We use cookies to improve our service and to tailor our content and advertising to you.More infoYou can manage your cookie settings via your browser at any time. To learn more about how we use cookies, please see our cookies policy.
In a study published in J Neurol Neurosurg Psychiatry, Xu et al.1
aimed to investigate the relation between microbleeds (CMBs) and
Neuropsychiatric symptoms (NPS) in an elderly population, through a cross-
sectional study related to 802 participants. Interestingly, they found a
statistically significant increment of the incidence of depression, with
the presence of multiple CMBs, in particular lobar CMBs. This finding is...
In a study published in J Neurol Neurosurg Psychiatry, Xu et al.1
aimed to investigate the relation between microbleeds (CMBs) and
Neuropsychiatric symptoms (NPS) in an elderly population, through a cross-
sectional study related to 802 participants. Interestingly, they found a
statistically significant increment of the incidence of depression, with
the presence of multiple CMBs, in particular lobar CMBs. This finding is
in line with the previous research by Tang et al..2 However, a recent
study by Zhang et al.3 did not find the similar increment trend in deep
CMBs in patients with post-stroke depression, indicating that the presence
of lobar CMBs, not deep CMBs, was a potential predictor maker of
depression. While CMBs is one of the MRI biomarkers of cerebral small
vessel disease (cSVD) and was often accompanied by other cSVD-related
brain changes, such as lacunar infarcts, white matter lesions, and
enlarged perivascular spaces.
The available evidence suggests that cSVD was a principal determinant
in the pathogenesis and development of post-stroke depression,4 and
depression in patients with a prevalence of cerebrovascular disease burden
may be related more to cumulative vascular pathology than to the location
and severity of a single risk factor. Investigating the role of a total
MRI burden of cSVD in its pathogenesis may help to understand this disease
better. As the previously mentioned, Zhang et al. found that higher total
MRI burden of cSVD was an independent predictor of depression, even
without detecting an apparent association between deep CMBs and
depression. Similar to the study by Zhang et al., a recent research
investigated total MRI burden of cSVD in cerebral amyloid angiopathy
(CAA), in univariable analysis, total cSVD score was associated with the
presence of CAA-related changes on pathologic analysis and CAA
presentation with ICH, but none of the different MRI markers comprising
the score were individually linked to vasculopathic changes in univariable
or multivariable logistic regression analyses.5 These suggest that an
assessment of total MRI burden of cSVD has several potential advantages
because it avoids overreliance on any one individual marker of small
vessel disease.5 Hence, a complete evaluation of the total MRI burden of
cSVD may be important to understand the effect of cSVD on clinical
outcomes, such as depression.
Conflict of Interest Disclosures: None.
Reference:
1. Xu X, Chan QL, Hilal S, et al. Cerebral microbleeds and
neuropsychiatric symptoms in an elderly Asian cohort. Journal of
neurology, neurosurgery, and psychiatry 2017;88(1):7-11. doi: 10.1136/jnnp
-2016-313271
2. Tang WK, Chen Y, Liang H, et al. Cerebral microbleeds as a predictor of
1-year outcome of poststroke depression. Stroke; a journal of cerebral
circulation 2014;45(1):77-81. doi: 10.1161/STROKEAHA.113.002686
3. Zhang X, Tang Y, Xie Y, et al. Total magnetic resonance imaging burden
of cerebral small-vessel disease is associated with post-stroke depression
in patients with acute lacunar stroke. Eur J Neurol 2016 doi:
10.1111/ene.13213
4. Pavlovic AM, Pekmezovic T, Zidverc Trajkovic J, et al. Baseline
characteristic of patients presenting with lacunar stroke and cerebral
small vessel disease may predict future development of depression. Int J
Geriatr Psychiatry 2016;31(1):58-65. doi: 10.1002/gps.4289
5. Charidimou A, Martinez-Ramirez S, Reijmer YD, et al. Total Magnetic
Resonance Imaging Burden of Small Vessel Disease in Cerebral Amyloid
Angiopathy: An Imaging-Pathologic Study of Concept Validation. JAMA
neurology 2016;73(8):994-1001. doi: 10.1001/jamaneurol.2016.0832
We are very grateful to Dr Keller for his comments and support for
the feedback control approach to deep brain stimulation for Parkinson's
disease. As he points out, "reducing or turning off the stimulation
current when it is not needed conforms to the clinical axiom if it ain't
broke, don't fix it". This is further borne out by a publication currently
in press in this journal in which we show that feedback-controlled dee...
