I read the article by Alonso on smoking and risk of amyotrophic
lateral sclerosis (ALS) with interest (1)
While the meta-analysis may not support a strong association with smoking
and ALS, there may be a relationship with the combination of smoking and
exercise.
Smoking increases carbon monoxide (CO) levels (2) and cyanide (3) in the
blood.
Cyanide binds with cytochrome oxidase in the mitochondria, and CO
interferes wi...
I read the article by Alonso on smoking and risk of amyotrophic
lateral sclerosis (ALS) with interest (1)
While the meta-analysis may not support a strong association with smoking
and ALS, there may be a relationship with the combination of smoking and
exercise.
Smoking increases carbon monoxide (CO) levels (2) and cyanide (3) in the
blood.
Cyanide binds with cytochrome oxidase in the mitochondria, and CO
interferes with the mitochondrial respiratory chain as well.
Mitochondria are also dynamically involved with exercise, with alteration
in mitochondrial network function induced by exercise (4).
Mitochrondrial protein composition is altered by ALS linked mutant
superoxide dismutase-1 (5), indicating a target organelle in ALS is the
mitochondria.
The interactions of smoking products such as CO and cyanide, causing
reduced oxygen availability from formation of carboxyhaemoglobin, causing
oxygen starvation of tissues, and poisoning of mitochondrial respiratory
chain function through interactions with CO and cyanide, when combined
with the increased oxygenation/reduction demands of exercise all may
interact on mitochrondrial genesis and energy production in the motor
neuron, to produce neurodegeneration and development of ALS in
susceptible individuals.
References:
1. Alonso A, Logroscino G, Hernan M. Smoking and the risk of amyotrophic
lateral sclerosis: a systematic review and meta-analysis. J Neurol
Neurosurg Psychiatry 2010;81: 1249-1252.
2. Klausen K, Anderson C, Nandrup S. Acute effects of cigarette smoking
and inhalation of carbon monoxide during maximal exercise. Eur J Appl
Physiol Occup Physiol 1983; 51: 371-379.
3. Lundquiest P. Rosling H, Sorbo B, Tibbling L. Cyanide
concentrations in blood after cigarette smoking, as determined by a
sensitive fluorimetric method. Clin Chem 1987; 33: 1228-1230
4. Bo H, Zhang Y, Ji LL Redefining the role of mitochondria in
exercise: a dynamic remodeling. Ann N Y Acad Sci 2010; 1201: 121-128
5. Li Q, Vande Velde C, Israelson A, Xie J, Bailey AO, Dong MQ. Et
al. ALS-linked mutant superoxide dismutase 1 (SOD1) alters mitochondrial
protein composition and decreased protein import Proc Natl Acad Sci USA
2010; 107: 21146-21151. Epub 2010 Nov 15.
We read with great interest the review article by McCarron et al. [1] concerning Terson’s syndrome. Having recently realised a prospective study in the subject, we feel interested to share our experience and to add some
information.
1- Although the original description of the syndrome by Dr Terson in 1900 concerned only intravitreous haemorrhages in association with subarachnoid haemorrhage, in o...
We read with great interest the review article by McCarron et al. [1] concerning Terson’s syndrome. Having recently realised a prospective study in the subject, we feel interested to share our experience and to add some
information.
1- Although the original description of the syndrome by Dr Terson in 1900 concerned only intravitreous haemorrhages in association with subarachnoid haemorrhage, in our opinion limiting the definition to the original description could be misleading today. The association of the intraocular haemorrhage with other situations with increased ICP such as head trauma is well documented. Thus we suppose that Terson’s syndrome definition should be enlarged to all the intraocular haemorrhages occurred in
association with acute intracranial hypertension.
2- The authors stated that “the greater proportion of patients developing Terson’s syndrome in the prospective studies may partly have resulted from delay in the appearance of vitreous haemorrhage”. In our experience with a prospective study of 100 patients with subarachnoid haemorrhage (non published data), all patients who demonstrated an intraocular haemorrhage during hospitalisation had an abnormal fundoscopic examination just after the acute episode and any tardive development of intraocular haemorrhage has not found. The only exception to this finding was the patients who had re-bleeding during hospitalisation period. This observation may lend in part some insight into our understanding of the pathophysiological mechanisms of intraocular haemorrhage and also has clinical importance. It
has been demonstrated that the intraocular venous pressure has a linear relationship with intracranial pressure, so that intraocular venous system is the equivalent of the intracranial bridging veins. This concept is the
principle of venous ophthalmo-dynamometry which has been showed to be a reliable method for estimation of intracranial pressure[2]. With regard to these explanations, we agree with the authors that a sudden intracranial pressure increase due to aneurismal rupture seems to be the leading cause of the intraocular haemorrhage, however this explanation remains controversial.
