I thoroughly enjoyed the article by Zanette et al (2014;14:351-353).
The authors are to be congratulated for their skilful history taking
skills, specifically the key observation that the pain coincided with
menses, suggesting the diagnosis, and thus confirming that a neurology
opinion, far from being "the last resort", should have been the "first
resort". I am troubled by the distribution of the pain however; the
autho...
I thoroughly enjoyed the article by Zanette et al (2014;14:351-353).
The authors are to be congratulated for their skilful history taking
skills, specifically the key observation that the pain coincided with
menses, suggesting the diagnosis, and thus confirming that a neurology
opinion, far from being "the last resort", should have been the "first
resort". I am troubled by the distribution of the pain however; the
authors' thesis, elegantly supported by the neurophysiology and exquisite
imaging, is that the pain was due to endometriosis affecting the left L4
root. However, the distribution of the pain appears more suggestive of
mainly L2, and perhaps a contribution from L1 and L3 - they also mentioned
a depressed knee jerk, which is mainly L3. Most of us regard the L4
dermatome as being below the knee and medial. Whilst I do not dispute the
diagnosis of endometriosis, I am intrigued by this, and wonder how the
authors explain the dermatomal discrepancy?
With kind regards
Richard J Davenport DM FRCP Edin
Consultant Neurologist
rjd@skull.dcn.ed.ac.uk
Voicemail: 0131 537 3590
NHS PRACTICE
Department of Clinical Neurosciences
Western General Hospital
Edinburgh EH4 2XU
Secretary telephone: 0131 537 2072
Fax: 0131 537 1132
Royal Infirmary of Edinburgh
MOPD 2
51 Little France Crescent
Old Dalkeith Road
Edinburgh EH16 4SA
Secretary telephone: 0131 242 1487
PRIVATE PRACTICE
Spire Murrayfield Hospital
122 Costorphine Road
EDINBURGH EH12 6UD
Telephone: 0131 334 0363
Spire Shawfair Park Hospital
10 Easter Shawfair
Edinburgh EH22 1FE
Telephone: 0131 654 5600
We thank Dr. Davenport for his interest in our case report [1] and
the opportunity to better explain our clinical reasoning.
In his e-letter Dr. Davenport argues that there is a discrepancy between
the distribution of the pain, which appeared more suggestive of L2 and
perhaps a contribution of L1 and L3, and the involvement of L4 root as
documented by clinical neurophysiology and neuroimaging. The patient was
asked to d...
We thank Dr. Davenport for his interest in our case report [1] and
the opportunity to better explain our clinical reasoning.
In his e-letter Dr. Davenport argues that there is a discrepancy between
the distribution of the pain, which appeared more suggestive of L2 and
perhaps a contribution of L1 and L3, and the involvement of L4 root as
documented by clinical neurophysiology and neuroimaging. The patient was
asked to draw the distribution of pain on a body diagram with no
suggestion from any of us,[2] and some degree of inaccuracy in drawing
pain distribution cannot be completely ruled out. However, the most likely
explanation for the discrepancy between the reported pain distribution and
the anatomical dermatome charts is the presence of referred pain and
central sensitization, two phenomena that are known to contribute to the
presence of non-anatomical and/or enlarged distribution of neuropathic
pain.[3] A pain duration longer than 2 years, as in our case, strongly
supports the view of central sensitization.
The second point raised by Dr. Davenport concerns the notion that a
depressed knee jerk mainly suggests L3 instead of L4 damage. The knee jerk
is mediated by the L3 and L4 roots, and its depression, as in the present
case, might be secondary to L4 radiculopathy.[4]
With best regards,
Giampietro Zanette MD,
Francesca Magrinelli MD,
Stefano Tamburin MD
References
1. Zanette G, Magrinelli F, Tamburin S. Periodic thigh pain from radicular
endometriosis. Pract Neurol 2014;14:351-3.
2. Magrinelli F, Zanette G, Tamburin S. Neuropathic pain: diagnosis and
treatment. Pract Neurol 2013;13:292-307.
3. Zanette G, Cacciatori C, Tamburin S. Central sensitization in carpal
tunnel syndrome with extraterritorial spread of sensory symptoms. Pain
2010;148:227-36.
