Ringleb and co-authors concluded that the use of magnetic resonance imaging to select octogenarian patients with acute ischaemic stroke for thrombolytic therapy increases safety(1). They dismiss the possibility that this apparent benefit of MR selection may have been due to selection bias since the NIHSS scores were similar in those in whom MRI was applied versus those not(1). However, we have shown...
Ringleb and co-authors concluded that the use of magnetic resonance imaging to select octogenarian patients with acute ischaemic stroke for thrombolytic therapy increases safety(1). They dismiss the possibility that this apparent benefit of MR selection may have been due to selection bias since the NIHSS scores were similar in those in whom MRI was applied versus those not(1). However, we have shown that a significant proportion of older patients have relative or absolute contraindications
to MR scanning unrelated to the severity of their stroke (2). Hence, in our view, the apparent reduction in intracerebral haemorrhage by the use of MR selection could well be mainly accounted for by the MR patients having less non-stroke co-morbidity and frailty (eg the need for a pacemaker); these non-stroke co-morbidities were not assessed in the paper. Furthermore, overall outcome, in terms of survival or survival free of disability was not significantly better in those selected by MR compared with those selected by CT.
We would also take issue with their description of their own study and the observational studies included in their systematic review as trials. This is misleading, since, in common usage, ‘trial’ is usually restricted to study designs in which a treatment allocation is determined
strictly randomly and the next allocation is concealed from the clinician.
We therefore conclude that this paper does not support the argument that patients (of any age) presenting more than 3 hours after stroke onset should be selected by the use of MR DWI/PWI imaging. Furthermore, the DIAS-2 trial, among patients with an acute ischaemic stroke 3-9 hours after stroke onset, selected for the presence of mismatch on MR DWI-PWI, did not provide evidence that thrombolysis (with i.v. desmoteplase) was of net benefit.(3) This result does throw the 'mismatch' concept into some doubt.
Furthermore, immediate access to MR scanning for acute stroke patients is problematic in many non-specialist hospitals admitting patients with stroke, so any requirement for MR pre-selection might exclude many patients from thrombolytic therapy. We should therefore await further randomised evidence (e.g. from the ongoing EPITHET study) on the utility of ‘mismatch’ on MR as a selection criteria for thrombolysis before making recommendations.
In the meantime, we do, however, agree with the concluding sentence of Ringleb’s article which states the only way to obtain reliable evidence on the effects of thrombolytic therapy beyond 3 hours, especially in octogenarians, is to include such patients in IST-3,(4) the only ongoing randomised trial which permits recruitment of patients over 80.
Peter Sandercock, DM
Joanna Wardlaw, MD
Richard Lindley, MD
Stefano Ricci, MD
On behalf of the IST-3 collaborative group
References
(1) Ringleb PA, Schwark C, Kohrmann M, Kulkens S, Juttler E, Hacke W, et al. Thrombolytic therapy for acute ischaemic stroke in octogenarians: selection by magnetic resonance imaging improves safety but does not improve outcome. J Neurol Neurosurg Psychiatry 2007 Jul 1; 78(7):690-3.
(2) Hand PJ, Wardlaw JM, Rowat AM, Haisma JA, Lindley RI, Dennis MS. Magnetic resonance brain imaging in patients with acute stroke: feasibility and patient related difficulties. J Neurol Neurosurg Psychiatry 2005 Nov; 76(11):1525-7.
(3) Hacke W, Furlan A. Results From The Phase III Study Of Desmoteplase In Acute Ischemic Stroke Trial 2 (Dias 2). Cerebrovasc Dis 23 (suppl 2), 54. 2007.
(4) Whiteley W, Lindley R, Wardlaw J, Sandercock P, International Stroke Trial Collaborative Group. Third International Stroke Trial. International Journal of Stroke 1, 172-176. 2006.
