Having received treatment for PMSAH in 2006, I agree vigorously with
the conclusion that there needs to be additional study on the long term
outcomes of individuals who have suffered this type of non-aneurysmal
brain bleed.
In my particular case, my in-hospital treatment was excellent, but I
had no idea what to expect afterwards, what complications might arise, how
long it would take for my headaches to subside...
Having received treatment for PMSAH in 2006, I agree vigorously with
the conclusion that there needs to be additional study on the long term
outcomes of individuals who have suffered this type of non-aneurysmal
brain bleed.
In my particular case, my in-hospital treatment was excellent, but I
had no idea what to expect afterwards, what complications might arise, how
long it would take for my headaches to subside, or whether I would have
continuing difficulties returning to my everyday functions. (In general, I
did not, but there are significant caveats.)
After I was discharged, the early recovery phase included periods of
intense pain that was not well managed by the highest prescribed dosage of
Vicodin. The neurosurgeon who treated me did not seem particularly
interested in my follow-up care, although while I was still in-hospital he
seemed quite attentive.
I was fortunate to have my wife as a home caregiver - she happens to
be a family medicine practitioner - and without her critical eye with
regard to managing my pain, I would have fared worse.
In the years since, I have ongoing concerns related to short-term
memory loss, fatigue, headaches, and difficulty concentrating - symptoms I
did not experience in any significant way before. I have had an extended
but temporary period of anosmia several years after the bleeding incident,
but have no idea whether this was connected to the hemorrhage or not.
Health care professionals need to recognize that this type of brain
bleed (laughably referred to as 'benign' in much of the literature) is a
pivotal event in a patient's life. The experience itself is highly
traumatic, and the recovery (especially the early phase) is difficult,
even though the outcome is likely good.
One of the main challenges I faced recovering from PMSAH was/is
uncertainty. There are few resources available to help identify the
situations/symptoms that one is likely to encounter in the years following
the hemorrhage, and it seems to me that the medical community ought to be
able to provide this information.
I applaud anyone willing to undertake this follow-up research that
could help provide patients like me recovering from PMSAH with some much-
needed answers.
We read an interesting review and meta-analysis of published articles
pertaining to cerebral amyloid angiopathy (CAA) by Samarasekera and
collegues published in March 2012 issue of our esteemed journal1. The
effforts made by the authors are worth appreciation. The previously
considered to be a rare neurological curosity, CAA is now recognised as an
important cause of spontaneous intracerebral haemorrhage and cognitive
im...
We read an interesting review and meta-analysis of published articles
pertaining to cerebral amyloid angiopathy (CAA) by Samarasekera and
collegues published in March 2012 issue of our esteemed journal1. The
effforts made by the authors are worth appreciation. The previously
considered to be a rare neurological curosity, CAA is now recognised as an
important cause of spontaneous intracerebral haemorrhage and cognitive
impairment in the elderly but still under-recognised2. Further
prospective studies in this direction are mendatory to strengthen the
diagnostc criteria with the help of modern neuroimaging and biopsy of
brain and leptomeninges as and when possible. New treatment and management
options described in earlier issue of this article in form of reduction of
blood pressure, statins, anti-inflammatory, immunomodulators and surgery
requires further trials in this direction2,3. Results of surgery are not
as dismal as it was thout to be previously as described earlier2 and our
own observation3.
REFFRENCES-
1-Samarasekara N, Smith C, Salman R Ai-Shahi. The asssociation between
cerebral amyloid angiopathy; systematic review and meta-analysis. J.
Neurol Neurosurg Psychiatry 2012; 83: 275-281.
2-Andreas Charidimou, Qiang Gang, David J Werring. Sporadic cerebral
amyloid angiopathy revisited: recent insights into pathophysiology and
clinical spectrum. J Neurol Neurosurg Psychiatry.2012;83:124-137.
3-Khichar Shubhakaran. Personal onservation.
We read with great interest a recent article by Morgante et al1
concerning the prevalence of psychosis associated with Parkinson disease.
Psychotic symptoms, mainly visual hallucinations (VHs), occur in about one
-third of patients, and thought to be a complication of antiparkinsonian
treatment. However, they reported that psychotic type symptoms of PD, such
as VHs, might occur more frequently in the early stage compared w...
We read with great interest a recent article by Morgante et al1
concerning the prevalence of psychosis associated with Parkinson disease.
Psychotic symptoms, mainly visual hallucinations (VHs), occur in about one
-third of patients, and thought to be a complication of antiparkinsonian
treatment. However, they reported that psychotic type symptoms of PD, such
as VHs, might occur more frequently in the early stage compared with later
stages.
In population-based, case-control study, PD patients historical records
were examined for depression and anxiety in pre-motor phase of PD.2-4
Notably, Shiba et al3 described that the association with anxiety was
significant even when the analysis went as far back as 20 years before the
onset of motor symptoms.3 These studies show that anxiety and depression
are associated with PD and suggest that the causative process or risk
factors underlying PD may be present many years before motor symptoms
onset.
