Does aspirin increase the risk of bleeding from cerebral aneurysms?

Aspirin and risk of subarachnoid hemorrhage: systematic review and meta-analysis

Phan K, Moore JM, Griessenauer CJ, Ogilvy CS, Thomas AJ.

Stroke 2017; 48:1210-1217.



Recent studies have suggested that the use of low-dose aspirin may reduce the risk of aneurysmal subarachnoid hemorrhage (aSAH). We aimed to evaluate any association between aspirin use and risk of aSAH based on the literature, and whether this is influenced by duration or frequency of aspirin use.


A search of electronic databases was done from inception to September 2016. For each study, data on risk of aSAH in aspirin versus nonaspirin users were used to generate odds ratios and 95% confidence intervals, and combined using inverse variance–weighted averages of logarithmic odds ratios in a random-effects models.


From 7 included studies, no significant difference was noted between aspirin use of any duration or frequency and nonaspirin users (odds ratio, 1.00; 95% confidence interval, 0.81–1.24; P=0.99). We found a significant association between short-term use of aspirin (<3 months) and the risk of aSAH (odds ratio, 1.61; 95% confidence interval, 1.20–2.18; P=0.002). No significant difference was found in terms of risk of aSAH for 3 to 12 months, 1 to 3 years, and >3 years of durations of use. No significant association was found between infrequent aspirin use (≤2× per week) or frequent use (≥3× per week) with risk of aSAH.


Current evidence suggests that short-term (<3 months) use of aspirin is associated with increased risk of aneurysmal subarachnoid haemorrhage. Limitations include substantial heterogenity of the included studies. The role of long-term aspirin in reducing risk of aSAH remains unclear and ideally should be addressed by an appropriately designed randomized controlled trial.

This abstract is cited in the neurochecklist:

Cerebral aneurysms: risk factors for rupture

Abstract link

By Hellerhoff – Own work, CC BY-SA 3.0,

Is the ketogenic diet useful for super-refractory status epilepticus?

Phase I/II multicenter ketogenic diet study for adult superrefractory status epilepticus

Cervenka MC, Hocker S, Koenig M, et al.

Neurology 2017; 88:938-943.



To investigate the feasibility, safety, and efficacy of a ketogenic diet (KD) for superrefractory status epilepticus (SRSE) in adults.


We performed a prospective multicenter study of patients 18 to 80 years of age with SRSE treated with a KD treatment algorithm. The primary outcome measure was significant urine and serum ketone body production as a biomarker of feasibility. Secondary measures included resolution of SRSE, disposition at discharge, KD-related side effects, and long-term outcomes.


Twenty-four adults were screened for participation at 5 medical centers, and 15 were enrolled and treated with a classic KD via gastrostomy tube for SRSE. Median age was 47 years (interquartile range [IQR] 30 years), and 5 (33%) were male. Median number of antiseizure drugs used before KD was 8 (IQR 7), and median duration of SRSE before KD initiation was 10 days (IQR 7 days). KD treatment delays resulted from intravenous propofol use, ileus, and initial care received at a nonparticipating center. All patients achieved ketosis in a median of 2 days (IQR 1 day) on KD. Fourteen patients completed KD treatment, and SRSE resolved in 11 (79%; 73% of all patients enrolled). Side effects included metabolic acidosis, hyperlipidemia, constipation, hypoglycemia, hyponatremia, and weight loss. Five patients (33%) ultimately died.


KD is feasible in adults with SRSE and may be safe and effective. Comparative safety and efficacy must be established with randomized placebo-controlled trials.


This study provides Class IV evidence that in adults withsuperrefractory status epilepticus, a ketogenic diet is effective in inducing ketosis.

This reference is cited in the neurochecklist:

Super refractory status epilepticus

Abstract link

Unwich. Kim Knoch on Flikr.

Do statins really increase the risk of Parkinson’s disease?

Statins are famous, and their fame lies in their ability to bust cholesterol, the villain in many medical disorders such as heart attack (myocardial infarction) and stroke. Some may add that statins are infamous, and this is partly because of their side effects such as muscle pain. Love them or hate them, we can’t get away from […]

via Do statins really increase the risk of Parkinson’s disease? — The Neurology Lounge

The 50 most fascinating neuroradiological pareidolias

Humans have a tendency to see patterns and images where none exist. Many of these patterns were created (or evolved, depending on your view) as early warning systems against the many predators that plot our early demise whilst lurking in dark and sinister shadows.

By Diego Delso, CC BY-SA 4.0, Link

The commonest image the brain imagines is of the face, and it doesn’t require much prompting for the brain to make faces at you. Take the image below for example:

Pareidolia. Tup Wanders on Flikr.