We thank Drs. Yuki and Wong for their interest in our paper. We agree
that the finding that anti-CNTN1 autoantibodies in patients are mostly of
the IgG4 subtype is important for our understanding of the pathophysiology
of anti-CNTN1-associated neuropathy. However, in the study by Miura as
well as in our study, IgG2 and IgG3 autoantibodies were detected in some
patients (1, 2). The two patients from our study with predomina...
We thank Drs. Yuki and Wong for their interest in our paper. We agree
that the finding that anti-CNTN1 autoantibodies in patients are mostly of
the IgG4 subtype is important for our understanding of the pathophysiology
of anti-CNTN1-associated neuropathy. However, in the study by Miura as
well as in our study, IgG2 and IgG3 autoantibodies were detected in some
patients (1, 2). The two patients from our study with predominance of IgG3
autoantibodies were tested in the acute phase of disease (1). It would be
of interest to learn if the samples of the patients with IgG2/IgG3
autoantibodies from Miura's study might also have been taken at the
beginning of disease, as this might suggest a switch of IgG subclasses
during the course of disease.
As pointed out by Yuki and Wong, the study by Miura et al. provides
additional findings shedding further light on the pathogenicity of anti-
CNTN1 IgG4 autoantibodies (2). Although fulfilling clinical and
electrophysiological criteria of chronic inflammatory demyelinating
polyneuropathy (CIDP), neuropathy with anti-CNTN1 autoantibodies more and
more evolves to be an independent disease differing from classical CIDP.
Yuki and Wong addressed the binding of sera of patients with anti-CNTN1
IgG4 autoantibodies to dorsal root ganglia (DRG), a finding that was first
described in the study by Miura et al. (2). This raises the question if
anti-CNTN1-IgG4-associated neuropathy should be categorized as a
ganglionopathy rather than a neuropathy or paranodopathy. Indeed, several
studies provide evidence that binding of anti-CNTN1 autoantibodies is not
restricted to the paranodes but can also be found on hippocampal neurons,
in the cerebellum and DRG, presumably correlating with clinical symptoms
like tremor or sensory ataxia (1-3). Nevertheless, in our opinion, anti-
CNTN1-IgG4-associated neuropathy should be considered a paranodopathy as
there is ample evidence that the paranodes are the major site of action in
this disease: Neuropathic symptoms are the first and predominant symptoms
in all patients described so far (1, 3). Morphological analysis of
paranodes shows severe destruction of paranodal architecture as a
correlate of impaired nerve conduction (1). Electrophysiological studies
showing conduction block, prolonged distal motor latency and slowing of
nerve conduction velocities are well in line with the concept of
paranodopathy (4). Distal onset of sensory symptoms further strengthens
this notion and argues against a ganglionopathy as a major cause of
sensory loss. Damage to DRG might contribute to sensory ataxia, especially
in truncal forms as decribed by Miura et al. (2), but all in all the
clinical and electrophysiological phenotype of these patients suggests to
consider anti-CNTN1-IgG4-associated disease a paranodopathy (or
paranodopathy plus). Further studies are needed to 1) elucidate the
pathogenesis of this disease on the molecular level and to 2) better
characterize the clinical phenotype in a larger cohort of patients.
1. Doppler K, Appeltshauser L, Wilhelmi K, et al. Destruction of
paranodal architecture in inflammatory neuropathy with anti-contactin-1
autoantibodies. J Neurol Neurosurg Psychiatry 2015.
2. Miura Y, Devaux JJ, Fukami Y, et al. Contactin 1 IgG4 associates to
chronic inflammatory demyelinating polyneuropathy with sensory ataxia.
Brain 2015.
3. Querol L, Nogales-Gadea G, Rojas-Garcia R, et al. Antibodies to
contactin-1 in chronic inflammatory demyelinating polyneuropathy. Ann
Neurol 2013;73:370-380.
4. Uncini A, Susuki K, Yuki N. Nodo-paranodopathy: beyond the
demyelinating and axonal classification in anti-ganglioside antibody-
mediated neuropathies. Clin Neurophysiol 2013;124:1928-1934.
