The 7 most devastating viral neurological infections

One may be forgiven for thinking that neurology is all about neuroinflammatory and neurodegenerative diseases. This is because these disorders seem to get a lot of attention. But nothing could be further from the truth-globally, infections impose a heavier burden on neurological practice than say Multiple Sclerosis (MS) or Parkinson’s disease (PD). And medical advances have done very little to deter all sorts of creatures from invading the nervous system.

Bacteria. Cesar Herada on Flikr. https://www.flickr.com/photos/worldworldworld/4095866396/

The major types of organisms that infect the nervous system are viruses and bacteria, but fungi and parasites also take their toll. In this blog we will focus on the 7 most devastating viral neurological infections.

CC BY-SA 3.0, Link

1.  Viral encephalitis

Encephalitis is infection of the brain substance, as opposed to meningitis which is infection of the covering of the brain. Viral encephalitis, for some reason, tends to favour the temporal lobes of the brain causing seizures and memory problems, amongst other symptoms. The main villain responsible for viral encephalitis is herpes simplex type 1 (HSV1), but almost every other virus can carry out the job with deadly precision. The list is long and includes geographically specific viruses as West Nile and Japanese B. Check out the full list of causes of viral encephalitis and its management.

Herpes Simplex Virus Type 1: Procapsid and Mature Capsid. NIH Image gallery on Flikr. https://www.flickr.com/photos/nihgov/28295539863

2. HIV associated neurological infections

No part of the nervous system is immune to the ravages of the dreaded HIV. The list includes HIV  associated neurocognitive disorders (HAND)myelopathiesneuropathies, drug-induced syndromes, and tumours. The worst aspect of HIV, of course, is that it opens the flood gates for opportunistic infections to invade the nervous system.

By BruceBlausOwn work, CC BY-SA 4.0, Link

3. Hepatitis E virus (HEV)

Hepatitis E virus is just emerging as a scourge of neurology. It is particularly villainous because of its protean manifestations, from Guillain Barre syndrome (GBS) to neuralgic amyotrophy (brachial neuritis), from transverse myelitis to idiopathic intracranial hypertension (IIH). Check out the full neurological manifestations of HEV.

By Transferred from en.wikipedia to Commons.This media comes from the Centers for Disease Control and Prevention‘s Public Health Image Library (PHIL), with identification number #5605.Note: Not all PHIL images are public domain; be sure to check copyright status and credit authors and content providers.English | Slovenščina | +/−, Public Domain, Link

4. Influenza H1N1

Influenza is bad, and H1N1 is a particularly nasty variant. This subtype of Influenza A is epidemic in pigs and birds, and unleashes havoc when it crosses over to humans. Its nervous system manifestations include encephalopathyGuillain Barre syndrome (GBS), acute demyelinating encephalomyelopathy (ADEM), and stroke. Not one to be treated lightly at all. Check out everything about Influenza H1N1 and the different ways influenza affects the nervous system.

H1N1 influenza viral particles. NIAID on Flikr. https://www.flickr.com/photos/niaid/8414750984

5. Zika virus infection (ZIKV)

This new kid on the infection block is fast establishing itself as a menace. Apart from causing myelitis, meningoencephalitis, encephalitis, encephalomyelitis, Guillain-Barre syndrome (GBS), and myasthenia gravis (MG), it is responsible for a variety of congenital defects, particularly microcephaly. Zika virus pathology and management are extensively covered in neurochecklists. Or check out 20 things we now know for certain about the Zika virus on our sister blog, The Neurology Lounge.

By Manuel Almagro RivasOwn work, CC BY-SA 4.0, Link

6. Ebola virus disease (EVD)

This ancient virus gained recent notoriety when it ravaged a large section of West Africa, sending chilling waves across the world. It is an RNA filovirus whose main reservoir is bats. It causes, among other things, an encephalitis and meningoencephalitis. It appears to be on vacation in the meantme, but it will surely rear its ugly head sometime soon. Check out the comprehensive clinical features and management of Ebola virus disease on neurochecklists.

By Scientific Animations – http://www.scientificanimations.com/wiki-images/, CC BY-SA 4.0, Link

7. Varicella zoster virus (VZV)

The varicella virus must take the prize for the most diverse ways a virus affects the nervous system. Neurochecklists has listed >20 neurological manifestations of VZV, ranging from herpes zoster to post herpetic neuralgia (PHN), from meningitis to encephalitis. VZV also causes all forms of cranial and peripheral neropathy, and may result in stroke, aneurysms, and giant cell arteritis (GCA). Not to mention the curiously named progressive outer retinal necrosis (just don’t mention its acronym!). Check out the full VZV on neurochecklists.