Neither the mechanism of VHs nor frequency of VHs in pre-motor phase are
not clear in PD. One potential explanation for VHs is the imbalance with
cholinergic neurotransmission rather than dopaminergic overactivity due to
antiparkinsonian treatment. Loss of dopaminergic nigrostriatal function
occurs before motor symptoms onset in PD and influences the serotonergic,
noradrenergic and cholinergic systems.
We suspect that imbalance of cholinergic system induces the VHs in the
early motor stage of PD. The beneficial effect of cholinesterase inhibitor
on VHs supports our suggestion.5
REFERENCES
1. Morgante L, Colosimo C, Antonini A, et al. Psychosis associated to
Parkinson's disease in the early stages: relevance of cognitive decline
and depression. J Neurol Neurosurg Psychiatry 2012;83:76-82.
2. Alonso A, Rodriguez LA, Logroscino G, et al. Use of antidepressants and
the risk of Parkinson's disease: a prospective study. J Neurol Neurosurg
Psychiatry 2009;80:671-4.
3. Shiba M, Bower JH, Maraganore DM, et al. Anxiety disorders and
depressive disorders preceding Parkinson's disease: a case-control study.
Mov Disord 2000;15:669-77.
4. Weisskoph MG, Chen H, Schwarzschild MA, et al. Prospective study of
phobic anxiety and risk of Parkinson's disease. Mov Disord 2003;18:646-51.
5. Kurita A, Ochiai Y, Kono Y, et al. The beneficial effect of donepezil
on visual hallucinations in three patients with Parkinson's disease. J
Geriatr Psychiatry Neurol 2003;16:184-8.
CEREBRAL AMYLOID ANGIOPATHY- NOT SO AVOIDABLE - NOT SO DISMAL A NEW HOPE
Honourable Editor Sir,
I read an intresting article by Cheridimou A and collegues published in February 2012 issue of our estttmed journal1. The authors have very nicely reviewed the sporadic cerebral amyloid angiopathy (CAA) in a very excellent and precise way. The efforts made by authors are worth appriciation by the readres. Here I would like to share...
CEREBRAL AMYLOID ANGIOPATHY- NOT SO AVOIDABLE - NOT SO DISMAL A NEW HOPE
Honourable Editor Sir,
I read an intresting article by Cheridimou A and collegues published in February 2012 issue of our estttmed journal1. The authors have very nicely reviewed the sporadic cerebral amyloid angiopathy (CAA) in a very excellent and precise way. The efforts made by authors are worth appriciation by the readres. Here I would like to share my views as under-
1- Age and hypertension are the two most important risk factors for stroke of either ischaemic or haemorrhagic type. Age probably is a strong risk factor because of cerebral amylod angiopathy. Hypertension almost always can worsen the stroke or cognitive impairment but age may not depending upon presence or abscence of cerebral amyloid angiopathy.
2- Further insight into the link between neurons and vascular system named as "neurovascular link" will also help understand the cerebral amyloid angiopathy better2.
3- Role of anti-inflammatory or disease modifying agents may have a promising role which requires prospective double blinded large scale trials. Further more the same may be studied in the patients taking anti-inflammatory or disease modifying drugs for some other purposes. The factor of bias may be calculated by means of stanndard satatistical mathods.
4- Bloob pressure may be kept on lower side in susceptible population.
5-Patients of stoke with microbleeds be managed carefully so as to avoid haemorrhagic comlications3. If Magnetic resonance imaging facility is not available or not affordable, the topography of the ischaemic lesions and leukoaraiosis along with other stroke risk factors may help guide regarding the possibility of cerebral amyloid angiopathy and the precautions accordingly for judicious use of antithrombotic therapy or thrombolysis. This is implicable for resource poor third world countries.
REFFRENCES-
1- Andreas Charidimou, Qiang Gang, David J Werring. Sporadic cerebral amyloid angiopathy revisited: recent insights into pathophysiology and clinical spectrum. J Neurol Neurosurg Psychiatry.2012;83:124-137.
2-Quaegebeur A, Lange C, Carmellet P. The neurovascular link in health and disease: molecular mechanism and therapeutic implication. Neuron. August 2011,Vol 11, issue 3-406-422.
3-Van Es C A G M et al. Cerebral microbleeds and cognitive functioning,the "PROPOSAL" study. Neurology October 11, 2011,Vol 77,No.15; 1446-1452.
The dorsal horns are not merely passive transmission stations but
sites at which dynamic activities (inhibition, excitation and modulation)
occur. [18]
Via a series of filters and amplifiers, the nociceptive message is
integrated and analysed in the cerebral cortex, with interconnections with
various areas. [1]
The processing of pain takes place in an integrated matrix throughout...
The dorsal horns are not merely passive transmission stations but
sites at which dynamic activities (inhibition, excitation and modulation)
occur. [18]
Via a series of filters and amplifiers, the nociceptive message is
integrated and analysed in the cerebral cortex, with interconnections with
various areas. [1]
The processing of pain takes place in an integrated matrix throughout
the neuroaxis and occurs on at least three levels, at peripheral, spinal,
and supraspinal sites. [9]
Knowledge of the modalities of pain control is essential to correctly
adapt treatment strategies (drugs, neurostimulation, psycho-behavioural
therapy, etc.).