We are very grateful to Dr Keller for his comments and support for
the feedback control approach to deep brain stimulation for Parkinson's
disease. As he points out, "reducing or turning off the stimulation
current when it is not needed conforms to the clinical axiom if it ain't
broke, don't fix it". This is further borne out by a publication currently
in press in this journal in which we show that feedback-controlled deep
brain stimulation has the potential to avoid the speech side-effects of
stimulation sometimes experienced by patients with Parkinson's disease
[1].
A case report from an independent group provides evidence that this
approach may also limit the dyskinesias that can be experienced by
patients receiving deep brain stimulation in combination with levodopa
[2]. Feedback-controlled deep brain stimulation is an exciting area of
development, but it still remains unclear whether the superior acute
efficacy and selectivity of such stimulation over conventional continuous
deep brain stimulation will be carried over in to the chronic state.
[1] Little S, Tripoliti E, Beudel M, Pogosyan A, Cagnan H, Herz D,
Bestmann S, Fitzgerald J, Aziz T, Cheeran B, Zrinzo Z, Hariz M, Hyam J,
Limousin P, Foltynie T, Brown P. Speech side effects are ameliorated in by
adaptive compared to conventional deep brain stimulation for in
Parkinson's disease. Journal of Neurology, Neurosurgery and Psychiatry, In
Press.
[2] Rosa M, Arlotti M, Ardolino G, Cogiamanian F, Marceglia S, Di
Fonzo A, Cortese F, Rampini PM, Priori A. Adaptive deep brain stimulation
in a freely moving Parkinsonian patient. Mov Disord. 2015 30:1003-5.
Conflict of Interest:
SL has been a participant in a DBS teaching course funded by Medtronic.
PB has received fees and non-financial support from Medtronic and personal fees from Boston scientific.
It is mentioned that Sherrington introduced the term Synapse. In fact
the word synapse was introduced By Macheal Foster,then Professor of
Physiology at Cambridge along with his mentor Arthur Woodllgar Verrall
coined the word Synapse,meaning Clasp.Thus Sherrington made no such
discovery,and is ti be credited only with having solicited the name. As he
was working on Reflexes,he has advocated the physiological concept of
Syn...
It is mentioned that Sherrington introduced the term Synapse. In fact
the word synapse was introduced By Macheal Foster,then Professor of
Physiology at Cambridge along with his mentor Arthur Woodllgar Verrall
coined the word Synapse,meaning Clasp.Thus Sherrington made no such
discovery,and is ti be credited only with having solicited the name. As he
was working on Reflexes,he has advocated the physiological concept of
Synapses.
Even Sigmund Freud, has visualized the gap between the nerve cells,before
Sherrington and called it "Contact barrier". His sketch is published. With
the fact mentioned above, why the contributions were not recognized,by the
scientific community? Their contributions has gone un-noticed for a long
time by the community,it should not happen for ever.Soceity will loose
faith in the scientific community for ever. By this we do not undermine
Sherrington 's contributions, he shared the Nobel Prize in 1932 along with
Edgar Douglas (Lord) Adrian.
Hence the credit should be given to Macheal Foster, Arthue Woodllgar and
Sigmund Freud. If down,scientific community is justified.
As a physician with Parkinson's disease, and as a former Bell Labs
electrical engineer, I recognize that Professor Brown's group is pursuing
an important and fundamental improvement to deep brain stimulation. The
theory of electronic feedback control systems has been extensively studied
and applied in areas such as aircraft and missile guidance; Brown's work
may expand the existing theoretical domain of control systems,...
As a physician with Parkinson's disease, and as a former Bell Labs
electrical engineer, I recognize that Professor Brown's group is pursuing
an important and fundamental improvement to deep brain stimulation. The
theory of electronic feedback control systems has been extensively studied
and applied in areas such as aircraft and missile guidance; Brown's work
may expand the existing theoretical domain of control systems, as well as
find new application for established theorems.