3- Another importance of the Terson’s syndrome that had not been discussed by the authors is the diagnostic value of the intraocular haemorrhage in diagnosis of intracranial vascular malformations. In general, between 15% to 20% of patients with a spontaneous subarachnoid haemorrhage have no aneurysm on the initial cerebral angiogram.[3] This may lead to difficulties of the diagnosis and necessity of repeating angiographies. In our
experience, all patients with intraocular haemorrhage had an aneurismal subarachnoid haemorrhage, and any patient with non-aneurismal subarachnoid haemorrhage developed intraocular haemorrhage. This means that in a patient with subarachnoid haemorrhage, the presence of intraocular
haemorrhage is an important indicator of aneurismal origin. In these cases, if initial angiograms are normal, repeated angiographies could be justified.
References:
1. McCarron M O, Alberts M J, McCarron P. A systematic review of Terson’s syndrome: frequency and prognosis after subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 2004; 75: 491-493.
2. Firsching R, Schutze M, Motschmann M, Behrens-Baumann W. Venous opthalmodynamometry: a noninvasive method for assessment of intracranial pressure. J Neurosurg. 2000 ;93:33-36.
3. Rinkel GJ, Van Gijn J, Wijdicks EF. Subarachnoid hemorrhage without detectable aneurysm. A review of the causes. Stroke 1993;24:1403-1409
I enjoyed reading Sun et al.’s (2004) article regarding effects of
the tongue acupuncture (invasive treatment) on children with cerebral
palsy. But I note that some important issues were not covered in the
article.
The authors reported "the treatment group received 40 sessions of TAC
(tongue acupuncture) in a daily basis" and "Sterile gauze was used to pick
and station the tongue with the ac...
I enjoyed reading Sun et al.’s (2004) article regarding effects of
the tongue acupuncture (invasive treatment) on children with cerebral
palsy. But I note that some important issues were not covered in the
article.
The authors reported "the treatment group received 40 sessions of TAC
(tongue acupuncture) in a daily basis" and "Sterile gauze was used to pick
and station the tongue with the acupuncturist's left hand and quick and
accurate insertion into the acupoints was performed with the right".
1) Since the subjects are children, their tongues are tiny and soft,
and nine of them with mental retardation. How did the authors measure the
accuracy and repeatability of the needle insertion, in terms of angle,
depth and location, by naked eyes? Particularly the tongues were being
grabbed and deformed.
2) The sensitive tongues being stabbed daily for 8 weeks, any local
inflammation or nerve damage was resulted? Especially the authors claimed
they could accurately stab the same acupoints daily. Were all the children
able to express their possible discomfort, e.g. numbness?
Regardless of my comments, the authors have presented an interesting
study. I admire their attempt at establishing an evidence-based
alternative therapy and would not hesitate to recommend their article to
anyone who is interested in the field of neurology or Chinese medicine.
Michael Wong
Hong Kong
Reference
1. Sun JG, Ko CH, Wong V, Sun XR. Randomised control trial of tongue
acupuncture versus sham acupuncture in improving functional outcome in
cerebral palsy. J Neurol Neurosurg Psychiatry 2004; 75: 1054-1057.
This review confirms that ICP monitoring provides no information
about intracerebral tissue energetiics except by inference in extremis.[1]
This informtion is vital if the management of the disorders listed in
this review and many others is to be significantly improved beyond
optimal care today. There is an opportunity to obtain this information in
conjunction with the ICP with the same ease and...
This review confirms that ICP monitoring provides no information
about intracerebral tissue energetiics except by inference in extremis.[1]
This informtion is vital if the management of the disorders listed in
this review and many others is to be significantly improved beyond
optimal care today. There is an opportunity to obtain this information in
conjunction with the ICP with the same ease and risks. The opportunity is
readily available but, despite the relevant parties in the US having been
informed of these opportunities more than 10 years ago, has been
exploited in ways that raise significant questions about the quality of
the data obtained. This would seem to be because of a lack of appreciation
of the relevant technical considerations and metabolic determinants of
cellular dysfunction, apoptosis and necrosis.