Response to letter regarding article, "The prognosis of acute
subdural haematoma from intracranial aneurysm rupture."
J. Matthijs Biesbroek1, MD; Jan Willem Berkelbach van der Sprenkel1,
MD, PhD; Ale Algra1,2, MD; Gabriel J.E. Rinkel1, MD.
1. Utrecht Stroke Centre, Department of Neurology and Neurosurgery,
Rudolf Magnus Institute of Neuroscience, University Medical Center
Utrecht, Utrecht, the Netherla...
Response to letter regarding article, "The prognosis of acute
subdural haematoma from intracranial aneurysm rupture."
J. Matthijs Biesbroek1, MD; Jan Willem Berkelbach van der Sprenkel1,
MD, PhD; Ale Algra1,2, MD; Gabriel J.E. Rinkel1, MD.
1. Utrecht Stroke Centre, Department of Neurology and Neurosurgery,
Rudolf Magnus Institute of Neuroscience, University Medical Center
Utrecht, Utrecht, the Netherlands.
2. Julius Center for Health Sciences and Primary Care, University Medical
Center Utrecht, Utrecht, the Netherlands.
Corresponding author
J. Matthijs Biesbroek, MD.
University Medical Center Utrecht
Department of Neurology
Heidelberglaan 100
Room G03.323
3508 GA Utrecht
The Netherlands
Tel. +31 88 755 5555
Fax. +31 30 254 2100
E-mail: J.M.Biesbroek@umcutrecht.nl
Word count: 512
References: 4
RESPONSE
We thank Dr Gelabert-Gonz?lez and co-workers for their interest in
our study, in which we concluded that the presence of acute subdural
hematoma (aSDH) in patients with aneurysmal subarachnoid haemorrhage (SAH)
is an independent risk factor for poor outcome. These findings were based
on 713 patients with SAH admitted from 1986 through 2009, of whom 53 had
aSDH.1
Dr Gelabert-Gonz?lez and co-workers raised two questions regarding
our treatment protocol for patients with SAH. Firstly, they wondered why a
large number of patients were not subjected to arteriography and stated
that arteriography is important in identifying the exact location of
aneurysms as well as any possible anatomical variation in brain arteries.
Until 1995 the policy in our hospital was to perform arteriography only in
case aneurysm surgery was considered. Surgery was until then mostly
performed in the late phase. In patients who were (initially) not in a
good clinical condition, arteriography was not performed until patients
had recovered. Thus, those patients who did not recover did not undergo
arteriography. From 1995 onwards, all patients with SAH undergo CT
angiography (CTA) on admission and most patients are operated upon in the
early phase. In our experience this CTA often provides sufficient
information for surgical planning of the operation, thus obviating the
need for arteriography in many of these patients.2,3
Secondly, the authors wondered why the majority of patients with aSDH
and poor clinical condition on admission did not undergo decompressive
surgery and noted that in their experience urgent surgical decompression
and immediate aneurysm clipping results in better outcomes than delayed
treatment or non-treatment. They refer to their retrospective study on
four patients with aneurysmal aSDH who underwent decompressive surgery and
clipping of the aneurysm.4 Despite this aggressive approach, 2 patients
died, 1 was disabled and dependent and 1 patient had good clinical outcome
at discharge. In our series, 13 out of 53 patients with aSDH underwent
decompressive surgery (eight of whom within 24 hours), which was combined
with clipping of the aneurysm in 11 cases. Out of 53 patients with aSDH,
79% had poor outcome at discharge and 75% had poor outcome at 3 months.