 Watch out for the top 7 bacterial neurological infections in a future blog post.
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What is the promise of macuna pruriens for people with Parkinson’s disease?

Mucuna pruriens in Parkinson disease: a double-blind, randomized, controlled, crossover study

Cilia R, Laguna J, Cassani E, et al.

Neurology 2017; 89:432-438.

Abstract

OBJECTIVE:

To investigate whether Mucuna pruriens (MP), a levodopa-containing leguminous plant growing in all tropical areas worldwide, may be used as alternative source of levodopa for indigent individuals with Parkinson disease (PD) who cannot afford long-term therapy with marketed levodopa preparations.

METHODS:

We investigated efficacy and safety of single-dose intake of MP powder from roasted seeds obtained without any pharmacologic processing. Eighteen patients with advanced PD received the following treatments, whose sequence was randomized: (1) dispersible levodopa at 3.5 mg/kg combined with the dopa-decarboxylase inhibitor benserazide (LD+DDCI; the reference treatment); (2) high-dose MP (MP-Hd; 17.5 mg/kg); (3) low-dose MP (MP-Ld; 12.5 mg/kg); (4) pharmaceutical preparation of LD without DDCI (LD-DDCI; 17.5 mg/kg); (5) MP plus benserazide (MP+DDCI; 3.5 mg/kg); (6) placebo. Efficacy outcomes were the change in motor response at 90 and 180 minutes and the duration of on state. Safety measures included any adverse event (AE), changes in blood pressure and heart rate, and the severity of dyskinesias.

RESULTS:

When compared to LD+DDCI, MP-Ld showed similar motor response with fewer dyskinesias and AEs, while MP-Hd induced greater motor improvement at 90 and 180 minutes, longer ON duration, and fewer dyskinesias. MP-Hd induced less AEs than LD+DDCI and LD-DDCI. No differences in cardiovascular response were recorded.

CONCLUSION:

Single-dose macuna pruriens intake met all noninferiority efficacy and safety outcome measures in comparison to dispersible levodopa/benserazide. Clinical effects of high-dose macuna pruriens were similar to levodopa alone at the same dose, with a more favorable tolerability profile.

This reference is now cited in the neurochecklist:

Parkinson’s disease (PD): emerging treatments

 

Abstract link

By Ton Rulkens from Mozambique – Mucuna pruriens – podsUploaded by Jacopo Werther, CC BY-SA 2.0, Link

How does minocycline influence the risk of developing MS?

Minocycline in MS Study Team. Trial of minocycline in a clinically isolated syndrome of multiple sclerosis

Metz LM, Li DKB, Traboulsee AL, et al;

N Engl J Med 2017; 376:2122-2133.

Abstract

BACKGROUND:

On the basis of encouraging preliminary results, we conducted a randomized, controlled trial to determine whether minocycline reduces the risk of conversion from a first demyelinating event (also known as a clinically isolated syndrome) to multiple sclerosis.

METHODS:

During the period from January 2009 through July 2013, we randomly assigned participants who had had their first demyelinating symptoms within the previous 180 days to receive either 100 mg of minocycline, administered orally twice daily, or placebo. Administration of minocycline or placebo was continued until a diagnosis of multiple sclerosis was established or until 24 months after randomization, whichever came first. The primary outcome was conversion to multiple sclerosis (diagnosed  on the basis of the 2005 McDonald criteria) within 6 months after randomization. Secondary outcomes included conversion to multiple sclerosis within 24 months after randomization and changes on magnetic resonance imaging (MRI) at 6 months and 24 months (change in lesion volume on T2-weighted MRI, cumulative number of new lesions enhanced on T1-weighted MRI [“enhancing lesions”], and cumulative combined number of unique lesions [new enhancing lesions on T1-weighted MRI plus new and newly enlarged lesions on T2-weighted MRI]).