Further information may be obtained from a review I had published on
a popular Canadian medical website last year.[2] My insight into the
relevant issues has been refined considerably since then [3] and will no
doubt continue to be refined.
References
1. M Czosnyka and J D Pickard
Monitoring and interpretation of intracranial pressure
J Neurol Neurosurg Psychiatry 2004; 75: 813-821
I have read with great interest the article by Edison et al about the
amyloid load in patients with Parkinson´s disease (PD), PD with dementia
(PDD) and dementia with Lewy bodies (DLB) (1). Authors hypothesised that
amyloid pathology would be uncommon in PD without dementia, an occasional
feature of PDD and present in the majority of DLB cases. This hypothesis
was clearly demonstrated (1). However,...
I have read with great interest the article by Edison et al about the
amyloid load in patients with Parkinson´s disease (PD), PD with dementia
(PDD) and dementia with Lewy bodies (DLB) (1). Authors hypothesised that
amyloid pathology would be uncommon in PD without dementia, an occasional
feature of PDD and present in the majority of DLB cases. This hypothesis
was clearly demonstrated (1). However, there are some points which are at
variance with previous imaging and pathological data. I am going to focus
in two of them which can be considered as paradigmatic of similar studies.
The first study used [11C]PIB scan and showed that 22% of cognitively
normal people had amyloid deposition in their brains (2) (This percentage
was of 15% in another study including 20 subjects after adjusting for age
(3)). These subjects were comparable in terms of age and MMSE scores, to
the ones included in the study by Edison et al. However, [11C]PIB scans
were normal in all the 41 control individuals and 10 PD patients without
dementia studied. The second one refers to the pathological analysis of
the brains of patients of the Sidney cohort (4). In this study, between 50
and 80% of the patients with a clinical diagnosis of PDD showed amyloid
plaques in their brains. The shorter the duration of PD, the higher the
percentage of plaques. Amyloid plaques were also found in 83% of patients
dead with a clinical diagnosis of DLB (4).
The purpose of this letter is not to discuss the psysiopathological
basis of dementia associated with PD, the position of DLB in the clinical
spectrum of Lewy body disorders or the value of [11C]PIB scanning for the
preclinical detection of AD, but to point out the fact that these results
do not fit with previous imaging data obtained in a similar way, as well
as with pathological studies. These discordant aspects are not discussed
by Edison et al yet they have been used to raise some conclusions quite
relevant to the concepts of AD and PD, such as the possibility of
preclinical diagnosis and the contribution of aging and AD-like pathology
to the development of dementia in PD. Moreover, one of the authors took
part in one of the prior studies with [11C]PIB imaging (2). How to
reconcile these data? Is this a diagnostic problem or a technical issue?
Is [11C]PIB imaging useful to diagnose amyloid deposition in cognitively
normal subjects? Is [11C]PIB deposition the reflection of the presence of
amyloid plaques? Was the diagnosis of DLB or PDD incorrect? Are the
conclusions of the Sidney study valid or more than 50% of the patients
included in this cohort actually had DLB instead of PD or PDD? It is
necessary to clarify the relationships between symptomatology, imaging and
pathology in degenerative diseases to avoid misinterpretations.
References
1. Edison P, Rowe CC, Rinne JO, et al. Amyloid load in Parkinson’s disease dementia and Lewy Body dementia
measured with [11C]PIB PET.
J Neurol Neurosurg Psychiatry 2008; doi:10.1136/jnnp.2007.127878
2. Rowe CC, Ng S, Ackermann U et al. Imaging beta-amyloid burden in aging and dementia.
Neurology 2007;68:1718-1725
3. Mintun MA, Larossa GN, Sheline YI et al. [11C]PIB in a nondemented population: potential antecedent marker of
Alzheimer disease.
Neurology 2006;67:446-452
4. Halliday G, Hely M, Reid W, Morris J. The progression of pathology in longitudinally followed patients with
Parkinson’s disease.