Dysfunction of pain control systems causes neuropathic pain. [1]
Spinal Cord Stimulation modalities evolved from the gate-control
theory postulating a spinal modulation of noxious inflow. [16] [2] [7]
[11] [12] [15] [17] [20] [22] [23] [24] [25] [26]
It has been demonstrated in multiple studies that dorsal horn
neuronal activity caused by peripheral noxious stimuli could be inhibited
by concomitant stimulation of the dorsal columns. [8]
Pain relief was more prominent at pain ascending through C fibers
than pain ascending through Adelta fibers [21]
Many theories on the mechanism of action of Spinal Cord Stimulation
have been suggested, including activation of gate control mechanisms,
conductance blockade of the spinothalamic tracts, activation of
supraspinal mechanisms, blockade of supraspinal sympathetic mechanisms,
and activation or release of putative neuromodulators. [14]
At present, Spinal Cord Stimulation is a well established form of
treatment for failed back surgery syndrome, complex regional pain
syndromes (CRPS), low back pain with radiculopathy and refractory pain due
to ischemia. [4] [3] [8] [13]
Stimulation produced analgesia can provide a level of analgesia and
efficacy that is unattainable by other treatment modalities. [19]
Spinal Cord Stimulation for the treatment of chronic pain is cost-
effective when used in the context of a pain treatment continuum. [14]
Precise subcutaneous field stimulation is targeted to specific areas
of neuropathic pain. [6]
We aim at attenuation or blockade of pain through intervention at the
periphery, by activation of inhibitory processes that gate pain at the
spinal cord and brain. [9]
Segmental noxious stimulation produces a stronger analgesic effect
than segmental innocuous stimulation. [10]
That is exactly what intradermal sterile water or subcutaneous saline
injections do!
Chloride, used in subcutaneous "sham" injections, independently
regulates the pain pathway. [5]
Intraspinal steroids should no longer be used since we can obtain
better results using sterile water intradermal injections, especially for
back pain.
Furthermore, intradermal injections are minimally invasive and
absolutely NOT neurotoxic.
References
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Labat JJ, Robert R, Delavierre D, Sibert L, Rigaud J.
Centre federatif de pelviperineologie, clinique urologique, CHU Hotel-
Dieu, 1, place Alexis-Ricordeau, 44093 Nantes, France.
http://www.ncbi.nlm.nih.gov/pubmed/21056357
[2] Int J Rehabil Res. 2010 Sep;33(3):211-7.
Effect of transcutaneous electrical nerve stimulation on sensation
thresholds in patients with painful diabetic neuropathy: an observational
study.
Moharic M, Burger H.
Department of Physical and Rehabilitation Medicine, Linhartova 51, SI-1000
Ljubljana, Slovenia.
http://www.ncbi.nlm.nih.gov/pubmed/20042866
[3] Conf Proc IEEE Eng Med Biol Soc. 2009;2009:2033-6.
Spinal cord stimulation for complex regional pain syndrome.
Shrivastav M, Musley S.
Medtronic Neuromodulation, 7000 Central Ave NE, Minneapolis, Minnesota,
55432 USA.
http://www.ncbi.nlm.nih.gov/pubmed/19964771
[4] J Clin Monit Comput. 2009 Oct;23(5):333-9.
Spinal cord stimulation: principles of past, present and future practice:
a review.
Kunnumpurath S, Srinivasagopalan R, Vadivelu N.
St George's School of Anaesthesia, Tooting, London, UK.
http://www.ncbi.nlm.nih.gov/pubmed/19728120
[5] Brain Res Rev. 2009 Apr;60(1):149-70. Epub 2008 Dec 31.
Chloride regulation in the pain pathway.
Price TJ, Cervero F, Gold MS, Hammond DL, Prescott SA.
University of Arizona, Department of Pharmacology, USA.
[6] Curr Pain Headache Rep. 2008 Jan;12(1):28-31.
Peripheral nerve stimulation for chronic pain.
Henderson JM.
Stereotactic and Functional Neurosurgery, Stanford University School of
Medicine, 300 Pasteur Drive, Edwards Building/R-227, Stanford, CA 94305,
USA.
http://www.ncbi.nlm.nih.gov/pubmed/18417020
[7] Schmerz. 2007 Aug;21(4):307-10, 312-7.
From Descartes to fMRI. Pain theories and pain concepts.
Handwerker HO.
Institut fur Physiologie und Pathophysiologie, Universitat
Erlangen/Nurnberg, Deutschland.
http://www.ncbi.nlm.nih.gov/pubmed/17674057
[8] Pain Physician. 2002 Apr;5(2):156-66.
Spinal cord stimulation.
Stojanovic MP, Abdi S.