The brains of social media users require even less prompting to conjure up a smiley or a frownie (if that is the word for it). All it takes is a comma and a colon.



The ‘ability’ to see what isn’t there has also served less life-preserving functions than gearing us up for the flight or fight response. Where, for example, would astronomy be without this important delusion?

Sky walk constellations. John on Flikr.

Medicine, surely more important than astronomy, has also made excellent use of this self-deception. This phenomenon was discussed in our sister (or brother) blog, The Neurology Lounge, under the title Pareidolias: why we see non-existent faces.

By Aleph79Own work, CC BY-SA 3.0, Link

There are many very useful clinical pareidolias in neurology, for example the classical inverted champagne bottle appearance which describes the shape of the leg in Charcot Marie Tooth disease (CMT). The most intriguing patterns are however seen on brain imaging. And the favourite neuroradiological pareidolias are, no surprise here, of animal shapes and faces. How many of these signs do you know? What diseases do they signify? Test yourself with our 50 most fascinating neuroradiological pareidolias. Links to the answers are at the end of the list.

Banana sign

Bare/empty orbit sign

Bright tongue sign

Boxcar ventricle sign

Butterfly sign

Champagne bottle neck sign

Chasing the dragon sign

By David Revoy / Blender FoundationOwn work, CC BY 3.0, Link

Corpus callosum splenium sign

Dense middle cerebral artery sign

Double panda sign

Double rim sign

Dural tail  sign

Ears of the lynx sign

Profile of the lynx. Tambako the Jaguar on Flikr.

Elephant sign

Empty delta sign

Eye of the tiger sign

Face of the giant panda sign

Smithsonian’s National Zoo’s Giant Panda Turns Four! Smithsonian’s National Zoo on Flikr.

Figure of eight sign

Haemosiderin cap sign

Harlequin eye sign

Hockey stick sign

Hot cross bun sign

Hummingbird sign

By Joseph C BooneOwn work, CC BY-SA 4.0, Link

Hypodense artery sign

Infundibulum sign

Ivy sign

Lemon sign

Lentiform fork sign

Leopard skin sign

Medusa head sign

By Miguel Hermoso CuestaOwn work, CC BY-SA 4.0, Link

Middle cerebellar peduncle (MCP) sign

Molar tooth sign

Omega/trident sign

Puff of smoke sign

Pulvinar sign

Punched-out corpus callosum sign

Radial band sign

Salt and pepper sign

Scalpel sign

Snake eyes sign

Snake eyes. Thomas Hawk on Flikr.

Spot sign

Spring sign

Starfield sign

Starry sky/swiss cheese sign

Swallow tail sign

Swirl sign

Tigroid sign

Tram track sign

Wine glass sign

Zebra sign

By ClipartqueenOwn work, CC0, Link

OK, we admit a few of the signs are not really pareidolias, but they do help to take the number up to a round 50! How many did you know? Why not check the answers and references in these neurochecklists:

Neuroradiological signs: classic types

Neuroradiological signs: miscellaneous types

And why not explore other neuroradiology pearls in our other 26 neuroradiology checklists such as:

Basal ganglia calcification

Bilateral thalamic lesions

Cerebellopontine angle (CP angle) lesions

Cortical abnormalities

Corticospinal tract hyperintensity

Enhancing meningeal lesions

Headache imaging checklist


MRI T1 high signal lesions

Radiation necrosis v tumour recurrence

Reversible splenial lesions

Sellar and parasellar lesions

Third ventricle lesions

White matter lesions

By Thomas Schultz – Own work, CC BY-SA 3.0, Link

And that’s not all: neuroradiology gems are sprinkled extensively in all the neurology topics covered by neurochecklists. Go on then, explore and please leave a feedback!

What factors predict the clinical progression of MS?

The following abstract is based on the Neurochecklist:

Multiple sclerosis (MS): risk factors

A systematic review of modifiable risk factors in the progression of multiple sclerosis

Hempel S, Graham GD, Fu N, et al.

Mult Scler 2017; 23:525-533.

The presenting symptoms and rate of progression of multiple sclerosis (MS) are very heterogeneous. The diverse clinical manifestations and the clinical course of the disease may vary with modifiable risk factors.


To systematically review modifiable risk factors and exposures associated with MS progression.


We searched six databases till March 2015, reference-mined reviews, and consulted with experts (PROSPERO 2015:CRD42015016461). Two reviewers screened and extracted data. We used random meta-analysis models and Grading of Recommendations Assessment, Development, and Evaluation (GRADE) to assess the quality of evidence.