The concept of "on demand" stimulation makes intuitive biological
sense. Reducing or turning off the stimulation current when it is not
needed conforms to the clinical axiom "if it ain't broke, don't fix it".
DBS, like other therapeutic interventions, should be applied to the point
of maximum benefit but not beyond, in order to limit side-effects.
Feedback control is the ideal way to accomplish this.
Will the DBS leads currently being implanted in Parkinson's patients
require replacement with leads optimized for sensing the feedback signal
as well as stimulation? If so, this may be a consideration for patients
with milder symptoms who might wish to wait for the availability of
adaptive DBS, to avoid the need for lead replacement.
We physicians are trained to push Rx medicines but increasingly we
find that supplements are efficacious and safer.
That melatonin is associated with weight loss is news to me. This paper
does an excellent job summarizing the clinical implications and cautions
in using melatonin. The dosage information is helpful as well.
In an editorial commentary accompanying a recent study on the
prevalence of apraxia in dementia patients [1], Bak emphasizes two facts:
1) research in cognitive neuroscience is contributing to increase the
awareness of a close relationship between cognitive and motor functions
and, by extension, cognitive and motor disorders in clinical populations;
2) despite so, the examination of motor functions in patients with
cogn...
In an editorial commentary accompanying a recent study on the
prevalence of apraxia in dementia patients [1], Bak emphasizes two facts:
1) research in cognitive neuroscience is contributing to increase the
awareness of a close relationship between cognitive and motor functions
and, by extension, cognitive and motor disorders in clinical populations;
2) despite so, the examination of motor functions in patients with
cognitive disorders is not part of the routine clinical evaluation.
Apraxia is a disorder in executing voluntary motor programming, in the
absence of deficits in primary motor or sensory processes, comprehension
of task instructions, object recognition or frontal inertia. Bak
identifies apraxia as the critical disorder to address in routine clinical
evaluation of patients with cognitive symptoms, as "it is exactly at the
intersection between both [movement and cognition]". In Bak's view, a
major obstacle to the improvement of clinical practice in this direction,
is the absolute lack of tests for apraxia, practical and fast to use as
part of routine evaluation. The Edinburgh Motor Assessment, in preparation
by Bak and colleagues, is thus introduced as the first tool to respond to
this urge.
We could not agree more with the importance of considering apraxia in the
routine clinical evaluation of cognitive functions in neurological
patients, including those with dementia. Apraxia is indeed a cognitive
deficit, affecting the higher-order mechanisms that govern purposeful
motor production.
However, if poverty or absence of tools is the problem, then we might not
have a problem. Researchers have long since recognized apraxia as a
cognitive disorder (with consequences on motor production). Moreover,
efforts have been made to offer handy, standardized tests of praxis
functions (e.g., the test TULIA [2]), based on models of apraxia, whose
anatomo-functional correlates have been extensively studied in brain-
damaged patients and in healthy individuals, with neuroimaging research. A
problem with most previous tests, evaluating gesture recognition,
identification and production in great detail, is the administration time,
usually so long as to advise their use in a post-screening phase (i.e.,
after the patient received a diagnosis of apraxia). Addressing this
problem, Tessari et al. [3] have developed STIMA (short test for ideomotor
apraxia), a standardized test for an accurate but quick diagnosis of
apraxia. The test, also usable for bedside screening, requires the patient
to imitate 36 gestures that form eight subscales. The test and each
individual subscale are accompanied by tables to correct raw-scores for
age and education, and convert raw-scores into equivalent scores (useful
for clinicians to estimate deficit severity) and percentiles (more often
used for diagnosis in research). Different subscales test for different
praxic impairments. In particular, STIMA emphasizes the distinctions
between: 1) imitation errors indicative of cortical damage (e.g., sequence
errors or unrecognizable gestures) versus subcortical damage (e.g.,
postural or timing errors); 2) producing distal (fingers/hand) versus
proximal (arm) components of gesture; 3) producing known gestures, which
recruits semantic structures in the left temporo-parietal cortex, versus
producing novel gestures, which relies on a bilateral cortical network, to
transform the visual input (the seen gesture) in a motor act. The
evaluation of novel gestures is also crucial to detect praxis deficits in
patients who can properly use objects and tools in their domestic context.