Interventional Pain Program, MGH Pain Center, Department of Anesthesia and
Critical Care, Massachusetts General Hospital, Harvard Medical School,
Cambridge, MA 02135, USA.
http://www.ncbi.nlm.nih.gov/pubmed/16902666
[9] J Bone Joint Surg Am. 2006 Apr;88 Suppl 2:58-62.
Basic science of pain.
DeLeo JA.
Dartmouth-Hitchcock Medical Center, Dartmouth Medical School, Neuroscience
Center at Dartmouth, Department of Anesthesiology, Lebanon, NH 03756, USA.
http://www.ncbi.nlm.nih.gov/pubmed/16595445
[10] Pain. 2005 May;115(1-2):152-60.
Segmental noxious versus innocuous electrical stimulation for chronic pain
relief and the effect of fading sensation during treatment.
Defrin R, Ariel E, Peretz C.
Department of Physical Therapy, School of Allied Health Professions,
Sackler Faculty of Medicine, Tel-Aviv University, 69978 Ramat Aviv,
Israel.
http://www.ncbi.nlm.nih.gov/pubmed/15836978
[11] Annu Rev Neurosci. 2003;26:1-30. Epub 2003 Mar 6.
Pain mechanisms: labeled lines versus convergence in central processing.
Craig AD.
Atkinson Pain Research Laboratory, Barrow Neurological Institute, 350
W.Thomas Road, Phoenix, AZ 85013, USA.
http://www.ncbi.nlm.nih.gov/pubmed/12651967
[12] Sports Med. 2002;32(4):251-67.
Return-to-work interventions for low back pain: a descriptive review of
contents and concepts of working mechanisms.
Staal JB, Hlobil H, van Tulder MW, K?ke AJ, Smid T, van Mechelen W.
Department of Social Medicine and Research Centre on Work, Physical
Activity and Health, VU University Medical Center, Van der Boechorststraat
7, Amsterdam, The Netherlands.
http://www.ncbi.nlm.nih.gov/pubmed/11929354
[13] Curr Pain Headache Rep. 2001 Apr;5(2):130-7.
Stimulation methods for neuropathic pain control.
Stojanovic MP.
MGH Pain Center, Department of Anesthesia and Critical Care, Massachusetts
General Hospital, Boston, MA 02114, USA.
http://www.ncbi.nlm.nih.gov/pubmed/11252147
[14] Curr Rev Pain. 1999;3(6):419-426.
Spinal Cord Stimulation: Indications, Mechanism of Action, and Efficacy.
Krames E.
Pacific Pain Treatment Centers, 2000 Van Ness Avenue, Suite 402, San
Francisco, CA 94109, USA.
http://www.ncbi.nlm.nih.gov/pubmed/10998699
[15] Ann Pharm Fr. 2000 Mar;58(2):77-83.
Pain and its main transmitters.
Costentin J.
Unite de Neuropsychopharmacologie Experimentale, ESA 6036 CNRS, Institut
Federatif de Recherches Multidisciplinaires sur les Peptides=IFR 23,
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http://www.ncbi.nlm.nih.gov/pubmed/10790600
[16] Neurol Res. 2000 Apr;22(3):285-92.
Mechanisms of spinal cord stimulation in neuropathic pain.
Meyerson BA, Linderoth B.
Department of Clinical Neuroscience, Karolinska Institute, Stockholm,
Sweden.
http://www.ncbi.nlm.nih.gov/pubmed/10769822
[17] Pain. 1999 Aug;Suppl 6:S149-52.
Regulation of spinal nociceptive processing: where we went when we
wandered onto the path marked by the gate.
Yaksh TL.
Department of Anesthesiology, University of California, San Diego, USA.
http://www.ncbi.nlm.nih.gov/pubmed/10491984
[18] Pain. 1999 Aug;Suppl 6:S121-6.
From the gate to the neuromatrix.
Melzack R.
Department of Psychology, McGill University, Montreal, Quebec, Canada.
http://www.ncbi.nlm.nih.gov/pubmed/10491980
[19] J Clin Neurophysiol. 1997 Jan;14(1):46-62.
Stimulation of the central and peripheral nervous system for the control
of pain.
Stanton-Hicks M, Salamon J.
Anaesthesia Pain Management Center, Cleveland Clinic Foundation, OH 44195,
USA.
http://www.ncbi.nlm.nih.gov/pubmed/9013359
[20] Percept Psychophys. 1996 Jul;58(5):693-703.
An investigation of the gate control theory of pain using the experimental
pain stimulus of potassium iontophoresis.
Humphries SA, Johnson MH, Long NR.
Department of Psychology, Massey University, Palmerston North, New
Zealand.
http://www.ncbi.nlm.nih.gov/pubmed/8710448
[21] J Peripher Nerv Syst. 1996;1(3):189-98.
Pain relief by various kinds of interference stimulation applied to the
peripheral skin in humans: pain-related brain potentials following CO2
laser stimulation.
Kakigi R, Watanabe S.
Department of Integrative Physiology, National Institute for Physiological
Sciences, Okazaki, Japan.
http://www.ncbi.nlm.nih.gov/pubmed/10970109
[22] Nurs Stand. 1993 Jul 28-Aug 3;7(45):25-7.