Thus, clinical outcome of patients with aSDH was essentially the same in
both series. We favour a tailored approach in patients with aSDH after
aneurysmal rupture. In patients in whom we consider the aSDH to be
(partially) the cause of the poor condition, we advocate surgery; in case
it is highly unlikely that the aSDH contributes to the poor clinical
condition, we are reluctant to perform decompressive surgery. We do agree
with the authors that in case of an aSDH after aneurysmal rupture not all
is lost and an aggressive approach is needed. Patients with an aSDH after
aneurysmal rupture should always be transferred to a tertiary referral
centre where the pros and cons of decompressive surgery should be decided
on an individual basis. We hope that our study and the letter from Dr
Gelabert-Gonz?lez and co-workers contribute to a more aggressive approach
and thereby to a higher chance of good outcome for patients with aSDH
after aneurysmal rupture.
REFERENCES
1. Biesbroek JM, Berkelbach van der Sprenkel JW, Algra A, et al. Prognosis
of acute subdural haematoma from intracranial aneurysm rupture. J Neurol
Neurosurg Psychiatry. doi: 10.1136/jnnp-2011-302139. Published Online
First: 31 October 2012
2. Velthuis BK, Van Leeuwen MS, Witkamp TD, et al. Computerized tomography
angiography in patients with subarachnoid hemorrhage: from aneurysm
detection to treatment without conventional angiography. J Neurosurg
1999;91:761-7.
3. Velthuis BK, Rinkel GJ, Ramos LM, et al. Subarachnoid hemorrhage:
aneurysm detection and preoperative evaluation with CT angiography.
Radiology 1998;208:423-30.
4. Gelabert-Gonz?lez M, Iglesias-Pais M, Fernandez-Villa JM. Acute
subdural haematoma due to ruptured intracranial aneurysms. Neurosurg Rev
2004;27: 256-62.
I read with interest the case report by Schulze-Bonhage et al.
documenting the termination of complex partial status epilepticus in a
patient following the intravenous administration of levetiracetam 1.
Schulze-Bonhage’s patient had seizures refractory to multiple frontline
anti-epileptic medications and lapsed into complex partial status
epilepticus when her pre-admission seizure medications were...
I read with interest the case report by Schulze-Bonhage et al.
documenting the termination of complex partial status epilepticus in a
patient following the intravenous administration of levetiracetam 1.
Schulze-Bonhage’s patient had seizures refractory to multiple frontline
anti-epileptic medications and lapsed into complex partial status
epilepticus when her pre-admission seizure medications were held during
the course of an elective admission for video EEG monitoring. This
admission was carried out as a part of epilepsy surgery work-up.
Intravenous loading of phenytoin and oral administration of lorazepam
failed to abort the status. A gratifying clinical response was achieved
within 35 minutes of intravenous levetiracetam administration.
The mechanism for the anticonvulsant effect of levetiracetam is
unique and still not fully understood. It does not seem to act through the
traditional mechanisms of ion channel blockage but rather is thought to
inhibit burst firing and propagation of seizure activity. This unique
mechanism of action may make it effective where other traditional anti-
epileptic drugs fail.
Schulze-Bonhage et al. report adds to the growing body of literature
demonstrating the effectiveness of levetiracetam in status epilepticus of
various types 2,3. Maybe it is time that conventional status epilepticus
abatement protocol of benzodiazepine->phenytoin- >phenobarbital
followed by either midazolam, propofol or pentobarbital infusion be
modified to give levetiracetam its just due.
Disclosure: None
References
1. Schulze-Bonhage A, Hefft S, Oehl B. Termination of complex partial
status epilepticus by intravenous levetiracetam.
J Neurol Neurosurg
Psychiatry 2009; 80: 931-933.
2. Möddel G, Bunten S, Dobis C, Kovac S, Dogan M, Fischera M, Dziewas
R, Schäbitz WR, Evers S, Happe S. Intravenous levetiracetam: a new
treatment alternative for refractory status epilepticus.
J Neurol
Neurosurg Psychiatry. 2009 Jun; 80(6):689-92.
3. Altenmüller DM, Kühn A, Surges R, Schulze-Bonhage A. Termination
of absence status epilepticus by low-dose intravenous levetiracetam.