4. Mumenthaler M. Neurologic Differential Diagnosis; translated and
annotated by Otto Appenzeller, 2nd ed. New York, NY: Thieme Publishing
Group. 1992:26-27.
With great interest I read Coebergh et al. piece on how to undiagnose
neurological disease. 1 My experience as a neurologist with subspecialty
training in epilepsy has taught me that diagnostic labels such as seizure
disorder or epilepsy once attached are very hard to purge either from the
patient's medical records or his memory. I frequently encounter patients
carrying a diagnostic label of epilepsy in whom continuous vi...
With great interest I read Coebergh et al. piece on how to undiagnose
neurological disease. 1 My experience as a neurologist with subspecialty
training in epilepsy has taught me that diagnostic labels such as seizure
disorder or epilepsy once attached are very hard to purge either from the
patient's medical records or his memory. I frequently encounter patients
carrying a diagnostic label of epilepsy in whom continuous video-EEG
monitoring reveals non-epileptic events. The record shows no interictal
epileptiform features and I feel reasonably confident in undiagnosing
their seizure disorder. Taking away their diagnosis of epilepsy is though
easier said than done as frequently an abnormal EEG has been reported in
the past. Maybe the patient suffers from epileptic as well as non-
epileptic events. Maybe I should continue the anticonvulsant to be on the
safe side. My patient too is apprehensive and not keen on shedding his
diagnostic label. Status quo is maintained.
References
1. Coebergh JA, Wren DR, Mumford CJ. Undiagnosing' neurological
disease: how to do it, and when not to. Pract Neurol 2014;14:436-439.
I read the article "Brain Injury and deprivation of liberty on
neurosciences wards" with interest - it is well-timed and provides a
helpful introduction to the the recent changes to deprivation of liberty
safeguarding criteria. Working in a residential neurorehabilitation centre
I am very familiar with the DoLS process as the majority of our client
group are admitted under this safeguard. As mentioned in the article, the...
I read the article "Brain Injury and deprivation of liberty on
neurosciences wards" with interest - it is well-timed and provides a
helpful introduction to the the recent changes to deprivation of liberty
safeguarding criteria. Working in a residential neurorehabilitation centre
I am very familiar with the DoLS process as the majority of our client
group are admitted under this safeguard. As mentioned in the article, the
recent changes have led to an increase in the number of requests for DoLS
assessment, as many of our clients lack the capacity to consent to their
admission and meet the "acid test", but are not actively seeking to leave.
The local authority has been overwhelmed by requests and as such it can
take considerable time for the assessment to be completed, as the article
mentions.
A particular concern for the service is the lack of brain-injury
specific knowledge in DoLS assessors. In my experience the professionals
sent out to complete assessments are frequently from either a mental
health or learning disability background. They can require considerable
support in understanding the complexity of acquired brain injury,
particularly with relation to individuals who have impairments that are
not immediately apparent at a first meeting. It is frustrating that DoLs
assessors are required to give a "diagnosis" of a mental disorder
(frequently "organic personality disorder" is the only available label) as
part of the DoLS process when commonly the reason for referral is a
cognitive impairment (i.e. impaired insight, attention or memory) rather
than a psychiatric condition. Understandably these teams have a colossal
workload but I would suggest that it is to their advantage to make contact
with local brain injury services and seek consultation and training. This
can enable DoLs professionals to feel confident to meet the needs of a
population from whom they are likely to now receive ever increasing
referrals.
Dear Sirs,
Myasthenia gravis: Association of British Neurologists' management
guidelines We read with interest the ABN's management guidelines on
Myasthenia
Gravis[1] and commend the authors for putting toget
her guidelines for this condition where the evidence base is limited. The
comments here reflect our experience of managing a large number of
patients with ocular myasthenia gravis (OMG). Moor
fields Eye Hospital is th...
Dear Sirs,
Myasthenia gravis: Association of British Neurologists' management
guidelines We read with interest the ABN's management guidelines on
Myasthenia
Gravis[1] and commend the authors for putting toget
her guidelines for this condition where the evidence base is limited. The
comments here reflect our experience of managing a large number of
patients with ocular myasthenia gravis (OMG). Moor
fields Eye Hospital is thelargest and only 24-hour eye casualty in London
and as such patients with OMG
often present early to us.