Acta Neuropathol 2008; 115:409–415
In their recent meta-analysis of genetics of cerebral amyloid
angiopathy (CAA), Rannikmae et al,[1] focusing on the association between
APOEe4 and sporadic CAA, stated that there is no widely accepted
standardised histopathological grading system for CAA. Although this is
true, several methods are currently used to describe the severity of CAA
in postmortem brain,[2, 3] and recently a semiquantitative scoring method
has...
In their recent meta-analysis of genetics of cerebral amyloid
angiopathy (CAA), Rannikmae et al,[1] focusing on the association between
APOEe4 and sporadic CAA, stated that there is no widely accepted
standardised histopathological grading system for CAA. Although this is
true, several methods are currently used to describe the severity of CAA
in postmortem brain,[2, 3] and recently a semiquantitative scoring method
has been suggested:[4] amyloid-beta (A-beta) deposition is scored
separately in meningeal and intracortical blood vessels on sections from
occipital, parietal, temporal, and frontal cortices: absent (0), scant A-
beta deposition (1), some circumferential A-beta deposition (2), and
widespread A-beta deposition (3). These scores are stated separately for
meningeal and intracortical blood vessels. In addition, the presence of
CAA in capillaries (capCAA) is noted (i.e., 0 and 1) and vasculopathy,
including fibrinoid necrosis, thrombosis, hemorrhage and double barreling
is assessed semiquantitatively with absent (0), occasional vessels (1),
and many vessels (2). The addition of respective scores gives a regional
total score and the overall severity of CAA across the brain may be
described by stating the mean value of all regional total scores (for
review see:[5]). Further research efforts using these or newly developed
methods will facilitate comparisons between different studies and will be
useful for the pooling of new data.
References
1. Rannikmae K, Samarasekera N, Martinez-Gonzalez NA, et al. Genetics
of cerebral amyloid angiopathy: systematic review and meta-analysis. J
Neurol Neurosurg Psychiatry 2013;84:901-908.
2. Vonsattel JP, Myers RH, Hedley-Whyte ET, et al. Cerebral amyloid
angiopathy without and with cerebral hemorrhages: a comparative
histological study. Ann Neurol 1991;30:637-649.
3. Olichney JM, Hansen LA, Hofstetter CR, et al. Cerebral infarction
in Alzheimer's disease is associated with severe amyloid angiopathy and
hypertension. Arch Neurol 1995;52:702-708.
4. Chalmers K, Love S, Ince P, et al. Validation of international
consensus criteria for the assessment of cerebral amyloid angiopathy in
post-mortem brain. In 6th Interantional Conference on Vascular Dementia
2009; Barcelona, Spain.
5. Attems J, Jellinger K, Thal DR, Van Nostrand W. Review: sporadic
cerebral amyloid angiopathy. Neuropathol Appl Neurobiol 2011;37:75-93.
We appreciate the comment regarding our study on ulcerated plaque
in the aortic arch.
As the commenter pointed, vascular neurologists might have
believed that the aortic plaque configuration was as important as the
plaque
thickness when aortogenic embolism was assessed. Our study could identify
a strong association between ulcerated plaque and recent multiple brain
infarction, which was possibly caused by rec...
We appreciate the comment regarding our study on ulcerated plaque
in the aortic arch.
As the commenter pointed, vascular neurologists might have
believed that the aortic plaque configuration was as important as the
plaque
thickness when aortogenic embolism was assessed. Our study could identify
a strong association between ulcerated plaque and recent multiple brain
infarction, which was possibly caused by recent plaque rupture.
Moreover, the aortic plaque tissue quality may be as important as
the plaque configuration to detect vulnerable plaque before plaque
rupture,
as mentioned about coronary artery and carotid artery. A study with
repeated
aortic MRI,enhanced CT and TOE examination may be required to solve this
problem.
I most enjoyed reading this paper about white matter disruption <Journal of Neurology, Neurosurgery, and Psychiatry 2006;77:850-855>
I have especially found the tractography image (figure 4) both an elegant image, and very helpful in explaining to my patients who have not understood why their brain injury was not revealed by standard brain imaging scans. So thank you for this useful cl...
I most enjoyed reading this paper about white matter disruption <Journal of Neurology, Neurosurgery, and Psychiatry 2006;77:850-855>
I have especially found the tractography image (figure 4) both an elegant image, and very helpful in explaining to my patients who have not understood why their brain injury was not revealed by standard brain imaging scans. So thank you for this useful clinical resource!