Epilepsia. 2008 Jul; 49(7):1289-90.
Thank you for your enthusiasm for our study, and for your questions.
In our opinion, an extensive neuropsychological test battery is
mandatory for diagnosis of probable AD dementia. An MMSE score alone is
not sufficient for the assessment of cognitive impairment.
We used MMSE as indicator for disease severity, within our sample of
already diagnosed probable AD patients. It is an interesting suggestion t...
Thank you for your enthusiasm for our study, and for your questions.
In our opinion, an extensive neuropsychological test battery is
mandatory for diagnosis of probable AD dementia. An MMSE score alone is
not sufficient for the assessment of cognitive impairment.
We used MMSE as indicator for disease severity, within our sample of
already diagnosed probable AD patients. It is an interesting suggestion to
use the MoCA for this purpose, because this test focuses more on several
non-memory domains. However, we preferred MMSE because it is commonly used
and easy to interpret.
Mean age of the patients in our cohort was 69+/-9 years old (shown in
table 1). Mean ages per cluster are given in table 4.
I am pleased to respond to Dr Sandip Kumar Dash’s letter dated 3rd July 2007. I wish to reassure Dr Kumar Dash that the home based exercise programme used in the trial was built on the published evidence and the consensus of physiotherapists at the time. It included six levels of
exercise progression and strategies for movement initiation and compensation as well as fall prevention.
I am pleased to respond to Dr Sandip Kumar Dash’s letter dated 3rd July 2007. I wish to reassure Dr Kumar Dash that the home based exercise programme used in the trial was built on the published evidence and the consensus of physiotherapists at the time. It included six levels of
exercise progression and strategies for movement initiation and compensation as well as fall prevention.
I must draw to Dr Kumar Dash’s attention the limitations of the two papers to which he makes reference. Sidaway’s paper (2006) was an account of a single subject and therefore, although interesting, was not generalisable. Morris’ paper (2000) was a theoretical paper on modelling
therapy. In her concluding paragraph she states ‘Randomised clinical trials are now needed to evaluate the specific effects of physiotherapy and to validate this model of care for people with PD’.
Our RCT was testing therapy and did where appropriate include techniques for initiating movement (cues)as part of the management. The results of our study and those of Nieuwboer et al JNNP 2007; (78) 2: 134-140 (specific focus on cueing techniques), which were published within months of each other, will make major contributions to what was previously a spartan evidence base for physiotherapy for people with PD.
Dear editor: We read with interest the paper by Biesbroek et al. "Prognosis of acute subdural haematoma from intracranial aneurysm rupture".
We think that, in order to avoid possibile misinterpretations, a clear distinction should be made between acute subdural haematoma (aSDH) associated with subarachnoid haemorrhage (SAH) and aSDH as the sole manifestation of a ruptured intracranial aneurysm, in the absence of SAH. THe latter is...
Dear editor: We read with interest the paper by Biesbroek et al. "Prognosis of acute subdural haematoma from intracranial aneurysm rupture".
We think that, in order to avoid possibile misinterpretations, a clear distinction should be made between acute subdural haematoma (aSDH) associated with subarachnoid haemorrhage (SAH) and aSDH as the sole manifestation of a ruptured intracranial aneurysm, in the absence of SAH. THe latter is a rare, but reported condition. We had the opportunity to describe such a case and reviewed the literature on this topic (1). The only explanation for a pure aSDH is that previous small bleedings cause adhesion of the aneurysm to the adjacent arachnoid membrane and the final rupture occurs into the subdural space. Conversely, ASDH with SAH or parenchymal haemorrhage can be due to a high pressure haemorrhage leading to pia-arachnoid rupture and extravasation of blood into a subdural or parenchymal location. Alternatively, a rapid accumulation of blood can distend the subarachnoid space, thus causing a tear of the arachnoid membrane. ASDHs with and without SAH do not share the same pathogenetic mechanisms, and their prognosis can be quite different. As a consequence, they should be treated as distinct disorders.