Evaluation of praxis solely based on execution or reports of daily
activities may leave those cases unnoticed. STIMA has been used and proven
sensitive to apraxic deficits in patients with stroke [4], as well as
neurodegenerative pathologies [5].
Our short (and non-exhaustive) overview of available standardized tests of
apraxia shows a scenario brighter than the total absence of suitable tools
depicted by Bak, and does justice to the numerous research teams in
cognitive neuropsychology and neuroscience, who have paid more attention
than Bak fears, to the clinical scopes of their activity and the
constraints of the clinical setting (i.e., time pressure).
Since the Edinburgh Motor Assessment by Bak et al. comes after recent and
less recent attempts to provide clinicians with a fast and accurate test
of apraxia, one may ask: do we really need this new tool? Perhaps, the
Edinburgh Motor Assessment introduces features that make it more suitable
to dementia patients, than other tests; or it relates to a model of
apraxia, not represented in the other tests. Presenting the Edinburgh
Motor Assessment as the first step toward an apraxia test for clinical
practice precludes the possibility to clarify those or other potentially
important aspects of that test. Considering its relation to extant tools
rather appears as a good method to provide clear indications about which
tool one (e.g., a clinician) should select in which case. This may help
reducing the noise in the exchange between researchers and clinical
practitioners as well as within our research field.
References
1. Ahmed S, Baker I, Thompson S et al. Utility of testing for apraxia
and associated features in dementia. J Neurol Neurosurg Psychiatry 2016;
doi:10.1136/jnnp-2015-312945
2. Vanbellingen T, Kersten B, Van Hemelrijk B et al. Comprehensive
assessment of gesture production: a new test of upper limb apraxia
(TULIA). Eur J Neurol 2010;17:59-66.
3. Tessari A, Toraldo A, Lunardelli A, et al. STIMA: a short
screening test for ideo-motor apraxia, selective for action meaning and
bodily district. Neurol Sci 2015;36: 977-984.
4. Mengotti P, Corradi-Dell'Acqua C, Negri GA, et al. Selective
imitation impairments differentially interact with language processing.
Brain 2013;136:2602-2618
5. Papeo L, Cecchetto C, Mazzon G et al. The processing of actions
and action-words in amyotrophic lateral sclerosis patients. Cortex 2015;
64:136-147.
Sir,
We thank Kumar et al. for their interest in our recent article on retinal
nerve fibre layer thickness (RNFL) in people with epilepsy. In their
letter they raise a few points that we would like to address.
1. Comparison between people with epilepsy and healthy controls. They
suggest that a comparison between people with drug-resistant versus non-
resistant epilepsy might have been more appropriate. However, a...
Sir,
We thank Kumar et al. for their interest in our recent article on retinal
nerve fibre layer thickness (RNFL) in people with epilepsy. In their
letter they raise a few points that we would like to address.
1. Comparison between people with epilepsy and healthy controls. They
suggest that a comparison between people with drug-resistant versus non-
resistant epilepsy might have been more appropriate. However, as described
in the paper itself, in Methods - Statistics, we first compared cases
versus controls and then tested for differences in the distribution of
average RNFL thickness as a continuous variable according to each
demographic and clinical factor, including drug-resistance. The results of
this comparison are presented in Results - Average RNFL thickness across
all quadrants and exposure to AEDs or non-medical treatments, and showed
thinner average RNFL in people with drug-resistant epilepsy compared with
non-resistant epilepsy.
2) Kumar et al. state that the aetiological spectrum of epilepsy is
not described. We report the epilepsy aetiology in Supplementary material,
Table S2, classified according to the "Commission on Classification and
Terminology of the International League Against Epilepsy, 1989". We also
tested for difference in the distribution of RNFL thickness according to
the epilepsy type (see Results - Average RNFL thickness and clinical
characteristics--univariate associations). This information was all
present in the publication.
3) We agree with the fact that age is a major factor determining the
RNFL thickness. We analysed correlation of average RNFL thickness with age
in both cases and controls. We included only epilepsy duration in the
regression models because of high collinearity with age. We did not
consider age group distribution as this would have significantly limited
the sample size.