Diagnostic tests
In addition to thyroid function, we also routinely
test for thyroid antibodies, as thyroid eye disease (TED) may coexist with
OMG. Thyroid function may benormal in such circumstances, and the presence
of TED may affect the response to treatment. There are two reasons for
this. Firstly the presence of thyroidantibodies is circumstantial evidence
for an autoimmune phenotype. Secondly patients with thyroid antibodies may
be euthyroid and still have dysthyroid eyedisease. The coexistence of TED
and OMG is important to recognize as the two
conditions are managed differently.
Approximately 50% of OMG patients are seronegative to anti-AChR
antibodies[2]. In addition to anti-MuSK antibodies
(MuSK+ MG can present as OMG only[3]), newer tests using the cell-based
assays can be helpful, and willlikely become more widely available, which
include:clustered anti-AChRantibodies (positive in up to 50% of
seronegative OMG[2]) and LRP4 antibodies(which is part of the MuSK
complex) [3].
At the time of writing, edrophonium (Tensilon) test
is no longer available.
Alternative methods of performing an anti-cholinest
erase test may includeneostigmine or pyridostigmine: Neostigmine adminis
tered intramuscularly has a long duration of action that allows pre- and
post
-test comparison and careful
documentation of ocular motility; a trial of oral pyridostigmine can also
be useful
as a diagnostic test. We tend to perform the pyrid
ostigmine challenge in the
following manner: For in-patients, we start with a
single oral dose of 30mg pyridostigmine and examine the patient one hour
later. A sequential increase by30mg is administered every 4 hours, i.e. up
to a single dose of 120mg. With the
four hour interval between each dose, the test may
therefore take two days to
complete. This method also allows observation of any dose-related adverse
effects e.g. diarrhoea. For the out-patient setting, pyridostigmine
challenge is performed over 8-12 weeks, with 2-3 cycles of two-weeks on,
two-weeks off pyridostgmine. The patient keeps a careful diary comparing
their symptoms during the two weeks on pyridostigmine, and the two weeks
off pyridostigmine. We prescribe a dose of 30mg three times daily, which
is increased over days to 120mg three times daily, and continue the
pyridosti
gmine challenge on 120mg three times daily if tolerated by the patient.
Treatment of ocular myasthenia gravis
In addition to symptomatic treatment with pyridostigmine, other
symptomatic treatments potentially useful include monocular occlusion (use
of an eye patch, or frosting of one lens on the spectacles) and prisms
(usually more useful if the
deficits become more fixed after long term OMG).
We prefer a daily dose of corticosteroid compared to alternate day dosing,
as is the preference or recommendations by other MG experts[4]. The
evidence for a better risk profile for alternate day dosing is limited.
The literature on this
seems to come predominantly from renal transplant in children, with
regards to
growth, although the evidence for this is mixed[5,6
]. In our experience, dailydosing can help with medication compliance At
present, we do not routinely refer our patients
with OMG for thymectomy, unless imaging suggests that a thymoma may be
present. This is an area that has unresolved questions. Some recent
retrospective studies suggest that early
thymectomy in non-thymomatous OMG could potentially improve outcome, but
this question remains to be addressed in a randomised controlled trial
[3]. The
MGTX trial studied the effect of thymectomy in MG,
is due to be reported in January 2016, but excluded patients with OMG[7].
It is also our practice to start azathioprine early
(i.e. approximately 1-2 months)
in patients who have response to corticosteroids.
In our experience, patients often relapse below 15-20mg prednisolone, and
there
fore find the relatively early introduction of azathioprine may help
weaning off prednisolone earlier. One argument against starting
azathioprine early is that some patients will be able to come off
prednisolone and remain in remission. In our experience this is an unusual
eventuality. After our patients have been in remission, we then start
to consider weaning off the corticosteroid-sparing
agent such as azathioprine if they have been on this alone for
approximately two years. The ABN guidelines by Sussman et al are a useful
resource for practicing neurologists, and we hope that our experience in
the management of large
numbers of patients with OMG described above could also be of value.
References
1 Sussman J, Farrugia ME, Maddison P,
et al.Myasthenia gravis: Association of
British Neurologists' management guidelines.