Pain: opening up the gate control theory.
Davis P.
http://www.ncbi.nlm.nih.gov/pubmed/8398721
[23] Bull Acad Natl Med. 1989 Oct;173(7):855-60; discussion 860-1.
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pain.
Cambier J.
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[24] Brain Res. 1983 Dec 5;280(2):217-31.
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Benabid AL, Henriksen SJ, McGinty JF, Bloom FE.
http://www.ncbi.nlm.nih.gov/pubmed/6652483
[25] Psychosom Med. 1979 Mar;41(2):101-8.
A signal detection analysis of the effects of transcutaneous stimulation
on pain.
Malow RM, Dougher MJ.
http://www.ncbi.nlm.nih.gov/pubmed/441227
[26] GATE CONTROL OF ION FLUX IN AXONS.
GOLDMAN DE.
J Gen Physiol. 1965 May;48:SUPPL:75-7.
I understand Dr Bourne's concerns regarding my criticism of the
survey of NIV reported from Sheffield. My Editorial Commentary was
prompted by the very evident shortcomings in the survey reported, relying
as it does on unverified data. We have reached a stage in epidemiological
work when accurate data are needed to assess the uptake of medical
interventions and their outcomes. Surveys cannot provide this essential
evide...
I understand Dr Bourne's concerns regarding my criticism of the
survey of NIV reported from Sheffield. My Editorial Commentary was
prompted by the very evident shortcomings in the survey reported, relying
as it does on unverified data. We have reached a stage in epidemiological
work when accurate data are needed to assess the uptake of medical
interventions and their outcomes. Surveys cannot provide this essential
evidential database.
We are concerned that the article by Professor Swash [1]
misrepresents both the nature and findings of our recent UK national
survey of the use of NIV in patients with MND/ALS. Although entitled an
"editorial commentary", the article is essentially restricted to a
critique of our study alone. In particular, he criticises the response
rate to the survey (63%) and the lack of verification of the data in a sub
-population;...
We are concerned that the article by Professor Swash [1]
misrepresents both the nature and findings of our recent UK national
survey of the use of NIV in patients with MND/ALS. Although entitled an
"editorial commentary", the article is essentially restricted to a
critique of our study alone. In particular, he criticises the response
rate to the survey (63%) and the lack of verification of the data in a sub
-population; he grudgingly acknowledges that the study "contains some
hints of changing practice" but concludes that "it would be unwise to
place too much reliance on these suggestions."
Most of the criticisms have already been refuted or acknowledged in our
paper. In the light of recent evidence showing the benefits of NIV in this
population,[2-4] the main aim of the survey was to compare present
practice with that found in a virtually identical survey we performed 9
years earlier.[5] To ensure comparability between the two surveys, we used
the same methodology; questionnaires were posted to all practising
neurologists in the UK, identified through the Association of British
Neurologists, with a second mailing to non-respondents. In this respect,
ours is a more complete survey of national practice than others, which
have largely been limited to specific regions, specialist centres or
neurologists who elected to participate. The number of new cases of MND
diagnosed in the preceding year was virtually identical in our two
surveys, reflecting the relatively stable incidence of MND, and in line
with the expected incidence in the UK. This implies that most of the
neurologists involved in the care of MND patients responded. In the paper,
we acknowledged that, as with most such surveys, the data were not
independently verified in a sub-group of neurologists; it should be noted
that the survey was anonymous and most of the information collected
reflects aspects of practice that could not have been gleaned from a
database. Where specific numbers of patients were requested, the scope for
error is much smaller than suggested by Swash as, in MND, NIV is initiated
only after careful consideration, the number referred by individual
neurologists is small and any individual errors are mitigated by the large
number of responses.
Our results showed a very large increase in the number of patients
referred for, and successfully initiated on, NIV (2.6 and 3.4 fold
respectively), as well as other improvements in respiratory care. These
impressive increases over a short period are much greater than any
potential reporting error by individual neurologists.
With regard to data on quality of life (QoL), the author seems to have
misunderstood the purpose of our study, which was a large-scale survey of
national practice rather than a study of the benefits of treatment. We
have previously shown that NIV improves the QoL of patients with MND;[3]
clearly, it was not our aim to show this again, nor would it have been
feasible to gather QoL data on a representative cohort of patients in the
practice of each neurologist.
We acknowledge that we did not compare the practice of individual
neurologists to national guidelines. We highlight that the National
Institute of Clinical Excellence (NICE) guidelines,[6] were in
development, but they were not available over the time period to which the
survey referred. Judging the practice of neurologists against these
guidelines would clearly have been inappropriate. We would suggest that
our approach provided much more worthwhile information: we assessed the
actual practice of each neurologist, including whether referral for NIV
was based on symptoms alone or in combination with physiological
impairment, whether they consider early intervention (physiological
impairment with no or only minimal symptoms) and, if respiratory function
was assessed, which specific tests were applied, whether they were
performed at presentation, routinely or only if symptomatic, and the
specific threshold that triggered referral. We showed that, compared to
the main body of neurologists, those with the highest rates of referral
for NIV were more likely to monitor respiratory function routinely and (in
addition to vital capacity) they were more likely to measure sniff nasal
inspiratory pressure and arterial blood gases and to consider early
intervention. Assessment along these lines is supported by the recently
published National Institute of Clinical Excellence guidelines.