RESULTS:

A total of 142 eligible participants underwent randomization at 12 Canadian multiple sclerosis clinics; 72 participants were assigned to the minocycline group and 70 to the placebo group. The mean age of the participants was 35.8 years, and 68.3% were women. The unadjusted risk of conversion to multiple sclerosis within 6 months after randomization was 61.0% in the placebo group and 33.4% in the minocycline group, a difference of 27.6 percentage points (95% confidence interval [CI], 11.4 to 43.9; P=0.001). After adjustment for the number of enhancing lesions at baseline, the difference in the risk of conversion to multiple sclerosis within 6 months after randomization was 18.5 percentage points (95% CI, 3.7 to 33.3; P=0.01); the unadjusted risk difference was not significant at the 24-month secondary outcome time point (P=0.06). All secondary MRI outcomes favored minocycline over placebo at 6 months but not at 24 months. Trial withdrawals and adverse events of rash, dizziness, and dental discoloration were more frequent among participants who received minocycline than among those who received placebo.

CONCLUSIONS:

The risk of conversion from a clinically isolated syndrome to multiple sclerosis was significantly lower with minocycline than with placebo over 6 months but not over 24 months.

This reference is now cited in the neurochecklist:

Multiple sclerosis (MS): emerging treatments

Abstract link

By ElbreapolyOwn work, Public Domain, Link

What is the influence of high altitude on migraine?

Migraine associated with altitude: results from a population-based study in Nepal.

Linde M, Edvinsson L, Manandhar K, Risal A, Steiner TJ.

Eur J Neurol 2017; 24:1055-1061.

Abstract

BACKGROUND AND PURPOSE:

A 1988 pilot study in Peru suggested an association between migraine and chronic exposure to high altitude. This study provides epidemiological evidence corroborating this.

METHODS:

In a cross-sectional nationwide population-based study, a representative sample of Nepali-speaking adults were recruited through stratified multistage cluster sampling. They were visited at home by trained interviewers using a culturally adapted questionnaire. The altitude of dwelling of each participant was recorded.

RESULTS:

Of 2100 participants, over half [1100 (52.4%)] were resident above 1000 m and almost one quarter [470 (22.4%)] at ≥2000 m. Age- and gender-standardized migraine prevalence increased from 27.9% to 45.5% with altitude between 0 and 2499 m and thereafter decreased to 37.9% at ≥2500 m. The likelihood of having migraine was greater (odds ratio, 1.5-2.2; P ≤ 0.007) at all higher altitudes compared with <500 m. In addition, all symptom indices increased with altitude across the range <500 m to 2000-2499 m, i.e. median attack frequency from 1.3 to 3.0 days/month (P < 0.001), median duration from 9 to 24 h (P < 0.001) and pain intensity [the proportion reporting ‘bad pain’ (highest intensity)] from 35.5% to 56.9% (P = 0.011). Each of these showed a downward trend above 2500 m.

CONCLUSIONS:

Dwelling at high altitudes increases not only increase migraine prevalence but also the severity of its symptoms.

This reference contributes to the neurochecklist:

Migraine risk factors

Abstract link

By George Cruikshankhttp://metmuseum.org/art/collection/search/393320, Public Domain, Link

How does body weight influence the risk of migraine?

Body composition status and the risk of migraine: a meta-analysis

Gelaye B, Sacco S, Brown WJ, Nitchie HL, Ornello R, Peterlin BL.

Neurology 2017; 88:1795-1804.

Abstract

OBJECTIVE:

To evaluate the association between migraine and body composition status as estimated based on body mass index and WHO physical status categories.

METHODS:

Systematic electronic database searches were conducted for relevant studies. Two independent reviewers performed data extraction and quality appraisal. Odds ratios (OR) and confidence intervals (CI) were pooled using a random effects model. Significant values, weighted effect sizes, and tests of homogeneity of variance were calculated.

RESULTS:

A total of 12 studies, encompassing data from 288,981 unique participants, were included. The age- and sex-adjusted pooled risk of migraine in those with obesity was increased by 27% compared with those of normal weight (odds ratio [OR] 1.27; 95% confidence interval [CI] 1.16-1.37, p < 0.001) and remained increased after multivariate adjustments. Although the age- and sex-adjusted pooled migraine risk was increased in overweight individuals (OR 1.08; 95% CI 1.04, 1.12, p < 0.001), significance was lost after multivariate adjustments. The age- and sex-adjusted pooled risk of migraine in underweight individuals was marginally increased by 13% compared with those of normal weight (OR 1.13; 95% CI 1.02, 1.24, p < 0.001) and remained increased after multivariate adjustments.

CONCLUSIONS:

The current body of evidence shows that the risk of migraine is increased in obese and underweight individuals. Studies are needed to confirm whether interventions that modify obesity status decrease the risk of migraine.