In total, 59 studies met inclusion criteria. Lower vitamin D levels were associated with higher Expanded Disability Status Scale (EDSS) scores (r = −0.22; confidence interval (CI) = −0.32, −0.12; 11 studies; I2 = 66%), smokers had an increased risk of MS progression (hazard ratio (HR) = 1.55; CI = 1.10, 2.19; I2 = 72%; seven studies), and there was no association of MS progression with the use of epidural analgesics during childbirth delivery (three studies). There was insufficient evidence to draw conclusions for 11 risk factors due to conflicting results or use of different predictor and outcome measures.


MS progression was consistently associated with low vitamin D levels, and smoking was associated with a more rapid decline in MS disability. Studies used a variety of methods, predictors, and outcomes making it difficult to draw conclusions. Future studies should focus on prospective assessments.

Abstract link

Is the growth of cerebral aneurysms predictable?

ELAPSS score for prediction of risk of growth of unruptured intracranial aneurysms

Backes D, Rinkel GJE, Greving JP, et al.

Neurology 2017; 88:1600-1606.



To develop a risk score that estimates 3-year and 5-year absolute risks for aneurysm growth.


From 10 cohorts of patients with unruptured intracranial aneurysms and follow-up imaging, we pooled individual data on sex, population, age, hypertension, history of subarachnoid hemorrhage, and aneurysm location, size, aspect ratio, and shape but not on smoking during follow-up and family history of intracranial aneurysms in 1,507 patients with 1,909 unruptured intracranial aneurysms and used aneurysm growth as outcome. With aneurysm-based multivariable Cox regression analysis, we determined predictors for aneurysm growth, which were presented as a risk score to calculate 3-year and 5-year risks for aneurysm growth by risk factor status.


Aneurysm growth occurred in 257 patients (17%) and 267 aneurysms (14%) during 5,782 patient-years of follow-up. Predictors for aneurysm growth were earlier subarachnoid hemorrhage, location of the aneurysm, age >60 years, population, size of the aneurysm, and shape of the aneurysm (ELAPSS). The 3-year growth risk ranged from <5% to >42% and the 5-year growth risk from <9% to >60%, depending on the risk factor status.


The ELAPSS score consists of 6 easily retrievable predictors and can help physicians in decision making on the need for and timing of follow-up imaging in patients with unruptured intracranial aneurysms.


This abstract is cited in the Neurochecklist:

Cerebral aneurysms: risk factors for rupture

Abstract link

Aneurysm with a surgical clip across the the neck or base. UMHealth System on Flikr.

What are the 4 syndromes of IgLON5 antibody disease?

The following abstract is based  on the Neurochecklist:

Anti IgLON5 antibody syndrome

Clinical manifestations of the anti-IgLON5 disease

Gaig C, Graus F, Compta Y, et al.

Neurology 2017; 88:1736-1743.



To report the presentation, main syndromes, human leukocyte antigen (HLA) association, and immunoglobulin G (IgG) subclass in the anti-IgLON5 disease: a disorder with parasomnias, sleep apnea, and IgLON5 antibodies.


This was a retrospective clinical analysis of 22 patients. The IgG subclass was determined using reported techniques.


Patients’ median age was 64 years (range 46-83). Symptoms that led to initial consultation included sleep problems (8 patients; 36%), gait abnormalities (8; 36%), bulbar dysfunction (3; 14%), chorea (2; 9%), and cognitive decline (1; 5%). By the time of diagnosis of the disorder, 4 syndromes were identified: (1) a sleep disorder with parasomnia and sleep breathing difficulty in 8 (36%) patients; (2) a bulbar syndrome including dysphagia, sialorrhea, stridor, or acute respiratory insufficiency in 6 (27%); (3) a syndrome resembling progressive supranuclear palsy (PSP-like) in 5 (23%); and (4) cognitive decline with or without chorea in 3 (14%). All patients eventually developed parasomnia, sleep apnea, insomnia, or excessive daytime sleepiness. HLA-DRB1*10:01 and HLA-DQB1*05:01 were positive in 13/15 (87%) patients; the DRB1*10:01 allele was 36 times more prevalent than in the general population. Among 16 patients with paired serum and CSF samples, 14 had IgLON5 antibodies in both, and 2 only in serum (both had a PSP-like syndrome). Twenty of 21 patients had IgG1 and IgG4 antibodies; the latter predominated in 16.


Patients with IgLON5 antibodies develop a characteristic sleep disorder preceded or accompanied by bulbar symptoms, gait abnormalities, oculomotor problems, and, less frequently, cognitive decline. IgG4 subclass antibodies predominate over IgG1; we confirm a strong association with the HLA-DRB1*10:01 allele.

Abstract link

By by Reggaeman – photo by Reggaeman, CC BY-SA 3.0, Link

How good is gamma knife radiosurgery for essential tremor?