Reference: Lucio Marinelli, Roberto Carlo Parodi, Paolo Renzetti, Fabio Bandini: Interhemispheric subdural haematoma from ruptured aneurysm: a case report. J Neurol (2005) 252 : 364-366
We read with interest the manuscript by Bannier et al[1] describing
weight gain at 16 months following bilateral subthalamic nucleus deep
brain stimulation (STN DBS) placement in patients with Parkinson's disease
(PD). The authors concluded that weight gain following DBS is “life-
threatening,” increases cardiovascular risk, and is more than a mere
normalization towards a baseline weight in the absenc...
We read with interest the manuscript by Bannier et al[1] describing
weight gain at 16 months following bilateral subthalamic nucleus deep
brain stimulation (STN DBS) placement in patients with Parkinson's disease
(PD). The authors concluded that weight gain following DBS is “life-
threatening,” increases cardiovascular risk, and is more than a mere
normalization towards a baseline weight in the absence of parkinsonism.
Obviously due to the short follow-up and small sample size, they were
unable to examine the rate of cardiovascular events or other surrogates
for cardiovascular health post-operatively. It is certainly difficult to
assess the impact of a 5.5 kg increase in weight on cardiovascular risk
factors. Figure 3 in their manuscript shows a negative correlation
between the preoperative weight and weight gain. Since the preoperative
weight is part of the change, this could indicate regression towards the
mean or that the subjects were relatively underweight preoperatively; it
is difficult to know what the baseline weights of these patients would
have been in the absence of advanced PD. Indeed, weight loss associated
with PD has been described in many studies[2], and it seems likely that
the patients most under their normal weight would gain the most weight
following symptom control. Additionally, it remains unclear if the weight
gain reported by Bannier et al and other authors will persist over years
in these patients as PD progresses; there is some data that this weight
gain is in fact not sustained[3]. Although obesity is an independent risk
factor for cardiovascular disease, previous studies have associated
chronic obesity rather than subacute weight gain with risk of
cardiovascular events[4, 5]. Furthermore, Bannier et al. argue that the
lack of correlation between motor improvement from DBS and weight gain in
prior studies indicates that the weight change is not related
mechanistically to relief of motor symptoms by DBS. Such a situation may
arise when there are floor or ceiling effects on one of the correlation
variables, and the large effect size and small standard deviations suggest
that nearly universal adequate motor improvement is occurring. Almost all
studies evaluating weight change after stereotactic surgery for PD are
uncontrolled, therefore an association between weight change and the
Unified Parkinson Disease Rating Scale (UPDRS) “off” change may be elusive
since the majority the DBS patients will sustain both remarkable
improvement in motor function and some degree of weight gain. If matched
controls with advanced PD and no DBS were incorporated into the
correlation analysis, they would likely show worsening of the UPDRS “off”
medications and weight loss over the same time interval, increasing the
likelihood of the demonstration of a significant correlation. While
excessive post-operative weight gain is undesirable in some patients,
future studies should examine if weight gain associated with DBS is
sustained and if it has a significant impact on cardiovascular health
before the conclusions of Bannier et al. can be drawn. The results of
such efforts have the potential to shift the benefit versus risk equations
for patients in whom this treatment may dramatically impact quality of
life.
Competing interests: None.
REFERENCES
[1] Bannier S, Montaurier C, Derost PP, et al. Overweight after deep
brain stimulation of the subthalamic nucleus in Parkinson disease: long
term follow-up.
J Neurol Neurosurg Psychiatry 2009;80(5):484-488.
[2] Chen H, Zhang SM, Hernan MA, et al. Weight loss in Parkinson's
disease.
Ann Neurol 2003;53(5):676-679.
[3] Novakova L, Ruzicka E, Jech R, et al. Increase in body weight is a non
-motor side effect of deep brain stimulation of the subthalamic nucleus in
Parkinson's disease.