4) We recognise that refractive errors may affect RNFL thickness. For
this reason, we excluded people with a distance refractive error of
>4.50 dioptres mean sphere/>2.5 dioptres cylinder.
5) We attempted to account for all known factors known to be
associated with changes in RNFL (exposure to vigabatrin, diabetes,
glaucoma or other known ocular disease, concurrent diagnosis of multiple
sclerosis, history of trauma or surgery to the eye or orbit, refractive
errors, brain MRI evidence of visual pathway involvement), as stated in
Methods, Participants.
The points raised by Kumar et al. were therefore all already
addressed in the original paper.
Sir,
The recently published article titled "Retinal nerve fibre layer thinning
is associated with drug resistance in epilepsy" by Balestrini S et al has
been a refreshing approach into a common menace - refractory epilepsy. 30
to 40% of patients with seizure are classified as persistent seizures
under AEDs among which refractory epilepsy is included. (1) Retinal nerve
fibre layer (RNFL) thinning is an easy and non invas...
Sir,
The recently published article titled "Retinal nerve fibre layer thinning
is associated with drug resistance in epilepsy" by Balestrini S et al has
been a refreshing approach into a common menace - refractory epilepsy. 30
to 40% of patients with seizure are classified as persistent seizures
under AEDs among which refractory epilepsy is included. (1) Retinal nerve
fibre layer (RNFL) thinning is an easy and non invasive analysis which
would point towards possible refractory epilepsy leading to shortening of
lead time to diagnosis. The present paper opens a whole new arena of
thought process for evaluation of refractory epilepsy but leaves the
promise open ended.
Few points we would like to point out are mentioned below
(1) Study groups: This retrospective case control analysis based on
hospital records compares two groups including those with epilepsy as the
case group and healthy individuals as controls. This comparison has its
flaws in comparing two different groups with inherent differences in
itself. The case group (epileptics) includes both refractory and non-
refractory epileptics, with the control groups being healthy controls.
Comparing the case group (patients of refractory epilepsy) with non
refractory epileptics might have been more prudent.
(2) Etiology of refractory epilepsy and its implications: Effectiveness of
AEDs in management of epilepsies is heavily weighted on the underlying
etiology. The present study has not mentioned the etiological spectrum of
epilepsy which would have further helped in enumerating subgroups adding
to strength and validity. Over reliance on the retrospective data for
delineating refractory epilepsy takes out the possibility of fixing an
appropriate etiology for refractoriness
(3) Variation in RNFL among the study population: Age group distribution
among the study group has not been mentioned. Literature points the role
of age as a major factor in determining the RNFL thickness. (2) Even
refractive errors has been noted to have an effect on RNFL thickness. (3)
The study excludes only few obvious factors noted to be associated with
reduction in RNFL thickness namely multiple sclerosis, Alzheimer's
disease, previous optic neuritis and angle closure glaucoma.
References
1. Beleza P. Refractory epilepsy: a clinically oriented review. Eur
Neurol. 2009;62(2):65-71.
2. Celebi AR, Mirza GE. Age-related change in retinal nerve fiber layer
thickness measured with spectral domain optical coherence tomography.
Invest Ophthalmol Vis Sci. 2013;54(13):8095-103.
3. Pawar N, Maheshwari D, Ravindran M, Ramakrishnan R. Retinal nerve fiber
layer thickness in normal Indian pediatric population measured with
optical coherence tomography. Indian J Ophthalmol. 2014;62(4):412-8.
Roalf et al. describe a short form of the Montreal Cognitive
Assessment (s-MOCA) comprising 8 items (score range 0-16) from the
original MoCA.
Data from a historical cohort administered the MoCA (n = 150)1 were
examined to extract s-MoCA scores. There was high correlation between s-
MoCA scores and MoCA and MMSE scores (0.94, 0.80 respectively).
Roalf et al. describe a short form of the Montreal Cognitive
Assessment (s-MOCA) comprising 8 items (score range 0-16) from the
original MoCA.
Data from a historical cohort administered the MoCA (n = 150)1 were
examined to extract s-MoCA scores. There was high correlation between s-
MoCA scores and MoCA and MMSE scores (0.94, 0.80 respectively).
s-MoCA scores differed significantly (null hypothesis rejected)
between dementia and mild cognitive impairment (MCI), and between MCI (t =
2.6, p = 0.01) and subjective memory complaint (SMC; t = 6.6, p <
0.001).