Practical Neurology2015;15
:199-206. doi:10.1136/practneurol-2015-001126
2 Jacob S, Viegas S, Leite MI,
et al.Presence and pathogenic relevance of
antibodies to clustered acetylcholine receptor in o
cular and generalized
myasthenia gravis.
Arch Neurol
2012;69:994-1001.doi:10.1001/archneurol.2012.437
3 Wong SH, Huda S, Vincent A,
et al. Ocular myasthenia gravis: controversies
and updates.Curr Neurol Neurosci Rep
2014;14:421. doi:10.1007/s11910-013-0421-9
4 Kumar V, Kaminski HJ. Treatment of myasthenia gravis.Curr Neurol
Neurosci Rep
2011;11:89-96. doi:10.1007/s11910-010-0151-1
5 Feldhoff C, Goldman AI, Najarian JS,
et al. A comparison of alternate day and daily ster
oid therapy in children following renal transplantation. Int J Pediatr
Nephrol
1984;5:11-4.
6 Diethelm AG, Sterling WA, Hartley MW,
et al. Alternate-day prednisone therapy in recipients of renalallografts.
Risk and benefits.
Arch Surg 1976;111:867-70.
7 Aban IB, Wolfe GI, Cutter GR,
et al.The MGTX experience: challenges in planning and executing an
international, multicenter clinical trial. J Neuroimmunol 2008;201-202:80-
4. doi:10.1016/j.jneuroim.2008.05.031
I am grateful to Drs Wong and Plant for their invaluable comments,
based on their enormous experience of patients presenting with suspected
ocular myasthenia.
The Guidelines are intended to offer non-specialists an approach to
management that will work, safely, in the majority of patients. Within
them, we stressed repeatedly the need to seek specialist opinion when in
any doubt, and their letter emphasises the benefit of...
I am grateful to Drs Wong and Plant for their invaluable comments,
based on their enormous experience of patients presenting with suspected
ocular myasthenia.
The Guidelines are intended to offer non-specialists an approach to
management that will work, safely, in the majority of patients. Within
them, we stressed repeatedly the need to seek specialist opinion when in
any doubt, and their letter emphasises the benefit of seeking such help.
Their views, by and large, don't contradict our basic approach, except
with respect to the timing of the introduction of azathioprine. With
respect to the specific issues that they raise:
Thyroid function should be assessed in all patients. We agree that if the
diagnosis of myasthenia is not secure, then it is appropriate to look for
evidence of thyroid ophthalmopathy, which would include antibody testing
and imaging studies.
Some patients seronegative for acetylcholine receptor antibodies may be
seropositive using other techniques, as they describe. However, if the
clinical diagnosis is of purely ocular myasthenia then the result will not
affect the immediate management as proposed in the Guidelines
We are not enthusiasts for the Tensilon? test and don't mourn its non-
availability! We have seen numerous patients incorrectly diagnosed as
having myasthenia on the basis of a test performed by somebody without
appropriate experience. We agree that other forms of anti-cholinesterase
testing may occasionally be helpful, and are grateful for their detailed
proposals. However, we have doubts about these being undertaken by non-
specialists.
We agree that physical treatments (e.g. eye patches and prisms) have their
place both acutely and in some patients with persisting diplopia despite
optimal drug treatment, but of course they become unnecessary inn the
majority of patients who respond extremely well to drug therapy.
We also agree that the evidence base for using alternate-days steroids, in
terms of reducing long-term side-effects, is minimal. At very high doses,
as may be needed in generalised myasthenia, steroid-induced myopathy may
be difficult to differentiate from myasthenic weakness. We have never seen
steroid-induced myopathy on an alternate day regime. In patients with
marked symptomatic fluctuation between steroid and non-steroid days, and
those with diabetes, we would often have a preference for a daily steroid
regime.
In the past, thymectomy has not been used widely for non-thymomatous
ocular myasthenia, perhaps largely because sternotomy represents major
surgery, with unacceptable cosmetic consequences, particularly for the
dominant young-female population. However, if the less invasive technique
of video-assisted thymectomy reduced the risk of generalisation, and for
some negated the need for immunosuppressant drug therapy, then it would
potentially be very valuable. Unfortunately, the International Thymectomy
Trial will not address these issues, and a further trial, at least in the
foreseeable future, seems unlikely. We think it is an option that is
appropriate to discuss with the patient.