Neuro Endocrinol Lett 2007;28(1):21-25.
[4] Garrison RJ, Castelli WP. Weight and thirty-year mortality of men in
the Framingham Study.
Ann Intern Med 1985;103(6(Pt 2)):1006-1009.
[5] Manson JE, Willett WC, Stampfer MJ, et al. Body weight and mortality
among women.
N Engl J Med 1995;333(11):677-685.
As a research intern aspiring to be a neurologist, I found Dr. Mathew
et al. article highly interesting and thought provoking [1]. Multiple
sclerosis is a complex neurological condition to manage, given its
numerous phenotypes.
It was very interesting to note that the authors found similar
imaging features on conventional MR brain scan in patients with multiple
sclerosis (MS)-like disease in association with LH...
As a research intern aspiring to be a neurologist, I found Dr. Mathew
et al. article highly interesting and thought provoking [1]. Multiple
sclerosis is a complex neurological condition to manage, given its
numerous phenotypes.
It was very interesting to note that the authors found similar
imaging features on conventional MR brain scan in patients with multiple
sclerosis (MS)-like disease in association with LHON (LMS) as well as
multiple sclerosis (MS) and hypothesized that mitochondrial dysfunction
could be a common pathophysiological pathway in the formation of white
matter lesions in these disorders [1].
Diffusion tensor MR imaging (DT MRI) has shown to be useful in
detecting micro-structural alterations in white matter and grey matter in
MS, in seemingly "normal -appearing white matter and gray matter" on
conventional MR images [2,3]. Recent studies also indicate that DT MRI may
demonstrate characteristic features in LHON such as decreased fractional
anisotropy (FA) and an increased mean diffusivity and radial diffusivity,
affecting exclusively the optic tracts and optic radiations, and in some
patients the acoustic radiations [4,5]. In that regard, it would be
useful to know if DT MRI could further identify any specific micro-
structural alteration that are common in these two conditions, which may
indeed act as a biomarker, and perhaps fuel future research in genotype-
phenotype correlation utilizing advanced MRI techniques including DT MRI
and functional MRI techniques.
References
1. Matthews L, Enzinger C, Fazekas F et al. MRI in Leber's hereditary
optic neuropathy: the relationship to multiple sclerosis. J Neurol
Neurosurg Psychiatry. 2015 May; 86(5):537-42
2. Fox RJ. Picturing multiple sclerosis: conventional and diffusion
tensor imaging. Semin Neurol. 2008 Sep; 28(4):453-66
3. Goldberg-Zimring D, Mewes AU, Maddah M, Warfield SK. Diffusion
tensor magnetic resonance imaging in multiple sclerosis. J Neuroimaging.
2005;15(4 Suppl):68S-81S.
4. Milesi J, Rocca MA, Bianchi-Marzoli S et al. Patterns of white
matter diffusivity abnormalities in Leber's hereditary optic neuropathy: a
tract-based spatial statistics study. J Neurol. 2012 Sep; 259(9):1801-7
5. Manners DN, Rizzo G, La Morgia C et al. Diffusion Tensor Imaging
Mapping of Brain White Matter Pathology in Mitochondrial Optic
Neuropathies. AJNR Am J Neuroradiol. 2015 Mar 19.
I greatly enjoyed reading the paper ePublished on June 19th. The finding that plaque inflammation, detected by USPIO MR imaging, is present even within contralateral asymptomatic plaques is similar to that noted in
recent FDG PET studies of atherosclerosis. Using plaque FDG uptake as a marker of inflammation, we (Rudd et al Circulation 2002) found that symptomatic lesions had about 30% more inflammat...