However I was puzzled by findings set alongside the discussion. I would find helpful any further comments (beyond the 3rd paragraph of the discussion) why the authors did not correlations with the WMS memory
assessment? <"because of characteristic differences between the MMSE and the others"> seemed to me to be contradictory to the point in the first paragraph about the importance of limbic circuitary in memory.
I read with interest the article looking at headache as an isloated
symptom of venous thrombosis.
As a radiologist, I was interested in the assertion that a "normal CT
scan" necessitated a MRI/MRV scan. In my experience if the symptomatology
is atypical, performing a CT venogram, particularly on the multislice CT
scanner can give an accurate result in a large proportion of cases.
We perform CT venog...
I read with interest the article looking at headache as an isloated
symptom of venous thrombosis.
As a radiologist, I was interested in the assertion that a "normal CT
scan" necessitated a MRI/MRV scan. In my experience if the symptomatology
is atypical, performing a CT venogram, particularly on the multislice CT
scanner can give an accurate result in a large proportion of cases.
We perform CT venography on a 16 slice scanner and the multiplanar
reconstructions of the 1.25mm images in sagittal and coronal reformats
enables visualisation of the venous sinuses adequately.
Secondly, what technique was used for MRV studies? A difference can
be seen if phase contrast technique (more accurate) is used in preference
to time of flight protocol. Also, 3-D MR venography is often superior to
2D MR venography in the delineation of major cerebral venous structures in
children, because artifactual loss of signal is seen with the use of 2D MR
venography in nondominant transverse sinuses.
Thirdly, mention should be made of cases which can present on
unenhanced CT with areas of infarction secondary to venous thrombosis and
further imaging may be directed accordingly in these cases.
References
1. Leach JL, Jones BV, Tomsick TA, Stewart CA, Balko MG. Normal
appearance of arachnoid granulations on contrast-enhanced CT
and MR of the brain: differentiation from dural sinus disease. Am J
Neuoradiol 1996; 17:1523-32.
2. Casey SO, Alberico RA, Patel M, Jimenez JM, Ozsvath RR, Maguire
WM, et al. Cerebral CT venography. Radiology 1996; 198:163-70.
3. Ayanzen RH, Bird CR, Keller PJ, McCully FJ, Theobald MR,
Heiserman JE. Cerebral MR venography: normal anatomy and
potential diagnostic pitfalls. Am J Neuoradiol 2000; 21:74-8.
4. Huisman TA, Holzmann D, Martin E, Willi UV. Cerebral venous
thrombosis in childhood. Eur Radiol 2001; 11:1760-5.
5. Rollins N, Ison C, Reyes T, Chia J.- Cerebral MR venography in
children: comparison of 2D time-of-flight and gadolinium-enhanced 3D
gradient-echo techniques- Radiology. 2005 Jun;235(3):1011-7. Epub 2005 Apr
28.
Chang et al.[1] give an excellent analysis of pathophysiology of
syringomyelia associated with adhesive arachnoiditis (SAA). This
is a complex problem with a very few effective treatment options. In
countries like India where tuberculous arachnoiditis is an often
seen entity, SAA can frustrate the treating neurosurgeon. As
suggested in article subarachnoid bypass is a feasible alternative.
We...
Chang et al.[1] give an excellent analysis of pathophysiology of
syringomyelia associated with adhesive arachnoiditis (SAA). This
is a complex problem with a very few effective treatment options. In
countries like India where tuberculous arachnoiditis is an often
seen entity, SAA can frustrate the treating neurosurgeon. As
suggested in article subarachnoid bypass is a feasible alternative.
We have used theco-peritoneal shunts as one of the treatment
modalities in these patients.
Theco-peritoneal shunting is used in the treatment of
syringomyelia with [2] or without myelotomy.[3] Although this has
been used in syringomyelia associated with Chiari malformation,
the results are satisfactory. We have used percutaneous theco-
peritoneal shunting distal to the point of blockage in 2 patients who
suffered from SAA secondary to tuberculous arachnoiditis after the
procedures like arachnoid lysis and myelotomy failed. Both the
patients showed improvement in their MRI picture and clinical
picture.
Percutaneous theco-peritoneal shunting distal to the point of
blockage is a procedure with minimal surgical morbidity and is
effective in the treatment of SAA.
