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.
We read the viewpoint on leg stereotypy1 by Joseph Jankovic with great interest. He has described leg stereotypy as repetitive, 1-4 Hz flexion extension, abduction-adduction movement at hips when the patient is seated and the feet rest on the floor.1 This movement has also been described to manifest as flexion extension at the knee joint or as tapping movement of foot.1 Patients as per this description have also been found to have...
We read the viewpoint on leg stereotypy1 by Joseph Jankovic with great interest. He has described leg stereotypy as repetitive, 1-4 Hz flexion extension, abduction-adduction movement at hips when the patient is seated and the feet rest on the floor.1 This movement has also been described to manifest as flexion extension at the knee joint or as tapping movement of foot.1 Patients as per this description have also been found to have some anxiety when asked to control these movements and also have an inner need to move their legs due to mounting tension. Additionally this movement has been described to reappear on distracting the patient.
Stereotypy has been defined as a non-goal-directed movement pattern that is repeated continuously for a period of time in the same form and on multiple occasions, and which is typically distractible.2,3 The key word discernable from this definition is its distractibility. These movements usually disappear when the patient is distracted with various stimuli especially when observed upon by others. This is in contrast with the above mentioned article where the patient's movements reappeared on distracting the patient. Second, stereotypic movements are not associated with an inner urge to perform the movement or to reduce an inner tension by performing the movement. This feature again contradicts with findings described in the above mentioned article in which patients experience an inner need to make the movement in response to an inner need. Such premonitory urges have however been described in the phenomenology of tics.4 Hence the reappearance of movement on distraction and presence of an inner urge to perform the movement create an uncertainity whether the described leg movement should be termed as stereotypy.
References
1. Leg stereotypy disorder. Jankovic J. J Neurol Neurosurg Psychiatry 2015;0:1-2.
2. Stereotypies: A Critical Appraisal and Suggestion of a Clinically Useful Definition. Mark J. Edwards, Anthony E. Lang,Kailash P. Bhatia. Movement Disorders, Vol. 27, No. 2, 2012.
3. Pandey S, Sarma N. Stereotypy After Acute Thalamic Infarct. JAMA Neurol. 2015;72(9):1068.
4. Christos Ganos, Davide Martino. Tics and Tourette Syndrome. Neurol Clin 33 (2015) 115-136.
The meta-analysis by Xu et al is a valiant effort to map the evidence
for modifiable risk factors of Alzheimer's disease (AD) (1). We
acknowledge this huge effort, however, we have serious concerns regarding
the systematic appraisal and the synthesis of the available data.
On top of the critique by Drs. Wu and Brayne (e-letter), a
comprehensive assessment of the article and its results can reveal
critical error...
The meta-analysis by Xu et al is a valiant effort to map the evidence
for modifiable risk factors of Alzheimer's disease (AD) (1). We
acknowledge this huge effort, however, we have serious concerns regarding
the systematic appraisal and the synthesis of the available data.
On top of the critique by Drs. Wu and Brayne (e-letter), a
comprehensive assessment of the article and its results can reveal
critical errors in data collection and the analysis of the available
evidence. An experienced methodologist could easily spot from the forest
plots in the supplementary material that all risk factors are in the same
direction, an observation that cannot be explained by chance.
Therefore, we tried to re-analyze the meta-analyses using data
reported in the supplementary material of this paper and, indeed, the
summary effect estimates could not be replicated. We figured out that the
authors have inadvertently used the extracted ORs (at least for binary
exposures) derived from the individual studies as is, without transforming
them into the logarithmic scale as it is required, leading to
miscalculations of the summary effect sizes. Thus, most if not all
inferences in the paper are based on these false summary estimates
resulting in misleading conclusions.
Besides the aforementioned analytical errors, we are afraid that the
extraction of relevant data points from the primary studies may suffer
from crucial errors as well. We summarise here potential problems for the
association between "ever vs never alcohol use" and AD as it illustrated
in supplementary material (page 184). Unfortunately, in 4 out of the 11
eligible studies the extracted estimates were wrong. Specifically, in 2
studies the authors included an estimate for the comparison of "wine
drinkers vs no drinkers" even though an estimate for "ever vs never
alcohol consumption" was available (2,3). In one study they inadvertently
reported the estimate for a comparison of tuberculosis history (4) instead
of the alcohol use, whereas in another study they extracted an estimate
for an occupational exposure to alcohols and phenols (as organic solvents)
(5). Moreover, it seems that the study "Lindsay, 2002" (3) has overlapping
populations with the study "CHSA, 1994" (6) and therefore it should not be
considered twice. Additionally, in one of the included studies (7) the
authors have captured an estimate that is most probably is a typo. In the
primary study, an OR of 4.10 (95% CI 0.60-80.50) is reported. Our back
calculations (based on the point estimate and the lower confidence
interval) have shown that the upper CI most probable was 28.05 and this
was not corrected by Xu et al, influencing the weight of this study in the
meta-analysis.