Although azathioprine is often considered a relatively safe drug, and its
steroid-sparing effect potentially valuable to the patient, our experience
suggests that many patients have their myasthenia controlled on a modest
dose of prednisolone and that azathioprine is unnecessary. We are
concerned by long-term side-effects, particularly cutaneous malignancies,
increased risk of infection (including shingles) and the occasional case
of late-myelosuppression.
The points raised by Drs Wong and Plant emphasise the lack of data
concerning the treatment of MG and should encourage us to design studies
to help answer the really important questions in MG, such as whether it is
possible to determine initial optimal treatment requirements from clinical
or immunological features.
As a jobbing MS neurologist in Southampton I am really not sure how
these guidelines are going to assist in my clinical practice.
Perhaps first and foremost, if I was to follow these guidelines I
would find myself frequently in breach of NHS commissioning criteria with
perhaps severe implications for both myself and my hospital trust given
the cost of these therapies. As such I feel the authors should have give...
As a jobbing MS neurologist in Southampton I am really not sure how
these guidelines are going to assist in my clinical practice.
Perhaps first and foremost, if I was to follow these guidelines I
would find myself frequently in breach of NHS commissioning criteria with
perhaps severe implications for both myself and my hospital trust given
the cost of these therapies. As such I feel the authors should have given
a little more attention to this issue, highlighting where guidance is
against what we are actually allowed to do.
My experience of multiple sclerosis patients is that they do not
simply fall into two broad categories of active vs more active and
therefore I find the division of the drugs into two broad categories
equally unhelpful and unnecessary. Perhaps the most obvious example is
that fingolimod has considerably more potency than some of the other
category one drugs and by these guidelines own definitions fingolimod
could easily be classed as a category two treatment and therefore be a
good option for more active patients, as it is already under the NHS
commissioning criteria.
The guidelines recommend using alemtuzumab or natalizumab in patients
with more active disease as defined by one relapse in the previous year on
interferon with MRI criteria. In clinical practice treatment decisions in
such patients are heavily influenced by factors such as disease duration,
treatment duration, relapse severity, prior relapse frequency on and off
treatment, and gadolinium enhancement on MRI (with number of T2 lesions
not being particularly useful). These guidelines could and should have
been more progressive in discussing a correct approach for different
patient types. Among other considerations that should have been discussed
include treating young women with highly active multiple sclerosis for
whom alemtuzuamb now provides the possibility of potent treatment and
pregnancy at the same time, and JC virus negative patients for whom
natalizumab offers a virtually risk free high potency therapy assuming
that JCV status is regularly monitored whilst on treatment.
Finally in non-relapsing established progressive disease there is
absolutely no evidence to support immunomodulation and given the costs of
therapy I really think this guidance could have taken a bolder approach in
making firm recommendations about cessation of treatment to support
clinicians in their discussions with such patients.
Overall I feel these guidelines offer a fairly simplistic and non-
commital approach, that as UK neurologists we are often unable to follow
due to commissioning restrictions, and with the wide range of therapies
now available a more progressive, customised approach that addresses a
wide range of patient characteristics is what is required.
Dear Sirs,
We welcome Dr Leach's comments and a call for action from Neurologists,
regarding service provision for women of childbearing age with
neurological disorders1. We would also like to highlight that quietly, a
number of us are grasping the nettle.
Risk is inherent in clinical practice. Managing risk effectively and pro-
actively in preference to reactively minimises the likelihood of a poor
outcome. This can be...
Dear Sirs,
We welcome Dr Leach's comments and a call for action from Neurologists,
regarding service provision for women of childbearing age with
neurological disorders1. We would also like to highlight that quietly, a
number of us are grasping the nettle.
Risk is inherent in clinical practice. Managing risk effectively and pro-
actively in preference to reactively minimises the likelihood of a poor
outcome. This can be achieved by identifying those at risk and adapting
practices to avoid that risk. This has not often been more concisely put
than by Cicero who is quoted as stating that "To make a mistake is only
human; to persist in a mistake is idiotic". We agree that at the very
least, missing an opportunity to avoid a maternal death is idiotic, and
certainly tragic.