References
1. Chang H S, Nakagawa H: Theoretical analysis of the
pathophysiology of syringomyelia associated with adhesive
arachnoiditis. J Neurol Neurosurg Psychiatry 2004; 75: 754-757.
2. Park TS, Cail WS, Broaddus WC, Walker MG. Lumboperitoneal
shunt combined with myelotomy for treatment of
syringohydromyelia. J Neurosurg. 1989;70(5):721-7.
3. Vengsarkar US, Panchal VG, Tripathi PD, Patkar SV, Agarwal A,
Doshi PK, Kamat MM. Percutaneous thecoperitoneal shunt for
syringomyelia. Report of three cases. J Neurosurg.
1991;74(5):827-31.
I read the article by Alonso on smoking and risk of amyotrophic lateral sclerosis (ALS) with interest (1) While the meta-analysis may not support a strong association with smoking and ALS, there may be a relationship with the combination of smoking and exercise. Smoking increases carbon monoxide (CO) levels (2) and cyanide (3) in the blood. Cyanide binds with cytochrome oxidase in the mitochondria, and CO interferes wi...
Dear Editor,
We read with great interest the review article by McCarron et al. [1] concerning Terson’s syndrome. Having recently realised a prospective study in the subject, we feel interested to share our experience and to add some information.
1- Although the original description of the syndrome by Dr Terson in 1900 concerned only intravitreous haemorrhages in association with subarachnoid haemorrhage, in o...
Dear Editor,
I enjoyed reading Sun et al.’s (2004) article regarding effects of the tongue acupuncture (invasive treatment) on children with cerebral palsy. But I note that some important issues were not covered in the article.
The authors reported "the treatment group received 40 sessions of TAC (tongue acupuncture) in a daily basis" and "Sterile gauze was used to pick and station the tongue with the ac...
Dear Editor
This review confirms that ICP monitoring provides no information about intracerebral tissue energetiics except by inference in extremis.[1]
This informtion is vital if the management of the disorders listed in this review and many others is to be significantly improved beyond optimal care today. There is an opportunity to obtain this information in conjunction with the ICP with the same ease and...
Dear Editor,
I have read with great interest the article by Edison et al about the amyloid load in patients with Parkinson´s disease (PD), PD with dementia (PDD) and dementia with Lewy bodies (DLB) (1). Authors hypothesised that amyloid pathology would be uncommon in PD without dementia, an occasional feature of PDD and present in the majority of DLB cases. This hypothesis was clearly demonstrated (1). However,...
In their recent meta-analysis of genetics of cerebral amyloid angiopathy (CAA), Rannikmae et al,[1] focusing on the association between APOEe4 and sporadic CAA, stated that there is no widely accepted standardised histopathological grading system for CAA. Although this is true, several methods are currently used to describe the severity of CAA in postmortem brain,[2, 3] and recently a semiquantitative scoring method has...
We appreciate the comment regarding our study on ulcerated plaque in the aortic arch.
As the commenter pointed, vascular neurologists might have believed that the aortic plaque configuration was as important as the plaque thickness when aortogenic embolism was assessed. Our study could identify a strong association between ulcerated plaque and recent multiple brain infarction, which was possibly caused by rec...
Dear Editor,
I most enjoyed reading this paper about white matter disruption <Journal of Neurology, Neurosurgery, and Psychiatry 2006;77:850-855>
I have especially found the tractography image (figure 4) both an elegant image, and very helpful in explaining to my patients who have not understood why their brain injury was not revealed by standard brain imaging scans. So thank you for this useful cl...
Dear Editor,
I read with interest the article looking at headache as an isloated symptom of venous thrombosis. As a radiologist, I was interested in the assertion that a "normal CT scan" necessitated a MRI/MRV scan. In my experience if the symptomatology is atypical, performing a CT venogram, particularly on the multislice CT scanner can give an accurate result in a large proportion of cases. We perform CT venog...
Dear Editor
Chang et al.[1] give an excellent analysis of pathophysiology of syringomyelia associated with adhesive arachnoiditis (SAA). This is a complex problem with a very few effective treatment options. In countries like India where tuberculous arachnoiditis is an often seen entity, SAA can frustrate the treating neurosurgeon. As suggested in article subarachnoid bypass is a feasible alternative. We...
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