The following abstract is based on the Neurochecklist:

Essential tremor (ET): non-drug treatment

Stereotactic radiosurgery for essential tremor: retrospective analysis of a 19-year experience

Niranjan A, Raju SS, Kooshkabadi A, Monaco E 3rd, Flickinger JC, Lunsford LD

Mov Disord 2017; 32:769-777.



Essential Tremor (ET) is a common movement disorder that can be disabling. Initial treatment is in the form of medical therapies. Patients with medically refractory ET seek surgical intervention which include radiofrequency thalamotomy, deep brain stimulation, and radiosurgical thalamotomy. Radiosurgical thalamotomy is a minimally invasive surgical option which is especially valuable for elderly and high surgical risk patients.


The purpose of this study was to retrospectively analyze the outcomes of stereotactic radiosurgery for patients suffering from medically refractory essential tremor.


During a 19-year period (1996-2015), 73 patients underwent gamma knife thalamotomy for intractable essential tremor. A median central dose of 140 Gy (range, 130-150) was delivered to the nucleus ventralis intermedius through a single 4-mm isocenter. We used the Fahn-Tolosa-Marin clinical tremor rating scale to score tremor, handwriting, drawing, and ability to drink fluids. The median time to last follow-up was 28 months (range, 6-152).


After gamma knife thalamotomy, 93.2% improved in tremor. Forty-four patients (60.3%) experienced tremor arrest or barely perceptible tremor. Eighteen patients (24.7%) noted tremor arrest and complete restoration of motor function. Tremor improvement was sustained at last follow-up in 96% of patients who experience tremor relief. Mean tremor score improved from 3.19 before to 1.27 after gamma knife thalamotomy (P < 0.0001). Mean handwriting score improved from 2.97 to 1.25 (P < 0.0001). Mean drawing score improved from 3.16 to 1.26 (P < 0.0001). Mean drinking score improved from 3.14 to 1.56 (P < 0.0001). Imaging follow-up showed three types of lesions: enhancing lesion, streaking along internal capsule on fluid-attenuated inversion recovery, and significant reactive changes. Three patients (4%) experienced temporary adverse radiation effects.


Radiosurgery is a safe and valuable treatment option for medically refractory essential tremor, especially for the elderly or those with high surgical risk for DBS or radiofrequency thalamotomy.

Abstract link

Heading into the gamma knife machine. Eric Gilliland on Flikr.

How does alcohol affect the risk of intracerebral haemorrhage?

The following abstract is based on the Neurochecklist:

Alcohol use and risk of intracerebral hemorrhage

Chen CJ, Brown WM, Moomaw CJ, et al; ERICH Investigators.

Neurology 2017; 88:2043-2051.



To analyze the dose-risk relationship for alcohol consumption and intracerebral hemorrhage (ICH) in the Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study.


ERICH is a multicenter, prospective, case-control study, designed to recruit 1,000 non-Hispanic white patients, 1,000 non-Hispanic black patients, and 1,000 Hispanic patients with ICH. Cases were matched 1:1 to ICH-free controls by age, sex, race/ethnicity, and geographic area. Comprehensive interviews included questions regarding alcohol consumption. Patterns of alcohol consumption were categorized as none, rare (<1 drink per month), moderate (≥1 drink per month and ≤2 drinks per day), intermediate (>2 drinks per day and <5 drinks per day), and heavy (≥5 drinks per day). ICH risk was calculated using the no-alcohol use category as the reference group.


Multivariable analyses demonstrated an ordinal trend for alcohol consumption: rare (odds ratio [OR] 0.57, p < 0.0001), moderate (OR 0.65, p < 0.0001), intermediate (OR 0.82, p = 0.2666), and heavy alcohol consumption (OR 1.77, p = 0.0003). Subgroup analyses demonstrated an association of rare and moderate alcohol consumption with decreased risk of both lobar and nonlobar ICH. Heavy alcoholconsumption demonstrated a strong association with increased nonlobar ICH risk (OR 2.04, p = 0.0003). Heavy alcohol consumption was associated with significant increase in nonlobar ICH risk in black (OR 2.34, p = 0.0140) and Hispanic participants (OR 12.32, p < 0.0001). A similar association was not found in white participants.


This study demonstrated potential protective effects of rare and moderate alcohol consumption on ICH risk. Heavy alcoholconsumption was associated with increased intracerebral haemorrhage risk. Race/ethnicity was a significant factor in alcohol-associated ICH risk; heavy alcohol consumption in black and Hispanic participants poses significant nonlobar ICH risk.

Abstract link

By Nik Frey (niksan) – stock.xchng: [dead link], CC BY 2.5,

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