Using the specified s-MoCA cutoff of <12/16, the test was very
sensitive (0.94) but not specific (0.25) for diagnosis of dementia versus
MCI, with a better balance for diagnosis of MCI versus SMC (sensitivity
0.75, specificity 0.66).
Effect sizes (Cohen's d) were medium for diagnosis of dementia versus
MCI (0.65) but large (1.19) for diagnosis of MCI versus SMC. All outcome
measures were similar to those for the MoCA.
This retrospective study suggests s-MoCA has utility as a cognitive
screening instrument for diagnosis of dementia and MCI in a dedicated
cognitive disorders clinic. Validation of s-MoCA in a prospective cohort
from this clinic (n > 200) is now being examined.
Reference
1. Larner AJ. Screening utility of the Montreal Cognitive Assessment
(MoCA): in place of - or as well as - the MMSE? Int Psychogeriatr
2012;24:391-6.
We read with interest the findings and recommendations by the
authors. (1)
Cerebrovascular disease accounts for the increasing burden of
seizures and epilepsy in people over the age of 65 years. The distinction
between acute and remote symptomatic seizures is highly relevant with
implications both for prognosis and clinical management. Acute
symptomatic seizures (ASS) following a cerebrovascular event are def...
We read with interest the findings and recommendations by the
authors. (1)
Cerebrovascular disease accounts for the increasing burden of
seizures and epilepsy in people over the age of 65 years. The distinction
between acute and remote symptomatic seizures is highly relevant with
implications both for prognosis and clinical management. Acute
symptomatic seizures (ASS) following a cerebrovascular event are defined
as seizures that occur within 7 days of the ictus while remote symptomatic
seizures (RSS) occur out with this time frame. (2) ASS occur in around 6%
of acute cerebrovascular events and are more likely in elderly patients,
in those with large strokes, stroke involving the cortex or multiple
vascular territories, cardioembolic events, and haemorrhagic stroke. (3)
Data from the Rochester Epidemiology Project showed a risk for subsequent
seizures at 10 years of 33% for ASS, (4) similar to the 28% at 8 years in
the Leung Study. Both fall well below the 2014 ILAE operational definition
of epilepsy - an enduring predisposition of the brain to generate
seizures, defined as a probability of further seizures of at least 60%
over the next 10 years. In contrast, following a RSS the 10year risk of
further seizures is 71.5%. (4) Thus a diagnosis of epilepsy is not
justified for ASS in the context of stroke.
A decision to commence treatment with anti-epileptic drugs (AEDs)
should not be taken lightly; AEDs are commonly implicated in adverse drug
reactions, and those with a new brain insult may be particularly
susceptible to the mood and cognitive side effects, potentially
interfering with rehabilitation. AEDs have known effects on bone health,
together with an increased risk of drug interactions in patients who
already take numerous drugs to address their many comorbidities, and
economic and psychosocial impact. (5)
While short-term treatment of frequent seizures and status
epilepticus occurring within seven days of an acute stroke is appropriate,
the overwhelming evidence is that beyond one month there is no benefit
from treatment with AEDs. Data from the Rochester Epidemiology Project
showed that patients with ASS have a higher mortality during the first 30
days compared to subjects with RSS. (4) This is obviously related to the
severity of the underlying stroke but can justify the treatment of ASS in
order to minimize the additional contribution to mortality and morbidity
due to seizures. However, any recommendation for long-term treatment with
antiepileptic drugs beyond a period of a few weeks is against the
available evidence. For this reason treatment for four years, as
recommended by Leung et al (2016), risks unnecessary exposure of these
patients to medication they may not need for many years.
References:
1. Leung T, Leung H, Soo YOY, Mok VCT, Wong KS. The prognosis of acute
symptomatic seizures after ischaemic stroke. J Neurol Neurosurg
Psychiatry. 2016 Jan 27;
2. Beghi E, Carpio A, Forsgren L, Hesdorffer DC, Malmgren K, Sander JW,
et al. Recommendation for a definition of acute symptomatic seizure.
Epilepsia. 2010 Apr;51(4):671-5.