Swash interprets our analysis by practice size incorrectly. We ranked the
size of neurologists' practice in quartiles according to the number of new
patients seen. Compared to neurologists in the quartile with the largest
practice, those with practices in the lowest quartile had a similar NIV
referral rate (corrected for practice size), but the proportion of
patients successfully established on NIV was lower (an outcome of
importance to patients and their carers). Also, we found that neurologists
within the lowest practice quartile were less likely to monitor
respiratory function and less likely to rely on the combination of
symptoms and respiratory function, both factors likely to influence
appropriate selection of patients for NIV.
With regard to oxygen therapy, the potential for varying
interpretation of the commonly used phrase "end of life" is covered in our
paper. Neurologists were asked about their use of oxygen 1) at the end of
life, 2) prior to the end of life, NIV not tolerated / inappropriate and
3) prior to the end of life, before a trial of NIV. We think this is
clear. We only highlighted the use of oxygen in the latter group (26% of
responding neurologists). The humane and reasonable use of oxygen to which
Swash refers applies to the former two groups (full data shown in our
paper, Table 6). Whilst it is well documented that patients with
hypercapnia due to respiratory muscle weakness share the propensity of
others with hypercapnia to develop more severe and potentially life-
threatening carbon dioxide retention when breathing uncontrolled oxygen,
our experience, and now the results of our survey, suggest that this is
not widely recognised by clinicians.
References
1. Swash M. Survey of non-invasive ventilation use in ALS in Britain.
J Neurol Neurosurg Psychiatry Published Online First: 2 September 2011.
doi:10.1136/jnnp-2011-300990.
2. Mustfa N, Walsh E, Bryant V et al. The effect of noninvasive
ventilation on ALS patients and their caregivers. Neurology 2006;66:1211-
17.
3. Bourke SC, Tomlinson M, Williams TL et al. Effects of non-invasive
ventilation on survival and quality of life in patients with amyotrophic
lateral sclerosis: A randomised controlled trial. Lancet Neurology
2006;5:140-47.
4. Farrero E, Prats E, Povedano M et al. Survival in amyotrophic
lateral sclerosis with home mechanical ventilation: The impact of
systematic respiratory assessment and bulbar involvement. Chest
2005;127:2132-38.
5. Bourke SC, Williams TL, Bullock RE et al. Non-invasive ventilation
in motor neuron disease: Current UK practice. Amotroph Lateral Scler Other
Motor Neuron Disord 2002;3:145-49.
6. National Institute for Health and Clinical Excellence. Motor
neurone disease - non-invasive ventilation. London: (CG105) National
Institute for Health and Clinical excellence, 2010.
We thank Dr. Kengo Maeda for his comments regarding our case report
of a patient with Kansai-type proximal-dominant hereditary motor and
sensory neuropathy (HMSN-P).[1] He argues that upper motor neuron (UMN)
involvement has not been established in HMSN-P because of the following
reasons: UMN signs were absent in his 15 patients with Brazilian and
Kansai-type HMSN-P; previous studies did not suggest UMN involvement in
H...
We thank Dr. Kengo Maeda for his comments regarding our case report
of a patient with Kansai-type proximal-dominant hereditary motor and
sensory neuropathy (HMSN-P).[1] He argues that upper motor neuron (UMN)
involvement has not been established in HMSN-P because of the following
reasons: UMN signs were absent in his 15 patients with Brazilian and
Kansai-type HMSN-P; previous studies did not suggest UMN involvement in
HMSN-P; and bilateral Babinski sign and corticospinal tract degeneration
in our case might be explained by multiple cerebral infarction. We agree
with Dr. Maeda in that UMN involvement has to be carefully assessed in
HMSN-P patients. However, we do not exclude the potential UMN involvement
in this disease. Detailed examination of the distribution of infarction
revealed that it could not explain the diffuse symmetrical involvement of
the corticospinal tract seen in our case. Furthermore, another case with
Kansai-type HMSN-P had a positive Babinski sign despite the lack of focal
lesions in brain magnetic resonance imaging. Abnormal protein aggregation,
even if not in UMNs, is also important for the understanding of the
pathogenesis of this disease. Although we reported that TAR DNA-binding
protein 43 kDa (TDP-43)-positive inclusions were not seen in our case,
further investigation under different staining conditions has revealed TDP
-43-positive inclusions in neurons of the brainstem nuclei, the anterior
horn of the spinal cord, Clarke's nucleus, and the dorsal root ganglia,
suggesting another link between HMSN-P and amyotrophic lateral sclerosis
(ALS). Clinically, early presentations with prominent fasciculations in
proximal muscles without sensory involvement in our series most commonly
lead to the diagnosis of ALS by neurologists, although the progression is
gradual. Together, we believe that the understanding of HMSN-P in the
context of ALS spectrum should contribute to the elucidation of the
pathomechanism of the disease.