Taking all these discrepancies into account we tried to repeat the
meta-analysis for the exposure to alcohol and AD. The summary OR
(estimated by our team using correct analytical methods, correct effect
estimates and after the exclusion of the study with overlapping sample)
was 0.79 (95% CI: 0.63-0.98) for fixed effects and 0.84 (95% CI: 0.57-
1.24) for random effects models with I2=57%. In contrast the authors
presented a summary OR of 0.63 (95% CI, 0.48-0.79) under the fixed-effects
model with I2=11.3%. We have observed similar discrepancies for several
other risk factors. Obviously using these effects to calculate the
population attributable fractions led to the false conclusion that 66% of
the Alzheimer's disease cases could be prevented. Indeed, a more
conservative and thorough estimation of the population attributable risk
for modifiable risk factors of AD indicated that known risk factors are
responsible for only 28.2% (95% CI, 14.2% to 41.5%) of total AD cases
worldwide (8).
Furthermore, inclusion of studies with overlapping samples was also
observed in meta-analyses of key risk factors. For example, in the meta-
analysis of type 2 diabetes mellitus, the authors included three studies
on Cardiovascular Health Cognition Study (Kuller et al 2003, Becker et al
2009 and Irie et al 2008) and another two studies on Baltimore
Longitudinal Study of Aging (Moffat et al 2004, Dal et al 2005). However,
only the study with the longest follow-up period should be included in the
analysis for each of these cohort studies. The same caveat was observed in
the meta-analysis for educational attainment.
Additionally, for other risk factors (e.g socioeconomic status and
educational attainment) the authors have not harmonized the exposure of
interest, presenting separate meta-analyses for "high level versus low
level" and for "low level versus high level" of exposure.
Finally, we should express our concerns regarding the search strategy
applied from the authors. For example in the case of coffee or caffeine
drinking, a previous published meta-analysis in 2015 (9) includes more
studies and yields non-significant effect estimates (5 studies in the
paper by Kim et al and 4 studies in the paper by Xu et al). The authors
report a significant random-effects OR of 0.54 (95% CI: 0.39 to 0.69)
compared to 0.78 [95% CI: 0.78 to 1.22) by Kim et al which is clearly non-
significant. Several similar examples exist throughout the manuscript
(e.g. current vs. never statin use, NSAIDs use, ever vs. never smokers).
Having all these caveats in mind the editorial team of the journal
should thoroughly re-assess all the available evidence presented in this
paper.
References
1. Xu W, Tan LL, Wang H-F, Jiang T, Tan M-S, Tan LL, et al. Meta-
analysis of modifiable risk factors for Alzheimer's disease. J Neurol
Neurosurg Psychiatry. 2015;86(12):1299-306.
2. Tyas SL, Manfreda J, Strain LA, Montgomery PR. Risk factors for
Alzheimer's disease: a population-based, longitudinal study in Manitoba,
Canada. Int J Epidemiol. 2001 Jun;30(3):590-7.
3. Lindsay J, Laurin D, Verreault R, H?bert R, Helliwell B, Hill GB,
et al. Risk factors for Alzheimer's disease: a prospective analysis from
the Canadian Study of Health and Aging. Am J Epidemiol. 2002;156(5):445-
53.
4. Harmanci H, Emre M, Gurvit H, Bilgic B, Hanagasi H, Gurol E, et
al. Risk factors for Alzheimer disease: a population-based case-control
study in Istanbul, Turkey. Alzheimer Dis Assoc Disord. 2003;17(3):139-45.
5. Kukull WA, Larson EB, Bowen JD, McCormick WC, Teri L, Pfanschmidt
ML, et al. Solvent exposure as a risk factor for Alzheimer's disease: a
case-control study. Am J Epidemiol. 1995;141(11):1059-71.
6. The Canadian Study of Health and Aging: risk factors for
Alzheimer's disease in Canada. Neurology. 1994;44(11):2073-80.
7. Harwood DG, Barker WW, Loewenstein DA, Ownby RL, St George-Hyslop
P, Mullan M, et al. A cross-ethnic analysis of risk factors for AD in
white Hispanics and white non-Hispanics. Neurology. 1999;52(3):551-6.
8. Norton S, Matthews FE, Barnes DE, Yaffe K, Brayne C. Potential
for primary prevention of Alzheimer's disease: An analysis of population-
based data. Lancet Neurol. 2014;13(8):788-94.
9. Kim Y-S, Kwak SM, Myung S-K. Caffeine intake from coffee or tea
and cognitive disorders: a meta-analysis of observational studies.
Neuroepidemiology. 2015;44(1):51-63.
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...
The meta-analysis by Xu et al is a valiant effort to map the evidence for modifiable risk factors of Alzheimer's disease (AD) (1). We acknowledge this huge effort, however, we have serious concerns regarding the systematic appraisal and the synthesis of the available data.
On top of the critique by Drs. Wu and Brayne (e-letter), a comprehensive assessment of the article and its results can reveal critical error...
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