3. Leone MA, Tonini MC, Bogliun G, Gionco M, Tassinari T, Bottacchi E, et
al. Risk factors for a first epileptic seizure after stroke: a case
control study. J Neurol Sci. 2009 Feb 15;277(1-2):138-42.
4. Hesdorffer DC, Benn EKT, Cascino GD, Hauser WA. Is a first acute
symptomatic seizure epilepsy? Mortality and risk for recurrent seizure.
Epilepsia. 2009 May;50(5):1102-8.
5. Mula M, Cock HR. More than seizures: improving the lives of people
with refractory epilepsy. Eur J Neurol. 2015 Jan;22(1):24-30.
In a study published in J Neurol Neurosurg Psychiatry, Xu et al.1 aimed to investigate the relation between microbleeds (CMBs) and Neuropsychiatric symptoms (NPS) in an elderly population, through a cross- sectional study related to 802 participants. Interestingly, they found a statistically significant increment of the incidence of depression, with the presence of multiple CMBs, in particular lobar CMBs. This finding is...
We are very grateful to Dr Keller for his comments and support for the feedback control approach to deep brain stimulation for Parkinson's disease. As he points out, "reducing or turning off the stimulation current when it is not needed conforms to the clinical axiom if it ain't broke, don't fix it". This is further borne out by a publication currently in press in this journal in which we show that feedback-controlled dee...
It is mentioned that Sherrington introduced the term Synapse. In fact the word synapse was introduced By Macheal Foster,then Professor of Physiology at Cambridge along with his mentor Arthur Woodllgar Verrall coined the word Synapse,meaning Clasp.Thus Sherrington made no such discovery,and is ti be credited only with having solicited the name. As he was working on Reflexes,he has advocated the physiological concept of Syn...
As a physician with Parkinson's disease, and as a former Bell Labs electrical engineer, I recognize that Professor Brown's group is pursuing an important and fundamental improvement to deep brain stimulation. The theory of electronic feedback control systems has been extensively studied and applied in areas such as aircraft and missile guidance; Brown's work may expand the existing theoretical domain of control systems,...
We physicians are trained to push Rx medicines but increasingly we find that supplements are efficacious and safer. That melatonin is associated with weight loss is news to me. This paper does an excellent job summarizing the clinical implications and cautions in using melatonin. The dosage information is helpful as well.
Conflict of Interest:
None declared
In an editorial commentary accompanying a recent study on the prevalence of apraxia in dementia patients [1], Bak emphasizes two facts: 1) research in cognitive neuroscience is contributing to increase the awareness of a close relationship between cognitive and motor functions and, by extension, cognitive and motor disorders in clinical populations; 2) despite so, the examination of motor functions in patients with cogn...
Sir, We thank Kumar et al. for their interest in our recent article on retinal nerve fibre layer thickness (RNFL) in people with epilepsy. In their letter they raise a few points that we would like to address.
1. Comparison between people with epilepsy and healthy controls. They suggest that a comparison between people with drug-resistant versus non- resistant epilepsy might have been more appropriate. However, a...
Sir, The recently published article titled "Retinal nerve fibre layer thinning is associated with drug resistance in epilepsy" by Balestrini S et al has been a refreshing approach into a common menace - refractory epilepsy. 30 to 40% of patients with seizure are classified as persistent seizures under AEDs among which refractory epilepsy is included. (1) Retinal nerve fibre layer (RNFL) thinning is an easy and non invas...
Roalf et al. describe a short form of the Montreal Cognitive Assessment (s-MOCA) comprising 8 items (score range 0-16) from the original MoCA.
Data from a historical cohort administered the MoCA (n = 150)1 were examined to extract s-MoCA scores. There was high correlation between s- MoCA scores and MoCA and MMSE scores (0.94, 0.80 respectively).
s-MoCA scores differed significantly (null hypothesis r...
We read with interest the findings and recommendations by the authors. (1)
Cerebrovascular disease accounts for the increasing burden of seizures and epilepsy in people over the age of 65 years. The distinction between acute and remote symptomatic seizures is highly relevant with implications both for prognosis and clinical management. Acute symptomatic seizures (ASS) following a cerebrovascular event are def...
Pages