I greatly enjoyed reading the paper ePublished on June 19th. The finding that plaque inflammation, detected by USPIO MR imaging, is present even within contralateral asymptomatic plaques is similar to that noted in
recent FDG PET studies of atherosclerosis. Using plaque FDG uptake as a marker of inflammation, we (Rudd et al Circulation 2002) found that symptomatic lesions had about 30% more inflammation within them than contralateral asymptomatic lesions, a finding since replicated by other
groups (Davies et al Stroke 2005, Tawakol et al JACC 2006).
I agree with the authors' conclusions that arterial inflammation is likely to be a pan-vascular phenomenon, and hence the urgent need for systemic rather than local therapies aimed at plaque stabilisation.
The next generation of studies aimed at functional imaging of plaque over time, and correlation with subsequent clinical events will be crucial, however, to validate this important area of research.
Dear Editor
Ringleb and co-authors concluded that the use of magnetic resonance imaging to select octogenarian patients with acute ischaemic stroke for thrombolytic therapy increases safety(1). They dismiss the possibility that this apparent benefit of MR selection may have been due to selection bias since the NIHSS scores were similar in those in whom MRI was applied versus those not(1). However, we have shown...
We thank Drs. Yuki and Wong for their interest in our paper. We agree that the finding that anti-CNTN1 autoantibodies in patients are mostly of the IgG4 subtype is important for our understanding of the pathophysiology of anti-CNTN1-associated neuropathy. However, in the study by Miura as well as in our study, IgG2 and IgG3 autoantibodies were detected in some patients (1, 2). The two patients from our study with predomina...
Response to letter regarding article, "The prognosis of acute subdural haematoma from intracranial aneurysm rupture."
J. Matthijs Biesbroek1, MD; Jan Willem Berkelbach van der Sprenkel1, MD, PhD; Ale Algra1,2, MD; Gabriel J.E. Rinkel1, MD.
1. Utrecht Stroke Centre, Department of Neurology and Neurosurgery, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, the Netherla...
Dear Editor,
I read with interest the case report by Schulze-Bonhage et al. documenting the termination of complex partial status epilepticus in a patient following the intravenous administration of levetiracetam 1. Schulze-Bonhage’s patient had seizures refractory to multiple frontline anti-epileptic medications and lapsed into complex partial status epilepticus when her pre-admission seizure medications were...
Thank you for your enthusiasm for our study, and for your questions.
In our opinion, an extensive neuropsychological test battery is mandatory for diagnosis of probable AD dementia. An MMSE score alone is not sufficient for the assessment of cognitive impairment.
We used MMSE as indicator for disease severity, within our sample of already diagnosed probable AD patients. It is an interesting suggestion t...
Dear Editor
I am pleased to respond to Dr Sandip Kumar Dash’s letter dated 3rd July 2007. I wish to reassure Dr Kumar Dash that the home based exercise programme used in the trial was built on the published evidence and the consensus of physiotherapists at the time. It included six levels of exercise progression and strategies for movement initiation and compensation as well as fall prevention.
I mu...
Dear Editor,
We read with interest the manuscript by Bannier et al[1] describing weight gain at 16 months following bilateral subthalamic nucleus deep brain stimulation (STN DBS) placement in patients with Parkinson's disease (PD). The authors concluded that weight gain following DBS is “life- threatening,” increases cardiovascular risk, and is more than a mere normalization towards a baseline weight in the absenc...
As a research intern aspiring to be a neurologist, I found Dr. Mathew et al. article highly interesting and thought provoking [1]. Multiple sclerosis is a complex neurological condition to manage, given its numerous phenotypes.
It was very interesting to note that the authors found similar imaging features on conventional MR brain scan in patients with multiple sclerosis (MS)-like disease in association with LH...
Dear Editor,
I greatly enjoyed reading the paper ePublished on June 19th. The finding that plaque inflammation, detected by USPIO MR imaging, is present even within contralateral asymptomatic plaques is similar to that noted in recent FDG PET studies of atherosclerosis. Using plaque FDG uptake as a marker of inflammation, we (Rudd et al Circulation 2002) found that symptomatic lesions had about 30% more inflammat...
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