Otorhinolaryngol 2010;74:991-994.
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...
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...
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...
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...
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 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...
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...
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...
The borderland between functional diseases and neurological diseases gets blurred especially when the patient presents with a myriad of symptoms which do not localize to any one level of the neural axis.1 If in addition the neurological examination is normal (especially the lack of 'hard' neurological signs such as upgoing plantars, cranial nerve signs, definite asymmetry of the deep tendon reflexes, cerebellar signs and...
We enjoyed the review by our colleagues Finlayson et al 1 from the United Kingdom, Congenital Myasthenic service, covering all aspects of the congenital myasthenic syndromes. We would, however, suggest that the section on neurophysiology could have been expanded and elaborated more. To state that the neurophysiological findings in congenital myasthenic syndromes are similar to those in autoimmune myasthenia gravis is corr...
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