This reference is contributes to the neurochecklist:

Abstract link

Different Shades of Migraine. Tudor Barker on Flikr. https://www.flickr.com/photos/tudedude/4326739234

What is the outcome of thrombolysis for stroke of unknown onset time?

Intravenous thrombolysis in unknown-onset stroke: results from the safe implementation of treatment in Stroke-International Stroke Thrombolysis Registry.

Dorado L, Ahmed N, Thomalla G, et al.

Stroke 2017; 48:720-725.

Abstract

Background:

Stroke patients with unknown onset (UKO) are excluded from thrombolytic therapy. We aim to study the safety and efficacy of intravenous alteplase in ischemic stroke patients with UKO of symptoms compared with those treated within 4.5 hours in a large cohort.

Methods:

Data were analyzed from 47 237 patients with acute ischemic stroke receiving intravenous tissue-type plasminogen activator in hospitals participating in the Safe Implementation of Treatment in Stroke-International Stroke Thrombolysis Registry between 2010 and 2014. Two groups were defined: (1) patients with UKO (n=502) and (2) patients treated within 4.5 hours of stroke onset (n=44 875). Outcome measures were symptomatic intracerebral hemorrhage per Safe Implementation of Treatment in Stroke on the 22 to 36 hours post-treatment neuroimaging and mortality and functional outcome assessed by the modified Rankin Scale at 3 months.

Results:

Patients in UKO group were significantly older, had more severe stroke at baseline, and longer door-to-needle times than patients in the ≤4.5 hours group. Logistic regression showed similar risk of symptomatic intracerebral hemorrhage (adjusted odds ratio, 1.09; 95% confidence interval, 0.44–2.67) and no significant differences in functional independency (modified Rankin Scale score of 0–2; adjusted odds ratio, 0.79; 95% confidence interval, 0.56–1.10), but higher mortality (adjusted odds ratio, 1.58; 95% confidence interval, 1.04–2.41) in the UKO group compared with the ≤4.5 hours group. Patients treated within 4.5 hours showed reduced disability over the entire range of modified Rankin Scale compared with the UKO group (common adjusted odds ratio, 1.29; 95% confidence interval, 1.01–1.65).

Conclusions:

Our data suggest no excess risk of symptomatic intracerebral hemorrhage but increased mortality and reduced favorable outcome in patients with unknown onset stroke compared with patients treated within the approved time window.

This reference is now included in the neurochecklist:

 

Abstract link

By Blausen Medical Communications, Inc. – Donated via OTRS, see ticket for details, CC BY 3.0, Link

What is the effect of venous sinus stenting for IIH?

Dural venous sinus stenting for medically and surgically refractory idiopathic intracranial hypertension

Satti SR, Leishangthem L, Spiotta A, Chaudry MI.

Interv Neuroradiol 2017; 23:186-193.

Abstract

Idiopathic intracranial hypertension (IIH) is a syndrome defined by elevated intracranial hypertension without radiographic evidence of a mass lesion in the brain. Dural venous sinus stenosis has been increasingly recognized as a treatable cause, and dural venous sinus stenting (DVSS) is increasingly performed.

A 5 year single-center retrospective analysis of consecutive patients undergoing DVSS for medically refractory IIH.

There were 43 patients with a mean imaging follow-up of 6.5 months and a mean clinical follow-up period of 13.5 months. DVSS was performed as the first procedure for medically refractory IIH in 81.4% of patients, whereas 18.6% of patients included had previously had a surgical procedure (ventriculoperitoneal (VP) shunt or optic nerve sheath fenestration (ONSF)). Headache was present in all patients and after DVSS improved or remained stable in 69.2% and 30.8%, respectively. Visual acuity changes and visual field changes were present in 88.4% and 37.2% of patients, respectively. Visual field improved or remained unchanged in 92%, but worsened in 8% after stenting. There was a stent patency rate of 81.8%, with an 18.2% re-stenosis rate. Of the 43 procedures performed, there was a 100% technical success rate with zero major or minor complications.

Based on this single-center retrospective analysis, dural venous sinus stenting can be performed with high technical success and low complication rates. A majority of patients presented primarily with headache, and these patients had excellent symptom relief with DVSS alone. Patients presenting with visual symptoms had lower success rates, and this population, if stented, should be carefully followed for progression of symptoms.