A joint approach is needed and at St George's University Hospitals NHS
Foundation Trust, Consultants in Obstetrics, Obstetric anaesthetics,
Neurology, Neurosurgery and Neuroradiology have together with excellent
support from Maternal Medicine Midwifery and Neurology Clinical Nurse
Specialists, been working collaboratively for some time.
Our Epilepsy Group run a regular clinic together with Maternal Medicine
Midwives for all women with Epilepsy delivering at St George's, and there
is a monthly joint Neurology and Obstetric clinic in maternal medicine
where women with complex (and sometimes more simple) neurological
disorders can be advised regarding pregnancy, delivery and breastfeeding.
Careful individualized plans for Neurological (including surgical and
vascular), Obstetric, Anaesthetic and midwifery led care are made for
these women.
We know from prospective data collection (risk also comes from not knowing
what you are doing) that unplanned episodes and adverse outcomes have been
avoided.
We are also aware that similar clinical services are available at other
Hospitals including University College London Hospitals, at Queen
Charlotte's and Chelsea Hospital, part of Imperial College Healthcare NHS
Trust, and has long been available at Birmingham Women's NHS foundation
Trust.
A call from the NHS England Strategic Clinical Networks was recently made
for a Neurologist advisor to join the London Maternity morbidity and
mortality expert panel. This is an opportunity to act and work together
that the clinicians at St George's will not be missing.
Yours sincerely,
Dr Dominic Paviour, Consultant Neurologist
Dr Ingrid Watt Coote, Consultant in Obstetrics and Maternal Medicine
Dr Hannah Cock, Consultant Neurologist and Epileptologist,
Ms Amanda Reeve, Clinical Nurse Specialist, Atkinson Morley Epilepsy Group
Trudy Williams, Specialist Midwife in Maternal Medicine
St George's University Hospital NHS Foundation Trust, London
References:
1. Death in pregnancy: a call for neurological action
John Paul Leach, Pract Neurol 2015;15:244-245 doi:10.1136/practneurol-2015
-001097
The outlined model of cooperative and integrative services for
pregnant women with neurological conditions is warmly welcomed (and not a
little envied!). While such services are provided the English centres
mentioned, it is sad that such high quality provision remains patchy and
incomplete. This nettle-grasping should no longer be quiet, but should be
loudly heralded and made the norm. The recently updated SIGN guideline...
The outlined model of cooperative and integrative services for
pregnant women with neurological conditions is warmly welcomed (and not a
little envied!). While such services are provided the English centres
mentioned, it is sad that such high quality provision remains patchy and
incomplete. This nettle-grasping should no longer be quiet, but should be
loudly heralded and made the norm. The recently updated SIGN guidelines
recommend a joint approach from all corners, and disparate organisations
such as the ILAE, the ABN, the Medical Royal Colleges, and the RCOG need
to come together to make such synergy routine. Only then can we ensure
that complications of epilepsy during pregnancy and the first post-partum
year follow other obstetric complications in decreasing incidence.
While reading Pennington et al's (2015) article on Functional
Cognitive Disorder, I was struck by the similarity between their
descriptions and a patient seen in clinic (patient X), with the exception
that X's symptoms appeared over the course of a few days with no
identifiable precipitating event. Extensive physical tests and brain
imaging investigations were carried out and no organic disease was found
yet symptoms we...
While reading Pennington et al's (2015) article on Functional
Cognitive Disorder, I was struck by the similarity between their
descriptions and a patient seen in clinic (patient X), with the exception
that X's symptoms appeared over the course of a few days with no
identifiable precipitating event. Extensive physical tests and brain
imaging investigations were carried out and no organic disease was found
yet symptoms were reportedly severe and having a major impact on X's
functioning. Here I discuss X's case (with identifiable information
changed in order to respect patient confidentiality) and propose that
there may be a sub-type of functional cognitive disorder with an acute
onset.
Patient X is a 48 year old house-wife and local preacher. She
presented to clinic with her husband after being referred by her GP due to
the development of severe confusion and cognitive impairment developing
from a previously high level of functioning just a few days earlier.
Symptoms began to appear on the Sunday evening and peaked on the Tuesday,
with no change between then and the clinic assessment (Thursday). X
reported completely 'losing track of time' and reported severe memory loss
which her husband had first noticed. During the assessment, she claimed
inability to answer any of our questions herself and repeatedly looked to
her husband for answers. When asked why she could not answer the
questions, she said that she 'could not remember' and described problems
with attention, concentration and executive function. This appeared
inconsistent with her performance in daily life as she had managed to
maintain her previous social roles, although we had no objective baseline
for comparison.