References
1. Fujita K, Yoshida M, Sako W, et al. Brainstem and spinal cord motor
neuron involvement with optineurin inclusions in proximal-dominant
hereditary motor and sensory neuropathy. J Neurol Neurosurg Psychiatry
2011;82:1402-1403.
We read with great interest, the article by Tsuang et al. (Occipitocervical malformation with atlas duplication) published in the Journal of Neurology, Neurosurgery and Psychiatry (2011 82:1101-1102). In this report, a patient with spastic gait is presented. The imaging studies revealed an atlas-like vertebra below the occipital bone. The authors referred to this anomaly as "atlas duplication". However, we believe that the anomalo...
We read with great interest, the article by Tsuang et al. (Occipitocervical malformation with atlas duplication) published in the Journal of Neurology, Neurosurgery and Psychiatry (2011 82:1101-1102). In this report, a patient with spastic gait is presented. The imaging studies revealed an atlas-like vertebra below the occipital bone. The authors referred to this anomaly as "atlas duplication". However, we believe that the anomalous vertebra is in fact a "persistent proatlas". The proatlas is found in some lower vertebrates as a separate, atlas-like vertebra between the occipital bone and atlas (Rao, 2002; Scheuer and Black, 2004). In man and during the embryonic period, the occipital sclerotome 4 is segmented in a manner that its proximal portion (hypochordal bow) is integrated into the caudal part of the basiocciput and its distal portion is integrated to the odontoid process of axis (Muller and O'Rahilly, 2003). Although proatlas segmentation malformation has been described in man, the "persistent proatlas" has never been reported before. We would like to congratulate the authors for recording this historically significant observation, which will remain a landmark in the developmental anatomy of the craniovertebral junction.
References
Rao PV. Median (third) occipital condyle. Clin Anat 2002;15:148-51.
Scheuer L, Black SM. The Juvenile Skeleton. San Diego, CA: Elsevier Academic Press, 2004, p. 195.
Muller F, O'Rahilly R. Segmentation in staged human embryos: the occipitocervical region revisited. J Anat 2003;203:297-315.
Ioannis Mavridis, M.D., Sophia Anagnostopoulou, M.D., Ph.D., Assoc.
Professor
Department of Anatomy, University of Athens School of Medicine
Corresponding author:
Ioannis N. Mavridis, M.D.
Department of Anatomy, Medical School, University of Athens,
Mikras Assias str. 75, Goudi, 11527 Athens, Greece
Tel.: 0030-210 74 62 404
Fax: 0030-210 74 62 398
e-mail: pap-van@otenet.gr
Ioannis Mavridis, M.D., Sophia Anagnostopoulou, M.D., Ph.D., Assoc.
Professor
Department of Anatomy, University of Athens School of Medicine
Corresponding author:
Ioannis N. Mavridis, M.D.
Department of Anatomy, Medical School, University of Athens,
Mikras Assias str. 75, Goudi, 11527 Athens, Greece
Tel.: 0030-210 74 62 404
Fax: 0030-210 74 62 398
e-mail: pap-van@otenet.gr
Dear Sir/Madam,
We read the article by Mok et al (2011) on cortical and
frontal atrophy associated with cognitive impairment in age-related
confluent white-matter lesion (WML).[1] They interestingly reported
that cognitive impairment in patients with confluent WML is
mediated by global and frontal cortical atrophy and that the
mechanisms whereby WML induces cognitive impairment are
uncertain.[1] They also mentioned that factors such as infarct
load and location, microbleed, global atrophy, central atrophy,
regional brain atrophy and Alzheimer's pathology may also affect
cognition.[1] They concluded that cognitive impairment in confluent
WML is probably mediated by frontal and global cortical atrophy.
We agree with the authors and we would like to comment on the
relation between regional brain atrophy and cognitive impairment.
We experienced a case of a 94-years-old female who had suffered
a stroke (a few years prior to her death) which caused focal
brain atrophy and was followed by the clinical expression of a
psychotic syndrome. The brain atrophy was found during a
cadaveric study in the dissection room of our Department. During
our macroscopic pathological investigation we noticed a fossa,
surrounded by a few petechiae, on the external surface of the
right parietal lobe, at the posterior end of the Sylvian
fissure. At this area, the cerebral gyri were excessively
atrophic and the fossa so deep that almost reached the external
wall of the lateral ventricle. The minimum gyri thickness was
approximately 1 mm, after removing the meninges. The tissue of
the atrophic gyri was soft like a chewing gum, despite the rest
gyri of the same brain. Checking out the arteries of the Willis
circle, we found a 25 mm long red fussiform thrombus occluding
the right middle cerebral artery (MCA). It was beginning from
the bifurcation of the right internal carotid artery and
extending within the MCA, occluding it completely. The microscopic
pathological investigation of the atrophic gyri revealed
degenerative lesions with microcycts, edema and many PAS(+)
amyloidal bodies. Oxymoronically, clear microscopic findings of an
infarct were absent.
