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.
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 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.
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.
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.
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
I read with interest Allen et al. approach to starting a new patient
consultation1. Apart from a few minor differences the basic methodology
employed by all four physicians is essentially the same. Across the pond,
I start a new patient consultation in much the same way. I walk into the
reception area, call out the patient's name and upon acknowledgement
("right here" or "yes" is the usual response, rarely "yo" and I hav...
I read with interest Allen et al. approach to starting a new patient
consultation1. Apart from a few minor differences the basic methodology
employed by all four physicians is essentially the same. Across the pond,
I start a new patient consultation in much the same way. I walk into the
reception area, call out the patient's name and upon acknowledgement
("right here" or "yes" is the usual response, rarely "yo" and I have still
to hear someone say "present); I introduce myself to the patient and then
proceed to walk the patient and the accompanying caregiver or friend to
the examination room assigned to me for that day. During the short walk I
may exchange a few brief pleasantries, the weather or the traffic always
are safe bets to elicit an answer from even the most stoic of patients!
("It sure is hot today" or "did you have a tough time driving into the
city today?"). This helps to break the ice and my next question after
everyone is seated comfortably in the room is "So Ms Watson what brings
you in to see my today?" I then allow the patient or the caregiver (both
at times) to speak uninterrupted for the next few minutes as I record
their words verbatim on a piece of paper. I make it a point to look up at
the patient from time to time to acknowledge that he or she has my rapt
attention. This is contrary to some of my colleagues who prefer to type
the history into the electronic health record (EHR) at the same time. I
feel this makes the encounter rather aseptic (with the physician typing
vigorously into the computer at times with his back to the patient) and so
I prefer to type my notes into the EHR either immediately after the
conclusion of the patient encounter or at the end of the day. I then ask a
few direct questions frequently to clarify some aspects of the patient's
history and then move on to the relevant past medical history, list of
current medications, social and family history and finally a brief review
of the systems. Then follows the neurological examination and it is not
infrequent that I may ask a few direct questions at this stage too ("does
it hurt here" "where does the pain radiate?"). I devote the last 10-15
minutes of a new patient consultation (a new patient consultation is
typically an hour in duration) to explain my assessment and plan and
answer any questions. I end the encounter by walking the patient over to
my secretary so that she can help schedule the tests ordered and a follow
up consultation if warranted.
References
1. Allen C, Scolding N, Mumford C, Smith P, Fuller G. How I start a
new patient consultation. Pract Neurol 2013; 13:254-7.
I read with interest the debate between Nightingale el al. and Schott
about whether we should routinely test for HIV in patients presenting with
cognitive impairment 1,2 . I assume that while the authors have taken
rather polarized views to state their point, the correct answer lies
somewhere in between. Testing for HIV shall not be the foremost in my
mind in a 75-year-old male presenting with slowly progressive cognitive...
I read with interest the debate between Nightingale el al. and Schott
about whether we should routinely test for HIV in patients presenting with
cognitive impairment 1,2 . I assume that while the authors have taken
rather polarized views to state their point, the correct answer lies
somewhere in between. Testing for HIV shall not be the foremost in my
mind in a 75-year-old male presenting with slowly progressive cognitive
impairment for the past few years accompanied with typical features of a
cortical dementia (aphasia, apraxias and agnosias). In such a patient I
shall rather harness my clinical and diagnostic skills to differentiate
between Alzheimer's disease, frontotemporal dementia and Lewy body
dementia. On the other hand a 45-year-old male presenting with cognitive
impairment accompanied by a movement disorder, certainly HIV testing shall
be included in my diagnostic armamentarium. One must though not forget
that positive HIV serology is not synonymous with HIV encephalopathy or
AIDS dementia complex which is a clinical syndrome comprising of a
combination of cognitive, behavioral and motor dysfunction. Testing a
patient with cognitive impairment for HIV shall have a high positive
predictive value only when the test is carried out after taking the
patient's age at presentation, history (not just of risk factors but also
of the rate of progression of symptoms) and examination findings into
consideration.
References
1. Nightingale S, Michael BD, Defres S, Benjamin LA, Solomon T. Test
them all; an easily diagnosed and readily treatable cause of dementia with
life-threatening consequences if missed. Pract Neurol. 2013;13:354-6.
2. Schott JM. HIV testing in dementia: test some, perhaps more, but
not all. Pract Neurol. 2013;13:357-8.
Can myoclonus involve large muscles like the trunk muscles giving out
just one jerk with a duration of a fraction of a second?Would it be
justified to term this phenomena as a myoclonic seizure or a complex
myoclonus when there is LOC for that fraction of a second;happening while
falling asleep only.Or can it be a sleep disorder,a hypnic jerk?
Can myoclonus involve large muscles like the trunk muscles giving out
just one jerk with a duration of a fraction of a second?Would it be
justified to term this phenomena as a myoclonic seizure or a complex
myoclonus when there is LOC for that fraction of a second;happening while
falling asleep only.Or can it be a sleep disorder,a hypnic jerk?
Conflict of Interest:
without reading the entire text how can I declare any competing interests.
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...
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 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...
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...
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...
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...
Is there any reason you can think of when the CSF protein and the CSF glucose should be evaluated from different tubes of CSF and not the same tube?
Conflict of Interest:
None declared
I read with interest Allen et al. approach to starting a new patient consultation1. Apart from a few minor differences the basic methodology employed by all four physicians is essentially the same. Across the pond, I start a new patient consultation in much the same way. I walk into the reception area, call out the patient's name and upon acknowledgement ("right here" or "yes" is the usual response, rarely "yo" and I hav...
I read with interest the debate between Nightingale el al. and Schott about whether we should routinely test for HIV in patients presenting with cognitive impairment 1,2 . I assume that while the authors have taken rather polarized views to state their point, the correct answer lies somewhere in between. Testing for HIV shall not be the foremost in my mind in a 75-year-old male presenting with slowly progressive cognitive...
sir/madam,
Can myoclonus involve large muscles like the trunk muscles giving out just one jerk with a duration of a fraction of a second?Would it be justified to term this phenomena as a myoclonic seizure or a complex myoclonus when there is LOC for that fraction of a second;happening while falling asleep only.Or can it be a sleep disorder,a hypnic jerk?
Conflict of Interest:
...Pages