X had no previous psychiatric history and no significant medical
history. She was not taking any regular medications except for the oral
contraceptive pill. She reported a normal upbringing. The only
identifiable recent stressor was that X had recently started a new
university course, part of which involved looking at different personality
types, which she said had 'confused' and 'worried' her.
It was first thought that she may have organic disease as her
symptoms came on suddenly, however she returned to psychiatry clinic
following extensive tests as no physical cause could be found. Could this
be a case of functional cognitive disorder with acute onset? Further
assessment and follow-up of patient X and others like her could unravel a
subgroup of patients who fall into this category.
I thoroughly enjoyed the article by Zanette et al (2014;14:351-353). The authors are to be congratulated for their skilful history taking skills, specifically the key observation that the pain coincided with menses, suggesting the diagnosis, and thus confirming that a neurology opinion, far from being "the last resort", should have been the "first resort". I am troubled by the distribution of the pain however; the autho...
We thank Dr. Davenport for his interest in our case report [1] and the opportunity to better explain our clinical reasoning. In his e-letter Dr. Davenport argues that there is a discrepancy between the distribution of the pain, which appeared more suggestive of L2 and perhaps a contribution of L1 and L3, and the involvement of L4 root as documented by clinical neurophysiology and neuroimaging. The patient was asked to d...
With great interest I read Coebergh et al. piece on how to undiagnose neurological disease. 1 My experience as a neurologist with subspecialty training in epilepsy has taught me that diagnostic labels such as seizure disorder or epilepsy once attached are very hard to purge either from the patient's medical records or his memory. I frequently encounter patients carrying a diagnostic label of epilepsy in whom continuous vi...
I read the article "Brain Injury and deprivation of liberty on neurosciences wards" with interest - it is well-timed and provides a helpful introduction to the the recent changes to deprivation of liberty safeguarding criteria. Working in a residential neurorehabilitation centre I am very familiar with the DoLS process as the majority of our client group are admitted under this safeguard. As mentioned in the article, the...
Dear Sirs, Myasthenia gravis: Association of British Neurologists' management guidelines We read with interest the ABN's management guidelines on Myasthenia Gravis[1] and commend the authors for putting toget her guidelines for this condition where the evidence base is limited. The comments here reflect our experience of managing a large number of patients with ocular myasthenia gravis (OMG). Moor fields Eye Hospital is th...
I am grateful to Drs Wong and Plant for their invaluable comments, based on their enormous experience of patients presenting with suspected ocular myasthenia. The Guidelines are intended to offer non-specialists an approach to management that will work, safely, in the majority of patients. Within them, we stressed repeatedly the need to seek specialist opinion when in any doubt, and their letter emphasises the benefit of...
As a jobbing MS neurologist in Southampton I am really not sure how these guidelines are going to assist in my clinical practice.
Perhaps first and foremost, if I was to follow these guidelines I would find myself frequently in breach of NHS commissioning criteria with perhaps severe implications for both myself and my hospital trust given the cost of these therapies. As such I feel the authors should have give...
Dear Sirs, We welcome Dr Leach's comments and a call for action from Neurologists, regarding service provision for women of childbearing age with neurological disorders1. We would also like to highlight that quietly, a number of us are grasping the nettle. Risk is inherent in clinical practice. Managing risk effectively and pro- actively in preference to reactively minimises the likelihood of a poor outcome. This can be...
The outlined model of cooperative and integrative services for pregnant women with neurological conditions is warmly welcomed (and not a little envied!). While such services are provided the English centres mentioned, it is sad that such high quality provision remains patchy and incomplete. This nettle-grasping should no longer be quiet, but should be loudly heralded and made the norm. The recently updated SIGN guideline...
While reading Pennington et al's (2015) article on Functional Cognitive Disorder, I was struck by the similarity between their descriptions and a patient seen in clinic (patient X), with the exception that X's symptoms appeared over the course of a few days with no identifiable precipitating event. Extensive physical tests and brain imaging investigations were carried out and no organic disease was found yet symptoms we...
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