This reference is cited in the neurochecklist:

Idiopathic intracranial hypertension (IIH): surgical treatment

Abstract link

Annotated Sagittal ATECO MR Venogram. Reigh LeBlanc on Flikr. Annotated Sagittal ATECO MR Venogram

Why is the diagnosis of cervical artery dissection difficult in older people?

CADISP-Plus Study Group. Cervical artery dissection in patients ≥60 years: often painless, few mechanical triggers

Traenka C, Dougoud D, Simonetti BG, et al;

Neurology 2017; 88:1313-1320.

Abstract

OBJECTIVE:

In a cohort of patients diagnosed with cervical artery dissection (CeAD), to determine the proportion of patients aged ≥60 years and compare the frequency of characteristics (presenting symptoms, risk factors, and outcome) in patients aged <60 vs ≥60 years.

METHODS:

We combined data from 3 large cohorts of consecutive patients diagnosed with CeAD (i.e., Cervical Artery Dissection and Ischemic Stroke Patients-Plus consortium). We dichotomized cases into 2 groups, age ≥60 and <60 years, and compared clinical characteristics, risk factors, vascular features, and 3-month outcome between the groups. First, we performed a combined analysis of pooled individual patient data. Secondary analyses were done within each cohort and across cohorts. Crude and adjusted odds ratios (OR [95% confidence interval]) were calculated.

RESULTS:

Among 2,391 patients diagnosed with CeAD, we identified 177 patients (7.4%) aged ≥60 years. In this age group, cervical pain (ORadjusted 0.47 [0.33-0.66]), headache (ORadjusted 0.58 [0.42-0.79]), mechanical trigger events (ORadjusted 0.53 [0.36-0.77]), and migraine (ORadjusted 0.58 [0.39-0.85]) were less frequent than in younger patients. In turn, hypercholesterolemia (ORadjusted 1.52 [1.1-2.10]) and hypertension (ORadjusted 3.08 [2.25-4.22]) were more frequent in older patients. Key differences between age groups were confirmed in secondary analyses. In multivariable, adjusted analyses, favorable outcome (i.e., modified Rankin Scale score 0-2) was less frequent in the older age group (ORadjusted 0.45 [0.25, 0.83]).

CONCLUSION:

In our study population of patients diagnosed with CeAD, 1 in 14 was aged ≥60 years. In these patients, pain and mechanical triggers might be missing, rendering the diagnosis more challenging and increasing the risk of missed cervical artery dissection diagnosis in older patients.

This reference is cited in the neurochecklist:

Cervical artery dissection (CEAD): clinical features

Abstract link

By Henry Vandyke CarterHenry Gray (1918) Anatomy of the Human Body (See “Book” section below)Bartleby.com: Gray’s Anatomy, Plate 513, Public Domain, Link

What are the downsides of mechanical thrombectomy for stroke?

Thrombectomy for ischemic stroke: meta-analyses of recurrent strokes, vasospasms, and subarachnoid hemorrhages.

Emprechtinger R, Piso B, Ringleb PA.

J Neurol 2017; 264:432-436.

Abstract

Background:

Mechanical thrombectomy with stent retrievers is an effective treatment for patients with ischemic stroke. Results of recent meta-analyses report that the treatment is safe. However, the endpoints recurrent stroke, vasospasms, and subarachnoid hemorrhage have not been evaluated sufficiently. Hence, we extracted data on these outcomes from the five recent thrombectomy trials (MR CLEAN, ESCAPE, REVASCAT, SWIFT PRIME, and EXTEND IA published in 2015). Subsequently, we conducted meta-analyses for each outcome.

Methods:

We report the results of the fixed, as well as the random effects model. Three studies reported data on recurrent strokes. While the results did not reach statistical significance in the random effects model (despite a three times elevated risk), the fixed effects model revealed a significantly higher rate of recurrent strokes after thrombectomy.

Results:

Four studies reported data on subarachnoid hemorrhage. The higher pooled rates in the intervention groups were statistically significant in both, the fixed and the random effects model. One study reported on vasospasms. We recorded 14 events in the intervention group and none in the control group.

Conclusions:

The efficacy of mechanical thrombectomy is not questioned, yet our results indicate an increased risk for recurrent strokes, subarachnoid hemorrhage, and vasospasms post-thrombectmy. Therefore, we strongly recommend a thoroughly surveillance, concerning these adverse events in future clinical trials and routine registries.

This reference is cited in the neurochecklist:

Ischaemic stroke: thrombectomy

Abstract link

By Neilbarman at English Wikipedia, CC BY-SA 3.0, Link

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