Persson et al (1989) supported that focal ischemic changes
produced by MCA occlusion constitute a dynamic process in which
several pathophysiologic events occur over an extended period.[2]
Tamura et al (1991) reported that delayed neuropathologic changes
following cerebral ischemia have attracted widespread attention and
their results demonstrate the significance of remote changes over
a long period of time following focal brain injury. This
phenomenon could be important in understanding the pathophysiologic
changes during the chronic phase of cerebral infarction.[3] We
believe that, in our case, the dynamic pathophysiologic process
followed MCA occlusion, combined with delayed neuropathologic
changes during the chronic phase of the stroke, resulted to the
regional atrophy and the cognitive impairment (regarded as a
'psychotic syndrome').
Finally, we support that major cerebrovascular accidents can
rarely cause regional brain atrophy. Perhaps the microvascular
condition of an old brain could partially help in understanding
not only the pathogenesis of this unusual phenomenon, but also
the developed cognitive impairment. Moreover, the pathophysiologic
mechanism which resulted to the observed atrophy could be also
involved in the clinical expression of cognitive impairment. We
hope that future studies will illuminate such paths of the human
brain physiology and pathophysiology, which are still remaining
dark and mysterious and therefore challenging and admirable.
References
1. Mok V, Wong KK, Xiong Y, et al. Cortical and frontal
atrophy are associated with cognitive impairment in age-related
confluent white-matter lesion. J Neurol Neurosurg Psychiatry
2011;82:52-7.
2. Persson L, Hardemark HG, Bolander HG, et al. Neurologic and
neuropathologic outcome after middle cerebral artery occlusion in
rats. Stroke 1989;20:641-5.
3. Tamura A, Tahira Y, Nagashima H, et al. Thalamic atrophy
following cerebral infarction in the territory of the middle
cerebral artery. Stroke 1991;22:615-8.
Having received treatment for PMSAH in 2006, I agree vigorously with the conclusion that there needs to be additional study on the long term outcomes of individuals who have suffered this type of non-aneurysmal brain bleed.
In my particular case, my in-hospital treatment was excellent, but I had no idea what to expect afterwards, what complications might arise, how long it would take for my headaches to subside...
We read an interesting review and meta-analysis of published articles pertaining to cerebral amyloid angiopathy (CAA) by Samarasekera and collegues published in March 2012 issue of our esteemed journal1. The effforts made by the authors are worth appreciation. The previously considered to be a rare neurological curosity, CAA is now recognised as an important cause of spontaneous intracerebral haemorrhage and cognitive im...
We read with great interest a recent article by Morgante et al1 concerning the prevalence of psychosis associated with Parkinson disease. Psychotic symptoms, mainly visual hallucinations (VHs), occur in about one -third of patients, and thought to be a complication of antiparkinsonian treatment. However, they reported that psychotic type symptoms of PD, such as VHs, might occur more frequently in the early stage compared w...
Dear Editors,
The dorsal horns are not merely passive transmission stations but sites at which dynamic activities (inhibition, excitation and modulation) occur. [18]
Via a series of filters and amplifiers, the nociceptive message is integrated and analysed in the cerebral cortex, with interconnections with various areas. [1]
The processing of pain takes place in an integrated matrix throughout...
I understand Dr Bourne's concerns regarding my criticism of the survey of NIV reported from Sheffield. My Editorial Commentary was prompted by the very evident shortcomings in the survey reported, relying as it does on unverified data. We have reached a stage in epidemiological work when accurate data are needed to assess the uptake of medical interventions and their outcomes. Surveys cannot provide this essential evide...
We are concerned that the article by Professor Swash [1] misrepresents both the nature and findings of our recent UK national survey of the use of NIV in patients with MND/ALS. Although entitled an "editorial commentary", the article is essentially restricted to a critique of our study alone. In particular, he criticises the response rate to the survey (63%) and the lack of verification of the data in a sub -population;...
We thank Dr. Kengo Maeda for his comments regarding our case report of a patient with Kansai-type proximal-dominant hereditary motor and sensory neuropathy (HMSN-P).[1] He argues that upper motor neuron (UMN) involvement has not been established in HMSN-P because of the following reasons: UMN signs were absent in his 15 patients with Brazilian and Kansai-type HMSN-P; previous studies did not suggest UMN involvement in H...
Ioannis Mavridis, M.D., Sophia Anagnostopoulou, M.D., Ph.D., Assoc. Professor
Department of Anatomy, University of Athens School of Medicine
Corresponding author: Ioannis N. Mavridis, M.D. Department of Anatomy, Medical School, University of Athens, Mikras Assias str. 75, Goudi, 11527 Athens, Greece Tel.: 0030-210 74 62 404 Fax: 0030-210 74 62 398 e-mail: pap-van@otenet.gr
Dear Sir/Madam,...
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